THE WAIKATO HOSPITAL

INTENSIVE CARE UNIT GUIDELINES

VERSION 3.4
DECEMBER 2007
Foreword 1
Caring for patients in the intensive care setting is a challenging but potentially rewarding experience. As we enter the intensive care
environment each one of us brings a unique mix of skills and knowledge. Inevitably though we must find a common ground on which to base
our management, without which optimal patient care and safety cannot be achieved.
The purpose of this manual is not to provide definitive answers for each problem, nor is it meant to be prescriptive in nature, but rather it
describes a number of standardised approaches and helpful guidelines to facilitate good patient care.
While you are working in this unit, no matter what your level of experience, you will encounter situations where you feel uncomfortable,
confused or even scared. While this manual is intended to assist you in caring for your patients, you should not be embarrassed to seek help
from those around you, including the staff specialist on duty and senior nursing staff.
Colleagues outside of the Waikato Hospital ICU that make use of these guidelines do so at their own risk. Furthermore, editions older than 12
months may vary significantly from current practice.
I would welcome your suggestions for future versions. You will find under reference sections in each chapter, references to articles which are
useful further reading.

Acknowledgements 2
Many Intensive Care Units have developed their own sets of guidelines and medical officer handbooks, particularly the Royal Adelaide
Hospital ICU handbook which for years was a useful companion. It is not surprising therefore that these guidelines draw on that document
and similar documents for structure and content. The guidelines represented herein are a result of the contributions of a number of the staff
of the unit, subjected to peer and colleague review. Dr Grant Howard was the driver and effector of the first several editions of this handbook
at Waikato Hospital. A large debt of gratitude is owed him for this.
Dr Nicholas Barnes, Editor 2007.

Format, Figures & Style 3

The discipline of intensive care revolves around;
the reconstruction of homeostasis when patients homeostatic control mechanisms fail.
& the withdrawal of this support in a manner which enables bodily homeostatic mechanisms to resume control.
It is acknowledged that the reflexual feedback control systems of the body form a complex topographical problem space over which it is the
skill and vision of Intensive Care Specialist that enables navigation. It is noted there are many different paths to similar conclusions and
there are many different styles of problem resolution. This manuscript serves to document useful guidelines and illustrate in part the styles of
the involved Intensivists. It is in no way to be used as a directive for a definitive course of action without first taking into consideration each
individual patient and their personal situation.
Dr Edward Coxon MBChB BMedSci (dist)

Waikato Hospital Intensive Care Unit 4

Waikato Hospital is the 600 bed tertiary referral hospital and trauma centre of the midland region of New Zealand and serves a population
area of 800 000. Waikato Hospital has specialist services in most fields apart from paediatric cardiac surgery. The Waikato Intensive Care
Unit has 15 beds and admits over 1100 patients a year.
The Waikato Intensive care unit is a mixed unit with 15% paediatric and 85% adult admissions. Approximately 30% of the admissions are
post cardiac surgical. The remainder are a mixture of trauma, medical and surgical patients. 76% of admissions are ventilated. Our average
APACHE II score is 16 and we have a mortality rate of about 9%.
The intensive care staff also assist in the management of patients in the High Dependency Unit which has 12 beds and admits over 1600
cases per year. The intensive care provides medical and nursing transport teams for inter-hospital transfers and oversees parenteral nutrition
within the hospital and home parenteral nutrition for the Waikato and Midland communities. Staff also participate in trauma and cardiac
arrest rosters.
The Waikato Intensive Unit has C24 classification from the Faculty of Intensive Care of the Australian and New Zealand College of
Anaesthetists and as such is recognised for unlimited core intensive care specialist training.
The Intensive Care unit medical staff consists of 5 consultants, one senior registrar and ten registrars. We have a nursing staff of about 65 full
time equivalents for ICU, 25 for HDU and 3 full time respiratory technicians.
The unit has an active research and teaching programs. We have a number of safety and quality initiatives in place
Contents 5
Table of Contents 6

Foreword 1.................................................................................................................................................................................2
Waikato Hospital Intensive Care Unit 4....................................................................................................................................2

Contents 5......................................................................................................................................................................................3

Table of Contents 6.....................................................................................................................................................................3

Administration 7...........................................................................................................................................................................6

Staffing 8....................................................................................................................................................................................6
Daily Program 24.......................................................................................................................................................................6
Orientation 31............................................................................................................................................................................7
Patient admission policy 32.......................................................................................................................................................7
Patient discharge policy 36.......................................................................................................................................................8
Clinical duties in the Intensive Care 39....................................................................................................................................9
Clinical Duties outside the Intensive Care Unit 50.................................................................................................................10
Trauma Call 56.........................................................................................................................................................................10
Intra-hospital patient transport 65...........................................................................................................................................11
Patient Retrieval 66.................................................................................................................................................................12
Infection Control 68.................................................................................................................................................................14
Research in the Intensive Care Unit 73...................................................................................................................................14
Information technology 80.......................................................................................................................................................15
Consent in the Intensive Care Setting 81.................................................................................................................................15
Hospital Emergencies 86.........................................................................................................................................................16

Clinical Procedures 88...............................................................................................................................................................17

Introduction 89.........................................................................................................................................................................17
Peripheral IV Catheters 92......................................................................................................................................................17
Arterial Cannulae 96...............................................................................................................................................................17
Central Venous Cannulae 101.................................................................................................................................................18
Cardiac Pacing 120.................................................................................................................................................................19
Intra-aortic balloon counterpulsation (IABP) 126.................................................................................................................20
Pleural Procedures 141............................................................................................................................................................21
Pericardiocentesis 152.............................................................................................................................................................22
Endotracheal Intubation 155...................................................................................................................................................22
Fibre-optic Bronchoscopy 183.................................................................................................................................................25
Cricothyroidotomy 186............................................................................................................................................................25
Tracheostomy-Percutaneous 191.............................................................................................................................................26
Nasojejunal tube insertion 203................................................................................................................................................27
Intra-abdominal pressure manometry 207...............................................................................................................................27
Intra-Cranial Pressure Monitoring 211...................................................................................................................................28
Jugular Bulb Oximetry 216......................................................................................................................................................28

Drugs and Infusions 222............................................................................................................................................................30

Introduction 223.......................................................................................................................................................................30
Cardiovascular Drugs 225.......................................................................................................................................................30
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Anti-hypertensive Agents 244..................................................................................................................................................32
Antiarrhythmic Drugs in Critical Care 248............................................................................................................................33
Respiratory Drugs 268.............................................................................................................................................................36
Sedation 275.............................................................................................................................................................................37
Anticoagulation 282.................................................................................................................................................................38
Endocrine Drugs 299...............................................................................................................................................................41
Renal Drugs 322.......................................................................................................................................................................43
Gastro-intestinal drugs 328.....................................................................................................................................................43
ICU Antibiotic Guidelines 336...............................................................................................................................................45

Fluids and Electrolytes 347.......................................................................................................................................................48

Principles of Fluid Management in Intensive Care 348.........................................................................................................48

Electrolyte Abnormalities 362.................................................................................................................................................49
Acid-Base Disturbances in the ICU 389..................................................................................................................................52
Nutrition 415............................................................................................................................................................................54
Blood and Blood Products 434................................................................................................................................................56

Clinical Management 4620........................................................................................................................................................60

Introduction 463.......................................................................................................................................................................60
Cardio-Pulmonary Resuscitation 464......................................................................................................................................60
Respiratory Therapy 472.........................................................................................................................................................61
Aspects of Renal Failure in Intensive Care 536......................................................................................................................67
Neurosurgical Guidelines 554..................................................................................................................................................70
Cardiothoracic Guidelines 580................................................................................................................................................74
Microbiology Guidelines 600...................................................................................................................................................76
Drug / Toxin Overdose 633......................................................................................................................................................78
Withdrawal of Treatment in the Intensive Care 642................................................................................................................80
Brain death and organ donation 647.......................................................................................................................................81

Paediatrics 6.11 ..........................................................................................................................................................................83

Introduction 6.11.1 ..................................................................................................................................................................83

Paediatric admission policy 6.11.2..........................................................................................................................................83
General Paediatric Care in ICU 6.11.2.1 ..............................................................................83
Bronchiolitis 6.11.3............................................................................85
Croup 6.11.4 ..................................87
Clinical Features of Severe Croup 6.11.4.1 .........................................87
Seizures in Children 6.11.5 ....................................................................88
Meningitis 6.11.6 ..................................89
Guidelines for the Management of a child with DKA 6.12................................................................................92

Spinal Injuries 6.13...........................................................................................................94

ICU Admission Policy 6.13.1............................................................................94

Appendices 7.0............................................................................................................................................................................95

Haemodynamic Principles 7.1............................................................................95

The Pulmonary Artery Catheter 7.3........................................................................................................................................96
“The PiCCO-catheter / monitor” 7.4......................................................................................................................................97
Principles of ventilation 7.5...................................................................................................................................................100

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The Sedation - Agitation Score 7.9........................................................................................................................................102
Classification of anti-arrhythmic drugs 7.10........................................................................................................................102
Useful equations in Intensive Care 7.11...............................................................................................................................104
Content of commonly used enteral feeds 7.12.......................................................................................................................105
Guidelines for the use of patient controlled anaesthesia (PCA) 7.13.................................................................................105
Guidelines for Performance of Sensory Evoked Potentials 7.14..........................................................................................107
MRI – Practical aspects of MRI transport 7.15....................................................................................................................108

Index..........................................................................................................................................................................................109

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Administration 7
Staffing 8
Director 9
Dr Nicholas Barnes
Consultant Medical Staff 10
Dr Frank Van Haren
Dr Nicholas Barnes
Dr Grant Howard (SOT)
Dr Rob Frengley
Dr John Torrance
Dr Peter Marko
Clinical Nurse Leaders 11
Mathew Hughes
Simon Mehari
Christine Craig
Diana Mallett
Alison McAlley
Senior Typist / Unit Secretary 12
Dianne Takiari-Dawson
Administrative Assistant 13
Jill Brough
Research Nurse 14
Mary La Pine
Respiratory Technician-Charge Technical Advisor 15
Paul Goble
Nurse Educator 16
Sarah Walker
Mark Reynolds
Organ Donor Co-ordinators 17
Alison McAlley
Sue MaCaskill
Operations Manager – Critical Care 18
Delwyne Board
Registrars 19
There are two levels of Registrar in the unit.
Senior Registrar 20
Advanced vocational trainees, rostered according to seniority and experience.
Registrars: vocational trainees (×2-4) or Registrars (×6-8) 21
Staff seconded from other disciplines to gain experience in Intensive Care Medicine.
Portfolios and autonomy of practice will be determined by trainee experience and rostering requirements.
Training positions 22
The Joint Faculty of Intensive Care Medicine, as a representative of both The Australian and New Zealand College of Anaesthetists and
The Royal Australasian College of Physicians, has accredited The Waikato Hospital Intensive Care Unit for training towards the
Fellowship in Intensive care. Trainees registered with the Faculty may have up to 24 months of service accredited towards their training.
Non-intensive Care Trainees 23
Rotation through the intensive care is made by the following specialty based training programs;
Physician trainee
Emergency Medicine trainee
Anaesthesia trainee

Daily Program 24
08h00 Morning handover (45 minutes)
09h30 Consultant led bedside ward round, followed by HDU administrative review
11h30 X-ray meeting (10h30 at the weekend) (30min)
16h00 Afternoon ward round and HDU review. (30min-1hr)
21h00 Evening hand over and HDU review
All time other than that allocated above should involve patient review, not only in response to request by nursing staff, but also in the
interests of optimising patient care and progress.
Weekly meetings 25
Monday Business Meeting 26
Alternating
ICU business Meeting
ICU Specialists meeting
Incident Meeting
ICU Microbiology meeting 27
Day: Thursday

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Time: 08h00 (before handover)
Venue: ICU meeting room
Hospital grand rounds (60min) 28
Day: Thursday
Time: 12h30
Venue: Hospital auditorium
Journal Club and ICU mortality meeting (Alternate Mondays) 29
Day: Monday
Time: 1200h
Venue: ICU meeting room
Critically Appraised Topics 30
Day: Tuesday
Time: 0800h
Venue: ICU meeting room

Orientation 31
At the start of the intensive care run, there is a 2 day formal orientation to the unit for all new registrars.
Introductory sessions are conducted by the senior medical staff, the unit manager, senior registrar, head technician and senior nursing
staff.
Topics covered include:
General orientation to the unit
Orientation to the helicopter and safety issues
Data collection and computer programs
Transport
Invasive and non-invasive ventilation
Organ donation
Intubation including difficult and failed intubation
Cardiac Surgery
Neurological/neurosurgical emergencies
In addition, attempts will be made to allow those registrars who feel that they require further experience with airway management and
intubation to attend anaesthetic lists in theatre early in the run. On these days, the duty anaesthetist should be approached and asked if
there are suitable lists available.
A simulator based teaching program is being developed and should form part of the orientation in the near future.

Patient admission policy 32

No patient may be accepted into the Intensive Care Unit without the knowledge and consent of the duty ICU specialist
Resuscitation or admission must however not be delayed where the presenting condition is imminently life threatening unless specific
advance directives exist.
In general patients should be admitted to the Intensive Care where it is perceived they would benefit in some way as a result. Usually this
means patients with actual or potential organ system failure, which appears reversible with the provision of intensive support measures.

Patient Triage: 33
ICU admission criteria should select patients who are likely to benefit from ICU care. Patients not admitted should fall into two
categories, “too well to benefit” and to “sick to benefit”. Defining substantial benefit is difficult, and no pre-admission model exists to
predict outcome in a given patient. Rather than listing arbitrary objective parameters, patients should be assigned to a prioritization model
to determine appropriateness of admission.
Priority 1: Critically ill patients in need of intensive treatment and monitoring that is not available outside of the ICU. Generally these
patients would have no limits placed on their care.
Priority 2: Patients that require intensive monitoring, and may need immediate intervention. No therapeutic limits are generally
stipulated for these patients.
Priority 3: Unstable patients that are critically ill but have a reduced likelihood of recovery because of underlying disease or the nature
of their acute illness. If these patients are to be treated in ICU, limits on therapeutic efforts may be set (such as not for intubation).
Examples include patients with metastatic malignancy complicated by infection.
Priority 4: These patients are generally not appropriate for ICU admission as their disease is terminal or irreversible with imminent
death. Included in this group would be those patients not expected to benefit from ICU based on the low risk of the intervention
that could not be administered in a non-ICU setting (eg: haemodynamically stable DKA, or an “awake patient following an
overdose).
Elective admissions 34
Where possible, elective surgical admissions should be booked at least 48hrs in advance. A book exists into which the names of
prospective patients must be entered, following discussion with the surgical team (or anaesthetist) responsible for that patient and the ICU
Consultant on duty for Unit 2 on the day the discussion is initiated. Bed availability must be confirmed by the anaesthetic team prior to
commencing the anaesthetic on the morning of surgery.
.

Management of patients in ICU 35

Patients in The Waikato Hospital Intensive Care Unit are managed primarily by the ICU staff. Visiting Teams should be discouraged
from charting drugs, fluids or other treatment directly.The exception is for elective paediatric ENT patients, where the team is
permitted to prescribe medicines to be given in ICU on a ward chart, but only prior to admission to ICU
The opinion of all Specialists involved in the case is however valued.
The Duty ICU Consultant must be kept fully informed of their opinion.

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Patient discharge policy 36

Discharge procedure 37
All discharges must be approved by the Duty ICU Specialist.
The parent team must accept care of the patient, this acceptance must be recognised at Specialist level, either through their Registrar, or
in some cases to the Specialist directly.
Other teams involved may need to be advised, e.g. the pain team, Renal Service
A careful plan for the immediate discharge period must be discussed with the accepting team, and be clearly documented in the notes
including:
Limitation of treatment where appropriate
Non-return orders
Clear medical management plan, including charting of the following for the next 24hrs:
Fluids
Feeding
Analgesia
Documentation to be completed prior to discharge:
database form
Discharge sheet/notes
Nurses will not send patients to the ward without first checking with the on duty Registrar
Reference:
SCCM Guidelines for ICU Admission, Discharge and Triage. Critical Care Med 1999 Mar: 27(3): 633-638

Deaths in the ICU 38

Withdrawal of therapy is a Consultant-only decision.
The duty consultant must be notified as soon as the patient has been examined and certified dead, unless other specific arrangements exist
(eg. where death is the expected outcome and the issue of a death certificate issue has been discussed).
The ICU Registrar must ensure:
A death certificate has been completed if applicable
The parent team is notified
Referring colleagues (including GP’s) are notified
Post-mortem consent has been acquired from the family (if indicated).
The Coroner must be notified as below:
Every death that appears to have been without known cause, as a result of suicide, or unnatural or violent death.
Every death in respect of which no doctor has given (or is prepared to give) a death certificate.
Every death that occurs while the person concerned was undergoing a medical , surgical or dental procedure, or some similar operation
or procedure.
Death that appears to have been a result of any such operation or procedure.
Death that occurred while the person was affected by an anaesthetic or that appears to have been a result of the administration to the
person of an anaesthetic.
Death of any patient detained in an institution pursuant to an order under section 9 of the Alcoholism and Drug Addiction Act of 1966
Any death of a child or young person in the care or oversight of an Iwi Social Service, a Cultural Social Service or The Child and
Family Support Service.
Death of any patient committed in a hospital under the Mental Health Act of 1969.
The death of any inmate within the meaning of the Penal Institutions Act of 1954
The death of any person in police custody, or in the custody of a security officer.
Where a death is referred to the coroner, no death certificate may be issued by the ICU Registrar.
Reference:
Taken from The Coroners Act , 2007.

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Clinical duties in the Intensive Care 39

General comments 40
Resident Staff will always shoulder a major part of the burden of continuity. Continuity is central to quality patient care and this
expectation is not diminished with a decrease in working hours. The consultant staff also play a pivotal role in this process, but because of
the prolonged periods of continuous call that they are expected to cover, they are not resident in the hospital and are therefore not
continually in the unit. The responsibility for maintaining continuity and for effective communication both with other unit staff and with
outside teams rests largely with the registrars. Effective communication is a basic medico-legal requirement.
There are guidelines covering the medical procedures and the administration of most of the drugs used in the ICU. These guidelines are
under constant review. The resident staff are required to be familiar with these guidelines and to consult them when required. In addition,
any inconsistencies or discrepancies within them should be brought to the attention of the consultant staff.
When asked by a team to review a patient, registrars are required to obtain a full history from the patient and the patient notes, to perform
a comprehensive examination of the patient and to formulate a differential diagnosis. They should then have an outline of a suggested
investigation and treatment plan. The parent team should be consulted concerning their expectations for the patient, in particular what
they are asking for from the ICU team. This information should be clearly documented in the patient record. This information is critical
when presenting a patient at handover and to consultant staff as it is not possible to make quality decisions based on incomplete
information.
It is important that there is a complete transfer of information at the handover between shifts. This will be facilitated by
Comprehensive admission note. Proforma sheets are available for cardiac and trauma admissions
Completion of a standardised daily update note.
Daily review of all clinical laboratory tests, microbiology and radiological tests
An update of the computerised problem list or daily progress notes by the night registrar. This will contain details of the presentation,
the provisional diagnosis, investigations, consults and opinions and unresolved issues that require follow up
Registrars should briefly familiarise themselves with the patients before the formal ward rounds
When leaving the unit, registrars must inform their registrar colleague if applicable. The ICU floor must never be left unattended without
proper reason, and the knowledge of the nursing team leader.

Patient Admission 41
Primary patient survey 42
A: Ensure patient protecting airway / GCS / cognition
B: Breathing pattern acceptable, Pulse Oximetry acceptable
C: Patient cardiovascularly stable, venous access acceptable
Obtain hand over information from the referring doctor
Secondary survey 43
Examine patient thoroughly 44
Notify Duty Specialist if this has not already been done.
Document essential orders:
Ventilation
Sedation, analgesia, drugs and infusions
Fluid therapy
Discuss management with nursing staff and team: Everyone must be aware of the plan !
Basic monitoring and procedures:
ECG
Invasive / non-invasive monitoring
Urinary catheter / NG tube
Basic Investigations (usually a full blood count, coagulation profile, ICU specific electrolyte profile)
Advanced Investigations; CT, MRI, Angiogram as indicated
Case note documentation (see below)
Inform and counsel relatives in general terms
Registrar Documentation 45
Registrars are responsible for documenting an admission note for all patients and a daily entry into the clinical notes as well as;
Discharge summary
Death certificate
Database form collection
Admission Note: Where a pro forma sheet exists this should be used (Cardiac and Trauma), otherwise include:
Date / time
Name of admitting officer
Reason for admission
Standard medical history including current medications
Thorough examination findings
Results of important investigations
Assessment / severity / differential diagnosis
Management plan
Document notification of parent team and duty senior.
Parent teams should be encouraged to write a short note at least.
Daily entry in clinical notes 46
Ensure each page is dated and labelled with the patients name and hospital number.
Date / time / name of ICU Staff Specialist conducting the round
A: Mental state, GCS, airway
B: Ventilation, saturation (or PaO2), chest findings
C: Pulse / BP / peripheral perfusion / Precordial exam.

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Abdominal examination and description of feeding mode.
Peripheries
Assessment or Impression
Plan
Immediately after completion, notes must be filed in the clinical record
Additional notation must be made in the notes when 47
Invasive procedures are undertaken
Important management decisions are made
Significant interaction is made with patient family.
ICU Problem List Formulation 48
Previously we have attempted to run a computerised problem list database.This has been inconsistently used and is in abeyance.This does
not however remove the obligation on the night registrar to have an awareness of active and resolved problems that an individual patient
has.
The Night Registrar is not on duty to simply fight fires until the next day dawns, but actually is the most important continuity pivot for
the ICU.

Daily management issues 49

The daily handover ward round at 08h00 is attended by the night Registrars, the incoming day staff, the duty consultant and
representatives of the nursing staff (CNL and team leader).
The night Registrar will prepare a report and present in a concise and professional manner on the handover round.
Important decisions regarding patient discharge and specialist investigations are made at this meeting and it is important that junior staff
have a good understanding of the patient status, including:
Patient details and demographics
Day of admission
Diagnosis and major problems
Relevant pre-morbid problems
Progress and significant events
Important results
Plan for the next 24 hours
Most of the above will appear on your daily “Problem List Report”.

Clinical Duties outside the Intensive Care Unit 50

Request for insertion of central venous access 51
Intensive Care Staff may be approached to facilitate central venous access in a patient not residing in intensive care
⋅ Request for CVC lines should come from Registrar level or above
⋅ The person performing the line insertion is responsible for gaining informed consent
⋅ CVC’s are generally elective procedures and do not take priority over ICU duties
⋅ The indication for insertion must be reviewed, and alternatives discussed if appropriate.
⋅ The safety of the procedure must be reviewed, in particular the determinants of haemostasis (see relevant section on procedures)
⋅ The patient is currently brought to the ICU for insertion when possible
⋅ For those familiar with the equipment, the old Sonosite may be borrowed from the Department of Anaesthesia
Cardiac Arrest Calls 52
Indications 53
Cardiac arrest calls may be called for the following:
In-hospital cardiac arrest or any severe clinical deterioration
Collapse of unknown origin in the hospital environs
Out of hospital arrest arriving in the emergency department
Arrest team Members 54
ICU Registrar
Cardiology, Cardiorespiratory or Medical Registrar according to time of day
Nurse practitioners: CCU nurse, Clinical resource nurses, ward staff.
CPR (Cardio Pulmonary Resuscitation) 55
The Waikato Hospital encourages the use of the International Consensus on Resuscitation guidelines for cardiopulmonary resuscitation
.The ICU Registrar is responsible for securing the airway and establishing effective ventilation, whilst the Medical Registrar should
concern themselves with cardiac and general aspects. It would be expected however that directing advanced life support be the
responsibility of the more senior Registrar present.
Where CPR has been “successful” but further active treatment may not be in the interests of the patient, the admitting medical officer and
ICU specialist must be consulted prior to withdrawing care.
All involvement in an arrest call must be documented in the patient case notes.

Trauma Call 56
After receiving details from ambulance personnel patients will be designated according to ACEM triage category. The Emergency
Department will initiate the call to the Hospital Operator. A 777 call is placed on the emergency pager, and you are required to confirm by
calling the operator back on 777.
During the day, one registrar (nominated by Co-ordinating registrar if rostered) will attend trauma calls. Ensure that the ICU nursing co-
ordinator for the day are aware of where you are going, and communicate with the ICU nursing team once the patient has been assessed
and the likely admission destination known. There is a registrar cellphone available to facilitate ongoing communication, and you should
carry this with you on leaving the unit. Remember to keep this phone charged when the opportunity arises.

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Trauma team member: 57
The team assembled will vary according to the number of cases expected, as below.
Trauma I (1 Case) 58
Emergency Department Senior (Trauma Leader)
ICU Registrar
Emergency Department Registrar (initiates resuscitation, assists with the management of the patient and makes sure all staff that have
been called, attend)
Surgical Registrar-(primary and secondary survey)
Trauma II (2 Cases simultaneously): 59
Emergency Department Senior (Trauma Leader)
ICU Registrar (Team leader in absence of ED/ICU Senior)
Emergency Department Registrar
Surgical Registrar
Anaesthetic Registrar
The ICU Senior is called in to lead the second trauma case if both cases ACEM Triage 1 or 2 or if ICU Registrar or Emergency Physician
request
Trauma III (3 Cases): 60
Call as for Trauma II with the addition of the Specialist Anaesthetist on call, Surgeon on call, and the orthopaedic registrar.
Trauma call procedure 61
The trauma call usually precedes the patient arrival in ED. It is worthwhile to prepare everything that might be needed (ie calculate and
draw up drugs, check intubation equipment and communicate with the rest of the team). It is particularly important to identify which
nurse is helping with the airways.
On arrival in the E.D. the patient should be assessed according to ATLS Guidelines (ABCD...).
Primary Survey 62
Airway: and total spine control. Do not forget to look in the mouth. Do not neglect the C-spine.
Breathing
Circulation: and haemorrhage control. Resuscitation without controlling bleeding control is at best a temporary measure. Techniques
such as FAST ((Focused Abdominal Sonography for Trauma) or DPL may be required before secondary survey.
Disability: brief neurological evaluation
Exposure: completely undress the patient
Adjuncts to primary survey include: Chest X-ray, Pelvic X-ray and cervical spine
Secondary Survey 63
Cover in the following order:
Head and scalp/ maxillofacial
Cervical Spine and Neck
Chest
Abdomen and Pelvis
Back and Perineum
Extremities
Neurology
Role of the ICU Registrar at the trauma call: 64
Primarily as a back-up for acute life threatening situations
ICU staff manages the patients airway, providing they are adequately experienced to do so
Secure the airway
Establish ventilation
Assist with vascular access
Do not leave ICU unattended for more than 30 minutes. Once the patient is stable and sufficient trauma team members present, you may
seek permission from the trauma team leader to return to the ICU. If this is not possible within 30 minutes the on-call registrar should be
called in so that the ICU is not left without medical staff.
ICU Registrars usually escort patients to the ICU from the emergency department. They may also be required to transport the patient to
radiology if the patient is destined for ICU thereafter.
Always
Document your involvement in the case notes.
Keep ICU senior medical and nursing staff up to date with patient progress, particularly if ICU admission is likely.
Reference:
Handbook of Trauma Care. The Liverpool Hospital Trauma Manual, 6the edition. Ed: S D’Amours, M Sugrue, R Russell, N Nocera.

Intra-hospital patient transport 65

No patient may be transported from the unit without the direction of the Duty ICU Specialist.
Medical escort is the rule. In a minority of circumstances a nurse escort may be sufficient, providing it is acceptable to the Duty ICU
Specialist and the Nursing leader.
Registrars should ask the Senior registrar to accompany them on their first in-hospital transport if (s)he is available. It may not be
appropriate for all registrars to undertake prolonged transport, or transport to unfamiliar areas (eg MRI). Always ask the duty ICU
specialist if you are unsure.
Prior to embarking on an escort all equipment, oxygen supply and emergency drugs must be checked.
All problems encountered on the escort must be recorded in the notes, and an incident form completed if appropriate.
If a test is deemed urgent the medical escort should endeavour to get an informal report written in the notes, failing which they should
request formal review and notification to the unit as soon as possible.
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Patient Retrieval 66
Introduction 67
The Waikato ICU is frequently involved in interhospital patient transport within (and occasionally beyond) the North Island. Note that our
formal involvement is limited to transport between public hospitals ONLY. The exception is attendance at unexpected emergencies while
en route to another site. Retrievals may be undertaken from Private Hospitals in Hamilton.
The Waikato ICU Transport Service is a consultative and consultant lead service concerned with the safe transport of seriously and
critically ill patients beyond the immediate newborn period, when we are able to and deem it appropriate. ICU Registrars with Transport
Team Nurses perform the vast majority of these transports under the supervision of the appropriate Intensivist who is responsible for the
Registrar’s performance. In every case, the appropriate Intensivist must be notified of the intention to perform a particular interhospital
transport and authorise it.
It must also be stressed that in every case, another team must be expecting to assess and where necessary accept care of a patient
transferred by our team, whether the patient is being admitted to our ICU or not.Exception: “single doctor on duty hospitals” within
WDHB
Effective and explicit communication is the principle that underlies interhospital patient transfer and every attempt must be made to
foster this by team members.

Specific Situations 2.10.2

Balloon pump-see transport compendium
Children-see table below and transport compendium.Between 5-10 kg, a Servo 300 is the most suitable ventilator.Beyond 10kg , either
Parapac or Pulmonetics are suitable.Transport of critically ill children by our team is a rare event indeed, and yet is required from
time to time.Whenever possible, children leaving our ICU bound for an Auckland hospital should be transported by Starship
Hospital Retrieval Services or Lifeflight if not destined for PICU at Starship
Dysbaric illness-if mild, transport should happen by standard escort and road ambulance.If severe, critical care transport as close to sea
level as possible.
Diversion to roadside-perform in usual doctor “Good Samaritan” role
ED destination-make sure ED physician on duty is aware the patient is coming to ED
HDU destination-check bed availability with HDU Co-ordinator.If no bed available, inform accepting team
Obstetric Patients-strict control of transport of these patients is required. Patients notified to us from the Obstetric Unit should already
have an appropriate decision made by duty Obstetrician as to what type of obstetric escort is necessary.If not, this should be
encouraged as a matter of urgency.If a referring clinician rings our ICU initially, we will take details and call Consultant
Obstetrician on duty who will be asked to specify the obstetric escort.Callers notifying of patients who are not in a public hospital
should be referred to St John’s ambulance and advised to dial 111.
Rapid response turnout-use whenever extreme emergency-notify all concerned to facilitate rapid transport.If sole registrar on duty, give
pager to ED registrar prior to leaving hospital
Relatively well patients-after verification that the patient can be transported without a critical care transport team (achieved by
assessing patient and liasing with duty Intensivist), ward staff are advised to explore other options with Duty Manager
Trauma within 48 hours injury-should be taken through the ED.For ICU patients beyond this period , transport direct to ICU is
preferable
Weight over 150kg-fixed wing or road ambulance necessary for at least return trip
When suitable transport or team unavailable- responsibility lies with medical staff attending patient to continue exploring other ways to
transport patient.This may involve liasing with transport services in other cities.

SUMMARY OF TRANSPORTING SERVICES

Referral Source Trauma In All admitted and non- trauma All Interhospital Transfers
ED Patients

Taupo, Tokoroa, Taumarunui, Thames ED A Zero ICU Transport Team

Te Kuiti ED A Zero

All other Midland Hospitals (Tauranga, Rotorua, Gisborne, New ICU Transport Team
Plymouth)

Neonates and children <5kg Neonatal Transport Team

Obstetric Referrals from hospital ICU Transport Team /

obstetrics

Interhospital transfers but not to Waikato ICU Transport Team

Roadside Retrievals ED A Zero

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Summary of the Transport Process

Initial call to ICU by

referring hospital

Clinical details
obtained by
Registrar/Specialist

Acceptance of transport by ICU Specialist

Pilot contacted by ICU

ICU coordinator Helicopter 06 100 663 ICU transport
notified Fixed wing 026 107 380 doctor notified
Ambulance control 8055

ICU transport
nurse notified

Duty Manager notified

Additional material:
The transport compendium, held in a red folder in the bay of ICU2 is the most comprehensive reference on our retrieval services.

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Infection Control 68
Introduction 69
Patients requiring intensive care are highly susceptible to infection due to immunosuppressive effects of drugs and disease, the use of
invasive monitoring techniques and the severity of the underlying illness requiring admission. The use of broad-spectrum antibiotics may
predispose to infection with resistant organisms.
Nosocomial infection delays patient discharge from the intensive care unit (ICU) and contributes significantly to morbidity. The
prevalence of hospital-acquired (nosocomial) infection in the ICU can be considerably higher than other clinical areas of the hospital.
Significant risk factors for infection include:
mechanical ventilation
prolonged length of stay
trauma or burns
intravascular catheterisation
urinary catheterisation
The four most common nosocomial infections seen in ICU are:
Pneumonia
urinary tract
intra-vascular catheter-related bacteraemia
surgical wound infection
All ICU staff are responsible for ensuring good infection control policies are adhered to, in particular good hand hygiene practice.

Hand Hygiene and Standard Precautions 70

Hand washing and hand disinfection remain the most important measures in the prevention of cross infection. Hands should be cleaned
before and after contact with every patient and after manipulation of the patient environment. Either a 15-second handwash with soap and
water, or alternatively the waterless hand gel may be used if hands are not visibly soiled.
A longer handwash with antibacterial soap is required prior to any major invasive procedures such as insertion of central venous catheter.
In addition to hand hygiene standard precautions are used for all patients:
Wear gloves for all contact with blood and body fluids including dressings and wounds. Gloves must be changed between patients.
Hands must be decontaminated after the removal of gloves.
Wear a disposable plastic apron or fluid-resistant gown to protect the skin and clothing for procedures likely to generate splash or cause
soiling.
Wear a mask and eye protection to protect mucous membranes of the eyes, nose and mouth during procedures likely to generate splash
or cause soiling.
Ensure patient-care equipment is cleaned and disinfected appropriately between patient use.
Staff who generate a sharp product (eg: needle or blade) are responsible for its safe disposal into an approved puncture resistant sharps
container.
Isolation and transmission-based precautions 71
In addition to standard precautions, isolation and appropriate transmission-based precautions are to be used with the following:
Multi-resistant organisms (MRO)
Patients infected or colonised with the following MRO’s require isolation and contact precautions (gloves and gown/apron for direct
patient care):
Methicillin Resistant Staph. Aureus (MRSA)
Vancomycin Resistant Enterococcus (VRE)
Multi-resistant gram negative organisms
Meningococcal disease - proven or suspected
Patients require isolation and droplet precautions (surgical mask within 1 metre of the patient) until 24hrs of completed antibiotic
treatment.
Miscellaneous
Burns patients require isolation and contact precautions
Febrile neutropaenic patients require isolation and contact precautions
High risk immunosuppressed patients require isolation and contact precautions
Respiratory syncytial virus require contact precautions
General Measures 72
The ICU should be kept tidy and uncluttered. Equipment not in use should be stored in a clean area.
Movement of people through the unit should be kept to a minimum. This applies equally to colleagues and relatives.
All visitors are to be encouraged to wash their hands before and after visiting the patient.
Staff with communicable diseases should take sick leave.
Further reading:
Please refer to the HW Infection Control Policy and Procedures Manual for further information.

Research in the Intensive Care Unit 73

Introduction 74
Research in The Waikato Hospital ICU is strongly encouraged. Applications for research, or ideas which may lead to an application
should be discussed with Dr Van Haren.

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Personnel 75
Coordinator of Research Dr Frank Van Haren
Nursing Research Mary La Pine
Research Committee Interested parties and medical / nursing staff involved in trials.
The research committee meets once a month to discuss ongoing issues regarding research, assess validity of proposed projects and
managing funding of studies appropriately.
Members of the medical and nursing staff are encouraged to become involved in research during their stay in the unit. Registrars are
expected to be aware of active studies in the unit, obtaining consent for which is seen as part of their responsibility within the unit.
Information on active studies can be obtained from the Director of Research, or the research coordinator. Research in the unit falls into 3
categories:
“In House”: Research that originates, and is conducted by staff within the unit
Contract research: Research conducted and funded by drug companies
ANZICS Clinical Trials Group (CTG) trials-these should be of particular interest to trainees
Presentation 76
Medical progress relies on dissemination of information to colleagues, and many training programs indeed require presentation of a
completed project to a suitable audience as part of training. For this reason completed projects should be presented at a scientific meeting
and, if appropriate, publication sought. Some funding will be available for medical / nursing staff who present at any meeting.
Suitable forums for presentation 77
Annual Scientific Meeting on Intensive Care (Held in October each year)
Abstracts to be submitted by preceding July
Prizes are awarded for
Best free paper (med / nurse)
Best review (med / nurse)
Best Poster
Best paper by a trainee
Thoracic Society of Australia and New Zealand (March)
International Meetings 78
Society of Critical Care Medicine , North America (Feb)
International Symposium on Intensive Care and Emergency Medicine, Brussels (March)
European Society of Intensive Care Medicine, various (Sept)
Ethics Submissions 79
Worldwide, the trend towards gaining ethical approval prior to commencing a study is becoming increasingly important. Many journals
will not publish research done without prior ethics committee approval.
With the exception of some audits, most projects must obtain approval from the Regional Ethics Committee prior to commencement. The
clinical trials coordinator should be viewed both as a resource person and an advisor in negotiating ethics committee approval.
Research is a slow process, therefore registrars that wish to do their college project whilst in ICU should obtain ethics approval, and in
some cases funding, before the start of the ICU rotation.
Assistance with the formal project may be requested from Dr van Haren

Information technology 80
There are numerous terminals in the intensive care unit that offer access to the hospital network from which patient results can be
obtained.
There is a hospital intranet which allows access to the library which has an excellent selection of on line journals available. All critical
care drug protocols are currently available on the intranet. Further medical and nursing protocols for critical care will be added in the near
future.
You will be given a login by the IT department. This allows you access to the laboratory data and to your own account. You will have an
e-mail address with access to the groupwise mail program and its address book which has a list of most company employees and their
contact details.
The local area network provides access to the “World Wide Web”. This is controlled and closely monitored by the IT department.
Numerous sites of medical interest are readily accessible. Other sites are however blocked by “border manager”. If you feel that a
particular site should be available, the URL should be submitted to the system controller who will look and the site and unblock access to
it if appropriate.
The ICU has its own web site which is held on a server outside the hospital. This can be found at
http://www.anaes-icu-waikato.org.nz. This contains basic information on the unit and has a collection of previous registrar topic
presentations that can be accessed. Any suggestions and all electronic presentations should be forwarded to John Torrance.

Consent in the Intensive Care Setting 81

Introduction 82
A competent patient may give or withhold consent for any medical treatment (Code of Health and Disability Consumer’s Rights).
Unfortunately, patients in ICU often cannot have their competency established with certainty. When a patient cannot give consent in an
emergency, in the absence of convincing evidence to the contrary (e.g. presence of a person with enduring power of attorney who can
categorically state that the person does not wish to receive the treatment in question, or applicable advance directive) consent to treatment
is implied.

Consent by relatives 83
Relatives or friends cannot give or withhold consent for the performance of a medical treatment.

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New Zealand statute does however mandate that the treating doctor takes the family views into account in deciding whether to perform a
particular treatment.

Consent at The Waikato Hospital 84

A “Right 7(4) Consent Form” is available to try to take the frequent inability of others to give consent for an incompetent adult into
account. Completion of the appropriate form is necessary to comply with hospital policy in certain procedures (see Waikato Hospital
Policy for Informed Consent).
A written record of informed consent is unnecessary for the vast majority of bedside procedures in ICU-in practice it is only universally
obtained for elective percutaneous tracheostomy.
When it is necessary to obtain consent for a particular procedure to be performed on an ICU patient, it is appropriate for ICU medical staff
to play a role in this process. This may mean ensuring that the staff intending to perform a procedure make the requisite information
available to the ICU registrar to enable them to get consent, or in many cases obtain consent themselves.
Miscellaneous: 85
Consent to participate in research is a specialised area which this document cannot cover.
Issues of a child’s competence to give or withhold consent are likewise too complex to cover here.
Consent is additionally required for a patient to participate in teaching.
A medical practitioner working in a hospital does not require a patients consent to take a blood alcohol level if requested by an
enforcement officer, providing taking the sample is not prejudicial to the patients care (Land Transport Act,1998).
Reference:
“Health Care Law in New Zealand” Johnson,S (held in ICU and main library).

Medico-Legal Assistance 2.14.3.2

In those situations where you may require medico-legal advice, a legal advisor may be contacted through the switchboard.

Hospital Emergencies 86
There is a Waikato Hospital Emergency Response Wall Chart in both ICU units which will guide you in any of the following situations:
Mass casualty
Communications or utility failure
Cardiac Arrest
Earthquake
Fire (or smoke smell)
Hazardous substance spill
Personal safety threat
Threat from telephone, letter or suspicious object
Bomb or arson
Radiation spill
Dialling “777” and thereby contacting the switchboard will in most circumstances allow you to initiate an emergency response that is
appropriate to the threat

Fire and building emergencies 87

Attend formal fire training sessions
Become familiar with location of fire exits
Assess medical condition of persons in an emergency area, and the likely effects of evacuation on them.
Advise the Floor warden of any special requirements
Follow instructions of trained accredited staff.

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Clinical Procedures 88
Introduction 89
It is inevitable that during your stay in the Intensive Care Unit you will be exposed to a number of procedures with which you are not
familiar. All staff are encouraged to become proficient with routine procedures:
ICU Procedures 90
Endotracheal intubation
Peripheral venous catheterisation
Central venous catheterisation
Arterial cannulation / PiCCO insertion
Pulmonary artery catheterisation
Urinary catheterisation
Lumbar puncture
Intercostal drain insertion or pleurocentesis
Naso-gastric / jejunal tube insertion
Patient consent should be obtained as outlined elsewhere in these guidelines.
No member of staff is permitted to attempt a procedure without adequate training. No matter how experienced you are, repeated
unsuccessful vascular punctures are unacceptable and a more experienced member of staff should be asked to help.
All procedures must be annotated in the case notes, including the indication / complications for the procedures.
Restricted procedures 91
Specialised procedures are generally performed by the Senior Registrar or Duty Specialist. They may not be attempted without prior
discussion with the Duty Specialist.
Percutaneous tracheostomy
Fibreoptic bronchoscopy
Transvenous pacing
Pericardiocentesis
Oesophageal tamponade tube insertion

Peripheral IV Catheters 92
Indications 93
Initial IVI access for resuscitation
Stable or convalescent patients where more invasive access is not warranted.
Management 94
All lines placed in situations where aseptic technique was not followed must be removed (eg. Placement by emergency staff at the roadside)
Acceptable aseptic technique must be followed including:
Thorough hand-washing
Skin preparation with alcohol swab
Occlusive but transparent dressing
All lines should be removed if not being actively used, or if > 2 days old. An exception may be made where venous access is challenging
(eg. paediatric patients)
Complications 95
Infection
Thrombosis
Extravasation

Arterial Cannulae 96
Indications 97
Invasive measurement of systemic blood pressure
Multiple blood gas sampling and laboratory analysis
Site and catheter choice 98
1st choice: Radial artery
2nd choice: Femoral.
Site of choice for PiCCO catheter monitoring (Pulsiocath 5F 16 cm catheter) is generally the femoral artery.
The axillary artery may be considered (usually 4F catheter).
The Brachial artery is an end-artery, and catheterisation has been considered a risk for distal arterial complication (although this has also
been disputed). It may be used if there are no alternatives.
Technique 99
⋅ All catheters should be inserted with full sterile technique (gown, sterile gloves, topical antiseptic)
⋅ The arterial line must be firmly anchored (eg. sutured)
⋅ The insertion site and all connectors must be visible through the applied dressing.
Complications 100
Infection
Thrombosis
Digital Ischaemia
Vessel trauma and fistula formation.

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Central Venous Cannulae 101

Training 102
Central venous catheterisation may not be attempted by any member of staff without adequate training or supervision.
Indications 103
Reliable IVI access in ICU patients:
Fluid administration
TPN, hypertonic solutions (amiodarone, nimodipine)
Infusions of inotropes or other vasoactive substances
Monitoring of right heart pressures (CVP, Pulmonary Artery Catheter)
Access for renal replacement therapy
Large bore resuscitation catheter: PA sheath or dialysis catheter.
Technique 104
All staff are expected to view and familiarize themselves with insertion techniques as described in standard texts.
All procedures must be performed under conditions of strict “asepsis”.
Where a junior member of staff is familiar with a certain technique, they should continue to use that technique.
If you suspect that you have mistakenly cannulated an artery rather than a vein, seek assistance from the senior Registrar or duty
ICU specialist prior to removing the offending line.

Choice of route 105

The internal jugular route represents less risk than subclavian in un-practised hands. Subclavian catheterisation may be the route of choice
from an infective risk perspective, followed by internal jugular and then femoral. Each site has characteristics that make it preferable under
certain circumstances and where the operator is in any doubt this should be discussed with senior staff members.
Subclavian 106
Avoid in situations where pneumothorax would be fatal. (i.e. severe respiratory failure, lung hyperinflation).
Avoid in patients therapeutically anticoagulated or coagulopathic
Platelet count < 50 000
INR > 2.0
APTT > 50 sec
It may be appropriate to attempt to reverse abnormal clotting prior to insertion of a CV catheter, however this should be discussed with the
Duty Specialist.
Always choose side of chest that is least effective for ventilation, or in which there is already an intercostal catheter.
Internal Jugular 107
This route is associated with a higher risk of infection than subclavian access. However there is a lower risk of pleural puncture (for high
jugular approach) and better control of haemorrhage than the subclavian approach.
Internal Jugular approach is the route of choice for dialysis catheter insertion, although femoral access is also acceptable.
The safety of jugular puncture is improved with ultra-sound guidance.
External Jugular 108
In certain circumstances it may be appropriate to attempt cannulation of the external jugular vein in order to achieve central venous access.
This route may be advantageous when the patient is coagulopathic, or in certain emergency situations where other access may be difficult.
This route has the lowest rate of complications, but is associated with a 20% failure rate due to inability to cannulate vein or malposition.
EJ access is less suitable for PA Catheter or Dialysis catheter insertion.
Femoral 109
Femoral catheterisation has traditionally been thought to confer a high risk of infection relative to subclavian access. This has not been
proven, although in certain patients (eg: the obese, or those with infected/open abdominal wounds) this may still hold true. The incidence of
thrombosis is probably similar to other sites.
Good flow characteristics for dialysis catheters, using a 20 cm or longer catheter.
Relatively low risk route for inexperienced operators in high risk patients (i.e. uncorrected coagulopathy, severe respiratory failure).
Reference:
Merrer J et al. Complications of femoral and subclavian venous catheterisation in critically ill patients. JAMA 2001. Aug 286(6):700-707
Line management 110
Routine line replacement is not required.
Lines should be removed as soon as:
They are not required any longer.
The patient has evidence of unexplained systemic infection (pyrexia, ↑WCC)
Insertion site infection or positive blood culture with likely organism (S epidermidis)
Guide-wire exchanges should not be performed unless discussed with the Duty Specialist.
Antibiotic coated CV lines should be used when access required beyond 2-3 days.
Complications 111
At insertion 112
Arterial puncture
Pneumothorax
Neural injury (phrenic nerve, brachial plexus, femoral nerve, cervical plexus)
Guidewire induced atrial ectopy, arrhythmia
During catheter presence 113
Infection: Infection risk increased with increased catheter size, choice of site (femoral > jugular > subclavian) and use of TPN or dextrose
containing fluids.
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Thrombosis
Embolism
Pulmonary infarct or pulmonary arterial rupture (PA Catheter)
Pulmonary artery catheterisation 114
The PA Catheter is not a resuscitation tool and should only be inserted in a controlled environment after discussion with the Duty Specialist.
Dwindling use of the PA catheter has resulted in a loss of familiarity with its use. Junior medical staff and nursing staff not familiar with this
instrument should not manipulate / advance / inflate the PA catheter balloon.
Indications 115
Haemodynamic measurement: (cardiac output, stroke volume, systemic vascular resistance)
Measurement of right heart pressures (pulmonary hypertension, pulmonary embolus)
Estimation of preload to the left ventricle-controversial.
Insertion 116
PA Catheter insertion is technically difficult and requires a working knowledge of right heart pressures and waveforms. See appendix on
pulmonary artery catheterisation
Monitoring PA trace 117
An adequate tracing should be visible on the monitor at all times. A damped tracing may represent a wedged catheter, clot at the catheter tip
or inappropriate equipment set-up (wrong monitor calibration, faulty pressure transducer).
⋅ Flush the distal lumen generously (using closed mechanism)
⋅ Withdraw catheter until a trace is present.
NB Never withdraw the catheter with an inflated ballon.
Measurement of pressures 118
Pressure should be referenced to the mid-axillary line
The true wedge pressure is measured at end-expiration
PEEP may influence wedge pressures, however this is not a factor at PEEP < 10 mmHg, and patients should not be disconnected from the
ventilator to measure PAC pressures.
Measurement of haemodynamics 119
Cardiac output measurement should only be attempted by staff familiar with the use of PA Catheters.
10 ml 5% dextrose at room temperature is rapidly injected into the appropriate lumen.
This is usually repeated three times, with results varying > 10% from average discarded.

Cardiac Pacing 120

Introduction 121
Most commonly, temporary cardiac pacing is encountered post cardiac surgery with epicardial leads.
Transvenous pacing is most often accomplished using a modified pulmonary artery catheter or by a cardiologist using a suitable lead.
Indications 122
In circumstances where “medical” pacing with a chrono(- ino) trope has failed or is inappropriate
Symptomatic bradycardias, including β-blocker intoxication
Complete heart block
Bifascicular block in association with evolving infarct (particularly anterior)
Elective: following cardiac surgery in “at risk” patients
Valve replacement or repair, VSD repair or repair papillary muscle rupture
Acute myocardial ischaemia
Persistent A-V block: A temporary pacing wire may be required as a bridge to sequential pacing.
Tachyarrhythmia’s may respond to overdrive suppression pacing.
Types 123
Balloon flotation lead
Modified PA catheters
Epicardial leads. Usually placed electively during cardiac surgery. Depending on surgeons preference and patient selection these may be
uni-or bi-polar and either ventricular alone or atrial and ventricular. Where leads have been placed at the time of surgery, their nature
and use should be clearly documented in the patient case notes.
Bipolar pacing lead placed under image-intensifier guidance, usually by cardiology team.
Flotation Catheter insertion 124
Flotation placed transvenous pacing wires should be placed using ECG guidance
Use aseptic technique and local anaesthesia where appropriate
⋅ Insert pacing wire using a peel away sheath, or if necessary a PA Catheter introducer (although this may leak).
⋅ Connect pulse generator but do not activate
⋅ Attach V5 lead of an ECG to the distal electrode of the catheter and advance noting QRS wave form change as the catheter advances
to the RV. Advance the catheter 2 cm, deflate the bulb and advance a further 1-2 cm.
⋅ Set output and sense of pulse generator to minimum value, and rate 20 bpm > than the patients own.
⋅ Turn generator on and gradually increase output while observing the ECG for capture
If there is no capture, or a high output is required then:
⋅ Place generator on demand mode.
⋅ Turn output down, advance or reposition the wire slightly
⋅ Attempt re-capture by increasing output. An ideal capture setting would be approx 2 mA, with a routine setting placed 2-3 mA higher
than capture threshold.
⋅ Secure wire in place
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A control CXR must be performed post insertion.
Pulse generator 125
All staff should familiarise themselves with the code of pacing and the pacing box.
References:
Reade MC. Temporary epicardial pacing after cardiac surgery.Part 1: General considerations in the management of cardiac pacing in the perioperative
period.Anaesthesia 2007 (62):264-271.
Reade MC. Temporary epicardial pacing after cardiac surgery. Part 2: Selection of epicardial pacing modes and troubleshooting. Anaesthesia 2007 (62):364-373.

Intra-aortic balloon counterpulsation (IABP) 126

Introduction 127
IABP’s are used at times in the unit, usually in patients returning from cardiac surgery, but occasionally as an optimising procedure prior to
surgery or in severe potentially reversible cardiogenic shock.
IABP study days and education sessions occur from time to time and are co-ordinated by the Unit Nurse Educator. If you are unable to attend
one of these sessions you should familiarise yourself with the equipment by asking senior staff (including nursing staff) and consulting the
unit IABP introduction folder kept in unit 2 area.
Usually IABP’s are sited by the Cardiothoracic Team or a Cardiologist. If they are to be inserted by ICU staff, it is only to be performed by
consultant staff or advanced ICU vocational trainees.
Indications 128
Ischaemic Heart Disease
Low cardiac output states following cardiac surgery
Cardiogenic shock associated with angiography, stenting or PTCA
Acute mitral incompetence (papillary rupture) or VSD associated with septal infarct.
Myocardial disease
Severe contusion
Myocarditis with cardiac failure
Cardiomyopathy
Severe beta blocker overdose
Contra-indications 129
Absolute 130
Aortic regurgitation
Aortic dissection or unstable aneurysm
Relative 131
Severe peripheral vascular disease
Tachyarrhythmias
Coagulopathic states
Procedure preparation 132
⋅ IABP insertion should only be performed by staff familiar with the equipment and personnel requirements.
⋅ Strict aseptic technique should be maintained
⋅ Check IABP function prior to insertion
⋅ Confirm that the helium cylinder volume is adequate
⋅ Reference the arterial pressure manifold to the mid axillary line and calibrated.
⋅ Connect a dedicated 5 lead ECG to the IABP
⋅ Machine in standby mode at the following settings:
ECG sense trigger
1:2 ratio augmentation
max. augmentation selected
inflate and deflate time at zero.
Insertion procedure 133
⋅ Use local anaesthesia in awake patients
⋅ An assistant who is scrubbed should be available
⋅ Select a balloon size: 34 ml balloon for patients under 165cm tall, 40 ml balloon if taller.
⋅ Cannulation the femoral artery using the Seldinger technique
⋅ Insert IABP using sheathless technique (catheter over wire) or large bore cannula supplied.
⋅ Insert to point approximating T4 (ie distal to origin of left subclavian artery) as an anatomical marker (2nd black marker on the IABP
itself), with a subsequent control X-ray once procedure complete
⋅ Aspirate blood from arterial port to confirm position
⋅ Connect to pressure transducer and pump, then turn on.
Trigger 134
The ballon inflation may be triggered in a number of ways:
ECG: Inflation at peak of T-wave and deflation before next QRS.
Arterial waveform
External pacemaker
Timing 135
Check balloon inflation against pressure wave-set to peak of dicrotic notch
Check ballon deflation against ECG-prior to QRS complex
Check diastolic augmentation on pressure wave
Select augmentation ration 1:1 or 1:2
Maintenance 136
Some surgeons wish the patient to be heparinised while the IABP is in situ

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The surgeon’s preference should be confirmed, and clearly documented in the patients notes.
Control CXR: the tip of the IABP is radiologically opaque and should be sited at the level of T4 (= carina on centred film)
The limb distal to the insertion site should be monitored neurologically and for adequate distal perfusion.
IABP function during arrhythmias 137
Arrhythmias markedly affect IABP function and they should be actively treated.
Ectopics: IABP should remain on ECG trigger, causing automatic deflation on an ectopic.
Atrial Fibrillation: move deflate slide to far right, which cancels automatic R-wave inflation.
VF / VT: proceed as per ACLS guidelines, IABP mechanism is not affected by cardioversion.
Cardiac arrest in a patient with an IABP in-situ: proceed to external cardiac massage.
Where CPR or arrhythmia is associated with effective cardiac output: Change IABP to pressure trigger
No cardiac output with CPR or arrhythmia: Set internal IABP mode to fixed rate of 40 inflations per minute and 20 ml augmentation.
Weaning 138
The IABP should only be removed once the patient has stabilised and the Duty ICU Specialist and Cardiothoracic Surgeon / Cardiologist
agree.
Generally the augmentation rate is sequentially decreased to 1:4 and then removed.
If the patient has been anti-coagulated then the heparin should be discontinued for 3 hours prior to removal of the IABP.
Catheter removal 139
Do not turn off the IABP and leave in situ.
⋅ If open arteriotomy has been used, surgical closure will be necessary
⋅ Disconnect IABP tubing but do not manually aspirate the balloon before withdrawal.
⋅ Apply manual pressure until haemostasis achieved. Do not apply occlusive dressing
If pressure bag or “fem-stop” pressure device applied then this must not be done in a way that might obscure ongoing haemorrhage.
Complications 140
Limb ischaemia
Haemorrhage
Infection
Aortic or femoral dissection
Aortic arch vessel or splanchnic arterial occlusion if balloon improperly sited.
Thrombocytopaenia
Balloon rupture with gas embolism

Pleural Procedures 141

Indications for accessing pleural space 142
Pneumothorax (± temporising procedure if under tension)
Haemothorax
Symptomatic or infected pleural effusion
Needle Thoracostomy for Tension Pneumothorax 143
⋅ 16G cannula placed in mid clavicular line, 2nd intercostal space
⋅ Proceed to formal intercostal drain insertion.
Pleurocentesis 144
Indications 145
Diagnostic procedure
Therapeutic procedure: Drainage of an infected collection requires an underwater seal drain. It may not be appropriate to perform “once-
off” drainage. The practice of draining non-infected pleural collections by pleurocentesis is controversial and should not be performed
without direction by the Duty ICU Specialist.
Technique 146
Local anaesthesia and sterile technique
Unless the fluid collection is grossly detectable on clinical examination and on plain radiology, pleurocentesis should be ultrasound directed.
Investigation of pleurocentesis fluid 147
Aspirated fluid should, at the very least, be submitted for:
pH: analysed in ICU blood gas analyser (pH < 7.20 = empyema, 7.20-7.25 = equivocal)

Intercostal Catheter / Underwater Sealed Drain 148

Insertion 149
⋅ Local Anaesthesia is mandatory in awake patients, and should be used in sedated patients
⋅ Strict aseptic technique
⋅ 28F catheter inserted into 3-4th intercostal space, mid-axillary line, using blunt dissection as described and recommended in the
ATLS guidelines.
⋅ The catheter must be guided through the ribs without use of sharp instruments (preferably finger). Trochar aided insertion techniques
are not acceptable.
Maintenance 150
Drains placed in un-sterile environs should be removed as soon as possible.
Drains should remain in-situ until radiological resolution has occurred and there is no further bubbling or drainage of significance ( < 150 ml
/ 24hrs)
Drains placed electively in theatre are the responsibility of the surgeon

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Complications 151
Incorrect placement
Pulmonary laceration
Pneumothorax
Bleeding as a result traumatic drain insertion (intercostal or, lateral thoracic artery, lung etc)
Empyema

Pericardiocentesis 152
Indications 153
Haemodynamically significant pericardial effusion
Traumatic pericardial tamponade
Technique 154
Pericardial access and drainage may not be performed in ICU except under the most dire circumstances. Echocardiographic guidance by staff
experienced is the technique is the preferred method.
Suspected cardiac tamponade in a patient who has undergone cardiac surgery is an indication for chest re-opening and not needle aspiration.

Endotracheal Intubation 155

Introduction 156
Endotracheal intubation in ICU patients is a high risk but vital emergency procedure in patients who often have limited reserve, are difficult
to position and may have a difficult airway.
All staff should familiarise themselves with the intubation trolley and equipment.
Whenever possible make sure that you have capable and trained staff to assist you. If you are inexperienced (e.g fewer than 20 intubations),
always call for assistance. If the duty specialist cannot be reached for some reason, or is detained, then assistance should be sought from an
anaesthetic colleague.
Rapid sequence induction is the rule in ICU patients.
Indications 157
Institution of mechanical ventilation
To maintain an airway
Upper airway obstruction or threat
Control of arterial carbon dioxide content (eg. in the setting of traumatic brain injury)
Patient transportation
To protect an airway
Patients at risk of aspiration
Altered conscious state
Tracheal toilet
Techniques 158
Orotracheal intubation is the rule.
Blind nasal awake intubation, or fibreoptic awake intubation, may be indicated in selected patients with cervical spine injury, limited mouth
opening or oro-facial surgery / trauma. These techniques should only be undertaken by staff with current experience of these techniques, and
only after discussion with the duty ICU specialist.
Standard endotracheal tube choice 159
All patients in the Waikato Hospital Intensive Care Unit should be intubated with a low pressure high volume PVC tube (eg Portex blue line
oral nasal tube)
Non-standard tubes 160
Patients returning from theatre may have a different ET tube (eg. armoured ETT) in situ. Where there is no good reason for this to remain, it
should be changed to the standard ETT if it is anticipated that the patient will require intubation > 48 hrs, and would not be exposed to
significant risk during the ETT change.

Intubation Guideline 161

Personnel 162
Skilled assistance is mandatory; where possible a team of 4 is required.
“Intubator” who controls and co-ordinates the procedure.
“Drug administration”
A person to apply in-line traction where the stability of the cervical spine is unclear.
Cricoid pressure (CP) is recommended in all emergency situations and should be applied at the commencement of induction.CP may
distort the larynx requiring it’s removal.
.
Preparation 163
⋅ Secure adequate IVI access
⋅ Check all equipment prior to intubation:
Adequate lighting
Selection of oropharyngeal airways
Working suction with Yankauer attachment
AMBU bag assembly and appropriate mask
100% oxygen with flow capability > 15 l/min
2 working laryngoscopes with appropriate choice of blade
Magill forceps
Malleable introducer and gum-elastic bougie
2 × ETT: estimated patient size and one smaller size. (Female = 7-8 mm, Male = 8-9 mm)
A selection of laryngeal masks
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Emergency cricothyrotomy kit: (#15 scalpel and 6.0mm cuffed ETT)
⋅ Ensure adequate monitoring
Pulse oximetry
Reliable blood pressure monitoring (eg. invasive if necessary)
ECG telemetery
Capnography must always be immediately available.
Difficult intubation Kit 164
A kit can be found in a yellow bag on the side of the Unit 2 intubation trolley containing:
An intubating LMA
McCoy laryngoscope
Light wands
Emergency cricothyrotomy kit
Jet ventilation system
Drugs 165
Induction agent 166
eg. Thiopentone, Fentanyl, Ketamine, Midazolam
Muscle relaxant 167
Suxamethonium 1-2 mg/kg
Consider rocuronium 1-2 mg/kg if suxamethonium contra-indicated i.e.
Burns patients > 48 hrs post injury
Spinal cord injury patients >72h injury or where spasticity is present
Some acute neuromuscular disease (e.g. GBS)
Hyperkalaemic states
Miscellaneous 168
Atropine 0.6-1.2 mg
Adrenaline 10 ml of 1:10 000 solution.
Phenylephrine 0.5 mg/ml (usually in 10 ml)
Procedure-Rapid sequence induction and orotracheal intubation 169
⋅ Pre-oxygenate for 3-4 minutes with 100% oxygen. Patients receiving non-invasive ventilation should continue on this form of
ventilation until the point of induction, and a PEEP valve applied to the AMBU-bag mask assembly.
⋅ Administer induction agent and suxamethonium
⋅ Apply cricoid pressure
⋅ Intubation under direct visualisation
⋅ Inflate ETT cuff until there is no air leak during ventilation
⋅ Confirm ETT placement with capnograph and chest auscultation with manual ventilation.
⋅ Release cricoid pressure
⋅ Secure ETT at correct length (Female = 19-21cm at incisors, Males = 21-23 cm at incisors)
⋅ Do not cut ETT
⋅ Connect patient to ventilator
⋅ Ensure adequate sedation and analgesia to cover period of muscle relaxant and continue as indicated by clinical scenario.
⋅ Insert naso-/-orogastric tube if not already present.
A follow-up CXR should be performed as soon as convenient.

Failed Intubation and difficult Airway Algorithm 170

Assess the likelihood and clinical impact of basic management problems
Difficult ventilation
Difficult intubation
Difficulty with patient co-operation or consent
Difficult tracheostomy
Actively pursue opportunities to deliver supplemental oxygen throughout the process of difficult airway management
Consider the relative merits and feasibility of basic management choices
Awake intubation vs. Intubation after induction of general anaesthesia
Non-invasive techniques as an initial approach vs. Invasive technique as initial approach
Preservation of spontaneous ventilation Vs ablation of spont vent.
Develop primary and alternative strategies
Awake Intubation 171
Awake intubation in the ICU setting occurs less commonly than in the operating theatre. An awake intubation in the ICU should be directed
by the duty ICU specialist, or directly delegated by the same. Intubation with the patient awake may be achieved by a variety of methods.
Establishment of a surgical airway is an alternative.

Failed Intubation 172

Approach to failed intubation

Consider
other
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Intubation attempts after induction of General anaesthesia

Success Initial attempts unsuccessful, consider

Calling for help
Return to spontaneous ventilation
Awakening the patient

Face-mask
ventilation Face-mask ventilation not adequate
adequate
LMA adequate
LMA
Not adequate
or feasible

Non-emergency pathway Emergency Pathway

Ventilation adequate Ventilation not adequate
Intubation unsuccessful Intubation unsuccessful

Alternative approaches to intubation: Call for help

Different laryngoscope blade
LMA as intubating conduit Emergency non-invasive vent:
Fibre-optic intubation Combitube
Stylette ot ETT exchanger Transtracheal jet vent.
Light wand Rigid bronchoscope
Blind oral or nasal

success
Fail after multiple Successful
attempts ventilation

Invasive airway Emergency invasive

access Awaken airway access:
patient
Maintenance of endotracheal tubes 173
Tapes 174
ETT are generally secured with white tape.
Tapes are changed daily or PRN by nursing staff.
In certain circumstances personalised ETT security may be required.
Cuff integrity 175
Sufficient air should be placed into the cuff to prevent an air leak, as assessed by auscultating over the trachea.
A technique which prevents cuff overinflation should be used.
Persistent cuff leakage 176
Any ETT that constantly requires additional air instilled into the cuff should be reviewed for:
Herniation above the cords
Cuff damage (rare)
Malfunctioning pilot tube valve (which can be excluded by placing distal pilot tube into container of water and observing for bubbling)
Airway suctioning 177
Airway suction is performed every prn.
Routine suctioning should be avoided especially where:
it requires disconnection of PEEP (open suction system)
May exacerbate the patient’s condition (asthma, reactive Intra-cranial pressure, florid pulmonary oedema).
Endotracheal tube change 178
Equipment and assistance 179
The procedure / setup is the same as for intubation de novo
Ensure patient is adequately oxygenated.
Ensure adequate anaesthesia and muscle relaxation

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Procedure 180
Perform direct laryngoscopy:
If a good view of the larynx and vocal cords is obtained then proceed to manual exchange of ETT with application of cricoid pressure, or
proceed as below using gum-elastic bougie
If direct laryngoscopy reveals abnormal or swollen anatomy, or only partial view of anatomy, then proceed as follows:
⋅ Place gum elastic or ventilating bougie through the ETT and insert to a length corresponding to a few cm distal to the end of the ETT.
⋅ With an assistant stabilising the bougie, and applying cricoid pressure, remove faulty ETT under direct laryngoscopy, while
maintaining bougie in the same position.
⋅ Confirm the bougie is still in place through cords once ETT removed, and then replace new ETT over the top of the bougie apparatus.
⋅ If the ETT does not progress smoothly through the cords, rotate 90 deg anti-clockwise and attempt again (i.e. Realign bevelled edge
of ETT along upper border of bougie)
⋅ Check position of ETT and secure as for de novo intubation procedure.
Extubation guideline 181
Ensure adequate assistance, monitoring and equipment as for intubation
Extubation should generally not be performed overnight if the responsibility to re-intubate might fall on a less experienced staff member.
Patients may be extubated if this action is part of an established care plan or algorithm (eg. cardiothoracic), or at the direction of the duty
specialist.
No patient should be extubated without medical staff being aware and available to assist.
Patient Selection 182
For a more extensive description see section on mechanical ventilation
The patient must be awake enough to maintain their own airway.
Any threat to airway patency as a result of surgery or injury may require consultation with the co-managing team (ENT or Plastic surgery)
prior to extubation.
Patient should demonstrate adequate pulmonary reserve. There are a number of ways of assessing pulmonary reserve although none is
perfect:
Resp rate < 30
FVC > 15 ml/kg
Pa02 / FiO2 ratio > 200
Resp rate / tidal volume 1 min after disconnection from ventilator (use T-piece )
The last method has the best predictive value.
Reference:
Walz JM et al. Chest 2007 ; (131):608-620.

Fibre-optic Bronchoscopy 183

Policy 184
Only to be performed by adequately trained staff, after authorisation by the duty ICU consultant.
Indications 185
Persistent lobar collapse that is refractory to normal bronchial toilet
Foreign body in airway
Diagnostic broncho-alveolar lavage (BAL)
Fibre-optic intubation

Cricothyroidotomy 186
Policy 187
The recommended procedure for urgent surgical airway access (not percutaneous tracheostomy)
When urgent surgical airway is required, call for help then proceed without delay.
Indications 188
Failed intubation drill
Inability to maintain an airway despite basic manoeuvres.
Equipment 189
Purpose made kits exist in the unit using direct access and/or a Seldinger technique. In the event of these not being available, the simplest
technique is described below.
# 15 scalpel and handle
Size 6.0 cuffed ETT
Oxygen delivery circuit and ventilation device (eg. Laerdal bag)
Procedure 190
Palpate cricothyroid membrane
Perform 2cm horizontal incision through skin and cricothyroid membrane
Insert blade handle into wound and turn vertically to enlarge wound (do not use blade or sharp instrument such as a pair of scissors)
Insert ETT into trachea
Connect oxygen circuit
Confirm correct placement with end-tidal CO2, auscultation, and if possible CXR.
Perform tracheal toilet as soon as adequate oxygenation achieved
Arrange definitive surgical airway as soon as possible.

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Tracheostomy-Percutaneous 191
Policy 192
Percutaneous tracheostomy is the preferred method for elective tracheostomy in suitable critically ill patients.
The decision to perform percutaneous tracheostomy rests with the duty ICU consultant.
Where appropriate the co-managing team should be consulted prior to performing the procedure.
Consent should be obtained as outlined in the unit guidelines.
Percutaneous tracheostomies may only be performed by experienced specialist staff or ICU vocational trainees under supervision.
Indications 193
as for surgical tracheostomy
Airway maintenance:
Prolonged intubation (> 10 days) or anticipation thereof.
Prolonged upper airway obstruction
Laryngeal pathology
Subglottic stenosis
Airway protection
Delayed return of glottic reflexes
Tracheal toilet / ineffective cough mechanism
Relative Contraindications 194
Elevated or unstable measured intra-cranial pressure
Coagulopathic state
Platelets < 100 000 (or abnormal function eg. following aspirin)
APTT > 40 sec
INR > 2.0
Renal failure with uncorrected uraemic state
Previous neck surgery
Unstable cervical spine injury
Unsuitable anatomy
Procedure 195
Percutaneous tracheostomy is commonly performed using two experienced operators
Anaesthetist / endoscopist: Responsible for administering a suitable anaesthetic and managing the airway.
Surgeon-operator
Equipment
Monitoring and drugs are as for standard endotracheal intubation, with the recommended addition of the fibreoptic bronchoscope.
Adequate lighting essential
Patient ventilated on 100% oxygen and a pressure controlled ventilation mode.
Equipment 196
A Cook kit using a “blue rhino” dilatational technique is standard. The guide-wire forceps technique using the Griggs forceps should only be
used by operators trained in this technique.
Tracheostomy tubes: The “Portex” tracheostomy tube is the standard tube used in this unit.
No patient should leave the ICU without the inner cannula being inserted prior to discharge in an effort to confirm patency.
Education and training 197
Senior Registrars and selected advanced trainees will be invited to learn how to perform percutaneous tracheostomies. This will involve
hands-on training with a skilled operator scrubbing alongside the trainee.
Airway management 198
Endoscopic confirmation of surgical technique is not practiced universally, but it is a useful adjunct to correct placement.
Method 1 199
⋅ Place the fibreoptic bronchoscope in the trachea beyond the distal tip of the ETT.
⋅ Under direct laryngoscopy retract the ETT (with deflated cuff) so that the cuff is above the vocal cords and inflate the cuff with 10-15
ml of air.
⋅ Use an assistant to secure tube in place and apply slight downward force on the ETT to maintain a seal to ventilate the patient.
⋅ Retract bronchoscope to a point proximal to planned tracheal puncture.
Method 2 200
⋅ Place the fibreoptic bronchoscope in the trachea beyond the distal tip of the ETT
⋅ Withdraw the ETT 2-3 cm with the cuff deflated, then reinflate cuff.
⋅ Request the surgeon-operator apply digital pressure over intended tracheal puncture site, and confirm this is distal to ETT tip and
bronchoscope.
⋅ Beware ETT puncture or bronchoscope damage.
⋅ Observe correct placement of needle-guidewire by Seldinger technique, and sequential dilatation.
⋅ Once tracheal tube in situ, connect to ventilator and insert bronchoscope into tracheostomy.
⋅ Confirm tip of tracheostomy clear of carina, and absence of ongoing haemorrhage.
Tracheostomy insertion technique 201
⋅ Position patient: 30 deg head up, with neck in extension but supported.
⋅ Adopt strict aseptic technique
⋅ Infiltrate with 10 ml of 1% lignocaine / 1:100 000 adrenaline over the pre-tracheal rings
⋅ Check trachy cuff, lubricate and insert dilator into trachy tube making sure there is a good fit.
⋅ Perform a 1-2cm incision over the 2nd tracheal ring.

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⋅ Dissect bluntly to fascia.
⋅ Insert sheathed needle catheter in to trachea at midline. Confirm placement by aspirating air and confirming with endoscopist.
⋅ Remove needle, and feed guidewire through sheath.
⋅ Remove sheath and dilate with mini-dilator.
⋅ Place white dilator -guide over sheath.
⋅ Proceed to dilatation with “rhino” (to appropriate size according to desired size tracheostomy)
⋅ Remove dilator and use guidewire to insert dilator and tracheostomy into the trachea.
⋅ Remove dilator and wire, inflate cuff and confirm placement with bronchoscope.
⋅ Secure with tapes.
⋅ Perform a control CXR if the procedure has been difficult or accomplished without bronchoscopy.
Complications 202
Haemorrhage (may be delayed as lignocaine / adrenaline wears off)
False passage, posterior wall tear
Loss of airway
Pneumothorax
Cricoid fracture (often tracheal ring fracture occurs as “normal part of procedure”)
Laryngeal dysfunction
Tracheal stenosis
Infection
Cuff leak (see cuff leak policy under intubation)
Dilatation of Murphy’s eye.

Nasojejunal tube insertion 203

Indications 204
Instillation of feed into the jejunum is an effective way of feeding patients with:
Prolonged gastric stasis ( > 3 days)
Gastric stasis resistant to treatment with pro-kinetic agents (erythromycin, metoclopramide)
Pancreatitis or other scenario’s where feeding distal to the duodenum is desired.
Procedure 205
⋅ Position the patient Rt side down to at least 45o, Remove any gastric tube.
⋅ Use a Corpak 10 Fr tube 140 cm long with stylet.
⋅ Close tube sideport and attach 3 way tap to flow through stylet hub.
⋅ Measure out Xiphisternum to ear plus ear to nose distance from the tip of the tube.
⋅ Insert tube to this distance, confirm intragastric placement by auscultation during air injection.
⋅ Administer 200 mg of erythromycin or 10-20 mg of metoclopramide as slow IVI “push”.
⋅ Inflate the stomach with 500 ml of air while the prokinetic is being administered.
⋅ Gently advance the tube. You should feel a steady resistance. If there is increasing then sudden loss of resistance this means you have
thrown the tube into a loop in the stomach. Withdraw the tube until resistance is felt and start slowly advancing the tube again. Insert
the tube to the 120-125 cm mark if possible.
⋅ Try to aspirate fluid from the tube. If fluid can be aspirated check the pH with a urine dipstick. An alkaline pH suggests duodenal or
further insertion.
⋅ Position the patient flat again and order an upper abdomen-lower chest x-ray.
⋅ Just before x-ray exposure inject 10 mls of contrast (Gastroview) down the tube.
Check tube position on x-ray.
If the tube is in a satisfactory position a gastric tube can now be inserted to decompress the stomach if this is desired.
Remember to leave the stylet in any fine bore tube during manipulation of the nasogastric tube. Keep the stylet in a plastic bag at the head of
the bed so it can be reinserted into the oesophageal and gastric segment of the fine bore tube during procedures such as NG tube or ET tube
removal to stiffen the fine tube and prevent its accidental partial removal.
Complications 206
Endobronchial placement
Other ectopic placement
Migration, kinking or knotting

Intra-abdominal pressure manometry 207

Policy 208
Renal perfusion pressure may be compromised by raised intra-abdominal pressure following:
Surgery
Trauma
Intra-abdominal pathology (eg: pancreatitis)
The occurrence of acute renal failure in an intensive care patient significantly increases the risk of adverse outcome.
The measurement of intra-abdominal pressures in patients that are at risk of developing abdominal compartment syndrome may allow renal
salvage in patients where there is a remedial cause.
A measured pressure of > 20 mmHg (referenced to the symphysis pubis) may precipitate acute abdominal compartment syndrome and renal
failure.
Procedure 209
⋅ Connect a 100ml bag of saline to a “metriset” which is then connected to a manometer. A 20G needle is then attached to the
manometer tubing.
⋅ Place patient supine

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⋅ Empty bladder
⋅ Clamp indwelling catheter distal to the culture aspiration point. Clean aspiration point with an alcohol swab and insert 20G needle
(prepared as above).
⋅ Inject 100 ml warmed sterile saline into patient’s bladder.
⋅ Open stopcock to transducer and allow 30 seconds to equilibrate.
⋅ Once pressure measurement completed, remove 20G needle from aspiration point, unclamp urinary catheter and allow free drainage
of the bladder.
Complications 210
Instillation of bacteria into the bladder
Triggering autonomic dysfunction (NB vagal) on injecting into the bladder, particularly if the bladder is incompletely drained.
Patient discomfort (if awake)
Artificially elevated readings due to bladder spasm or local pelvic haemorrhage may precipitate interventions that are associated with
significant morbidity.
Reference
Sugrue,M. Intra-abdominal pressure: time for clinical practice guidelines ? Intensive Care Med (2002) 28: 389-39 1.

Intra-Cranial Pressure Monitoring 211

Introduction 212
For expanded discussion on the role of ICP monitoring in the management of head injury and raised intra-cranial pressure refer
Neurosurgical guidelines (Chapter 6, section 6.5).
Insertion of an ICP monitor is generally performed by neurosurgical staff.
Procedure 213
⋅ Confirm valid indications for monitoring
⋅ With the head stabilised in a neutral position, select insertion site: usually mid pupillary line (commonly right side) and 3cm anterior
to coronal suture.
⋅ Shave the scalp, infiltrate with local anaesthetic (5 – 10 ml lignocaine with adrenaline).
⋅ Incise scalp sufficient to insert mini retractor.
⋅ Use drill to create a burr hole, using spacer guard to guide depth.
⋅ Remove retractor and using a Touhy needle burrow 2 – 3 cm medially under the galea.
⋅ Thread the micro-sensor from the tip of the Touhy towards the burr hole, remove the Touhy needle, leaving the sensor under the skin.
⋅ Insert the retractor again.
⋅ Puncture the dura
⋅ The microsensor should have been zeroed before procedure, or do it now !
⋅ Kink the micro-sensor at the require depth (generally 2 – 2.5 cm) so that the microsensor tip is within the cranial vault, and preferably
within brain parenchyma.
⋅ Insert sensor so that kink is flush with outer skull table. Retract excess cable subgaleally.
⋅ Bone wax may be useful in sealing the burr hole if desired.
⋅ Secure sensor to scalp. Additional strain relief can be provided by coiling excess line and suturing to scalp.
Monitor Set-up and Calibrating the sensor 214
⋅ Connect the microsensor to the ICP express cable without touching the transducer tip.
⋅ Place the tip of the microsensor just under the surface of sterile water placed in the microsensor pack tray.
⋅ Now switch on the unit.
⋅ Press the P›0 button on the panel. A reference number will appear. Record this in the patient records and on the white microsensor.
⋅ Press the menu button- an ICP reading should appear with an appropriate wave form.
⋅ Calibration with the main monitor can be performed at a suitable stage using the 20’ or100’ button as appropriate.
Complications 215
Apart from the procedure itself, infection remains the main risk. The manufacturers of the Codman system claim an infection rate of 1.5
episodes per 100 days use.

Jugular Bulb Oximetry 216

Introduction 217
Whilst not proven to affect outcome following severe head injury, jugular bulb oximetry may be useful in the monitoring and manipulation
of cerebral perfusion. See Chapter 6, Neurosurgical guidelines for further information.
Indications 218
Use is controversial.
Closed head injury, with:
GCS < 8
Injury less than 24 hrs old (relative)
ICP monitoring established
Procedure 219
⋅ Prepare using aseptic technique as for central line insertion.
⋅ Connect connect 3 way tap to catheter and flush with heparinised saline.
⋅ Cannulate internal jugular vein on side of maximal injury (or on left in case of diffuse injury).
⋅ Insert guidewire in retrograde fashion (i.e. towards cranial vault).
⋅ Using Seldinger technique insert introducer and “peel away” sheath.
⋅ Remove wire and introducer.

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⋅ Insert catheter until resistance is felt
⋅ Aspirate to confirm vascular placement and then flush catheter.
⋅ Secure with a tegaderm dressing without coiling catheter.
⋅ Confirm catheter position with a C-spine X-ray (tip opposite C1).
⋅ Continuous flush with hep saline at 3ml / hr.
Calibration 220
Continuous oximetric measurement of jugular bulb blood is not currently available in our ICU.Intermittent sampling may still be used to
measure saturation and lactate extraction.
Complications 221
As for central venous cannulation.
Thrombosis: approximately 40 % association within 3 days.
Poor reliability: readings from contralateral jugular vein may differ by as much as 15 %.

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Drugs and Infusions 222
Introduction 223
Most patients admitted to the ICU will have had medications prescribed for concurrent or pre-morbid conditions. A new chart for each drug
must be started on each patient’s arrival in ICU. Re-charting of all drugs implies an active review of the appropriateness of drug
administration and dosage, in changing clinical conditions.
It is important that drug charts are accurate, legal and legible. Use of drug trade names is not acceptable practice. Similarly only drugs which
are approved by the ICU medical staff may be given to ICU patients. For this reason only ICU medical staff may write (prescribe) in the
patient’s drug chart while the patient is in the ICU.
Charting of drugs by outside teams must be discouraged.
On discharge to the ward it is the responsibility of the discharging medical person to review patient drug and fluid orders.

Prescription practice 224

In general the following principles should be considered when prescribing any drugs for ICU patients.
A drug should only be instituted where the potential benefit is well described, or the risk for adverse effects low when benefit is unproven.
Unit protocols and guidelines should be used where these exist for a given drug.
ICU patients often have vastly altered drug pharmacokinetics (what the body does to the drug) and pharmacodynamics (what the drug does
to the body).
The role of therapeutic drug monitoring should be understood
Good drug prescribing practice is mandatory, including: Legible hand writing, use of generic (not trade) names for drugs, clear delineation
of dose, frequency and duration of treatment.
Prescribing in Pregnancy 4.1.2
Prescribing in pregnancy requires knowledge of teratogenicity and suitability for the fetus.
A website which can provide this information is www.tga.gov.au/docs/html/medpreg.htm

Cardiovascular Drugs 225

Inotropes 226
General Principles 227
In general the following rules should be followed where possible before instituting inotropic support.
Establish the presence of hypotension 228
Absolute: Systolic Blood Pressure < 90 mmHg
Relative: Systolic Blood Pressure decrement > 30 mmHg below normal for that patient.
Despite these definitions, we often quote mean arterial blood pressure (MAP) as being more relevant to organ perfusion. A MAP of > 60-70
mmHg would be considered adequate in most instances.
Organ perfusion 229
When hypotension is deemed to exist, assess organ perfusion:
Renal: urine output (minimum 0.5 ml/kg/min)
Cerebral: cognitive state
Peripheries (unreliable in septic patients)
Surrogate markers: eg Metabolic acidosis on a blood gas, measured lactate or venous oxygen saturation..
Assess and correct hypovolaemia 230
This simple concept is in practice very difficult to perform accurately. In the ICU there are a number of ways to assess intravascular volume
status although each has shortcomings.
Clinical assessment of fluid status including JVP
Variation of arterial waveform characteristics with mechanical ventilation.
Measurement of dynamic and static measurements CVP.
Blood pressure response to passive leg elevation
Right heart catheterisation.
Calculation of intrathoracic blood volume and extrapolation to extravascular lung water using PiCCO.
Echocardiographic techniques.
Except in very clear-cut cases (ie gross fluid overload or cardiac failure), in a situation where there is doubt as to the patients fluid status a
trial of fluid administration should be considered.Blood pressure response to passive leg elevation may be a useful predictor of fluid loading
without the risk of fluid overload.
Instituting inotropic therapy 231
Only once the above steps have been considered should inotrope therapy be considered.
No single inotrope (or mixture of inotropes) has been shown to be superior to another.
Please consult appendix on haemodynamic principles.

Catecholamines 232
Introduction 233
There is marked inter-individual variation in response to a chosen inotrope, due to:
Qualitative and quantitative changes in adrenergic receptor kinetics in both acute illness (sepsis) and chronic conditions (heart failure).
Underlying variability in disease state (ie cardiogenic shock, sepsis, hypovolaemia.)
Clinical Applications 234
Short notes on using common agents 235
Dopamine / adrenaline / noradrenaline: For ease of application many claim these three agents have a β-adrenergic action in low dose and a
progressive α-effect in increasing doses. Each however has a characteristic feature worth noting
Dopamine in low doses (2.5 µg / kg / min) has a direct diuretic effect which may result in increased urine volume; there is no evidence of a
reno- protective effect.
Adrenaline is a useful α / β-agonist, however it does have significant β2-effect which may result in unwanted metabolic effects
(hyperglycaemia, lactic acidosis).
Noradrenaline is generally held to have a predominant α-effect and is therefore useful as an inotrope-vasopressor, particularly in septic
shock.
Dobutamine, a synthetic inotrope, does not have significant α-effects (may have some myocardial α-effect) and is therefore useful in
increasing heart rate and stroke volume, but may cause a paradoxical fall in blood pressure due to peripheral β-adrenergic activity.
Adrenaline and noradrenaline, when mixed in ratio’s of 3 mg : 50 ml 5% dextrose will administer a dose in ml / hour equivalent to a dose of
micrograms per min. Individualising patient doses per kg is not a useful practice, but is traditionally used to quantify dopamine
administration.
Adrenaline and noradrenaline infusions should be started at 3-5 µg / min and titrated to response. Infusions of these agents require 3-5
minutes to achieve steady state. Changes in rate more frequently than every 3-5 minutes (unless in an emergency) should be discouraged as it
may lead to a “roller-coaster” effect.

Phosphodiesterase inhibitors 236

Phosphodiesterase inhibitors increase cAMP by non-adrenergic mechanisms. They are not therefore affected by down-regulation of
adrenoreceptors as occurs in sepsis or heart failure. For this reason milrinone is useful for refractory (ie following adequate volume
resuscitation) low cardiac output states.
They result in:
Increased myocardial contractility
Systemic and pulmonary vasodilatation (often requires co-administration of a vasopressor / noradrenaline)
Improved diastolic relaxation (useful in patients with diastolic heart failure)
Notes on pharmacology of milrinone 237
These drugs usually require a loading dose on commencement which may predispose to additional hypotension by virtue of vasodilatation.
The relatively long half-life of these agents requires forethought before administration, as their action is not easily reversed, and titration of
infusions to effect cannot be effected rapidly.
INOTROPIC AGENTS COMMONLY USED IN ICU TABLE 1
Agent Standard Infusion Indications
Adrenaline 1 mg / 50 ml D5W ratio. CPR
Severe sepsis syndrome / shock
Cardiogenic shock
Acute severe asthma (adjunct)
Anaphylaxis (correct hypovolaemia !!)
Medical Pacing (1st line drug)
Noradrenaline 4 mg / 50 ml D5W ratio Conditions where mixed -/ -effect is required with a predominant -
(ml/hr = g / min) effect
Multiples of base dose may be used ie. septic shock
Dopamine 200 mg / 50 ml D5W No advantage over adrenaline or noradrenaline
(ml/hr approximates g / kg / min in 70kg person) May induce more tachycardia than adrenaline (through stimulation of D-
receptors)
Not reno-protective, but may have direct diuretic effect.
Dobutamine 250 mg / 50 ml D5W Pure  adrenergic agent used in low cardiac output / high vascular
(ml/hr = g / min) resistance states.
Effect may be diminished in sepsis and chronic heart failure due to down
regulation of receptors.
Levosimendan 12.5 mg in 500ml 5 % dextrose. Ionotrope, predominantly by Ca2+ sensitisation of myocardium.
Run at 0.05 to 0.2 µg/kg/min until bag empty (approx 24 Recommended loading dose (up to 24 µg/kg in 10 min) often omitted or
hrs). given more slowly

Milrinone Loading dose: Cardiogenic shock due to diastolic failure

12.5 - 50g / kg over 20 min Pulmonary hypertension following cardiac valve replacement.
Infusion: Rescue following catecholamine induced down regulation of receptors in
10 mg / 50 ml D5W (200ug / ml) patients requiring ongoing chrono-inotropy.
in fuse at 0.375 – 0.75 ug / kg / min. These agents may accumulate in renal failure
(8-15 ml / hr in 70 kg pt)

Vasopressor agents 238

Introduction 239
Noradrenaline is the vasopressor of choice in the ICU. Indirect acting agents such as metaraminol and phenylephrine should generally be
restricted to peri-operative practice where temporary vasodilatation results from specific intervention (spinal, epidural, local block)
General principles 240
These agents are used primarily to induce vasoconstriction and thus elevate blood pressure.
They may increase cardiac afterload and thus cardiac wall stress
These agents should not be used to treat hypotension due to hypovolaemia.
Indications 241
Hypotension following sympathetic block (epidural anaesthesia), where vasodilatory effect is likely to be temporary, and excessive fluid
administration is not recommended.
Hypotension resistant to catecholamine use (ie. vasopressin).
Complications 242
Rebound hypertension
Vagal response (with possible bradycardia)
Tachyphylaxis
VASOPRESSOR AGENTS COMMONLY ENCOUNTERED IN ICU TABLE 2
Agent Standard Infusion Indications
Phenylephrine 10 mg made up to 50 ml 5 % dextrose. Start Predominantly used in anaesthetics for short periods of predictable hypotension
infusion at 5 ml / hr. Titrate to BP at 1 – 10 ml associated with epidural or spinal anaesthesia.
/ hr
Ephedrine IVI:30 mg / 10 ml D5W titrated to effect IVI No longer commonly used outside operating theatres.
(1-3 mg).
Oral: 25-50 mg 8hrly po.
Vasopressin 20 units / 40 ml D5W at 2.0 ml/hr (approx Catecholamine resistant hypotension-limited availability
=0.04 units / min) Efficacy appears to be above a given threshold and not linear – “do not titrate” to
effect.

Steroid use in patients requiring vasopressors: 243

Following the Corticus study, it is generally accepted that steroids have a li mited role in septic shock.

Anti-hypertensive Agents 244

General Principles 245
Elevated blood pressure should be viewed in the context of each patient, and should include an appraisal of pre-morbid blood pressure.
Acute hypertension in the intensive care should not elicit direct treatment, but rather a review of the cause of blood pressure elevation:
Elevated blood pressure is commonly seen in patients who are agitated, delirious, or who have some other cause for overt sympathetic drive.
This should be addressed with analgesia and sedation where appropriate. A dual purpose drug such as an α 2-agonist (clonidine or
dexmedetomidine) may be useful.
Hypertension in the setting of intracranial pathology may be self limiting. No attempt should be made to actively lower elevated blood
pressure with anti-hypertensive agents unless cerebral perfusion pressure is not threatened. Vasodilators may increase intracranial pressures
further while dropping cerebral perfusion pressure to dangerous levels.
Indications 246
Acute
Peri-operative control of hypertension post-cardiac, carotid or other vascular surgery, or for patients with critical myocardial
ischaemia. In this instance target blood pressures should be discussed with the surgeon involved, and confirmed with the Duty ICU
Specialist.
Accelerated hypertension: “Malignant Hypertension”
Hypertensive Proteinuric Pregnancy states (Eclampsia)
Active Phaeochromocytoma (NB: always preceed β-blockade with alpha blocker)
Non-hypertensive indications
Reduction of afterload in cardiac ischaemia and failure
Decrease ΔP / Δt in patients with aortic dissection
Complications 247
Hypotension
Tachyphylaxis
Cyanide Toxicity-Sodium Nitroprusside
Pulmonary vasodilatation causing increased pulmonary shunting and hypoxia
VASODILATORS AND OTHER ANTI-HYPERTENSIVE AGENTS IN THE ICU
Agent Dose Uses
GTN (glyceryl tri- 50 mg in 50 ml. Use non-PVC giving set. Venodilation > arterial. Unpredictable hypotensive effects.
nitrate) Range 1-20 ml / hr (0-20 mg / hr) Useful in cardiac ischaemia (no proven effect on outcome)
Tachyphylaxis when used > 24hrs
Sodium Nitroprusside 50 mg / 50 ml D5W. Rapid control hypertension by direct arteriolar action.
Range 0- 20 ml / hr IVI Cyanide toxicity may be seen at total dose > 1.5 mg/kg/24hrs
(tachyphylaxis and metabolic acidosis)

Captopril Dose 6.25-50 mg up to 6 hrly po After load reduction / anti-hypertensive

Syrup 5 mg/ml also available for smaller dose adjustment Dose adjustment required in renal failure
May aggravate renovascular insufficiency
Beware first dose effect ( BP > expected).
Enalapril 2.5-40 mg daily po Longer acting than captopril, only use once patient stable, or captopril
therapy established.
Amlodipine 5-10 mg daily po Long acting dihydropyridine Ca channel blocker.
Use as anti-hypertensive in stable patients (not anti-arrhythmic)
Labetalol Bolus: Non-selective -blocker, some -blocker activity.
5 mg bolus. No faster than 20- 50 mg over 1-5 min. ( < Useful in bolus temporising treatment of acutely elevated blood pressure.
300 mg / d) Not shown to increase ICP in head injured patients (unlike GTN and
Infusion: Nitroprusside)
200 mg in 40 ml D5W, infuse at 5 – 30 ml / hr (25 – 150
mg / hr)
Atenolol 25-100 mg bd po Useful in blunting sympathetic overdrive
( Head injury, agitation, thyroid crisis)
Renally cleared, reduce dose in renal failure.
Use all -blockers with caution in patients with asthma or peripheral
vascular disease
Avoid concomitant use with Calcium channel blocking agents
Metoprolol Oral: 47.5 mg – 190 mg per day in 1 –2 doses (CR Commonly used β-blocking agent
formula). Metabolised by the liver, useful in conditions where renal function
NG: 25 – 200 mg / day in divided doses uncertain or deteriorating
IVI: 1-5 mg slowly up to 15 mg.
Esmolol Bolus: 0.25 – 0.5 mg / kg IVI Ultra short acting -blocker used in cardiac surgery, and where a short trial
Infusion: 50 – 200 ug / kg / min. (2.5 g in 50 ml D5W = of the patients ability to tolerate a negative inotrope is useful
50 mg / ml)
Clonidine Bolus: 150g diluted in 10 ml NS, administer 1-5 ml IVI Centrally acting 2-agonist.
prn Useful in peri-operative centrally mediated hypertension, with anti-
agitation benefits.
Hydralazine 10-20 mg as a bolus IVI Direct acting arterial vasodilator
20-40 mg 6-8 hrly Mild positive inotrope but often associated with a reflex tachycardia.
Very rarely administered as an infusion 1.5-5.0 g / kg / Half-life 4-6 hrs - Metabolic slow acetylators at risk to develop Lupus
min in cardiac surgery. (not recommended by Syndrome with prolonged use, or dose > 200 mg / day.
manufacturer)
Methyldopa 250 mg - 2 g / day bd po Traditional agent still useful in gestational proteinuric hypertension
MgSO4 Bolus: 10-20 mmol IVI slowly (may cause sensation of Gestational proteinuric hypertensive states (“eclampsia”)
flushing, and hypotension) Torsades
Infusion: 40 mmol in 500 ml of D5W 6 hrly IVI Phaeochromocytoma,
? Status Asthmaticus, siezures
Beware of hot flush on administering IVI bolus in awake patients.
Toxicity: monitor for “weakness” in non-ventilated patients: ie falling
respiratory rate and loss of deep tendon reflexes.

Antiarrhythmic Drugs in Critical Care 248

General Principles of Treatment 249
In therapy of arrhythmias, prior consideration should be given to causal or aggravating factors:
Hypoxæmia
High, occasionally low, pH
Hypokalæmia, hypomagnesæmia
Pre-existing drug effects or toxicity (including bronchodilators and inotropes)
Presence of right heart lines (including pacemakers)
Myocardial or coronary compromise, especially pulmonary œdema
The need for therapy should be carefully evaluated. For instance atrial tachyarrhythmias with a ventricular response similar to that of the
preceding sinus rhythm need not be slowed down or abolished at the cost of additional hypotension. Reperfusion VT associated with
myocardial infarction (fascicular or otherwise) or non-paroxysmal junctional tachycardia (NPJT) at 130 / min may be as acceptable as sinus
or junctional bradycardia at 40 / min and equally self-limiting.
Non-pharmacological therapy should also be always considered-if only to be dismissed, as in the case of precordial thump for VT (repeated
thumps for pacing asystole may be OK). In patients with permanent pacemakers, a magnet may abolish both VT or SVT by fixed overdrive
pacing; post-CABG patients with temporary wires may be more reliably overdriven. DC cardioversion is always available.
The value of precise diagnosis is increasingly deconstructed by the likes of sotalol or amiodarone. Still, as a general rule, if antiarrhythmics
are to be used, a 12-lead ECG should be obtained.
Arrhythmias can only be defined electrocardiographically. On the other hand, a full ECG obtained on a pulseless patient is medico-legally
indefensible.
In many ICU patients the need for continued therapy ceases as they improve and the drug-often the ubiquitous amiodarone-can be stopped.
Reference:
Throhman RG, Parillo JE (Eds). Arrhythmias in the critically ill patient. Crit Care Med 2000; 28(10): Suppl

Drug Therapy of Bradyarrhythmias 250

Pacing is preferred, but there are clinical situations when pacing is either impracticable or fails. A number of drugs have some utility in the
setting of bradycardia – bradyarrhythmia.
Adrenaline 251
A mixed β- / α- agonist, adrenaline has declined in popularity mainly due to its metabolic side effects mediated by β-receptor stimulus
(increased lactic acid production, hyperglycaemia). In emergency situations where bradycardia is asscciated with hypotension and patient
compromise adrenaline remains the first line agent, at least in the short term.
Atropine 252
Alkaloid from Atropa belladonna, competitive acetylcholine antagonist at post-ganglionic parasympathetic endings. It comes in 0.6 mg
ampoules.Doses smaller than 0.6 mg in an adult may paradoxically cause bradycardia.
Its vagolytic action is useful in the very early stages of (usually inferior) myocardial infarction complicated by significant bradycardia or
block; later stages of AV block are more likely to respond to aminophylline. Intraventricular, Möbitz II block is made worse. Escape-capture
bigeminy may be replaced by slower 2:1 block.
It may also be used in reflex bradycardia associated with upper airway manœuvres, such as suctioning.
In brady-asystolic cardiac arrest, it is next to useless.
Isoprenaline 253
Isoproterenol is a “pure” ß agonist producing marked vasodilatation and cardiac stimulation; these actions have long ago necessitated its
replacement by selective ß-2 bronchodilators in asthma. It is sometimes used for:
3o or advanced 2o AV block as a bridge to pacing;
to promote tachycardia and shorten the QT interval, against potential or manifest torsade de pointes. Here, too, pacing offers greater
flexibility and stability.
Aminophylline 254
o o
It may be indicated for symptomatic 2 or 3 AV block in later stages of inferior myocardial infarction, as mentioned above.

Supraventricular Arrhythmias 255

Some agents control the ventricular response through AV blocking action, some interrupt the reentry circuit and abolish the paroxysm; many
do both.
Adenosine 256
Endogenous adenosine production is enhanced by ischæmia and it may well be the mediator of sustained AV block following inferior
infarction. Its half-life is only 0.6-1.5 sec, requiring larger dose with peripheral access, e.g. 6 mg where 3 mg given centrally would do.
In SVT, both AV nodal and non-nodal re-entrant tachycardias (AVNRT and AVRT), the slow pathway is blocked and cycle length alternans
may occur. With incremental doses, over 90 % effectiveness is seen. The response can also be used to differentiate broad complex tachycardia
due to aberrancy from its ventricular look-alike, even though adenosine-sensitive VT needs consideration.
Chest pain induced by adenosine, like that of dipyridamole, can be severe; other side effects include flushing, headache, dyspnœa and cough.
Sinus bradycardia or arrest and ventricular arrhythmias are frequent, but almost never actionable. AF or flutter may follow cardioversion of
SVT; they are less durable than with verapamil. SVT recurs early in 10-30% of cases.
Indications for adenosine 257
Narrow complex tachycardia: Adenosine may be the drug of choice in investigating and or treating such arrhythmia. It may terminate AV-
nodal and AV re-entry tachycardia, or reveal underlying atrial flutter or fibrillation.
Broad complex tachycardia: Adenosine may terminate SVT with intra-ventricular conduction block. It will not cardiovert true VT. It may be
useful therefore in treatment of regular broad complex tachycardia not thought to be of ventricular origin.
Dose:
Adults: Incremental 3 mg, 6 mg, 12 mg, 18 mg. Given via large peripheral or central vein followed by saline flush. Some practitioners use
6mg as first dose.
Please be aware that administration of adenosine may cause the patient to feel very unwell (“hot, flushed, nauseous”) and you should warn
the person beforehand if possible
Reference:
Ganz LI, Friedman PL. Medical progress: Supraventricular tachycardia. N Engl J Med 1995;332:162.
Verapamil 258
Verapamil inhibits the slow inward Calcium channel and blocks the slow antegrade pathway in AVNRT; it stops AVRT by AV block. Its effect
on SVT should be apparent within three minutes. If a 1-5 mg bolus (tailored to age and co-morbidity) is ineffective, a bigger (5-10 mg) dose
10 minutes later is recommended. Before adenosine, verapamil was the drug of choice in treatment of SVT.
It can be used to slow the ventricular response in AF, but this is rarely done now. It remains quite useful for the same purpose in multifocal
atrial tachycardias (where atrial rate may also be slowed), usually as an infusion.
Hypotension may be a problem. It is obviated by preceding the bolus by 5 mmol of Calcium; there is no loss of anti-arrhythmic activity.
Verapamil should be given slowly in patients with known myocardial disease.
Other side effects are similar to those of adenosine-sinus pauses, bradycardia and occasionally AF. Unlike adenosine, it should never be
given to diagnose a broad-complex tachycardia: cardiogenic shock or cardiac arrest may result.
Amiodarone 259
This is currently the drug of choice for AF with rapid response in the ICU, given as a 5-10 mg/kg loading dose over 20 – 60 minutes
(occasionally bolus) and followed by 1200 mg / day infusion. Its advantage over digoxin is the rapid (within one hour) control of the
ventricular rate; unlike digoxin, it may aid return of sinus rhythm. It is also quite successful for cardioversion of SVT although it is rarely
used for this purpose
Acutely, amiodarone blocks the AV node (prolonging the PR interval in sinus rhythm); there is no immediate effect on the sinus rate, QRS
duration or QT interval. It prolongs action potential and lengthens the effective refractory period throughout the heart; hence slowing of the
sinus rate and prolongation of the QT interval follow.
Amiodarone is best given via a central vein as it causes severe thrombophlebitis. Other side effects are flushing, nausea and transient
hypotension. In patients with LV dysfunction, overt failure and shock may occur. In these patients it is wise to omit the bolus and start with
an infusion.
Long-term side effects are serious and well known; they are rarely of great moment in the ICU.
Flecainide 260
It slows the phase zero of the action potential, interfering with the fast inward Sodium current; it depresses the diastolic repolarisation. The
action potential is not prolonged-hence its 1C classification. PR, QRS and QT are prolonged.
It is a potent “PVC killer” but has suffered greatly in the CAST trial: its pro-arrhythmic propensity precludes its long-term use in post-MI
patients. The bad reputation has spread. This has little to do with its benefits in the ICU, where it remains the drug of choice for both SVT
and AF & flutter in patients with WPW syndrome. It slows conduction in the atrium. It is also a good drug for pharmacological cardioversion
of AF and flutter in patients with normal conduction. Its pro-arrhythmic effects are of less moment in continuously monitored ICU patients.
Preferred dose in the ICU = 150 mg in 5% dextrose IVI over 30 minutes.
One important side effect is the elevation of the pacing threshold; the patient may become un-paceable. This limits its use in the pacemaker-
dependent post-CABG patients. Flecainide is a “consultant only” restricted drug in New Zealand.

Ventricular Arrhythmias 261

The pharmacological therapy is mostly concerned with treatment of VT and prevention of VF. Isolated VEBs, accelerated idiofocal rhythms,
escape beats or parasystole are usually treated by mistake.
Lignocaine 262
Lignocaine has for a long time been the drug of choice for the emergency treatment of ventricular arrhythmias.
Its great advantage is its relative lack of toxicity; its equally great disadvantage is the frequent (80-90%) ineffectiveness in VT.
The toxicity is mostly on the CNS, with slurred speech, twitching and seizures; a rare change in intraventricular conduction is usually trivial,
but interesting.
The standard dose is 75 mg, followed by 2-4 mg / min infusion in 5% D.
Amiodarone 263
The drug is effective for sustained monomorphic VT and has some activity in VF. It is the drug of choice for VT in ICU.
Sotalol 264
Sotalol, in addition to its amiodarone or bretylium-like class activity, is also a non-selective ß blocker (in its l-isomer). It prolongs QT and
PR intervals and appears to produce more episodes of torsade de pointes than amiodarone (but probably less than flecainide). It is excreted
unchanged in the urine.
A loading dose is 0.5-1.5 mg/kg over 10 minutes, followed by infusion of 0.2-0.4 mg/kg/hour in 5% D or by oral tablets. It is a significant
negative inotrope; some VT patients in the emergency department setting had to be shocked “at the end of the needle”. A lower initial dose is
prudent. Other side effects, like asthma, are shared with ß-blockers. On the other hand, the ß blockade is a reason for its being the drug of
choice for VT in patients with IHD.
Its use in the treatment of supraventricular tachycardias is not recommended.
Magnesium 265
A major indication is true torsade de pointes VT, where 2-4 g bolus is followed by 3-20 mg / min infusion.
Polymorphic VT with normal preceding QT is usually seen in the setting of acute ischæmia and responds to magnesium with the same
frequency as sustained monomorphic VT- very rarely. Amiodarone, ß-blockers and urgent revascularisation are the best strategy here.
Procainamide 266
Its effects are very similar to those of quinidine; it is a Class 1A Sodium channel blocker, prolonging the QRS complex (25 % “effect”, 50%
“toxicity”) and the QT interval. It is less vagolytic than quinidine and has little, if any, ganglion-blocking properties.
Dose:
loading dose: 1 g in 50 cc 5% D (20 mg / cc) at 10-20 mg / min.
Alternatively, 100 mg boluses over 1 minute can be repeated at 5 min intervals, watching the BP.
It is quite effective drug for VT and probably most effective of all drugs to slow down the conduction by an anomalous pathway in WPW, AF
or flutter. It is rarely used; part of the problem is the relatively long time (20 min) to load an effective dose.
Phenytoin 267
Beside KCl, diphenylhydantoin is the drug of choice for VT caused by digoxin toxicity; it is also effective for digitalis-induced paroxysmal
atrial tachycardia with block, but less so for non-paroxysmal junctional tachycardia. It is best given, like procainamide, as 100 mg boluses
every 5 min; the usual antiarrhythmic dose is approximately 700 mg (beyond 1000 mg it is unlikely to succeed).
COMMONLY ENCOUNTERED ANTIARRHYTHMIC AGENTS
Agent Administration Uses
Amiodarone Acute: Drug of choice for AF with rapid ventricular response.
5 mg / kg (commonly 300 mg) IVI over 30-60 Drug of choice in ICU for ventricular tachycardia
minutes. May have some effect in treatment of ventricular fibrillation.
Followed by 1200 mg over the remainder of the Highly irritant given IVI into peripheral veins
next 24 hours. Diverse and relatively common side effects with prolonged use.
Chronic: decremental dosing.
200 mg 8hrly po for 1 week.
200 mg 12 hrly po for 1 week
200 mg daily po as long as required.
Magnesium 5-10 mmol IVI slow bolus Best proven indication in torsade de pointes.
(1 ampoule = 10 mmol = 2.5 g) Probably works by physiological Calcium antagonism
May be helpful in treatment of some supra-ventricular tachycardias, such as
multifocal atrial tachycardia.
Low risk-benefit profile

Adenosine Incremental dose IVI until desired effect: Drug of choice in version of AVNRT and AVRT.
3 mg  6 mg  12 mg  18 mg Useful diagnostic / therapeutic test to differentiate broad complex tachycardia
(SVT with aberrant conduction versus true VT)
May induce short period of sinus bradycardia or even arrest-almost never requires
intervention.
Verapamil Bolus: Prior to adenosine was drug of choice for AVNRT or AVRT.
5 mg IVI Rarely used as rate control agent in AF.
if ineffective follow with 10 mg 10 minutes later. Should not be used to diagnose a broad complex tachycardia as adenosine may.
Consider alternative agent in the presence of severe left ventricular dysfunction.
Digoxin Loading dose: May assist in rate control for stable patients with CCF.
0.25 to 0.5 mg  3 doses, 4 hours apart. Narrow therapeutic range.
Total dose 1.0-1.5 mg Long half life.
IVI or PO Difficult to use in acutely ill patients and those with renal impairment.
Minor positive inotropic effect

Respiratory Drugs 268

Nebulised bronchodilators 269
General principles 270
These agents are used in the treatment of bronchospasm in Intensive Care (including acute severe asthma).
These agents do not necessarily need to be delivered by nebuliser, but can be administered as a metered dose inhaler into the appropriate port
on the inspiratory limb of the ventilator circuit.
Once these agents have been commenced they should be reviewed daily or more often, as is the case with all prescribed drugs. This is
usually assessed by improvements in audible wheeze, lung compliance, respiratory rate and blood gases.
Indications 271
Pre-existing obstructive airways disease where reversibility is suspected
Acute severe asthma
Acute exacerbation of obstructive airways disease
Parenteral Therapy in treatment of reversible obstructive airways disease 272
Indications 273
Adjunctive therapy for acute severe asthma in patients not responding to nebulised agents
Complications 274
Hypokalaemia, metabolic alkalosis
Arrhythmias (theophylline)
Intercurrent infection
Polyneuropathy
Lactic acidosis (β2-stimulants)

DRUGS COMMONLY USED TO TREAT ASTHMA AND AIRWAY OBSTRUCTION

Drug Infusion / dose Clinical uses
Salbutamol Nebulised in N Saline (5 mg:1ml) First line bronchodilator
Continously, 2 or 4 hourly Acute or chronic airway obstruction
Asthma
Adjunct in severe hyperkalaemia
Ipratroprium Nebulised (500ug) alone or in addition to Salbutamol Chronic airflow obstruction (CAO)
Administered qid or rarely q4h Bronchorrhoea
 Budesonide Nebulised 1 mg bd Steroid dependent obstructive airways disease
(nebulised steroid)
Adrenaline 1 mg / 50 ml 5% dextrose Acute severe asthma
(= 20 g / ml) Rapid onset an d offset of action
Titrate until demonstrate pressor response
(may require up to 100 g / min)
Salbutamol 3- 20 g / kg / hr in 5% dextrose Acute severe asthma
IV infusion (usual adult dose 0.5 – 1.0 mg / hr) Longer duration of action
Hydrocortisone 100 mg IV 4-8 hourly All patients with acute severe asthma;
wean off over 48-72 hrs once broken
2. Steroid dependent COPD
Theophylline 1000 mg / 100 ml 5% dextrose No longer 1st line drug.
Intra-venous infusion Loading: 5-7 mg/kg over 30 minutes to an hour. Omit if patient May improve respiratory drive in COPD
normally on theophylline. Narrow therapeutic index: proarrhythmic
Maintenance: infusion 2-4 ml/hr (0.6-0.9 mg/kg/hour or max 1 Levels no longer able to be measured at Waikato Hospital.
gm / day)
Levels: 55-110 mol/L

Sedation 275
Introduction 276
Historically patients in intensive care were heavily sedated and often paralysed. As modes of ventilation have evolved, it has become
desirable for patients to be more neurologically accessible. Anxiolysis and analgesia, not sedation, are the primary goals in the management
of the critically ill patient.
Pain and anxiety are associated with significant adverse physiological responses:
Sympathetic activity
Intracranial hypertension
Gastritis and gastric erosion
Excessively catabolic state.
This needs to be weighed against the adverse effects associated with over-sedating a patient:
Respiratory depression
Prolonged ventilation and associated risk of nosocomial infection.
Eventual emergence phenomena with sympathetic overdrive, delirium and withdrawal.
Hypotension
Gastroparesis
Prolonged stay with unnecessary use of resource, and increased risk of complications.
Approach to analgesia 277
No patient should be required to endure excessive pain.
If the patient is awake and alert consider in step-wise fashion the following:
Regular paracetamol
Codeine preparations (with or without paracetamol)
Non-steroidal anti-inflammatory drugs unless contra-indicated. (ie bleeding diathesis, gastric ulcer / erosion, renal dysfunction).
Patient controlled analgesia (PCA-see later section)
Where the patient is unable to co-ordinate the PCA mechanism, bolus analgesia should be administered by the nursing staff, titrated to the
patients request for pain relief.
In exceptional circumstances an infusion of narcotic may be appropriate.

Approach to Sedation 278

Patient sedation should be goal-directed. Generally sedation should fall into one of the categories listed below:
Patient and nursing safety in the event of patient agitation: To enable effective care to be delivered and prevent occurrence of accidental
extubation or removal of vascular access catheters.
Treat unacceptable treatment-related distress
Where agitation or restlessness compromises patient haemodynamics.
To facilitate ventilation or minimise patient-ventilator dysharmony.
Control intra-cranial pressure.
Reduce metabolic rate (oxygen consumption) and sympathetic drive.
In mild cases adequate sedation can be administered by regular and / or “prn” administration of one or more of:
Haloperidol 2.5-20 mg 6 hrly (PO / NG / IVI) ±2.5-10 mg prn IVI
Clonidine 50-200 µg 6-8hrly PO ± 15-30 µg prn IVI (max 600 µg / day)
Diazepam 2.5-10 mg 8rly (PO / NG / IVI) ± 5-10 mg prn IVI
Where an infusion is deemed necessary, this should be goal directed with a sedation end-point specified according to a designated sedation
score. ( See appendix – Sedation-Agitation score)
All sedation in patients with a sedation score of – 2 or – 3 should be stopped at 07h30 everyday to allow neurological assessment
unless doing so would expose the patient to excessive risk as determined by the Medical Staff (eg: sedation for ICP control)
In the Waikato Hospital ICU, propofol ± bolus opioid or infusion of short acting opioid, is the first line sedative agent where an infusion is
required.
COMMONLY ENCOUNTERED SEDATIVE AGENTS AND OPIOIDS IN ICU
Drug Infusion / Dose Clinical uses
 Propofol 10 mg/ml (neat solution), Short term sedation of intubated and ventilated patients.
Start at 3 ml/hr and titrate against effect Anaesthesia for minor procedures where prompt return of consciousness is required (eg
Max dose < 5mg/kg/ hr tracheostomy, CVC)
Potential myocardial depressant and vasodilator
No analgesic effect.
Midazolam Bolus: 1-5 mg prn IVI Review rate / sedation daily or more often
Infusion: Midazolam 60 mg in 60 ml 0.9% Effects prolonged in renal failure
saline: 1-15 ml/hr Anticonvulsant
Morphine Bolus: 0.5-5 mg IVI prn, or PCA. First line analgesic
Infusion: Morphine 60 mg in 60 ml 0.9%
saline at 1-10 mg/hr
Fentanyl Bolus 12.5-200 g IVI Haemodynamic stability
Infusion: 500 g in 50 ml. At 10 –200 ug / hr Potent medium acting narcotic
(1-20ml) Used for procedures in ventilated patients
Useful in patients with renal failure where the active metabolites of Morphine may pose
a sedative risk
Diazepam 2.5-20 mg IVI / po prn Antoconvulsant
Dexmed-etomidine Loading dose: 1  g / kg over 10 min. Selective -2 agonist causing sedation and analgesia.
Infusion: 0.2 – 0.7 g / kg / hr Dose related hypotension limits effective loading dose (often omittted)
(make up 4 g / ml sol in 50 ml syringe) Useful in agitation states where some analgesia is required but airway reflexes relatively
maintained.
Haloperidol 2.5-10 mg IV prn First line major tranquilliser, use for delirium, agitation esp. in opioid / benzodiazepine
withdrawal.
 blocker: hypotension
Chlorpro-mazine 5-10 mg IV prn, or 50 mg / 50 ml D5W @ 1- As for haloperidol; 2nd line tranquilliser
10 ml/hr More sedating, unpredictable & longer acting agent
Potential for marked hypotension esp given IV

Approach to muscle relaxants in the Intensive Care Unit 279

Introduction 280
Muscle relaxant use in the intensive care setting is to be discouraged unless specifically indicated.
There is no circumstance where a patient should receive muscle relaxant without covering sedation where the possibility of consciousness
exists. Where doubt exists with regard lingering effects of muscle relaxant, this should be confirmed with a nerve stimulator, prior to
stopping sedation.
The indications for using muscle relaxants in ICU are limited to:
Endotracheal intubation and acute control of ventilation post intubation
Patient transport
Selected patients with complicated ventilatory parameters
Facilitate acute procedures: tracheostomy, bronchoscopy.
In selected patients with severe head injury and uncontrolled intra-cranial pressure.
Complications 281
Hyperkalaemia (suxamethonium)
Polyneuropathy and myopathy
COMMONLY USED MUSCLE RELAXANTS IN THE INTENSIVE CARE
Relaxant Dose Comment
Suxamethonium 100-200 mg Consider pre-treatment with atropine (0.6-1.2 mg) if potential bradycardia and always with
or second dose.
1-2 mg/kg Contraindicated in burns ( > 3 days post burn), chronic spinal and neuromuscular
syndromes, hyperkalaemic states (K  5.5)
Vecuronium 2-8 mg IVI Firstline non-depolarising agent
No real advantage over pancuronium, although less tendency to cause tachycardia.
Repeated dosing leads to accumulation and increased risk of myo-/ neuropathy.
Atracurium 0.5 mg / kg IVI Clearance independent of renal or hepatic metabolism
Rocuronium 0.6 mg / kg IVI Rapid onset (60 secs) non depolariser
Duration of action: 30-40 minutes
Used as alternative to suxamethonium for emergency intubation

Anticoagulation 282
General Principles 283
Anticoagulation in critically ill patients is a challenging issue, with patients at risk of bleeding diatheses as well as hypercoagulable states.
Often a single patient will move through a state with a high risk of bleeding (including surgical sites) to one of high risk of developing
venous stasis and thrombosis. The decision to administer anticoagulation is often based on a relative risk-benefit assessment.
Where anticoagulants are contra-indicated, alternative methods should be employed to prevent venous stasis in the lower limbs (graded
compression stockings and sequential calf compressors), although it is unclear as to whether these confer adequate protection against
thrombosis and embolisation.
As a general rule heparin infusions should be used to effect anticoagulation, titrated intravenously to a therapeutic APTT where this is
required, or administered subcutaneously for DVT prophylaxis. Low molecular weight heparins may require measurement of anti-factor Xa
to quantify effect, and are more difficult to reverse than unfractionated heparin.
Where any doubt exists with regard the use of an anticoagulant in a given surgical or trauma patient, this should be confirmed with the
Surgeon involved.
Indications for the use of warfarin 284
Post operative prosthetic valve (According to cardiothoracic guidelines)
Previous thrombo-embolism: Selected cases only
Maintenance of thromboprophylaxis in selected high risk patients only
Indications for the use of heparin 285
DVT prophylaxis (LMWH)
Proven venous or arterial thrombo-embolism
Myocardial ischaemia syndromes
Prosthetic heart valves
Prior to commencing oral anticoagulants
During an acute illness where oral anticoagulation is unsuitable
Atrial Fibrillation-sustained
Intra-Aortic Balloon Counterpulsation: (See guidelines on IABP. Heparin use not routine).
Continuous Renal replacement therapy (See below)
Prophylactic use of heparin 286
DVT prophylaxis should be commenced within 24- 36 hrs of admission to the ICU. Low molecular weight heparin is generally considered as
safe, and in some instances marginally superior (eg. orthopaedic patient populations) to unfractionated heparin. Enoxaparin (Clexane) is the
chosen LMWH in the Waikato Hospital ICU (40mg daily).
Non-pharmacological methods of DVT prophylaxis :elasticated compression stockings (ECS) or sequential compression devices (SCD) may
confer some protection against DVT formation.
Exclusions to heparin DVT prohylaxis 287
Clinical coagulopathy or thrombocytopaenia
Therapeutic anticoagulation (eg Warfarin, heparin)
Significant intra-cerebral haemorrhage
Heparin Induced Thrombocytopaenia.
DVT prophylaxis by category 288
Medical ICU patients: Enoxaparin when bleeding risk felt to be minimal. When bleeding risk high (e.g. first three days after intracerbral
haemorrhage), use ECS and SCD.
Non-neurosurgical, non cardiac Surgical patients: ECS plus enoxaparin when possible. Use SCD if enoxaparin contraindicated.
Head injury with CT evidence of frank haemorrhage or haemorrhagic stroke: ECS and SCD for 72 hrs. Substitute enoxaparin for SCD at
72 hours if appropriate.Check if EVD in place; consider not using enoxaparin If EVD placement seems likely
Neurosurgical patients-tumours, SAH-ECS alone; meningiomas- ECS, enoxaparin delayed at least 7 days;anerysm surgery –ECS;
enoxaparin delayed at least 10-15 days or longer if intracerbral haematoma; chronic SDH-ECS, anticoagulants restarted 15-21 days,
possibly after repeat CT
Spinal Cord injury with intra-spinal haemorrhage on MRI: As for intra-cerebral haemorrhage above.
Pelvic fractures and patients with significant trauma: Thrombotic and initial bleeding risk high. If enoxaparin felt inappropriate at 24-
36hrs then consider placement of temporary caval filter.
Reference:
Sixth ACCP Consensus Conference on Anti-thrombotic Therapy. Chest 2001:119; 132-175 S

Systemic anticoagulation using unfractionated heparin 289

Weight based nomograms are more effective in achieving therapeutic anti-coagulation in a shorter period of time.
Proceed with loading dose if safe: 70 units / kg.
Continue with 20 units / hr / kg as continuous infusion (10 000 units heparin in 100 ml Normal Saline = 100 iu / ml
Check aPTT 4-6 hrly and adjust infusion rate according to chart:

UNFRACTIONATED HEPARIN NOMOGRAM

APTT Change in Heparin Infusion Rate
> 150 Reduce by 500 iu/hr (5mls/hr)
121 – 150 Reduce by 300 iu/hr (3mls/hr)
101 – 120 Reduce by 100 iu/hr (1ml/hr)
60 – 100 No change – Therapeutic
45 – 60 Increase by 100 iu/hr (1ml/hr)
36 – 44 Increase by 200 iu/hr (2mls/hr)
< 36 Increase by 400 iu/hr (4 mls/hr)
N.B. For APPT’s within 12 hours of starting thrombolytic therapy do not discontinue or decrease the infusion unless:
significant bleeding occurs
APPT is > 150 secs
Adjust the infusion as per nomogram if APPT < 50 secs.
Heparin toxicity (prolonged APTT) in a patient that is actively bleeding should be reversed with Protamine Sulphate 50 mg aliquots IVI
(usually diluted). Administration of protamine may aggravate peripheral vasodilatation and hypotension in susceptible patients.
Recombinant Factor VIIa 290
Introduction 291
The intrinsic and extrinsic pathways of coagulation serve as useful laboratory models for in-vitro coagulation tests. In vivo, the critical
pathway involves exposure of tissue factor (TF) which then binds with factor VIIa (endogenous activated VII ususually only 1% of total
fVII). Exogenous VIIa therefore initiates vigorous coagulation in patients with endothelial injury and exposed TF, but only where sufficient
fibrinogen exists in serum.
Pre-conditions for use 292
Intractable bleeding in the setting of :
Surgery
Trauma
Medical indications (oesophageal varices, pulmonary haemorrhage, selected haematological disorders, possibly warfarin related
intracranial haemorrhage)
Every effort has been made to address a surgical bleeding point (i.e. surgical exploration or angiography-embolisation)
Clotting factor replacement is optimal including platelets (> 50 × 109/L): fVIIa will only enhance in-vivo clotting, not replace it!
If enhanced fibrinolysis is suspected, then anti-fibrinolytic agents should be given before fVIIa.
Duty ICU Specialist approval required for use in ICU.
All “off-label” use must be recorded for audit purposes
Contra-indications 293
fVIIa use in non-haemophiliac populations, particularly the critically ill, is relatively new. Its safety has not been established in:
DIC
Sepsis
Recent unstable angina
Pregnancy
Its pro-thrombotic effect clearly requires caution where further thrombosis may lead to mortality/morbidity.
Dose 294
20 – 100 µg/kg as an IVI bolus. A second dose 2 hours later may be of some benefit, but further doses thereafter are unlikely to help.
Reference:
Novoseven online. Available at http:www.novoseven.com

Heparin Induced Thrombocytopaenia 295

Introduction 296
HITS occurs in two forms.
Dose related: Platelet clumping as an effect of the larger glycosaminoglycans containing the active pentasaccharide of heparin.
Immediately obvious, dose related and usually mild.
Auto-immune: IgG antibody mediated. Therefore usually occurs 7-10 days after exposure in non-sensitised patients. Idiosyncratic, often
severe.
HITS may appear more common in the setting of continuous renal replacement therapy. This might reflect patient condition and platelet
adsorption to dialysis filter.
Diagnosis 297
Decrease in platelet count: Usually < 50 000×109 / L. Rarely < 20 000×109 / L
Skin lesions at heparin injection sites
Dominant finding of thrombosis (not bleeding)
Formation of Heparin antibodies (heparin – PF4 ELISA = Sensitive but not specific).
Treatment Measures 298
Stop all Heparin immediately and reconsider indication for anti-coagulation. Warfarin, if commenced, should not be used alone as it
exacerbates thrombotic risk.
Use of Low Molecular Weight Heparin in these patients is not considered safe (cross-reactivity rates in excess of 90% reported).
Institute alternative anticoagulant (eg: Thrombin inhibitors or Danaparoid Sodium)
DANAPAROID SODIUM DOSING TABLE 9
IVI loading dose: (body weight adjusted) < 60 kg 1500 U
60-75 kg 2250 U
75-90 kg 3000 U
> 90 kg 3750 U
Infusion: Danaparoid in 250 ml 5% dextrose Infuse 400 U / hr (44 ml/hr) for 4 hours
decrementally 300 U / hr (33 ml/hr) for 4 hours
200 U / hr (22 ml/hr) titrated to a anti-Xa level target 0.5-0.8
Subcutaneous: anti-Xa U / ml 750 U 8-12 hrly
NB: Danaparoid Sodium is renally cleared and dose adjustment may be necessary in patients with renal dysfunction.
Reference:
Pravinkumar, E. HIT/HITT and alternative anticoagulation: current concepts. BJA 2003 90(5):676-85
Endocrine Drugs 299
Insulin 300
Introduction 301
Glycaemic control in the critically ill has become one of the most debated aspects of care. There is some evidence that tight control of blood
sugar (4.4 – 6.0 mmol /L) is associated with improved outcome. This effect may be preserved at levels less than 8 mmol/L. This area of ICU
practice is evolving and requires regular review.
Target blood sugar level = 4.4 – 6.0 mmol/L in the Waikato Hospital ICU
Indications for insulin in the ICU 302
Diabetic emergencies: NB Rapid glycaemic control is not a priority in patients with either hyperosmolar or ketotic diabetic states. In fact
rapid correction of severe hyperglycaemic states may aggravate cerebral oedema.
Hyperglycaemia in diabetics and non-diabetics, particularly with AMI or neurological conditions
Treatment of hyperkalaemia: ie 50 ml 50% dextrose administered with 10 units actrapid insulin.
Administration of insulin 303
Mix regular short acting insulin (actrapid) with normal saline to a concentration 1 IU/ml.
Administer in a 50 ml syringe via syringe driver.
Maximum infusion rate never to exceed 25 IU/hr.
Discard at 24 hrs of use.
Monitoring of blood glucose 304
Blood sugar levels should be monitored hourly until stable within desirable range. Once stable, monitor at least 2 hrly in the first 48 hrs of
ICU admission, and 4 hrly thereafter.
TIGHT GLYCAEMIC CONTROL IN WAIKATO ICU
Blood sugar on first assessment
< 3.3 mmol/L Administer 20 ml 50 % dextrose, stop insulin administration if any.
Ensure adequate glucose intake ( 1 ml/kg 5 dextrose or equivalent enteral feed)
Repeat BSL in 30 min
3.4 – 4.3 mmol/L Ensure adequate glucose intake. Repeat BSL in 30 min
4.4 – 6.0 mmol/L Repeat blood sugar in 1 hr
6.1 – 12.2 mmol/L Start actrapid infusion at 1 IU/hr. Repeat BSL in 1 hr
> 12.2 mmol/L Start actrapid infusion at 2 IU/hr. Repeat BSL in 1 hr
Ongoing sugar control management
< 3.3 mmol/L Stop insulin and administer 20 ml 50 % dextrose
Ensure adequate glucose intake ( 1 ml/kg 5 dextrose or equivalent enteral feed)
Repeat BSL in 30 min
3.4 - 4.3 mmol/L Decrease insulin infusion by half
Ensure adequate glucose intake
Repeat BSL in 30 min
4.4 - 6.0 mmol/L Insulin infusion unchanged
Repeat blood sugar in 1 hr
Once stable in range repeat 2 hrly (or 4 hrly if > 48 hrs post admission)
6.1 – 7.8 mmol/L Increase infusion rate by 0.5 IU/hr. Repeat BSL in 1 hr
7.9 – 12 mmol/L Increase infusion rate by 1 IU/hr. Repeat BSL in 1 hr
> 12 mmol/L Increase infusion rate by 2 IU/hr
Insulin-dextrose in exceptional circumstances 305
The above guideline only applies to patients receiving IVI dextrose or significant enteral caloric intake. Should this be interrupted, insulin is
to be stopped and a BSL checked after 1 hr.
Where the desired patient maintenance fluid does not contain dextrose (i.e Normal Saline), 10 ml/hr of 50% dextrose should be run
concurrently, and insulin administration continued as above.
Tight glycaemic control is not practised in children or in neurosurgical patients requiring ventriculostomy or ICP monitoring (the
latter at neurosurgical request because of concerns over the effect of low normal glucose levels on the injured brain)
Ongoing requirement for insulin beyond acute phase: 306
Patients requiring insulin for established or known diabetes should be converted to subcutaneous insulin as a medium or long acting form
with / without short acting insulin constructed according to subcutaneous sliding scale. As these patients may need long term follow-up, they
should be referred to the endocrine service for assistance.
Reference:
Van Den Berghe G, et al. Intensive Insulin Therapy in Critically Ill Patients. NEJM 2001, Nov 8;345(19):1359-1367

DDAVP 307
For Diabetes Insipidus 308
General 309
DI may occur in the following settings:
Evolving brain death or severe brain injury
Post ablative pituitary surgery, or injury to pituitary stalk (anterior cranial fractures)
Nephrogenic causes are typically mild and do not require treatment.
Fluid mobilisation during convalescent phase of injury should not be mistaken for DI.
Indications for DDAVP in diabetes insipidus 310
Persistent polyuria > 300 ml/hr for more than 3-4 hours with incremental hypernatraemia.
 Low urine osmolality in the presence of high plasma osmolality (or hypernatraemia)
Pre-existing hyperosmolar state or intravascularly deplete patient.
Dose of DDAVP in diabetes insipidus 311
1-2 µg IVI bd as required.
Fluid orders: 312
Isotonic fluid replacement in under-resuscitated patients.
5% Dextrose or 0.45% Saline in patients where hypernatraemia exists (maximum decrease in serum Sodium should not exceed 2 mmol/L/hour)
For Platelet dysfunction 313
Indications 314
Adjunctive treatment in bleeding patients with platelet dysfunction as a result of
Uraemia
Cirrhosis
Von-Willebrand’s Disease
Drug (NSAID-s or aspirin) or cardiac surgery related platelet dysfunction
Contraindications 315
Use in patients with severe coronary or cerebrovascular atherosclerosis may cause arterial thrombosis.
Dose 316
0.3 µg / kg IVI over 30 minutes or 300 µg intra-nasally.
In some instances a second dose may be administered, although a rapid “fall-off” in effect per dose (tachyphylaxis) is the norm.

Steroids 317
General 318
The use of steroids in the critically ill has been the subject of much debate and some research. The CORTICUS study results would suggest
that steroids do not reduce mortality in septic shock.
Proven Indications 319
Hypoadrenalism (Addison’s disease or crisis)
Acute severe asthma
Panhypopituitarism
Haemophilus meningitis in children (discuss with paediatric team first)
Pneumocystis Carinii pneumonia (Pa02 < 60 mmHg)
Collagen Vascular diseases
Active Immunosuppression (GVHD, solid organ transplant)
Myasthenia Gravis
Treatment peritumoral oedema in the central nervous system
Unproven ICU indications 320
Non-infected (fibroproliferative) ARDS: Meduri protocol = Methylprednisolone 2 mg/kg for 14 days, tapered 1.0-0.5 mg/kg for next 14
days.
Shock associated with vasodilated states which are refractory to high dose, or prolonged administration of, inotropes.
Myocarditis
Exacerbation of chronic airway obstruction
Bronchiolitis obliterans
Anaphylaxis
Conditions where steroids are not indicated or actively contra-indicated 321
Active infection
Head injury
Guillain-Barre Syndrome
Fat embolism syndromes
RELATIVE STEROID POTENCIES
Steroid Equivalence (mg) Glucocorticoid activity Mineralocorticoid activity
Hydrocortisone 100 mg 1 1
Prednisone 25 4 0.3
Methylpred. 20 4 0
Dexamethasone 4
Fludrocortisone 1 10 250
Renal Drugs 322
General Principles 323
Acutely ill patients are at risk for developing, or exacerbating, renal dysfunction. Good intensive care practice, and renal care, encompasses:
Avoiding renal hypoperfusion: ICU patients generally do not have the ability to autoregulate renal blood flow and GFR, as these become
increasingly dependent on systemic perfusion pressures. For this reason urinary output is a sensitive marker of total body perfusion,
and resuscitation status.
Ensure adequate volume resuscitation
Avoid renal toxins if possible: aminoglycoside antibiotics, contrast mediums etc
Consider local complicating conditions: eg. abdominal compartment syndromes.
Administration of agents such as dopamine in low dose, or frusemide, may help maintain urine output with some inherent advantages in
fluid management. They are not however reno-protective, and their use should be carefully weighed up in each clinical scenario.

Diuretics 324
Indications 325
Symptomatic fluid overload without intravascular depletion
Pulmonary oedema
Congestive Cardiac Failure / Cor Pulmonale
Ascitic states where abdominal volume is thought to be a compromising factor
Hypertension
Conjunctive therapy in Cardiac failure (not primarily diuretic): ACE-I and thiazide, Low dose (25 mg / day) spironolactone.
Metabolic alkalosis: eg recovering ventilated patients allowed permissive hypercapnoea, prolonged renal replacement therapy with
bicarbonate overshoot. (ie. acetazolamide).
Contraindications 326
Hypovolaemia
Anuria: Frusemide in particular acts on the luminal side of the renal tubule. States where there is no, or low, GFR will not respond to drug
administration, and may complicate hypotension by direct afterload reduction.
Failure to respond to trial dose
Drug hypersensitivity: NB Sulphonamides
Complications 327
Hypovolaemia (often hyperosmolar)
Hyponatraemia or hypernatraemia
Electrolyte disturbance of K+, Mg2+ and PO43-.
COMMONLY ENCOUNTERED RENAL DRUGS
Drug Administration Comments
Frusemide Bolus: 20-100 mg PO / IVI prn. Potent loop diuretic
Infusion: 2.5-10 mg/hr (larger doses have also been More effective administered as infusion
in used, however this practice is not well Toxicity (deafness and interstitial nephritis) increased with co-administration
documented in standard literature) of aminoglycosides.
K+, Mg2+ P043-common.
Spironolactone 25-100 mg bd Potassium sparing diuretic.
May prevent pathological cardiac modelling in low dose.
2nd line agent, diuretic resistant heart failure.
Mannitol 20% solution (200 mg/ml) Potent osmotic diuretic
Bolus: 100 ml prn IVI. May cause hyper-osmolal state, with increased osmolal gap (measured-
Traditional doses of 0.5-1.0 g/kg body weight are calculated osm)
probably excessive. Dose limited by ceiling of 300 mosm/L
Max dose 3 g/kg/day or see opposite. Limited role: acute head injury with raised ICPn
Has been used but has no proven role in treatment of myoglobinaemic /-uric
states.

Gastro-intestinal drugs 328

Prophylaxis of gastric “stress ulceration” 329
Not indicated in enterally fed patients, even at low volumes, unless the patient is known to have pre-existing or subsequently (in-hospital)
proven peptic ulceration.
Consider use of a prophylactic agent (ranitidine 50 mg IVI 8 hrly) if patient is not enterally fed and:
Pre-existing or intercurrent coagulopathy
Mechanical ventilation > 48hrs
Active GI Bleeding 330
Diagnosis 331
Revealed blood: Nasogastric blood, haematemesis, malaena
A fall in systolic blood pressure > 20 mmHg
Drop in Hb > 20 g / l in 24 hours, or requiring transfusion of blood
Management 332
ABC / resuscitate
Correct coagulopathy / cease heparin
Omeprazole 40-80 mg IVI 12-8 hrly, consider oral / nasogastric once stable.
Endoscopy ± sclerotherapy / colonoscopy / angiography and attempted vessel embolism if clinically appropriate.
Use of gastro-intestinal pro-kinetic agents 333
General 334
Gastric stasis, colonic and small intestinal ileus are common management problems in the intensive care unit. It may be necessary to explore
jejunal feeding tube placement and or the use of prokinetic agents to facilitate enteral feeding (see algorithm on enteral feeding).
Contra-indications 335
Erythromycin, sometimes used in this setting, interacts significantly with other drugs metabolised by the Cytochrome P450 enzyme system,
with potentially lethal side effects (eg. arrhythmia).
Potential drug interactions must be reviewed prior to commencing erythromycin.
GI DRUGS COMMONLY USED IN THE WAIKATO ICU
Drug Dose Comments
Metoclopramide (maxalon) 10 mg 6 hrly prn May be a useful first line agent in mild-moderate nausea and vomiting
May reduce gastric stasis (not first line)
Ondansetron 4-8 mg IVI 8hrly prn Potent alternative anti-emetic (expensive)
Cyclizine 25-50 mg IVI 8hrly prn Useful second line anti-emetic.
Histamine-1 receptor antagonist
Possible anticholinergic side effects, including tachycardia
Erythromycin 100 mg IVI Q.I.D Proven pro-kinetic agent
Limited by drug interactions (eg. fluconazole, aminophylline)
Ranitidine 50 mg 8hrly IVI H2-receptor blocker
150 mg bd po Less effective acid suppression during feeding
Ill defined link with increased rates of nosocomial infection
Useful prophylactic agent
Omeprazole Active Bleeding: 80 mg IVI bolus (own diluent) Proton pump inhibitor
followed by 8 mg / hr of infusion (40 mg in 100 Effective acid suppression for 24hrs
ml NS) Proven efficacy in Rx of actively bleeding ulceration
Acute Rx: 40 mg bd IVI
Established: 40 mg dly po
Octreotide Bolus: 50g IVI Somatostatin analogue
Plasma half life 100min Varices: 50g / hr Proven as effective as sclerotherapy in ameliorating variceal bleeding
Duration of action up to 12 (decreases portal pressure)
Fistulae: 100-200g IVI or SC 8 hrly
hrs Decreases GI secretion volume in treatment of enteric and pancreatic fistulae
(attenuated after approx.1 week)
ICU Antibiotic Guidelines 336
Prologue 337
Emerging bacterial resistance is one of the major challenges facing modern intensive care. It is the duty of all members of staff to actively
participate in the appropriate use of anti-microbials, while adopting proven infection control behaviour.

Introduction 338
The Waikato Hospital Intensive Care Unit supports in general the Waikato Hospital Antimicrobial Guide. Another useful reference is the
Australian Therapeutic Guidelines: Antibiotic Version 11, 2000, Chairman, Writing Group: Associate Professor J Spicer. These guidelines
and updated versions are available at www.tg.au
This section cannot be a comprehensive guide, but should aid staff as to the unit preferences in antibiotic prescribing practice.
Resident staff may not change antibiotics without prior discussion with the duty ICU specialist.
All antibiotic charting must be reviewed daily.The indication should be recorded on the drug chart.
The unit microbiological results must be reviewed daily and recorded in the patient notes.
All suggested drug dosages (magnitude and frequency) given in this section are intended for the general population, with normal
renal function. When prescribing drugs in the elderly, and any patients with significant renal or hepatic insufficiency, you must
allow for modified drug handling.

Principles of prescription 339

Prophylaxis 340
General 341
Prophylactic antimicrobial therapy should be restricted to situations in which it has been shown to be effective, or where the consequences of
infection are disastrous.
Antimicrobials should be directed against likely causative organisms, however it is not rational to attempt to cover all possible microbes.
Timing 342
Antibiotics for the purpose of prophylaxis should be administered at the time of anaesthetic induction, and to cover the period of surgery and
/ or microbe implantation.
A second dose of antibiotic may be warranted if the operation continues beyond one half of the normal dosing interval for the agent being
used.
There may be some evidence in specific types of surgery (eg. vascular surgery) for extending prophylactic cover beyond the immediate
operative period, however in general there is little evidence to support such a practice.
Preferred antibiotics 343
Please confirm antibiotic choice and duration with each individual surgeon at the time of admission of the patient to the Intensive Care Unit.
The antibiotic choices given below would constitute a rational approach; however it is generally not the role of the ICU staff to direct
surgical choice of agent or duration of prophylaxis.
PROPHYLACTIC ANTIBIOTICS BY SURGICAL SPECIALTY
Specialty Procedure Antibiotic Choice

Cardiac Surgery Cephazolin 1g q8h until chest drains removed

Orthopaedics Prosthetic large joint replacement Refer surgeon

Insertion of prosthetic or transplant material
Internal reduction and fixation of bones
Neurosurgery Antimicrobial prophylaxis is not indicated for CSF leakage following Single dose 3rd generation cephalosporin prior to placement
trauma unlessit results from an open cranial vault fracture. shunt, EVD or ICP monitor or craniotomy.
The value of routine prophylaxis for the insertion of shunts, 3rd generation cephalosporin on induction and for 5 days post
ventricular drains or pressure monitors remains uncertain, but is cranioplasty.
widely requested.
Abdominal Surgery Single dose antibiotic is usually sufficient. If the duration of surgery Metronidazole 500 mg IVI timed to end at induction
is > 3hrs consider a second dose. + one of the following
If abdominal cavity soiled then a full course of therapy is warranted Cephazolin 1 g IVI or
(see empiric treatment) Gentamicin 3-5 mg/kg IVI
Or single agent
Cefotetan 1-2 g IVI
Vascular Surgery Elective cases involving head and neck Antibiotic prophylaxis is not supported in the literature
Reconstruction of the aorta and / or lower limb vasculature, One of the following:
particularly where groin incision involved Cephazolin 1 g at induction and 8hrly IVI
Surgical preference is usually for antibiotics to continue until central Note: Vascular surgery may be one of the few disciplines
access or other portals for infection removed. where some evidence exists for “prophylactic” antibiotic
administration for up to 48 hrs post-op.
General 344
The institution of antibiotic therapy prior to definitive bacteriological diagnosis should be based on local epidemiological data, potential
pathogens and their known antimicrobial sensitivity patterns.
Whenever possible material (blood, sputum, urine or directly infected tissue) should be obtained before institution of antibiotics, however in
life-threatening situations (eg. meningitis) it may be appropriate to administer antibiotics immediately rather than delay pending culture.
With the progression of diagnostic techniques such as PCR and other DNA probe techniques it may be possible to identify organisms despite
prior antibiotic administration.
Where the there is doubt as to the likely source of infection, or the appropriate choice of empiric antimicrobial, it would be prudent to
consult the Department of Infectious Diseases.
Well chosen anti-microbials should be continued for at least 48 hours before another empiric antibiotic is added or substituted.
Once gram stain or culture results become known, the choice of agent should be rationalised appropriately.
NB: No ICU antibiotic regimen may be changed or altered without prior knowledge, and consent, of the duty ICU specialist.
SCENARIO’S REQUIRING EMPIRICAL USE OF ANTIBIOTICS IN THE INTENSIVE CARE
Infection Comment Antibiotics
Pneumonia Community acquired severe pneumonia: 2 or more of Erythromycin (or equivalent) 500 mg to 1 g 6 hrly IVI +
Community Acquired RR > 30 / min Augmentin 1.2 g 8hrly
Pa02 < 60 mmHg on ABG When available in IVI formulation, the newer generation
PaCO2 > 50 mmHg fluoroquinolones moxifloxacin or gatifloxacin may be
appropriate as monotherapy
Diffuse or multi-lobar infiltrate on CXR
Haemodynamic compromise
Mechanical ventilation
Pneumonia Pneumonia developing in a ventilated patient, that was not Tobramicin 5 mg/kg daily adjusted for age and renal function
Ventilator Acquired evident on initiating respiratory support, in a patient ventilated +
for > 48hrs. Piperacillin + tazobactam (Tazocin) 4.5 g IVI 8 hrly
Pneumonia
Or Or single agent
Hospital Aquired pneumonia Meropenem 500 mg - 1 g 8-12 hrly may be used as
giving rise to ICU admission monotherapy.
Where an aminoglycoside cannot be used, or Legionella is
suspected:
substitute erythromycin 500 mg - 1 g 6 hrly IVI. (or newer
generation fluoroquinolone eg. moxifloxacin)
Aspiration Pneumonia Antibiotics are not indicated for cases of mild to moderate Augmentin 1.2g 8 hrly IVI
aspiration lung injury.
Where severe aspiration has occurred or abscess cavity
suspected treat as opposite.
Exacerbation COAD Routine use of antimicrobial agents not proven beneficial. Amoxycillin 500 mg 8hrly IVI for 5 days
Consider treatment if increased cough and dyspnoea associated
with increased sputum volume and purulence
Positive sputum culture (H.Influenza, S.Pneumoniae, M.
Catarrhalis) may indicate colonisation only.
Intra-abdominal Sepsis Faecal peritonitis or perforated viscus Amoxicillin 2 g IVI 6 hrly +
Gentamicin 5 mg/kg IVI daily +
Metronidazole 500 mg 12 hrly IVI
Or if patient penicillin sensitive / aminoglycoside contra-
indicated
Metronidazole 500 mg 12 hrly IVI +
Cefipime 1-2g 12hrly IVI
Pancreatitis (resulting in Without evidence of extensive necrosis. Meropenem 500 mg IVI 8 hrly
ICU admission) Where enhanced CT evidence suggests infected necrosis,
surgical drainage is indicated
Biliary sepsis Acute Cholecystitis Amoxycillin 1 g IVI 6 hrly +
Ascending Cholangitis Gentamicin 4-6 mg/kg daily IVI +
Antibiotic therapy should be seen as an adjunct to drainage Metronidazole 500 mg 8hrly IVI
Line Sepsis complicated If patient clinically septic from invasive catheter, or at risk of Vancomycin 1g IVI. 12 hrly  2 doses
devastating infection (ie. prosthetic valve or graft) then remove Consider adding Gentamicin 4-6 mg/kg daily IVI if patient is
catheter and commence treatment accordingly not already receiving gram negative cover.
Removal of infected catheter is often sufficient to “treat” Review ongoing treatment with cultures according to patient
localised access infection. progress.
Viral (HSV) encephalitis or Empirical cover viral meningitis / encephalitis where there is a Acyclovir 10 mg/kg IVI 8 hrly
meningo-encephalitis clinical index of suspicion. Review treatment at earliest possible time when gram stain and
CSF (+PCR) examination complete.
Urinary infection Treat as for severe pyelonephritis Gentamicin 4-6 mg/kg IVI daily according to age and renal
precipitating ICU admission function +
Ampicillin 2 g 6 hrly IVI.
Or if aminoglycoside undesirable
Ceftriaxone 1-2 g IVI daily
Bacteruria in Intensive Care Treatment should only be considered if patient shows signs of Remove urinary catheter if possible
Patients systemic illness / sepsis, supported by significant pyuria
Hospital Aquired or Particularly associated with instrumentation Cefipime 1-2g 12 hrly
complicated UTI Or
Meropenem 1g 12hrly
 Suspected Bacterial All patients with suspected endocarditis should have at least Benzylpenicillin 1.8 g IVI 4 hrly +
Endocarditis three sets of blood cultures taken, each from a separate Di(flu)cloxacillin 2 g 4 hrly +
venepuncture site prior to starting treatment. Gentamicin 5mg/kg daily for 1-3 days may clear bacteraemia
Consult Infectious Diseases team earlier
Where a patient has a prosthetic heart valve, or has been in
hospital for > 48hrs, substitute vancomycin 1g 12 hrly for
flucloxacillin.
Cellulitis or soft tissue Simple cellulitis Flucloxacillin 1g 6 hrly
infection Cellulitis complicating pre-existing ulcer Add Augmentin 1.2g 8 hrly IVI
Suspected necrotising fasciitis See below
Burns No antibiotics indicated unless infection proven
Suspected Systemic Fungal Suspected Candidiasis Fluconazole 200-400 mg IVI daily, adjusted to renal function
Disease Suspected Aspergillosis or
Caspofungin 75mg then 50mg daily
Amphotericin 0.5-1.5 mg/kg/day IVI
Microbe specific antibiotic use in the ICU setting 345
Where a specific microbe (pathogen) has been isolated, therapy should be tailored as outlined below.
MICROBE SPECIFIC ANTIMICROBIAL CHOICES IN THE ICU
Organism 1st choice 2nd choice
Pneumococcus Benzyl penicillin 1.2 g IV 4-6 hrly Ceftriaxone 1 g IVI daily
Staphylococcus aureus Flucloxacillin 2 g IV 6 hrly Cephalothin 1 g 6 hrly IVI
MRSA (alert ID team and infection Vancomycin 1 g IVI 12 hrly Teicoplanin 400-600 mg loading dose IVI, 200-600
control) mg daily IVI maintenance.
Meningococcus Benzyl penicillin 1.2 g IVI 4-6 hrly Ceftriaxone 2 g IV daily
Household contacts Rifampicin 600 mg oral bd x 2 days Ciprofloxacin 500 mg po x 1
Enterococcus (bacteraemia or Amoxycillin 1-2 g IV 6 hrly + Vancomycin 1 g IVI daily +
severe infection) Gentamicin 5 mg/kg IVI dly Gentamicin if SBE
Gp A Strep. Infection Benzylpenicillin 1.8 g 4 hrly IVI
If severe infection consult ID And consider adding;
Clindamycin 600 mg IVI 8 hrly + Intragam 150 mg/kg/day x 5 days
Cease IG when pt. Improves
Haemophilus influenzae Ceftriaxone 1g IVI dly Amoxycillin 1-2 g IVI 6 hrly
E. Coli Gentamicin 5 mg/kg IVI dly Ceftriaxone 1 g IVI dly
Enterobacter Gentamicin 5 mg/kg IVI dly Ciprofloxacin 200-400 mg 12 hrly IVI
Klebsiella Gentamicin 5 mg/kg IVI dly Ceftriaxone 1g IVI dly
Pseudomonas aeruginosa Piperacillin 3 g IVI 6 h + Cefipime 1.0-2.0 g 12 hrly IVI
Gentamicin 5 mg/kg IVI dly & either
Tobramicin 5mg/kg IVI dly
or
Ciprofloxacin 200-400 mg 12 hrly
Legionella spp Erythromycin 500 mg -1 g IVI 6 hrly Consider newer fluoroquinolone when available in
IVI formulation
Pneumocystis Carinii Co-trimoxazole 320 / 1600 mg IVI 6 hrly + Pentamidine 4 mg/kg/day IVI +
Infection complicating or causing methylpred 40 mg bd x 5 days, Steroid therapy as noted opposite.
ICU admission qualifies as severe, methylpred 40 mg daily x 5 days,
requiringe steroid therapy. methylpred 20 mg daily x 11 days
Clostridium difficile: Cease other antibiotics if possible Vancomycin 125 mg 6 hrly given enterally
1.Mild / moderate 1.Metronidazole 400 mg po bd
2.Severe, or relapse after Rx (or 500 mg IVI 12 hrly if nil by mouth)
x 7-14 days
2.Repeat above
Clostridial infection Surgical debridement Meropenem 1g b.d.
(Polymicrobial Infection) Benzylpencillin 2.4 g IVI 4 hrly +
Gentamicin 5 mg/kg IV daily +
Metronidazole 500 mg IV bd
Complications of antibiotic use 346
Drug hypersensitivity: Dermal eruptions, anaphylactoid / anaphylactic reactions
Drug toxicity: Idiosyncratic (non-dose related) or dose related.
Flucloxacillin-hepatotoxicity
Aminoglycoside-renal toxicity
Emergence of bacterial resistance
Selection of nosocomial colonising organisms (and potential pathogens)
Pseudomembranous colitis
Fluids and Electrolytes 347
Principles of Fluid Management in Intensive Care 348
Fluid charting 349
Prologue 350
All fluid prescriptions must be reviewed daily.
Non-standard / bolus fluid orders must be charted individually
Fluid orders should be considered in two components
Maintenance or replacement fluids 351
Daily total fluid administration including enteral feeding = 30-40 ml/kg / day or 80-120 ml/hr, selected according to patient serum Sodium
and / or glucose tolerance + additional fluid tailored to excessive losses where appropriate.
4% dextrose and one 5th normal saline
normal saline
5% dextrose
Patients who are anuric or fluid overloaded should not necessarily receive “maintenance” fluids.
Resuscitation fluids 352
The intensive care community is divided on the relative suitability of each fluid in the resuscitation of a critically ill patient. In general if
crystalloid (normal saline or Hartmann’s solution) is chosen in the first instance, no more than 2000 ml should be administered, followed by
colloid.
Fluid boluses should optimally be titrated against a measurable end-point, although most in current use are at best imperfect (see appendix
on pre-load).
COMPOSITION OF COMMONLY USED FLUIDS
Solution Concentration of solute in mmol / L
Na K Cl Ca Lact Glu (g) Osm Prot (g)
Normal Saline 0.9% 150 150 300
Half-Normal Saline 75 75 150
1 / 5 Normal Saline +
4% Dextrose 30 30 40 282
(D4S, 4% and a fifth)
5% Dextrose 50 278
Hartmanns (lactated
129 5.0 109 2.0 29 274
ringers solution)
Gelofusine (500 ml) 144 120 283 Gelatin 20
Albumex 70 62.5 25
Hemohes (500ml) 150 150 310 starch 10

Assessment of fluid balance and hydration 353

Clinical markers 354
Skin turgor, mucous membrane hydration (poor indicator)
Heart rate and blood pressure
Peripheral perfusion, capillary refill
Biochemical markers
Serum Na+, Cl-, osmolality
Urea / creatinine
Bicarbonate
Haematocrit
Charted fluid balance - at best a rough guide
Charted intake – (Charted losses of all types + Insensible losses)
Predictors of increased cardiac output in response to administration of fluid 355
JVP / CVP: Useful in patients with “normal” lungs and right heart function. In other patients a trend in pressures may be useful.
Pulmonary artery pressures (particularly diastolic), and pulmonary capillary pressure. At best these are poorly related to a response to
further fluid (pre-load), but are still widely employed.
PiCCO derived estimates of intra-thoracic blood volume and extra vascular lung water.
Variation in arterial wave form peak with positive pressure ventilatory cycle
This is a notoriously difficult aspect of critical care practice. Please consult the appendices on haemodynamic principles. Often the decision
to administer fluid is governed by a conglomeration of each of the following. If you are in any doubt consult the duty ICU specialist, but do
not delay the administration of fluid in the acute resuscitation phase.

Body Fluid and Electrolyte Physiology 356

A working knowledge of the distribution of fluid and electrolytes throughout the body is required before any rational prescribing process can
begin. It is beyond the scope of this handbook to describe in detail the physiology involved. What follows are salient notes on fluid and
electrolyte distribution, and some of the more common disorders encountered in the intensive care setting.
Fluid distribution 357
FLUID DISTRIBUTION IN THE NORMAL PERSON
Fluid Compartment Volume (ml/kg) Volume (l / 70 kg) male %
total body weight
Plasma 45 3.150 4.5
Blood 75 5.250 7.5
Interstitial 200 14.000 20
Extracellular 250 17.500 25
Intracellular 350 24.500 35
Total body fluid volume 600 42.000 60
NB: These figures apply to a normal person, and may be significantly altered in a critically patient
Electrolyte distribution 358
ELECTROLYTE DISTRIBUTION IN THE NORMAL PERSON
Electrolyte Extracellular Fluid Compartments Intracellular Fluid
Plasma Interstitium
Whole plasma Plasma “water”
Sodium 140 150 143 10
Potassium 3.7 4 3.8 155
Chloride 101 109 114 3
Bicarbonate 27 29 30 10
Calcium (ionised) 1.1 1.2 1.2 < 0.01
Magnesium 0.7 0.8 0.8 2
Phosphate 1.1 1.2 1.1 100
Osmolality 291 291 290 290
Determinants of solute movement and concentration 359
Passive transport mechanisms 360
Diffusion: movement of a solute from an area of higher concentration to one of lower
Non-ionic diffusion
Gibbs-Donnan effect: The unequal distribution of diffusible ions on either side of a membrane can be explained if one side contains a
poorly diffusible ion (eg. albumin-anion), since at equilibrium;
The product of the diffusible ions in one compartment will equal the product of the same ions in the other compartment.
Within each compartment the total cationic charges equal the total anionic charges-electrical neutrality must be maintained in
passive systems.
Active transport mechanisms 361
Energy requiring mechanisms which distribute a substance across a membrane, in a manner not achievable by physical forces alone. These
are essential for establishing electrical and ionic differences across membranes, the basis for tissue excitability and other fundamental
functions of the body.

Electrolyte Abnormalities 362

Approach 363
Electrolyte derangement should be viewed as resulting from one of the following.
Erroneous results:
Lab error
Haemolysed specimen
Factitious results: eg hyperglycaemia and hyponatraemia; lipaemic serum.
Blood taken in proximity to an intravenous infusion
Decreased or increased intake
Decreased or increased loss (renal versus extra-renal)
Shifts between compartments: eg potassium driven intra-cellularly by insulin.
Treatment of electrolyte disturbance should be aimed at not only the apparent problem but also the underlying cause.
Consideration should be given to the consequences of rapid correction of measured plasma electrolyte imbalances. Particularly those which
have developed over a longer period of time, for which there may have been some intracellular accommodation.

Hyponatraemia: Na+ < 130 mmol/L 364

Aetiology 365
Factitious 366
Measured plasma osmolarity > 290 mmol/L:
Hyponatraemia in hyperglycaemia: For every 10 mmol/L increase in glucose, serum Sodium falls 3 mmol/L. It is in a sense a real
hyponatraemia, however treatment aimed at correcting the blood glucose will resolve the hyponatraemia.
Mannitol: not usually a clinical issue, however later diuresis and hypernatraemia may be.
Alcohol (including methanol)
Measured plasma osmolarity 270-290 mmol/L
Hyperlipidaemia
Hyperproteinaemia
Neither of the above should be a problem with current ion-specific electrodes.
Measured plasma osmolarity < 270 mmol/L 367
Hypovolaemia with Sodium depletion
Renal
diuretics
Addisons
Polyuric renal failure or diuretic recovery phase of renal dysfunction
Extra-renal
 GIT loss
Burns
Hypervolaemia (water excess)
Renal failure: acute or chronic
Extra-renal
Excessive intake (IVI 5% dextrose)
Oedematous states: CCF, cirrhosis, nephrotic syndrome, hypoalbuminaemia.
Normovolaemia
Psychogenic polydipsia
SIADH
Hypothyroidism
Acute adrenal insufficiency
Management of Severe Hyponatraemia with fitting or decreased LOC 368
Resuscitative measures and ABC principles should not be delayed.
Hypertonic saline (3, 20% ) may be indicated but should not be used without prior discussion with the ICU duty consultant, unless the patient
is actively fitting
Hypertonic saline is very irritant and is best administered via central venous access where time allows.
An infusion of 50-70 mmol / hr of Sodium should increase the serum Sodium by approximately 2 mmol/L / per hour.
The serum Sodium should not be allowed to increase more than 20 mmol/L in the first 24 hours, and certainly should not be overcorrected
(serum Sodium > 130 mmol/L).
In very rare circumstances where fitting or encephalopathy are life threatening, 500 ml of 20% mannitol has been used.
Reference:
Worthley LIG. Hyponatraemia and speed of correction. Why is there a dilemma ? Critical Care and Resuscitation 2000;2:173-180
Hypovolaemic states 369
Restore volume with normal saline or colloid according to clinical estimate (fluid balance, weight, JVP, CVP)
Urine Sodium may be misleading in the context of diuretic administration or use of catecholamines.
Hypervolaemic states-most common scenario clinically 370
Fluid restriction if safe to do so ( < 15 ml/kg / day)
Excess should correct as ADH levels re-set (often ADH ↑ post surgery)
Address underlying cause (cardiac failure etc)
SIADH-often misdiagnosed 371
Diagnosis:
Low serum osmolarity
Urine osmolarity > plasma osmolarity
Urine Sodium > 40 mmol/L with normal renal, hepatic and cardiac function, and no diuretic use.
Management:
Fluid restriction ( < 1000 ml / day)
Hypernatraemia: Na+ > 145 mmol/L 372
Aetiology 373
Water depletion 374
Virtually all body fluids have a Sodium concentration less than that of plasma
Renal loss:
Diuretics or osmotic diuresis
ARF / CRF
Diabetes insipidus:
Neurogenic (including Guillain-Barre)
Nephrogenic: Hypercalcaemia, hypokalaemia, drug related (lithium), congenital
GIT losses: diarrhoea, vomiting fistulae, small bowel obstruction
Skin losses: fever, vasodilated states, burns, thyrotoxicosis
Inappropriate fluid restriction or under administration (elderly, post operative nil by mouth)
Salt gain 375
Iatrogenic administration of Sodium containing feed or IVI fluids.
Mineralocorticoid excess
Management 376
Water depletion / hypovolaemia 377
Resuscitate if necessary
“Restore” volume over 24-28 hrs using a relatively hyponatraemic fluid (half normal saline or 5 % dextrose), if necessary a rough estimate of
fluid deficit can be calculated:
(measured serum Na+ - 140) x (Body Weight x 0.6)
Water deficit =
140
eg; a 70kg male with a serum Sodium of 160 mmol/L might be expected to have a fluid deficit of 6 litres.
Do not correct Sodium by more than 2 mmol / hr.
Consider DDAVP if central diabetes insipidus has been confirmed
Excess salt intake. 378
Address cause
Hypokalaemia: K+ < 3.5 mmol/L 379
Aetiology / classification 380
Increased loss
Renal
Diuretics
↓serum Magnesium, ↓ serum Calcium
Steroids and mineralocorticoid excess
Renal tubular acidoses
GIT: diarrhoea, hypersecretory states (villous adenoma, small bowel fistulae)
Inadequate dietary intake or daily administration
Transcellular shifts:
β-stimulants (catecholamines, salbutamol)
Insulin (endogenous or exogenous)
Familial periodic paralysis and related syndromes (consider thyrotoxic states).
↑pH
Management 381
Potassium replacement intravenously or orally.
Intravenous replacement should not exceed 40 mmol / hr, concentrated solutions should be administered centrally and the patient carefully
monitored.
Concentrated solutions should not be administered peripherally.
Address cause of K+ loss.
A low threshold should be adopted for co-administration of Magnesium as an essential co-factor in Na +-K+ pumps. Patients that are
Magnesium deficient will remain hypokalaemic despite generous administration of potassium.

Hyperkalaemia: K+ > 5.0 mmol/L 382

Aetiology / classification 383
Factitious
Sampling in proximity to venous infusion
Haemolysis: ie collection using vacuum tube systems (venous sampling via vacutainer with narrow gauge needle)
Extremes of thrombocytosis and leukocytosis.
Release from intra-cellular compartments:
Acidosis: ↓pH by 0.1 ≅ serum K+ ↑ by 0.5 mmol/L
Tissue disruption: tumour lysis syndromes, rhabdomyolysis, intravascular haemolysis, burns
Suxamethonium (note: see section on drugs for intubation 3.9.3.1.2)
“Insulin deficiency”: the hyperkalaemia associated with diabetic ketoacidotic states is related to lack of insulin and a change in
serum pH but is usually associated with a total body potassium deficit.
Increased intake: Not usually a problem unless patient has impaired renal function.
Reduced potassium clearance:
Acute renal failure
Renal tubular acidosis: type 4
Potassium sparing diuretics: (spironolactone, amiloride)
Management 384
Patients with a slow rise in serum potassium usually tolerate elevated levels better than following an acute rise.
Where elevated serum potassium (generally > 6.0 mmol/L) is associated with acute ECG changes or haemodynamic compromise this should
be considered a medical emergency and treated as follows:

EMERGENCY TREATMENT OF HYPERKALAEMIA

Intervention Mode of administration Mechanism of action Comment
Calcium Chloride 10 ml IVI stat, repeated in 20 minutes if Membrane stabilisation First line action
appropriate Has no effect on serum potassium
concentration
Insulin Bolus: 10 units actrapid equivalent insulin Intracellular transfer of potassium Temporising measure
with 50 ml 50% dextrose Probable decrease in serum potassium
Infusion:20 units of actrapid insulin in concentration of 1 mmol/L for 30-60 minutes
500 ml 10 dextrose over 30-60 min.
%
with some effect up to 3 hours (either method)
Calcium and a dextrose-insulin preparation are appropriate measures to institute in the short term, pending use of definitive treatment (eg. resuscitation, exchange
resin, or haemodialysis).
Bicarbonate Bolus equivalent to 50-100 mmol. Promotes cellular uptake of Temporising measure only
potassium by reducing hydrogen- Do not administer with Calcium salts
potassium exchange Not appropriate in hypovolaemic acidotic
patients
Exchange resins: Sodium (or Calcium) resonium Exchanges K+ for alternative cation Definitive but delayed treatment.
resonium 30-60g orally or rectally 8 hourly in gut, therefore action delayed for > May be difficult to administer in ICU patients
120 minutes with abnormal gut motility.
Sometimes given with lactulose 20ml

2 stimulants Nebuliser: 10-20 mg by nebuliser over 10 Intra-cellular transfer of potassium Temporising agent although concern exists
minutes over the use of an arrhythmogenic agent the
IVI: 0.5 mg IVI over 10-15 minutes critically ill.

Hypophosphataemia: Serum Phosphate < 0.7 mmol/L 385

Low serum phosphate is associated with serious clinical consequences, and is probably under-appreciated in critically ill patients.
Some studies suggest an incidence of up to a third of all ICU patients may be phosphate deficient.
Aetiology 386
Inadequate input
GIT phosphate binders (eg. laxatives, antacids)
Starvation
Vomiting or nasogastric suctioning
Relative or absolute Vit D deficiency
Transcellular shifts
Carbohydrate loading, re-feeding phenomenon.
Drugs: Insulin, catecholamines, steroids, β2-agonists
Excessive losses
Massive diuresis
Dialysis, including continuous replacement modalities.
Clinical effects 387
All energy requiring processes may be involved.
Cardiac: Decreased contractility.
Respiratory: Failure to wean.
Muscle / bone: Myopathy, Rhabdomyolysis, Osteomalacia.
Haematological: Dysfunction of all formed elements of blood.
Renal: Acute tubular necrosis.
Phosphate replacement 388
PHOSPHATE REPLACEMENT IN THE ICU
Serum phosphate: Dose (IVI):
> 0.7 mmol/L 0.16 mmol/kg over 4-6 hrs
0.5-0.7 mmol/L 0.32 mmol/kg over 4-6hrs
< 0.5 mmol/L 0.64 mmol/kg over 8-12hrs.

Acid-Base Disturbances in the ICU 389

Introduction 390
Critically ill patients commonly have a deranged acid base status. Despite this, explanations of the physiology behind the process are not
universally accepted. It is necessary to have an approach to the clinical importance of each of the common major abnormalities, even given
the complex and often mixed scenario’s you might encounter. You are encouraged to read widely on the subject of acid-base disorders and
the opposing ideologies put forward to explain them.
Correction of acid-base disturbance should be aimed at the underlying cause, and not at correction of the superficial abnormality.

General principles 391

The concept of pH:
pH = negative log of the hydrogen ion concentration. Normal range = 7.36 -7.40
Regulation of pH 392
Without regulation of acid-base, the daily production of non-volatile H + in a normal person (about 70 mmol) would reduce the pH in a
volume of water similar to that of a 70kg man (42 l) from 7.4 to a pH of 2.78.
The human body is an “open” system in which other organ systems and tissues contribute to the maintenance of the free [H +] within a
narrow, biologically tolerable range.
K x CO2
Henderson Equation [H+] =
[HCO3 - ]
-
6.1 + log[HCO3 ]
Henderson / Hasselbach Equation pH =
PaCO2 x 0.03
From both the above it is clear that any mechanism responsible for regulating or affecting pH does so by changing the relative concentrations
of HCO3- , PaCO2 or H+ directly.
The response of the body to an enforced change in one of these parameters takes place in three broad groups:
Adjusting minute ventilation (increasing respiratory rate or tidal volume) to manipulate PaCO2
Buffering systems:
Bicarbonate ion
Haemoglobin
Protein substrates
Phosphate
Renal compensation: delayed > 6-12hrs
Primary and secondary acid-base derangements 393
End point: “constant” PCO2 : HCO3- ratio
CHARACTERISING ACID -BASE DISTURBANCES
Acid-Disorder Primary Change Compensation
Respiratory acidosis PCO2 HCO3-
Respiratory alkalosis PCO2 HCO3-
Metabolic acidosis HCO3 -
PCO2
Metabolic alkalosis HCO3- PCO2
Compensatory changes are “never” complete, and certainly “overcompensation” does not occur.
Adequacy of compensation 394
Expected magnitude of compensation for a primary abnormality is given below. In critically ill or ventilated patients compensation may not
be possible, presenting as a mixed or complex problem.
EXPECTED COMPENSATION FOLLOWING ACID-BASE DISTURBANCE
Primary disorder Expected Change
Metabolic acidosis PCO2 in mmHg = ( 1.5  HCO3- in mmol/L) + 8
Metabolic alkalosis PCO2 = (0.7  HCO3-) + 21
Acute respiratory acidosis pH = 0.008  (PCO2-40) or approx 1 mmol/L  in HCO3- per 10 mmHg increase in PaCO2
Chronic respiratory acidosis pH = 0.003  (PCO2-40) or approx 4 mmol/L  in HCO3- per 10 mmHg increase in PaCO2
Acute respiratory alkalosis pH = 0.008  (40-PCO2)
Chronic respiratory alkalosis pH = 0.017  (40-PCO2)

Metabolic Acidosis 395

The anion gap 396
Classically metabolic acidoses are classified according to the concept of anion gap. Whilst the body must maintain overall electrical
neutrality there are a number of unmeasured ions which result in a difference when the major cations are compared to the major anions.
ie. Anion Gap = {Na+ + K+]-[Cl- + HCO3- ] = 12-17 mmol/L = unmeasured anions
DETERMINANTS OF THE ANION GAP TABLE 24
Unmeasured anions Unmeasured cations
Proteins (albumin) 15 mmol/L Calcium 2.5 mmol/L
Organic acids (lactate, ketones) 5 mmol/L Magnesium 1.2 mmol/L
Phosphates 2 mmol/L IgG
Sulphates 1 mmol/L Other
An increase in anion gap usually means an increase in an organic acid. In some patients with low serum albumin this may be masked unless you adjust accordingly.
Aetiology 397
Raised anion gap metabolic acidosis 398
Lactic acidosis
Ketoacidosis
Rhabdomyolysis
Drugs or toxins:
Aspirin (may result in elevated salicylate, lactate, ketones)
Ethanol
Methanol
Ethylene glycol
Paraldehyde
Renal failure: usually only mildly elevated anion gap ( < 23)
Low or normal anion gap acidosis 399
Hyperchloraemic metabolic acidosis:
Infusion IVI of NaCl
Resolving renal failure
Renal tubular acidosis / carbonic anhydrase inhibitors
GIT losses including fistulae
Hypoalbuminaemia
Myeloma
Management 400
High anion gap 401
Address cause. Bicarbonate administration is not indicated
Normal anion gap 402
Address underlying cause.
In some situations (eg. renal tubular acidosis) it may be appropriate to replace / administer bicarbonate directly.
Approx deficit = (24-[HCO3-]) × (body weight × 0.6) in mmol.
Generally one third to one half of the estimated deficit should be replaced and then acid-base status reviewed.

Metabolic Alkalosis 403

Aetiology 404
Common causes 405
Diuretics
Vomiting
Post hypercapnoea > 48 hrs
Any fluid loss replaced with insufficient Na+, associated with H+ loss (contraction alkalosis).
Association with hypovolaemia and / or hypokalaemia
H+ / Proton loss. 406
Renal
↑ Na+ reabsorption
Cushings syndrome including exogenous steroid administration
Proximal tubulopathies: Bartter’s syndrome, Liddle’s syndrome
Hypercalcaemia / hypomagnesaemia associated with diabetes insipidus
Diuretics
GIT
 NG suctioning or protracted vomiting
Diarrhoea (acidosis more likely)
Increased administration of bases 407
CVVHDF-lactate buffered solution
Management 408
Correct hypovolaemia and electrolyte abnormalities
Review drugs, and administration of exogenous bases (lactate buffered dialysate, citrate)
Acetazolamide has been used to increase renal losses of bicarbonate, however this should not be considered routine practice.

Respiratory Acidosis 409

Aetiology 410
Any cause of hypoventilation, whether respiratory failure or planned (permissive hypercapnoea ventilation).
Treatment 411
Address underlying respiratory pathology

Respiratory Alkalosis 412

Aetiology 413
Any cause of hyperventilation in ICU eg. early sepsis
Early hypoxic situations
Anxiety
Hysteria (NB this is a diagnosis by exclusion, and presumes normal oxygenation)
Neurogenic hyperventilation: usually a marker of severity of head injury.
Treatment 414
Treat underlying problem.

Nutrition 415
Enteral Nutrition 416
The prevalence of malnutrition is increasing in hospitalised patients due to the aging process of the general population and the development
of aggressive medical and surgical treatments for chronic debilitating diseases.
The positive consequences of enteral feeding however may go beyond nutrition and extend to immune modulation, and possibly bacterial
translocation through the gut.
Enteric feeding is the preferred mode of nutritional support and should be considered in all patients admitted to the ICU.
Reference
Jolliet P et al. Enteral nutrition in intensive care patients: a practical approach. Working group on nutrition and metabolism, European Society of Intensive Care.
Intensive Care Medicine 1998.24(8): 848-59.
Advantages 417
In some patient subgroups (trauma) early enteral feeding improves patient outcome.
Enteral feeding helps retain gut integrity and reduce atrophic changes.
May reduce the incidence of gastric erosions and stress ulceration
Cost effective: Cheaper than TPN !
Complications of central access for TPN are reduced (invasive procedures, infective risk)
Disadvantages 418
Regurgitation / aspiration (no difference gastric versus distal feeding)
Diarrhoea: diarrhoea may be a result of osmotic load to the gut, however it is not the most likely reason for diarrhoea in critically ill
patients, and other causes should be sought and excluded.
Indications 419
All ICU patients with a secure airway and functioning gut may receive enteral feeding.
Patients admitted post surgical intervention should have the intention to feed cleared with the surgeon in charge.
Patients with operatively placed jejunostomy may commence feeding within 6 hours of placement (again, confer with the surgeon)
Where gastric feeding has not been established by day 5 of ICU admission (or earlier if undernourished), a post-pyloric (duodenal / jejunal)
tube should be considered for distal feeding. Use of hypercaloric feeds may be considered to ensure reasonable intake.
Consider placing a fine bore feeding tube, to reduce irritation and ulceration, once feeding has been established for a reasonable length of
time (5-7 days).
Contra-indications 420
Absolute: 421
Non-functional gut: anatomical disruption, obstruction, gut ischaemia
Generalised peritonitis
Severe shock states
Relative 422
Expected short period of fasting (except trauma patients)
Abdominal distension while feeding enterically
Localised peritonitis, intra-abdominal abscess, severe pancreatitis
Comatose patients at risk of aspiration
Extremely short bowel ( < 30 cm)
Feeding Guideline 423
(see algorithm below)
 ⋅ Place a 12F or larger nasogastric tube to allow reliable aspiration (orogastric tube should be considered in patients with anterior and
middle cranial fossa trauma).
⋅ Check position of feeding tube with abdo X-ray prior to feeding. It may not be obvious from standard CXR or AXR that the tube is
adequately placed, requiring a modified film or both views.
⋅ Nurse the patient at 30-45 degrees head up.
⋅ Commence feeds at 30 ml/hr and feed continuously according to the attached protocol.
⋅ Aspirate the tube 4 hrly (do not attempt routine aspiration of jejunostomies, naso-duodenal or naso-jejunal tubes.
⋅ Flush jejunostomy or gastrostomy tubes with 10-20 ml of saline 6 hourly if not being used.

The Waikato Hospital Enteral Feeding Algorithm

Aspirate > 300 ml: start entral feed 20 ml/hr

Discard. Stop feed.
Reassess appropriateness
of entral feeding

Aspirate after 4 hrs:

is volume > 200 ml ?
Yes No

Return all aspirate

Return 200 ml only increase rate to
continue at same rate 40 ml/hr

Aspirate after 4 hrs:

is volume > 200 ml ?
Yes No

If aspirate consistantly > 200 ml for 24 hrs, consider: Return all aspirate and increase
Reassess appropriateness of entral feeding feed by 10 ml / hr at each test
Prokinetic (erthromycin 100 mg 6 hrly IVI) aspirate until goal rate achieved
Post - pyloric feeding (jejunal) or aspirate > 200 ml.

Prokinetics: 424
If feeding is persistently not tolerated > 48hrs then consider
Reduction in narcotic dosage
Use of a prokinetic agent: metoclopramide 10 mg IVI 6 hrly, then if necessary erythromycin 100 mg IVI 4hrly.
Post-pyloric feeding
Choice of enteral feed 425
Most patients should be commenced on a standard isocaloric feed such as Nutrison standard multifibre.
Nutritional supplementation should be adjusted to provide approximately 25-35 kCal / kg weight / day of non protein energy, and 1.0-1.5 g /
kg body weight of protein per day.
Immuno-fortified feeds (with glutamine, arginine, nucleotides, omega-3-fatty acids) have shown some benefit in small studies to date. Their
use is accepted to be of benefit in polytrauma patients. Despite this there is as yet no defined place for these feed types in the ICU setting.

Parenteral Nutrition 426

General 427
Historical attempts at hyper-alimentation may have resulted in the role of PN in the ICU diminishing over the last 10 – 20 years. Concerns
still exist over potential immuno-suppression, hyperglycaemia and the infection risk coupled with central venous access.
PN should not be ordered unless requested by the duty ICU specialist.
Indications 428
Parenteral nutrition should only be considered in patients who are not suitable for adequate enteral feeding.Indications for specialised
nutritional support apply; route selection is based on specific pathology present which might contraindicate enteral feeding.
Short term:
No enteral intake likely >7-10 days in previously well or mildly malnourished
No enteral intake likely >5-7 days if previously malnourished or currently catabolic
Weight loss > 10 % starting body weight
Long term:
 Structural or functional short bowel syndrome
Vascular access 429
TPN may be administered by central or peripheral access if an appropriate formula is used.
Complications 430
Depression of immune function
Gut villous atrophy
Metabolic imbalance:
Electrolyte disturbance
Glucose intolerance
Hyperosmolar dehydration syndrome
Rebound hypoglycaemia on ceasing TPN
Hyperbilirubinaemia
Fluid imbalance
Trace element and vitamin deficiency
Complications of central venous access.
Charting TPN 431
Choice of formula 432
Waikato Hospital commonly uses 2 pre-mixed ‘3-in-1’formulae.
“Parenteral nutrition -glutamine supplemented” (should be charted in this way). Must be given centrally. Usually commenced at 60ml/hour.
Final hourly infusion rate approximates patient weight if non-catabolic or add 20ml/hour if catabolic.
Peripheral parenteral nutrition- 0.6 kCal/ml. Start at 80 ml/hr and increase to 120 ml/hr as tolerated. Beware extra volume.
Points to note:
Referral is made on a customised referral form
If patients blood sugar estimation exceeds 10 mmol/ L, the managing team should be encouraged to commence an insulin sliding scale
A sticker in the TPN folder outlines the expectation for blood sampling and approach to possible line infection.This should be stuck in the
patient notes on commencement
A note should be made in the patient notes if TPN is refused or discontinued
A daily round is generally appropriate, but for longer courses or where cessation has been recommended by ICU staff, the patient may not
be rounded on
During the week the receptionist will fill out the lab results sheet; at the weekend this should be done by the short day registrar
Suspected vascular access infection in TPN patient 433
See TPN folder

Blood and Blood Products 434

Introduction 435
The decision to transfuse a patient, or administer other blood products, outside of these guidelines is the prerogative of the duty ICU
specialist.
Whenever reasonable, the patient’s informed consent to proceed with transfusion should be obtained.

Blood transfusion 436

Acute resuscitation 437
Excessive ongoing haemorrhage is usually surgical in origin. In these circumstances transfusing blood products should be viewed as a
bridging procedure until definitive treatment is undertaken.
Platelet count and coagulations studies should be performed, and if abnormal addressed as required.
Blood replacement in an otherwise fit patient should be considered once blood loss is anticipated to exceed 25 % of total blood volume (or
1000-1500ml).
A full cross match may take up to 20 minutes, if blood is required faster than this consider one of the following:
Group specific (ABO, Rh+) blood without full compatibility testing may be available faster (5-10 minutes).
“O negative” blood can be issued immediately in a true emergency, while similarly “O positive” blood can be used for men, or women past
child bearing age.
Elective transfusion 438
%
Traditionally a haematocrit of 30 or absolute haemoglobin of 10 g/L have been used as a trigger to transfuse a patient. In stable patients with
adequate oxygenation there is no need to transfuse until Hb ≤ 70.0 g/L. Critically ill patients with poor oxygenation, myocardial ischaemia,
acute head injury or ongoing risk of blood loss may require earlier transfusion.
Elective transfusion in the Waikato Hospital ICU should be conducted according to the algorithm below:

Elective transfusion of ICU patients

 ADULT PATIENT WITH ANAEMIA

POST CABG ? Maintain

YES Hb > 80 g/dl

NO

UNSTABLE
CARDIAC
CORONARY
DISEASE ? YES SYNDROME?

YES N
NO
O

Maintain Maintain
Hb > 80 g/dl Hb > 70 g/dl if no
ONGOING (? 90 g/dl) active bleeding
BLEEDING ?

N
YES

Attempt to maintain
ACCEPT
Hb > 70 g/dl
Hb > 70 g/dl

Reference:
Hebert PC. Transfusion requirements in critical care. British Journal of Anaesthesia 1998. 81,Suppl 1:25-33.
Bracey et al. Lowering the hemoglobin threshold for transfusion in coronary bypass procedures: effect on patient outcome. Transfusion, 1999, 39(10): 1070-1077

Platelet transfusion 439

Indications 440
Permission may have to be sought from a Haematologist prior to platelets being issued.
Spontaneous haemorrhage is rare at platelet counts of > 10 ×109 / µl (or > 20 ×109 / µl in febrile patients)
Prophylactic transfusion before surgery or invasive procedure:
Platelet count < 50 × 109 / µl
Platelet count > 50 × 109 / µl where there is evidence of abnormal platelet function (eg. uraemia, aspirin therapy)
Uncontrolled haemorrhage:
Transfuse platelets at platelet count < 100 × 109 / µl
Consider transfusing platelets at any threshold if there is reason to suspect platelet dysfunction.
Bone Marrow failure, TTP ,ITP, or H.I.T.S.
Seek advice from haematology team.
Dosing of platelets 441
One dose of platelets usually means pooled donor platelets from 4 or more donors.
One dose approximates 3-3.5 × 1011 platelets, or enough to increase the platelet count by 20-25 × 109 / µl at 24 hours, in the absence of
further problems.
Risk of transfusion 442
In general the risk is similar to that for blood transfusion with the following addition:
There is a higher risk of bacterial contamination than whole blood (0.6 / 1000 cases per dose)
HLA allo-immunisation may occur in 45-62% of long term recipients, resulting in transfusion resistant thrombocytopaenia.
Platelet specific antibodies may develop (4% of patients)
Adjunctive treatment 443
Administration of DDAVP 0.3-0.4 µg/kg over 30 minutes may increase levels of factor VIII:C and VIII:vWF with increased platelet
adhesion.
Indication 444
Haemophilia A, type I von Willebrand’s Disease.
Bleeding post cardio-pulmonary bypass
Uraemia
Platelet dysfunction secondary to aspirin
Other scenarios where platelet dysfunction is suspected and platelet transfusion might be delayed, or stock exhausted.
Fresh Frozen Plasma 445
Indications 446
Prophylactic transfusion prior to surgery or other invasive procedure
Patients on warfarin ro vit K deficiency: consider partial reversal with 1 mg Vit K or full reversal with 10 mg Vit K if time allows
(24-36hrs).
Prolonged INR or APTT in patients with liver disease
Inherited coagulation factor deficiency when factor concentrates not available.
Haemorrhage
Warfarin or Vit K deficiency
Prolonged INR or APTT in patients with liver disease
Inherited coagulation factor deficiency when factor concentrates not available
DIC
Massive transfusion:
Consider administering calcium as citrated stored blood is calcium deficient, retarding the clotting cascade.
Whole stored blood does not contain clotting factors in any appreciable number
Consider transfusion when INR > 1.5 or APTT > 40 seconds.
Plasma exchange in TTP and related syndromes.
Dosing of FFP 447
10-15 ml/kg (average 2-4 units) according to clotting profile.

Cryoprecipitate 448
Indications 449
Diffuse microvascular bleeding and fibrinogen < 1.0 g / L
DIC
Massive transfusion
Hereditary hypofibrinogenaemia
Dose 450
Generally 2-4 units.

DIC 451
Definition: 452
A process representing disordered balance of the haemostatic and fibrinolytic systems, usually in response to severe pathophysiological
stimuli as part of multisystem organ dysfunction. Characterised by:
Microthrombi formation causing microvascular obstruction
Consumption of platelets and clotting factors
Thrombocytopaenia
Diagnosis-DIC screen 453
Blood smear examination for evidence of red cell fragmentation, haemolysis, thrombocytopaenia.
Extended coagulation screen:
Prolongation of thrombin clotting time, APTT, Prothrombin time.
Hypofibrinoginaemia
Low factor VIII
Elevated fibrin breakdown products (FDP’s).
Liver function tests and renal function review.
Treatment 454
Treat the underlying cause
Replace blood components as assessed by above DIC screen if patient bleeding or at risk of bleeding.
Controversial therapies 455
Heparin, fibrinolytics, antifibrinolytics (aminocaproic acid) and other agents have been described in the literature. They do not form part of
standard therapy and should not be attempted without ICU consultant approval, and not before exhausting other therapies at the advice of the
haematology specialty service.

Blood transfusion reaction guidelines 456

Introduction 457
A wide range of reactions can be manifest upon infusion of blood products.
The response to a suspected reaction depends on the urgency of the transfusion and the magnitude of the adverse reaction.
Suspected transfusion reaction 458
Stop the infusion and check the patient details against that of the blood product. If there is any discrepancy then discontinue the transfusion.
If patient and product details are correct then proceed as follows.
Mild reactions 459
Temperature rise < 1.5 oC without hives, rash, bronchospasm or cardiovascular compromise: restart transfusion at slower rate.
Moderate reactions 460
If temperature rise > 1.5 oC other manifestations, administer antipyretic (paracetamol 1g) and restart transfusion of the same unit after 20
minutes.
Severe reactions 461
If any signs or symptoms in addition to temperature rise, discontinue the transfusion and return the blood product to blood bank for re-
crossmatch and culture.
Treat as for anaphylaxis:
Volume resuscitation
Adrenaline or vasopressor as necessary.
Bronchodilators if significant airway outflow obstruction.
Adjuncts: anti-histamine, theophylline, corticosteroids may not be appropriate in ICU population and should be discussed with duty ICU
specialist.
Clinical Management 4620
Introduction 463
The purpose of this chapter is not to dictate rigid policies on the most appropriate way to manage every patient. Rather it is to provide
guidelines on reasonable clinical practice based on the available evidence and where that is lacking, based on consensus practice.
As you will come to realise during your stay in the ICU very few patients read the appropriate textbooks prior to becoming ill. Patients
therefore may not behave in a “classical” or expected manner. It is in these patients that these guidelines may help you to adopt a reasonable
and standardised approach.

Cardio-Pulmonary Resuscitation 464

Introduction 465
Whilst we have little control at present over community cardiac arrests, and to a lesser extent hospital cardiac arrest, it must be stressed that
vigilance and pro-active management of critically ill patients may abort a process precipitating a cardiac arrest within the ICU.

Key Points in the management plan for an adult collapse 466

In adult cardiac arrest, VF / VT is the most likely rhythm, and a defibrillator the only effective treatment.
⋅ Start effective CPR as soon after the circulatory arrest as possible. Effective artificial circulation requires controlled, uninterrupted
chest compression. The ratio of compressions to ventilation is 15:2 in all instances except when an ETT is in place, when it is 5:1
with no compression pause. The rate of compression is 100 / min.
⋅ As soon as possible (especially in unmonitored patient) switch the defibrillator on and check or confirm the rhythm via the paddles.
⋅ Defibrillate as soon as possible. Defibrillation should take precedence over all other interventions. Assess for, and shock, VF /
pulseless VT, up to 3 times (200J, 200J to 300J, 360J or equivalent biphasic) if necessary.
Endotracheal intubation, IV insertion and ECG electrode placement / replacement should occur between defibrillation attempts. The order of
priority for these adjuncts is
⋅ secure airway
⋅ ventilate with 100% oxygen
⋅ IV administration.
Augmentation of aortic diastolic pressure should be an adjunctive goal of therapy since coronary perfusion is low during conventional CPR.
Adrenaline and other alpha agonists will significantly increase aortic diastolic pressure. Administer adrenaline to maintain coronary blood
flow if the first three defibrillations fail. 1 mg of adrenaline every 3 minutes is an acceptable minimum. Vasopressin 40.i.u IV is a suitable
alternative in VF / VT arrests.
Consider and correct if possible any reversible causes of circulatory arrest. (see 5H’s and 5T’s on algorithm below)
During CPR, adequate ventilation is the mainstay of therapy for acid-base abnormalities. The indications for Sodium Bicarbonate are:
Hyperkalaemia
Tricyclic antidepressant overdose where metabolic acidosis existed prior to arrest.
Late in cardiac arrest situation (at least > 10 minutes) in intubated hyperventilated patients.
If VT / VF persists after 9 defibrillating shocks, give amiodarone 150 mg IVI or lignocaine 1-1.5 mg/kg. Give earlier if a defibrillating shock
seems transiently successful.
Reference:

Basic and Advanced CPR: Management Plan for Adult Collapse

 Adult Cardiac Arrest

Basic Life Support Algorithm if appropriate ABC

Consider Praecordial Thump

Attach defibrillator / monitor and assess rhythm

VF/VT Check Pulse non VF/VT

Attempt defibrillation x3
as necessary
During CPR
Check electrode/paddle position and contact

CPR up to 3 mins
secure airway, attempt and verify IVI access
VT/VF refractory to initial shocks
CPR 1Min

Adrenaline 1 mgIV every 3-5 min

(or vasopressin 40U IV single dose x1 only)
Paients with non-VF/VT rhythms
Adrenaline 1mg IV every 3-5 mins
Consider antiarrhythmics, pacing, buffers
Search for correctable causes

Consider Cuases that are potentially reversable

Hypovolaemia Tablets
Hypoxia Tamponade, cardiac
Hydrogen ion - acidosis Tension Pneumothorax
Hyper / Hypo - kalaemia Thrombosis (acute cononary syndromes
Hypothermia Thrombosis (pulmonary embolism)

Induced hypothermia following cardiac arrest 467

Introduction 468
Patients subjected to therapeutic hypothermia as soon as possible following resuscitation from cardiac arrest may have a better outcome (15-
25% absolute survival advantage). Following consultation with the Duty Intensivist, short term hypothermia should be induced as below.
Patient selection 469
Apply to patients with
Suspected hypoxic-iscaemic encephalopathy.
Motor score of GCS 4 or less (ie flexion to pain or worse)
Cooling guideline 470
⋅ Cool as soon as possible following return of circulation.
⋅ Use up to 40ml/kg of fridge cold isotonic crystalloid if necessary
⋅ Sedate with propofol, with intermittent muscle relaxant to ablate shivering if prominent
⋅ Actively cool, using water cooled blanket to temperature target of 33 (32.5-33.5) deg centigrade for 12 hours, as measured with rectal
temp probe.
⋅ After 12 hours actively re-warm to 37 degrees.
⋅ Conduct sedative free neurological assessment. Progress to somato-sensory evoked potentials if awakening slow or absent.
Rapid Cooling 471
Rapid onset cooling can be achieved by administering up to 40ml / kg of Ringers lactate or other isotonic crystalloid, cooled to 4 degree
centigrade, over a 30 minute period
Reference:
Bernard et al. Induced Hypothermia in Critical Care Medicine: A review. Critical Care Medicine 2003; 31(7):2041-2051.

Respiratory Therapy 472

Introduction 473
Traditionally the major reason for referral to intensive care, respiratory failure and our understanding of how best to manage it is constantly
evolving.
Recent advances in ventilatory strategy, and their impact on not only lung injury but also on other organ dysfunction, necessitates that all
staff within the ICU acquire some understanding of the pathophysiology involved.
While Registrars and residents are encouraged to understand the principles of ventilation, and indeed participate in the management of
ventilated patients; decisions regarding ventilation, weaning, extubation and other extra-ordinary actions (such as patient proning) remain
the domain of the duty ICU specialist.
Respiratory Failure 474
Definition:-Failure of efficient gas exchange. Either failure to oxygenate adequately, or failure to ventilate.
Failure to oyxygenate adequately 475
PaO2 < 60 mmHg under the following conditions:
FiO2 21% (i.e. room air)
Barometric Pressure 760 mmHg (sea level)
No intracardiac shunt
NB: This does not mean taking a patient off oxygen to perform and arterial blood gas, but rather inferring the need for “assistance” as stated
below.
Failure to ventilate adequately 476
PaCO2 > 50 mmHg, unless in the presence of a primary metabolic alkalosis (pH normal or elevated)

Aetiology 477
Lung insult
Pulmonary oedema (hydrostatic-cardiogenic, or leaky capillary-ARDS)
Pneumonia
Contusion
Haemorrhage
Airway pathology
Proximal
Distal: COAD, asthma, bronchiectasis, sputum retention
Neuromuscular
Depressant drugs
Intra-cranial pathology
Guillan Barré
Myasthenia Gravis
Skeletal
Loss of chest wall integrity: flail chest
Loss of chest wall elasticity: severe kyphosis or scoliosis
Intra-thoracic space occupying lesion: Pneumo-/ Haemothorax, pleural effusions.

When Should I Consider Ventilating ( intubating) Patients ? 478

Indicators 479
Clinical assessment outweighs any “result” such as an ABG / CXR or other objective measurement (see below)
Consider institution of ventilation in the presence of:
Threatened airway
Fatigue or imminent exhaustion
Inability to effectively cough or clear secretions
Respiratory failure
Objective measurements 480
In the appropriate clinical setting, and where time allows a combination of the following may assist your decision.
Resp rate > 35 breaths per minute
Tidal volume < 5 ml/kg
Vital capacity < 15 ml/kg
Abnormal oxygenation as indicated by:
PaO2 < 75 mmHg on an FiO2 > 0.4 (40% O2)
PaO2 to FiO2 ratio < 150
Abnormal ventilation as indicated by:
PaCO2 > 60 mmHg
OXYGEN DELIVERY SYSTEMS
Classification Device Oxygen Flow (l/min) Approx FiO2 as percent Comment / Indication
Variable delivery devices Nasal Catheters 2 28% Not suitable for acutely ill patients.
4 35% Indicated to provide supplementary oxygen only in
6 45% stable patients
Semi-rigid masks 5 35% Inspired fraction of oxygen variable with minute
(eg Hudson) 6 50% volume
8 55% Popular because of low cost, not accurate oxygen
delivery
10 60%
12 65%
Reservoir plastic 6-15 FiO2 = 21% + 4% per l/min
masks
Fixed Delivery Devices Venturi type masks 2-8 24-50% according to Fixed delivery device at all but extreme of
manufacturer instructions respiratory effort.
More expensive than hudson type mask, but
preferable in unstable patients
CPAP devices Most of these devices make use of turbine devices or high wall flow to provide oxygen / gas mixtures at
BiPAP system flow rates in excess of that achieved at peak respiratory effort. They usually all allow reasonably accurate
oxygen / gas blending and therefore control of patient FiO2
Ventilators

Humidification 481
General 482
Poor conditioning of the temperature and humidity of inspired gases leads to airway damage, sputum plugging and may even increase
morbidity and mortality of during an ICU stay.
All patients that are intubated / tracheostomised must have adequate humidification of inspired gases using one of two mechanisms
Heat and Moisture Exchangers (HME’s) 483
Effective first line humidifier: Conserves patients exhaled water vapour and temperature (gas re-inspired at about 20 deg C). Still requires
patient to be able to warm and humidify inspired gas to some degree.
Not effective at minute volume in excess of 10 l/min.
Must be changed daily
Cannot be used with an in-line nebuliser.
Incorporates a bacterial filter.
Heated water humidifiers (Fisher and Paykel evaporative humidifier) 484
Where any doubt exists about adequate humidification, a heated water humidifier should be the default humidifier, particularly those patients
in whom there is bronchorrhoea, sputum inspissation or haemoptysis.
Generally these devices supply gas to the upper proximal airways at 29-32 oC and 95-100% relative humidity, requiring minimal modification
within the lungs.

Mechanical Ventilation 485

Introduction 486
Mechanical ventilation is one of the mainstays Intensive Care Medicine and you should attempt during your stay to develop an
understanding of the basic principles and practice of ventilation.
Registrars are not expected to manage patient ventilation alone. While most patients can be ventilated using a “default” setting (see below),
ventilation of complex patients remains the domain of the duty ICU specialist.
Senior Critical Care Nursing Staff may be useful resource people to aid in troubleshooting, and assisting with instituting ventilation using a
default setting.
No change may be made to a ventilator without clear written order on the appropriate chart and communication with bedside staff.
Indications for mechanical ventilation 487
Respiratory failure
Maintenance of cardiopulmonary homeostasis in an unstable or high risk environment:
Following cardiac arrest
Post-operative support in high risk surgical patients
Control of intracranial pressure
Patient Transport / assessment
Relaxant anaesthesia
Objectives of mechanical ventilation 488
Improve patient oxygenation and improve ventilation perfusion mismatch.
To improve alveolar ventilation and reduce PaCO2
To increase end expiratory lung volume, preventing or treating lobar or pulmonary collapse and atelectasis.
To increase functional residual capacity: PEEP may help improve oxygenation through lung recruitment, and reduce lung injury with the
prevention of repeated opening and closing of alveoli.
To unload the respiratory muscles when there is respiratory muscle insufficiency or ventilatory failure.
To allow adequate sedation and paralysis of the patient to aid control to enable the underlying disease state to be adequately treated.
In some conditions such as trauma where there is loss of chest wall integrity such as in a flail chest, ventilation may be needed to stabilise
the chest wall and to initiate other treatment such as analgesia with safety.
Complications of mechanical ventilation: 489
Haemodynamic 490
Increased intrathoracic pressure-unmasking of hypovolaemia (although there is significant benefit to LV performance with application of
PEEP).
Respiratory 491
Nosocomial pneumonia
Volutrauma
Barotrauma
Ventilator dependency
Metabolic 492
Post-hypercapnoeic metabolic alkalosis
SIADH
Local 493
Pressure effects from ETT, tracheostomy or face masks.
Ventilator settings 494
Default ventilator settings, and principles in optimizing ventilation in ICU patients 495
(see appendix for explanation of ventilation modes and terminology)
Where there is no reason to expect mechanical ventilation will be complex the following settings should be chosen:
Mode 496
SIMV, volume control.
Oxygen 497
Titrate delivered oxygen to provide an oxygen saturation > 90% (an equivalent arterial PO2 of > 60 mmHg), unless otherwise specified by the
duty ICU specialist.
Tidal Volume 498
The ARDS-net trial suggested 6-8 ml per kilogram ideal body weight per breath (450-550 ml per delivered breath in a 60 kg woman, 500-650
ml in a 70 kg male). Generally in the Waikato Hospital ICU 8-10 ml / kg is the preferred volume.
Peak and plateau airway pressures resulting from instilling the chosen tidal volume should not exceed 40 cmH2O and 32 cmH2O respectively
in the short term, and preferably not more than 35 cmH2O and 28 cmH2O respectively for more than a few hours.
Reference:
Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. New England Journal
of Medicine 2000, May 4. 342(18):1301-8
Respiratory rate 499
10 to 25 breaths per minute adjusted to an arterial blood gas PaCO2 in the normal range or approximating pre-morbid level.
Rapid ventilatory rates are not appropriate in patients with prolonged expiratory phase (ie Acute status asthmaticus: 5-8 breaths per minute
adequate and perhaps desirable).
In some patients attempting to normalize arterial carbon dioxide content may expose the patient to the risk of barotrauma and / or volu-
trauma. It is important that the duty ICU specialist is notified if this is suspected.
PEEP 500
As a guideline, PEEP may be applied using the nomogram below, titrated to arterial oxygen content:
FIO2 0.3 0.4 0.4 0.5 0.5 0.6 0.7 0.7 0.8 0.9
PEEP 5 5 6 6 10 10 10 12 14 16
Spontaneous mode of ventilation 501
Indications 502
Consider allowing the patient to breathe spontaneously if:
FiO2 ≤ 0.4 and PEEP ≤12 cmH2O and
PEEP and FiO2 values are trending downwards.
The patient has spontaneous breathing efforts
Haemodynamically stable
Newer generation ventilators may facilitate the use of spontaneous modes in patients who are sicker, generally however this should be
discussed with the duty ICU specialist.
Mode 503
“Pressure support”
Support level 504
Titrate level of pressure support 5-15 cmH2O to achieve acceptable tidal volume (see above) and respiratory rate below 30 breaths per minute
(preferably < 25 / min).
PEEP 505
5-12 cmH2O according to FiO2, see chart above

Positive Pressure Ventilation and Hypotension 506

Positive pressure ventilation may exacerbate or induce hypotension by increasing relative intrathoracic pressure and therefore decreasing
venous return to the heart. ie
Mild – moderate: Loss of negative phase of inspiration and initiation of PEEP
Extreme: Excessive increase in intrathoracic pressure (auto-PEEP or tension pneumothorax)
Weaning from Mechanical ventilation 507
Introduction 508
In many patients, especially those requiring short-term support, mechanical ventialtion can be removed quickly and easily. In more complex
cases however considerable difficulty may be encountered
The actuarial risk of nosocomial pneumonia increases by about 1 % per each day of MV, being 6.5% at 10 days and 19% at 20 days. It is crucial
to discontinue ventilatory support and extubate at the earliest time that a patient can sustain spontaneous ventilation safely. Planning for
weaning should start as soon as the patient is intubated, using the following parameters:
How long can we expect this patient to require mechanical ventilation (MV)? Is a tracheostomy likely to be needed?
What is the underlying disease process and how may this impact on weaning?
Premature attempts at weaning can result in respiratory muscle fatigue and atelectasis.
Premature extubation with resultant reintubation carries an appreciable risk to the patient.
Minimum requirements for extubation 509
Improving clinical condition.
Patient stable on FiO2 < 0.4 with a PaO2 > 60 mmHg
PEEP < 5-8 cmH2O
Acceptable neurological state: ie the expectation exists that the patient will be awake enough to protect their airway, and have the local
ability (intact cranial nerve function or tracheostomy) to do so.
Haemodynamically stable
No prospect of major intervention planned in the ensuing 24 hours
Predicting successful weaning from mechanical ventilation 510
In a small percentage of patients, there may be some doubt as to whether the patient will cope with removal of respiratory support despite
meeting the above criteria. A number of parameters have been studied, however at present a “spontaneous breathing trial is considered the
most useful, with a positive predictive value of about 80%.
Spontaneous breathing trial 511
⋅ The patient should receive no more than a PEEP of 5 cmH2O through a T-piece system. Generally if an SBT is conducted while on the
ventilator, no more pressure support than is sufficient to overcome “system” resistance to flow should be allowed (see ETT
compensation mode on newer generation Puritan-Bennett).
⋅ Allow 120 minute trial (some suggestion 30 minutes may predict adequately)
⋅ If trial successful extubate
Markers of successful Spontaneous Breathing Trial 512
Objective
Gas exchange acceptable ( Oxygen sat > 90% , PaO2 > 50 – 60 mmHg , Increase in PaCO2 < 10 mmHg)
Stable ventilatory pattern (RR < 30 – 35 / min , RR not changed > 50%)
Haemodynamically stable
Subjective
No onset or worsening of discomfort
Diaphoresis
Clinical evidence increased work of breathing
Reference:
Collective task force. Evidence-Based Guidelines for Weaning and Discontinuing Ventilatory Support. Chest Dec 2001 120(6): 375S-395S.
Chosen mode of weaning to extubate 513
There is no evidence that a trial of unsupported breathing using a T-piece apparatus is any better or worse than decremental levels of pressure
support ventilation. Both may be used in The Waikato Hospital ICU prior to planned extubation.
The duration of the trials is not defined but those that fail usually do so early on. Probably 30 minutes to two hours is all that is needed.
Clinical signs of failure include tachypnoea, tachycardia, hypertension, obtundation, and desaturation.
Factors that influence success of weaning 514
Increase in work of breathing
Increase metabolism (increasing CO2 production)
Fever, sepsis, carbohydrate excess
Reduction in pulmonary or chest wall compliance
Pulmonary oedema, acute respiratory distress syndrome, atelectasis, pneumonia
Bronchospasm, retention of secretions
Obesity, abdominal distension
Unfavourable respiratory circuit characteristics
Delayed response and high negative pressure to ‘trigger’ high resistance circuitry
Inspiratory flow rate unable to match peak inspiratory flow
Reduction in respiratory muscle power
Electrolyte abnormalities (Hypokalaemia, hypomagnesaemia, hypophosphataemia, metabolic alkalosis)
Cardiovascular failure (Left ventricular failure, shock, anaemia)
Polyneuropathy of the critically ill
Myopathy (eg endocrine or carcinomatous)

Depression in respiratory centre

Excess respiratory depressant drugs
Hypothyroidism
Pain
Brain Injury
Ventilation in the prone position 515
Introduction: 516
Ventilating a patient in the prone position has not been shown to improve mortality, however in up to 60 % of selected patients there is a
significant improvement in oxygenation, often persisting beyond the period spent prone.
It is unclear how long a patient should be ventilated in the prone position. The majority of patients that do respond do so quickly, however up
to 30% may exhibit delayed improvement. Available evidence suggests > 12hrs is recommended.
The decision to prone a patient should not be made lightly, and is the domain of the ICU specialist.
Once the decision has been made to prone a patient, this should be done following ICU nursing guidelines, under the direction of an
experienced nursing team.
Rationale for prone ventilation: 517
Increased uniformity of regional pleural pressure gradient.
Improvement in dorsal ventilation with a reduction in shunt fraction
Improved ventilation-perfusion heterogeneity.
Uniform distribution of lung water and exudate
Improvement in FRC with further alveolar recruitment
Reduction in diaphragmatic splinting and improved movement of the posterior diaphragm
Non-restriction of abdominal contents
Indications: 518
Severe ARDS as given by: PaO2: FiO2 ratio < 100
Non response to standard supportive / ventilatory care
Local or anatomical factors (eg. posterior burns)
Relative Contraindications: 519
Inadequate staff to perform procedure safely
Anterior intercostal catheter
Continuous renal replacement therapy
Intra-aortic balloon counterpulsation
Morbid obesity
Hazards: 520
Difficult airway management and access (including ETT kinking and dislodgement)
Accidental removal of invasive catheters (and possible occult haemorrhage)
Obstruction or disconnection of abdominal / thoracic drains.
Pressure necrosis, pressure neuropraxia and blindness
Labour intensive procedure-distraction from other patients
Reference:
Tobin A, Kelly W. Prone Ventilation-it’s time. Anaesth Intensive Care 1999, April 27(2): 194-201
Chatte G et al. Prone Position in Mechanically Ventilated Patients with Severe Acute Respiratory Failure. Am J Respir Crit Care Med. 1997. 155:473-478
McAuley DF et al. What is the optimal duration of ventilation in the prone position in acute lung injury and acute respiratory distress syndrome. Intensive Care Med
2002.28: 414-418.

Non-invasive ventilation (NIPPV) 521

Introduction 522
Strict control of application of NIV exists for HDU Patients-see relevant Procedure on Intranet for current version
Mechanical ventilation not requiring endotracheal intubation may avoid many of the complications of invasive ventilation (ie. generally
associated with less ICU acquired infection, results in shorter ICU and hospital length of stay, and may be more acceptable to patients.
Appropriate patient selection is important (restrict to indications below), as is appropriate monitoring and a controlled environment with the
capacity to initiate invasive ventilation without delay where necessary.
Modes 523
Continuous positive airway pressure (CPAP)
Single continuous positive airway pressure
No augmentation of tidal volume
Generally seen to be useful in hypoxic states
Biphasic positive airway pressure (BiPAP)
Usually PEEP plus augmentation of tidal volume
Useful in the treatment of hypercarbic states
Indications 524
This section does not attempt to address the role of NIPPV outside of acute conditions. The groups outlined below are those that have been
studied, often in a limited way.
Accepted indications 525
Acute exacerbations COAD: Good evidence that NIPPV useful in hypercapnoeic patients.
Pulmonary oedema.
Patients with underlying neuromuscular, parenchymal or restrictive lung disease: NIPPV useful only if decompensation is a result of
reversible infection and not disease progression.
Less accepted indications 526
NIPPV should only be applied in the following situations on a trial basis, with well defined end points, and in a well controlled environment
(ICU generally).
Weaning or early discontinuation of invasive ventilation.
Stable airway obstruction (eg: post operative patient with obstructive sleep apnoea).
Pneumonia or ARDS
Asthma
Contra-indications to NIPPV 527
Patient with impaired level of consciousness, including those that are in-extremis
 Haemodynamic instability
Bowel obstruction or upper GI haemorrhage (increased risk of aspiration)
Agitation such that mask not tolerated well
Impaired cough, including low GCS and bulbar dysfunction
Non-reversible disease process
Untreated pneumothorax
Pre-requisites 528
The patient must be able to protect their own airway sufficiently.
The patient must be accepting of the face mask
There must be a reversible problem requiring “bridging” respiratory support.
There must be adequate monitoring:
Continuous pulse oximetry, telemetry and at least intermittent blood pressure and ABG recording.
Nursing ratio no worse than 1:2.
Complications 529
Aerophagia or gastric distension - Aspiration lung injury
Mask intolerance and heightened anxiety
Pressure necrosis of the face
Reference:
International Consensus Conference in Intensive Care Medicine. Non-invasive ventilation in acute respiratory failure. Intensive Care Medicine 2001; 27:166-178.

Extra-corporeal Lung Support 530

Introduction 531
ECLS is a system of veno-venous extracorporeal gas exchange treatment. While not especially difficult to implement, it is highly resource
intensive (staff, disposable costs, blood product usage). Its implementation may impact on our ability to care for other patients, and therefore
deserves careful consideration before implementation.
Indications for ECLS 532
ECLS has not been proven beneficial in any randomised controlled trial.
Hypoxia. Fulfilling both criteria below
PaO2 : FiO2 ratio < 60 measured on at least 2 occasions 2 hours apart, despite appropriate ventilator management (including
recruitment manoeuvres, patient positioning, NO etc).
Tidal volumes of 5 ml / kg produce plateau pressures above 35cm H2O.
Supercarbia: When hypercarbia considered unacceptable in acute situation (asthma).
Reversible circulatory failure: Veno-arterial ECMO may rarely be implemented when reversible circulatory failure is present (cardio-
depressant drug overdose or post cardiotomy)
Exclusions to ECLS 533
Treatment failure is associated with
Age > 50 years
Mechanical ventilation > 1 week
Presence and severity of other organ dysfunction
Actioning ECLS 534
ECLS is no longer performed at Waikato Hopsital. Referral to the Intensivist on call for the CVICU is required for consideration of a patient
for ECLS.
Reference:
Alpard K A, ZwischenbergerJB. Perfusion 1998; 13: 3-15
Anderson H L, Advances in Surgery 1998;31:189-215

Hyperbaric Oxygen Therapy (HBO) in Critically Ill Patients 535

Hyperbaric oxygen treatment is indicated in significant air embolism and severe decompression illness. It may be indicated in carbon
monoxide poisoning and clostridial soft tissue infections. Hyperbaric oxygen therapy is accessed through HMS Philomel at the Devonport
Naval Base. Even in patients where HBO may be indicated, the isolated nature of the facility and the unfamiliarity of our staff with the
hyperbaric environment make this mode of therapy less feasible.
Unintubated, non-ICU patients can be referred by their managing services to the North Shore Hospital or Auckland Hospital for subsequent
management.
Reference:
Weaver Lk et al. NEJM 2002; 347:1057

Aspects of Renal Failure in Intensive Care 536

Introduction 537
Renal failure in ICU almost invariably involves at least one other organ dysfunction or failure, and carries a mortality of up to 70 % in this
setting.
The advent of continuous renal replacement therapiesand othe low efficiency dialytic modalities (SLEDD) have revolutionised this aspect of
care.
Conversely “renal protective” strategies have not been proven beneficial in large multi-centre trails.
The decision to commence a patient on continuous renal replacement therapy is often not based on clear indicators (see below) and it should
always be discussed with the duty ICU specialist.
The renal unit should be alerted as early as possible to review any patient that might need ongoing renal support beyond the acute critical
care period.
Aetiology of renal failure in the ICU 538
The classical compartmentalisation of pre-renal, intra-renal and post-renal factors hold true in ICU with the following considerations:
A missed, but reversible, cause of renal failure has dire consequences-“time is kidney”.
Renal perfusion (blood flow and GFR) in critically ill patients may become directly related to systemic blood pressure as local
autoregulation fails. Hypotension, even a marginal decrease, will not be well tolerated.
The renal interstitium is relatively hypoxic even under optimal conditions. When subjected to a multilevel endothelial insult as a result of
sepsis or SIRS there is a ready predisposition to a vasomotor nephropathy and progession to overt ATN.
The pharmacokinetics of many drugs in ICU are severely deranged, exposing the patient to a much greater risk of nephrotoxic effects.
Drugs and toxins (including radio-contrast) should not be administered without consideration of their toxicity.
Occult or overt increases in intra-abdominal pressure should always be considered in patients with abdominal distension with or without
previous surgery. When considered it should be measured and if necessary addressed (see Intra-abdominal pressure measurement,
section 3.1.4).
Assessment of renal function in a given patient 539
Biochemical markers 540
Serum creatinine is a poor marker of renal reserve. A rise in serum creatinine > 120umol / L may not occur until more than 75 % of renal
function is lost.
All patients should have their renal function calculated, and drugs tailored according to the Cockroft and Gault equation:
(140-patient age) x weight in kg x 0.8 for females
Creatinine Clearance (ml/sec) =
50 000 x Serum creat. conc in mmolL-1
From this equation it can be appreciated that a 20 year old 100kg male will have 6 times the creatinine clearance of an 80 year old 50kg
woman, even though they have the same serum creatinine concentration.
Urine 541
The minimum urine output required to excrete obligatory daily solute load is 0.5 ml/kg / hr
Urine electrolyte analysis is of little use in ICU to diagnose aetiology of renal failure but maybe useful in specific electrolyte abnormalities.
Urine sediment: Unhelpful unless a specific reason exists (true vasculitis, nephritis)
Renal imaging 542
Ultrasound or nuclear imaging techniques may be useful where pre-existing pathology is suspected, or the renal vasculature has been
compromised by surgery or trauma.
Thoracic aortic dissection may extend distally and compromise renal blood flow, particularly where a significant false lumen exists. As soon
as is practical following acute repair, investigation of aorto-renal vascular anatomy should be performed to facilitate a fenestration procedure
if necessary.
Post -renal pathology, whilst uncommon in ICU, is embarrassing to miss and should be excluded where there is any doubt about the cause of
renal failure.

Renal protective strategies 543

Good practice 544
The cornerstones of good renal protection are not the administration of various drugs, but critical care practice ie.
Adequate fluid resuscitation (sometimes a difficult concept)
Haemodynamic support to maintain both a good renal perfusion pressure and adequate blood flow. Where necessary this may involve
inotrope and / or vasopressor support. Despite historical anxiety about the use of vasopressors (noradrenaline), it is not harmful to the
kidneys and may in fact increase renal blood flow in animal studies.
Avoid nephrotoxic drugs where necessary
Treat intercurrent infection
Active surveillance for abdominal compartment syndrome, where this is appropriate.
Drug therapy 545
The following drugs have been used to promote urine output, but have not been found to impact in a positive way on progression to dialysis
or mortality.
Low dose dopamine (increase in urine output secondary to direct tubular effect and minor increase in β-effect)
Frusemide (must be delivered to lumen of tubule to be effective)
Mannitol
Aminophylline
The routine use of these drugs is not advocated.

Renal Replacement Therapy 546

Indications for dialysis
The threshold for dialysis in a critically ill patient is different from that of an ambulatory ward patient. Mortality in critically ill patients is
related to time averaged urea during their stay, so that dialysis should be started earlier with the aim of maintaining a optimal state,
rather than cyclical clearance of urea and metabolites.
The presence of two of the following would suggest dialysis should be considered
Oliguria < 200 ml / 24hrs
Oliguria < 50 ml / 12hrs
Sever acidaemia
Hyperkalaemia
Plasma Urea > 30 mmol/L or uraemic syndrome (pericarditis, pneumonitis, bone marrow suppression)
Plasma Creatinine > 300umol / L
Pulmonary oedema
Diuretic resistant cardiac failure
Anasarca (generalised oedema)
Selected overdose (salicylates, methanol, theophylline)
 Imminent or ongoing massive blood product administration
The attempted removal of cytokines and inflammatory mediators is not yet proven to reduce mortality in humans.
Modes of dialytic therapy in the ICU 547
Standard intermittent dialytic therapy: Although still used in this ICU, it is limited by resource availability and is probably not suitable for
use in unstable patients
Sustained low efficiency dialysis: essentially slow intermittent dialysis
Continuous veno-venous renal replacement therapy: A growing field of therapy in the ICU, this modality has become the mainstay of renal
replacement in the critically ill at The Waikato Hospital.
Continuous renal replacement:-Default Prisma settings 548
Mode
CVVHD
Blood flow rate
150 ml/min
Dialysate flow rate
2000 ml/hr
Anticoagulation 549
The filter is primed with 5000 units of unfractionated heparin as part of the start up procedure.
If considered safe, a bolus of 2000-5000 units of heparin is administered to the patient IVI at the commencement of dialysis.
There is no evidence that anticoagulation prolong filter life and prevents clotting in the filter. Anticoagulation is however widely practiced,
the aim being to anti-coagulate the filter but not the patient. Therefore:
Heparin 10 000 IU is made up to 50ml with Normal Saline, and starting at 5 ml / hr is infused via stand alone syringe pump “pre-filter”.
Protamine 100 mg made up to 50 ml with Normal Saline, starting at 5 ml / hr is infused via separate syringe pump into the patient.
The aim of the titration between heparin and protamine infusions is to achieve an APTT across the filter of > 100 sec, while maintaining a
patient APTT < 50 sec.
Patients with deranged coagulation due to sepsis or low / abnormal platelet function may not require heparin administration at all.
Potassium replacement 550
The haemodialysis counter current should mean that with an effective filter in situ, the plasma exiting the filter has the same potassium
concentration as the dialysate entering the filter. Potassium supplementation should therefore only occur in the dialysate fluid.
Standard haemofiltration fluid is lactate buffered and contains [K+] = 1 mmol/L. Add K= according to the table below
POTASSIUM SUPPLEMENTATION IN RENAL REPLACEMENT (CVVHD)
Plasma potassium conc Add to 5l standard dialysate solution Final dialysate K+ conc.
> 6.0 mmol/L Nil to first bag and repeat serum K+ at 4 hours 1 mmol/L
3.0-6.0 15 mmol 4 mmol/L
< 3.0 20 mmol to first bag and repeat serum K+ at 4 hours 5 mmol/L
If potassium supplementation exceeds that described above, it should be given parenterally in the normal way until a desired serum
potassium concentration is achieved.
Buffering solution 551
The most dialysate solutions contain lactate as a buffer, as this results in a stable solution. Lactate is then metabolised to bicarbonate in the
liver. Commonly therefore patients on CVVHDF will have moderately elevated lactate levels. In the context of a stable patient (unchanged or
improving whole blood pH) this should not cause alarm.
Solutions using bicarbonate as a buffer need to be prepared just prior to use. They are more expensive, and more prone to contamination.
Bicarbonate buffer fluid is not indicated unless there is significant hepatic impairment causing or contributing to a lactate of over 7.0mmol/l.
Fluid removal 552
The machine will allow you to set a net fluid removal volume per hour. This is calculated by the machine based on the weight of the
ultrafiltrate bag (i.e. gravimetric method), and the set flow rates of replacement and dialysate fluids. The volume to be removed from the
patient must be discussed with the duty ICU specialist, and form part of the daily management plan.
Complications of continuous renal replacement therapy: 553
Haemorrhage (and other consequences of exposure to heparin (H.I.T.S.)
Hypothermia, or masking of hyperthermia (prevention of hyperthermia may be clinically useful)
Complications of (prolonged) venous access.
Exposure to extracorporeal circuits and filter (activation of complement, sequestering of platelets)
Air embolism
Increased requirement for experienced staff, and increased nursing workload.

The CVVHDF circuit: A simplified representation of CVVHD

 CVVHD

Roller
Pump Roller
Pump

Heparin Protamine

Diffusion:
Roller Semi-permeable membrane Roller
Pump Dialysis counter current Pump

Filtrate out Dialysate in

Reference:
Bellomo R, Ronco C. Renal replacement therapy in the intensive care. Critical Care and Resuscitation 1999. 1(1):13-25.

Neurosurgical Guidelines 554

Neurotrauma 555
The effective management of neurotrauma relies upon early notification of the neurosurgical team, and close liaison at all times.
For obvious reasons we have no control over the magnitude and mechanism of the primary injury, however we can influence patient outcome
by preventing a secondary insult through hypoxia, hypotension, or electrolyte / metabolic derangement.
Acute trauma resuscitation 556
Safe retrieval and transport around the hospital, and during emergency surgery
Cardio-pulmonary / renal / metabolic homeostasis
Maintenance of cerebral perfusion.
Monitoring the head injured patient 557
Real time (invasive) arterial blood pressure monitoring
CVC accessed and pressure transduced.
End-tidal CO2 monitoring (calibrate and establish arterial-end tidal difference).
ICP monitoring
Jugular Bulb oximetry
Brain tissue oxygen measurements
There is general consensus regarding the benefit of generic ICU monitoring (arterial oxygenation, blood pressure etc) to prevent secondary
brain insult. The role of intracranial pressure monitoring appears accepted, what is less clear is the threshold for therapeutic intervention and
the benefits thereof. Where possible, an ICP maintained less than 20 mmHg in adults and lower in children seems beneficial. An increase in
ICP despite active measures would normally lead to an attempt to manipulate cerebral perfusion pressure (generally maintained > 70
mmHg). The addition of jugular venous oximetry has introduced a cerebral blood flow aspect, however added benefit has not been clearly
shown. A SjVO2 < 55 % may be suggestive of a low perfusion state, and is associated with poorer prognosis. A high SjVO2 however may
equally be evidence of hyperemia or decreased tissue extraction, although the significance of this observation is less clear in a therapeutic
sense.
Indications for ICP (intra-cranial pressure) monitoring 558
Severe closed head injury GCS < 8 / 15 after adequate resuscitation
Abnormal CT scan head (haematoma, contusion, oedema, effaced basal cisterns)
Consider in patients where cerebral status cannot be determined for other reasons (ie sedation for ventilation in polytrauma).
Consider in patients with a normal CT scan in the presence of a GCS < 8 if the patient is older than 40 years, has motor posturing, or is
prone to marginal hypotension (SBP < 90 mmHg).
Measurement of Jugular venous saturation may be of additional use in titrating cerebral perfusion pressure where:
A sustained rise in ICP cannot be reduced with maximum medical therapy and cranial decompression may not be possible or
appropriate.
Doses of vasopressor required to sustain a CPP > 70 mmHg become non-sustainable or dangerous.
Ventilation of the head injured patient 559
Maintain PaO2 > 80 mmHg
Maintain normocapnia: PaCO2 between 35-40 mmHg. Hyperventilation to PaCO2 as low as 25 mmHg may decrease ICP temporarily, however
there is a short term trade off in cerebral blood flow, and after 6 hours tachyphylaxis occurs with a potential hyperaemia on correction to a
normal PaCO2. Hyperventilation should not be used therefore unless it forms a short term bridge to definitive treatment (ie. impending
surgery), or unless guided by jugular bulb oximetry.
Low level PEEP has not been proven to affect outcome of head injury adversely, and is beneficial in the prevention of secondary pulmonary
pathology.
Haemodynamic priorities 560
Maintain perfusion pressure:
Mean arterial pressure (MAP) > 90 mmHg in the absence of an ICP monitor,
 Cerebral perfusion pressure (see algorhythm below) > 70 mmHg where ICP is being monitored (CPP = MAP-ICP).
Avoid inotrope or vasopressor use until patient adequately fluid resuscitated.
Fluid maintenance
Aim for euvolaemia
Use crystalloid (usually normal saline) unless a specific contra-indication exists
Osmotherapy 561
Indications:
Signs of trans-tentorial herniation
Progressive neurological deterioration not attributable to systemic pathology.
The patient should be euvolaemic prior to initiating osmotherapy.
Bolus therapy may be better than infusions: consider-
Mannitol 0.25 g / kg or (100 ml of 20% )
Hypertonic saline: 10-20 ml of 4M saline to a serum Sodium concentration of 150-155 mmol/L
Measured osmolality should generally not exceed 320 mmol/L.
Prolonged serum hyperosmolality will promote intracellular generation of “idiogenic osmoles” leading to a rebound in cellular fluid
uptake (and ICP) if osmolality is allowed to correct rapidly beyond day 3 of therapy.
Sedation 562
First 24-48hrs: It may be appropriate to use a short acting agent such as propofol to facilitate repeated neurological assessment,
particularly where no ICP measurement exists.
Labile neurogenic hypertension, sympathetic storming or emergence agitation: Consider β-blockade or clonidine.
Barbiturate use:thiopentone may be used, however levels are no longer measured at Waikato Hospital. Phenobarbitone is an alternative.
Other management issues relating to neurotrauma 563
Steroids 564
not proven useful and likely harmful in the trauma setting.
Antibiotics 565
A single dose of antibiotic is sufficient to cover insertion of monitoring catheters.
A fracture base of skull is not an indication for antibiotic prophylaxis in the absence of a CSF leak.
CSF should be sent for MC&S every second day. All sampling of CSF, or other disruption of the drainage system should be performed
using aseptic technique and according to EVD guidelines
Intrathecal antibiotics should be given by neurosurgical staff
Seizure prophylaxis 566
Waikato Neurosurgeons have asked for the following patients to have prophylactic phenytoin:
Moderate head injuries with haematomas, contusion
Depressed skull fracture with dural tear , CSF leak and/or cortical injury

Thromboprophylaxis 567
All patients should be fitted with thigh length ECS
See section on anticoagulants for details
Patients unsuitable for drug prophylaxis should have SCD when available
Stress ulcer prophlaxis 568
consider if patient likely to be ventilated for > 48hrs, and not tolerating enteral feeding
Avoid hyperthermia 569
Hyperthermia should be avoided and treated as possible
Tight Glycaemic control 6.5.1.7.7
This is currently not practised in neurosurgical patients requiring ventriculostomy or ICP monitoring (i.e. as a marker of significant brain
injury) because of microdialysis studies showing eveidence of cellular distress at low normal glucose levels.

Reference:
Evidence based guidelines for the treatment of traumatic brain injury. The Brain Trauma Foundation: www.braintrauma.org
Qureshi AI. Use of hypertonic saline solutions in treatment of cerebral edema and intracranial hypertension. Crit Care Med 2000, 28(9):3301-3311

Cerebral Perfusion Pressure Algorithm

 Optimise Cerebral Perfusion Pressure - Goals
1) Maintain euvolemia using IVI crystalloid or colloid
2).Ensure normocarbia: PaCO2 35-40mmHg
3).Maintain measured serum osmolality between 310-320 mmolL-1
4).Commence inotrope infusion to a Cerebral perfusion pressure
(Mean arterial pressure - intracranial pressure) > 70mmHg.

ICP

If ICP > 20mmHg ICP < 20mmHg

> 10 minutes
Nil further required
1.Consider CSF drainage if intraventricular
catheter in situ.
2.Ensure adequate sedation with morphine
and midazolam (or propofol and narcotic)
3.Exclude contributing factors:
- Non-neutral head position
- Check pt 30 deg. head up
- Keep PaCO2 approx 35mmHg
- Maintain normothermia
- Occult seizure activity
- Obstructed venous drainage (cervical
collars or ETT ties)

ICP not responsive No surgically remedial lesion

Urgent CT Scan and alert Maintain CPP > 70mmHg
neurosurgical team

Temporary measures:
If ICP < 25-30mmHg and static, but
Hyperventilation (short term): PaCO2 30mmHg requiring large doses of catecholamines
%
Bolus mannitol (100ml of 20 ) Consider resetting CPP at > 60mmHg with guidance
or hypertonic saline 10-20ml of 20% per hour of a jugular venous oxygen saturation device

Surgical Intervention ICP > 25 -30mmHg

Consider:
Barbiturate Coma
Induced Hypothermia
Craniectomy or insertion EVD

Status Epilepticus 570

Definition 571
Prolonged or repetitive seizures that occur without a period of recovery between attacks.
Refractory status epilepticus refers to ongoing seizures for more than 20-30 minutes.
Serial seizures may occur within a brief period, but as long as the patient regains consciousness in between this is not an indication for
ICU admission.
Principles of ICU management 572
Basic resuscitation protocol: Secure Airway, Breathing, Circulation
Acquire IVI access.
Control Seizures using drugs described in table below
Consider precipitating causes and treat as appropriate:
Glucose: administer an empiric dose if in doubt, or estimation delayed.
Electrolytes: Ca2+, Mg2+, K+, PO43-
Metabolic derangement: hypoglycaemia, thiamine deficiency, intoxication or withdrawal
Known epileptic: review medication compliance and recent changes.
Intracranial pathology: CVA, tumour, infection
Prevent secondary insult: Hypoxia, hyperpyrexia, prolonged seizures-rhabdomyolysis.
Further investigations:
CT scan head: where cause of seizure unknown, and of new onset.
EEG. May be useful where pseudoseizures are suspected, the patient has complex partial seizures with intermittent generalisation,
or where muscle relaxants have been administered to the patient.
Lumbar Puncture: LP’s are generally not indicated.
USEFUL DRUGS IN THE TREATMENT OF STATUS EPILEPTICUS
Drug Comment Dosage
Diazepam First line acute treatment 5-10 mg prn IVI
Midazolam Consider only in patients with protected airway in ICU setting. 1-10 mg/hr via infusion
Clonazepam Alternative to Diazepam in status epilepticus 1-2 mg prn IVI as bolus followed by 0.5-1.0 mg/hr IVI
Medium to long acting benzodiazepine, beware accumulation infusion.
Phenytoin First line treatment along with Diazepam (or other benzodiazepine) Loading dose 15-20 mg/kg IVI over 30 minutes with
telemetry.
Maintenance 300 mg/24hrs titrated to therapeutic range
Pheno- Consider if seizure uncontrolled within 20 minutes. Consider only if Loading dose 20 mg / kg over 30 min
barbitone benzodiazepine and phenytoin therapy have failed. 1.5 mg/kg/min as infusion
USEFUL DRUGS IN THE TREATMENT OF REFRACTORY STATUS EPILEPTICUS
Ketamine NMDA receptor antagonist, may be helpful when GABA receptor Loading dose: 1 – 5 mg / kg
response to other drugs less effective Infusion: 1 – 5 mg / kg / hr
Propofol Anaesthetic agent used to control refractory status in the intubated 1-2 mg/kg followed by 2-10 mg/kg/hour.
patient
Thiopentone: Reserved for failed “standard treatment”, where endotracheal Loading dose: 5 mg/kg
intubation is required Infusion: 1-3 mg/kg/hour (approx 150 mg/hr) titrated to
EEG activity at the bedside.
Once emergency treatment has been implemented it is expected that the assistance of the neurology team will be sought in adjusting treatment in known epileptics,
or those with focal or complex partial seizures.
Reference:
Durham D. Management of Status Epilepticus. Critical Care and Resuscitation1999; 1:344-353.
Lowenstein DH. Status Epilepticus. New England Journal of Medicine 1998,338(14):970-976.

Subarachnoid haemorrhage 573

Introduction 574
Patients will be admitted either electively following planned surgery or as a result of acute aneurysmal rupture, generally with impaired level
of consciousness. For patients with a sufficiently good prognosis, aneurysm isolation will be planned to occur within 48 hours of intial
rupture.
Planning of surgical intervention in patients with acute rupture 575
Early ( < 3 days):
Advantages: Prevents re-bleeding, may assist with reduction in associated vasospasm (blood products removed) and subsequent
cerebral ischaemia.
Disadvantages: More technically difficult, higher risk of intra-operative rupture.
Late ( > 11 days):
Advantages: Easier procedure. Allows a period of observation, avoiding surgery in potentially non-salvageable patients.
Disadvantages: re-bleed or rupture. Increased risk of vaso-spastic complications.
CLASSIFICATION OF SUBARACHNOID HAEMORRHAGE
Grade Description GCS
0 Non-ruptured 15
1 Asymptomatic, minimal headache, slight neck stiffness 13-15
2 Moderate headache, neck stiffness, neurology limited to cranial nerve pathology. 13-14
3 Drowsy, confused, mild focal defecit 13-14
4 Stupor, moderate to severe hemiparesis, early decerebrate rigidity 7-12
5 Deep coma, decerebrate rigidity, moribund patient 3-6
Principles of ICU management 576
Monitoring 577
Pulse oximetry
Invasive arterial monitoring
Central venous access (particularly during administration of nimodipine).
ICP monitoring in patients returning with a ventricular drain. Instructions for drain height and CSF drainage should be obtained from the
surgical team involved.
Neurological observations hourly: A deterioration in GCS that cannot be easily explained or corrected (eg. sedation) may be due to a re-
bleed, vasospasm or hydrocephalus in which case the neurosurgical team should be notified.
Anticonvulsant prophylaxis (generally with phenytoin) is given for the first 21 days after rupture.
Therapeutic interventions 578
Prior to definitive aneurysm management, MAP is kept in the range of 80-100. Following aneurysm isolation, the MAP may be allowed to
rise higher and on occaision deliberate hypertension will used in the management of vasospasm.
Aim to minimise secondary damage due to cerebral vasospasm, using Nimodipine preferably given orally or gastrically or if necessary IV
(Calcium channel antagonist) 10 mg/hr IVI (preferably via CVC)
Nimodipine administration may precipitate hypotension, in general noradrenaline is used to maintain the desired mean arterial pressure
(MAP)
Fluid administration:
Maintain at least normovolaemia using 0.9% saline IVI (generally minimum 2.5l/day)
Hypervolaemia has been advocated as a means of maintaining cerebral flow. Measures of adequate volume status should include:
Warm and well perfused patient
Urine output at least 0.5 ml/kg / hr, preferably > 1.0 ml/kg / hr
CVP > 12 mmHg
Maintain normal serum electrolytes and total osmolality
Adjuncts to treatment 579
Direct and chemical (papaverine) angioplasty may play a role in refractory cerebral vasospasm, and should be discussed with Neurosurgeon
and Neuroradiologist.

Approach to diagnosis and management of cerebral vasospasm

 Reference:
Al-Yamany M, Wallace MC. Management of cerebral vasospasm in patients with aneurysmal subarachnoid haemorrhage. Intensive Care Med 1999; 25:1463-1466.

Cardiothoracic Guidelines 580

Introduction 581
The Registrar on duty is expected to accept the patient on return from theatre.
The patient’s pre-operative condition taken together with intra-operative events will usually define the parameters required for a given
patient.
It is important to document and communicate clearly any expected deviation from the normal pathway of post-operative care.

Admission of a cardiothoracic patient 582

On accepting a patient into the unit the following must be clarified in addition to a general admission:
Pre-operative morbidity including:
Actual renal function (elderly people with normal creatinine may have less than 50 % residual renal function as calculated by
Cockroft and Gault)
Left ventricular function and effort tolerance.
Drug history, particularly the use of anti-platelet therapy leading up to surgery
Co-existant vascular disease, particularly neurovascular disease (eg carotid artery, previous TIA / CVA’s)
Intra-operative management issues:
Number of grafts, vessel harvesting, valve replacement (prosthetics or tissue)
LV appearance and behaviour
Fluid loading behaviour on table (ie some patients respond to higher “filling pressures”)
Surgical haemostasis: The surgeon may predict a patient will ooze, and therefore be willing to accept different blood loss parameters prior
to actioning re-opening of the chest.
Respiratory Care 583
Default ventilator settings on return to ICU 584
The nursing staff will prepare a Siemens Servo 900C (in consultation with the Cardiac Anaesthetic Staff delivering the patient) generally
consistent with the following:
FiO2 as decided by Cardiac Anaesthetic Staff
Mode: SIMV/IPS, at rate 10 breaths / min, 10ml/kg tidal volume, PEEP 5
Nursing Staff change to IPS 10/5 asfter intial observation period and ascertain whether respiration adequate
Extubation 585
Once the patient is awake and comfortable they may be converted to spontaneous ventilatory modes.
Extubation may be considered once the following criteria have been met:
Awake, comfortable patient
Normothermic (Temp > 36.0 oC)
Cardiovascular stability: Allowing only minimal inotropes, but accepting continued requirement for cardiac pacing.
Adequate gas exchange: PaO2 > 70 mmHg on FiO2 ≤ 0.4, with normal PaCO2.
Normal acid-base status: pH 7.35-7.45, HCO3- > 20 mmol/L, BE of -5 mmol/L to + 5 mmol/L.
Minimal Bleeding: < 100 ml/hr ideally. Do not extubate patient if blood loss > 200 ml / hr.
Management of Bleeding 586
Introduction 587
A set of baseline bloods including clotting profile are performed on accepting the patient from theatre. A TEG may have been performed
which may assist component transfusion therapy. Standard coagulation tests remain the main indicators for component therapy in the
bleeding post cardiac surgical patient.
Limits for initiating review by cardiac surgeons 588
Alert cardiac surgeons if the following is exceeded (note the threshold for this is less than that practiced in some other centres).
> 200 ml of blood in intercostal drains in the first hour in ICU.
> 400 ml of blood in any given hour thereafter would be indicative of surgical cause of bleeding and the surgeon should be notified
immedicately.
> 200 ml of blood per hour for any 2 consecutive hours.
Therapeutic interventions 589
In the presence of bleeding, treatment should be aimed at correcting the deficit ie.
TCT high, consider heparin reversal with protamine (TCT may be elevated in other conditions)
INR > 1.5 or APTT > 1.5 times normal: Consider FFP as first line treatment.
Platelets should be transfused at a low threshold following surgery with CPB even if quantitatively normal.
The role of DDAVP, postoperative aprotonin and other antifibrinolytics is not yet clear.Ask the Duty ICU Specialist prior to administering
these products.
Avoid hypertension, as it may exacerbate bleeding.
Using PEEP to reduce mediastinal bleeding is not an evidence based practice.It is likely to excacerbate hypotension due to hypovolaemia,
and should not be applied in a level above routine without discussion with the Duty ICU Specialist.
Reference:
Robinson KL et al. Practical Management of Anticoagulation, Bleeding and Blood Product Support for Cardiac Surgery. Part 1: Bleeding and Anticoagulation issues.
Heart Lung and Circualtion. 2001; 10:142-153.

Hypotension 590
Introduction 591
If you are concerned that the patient is about to have a cardiac arrest (or if they have had one), a “Cardiac Reopening” Call should
be put out via the operator. Only brief CPR should be given while preparation for resternotomy is made. Resternotomy should be
performed within five minutes of arrest, by staff attending the patient at the time, usually ICU Staff.

Patients should have their Blood Pressure maintained at a mean arterial pressure (MAP) of 70-90 mmHg, unless otherwise specified by the
surgeon and agreed to by the ICU specialist. Patients with longstanding mild hypotension (often with long-standing valvular disease) may be
tolerant of MAP’s as low as 60mmHg.
Only in exceptional circumstances and with agreement of the Duty ICU Specialist should a MAP of < 60mmHG be allowed to persist or be
aimed for.
Where a patient is returned to the ICU on an infusion of inotropes or vasopressor, clear direction should be sought as to their indication and
limits.
Where hypotension is not seen to respond to simple measures and checks given below consult the duty ICU specialist without delay.
Approach to Hypotension (systolic BP < 90 mmHg) in the cardiothoracic patient 592
Exclude hypovolaemia 593
Maintain CVP at least 8-10 mmHg
If a pulmonary artery catheter is in situ then maintain left atrial pressure as estimated by pulmonary capillary wedge pressure > 10-12
mmHg
Or maintain “filling” pressures at levels suggested as optimal during surgery (defined on accepting patient into ICU).
Patients may receive up to 2000 ml of colloid IVI according to the parameters defined above. No further fluid should be given beyond that
limit without informing the duty ICU specialist unless the patient is bleeding. In the case of excessive bleeding early Cardiac Surgical
consultation is advised.
Myocardial (pump) failure 594
Assess acute ischaemic changes on ECG
Consider tamponade:
Cardiac tamponade is a surgical emergency classically indicated by
refractory hypotension, with evidence of hypoperfusion (cold extremities, diminishing urine output, increasing acidosis, poor
response to increasing inotropes), and occasionally pulsus paradoxus.
Diminishing drainage from chest drains
Increasing right heart pressures (CVP or PA pressure)
Globular heart on chest X-ray
Echocardiographic evidence of tamponade.
If patient is electrically paced, ensure adequate capture, and rate of

Vasodilatation 595
Patients may have a systemic inflammatory response to the preceding surgery and bypass procedure.
A vasopressor ( usually noradrenaline) is required to defend perfusion pressure.

Hypertension 596
Introduction 597
A systolic blood pressure > 140 mmHg MAY be detrimental to the patient: ie
Increased afterload and myocardial oxygen consumption
Increased incidence of stroke
 Increased risk of bleeding and vascular graft suture line dehiscence.
Approach to hypertension in a cardiothoracic patient 598
Confirm veracity of reading, exclude pain, agitation, or other reversible cause not requiring antihypertensive.
Consider short acting agent as first line treatment:
GTN infusion (50 mg in 50 ml dextrose water) 1 mg/hr to 20 mg/hr max.
(Sodium nitroprusside may be considered if GTN unsuitable or ineffective)
Only if high blood pressure sustained or refractory consider:
Captopril 6.25 mg NG, repeat in 1-2 hours if necessary.
Metoprolol 1 mg IVI, (1mg dose increments to 10 mg max.) prn or 25-50 mg 8 hrly po / NG (or other β-blocker with which you are
familiar).
Clonidine 15-45 µg prn IVI.
Antibiotic administration 599
Routine prophylaxis for the non-allergic patient is cephazolin 1g q8h.This is discontinued after chest drain removal.

Special requests from Surgeons 6.6.8

In general, particular standing requests from invidual surgeons are undesirable.Requests should preferably be entered in the operation note
and remain negotiable.Nevertheless, the following standing requests are noted as a general guide to practise:
Mr Parkinson:GTN at 1 mg/hour for CABG patients unless hypotensive, frusemide 40mg and oral postassium supplements from first
postoperative day unless contraindicated, atrial pacing unless “contraindicated” for 24 h
Mr Lin: GTN at 1-3 mg hour for radial graft patients unless hypotensive.Will discuss request for blood pressure targets with aortic surgery
Mr Kerjiwal: “routine” atrial pacing and Hb target of 70g/l
At no time should these requests stand in the way of proper care of the patient as defined by the Intensivist on duty.

Microbiology Guidelines 600

Introduction 601
Sepsis is a common cause of death in critically ill patients. The detection of active infection, as opposed to colonisation with ICU flora, is
difficult but important.
Regular routine microbiological examination is not cost effective in the ICU, and infective screens should only be ordered for specific
indications, using the guidelines listed below.
Simple preventative measures are extremely important in the containment of infection and the prevention of bacterial resistance. i.e.
Compulsory hand washing by all staff who come into contact with patients. Hands should be washed both before and after patient contact.
Strict aseptic technique for all procedures
Rational prescription of antibiotics.

Glossary: 602
Systemic inflammatory response syndrome: “SIRS” 603
Describes clinical picture following any insult (trauma/major surgery, burns, pancreatitis, hypersensitivity reactions) activating a significant
inflammatory reaction.
Defined by the presence of at least 2 of the following:
Temp > 38 oC or < 36 oC
Heart rate > 90 bpm
Respiratory rate > 20 bpm (or PaCO2 < 32 mmHg spontaneously breathing)
Plasma WCC > 12000 /mm3 or < 4000 /mm3 or > 10% immature neutrophils (band cells)
Sepsis 604
The presence of SIRS as defined above in the presence of a proven microbiological pathogen
Septic Shock 605
Sepsis with hypotension, despite adequate fluid resuscitation, along with the presence of perfusion abnormalities that may include but are
not limited to
Lactic acidosis
Oliguria
Acute alteration in mental status
Nosocomial infection 606
Clinically evident infection that was neither present nor incubating at the time of admission to hospital (generally held to appear > 48hrs
after admission)
Colonisation 607
The detectable presence of micro-organisms on / in a patient that are not pathogenic or elicit an inflammatory response.

Screening for sepsis 608

Septic screen-empiric 609
COMPONENTS OF SEPSIS SCREEN-STANDARD
Site of specimen Comment
Urine microscopy and Pyuria is common in the ICU and may not be indicative of active infection.
culture Routine examination of urine is not indicated as asymptomatic bacteruria is common
Sequential courses of antibiotics will not eradicate infection while the catheter remains in situ.
Local instillation of antibiotics into the bladder is similarly ineffective.
 Candiduria alone is not significant but must be interpreted with fungal cultures of other parts of the patient.
Tracheal aspirate and Tracheal aspirates may yield false positives (30%), and false negatives.
Broncho-alveolar BAL should be undertaken to confirm suspicion of ventilator associated pneumonia (VAP). Specimens which yield > 5 % intracellular
lavage (BAL) organisms, and confirm presence of white cells without epithelial contamination indicate VAP.
Treatment should only be initiated if the patient is systemically unwell. Antibiotics will not eradicate colonising organisms, but may well
promote bacterial resistance.
Blood cultures Blood cultures must be taken by fresh venous or arterial puncture.
Skin organisms grown from a single bottle are usually considered a contaminant, but should not be dismissed lightly in the presence of a
deteriorating patient.
Components of sepsis screen-directed 610
Fungal cultures
CSF
Pleural Tap
X-ray sinuses
Directed or bronchoscopic examination of chest flora.
Investigation of Pneumonia 611
Community acquired pneumonia 612
Microbiology 613
Common organisms:
Strep pneumoniae, Haemophilus influenzae, Influenza A
Other organisms:
Bacteria: Legionella sp, Gram-bacilli, S. Aureus
Viral: Influenza B, Parainfluenza, Adenovirus, RSV
Other: Mycoplasma, Chlamydia Psittaci (birds), TB, Chlamydia pneumoniae
Investigations 614
Full blood count and differential
Biochem: ICU profile
ABG
CXR
Microbiology 615
Blood cultures ×2
Endotracheal aspirate or sputum for microscopy and culture (urgent gram stain)
Respiratory viral antigen and culture (if not intubated then use nasopharyngeal swab)
Serology: for atypical bacteria
Direct antigen detection: Urine (pneumococcal Ag), serum (Legionella Ag) by PCR .
Pleural fluid: where significant effusion present
In immuno-compromised host 616
Extend spectrum of detection on sputum: fungal stain and culture, Pneumocystis Carinii stain and acid fast bacilli.
Viral studies for CMV, HSV, EBV
HIV serology if appropriate
Consider broncho-alveolar lavage or lung biopsy if initial cultures negative.
Nosocomial pneumonia in the ICU 617
Introduction 618
% %
Incidence: Up 20 of all ICU patients, 70 of patients meeting criteria for ARDS.
Clinical diagnosis, including use of tracheal aspirates, has poor sensitivity and specificity.
Diagnosis 619
A diagnosis of nosocomial infection (including ventilator associated pneumonia) should be considered if:
New and persistent CXR changes
Tachycardia and tachypnoea
Fever or hypothermia
Leucocytosis or leucopaenia
Purulent sputum
Deteriorating lung function or increasing ventilatory requirement.
Confirmation of diagnosis:
Broncho-alveolar lavage: Only specimens with Epithelial cell count < 1 % considered
> 5 % intracellular organisms considered diagnostic
< 5 % intracellular organisms, treat with antibiotics only if patient unstable and subsequent culture reveals > 104 CFU / ml.
Treatment 620
Empiric treatment should be guided by the initial gram stain. See antibiotic guideline (ch 4.11)

Vascular Catheter Sepsis 621

Introduction 622
It is no longer common practice to remove or replace central access routinely, but only when infected or no longer required.
Suspect line sepsis in the presence of:
New or unexplained fever
Or ↑ in WCC
Deterioration in organ function
Positive blood culture with likely organism in a patient with sepsis.
Evidence of local infection (inflammation or pus at the insertion site)
Guidelines 623
Attempt to confirm bacteraemia by taking blood cultures from a peripheral vein (cultures from the line may only indicate colonisation)
Remove line on suspicion of infection. Intra-vascular catheters are not routinely submitted for culture.
Treatment 624
Removal of the infected line will usually result in resolution of clinical sepsis.
Antibiotics are indicated only if sepsis is severe, progressive following removal of the line, or if the patient is high risk (eg. prosthetic
implants)
Refer to antibiotic guidelines for selection of antibiotics.
Subsequent venous access 625
In ICU central access may be necessary for ongoing antibiotics or inotropes, so that a new line may have to be inserted immediately.
Where possible wait 24 hours before re-inserting a new line at a new site.
Guidewire exchanges may only be performed where mechanical problems complicate a new catheter site.
Antibiotic Locking of long term vascular access 626
Long stay, surgically implanted catheters may be precious, and should not be removed without consulting the duty ICU specialist.
Removing long term vascular access 627
Perform peripheral blood cultures, and remove the offending line if:
Patient unstable
Blood culture grows a fungus
There is obvious catheter tunnel infection is present.
Antibiotic locking 628
Stable patients with a positive blood culture should receive 3 days of appropriate antibiotic therapy. If they are judged to have responded
adequately to therapy, a trial of antibiotic line locking may be trailed to save the intravascular catheter.
Generally Gentamicin 5 mg/ ml or Vancomycin 1mg / ml is used depending on the microbe grown. Amikacin (1.5 mg / ml), ciprofloxacin,
flucloxacillin, linezolid and teicoplanin have all been described. Where groad spectrum is required, a combination of ciprofloxacin and
teicoplanin has been shown to be stable.
Procedure:
⋅ Dilute the appropriate antibiotic in normal saline
⋅ Inject 2ml of locking antibiotic (most lines have a capacitance of < 1ml – check if you are unsure).
⋅ Leave antibiotic lock in-situ for >12 hr per day.
Fungal infections 629
Introduction 630
The incidence of systemic fungal infections in Intensive Care has increased in recent years as a result of
Increased use of broad spectrum antibiotics
Increasing numbers of immunosuppressed patients being referred to ICU.
Prolonged use of intravascular catheters
Co-existent use of immunosuppressive therapy.
The Department of Infectious Diseases should be consulted where any doubt exists with regard initiation of antifungal therapy.
Indications for antifungal therapy 631
Prophylaxis in patients following bone marrow transplant or neutropaenic patients.
Single positive blood culture in a high risk patient
Isolation of candida from any sterile body site except urine, or isolation of fungi in two anatomically discrete sites in selected patients.
Histological evidence of yeast or mycelial forms in tissue from high risk patients.
Treatment 632
See antimicrobial guidelines.

Drug / Toxin Overdose 633

Introduction 634
The majority of overdoses are polypharmacological and respond to general supportive measures. Overall mortality is low and usually relates
to cardio-respiratory arrest and / or uncontrolled siezures prior to admission.
Despite an unreliable correlation between depth of coma and preservation of glottic reflexes, over the last decade emergency departments
have become more aggressive at intubating patients.
While specific reversal agents such as Naloxone (opioids) or flumazenil (benzodiazepines) have some short term use, their relatively short
half lives restrict their efficacy in definitive treatment.

Admission to ICU 635

Intubated patients
Uncontrolled siezures
Coma
Persistent hypotension
 ECG abnormalities consistent with significant ingestion (may be suitable for HDU monitoring in the absence of other features listed
above):
Ventricular or supraventricular tachyarrhythmias
Sinus tachycardia > 140 / min
2nd or 3rd degree heart block
QT-prolongation (preferably index QTc)
QRS duration > 0.12ms
Gastric lavage 636
The place of gastric lavage in acute poisoning is debatable, and is only of benefit in the hyperacute phase of poisoning (< 1 hour).
Patients must be awake with a preserved gag reflex, or already be intubated, failing which the risks and benefits of intubating specifically to
perform gastric lavage patient need to be evaluated.
Procedure 637
⋅ Insert 16G nasogastric tube (not a large bore sump)
⋅ Instil 1 ml/kg warm water only, and then attempt recovery of the lavage.
⋅ Do not continue to instil water until the previous volume has been removed.
⋅ Continue until lavage is clear.
Charcoal 638
Charcoal aspiration has a high morbidity and mortality. As for gastric lavage above, this should not be attempted in patients without a safe or
protected airway.
Instil 50g as soon as possible and 50g 4 hrly thereafter while indication persists. Co-administration with sorbitol has not been shown to
increase efficacy.
In general charcoal should be given in a ratio of 10:1, charcoal dose to drug ingested dose.
Indications for administering activated charcoal 639
Virtually all patients presenting with a drug overdose.
Contra-indications 640
Elemental metals (lithium, iron)
Pesticides
Strong acids or alkalis
Cyanide
Late presentations > 4-6 hrs post ingestion.
Specific Overdoses 641
The Hospital intra-net site contains a link to “Medline and other Biomedical Databases”, in which directory you will find “Micromedex”
which contains both “Poisindex” and “Drugdex” two accessible and readable databases relating to drug and toxin ingestion.
Consult the duty ICU specialist prior to commencing therapy not considered part of basic resuscitation measures.

Management of the unconscious, undetermined overdose

 Immediate adjuncts to consider;
Acute resuscitation: Hypoglycaemia Rx 50ml 50% dextrose
Airway Opiates Rx Naloxone ivi 200 mcg increments
Breathing Alcoholics Thiamine 100mg
Circulation Significant Paracetamol ingestion
(before 4 hours) Rx N-acetyl cysteine

Patient ABG

Exam exclude
History

Relatives Trauma Biochem: ICU profile

Ambulance staff Neurologic disease

Bloods
Drugs: Paracetamol
Circumstantial Metabolic Encephalopathy
(salicylates/theophylline)
Endocrinopathy
? Hepatitis Serology
? HIV (if strong suspicion)

Routine screen:
Barbiturates, opiates,

Urine
benzodiazepines, tricyclics
Specific if indicated:
ABG Cannabis, cocaine

No Metabolic Acidosis Metabolic Acidosis Increased anion gap

Sedatives Normal anion gap

Hypnotics
Paracetamol
Osmolar gap

?
Theophylline
Anticholinergics
Carbon Monoxide
Organophosphates
? Toluene sniffing
Acid Ingestion <10 >10

Phenothiazines Lactate Acidosis Methanol

Lithium (check ABG)
Diabetic Coma
Salicylates
? Ethanol
Ethylene

?
glycol
Cyanide

Withdrawal of Treatment in the Intensive Care 642

Introduction 643
Withdrawal of treatment, or the decision not to initiate treatment, is a consultant responsibility.
Junior staff are not expected, nor encouraged, to begin an end-of-life discussion with a patient or their family unless on the instruction of the
Duty Intensisvist.

Principles 644
Patients have a right to receive quality end of life care including appropriate palliative care and help making decisions regarding life-
sustaining treatment.
Health providers are not however obliged to provide treatments that would be perceived to be futile, or otherwise not in the best interests of a
given patient.

Deciding not to treat (or treat any further) 645

The goal of intensive care is to prevent unnecessary suffering and premature death by treating reversible illnesses for an appropriate period
of time.
Patients in whom treatment is to be withdrawn or not initiated generally fall into one of the following categories:
Imminent death: A patient with an acute illness whose reversal or cure would be unprecedented, and will certainly lead to death.
Lethal condition: Progressive, unrelenting terminal disease incompatible with survival longer than 3-6 months. Life sustaining treatment
should not be provided for the underlying disease. Where treatment is provided for superimposed, reversible illness, this should have
clear goals and limitations.
Severe irreversible condition: A patient has a severe and irreversible condition impairing cognition or consciousness, but where death may
not occur for many months. Life sustaining treatment should not be instituted for the underlying condition, but again may be used to
achieve a specific goal (eg. waiting for arrival of a family member).
The decision making process 646
Generally, there should be inter-professional team consensus to withdraw therapy.
The duty ICU specialist or primary specialist should:
As early as possible discuss with patients while capable, their prognosis and wishes for treatment.
Explore why the patient or substitute decision maker wishes treatment to be continued.
Discuss with the patient or decision maker the rationale for withholding or withdrawing of life support systems.
Describe palliative measures and emphasize patient comfort and dignity.
Offer hospital resources such as social work, chaplaincy or bioethics to assist the patient / family with their psychosocial, cultural,
spiritual and informational needs.
Document pertinent details of this communication in the patient notes.
Where there is not consensus between the patient/family and staff, then:
Negotiate a plan of care acceptable to all parties.
Obtain a second opinion should this be appropriate
Initiate a clearly defined trial of therapy
If none of these are successful then external mediation may become necessary although this would be extremely rare.
Reference:
“ANZICS” guidelines on withdrawal and limitation of intensive care therapy, draft format-unpublished
Singer PA et al. Hospital policy on appropriate use of life sustaining treatment. Critical Care Medicine 2001, 29 (1):187-191

Brain death and organ donation 647

Declaration of brain death 648
This procedure is an absolute requirement prior to organ donation
Where clinical examination is to be used alone, this must be performed by 2 doctors of the status prescribed by local jurisdiction
The two doctors may choose to present at each examination, however, each must perform ALL of the brain death studies independently, and
be responsible for one of the examinations.
In some circumstances, a clinical examination may be replaced by investigations as given below.

Clinical certification of brain death 649

as per ANZICS Working Party on Brain death and Organ Donation 1998
“ Recommendations concerning Brain Death and Organ Donation”)
Pre-conditions 650
A cause of coma must be identified and documented
Reversible causes of coma must be excluded
coma caused by drugs / poisons-Morphine, Midazolam, barbiturates etc
unresponsive state caused by neuromuscular blocking agents-vecuronium, pancuronium etc
coma caused by hypothermia-core temperature must be ≥ 35o C
coma caused by metabolic or endocrine disturbance-the patients should have:
normal renal function
normal hepatic function
normoglycaemia
normal electrolyte profile
Clinical assessment of brain stem function 651
It is recommended that this procedure is performed separately by 2 doctors in separate examinations (current guidelines recommend at least
two hours apart though this is likely to change) to ensure that death is not confirmed until a minimum of 6 hours after onset of coma (or 24
hours if due to hypoxic-ischaemic brain insult).
A minimum of four hours observation with confirmation of absence of pupilllary, corneal, gag/cough and breathing reflexes must occur,
during which the patient has been comatose (Glasgow Coma Score 3), had non-reactive pupils, absent cough and gag reflexes, and no
spontaneous breathing efforts
In some cases this period may be longer (eg. in primary hypoxaemic injuries)
Testing brain stem function 652
A response at any stage deems the patient is not brain dead and further testing does not proceed
absent pupillary responses to light (directional and consensual)
tests cranial nerve III
absent corneal reflexes (avoid unnecessary repetition so as not to injure the cornea)
tests cranial nerve V + VII
absent vestibulo-ocular reflex: (the tympanic membrane must be inspected and noted to be intact before proceeding).-no nystagmus (no
eye deviation to the stimulated side) on the injection of 50 ml of iced water into the ear
tests cranial nerve VII + VIII
absent gag reflex
tests cranial nerve IX + X
absent cough reflex
tests cranial nerve IX + X
absent response to painful stimuli within the cranial nerve distribution
absent respiratory function: should always be done last, and the following must be adhered to following the disconnection of the
ventilator:
pre-oxygenate the patient by placing oxygen tubing into the ET tube and insufflate with 100% oxygen at 2 l/min
look for apnoea clinically
sample ABG 10-15 minutes following disconnection from the ventilator.
the PaCO2 should be > 60 mmHg
Time of death 653
The legal time of death is at the time of the completion of the second test of brain death studies / or whatever time the doctor performing the
second set of brain death studies documents on the appropriate form and / or in the patient notes.
Non-clinical certification of brain death 654
Objective demonstration of the absence of cerebral blood flow is required if brain death is suspected and the preconditions (2b) for clinical
certification cannot be met. For example:
facial trauma or obstruction of the external auditory canals may not allow assessment of all the brain stem reflexes.
a high cervical injury will not allow assessment of all the brain stem reflexes
Where the effects of sedation agents cannot be excluded
A 6 hour period of observation of absent brain function is preferred prior to radiological examination when the absence of cerebral blood
flow may be established by either:
radionuclide cerebral perfusion scan
4 vessel angiography
Certification of brain death is then undertaken after the respective scan has been verified by a practitioner certified to do so.
The legal time of death is at the time of radiological testing.
Frequently asked questions: Exclusions to the diagnosis of brain death. 655
The following observations do not exclude a diagnosis of brain death:
spontaneous “spinal” movements of the limbs
respiratory-like movements (shoulder elevation and adduction, back arching or intercostal expansion without significant tidal volume)
sweating
blushing
tachycardia
absence of diabetes insipidus (normal osmolar control mechanism)
deep tendon reflexes
Up-going plantar reflex.

Admission to ICU of Potential Donors 6.10.3

Patients may be referred for admission where brain death seems very likely and the only potential gain for the patients’ family and society is
organ donation. In this section we are not talking about patients where the prognosis is unclear, but rather patients who currently are refused
admission to ICU and extubated in the ED/Ward instead.

In these cases, the registrar should make a complete assessment of all the relevant medical/radiological details as for any other patient prior
to discussion with the Intensivist on duty. In addition though, it would be reasonable to check the donor status on the drivers licence
(obtained through the phone number in the Organ Donation Folder in ICU-NOT by asking relatives).
Potential medical exclusions to donation should be sought discreetly including advanced age (e.g. over 75 years), some malignancies with
potential for distant spread, HIV, active viral heapatitis etc (see Organ Donation Folder).

It is not an expectation of registrars that they initiate a formal examination to establish brain death or initiate a request for organ
donation or discussion about organ donation or brain death in the Emergency Department (or indeed ICU), unless directed to by the
Duty Intensivist and when willing and sufficiently experienced to do so. In nearly every instance, this discussion would be
conducted directly by the specialist.
The focus must remain on the medical needs of the patient and the psychological needs of family at all times.

An indication that survival seems highly doubtful at this stage (once confirmed by the Intensivist in person or by phone) should suffice at this
stage when it is felt inappropriate to intiate more direct discussion in the ED. It is currently not unusual to admit patients in this circumstance
irrespective of their potential donor status.
The Intensivist may decide not to admit the patient if it suspected that the patient may not progress to brain death, or in relation to any
medical or social factors that would make donation unlikely, or if there is an immediate prospect that another patient’s life would be
jeopardised by admitting this patient. The Link Nurse should be involved by Nursing or other staff to examine staffing possibilities if
insufficient nurses are available and/or to provide assistance in any discussion subsequent to the Intensivists assessment/family discussion.
It is not intended at this stage to intervene in a different way for patients presenting to the ED in collapse in terms of the decision whether to
intubate or not, i.e. there is no plan to intubate/ventilate patients in the hope that their families/society at large may benefit in the instance
that the patient becomes a potential donor.
Sound clinical decision making as prevails currently must continue to apply.
Paediatrics 6.11
Introduction 6.11.1
A number of paediatric patients (usually around 200) are admitted to the Waikato Hospital ICU each year. Registrar staff need to maintain
full involvement with these patients irrespective of their previous experience with children. Liberal involvement of the Paediatric Specialist
responsible for the child and their resident staff may be required to assist in management.
However, as with the adult patients in the ICU and unless the question is clearly outside the provenance of intensive care (e.g. napkin rash,
questions of dietary intolerance, immunisation etc.), the intensivist should be involved first. Many patients (particularly postoperative
patients) are here for nursing care, but the ICU registrar will meet many of their basic medical needs.

Paediatric admission policy 6.11.2

Policy 6.11.2.1
Definition of paediatric patient 6.11.2.1.1
A patient under the age of 15, or if under the care of a paediatrician, is considered paediatric. While patients under the age of 15 years
requiring HDU care are generally managed in the ICU, common sense needs to prevail. Conditions commonly managed in the HDU and
never in the ICU (eg: venous thrombosis) in a child close to the cut-off age should logically be managed in the HDU.Older diabetic children
are frequently under the care of an adult Diabetologist, and care in HDU may be appropriate.
At the other end of the spectrum, it may be appropriate for carefully selected neonates who have already left hospital or who were “outborn”
to be managed in the Newborn unit. The responsible Paediatrician, Neonatologist and Intensivist should liase to determine appropriate
disposition. Clinical assessment is based significantly on the derangement of physiological parameters from normal. In health these values
are determined by the child's age, settling at what can be considered adult values in the early teenage years.
Patients younger than their eigth birthday, anticipated to need >24 hours invasive ventilation should be discussed with Starship with a view
to transfer when possible. Patients older than their eigth birthday (but of course prior to their 15 th birthday) who in addition to a projected
requirement for invasive ventilation > 24h require inotrope/vasopressor infusion or renal replacement therapy should be discussed with
Starship with a view to transfer when possible. Clearly there are patients of 13 to 14 years age who may be considered adult and some
flexibility is important, without constantly “pushing” the lower limit of this age criterion. Such 13 and 14 year olds may be considered
“adult” if: they present with adult diseases (e.g. overdose, alcohol intoxication, driver involved in road accident), and to some extent if they
will be likely be managed by adult specialists at the hospital during their entire stay.
The reader is referred to the very detailed document in the Paediatric Guideline folder for guidance on the specifics of management of
paediatric patients within ICU, including so called HDU admissions to ICU and the details of drug prescription, responsibility for discharge
etc.
HDU have a complementary policy which describes management of that age group in that unit.
What follows is an ABCD approach to the physiological and anatomical factors that affect assessment and management of the paediatric
patient.

General Paediatric Care in ICU 6.11.2.1

Airway 6.11.2.1.1
Tracheal tube size selection can be estimated from the formula: Age/4 + 4.
The expected orotracheal tube length can be estimated by: Age/2 + 12 and nasally by Age/2 + 15
Traditionally cuffed tubes have been avoided in very young children over concerns of sub-glottic trauma, although this is contentious.
Cuffed tubes can allow greater protection against pulmonary aspiration and minimise ventilator leak by creating an airtight seal with
the tracheal wall.
At Waikato Hospital the smallest cuffed tracheal tubes we have are size 4.0, so from a practical point of view any child under 4 years
should probably have an uncuffed tracheal tube.

Any child that will require a size 5.0 ETT or larger should have a cuffed tube.

Please remember this, especially in the ED.

If choosing a cuffed tube consider using a “half-size” smaller ETT.
NB The narrowest part of a child's airway is at the level of the cricoid cartilage. If resistance is encountered having passed the tracheal
tube through the glottis, select a smaller tube size.
In children less than 5 years old a nasal ETT is usually inserted after orotracheal intubation to assist with tube stability unless a
contraindication exists. If such a child is being transferred to ICU from theatre or from another hospital, please ask for this.

Breathing 6.11.2.1.2
Respiratory rate should be assessed at rest in isolation of medical or nursing cares.
Also note the extent of chest excursion, use of accessory muscles, tracheal tug, nasal flaring, sternal or subcostal recession, the presence of
inspiratory or expiratory noises and the presence of cyanosis.
Normal age related respiratory rate is tabulated below:
NORMAL RESPIRATORY RATES
Age Respiratory rate
<1 30-40
1-2 25-35
2-5 25-30
5-12 20-25
>12 15-20
Having given these values, infants are not usually considered significantly tachypnoeic until RR exceeds 60.

Don't get caught out: 6.11.2.1.2.1

Normal oxygen saturation on oxygen therapy does not preclude significant respiratory embarrassment.
A slow respiratory rate in a sick child should be considered pre-terminal.
It is common for a referral to include the statement:”(s)he is getting tired”. If clinical exhaustion is occurring it is highly significant and
should be acted on. Don’t forget though that a child whose general condition is improving (e.g. response to bronchodilators) or even
one who is not so well may be catching up on lost sleep. The more reliable signs of clinical exhaustion include obtundation and
confusion. Conscious level impairment should be formally and carefully evaluated as in any other patient. Hunger, handling, parental
absence and performance of monitoring / procedures is usually distressing to children. Agitation then is neither sensitive nor specific
as a measure of serious disease in children without other objective measures.
Tachypnoea with a clear chest x-ray often signifies acidosis or shock
A study of grunting respiration in paediatric patients revealed a high level of serious disease-not all of it was pulmonary in origin
Issues surrounding artificial ventilation6.11.2.1.2
Under normal conditions aim for tidal volumes of 10mls/kg and rate as suggested above.
PEEP “dose” is the same at any age.
Positive pressure ventilation with an uncuffed tube often results in a significant air leak. Monitor expiratory gas volumes to assess
adequacy of ventilation. Pressure controlled ventilation may provide greater constancy of tidal volume under these circumstances.
Setting a larger tidal volume, in volume control modes, to accommodate the leak could be dangerous should the leak disappear eg with
re-positioning of the child.
It may, of course, be appropriate to change the tracheal tube to a cuffed version or larger size.
Blood gas analysis, capnography or transcutaneous carbon dioxide measurement can assess adequacy of ventilation. Pulse-oximetry does
not allow assessment of ventilation.

It is mandatory to use capnography in every intubated paediatric patient in Waikato Hospital ICU unless overriding reasons exist.

Sedation involves opiates, benzodiazepines and sometimes other agents such as chloral hydrate. Propofol may be used but never in high dose
or prolonged periods.

Circulation 6.11.2.1.3
Assess for signs of end-organ hypoperfusion such as cool peripheries, delayed capillary refill, oliguria (<1ml/kg/hour), agitation, drowsiness
and coma. Tachypnoea is an early sign of shock. Tachycardia can be difficult to interpret in the distressed child, but should be taken
seriously, especially if there is other evidence of shock.
NORMAL AGE RELATED HEAR RATE
Age Heart rate
<1 110-160
1-2 100-150
2-5 95-140
5-12 80-120
>12 60-100

Expected systolic blood pressure can be calculated by: 80 + (age x 2)

Normal blood volume is estimated at 80mls/kg (neonate 90ml/kg, adult 70ml/kg)
Initial fluid challenge in shocked child should be 20mls/kg of warmed 0.9% saline. Repeat as necessary. If in a hurry or using an IO access
use a 3-way tap and syringe.
Calling for someone more experienced to put a drip in during a life-threatening emergency is an indication for you to place an IO access
before they arrive. No one you know has done this frequently, but many should have done it more often. The technique is an old one that was
reintroduced because of practical difficulties and frequent failures involved in venous access in collapsed paediatric patients.
4ml/kg packed cells can be expected to raise Hb by 10g/l.
Don't get caught out:
• Hypotension is a late sign and thus not required for a diagnosis of shock.

Disability 6.11.2.1.4
Defining level of consciousness can be difficult in young children. A modified version of the GCS can be used, but remember this is not what
it was developed for. Valuable information can be gained from the parents.
AGE APPROPRIATE COMA SCORING
Eye Score Response
4 Spontaneous
3 Speech
2 Pain
1 None
Motor Score < 12 months > 12 months
6 Normal movement Obeys commands
5 Localises to supraocular pain Localises to supraocular pain
4 Flexion withdrawal from nailbed pressure Flexion withdrawal from nailbed pressure
3 Abnormal flexion to supraocular pain Abnormal flexion to supraocular pain
2 Extension to supraocular pain Extension
1 No response to supraocular pain No response to supraocular pain

Verbal Score < 2 years 2-5 years > 5 years

5 Babbles, words or sentences as normal Appropriate Orientated
4 Less than usual ability Inappropriate Confused
3 Cries to pain Cries/ screams Inappropriate
2 Moans to pain Moans to pain Moans to pain
1 None None None

Simpler systems like the AVPU system may be preferred.

A child with a GCS of 8 (or unresponsive to pain in the AVPU system)or under should be considered unconscious and unable to protect their
own airway. This may necessitate tracheal intubation. Don't forget to exclude hypoglycaemia as a cause of decreased consciousness.

Hypoglycaemia is an ever present risk in critically ill children especially if not fed enterally.
Regular glucose monitoring is necessary. See nursing policies.

Drugs 6.11.2.1.5

Use Drug Doses book or other recognized sources for drug dosing.
Try and give or supplement potassium intake enterally whenever possible. It is rarely practical to put a central line in conscious children. Use
your common sense-concentrated potassium infusions are never given via peripheral vein in any patient irrespective of age.

Investigations 6.11.2.1.6
It may well be reasonable for paediatric patients to receive few blood tests or chest X-rays on admission to hospital or during their stay.
When however they are referred for consideration of intensive care admission a more liberal, yet still considered approach is necessary.
Basic haematology, biochemistry and blood culture tests are often necessary. A chest X-ray is commonly required, but always for respiratory
conditions.
“Microcollects” can be arranged for the morning bloods and will often be performed by lab staff if the Night ICU registrar speaks kindly to
the Nursing staff to arrange.

Sources of Help 6.11.2.1.7

Lines of communication are established above and in the Paediatric Admission policy.
The same offer made to contact the Intensivist on duty for matters of concern exists as for any patient in or referred to ICU.
Informal contact with paediatric resident staff may be helpful over some matters, but needs to be treated with the same caution as when
you are informally approached by other resident staff for advice.
These guidelines.
Two specific references are chained in the workroom for your use.
Shann’s “Drug Doses” is very useful to carry with you
A copy of Nelsons is locked in the library cupboard, but is largely supplanted by Internet resources available now

References: Macnab A et al. Care of the Critically ill child. Churchill Livingstone, 1999.

Bronchiolitis 6.11.3
Children may be admitted to the ICU/HDU for ventilation, CPAP or observation if there is sufficient concern that they are likely to require
emergency respiratory support.
As with all ICU admissions, the Intensivist must be involved.
All admissions must be notified to the Paediatrician on call by on-call paediatric staff, who have the ability to attend as they see fit or are as
they are requested to.
The most likely infecting organism is respiratory syncytial virus (RSV) which is isolated in 75% of children less than two years of age
hospitalized for bronchiolitis.

Clinical Features 6.11.3.1

Profuse coryza, congestion and a low-grade fever
Signs of lower respiratory tract involvement include cough, dyspnoea, wheezing and feeding difficulties Severe cases - respiratory distress
with tachypnoea, nasal flaring, retractions, head bobbing, obtundation and possibly cyanosis.
Infants under six month of age are the most severely affected due to smaller, more easily obstructed airways and decreased ability to clear
secretions.
Apnoeas are common in infants – central non-obstructive - may require intubation in 10%
 otitis media, retractions, fine rales and diffuse, fine wheezing.
Rarely - myocarditis, supra-ventricular and ventricular dysrhythmias and inappropriate secretion of antidiuretic hormone
Chest radiographs - usually reveal hyperinflation and 20-30% will show lobar infiltrates and/or atelectasis. May be normal.
Laboratory 6.11.3.2
Blood CBC and electrolytes just prior to or at admission and electrolytes daily
Microbiology Blood cultures are advisable (incidence of bacteraemia 9% ICU admissions with bronchiolitis in one study)
Nasopharyngeal aspirates for RSV antigen – more sensitive than nasal swabs

Treatment 6.11.3.3
If severe enough for ICU admission, the child will require:
Oxygen to maintain saturation 92-94%
Barrier nursing
Disturbance of the child is minimized
Secure IVI access and appropriate dextrose containing fluid infusion-paediatric/other staff may need to assist with this before or after
ICU admission
Keep NPO until confident intubation will not be required
Bronchodilators –see below
CPAP is used as a trial of treatment for children with moderate to severe respiratory distress or frequent relatively brief apnoeas.
Prolonged apnoeas do not usually respond satisfactorily to CPAP. 5cm H20 usually prescribed and adjusted upwards if felt necessary.
CPAP has not been proven to have a role in bronchiolitis in any clinical trial, but at the least seems to provide symptomatic benefit.
Caffeine or aminophylline are prescribed if requested by Intensivist or Paediatrician
Appropriate monitoring-If on CPAP or unstable, monitor PaCO2 transcutaneously continuously if available
If ventilated, an arterial line should be inserted if possible. Papaverine added as per guideline.
Ventilatory support – these patients should be nasally intubated with the appropriate size tube
The ventilator should initially be set on a pressure regulated mode with a pressure of 20cm H 2O (volumes may be misleading in children
with large leaks)
Look for chest movement and EtCO2 trace – adjust the ventilator as appropriate to ensure PaO 2>60mmHg and the desired PaCO2. Higher
PaCO2 may be tolerated. End-tidal C02 monitoring must be used (see separate guideline).
Insert a nasogastric tube and feed enterally
Treatment is largely symptomatic
Sedation - would involve the use of morphine 0.5mg/kg diluted in 50ml 5% dextrose plus/minus midazolam 0.5mg/kg diluted in 50 ml
dextrose at 0 – 10ml per hour. Phenobarbitone and chloral hydrate may be considered. Muscle relaxants are often used for the first several
hours.

Emergencies in Ventilated Children with Bronchiolitis 6.11.3.4

Prolonged, disturbing episodes of arterial desaturation often accompanied by frank cyanosis, bradycardia and even cardiac arrest are
relatively frequent in children ventilated for respiratory distress .A simple plan is followed to try and safely manage this disturbing problem:
“Bag” the child with 100% oxygen using a Laerdal bag-sometimes this action, plus suction relieves the situation. Note whether a
suction catheter passes fairly easily or not at all.
Rapidly confirm ETT position using capnography and/or direct laryngoscopy and visual inspection of depth of insertion compared
to known previous position.
Remove ETT rapidly if it appears oesophageally misplaced or blocked based on above tests.

Reoxygenate and reintubate, calling for help as necessary and confirming ETT position with capnography and if necessary direct
laryngoscopy.

Commence cardiac compressions and use appropriate drug treatment if indicated.

Consider a chest X-ray even if you do not reintubate-most frequently this does not lead to a change in treatment or even show a
change however.

Reconsider the ventilation strategy, sedation and paralysis regimen in consultation with the Intensivist.

Frequently, the problem is recurrent and despite its disturbing nature, has to be accepted as part and parcel of what has become a life-
threatening condition. Maintaining ETT security and patency, not unduly prolonging the period of sedation/paralysis and appropriate
ventilatory treatment minimizes problems.

Drugs 6.11.3.5
Bronchodilators - despite negative results in well designed trials there remains enthusiasm in some clinical quarters for use of
bronchodilators. These are administered if requested by Intensivist or Paediatrician.
Antibiotics - should be strongly considered in a sick young infant, especially presenting with apnoeas
- Use in other admissions to ICU with bronchiolitis is controversial, but the incidence of bacteraemia in this group is said to
be about 9% which may justify relatively liberal initial empirical use until blood cultures are proven negative. Antibiotics
are given if requested by Intensivist or Paediatrician.
Ribavirin is not used.
The role of Methylxanthines is unclear. A single non-randomised, retrospective trial of intravenous caffeine in a group of 7 infants between
32-38 weeks post gestation suggested benefit.

Reference:
Fitzgerald D and Kilham H. Bronchiolitis: assessment and evidence based management. MJA 2004; 180: 399-404.
McNamara d et al. Methylxanthines for the treatment of apnoea associated with bronchiolitis and anesthesia. Pediatric Anesthesia 2004; 14:541-550.

Croup 6.11.4

Croup refers to the clinical syndrome of harsh "barking" cough and inspiratory stridor".
The commonest cause is a viral laryngotracheobronchitis (LTB).
Other causes of stridor must be considered
Foreign body
Typically sudden onset
Epiglottitis (very rare in usually well, immunized children-no childhood cases in the Waikato since 1996)
Short history (over a few hours), high fever, sitting and drooling saliva. Child “refuses” to cough or swallow (too painful). External
laryngeal tenderness often present. Not so much inspiratory stridor as muffled expiratory noise. Difficult to confuse with croup
Retropharyngeal abscess
Acute tonsillar hypertrophy
Bacterial tracheitis-starts with typical croup followed not by improvement over 1-2 days but by deterioration , with sick, toxic child (rare)
Laryngomalacia-subacute/chronic history
Tumour/subglottic haemangioma
Trauma

LTB typically affects children aged between 6-36 months with a peak incidence at 12-24 months. It is usually a mild self-limiting illness but
may occasionally cause severe airway obstruction. Typically it develops over several days along with a concurrent coryzal illness.
Spasmodic croup, thought related to “allergy”to viral antigens, often arises suddenly in the middle of the night, rarely requires hospital
admission or indeed any specific treatment and often resolves within a few hours.

Clinical Features of Severe Croup 6.11.4.1

• inspiratory AND expiratory stridor at rest
• tachypnoea
• marked tracheal tug and chest wall retraction
• agitation or exhaustion

Signs of imminent airway obstruction / cardiorespiratory arrest include: 6.11.4.1.1

decreasing level of consciousness
cyanosis , especially if on oxygen
bradycardia
ineffectual respiration
slowing respiratory rate (without other signs of improvement)

Examining the child with severe stridor 6.11.4.1.2

Do not lie the child flat
Do not instrument the airway (eg with wooden spatula)
Do not distress the child unnecessarily (eg separating from parents)
Do not send or allow to be sent unaccompanied to Xray department (e.g. for lateral neck Xray).

Management of severe croup 6.11.4.2

Exclude alternative diagnoses eg foreign body, epiglottits etc.
Oxygen
Often poorly tolerated by young children, but deliver by method best tolerated
Humidification has not been shown to be of any benefit.
IV access
If ICU admission is seriously being sought because the risk of requirement for intubation is thought high, serious consideration must be
given to IV access placement in the ED. If the child is being transported to theatre for laryngoscopy under GA, the timing of IV access can be
discussed with the responsible Anaesthetist.
Steroids
Dexamethasone 0.3mg/kg PO/IV/IM, then 0.15mg/kg 6hly. Prednisone is often given, as it is more readily available.
• Nebulised adrenaline
0.5ml/kg 1:1000 adrenaline nebuliser (max 5mls = 5mg) will give temporary improvement only and may "buy time" for steroids to become
effective.
• Intubation
Indications include:
increasing respiratory distress
cyanosis unresponsive to oxygen
exhaustion or confusion
high oxygen requirement (>60-70%)
cardiorespiratory arrest
poor response or transient (<1hour) response to adrenaline

Intubation will be performed in theatre by an Anaesthetist-contact Intensivist first if you think intubation may be required.
Issues surrounding drug prescription:

Systemic corticosteroids are the mainstay of drug treatment.

Nebulised budesonide is used in mild to moderate croup of all types-i.e. unsuitable for children thought to require ICU admission.
Nebulised adrenaline is an emergency rescue treatment. It buys you time (up to 2 hours) to allow the corticosteroid to become effective.
Any child receiving nebulised adrenaline will have already received or will immediately receive systemic corticosteroids.
Antibiotics are not indicated in uncomplicated croup.

No patient may leave the emergency department bound for ICU without having received systemic corticosteroids, be they orally,
intravenously or intramuscularly administered.

Drug doses 6.11.4.3

Dexamethasone 0.3 mg/kg PO/IV then 0.15mg/kg/12hourly for maintenance
Prednisone 2mg/kg PO then 1mg/kg/12hourly for maintenance
Budesonide 2-4mg Neb then 2mg/12 hourly for maintenance
Adrenaline (1:1000 ie 1mg/ml)-1ml 1:1000 starting minimum dose up to 0.5ml/kg (max 5mls) Neb

Reference:
Duncan A in Oh’s Intensive care manual 5e, 2003; 1007-1014.
Fitzgerald D and Kilham H.Croup: assessment and evidence-based management. MJA: 2003 Oct 6; 179(7): 372-7.

Seizures in Children 6.11.5

Definition of status epilepticus 6.11.5.1
Generalised convulsion lasting >30 minutes, or repeated convulsions occurring over a 30 minute period without recovery of consciousness
between each convulsion.
(N.B. cf. definition of typical febrile convulsion up to 20 mins)
Many children arrive having received rectal diazepam from parents or paramedics. The general consensus is this should NOT be considered
and that treatment should commence at the start of the algorithm.
Step 1
Initial assessment should follow ABCDEFG (Don't Ever Forget Glucose) principle
Oral or nasal (teeth clenching or “too awake” to tolerate oral airway) airway if necessary.
Many seizure patients you are called to will not require consideration of intubation.
High flow oxygen
Brief bag mask ventilation is sometimes required after benzodiazepine administration
Take brief history & exam (considering differentials such as tonic spasm secondary to RICP, drug-induced dystonia).
Most seizures will stop within 5 minutes, but treatment should begin within 10 minutes.

If intravenous access is immediately established give 0.1–0.25 mg/kg diazepam over 60 seconds.
Midazolam 0.1mg/kg IV is an alternative if the attending doctor is more familiar with this.
If no IV access then give rectal diazepam 0.5mg/kg or midazolam intramuscularly as above. Consider intraosseous access.

If after 10 minutes the initial seizure has not stopped or another has begun then progress to step 2

Step 2
Establish IV or IO access and give phenytoin 20mg/kg unless child already on it. Max rate 1mg/kg/min-usually given over 30-45 minutes
however. Further doses of benzodiazepine may be necessary during this period.

Step 3
Discuss case with Intensivist if ICU admission is sought by Paediatric staff, it is clear seizures are not controlled or if a severe acute
underlying condition is suspected based on history.
IV phenobarbitone 20mg/kg over 10 minutes or sodium valproate 15mg/kg over 45 mins are alternatives if phenytoin cannot be given for
some reason.
Optimise phenytoin dosage as necessary when levels available
Step 4
Intubation may prove necessary if seizures continue, respiration becomes inadequate or if further barbiturate dosing is envisaged.
Further investigation as appropriate and directed by Paediatrician/Intensivist.

Several approaches are possible:

midazolam infusion (0.15mg/kg over 30 mins, followed by 1mcg/kg/min infusion, increasing by 1mcg/kg/min every 15 mins if seizures
do not abate).
further phenobarbitone, valproate etc.

No child may leave the ed bound for icu with a diagnosis of status epilepticus without a firm reason for not receiving an adequate
loading dose of long acting anticonvulsant. this applies to children where the status abates prior to ed arrival or with the use of
benzodiazepines.

In these patients, seizures frequently recur and often “needlessly” so. Rare patients are on multiple anticonvulsants or cannot receive
standard long acting anticonvulsants for some reason. A different approach is needed for these children.

Reference:
Scott R and Neville B. Pharmacological management of convulsive status epilepticus in children. Dev Med Child Neurol 1999; 41:207-210.

Meningitis 6.11.6

This condition is particularly challenging in the paediatric population as symptoms and signs are often non-specific, especially in infancy. A
high index of suspicion should be maintained, and empirical treatment commenced until the diagnosis can be excluded.
Meningitis is classically subdivided into bacterial and aseptic forms depending on the appearance of CSF at microscopy.

Bacterial Meningitis 6.11.6.1

Likely causative organisms for bacterial meningitis depend on age.

LIKELY ORGANISM INVOLVEMENT ACCORDING TO AGE

Age Common organisms

< 1 month Grp B Streptococci
Enterococci
Gram -ve bacilli
Listeria monocytogenes
1 to 3 months As above & below
> 3 months S. pneumoniae
N. meningitidis
H. influenzae

• Antibiotic resistance
Penicillin and cephalosporin resistant strains of S.pneumoniae are becoming increasingly prominent throughout the world although
uncommon in the UK and Australasia.

Add vancomycin if Gram +ve diplococci are seen on Gram stain.

• The steroid controversy

The contention is that corticosteroids may attenuate the inflammatory meningitic process thus reducing the incidence of long-term
neurological sequelae.

Steroids are given if requested by Paediatrician or Intensivist.

• Meningococcal disease
A high index of suspicion allows early recognition of the disease and institution of aggressive treatment.
Meningococcal disease presents as meningitis in ~50%, septicaemia in ~10% and mixed picture in the remaining~40% of cases.
20% of cases will not have a petechial, rash. It is also important to note that other bacteria and viruses can present with petechiae, albeit less
commonly.
From a practical point of view any child with a fever and petechial rash should be assumed to have meningococcal disease until proven
otherwise. Give cefotaxime or ceftriaxone immediately, DO NOT wait for laboratory results.

Aseptic meningitis 6.11.6.2

Causes can be subdivided into infectious and non-infectious causes.

Clinical features 6.11.6.3

The classic triad of headache, neck stiffness and photophobia may be present in older children but often absent in infants. A history of poor
feeding, high temperature, vomiting, apnoeas, convulsions, irritability and lethargy should raise suspicion. Don't forget to ask about
immunisations.
Classical signs (Kernig’s, Brudzinski and nuchal stiffness) are often absent. If these signs are present they are neither sensitive nor specific
for differentiating between viral and bacterial meningitis.
Petechial rash is often said to be pathognomonic of meningococcus but does occur with viral and other bacterial causes. Don't forget to
examine the fontanelle (if appropriate) and ears, nose and throat for possible septic focus.

Differential diagnoses 6.11.6.4

• Viral encephalitis
Classically presents with fever, headache and decreasing GCS. Focal neurology and seizures are common findings. With a compatible
history, acyclovir is commonly given.
• Viral meningitis
Usually mild and self limiting, but severe forms can be easy to confuse with bacterial meningitis. CSF analysis will help
• Other causes of non-traumatic coma (see separate section)
A GCS < 13, complex seizures or focal neurology should raise the suspicion of a diagnosis other than bacterial meningitis the most
important of which include cerebral oedema or space occupying lesion. CT scan, and not LP, is indicated under these circumstances.

Investigations 6.11.6.5
This is a guide to the initial investigations that you should consider. Obviously CSF will not be available in all cases.

INVESTIGATIONS IN CNS INFECTIONS

Sample Test
Blood Routine haematology, coagulation, biochemistry, renal & hepatic function
Culture & sensitivity
Blood & urine Influenza A, CMV, mycoplasma, chlamydia serology
Urine Pneumococcal antigen
Blood +/- CSF PCR meningococcus, enterovirus & HSV
CSF Microscopy & Gram stain
Biochemistry (glucose & protein) nb don't forget serum glucose at same time
as LP
Culture & sensitivity
Enterovirus PCR

Other investigations Indication

CT scan GCS <13 with sudden, subacute(>24 hours) or chronic symptoms (these
suggest other aetiologies)
complex seizures
focal neurology
MRI & EEG Viral encephalitis a possibility
CSF TB & cryptococcus if history suggestive

Other disease mimicking meningitis 6.11.6.6

A proportion of children with symptoms or signs suggestive of meningitis will have another diagnosis eg tumour, encephalitis, abscess or
haemorrhage. The onset and duration of symptoms, presence of focal signs, complex seizures or depressed level of consciousness indicate
the possibility of these diagnoses.
Under these circumstances CT scan is the first investigation of choice.

Lumbar Puncture 6.11.6.7

Lumbar puncture is the definitive investigation for diagnosing meningitis and should be performed in all cases of suspected meningitis
unless there are specific contraindications before antibiotics are given.
Contraindications to LP
 Signs of raised intracranial pressure
complex convulsive seizures
focal neurological signs
GCS<13
coagulopathy
obvious shock or respiratory failure
local superficial infection

Benefits of lumbar puncture:

A definitive diagnosis of meningitis is made, organisms being seen in approximately ¾ of cases.
Allows identification of unusual organisms (especially at the extremes of age and immunocompromised).
Allows identification of resistant organisms (eg resistant pneumoncocci).
Once sensitivities are known, broad spectrum antibiotics can be replaced with narrow spectrum monotherapy.
Allows discontinuation of antibiotics if the CSF is clear.
Removes differential diagnoses eg encephalitis

Beware:
It seems to have become common practice to perform a CT scan prior to LP over concerns regarding intracranial hypertension and the risk of
herniation, but:
A "normal" CT scan does not exclude raised ICP especially in children.
Death from herniation following LP can occur despite a normal CT scan
So the decision to perform a lumbar puncture should be based purely on clinical findings.
An LP is performed at the discretion of Paediatric staff prior to ICU admission (and generally performed by those staff if felt indicated) or at
the direction of Intensivist and Paediatrician after ICU admission.
If the ICU resident staff lack the requisite experience to perform this (e.g. in a small infant), Paediatric staff will usually be asked to perform
the LP.

Management 6.11.6.8
Airway-If the child is obtunded and unable to protect their own airway then intubate the trachea.
Breathing-If spontaneous respiratory effort is inadequate then support with positive pressure ventilation.
Circulation-If there is evidence of poor peripheral perfusion or overt shock give a 20mls/kg bolus of warmed 0.9% saline and reassess.
This may need to be repeated. Shock resistant to fluid therapy will necessitate inotropic support. (See section on shock).
Observe for seizures and evidence of raised ICP. Treat these aggressively (see separate sections on non-traumatic coma & status
epilepticus).

AGE APPROPRIATE ANTIBIOTIC TREATMENT FOR CNS INFECTIONS

Age Empiric treatment

< 1 month Cefotaxime

&
Amoxycillin /penicillinG

1 to 3 months Ceftriaxone
&
Amoxycillin /penicillin G

> 3 months Ceftriaxone

Additional feature Consider adding to above

guideline

Complicated case Vancomycin

Recent head trauma or neurosurgery
Indwelling CSF shunt
Immunosuppression

Gram +ve cocci or diplococci seen in Vancomycin

CSF

HSV Encephalitis not excluded Acyclovir

Once sensitivities are known, broad-spectrum antibiotic cover can be changed to narrow spectrum monotherapy

Duration of treatment is at discretion of Paediatrician or Intensivist

Don't forget to inform public health if meningococcal disease is strongly suspected or proven or if other notifiable diseases are implicated.
 Reference:
Correiea J and Hart C. Meningococcal disease. Clin Evid. 2004 Dec; (12): 1164-81.

Guidelines for the Management of a child with DKA 6.12

Clinical Findings 6.12.1

dehydration
hyperglycaemia
ketoacidosis
electrolyte derangement
hyperosmolar state

Treatment Rationale 6.12.2

The greatest mortality and morbidity in the setting of paediatric DKA is as a consequence of cerebral oedema. It is thought that
rapid correction of the hyperosmolar state produces an osmotic dysequilibrium and can result in cerebral oedema. This occurs in
approximately 7 per 1000 paediatric DKA episodes. It is more common in newly diabetics.
In view of this, there has been a recent trend to replacing volume deficit slowly, as well as slowly correcting hyperosmolality.

Initial management 6.12.3

Ensure adequacy of airway and breathing.
If shocked give 20mls/kg bolus 0.9% saline and reassess
If not shocked give 10mls/kg bolus 0.9% saline.
Assess conscious level.

Investigations 6.12.4
Electrolytes, urea, creatinine, serum osmolality, glucose, CBC, blood gas (venous if not arterial), blood cultures, plasma
betahydroxybutyrate, urinalysis and CXR.
Lines & tubes 6.12.5
X2 IV lines and consider a urinary catheter.
Consider central venous access (rarely practical) and/or arterial line as regular sampling will be necessary.
Volume resuscitation 6.12.6
Prescriptive volume resuscitation can not accommodate the wide variation of clinical presentation, but may be used to guide
treatment.
Remember the principle of low volume resuscitation and slow (36-48hours) correction of deficit.
Estimate volume deficit 6.12.7
Based on clinical assessment of the child.
Calculate deficit as 10mls/kg for every % point dehydrated:
Total Deficit = Estimated % dehydration x 10 x weight (kg)
Subtract volume of any fluid boluses given and replace remaining deficit over 36-48 hours (depending on osmolality at
presentation) in addition to maintenance fluids.
Remember this is purely an estimate, but will help guide initiation of therapy

Choice of fluid 6.12.8

Use 0.9% Saline for replacement and maintenance while glucose > 15mmol/l
Use 0.45%Saline/ 5%Dextrose (equal volumes 0.9%Saline & 10%Dextrose) when glucose < 15mmol

Correcting hyperglycaemia 6.12.9

Should be done slowly. Aim for 2-4mmol/l/hour.
In practice, glucose tends to drop much quicker than this on initiation of volume resuscitation. On the basis of this, commence insulin
infusion 30-60 minutes after fluid initiation.
Start insulin (Actrapid) infusion at 0.05units/kg/hour (titrate +/- 0.025units/kg/hour)
No bolus of insulin, unless life threatening hyperkalaemia.
Aim to keep glucose 10-20mmol/l until acidosis resolving (pH>7.3, HCO3- > 15)
Note that prescription of normal sliding scale insulin is inappropriate.

Correcting osmolality 6.12.10

Should be done slowly. Aim for drop of less than 5mosmol/l/hour. For the same reasons as mentioned above, this is difficult to achieve in

the first couple of hours.

 Calculated Osmolality = ([Na+] x2) + [urea] + [glucose]
From a practical view, ensure Na+ is not falling.
N.B. a blood sample should be sent to the lab to measure osmolality, in case unmeasured osmoles (e.g. ketones or lactate)

present in significant amounts.

Correcting acidosis 6.12.11

Bicarbonate is rarely indicated. Consult Intensivist.

Potassium replacement 6.12.12

Potassium deficit is often very large. On presentation, however, it is common for plasma potassium to be normal or even high, but as
acidosis resolves it drops rapidly

If K+ > 5mmol/l then do not give potassium

If K+ 4-5mmol/l give 0.1mmol/kg/hour (approximately equivalent to 20mmol/l KCl)
If K+ 3-4mmol/l give 0.2mmol/kg/hour 40
If K+ < 3mmol/l give 0.3 mmol/kg/hour 60
If patient anuric give half the amount of potassium suggested above.

Phosphate 6.12.13
Hypophosphataemia is common and can be corrected if desired with potassium dihydrogen.

Observe for signs of raised ICP 6.12.14

Hourly neuro observations should be undertaken for the first 24 hours, and half hourly if GCS <15.
Persistently low or deteriorating scores are highly suggestive of cerebral oedema.
Give mannitol 0.25g/kg = 1.25ml/kg of 20%solution and repeat as necessary (guided by senior staff).
If hyponatraemic consider 4M Saline 0.25mls/kg (up to 20ml)
Liaise with senior staff.

Pitfalls 6.12.15
In severe ketoacidosis betahydoxybutyrate predominates over acetoacetate. Ketostix react with acetoacetate NOT betahydoxybutyrate. So
may underestimate severity of ketonuria.
Don't forget to correct sodium for presence of hyperglycaemia Corrected sodium = measured sodium +
(Glucose-5)/3
Osmolality and glucose often drop rapidly on initiation of treatment, but thereafter decrease insulin infusion rate if falling faster than 2-
4mmol/l/hour.
Spinal Injuries 6.13
ICU Admission Policy 6.13.1
Assessment and admission to ICU 6.13.1.1
Patients with clinically complete or near complete cord injury at or above C5 in the cervical region near-complete signalled by motor
power less than 3 in majority of muscle groups below level of injury are assessed with a view to routine ICU admission.
In thoracic cord injuries, injuries above T6 producing clinically complete or near complete lesion as above are assessed with a view to
routine ICU admission.
Exceptions in both cases are patients with such severe associated morbidity or comorbidity that the Intensivist on duty explicitly advises
against ICU admission.
In every case of spinal cord or significant spinal column, an Orthopaedic team’s advice will have been sought if the referral did not come
from that Orthopaedic team directly.
Radiological Assessment of the Spine 6.13.1.2
This vexed area remains incompletely resolved. What is clear is that complete radiological clearance of the cervical spine is required in those
patients where clinical examination cannot be relied upon to do so. The issue of when to attempt screening clearance of the thoracic and
lumbar spine is becoming clearer from the literature, but no guidelines are in current use at Waikato Hospital. An individual decision is thus
required.

Critical Care Management of Spinal Cord Injury 6.13.1.3

As in other injuries and critical illnesses, priorities revolve around airway, breathing and circulation as the starting point of treatment.
In an emergency or with an unco-operative patient a rapid sequence induction with MILS and avoiding suxamethonium beyond the first 48 or
so hours is the norm. In the relatively uncommon critical care scenario of elective intubation, awake fibreoptic intubation may be considered.
The evidence base for preferring this over careful conventional laryngoscopic intubation seems weak.
The concept of preventing secondary neurological injury in the spinal cord is also accepted despite an incomplete evidence base. This is
usually achieved with appropriate fluid loading and use of chronotropes, inotropes and vasopressors.
Appendices 7.0
Haemodynamic Principles 7.1
Introduction 7.1.1
When faced with a patient who may have some haemodynamic impairment you should have a systematic approach to assessing and
managing this important issue. The following is one way:
Ask four questions:
Is the blood pressure actually low?
Is there any evidence of shock (or poor tissue perfusion)?
Does this patient require more fluid?
Do I need to introduce an inotrope, a chronotrope or a vasopressor?
Diagnosing hypotension 7.1.2
Absolutely low blood pressure 7.1.2.1
Low blood pressure is variously defined as
Systolic BP < 90 mmHg or Mean arterial pressure < 60 mmHg.
These are implied limits at which vital organs continue to autoregulate blood flow.
Relatively low blood pressure: 7.1.2.1
Individual patients may “normally” have elevated or indeed low blood pressure. Hypotension would then be considered as:
Systolic BP 30% lower than known values for that patient (or an absolute drop of 20 mmHg).

Is there any evidence of shock ? 7.1.3

Bedside indicators: 7.1.3.1
Cerebral perfusion: restlessness or confusion
Renal blood flow: oliguria ( < 0.5 ml/kg / hr)
Cool peripheries (unreliable)
Simple investigations 7.1.3.2
ECG: evidence of regional ischaemic changes
↓pH on arterial blood gas
↑ Serum lactate
Central venous oxygen saturation.
Surrogate end-points 7.1.3.3
Generally unwieldy eg. gastric tonometry and measurement of gastric mucosal pH.

Does this patient require more fluid resuscitation? 7.1.4

Introduction-Assessment of Cardiac Preload 7.1.4.1
This is the hardest question to answer.
All texts and wise men will urge you to adequately volume resuscitate the patient, while simple to say, it is difficult to fulfil.
Defining preload 7.1.4.2
Pre-load refers to the degree of ventricular filling which infers the degree of stretch of myocytes during diastole.
Starling Curve 7.1.4.3
The more fluid returned to the heart (venous return), the greater the contractile force of the heart and the greater the volume of blood
expelled.
At some point the distension of the heart exceeds its ability to contract and the ventricle will fail.
THE FRANK STARLING CURVE FIGURE 1
Ventricular Contractile Energy

Volume responsive
cardiac performance

Ventricular End-Diastolic Volume

Should I give more fluid ? 7.1.4.4

Patients on the volume responsive part of the Starling curve should increase their cardiac output in response to further intravenous fluid.
How do I know where the patient is on the curve ? 7.1.4.5
In a number of patients this is not problematic as they have haemorrhagic shock, vomiting, diarrhoea or some other reason for absolute or
relative (eg. epidural, anaphylaxis) intra-vascular volume contraction
There are a number of techniques for assessing or inferring left ventricular end-diastolic volume as the determinant of pre-load in patients
where this is not clear-cut. Two of these, the pulmonary artery catheter and the PiCCO are described separately in this appendix.
Clinical estimates of hydration (moist mucous membranes, skin turgor….) are almost useless in ICU.
Estimation of JVP, or indeed invasive measures of right heart (CVP) or left heart(pulmonary capillary wedge pressure) filling pressures have
some relevance in patients with hearts that have normal structure and function. Often this is not the case in ICU.
So what should I do ? 7.1.4.6
Often clinical practice relies on your impression and an assessment of the risk of giving more fluid than not doing so. ie. It would be “easier”
to give fluid to a hypotensive person with a clear chest who is ventilated, than one with chest crackles who is developing respiratory failure,
even if this is due to some other pathology.
The decision to implement a fluid challenge is inextricably linked with a duty to closely observe the results and act accordingly.
Do I need to introduce an inotrope, a chronotrope or a vasopressor ? 7.1.4.7
Once the three questions above have been addressed adequately it may become necessary to use an agent to bring about an increase in blood
pressure and therefore organ perfusion. ie.
Organ perfusion: Q = (Pi-Po)×C , where
Q = organ perfusion
C = regional conductance (a function of vascular radius, and blood rheology)
Pi-Po = pressure gradient across the tissue bed or organ (generally blood pressure, BP)
BP = Systemic vascular resistance (SVR) × cardiac output , (ie = HR × Stroke volume × SVR).
Manipulation of blood pressure and therefore organ perfusion relies on changing one of the following three parameters therefore: heart rate,
stroke volume and vascular resistance.
While the response to a given agent is not always totally predictable, the commonly used drugs would be used with the following
expectation:
INOTROPIC SUPPORT
Drug Action Comment
Adrenaline Mixed alpha and beta receptor activity Will usually result in increased cardiac output.
Vasopressor effect unreliable, but dominant beta effect not seen as for
dobutamine.
Associated with beta-2 activity and unwanted metabolic effects
(hyoperglycaemia, lactate production)
Noradrenaline Predominant alpha activity Used as a vasopressor with some increase in cardiac performance.
Milrinone Methylxanthine. Non-adrenergic receptor activity. Cardiogenic shock due to diastolic failure
Increases cAMP intracellularly by modulating Pulmonary hypertension following cardiac valve replacement.
phosphodiesterase activity. Rescue following catecholamine induced down regulation of receptors in
May also facilitate diastolic relaxation patients requiring ongoing chrono-inotropy.
These agents may accumulate in renal failure
Dobutamine Synthetic beta agonist Chronotrope and inotrope
May result in a fall in blood pressure due to peripheral vasodilatation.
Dopamine 1 < 2.5 g / kg / min Diuretic
(D-receptor stimulus) Chronotropic
Dopamine 2 2.5-10 g / kg / min Add beta stimulus as for dobutamine
Dopamine 3 > 10 g / kg / min Increasing alpha stimulus.
Phenylephrine Vasopressor Predominantly used in anaesthetics for short periods of predictable
Potent post- synaptic adrenergic agonist hypotension associated with epidural or spinal anaesthesia.

The Pulmonary Artery Catheter 7.3

Introduction 7.3.1
The “PAC” was designed in an effort to quantify and therefore manipulate haemodynamic parameters ie.
1] Estimation of cardiac pre-load by measuring pulmonary artery occlusion pressure
2] Estimation of cardiac output by thermodilution
Pulmonary artery occlusion or wedge (PCWP) pressure 7.3.1.1
Under conditions described in the clinical procedures section of this guideline the PA catheter is inserted into a central vein.
The PA catheter is introduced into a segmental pulmonary artery using a flow directed technique described below.

Swan-Ganz-Haemodynamic Waveforms
A typical Pressure trace during Pulmonary Artery Catheterisation (from left to right) and corresponding diagrammatic representations of
compartments; RA Right Atrium, RV Right Ventricle, PA Pulmonary Artery and PAOP Pulmonary Artery Occlusion Pressure.
The premise behind the use of this catheter is that PAOP is determined by left atrial pressure which bears a relationship to left ventricular
end diastolic pressure and this in turn relates to left ventricular end-diastolic volume as the final arbiter of pre-load.
This relationship does not hold true if;
There is not a continuous column of fluid between sensor and left atrium.
There is mitral regurgitation.
The compliance characteristics of the left ventricle are abnormal.
Given the above it is not surprising that the PAOP has proven to be an unreliable predictor of preload in clinical practice.
Complications of Pulmonary Artery Catheterisation 7.3.1.2
Time spent inserting the catheter may distract from resuscitating the patient.
Insertion and mechanical problems, thrombosis and infection are similar to those observed with central access cannulation.
Balloon induced problems:
Balloon rupture
Catheter knotting
Pulmonary infarction
Pulmonary artery rupture
Pulmonary and tricuspid valve damage
Endocarditis
Arrhythmia’s
Place in therapy 7.3.1.4
The impact of a PA catheter, and the haemodynamic variables obtained with it on management, and outcome, are not well defined.
Particularly disappointing has been the inability of pulmonary wedge (or occlusion) pressure to reflect in any useful way the pre-load status
of a given patient.
Understanding of the catheter’s limitations and usefulness varies widely among doctors and nursing staff and requires ongoing education to
reduce morbidity associated with its use, and correct interpretation of the data it provides.
Proponents of its use argue that failure of clinical judgement in diagnosing type of shock, or instituting successful treatment is an indication
for catheterisation of the right heart, to assess haemodynamic and metabolic variables reflecting type, severity and course of circulatory
compromise.
Those who do not favour use of the PA catheter argue that clinical judgement (or less invasive monitoring) is not inferior to catheterisation of
the right heart.
The lack of direct evidence to support the use of this type of catheter, and the increasing body of evidence documenting its inability to
predict response to fluid loading have resulted in declining use of the PA catheter in clinical practice.
A PA catheter is infrequently inserted within the ICU at Waikato Hospital. Other methods of monitoring are generally preferred.
Reference:
Synopsis of Intensive Care Medicine, L I G Worthley. Churchill Livingston, Chapter 8, Vascular Cannulation and hemodynamic pressure measurements 1994.
Oxford Textbook of Critical Care. Webb, Shapiro, Singer and Suter editors. Chapter 16, Monitoring equipment and techniques. Oxford Medical Publications 1999.

“The PiCCO-catheter / monitor” 7.4

Introduction 7.4.1
This method evolved as an alternative to cathterisation of the right heart in an attempt to elucidate further the concept of cardiac pre-load,
and patient fluid status.
Aims 7.4.1.1
Measurement of cardiac output by less invasive means than catheterisation of the right heart.
Estimation of pre-load, intra-thoracic blood volume and by inference “extra-vascular lung water”.
Technique: 7.4.1.2
Trans-pulmonary thermodilution measurement and analysis of pulse contour.
Estimation of cardiac output 7.4.1.3
A bolus of injectate, usually cold fluid, given into a large central vessel (eg. superior vena cava) can be detected in a large artery (eg. femoral
or axillary) as a temperature change, giving rise to a pulse contour.
This is similar in theory to the thermodilution principle used in the PA catheter where cold fluid of a known volume and temperature is
injected proximally into the catheter and a temperature change detected more distally by a temperature sensor as the colder fluid mixes with
blood. The magnitude of the temperature change detected at the thermistor can be used to estimate the volume of blood into which the cold
fluid was diluted, and hence the cardiac output.
When this is done across the entire pulmonary circulation however, and is detected in an artery the “pulse contour” generated by the
temperature change is flatter and longer, but nevertheless still gives reliable results when extrapolated to predict cardiac output.
Estimation of pre-load, intra-thoracic blood volume and extra-vascular lung water 7.4.1.4
The derivation of these parameters using this technique is not simple, nor intuitive, and requires extensive extrapolation of data.
Inferences inherent in estimation of cardiac pre-load using the PiCCO technique 7.4.1.5
By examining the contour of the temperature “pulse wave” generated in the systemic arterial tree by injecting cold fluid centrally, it is
possible to make some inferences relating to given blood volumes.
Inference 1 7.4.1.6
An injected indicator (cold fluid) always mixes with largest volume accessible.
Cold water injected into a central vein will mix into fluid in the following spaces, which together comprise the intra thoracic thermal volume
or ITTV.

PICCO Dilution and Redistribution Of Temperature

CV Bolus Injection Arterial Catheter

RAED RVED EVLW LAED LVED

PBV
V V V V

Where:
GEDV = The volumes of each of the heart chambers are visualised in diastole as representing the state of largest volume. The sum of all
fluid in all the chambers is called the global end diastolic volume.
PBV = Pulmonary blood volume, or that volume of blood in the lung vasculature.
EVLW = Extra vascular lung water. The volume of fluid in the lung, that is not in the lung vasculature.
ITBV = intra thoracic blood volume is the sum of all blood in the heart chambers and that in the pulmonary vasculature (PBV)
Inference 2 7.4.1.7
By analysing the shape and time characteristics of the temperature wave form (or pulse) it is possible to make certain assumptions with
regard to the volumes of mixing as given above.

PICCO The Fudge Factor

Where:
At = Arrival time. Time taken for cold injectate given centrally to be first detected in the systemic arterial tree.
MTt = Mean transit time. Time taken for a defined amount of the cold injectate to have passed the thermistor.
DSt = Down Slope time. Exponential down slope time, equivalent to the rate of decline of the temperature pulse form as extrapolated by
the PiCCO software.
Intra thoracic thermal volume (ITTV) as defined above can be calculated by the derivation:
ITTV = MTt × the cardiac output.
Pulmonary Thermal volume (PTV) can be calculated by the derivation
PTV = DSt × the cardiac output.
By subtracting PTV from ITV the global end diastolic volume (GEDV) can be calculated. GEDV has been proven to correlate with intra
thoracic blood volume (ITBV) in a linear fashion.
The leap of faith is that wave form analysis produced by a transpulmonary thermodilution technique, can be used to calculate cardiac output.
Derived fluid volumes may allow estimation of both preload (using global end diastolic volumes or intra thoracic blood volumes), and the
amount of extravasated fluid into the lungs (given by extra vascular lung water).
Once you accept this principle you can the use these numbers to guide both further fluid therapy and administration of inotropes or
vasopressors.
NORMAL RANGES FOR PICCO EVALUATION
Variable Normal range Unit
Cardiac Index ( CI ) 3.0 – 5.0 L / min / m2
ITBI 850 – 1000 ml / m2
EVLWI 3.0 – 7.0 ml / kg
SVRI 1200 - 2000 dyn / sec / cm-5 / m2
Principles of ventilation 7.5
Introduction 7.5.1
Mechanical ventilation serves two basic functions: ventilatory support and oxygenation support.
Ventilatory support is designed to provide either total or partial gas transport between the environment and the alveoli. Usually this is done
by providing positive airway pressure in a manner that mimics the normal tidal volume and breathing frequency pattern.
In contrast oxygenation support is designed to supplement the F IO2 and to optimise ventilation perfusion matching to effect alveolar gas
transport. The most common technique to accomplish this is the application of positive end expiratory pressure (or PEEP), but manipulations
of the ventilatory pattern and other strategies can also be used.
Classification of ventilators 7.5.1.1
Mechanical ventilators have been classified according to the characteristics of the inspiratory phase.
If they provide a constant inspiratory pressure they are known as pressure generators.
If they provide a constant inspiratory flow they are known as flow generators.
Flow Generators 7.5.1.1.1
These usually deliver a preset volume of gas to the lung independent of the change in pulmonary or chest wall compliance or airway
resistance.
The pulmonary and chest wall compliance and airway resistance determine the proximal airway pressure produced by these machines.
Pressure Generators 7.5.1.1.2
These deliver gas at a preset pressure.
They are often simple, small, robust and cheap.
The volume of gas that they deliver can be altered by a change in the patient’s lung or chest wall compliance or airway resistance.
Modern ventilators encompass both types of generator. They can ventilate the patient either by preset volume, independent of compliance, or
preset pressure which is interactive with pulmonary compliance and resistance, thus altering tidal volume.
It is important to become familiar with the mechanics of both modes.

Ventilatory strategies to provide total ventilatory support 7.5.2

Current approaches to total ventilatory support generally attempt to duplicate the normal bulk flow ventilatory pattern and use tidal volumes
(VT) of 5-10 ml/kg.
Machine breath rates of 10-30 breaths per minute and inspiratory to expiratory ratios (I:E) of 1:4 to 1:2.
These positive pressure breaths are generally delivered as either flow limited volume cycle breaths or pressure limited time cycle breaths.
Positive pressure ventilatory support is usually used in conjunction with elevations in baseline (end expiratory) pressure (PEEP) and
supplementary oxygen.
These settings generally provide safe and effective total ventilatory support in most patients in respiratory failure.
In more complex patients, conventional approaches do not provide ideal blood gas values, or airway pressures may be excessively high.
Under these circumstances other strategies may be considered.
Controlled mechanical ventilation 7.5.2.1
This is the most basic form of mechanical ventilation supplying all ventilation in the apnoeic patient.
Spontaneous breaths are not available.
During pressure control ventilation (PCV) each breath is delivered as time pressure controlled breaths and tidal volume varies, dependent on
the resistance of the airway, elastance and the total PEEP.
Assist control ventilation (ACV) 7.5.2.2
In addition to a preset background rate of CMV breaths the patient’s inspiratory effort initiates a standard CMV breath.
The ability to control respiratory rate means that less sedation is required, however the respiratory muscles continue to contract during these
assisted breaths with only a small reduction in work compared to unassisted spontaneous breaths.
Intermittent mandatory ventilation (IMV) 7.5.2.3
This was introduced to allow unimpaired spontaneous breaths while still ventilated with intermittent CMV breaths to minimise sedative use
and to reduce respiratory muscle discoordination, allowing more rapid weaning.
Synchronised intermittent mandatory ventilation (SIMV) 7.5.2.4
Is designed to avoid “breath stacking” by partitioning the inspiratory time into patient initiated or spontaneous breaths.
Neither IMV nor SIMV has been clearly shown to allow easier weaning than T-piece trials.
Pressure support ventilation (PSV) 7.5.2.5
During this type of ventilation the patient breaths are supported to a preset pressure using additional gas flow.
Inspiration is usually terminated when the inspiratory gas flow falls to about 25% of the initial flow rate.
The main disadvantage of pressure support ventilation is that the tidal volume may alter so that minute volume will alter depending on
respiratory drive, pressure support level and respiratory system compliance.
Excessively large tidal volumes resulting in overstretch of the lung may occur, possibly contributing towards ventilator associated lung
damage.
On some ventilators there is a similar type of ventilation called volume support (VS) which is a mode of adaptive pressure support
ventilation where breath to breath logic is used to assure preset tidal volume.
There are many other forms of ventilation which at the moment are still being investigated. These include airway pressure release
ventilation, bilevel ventilation and proportional assist ventilation.
 Note: PSV and VSV are spontaneous modes. They cannot be used in paralysed patients.

Objectives of mechanical ventilation 7.6

To improve alveolar ventilation and reduce PaCO2.
To improve oxygenation and ventilation perfusion mismatch.
To increase end expiratory lung volume to prevent or treat lobar or pulmonary collapse and atelectasis.
To increase functional residual capacity through the use of PEEP, which may help improve oxygenation or reduce lung injury through
adequate recruitment with the prevention of repeated opening and closing of alveoli.
To unload the respiratory muscles when there is an unbalance between load and the ability to cope. This results in respiratory muscle
insufficiency or ventilatory failure.
To allow adequate sedation and paralysis of the patient to aid control to enable the underlying disease state to be adequately treated.
In some conditions such as trauma where there is loss of chest wall integrity such as in a flail chest, ventilation may be needed to stabilise
the chest wall and to initiate other treatment such as analgesia with safety.
Other Ventilatory strategies 7.7
Reverse I:E Ratio 7.7.1
The conventional inspiratory to expiratory (I:E) ratio is generally 1:2 to 1:4.
This range of I:E ratio tends to synchronise with the patient’s spontaneous ventilatory drive and permits adequate expiratory time for the
lung to return to functional residual capacity (FRC) using the recoil pressure of the lung.
Lengthening the inspiratory time to I:E ratios approaching 1:1 or even exceeding it (inverse ratio ventilation) can be accomplished in either
volume or pressure cycled modes.
Prolonging inspiration has several physiological effects.
The alveolus is held at its inspiratory volume for a longer period. This should allow more mixing time between the alveolus and the
conducting airway and more exposure of the capillary blood to fresh gas. Some studies have shown an improvement in ventilation
perfusion (V / Q) mismatching with this technique and increases in the PaO2.
Incomplete lung emptying. Under these conditions the lung cannot return to its normal FRC and intrinsic PEEP or auto-PEEP develops.
Many of the studies on long inspiratory time and inverse ratio ventilation showing an improvement in gas exchange have probably had this
occur as a consequence of auto or intrinsic PEEP.
Long inspiratory times with air trapping may also improve V / Q mismatching because it functions like applied PEEP, however there is often
a trade-off to allow permissive hypercapnoea. This is largely a consequence of lower set respiratory rates to allow adequate expiration per
breath.
Baseline alveolar pressure rises and thereby this raises maximum alveolar pressure for a constant tidal volume.
The main role of inverse ratio ventilation is in alveolar recruitment in acute lung injury and ARDS. In these conditions it is used as a
ventilatory strategy in an attempt to improve oxygenation.
It is important to realise that once the I:E ratio has been inverted the need for increased sedation and neuromuscular paralysis starts to
increase.
The mode is inherently uncomfortable and is poorly tolerated in lightly sedated patients.
There may be negative effects on cardiac output (increased intrathoracic pressure impeding venous return)

Ventilation Mechanics 7.8

Tidal volumes: 7.8.1
Traditionally an average tidal volumes of around 10-15 ml/kg were used, and 10 ml/kg can be considered a reasonably safe tidal volume in
most patients including children. In patients with poorly compliant lungs or acute respiratory distress syndrome lower tidal volumes should
be used ( < 8 ml/kg).
Respiratory frequency 7.8.2
The respiratory frequency required in an adult varies between 8 and 25 inflations per minute and depends on the patient’s expiratory time
and lung compliance.
Peak inspiratory airway pressure 7.8.3
Generally this should be set on the ventilator to at or below 35 - 40 cmH 2O to reduce side-effects of barotrauma. Plateau pressure is probably
a more reliable guide to risk of barotrauma than peak pressure.
Positive end expiratory pressure 7.8.4
Introduction 7.8.4.1
PEEP is defined as the pressure above atmospheric maintained at the airway at the end of expiration.
It is a supportive technique used to increase arterial oxygen content without increasing the FiO2 and maintain alveolar / small airways
recruitment.
Using PEEP 7.8.4.2
PEEP may be indicated in patients with pulmonary oedema of cardiogenic or non cardiogenic origin.
The usual range of applied PEEP varies anywhere from 5 to 15 cmH2O and rarely up to 20.
Problems with using PEEP 7.8.4.3
PEEP is generally contraindicated in patients with a bronchopleural fistula, or severe barotrauma as it may further predispose to barotrauma
including mediastinal air leak and pneumothorax.
PEEP may also
Increase physiological dead-space
Reduce the capacity to excrete carbon dioxide
Reduce cardiac output, which is due in part to a decrease in venous return and an increase in alveolar and therefore pulmonary blood
pressure, ie an increase in RV afterload, and alteration of left ventricular geometry (intraventricular septum shifted towards the left).
Other complications may include a decrease in renal blood flow and possibly a reduction in portal blood flow.
Weaning from PEEP 7.8.4.4
In general to wean from PEEP we usually reduce the fractional inspired oxygen concentration first until it is down to approximately an F I02
of 0.5
The PEEP is then slowly removed 3-5 cmH2O at a time, providing the PaO2 is > 60 mmHg.
Reference:
Synopsis of Intensive Care Medicine, L I G Worthley, Churchill Livingston, Ch 41, Mechanical Ventilation 1994.
The Australian Short Course on Intensive Care Medicine, 1997 Handbook, pp 81, Principles of Mechanical Ventilation (A Bersten).
Current Therapy in Critical Care Medicine, 3rd Ed, Parrillo Ed. Mechanical Ventilation Strategies p 27-32 (1997).

The Sedation - Agitation Score 7.9

One of many sedation scores developed to assess and target depth of sedation.
This score is not interchangeable with Glasgow Coma Score, the purpose of which is to assess depth of coma following an insult to the brain.
THE SEDATION - AGITATION SEDATION SCORE
Agitation Scale Dangerous Agitation +3 Pulling at ETT, trying to remove equipment, climbing out of bed, thrashing side to side or striking at
staff
Very agitated +2 Does not calm despite frequent verbal reminding of limits, requires physical restraints, biting ETT
Mildly agitated +1 Anxious or mildly agitated, attempting to sit up, calms down to verbal instruction
Calm or asleep 0 Calm, awakens easily, follows commands.
Sedation Scale Mildly sedated -1 Difficult to arouse, awakens to verbal stimuli or gentle shaking, follows simple commands
Very sedated -2 Arouses to physical stimuli,but does not communicate or follow commands. May move
spontaneously.
Unarousable -3 Minimal or no response to noxious stimuli, does not communicate or follow commands.
Paralysed P When muscle relaxants are used, measurement of sedation is not possible.

Classification of anti-arrhythmic drugs 7.10

Classification of Antiarrhythmic Drugs by Their Action 7.10.1
The standard classification of antiarrhythmic drugs was developed by Singh and Vaughan Williams based upon the drug's
electrophysiological mechanisms of action:
Class I drugs act by blocking the Sodium channel, and are divided into 3 groups, IA, IB, and IC based on their effects on repolarization and
potency towards blocking the Sodium channel
Subclass IA drugs are potent Sodium channel blockers (prolong QRS interval), and also usually prolong repolarization (prolong QT
interval) through blockade of potassium channels
Subclass IB drugs have the lowest potency as Sodium channel blockers, produce little if any change in action potential duration (no effect
on QRS interval) in normal tissue, and shorten repolarization (decrease QT interval)
Subclass IC drugs are the most potent Sodium channel blocking agents (prolong QRS interval), and have little effect on repolarization (no
effect on QT interval)
Class II drugs act indirectly on electrophysiological parameters by blocking beta-adrenergic receptors (slow sinus rhythm, prolong PR
interval, no effect on QRS or QT intervals)
Class III drugs prolong repolarization (increase refractoriness) by blocking outward potassium conductance (prolong QT interval), with
typically little effect on the rate of depolarization (no effect on QRS interval)
Class IV drugs are relatively selective AV nodal L-type Calcium-channel blockers (slow sinus rhythm, prolong PR interval, no effect on
QRS interval)
Miscellaneous In addition to the standard classes, IA-C, II, III, and IV, there is also a miscellaneous group of drugs that includes digoxin,
adenosine and Magnesium with actions that don't fit the standard four classes.

VAUGHAN WILLIAMS CLASSIFICATION OF ANTIARRHYTHMIC DRUGS

Class Action Drugs
I Sodium Channel Blockade
Ia Prolong repolarization Quinidine, procainamide, disopyramide
Ib Shorten repolarization Lignocaine, mexiletine, tocainide, phenytoin
Ic Little effect on repolarization Encainide, flecainide, propafenone
II Beta-Adrenergic Blockade Propanolol, esmolol, acebutolol, l-sotalol
III Prolong Repolarization (Potassium Channel Blockade; Other) Ibutilide, dofetilide, sotalol (d,l), amiodarone, bretylium
IV Calcium Channel Blockade Verapamil, diltiazem, bepridil
Misc Miscellaneous Actions Adenosine, digitalis, Magnesium

The Vaughan Williams Classification –an explanation 7.10.2

The Vaughan Williams classification is relatively simple and is useful as a conversational shorthand based on mechanism of action, for its
ability to predict adverse effects, and for preliminary decisions regarding drug therapy, but it has a number of important drawbacks:
Drugs within a class are not necessarily clinically similar; a patient may respond well to one drug in a given class, but not another
Almost all of the currently available drugs have multiple actions; it is rarely apparent which of these actions is responsible for suppression of
an arrhythmia in a given patient
The metabolites of many of the drugs contribute to or are primarily responsible for their antiarrhythmic actions (e.g.-procainamide and its
metabolite, N-acetylprocainamide; encainide and its metabolite, 3-methoxy-O-desmethylencainide)
The stereoisomers of several drugs can have different actions:
The stereo isomers of disopyramide (Class IA) have opposite effects on repolarization; the predominant effect in a given patient
depends on the degree of stereospecificity exhibited in elimination of the drug by that patient
Only the l-isomer of sotalol has beta-adrenergic blocking activity
Some of the most widely used drugs (procainamide, disopyramide, amiodarone, sotalol) have multiple actions which might explain their
utility in treating a broad range of arrhythmias.
Class Toxicities 7.10.3
CLASS TOXICITIES OF ANTIARRHYTHMIC DRUGS
Class I Class II Class III Class IV
Proarrhythmic effects: Sinus bradycardia Sinus bradycardia Sinus bradycardia
IA-Torsades de pointes AV block Torsades de pointes AV block
IC-CAST proarrhythmia Depression of LV function (adrenergic- Negative inotropic effect
Negative inotropic effect dependent)
Infranodal conduction block

ANTIARRHYTHMIC ACTIONS OF ANTIARRHYTHMIC DRUGS

Drug (Class) Class I ActionsClass II Actions Class III Class IV Other Actions
Actions Actions
Quinidine (IA) ++ + ++ + Alpha-adrenergic blockade
Procainamide (IA) +++ + + Ganglionic blockade
Disopyramide (IA) +++ + + Anticholinergic
stereo
specific
Lignocaine (IB) +++
Mexiletine (IB) +++
Phenytoin (IB) + + +
Encainide (IC) +++
Flecainide (IC) +++ + +
Propafenone (IC) ++ + +
Moricizine (I) ++
Propranolol (II) + +++
Esmolol (II) + +++
Sotalol (II / III) ++ +++ Class II actions stereo specific
Amiodarone (III) +++ + ++ + Alpha-adrenergic blockade
Muscarinic blockade
Ibutilide (III) +++
Verapamil (IV) + + ++++
Diltiazem (IV) +++
Adenosine (Misc.) + ++ Enhances potassium conductance
Inhibits cAMP-induced Ca2+ influx
Useful equations in Intensive Care 7.11
STANDARD HAEMODYNAMIC VARIABLES

Variable Formula Normal Range

CO
Cardiac Index CI = 2.5 – 5 l/min/m2
BSA
MAP - RAP
SVR = x 79.9
Systemic Vascular CO 750 – 1500
Resistance dyn.sec/cm3/m2
MAP - RAP
SVRI = x 79.9 x BSA
Systemic Vascular CO 1400 – 2400
Resistance Index dyn.sec/cm3/m2
MAP - RAP
PRV = x 79.9
Pulmonary Vascular CI 150 – 250
dyn.sec/cm3/m2
CI
SVI =
Stroke Volume Index HR 33 – 47 ml/beat/m2
LVSWI = ( MAP - PAOP ) x SVI x 0.0136
Left Ventricular Stroke 50 – 120 g/m2/beat
Work Index
RVSWI = ( MAP - RAP ) x SVI X 0.0136
Right Ventricular Stroke 25 – 55 g/m2/beat
Work Index
CaO2 = ( Hb x 1.34 x SaO2 ) + ( PaO2 x 0.0003 )
Arterial Oxygen Content 17 – 20 ml/100ml
CvO2 = ( Hb x 1.34 x SvO2 ) + ( PvO2 x 0.003 )
Venous Oxygen Content 12 – 15 ml/100ml
DO2I = CI x CaO2 x 10
Oxygen Delivery Index 550 – 750 ml/min/m2
VO2I = CI x ( CaO2 - CvO2 ) x 10
Oxygen Consumption 115 – 160 ml/min/m2
Index
VO2I
Oxygen Extraction Ratio O2ER = 0.24 – 0.4
DO2I

Qs ( CcO2 - CaO2 )
Shunt Equation = x 100 5 – 15 %
Qt ( CcO2 - CvO2 )
CcO2 = ( Hb x 1.34 x 1.0 ) + ( PAO2 x 0.003 )
End Capillary Oxygen 80 – 100 ml/100ml
Content
PAO2 = FiO2 ( 760 - 47 ) - ( PaCO2 x 1.25 )
Aveolar Gas Equation 100 – 650 mmHg
Content of commonly used enteral feeds 7.12
NUTRITIONAL COMPARISON OF ENTERAL FORMULAS (PER LITRE)
Per Litre Nutrison Protein Nutrison Standard N-source Pulmocare Resource Nova
Plus Multifibre Multifibre Renal For kids Source 2
Kcal 1250 1000 2000 1500 1000 2000
Protein (g) 63 40 74 62.4 30 90
Fat (g) 49 39 100 92.0 50 88
CHO (g) 141 123 200 106 110 214
Na mmol 48 43 43.5 57 17 35
K mmol 43 38 20 48.6 33 43
Phos (mg) 29 720 650 1055 800 1050
Osmolarity 280 330 700 390 790
Fibre (g) 15 15 - - - -

Guidelines for the use of patient controlled anaesthesia (PCA) 7.13

Introduction 7.13.1
PCA is a useful analgesic technique:
Small and frequent intravenous bolus doses of opioid can be given whenever the patient becomes uncomfortable, or when a painful
stimulus is anticipated, enabling individual titration of pain relief. This flexibility helps to overcome the wide interpatient variation in
opioid requirements.
The intensity of acute pain is rarely constant, and PCA means that the amount of opioid delivered can be rapidly titrated.
Patients can also titrate the amount of opioid delivered against dose-related side effects.
The inherent safety of the technique lies in the fact that, as long as the machine is in PCA mode only (ie. there is no continuous infusion),
further doses of opioid will not be delivered should the patient become excessively sedated.
Contraindications 7.13.1.1
Patient confusion
Inability to understand the technique.
Untrained staff (medical and nursing)
Standard PCA use in ICU 7.13.2
If patients commence a PCA within ICU from an ICU Medical Staff members prescription, either the APS acute pain nurse may be
told or the pink form returned to Level 3 recovery so appropriate follow-up may take place .
Oxygen is generally admisnistered, but is not required if oximetry is satisfactory.
Caution with other opioids and sedatives.
It must be clear that if others press the button for the patient, some advantages are lost.
The IV line must contain a non-return valve.
Change syringe every 24 hours and line every 48 hours.
It is customary to chart oxygen, naloxone and an antiemetic on discharge to the ward. Acceptable physiological parameters must also be
entered on the PCA chart for ward use.
Observations 7.13.2.1
Pain score, sedation score and respiratory rate need continuous measurement appropriate to the overall condition of the patient, but with a
minimum of q 2-4 hourly recordings.
Data on total demands, “good” demands, amount in syringe, and cumulative dose hourly should be able to be accessed by the bedside nurse.

Programmable Variables 7.13.3

Loading Dose 7.13.3.1
Patient controlled analgesia may not be effective for some time if moderate to severe pain is present from onset.
During the recovery period, to make the patient comfortable before PCA is commenced, a loading dose of opioid may be required.
Bolus Dose 7.13.3.2
The optimum bolus dose is that which results in appreciable analgesia without significant side effects. A dose of 1mg is the usual intial dose.
The dose may be increased or decreased by 0.5mg if effect is insufficient or excessive respectively.
Lock-out interval 7.13.3.3
This is the time from the end of delivery of one dose until the machine will respond to another demand. This allows the patient to feel the
effect of one dose before receiving a subsequent dose. Most patients have an inherent maximum frequency of demand-the average rate is 3-5
doses per hour.
Continuous (background) infusion 7.13.3.4
A continuous infusion decreases the inherent safety of PCA, as opioid will be delivered regardless of how sedated the patient may be.
Drug concentration 7.13.3.5
Standard prescriptions are employed (see PCA chart).
Total Dose Limit / 4 hourly Limit 7.13.3.6
The use of dose limits is not usual practice. The inherent safety mechanism of PCA lies in the belief that somnolence or even drowsiness
should supervene before overt narcosis. This may not be true where drug clearance is altered (morphine -6 – glucuronide in renal failure), but
the clinical significance is unclear.
Standard Prescriptions for PCA 7.13.4
Morphine 7.13.4.1
Usually the opioid of first choice.
Fentanyl 7.13.4.2
Indications: 7.13.4.2.1
The use of Fentanyl in PCA’s is generally reserved for:
Patients who are unable to tolerate Morphine
Patients with renal impairment, in whom accumulation of Morphine 6 glucuronide can lead to over sedation, although the rationale for this
is questionable
Tramadol 7.13.4.3
Indications 7.13.4.3.1
Elderly
Patients with respiratory depression or compromise
Excessive drowsiness with narcotic PCA
Miscellaneous Agents 7.13.4.4
Pethidine 7.13.4.4.1
Is not used in PCA’s in The Waikato Hospital Intensive Care Unit. This is because norpethidine toxicity is a very real possibility with the
doses which could be used in a PCA.
Methadone 7.13.4.5
Has an extremely long half life compared to other opioids (15 to 40 hours). This makes fast titration with methadone more difficult, and may
lead to significant accumulation of the drug.
Methadone is not used in PCA’s in The Waikato Hospital ICU for the above reasons.
Methadone is most commonly used for the management of chronic pain, or in suppressing withdrawal symptoms in individuals addicted to
opioids.
Special Situations 7.13.4.6
PCA and the opioid tolerant patient 7.13.4.6.1
These patients are likely to require much larger doses of opioids and a background infusion benefits many. To calculate an appropriate
background infusion, base it upon 50-100% of the patients usual opioid requirements.
The bolus dose which is ordered (in mg.) is normally the same as the background infusion in mg/hr.
Incomplete Cross Tolerance 7.13.4.6.2
The degree of cross tolerance that occurs between opioids is unpredictable, and appears to be incomplete. If a change is made from one
opioid to another, especially when doses have been high, it may be best to commence the new opioid at a dose that is about 50 % of the
calculated equianalgesic dose of the new opioid. The equianalgesic doses given above are based on single dose studies in opioid naïve
patients and should be used cautiously in patients on long term opioids.
In particular, if changing opioid therapy to oral methadone, doses that are about 10-15 % of the expected equianalgesic dose may be more
appropriate. This lower than expected dose may be due to the long and variable half life of methadone and also because methadone is
thought to have NMDA receptor antagonist properties.
Illicit Opioids 7.13.4.6.2
Where a patient has been using illicit opioids the amount and purity of the drug they have been using is difficult to ascertain. As a rough
guide, one should assume purity to be no more than 50%. It is safer to be conservative.
Problem Solving and PCA’s 7.13.4.7
Patient Confusion 7.13.4.7.1
Patient confusion and inability to understand the use of a PCA is an absolute contraindication and other means of analgesia should be used.
Inadequate Analgesia 7.13.4.7.2
Assess the patient.
Exclude technical issues, including pump programming and function, and reliability of vascular access.
If there is increasing pain, increasing analgesic requirements, or pain out of proportion to that expected for the procedure or for the number
of days elapsed since the procedure, then there may be another cause for the pain. A complication may have developed (eg. a leaking
anastomosis following bowel surgery, compartment syndrome), or the patient may have colicky “wind” pain which responds poorly to
opioids.
If these are excluded and the patient is receiving 3 bolus doses per hour on average, encourage the patient to use the demand button more
frequently. If side effects are limiting use of the PCA, treat these.
If the patient is receiving 3 bolus doses per hour, and still has inadequate analgesia, increase the size of the bolus dose (usually double).
Nausea and Vomiting 7.13.4.7.3
An appropriate antiemetic should be given.
If the patient has low analgesic requirements, then a decrease in the size of the bolus dose should be tried.
Non-opioid analgesia such as regular paracetamol and NSAID suppositories (if no contraindications such as lower GI surgery) should be
added.
Individual patients may be more sensitive to a particular opioid. If other measures have failed, then it is worth considering a change to a
different opioid. However, remember that opioids are not the sole cause of post-operative vomiting.
Pruritus 7.13.4.7.4
Pruritus may be caused through both histamine release and u-receptor activation. It is more commonly seen with Morphine that Fentanyl. In
the hospital setting, pruritus is most often caused by lying on a plastic covered mattress! (pruritus is present on the back only).
If the distribution of the pruritus is on the face and trunk, then it is likely to be due to the opioid.
Treatment options are:
 Change the opioid. Eg. Morphine to Fentanyl.
Titrate small (50-100 mcg) doses of Naloxone.
Antihistamines-but these may lead to sedation and respiratory depression.
Sedation and Respiratory Depression 7.13.4.7.5
These are unusual with a “pure” PCA-i.e. with no background infusion, with an appropriate size of bolus dose and no additional sedative
agents.
If a patient does have a sedation score of -1 (constantly or frequently drowsy-falls asleep during conversation but easy to rouse), then a
reduction in bolus dose (usually by half) and ceasing any background infusion is indicated.
If the patient has a respiratory rate of 8 or less, in addition to sedation score of -1, then titration of Naloxone in 100mcg doses should be
considered, in addition to the above.
If the patient has a sedation score of -2 or less (somnolent, difficult to rouse) then Naloxone should be administered regardless of the
respiratory rate.
Problems not infrequently arise in the opioid dependent patient, who becomes sedated, yet complains of high pain scores. It should be
explained to these patients that they cannot be safely given more opioid, and that complete pain relief may be an unrealistic aim for them.
Addition of non-opioid pain relief may be of value.
Urinary Retention 7.13.4.7.6
Urinary retention can occur, and should be treated with catheterisation. Be wary of the possibility of sedation / respiratory depression in the
patient who has been treating the pain of a distended bladder with their PCA, who then has the pain relieved by a catheter.
Inhibition of Bowel Motility 7.13.4.7.7
To some extent, inhibition of bowel function is inevitable. Patients should be discouraged from using their PCA to treat “wind” pains.
Hypotension 7.13.4.7.8
Opioids will not in themselves cause hypotension, but may unmask hypovolaemia (through a reduction in sympathetic tone).
Reference:
Dr Cliff Peady, Coordinator, Acute Pain Service, The Canberra Hospital. (Reviewed: Dr John Torrance April 2004)
Acknowledgement: These guidelines contain material heavily plagiarised from “Acute Pain Management-A practical guide” Macintyre and
Ready, 2nd Edition 2001. And also “Guidelines for Anaesthetists”, Acute Pain Service, Royal Adelaide Hospital (revised February 1998)

Guidelines for Performance of Sensory Evoked Potentials 7.14

Introduction 7.14.1
Short and long latency sensory evoked potentials (SEPs) have shown utility for prognostication in severe diseases of the central nervous
system. In particular, SEP’s are a very useful adjunct to clinical assessment in patients with hypoxic-ischaemic encephalopathy and traumatic
brain injury.
Patient Preparation 7.14.2
test is preferably performed with a core temperature of > 36 degrees centigrade.
patients not ventilated with controlled modes will require a controlled mode, minimal sedation as below and paralysis (generally 0.1
mg/kg vecuronium will produce up to 30 minutes paralysis, with additional smaller doses sometimes required to complete recording)
to reduce artefact during recording.
heavy sedation should not be used. Long latency potentials are affected by sedatives at high dose. However, a dose of 10ml/hour maximum
of propofol would not be expected to significantly delay or abolish even long-latency potentials. Remember that this is a test used
almost exclusively when the patient is in coma and one that is performed in outpatients with minimal discomfort.

Recording 7.14.3
request is made to the Technicians specifying whether N20’s alone or N20’s and N70’s are to be performed. This is at the discretion of the
Intensivist.
N20’s are recorded using an 8 mV stimulus of the Median nerve delivered at 5Hz for 100 seconds resulting in waveforms averaged from
500 sweeps of 50 ms duration.
N70’s require a 250 ms sweep duration and a 3 Hz stimulus rate to accommodate the recording of the longer latency potentials. 300
sweeps are averaged to derive the waveforms.
Precautions 7.14.4
an assurance of spinal column stability prior to the procedure is preferred, but not essential
in post craniectomy patients, the technique may still be performed in the usual way. Ensuring the electrodes are sub dermal only is more
important here. Keeping as far away from an actual wound as possible is prudent (personal Communication, James Judson, DCC,
Auckland City Hospital, Linda Hill, Charge Neurophysiology Technician, Auckland City Hospital).

Interpretation 7.14.5
clinical correlation is vital. Individual intensivists may appropriately interpret recordings they have requested. There is an expectation
within this particular ICU for Intensivists to acquire or maintain some expertise in clinical correlation and interpretation of SEPs.
the threshold for reporting absence of a potential is difficult. Some authorities quote minimal amplitude that needs to be achieved before
regarding a potential as present. Other authorities simply report a potential as present if they believe it to be discernible. It is important
to note that some potentials occur earlier than 13ms after stimulation, and their presence should not be confused with presence of an
N20.
if the Intensivist is not comfortable with interpretation, they may ask for a Neurologist interpretation, either directly by ringing the person
concerned then faxing the result, or asking the technician to do so. Either way, this person must be contacted directly to be able to
report the test.

Reference:
Practice Parameter: Prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence based review): Report of the Quality Standards
Subcomittee of the American Academy of Neurology. Wijdicks EFM et al.Neurology 2006; 67; 203-10.
MRI – Practical aspects of MRI transport 7.15
Introduction 7.15.1
Referral and transport of a patient to the MRI scanner should be initiated by the duty ICU specialist, who will also take responsibility for the
transport unless able to delegate to a suitably qualified registrar. A number of factors make the MRI a technically demanding area to work in:
The MRI scanner is remote from the ICU.
Indications for MRI scanning usually involve pathology of the spinal cord, or areas of the brain not well visualised on CT scan.
There are specific restrictions on practice by virtue of the MRI technology.
Safety 7.15.1.1
There are three main mechanisms, in addition to the standard risks of patient transport, by which patient and staff may be injured
The effects of magnetism: The magnetic strength of an MRI is measured in Tesla, with an average machine developing 1.5 -2.0 T. This is
similar that required in a scrapyard to lift a car of the ground. The more ferrous an object, the more likely it is to be affected by the
magnetic coil. All metallic objects should be removed if possible. Those that cannot be must be discussed with the MRI staff. Of note,
metallic heart valves are non-ferrous, and are said to experience less shear stress than that exerted by heart contractility.
Magnetic flux: A changing magnetic field strength induces electrical current in conductors with consequences such as heating in a
prosthesis. Rapidly changing fields may even cause nerve depolaristaion.
Radio-frequency: Generally in the region of 15-20 kW. This may cause heating or electrical conduction where a coil exists. For this reason
cables etc should not be coiled or kinked if excessively long.
Relevance for ICU 7.15.1.2
MRI transport is a team event, requiring a competent nurse, an ICU technician, and an experienced medical escort.
Basic ICU equipment must be removed from the room, with consequences for ventilation (dead space in tubing), infusions (long lag time for
any change to take effect), and monitoring (damping of trace)
Some ICU indwelling equipment such Codman ICP monitors and PiCCO catheters are considered unsafe in the MRI and may have to be
replaced or removed.

Procedure 7.15.2.1
Complete patient consent issues and MRI risk screening document.
In ICU 7.15.2.1.1
Liaise with nursing and technical staff so that adequate preparation time is available and an appropriate ventilator is available in MRI.
Careful planning is mandatory to ensure adequate sedation, vasopressor or other substance is available, as these may not be able to be
sourced in the MRI scanner rooms. In addition to a standard transport, note the following:
⋅ Non-vital infusions are disconnected and capped.
⋅ Vital infusions (vasopressors and sedation) will require the addition of 3 ×2 m rigid extension sets, which are coiled with micropore
(may require preparation of new syringes and pumps).
⋅ Add 3 extra rigid lines to the arterial line. The resulting trace will be damped, but with a reasonably active mean pressure.
⋅ Take two further 3 way taps for attachment to the infusion lines outside of the MRI room (for boluses) and 4 extra luer plugs for
keeping the extension lines sterile during their passage through the scanner wall
In the MRI ante-room 7.152.1.2
⋅ Transfer onto the MRI gurney.
⋅ Remove and exchange ICU non-invasive BP cuff for MRI equivalent.
⋅ Remove ECG dots.
In the MRI 7.15.2.1.3
⋅ Attach the MRI oximeter, NIBP and capnograph.
⋅ In an aseptic manner, disconnect arterial line extensions using luer plugs, prior to patient movement into scanner gantry.
⋅ Where vasopressors are in use, the pump should be left infusing (i.e not turned off), the line disconnected using a luer plug and passed
through the wall for immediate re-attachment.
⋅ Use a paper tape measure to establish height of phlebostatic axis prior to movement of patient into scanner gantry.
⋅ Move patient into scanner gantry, check there is no fouling of lines or equipment through the range of movement required.
⋅ Pass through any further lines required for use outside the scanning room itself.
⋅ Pass through the arterial line extension set for re-attachment to transducer and monitor outside the room. Use height measurement as
above to “level” transducer.
When departing from the scanner perform above in approximately reverse order.
Index
Acid - Base.......................................................................................... Cardiothoracic....................................................................................
characterisation..........................................................................52 guidelines....................................................................................74
compensation for........................................................................53 hypertension following surgery.................................................75
Activated charcoal.........................................................................79 hypotension following surgery..................................................75
Acute hypertension............................................................................. Management of bleeding...........................................................75
treatment.....................................................................................32 patient admission.......................................................................74
Adenosine.......................................................................................34 respiratory care...........................................................................74
dosage.........................................................................................34 caridac pre-load..................................................................................
Admission to ICU............................................................................... PiCCO estimation of,.................................................................98
criteria for.....................................................................................7 Catecholamines..............................................................................30
Adrenaline......................................................................................31 Central Venous Cannulae...................................................................
and bradycardia..........................................................................34 insertion......................................................................................18
Aminophylline.................................................................................... request for insertion...................................................................10
and bradyarrhythmia..................................................................34 Cerebral perfusion pressure...........................................................71
Amiodarone........................................................................................ Chlorpro-mazine............................................................................38
AF and.........................................................................................35 Clonidine.............................................................................................
dose.............................................................................................36 anti-hypertensive........................................................................33
VT / VF.......................................................................................35 Clostridium difficile.......................................................................47
Amlodipine.....................................................................................33 Cockroft and Gault equation.........................................................68
Analgesia........................................................................................37 Consent...........................................................................................15
Anion Gap.......................................................................................53 Cricothyroidotomy.........................................................................25
anti-arrhythmic drugs......................................................................... Croup.............................................................................................. .87
Vaughn-Williams classification..............................................102 Cryoprecipitate...............................................................................58
Antibiotic............................................................................................ Cyclizine.........................................................................................44
empiric, biliary sepsis................................................................46 Danaparoid Sodium........................................................................40
empiric, burns.............................................................................47 DDAVP................................................................................................
empiric, endocarditis.................................................................47 diabetes insipidus.......................................................................41
empiric, line sepsis.....................................................................46 platelet dysfunction....................................................................42
empiric, soft tissue infection.....................................................47 Death...................................................................................................
empiric, UTI...............................................................................46 notification...................................................................................8
empirical, intra-abdominal sepsis.............................................46 Dexmedetomidine..........................................................................38
empirical, pancreatitis...............................................................46 dialysis............................................................................................68
empirical, pneumonia................................................................46 Diazepam........................................................................................38
prophylaxis, abdominal surgery................................................45 DIC..................................................................................................58
prophylaxis, orthopaedics..........................................................45 Digoxin...............................................................................................
prophylaxis, vascular surgery....................................................45 dosage.........................................................................................36
Antibiotics.......................................................................................... Disaster plan...................................................................................16
principles of prescription...........................................................45 Discharge..........................................................................................8
prophylaxis with.........................................................................45 Diuretics..........................................................................................43
Anticoagulation..............................................................................38 Dobutamine....................................................................................31
Arrhythmia.......................................................................................... Dopamine........................................................................................31
treatment of................................................................................33 Drug / Toxin Overdose...................................................................78
Arterial Cannulae...........................................................................17 Drug overdose....................................................................................
Aspergillosis...................................................................................47 management of...........................................................................79
Asthma................................................................................................ Drugs...................................................................................................
treatment.....................................................................................36 prescription.................................................................................30
Atenolol..........................................................................................33 DVT prophylaxis............................................................................39
Atracurium......................................................................................38 Dysbaric illness..............................................................................12
Atropine..........................................................................................34 E. Coli.............................................................................................47
Aveolar Gas Equation..................................................................104 ECMO.............................................................................................67
Beta 2 stimulants................................................................................ Enalapril..........................................................................................33
and hyperkalaemia.....................................................................51 Endotracheal intubation.....................................................................
Bicarbonate......................................................................................... difficult intubation kit................................................................23
and hyperkalaemia.....................................................................51 drugs for......................................................................................23
Blood transfusion...........................................................................56 guideline.....................................................................................22
transfusion algorythm................................................................56 Endotracheal Intubation.................................................................22
Blood transfusion reaction.............................................................58 Endotracheal tube...............................................................................
Bradyarrhythmias...........................................................................34 exchange of.................................................................................24
Brain death......................................................................................81 enteral formulas..................................................................................
brainstem testing........................................................................81 content of..................................................................................105
non-clinical confirmation of......................................................82 Enteral Nutrition............................................................................54
Bronchiolitis...................................................................................85 feeding algorithm.......................................................................54
Bronchoscopy.................................................................................25 prokinetic use.............................................................................55
Budesonide.....................................................................................37 Enterobacter....................................................................................47
Calcium Chloride............................................................................... Enterococcus..................................................................................47
in hyperkalaemia........................................................................51 Erythromycin......................................................................................
Candidiasis.....................................................................................47 pro-kinetic GI.............................................................................44
Captopril.........................................................................................33 Esmolol...........................................................................................33
Cardiac arrest...................................................................................... Extra-corporeal oxygenation.........................................................67
arrest call....................................................................................10 extubation.......................................................................................65
Cardiac Arrest..................................................................................... Extubation...........................................................................................
therapeutic hypothermia............................................................61 guideline.....................................................................................25
Cardiac Index...................................................................................... Factor VIIa.........................................................................................
calculation................................................................................104 conditions for use.......................................................................40
cardiac pre-load..............................................................................95 Factor VIIa......................................................................................40
Cardio-Pulmonary Resuscitation..................................................60 dose.............................................................................................40
Fentanyl..........................................................................................38 principles of..............................................................................100
Flecainide.......................................................................................35 tidal volume..............................................................................101
Fresh Frozen Plasma......................................................................58 when to,.......................................................................................62
Frusemide.......................................................................................43 Mechanical Ventilation..................................................................63
Fungal infections............................................................................78 medico-legal advice.......................................................................16
Gastric lavage.................................................................................79 Meningitis.......................................................................................89
Gastric ulceration............................................................................... Meningococcus...............................................................................47
prophylaxis.................................................................................43 Metabolic Acidosis.........................................................................53
Gibbs-Donnan.................................................................................49 Metabolic Alkalosis.......................................................................53
GTN................................................................................................33 Methyldopa.....................................................................................33
Haemophilus influenzae................................................................47 Metoclopramide.............................................................................44
Haloperidol.....................................................................................38 Metoprolol......................................................................................33
Hartmanns........................................................................................... Microbiology......................................................................................
composition................................................................................48 guideline in ICU.........................................................................76
Hemohes............................................................................................. Midazolam......................................................................................38
composition................................................................................48 milrinone.........................................................................................31
Henderson / Hasselbach Equation.................................................52 Morphine.........................................................................................38
Heparin............................................................................................. ... MRI transport...............................................................................108
IABP, use with............................................................................20 Muscle relaxant..............................................................................38
indications..................................................................................39 Nasojejunal tube.................................................................................
systemic anticoagulation, dosage..............................................39 insertion......................................................................................27
Heparin Induced Thrombocytopaenia...........................................40 ndotracheal tube.................................................................................
Hydralazine....................................................................................33 cuff leakage................................................................................24
Hydrocortisone................................................................................... Neurotrauma...................................................................................70
asthma, use in.............................................................................37 Cerebral perfusion pressure algorithm.....................................71
Hyperbaric oxygen therapy...........................................................67 sedation for.................................................................................71
Hyperglycaemia.............................................................................41 Non-invasive ventilation................................................................66
Hyperkalaemia...............................................................................51 Noradrenaline.................................................................................31
Hypernatraemia..............................................................................50 Novasource 2................................................................................105
water deficit calculation............................................................50 Novosource renal.........................................................................105
Hypertonic saline...........................................................................71 Nutrison multifibre......................................................................105
Hypokalaemia.................................................................................51 Obstetric Patients...........................................................................12
Hyponatraemia...............................................................................49 Octreotide.......................................................................................44
management of fitting or coma.................................................50 Omeprazole....................................................................................44
Hypophosphataemia.......................................................................51 Ondansetron....................................................................................44
hypotension......................................................................................... organ donation................................................................................81
definition....................................................................................30 Orientation........................................................................................7
ICP.................................................................................................
..70 Oxygen Delivery Systems.............................................................63
ICP monitor......................................................................................... Pacing.............................................................................................. ....
insertion......................................................................................28 cardiac.........................................................................................19
Inotropes.........................................................................................30 Paediatric admission policy...........................................................83
Inotropic Support...........................................................................96 Parenteral Nutrition........................................................................55
Inra-aortic balloon counterpulsation................................................. formula choice............................................................................56
removal of catheter....................................................................21 patient controlled anaesthesia.....................................................105
Insulin................................................................................................. PCA.....................................................................................................
administration with non-dextrose IVI fluids............................41 dose variables...........................................................................105
and hyperkalaemia.....................................................................51 morphine...................................................................................106
Intercostal Catheter........................................................................21 problem solving.......................................................................106
Intra-abdominal pressure manometry...........................................27 standard script..........................................................................106
Intra-aortic balloon counterpulsation............................................20 tramadol....................................................................................106
Intubation............................................................................................ Pericardiocentesis..........................................................................22
Awake.........................................................................................23 pH....................................................................................................52
difficult.......................................................................................23 Phenobarbitone...............................................................................72
Failed, ASA guideline................................................................23 Phenytoin........................................................................................72
Ipratroprium....................................................................................36 Phenytoin............................................................................................
Isoprenaline....................................................................................34 treatment of VT..........................................................................35
Jugular Bulb Oximeter....................................................................... PiCCO.................................................................................................
Insertion......................................................................................28 cardiac output.............................................................................97
Jugular venous saturation..............................................................70 EVLW.........................................................................................98
Klebsiella........................................................................................47 ITBV...........................................................................................98
Labetalol.........................................................................................33 preload........................................................................................48
Legionella.......................................................................................47 reference ranges.........................................................................98
Levosimendan................................................................................31 siting...........................................................................................17
Lignocaine.......................................................................................... PiCCO-catheter..............................................................................97
treatment of arrhythmia.............................................................35 Platelet transfusion.........................................................................57
Magnesium.....................................................................................35 dosing of.....................................................................................57
anti-hypertensive........................................................................33 Pleurocentesis.................................................................................21
dose in VT...................................................................................36 Pneumococcus................................................................................47
Management of a child with DKA 7.8.......................92 Pneumocystis Carinii.....................................................................47
Mannitol...................................................................................43, 71 Pneumonia..........................................................................................
mechanical ventilation....................................................................... investigation of...........................................................................77
objectives of.............................................................................101 ventilaor associated....................................................................77
Mechanical ventilation....................................................................... Prescribing in Pregnancy...............................................................30
applied PEEP..............................................................................64 Pressure support...........................................................................100
default ventilator setting............................................................64 Pro-kinetic GI agents.....................................................................44
I Propofol..........................................................................................38
E ratio...................................................................................101 Pseudomonas aeruginosa...............................................................47
peak airway pressure................................................................101 Pulmocare.....................................................................................105
PEEP.........................................................................................101 Pulmonary Artery Catheter............................................................96
Pulmonary artery catheterisation...................................................... Vasopressor agents.........................................................................31
insertion......................................................................................19 Vecuronium.........................................................................................
Pulmonary Artery Catheterisation..................................................... dose.............................................................................................38
Pressure trace.............................................................................96 Ventilation......................................................................................63
Pulmonary Capillary Wedge Pressure...........................................96 Ventricular Arrhythmias................................................................35
Ranitidine.......................................................................................44 Verapamil............................................................................................
Rapid response turnout..................................................................12 and arrhythmia...........................................................................34
Rapid sequence induction..............................................................23 dosage.........................................................................................36
Renal Failure..................................................................................67 Withdrawal of Treatment...............................................................80
assessment of..............................................................................68
protective strategies...................................................................68
Renal Replacement therapy...............................................................
indications for............................................................................68
Renal Replacement Therapy..........................................................68
anticoagulation and,...................................................................69
default dialysis settings............................................................69
Potassium and,...........................................................................69
Research..........................................................................................14
Resonium........................................................................................51
Respiratory Acidosis......................................................................54
Respiratory Alkalosis.....................................................................54
Respiratory Failure........................................................................62
Rocuronium....................................................................................23
dose.............................................................................................38
Salbutamol......................................................................................36
IV infusion..................................................................................37
Sedation..........................................................................................37
approach to,................................................................................37
daily cessation............................................................................37
Sedation - Agitation Score...........................................................102
Seizures in Children.......................................................................88
Sensory Evoked Potentials..........................................................107
Sepsis..................................................................................................
sepsis screen...............................................................................76
vascular catheter.........................................................................77
Septis.............................................................................................
......
septic shock................................................................................76
SIADH............................................................................................50
Siezure................................................................................................
clonazepam, treatment with......................................................72
diazepam, treatment with..........................................................72
midazolam, treatment with........................................................72
SIMV.............................................................................................100
SIRS................................................................................................76
Sodium Nitroprusside....................................................................33
Sotalol.............................................................................................35
Spinal Injuries................................................................................94
Spironolactone................................................................................43
Spontaneous breathing trial...........................................................65
Staphylococcus aureus...................................................................47
Starling Curve................................................................................95
Status Epilepticus...........................................................................72
refractory, drug treatment of.....................................................73
Steroid.................................................................................................
and septic shock.........................................................................32
relative potencies.......................................................................42
use in ICU...................................................................................42
Streptococcus,Group A..................................................................47
Subarachnoid haemorrhage...........................................................73
classification of..........................................................................73
Supraventricular Arrhythmias.......................................................34
Suxamethonium..............................................................................23
dose.............................................................................................38
Suxemethonium..................................................................................
contraindications........................................................................23
Systemic inflammatory response syndrome.................................76
Systemic Vascular Resistance............................................................
calculation................................................................................104
Theophylline...................................................................................37
Tracheostomy.....................................................................................
discharge safety..........................................................................26
percutaneous...............................................................................26
Transport.............................................................................................
in hospital...................................................................................11
Trauma Call....................................................................................10
Underwater Sealed Drain...............................................................21
Vascular Catheter Sepsis....................................................................
antibiotic locking.......................................................................78
Vasopressin.....................................................................................32