Intern Survival Guide 2014-2015

Internal Medicine
Intern Guide
2014-2015
University of Colorado Guide to Internal Medicine
Editors
Mim Ari, M.D.
Joseph Burke, M.D.
T. Ray Foley, M.D.
Ryan G. Webb, M.D.
David Williams, M.D.
Contributors
Eva Aagaard, M.D.
Rebecca L. Adochio, M.D.
Rebecca Allyn, M.D.
Amrut Ambardekar, M.D.
Virginia Borges, M.D.
Sarah Bull, M.D.
Jessica Campbell, M.D.
Warren Capell, M.D.
Mark J. Fesler, M.D.
Rachel Groff, M.D.
Kristin Harmon, M.D.
Kennon Heard, M.D.
Justin Hopkin, M.D.
Lynsee Hudson, M.D.
Timothy Jenkins, M.D.
Jessica Kendrick, M.D.
Andrew J.P. Klein, M.D.
Andrea Krumholz, M.D.
Elaine T. Lam, M.D.
Christopher Lieu, M.D.
Mike Loughner, M.D.
Daniel D. Matlock, M.D.
Timothy Oster, M.D.
Edward Stenehjem, M.D.
Rachel Swigris, M.D.
Cecilia Wang, M.D.
Faculty Editor
Suzanne Brandenburg, M.D.
Funding for this publication was paid for by the University of Colorado Department of Internal Medicine.
Based on a 2007 Gray/Connors Publication
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Disclaimer
This handbook is meant to serve as a guide to the practice of internal medicine. All
information contained within is believed to be reliable and accurate but is by no means
exhaustive on any one topic. The guidelines found within are only recommendations as to
the practice of medicine. The editors of this book do not provide any guarantee of their
accuracy or completeness.
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TABLE OF CONTENTS
Message from the Chiefs ....................................................................................................... 8
The Eightfold Path through Internship .................................................................................. 9
Mentorship Program .............................................................................................................. 10
Wellness Program .................................................................................................................. 12
Hospital Breakdown
University/AIP ........................................................................................................... 15
Denver Health ............................................................................................................ 16
VA.............................................................................................................................. 17
PSL ............................................................................................................................ 18
Rose ........................................................................................................................... 19
Basic Intern Stuff
Conducting Yourself on the Wards ........................................................................... 21
General Order Writing ........................................................................................................... 21
Admit Orders ............................................................................................................. 22
Sign-out...................................................................................................................... 23
Pagers......................................................................................................................... 24
How to Page ................................................................................................... 24
Changing the Message on Your Pager........................................................... 24
Ideal Admission Note ................................................................................................ 25
Ideal Progress Note .................................................................................................... 26
Procedure Notes ......................................................................................................... 27
Death Note ................................................................................................................. 27
The Bane of Residency Discharge Summaries ................................................................... 28
The Experienced Approach to: Common Night Float/Cross Cover Issues ........................... 29
Tachycardia.................................................................................................... 29
Bradycardia .................................................................................................... 29
Hypotension ................................................................................................... 30
Hypertension .................................................................................................. 30
Fever .............................................................................................................. 31
Low Urine Output .......................................................................................... 33
Hypoxia.......................................................................................................... 33
Electrolyte Replacement ................................................................................ 34
Heparin Drip Adjustment .............................................................................. 35
Nausea/Vomiting ........................................................................................... 35
Chest Pain ...................................................................................................... 36
Falls................................................................................................................ 36
Insomnia ........................................................................................................ 37
Altered Mental Status .................................................................................... 37
Dyspnea ......................................................................................................... 38
Combative Patient.......................................................................................... 38
Deceased Patient ............................................................................................ 39
The Experienced Approach to: Procedures .......................................................................... 40
Central Lines .................................................................................................. 40
Thoracentesis ................................................................................................. 41
Paracentesis.................................................................................................... 42
Lumbar Puncture ........................................................................................... 43
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The Experienced Approach to: Common Subspecialty Issues ............................................. 45

Cardiology ................................................................................................................. 45
Chest Pain ...................................................................................................... 45
Acute Coronary Syndrome ............................................................................ 47
Atrial Fibrillation ........................................................................................... 47
Stress Testing ................................................................................................. 48
Cardiac Catheterization ................................................................................. 49
CHF................................................................................................................ 50
Heart Transplant Basics ................................................................................. 51
Advanced ECG Reading ................................................................................ 52
Post Cardiac Arrest Hypothermia .................................................................. 57
Endocrinology............................................................................................................ 58
DKA............................................................................................................... 58
Hyperglycemic hyperosmolar state ............................................................... 59
Hypoglycemia ................................................................................................ 60
Hyperglycemia ............................................................................................... 60
Thyroid Storm ................................................................................................ 62
Myxedema Coma ........................................................................................... 63
Euthyroid Sick Syndrome .............................................................................. 64
Adrenal Insufficiency .................................................................................... 65
Pituitary Apoplexy ......................................................................................... 66
Hypertriglyceridemia ..................................................................................... 66
Hypercalcemia ............................................................................................... 67
Hypocalcemia ................................................................................................ 68
Hypernatremia/Diabetes Insipidus................................................................. 68
Hyponatremia/SIADH ................................................................................... 69
Appendix A - DKA Protocol ......................................................................... 69
Appendix B - HHS Protocol .......................................................................... 70
Appendix C - Scoring System for Thyroid Storm ......................................... 71
Gastroenterology........................................................................................................ 72
GI Bleed ......................................................................................................... 72
Evaluation of Ascites ..................................................................................... 73
Spontaneous Bacterial Peritonitis .................................................................. 73
Geriatrics.................................................................................................................... 74
Medications.................................................................................................... 74
Sundowning/Agitation ................................................................................... 74
Medicare ........................................................................................................ 74
Nursing Homes .............................................................................................. 74
Heme/Onc .................................................................................................................. 75
Anemia........................................................................................................... 75
Pancytopenia .................................................................................................. 77
Thrombocytopenia ......................................................................................... 77
Fever and Neutropenia ................................................................................... 78
Tumor Lysis Syndrome ................................................................................. 82
Spinal Cord Compression .............................................................................. 82
Brain Metastasis............................................................................................. 84
Hypercalcemia ............................................................................................... 84
SIADH ........................................................................................................... 86
Superior Vena Cava Syndrome ..................................................................... 86
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Blood Products............................................................................................... 87
Transfusion Reactions ................................................................................... 90
Hospitalist Medicine .................................................................................................. 92
Surgical Clearance ..................................................................................... 92
Peri-op Cardiac Risk Assessment/Beta Blockers .......................................... 92
Peri-op Pulmonary Risk Assessment ............................................................. 92
Peri-op Diabetes Management ....................................................................... 92
Peri-op Steroid Management ......................................................................... 93
Infectious Diseases .................................................................................................... 94
S. aureus Bacteremia ..................................................................................... 94
Endocarditis ................................................................................................... 99
Osteomyelitis ................................................................................................. 100
HIV/AIDS ...................................................................................................... 102
Tuberculosis ................................................................................................... 105
Nephrology ................................................................................................................ 106
Acid/Base Disturbances ................................................................................. 106
Hyponatremia ................................................................................................ 107
Hypernatremia ............................................................................................... 109
Hypokalemia .................................................................................................. 110
Hyperkalemia ................................................................................................. 110
Hypomagnesemia .......................................................................................... 111
Hypophosphatemia ........................................................................................ 111
Acute Renal Failure/Acute Kidney Injury ..................................................... 111
Renal Replacement Therapy .......................................................................... 113
Neurology .................................................................................................................. 115
New-Onset Seizure ........................................................................................ 115
Headache Emergencies .................................................................................. 117
CNS Infections............................................................................................... 119
Anoxic Brain Injury ....................................................................................... 122
Acute Spinal Cord Injury/Compression......................................................... 123
Status Epilepticus........................................................................................... 124
Pulmonary/Critical Care ............................................................................................ 126
Basics of CXR Reading ................................................................................. 126
Hypoxia .127
Hypercarbia ...127
Pleural Effusions ............................................................................................ 128
COPD Exacerbations ..................................................................................... 129
Sepsis ............................................................................................................. 129
Important Drips ............................................................................................. 131
Rheumatology ............................................................................................................ 133
Arthrocentesis/Synovial Fluid Analysis ........................................................ 133
Toxicology ................................................................................................................. 134
General Consult Information ......................................................................... 134
Aspirin Overdose ........................................................................................... 134
Tylenol Overdose........................................................................................... 134
Lithium Overdose .......................................................................................... 135
TCA Overdose ............................................................................................... 136
Withdrawal Syndromes ............................................................................................. 137
Alcohol Withdrawal....................................................................................... 137
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How to think about Differential Diagnoses ........................................................................... 138

The Patient-Centered Approach ............................................................................................ 140
Info for the Program
Chiefs Pagers ............................................................................................................ 141
Housestaff Office Information ................................................................................... 141
Library information (pocket guide)142
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A Message From The Chiefs

We think that Colorado is an amazing place to train in medicine, full of a varied array
of both medical and non-medical gems. To find them you have to be fully invested in life, both
in and out of the hospital. We hope your time here is filled with as much personal and
professional satisfaction as ours has been. As your Chief Medical Residents, it is our job to
assure this promise is fulfilled. We are committed to helping you in any way we can.
This guidebook has been published annually since 2007 and given to each incoming
class of interns. When the guide was described to a non-medical friend of ours he said, Oh,
you mean like CliffsNotes for doctors? Exactly. Its meant to serve as a quick reference
during the night and to help give you a push in the right direction toward the correct
management of many of the common diagnoses and issues with which you will be confronted
this year. That said, it should function as a jumping off point: something to get you started
while you dig deeper into the problem.
Keep this reference guide in your pocket and know that you are never more than a page
flip away from all those who came before you. Know that, along with your resident, you are
following the path of countless doctors who were in your same situation not long before. Feel
secure in the understanding that every unusual night float call or patient you see has been dealt
with before that there are answers out there and that you will find them.
You are starting out on something that will change the way you think. It is an
experience that cannot be replicated or repeated so take advantage of this opportunity while it
is available to you. Call upon those above you. Be judicious, confident and decisive, but never
cavalier.
The mastery of medicine takes two things: knowledge and experience. The first will
come from the time you are willing to put in to mastering your craft. We want this book to be
one of many sources to help you toward your first goal. The second is just that: experience. It
will come over time and cannot be rushed, so dont worry about trying to speed up the process.
Its a life-long learning process, and we promise, its happening for you already. You will look
back on these years as some of the most difficult and rewarding of your career. We hope that
you come away from the process of internship a stronger, more confident person, but realize
that you may not necessarily start out that way. Any help that we as the chiefs can provide is
yours. Anytime, day or nightjust ask.
The Chief Medical Residents
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The Eightfold Path Through Internship

1. Play Nice. Keep your head. There will be many situations where you may feel the urge to
blow up or be less than cordial to your colleagues. Dont. Youre the doctor now, the leader of
the team. People will look to you for calm and confidence during the stressful timeslead by
example.
2. Rely on those above you. Youre never alone in the hospital, your clinic, or on any other
rotation. Call your resident with any and all questions you are unsure of the answer to and the
chiefs with any problems that come upthats what theyre there for. Remember the old
adage: its better to wake your resident at 2 AM with a question than at 4 AM to intubate
someone.
3. Pay yourself first. Its an old maxim from the economic world and very relevant to the
busy lifestyle you have chosen. Get up 15 minutes early and have breakfast; its worth hours of
fatigue later in the day. If you exercise (and you should), do so the second you get home before
the urge to nap sets in. Do something enjoyable on your days off (after sleeping in a little, of
course).
4. Have fun. Internship is difficult, but fun, especially here in Colorado. When youre on,
youre on, but on your days off, be off. If you dont know what to do, call a colleague or
friendyoure all in the same boat and will find plenty of fun ways to spend your free time in
this state of ours.
5. Make time to go to conferences and morning reports. Time wont just fall into your lap
during your intern year; you will have to carve it out. Most of your payment over these three
years comes in the form of educational conferences and lectures from senior faculty. Tap this
resource till its dry. With the exception of an emergency situation demanding immediate
patient care, conference should take priority over all other activities, including rounding.
6. Communicate. Effective communication solves just about every misunderstanding in the
hospital; conversely, ineffective talk between colleagues and staff will cause plenty of turmoil.
When you are having trouble seeing eye to eye with someone, start over by asking what that
person is saying, what it is specifically that they want from you and how you can help them
solve their (and your) problem. Along these same lines, be honest in all your dealings. If you
havent done something, own up to it. Lying undermines all communications and puts future
dealings between you and others in question. Every resident and attending above you has made
mistakes; admitting them in a timely manner will serve you and your patients better than an
attempt at concealment.
7. Learn from your patients. In the morning, on rounds and every second you can make to
have contact with them. This also includes reading after work on the conditions you have seen
that day, especially those you may have initially misdiagnosed or were unsure about. Patients
have more to teach you (if you listen) than any lecture series or book.
8. Keep a sense of self. Internship can be a tough time and it is easy to let the work define
you. While we are all here for the primary purpose of becoming great doctors, you were all
selected because you were already great people. Dont let the diversity you demonstrated to get
here fall by the wayside. Keep something from your prior life (working out, reading, playing
basketball on Saturday, your pre-residency friendships) and always find time for it, even on the
busy months. You got here because of who you are and, while internship is certainly
transforming in a lot of ways, no job should change your fundamental beliefs or inner self. If
you find this happening, come talk to one of the chiefs.
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Resident Mentoring Program

Residents in the Department of Medicine participate in a mentoring program with four distinct
components. The components and the key mentors for each are described below.
1.
Bi-annual career advising and performance review: residents are required to meet with
an assigned core residency faculty member a minimum of twice each year (and interns will be
scheduled for an additional meeting during the first 2 months of training). The purpose of these
meetings is threefold:
To review and provide specific feedback on the residents performance and overall
well-being to date with a focus on educational and professional goal setting for the short
and long-term.
To monitori progress towards meeting ABIM requirements to be board-eligible
To inquire about their personal well-being
To discuss future career aspirations and discuss opportunities within and outside the
program to assist the resident in meeting or further investigating career interests
To obtain feedback and suggestions from residents on rotations and other aspects of
the overall program in order to best meet resident needs over time.
All residents are initially assigned to either the program director or an associate program
director. However, they may be referred to others either within or outside of this group for
specific career and/ or personal mentoring and advising. All of these faculty members have
open door policies and encourage meeting regularly with housestaff regarding any issues of
concern. The core faculty advisors are:
Name
Suzanne Brandenburg
Title
Program Director
Karen Chacko
Didi Mancini
Associate Program Director;

Director of Primary Care
Program
Associate Program Director
Mel Anderson
Jeff Glasheen
Director, Hospitalist Program
Darlene Tad-y

Hospitalist Training Program
Katie Heist
Assistant Program Director
Jennifer Adams
Assistant Program Director

Primary Care Program
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Contact Information
Suzanne.Brandenburg@ucdenver.edu
303-266-7203 pager
303-724-1787 office
Karen.Chacko@ucdenver.edu
303-266-3299 pager
303-724-2257 office
Diana.Mancini@dhha.org
303-201-2607 pager
Melver.Anderson@va.gov
303-360-7644 pager
303-393-2840 office
Jeffrey.Glasheen@ucdenver.edu
303-266-4263 pager
Darlene.Tad-y@ucdenver.edu
303-266-2509
720-848-4289 office
Kathleen.Heist@ucdenver.edu
303-266-0100 pager
303-724-2250 office
Jennifer.adams@dhha.org
303-206-9784 pager
303-436-4200 office
2.
Confidential Advising: This voluntary advising system provides residents with an
opportunity to speak to a faculty member regarding any number of issues important to career
development, work stresses, health, family and/or personal issues they prefer not to discuss
with the program administration. They have no significant role in resident promotion,
fellowship selection or hiring and all conversations with them are completely
CONFIDENTIAL and SAFE.
Name
Rachel
Swigris
Adam
Trosterman
Rita Lee
Jeremy
Long
Sopheap
Na
Melanie
Stickrath
Mentoring Areas of Interest/ Focus

Physician wellness and resilience;
work-life balance; Womens Health,
weight management, preventative
medicine
Resident and medical student education;
curriculum development; resource
utilization
Provider well-being; advocacy; health
disparities; substance abuse; gay,
lesbian, bisexual, transgender, intersex
healthcare
Provider wellness, life balance, resident
education, quality improvement, health
policy and community involvement in
healthcare
Provider wellness, life balance, and
resident education
Work-family balance, career
development and wellness
Contact Information
Rachel.Swigris@ucdenver.edu
303-266-1764 pager
720-848-9500 office
Adam.Trosterman@ucdenver.edu
303-266-0586 pager
720-848-4289 office
Rita.Lee@ucdenver.edu
303-266-6267 pager
720-848-2340 office
Jeremy.Long@dhha.org
303-892-0132 pager
303-436-8767 office
Sopheap.Na@va.gov
303-332-8715 pager
303-399-8020 x3236 office
Melanie.Stickrath@ucdenver.edu
303-560-7644 pager
303-399-8020 x2321 office
3.
Project or Research-Focused Mentoring: All faculty within the Department of Medicine
have a demonstrated interest in and commitment to mentoring the housestaff. One clear
purpose of the bi-annual advising meetings is to help residents identify specific individuals
with whom they may share research or other project interests and to facilitate contact with
those individuals. For research specific interests, there are also specific meet and greet events
incorporated into the research curriculum. These provide excellent opportunities to meet with
faculty who are interested in having housestaff work with them, and to learn about projects that
are currently occurring within the department. Additionally, there is now a database including
the faculty members in internal medicine and internal medicine subspecialties and their
respective research projects; this is available upon request.
4.
Chief Resident Mentorship Groups: All the interns will be assigned to one of five chief
residents with whom theyll meet casually throughout the year to discuss personal and career
development. These groups will meet on an ad hoc basis, 4-6 times per year, as their members
are available.
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MENTAL WELLNESS
The teaching of good doctoring of patients, of colleagues, of oneself should begin in
the house staff years.-R. Levin
Your medical training years will be filled with high demand stressors. The importance
of simple stress management strategies like making time for some physical exercise, taking
advantage of times to catch up on sleep, fueling your body with the most nutritious food you
can and scheduling frequent visits with family and friends are vital to your wellness. The
following are some of the available resources for you divided up into four categories of
wellness: mental, spiritual, physical and nutritional.
Center for Integrative Medicine - 720-848-1090
This clinic emphasizes the wellness and healing of the entire person, drawing on both
conventional medicine and complementary and alternative medicine (CAM). The services they
offer are listed below.
Acupuncture
Biofeedback
Chinese Herbals
Chiropractic Care
Educational Workshops
and Classes
Health and Wellness
Consultations
Herbal
Supplement/Pharmaceutical
Consultations
Lifestyle/Relaxation
Counseling
Massage Therapy
Nutrition Counseling
Psychological Counseling
Spiritual Counseling
Tai Chi - Yang Style
CPHP (Colorado Physician Health Program) - 303-860-0122

http://www.cphp.org/
The mission of Colorado Physician Health Program is to assist physicians, residents,
medical students, physician assistants and physician assistant students who may have health
problems which if left untreated, could adversely affect their ability to practice medicine safely.
***Everything you do through CHCP is completely confidential***
CPHP is a non-profit independent organization that is separate from other entities such
as the Board of Medical Examiners or the Colorado Medical Society.
Who needs CPHP? Residents with health problems, including medical conditions,
psychiatric illnesses, substance abuse, and personal problems.
Counseling services
For more information or for an appointment, call the office of Margaret Roath, (303) 315-8159.
Biofeedback for stress management is also available. All services are completely confidential.
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Students not enrolled in the HSC Student Health Insurance may contact Margaret Roath for
assistance in finding a provider.
Student Assistance Office (for referral only) (303) 724-2866
University Mental Health Services
(303) 724-1000
Colorado Physician Health Program
(303) 860-0122
Housestaff Family Support Group
(303) 724-3039
Student Insurance Office
(303) 724-7674
Spiritual Wellness
Chaplains are available 24 hours a day, 7 days a week (720) 848-4063. They
...are here to be spiritually and emotionally helpful to you.
...will assist you with prayer, sacraments and other religious rituals.
...will help in the search for meaning in the experience of illness or injury.
...are a resource to reach particular faith group representatives.
...listen, encourage, comfort, care, and support.
...advocate.
The Chapel at Anschutz Inpatient Pavilion, located at the Anschutz Medical Campus is
designed for comfort, peace and healing and is open at all times for meditation, prayer or just
solitude.
http://www.uch.edu/your-visit/patient-services/spiritual-care/index.aspx
Physical Wellness
Anschutz Health and Wellness Center- 303-724-9030
Campus gym and recreational facility with resident rates of approximately $30/month.
CU Sports Medicine - 303-871-2250
http://www.uch.edu/conditions/bones-joints-muscle/sportsmedicine/index.aspx
Campus Recreation at Auraria
Health Sciences Students are welcome to join the Recreation Center at the Auraria Campus
(UCD, MSCD, CCD) for $40/semester.
Spouses/Significant Others/Roommates/etc. are also allowed to join with an HSC Student
sponsor, for $100/semester.
http://www.mscd.edu/~cra/#
Fitzsimons Golf Course
www.golfaurora.com/fitz.htm
(303) 397-1818 (4 days advance notice is required).
Running/Walking
Jogging Trail a partially paved walking/running pathway follows the inside perimeter of the
entire Fitzsimons site
Intramural Sports - www.uchsc.edu/studentassistance
HSC offers the following for all students on both campuses:
Flag Football.. .Fall
VolleyballFall and Winter
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BasketballFall and Winter
SoftballSpring
Nutritional Wellness
Nutritionist at the Center for Integrative Medicine:
http://www.uch.edu/conditions/integrative-medicine/index.aspx
www.eatright.org - the ADA web site
www.quickandhealthy.net - healthy nutrition for busy people
www.rd411.com - wonderful links and tips
Discount programs
The Advantage Program is sponsored by the HSC Human Resources. The various discounts
are listed on this website:
http://www.ucdenver.edu/about/departments/HR/EmployeeDiscount/Pages/index.aspx
Discounts are available to Students/Faculty/Staff at HSC.
Websites
Finding balance in medical life:
http://www.findingbalanceproductions.com/aboutus.asp?SessionID=%7BB2D97EEF-5240-4BF0-8825-A1976619023A%7D
Healing the Healer:
Mothers in Medicine:
https://www.amsa.org/healingthehealer/index.cfm?secure=yes
http://mommd.com/books.shtml
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Hospital Breakdown
University Hospital/Anschutz Inpatient Pavilion
AIP1 / AIP2
Call Rooms:
Ward teams: There are 2 call rooms located on the second floor of AIP1 next to the East
service elevators and the staff lounge. The door code is 0623.
MICU call rooms are located in the MICU on the 10th floor of AIP2. The door code is
4444 and badge activated.
CICU call rooms are located in the CICU on the 3rd floor of AIP2. The door code is
3000 and badge activated.
Each unit has a staff lounge with lockers to store personal items
There is a faculty lounge on the 2nd floor of AIP2 across from the East service elevator.
The door code is 0623
Computer: The Universitys EMR is Epic-based. Login codes are identical and linked to your
UCD Webmail login ID and password.
Locations:
General Medicine Floors:
AIP2 9th floor
AIP1 6,9,10,12, THRU
MICU AIP2 10th floor
CICU AIP2 3rd floor
SICU/NICU AIP2 2nd floor
ACE- AIP1 12th floor
Step-Down AIP1 10th floor
BMT/Oncology AIP1/AIP2
11th floor
ED: Main Floor of AIP2.
Dialysis Unit (inpatient): Main
floor of AIP1
Radiology: Basement of AIP1
Clinical Laboratory services:
Leprino 2nd floor
Food:
Garden View Caf (main cafeteria): located in AIP 1, 1st floor, all days 6:30A-1:00A.
Courtyard Caf: located in AOP, 1st floor, M-F 7:00A-2:00P.
17th Avenue Restaurants: Jimmy Johns Dazbog, etc. Predominantly open M-F.
Important Numbers and Codes:
Main Hospital Line: 720-8480000
AIP2 10th floor MICU: 85492
AIP2 3rd floor CICU: 84500
AIP2 9th floor: 84601
AIP1 12th floor (ACE): 84751
AIP1 9th floor (Pulm/Med):
87579
AIP1 6th floor W (transplant):
84551
AIP1 6th floor E (Surg): 87680
AIP1 2nd floor THRU: 84301
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CMR office: x84246

Lab Main line: 84401
o Micro: 87084
o Path: 84421
Radiology 86343
Radiology OD: 303-266-6347
Interpretive Services: 80397
Pharmacy:81389
Social Work: 86640
o Swing (14:30-23:00)
303-266-1385
o Weekend 303-266-2038
Denver Health Medical Center

Call Rooms:
Ward team call rooms are located on the ground floor of the main hospital across from
the ED. The door code is 5210*. This bank of call rooms has a lounge with a TV,
refrigerator, microwave, and couches. It is a good place to relax during some down
time.
MICU call rooms are located in the second floor of the B Tower. Your ID badge is
needed to unlock the electronic lock on the door. There is also a very nice lounge with
TV and a small kitchen.
Computer: Codes and training will be provided. Lifelink Clinicals is the main program where
CPOE, labs, vitals, medications, I/Os and ancillary staff reports are located. Within Lifelink
you can access EDM, a program into which all of the notes (discharge summaries, H&Ps,
progress notes, clinic notes, etc.) are scanned. Daily progress notes and H&Ps are handwritten.
Radiology: PACS, accessible from your Desktop Portal. Codes will be assigned.
Locations:
General Medicine Floors: 9th, 8th, 6th in the main hospital.
MICU/CCU: 2nd Floor in the B Tower.
Step-Down: Several beds on the 3rd floor of the B Tower above the MICU
Cafeteria: Basement of main hospital.
ED: Main Floor of the hospital behind the elevator bank.
Adult Urgent Care Clinic (AUCC): Main floor of the hospital, next to ED
Correctional Care (CCMF): Basement of B Tower.
SICU: 2nd Floor of the main hospital, above the ED.
Radiology: Main floor of the hospital by the ED.
Food:
Cafeteria: M-F 6:30A-6:30 P; Holidays and weekends: 11:00A -2:00P.

SUBWAY: daily 6A-2A
Hospital Gift Shop (expensive, but nice snacks and drinks): Main floor of Pavilion C.
Vending Machines on the 2nd Floor of the main hospital.
Call rooms on the main floor of the hospital generally have bread, juice, milk, fruit,
cereal, and peanut butter/jelly.
Lunch at Conference every day- 9th floor!
Important Numbers and Codes:

Main Number: 303-436-6000
Main Call Room Door Code: 5210*
MICU Door Code: 159
CMR: 303-602-8626
Lab: 303-602-5200
Micro: 303-602-5205
MICU/CCU: 303-602-1460
Step-Down Unit: 303-602-1425
9th Floor: 303-602-8700

8th Floor: 303-602-8800
6th Floor: 303-602-8900
Inpatient Pharmacy: 303-602-9200
ED: 303-436-8100
Radiology: 2-4144, US: 2-4135, CT: 24149, MRI: 2-4128
Denver VA Medical Center

Call Rooms: Located on the 5th Floor VA, rooms 5A162, 5B106, 5B110, 5B111.
Door codes: 5A162 = 143
5B106, 5B110, 5B111 = 1430
Resident Lounge: 5A161, code 1430
OBMT: This is primarily an outpatient rotation with some overnight call to provide night float
to the VA floor teams. There is a separate morning report at 7:30 AM in 1B135 (Code 1-3-5-2)
on the first floor every weekday. Interns and residents will do various outpatient clinics during
the day as assigned at the beginning of the month.
Computer: Codes are assigned during an orientation on the first day of every month for new
interns and new residents. Computer problems: CPRS (2777) or Help Desk/IRMS (4681).
Data: Vitals: Essentris application, I&Os as well. Labs/Meds can be checked in CPRS.
Check CPRS administration record to determine med dosing.
Social Workers:
Teams A+C 303-687-0314
Teams B+D 303-613-0789
General Phone number for SW: 2558
Locations:
Basement:
1st floor:
2nd floor:
3rd floor:
4th floor:
5th floor:
6th floor:
7th floor:
8th floor:
Cafeteria/Canteen, prosthetics dept., path to the nursing home

Subspecialty 2 clinic, OBMT conference room, OBMT A,
Starbucks behind the police station
Radiology dept.
Dental dept., lab services
SICU, general med/surg on 4 south
Primary medicine/telemetry floors on 5 north and south, MICU
OBMT B clinic, subspecialty 3 & 4 clinics
Inpatient psych services
OBMT C clinic
Phone Numbers:
Main 303-399-8020
Inpatient CMR 2390
OBMT CMR 2058
MICU 3344
5N 2827
5S 2338
4S 3881
SICU 2879
Firm A OBMT 3862/3874/3878
Firm B OBMT 3082/4062/4112
Firm C OBMT 3570/5287
ED 2353
Lab 2213
Micro 2638
Path 2628
National Teleradiology Program 877-780-5559
After-Hours Radiology Tech 5909
Radiology 2430
US 2204
CT 2443
MRI 4166
Nuclear 2454
IR 2445
Cath Lab 5865
Echo 2378
- 17 -
Inpt pharmacy 303-613-0404

Endoscopy lab 4606
People to know:
PICC pager: 303-413-2286
Silver Bullet pager: 303-402-3717
Transfer Coordinator: 5284
CPRS help pager: 2777 call day or night with any problem with computer system
Cafeteria Hours: M-F 7:00AM-4:00PM in the basement.
Presbyterian/St. Lukes
Heres all the info you need to know at PSL.
Parking: Free parking in the underground lot. Use any of the spots except the handicap and
short term parking. Take the elevators on the right up to the main floor of the hospital.
Call Rooms: 4th floor. Take main elevator to 5th floor and then walk down to 4th floor. Code
is 2565. Computer, phone in each sleep room (code 2565). Refrigerator, lockers available.
Intern Lounge: Located on the 1st floor. Code is 2565.
Noon Report: 12:00 in Colorado South or alternate published room.
Daily Schedule:
6:00- 7:30AM: Cross cover signout and pre-rounding.
7:30-8:30AM-Morning Handoffs: Occurs in the doctors lounge.
8:30-9:30AM: Team Rounding
9:30-10:30AM: SIBR (interdisciplinary rounds)
Pagers should remain on until 6:00pm unless you are post-call.
Computers: The PACS helpline is X7721 (839-7721). PACS is available on most computers.
There is a larger screen in the C pod of the ICU. Physicians Help Desk #720-612-6022 (24/7)
Meditech helpline is X7898 for most Meditech issues. For Meditech passwords, Linda
Akbarzadeh is the contact at X 6329.
Data: HCarePortal for data collection, Dictations, prior admits.
Orders go on paper as do daily notes.
Locations:
ICU-2nd floor
Onc 3B.
Teaching Team Medicine 5th and 9th Floors
* B elevators are at the top of the escalators through the main entrance
Cafeteria Hours: 7am-7pm; 7am-2pm Weekends.
Food: $103 provided for the month. Max of $15/day. Just give your food code at the register
when you are checking out. PSL employees also get a 25% discount so make sure you get your
- 18 -
PSL badge and wear it. Lunch is provided >90% of the time M-F. Can use Dining money at
Jazzmans Coffee, which has great hours!
Dictation: INTERNS DICTATE ALL H&Ps. (Not as bad as it sounds. You will learn very
fast.) Make sure you use the complete format including family history and complete review of
systems for billing purposes. Upper level residents dictate the discharge summaries.
Protocols: PSL has protocols with associated order sets for ventilated patients, heparin drips,
sepsis, pneumonia, MI, electrolyte replacement, insulin drips and DKA, neutropenia, stroke,
bone marrow transplant, etc. Please use them.
Telephone numbers:
ER 4111
CT/MRI 6589
CMR 6376
Lab 6800
ER door code ____# (month/year)
Med Records 7474
ICU pod D 6471, pod A 6472, pod B 6470 10th floor 7090
5th floor 7590
9th floor 7990
3b onc 4936
CV lab/echo 6460
radiology 6522
GI lab 6066
rad report line 303-869-1800
echo report line 800-810-0342, then your ID#, then * for work type, then 2 to listen, then enter
account number followed by #
Long distance: 1+#+6277
Rose Medical Center

Format: Residents, generally R3, will be in the emergency department for 10 hour shifts
through the month
Computer: All codes for the Meditech system (also used at PSL) are given out on the first day
of your rotation. In the emergency department, there is a special computer system that you will
be trained to use for chart documentation on the first day of the rotation
Data: Vitals/Labs/Meds: computer. Codes for ED computer system are given at the beginning
of the rotation.
Radiology:
Radiology dictation line: 303-320-7421 or ext 7421

Enter ID#
Enter Password
Enter pts birthday (e.g., May 4, 1953. Enter 05041953)
Obtain codes via ext 2023 if not given to you at orientation.
Viewing: PACS in MICU. Codes given at beginning of rotation.
Locations:
Basement cafeteria, grand rounds room

1st floor ED, radiology dept., Little Miss Latte caf
- 19 -
2nd floor step down unit, OR suites, bridge to Pavilion area (long term
stay pts and some post op recovery)
3rd floor surg beds
4th floor main medical floor, medicine conference room, ICU
5th floor secondary medical floor
6th floor special VIP patient rooms
Phone Numbers:
Main: 303-320-2121
Information systems: 2776
Lab: 2364
Path: 2250
Cath Lab: 2238
Radiology: 2290
US: 2296
MRI: 2582
IR: 7540
MICU 2226
4 north: 2470
CMR: 2977
Endoscopy lab: 2066
Micro: 2360
Inpt pharmacy: 2167
Intermediate Care Unit: 2273
Rads back desk: 2574
CT: 2815
Nuclear med: 2295
2 PAV: 7200
4 central: 2475
5 central: 2575
ER door code: 6789 (subject to change) ED back line: 5400

Cafeteria Hours:
Breakfast: 6:30AM-10:30AM, 7 days a week

Lunch: 11:00AM-4:00PM M-F, 11:00AM-2:00PM Weekends.
Dinner: 4:30PM-7:00PM M-F
There are no food credits for residents during the Rose month
As mentioned above, there is a small coffee/sandwich shop on the first floor called
Little Miss Latte is open from 7:00am often until 02:00 am for sandwiches, breakfast
foods, coffee, and snacks.
- 20 -
Conducting Yourself On The Wards

The first and most important thing to remember is to be courteous. Everyone has a
common goal: taking care of the patient. This can be difficult to remember when tired and
under stress, but its true. When nurses call you, be polite and respond quickly. Answer all
pages in a timely manner. The person who needs something from you now may be the one you
need something from later.
Secondly, be professional. Dress professionally and act (even though you may not feel
like it the first few days) like a doctor should. Professionalism includes not only your attitude
and your dress but also taking care of all your tasks before you leave the hospital every day.
This includes getting all notes in the chart early, updating your sign-out, dictating any discharge
summaries that are assigned to you and making sure everything your patient needs has been
followed up on personally. You are ultimately the one the patient will look to for help,
guidance, compassion and answers make them feel comfortable and confident doing this.
Dont argue and complain, even if you think you are right about a trivial matter it doesnt do
you or the patients any good to have an angry, resentful staff surrounding you.
As for the people you work with in the hospitals, it is a great idea to introduce yourself
to as many of them as possible when starting a new rotationnurses, ward clerks, techs. Many
have been there for years and a good working relationship can be vital to getting things
accomplished in a friendly work environment.
These things can be tough to remember in the heat of battle, especially when you dont
see everyone else around you playing by the same rules. But youre the doctor now, the captain
of the team, and its your job to rise above all things petty and lead your team to victory.
General Order Writing

All medications need a dose, route (PO, PR, IV) and a schedule (q6 hours)
All blood pressure medications should have parameters for when they should be held
(i.e. hold labetalol for SBP < 120 or HR < 60)
Be careful with writing too many PRN medications on your admission orders;
while this can be a time saver later, there are many conditions you would
like to be called with (agitation, anxiety, hypertension) when they occur
Verbal orders are often required in emergency situations but should be avoided
otherwise as they are fraught with obvious problems; do not expect every
nurse to take a verbal order from you in the night if the situation does not
absolutely require it. These orders need to be signed within 24 hours.
Admit Orders
(Editors Note: While our major hospitals now have electronic order entry and admission
ordering templates, this section is still included for (a) historical reference and (b) because
- 21 -
computers can and do sometimes go down. The work of the intern will not go away just
because the computer did; you may need to refer to this section!)
While a specific patients needs may call for special orders to be written on admission, here is a
general guideline for what needs to be in every set of admit orders other things may need to
be added on but the following order categories have to be covered for every patient. The
mnemonic for this is usually referred to as ACDA VAN DISML.
Note: Many common diagnoses (community acquired pneumonia, myocardial
infarction) have order sets preprinted for you. These are not designed to take the thinking and
decision making out of your hands but rather to ensure that all important aspects of their care
are initiated from the time of admission. It is required of you that you use them if available, but
be sure to review them carefully for each individual patient as no order set can address every
individual patients needs.
A Admit to: the name of your service (Medicine) followed by attending name,
resident name, intern name and pager number
D Diagnosis
C Condition: critical, guarded, fair, stable, good are your options
A Activity: bed rest, ambulate with assistance, ad lib, etc.
V Vitals: how often you want vitals done (usually write per routine here)
A Allergies
N Nursing: a good place to list telemetry, Foley placement, NG usage, etc.
D Diet
I IV fluids: list the rate, type of fluid and how much. Always write an endpoint for
fluids.
S Studies: list all radiology and non-invasive cardiology stuff here (dont forget
to include a radiology order form for each study ordered)
M Medication Orders
L Labs: dont count on the ER to have done things for you, order everything
you think the patient needs, lab will call you if its a duplicate
End every set of admit orders with a Call House Officer Call H.O. section which gives the
nurses parameters that, when met, they are to call you about.
E.g. Call H.O. if temp > 101.5, SBP > 160 or < 100, DBP > 90 or < 60,
HR > 110 or < 60, new chest pain, altered mental status.
Sign, date and time your orders and stamp them.
- 22 -
Sign-out
Sign-out occurs differently across the various hospitals. In some situations a designated
time and place are arranged, in others you can sign-out whenever all your work for the day is
finished, so check with your chiefs on the first day to find out how its done in the hospital you
are rotating through.
Sign-out has the potential to be a place where the ball gets dropped; dont let this
happen to you. Use the form below which includes a general template as well as an example
patient to be sure everything that needs to be included is in there. This will be your last chance
to tell the on-call intern everything he or she needs to know about what to do for your patients
overnight so make it count.
Several sights have software in place for generating sign-out. Where this is not the case,
there are usually standardized templates similar to the one below.
Patient Name
MR number
Room number
Admit date
HPI: list
the age, sex,
admitting
diagnosis
and major
current
issues
Medications:
list all meds,
in order of
importance
Studies:
list all studies
to date and
their results
Allergies
Code Status
Active Issues:
list all
problems you
are currently
addressing as
well as active
chronic
problems
To Do:
list anything that
needs to be
followed up by
cross cover or
things to watch
out for
Primary Team:
list issues for the
primary team
that need to be
addressed the
next day
The most important aspect of the sign-out is assuring that the overnight person knows what to
do in case an issue with your patient occurs overnight. Dr. Eugene Chu, formerly at Denver
Health has developed a good sign-out method that should be observed every time you check
out for the evening. The mnemonic is SAIFIR:
S Summary (to be given in 1 or 2 sentences)
A Active issues (things the team is addressing that may come up overnight)
I If/then (a series of scenarios that may occur and what to do about it)
F Follow up (all labs, test, etc. specifically that need to be followed up)
I Interactive questions (from the receiving intern to the handing-off intern)
R Read back (confirmation by the receiving intern of all he/she has heard)
You will receive further signout training during your first week of internship.
- 23 -
Pagers
How To Page
Seems obvious but just in case:
1) Call the number you want and wait for the beep.
2) Put in the number at which you would like to be called back.
3) Press the * button and put the last 4 digits of your pager in. This way
if a call cannot be returned immediately, the person can page you back later
when you may not be by the same phone.
Changing Your Message
Find the 4 digit code on the back of your pager. It is the last 4 digits in the 9 digit number .
Once you have the code....
1. Call your pager.
2. Press "0"
3. Enter your 4 digit password. At this point, you can hit "3" to listen to voicemail, "2" to delete
voicemail, or "30" to record your message. If you hit 30....
4. Record message after the beep
5. Hit "0" again to save message.
This can be confusing the first couple times but the learning curve is steep. After that, its very
useful. Not only saves you from getting called at night, but helps direct the nurse/radiologist on
whom to call when you are off.
Forward Your Pager
As a rule of thumb, on inpatient months you should be either answering your pager or have it
forwarded to someone else. This streamlines nurse physician communications in off-hours.
To forward you pager:
1. Call your pager
2. Press 0 followed by your 4 digit password
3. Then press 16
4. Follow the prompts: Press 6 followed by the pager # you are forwarding to. Finish with
the # sign. It will then prompt you to confirm the number
5. To cancel pager forwarding, follow steps 1-3 then press 3 to cancel
An Ideal Admission Note (H+P)

- 24 -
This is the cornerstone of the patients admission as far as medical decision making
goes. It is the single most referred to note in the chart, the one every consultant, nurse, and coresident will turn to for information on your patient. As an internist, it is also your stage, the
place where your thoughts and conclusions shine, so take time with this document.
HPI: The first sentence should always be of the 67 y/o woman with known CAD and DM II
who presents with crushing, substernal chest pain variety. Keep it very short and to the point,
including only those facts which directly relate to your ultimate diagnosis.
The next paragraph should include a thorough analysis of the patients complaint using
the FAR COLDER system:
Frequency
Character
Associated symptoms
Onset
Radiations
Location
Duration
Exacerbating factors
Relieving factors
The next paragraph should follow from the conclusions youve derived from the first. In
it, ask and answer all the pertinent review of systems (+fever, +SOB, no N/V) that relate to the
condition you believe the patient has. The HPI, when done well, should generate the right
answer to a diagnostic dilemma before any test is ordered more than 90% of the time.
PMH: include medical conditions, when they were diagnosed, as well as surgeries and when
they occurred
Allergies: include the name of the offending agent as well as the specific reaction it causes
Meds: many patients do not know the meds they are taking; the best way to get this list correct
is to have a family member bring in all their pill bottles. Short of that you may have to use the
most recent clinic note available in the chart
Social History: include drug, alcohol, tobacco use status as well as family support system and
name of PCP.
Review of Systems: this section is designed to be the answer to the question, Is there anything
else bothering you today? It should not include any repetition of things already mentioned in
the PMH or the HPI.
Physical Exam, Vitals and Laboratory Studies
Assessment and Plan: this is where you put your money down on a diagnosis, explain why
you think it is correct, other things you considered and excluded and what you plan to do about
it.
write this out in a problem-based format touching on the chief complaint as well
as anything else you will be treating including chronic active conditions
explain your reasoning thoroughly, DO NOT JUST USE BULLET POINTS
address COR status
Sign, date and time your note and stamp it (if paper).
An Ideal Progress Note

- 25 -
While it may seem like a chore to write a note on each patient every day it is both
required and important. The progress note should be a concise record of the events of the last
24 hours in that patients hospitalization. It should be something that you and your colleagues
can refer to in order to know exactly what has happened to the patient, any recent changes or
events and what you have done or plan to do. Imagine that you are writing it so that a
consultant can be kept up to date or a cross cover intern in the middle of the night can know
exactly what is happening with a patient they may not be very familiar with.
Remember that cutting and pasting in our electronic records, while seemingly
convenient, encourages you to make errors of omission, increases mistakes, and perpetuates
old, possibly inaccurate information. Use the cut and paste very sparingly, if at all.
Date: xx/xx/xxxx
Time: 00:00
Service: primary medicine team
Subjective: a quick outline of important events in the last 24 hours, issues the nursing staff has
mentioned that the patient may not have, any updates on their condition that the patient
mentions to you (worsening nausea, improved pain)
Vitals: they are vital and must include numbers in a range of lows and highs over the last 24
hours; afebrile is not a vital sign.
I/Os: include totals in and out as well as specifics (what amount out was urine, how much was
stool, how much was vomitus)
Meds: copied into the note and updated daily from the most recent MAR (not from yesterdays
note even though it may be easier to find in the morning)
Physical Exam: you must document at least a 6 system exam every day at a minimum with
other areas examined as required based on the patients symptoms
Labs: include daily labs, pending or completed culture results including sensitivities, any new
radiographic studies, results of any procedures performed since the last note you wrote
Assessment: a quick, one-liner including the patients age, sex and primary problem
Plan: List this out by the issues or in the case of an ICU patient, in a system-based format.
each problem should be listed separately along with what you plan to do about
it that day and what was done about it the day before
any problem which has resolved in the last 24 hours should be listed one last time to
acknowledge its resolution and then can be dropped from the list
if you dont know the specific plan on an issue, you may write, to be further
discussed with team an addendum note can always be completed later
be sure to mention prophylaxis daily (nexium, SQ heparin, SCDs) in every note
always end your note with COR status
- 26 -
An Ideal Procedure Note

As an example a note for a thoracentesis follows although this note is acceptable for any
procedure with small changes.
Operator: Your name, name of supervising resident

Procedure: Left sided, diagnostic and therapeutic thoracentesis
Consent: Consent was obtained and on the chart at time of procedure.
Area was prepped and draped in the usual sterile fashion. Area was numbed with 1%
lidocaine using a 25 gauge needle and the procedure was begun. A catheter over a needle was
inserted over the rib until a clear, straw color fluid was obtained. The catheter was then
advanced as the guide needle was removed until the catheter was advanced fully into the
thorax. 1,500 cc of fluid was removed and the catheter was taken out. Estimated blood loss
(EBL) = 2 cc. The patient tolerated the procedure without issue. A CXR was ordered to assure
no complications.
Tests sent: cell count, gram stain, pH, AFB
An Ideal Death Note

Called to see patient at 00:00 by the nurse for complaint of (labored breathing,
decreased wakefulness, agitation). Found patient to be (unresponsive, Cheyne-Stokes
breathing, without signs of life). I examined the patient and noted no respirations, no heart
sounds, and no withdrawal to pain. Pupils were fixed and dilated. Telemetry confirmed no
signs of cardiac electrical activity; a strip was printed and placed in the chart.
Time of death: 00:00.
Next of kin was notified.
- 27 -
The Bane of Residency Discharge Summaries

OK, one of the least fun things you will have to do during your residency is a discharge
summaryin fact, lots of them. On the other hand, when a patient is admitted to your service,
the first thing you will scour the records for and read is the last discharge summary on that
person. So its important. If you dont feel like doing one right as the person is being
discharged, think about the next doc who will take over their care, how much having that
document will impact that patients care and reconsider.
When you are dictating a summary (done at some of our hospitals instead of typing),
speak reasonably slowly and clearly into the phone. Do not do them from home on a cell
phonethe reception is not adequate for dictation and youll end up having to do it again.
When you are done, write down the dictation number along with the patients name and
medical record number keep these for about a month after youre off service in case a file
gets lost (as it occasionally does). Having this record will keep you from having to do the
whole thing againfrom memorynot fun.
To make things a little easier for you and to help keep anyone from getting behind,
heres a template you can read from into the phone, adding in the details about your specific
patient as you go.
(Please see the sections on the specifics of each hospital for codes, instructions, etc.)
Your Name:
Attending Name:
Patients Name:
Medical Record Number:
Date of Admission:
Date of Discharge:
Admission Diagnosis: list the primary diagnosis first followed by all other conditions
which were acute and treated on that admission, leave out chronic conditions
Consultations Called: list all, if none, state None
Procedures Performed: same as above
Hospital Course: as descriptive as possible including how the patient presented, what you
did for them, how they responded, what you did next
Diagnoses at Discharge: list all conditions treated; in this section you will start with the thing
that brought the patient into the hospital, move on to other acute issues and then include all
chronic conditions for which a medicine or therapy will be provided on discharge, even if it is
the same one they came in on
Medications at Discharge: list all meds, old and new
Diet on Discharge
Activity on Discharge
Disposition: discharged to home, discharged to Autumn Sunset Nursing Home, etc.
Follow Up: list all follow up appointments with dates and times
- 28 -
The Experienced Approach to: Night Float/Cross Cover Issues

Your most important job at night, other than admitting and caring for your own patients,
is helping to care for others patients while they are out of the hospital. Whenever you are in
doubt about any issue over night, call your resident.
Tachycardia
1. Get vitals first. If unstable, manage patient via ACLS guidelines. Call a Rapid
Response or potentially a code if you need help.
2. Go see the patient. Is this new? Are they symptomatic? Order stat EKG.
3. Compare EKG to old. See cardiology section for algorithm on how to diagnose
rhythm and when to use adenosine and vagal maneuvers.
Bradycardia
1. Get vitals first. Go see the patient.
2. If they are symptomatic (dizzy, chest pain, syncope) or hemodynamically unstable,
follow ACLS guidelines. Put patient in Trendenlenberg. Call a Rapid Response or
potentially a Code if you need help.
3. If stable, order atropine to the bedside and consider placing the patient on telemetry.
4. Place pacer pads on the patient (can always take them off).
5. If ECG shows either Type II second degree or 3rd degree AV block, consider
transcutaneous pacing and possibly a transvenous pacer. Call Cardiology ASAP,
and transfer to ICU.
6. If patient is stable and not symptomatic, take a quick look at the chart to try and
determine why this might be happening.
7. DDX:
Meds: -blockers, Calcium-channel blockers, digoxin, amiodarone, clonidine.
Cardiac: sick sinus syndrome, inferior MI, vasovagal (usually transient), 2nd or
3rd degree AV block, junctional rhythm.
Autonomic N.S: neurocardiogenic syncope, carotid-sinus hypersensitivity,
cough/micturition/emesis/defecation induced.
Other: idiopathic degeneration (aging), infiltrative disease in the conducting
system (sarcoid, amyloid), collagen vascular disease, surgical trauma,
endocarditis, hypothyroidism, hypothermia, increased intracranial pressure
(Cushings reflex), hyperkalemia, hypokalemia, OSA, normal variant (marathon
runner).
8. Management (if stable):
Take a focused H&P and look at the medication administration record.
If you think this is medication induced, consider holding a dose of the med if
stable. Consider calcium or glucagon administration if you believe it to be
secondary to the calcium channel or beta blocker the patient is taking.
Put patient on telemetry to track trends.
Consider sending electrolyte panel.
- 29 -
Hypotension
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
Start with your ABCs. Is this person symptomatic (dizzy, chest pain,
unconscious)?
See the patient immediately. If unstable, call a Rapid Response or potentially a
Code.
Get the rest of the vitals. Is there evidence of shock (distributive, cardiogenic,
hypovolemic)?
Make sure the blood pressure is real (if the patient is stable). Measure it yourself
with a manual cuff. Make sure all vitals are current.
Is this patients blood pressure always 80/40 and they feel fine (you will
probably see this on the cardiology service)?
Calculate the MAP: MAP <60 is associated with decreased perfusion to vital
organs.
Determine what your IV access is: Make sure there are two large bore IVs and
start Normal Saline wide open while you are thinking, unless the patient is in
cardiogenic shock.
Consider need for a central line early. If you are going to give pressors, they
need a central line stat. Pressors are dangerous to use via peripheral access, and
some hospital policies flatly prohibit it.
Focused H&P if stable. Talk to the nurse.
If BP is undetectable, remember that if you can feel a femoral pulse the SBP is
>80 and if you can feel a carotid pulse the SBP is greater than 60.
Place patient in Trendelenburg.
Labs and Studies: CBC, chem.-7, LFTs, 2 sets of blood cultures, UA with
culture, lactate,? BNP, troponin (if you think is cardiac), CXR, EKG, ABG.
Broad-spectrum antibiotics if you think this is septic/distributive shock.
Hypertension
1. Take a deep breath. Urgent action is only required if you think the patient has
hypertensive emergency.
2. Re-check the reading manually. Check the other vital signs. Focused H&P. Quick
chart biopsy. What do they take at home?
3. Review the vital sign trends. Is this new? Occasionally you will be called with what
seems like a concerning blood pressure, when the patient lives at the BP.
4. Uncontrolled Hypertension (formerly Hypertensive Urgency): SBP > 220 or DBP
>125. No end organ damage.
5. Hypertensive Emergency: Hypertension + end organ damage. The BP does not have
to meet certain cut-offs. Look for end organ damage:
Brain: AMS, lethargy, stroke, seizure
Eye: change in vision, papilledema, flame hemorrhages
Heart: CP, heart failure, ECG with strain or ischemic changes, SOB
Renal: low urine output, edema, elevated Cr, hematuria.
6. DDX:
Withdrawal: ETOH, -blockers, ACE-I, clonidine. Did someone stop their meds
or lower their doses when they were admitted?
Drugs: cocaine, amphetamines
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Cushings reflex?
RAS, ESRD, renal failure
Drug Interactions
Pregnancy: eclampsia, pre-eclampsia
Aortic dissection, coarctation of the aorta
Endocrine: pheochromocytoma, Cushings syndrome, thyrotoxicosis.
7. Treatment:
Hypertensive Emergency: ICU admission. Lower BP by no more than 25% in
the first 6 hours and then to a goal of 105 DBP over 6-12 hours. Patient will
likely need nitroprusside (best choice for most) or labetalol gtt and an arterial
line. Consider nitroglycerine gtt if patient has cardiac ischemia. Also consider
giving an ASA if no contraindications.
Uncontrolled Hypertension (formerly Hypertensive Urgency): this must be
evaluated in the context of the patient with attention paid to the time course of
the hypertension. If felt to be a chronic problem, consider either not treating or
treatment with medications which would be appropriate for long-term use as an
outpatient (thiazide diuretics, ACEI, calcium channel blockers). If the time
course is felt to be more acute, consider use of hydralazing: 10 mg IV q 6 hours.
PO hydralazine can be used as well, but you will need to use higher doses such
as 25 mg PO. In the
Fever
1. Temp > 38.3C and greater than 38C in neutropenic/transplant/dialysis
patients.
2. Broad DDX:
Infection: PNA, UTI, line infection, cellulitis, VAP, osteomyelitis,
endocarditis, myocarditis, pericarditis, encephalitis, meningitis, abscesses
(esp. if post-op), sinusitis, prostatitis, C. difficile diarrhea, fungal (esp. if
immunosuppressed with lines), decubitus ulcers.
Inflammation: collagen vascular diseases, neoplastic, mucositis.
Drug Fever: beta lactams, amphotericin, chemotherapy, neuroleptic
malignant syndrome, malignant hyperthermia of anesthesia to name a
few.
Clot: PE, DVT, thrombophlebitis.
Neurologic: spinal cord injury, hypothalamic injury, intracranial
hemorrhage, seizures, subdural hematoma.
Endocrine: adrenal insufficiency, thyrotoxicosis.
Miscellaneous: Alcohol/drug withdrawal, aspiration, transfusion
reaction, hematoma, pancreatitis, MI, acalculous cholecystitis, ischemic
bowel, fat emboli, transplant rejection, gout/pseudogout, GI bleed.
Atelectasis does not cause a high fever; this is a myth, so keep looking.
3. If the patient develops fever after 72 hours in the hospital, then likely nosocomial
infection or drug-induced fever:
Common Infections: UTI (esp. with foley catheters), central venous or
peripheral catheter infections, pneumonia, wound infection, C.difficile
colitis.
Less Common Infections: decubitus ulcers, sinusitis, acalculous
cholecystitis.
- 31 -
4. Work-Up:
Determine whether patient is stable or unstable Ask nurse for V.S.
over the phone. Assess patient immediately at the bedside if hypotensive,
tachycardic, tachypneic. Document your findings in the chart with a short
note. If unstable, call your resident, as patient will likely need to be
transferred to the ICU. If hypotensive, start normal saline IV bolus and put
patient in Trendelenburg position.
Perform a focused history and physical.
Order two sets of peripheral blood cultures. If patient has a line, and
peripheral blood cultures are difficult to obtain, it is O.K. to get one of the
two sets through the line. If blood cultures have been done within 24 hours
and patient is stable, then only re-culture if unstable.
Determine what other tests should be ordered according to clinical
findings. If an infectious etiology seems likely, urine and lung sources can
be evaluated with a UA with culture and CXR.
Keep your differential broad. Consider non-infectious etiologies
including drug fever, PE, transfusion reactions (See above).
5. Treatment:
If patient is unstable, start broad-spectrum antibiotics or start directed
antibiotic therapies if you have identified the source of the fever (i.e. PNA,
UTI).
See Oncology section for neutropenic fever.
Follow algorithms for bone marrow/stem cell transplant patients.
If patient is stable and you do not have a source, you can withhold
antibiotics until the source is determined.
6. Specific Therapies:
If known neutropenic fever, see oncology section for recommended
regimens.
If suspected pulmonary source is this community acquired, hospital
acquired, health care associated, or ventilator associated? Next, consider
patients risk factors for multi-drug resistant organisms. These pieces of
information will help you determine an appropriate regimen.
If suspected intra-abdominal source, need to cover for polymicrobial infection
(gram negatives, enterococcus and anaerobes). Consider carbapenems or beta
lactam/beta lactamase inhibitor like piperacillin-tazobactam.
If urinary source, will need coverage for gram negatives.
If suspected soft tissue infection, add vancomycin for coverage of MRSA
(good first line therapy in cellulitis).
Antipyretics: acetaminophen 500 mg to one gram PO (write not to exceed 3
grams per day and if patient has liver disease not to exceed 2 grams per day).
Be careful with ibuprofen especially if patient has ARF, ESRD, surgery is
planned, GI bleed, anticoagulated.
Marik, PE. Fever in the ICU. Chest 2000; 117: 855 869.
- 32 -
Low Urine Output (UOP) defined as less than 0.5 cc/kg/hr

1. Fluids, not lasix. With rare exceptions (extreme volume overload such as in endstage CHF patients come to mind), the answer to low urine output is almost never to
give lasix.
2. Consider whether or not they have a Foley in place. In patients without a
Foley, not urinating for 4-6 hours may be normal (you dont give hourly
urine output normally, do you?). In this case, if you or the nurse are still
concerned about their urine output, order a quick bladder scan or PVR to
see how much is in there. If nothing, see #3. If a lot, see #4. If 100-200
ccs you can safely continue to monitor closely for another couple of
hours.
3. Determine the cause. Causes to consider:
Poor flow to the kidneys because of a bad or worsening pump (the heart)
Poor flow because of hypovolemia
Poor flow because of distribution (sepsis/shock)
Renal failure (a variety of causes, either new or worsening)
4. Obstruction not allowing any urine to get out. Place Foley or straight cath and
continue to assess.
Hypoxia
1. See the patient immediately! Start with ABCs. Does this patient need to be intubated
right now? What are the vital signs? How much oxygen are they on?
2. Look at the trend. Is this immediate or has their oxygen requirement steadily been
increasing?
3. Call a Code if patient has stopped breathing, is unstable, is blueafter making sure
of their cor status.
4. Make sure it is real. Switch extremities, switch probes.
5. Diagnostic tests: CXR, ABG stat (goal PaO2 is greater than 60). Then order: EKG,
CBC, chem.-7, troponins. Perform a focused history and physical- is this patient in
heart failure, no breath sounds on one side indicating a PTX
6. DDX:
Pulmonary: pneumonia, PTX, PE, aspiration, bronchospasm (asthma, COPD,
drug reaction), upper airway obstruction, ARDS, flash pulmonary edema.
Cardiac: MI/ischemia, CHF, arrhythmia, tamponade.
Metabolic: sepsis, acidosis
Hematologic: profound anemia, methemoglobinemia (low sat, normal PaO2)
CNS: stroke, medications (benzos, opiates), AMS.
7. Treatment
Give them as much oxygen as you can.
Consider Non-invasive positive pressure ventilation (BiPaP or CPAP) if they do
not have altered mental status and they are relatively stable (especially for
hypercapnea).
Intubate those who cannot protect their airway or who do not turn around with
oxygen- remember to check Cor Status.
RT can be our best friend in these situations.
Treat the underlying cause (i.e. furosemide and CPAP if heart failure, abx for
PNA).
Give albuterol nebs to those who are wheezing.
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Electrolyte Replacement
Rough goals for lytes replacement (especially in cardiac patients or anyone with a
history of arrhythmia) are K = 4.0, Mg = 2.0, Phos = 3.0.
Be very, very careful replacing lytes in a renal patient with poor ability to
process them.
Potassium: Can be given PO (very effective, a little hard on the stomach at doses above
40 meq) or IV (should be given with lidocaine as it burns going in).
Expect a result as follows:
K = 3.5 4.0..to raise the level by 0.1 will take 10 meq
Never give more than 10 meq IV per hour as it can cause arrhythmias/death.
Give via PO route whenever possible, by both routes if the K is less than 2.5 and there
is a high risk for the hypokalemia causing an arrhythmia or if multiple PVCs are noted
on telemetry.
If hypomagnesemia is present as well, this must also be corrected. Low magnesium
levels can cause patients to be refractory to potassium repletion.
Magnesium: Can be given PO (also a little hard on the stomach, may cause diarrhea)
500-1000 mg per dose, up to TID or IV 1-4 g per dose. Expect approximately
a 0.1 increase in Mg levels for every gram given IV. The max you can give in a
single IV dose is 4g if the Mg is < 1.5.
Phosphorus: Can be given via PO or IV routes, equally effective. A great way to raise the
phos in a patient who can eat is to add 1-2 containers of skim milk to each meal. PO
dosing is 500 mg BID TID, IV dose is 10 mmol IV x 1, repeat as needed.
Phosphorus IV comes in two flavors: NaPhos and KPhos. Both contain fairly
negligible (7 meq) of their respective carriers but avoid KPhos if the K is high
and NaPhos if the Na is high.
Never attempt to use KPhos to replete the K.
Calcium: Remember that calcium needs to be corrected for the patients albumin based
on the following formula prior to replacing it:
Ca = serum Ca + 0.8 mg/dL for every 1 g/dL of albumin < 4.0
If you are still unsure of the true Ca level or want to check more accurately, you
can order an ionized calcium prior to replacement.
Replacement can be accomplished via PO or IV routes. Either 1 gram of CaCl
(13.6 mEq of elemental Ca) or 1 gram Ca gluconate (approx. 4.5 mEq of
elemental Ca) are acceptable IV preparations, noting the difference in strengths.
- 34 -
Ca gluconate 500-1000 mg PO TID is a standard PO dosing (as is the use of

TUMS OTC 500 mg PO TID which will provide 30mEq of elemental Ca).
Heparin Drip Adjustment

Heparin drips are being used less and less frequently as low molecular weight heparin
becomes more acceptable for use in PE, DVT and other common conditions but you will still
need to know what to do with one for your post-cardiac cath patients, those with unstable
angina and some others.
Adjusting the drip is a little bit of science and a lot of art, with the final answer being to
check q6h PTTs and monitor carefully for bleeding. Most hospitals have protocols that allow
the nurse to adjust appropriately.
Loading dose: 60 - 80 units/kg IV x 1
60 units/kg for unstable angina and MI, 80 units/kg for treating a known
or suspected DVT or PE
Starting dose: 12- 18 units/kg/hr continuous infusion
again, the lower dose for UA and MI, the higher for known clot
Adjustment Table
apt
Rebolus
Stop Time
Drip rate change
< 35
80 units/kg
4 units/kg/hr
35 45
40 units/kg
2 units/kg/hr
46 59
2 units/kg/hr
60 80
-GOAL RANGE
81 100
30 minutes
1 unit/kg/hr
101-120
60 minutes
2 units/kg/hr
> 120
90 minutes
3 units/kg/hr
(Adapted from the original by Raschke RA, et al. Ann Int Med 1993; 119:874-881)
Hint: If you are called with a very high PTT (>200) on a recently started drip or on a
patient who has had a stable drip rate for days, the person drawing the level may have pulled
the blood out of a heparinized line. It is reasonable and OK to ask them to redraw it via a
peripheral stick before making any changes unless the patient is clinically over-heparinized
(i.e. bleeding).
Nausea/Vomiting
1. First of all figure out what they are vomiting and why. Could they be obstructed- if so,
get a 3-Way of the abdomen. Examine them and make sure something more serious isnt
going on. If they are not vomiting blood, consider the following recommended antiemetics.
Remember many of these drugs can have significant extra-pyramidal effects so be careful.
Zofran 4 mg IV q 8 hours
Phenergan 12.5 mg to 25 mg IV or PO q 6 hours prn. Can also be given as a
suppository.
Compazine 5 mg to 10 mg PO q 6 t o8 hours. 25 mg suppositories are also
available. Can be given IV/IM at doses of 5 to 10 mg.
- 35 -
Reglan (a good motility agent as well). Start 10 mg Q 6 hours. Try to avoid this
drug in elderly patients.
Low dose benzos such as ativan can be used, but again do not give to elderly.
Chest Pain
For more specific info see the cardiology section but this should get you started.
1. Order an EKG, CXR and a new set of vitals while you are on your way to see the
patient.
2. Obviously your first concern is the heart, lungs and vessels as they are the
things that could lead to acute collapse of the patient if missed or not addressed in a
timely fashion. Consider this as you review the nature of the pain and the patients
history.
3. Then, think about whats in the chest that could be hurting, layer by layer:
Derm herpes zoster (pain will start approx. 48-72 hours before the rash
appears).
Musculoskeletal fractured rib (coughing, trauma), pulled muscle,
costochondritis.
Nerves nerve root pain from a compressive spinal lesion (cancer).
Heart angina, MI, arrhythmia causing poor coronary perfusion,
pericarditis.
Vessels aortic dissection, pulmonary embolus.
Lung pneumothorax, pneumonia, pleurisy from an effusion.
4. Other potential etiologies of chest pain:
GI esophagitis (pill or other), GERD, esophageal spasm, peptic ulcer.
Hepatology hepatitis with capsular strain, Fitz-Hugh-Curtis syndrome.
Other pancreatitis, splenic rupture or infarct, gallstones.
Then go back and make sure its not the heart again.
Rising Creatinine/Acute Renal Failure see the renal section

Falls
1. See the patient and examine them with a full neurologic exam.
2. If at all in doubt about head trauma order a non-contrast head CT to be done
STAT.
3. Order any other radiology as directed by your exam (hip films, wrist films)
and make sure it gets done that night, not in the morning, unless you are
confident in splinting the joint appropriately until further evaluation.
4. Attempt to figure out if there is a correctable or treatable reason as to why
they fell. Look at the medicine list.
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Insomnia
1. First and foremost, find out why the patient cant sleep; theres usually a good
answer that might not require medication.
2. Choose a medicine designed for sleep; do not rely on the side effects of
medications for other conditions (i.e. Seroquel, Benadryl, amitriptyline,
Ativan)
Good Options:
Trazodone 25 mg po qhs PRN
Ambien 5 mg po qhs PRN (use with caution in elderly)
*Hint: Always remember to give people over age 65 half the dose you would
normally use.
3. Assure good day/night cycle in their room by asking the nurses to turn the TV
off after midnight, turn the lights out after 10 PM, turn the lights back on during the day
and have them open their blinds in the AM as well. This may help avert the same call
the next night.
Hypoglycemia/Hyperglycemia see the endocrinology section

Altered Mental Status
Needless to say, the causes are many and each needs to be carefully considered. The
mnemonic is not very helpful (probably easier to just flip this page open until these things stick
in your head as opposed to trying to memorize them cold). In the hospitalized patient, the cause
is usually multifactorial.
Mnemonic: SHE STOPs for TIPS on AEIOU
Sepsis
Hepatic Enceph.
Electrolytes
Stroke
Temp
Oxygen
Psych
Trauma
Infection
Porphyria
Seizure
Alcohol
Endocrine
Inflammation
Opiates
Uremia
*Hint: Finding one of these reasons in the chart does not rule out the
othersmake sure you have considered all the possibilities as there are many and
some patients will have more than one.
- 37 -
Dyspnea
Remember first of all that dyspnea is a symptom, not a diagnosis or disease. Your job
in the patient complaining of dyspnea, or shortness of breath, is to figure out why. A good
approach is to think of dyspnea in four broad categories, each of which can be investigated
quickly with just four tests.
Pulmonary Causes: the largest group, a good place to start
pneumonia
asthma
pneumothorax
aspiration
pulmonary embolus
mechanical obstruction
COPD
ARDS
Cardiac Causes: the next largest and most common
CHF
myocardial infarction
tamponade
arrhythmia
Hematologic Causes:
hemoglobinopathies
cyanide toxicity
very severe anemia
Acid/Base Disturbances:
metabolic acidosis
respiratory alkalosis
Psychiatric Causes:
panic attack
Using this list from the top down will not give you every answer, but it will allow you
to quickly reason through 18 of the more common causes.
As for figuring out which on it is, four tests will help rule in or out each of the above
listed disorders (with the exception of psych causes, which are always a diagnosis of
exclusion).
CBC
CXR
ABG
EKG
Order these over the phone or as soon as you get to the patient in all calls for new-onset
dyspnea; while you are examining them the results will be cooking and youll be well on your
way to solving the problem.
Hint: Do not disregard dyspnea in the face of a normal O2 sat; it takes a lot to change
the saturation and can fool you into thinking nothing is going on.
Adapted from J. Wiese, Tulane Internal Medicine Guide, 2003
Combative Patient
1. Go see the patient and figure out what is going on. Is this a psychiatric issue or is it
medical?
2. If you feel like you and the staff are in danger of physical injury, call security right
away. Do not try and restrain the patient yourself. It is not your job to physically
restrain anyone; dont attempt to do that. If the patient is trying to leave the hospital
and you believe them to be a danger to themselves AND you believe this to be
primarily psychiatric, place them on a Mental Health Hold. Remember that a MHH is
not necessary to prevent someone from leaving the hospital AMA when the cause is
- 38 -
medical; in this case, you must simply document the lack of capacity from a medical
cause (delirium, intoxication, etc).
3. If you feel this is not psych, then do the AMS work-up recommended in the
preceding section.
4. Try and re-orient the patient before using chemical or physical restraints.
5. Chemical restraints:
Haldol should be your first choice. Start at low doses especially in the elderly,
such as 0.5-1 mg IV X 1. Can be given IV/IM/PO. Do not give doses larger than 5
mg at one time.
If for some reason haldol cannot be used, try zyprexa. There is a fast acting form
Zydis that can be given in a pinch. However, remember that atypical antipsychotics
have been associated with increased mortality rates in the elderly.
Risperidone is another option, but this also carries to increased mortality rate
discussed above.
6. Physical restraints: if at all possible, try not to restrain a patient, but if needed try to
use the least restrictive. Try a Posey vest or a distraction apron first; a distraction
apron has a lot of buttons, zippers, and things for someone to play with and works
well for the elderly. Also consider using mittens if the concern is that the patient will
pull something out. The nurses are really the best at determining what will help a
patient. Please sign your restraint orders in a timely manner.
Deceased Patient
You will be called to pronounce a patient who has died at some point. The nurses know
that we dont do this a great deal and have streamlined the process for you. Interns may
pronounce death without their residents present but if you have concerns or it is your first time,
call your resident to assist.
1. Find the charge nurse, let them know you will be the doctor pronouncing the patient
and will need all the necessary paperwork.
2. Examine the patient for signs of life and note the time you finish your exam this is
the time of death.
- if the family is in the room and upset, speak with them before approaching their
recently-deceased relative; let them know what you will need to do and why. This
can be difficult, particularly when you are cross covering and have never met the
family. The vast majority of the time, they will be fine with you examining their
loved one once you explain your role. However, if the family is very upset with
your presence, leave the room and get a nurse to come back in with you to help
console the family while you make the pronouncement
- check heart and breath sounds with your stethoscope; while you are doing this, out
of sight of the family, firmly squeeze the patients nail bed between your fingers to
assess withdrawal from pain; then quickly check pupillary light reflexes in both eyes
- you do not say the time of death out loud like on TV, just note it in your head
3. Fill out the Death Packet provided for you by the charge nurse. It is very
self-explanatory but the charge can help if you have questions. However, do not
sign the form, only an attending can do that in the morning.
4. Call the coroner using the number provided in the death packet. Youll want to have
the patients chart with the face sheet for this as there are a lot of questions to be
answered.
- 39 -
5. You are in charge of asking the family for permission to do an autopsy and should
make an effort to obtain one in all cases.
6. Write the death note as outlined in the Ideal Death Note section of this guide
7. If appropriate and you feel it is needed, go back and offer your and the hospital
staffs support to the family, i.e. see if they need tissues, coffee, have any questions.
8. Ensure that next of kin is either present at the bedside or has already been notified. If
there is a question, call them yourself.
You do not get involved in the procurement of organs, it is a conflict of interest.
The Experienced Approach to: Procedures
Central Lines
Central lines are important ways to get access in a patient requiring pressors for any
reason, someone in whom immediate, multiple points of access are needed and in those for
whom no other sites of access are available in an emergency. They should always be
performed in a very sterile fashion (except in Code situations when time is of the essence) and
an ultrasound should be used whenever possible.
They are very useful when done correctly although inserting one carries with it a certain
amount of risk. The femoral approach is best reserved for Code situations when interosseous
access is unavailable for some reason, and when other access sites cannot be used. It is the least
sterile of the options in the long term. The other two sites, the internal jugular and the
subclavian, can be used interchangeably based on operator experience and the patient. For
example, an IJ is safest in a patient on positive pressure ventilation and in very thin patients. An
IJ has very few drawbacks, although a very agitated patient may thrash their head around a lot
and a person with a large neck can be technically challenging.
While the sites may vary, the technique is the same. Below is a description of the
Seldinger technique for reference and a few helpful hints to be reviewed prior to the procedure.
1) Obtain consent and place it on the chart.
2) Use the ultrasound to locate the vein if using the IJ. Compress the vasculature to identify
artery and vein.
3) Completely dress yourself for the procedure; this means sterile gown, gloves, protective
eyewear, and cap. This is required for all central lines.
4) Prep and drape the area in question in the usual sterile fashion.
5) Numb the skin over the area as well as your intended path to the vein with the 1% lidocaine
included in all the kits. For IJ approaches you can usually find the vein with this needle as
well.
6) Flush the catheter in all its ports with sterile saline so no air is left in it.
7) Cover the Ultrasound probe with a sterile sleeve.
8) Now use the insertion needle, the largest one in the kit, to follow the path you just numbed
in an effort to find the vein. Hold the Ultrasound in your other hand and keep an eye on
both your needle and the vein on the ultrasound monitor. Always draw back as you are
advancing so you will know when you are in the vein (the blood will fill the syringe
quickly).
9) Once you are in and getting good flow back, remove the syringe from the needle, leaving
the needle exactly where it is. Often blood will flow briskly from the back of the needle
but not in every case, depending on the pressure and volume status of your patient. If
blood is squirting from the needle in a pulsatile fashion you likely have canulated the
- 40 -
10)
11)
12)
13)
14)
15)
16)
artery if this happens, remove the needle and hold pressure for 10 minutes on the site.
Never dilate and place the line if you are unsure of where you are.
Insert the wire into the back of the needle and into the vein until there are 5-10 cm of wire
sticking out the back. NEVER LET GO OF THE WIRE. Never force the wire if it doesnt
go in easily. If you cant get it in easily attempt to tilt the needle more parallel to the
patient to facilitate the direction it takes inside the vein. If this doesnt work, you may have
to start over with another stick in a slightly different location as there may be scarring or
other obstruction within the vein itself at that site.
Remove the needle and make a small 0.5 cm skin nick where the wire is.
Slide the dilator over the wire and at least half way into the patient. A good deal of blood
may now flow out as you have made a large hole in a large vein. Have some gauze at the
ready on your sterile site. NEVER LET GO OF THE WIRE. Remove the dilator.
Slide your catheter over the wire. When you get the tip close to the skin you will have to
push the wire back into it so that you dont let go. The wire will come out the back of the
shortest port. When it does, grab the wire and push the catheter in the rest of the way and
remove the wire. For femoral lines, the catheter should go all the way in. For subclavian
and IJ line the catheter should go to about 20 cm if on the left side and 16 cm if on the
right side but you will have to judge by the size of your patient.
Now flush all ports with sterile saline to assure that they work easily. Place caps on their
ends. Suture the line into place, remove your sterile drape and ask the nurse to secure the
site with Tegaderm to assure that the line isnt pulled out.
For all subclavian and IJ lines, FAILED OR SUCCESSFUL, order a CXR to assure no
intrathoracic complications.
Write a procedure note for all lines, failed or successful.
Thoracentesis
Indications: therapeutic relief of dyspnea, diagnosis of unknown effusion
Complications: pain, bleeding, infection, hemothorax, pneumothorax, costal nerve damage,
damage to liver or spleen
Equipment needed: thoracentesis kit, extra lidocaine, sterile gown, sterile gloves, glasses or
mask, sterile cap
1) Obtain consent and place it in the chart.
2) Have patient sit with their legs over the side of the bed and have them lean over with their
head resting on their arms on a bed side table this is the ideal position and the one they
will be in during the procedure
3) Remember: as they can no longer see what you are doing and you plan to stick a large
needle into them, explain what you are doing before it happens
4) Tap out the effusions using your hands and determine a safe spot to insert your needle; a
good choice is one-two ribs below the top of the effusion so long as this is above the 9th rib.
Also, you can and should use ultrasound to visualize the effusion.
5) Prep and dress yourself in a sterile fashion
6) Prep and drape the area in a sterile fashion as well
7) Open the kit and anaesthetize the area you plan to invade do this by making a small skin
wheal of lidocaine with the little needle, then anaesthetizing deeper with the larger needle
until you obtain the pleural fluid (unless the patient is very obese you should hit it with your
lidocaine needle)
8) Make a small nick in the skin with the scalpel provided in the kit
- 41 -
9) Connect the 60 cc syringe to the drainage needle/catheter set up and advance along the
now-numb path you have made; always aim for the bone itself when entering with the large
needle when you hit it, move ever so slightly upward until you pass just over the bone, as
the neurovascular bundle lies just below the rib.
10) When fluid is noted, gently slide the catheter forward over the needle while pulling the
needle back ever so slowly this will allow for passage of the soft, plastic catheter into the
pleural space without allowing much of the needle in to cause complications.
11) Remove fluid as needed, first filling the syringe for studies, then connecting the large
volume removal bag; take no more than 1.5L at a single time to avoid the risk of reexpansion pulmonary edema.
12) When you remove the catheter, have the patient hum the entire time you do so this will
avoid having them take a deep breath as the catheter is coming out and possibly sucking a
large amount of air into the pleural space, causing a pneumothorax. A simple Band-Aid
closes the hole you have made.
13) Write a procedure note.
Studies to be sent:
All fluid: cell count and differential, glucose, albumin, total protein, gram stain,
culture, LDH, pH. Cytology, AFB, ADA, amylase, cholesterol and triglycerides may be
indicated if you are looking for special causes of effusion.
Paracentesis
Indications: diagnose cause of fluid, look for bacterial peritonitis, therapeutic relief
Complications: pain, bleeding, infection, bowel perforation, liver/spleen laceration, persistent
leakage of fluid
Equipment needed: paracentesis kit, extra lidocaine, sterile gown, sterile gloves, glasses or
mask, sterile cap, Vacutainers for fluid collection (1L per container)
- you do not need a whole kit for a diagnostic-only tap, an 18 gauge needle and
a 60 cc syringe will work fine
2) Have the patient supine in the bed in a comfortable position.
3) There is no reason to perform a blind tap. Always use ultrasound to identify an optimal
pocket.The standard location is in the RLQ, just superior to McBurney's point if the liver
is large, you can use the same spot on the other side which is just as safe. Before inserting
the needle, assure that the area does not have any large, superficial veins running through it
with these patient's portal HTN and poor coagulation, these will bleed a lot if stuck so
avoid them.
4) Prep and dress yourself in a sterile fashion.
5) Prep and drape the area in a sterile fashion as well.
6) Open the kit and anaesthetize the area you plan to invade with your needle do this by
making a small skin wheal of lidocaine with the little needle, then anaesthetizing deeper
with the larger needle until you obtain ascetic fluid note: the peritoneum is highly
innervated, use a good deal of lido here.
7) Make a small nick in the skin with the scalpel provided in the kit.
8) Connect the 60 cc syringe to the drainage needle/catheter set up and advance along the
now-numb path you have made; always hold the needle itself with your left hand, about 1
- 42 -
inch above the skin this way when you pop through the peritoneum the needle doesnt
drive deeply in.
9) When fluid is noted, gently slide the catheter forward over the needle while pulling the
needle back ever so slowly this will allow for passage of the soft, plastic catheter into the
peritoneal space without allowing much of the needle in to cause complications.
10) Remove fluid as needed, first filling the syringe for studies, then connecting the
Vaccutainer to remove the large volume; for patient with cirrhosis or portal hypertension,
never take more than 6L without administering 50g-100g of Albumin 25% soln. during the
procedure.
11) Close the wound with a Band-Aid or cover with an ostomy bag if continued leakage is a
problem.
Studies to be sent:
All Fluid: cell count and diff, total protein, albumin, glucose, LDH, gram stain
and culture. AFB, cytology, fungal cultures may be needed depending on what you're looking
for.
Lumbar Puncture
Indications: infection, subarachnoid hemorrhage, assessing the etiology of a headache or fever
of unclear origin
Complications: pain, bleeding, infection, post-procedure headache, brain herniation, persistent
leakage of fluid
Contraindications: Alteration in mental status or focal neuro deficits should get a non-con CT
of the head first to assure no elevated intracranial pressure; if this is the case, start the
antibiotics before the CT and do the procedure immediately afterward never wait to start
antibiotics if you suspect bacterial meningitis for any reason!!
Equipment needed: LP kit, extra lidocaine, sterile gown, sterile gloves, glasses or mask,
sterile cap
2) Have the patient sit on the edge of the bed with upper body bent over a bedside table so the
spine is readily identifiable always mark your intended point of entry in this position
before laying them on their side. This spot is midline in the spinal column, at the level of
the pelvic brim both easily identifiable in the seated position. Mark it with the tip of a
retractable pen with the pen part in so a small circle is pressed into the skin (this wont
wash away like ink when you clean the area).
3) Lay the patient on his side.
4) Prep and dress yourself in a sterile fashion.
5) Prep and drape the area in a sterile fashion as well.
6) Open the kit and anaesthetize the area you plan to invade with your needle do this by
making a small skin wheal of lidocaine with the little needle, then anaesthetizing deeper
with the larger needle. You will need most or all of the lidocaine as the bony structures as
well as the ligamentum are all sensitive,
7) The key to this procedure is positioning: Get someone to help you keep the patient in asclose to a fetal position as you can get them with their head tucked toward their knees.
Keep your needle parallel to the floor the whole time and aimed slightly rostrally (toward
the head).
- 43 -
8) Slowly advance the spinal needle along your anesthetized track, always parallel to the floor;
you will feel several layers of 'popping' which are the ligaments, as you enter. The classic
'pop' of the dura mater as you enter the fluid itself is truly louder/more pronounced than the
others and feels distinctly different. It is a feeling. Don't be surprised if you don't get it the
first pass, the canal is often deeper than you think. If you miss, remove the needle almost all
the way out but keep it under the skin and redirect inferiorly to your last pass a common
mistake is going too high.
9) When you feel the pop, remove the stylette from the needle and wait 2-3 seconds for fluid
return. If clear fluid comes out, catch it. If an opening pressure is important, now is the time
to connect the pressure column to the back of the needle and get a measurement before any
fluid is removed. If you're not sure about needing an opening pressure, get one you'd hate
to have to do all this again. They have to be in the lateral decubitus position to check an
opening pressure.
10) You'll need about 2cc per tube with 4-5 cc recommended in the 3rd one to be saved for later
studies if needed.
11) Remove the needle when done and place a small Band-Aid over your hole. Instruct the
patient not to sit up at all for at least 1-2 hours and not to walk around for 3-4 hours to
decrease thE chance of a headache.
Studies to be sent:
Tube #1: cell count and diff; Tube #2: glucose, protein, VDRL; Tube #3: culture
and gram stain (any special studies should be added to this one including cytology, TB,
viral panels, crypto latex agglutinin); Tube #4: cell count and diff (again)
- 44 -
The Experienced Approach To:

Subspecialty Issues
Cardiology
Basic Tips/Random Stuff
1. Keep K+ above 4 and Magnesium above 2 (dont replace with ESRD or
ARF unless cleared by UPPER LEVEL).
2. Always compare ECGs to old.
3. If on cardiology, make copies of all ECGs obtained and an old one and bring
to rounds.
4. PO to IV furosemide is 2:1 (i.e. 40 mg of PO furosemide is 20 mg IV)
5. PO hydralazine to IV hydralazine is 4:1.
6. Toprol XL to metoprolol is 1.4 mg to 1 mg.
7. Remember you are not alone. Have a low threshold to call your resident and
fellow.
8. Hold beta blockers for patients getting stressed with exercise or dobutamine at
least 12 hours prior to procedure.
9. Generally, most patients admitted to the cardiology service with chest pain
should be NPO after midnight and be on a no caffeine (in case persantine
will be used), cardiac diet the day prior in anticipation of a stress test.
10. If a patient on the cardiology service has had a cath at an outside hospital,
obtain cath report from the other hospital (can call the cath lab at outside
hospital).
Chest Pain
Assess vital signs immediately, including O2 sat. If unstable, see patient
immediately.
ECG immediately and always compare to old. Obtain new ECGs every time
the pain changes or goes away- look to see if there are dynamic changes.
Get a CXR (portable is O.K).
1.
DDX: Acute coronary syndrome (unstable angina, NSTEMI, STEMI), Aortic
dissection, Pneumothorax, PE, GERD, Musculoskeletal, pericarditis/myocarditis,
pneumonia/pleurisy, PUD, esophageal spasm, esophageal rupture or tear (Mallory- 45 -
Weiss), candidiasis, herpes zoster, costochondritis (Tietzes syndrome), anxiety

(diagnosis of exclusion).
Directed History and Physical (rule out the bad stuff):
ACS: typically pressure type of pain, associated with shortness of breath,
nausea, vomiting, diaphoresis, radiation. Assess for risk factors including history of
prior MI, prior stenting procedures, DM, HTN, tobacco use, FHX, hyperlipidemia. MI
can present atypically in women and diabetics.
Aortic dissection: tearing pain that usually radiates to the back. Associated with
HTN, smoking.
Pneumothorax: Associated with COPD, trauma, central lines. Decreased breath
sounds, hyperresonance. Deviation of the trachea away from the side of the PTX,
hypoxia.
PE: dyspnea, tachycardia, tachypnea, pleuritic chest pain, hypoxia, A-a gradient,
possible hemoptysis.
2.
If angina is suspected: start Oxygen by NC, cardiac monitoring (i.e. telemetry),
NTG (0.4 mg SL q 5 minutes X 3; hold for SBP <100; If has an RV infarct/inferior MI
or has taken a 5 PGE antagonist- i.e. sildenafil- NTG may cause hypotension because
pre-load is reduced). Nitropaste or nitroglycerine gtt, ASA 325 mg PO if no
contraindications or has not yet been administered. Get a CXR (portable is O.K.) Labs:
Troponins (if the chest pain just started, the test may not be positive yet, so cycle them
more rapidly than q 6 hours; generally order troponins q6 hours X 3 or until they peak).
Chem.-7, mg, phos, coags.
3.
If PE is suspected: CT with PE protocol (generally contrast is not O.K. in a
patient with ARF/AKI, CKD, contrast allergy) or V/Q scan. If have high level of
suspicion, start anticoagulation right away as long as not contraindicated.
4.
PTX: If tension, immediately place a 14 gauge angiocath into the 2nd intercostal
space in the midclavicular line (Dont wait for the CXR). Otherwise, obtain CXR and if
PTX present and patient is stable call pulmonary fellow or attending (if on cardiology
service, call the fellow) for chest tube placement (sometimes small ones can be treated
with high flow oxygen).
5.
If aortic dissection is suspected: transfer to ICU, give beta-blocker to reduce
heart rate and BP. Get an emergent CT scan with dissection protocol or echo ASAP. If
patient is not stable, dont send down for a CT scan unless OKd by someone more
senior than yourself.
Lee TH, Goldman L. Evaluation of the patient with acute chest pain. N Engl J Med 2000; 342:
1187 95.
- 46 -
ACS
STEMI
Troponins
Positive
NSTEMI
Positive
Unstable angina
Negative
ECG changes
ST elevations or
new LBBB
May have ST
depressions, T
wave inversions, or
ST elevations that
dont meet criteria
for STEMI.
+/- May have ST
depressions, T
wave inversions, or
ST that dont
meet STEMI
Atrial Fibrillation
1.
If symptomatic or unstable (CP/ischemia, SBP <90), proceed with cardioversion
(ACLS).
2.
If relatively stable, control rate, anticoagulate. Cardioversion may be considered further
down the road.
3.
Causes:
P (pulmonary, pericarditis/myocarditis, pain, post-op)
I (Ischemia)- rare unless large RCA infarct.
R (rheumatic heart disease/valvular heart disease)
A (alcohol)
T (thyroid)
E (emboli)
S (sepsis/sick sinus)
Other things that dont fit with the mnemonic: fever, CHF, HTN, cardiomyopathy,
congenital heart disease, changes in myocardial wall stress, diabetes.
*Hint: Almost anything you can think of that makes the heart go fast (drugs,
alcohol withdrawal) or anything that causes the atria to be stretched out of
shape (COPD, infiltrative disease) can cause atrial arrhythmias.
4.
Rate control:
Be careful when using -blockers and Calcium channel blockers together, as the
combination may cause excessive AV nodal blockade.
-blockers: dont give if actively wheezing or if in decompensated heart failure.
- Metoprolol PO if rate is relatively slow and patient is stable
- Metoprolol 5 mg IV X 3
- Esmolol gtt- good to consider in ICU patients/potentially unstable
because half-life is about 9 minutes.
Calcium channel blockers:
- 47 -
- Contraindicated with VT, 2nd /3rd degree heart block without pacer,
severe hypotension, cardiogenic shock, bypass tracts.
- Diltiazem: bolus administration and if does not work, then gtt.
Digoxin: caution in renal failure. Less hypotension. Controls rate at rest, but not
with exercise. Slower onset. Remember to check levels.
Amiodarone: long term side effects. Consider in unstable patients or patients with
CHF who need rhythm control as has short-term calcium channel blocking and
sympatholytic effects.
5.
Anticoagulation
Consider the use of unfractionated or LMWH in hospital. No LMWH for those with
CrCl less than 30. Overlap with warfarin until INR 2 3 achieved.
6.
Cardioversion
If in afib for longer than 48 hours or cannot document length of afib, patient will
need to be anticoagulated for 4 weeks before cardioversion to decrease risk of
embolization during procedure.
If TEE shows no atrial thrombus can proceed directly to cardioversion.
Following cardioversion, patients will need to be anticoagulated for at least 3 - 4
weeks.
1.
Who gets stress testing?

Intermediate probability for having had angina, or suspected arterial blockage
2.
Stress testing can be divided into the stress and the modality used to look to see if there
is ischemia.
Stress: modalities used to stress the patient.
a) Treadmill:
Requires a fair amount of work, increasing every 3 minutes in
speed and grade. GOAL: 85% of MPHR (therefore no BB or ratelimiting agents).
Everyone who can walk should be put on the treadmill, this will
give you not only functional capacity, but also allow for
assessment of ischemia.
Contraindications: Unstable angina, ACS, inability to ambulate.
Imaging: can be linked with ECG, echo, ECG with myoview.
b) Dobutamine:
Dobutamine either starts at 5 or 10 mcg/kg/min, increasing every 3
minutes like the Bruce in 10 mcg increments to a max of 50. At
times atropine is used to further increase heart rate, so watch for
urinary retention post procedure. Goal: 85% of MPHR (therefore
no BB or rate limiting agents).Use in cases where persantine
(RAD) is contraindicated and treadmill not possible.
Imaging: used with either Myoview (cardiolyte) or echo. Caution in
those at risk for dysrhythmia (electrolyte abnormalities, known
dysrhythmias).
c) Persantine:
Stress Testing
- 48 -
Works by causing vasodilation, and a coronary steal phenomenon

(i.e. blood goes to good areas and not to bad areas). You should see
drop in BP with a small rise in HR. Generally, no ECG changes.
Goal: No need to achieve HR here, therefore okay to give all the
patients meds, including BB, except for theophylline. The
methylxanthines negate the effect of Persantine, this is why you
cannot have caffeine for 12 hours prior to the test. Imaging:
always use myoview since you are not going for heart rate.
Contraindicated in patients with bronchospasm. Reversed with 75
mg (3cc) of aminophylline which can be given via IV push.
d) Adenosine
Shorter acting than persantine. Can be used when you are
concerned about bronchospasm. Same mechanism of action as
persantine. Can be reversed with aminophylline.
Imaging: pair with a stress above.
a) ECG:
Will be used with all stress tests to monitor the patient. Can be your
definitive modality if the baseline ECG is normal. Cannot use ECG to
assess ischemia when a) LBBB b)Dig effect c)LVH with repolarization
or any other resting ST depression (can use it in RBBB). Goal: looking
for ST depression which comes in 3 forms, upsloping (normal up to 2
mm), horizontal (abnormal + at 1mm), downsloping (abnormal again 1
mm); also need to look for ST segment elevation. Will stop the test if ST
segment elevation, if ST depression with any sxs, or electrical instability.
Note J point elevation should come down with exercise, also there are
some people who get rate-related RBBB and even LBBB.
b) Echo:
Can be paired with dobutamine or with exercise. Looking for
inducible wall motion abnormalities. Need to know that the patient
has good windows (i.e. if they are really obese, not a good idea).
Great test for the possible false positive ECG.
c) Myoview (cardiolyte):
Imaging agent for use with persantine/adenosine, also can be used
with ETT when there are baseline ECG abnormalities. Also can be
used with dobutamine when the patient hits the target heart rate
Cardiac Catheterization
1)
2)
Indications: Initial reperfusion therapy for acute STEMI or new LBBB MI. Or in
NSTEMI with uncontrolled chest pain, hemodynamic instability or electrical instability.
If you suspect someone is going to get cathed, hold their metformin.
- 49 -
3)
Types of stents placed: Bare metal stent (BMS) vs. drug eluting stent (Taxuspaclitaxel or Cypher- sirolimus or similar).
4)
If cardiac catheterization is planned and pt has CKD or recent renal insult, consider
NAC (600 mg PO BID X 4 doses- 2 before and 2 after procedure) before and after the
procedure and IV fluid hydration 12 hours prior to the procedure and following the
procedure.
5)
Basic anatomy:
Left main gives off the Left circumflex (LCX) and the LAD. LAD branches
include the septal arteries and the diagonal artery. Obtuse marginal artery branches off
the LCX.
Branches of the right coronary artery include the SA node artery, conus artery, acute
marginal artery, posterior left ventricular artery (PLV), posterior descending artery
(PDA). However, if left dominant, the LCX may give off the PDA.
6)
Post-cath care:
Check access site for oozing, bleeding, hematoma, or bruits after procedure.
Check distal pulses: If pulses are diminished or unequal consider acute limb
ischemia. Remember the 5 Ps of acute limb ischemia: pain, pallor, pulselessness,
paresthesia, paralysis. Call fellow immediately if suspected, as this is a medical
emergency.
If a continuous bruit is present, an AV fistula may have formed. If a systolic bruit is
present a pseudoaneurysm may have formed. Order US, call fellow.
If bleeding present, hold pressure cephalad to puncture site as ateriotomy is likely 1
2 cm above skin entrance. If bleeding does not stop contact fellow.
Oozing, hold pressure for at least 10 minutes.
Hematoma: check hct, platelets. Order type and cross. Follow size-outline
border with pen.
If hct drops, consider retroperitoneal bleed and order non-contrast CT to rule this out.
If Cr increases within 48 to 72 hours of cath, consider contrast-induced nephropathy.
CHF
1. The most important thing to recognize is when a patient is cold and wet (see below) as they
likely need inotropes- we usually give dobutamine. Do not start this without speaking to your
resident and fellow.
Learn this chart and classify all your CHF patients into one of these four categories.
Perfused? Yes
Congested? No
Warm and Dry
Congested? Yes
Warm and Wet
Perfused? No
Cold and Dry
Cold and Wet
*Signs/Symptoms of Congestion: orthopnea, high JVP, Increasing S3, Loud P2, edema,
Ascites, rales, Hepatojugular reflux.
- 50 -
*Signs/Symptoms of Low Perfusion: Narrow pulse pressure, pulsus alternans, Cool forearms
and legs, Sleepy/obtunded, low serum sodium, acute renal failure, symptomatic hypotension.
Digoxin level in heart failure patients should be 0.8 to 1.1 and needs to be
renally dosed.
Hold beta blockers if patient is in cardiogenic shock, otherwise can the beta blocker
continue unchanged in most situations
Do not re-start beta blocker until patient is euvolemic.
When adding an ACE inhibitor start with captopril, which is dosed q 8 hours. If
tolerated increase dose at each interval (you can sign this out). See conversion table
below to figure out how much lisinopril to discharge someone on. Never discharge
someone on captopril, unless fellow/attending instruct you to do so because it is
difficult for patients to take a drug TID.
Captopril
6.25 mg PO TID
12.5 mg PO TID
25 mg PO TID
50 mg PO TID
Lisinopril
5 mg PO Daily
10 mg PO Daily
20 mg PO Daily
40 mg PO Daily
Nohria A, Lewis E, Stevenson LW. Medical Management of Advanced Heart Failure. JAMA
2002; 287: 628 640.
Heart Transplant Basics

1.
Rejection: 4 types.
1. Hyperacute: minutes to hours. Secondary to preformed antibodies to HLA, ABO
blood group antigens, endothelial antigens that cause immediate rejection. You will not
see this unless you are on surgery.
2. Acute Cellular: may occur at any time, but most common 3 to 6 months
following transplant. T cell mediated. Dx made via endomyocardial biopsy where
lymphocytic infiltrate is present along with macrophages with resultant
myocytolysis. Patient may have no symptoms. Usual treatment is IV or oral
steroids, monoclonal or polyclonal anti-lymphocyte antibodies.
3. Acute Humoral (vascular): days to weeks following transplant. Less common
than acute cellular (7%). Mediated by antibodies against donor HLA or endothelial
cell antigens. Highest risk are women, high panel reactive antibody screen, CMV +,
sensitization to OKT3. DX on endomyocardial biopsy with immunoglobulin and
complement in the vessels or by swollen endothelial cells. Commonly associated with
severe LV dysfunction. Treat by intensifying immunosuppression and either by
modulating antibody production or removing antibodies (cyclophosphamide, IVIG,
plasmapheresis).
4. Chronic: months to years. Likely a combination of humoral and cellular.
Manifests as graft atherosclerosis with myointimal proliferation.
- 51 -
2.
The Immunosuppression Scheme:

Induction: Intense perioperative immunosuppression X 7 to 14 days. Lympholytic
agents (ATGAM, thymoglobulin). Increasingly, IL-2 receptor antagonists are being
used.
Maintenance: Combination of an antiproliferative agent (mycophenolate or
azathioprine), a calcineurin inhibitor (cyclosporine or tacrolimus) and steroids. Early
on, higher cyclosporine levels (300 350) and TAC levels (10-15) are desired. Later (2
years out), Cyclosporine levels should be about 200 and TAC levels 5 10. Prednisone
is generally tapered off in about 50% of transplant patients 6 to 12 months posttransplant.
Rejection: Intensity and type of regimen depends on severity of rejection and
whether T or B cell mediated.
3.
Anti-lymphocyte Agents: used in induction and steroid resistant rejection

ATGAM: polyclonal anti-lymphocyte Abs produced in horses.
Thymoglobulin: polyclonal anti-lymphocyte Abs produced in rabbits.
Muromonab CD3 (OKT3): murine antibody that recognizes epsilon chain of the
CD 3 molecule on T cells, rendering T cells unable to respond to antigen challenge or
bind to target cells.
4.
Anti-cytokine Receptor Antibodies: bind to subunit of IL-2 receptor, preventing

binding of IL-2 to the IL-2 receptor, thus inhibiting the proliferation of T cells.
Daclizumab and Basiliximab are the two on the market.
the
Lindenfeld J, et al. Drug therapy in the heart transplant recipient part I: cardiac rejection and
immunosuppressive drugs. Circulation 2004; 110: 3734 3740.
Advanced ECG reading

1.
LITANY OF CATEGORIZATION
The mean rate of the QRS complexes:
- Slow rate
- Normal rate
- Fast rate
The duration of the dominant QRS complexes
- Narrow (normal in adults 70-113 msec)
- Wide (>120 msec)
The spacing of the R-R intervals
- Regular
- Irregular
2.
REGULAR NARROW-COMPLEX TACHYCARDIAS

Take home points
- Adenosine can be used to help differentiate narrow complex tachycardias. Do
not use adenosine in wide-complex tachycardia that is irregular; use very
carefully in transplant patients (if at all) and patients on dipyridamole.
- Remember the differential: AVNRT is the most common and should
break with adenosine. The relationship between the QRS and P-waves is
important for narrowing the differential.
- 52 -
- The key to arrhythmia diagnosis is how it starts and how it ends, run a
continuous rhythm strip when giving adenosine.
Step 1: First make sure that the rhythm is narrow (QRS < 120 ms) or matches
the patients previous baseline QRS morphology and that it is a tachycardia (rate >
100).
Step 2: Is the dominant rhythm regular or irregular?
Regular narrow-complex tachycardia differential:
1. Sinus tachycardia
2. Atrial flutter
3. AV nodal reentrant tachycardia (AVNRT)
4. AV reentrant tachycardia (AVRT) (ORT)
5. Atrial tachycardia (AT)
6. Accelerated junctional tachycardia
7. Sinus node reentry tachycardia
Note: a very fast irregular rhythm (fast atrial fibrillation) can look like a regular
narrow complex tachycardia.
Approach:
What is the rate?
100-140: this will likely be sinus tachycardia, atrial tachycardia,
or an accelerated junctional tachycardia. Remember that the upper limit of
normal for sinus tachycardia is 220 age. Also remember that an
accelerated junctional tachycardia is usually at a rate of 100-120.
140-160: think of atrial flutter with 2:1 block or atrial
tachycardia, less likely AVNRT or AVRT.
160-220: think of an AVNRT, AVRT, AT.
Find the P waves:
No P waves seen: consider accelerated junctional tachycardia for
slower rhythms and AVNRT for faster rhythms.
P waves present and PR < RP (= P wave just before the QRS):Is
the P upright in lead I and the inferior leads (II, III, aVF). If the answer is
yes, youre probably dealing with a sinus tachycardia. If the answer is no,
youre probably looking at an atrial tachycardia. Remember that slow
sinus rates come from inferior portion of the sinus node, and fast sinus
rates more superiorly; hence, the P-wave becomes more peaked in the
inferior leads at higher sinus rates.
P waves present and PR > RP (= P wave just after the QRS): if
the rate is slower (100-120), think of an accelerated junctional tachycardia
with retrograde P waves. If the rate is fast (> 160), think of AVRT.
P waves present and going at a rate of 300: think of atrial flutter.
Clues for specific rhythms:
Sinus tachycardia: upright P wave in I and the inferior leads and
normal PR interval. The maximum rate is usually 220-age. In most cases,
the rhythm speeds up and slows down gradually.
Atrial flutter: look for saw-tooth waves in the inferior leads (II,
III, aVF). The rate is usually approximately 150 and there are P waves
going at a rate of 300.
- 53 -
AVNRT: look for the pseudo S wave in lead II and the pseudo
R wave in lead V1.
AVRT: the P-wave can have a variety of relationships with the
QRS.
AT: looks like a sinus tachycardia except that the P waves are
not upright in both I and II and the PR interval can be shortened or
prolonged.
Short RP, Long RP what are people talking about?
Short RP tachycardias
-most commonly AVNRT or Orthodromic Reciprocating Tachycardia (ORT)
-also can be atrial tachycardia with a long 1 AV block (usually at faster
rates)
Long RP tachycardias
-most commonly atrial tachycardia
-can also be uncommon AVNRT, ORT, or junctional tachycardia (PJRT)
A
- 54 -
P in R Tachycardia
-most commonly AVNRT
-Two major presentations
1) No discernable P waves (P wave buried in the QRS complex) (A)
2) Pseudo S waves (B):
a retrograde P wave blends with the end of the QRS complex in the
inferior leads, producing a pseudo S wave and Pseudo R
3) (C): A P wave blends with the end of the QRS complex in lead V1
producing a pseudo r wave.
3.
IRREGULAR NARROW COMPLEX TACHYCARDIAS

Irregularly Irregular Rhythm (four main causes):
1. Atrial Fibrillation: Most common cause. Chaotic atrial depolarization (atrial rate
~600 bpm) likely from pulmonary veins. Because of decremental nature of AV node,
ventricular rate 180s-200s
2. Atrial Flutter with variable block: Flutter waves in the inferior leads
3. Multi-focal atrial tachycardia: Often seen in patients with concomitant pulmonary
disease. Diagnostic criteria mandates 3 distinct P wave morphologies.
4. Frequent Premature atrial contractions
Regularly Irregular Rhythm: Grouped beating (clusters of mathematicallyspaced QRS complexes, separated by pauses of identical duration). Wenckebach
periodicity should always be considered either from AV block or during junctional
tachycardia with exit block (Digoxin toxicity).
1. 2nd degree AV Block, type I (Wenckebach) or Type II (Mobitz II)
2. PVCs in a repetitive pattern (trigeminy, quadrigeminy)
3. PACs in a repetitive pattern
4.
WIDE COMPLEX IRREGULAR TACHYCARDIAS

Take home points:
- These are rare, history of WPW or if patient has a known accessory
pathway, think afib with competing conduction down AP and some down
HP network (varying degrees of pre-excitation).
- Always note whether a pre-existing bundle is present, AFIB with a BBB
is likely the most common cause of an irregular WCT
- Principal: Wide complex supraventricular rhythms (excluding bundle
branch blocks) result from ventricular activation either partly or
completely from accessory pathway conduction. The electrical signal will
propagate across the myocardium from cell to cell using gap junctions etc.
This is in contrast to narrow complex QRS complexes which use the
slick His Purkinje system and therefore depolarize efficiently across the
myocardium in a fast manner. For example, a PVC has such a wide
QRS because the initial depolarization takes more time to spread across
the ventricle because it does not use the Purkinje system.
- 55 -
Steps:
1. Do all wide QRSs within any single lead have essentially identical
morphology?
If yes probably an existent RBBB or LBBB
If noExclude rate-related bundle branch block
5.
REGULAR WIDE COMPLEX TACHYCARDIAS

VT or not VT, this is the question
Take Home Points:
- Assume VT till proven otherwise, remember follow ACLS
- Remember what a bundle branch block looks like.
Helpful hints:
1. Remain calm, ensure what you are looking at it real, not motion
artifact.
2. If patient is hemodynamically unstable, follow ACLS guidelines (likely
VTSHOCK, remember some sedation).
3. If you shock a patient and the rhythm does not change, likely not VT.
4. Try to get a baseline ECG to see what you were starting with.
5. If the patient has a history of MI, likely VT.
6. Is there a history of WPW?
7. Remember what a bundle branch looks like, does the rhythm look like
a bundle, if not then likely VT.
8. Distinguish between a wide QRS and an elevated ST segment.
9. Apply the Brugada criteria, you are trying to distinguish between SVT
with aberrancy and VT.
Causes (Memorize this list):
1. ST with BBB: Leading cause of regular WCT. Looks like a bundle and
is fast and regular. Can see P waves with each QRS
2. Supraventricular tachycardia with BBB: May not see P waves. Use
Brugada criteria. Looks like a bundle. A history of SVT and a bundle
helps in the dx.
3. Ventricular Tachycardia: May see retrograde V-A conduction.
Brugada criteria.
4. Antidromic reciprocating tachycardia: History of WPW with AP
-should see retrograde P waves
References
Evans, Tom ECG Interpretation Cribsheets Ring Mountain Press, Corte Madera, CA available
through the UCSF bookstore.
Ganz LI, Friedman PL. Supraventricular tachycardia. N Engl J Med. 1995 Jan 19;332(3):16273.
Delacretaz E. Supraventricular tachycardia. N Engl J Med. 2006354;10:1039-51
- 56 -
Post cardiac arrest hypothermia

Current ACLS guidelines recommend mild hypothermia for comatose patients
resuscitated from prehospital cardiac arrest. This recommendation is based on two trials
published in the NEJM in 2002. These studies found an increased number of survivors and
improved neurologic outcomes with a number needed to treat of around 5.
All of our hospitals have protocols in place to help with this process. The general
process is that the patient is sedated and paralyzed (to prevent shivering) and then cooled with
cooling blankets to a core temperature between 32-34C. The temperature is maintained in this
range until 24 hours after the start of cooling, at which point the patient is allowed to gradually
rewarm over 6-10 hours.
Common complications include bradycardia, hyperkalemia, coagulopathy and
overshoot to below target temperature. The bradycardia is usually well tolerated and does not
require treatment. Electrolyte and coagulation abnormalities are monitored closely with
frequent lab checks.
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Endocrinology
Diabetic Ketoacidosis (DKA)

1.
Signs/Symptoms: polyuria, polydipsia, polyphagia, abdominal pain, nausea, vomiting,

dizziness, and confusion. Kussmauls respirations (i.e. rapid, large-volume breathing),
acetone or fruity breath. Tachycardia and orthostasis due to intravascular volume
depletion. Coma, respiratory arrest, death.
2.
Potential Causes: Infection is the most common precipitating factor, followed closely by
inadequate use of insulin. Alcohol abuse, myocardial infarction, pancreatitis, eating
disorders, trauma, hormonal changes (e.g., during pregnancy), undiagnosed diabetes, drugs
(e.g. corticosteroids), medication noncompliance.
3.
Initial Evaluation:
History: Look for precipitating factor(s)
Exam: Urgent evaluation with vital signs and orthostatics
Lab: BMP - calculate anion gap and corrected Na+, ABG, serum and/or urine ketones,
CBC+diff. Consider ECG, CXR, UA, troponins, pregnancy test, lipase, blood and urine
cultures.
4.
Treatment (see Appendix A. DKA Treatment Protocol)

Volume resuscitation
- An average of 6 L IVF is needed in the first 24 hr to replete
intravascular volume
- Initial bolus of NS 1-2 L followed by continuous infusion to achieve
euvolemia
Electrolyte repletion -- Follow electrolytes and AG every 2 to 4 hr
- Potassium - may be elevated initially but will fall after initiating
insulin
If <3.3 mEq/L on presentation, replete prior to initiating insulin
therapy. Otherwise supplementation should be initiated for K+ <5
mEq/L.
- Sodium - may be falsely low from hyperglycemia
Calculate actual serum Na+ by adding 1.6 mmol/L for every 100
mg/dL glu >100 mg/dL
- Phosphorous - may be elevated initially. Insulin therapy will cause rapid
intracellular shift; replete if <1 mg/dL
Glucose control
- Follow glucose level every hour
- Initiate insulin drip (for bolus and initial drip rate see flowsheet in
appendix or use the University of Colorado Hospital (UCH)
standardized order set for DKA/HHS.
- 58 -
- Add dextrose (D5) infusion when glucose falls below 250 mg/dl to
avoid hypoglycemia and to provide carbohydrate nutrition. Patient may
still require continued volume resuscitation.
Ketone resolution: follow ketones Q4hr initially and treat with fluids and
insulin as above. Ketonemia takes longer to clear than hyperglycemia. Clearance of
ketones should not be used as an indicator of response to therapy if the lab uses the
nitroprusside method to measure urine or serum ketones since it does not measure the
most prevalent acid in DKA (-OH-butyrate).
5.
Transition to subcutaneous insulin

Once DKA is resolved, time transition to coincide with reinstitution of PO
intake
Administer long-acting insulin 1-2hours PRIOR to stopping IV insulin
infusion. Start rapid-acting insulin at the next meal.
To calculate insulin doses
- Use outpatient insulin regimen OR
- Calculate Total Daily Dose (TDD) estimating from IV Insulin
infusion as follows: TDD = add up insulin used in the last 6 hr of
IV insulin gtt, multiply by 4 for 24 hr requirement, then take 80%
of that calculation. 50% of TDD given as Glargine once a day and
50% administered as rapid-acting insulin (e.g. Lispro) split among
3 meals. OR
- Estimate using body weight: If patient is overweight, initial TDD
= 0.3-0.5 units/kg/day. If patient is thin, initial TDD = 0.1-0.3
units/kg/day.
UCH has standardized orders for subcutaneous insulin that can be used
Strongly consider Endocrine/Diabetes physician team consult to recommend
dosing strategies or adjustments in insulin therapy.
Call inpatient Diabetes Clinical Educator as needed for patient education
Hyperglycemic Hyperosmolar Syndrome (HHS)

1. Signs/Symptoms: altered mental status or coma. Elevated serum osmolality without ketosis.
Often with h/o type 2 diabetes and insulin resistance. Serum glucose often much higher,
with more severe volume depletion than in DKA, leading to higher mortality rate (15%
versus <5%).
2. Potential Causes: similar to DKA. Often seen in elderly persons without easy access to PO
fluids
3. Initial Evaluation: same as for initial DKA evaluation
4. Treatment (see Appendix B. HHS Treatment Protocol or UCH standardized order set for
DKA/HHS
Volume resuscitation: Similar to DKA except that more IVF resuscitation is
typically required
Electrolyte repletion: see DKA section 4.b.
Carefully control rate of correction of serum osmolality and sodium
- 59 -
Serum osm should decrease by <3 mOsm/kg H2O/hr

Glucose control: see DKA section 4.c.
Monitor closely for signs of cerebral edema (mortality 70%) and follow these
guidelines to correct glucose and serum Osm levels:
Keep serum glucose between 250-300 mg/dL until serum Osm <315 mOsm/kg
Adding dextrose when glucose reaches 300 mg/dL may reduce risk of cerebral
edema
5. Transition to subcutaneous insulin see section I.A.5. above
Hypoglycemia
1. Signs/symptoms: Anxiety, diaphoresis, confusion, tremor, fatigue, loss of consciousness
2. Potential Causes: Drugs (sulfonylureas, insulin, alcohol), infection/sepsis, hepatic or renal
failure, adrenal insufficiency, malignancies (lymphomas/leukemias via IGF-2
secretion), insulinoma, prior gastric surgery, factitious.
3. Initial Evaluation and Treatment:
Confirm serum blood glucose <70 mg/dL
If patient is not diabetic, not on glucose-lowering diabetes agents or insulin and is
asymptomatic, do not treat the hypoglycemia. Recheck blood glucose prn
For patients on glucose-lowering diabetes agents or insulin, treat immediately as
follows:
1. If patient can take PO, give 15 grams of carbohydrate (4 oz of fruit
juice OR non-diet soda OR 15 grams glucose gel).
2. If patient unable to take PO and has IV access, give 1/2 amp D50 IV
3. If patient unable to take PO and has no IV access, give 1 mg (1 amp)
glucagon IM
4. Check BG in 15 minutes & repeat above until BG is 100mg/dL
5. D10 IV infusion may be required for persistent hypoglycemia
unresponsive to above
Search for underlying cause. Common causes of inpatient hypoglycemia are
sudden changes in nutritional status (e.g. NPO) without adjustment in insulin
dosing, and use of outdated insulin regimens such as Sliding Scale Regular
Insulin.
4. Call Endocrine consult for recurrent/persistent hypoglycemic episode(s). Labs helpful for
workup of recurrent hypoglycemia include glucose, C-peptide, insulin, sulfonylurea
level (all while hypoglycemic)
Hyperglycemia
(with or without a prior diagnosis of diabetes)
**Adjust insulin doses DAILY as needed, based on BG control and the amount of extra
insulin given in the previous 24 hr for high BG**
- 60 -
1. The Basics
Total Daily Dose (TDD) = sum total of all insulin scheduled to be given during a 24
hr period
Initial TDD for type 2 diabetes: 0.3 0.4 units/kg/day. For type 1, use 0.3 0.8
units/kg/day
50% of TDD is given as basal insulin, 50% as rapid-acting insulin distributed
across 3 meals
a) Basal Insulin = long acting insulin required to maintain normal BG
overnight and while NPO
b) Mealtime Bolus Insulin = rapid-acting insulin used to cover mealinduced rise in glucose
Patients on intensive insulin therapy use a carbohydrate to insulin (C:I) ratio for
meals. C:I ratio means that the patient takes 1 unit of rapid-acting insulin for every X
grams of carbohydrate eaten in a meal. Calculate C:I by dividing the correction factor
(see below) by 3.
- Correction Factor = rapid-acting insulin used pre-meal to correct
hyperglycemia
- CF means that 1 unit of rapid acting insulin will decrease the BG by X
mg/dl. CF is calculated by dividing the TDD into 1650.
- For patients on standard insulin therapy, correction factors can be used
in addition to meal dose insulin to customize hyperglycemia treatment
scales.
2. Treatment
If known diabetes, review outpatient diabetes management with patient and adjust
if needed
Fingerstick BG QAC and QHS (q4-6 hr if NPO); q1-2 hr on insulin drip. Goal <180
mg/dL
Goals: avoid hypoglycemia, severe hyperglycemia, and electrolyte abnormalities
- Critically ill patients: < 140 mg/dl, tight control 80-110 mg/dl may be
associated with increased mortality
- Noncritically ill patients: premeal BG levels between 90130 mg/dl, all
fasting BG < 180 mg/dl
Establish plan for treatment of hypoglycemia
- If patient is alert, treat with simple sugars (1/2 cup juice or 15 g glucose)
and recheck BG
Adjust scheduled insulin regimen accordingly. Do not discontinue basal
insulin.
Oral medications: hold metformin and sulfonylureas upon admission in most cases
3. Injectable insulin
Strongly consider IV insulin drip in the ICU since critically ill patients do not
absorb SQ insulin as well and require tighter glucose control
History of outpatient insulin use?
1. Continue basal insulin (glargine/Lantus, NPH) at outpatient doses or
cut in if NPO
- 61 -
2. Continue bolus insulin for meals using rapid acting insulin

(humalog/Lispro, novolog/Aspart, glulisine/Apidra)
3. If on insulin pump, continue in the hospital. Consult Diabetes Clinical
Educator
4. Start CF based on equation in previous section
No history of outpatient insulin use?
1. Initiate scheduled-dose insulin (basal +/- mealtime bolus) based on
previous days insulin requirements. May use weight to estimate TDD
see previous section
2. Initiate CF using rapid acting insulin see previous section
4.
Insulin Adjustment Pearls

If BGs for past 24 hr were mostly >180, incorporate the extra insulin
administered for hyperglycemia into the new scheduled dose insulin
regimen
If there was a BG <80 in the past hr, reduce total daily dose by 10-20%
If AM fasting BG is elevated, check a 3 am FSBG to make sure this is not
rebound hyperglycemia BEFORE increasing basal insulin dose
If AM fasting BG rises by >30 mg/dL above bedtime BG, increase basal insulin
If lunchtime BG is elevated, increase breakfast bolus. If dinnertime BG is
elevated, increase lunch bolus. If bedtime BG is elevated, increase dinner bolus
5. Call Diabetes Clinical Educator or Endocrine service with questions or consults

6. Discharge planning
Diabetes education prior to discharge
Restart oral medications unless contraindicated
Schedule outpatient evaluation and follow-up
Every patient admitted for DKA or HHS MUST be discharged on an insulin
regimen
References
Hirsch IB, Braithwaite SS, Verderese CA. Practical management of inpatient hyperglycemia. (monograph you
received at beginning of residency)
Kitabchi AE, et al. Hyperglycemic Crises in Adult Patients With Diabetes. Diabetes Care 29:2739-2748, 2006.
American Diabetes Association. Standards of Medical Care in Diabetes 2007. Diabetes Care 2007;30(Supp.
1):S27-S31. Section VIII. A.
Thyroid Storm
1.
Signs/Symptoms: Fever, tachycardia, tachypnea, arrhythmias, CHF, abdominal pain,

nausea, vomiting, diarrhea, hyperkinesis, psychosis, coma, goiter (not always present).
2.
Potential Causes: Often in patients with unrecognized/inadequately treated thyrotoxicosis

and a precipitating event: thyroid or nonthyroid surgery, infection, trauma, PE, MI, acute
iodine load.
3.
Initial Evaluation:
History: personal or family history of thyroid abnormalities, goiter, recent
iodine contrast, agitation, recent weight loss
- 62 -
PE: goiter +/- bruit, stare, lid lag, proptosis, tachycardia, agitation, tremor, brisk
relaxation phase of reflexes and hyperreflexia
Lab: TSH (undetectable), free T4 (high) OR total T4 and T3 resin uptake (both high),
total T3 (often high), CBC, BMP, LFTs.
Diagnosis: Labs alone are insufficient. If you have a high index of suspicion use
the Burch score which takes into account body temperature, CNS changes,
GI/hepatic dysfunction, and cardiovascular dysfunction (CHF, atrial-fib) to
determine need for aggressive intervention (Appendix C). Consult Endocrine.
Delayed/inappropriate treatment may result in death.
4.
Treatment:
First, reduce the heart rate and stabilize patient:
1. Esmolol drip - load with 250-500 g then 50-300 g/kg/minute
2. Support the circulation IVF
Once stable, decrease thyroid hormone synthesis:
1. Propylthiouracil (PTU) up to 800 mg/day in divided doses (PO, PR,
NG). Also blocks conversion of T4 to T3
2. Methimazole (Tapazole) up to 80 mg/day QDor BID (PO, PR, NG)
Inhibit thyroid hormone release give 1 hr after first dose of anti-thyroid drug
1. SSKI 5 drops PO q8h OR
2. Lugols solution 10 drops PO q8h
Block T4T3 conversion with steroids (?relative adrenal insufficiency)
hydrocortisone 100 mg IV q8hr
Finally, search for and treat the precipitating condition
Myxedema Coma
1.
Signs/Symptoms: altered mental state, hypothermia, precipitating event. Obvious physical

signs of hypothyroidism, respiratory depression, bradycardia, hypotension, low-voltage
non-specific ST changes on ECG, anorexia, abdominal pain, distention, constipation (may
be severe causing ileus & megacolon; carries a 20-30% mortality rate)
2.
Potential Causes: Complication of long-standing untreated or undertreated hypothyroidism

with a precipitating event: infection, MI, CVA, sedatives, trauma, GI bleed
3.
Initial Evaluation:
History: personal or family history of thyroid or pituitary disease, fatigue,
constipation, depression, weight gain
PE: Hypothermia, bradycardia, edema, dry skin, delayed relaxation of reflexes, loss
of lateral third of eye brows
Lab: TSH (high), Free T4 (low or undetectable) OR total T4 and T3 resin
uptake (both low), total T3 (often low), BMP, CBC, Cort stim, CPK
4.
Treatment:
- 63 -
Rapid institution of parenteral thyroid replacement is necessary in true myxedema

coma
Proper dosing and form of replacement (T4 alone, T3 alone, T4 + T3) is
controversial. CALL ENDOCRINE
5. Treatment of precipitating cause (e.g. broad-spectrum antibiotics)
Supportive care
Intensive care admission
Cautious IVF
Ventilatory support
Passive rewarming (active rewarming may produce peripheral vasodilation and could
contribute to hypotension or shock)
Hydrocortisone (often a degree of impaired adrenal function) until you verify intact
adrenal function with Cortisol Stimulation Test (see below)
Euthyroid Sick Syndrome/Nonthyroidal Illness

1. Defining the condition
Changes in thyroid function tests that occur in patients with a variety of
nonthyroidal illnesses including infections, malignancies, MI, trauma, surgery,
inflammatory conditions, and starvation
NOT a primary thyroid disorder. Results from changes in peripheral thyroid
hormone metabolism and transport induced by the nonthyroidal illness
2. Management:
NO data demonstrating recovery or survival benefit from thyroid hormone
treatment, so it is NOT recommended. Look for signs/symptoms of
hypothyroidism, and if in doubt, consult Endocrine.
Ross D. Thyroid function in non thyroidal illness. Up-to-date 2006
Thyroid Pearls
Figuring out a dose for thyroid hormone replacement:
- Full replacement dose for hypothyroidism: 1.6 mcg/kg PO QD (actual
body weight)
- Equivalent IV LT4 dose ~ 80% of PO dose
Factors that affect interpretation of TSH
Glucocorticoids and dopamine IV gtt can lower TSH values
TSH levels vary diurnally and are highest at night
- 64 -
Adrenal insufficiency
1.
Signs/symptoms - fatigue, weakness, anorexia, nausea/vomiting, abdominal pain,

orthostatic hypotension, cognitive: mild memory loss to psychosis, weight loss,
hyperpigmentation (for Addisons), hyponatremia, hyperkalemia
2.
Potential causes
Primary (adrenal)
Secondary/tertiary
(pituitary/hypothalamic)
Autoimmune adrenalitis
Infection TB, fungal, CMV, HIV
Bilateral adrenal hemorrhage
Adrenomyeloneuropathy
Metastases (lung, breast, GI)
Meds ketoconazole, rifampin
3.
Withdrawal from exogenous

glucocorticoids
Severe head trauma
Sheehans syndrome
Pituitary apoplexy
Pituitary or hypothalamic tumors
Infiltrative sarcoid, histiocytosis X
Infections TB. Histoplasmosis
Autoimmune lymphocytic
hypophysitis
Cranial irradiation
Initial evaluation
The usual diurnal variation of cortisol is lost in critical illness, so draw a
random cortisol
A random cortisol of <5 mcg/dL in a sick patient
8 am cortisol of <5 mcg/dL in noncritically-ill patients is diagnostic for adrenal
insufficiency
A cortrosyn stimulation test (cort stim) should be performed for definitive
diagnosis:
- Draw a baseline cortisol. In sick patients, anytime; in non critically-ill
patients, draw at 8 am
- Administer 250 mcg Cortrosyn (synthetic ACTH) IV/IM
- Re-draw cortisol at 30 and 60 minutes
- A stimulated cortisol of >20 mcg/dL excludes adrenal insufficiency
except in secondary or tertiary adrenal insufficiency developing within 2 weeks prior
(usually from pituitary trauma). In septic shock, increment of <9 mcg/dL is consistent
with functional adrenal insufficiency
- Hydrocortisone is the synthetic version of cortisol, so a patient who has
received hydrocortisone within 10 hr will have a cortisol level that may appear
normal or elevated
Suspect acute adrenal crisis in patients who are hypotensive despite aggressive fluid
resuscitation, or in septic shock
Suspect adrenal insufficiency in any patient whose supraphysiologic regimen of
glucocorticoids has been interrupted (prednisone >5 mg QD or dexamethasone >0.5
mg QD >1 month)
- 65 -
4.
Treatment for adrenal crisis: the 5 Ss (salt, sugar, steroids, support, search)
1. Volume resuscitation with D5NS
2. Dexamethasone 4 mg IV/PO if you want to give steroids before the cort stim test
has been performed OR hydrocortisone 100 mg IV q8h if you have already drawn the
baseline cortisol and/or performed the cort stim since hydrocortisone administration will
interfere with testing
3. Steroids can be tapered to maintenance doses after 1-3 days if the precipitating
event or associated illness is under control
4. ICU supportive care
5. Search for precipitating cause
References
Endocrine Secrets, 4th edition, 2005, chapter 31: Adrenal insufficiency
Harrisons Principles of Internal Medicine online (http://hslibrary.ucdenver.edu/ebooks/, Part
14, chapter 321: Disorders of the adrenal cortex)
www.endotext.org Adrenal Disease and Function chapter 13: Adrenal insufficiency
Pituitary Apoplexy
1.
Definition: hemorrhage or infarction of the pituitary gland, often in a preexisting adenoma

but may occur with head trauma, on anticoagulation, or immediately postpartum.
2.
Symptoms: Sudden and severe headache, visual and cranial nerve disturbances including
bitemporal hemianopsia, confusion, symptoms of 2 adrenal insufficiency
(N/V/hypotension).
3.
Lab/studies: Head CT scan will usually show pituitary enlargement or hemorrhage. MRI is
more sensitive for detecting adenoma and hemorrhage. Draw a pituitary panel LH, FSH,
estradiol or testosterone, alpha-subunit, IGF-1, cortisol, prolactin, TSH and free T4
4.
Management
Medical: Dexamethasone 4 mg IV BID for cerebral edema and adrenal insufficiency
Surgical: If headache and visual disturbances do not improve on steroids,
transsphenoidal pituitary decompression is indicated
Severe Hypertriglyceridemia
1. Signs/Symptoms: Often asymptomatic but may present with acute pancreatitis. May include
symptoms of the chylomicronemia syndrome: abdominal pain (can be chronic), malaise,
dyspnea, peripheral neuropathy, and memory loss. Abdominal tenderness, eruptive
xanthoma (usu. upper back, buttocks, extensor surfaces of extremities), lipemia
retinalis, hepatosplenomegaly.
2. Potential Causes: Usually an underlying genetic disorder of hypertriglyceridemia
complicated by one or more secondary factors. Possible secondary factors (more
common factors in bold):
- 66 -
Medications
Oral estrogens/SERMs
Glucocorticoids
HCTZ
HAART
Bile acid sequestrants
-blockers
Loop diuretics
Cyclosporine
Tacrolimus
Antipsychotics
Propofol
Cis-retinoic acid
Behavioral
Alcohol use
High-fat meal(s)
Metabolic
Uncontrolled DM (1 or 2)
Insulin resistance
Pregnancy
Hypothyroidism
Proteinuria (nephrotic range)
Hepatocellular disease
Cushings syndrome
Male hypogonadism
3. Initial Evaluation Search for secondary factors

History: alcohol use, recent food intake, medications, pregnant?
Labs: glucose, TSH, UA (for proteinuria), LFTs, hCG (females), lipase (if
suspect pancreatitis)
4. Treatment
NPO (if acute pancreatitis), or zero-fat diet (if asymptomatic/incidental diagnosis)
this is the most important treatment. Hypertriglyceridemia will not resolve if fat intake
continues
Eliminate or treat any identified secondary factors; insulin treatment of poorlycontrolled diabetes can be especially helpful.
Once pt. eating, initiate gemfibrozil 600mg BID or fenofibrate 160 mg QD
(renal-dose if needed)
Follow daily TG until goal (TG < 400 mg/dL) is achieved. Diet can include fat
(<20%) when TG <1000 mg/dL, and can be advanced to 30% when TG < 400
mg/dL
Severe Hypercalcemia
1. Signs/Symptoms: Confusion, Lethargy, Anorexia, Nausea, Constipation, Polyuria,
Arthralgias, Weakness, HTN, renal insufficiency, RTA, shortened QT interval
2. Potential Causes: VITAMINS TRAP
V = Vitamins
I = Immobilization
T = Thyrotoxicosis
A = Addisons disease
M = Milk-alkali syndrome
- 67 -
I = Inflammatory disorders
N = Neoplastic-related disease
S = Sarcoidosis
T = Thiazide Diuretics (Drugs)
R = Rhabdomyolysis
A = AIDS
P = Pagets disease, Parenteral nutrition, Pheochromocytoma, Parathyroid disease
3. Initial Evaluation
Serum BMP, calcium, albumin, phos, intactPTH, 25(OH)vitamin D, and
possibly 1,25(OH)_ vitamin D. If iPTH is low, draw PTH-related peptide
Follow Ca x Phos product Q2-4 hrs
4. Treatment
Saline infusion (250-1000 mL/h)
Bisphosphonate IV
Zolendronic Acid 4 mg IV over 15 min OR Pamidronate 30-90 mg IV over 2 hrs
Consider dialysis if severe
Severe Hypocalcemia
1. Signs/Symptoms: numbness, tingling, muscle cramps, depression, psychosis, tetany and
seizures, QT prolongation, papilledema
Chvosteks sign tap on facial nerve and look for upper lip twitch
Trousseaus sign inflate BP cuff and look for hand twitch
2. Potential Causes: hypoparathyroidism, hypoalbuminemia, hyperphosphotemia (rhabdo,
tumor lysis, renal failure), hungry bone syndrome (recent treatment for
hyperparathyroidism), chelation (citrate/transfusions), Mg depletion (decreased PTH
secretion, PTH resistance), Vitamin D deficiency, sepsis/severe illness, chemo drugs
3. Initial Evaluation
Serum BMP, Ca++, albumin, phos, Mg++, intact PTH, 25(OH)vitamin D. Ionized
Ca++ (in severe illness)
Correct Ca++ (Cacorrected = Cameasured + [(4-albumin) x 0.8)]
Urine Cr, Ca++ and Mg++
4. Treatment Treat symptoms, NOT a number!! Pts. with chronic hypoparathyroidism
often live at a much lower serum Ca level
Calcium carbonate PO (500 mg PO Q2-4 hr)
Active Vitamin D (calcitriol 0.25 0.5 micrograms PO BID)
Calcium gluconate IV bolus (1-2 gm IV bolus)
Calcium gluconate IV gtt call Endocrine prior to starting gtt!!
Magnesium sulfate 2 gm IV (if Mg low; follow with oral Mg)
Hypernatremia/Diabetes Insipidus See Renal Section

Key points:
Must have elevated serum Osm to be diagnosed with DI. If serum Osm is high normal
and DI is suspected, confirm diagnosis with a water deprivation test; call Endocrine.
Differentiate between central and nephrogenic
- 68 -
Monitor I/Os carefully and ensure pt has access to free water
Hyponatremia/SIADH See Renal Section, Onc Section

Key points:
Patient should be euvolemic even though they have excessive Total Body Water
Should have serum Osm <280 mOsm/kg and urine Osm >100 mOsm/kg
Look for underlying cause of SIADH and exclude pituitary, adrenal and thyroid
dysfunction before diagnosing
Appendix A. DKA Treatment Protocol
Kitabchi AE, et al. Hyperglycemic Crises in Adult Patients With Diabetes. Diabetes Care 2006;29:2739-2748.
** Protocol for the management of adult patients with DKA. *DKA diagnostic criteria: serum
glucose >250 mg/dl, arterial pH <7.3, serum bicarbonate <18 mEq/l, and moderate ketonuria or
ketonemia. Normal laboratory values vary; check local lab normal ranges for all electrolytes.
After history and physical exam, obtain capillary glucose and serum or urine ketones
(nitroprusside method). Begin 1 liter of 0.9% NaCl over 1 h and draw arterial blood gases,
- 69 -
complete blood count with differential, urinalysis, serum glucose, BUN, electrolytes, chemistry
profile, and creatinine levels STAT. Obtain electrocardiogram, chest X-ray, and specimens for
bacterial cultures, as needed. *Serum Na+ should be corrected for hyperglycemia (for each 100
mg/dl glucose >100 mg/dl, add 1.6 mEq to sodium value for corrected serum sodium value).
Appendix B. HHS Treatment Protocol
** Protocol for the management of adult patients with HHS. HHS diagnostic criteria: serum glucose
>600 mg/dl, arterial pH >7.3, serum bicarbonate >15 mEq/l, and minimal ketonuria and ketonemia.
Normal laboratory values vary; check local lab normal ranges for all electrolytes. After history and
physical exam, obtain capillary glucose and serum or urine ketones (nitroprusside method). Begin
1 liter of 0.9% NaCl over 1 h and draw arterial blood gases, complete blood count with differential,
urinalysis, serum glucose, BUN, electrolytes, chemistry profile and creatinine levels STAT. Obtain
electrocardiogram, chest X-ray, and specimens for bacterial cultures, as needed. Adapted from ref. 1.
*Serum Na+ should be corrected for hyperglycemia (for each 100 mg/dl glucose >100 mg/dl, add
1.6 mEq to sodium value for corrected serum sodium value).
Kitabchi AE, et al. Hyperglycemic Crises in Adult Patients With Diabetes. Diabetes Care 2006;29:2739-2748.
- 70 -
Appendix C. Scoring system for thyroid storm. Only for use in hyperthyroidism
Nayak B, Burman K. Thyrotoxicosis and thyroid storm. Endocrinol Metab Clin N Am

2006;35:663-686.
- 71 -
Gastroenterology
Gastrointestinal Bleed
Ddx: Upper: swallowed blood, gastritis/esophagitis, Mallory-Weiss tear, gastric or
esophageal varices, portal hypertensive gastropathy, ulcer, mass, Dieulafoys lesion
Lower: colitis, ischemic bowel, AVM, mass, hemorrhoids
Key history points: Acute vs. chronic, number of episodes, quality of emesis or bowel
movements, prior bleeding history, risk factors such as liver disease, alcohol use, or
NSAID/anticoagulant use
Physical exam: Vital signs (first to change, Hct may be normal for 8 to 24 hours), orthostasis
((+) with 20% loss), stigmata of chronic liver disease, abdominal pain/peritonitis, rectal
exam
Nasogastric lavage: Negative lavage does not rule out upper bleed unless there is bilious
return, G-tubes can be used instead if present, lavage is not contraindicated with varices,
can be used to monitor for active bleeding. Consider in patients with significant rectal
bleeding since a rapid UGIB can present as a LGIB as well.
Initial orders:
Vital signs at least every 4 hours, initial orthostatic VS

NPO
Insert two large bore IVs (at least 18 gauge)
Hct: repeat on assessment and every 4 hours
PTT/PT/INR
BUN: suggestive of GIB if elevated in absence of renal disease
Type and cross
Platelet count
ECG: especially if history of cardiac disease
IVF: NS or LR
Nasogastric tube: lavage until clear, low intermittent suction
Consult gastroenterology
Special Treatments:
Coagulopathy: Correct with FFP or vitamin K for goal INR < 1.5, platelets for goal > 50
Variceal bleed: Octreotide 50 g IV bolus followed by 50 g/hr continuous infusion for 48-72
hr, endoscopy, balloon tamponade or TIPS if endoscopy fails
PUD: Start with high dose PPI (80 mg IV bolus then 8mg/hr), endoscopy
Antibiotic prophylaxis: Reduces mortality as well as bacteremia, pneumonia, SBP, and UTIs
in cirrhotics with UGIB. Start with IV therapy daily (e.g., ceftriaxone) and then transition to
oral twice-daily norfloxacin or ciprofloxacin once GI bleeding is stabilized. Treat for a total of
7 days.
Prokinetics: Consider erythromycin 250 mg IV prior to endoscopy to improve visualization
Evaluation of Ascites
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Ddx of ascites by serum-ascites albumin gradient (SAAG):

(SAAG = serum albumin ascites albumin)
High gradient/portal HTN (> 1.1 g/dl)
Spontaneous bacterial peritonitis
Cirrhosis
Alcoholic hepatitis
Cardiac ascites
Mixed ascites
Fulminant hepatic failure
Budd-Chiari syndrome
Portal vein thrombosis
Veno-occlusive disease
Myxedema
Fatty liver of pregnancy
Low gradient (<1.1 g/dl)

Peritonitis from TB or rupture
Peritoneal carcinomatosis
Protein-losing enteropathy
Nephrotic syndrome
Bowel obstruction or infarct
Pancreatic ascites
Biliary ascites
Postoperative lymphatic leak
Serositis (connective tissue diseases)
Paracentesis:
Indications:
Contraindications:
Obtaining fluid for analysis

Decreasing respiratory or abdominal distress
Bowel obstruction or distension
Significant coagulopathy
Please note that paracenteses can be performed in the vast majority of patients with
ESLD despite elevated INRs and thrombocytopenia; transfusion of blood product to
reverse the coagulopathy before the procedure is not recommended in these patients.
Complications: secondary bacterial peritonitis, hemorrhage, abdominal wall hematoma,
ascitic fluid leak, bowel perforation, hypotension, renal failure, bladder perforation
Orders:
Gram stain
Aerobic and anaerobic cultures
Cell count and differential
Albumin
Total protein (If SAAG > 1.1, AFTP > 2.5 c/w cardiac ascites, > 2.5 c/w
cirrhosis)
+/- glucose, AFB, cytology, triglycerides, bilirubin
Adjustment for traumatic tap:
Subtract 1 WBC per 750 RBC

Subtract 1 PMN per 250 RBC
Albumin for large volume paracentesis: none if <5 liters, if >5 liters is to be
removed, give 50 gm (25% Solution)
Spontaneous Bacterial Peritonitis (SBP)
Ascitic fluid PMN count > 250 cells/mm3:

- Empiric antibiotic therapy (e.g., cefotaxime 2g IV q8h)
- Albumin infusion 1.5gm/kg body weight initially and 1.0 gm/kg on day 3
Ascitic fluid PMN count < 250 cells/mm3 with signs/symptoms of infection:
- 73 -
- Empiric antibiotic therapy while awaiting cultures results

- Can hold on albumin reasonably in this circumstance
After treatment for SBP, patient will require life-long prophylaxis
Geriatrics
1.
Guiding principles:
Less is more (i.e,. risk/benefit ratio as you age)
Evaluate function first (ADLs and IADLs)
The problem is often a side effect of a medication
With delirium think of infection and medications as the most likely causes in
hospitalized patients
Geriatric syndromes (falls, incontinence, weight loss) are generally
multifactorial
2.
Medications to avoid in the elderly:

Beers List Website: http://www.dcri.duke.edu/ccge/curtis/beers.html
Benzodiazepines/high dose sleepers
Diphenhydramine (Benadryl)
Amitriptyline
Metoclopramide (Reglan)
Ketorolac (Toradol)/Indomethacin (and other NSAIDs)
3.
Sundowning and agitation:

Reorientation is important!
Low dose haloperidol, 0.5-1 mg IV is a helpful adjunct
Think of alcohol (or BZD) withdrawal - dont assume that old folks dont drink
Look at the medication list and consider infection (especially UTI)
4.
Medicare:
Eligibility: 65, ESRD, ALS, disabled, > 40 quarters of medical-eligible work
by person or spouse, permanent resident
Part A (automatic, do not need to apply): Covers hospital, SNF, hospice (does
not pay room and board; Medicare pays for care and meds), some home health
care.
Part B (must apply, optional, costs extra): Covers 80% of doctor visits, home
health care, other services.
Part C: Medicare HMOs (alternative to Parts A & B).
Part D: Prescription drug plan. Automatic, but benefits are only available
through private companies at prices of $20 to $50 per month or through
Medicare HMO.
5.
Nursing Homes:
Two types of care: skilled/subacute rehab or custodial/long term care
Skilled care paid by Medicare and requires a 3 day hospital stay for them to pay
Custodial care is for patients who still need nursing care but are no longer able
to rehab. Payer is predominantly self-pay or Medicaid
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If patient has assets, patient (or spouse) must pay until poor enough to qualify
for Medicaid. This is termed spending down.
If Medicaid pays, they take the residents social security check
Cost of Aging Who Pays. Susan T Bray-Hall, M.D.
Hematology/Oncology
Anemia
Anemia is a common problem that you will be called with frequently. It is best to develop a systematic
way of responding to and evaluating the causes of anemia.
One helpful mental image for anemia is to liken it to a child splashing around in a bathtub. The reason
the tub isnt full (anemia) could be one of three broad categories:
1) the faucet is off and no water is going in (decreased production)
2) the child is splashing all the water out (destruction/hemolysis)
3) the plug in the bottom of the tub has been pulled out (blood loss)
In all cases it is correct to consider each of these three categories when evaluating a low hematocrit,
taking into account the historical information you know about the patient to help guide your thought
process.
Common causes of anemia by Production/Destruction/Loss categories
Cause to Consider
Associated Conditions
Decreased Production
Destruction/Hemolysis
Cancers
Myeloproliferative Disorders
Chronic Inflammatory Dis.
Acquired Intrinsic
PNH
liver disease
vitamin E deficiency
Hereditary Intrinsic
thalassemias
spherocytosis
G6PD
Warm Antibody Mediated
HIV
EBV
SLE
idiopathic (50-70%)
Cold Antibody Mediated
mycoplasma
EBV
lymphoproliferative d/o
Drugs
PCN, cephalosporin, sulfa
NSAIDs
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Substrate Deficiencies
Iron
B12
folate (rare but possible)
Mechanical Trauma
TTP/HUS
eclampsia
malignant HTN
cardiac valves
severe burn patients
march trauma
Other Infections
sepsis of any cause
acute viral infections
syphilis
malaria
babesiosis
clostridial infections
Other
splenomegaly
hypophosphatemia
transfusion reactions
snake/spider bite
Blood Loss
TCAs, phenothiazines
thiazides
sulfonylureas
GI bleeding
GU bleeding
trauma
surgery
repeated phlebotomy
menstruation
pregnancy
Common causes of anemia by MCV
Microcytic (MCV < 80): for w/u order ferritin, TIBC, smear, reticulocyte count.
1. Iron Deficiency: ferritin is low (usually < 30), TIBC is high. But, ferritin is an acute phase
reactant and may be elevated in inflammatory states. In early stages, MCV is also normal.
Normocytic (MCV 80 100): check reticulocyte count.
1. Decreased reticulocyte count: aplastic anemia/red cell aplasia, myelophthisis, MDS, anemia
of chronic disease, iron deficiency, chronic kidney disease, hypersplenism, hypothyroidism,
multiple myeloma, HIV/AIDS, Mixed (e.g. iron deficiency with B12 deficiency).
2. Increased reticulocyte count: acute blood loss, hemolysis.
Macrocytic (MCV >100)
1. Megaloblastic (hypersegmented neutrophils): B12 deficiency, folate deficiency, drug
induced (azathioprine, MTX, chemotherapy, hydroxyurea).
2. Non-megaloblastic: alcohol, liver disease, hypothyroidism, reticulocytosis, aplastic anemia,
MDS, drugs (AZT, anticonvulsants).
Hint: Hospitalized patients can drop their Hct by 1% per day by blood draws, so be aware.
Pancytopenia
P- Pernicious anemia/PNH
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I- Infection (HCV, EBV, Parvo B19, HIV, leishmaniasis, brucellosis), Infiltrative (lymphoma,
myeloma, carcinoma, hairy cell leukemia)
G- Granulomatous diseases (TB, Sarcoid)
H- Hypersplenism (CLL, lymphoma, ESLD)
A- Aplastic Anemia
M- Marrow infiltration/suppression (MDS, myelofibrosis, alcohol, toxins, medications).
Thrombocytopenia
1. Common in hospitalized patients and is defined as a platelet count less than 150,000/mcL.
2. The evaluation and management of thrombocytopenia should proceed in parallel when
confronted with this problem, as some disorders that cause thrombocytopenia do not cause
bleeding (HIT, some forms of DIC), and the transfusion of platelets in these disorders can worsen
the clinical course (TTP/HUS/HIT/DIC).
3. Immediate action is necessary when a patient is bleeding, requires an invasive procedure, or the
absolute platelet count falls to less than 10,000/mcL.
4. A peripheral smear is the first test that should be reviewed to rule out platelet clumping, or
pseudothrombocytopenia. If platelet clumping is present, blood should be sent to the lab in a
sodium citrate rather than an EDTA tube.
5. A focused physical examination should be directed at the vital signs, ocular fundi,
subconjunctival areas, nasal and oral cavity, extremities, and rectum to look for evidence of
retinal or subconjunctival hemorrhage, epistaxis, oral or cutaneous petechiae, raised ecchymotic
areas at heparin injection sites, and occult blood in stool.
6. Although there is some conflicting data, the presence of fever, physical exam evidence of minor
bleeding, and anemia appear to be risk factors for bleeding at a given level of thrombocytopenia.
Wet purpura, or mucosal hemorrhage, appears to be a stronger risk factor for clinically serious
bleeding than dry purpura, or petechiae and ecchymoses.
7. A brief differential should be considered: DIC, sepsis, HIT, TTP, massive blood transfusion
coagulopathy, post-transfusion purpura, pulmonary embolism, and medications.
8. Concurrent anemia and thrombocytopenia as a result of microangiopathic hemolytic anemia
occurs in DIC/TTP/HUS.
9. A review of clinical data should focus on the following: reason for DIC? (sepsis, pregnancy
complication, trauma, malignancy), vital sign abnormalities/known site of infection to suggest
sepsis, recent heparin administration (HIT development requires 5 days of continuous heparin
therapy in any form or heparin administration in the prior 100 days with new heparin exposure),
predisposing factors for TTP (recent organ transplant, transplant medications, clopidogrel), recent
transfusion of any kind, and a scan of the medication list for chemotherapy, antimicrobials (e.g.
piperacillin), H2 blockers, and GPIIb/IIIa antagonists.
10. Assessment of the temporal trend in platelet count and its relation to acute illness and medication
initiation is helpful in prioritizing the differential diagnosis.
Discontinue medications that inhibit platelet function such as aspirin, NSAIDs,
thienopyridines, GPIIb/IIIa antagonists. Ancillary laboratory studies that should be obtained
include an INR, PTT, full CBC, fibrinogen level, peripheral smear if not done initially, and
LDH.
11. A patient with HIT will require discontinuation of heparin and initiation of alternative
anticoagulation (lepirudin, bivalirudin). This disorder can be difficult to diagnose definitively in
the acute setting and typically hematologic consultation is necessary to assist in management.
12. Patients with TTP/HUS benefit from rapid institution of plasmapheresis.
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13. There is no consensus regarding management of DIC, although treatment of the underlying
disorder appears to be effective in most cases.
14. Drug-related thrombocytopenia requires discontinuation of the medication.
15. Thrombocytopenia related to sepsis typically resolves with treatment of the underlying infection.
16. A safe absolute platelet count has not been defined for many of the invasive procedures we
perform on hospitalized patients including central venous catheterization, lumbar puncture,
thoracentesis, paracentesis, and arthrocentesis. A good general dictum is to raise the platelet
count to greater than 30,000/mL for medical procedures and to greater than 50,000/mL for
surgical procedures.
17. Randomized clinical trials support the practice of withholding platelet transfusion in stable
oncology patients receiving chemotherapy until the platelet count falls below 10,000/mcL.
18. When to transfuse a patient with ITP is controversial but most experts would use 5-10,000/mcL
as the cutoff.
19. For more complicated patients, safe platelet count cutoffs and therefore transfusion triggers are
less well defined. Expert opinion currently recommends a primary prophylactic threshold of
20,000/mcL and a threshold of 50,000/mcL for those with active bleeding or prior to invasion.
20. Recent studies show that only 50% of ICU patients with a variety of disorders will have an
appropriate rise in the platelet count post transfusion, and therefore the risks and benefits in this
population need to be weighed carefully in the absence of a clear evidence-based strategy.
21. Platelets can be given as pooled platelet packs from multiple donors or as apheresis units from a
single donor. Some hospitals use only apheresis units while others use either six or ten unit
platelet packs, with variable numbers of actual platelets administered.
22. Dosing of platelets is entirely empiric, and a reasonable practice is to give an apheresis unit or
platelet pack and recheck the peripheral platelet count 1-4 hours later to determine whether more
units are required to achieve the desired platelet count. In general, an appropriate response to
platelet transfusion is an increase in the post transfusion count of between 10-50,000/mcL.
Fever & Neutropenia Hot n Low

Fever in the neutropenic cancer patient is one of the most common oncologic emergencies. If left
untreated, febrile neutropenia has a mortality rate as high as 70% at 48 hours. In the early days of
chemotherapy use, infections were responsible for 75% of the treatment-related mortality. Aggressive
cytotoxic therapy such as induction chemotherapy for leukemia has been made possible in large part
by the availability of effective broad-spectrum antibiotics.
Definitions
Neutropenia: Granulocyte count (polys + bands) < 500 or <1000 and expected to decline to <500
Fever: single temperature >101F or >/= 100.4 F for at least an hour
60% of patients with F+N are actually infected
16-20% with counts <100 are bacteremic
Sources of infection
Endogenous: translocation from GI tract due to mucosal damage from chemotherapy
Catheter-related
Environmental: food, water, air
Skin! Look everywhere! Check peri-rectal area but DO NOT DO rectal exam
Evaluation
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History: S+Sx of infection - classic signs of infection may be absent or subtle

Afebrile patients with signs or symptoms compatible with infection should be treated empirically
Estimate length of neutropenia: what kind of chemotherapy and how long ago?
Most common sites: gums, pharynx, esophagus, lung, perineum and anus, skin, catheter sites
Avoid rectal examination, suppository use
Blood cultures from all catheter ports and one set from periphery, UA, culture other sites as
indicated
CBC with diff, LFTs, lytes, CXR
Treatment
Begin therapy within 4 hours of fever spike
Empiric therapy: there are multiple effective regimens as seen below. Monotherapy is cheaper,
safer and as effective as dual therapy in uncomplicated F + N. Dual therapy offers synergy against
GNR and may be preferred in sicker patients or those with focal infections requiring broader
coverage (pneumonia).
Regimen must always include anti-pseudomonal coverage
Consider need for gram + coverage (see criteria below)
Remember to consider allergies, renal function and dose adjust
Initial Empiric Therapy of Fever/Neutropenia (Clinical Infectious Diseases 2002; 34:730-751)
Commonly used regimens:

Monotherapy: Cefepime, Imipenem, Meropenem. These all have excellent gram-negative coverage
as well as coverage of S. viridans, S. pneumo and Staph. Ceftazidime can be used but has no
gram-positive coverage.
Dual therapy: Aminoglycoside or quinolone + one of the agents above.
Add vancomycin if needed to any of the above combinations if criteria are met.
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If Afebrile
If Febrile
Continue initial antibiotics
Panculture, CXR
Examine lines, low threshold to
change
Consider adding vancomycin for
empiric line coverage
If source found: adjust abx as needed

If no source found:
if low risk switch to oral therapy (cipro +
amox/clavulanate) and consider discharge
if high risk, continue antibiotics
All have excellent gram-negative coverage as well

as coverage of S. viridans, S. pneumo and Staph.
Ceftazidime can be used but has no gram-positive
coverage.
Dual therapy: Aminoglycoside or quinolone + one
of the agents above.
Add vancomycin if needed to any of the above
combinations if criteria are met.
Duration of therapy
If afebrile by day 3:
ANC >500 for 2 consecutive days stop abx 48
hours after afebrile and ANC > 500
ANC <500 by day 7:
Low risk: stop abx when afebrile for 5-7
days
High risk: continue abx
If persistent fever:
ANC >500 stop after 4-5 days and reassess
ANC < 500: continue for 2 weeks and
reassess. Stop if no disease sites identified.
(Clinical Infectious Diseases 2002; 34:730-751)
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If still febrile on day 4-5

Repeat cultures, CXR
If progressive disease, change
antibiotics
Consider adding empiric fungal
coverage
(particularly for high risk-see risk
assessment above)
Empiric Therapy of Fever and Neutropenia

Initial Questions:
Is patient high risk?
High risk: ANC < 100, evidence of focal infection, inpatient when F + N develops, outpatient with
serious coexisting medical condition, clinically stable outpatient with uncontrolled cancer,
neutropenia expected > 10 days
Low risk: well appearing, no focal evidence of infection, no co morbidities, duration of neutropenia
< 7 days, etc. Two recent RCT have shown oral cipro/amoxacillin-clavulanic acid is as safe and
effective as IV antibiotics in selected low-risk inpatients. Outpatient therapy with vigilant
observation may be an option in selected patients, but this is not yet widely practiced.
Is vancomycin needed?
Indications include: cellulitis, severe mucositis, quinolone prophylaxis, colonized with MRSA,
obvious catheter infection, hypotension/sepsis, pneumonia
Consider anaerobic coverage for:
Gingivitis, rectal abscess, typhlitis
Use of GCSF
Shortened duration of neutropenia and length of hospital stay and cost savings in some studies
No effect on mortality
Consider if:
Worsening of course because of prolonged neutropenia expected: pneumonia, hypotension, severe
cellulitis, sinusitis, systemic fungal infection, multi-organ dysfunction due to sepsis
Antibiotic prophylaxis
Routine prophylaxis not recommended due to concern for resistance
Consider if: pt expected to be profoundly neutropenic (<100), significant lesions to mucous
membranes (periodontal disease, mucositis), catheters, etc.
Bactrim and quinolone prophylaxis well studied: reduce infection rate but not necessarily mortality
Goal: treat only high risk patients for as short a time as possible
Antiviral prophylaxis with acyclovir or ganciclovir and antifungal prophylaxis with fluconazole are
indicated in patients undergoing allogeneic BMT.
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Tumor Lysis Syndrome

The tumor lysis syndrome is an acute metabolic emergency resulting from massive cell lysis caused by
rapid cell turnover or rapid response to cytotoxic therapy. Cell lysis leads to hyperkalemia,
hyperuricemia and hyperphosphatemia. Hormonal and renal regulatory mechanisms as well as
phosphate binding cause serum calcium to fall. Hypoglycemia, hyponatremia, adrenal failure and lactic
acidosis can also be seen. The syndrome can develop spontaneously in patients with acute leukemia or
aggressive lymphoma (Burkitts), but is usually precipitated by treatment of hematologic malignancies
in which there is a large tumor burden. It can occur during treatment of some solid tumors, although
much less commonly.
Major dangers are:
Acute renal failure, which can be caused by uric acid nephropathy or nephrocalcinosis
Prior to allopurinol, 10% of patients treated for acute leukemia got uric acid nephropathy
Now hyperphosphatemia causing calcium-phosphate uropathy is more common
Cardiac arrhythmias from hyperkalemia or hypocalcemia
Management:
Prophylaxis
Pre-treat for at least 2 days before chemotherapy with:
Allopurinol or rasburicase
Aggressive hydration (with NS) to maintain urine output > 2.5L/day
Alkalinization is no longer recommended as it can enhance calcium/phosphate deposition
Do not begin therapy until Cr <1.6 and UA < 8.0 (sometimes dialysis is needed before
proceeding with therapy.)
Do not treat hypocalcemia unless pt is symptomatic (Increased risk of CaPO4 ppt).
Once therapy has begun
Check electrolytes, Ca, Mg, Po4 BID until stable
Use PRN:
Phosphate binders: lower serum phos either with calcium carbonate (taken with meals) or
aluminum based binders (amphogel, alternagel) if calcium-phosphorus product >60
Kayexalate
Dialysis
Spinal Cord Compression

Prevalence: 5-10% of cancer patients and in 10% of these it is the presenting complaint
Most common causes: lung, prostate, breast, multiple myeloma
Most common sites: thoracic spine (70%), LS spine (20%), cervical (10%).
Multiple sites common in breast, prostate; lung almost always a single site.
Classification:
Epidural spinal cord compression (most common)
Vertebral body metastasis, paravertebral soft tissue mass, epidural mets
Epidural cauda equina compression
Leptomeningeal mets
Intramedullary mets
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Presentation:
96% have pain as first symptom
Loss of bowel/bladder function, motor weakness, sensory deficits are late findings
Localized back pain worse with movement and also with lying supine (unlike disc disease)
Usually present for months before neurologic symptoms appear
Can have radicular pain but less common: unilateral or bilateral
Examination
Palpate vertebrae, flex and extend cervical/lumbar spine
Thorough neurologic examination including rectal tone and perineal sensation may localize lesion
Can check post-void residual. If PVR > 150cc suspect bladder dysfunction.
Example algorithm for work-up of back pain in patients with cancer:
Radicular pain only, normal neurologic examMRI within 24h

Pain + radiculopathy Admit, MRI within 24h then LP
Brachial plexopathyMRI, consider admission. If paraspinal mass, dexamethasone and XRT
Pelvic plexopathy MRI or CT, consider admission (if cannot walk), LP. If paraspinal mass,
dexamethasone and XRT
Myelopathy (upper motor neuron signs) MRI, admit, dexamethasone, XRT
Treatment
Pain control: narcotics plus NSAIDS, consider gabapentin/amitriptyline for neuropathic pain,
pamidronate.
Corticosteroids: help decrease cord edema, pain, preserve neurologic function, improve overall
outcome.
If high grade lesion and neurologic signs of compression consider high-dose therapy (one welldone RCT showed that 81% remain ambulatory vs., 63% with lower doses) 100 mg IV bolus then
24 mg QID x 3 days then taper over 10 days. Significant complication rate from steroids- discuss
with an attending before using high-dose.
If low grade lesion or not appropriate for high dose, use 10mg IV bolus then 4mg PO QID tapered
over 14 days.
Radiation therapy: equal success rate to surgery with similar duration of improvement.
Indications for surgery (laminectomy): to establish diagnosis, progression despite radiation therapy,
vertebral instability- recent data suggest early surgical intervention superior
Breast, prostate, myeloma, lymphoma have 70-88% chance of responding to radiation alone with
70-85% resolution of back pain.
Prognosis
Depends on primary tumor type
If patients treated while still ambulatory, there is an 89-94% chance of remaining ambulatory
If paraplegic, 10% chance of regaining ambulation
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Brain Metastasis
25% of patients with cancer die with intracranial mets
Lung, breast, melanoma most common
Melanoma, germ cell, renal cell most likely to hemorrhage
DDx of mass lesion: metastasis, intracerebral hemorrhage, brain abscess, hydrocephalus, subdural
hematoma, radiation necrosis
Location: multiple mets (50%) cerebral hemispheres (37%), frontal (12%) posterior fossa (14%)
Presentation
Focal signs (hemiparesis, hemisensory deficit, aphasia, etc) 50%
Headache 33%
Mental status change 22%
Seizure 20%
Hemorrhage into tumor: sudden seizure or focal neurologic symptoms followed by headache
Herniation syndromes
Examination
Thorough neurologic exam including fundoscopy and gait evaluation.
Work-up
CT and MRI are equally effective
CT with contrast has higher yield
If single metastasis or no lesions on CT, obtain MRI with gadolinium
MRI more sensitive for small mets and better for visualizing posterior fossa
Treatment
If symptomatic, treat with corticosteroids to lessen brain edema (see section on cord compression)
If multiple mets: whole brain radiation
If a single met and controlled extracranial disease can consider surgical excision prior to wholebrain radiation.
Selected patients with hydrocephalus may benefit from a shunt
If patient presents with seizure start phenytoin
Patients with no history of seizure have a 10% chance of developing one. Prophylactic
anticonvulsants considered for high-risk patients (frontal mets, focal hemispheric symptoms) but
the data does not support prophylaxis.
Hypercalcemia
Most common paraneoplastic syndrome. Prevalence is 10% in patients with advanced cancer.
Responsible for 40% of all hypercalcemia
Lung, breast, head and neck, renal and multiple myeloma most common causes
Etiology
Humoral hypercalcemia of malignancy (HHM) 80% of cases
Squamous cell lung ca, H+N ca, renal cell
PTHrP produced by tumor has homology with parathyroid hormone.
- 84 -
Causes hypercalcemia by increased bone resorption, decreased bone formation, increased renal
tubular resorption of Ca, increased excretion of phosphate, and increased urinary cyclic AMP.
Lymphoma can rarely produce vitamin D
Local osteolytic hypercalcemia (LOH) 20% of cases
Myeloma, leukemia, lymphoma, breast and other solid tumors
Caused by local production of hormones, cytokines which activate osteoclasts causing bone
resorption
In patients with breast cancer 50% have HHM and 50% have LOH
Presentation
Malaise, fatigue, confusion, anorexia, bone pain, polyuria, polydipsia, weakness, constipation,
nausea, vomiting
Severe hypercalcemia: confusion, lethargy, coma, and death.
Etiology
Primary
hyperparathyroidism
Humoral
hypercalcemia
Local osteolytic
Hypercalcemia
Calcium
High
Phos
Low
1,25 vit D
High or
normal
PTH
High or normal
Very
high
High
Low
Low or
normal
Low or
normal
Low to normal
Normal
Low or normal
Diagnosis
Check Ca, albumin, renal function, PO4, alk phos, EKG
R/o bony mets
Normal PTH and low PO4 suggest HHM
Normal PTHrP, normal PO4 in presence of bone mets suggests LOH
Check PTH prior to treatment (on admission).
Treatment
Moderate (12-13.5 mg/dL)
IV NS for hydration-at least 2-4 liters/day
Once euvolemic begin furosemide to prevent volume overload- only if able to carefuly match I/Os
Pamidronate 60-90mg IV over 2 hours (or Zolendronate-more effective, more expensive)
This therapy reduces Ca to normal in 80% by 7 days
If LOH, glucocorticoids may inhibit bone resorption and cytokine production
Severe (>13.5 mg/dL)
In addition to above add calcitonin 4-8 U/kg SQ qid
If refractory, gallium 200mg/meter squared in 1 liter IV QD x 5 d-careful if AKI
Plicamycin can be considered (toxic to liver, kidney, BM)
Prognosis
Median survival of patients with hypercalcemia only 1-3 months
Treatment may not be indicated if patient has end-stage disease unless it will improve quality of
life
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SIADH
Definition
Euvolemic hypotonic hyponatremia. Serum Na < 135, serum Osm < 280, urine Na >20 urine Osm
>100
Etiology
Production of ectopic ADH by tumor cells
Associated with many tumors. 38% of patients with small cell lung ca (this group has a poor
prognosis)
Cytotoxic drugs: vincristine, cyclophosphamide, cisplatin, ifosfamide, levamisole, melphalan
Other drugs: SSRIs, antineuroleptics, amitriptyline, carbamazepine etc.
High dose cyclophosphamide is a common cause of SIADH because:
Drug enhances ADH release and effect.
Patients receive large amounts of IVF to prevent hemorrhagic cystitis
Nausea can also stimulate ADH release
Other DDx: Renal, adrenal, thyroid insufficiency, CNS disturbance, major surgery
Presentation
Most often asymptomatic
Anorexia, depression, lethargy, irritability, confusion, muscle weakness, marked personality
change.
If Na < 110: seizure, areflexia, pseudobulbar palsy, coma, and death.
Treatment
Treat underlying disease/remove offending drug
Asymptomatic hyponatremia
Fluid restriction alone may be enough (1-1.5L day)
If patient requires IVF switch all IVF to NS and consider lasix to keep I = O
Liberalize salt in diet
Correct hypokalemia if present
If hyponatremia persists/worsens consider:
Lasix and salt tablets
Demeclocycline or lithium (decrease collecting tubule response to ADH)-watch for renal toxicity
Urea 30g day to increase solute excretion (if above doesnt work)
Symptomatic or severe hyponatremia
If mental status change, NA <115 in consider 3%NS, correcting of total Na deficit over 24h no
faster than 0.5meq/L/h. More rapid repletion occasionally indicated with severe cases.
Patients with mild chronic SIADH who do not respond to therapy may have reset osmostat and do
not need further treatment
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Superior Vena Cava Syndrome

Definition
SVC obstruction can result from compression, obstruction, or thrombosis of the SVC. Onset may
be rapid. Patients may have a significant degree of discomfort, fear and distress.
An increasingly common cause of SVC-like syndrome is thrombosis of the SVC in patients with
central venous catheters.
Other causes: granulomatous infections, goiter, aortic aneurysms, and fibrosing mediastinitis
Etiology
Neoplastic causes include bronchogenic, lymphoma, leukemia, and germ cell tumors.
70% are due to lung cancers
Presentation
Dyspnea, orthopnea, swelling of the face, limbs, and upper extremities, venous dilatation over the
anterior chest wall, cough +/- hemoptysis, chest pain.
Jugular venous distention, facial plethora, and cyanosis may be present.
Hoarseness, syncope, dizziness, and confusion may also be present.
Evaluation
CXR abnormal in >80% of cases. Widened superior mediastinum and pleural effusions.
CT scan with IV contrast- shows reduced or absent opacification of central venous structures, with
prominent collateral venous circulation.
No advantage of MRI over CT
Biopsy of the mass should be made if diagnosis or tumor type is unknown. Sputum cytology,
biopsy of lymph nodes, bronchoscopy, and thoracentesis may also be helpful for diagnosis of
tumor type.
Treatment
Glucocorticoids- Dexamethasone 4mg q6h may be helpful, esp. if lymphoma or thymoma
Elevate head of bed
Oxygen
Loop diuretics and low-salt diet
Radiation therapy is useful for radiosensitive tumors, e.g. NSCLC
Chemotherapy is useful for chemosensitive tumors, e.g. SCLC, Non-Hodgkins lymphoma
Remove any indwelling central venous catheters that may be causing or contributing
Other: Placement of intravascular stent, surgery
BLOOD PRODUCTS
PACKED RED BLOOD CELLS
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Indications for transfusion:

Symptomatic anemia in a normovolemic patient regardless of H/H
Acute blood loss w/ evidence of inadequate O2 delivery
Hemoglobin <7 in a hemodynamically stable hospitalized patient
Post-operative hemoglobin of <8
Consider transfusion for hemoglobin <8 in patients with CAD
Facts:
Each unit pRBC has volume ~300ml (200ml of red cells) and should raise hemoglobin by 1g/dL
and hematocrit by 3% unless active bleeding
Each unit of pRBC contains ~200mg iron; hemosiderosis can produce organ damage when total
iron load approaches 15-20grams (75-100 units)
Loss of 1 unit of blood causes -1.5 mEq K, but transfusion of 1 unit causes +10 mEq since K leaks
out of red cells in stored blood; monitor in CKD and massive transfusion
Citrate present in stored blood can result in metabolic alkalosis (citrate~bicarb). Ionized calcium
may be decreased from calcium+citrate complexing
PLATELETS
Indications for transfusion of platelets:
Platelet count of <10 in non-bleeding patient w/ marrow suppression; consider higher threshold
(<30,000) for patients who are febrile/septic
<50,000 if actively bleeding; <100,000 if CNS bleed
< 50,000 before surgery; < 100K before ocular or CNS procedure
<20,000 for most bedside procedures
Facts:
One apheresis unit of platelets is equivalent to 4-6 pooled donor units; most hospitals use this type
of product
One apheresis unit should raise platelet count by 30K within 1 hour
Platelets do not require ABO matching, but may have a more robust platelet response with matched
units
True platelet transfusion refractoriness is defined as increment of <10K on two or more occasions;
HLA antibodies may contribute, so HLA matched units may be helpful
FRESH FROZEN PLASMA

Plasma containing all coagulation factors; frozen within 8 hours of collection
Indications for transfusion of FFP:
Active bleeding in the setting of an INR >1.5 (includes in the setting of liver disease, DIC, warfarin
overdose, vitamin K deficiency)
INR>2 in non-bleeding patient scheduled for surgery or invasive procedure
TTP (plasma exchange is preferred)
Facts:
Dose is generally 10-15mL/kg (usually about 3-5 units)
FFP can have INR as high as1.3, and generally doesnt correct the INR to below 1.6
One unit of FFP raises coagulation factor levels by ~8% and fibrinogen by ~13
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CRYOPRECIPITATE
FFP that is thawed at 4 degrees C leading to separation of fibrinogen, Factor VIII, Factor XIII, and
vWF.
Indications for transfusion of cryoprecipitate:
Fibrinogen < 100 mg/dl in the setting of consumptive coagulopathy (DIC) or severe bleed
Facts:
10 units of cryo contain ~2g of fibrinogen and will raise the fibrinogen level by 1 point per kg of
patient weight
Cryo is no longer a standard therapy for Factor VIII deficiency hemophilia or VWD given
availability of more concentrated factor products
DIFFERENT PREPARATIONS:
Leukoreduced blood components Removal of leukocytes through filtration to <106. Done to prevent
complications of PRBC transfusion related to WBCs (transfusion reaction, CMV infection). Most
hospitals automatically do this for PRBCs now.
Indications for leukoreduced product:

Chronically transfused patients (HLA sensitization)
Potential or previous transplant recipients
Patients with previous febrile non-hemolytic transfusion reactions
CMV seronegative at-risk patients (b/c CMV lives in white cells)
Irradiated blood components - Red cells that are exposed to at least 2500cGy of Gamma radiation to
destroy the ability of T lymphocytes to divide. Done to avoid transfusion-associated GVHD.
Indications for irradiated product:
Severe congenital immune deficiency
Immunocompromised transplant recipients (especially BMT)
Transfusions from family members
CLL or other patients being treated with fludarabine chemotherapy
Hodgkin lymphoma
Consider in patients with solid tumors being treated with aggressive chemo
Washed blood components - Blood is washed to prevent infusion of proteins present in residual plasma
in red cell concentrates that may cause allergic reaction.
Indications for washed product:
Patients with severe or recurrent allergic reactions
Documented IgA deficiency (pts can have anti IgA antibodies)
Reduce plasma K levels in acute renal failure
CMV negative components - Includes leukoreduced and seronegative CMV products.
Indications for CMV negative components:
CMV negative allogeneic BMT
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Immunosuppressed CMV negative patients, potential transplant candidates

PREMEDICATIONS FOR TRANSFUSION:
Goal is to prevent transfusion reactions
Generally recommend APAP 650mg PO and benadryl 50mg PO
May use dexamethasone in patients with history of severe reaction
Be careful in patients at risk of complications from these therapies (ie liver disease, elderly)
Transfusion Reactions
Overall, 1-6% of all patients, and up to 10% of heme/onc patients who receive blood transfusions
experience an adverse reaction.
Overview
Immunologic Reactions:
Febrile non-hemolytic transfusion reactions
Acute hemolytic transfusion reactions
Delayed hemolytic transfusion reactions
Anaphylactic transfusion reactions
Urticarial transfusion reactions
TRALI
Post ransfusion purpura
Graft-versus-host disease (GVHD)
Chemical/Physical Reactions:
Volume overload
Citrate toxicity
Hyperkalemia, Hypokalemia/metabolic alkalosis
Febrile Non-hemolytic Reactions:
Most common reaction (0.5-1% of all pRBC transfusions)
Symptoms include fever, chills, mild dyspnea, and malaise 1-6 hours after transfusion
Etiology is from cytokines that are generated and accumulate during the storage of blood
components
Benign and without any lasting sequelae, but cannot distinguish initially from acute hemolytic
reactions so the initial treatment for both the same
Treat by stopping the transfusion, IVFs, draw appropriate labs, and antipyretics
Prevented by using leukoreduced or washed products
Acute Hemolytic Reactions:
1 per 40,000 transfused units of pRBCs
Medical emergency from rapid destruction of donor RBCs by preformed recipient antibodies
Most commonly due to ABO incompatibility from clerical erroron occasion can have acquired
alloantibodies like anti-Rh or anti-Jka
Symptoms: The classic triad of fever, flank pain, and red/brown urine (hemoglobinuria) is actually
rarely seen. Other symptoms include chills, flushing, nausea, chest tightness, malaise
Treatment includes stopping the transfusion, initiating protocol for transfusion reactions (i.e. blood
bank checks for clerical errors), maintain ABCs, start IVFs (Normal Saline), and check a direct
antiglobulin (Coombs) test, Hemoglobin, and repeat T&C from the other arm.
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Maintain UOP of 100-200 ml/hr with IVFs to avoid renal failureurinary alkalinization doesnt
really do much
Do not use Lactated ringers (calcium in this may initiate clotting of any remaining blood in the
line) or dextrose containing IVFs (dextrose may hemolyze any remaining RBCs in the line)
If massive hemolysis is present and there is concern for DIC, cautious early heparinization
(10units/kg/hour) for 12-24 hours may be indicated.
Delayed Hemolytic Reactions:

1 per 7000 pRBC transfusions
Anamnestic antibody response occurring after re-exposure to foreign red cell antigens previously
encountered by transfusion, transplantation, or pregnancy
Antibodies are often Kidd or Rh, and levels have fallen to undetectable levels on pre-transfusion
testing, but increase rapidly in titer following the transfusion
Time course is within 2 to 10 days after transfusion.
Signs/Symptoms are falling hematocrit, slight fever, mild increase in indirect bilirubin,
spherocytosis on smear
Often actually diagnosed by blood bank when a new antibody screen is done when more blood is
ordered.
Hemolysis is usually extravascular, gradual and less severe than with acute reactions
No treatment is required unless brisk hemolysis is present.
Anaphylactic Reactions:
1 per 20,000 to 50,000 transfused units
Occurs within few seconds to minutes following initiation of transfusion that contains any plasma
(often < 10 cc transfused)
Almost always due to the presence of class-specific IgG, anti-IgA antibodies in patients who are
IgA deficient
Selective IgA deficiency occurs in 1 in 300-500 people, but not all have developed antibodies.
Usually not a problem in patients with acquired IgA deficiency
Symptoms: Anaphylaxis (tachycardia, urticaria, flushing, laryngeal edema, hypotension,
respiratory distress)
Treatment: stop transfusion, Epinephrine (0.3 ml of 1:1000 solution IM), possible IV epinephrine
gtt, Airway, IVFs, occasionally pressors
Prevented by using washed blood products
Urticarial Transfusion Reaction:
1-5% of all reactions
Occurs when soluble allergic substance in plasma of donated blood product react with preexisting
IgE antibodies. Cause mast cells and basophils to release histamine leading to hives
Treatment: stop transfusion, give diphenhydramine. If hives resolving, can actually resume
transfusion
Transfusion-Related Acute Lung Injury (TRALI):

Actually under reportedone series found 1 in 2000 transfusions at a university hospital
ARDS type of picture 30 minutes to 6 hours post transfusionnot related to volume overload
Pathogenesis still unknownyoure never wrong if you blame cytokine
-elevated risk with increasing units of FFP
Treatment is supportive
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Post Transfusion Purpura:

Uncommon (~250 reported cases), female:male ratio 26:1
Severe thrombocytopenia 5-10 days following platelet containing product.
Prior sensitization to a foreign antigen by pregnancy or prior transfusion, most commonly
implicated is human platelet antigen 1a (HPA-1a)
Treatment is high dose IVIG
Graft-versus-host disease (GVHD):
Rare, primarily immunocompromised patients when viable donor lymphocytes attack recipient
tissues (prevented by using irradiated blood products in this patients)
Can also happen if recipient receives blood products from a relative who is a partial HLA match
(also prevented by irradiation)
Very poor prognosis
Hospitalist
Pre-Op Workup/Surgical Clearance
The first rule is never say in your note, The patient is OK to go to surgery. The goal of a
clearance is not to say whether a patient can or cannot go to surgery but rather what the risk level is
in taking them and what needs to be done immediately before, during, and after. All patients are OK
to go to surgery if the setting is right and the benefits outweigh the risks. Conversely, no patient
should go unless these criteria are met. Here are the issues that need to be addressed in every medical
evaluation prior to surgery.
Cardiac Risk Assessment for Non-Cardiac Surgery
(Circulation 2007;116:418-500 and Circulation 2009;54:2102-2128)
Emergent surgery?
Yes OR
No
Active cardiac
condition?
Yes Evaluate and treat,

then consider OR
No
Low-risk surgery?
Surgery-specific risk:
High
- Vascular, prolonged surgery with
anticipated large volume shifts
Intermediate
- Intraperitoneal, intrathoracic
- Head and neck, CEA
Yes OR
No
METs > 4
No symptoms
Active cardiac conditions:

- Unstable coronary syndromes
- MI within 30 days
- Decompensated HF
- Significant arrhythmia
- Severe valvular disease
- AS with valve area <1.0cm2
- Symptomatic mitral stenosis
Yes OR
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No
Clinical Risk Factors

(Calculate RCRI)
OR after need for

beta-blocker, statin,
and stress test
considered
(see below)
- Orthopedic, prostate
Low
- Breast, endoscopy, cataract
- Ambulatory surgery
METs > 4
- Climb a flight of stairs
- Heavy housework
Peri-operative cardiac risk should be calculated with the Revised Cardiac Risk Index (RCRI):
(Circulation 1999;100:1043-1049)
RCRI Score (1 pt for each risk factor):
- High-risk procedure
- Ischemic heart disease (h/o MI, Q waves on ECG, angina, +stress, NTG use)
- Congestive heart failure
- Cerebrovascular disease
- Insulin-dependent diabetes
- Creatinine > 2
The risk of major perioperative cardiac complications is 0.4% for 0 pts, 0.9% for 1 pt, 6.6% for
2 pts, and 11% for 3 pts. Include the RCRI score in your note.
Alternatively, you can use the new NSQIP risk calculator developed in 2011:
http://www.surgicalriskcalculator.com/miorcardiacarrest
In general, risk <1% is considered low, 1-5% is considered intermediate, and >5% is
considered high.
Now that you know the patients baseline cardiac risk, you need to make recommendations
about whether the patient needs any additional diagnostic studies or medical management prior
to surgery.
Perioperative Beta-Blockade
- Continue BB if patient already on BB
- If RCRI < 2, no need for BB unless patient has CAD
- If RCRI 2, start a BB if there is time to safely titrate to goal HR 50-60 pre-operatively.
Goal HR 60-80 post-op. Continue for 30 days post-procedure.
Perioperative Statin Therapy
- Continue statin if patient already on statin
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- Consider statin if vascular surgery or if should be on one as outpatient

Perioperative Stress-Testing
- Consider for RCRI 1 only if will change management (i.e., if it will help you decide about
more aggressive medical management; little reason for preoperative revascularization even if
+ stress therefore this is rarely done anymore)
Pre-Op ECGs
- Obtain in patients with any RCRI points unless undergoing low-risk surgery
How should you manage patients with a previous PCI?
- Bare Metal Stents
- <30-45 days delay surgery if not urgent; continue dual antiplatelet therapy if urgent
- >30-45 days OR with aspirin
- Drug-Eluting Stents
- < 12 months delay surgery if not urgent; continue dual antiplatelet therapy if urgent
- > 12 months OR with aspirin
Pulmonary Risk: Suggest things that can be done in the acute setting to lower surgical risk.
(NEJM 1999: 340:937-944)
1. Treat restrictive disease adequately if present
2. Obtain a CXR only if infection is suspected and treat if present
3. If severe pulmonary disease, suggest spinal or regional anesthesia
4. Encourage incentive spirometry use immediately after
5. Recommend CPAP and the settings if patient uses this at home
**Remember, while quitting smoking is good, it only helps with surgery if the
patient has quit 6-8 weeks prior to procedure. Recommend nicotine patch.
Diabetes Management: If diabetic, use the following guidelines.
(Arch. Int. Med. 1999: 159:2405-2411)
1. Hold all oral agents on the day of surgery
2. In theory, patients should be able to continue their normal long-acting (i.e., glargine) insulin
dose even while NPO since it covers their basal requirements. However, to be conservative,
consider giving patients 1/2 to 2/3 their usual morning insulin dose if they are dosed daily,
and 1/3 to 1/2 their morning dose if they are dosed 2-3 times per day.
3. Recommend QAC + QHS fingersticks for all diabetics
4. Recommend short-acting insulin at mealtimes + CF for all diabetics and adjust basal insulin
according to these needs
5. If a patient needs to go to surgery emergently and they already took a dose of long acting
insulin, using a dextrose drip of 50 cc/hr of 10% solution with frequent monitoring is wise
6. Consider continuous insulin drip if long, complex procedure
Perioperative Management of Patients on Chronic Steroids
Patients who have taken any dose of glucocorticoids for <3 weeks, who are on chronic alternate
day therapy, or who are on < 5 mg/day of prednisone are unlikely to have a suppressed HPA
axis and can continue their usual dose of steroids.
Patients taking prednisone doses >20mg/day for 3 weeks or who have Cushingoid appearance
should be assumed to have HPA axis suppression. Patients on 5-20 mg prednisone/day may or
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may not have adrenal insufficiency. Stress-dosing has been suggested according to surgical
intervention, though adrenal insufficiency without increased dosing is relatively rare. If highdose therapy is employed, replacement dose should be resumed within 48 hours.
If on baseline steroids 5 mg/day, supplement with: (JAMA 2002: 287 No.2:236-240)
1. Minor surgical stress Hydrocortisone 25 mg IV q8h on day of procedure only
2. Moderate surgical stress Hydrocortisone 50-75 mg q8h on day of procedure, taper
to baseline dose over 1-2 days
3. Severe surgical stress Hydrocortisone 100-150 mg IV q8h on day of procedure,
taper to baseline dose over 1-2 days
4. Critically ill patients get 50 mg IV hydrocortisone q8h + 50 g IV fludrocortisone
qday until shock resolves, then slow taper
Perioperative Medication Management
- Consider holding ACEI or ARB the night before or morning of surgery to minimize the risk of perioperative hypotension
- Hold NSAIDs preoperatively
Infectious Disease
General Considerations:
Consider what organisms the patient is at risk for; do they have a history of resistant
organisms, were they recently hospitalized, what is the source of infection (different drugs
for different bugs)
Whenever possible, narrow your antibiotics. If you have sensitivities, use them.
If the patient is not improving, do you have the wrong drug, the wrong bug, or is the bug
resistant?
Evaluation and Management of Staphylococcus

aureus Bacteremia (SAB)
1. Background
Staphylococcus aureus is one of the most common causes of bacteremia and is the most serious
About 1/3 have definite or possible endocarditis (modified Duke criteria1)
About 1/3 have deep-tissue infections due to hematogenous seeding (e.g., vertebral
osteomyelitis, septic arthritis, psoas abscess)
Mortality of SAB: 9% to 47%
Things to remember during the initial management of S. aureus bacteremia
S. aureus should not be considered a blood culture contaminant, unless discussed with the
Infectious Diseases (ID) consult service
Central venous catheters (if removable) should be removed and the catheter tip sent for culture
as soon as possible after the identification of S. aureus
o risk of relapse is increased when catheters are not removed2
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o use peripheral venous access until bacteremia has cleared whenever possible
All patients should have a follow-up blood culture drawn 2-3 days after the initial positive
culture, even if signs or symptoms of infection have resolved
o a positive follow-up blood culture is a strong predictor of endocarditis and deep-tissue
infections3
Echocardiography should be performed routinely4
Localizing signs or symptoms should be evaluated with the appropriate imaging study (e.g.,
MRI of spine to evaluate for osteomyelitis or epidural abscess in a patient with SAB and back
pain)
We recommend consultation of the ID service early in the inpatient course of all cases of
SAB for assistance with evaluation and management
Identifying patients at risk for complications

The following are predictors of endocarditis and/or deep-tissue infections:
o Positive follow-up blood culture
o Failure to remove intravascular catheter
o Persistent fever >3 days after initial culture
o Prior endocarditis or underlying valvular disease
o Prosthetic valve, pacemaker, implantable defibrillator, prosthetic joint, or other
prosthetic devices
o Time to blood culture positivity of 14 hours
o Community-acquisition of infection
o Unknown source of infection
Treatment of S. aureus bacteremia
Optimal treatment requires intravenous therapy
Oral therapy such as fluoroquinolones, linezolid, clindamycin, and beta-lactams should NOT be
used
Empiric coverage should be directed at methicillin-resistant S. aureus (MRSA) until
susceptibilities are known (33% of isolates are methicillin-resistant)
Antistaphylococcal penicillins (nafcillin/oxacillin) and cefazolin are superior to vancomycin
and daptomycin for the treatment of methicillin-sensitive S. aureus (MSSA) bacteremia5, 6
o consider cefazolin for patients with MSSA bacteremia who have a history of penicillin
allergy that does not include hives, symptoms of airway compromise, or anaphylaxis6
Adjunctive aminoglycoside use for 3-5 days in suspected endocarditis decreases time to
clearance of bacteremia but has not been shown to improve cure rates4 and increases the risk of
nephrotoxicity 5
Methicillin-sensitive S. aureus (MSSA) bacteremia treatment options
Nafcillin
Usual Dose
Considerations
Formulary Approx.
Cost
2gm Q4h
OR
10-12gm cont
infusion
(Adjust
hepatic*)
Standard therapy for MSSA

bacteremia/endocarditis.
Monitor: CBC, LFTs,
Creatinine
UCH
DHMC
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$57/10gm
Oxacillin
2gm Q4h
(Adjust
hepatic*)
Standard therapy for MSSA

bacteremia/endocarditis.
Monitor: CBC, LFTs,
Creatinine
$60/10gm
Consider for patients with

All
$6/3gm
concomitant gram negative
$10/5gm
infections
Monitor: CBC, Creatinine
*discuss hepatic insufficiency dose adjustments with ID and Pharmacy services
Cefazolin
2gm Q8h
(Adjust renal)
VA
- 97 -
Methicillin-resistant S. aureus (MRSA) bacteremia treatment options

Usual Dose
Considerations
Formulary
Approx.
Cost
Standard therapy for

MRSA
All
$10bacteremia/endocarditis.
15/day
Monitor: CBC,
Creatinine
FDA-approved for
Requires ID $170/day
Daptomycin, IV 6mg/kg Qday MRSA
(Adjust
bacteremia/endocarditis. approval(Cubicin)
hepatic*)
**NOT for use in cases All
with pulmonary
involvement.
Monitor: LFTs, CK
**NOT FDARequires ID $150/day
Linezolid, IV/PO 600mg Q12h approved for MRSA
(Adjust
bacteremia, use only in approval(Zyvox)
hepatic*)
consultation with ID
All
service
Monitor: CBC, LFTs
*discuss hepatic insufficiency dose adjustments with ID and Pharmacy services
Vancomycin, IV
See section
below
Dosing recommendations for vancomycin

I.
Initial Dose
All patients, irrespective of renal function, should receive an initial dose of 15mg/kg*
once
*Based on actual body weight unless patient is obese (>130% of ideal body
weight (IBW))
IBW (kg) = [50 (male) OR 45 (female)] + 2.3(patient height >60inches)
If patient >130% of IBW, then use Adjusted body weight (AdjBW (kg) = IBW
+ 0.4(Actual-IBW))
Please round all doses to the nearest 500mg dose
II.
Maintenance Dosing
The following are empiric maintenance regimens based on creatinine clearance (CrCl) by the
Cockcroft-Gault equation:
Renal function (ml/min)
Empiric Dose
ClCr>60
15mg/kg* Q8-12h
Clcr 40-60
1000mg Q12-24h
ClCr 10-40
1000mg Qday
CrCl<10 or intermittent HD
**
CVVH
1000mg Qday
*See weight-based dosing for obese patients above
**Serum TROUGH levels should guide therapy in patients with severely impaired or rapidly changing
renal function. Please refer to specific institution recommendations for maintenance dosing.
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III.
Pharmacokinetic (PK) Monitoring
In general, many acute care patients will be appropriate for PK monitoring of vancomycin serum
trough concentrations.
A trough level should be drawn within 30 minutes of the next dose, after a patient
has reached steady state (after approximately 3-5 doses have been administered).
Vancomycin serum concentrations may be increased by altering dose or
administration interval. Adjusting the interval is the preferred method for increasing
serum trough concentration (e.g., 1gm Q12hrs 1gm Q8hrs)
Goal serum trough concentration: 10-20mg/dl4 (15-20mg/dl for bacteremia
associated with MRSA pneumonia7)
o Note: each institution has specific policies for PK monitoring
Duration of therapy
The optimal duration of therapy for SAB remains unclear; consultation with the ID service is
recommended
Generally, a duration of therapy of least 14 days for uncomplicated infections and at least 28
days for complicated infections (positive follow-up blood cultures, endocarditis, deep-tissue
infections) can be expected
Patient follow-up
All patients discharged on intravenous antimicrobial therapy need weekly laboratory and
clinical monitoring
Contact the ID service to arrange appropriate follow-up at least 48 hours prior to discharge
References
1. Li JS, Sexton DJ, Mick N, et al. Proposed modifications to the Duke criteria for the diagnosis of
infective endocarditis. Clin Infect Dis. Apr 2000;30(4):633-638.
2. Fowler VG, Jr., Justice A, Moore C, et al. Risk factors for hematogenous complications of
intravascular catheter-associated Staphylococcus aureus bacteremia. Clin Infect Dis. Mar 1
2005;40(5):695-703.
3. Fowler VG, Jr., Olsen MK, Corey GR, et al. Clinical identifiers of complicated Staphylococcus
aureus bacteremia. Arch Intern Med. Sep 22 2003;163(17):2066-2072.
4. Baddour LM, Wilson WR, Bayer AS, et al. Infective endocarditis: diagnosis, antimicrobial
therapy, and management of complications: a statement for healthcare professionals from the
Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular
Disease in the Young, and the Councils on Clinical Cardiology, Stroke, and Cardiovascular
Surgery and Anesthesia, American Heart Association: endorsed by the Infectious Diseases Society
of America. Circulation. Jun 14 2005;111(23):e394-434.
5. Fowler VG, Jr., Boucher HW, Corey GR, et al. Daptomycin versus standard therapy for
bacteremia and endocarditis caused by Staphylococcus aureus. N Engl J Med. Aug 17
2006;355(7):653-665.
6. Stryjewski ME, Szczech LA, Benjamin DK, Jr., et al. Use of vancomycin or first-generation
cephalosporins for the treatment of hemodialysis-dependent patients with methicillin-susceptible
Staphylococcus aureus bacteremia. Clin Infect Dis. Jan 15 2007;44(2):190-196.
7. Guidelines for the management of adults with hospital-acquired, ventilator-associated, and
healthcare-associated pneumonia. Am J Respir Crit Care Med. Feb 15 2005;171(4):388-416.
Contributions by members of the Divisions of Infectious Diseases and Pharmacy
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Endocarditis
1. Infective Endocarditis -infection of the lining of the heart, including the heart valves
If you suspect someone has endocarditis, they should be evaluated using the modified Duke
criteria:
Definite endocarditis: Presence of 2 major criteria or 1 major criterion and 3 minor
or 5 minor criteria.
Possible endocarditis: Presence of 1 major criterion and 1 minor or 3 minor criteria
2. Major Criteria:
Positive Blood Cultures: Positive blood cultures for microorganisms that typically cause
endocarditis (Strep. viridans, Strep. bovis, HACEK organisms, Staph. aureus or community
acquired enterococci with no other primary focus).
Persistently positive blood cultures of one of the above organisms in blood cultures drawn more
than twelve hours apart or positive blood cultures in three out of four sets drawn at the same
time or single positive blood culture or serology test for Coxiella burnetii.
Evidence of Endocardial Involvement: Positive echocardiogram (oscillating intracardiac
mass on valve or supporting structures, abscess or dehiscence of prosthetic valve). New
valvular regurgitation (does not include change in pre-existing murmur).
3. Minor Criteria:
Predisposing heart condition or history of intravenous drug use.
Fever 38.0 C
Vascular phenomena (septic infarcts, Janeway lesions, mycotic aneurysms).
Immunologic phenomena (Oslers nodes, Roth spots, glomerulonephritis).
Positive blood culture not meeting major criteria and also excluding single positive set for
coagulase negative staphylococci and organisms that do not cause endocarditis.
4. Workup should include:
At least three sets of blood cultures: Depending on the severity of the illness, it may be
reasonable to initially withhold antibiotic therapy until sufficient cultures are obtained or until
diagnosis is made.
Electrocardiogram: Presence of a new conduction abnormality (i.e. first degree AV block)
may indicate a complication such as a perivalvular abscess.
Chest x-ray: Evidence of new heart failure or septic emboli may be detected.
Echocardiogram: This should be performed in all cases of suspected endocarditis. TTE can be
a reasonable first test, but TEE should be pursued if TTE is negative and clinical suspicion is
high. TEE should be considered as the first test if the likelihood of obtaining good windows
with TTE is low (morbid obesity, previous thoracic surgery, COPD) or if clinical suspicion of
endocarditis and its complications is fairly high (prosthetic valve or new conduction block on
EKG). However, if TEE needs to be delayed because of the clinical scenario, then TTE should
be performed without delay.
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5. Common Organisms:
Native valve, non-IV drug user: Strep. viridans > Staph. aureus > Enterococcus
Native valve, IV drug user: Staph. aureus > Strep. viridans > Enterococcus
Prosthetic valve, within 6 months: Staph. epidermidis > Staph. Aureus > gram negative rods
Prosthetic valve, after 6 months: Strep. Viridans > Staph. Epidermidis > Staph. Aureus and
enteroccocus
6. Initial Therapy:
Acute endocarditis with native valve: Typically start vancomycin and gentamicin and then
tailor based on culture results. Nafcillin is a superior agent to vancomycin if MRSA has been
ruled out because it is bactericidal instead of static (vancomycin).
Acute endocarditis with prosthetic valve: Typically start vancomycin, gentamicin, and
rifampin if within one year of valve replacement and then tailor based on culture data.
7. Continued Care:
Tailor antibiotic therapy as soon as culture data is available
Obtain two sets of blood cultures every 24-48 hours until cultures are negative
Duration of therapy should be based on counting the first day that blood cultures are negative
as the start of therapy
Duration of therapy is typically 4-6 weeks and can often be completed in the outpatient setting
once the patient is clinically stable
Repeat echocardiography should be obtained at the end of therapy to establish a new baseline
for the patient
8. Surgical Intervention:
This is often a complicated decision, made in conjunction with cardiothoracic surgery, but
should be considered in certain scenarios:
1. Fungal infection.
2. Heart failure from valvular dysfunction that is unresponsive to medical therapy
3. Persistent infection despite appropriate medical therapy (positive blood cultures after one
week or embolic events during the first two weeks of therapy).
4. Prosthetic valve dehiscence or perivalvular abscess.
Baddour LM, et al. Infective endocarditis: diagnosis, antimicrobial therapy, and management of
complications. Circulation 2005; 111: 394-434.
Osteomyelitis
1. Three Types:
1. Due to local spread from a contiguous contaminated source of infection. Usually secondary to
trauma, bone surgery, or joint replacement.
2. Secondary to vascular insufficiency. Predominantly in diabetics. Most cases start with a soft
tissue infection.
3. Hematogenous osteomyelitis: bacterial seeding.
2. Acute vs. Chronic
Acute: evolves over several days or weeks.
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Chronic: evolves over weeks to months to years. Characterized by persistence of

microorganisms, low-grade inflammation, presence of dead bone, and fistulous tracts. Hard to
treat and usually requires surgical intervention.
3. Microbiology
Clinical Scenario
Most common in any type
Foreign-body-associated
Associated with bite, diabetic feet,
and decubitus ulcers
Sickle-cell disease
HIV
Human or animal bites
Immunocompromised
Populations with high TB prevalence
Populations in which these organisms
are endemic
Microorganism
Staphylococcus aureus
Coagulase-negative Staph or propionibacterium spp.
Streptococci and/or anaerobic bacteria
Salmonella spp or Streptococcus pneumoniae
Bartonella henselae or B. quintana
Pasturella multocida, Eikenella corrodens
Aspergillus spp., Candida albicans, or Mycobacteria
spp
Mycobacterium tuberculosis
Brucella spp., Coxiella burnetii, cocci, blasto, histo.
4. Signs and Symptoms: range from open wounds exposing fractured bone, a draining fistula, local
swelling and bone pain tenderness without skin lesions. +/- fever. Joint instability or painful
joint in patients with prosthetic joints.
5. Diagnosis:
ESR and CRP will often be high. CRP goes up first and is more reliable to assess treatment
response.
WBC count may be normal.
Start with plain films (often normal early on) if they do not show anything, order an MRI.
If you can probe down to bone, the patient has osteomyelitis.
Getting tissue is the key: Bone biopsy/aspiration whether under CT guidance or during surgery
is critical as this will guide treatment.
6. Treatment:
Anything but acute or hematogenous osteomyelitis is almost impossible to treat without
surgery. Consult Ortho.
Antibiotics should be based on culture and sensitivity results. Hold therapy until after biopsy or
specimens from I&D obtained.
Antibiotic courses are generally long (4-6 weeks), so get ID involved early to facilitate
disposition, need for vascular access, and outpatient antibiotic coordination.
Lew DP, Waldvogel FA. Osteomyelitis. Lancet 2004; 364: 369-79.
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HIV / AIDS
1. Diagnosis:
ELISA is positive one month after infection in 80% of patients.
If considering acute HIV infection, check viral load.
Review risk factors and screen anyone between ages of 13 and
64.
Obtain accurate contact information for the patient who will be
tested for HIV in case discharged prior to test result.
AIDS: HIV + and CD4 < 200 or evidence of opportunistic
infection (OI)
Acute HIV Symptoms

Asymptomatic
(majority)
Rash
Fever
Fatigue
Rash
Headache
Pharyngitis
LAD
Aseptic Meningitis
Myalgias
Night Sweats
2. If diagnose new HIV infection:

Call and notify ID service.
Labs to obtain: Viral load, CD4 count, genotype, CBC/LFTs/Chem 7, Hep serologies, RPR,
Toxo IgG, lipids.
Vaccinate against pneumonia, flu, Hep A, Hep B and place ppd.
Talk to patient about diagnosis!
3. Treatment recommendations:
Symptomatic disease: Start treatment
Asymptomatic disease
CD4 > 500.. defer rx
CD4 350 500generally not recommended
CD4 200 350therapy considered and treatment
individualized
CD4 < 200.. therapy recommended
Drugs: Generally use 2NRTIs and 1 NNRTI or 2NRTIs and 1 PI.
NRTI
NNRTI
PI*
Emtricitabine (Emtriva, FTC)
efavirenz (Sustiva, EFV)
atazanavir (Reyataz, ATV)
lamivudine (Epivir, 3TC)
nevirapine (Viramune,
lopinavir/ritonavir (Kaletra,
NVP)
LPV/r)
zidovudine (Retrovir, AZT,
fosamprenavir (Lexiva, FPV)
ZDV)
didanosine (Videx EC, ddi)
tipranavir (Aptivus, TPV)
tenofovir (Viread, TDF)
indinavir (Crixivan, IDV)
stavudine (Zerit, d4T)
saquinavir (Invirase, SQV)
abacavir (Ziagen, ABC)
ritonavir (Norvir, RTV)
darunavir (Prezista, DRV)
nelfinavir (Viracept, NFV)
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- 104 -
Combination formulations:
Atripla: TDF + FTC + EFV
Truvada: TDF + FTC
Combivir: AZT + 3TC
Epzicom: ABC + 3TC
Trizivir: AZT + 3TC + ABC
*Ritonovir boosted PIs: ritonovir will elevate other PI drug levels due to its interaction with the CYP
-450 system.
4. When pts on HAART are admitted:
Notify the ID service, regardless of whether you want them to consult (not necessary to call
them in the middle of the night, but a courtesy call in the morning is appropriate).
If tolerating PO, may continue treatment unless you think their admission problem is directly
related to their medication.
If unable to take PO, stop ALL the HAART meds.
If unsure, stop all HAART meds and speak with ID.
Dont add a PPI until you check it does not interfere with HAART absorption.
5. Opportunistic Infections:
CD4 Count
<500
<200
<100
Possible OIs
Bacterial Infections, seborrheic derm, KS, oral/pharyngeal Candida, HSV,
TB
Esophageal candidiasis, Histoplasmosis, Blastomycosis, Cryptococcosis,
Coccidioidomycosis, PCP
CMV, MAC, invasive Aspergillosis, PML, CNS lymphoma, Toxoplasma
Prophylaxis:
OI
When to start (CD4)
PCP <200
Toxo <100
MAC <50
Histo <150 (Must live in
endemic area)
TB
At diagnosis check
PPD
1st Line
Bactrim DS one daily
(or SS daily or DS 3x
week)
Bactrim DS one daily
Azithro 1250mg qWeek
Itraconazole 200mg
daily
9 months INH
2nd Line
Dapsone, aerosolized pentamidine, or
atovaquone
Dapsone-pyrimethamine
Clarithromycin, Rifabutin
RIF + PZA x 2 months
6. PCP:
Consider PCP if CD4 <250, questionable compliance with prophylaxis, sub-acute course, dry
cough, exertional hypoxia, night sweats, etc.
Just because the patient has taken prophylaxis does not mean they cannot have PCP!
Especially if prophylaxis is not TMP/SMX.
CXR can be normal or with bilateral interstitial infiltrates.
DX: Have RT induce sputum to check PCP DFA. If suspicion high and sputums are negative,
bronchoscopy with BAL has sensitivity of 95-99%. Elevated LDH is also suggestive.
RX: TMP/SMX for 21 days.
- 105 -
If suspected, get an ABG! If PaO2 > 70: consider oral TMP/SMX 2 DS tabs PO TID. If PaO2
< 70: Steroids first (Prednisone 40 mg BID x 5d, then 40mg daily x 5d, then 20mg daily x 11d),
then IV TMP/SMX.
Alternative therapies: clindamycin + primaquine PO (check for G6PD first) OR pentamidine IV
(watch glucose, blood pressure, electrolytes) are usually best alternatives. Use atovaquone
when other therapies impossible.
7. Other organisms to keep in differential of pulmonary infections: TB, CAP pathogens, Nocardia,
fungal pneumonia (histo, blasto, coccidio, aspergillosis, etc), viral pneumonia (HSV, CMV),
KS, lymphoma. Consider all that you would in a patient without HIV (do not limit differential
to just infectious causes, i.e. PE, CHF, pericarditis, etc).
8. AIDS and Diarrhea:
Protozoal: Cyclospora/Microsporidium/Isospora, Cryptosporidium, Giardia, Entamoeba.
Bacterial: Salmonella/Shigella/Campylobacter, MAC, TB, C. diff.
Viral: CMV, HSV, HIV.
Fungal: Histoplasmosis, Coccidioidomycosis, Candida albicans.
Work up:
1. Stool: Culture, C. diff toxin, O and P, modified acid fast smear (crypto, cyclospora,
isospora), trichrome for microsporidium if CD4 <100, stool antigen for Giardia and
Cryptosporidium.
2. Blood: MAC blood cultures if suspected.
3. Endoscopy: If above is negative, endoscopy to evaluate for KS, CMV, lymphoma, TB,
microsporidiosis.
9. AIDS and Esophagitis: HSV, CMV, Pill induced, Candida.
10. AIDS and Proctitis: HSV, CMV, Chlamydia, Neisseria.
11. AIDS and Altered Mental Status:
Always perform a thorough H & P/neuro exam, lumbar puncture, and some form of neuro
imaging (preferably with contrast).
If CT negative, think meningitis: bacterial (Listeria, plus common meningitis organisms), viral
(CMV, HSV), Cryptococcus, TB.
If CT shows mass lesions: Toxo, Lymphoma, pyogenic abscess, PML.
Labs to check: RPR, serum crypto antigen, and typical cultures.
DDX:
1. Parenchymal: Toxo, CNS lymphoma, PML, HSV encephalitis, AIDS dementia.
2. Meningeal: cryptococcus, bacterial, syphilis, TB meningitis, lymphoma.
3. Other: metabolic, CVA, drugs, systemic infection, psychiatric.
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TUBERCULOSIS
1. Consider with high risk populations
Contact with known TB case
Homeless
Prisons
Chronically ill (ESRD, DM, Alcoholics, cancer)
HIV/AIDS
Healthcare workers
Foreign born or immigrant
2. Transmission via airborne droplets.ISOLATE ALL PATIENTS THAT YOU ARE GOING TO
RULE OUT WITH SPUTUMS! If you are suspicious enough to check sputums, isolate the patient.
3. Diagnosis: Induced sputum for AFB. Typically, need three negative AFBs and/or alternative
diagnosis to discontinue isolation. They have to be collected on different days, so dont delay in
ordering them. Make sure the lab has the specimen. Sometimes they will not tell you if they were
unable to collect the sample or if the sample is insufficient. Avoid use of fluoroquinolones for
suspected CAP when TB is considered as these drugs can cloud dx due to some activity against MTB.
4. Interpretation of PPD test: to detect Latent infection. 2-12 weeks is needed after an acute infection
for the PPD to be positive.
Size of PPD Considered positive
>5mm*
HIV +, immunosuppressed (pts on greater than 15mg/day of prednisone), close contact
with known active pulmonary TB case, CXR c/w prior TB.
>10mm**
IVDA, employees/residents of high risk congregate settings, chronic medical condition
>15mm
Everyone else
Previous
Interpret as if they never had the BCG vaccine.
BCG
* highest risk for developing active TB if they become infected with M. tuberculosis
** increased probability of recent infection or who have conditions that increase the risk for TB
5. +PPD with active disease ruled out:
NON HIV:
5% develop active disease in 2years
5% develop active disease in their lifetime
90% will be asymptomatic
HIV +:
5-12% will develop active disease PER YEAR!
6. Treatment of Latent TB: Many drug regimens available.
Most commonly used is: INH daily x 9months
7. What is MDR TB: TB that is resistant to at least INH and RIF. Risk Factors for having MDR-TB:
History of previous TB treatment
Direct contact with MDR-TB patient
HIV+
Persistent positive cultures after 3 months of therapy
People from areas with high MDR-TB prevalence
- 107 -
8. What is XDR TB: MDR TB that is also resistant to any fluoroquinolone and any of the injectable
drugs.
9. Clinical manifestations of TB are protean:
Primary pulmonary TB: this is asymptomatic in most (HIV pts have higher risk of symptomatic
primary disease).
Reactivation pulmonary TB: most commonly seen in apical segments of lungs, but can be
atypical, especially in HIV pts.
TB pleurisy: can cause pleural effusion. Typically lymphocyte predominant, high LDL,
exudative, and elevated ADA levels. Usually need to get pleural biopsy to diagnose.
Miliary TB: pulmonary disease secondary to hematogenous spread throughout the lung.
Extrapulmonary TB: lymphadenitis, peritonitis, pericarditis, meningitis, osteomyelitis, enteritis,
adrenal, etc. Dont be fooled, higher rates of extrapulmonary TB in HIV patients.
10. Treatment: This will be done in consultation with an ID specialist.
TB (known susceptible to standard agents):
1st line Therapy: INH, RIF, ETH, PZA.varying dosing schedules available.
2nd line agents: Ciprofloxacin, Ofloxacin, Cycloserine, PAS, Ethionamide.
Injectables: Streptomycin, Amikacin, Kanamycin, Capreomycin
MDR TB: Need 4 active drugs in regiment. At least one 2nd line agent and one injectable.
Nephrology
Acid-Base
1. A simple approach to acid-base disorders:
Rule 1: Look at the pH. Whichever side of 7.4 the pH is on, the process that caused it to
shift to that side is the primary disorder (i.e. acidosis or alkalosis). This is because the
body never fully compensates for the primary acid-base disorder.
Rule 2: Calculate the anion gap. Look at the compensation. For a metabolic process the
pCO2 should increase (metabolic alkalosis) or decrease (metabolic acidosis). For a
respiratory process, the bicarbonate should increase (respiratory acidosis) or decrease
(respiratory alkalosis).
Rule 3: Calculate the delta gap (if there is an anion gap present). Take the patients
anion gap and subtract it from a normal anion gap (12 or 3 X albumin) and add this to
the measured bicarbonate concentration. If sum is greater than 30, then there is also an
underlying metabolic alkalosis. If the sum is less than 23, then there is also an
underlying non-anion gap metabolic acidosis.
2. Most complicated acid-base disorder is a triple ripple.
3. Anion gap and protein: to get a patients normal anion gap, multiply their albumin by 3 (rough
estimate).
4. Compensation Formulas:
Metabolic Acidosis (can use either):
1. pCO2 decreases 1.2 for each mmol/L change in bicarbonate.
2. pCO2 should roughly equal last two digits of the pH.
Metabolic Alkalosis:
1. pCO2 increases 0.6 for each mmol/L change in bicarbonate.
Respiratory Acidosis:
- 108 -
5.
6.
7.
8.
9.
1. Acute: Bicarbonate increases 0.1 for every mmHg change pCO2.

2. Chronic: Bicarbonate increases 0.35 for every mmHg change in pCO2.
Respiratory Alkalosis:
1. Acute: Bicarbonate decreases 0.22 for every mmHg change in pCO2.
2. Chronic: Bicarbonate decreases 0.5 for every mmHg change in pCO2.
Causes of Respiratory Alkalosis: anxiety, hypoxia, lung disease with or without hypoxia
causing pulmonary receptor stimulation, CNS disease, Drugs (salicylates, catecholamines,
progesterone), pregnancy, sepsis, hepatic encephalopathy, liver disease, mechanical ventilation.
Causes of Respiratory Acidosis: CNS depression (drugs, CNS event), neuromuscular disorders
(myopathies, neuropathies), acute airway obstruction, severe pneumonia or pulmonary edema,
hemothorax/pneumothorax, thoracic cage injury, chest wall disorders, central hypoventilation,
COPD.
Causes of Metabolic Alkalosis:
Urine Chloride <10: emesis, NG suction, diuretics, post-hypercapneic, CF, villous
adenoma, congenital chloride diarrhea.
Urine Chloride >20: hypokalemia, primary aldosteronism, secondary aldosteronism
(CHF, cirrhosis, ascites), Cushings, Gitelmans, Liddles, licorice.
Misc: refeeding alkalosis, excess alkali administration, massive transfusions, milkalkali.
Causes of Non-anion Gap Metabolic Acidosis:
GI Bicarbonate Losses: Diarrhea, urinary tract diversions, ileus, fistulas, villous
adenoma.
Renal Bicarbonate Losses: RTA, renal failure, carbonic anhydrase inhibitors,
aldosterone inhibitors.
Misc: post-hypocapnea, HCl administration, TPN, urinary tract diversions.
Calculate the urine anion gap to differentiate between GI and renal causes. UAG:
UrineNa + UrineK UrineCl. If positive, then GI cause most likely. If negative, then
renal cause.
Causes of Anion Gap Metabolic Acidosis:
M-Methanol
U- Uremia
D- DKA/AKA/Starvation ketosis
P- Propylene glycol(lorazepam gtt), paraglutamic acid(APAP toxicity)
I- INH/Iron
L-Lactic Acidosis
E- Ethylene Glycol
R- Rhabdomyolysis
S- Salicylates
Haber RJ. A practical approach to acid-base disorders. West J Med. 1991; 155: 146-151.
Hyponatremia
1. Classify total body sodium status of the patient first
Edema, elevated neck veins, etc=total body sodium is elevated
Dry mucous membranes, orthostatic VS, etc=total body sodium is decreased
2. Then classify the patients total body water status in relation to sodium by the beaker principle
If the patient is hyponatremic and total body sodium is elevated (ie edema, elevated
neck veins), their total body water is even greater
- 109 -
3.
4.
5.
6.
7.
8.
If the patient is hyponatremic and total body sodium is decreased, (ie dry, tachy) their
total body water is relatively higher but may be normal or slightly low
Check serum osm, urine osm, urine sodium
Hypertonic hyponatremia is due to the gain of impermeable solute other than sodium (i.e.
glucose-no osmolar gap) or IV mannitol or glycine (will have osmolar gap).
Hypovolemic Hyponatremia: ADH is being secreted in order to maintain intravascular volume.
Renal sodium loss: Diuretics, osmotic diuresis (mannitol), adrenal insufficiency, salt
wasting nephropathy, bicarbonaturia (RTAs, emesis), ketonuria, cerebral salt wasting
syndromes. Serum osm < 280. Urine sodium > 20.
Extrarenal sodium loss: GI (vomiting, diarrhea), blood loss, surgical drains, excessive
sweating (marathon runners), fluid sequestration (bowel obstruction, pancreatitis,
peritonitis, burns, muscle trauma). Serum osm > 280, urine sodium < 10. These patients
will have to be getting free water in order to lower their sodium.
Euvolemic Hyponatremia:
Hypothyroid
Adrenal Insufficiency
Psychogenic polydipsia (need to drink at least 10 to 15 L/day, low urine osm), beer
potomania (low urine osm)
SIADH
1. Pulmonary: infection (PNA, TB), acute respiratory failure
2. CNS: mass lesions, stroke, inflammatory and demyelinating disorders, meningitis,
hemorrhage, trauma, acute psychosis.
3. Neoplastic: remember small cell lung CA, others.
4. Drugs: carbamazepine, vincristine, cyclophosphamide, opiate derivatives,
desmopressin, SSRIs, TCAs.
5. Other: post-op state, pain, severe nausea, HIV.
Hypervolemic Hyponatremia: Increased volume of extracellular fluid.
Cirrhosis, CHF, nephritic syndrome. Urine sodium < 20.
Treatment
Fire Water: Only give 3% NaCl (513 meq sodium per liter) if patient is seizing, in a coma,
or serum sodium is less than 110 to 115 meq/L (dont give if they are asymptomatic, as this
is likely chronic). Call renal fellow before initiating 3% NS! Initial goal is to correct at 1 to
2 meq/L per hour until sx resolve or sodium is 118 meq/L. Then, stop the 3% NaCl, call
renal fellow and discuss plan. From here the goal will be to correct no more than 8 to 10
meq/L over the first 24 hours from the initial sodium.
Correcting the serum sodium too quickly can result in central pontine myelinolysis (CPM)
manifested as flaccid paralysis, dysphagia, dysarthria.
General guideline for correction is 0.5 meq/hour. Goal is 8 to 10 meq/L over the first 24
hours. Monitor electrolytes q 4 hours at least. Based upon result may need to adjust fluid
rate or switch fluid altogether.
Hypovolemic Hyponatremia: use 0.9% NaCl or normal saline (154 meq/L). See above for
3% NaCl indications.
Euvolemic Hyponatremia: If asymptomatic, initiate fluid restriction to less than 1 Liter per
day. Watch free water in gtts and meds. See above for 3% NaCl indications.
Hypervolemic Hyponatremia: Fluid restriction. Diuresis. If unable to get volume off with
diuresis (i.e. diuretic resistance, tenuous hemodynamics, may need to call renal fellow to
discuss ultrafiltration or SCUF).
To calculate the change in serum sodium per liter of fluid (i.e. NS, NS etc):
- 110 -
Infusate Na+ - Serum Na+ / TBW + 1

Androgue HJ, Madias NE. Hyponatremia. NEJM 2000. 342 (21): 1581 9.
Hypernatremia
1. The majority of the time is due to free water loss, but can also be caused by hypertonic sodium gain.
In order to maintain the hypernatremia, requires impairment of thirst or inadequate access to free
water. Therefore, most commonly occurs in hospitalized patients such as those in the ICU, AMS, and
the elderly.
2. Assessment: volume status, urine output, urine osm, urine sodium, serum osm.
3. Symptoms: muscle weakness, confusion, coma, thirst.
4. Net Pure Water Loss as a cause
Unreplaced insensible losses (septic and febrile)
Not drinking due to impaired thirst or no access to water (on ventilator)
Diabetes Insipidus: patient is hypovolemic, urine output much greater than 1 Liter per day.
Urine osm < 250. Use DDAVP to differentiate central from nephrogenic.
1. Central DI: urine osm should increase with DDAVP. Causes include CNS trauma or infection, brain
tumors, cerebral aneurysms, granulomatous diseases (TB, sarcoid, histiocytosis X).
2. Nephrogenic DI: no change in urine osm with DDAVP. Causes include lithium, demeclocycline,
amphotericin B, V2 receptor antagonists, foscarnet, hypercalcemia, hypokalemia, renal disease.
5. Net Hypotonic Fluid Loss as a cause
Renal causes: loop diuretics, osmotic diuresis (e.g. glucose), post-obstructive diuresis,
polyuric phase of ATN, intrinsic renal disease. Generally, these patients are hypovolemic,
urine osm > 500, urine output > 1 L/day, urine Na+ > 20.
GI causes: emesis, diarrhea, NG suction, enterocutaneous fistula, use of osmotic cathartic
agents (lactulose etc.).
Cutaneous causes: burns, excessive perspiration
6. Net Hypertonic Sodium Gain as a cause
Hypertonic sodium bicarbonate infusion, hypertonic feeding preparations, ingestion of a lot
of sodium chloride (salt lick?), ingestion of sea water, primary hyperaldosteronism,
Cushings syndrome, hypertonic dialysis, infusion of hypertonic saline, sodium chloride
rich emetics. Patient is usually euvolemic to hypervolemic, urine osm > 500, urine Na+ >
100. It is hard to get this if patient has normal renal function!
7. Treatment
If sodium is corrected too rapidly, patient may develop cerebral edema.
Maximum correction per day is 10 meq/L.
Calculate the Water deficit and replace the deficit according to the above goal. May want to
check lytes q6 hours to make sure you are not over correcting or that you are correcting fast
enough. Also, add about 30 cc per hour of insensible losses.
Water Deficit: TBW X (1 140/serum sodium). TBW is weight in kg X 0.4 in women and
0.6 in men.
If patient is hypovolemic, fill the tank first with NS (sodium cannot get higher than 154
meq) and then work on the rest of the free water deficit with NS.
If patient is hypervolemic, D5W is usually the best IVF to use.
Remember to use NG/OG to give free water. As an example you can write: 250 cc of free
water NG q 6 hours.
With diabetes insipidus, it is a different story and you should call the renal fellow.
- 111 -
Androgue HJ, Madias NE. Hypernatremia. NEJM 2000; 342 (20): 1493 9.
Hypokalemia
1. Usually, patients with mild hypokalemia are asymptomatic. Non-specific symptoms include:
lassitude, constipation, generalized weakness. With levels less than 2.5, muscle necrosis can occur and
with levels less than 2, ascending paralysis is possible.
2. EKG changes: T wave flattening, ST segment depression, U waves, QT prolongation, arrhythmias.
3. Causes:
Decreased intake (i.e. alcoholics)
GI losses: infectious diarrhea, tumors (VIPoma, villous adenoma, ZE syndrome), jejunoileal
bypass, malabsorption, chemotherapy, radiation enteropathy.
Renal losses: Diuretics, mineralocorticoids (fludrocortisone), high dose glucocorticoids, drugs
associated with magnesium depletion (aminoglycosides, cisplatin, amphotericin), high dose
abx, mineralocorticoid excess (primary hyperaldosteronism, congenital adrenal hyperplasia,
rennin secreting tumor, Cushings syndrome, renovascular/malignant hypertension, vasculitis),
apparent mineralocorticoid excess (Liddles syndrome), impaired chloride associated transport
(Gitelmans and Bartters syndrome).
Transcellular Shift: 2 agonists (epinephrine, pseudoephedrine), bronchodilators, tocolytics,
theophylline, caffeine, insulin overdose, verapamil overdose, alkalosis.
4. Treatment:
Make sure you check the magnesium, because you need to replete that too- via IV.
Check the creatinine! Give K+ carefully to those with ARF/CKD. Call renal fellow if you have
any questions. Generally, you do not correct the K+ and Magnesium of patients with ESRD.
PO and IV are equivalent. In general, 10 meq of KCL will raise the serum K+ by 0.1 meq/L. If
the K+ is low enough, you will often want to combine PO and IV.
You can give 10 meq per hour of KCl through a peripheral IV and 20 meq per hour through a
central line.
Gennari FJ. Hypokalemia. NEJM. 1998; 339 (7): 451 8.
Hyperkalemia
1. ECG changes: peaked T waves, shortened QT PR and QRS lengthening disappearance of P

waves sine wave.
2. Symptoms: muscle weakness, abdominal distension.
3. Treatment: C BIG K DROP
C- 1 to 2 Amps of Calcium Chloride to stabilize myocardium if ECG changes
B- Beta agonists: albuterol given as 3 continuous nebs; Bicarb: 2 Amps NaHCO3
I- Insulin: 10 units regular insulin IV
G- Glucose: 1 to 2 AMPs of D50.
K- kayexalate: 30 to 60 grams PO- need to make em poop to work- overall controversial tx
D- Diuretics (lasix), Dialysis
R- Repeat the lab draw to make sure value is correct.
O- Observation via telemetry at least.
P- 112 -
3.Caution in ESRD!
-They can tolerate higher levels of K as it is a chronic issue-Check the ECG!
-Check Phos and Ca and calculate Ca/Phos product (multiply the 2 values) prior to giving
calcium- if higher than approximately 70 high risk of precipitation and ectopic calcification
Hypomagnesemia
1. ECG changes: PR and QT prolongation
2. Symptoms: tremor, fasicilulations, ataxia, tetany, seizure
3. Often associated with hypocalcemia, hypokalemia
4. Replete- if in the hospital use IV as PO is rarely effective-causes diarrhea.
5. If patient has ESRD, do not replete the magnesium unless cleared by fellow.
6. General Sliding Scale:
Serum Magnesium
1.8 to 1.9
1.5 to 1.7
1.2 to 1.4
< 1.2
Magnesium Sulfate Dose IV

1 gram
2 grams
3 grams
4 grams and recheck
Hypophosphatemia
1. Again, watch repletion in ARF/CKD and generally do not replete in someone with ESRD unless
cleared by renal fellow.
2. Follow Ca, K, and Mg levels as you are repleting.
3. IV repletion: 15 mmol of Kphos (has 22 meq of K+), Sodium phos.
4. PO repletion: Kphos or Neutraphos: one to two tabs TID to QID; can also give skim milk with meals
also.
Hyperphosphatemia
1. You will usually see this in patients with ESRD.
2. If really high, calculate the Calcium-Phos product by multiplying serum calcium and serum phos. If
> 70, worry about ectopic calcifications.
3. Treatment usually proceeds by giving a medication which binds phosphorus in the gut. If calcium is
high, do not give calcium-containing compounds. Give with meals. What you give will also depend
what is on formulary at the specific hospital.
Calcium carbonate
Calcium acetate (PhosLo)
Aluminum Hydroxide (Amphogel)
Renagel.
Hyper- and Hypocalcemia- see endocrine section.

Acute Kidney Injury (A.K.A. Acute Renal Failure)
1. Definition: Increase in Cr of 0.5 mg/dL, within 1 week or less, if baseline is less than 2.5 mg/dL or
an increase in serum Cr by more than 20% if baseline is greater than 2.5.
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2. Associated with a 20% mortality rate.

3. Three Causes:
Pre-renal: conditions leading to decreased renal perfusion.
1. Hypovolemia: GI, urinary, skin losses. Hemorrhage. Third spacing (Liver disease, burns).
Inadequate cardiac output.
2. Hypotension: sepsis, anesthesia and medication induced, hepatorenal syndrome, relative
hypotension.
3. Pharmacologic: NSAIDs, ACE inhibitors, contrast dye.
4. Large vessel: thrombosis, embolus, dissection, RAS.
Intra-renal: diseases or states that affect the nephron (e.g. glomeruli, tubules, vessels, or
interstitium). Most common is ATN.
1. Small vessel: atheroembolism, malignant hypertension, scleroderma, TTP/HUS, DIC.
2. Glomeruli: acute or rapidly progressive glomerulonephritis, vasculitis.
3. Tubules: ATN (causes include hypovolemia, hypotension, sepsis, IV contrast,
aminoglycosides, amphotericin B, cisplatin, myoglobin, hemoglobin), obstruction (uric acid,
calcium oxalate, acyclovir, indinavir, light chains).
4. Interstitium: AIN (NSAIDS, antibiotics, pyelonephritis, infiltration by lymphoma/sarcoid).
Post-renal: obstruction from renal pelvis to urethra.
1. Ureteral: tumors, calculi, clot, sloughed papillae, retroperitoneal fibrosis, lymphadenopathy.
2. Bladder neck: tumor, thromboemboli, calculi, prostatic hypertrophy or carcinoma,
neurogenic.
3. Urethral: strictures, tumors, obstructed indwelling catheters.
Diagnosis:
Post-renal
ATN
Acute GN
AIN
BUN:Cr
Urine Na
Prerenal
> 20:1
<20
>20:1
Varies
< 20:1
>40
>20:1
<20
Urine Osm
FeNa (%)
>500
<1
<400
Varies
<400
>2
>400
<1
<20:1
<20 (acute), >40
(few days)
Variable
<1 (acute), >1 (few
days)
FeUrea (%)
Urinary
Sediment
<35%
Benign
or
hyaline
casts
Varies
Normal or
red cells,
white
cells, or
crystals
>35%
Renal
tubular
epithelial
cells,
granular
and
muddy
brown
casts.
Dysmorphic
red cells
and red cell
casts.
White cells, white

cell casts, with or
without eosinophils.
+ Hansels stain.
4. Further Diagnostic Studies to Consider:

Renal Ultrasound.
Spot urine protein and creatinine to calculate the urine protein:Cr. Good estimate for 24 hour
protein excretion.
Place foley especially if anuric or worried about obstruction.
Follow urine output closely.
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CK if worried about rhabdomyolysis.
Singri N, Ahya SN, Levin ML. Acute renal failure. JAMA. 2003; 289 (6): 747-751.
Esson ML, Schrier RW. Diagnosis and treatment of acute tubular necrosis. Ann Intern Med. 2002;
137: 744 752.
CKD Stages
Stage 1: Kidney damage with normal or increased GFR. GFR 90 mL/min/1.73m2.
Stage 2: GFR 60 89 mL/min/1.73m2
Stage 3: GFR 30 59 mL/min/1.73m2
Stage 4: GFR 15 29 mL/min/1.73m2. Preparation for dialysis (i.e. access planning).
Stage 5: GFR < 15 mL/min/1.73m2 or on dialysis.
Renal Replacement Therapies (RRT)

1. Indications for emergent dialysis:
A- acidosis (esp. if pH < 7.2)
E- electrolytes (e.g. hyperkalemia- with EKG changes and/or level > 6.5)
I- Ingestion (such as ethylene glycol, lithium)
O- volume overload
U- uremia
2. RRT Modalities
There are two main types of dialysis, intermittent and continuous. The difference between the
two is duration. Intermittent is usually done 4-6 hours per day and continuous is done 24 hours
per day.
3. Indications
All RRT therapies have the same indications: severe acidemia, electrolyte abnormalities
(hyperkalemia), volume overload, uremia, and drug overdoses.
Continuous renal replacement therapies (CRRT) are primarily used in the ICU setting in
hemodynamically unstable patients. Intermittent hemodialysis (IHD) is used in
hemodynamically stable patients.
Both modalities are effective at removing solutes, but IHD allows for faster removal of solutes.
CRRT allows for slower removal of volume and solutes resulting in less fluctuation of solutes
and continuous volume control.
The disadvantages of CRRT include 1) immobilization, as patients are connected to a machine
24 hours per day; 2) clotting, therefore, there is a need for anticoagulation with heparin; 3)
higher costs; 4) higher demands on nursing time.
The disadvantage of IHD is more significant volume shifts which can result in hemodynamic
instability.
4. Three types of dialysis
1. Hemodialysis: Solute removal by diffusion. Solutes passively diffuse down their concentration
gradient. Dialysate is run countercurrent to the patients blood flow to increase the gradient.
Urea, creatinine, and potassium move from the blood to the dialysate. Calcium and bicarbonate
move from the dialysate to the blood. No volume is removed.
2. Hemofiltration or Ultrafiltration: Solute and volume removal, although the main purpose is to
remove volume. Solute removal is by convection (solute drag) and solutes are only
significantly removed if it is done for a prolonged period of time. Transmembrane pressure
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gradient drives water across a semi permeable membrane and drags solutes with it.
Replacement fluid is needed, as high ultrafiltration causes volume contraction and can lead to
hypotension.
3. Hemodiafiltration: Combination of both hemodialysis and hemofiltration. Solutes are removed
by both diffusion and convection. Volume is also removed and, therefore, a replacement fluid
is needed. This is typical of outpatient dialysis.
5. IHD
Standard IHD: Uses one of the above 3 types of dialysis, done 4-6 hours per day. This is the
type of dialysis mainly used in patients with ESRD in an outpatient setting.
Sustained Low Efficiency Dialysis (SLED): Is slower IHD done for a longer period of time(612 hours). Allows for hemodynamic stability as has slower removal of solutes and volume.
This is becoming more popular and used frequently at Rose Hospital.
6. CRRT (done 24 hours/day)
Slow continuous ultrafiltration (SCUF): Dehydrating procedure used only for volume overload.
No intention of removing solutes. Transmembrane pressure gradient slowly drives water
across a semi permeable membrane. No replacement fluid is needed as goal is to remove fluid.
6-7 L of fluid can be removed daily.
Continuous Venovenous Hemofiltration (CVVH): Hemofiltration only, no hemodialysis.
Solutes removed by convection only and are efficiently removed over 24 hours. Replacement
fluid is needed as a large amount of volume is being removed.
Continuous Venovenous Hemodialysis (CVVHD): Solutes removed by diffusion. Allows for
greater solute removal than CVVH. There is no volume removal as no hemofiltration is done
and therefore there is no replacement fluid.
Continuous Venovenous Hemodiafiltration (CVVHDF): Combination of CVVH and CVVHD.
Solutes removed by convection and diffusion. Volume can be removed and replacement fluid is
needed.
7. The choice of RRT needs to be individualized. Identify the primary goal for the patient, i.e. fluid
removal, solute removal, or both. Choice will also depend on what machines, nursing staff, etc are
available. Use the method with less side effects and greatest benefit in a given case. Treatment of the
underlying condition outweighs the choice of RRT.
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Neurology
Seizures
Seizures are a source of great excitement and drama for most nurses and housestaff, usually
unnecessarily so. No doubt they are difficult to watch, but if you can lend a little structure to the
inevitable chaos of the seizing patient, it will be easier on everyone. The first step is always the
sameensure the safety of the patient, then once the dust has settled you can figure out what triggered
the seizure.
The approach to the seizing patient:
1. Remain calm, and try to keep everyone around you calm as well.
2. Note the time of onset and duration of the seizurethis means looking at your watch, because
it will always seem longer than you think if youre just estimating.
3. Check a STAT finger-stick blood glucose.
4. Try to determine if the seizure was focal or generalized in its onset. This is often difficult
information to come by.
5. There usually isnt any reason to call a COR.
6. Keep the patient safe. Place them in the left lateral decubitus position to prevent aspiration, and
try to keep them from banging their head and limbs against bedrails, the floor, etc.
7. Dont put anything in the seizing patients mouth.
8. Most seizures are self-limited and brief, with most lasting less than one minute. When you get
called about a seizure, have the nurse have lorazepam 4 mg IV ready at the bedside, but you
DO NOT need to give it unless the seizure has not stopped by two minutes. If it hasnt selfterminated by two minutes, the patient is at relatively high risk for ongoing seizures and even
status, so must be treated.
9. If the seizure is still going at two minutes, give 2 mg of lorazepam IV. Repeat lorazepam 1-2
mg every one to two minutes as needed until seizures have stopped. Watch for respiratory
depression with higher doses of lorazepam. Consider transfer to higher level of care if needed.
Consider phenytoin load if long-lasting seizure.
10. Evaluate for underlying cause of seizure once seizure has terminated.
New-onset seizures in the hospitalized patient are usually provoked, meaning that there is some
underlying identifiable cause such as a metabolic abnormality, infection, etc. that will explain the
seizure.
Differential Diagnosis:
Metabolic: hypo- or hypernatremia, hypo- or hyperglycemia, hypo- or hypercalcemia,
hypomagnesemia, hyperosmolality, uremia, hyperammonemia, hyperthyroidism
Toxic: PCP, cocaine, or amphetamine intoxication; ETOH withdrawal
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History:
Drugs: haloperidol, TCAs, levofloxacin, imipenem, penicillins, cephalosporins,

bupropion, amantadine, meperidine, fentanyl, anticholinergics, lidocaine, procaine,
methotrexate, vincristine
Trauma: subdural or epidural hematoma, subarachnoid hemorrhage
Vascular: ischemic stroke, cerebral hemorrhage
Infection: meningitis, encephalitis
Tumor: metastatic disease, primary brain tumor
Obtain all available history regarding seizure from witnesses

Review chart
Any prior history of seizures or epilepsy?
What is the admitting diagnosis?
Any current infections? Any history of HIV?
What are the medical comorbidities, i.e. renal failure, hepatic failure, hypoxia?
Any h/o ETOH or drug abuse or withdrawal?
What are the recent labs?
Review the patients medications carefully
Physical Examination:
Vitals: look for interictal arrhythmias, fever, hypertension, hypoxia
Check lateral aspect of tongue for laceration after seizure
Check for any evidence of head injury
Check for papilledema
Check for meningismus
Perform careful pulmonary exam, listening for decreased breath sounds or rales that
may suggest aspiration during seizure
Look for urinary or fecal incontinence
Briefly assess level of alertness after seizureorientation, simple commands, counting
backwards, etc.
Look for any signs of hemiparesis, reflex asymmetry, etc.
Diagnostic Work-up:
CBC, CMP, Mg
Consider utox, lumbar puncture, TSH, alcohol level if clinically indicated
If on any antiepileptic medications, check appropriate levels
Check routine bedside EEG
If the patient has a focal deficit on neurological exam and/or no other cause is identified
on the above studies, obtain CT or MRI of brain with and without contrast
Serum prolactin levels may be elevated for up to one hour following a seizure
Seizures also result in mild peripheral leukocytosis due to demargination of neutrophils,
elevated CPK, anion gap metabolic acidosis, and elevated serum lactate; these are all
transient and resolve within a few hours
Treatment:
Make sure the patient has adequate IV access, i.e. two working peripheral IVs.
Treat any underlying metabolic, infectious, or other cause identified on the above
evaluation.
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For a single first-time seizure that has stopped on its own, no treatment is warranted
beyond treating any provoking factors.
Antiepileptic drugs are reserved for patients with status epilepticus, those with multiple
seizures, and those with risk factors that make them more likely to continue to
experience seizures.
If the patient is in status, treat as per the status epilepticus protocol provided in a
separate section.
If a structural lesion is found or if there is a metabolic insult that cannot be rapidly
treated, the patient should be loaded with phenytoin 20 mg/kg IV or fosphenytoin 20
PE/kg IV.
Place the patient on seizure precautions.
Headache Emergencies
Headache is one of the most common complaints among patients in the clinic, in the ED, and on the
wards, so its important to know when a headache indicates a life-threatening process. This is
sometimes easier said than done.
When someone says they have the worst headache of my life, what does that really mean? Thats
going to happen to everyone at some pointif youve never had a headache before, any headache will
be the worst headache of your life. Most of the time its nothing, and you dont need to proceed with
imaging, LP, labs, or any other workup.
However, there are the minority of headache cases that are something more major, with potentially
lethal underlying etiologies that must be diagnosed early and treated appropriately. So, what signs or
symptoms should you worry about?
There are several red flags in headaches that should push you to undertake a more thorough
evaluation of the headache patient. These include:
Focal neurological deficits
Fever
Meningismus
Papilledema
Associated seizures
Abrupt onset with pain maximal in intensity at onset (thunderclap headache)
Onset of frequent headaches after age 50 without prior history of headaches
Altered level of consciousness
Headache worsening with valsalva, bending over, cough
Headache awakening patient from sleep
Change from prior headache pattern
Subarachnoid hemorrhage
Intraparenchymal cerebral hemorrhage
Meningitis or encephalitis
Cerebral venous sinus thrombosis
Pituitary apoplexy
Brain tumor
Brain abscess
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Spontaneous intracranial hypotension

Subdural or epidural hematoma
Extracranial vascular dissection (carotid or vertebral arteries)
Complicated migraine
Careful History:
Ask about any prior headaches (character, location, quality, duration, associated
symptoms) for comparison to current headache
Ask about current headache (rate of onset, intensity, quality, location, associated
symptoms, alleviating factors, exacerbating factors)
Is it worse with Valsalva? Cough? Sneeze?
Are headaches worse in the morning or do they awaken the patient from sleep?
Are they associated with nausea and/or vomiting?
Is there any associated photophobia or phonophobia?
Is there any history of head trauma, either recent or remote?
Is there any seizure activity noted?
Is there any fever or other evidence of systemic illness or infection?
Careful Physical Examination:
Check the vitals: fever, tachycardia, Cushings reflex (hypertension with bradycardia,
associated with increased intracranial pressure)
Look for any focal neurological deficits on exam
Cranial nerve VI palsies are common false localizing signs with increased ICP
Diagnostic Work-up:
CT head without contrast is usually the first step, since intracranial hemorrhage is a
chief concern in abrupt-onset severe headaches.
o Sensitivity of CT for acute intracranial bleeds approaches 100% in the first 1224 hours, but drops after 24 hours as well as with small volumes of blood and
anemia (hematocrit <30).
If CT of the head is negative and clinical suspicion for subarachnoid hemorrhage
remains high, you MUST do a lumbar puncture to rule out this diagnosis.
o CSF will show elevated RBCs that do NOT clear from tube #1 to tube #4 and
elevated protein.
o Xanthochromia (yellowing of the CSF) may also be seen, but remember that this
takes 8-12 hours to occur as it is the result of the breakdown of the RBCs
within the CSF, which takes time.
LP if evidence of infection.
Consider MRI if CT has not provided definitive diagnosis.
Use your neurology consultants early and often.
Notes:
In general, migraines, cluster headaches, and tension headaches tend to be fairly stereotypical
within the same patient.
Seizures are decidedly uncommon as a feature of any of the primary headache syndromes (i.e.
migraine, cluster, tension) and suggest an underlying structural CNS lesion.
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Papilledema takes at least 24-48 hours to form and so will not be present in the acute setting. If
it is seen, it implies possible increased intracranial pressure.
Migraines, cluster HAs, and tension HAs are gradual in onset, building in intensity over
several minutes to even hours. True thunderclap headaches from subarachnoid bleeds, etc.
are dramatic and abrupt in onset, with pain that is maximal from the beginning.
Onset of primary headache syndromes after the age of 50 years is uncommon, so the older
patient with new-onset frequent headaches must be evaluated for potential sources such as
tumor or chronic subdural hematoma.
None of the primary headache syndromes should produce a frank alteration in consciousness.
While focal neurological deficits may be part of a patients migraine aura or even a complicated
migraine, remember that the patient will often have a history of similar events in the past to
help clarify this question. When in doubt, get a scan and work them up.
CNS Infections
Clinical Presentation:
Bacterial meningitis typically presents with fever, stiff neck, and headache with progressive
deterioration in level of consciousness. Seizures and focal neurological deficits can also occur.
Viral meningitis typically presents with fever, headache, stiff neck, and constitutional signs of
viral infection such as GI symptoms or URI. Significant alteration in consciousness does not
occur and should suggest another etiology.
Encephalitis typically presents with fever, headache, altered mental status, and focal
neurological signs.
Presence of a diffuse maculopapular rash suggests either enterovirus or meningococcus as the
causative organism.
o The rash of Neisseria meningitides begins as a maculopapular rash on the trunk and
lower extremities that rapidly becomes petechial or purpuric and spreads to involve the
conjunctivae and mucous membranes.
o The rash of enterovirus starts on the face and trunk then spreads to the extremities.
Rashes due to antibiotics usually start on the face, spread to the chest and trunk, and then to the
lower extremities. By the time it reaches the lower extremities, the rash on the face is often
nearly gone.
Epidemiology:
In adults 15-50 years, Streptococcus pneumoniae and N. meningitides are the most common
organisms causing community-acquired bacterial meningitis.
Pneumonia, acute sinusitis, and acute otitis media are common preceding illnesses for
pneumococcal meningitis.
Risk factors for pneumococcal meningitis: complement deficiency, hypogammaglobulinemia,
splenectomy, head trauma with basilar skull fracture, ETOHism, diabetes, sickle cell disease,
thalassemia major, multiple myeloma
Patients with defects in cell-mediated immunity must be covered against Listeria
monocytogenes. (This includes those with HIV, pregnancy, hematologic malignancies, chronic
steroid use, cancer, chemotherapy, organ transplantation, alcoholism, the elderly, and infants.)
In patients who have undergone neurosurgical procedures, excluding shunts and Ommaya
reservoirs, the most common organisms causing meningitis are gram-negative bacilli and
staphylococci.
In patients with CSF shunts and Ommaya reservoirs, coagulase negative staphylococci and
Staphylococcus aureus are the most common organisms.
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DDx for fever, headache, stiff neck: bacterial meningitis, viral meningitis, fungal meningitis,
tuberculous meningitis, drug-induced hypersensitivity meningitis, carcinomatous meningitis,
meningitis due to inflammatory disorders (SLE, sarcoidosis, Sjgren syndrome), subarachnoid
hemorrhage.
DDx for fever, headache, stiff neck plus altered level of consciousness, seizures, or focal
neurological deficit: bacterial meningitis, viral encephalitis, Rocky Mountain Spotted Fever,
fungal meningitis, brain abscess, epidural abscess, subdural empyema, venous sinus
thrombosis, subarachnoid hemorrhage.
Evaluation:
Immediate blood cultures and empiric antibiotic and adjunctive therapy should be initiated
prior to lumbar puncture and before head CT.
You do NOT need a CT prior to lumbar puncture in every patient!
In patients with suspected bacterial meningitis, you should get a CT before LP if one or more of
the following is present: (1) focal neurological deficit; (2) new-onset seizure; (3) papilledema;
(4) altered level of consciousness; or (5) immunocompromised state.
CT cannot reliably predict whether a patient will or will not herniate after LP in bacterial
meningitis in the absence of focal asymmetric parenchymal lesions!
Perform lumbar puncture if safe:
Never defer antibiotics until after the LP is done.
CSF gram stain and culture results may be affected if antibiotics are given for several hours
prior to LP, but CSF cell count and diff, glucose, and protein will not be affected enough that a
diagnosis of bacterial meningitis cannot be inferred.
Always obtain opening pressure on the LP.
Send CSF for cell count and differential on tubes 1 and 4, glucose, protein, Gram stain, and
culture to start. You can add viral PCRs, fungal cultures, VDRL, and other studies depending
on the initial CSF profile.
Typical CSF profile in bacterial meningitis: opening pressure greater than 18 cm H2O;
polymorphonuclear (PMN) leukocytosis; elevated protein; low glucose (CSF-blood glucose
ratio less than 0.6).
Typical CSF profile in viral meningitis: opening pressure usually normal (less than 18 cm
H2O); lymphocytic leukocytosis (may be PMN predominant in first 24 hours); normal to
slightly elevated protein; normal glucose.
Remember, LP is never a life-saving procedure!
1) If concerned about increased intracranial pressure, consider a bolus of IV mannitol 20
mg/kg, then LP 20 minutes later with careful measurement of opening pressure. If
opening pressure is markedly elevated (greater than 35-40 cm H2O), stop the LP and
collect the CSF in the manometer; this will usually give you enough fluid for basic CSF
studies to make a diagnosis.
2) If there is significant concern about herniation with LP, the procedure can be deferred
while the patient is empirically treated with antibiotics until the patient stabilizes
enough that LP is deemed safe or the organism if identified by blood culture.
Treatment:
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Empiric antibiotic selection based on age, associated premorbid conditions, and possibility that
a penicillin- and cephalosporin-resistant strain of S. pneumoniae is responsible for the patients
meningitis.
For patients 15-50 years: ceftriaxone 2 grams IV every 12 hours, vancomycin one gram IV
every 12 hours, and acyclovir 10 mg/kg IV every 8 hours.
For patients over the age of 50 and in immunocompromised patients, add ampicillin 2 grams IV
every 4 hours to the above regimen to cover against Listeria.
Dexamethasone 10 mg IV every 6 hours should be given for a total of four days, with the first
dose administered with or 15 to 20 minutes prior to the first dose of antibiotics.
If initial CSF profile is consistent with bacterial meningitis, acyclovir can be discontinued.
Antibiotic regimen can be refined once Gram stain and culture results with sensitivities return.
Duration of therapy: S. pneumoniae or H. influenzae 10-14 days IV abx, N. meningitides 5-7
days of IV abx followed by 2 days of oral rifampin, Listeria 3-4 weeks of IV abx.
Patients with suspected meningococcal meningitis must be placed in isolation for the first 24
hours after initiation of antibiotic therapy.
Anyone who has come into contact with a patient with meningococcal meningitis must receive
prophylactic antibiotics with rifampin 600 mg bid for 2 days, a single dose of ceftriaxone 250
mg IM, or a single dose of ciprofloxacin 500 mg PO.
Contacts of patients with H. influenzae meningitis must receive prophylactic treatment with
rifampin 600 mg daily for four days
Viral meningitis requires supportive care only.
Headache in viral meningitis may persist for months and is best managed with NSAIDs and
amitriptyline.
Prevention:
Those over age 65, those with asplenia, and those over age 2 years who are at risk for
pneumococcal disease as a result of chronic illness should receive the pneumococcal vaccine,
which confers protective antibody levels for 5 years in most adults.
The meningococcal conjugate vaccine is recommended prior to entry into high school.
Notes:
Mortality in bacterial meningitis remains 25% despite optimal therapy.
50% of patients develop complications such as cerebral edema, hydrocephalus, septic venous
sinus thrombosis, arteritis, seizures, cranial nerve palsies, septic shock, DIC, renal failure,
SIADH, cerebral salt wasting syndrome, and ARDS.
In HIV patients, opportunistic agents to consider include Toxoplasma, CMV, EBV, VZV, JC
virus (causes progressive multifocal leukoencephalopathy, PML), TB, syphilis, Nocardia,
Cryptococcus, Candida, Aspergillus, Coccidioides, and Histoplasma
In transplant patients, consider fungi, molds, toxo, CMV, VZV, EBV, HHV-6.
A brief word about herpes encephalitis:
o 90% of cases are due to reactivation of HSV-1, usually in previously healthy patients.
Fever, headache, and altered mental status are invariably present.
Other common findings include seizures, aphasia, weakness, impaired memory,
and hallucinations.
MRI reveals hyperintensities in one or both frontotemporal regions.
LP shows increased opening pressure, lymphocytic pleocytosis, elevated
protein, and normal glucose.
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CSF HSV PCR is 95% sensitive and 100% specific, but can be falsely negative
within the first 72 hours of symptoms. If clinical suspicion is high with a
negative HSV PCR, the patient should be treated empirically with acyclovir and
the LP and PCR repeated in 2-3 days.
Treatment is acyclovir 10 mg/kg IV every 8 hours for 14-21 days. Mortality is
70% without treatment, but drops to 19% with therapy. If the patient survives
the initial infection, morbidity is nearly 100% and varies from mild cognitive
impairments to more significant deficits such as hemiparesis or epilepsy.
A bloody CSF can alter some results of the LP:
WBC count is increased by 1 WBC/mm3 for every 700 RBCs/mm3.
CSF protein concentration will be increased by 1 mg/dL for every 1000 RBCs /mm3.
If CSF is contaminated by blood, a false-positive CSF EBV PCR and a false-positive CSF
VDRL may occur.
If CSF is contaminated by blood, a false-negative CSF HSV PCR may result.
Anoxic Brain Injury

Causes:
Cardiopulmonary arrest and other causes of decreased cardiac output, prolonged hypotension,
prolonged hypoxia, prolonged hypoventilation. It only takes 2-5 minutes of ANOXIA to cause
irreversible damage, but longer periods of hypoxia or decreased cerebral perfusion will cause
permanent injury as well.
Clinical Presentation:
Coma, lack of purposeful responsiveness to stimulation and pain, myoclonus, decorticate (flexor) or
decerebrate (extensor) posturing, loss of some or all brain stem reflexes (i.e. blown pupil, decreased
blink reflex, loss of gag/respiratory drive)
Initial Workup after patient stabilized:
Imaging: Head CT: r/o acute bleed, severe cerebral edema, or mass lesion as explanation.
Labs: LFTs, Chem 7, Mg, Phos, Ca, ABG. Important to r/o severe metabolic disturbances as
they confound the neurologic exam, but may be reversible
Initial Management:
Cooling Protocol, DONT WAIT. Goal: hypothermia initiated within 90 minutes, for patients
who have no ongoing cardiac dysrhythmia. Hypothermia to 33C with external cooling
blankets (or per hospital protocol) with use of paralytics. Hypothermia to be maintained for 24
hours followed by passive rewarming.
Avoid neuromuscular blockers, barbiturates, narcotics, and benzos OUTSIDE of the cooling
protocol. These medications can suppress brainstem reflexes and interfere with the
neurological exam and prognostication. If there truly is an anoxic injury, there should not be a
significant need to sedate patient.
If cerebral edema is present, elevate head of bed, hyperventilate, and avoid excess IVF. Serial
Head CTs q12-48 hours depending on severity. No evidence that mannitol or steroids improve
outcome if etiology is anoxia, but may be used in dire situations. If signs of impending
herniation (third nerve palsy or dropping brain stem reflexes) or head CT demonstrates severe
edema, neurosurgical consult for intervention.
Neurology consult for prognosis. They will want the patient to be OFF cooling protocol and
OFF all sedating medications to perform meaningful examination.
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Document type of arrest or arrhythmia if known, duration of CPR, and time to return to normal
vital signs. These things provide important information about prognosis.
Prognostic Hints (Evidence Level in parentheses):

1. Serum NSE (neuron specific enolase) levels >33 g/L at days one to three post-CPR accurately
predict poor outcome (Level B)
2. The assessment of poor prognosis can be guided by the presence of bilaterally absent cortical
SSEPs (N20 response) within one to three days (Level B).
3. The prognosis is invariably poor in comatose patients with absent pupillary or corneal reflexes,
or absent or extensor motor responses three days after cardiac arrest (Level A).
4. Patients with myoclonus status epilepticus within the first day after a primary circulatory arrest
have a poor prognosis (Level B).
5. There are inadequate data to support or refute whether neuroimaging is indicative of poor
outcome (Level U) .
Acute Spinal Cord Injury/Compression

Acute Spinal Cord Injury is most often due to trauma, with MVAs as the most common cause, and
will be recognized/managed in the ED, but acute nontraumatic compression can occur in the inpatient
setting.
Causes of Inpatient Acute Spinal Cord Injury or Compression: Epidural Abscess (think of those with
Diabetes, ETOH, IVDA or multiple comorbidities with prolonged hospital stay), SC ischemia
(operative complication, embolic infarct, or decreased perfusion), Metastatic tumor, Primary tumor, or
Epidural Hematoma (post procedure or coagulopathy)
Clinical Manifestation of Acute Cord Compression:
Can have symptoms stemming from nerve roots or the cord, depending on site of compression
Epidural abscess presents as neck or back pain that is relentless when patient lies in bed. It
often progresses to paresthesias, radiating pain that has radicular nature. Paralysis is late
finding.
If cord compressed before roots, usually see sensory loss, weakness, impairment of cutaneous
and proprioceptive sensation below the lesion. May have incomplete compression, so can have
crossed findings if Brown-Sequard syndrome (hemi-cord).
Poor control of bladder usually proceeds bowel dysfunction acutely.
In cauda equina or conus compression, pain in lower back, rectum, and legs with early loss of
bladder function and impotence. Saddle anesthesia.
In the first 24-48 hours of compression, expect a lower motor neuron pattern with flaccid tone
and hyporeflexia that transitions to spasticity and hyperreflexia. If left untreated, will progress
to wasting and atrophy at level of lesion and spastic paraplegia or quadriplegia below the
lesion.
Initial Evaluation:
EMERGENT MRI with and without contrast of region of spine of interest is GOLD
STANDARD. If spinal cord compromise is suspected, cannot wait until next day!! CT of
spine will not show soft tissue or abscess compression of cord unless bones are displaced and is
an inadequate study to r/o compression.
DO NOT LP if epidural abscess is suspected. LP can seed the CSF if needle transects pus
pocket. Wait for imaging and neurology consult to guide.
- 125 -
If abscess suspected, try to isolate etiology. Blood Cultures, Urine Cultures, Chest X-ray. ESR
(often elevated in epidural abscess).
Check Post Void Residual
Management:
Urgent Neurology and/or Neurosurgery Consult if appropriate.
Emergent Decompression indicated if cord compromise due to surgical lesion
Urgent Radiation therapy if non-resectable metastatic disease
If Epidural Abscess, start empiric antibiotics with MRSA coverage until bug isolated
In acute, noninfectious, SC injury, current recommendation is to treat with steroids within 8
hours of injury: starting methylprednisolone 30mg/kg bolus over 15 minutes followed by 5.4
mg/kg/h for 23 hours
Recommendations vary for subacute cord compression (i.e. epidural abscess, tumor), but most
use dexamethasone 4-20 mg q6h.
Status Epilepticus
Status Status epilepticus (SE) should be considered for:
Generalized tonic clonic (GTC) seizure lasting longer than 5 minutes. Look for stiffening with
or without rhythmic jerking, often bowel/bladder incontinence and/or tongue biting.
Any 2 or more GTC seizures without clearing of consciousness between them.
A GTC seizure followed by prolonged unconsciousness >15 minutes even after treatment.
Be suspicious of ongoing seizure activity for:
Unconsciousness with subtle rhythmic movements (eye or limb twitching) or fluctuating vital
signs.
Unconsciousness with a history of epilepsy AND history of noncompliance or NPO.
DONT PANIC:
Stay calm, near the head of the bed. Think of it like a code. Assess the situation, time the
seizure, and get assistance from the nurse immediately.
Do not try to restrain the patient. You (and the patient) will only end up hurt.
Err on the side of treating better to treat a non-seizure than to wait to treat SE.
Establish IV access ASAP if not already done.
Be prepared to intubate if necessary. Place oxygen once patient stable.
Notify the neurology resident for help with management.
EEG is not necessary unless inducing chemical coma.
Dont stop until the seizures stop!
Treatment protocol:
1. Benzos first! Choose one.
Ativan 0.1mg/kg IV: load 4mg, then 2mg IV q2 min up to 8mg; onset 6-7 min, off 12 hrs
Valium 0.2mg/kg IV: load 10mg, then 5mg IV q2 min up to 30mg; onset 2-3 min, off 15 min
2. Load Anti-Epileptic Drug (AED) at the same time! Choose one.
Dilantin (phenytoin/PHT): 20mg/kg IV load at 50mg/min (1500mg for 70kg)
Cerebyx (fosphenytoin/fPT): 20 PE/kg IV load at 150mg/min
Depakote (valproic acid/VPA): 25mg/kg IV load at 20mg/min
Phenobarbital (PB): 20mg/kg IV load at 75mg/min
- 126 -
Keppra (levetiracetam/LEV): 1500mg IV push over 5 minutes

3. Give more AED if still seizing! Use the same one. Check levels.
PHT 10mg/kg IV, goal serum level 25-30
fPT 10 PE/kg IV, goal serum level 25-30 (check phenytoin level)
VPA 10-25mg/kg IV, goal serum level 100-150
PB 10mg/kg IV, goal serum level 40-45
LEV 1500mg IV push over 5 minutes (no level)
4. Add a second AED (ask neurology resident for recs) if still seizing!
5. Give anesthetic if still seizing! EEG and intubate if not already done.
Versed (midazolam) 200mcg (microgram)/kg IV load, then 0.75-10mcg/min gtt
Propofol 1-2mg/kg load, then 2-10mg/kg/hr gtt
Pentobarbital 5-20mg/kg load, then 1-4mg/kg/hr gtt
Notes:
If no IV access, give Valium 10mg IM or PR to stop seizure and establish access
PHT/fPT/PB associated with arrhythmia and respiratory suppression stop infusion and reduce
rate
Phenobarbital can take up to 10 days to clear
VPA associated with platelet dysfunction, thrombocytopenia, and increased peri-surgical
bleeding risk
Beware of subclinical status uncover the patient and look for any rhythmic movement
- 127 -
Pulmonary & Critical Care

Basics of Chest X-ray Interpretation
Remember to be systematic every time. Avoid tunnel vision and look at the whole picture.
Step 1: Is the film correct?
Correct patient and exam?
Correct technique?
Check rotation The medial ends of the clavicles should be centered over the spinous
processes.
Penetration If correct, the vertebral bodies should be barely seen in the lower cardiac
silhouette, and intervertebral spaces are just visible. Over penetrated films look darker.
Check inspiration - The right diaphragm at full inspiration should be between the 5th and 7th rib.
If there are more than 10 ribs, then the lungs are hyperinflated.
Correct line placement (NG, central lines, pacemakers, swan-ganz, ETT)
Step 2: THE BONES (ribs, vertebrae, scapulae, and clavicles)
Compare symmetry and look for changes in opacity
? fractures, masses, arthritis
Step 3: THE SOFT TISSUES
Compare symmetry and look for changes in density
? edema, subcutaneous air, breasts, masses
Step 4: THE DIAPHRAGM
The right should be higher and both should look smooth.
Check the costophrenic angles for sharpness.
? air under the diaphragm
Step 5: THE HEART AND MIDELINE STRUCTURES
The cardiac silhouette should be less than half the
width of the thoracic cage.
? widened mediastinum, trachea midline
radiology.creighton.edu/basic/cxray/image84.gif
- 128 -
Step 6: THE LUNG FIELDS

Compare for symmetry and density
? lung markings to the chest wall. If not, think pneumothorax.
Identify horizontal fissure - ? fluid
Common chest x-ray findings
Pneumonia Consolidation: ill-defined opacity without loss of volume; look
for air bronchograms (a black tube within the white opacity); identify
which lobes involved
http://www.usfca.edu/fac_staff/ritter/chestxra.htm
Pulmonary edema - looks like consolidation, but usually bilateral and near
hilum; cephalization (larger lung markings in the upper fields)
Pneumothorax no lung markings and black at the periphery, tracheal shift
with tension
Atelectasis area of collapse or volume loss with increased opacity
COPD hyperinflated lung fields, flattened diaphragms, apical decreased
opacities with lung markings (bullae)
Pleural effusions - presence of a fluid level (may just be a gradual haze), blunted
costophrenic angles, fluid in the fissures
HYPOXIA
Think of 5 etiologies:
1. Alveolar Hypoventilation: will be hypercarbic and have a normal A-a gradient (Age / 4).
2. V/Q Mismatch: PNA, COPD, PE. Elevated A-a gradient. Reponds to supplemental Oxygen.
3. Shunt: Pulmonary Edema, PNA, atelectasis. Elevated A-a gradient. Wont correct with
supplemental oxygen.
4. Decreased FiO2: does not happen in Denver.
5. Decreased Diffusion
- 129 -
Hypercarbia
Remember that PCO2 = VCO2 (CO2 Production) / (minute ventilation - dead space ventilation)
Etiologies:
1) Decreased Minute Ventilation (RR X TV)
a. Cant Breath: Airway Obstruction (COPD, Asthma), Stiff Lungs/Pleura/Chest Wall
(Pulmonary Edema, ARDS, PNA, effusions), Weakness (neuromuscular disorders,
Hypophosphatemia)
b. Wont Breath: Narcotics, Benzos, Hypothyroidism, CNS Disease
2) Increased Dead Space: COPD, PEEP, PE without ability to increase minute ventilation
3) Increased CO2 production: Carbs or increased metabolic production
Pleural Effusions
Transudative effusions form when hydrostatic pressures favor fluid formation exceeding clearance.
Exudative effusions form through increased vascular permeability. Pleural effusions usually arent
visible on CXR until there is at least 300ml present. Exam is notable for decrease breath sounds,
dullness to percussion, decreased tactile fremitus, egophony, and possible friction rub.
When to tap:
When diagnosis is unknown, symptomatic relief, new effusion (max 1500mL) or unexplained
effusion
IF A PATIENT HAS A PNEUMONIA WITH EFFUSION THAT LAYERS OUT >1cm ON
LATERAL DECUB CXR, YOU HAVE TO TAP IT TO EVALUATE FOR EMPYEMA
What to order:
serum protein and LDH (if you have one within the past 24 hours, no need to repeat), pleural fluid
protein, LDH, glucose, gram stain, culture, pH, cytology if indicated
if you suspect TB, order adenosine deaminase (>40), IFN Gamma (>140) or PCR
if its a bloody effusion, order a hematocrit on the effusion to evaluate for hemothorax
pH needs to go to lab in an ABG syringe that is put on ice IMMEDIATELY
check pleural cholesterol or TG if suspect chylothorax (>110 is diagnostic)
pleural amylase if you suspect esophageal perforation
Lights Criteria: (exudate if any of 1 of the 3 is positive: 98% sensitive, 83% specific)
1. Pleural fluid (PF) to serum total protein ratio of >0.5
2. PF to serum LDH ratio of >0.6
3. PF LDH value of >2/3 of the upper limit of normal for serum LDH
-can also use serum albumin-pleural albumin >1.2 g/dL: more specific
Transudative Effusion: CHF, nephrotic syndrome, hypoalbuminemia, liver dx/cirrhosis, myxedema,
constrictive pericarditis
Exudative Effusion: Malignancy, PE, parapneumonic effusion, TB, RA, lupus, asbestosis, pancreatitis,
trauma, esophageal perf (high salivary amylase), radiation, drugs, chylothorax, yellow nail syndrome,
sarcoid
Other Effusion Tips/Pearls:
Hematocrit >50% of serum hematocrit = hemothorax
Hematocrit of 1-20% suggests cancer, PE or trauma
- 130 -
Anchovy paste effusion=amoebiasis

Stinks=empyema
Low glucose: complicated parapneumonic effusion, RA, CA, TB, hemothorax
Lymphocyte-predominant: lymphoma, sarcoid, TB, yellow nail, chylothorax
Eosinophilia: pneumothorax, asbestosis, TB, PE, fungal infxn, parasites, drugs
Management of Parapneumonic Effusions

Description
Features
Treatment
Insignificant
Typical
Borderline
parapneumonic parapneumonic complicated
effusion
effusion
parapneumonic
effusion
<1cm
>1cm, glucose pH 7.0-7.2
>40, PH>7.2
and/or
gram stain and LDH>1000;
cx negative
glucose>40
Gs and cx
negative
Antibiotics
Antibiotics
Abx plus serial
only
only
thoracentesis
No
thoracentesis
Complicated
empyema
parapneumonic
effusion
pH<7.0 and/or
glucose <40
and/or positive
GS or cx
no frank pus
pus
Chest tube plus Abx plus

antibiotic
large tube
+/decortication
Winshall, JS, Lederman, RJ. Tarascon Internal Medicine & Critical Care Handbook. 3rd Edition.
2004. pages 138-139.
COPD EXACERBATIONS
1. 1. Signs and Symptoms: change in amount or character of sputum production, +/- fever, viral
syndrome. Most common causes are viral, bronchospasm, and consider PE if you cannot explain
the cause.
2. Labs and tests: CXR, CBC, chem.-7, CXR, ABG.
3. Treatment:
a. Duonebs q 6 hours with prn albuterol nebs in between (can do continuous, Q 1 hour, Q 2 hour
etc.)
b. Azithromycin: IV if in the ICU or start a Z-pack.
c. Steroids: Start with prednisone 60 mg with a taper depending upon improvement. If admitted to
the ICU, give solumedrol 60 mg IV q 6 hours and then convert to oral prednisone.
d. Non-invasive positive pressure ventilation: BiPaP if respiratory distress/ hypercapneic. This
wont work if the patient is not conscious or obtunded.
e. Heliox is an adjunct which increases laminar flow in the airways.
f. Smoking cessation
1. Target oxygen therapy to achieve an O2 sat of 90 92%.
ARDS
Definition:
Acute hypoxic respiratory failure meeting the following criteria:
Bilateral infiltrates
No evidence of heart failure (ie, wedge pressure 18)
PaO2/FiO2 is 200 mmHg
- 131 -
SEPSIS
Definitions:
Systemic Inflammatory Response Syndrome Criteria (must have 2 to have SIRS):
1) 36C T 38C
2) RR 20 breaths per minute, PCO2 < 32 mm Hg
3) HR 90 beats/min,
4) 4,000 cells/mm3 WBC 12,000 cells/mm3 or > 10% bands
Sepsis: Two SIRS Criteria + Infection (+ UA, Infiltrate on CXR, etc)
Severe Sepsis: Sepsis with evidence of Organ Dysfunction, Hypoperfusion, Hypotension
Septic Shock: Severe Sepsis not responsive to fluids. Vasopressors Required.
Vasopressors and Sepsis (for dosing see table below):
Surviving Sepsis 2008 Recommendations (CCM, 2008)
a. MAP should be maintained greater than or equal to 65 mm Hg.
b. Norepinephrine as the first pressor of choice, can consider dopamine (Remember that
dopamine has more chronotropic effects).
c. Vasopressin can be added to norepinephrine in anticipation that its effects are
equivalent to norepinephrine alone
d. Epinephrine is the next pressor of choice if norepinephrine or dopamine are not
sufficient
e. Then think about phenylephrine, methylene blue At this point the pulmonary fellow
should be by your side.
- 132 -
Dose
Infusion Concentration
Set Pump to
Drug
Amiodarone
450 mg/250 mL D5W

33.3 mL/hr x 6 hours then
Bolus:
Pulseless VT/VF:
(Non PVC bag or glass
16.7 mL/hr x 18 hours
300 mg
bottle only)
Stable VT or Afib:
1.8 mg/ml for pump
150 mg
setting
Drip: 0.5-1 mg/min
200 mg/100 mL
Weight based
Cisatracurium Bolus: 0.2 mg/kg
Drip: 0.5-10 mcg/kg/min 2000 mcg/mL for pump
setting
Dexmedetomidine Bolus: 0.5-1 mcg/kg
200 mcg/50 mL
Weight based
Drip: 0.2-0.7 mcg/kg/hr
4 mcg/ml for pump setting
Dose delivered
Comments
Bolus: IV push if pulseless, After bolus dose, obtain continuous

otherwise over 10 min
infusion from PharmacyMaximum dose
Drip: 1 mg/min x 6 hours, of 2.2 g/24 hrs
then 0.5 mg/min x 18 hours
Drip: 0.5-10 mcg/kg/min
Train of four monitoring required. Goal

1-2 twitches.
Drip: 0.2-0.7 mcg/kg/hr
Titrate to desired Riker sedation score.

Bolus dose may cause hemodynamic
instability and may be omitted.
Max 1.5 mcg/kg/hr
May cause bradycardia and hypotension.
Monitor HR and BP.
Bolus: 0.1-0.25 mg/kg

100 mg/100 ml D5W
5 mg/hr = 5 ml/hr
Drip: 5-15 mg/hr
(Usual bolus dose 5-25
10 mg/hr=10 ml/hr
mg)
1 mg/ml for pump setting 15 mg/hr=15 ml/hr
Drip: 5-15 mg/hr
Drip: 2.5-20 mcg/kg/min 500 mg/250 mL or 1000 Weight based
Start 2.5-5 mcg/kg/min
Suggested dose 2.5-20 mcg/kg/min.
Dobutamine
mg/250 mL
Max 40 mcg/kg/min. May cause
2000 or 4000 mcg/mL for
tachycardia, PVCs, hypotension.
pump setting
Drip: 2.5-20 mcg/kg/min 800 mg/500 mL or 800
Weight based
Start 2.5-5 mcg/kg/min
Dopamine
mg/250 mL
Max 50 mcg/kg/min. May cause
tachycardia, arrhythmias, and tissue
pump setting
ischemia.
Drip: 0.01-0.5
8 mg/500 mL or 8 mg/250 Weight based
Start 0.01-0.05 mcg/kg/min Suggested dose 0.01-0.5 mcg/kg/min.
Epinephrine
mcg/kg/min
mL D5W
Central line only.
Max dose: 1 mcg/kg/min 16 or 32 mcg/mL for
May cause tachycardia, arrhythmias, and
pump setting
tissue ischemia.
Bolus: 0.5 mg/kg over 1 2500 mg/250 mL or 2000 Weight based
Start: 25-50 mcg/kg/min Suggested dose 50-200 mcg/kg/min.
Esmolol
min
mg/100 mL
Max: 300 mcg/kg/min
Drip: 50-200
10 or 20 mg/mL for pump
May cause bradycardia and hypotension.
mcg/kg/min
setting
80 mg/100 mL NS
10 ml/hr
Drip: 8 mg/hr
For nonvariceal upper GI bleed
Esomeprazole Bolus: 80 mg
Drip: 8 mg/hour
0.8 mg/mL for pump
setting
Drip: 0.01-0.15
2 mg or 4 mg/250 mL
Weight based
Start: 0.01-0.05
Suggested dose 0.01-0.15 mcg/kg/min.
Isoproterenol
mcg/kg/min
D5W
mcg/kg/min
Max 0.3 mcg/kg/min
(Non Wt based 2-20
8 or 16 mcg/mL for pump
May induce tachycardia and worsen
mcg/min)
setting
myocardial ischemia.
2000 mg/500 mL
1 mg/min= 15 or 7.5 ml/hr Drip: 1-4 mg/min
Monitor lidocaine levels and signs of
Lidocaine
Bolus:
1-1.5 mg/kg
Premixed in D5W or
2 mg/min= 30 or 15 ml/hr
toxicity: neurological, cardiovascular,
2000 mg/250 mL
3 mg/min= 45 or 22.5
and gastrointestinal
Drip:
1-4 mg/min
Concentrated
ml/hr
4 or 8 mg/ml for pump
setting
Bolus: 50 mcg/kg over 20 mg or 40 mg/100 mL Weight based
Start: 0.125-0.25
Milrinone
10min
D5W or NS
mcg/kg/min
Max 1.5 mcg/kg/min.
Drip: 0.125-1
May cause hypotension and
mcg/kg/min
pump setting
thrombocytopenia.
Bolus: None
25 mg/ 250 mL or
2.5 mg/hr = 25 or 5 ml/hr Start: 2.5-5 mg/hr; titrate Suggested dose 2.5-15 mg/hr
Nicardipine
Drip: 2.5-15 mg/hour
50 mg/100 mL
5 mg/hr =50 or 10 ml/hr every 5-15 minutes until
Max 15 mg/hr; higher doses have been
0.1 or 0.5 mg/mL for
10 mg/hr = 100 or 20 ml/hr desired blood pressure
used for eclampsia and
pump setting
15 mg/hr = 200 or 40 ml/hr achieved
pheochromocytoma
Bolus: None
50 mg or 200 mg/250 mL Dosing can be Weight
Start: 0.05-0.1 mcg/kg/min Suggested dose 0.05-3 mcg/kg/min or
Nitroglycerin
Drip: 0.05-3 mcg/kg/min D5W or NS
based or non-weight based or 5-10 mcg/min
5-200 mcg/min.
or 5-200 mcg/min
Titrate every 3-5 minutes Max 5 mcg/kg/min or 400 mcg/min.
pump setting
May cause headache
Bolus: None
50, 100, or 200 mg/250
Weight based
Start: 0.1-0.25 mcg/kg/min Suggested dose 0.25-5 mcg/kg/min.
Nitroprusside
Drip: 0.1-5 mcg/kg/min mL D5W
Titrate every 3-5 minutes Max 10 mcg/kg/min.
200, 400, or 800 mcg/mL
Monitor serum thiocyanate levels in
pump setting
renal failure.
Weight based
Start 0.05-0.1 mcg/kg/min Suggested dose 0.05-1 mcg/kg/min.
Norepinephrine Drip: 0.05-1 mcg/kg/min 8 mg or 16 mg/250 mL
Max: 1.5-3 mcg/kg/min D5W
Central line only.
32 or 64 mcg/mL for
May cause arrhythmias and tissue
pump setting
ischemia.
Bolus: 50 mcg
1000 mcg/100 ml NS
50 mcg/hr = 5 ml/hr
Start 50 mcg/hr
Suggested dose is 50 mcg bolus, then 50
Octreotide
Drip: 25-100 mcg/hr
10 mcg/mL for pump
mcg/hr for variceal bleed.
setting
Diltiazem
- 133 -
Co mment [SB1]:
Phenylephrine
Procainamide
Propofol
Vasopressin
Vecuronium
Drip: 0.2-2.5 mcg/kg/min 50 mg or 100 mg/250 mL

Max: 5 mcg/kg/min.
D5W
pump setting
Bolus: 17 mg/kg over 30 2000 mg/500 mL or
min
2000 mg/250 mL D5W or
(Max infusion rate 50
NS
mg/min)
4 or 8 mg/ml for pump
Drip: 1-6 mg/min
setting
Bolus: 0.5 mg/kg
1000 mg/100 mL
Drip: 5-50 mcg/kg/min 10 mg/mL for pump
setting
Bolus: 40 units (only for 200 units/250 mL NS
asystole or VF/pulseless
VT)
0.8 units/mL for pump
setting
Drip: 0.03 units/min
Bolus: 0.1 mg/kg
100 mg/250 mL D5W or
Drip: 0.5-2 mcg/kg/min NS
Weight based
Start 0.2 mcg/kg/min
1 mg/min= 15 or 7.5 ml/hr Drip: 1-6 mg/min

3 mg/min= 45 or 22.5
ml/hr
Weight based
Drip: 5-50 mcg/kg/min

Max: 150 mcg/kg/min
0.04 units/min= 3 ml/hr
Sepsis/BP: 0.01-0.04
units/min
GI Bleed: 0.2-0.4
units/min
HRS: 0.04-0.8 units/min
Drip: 0.5-2 mcg/kg/min
Weight based
Suggested dose 0.2-2.5 mcg/kg/min.

Central line only.
May cause arrhythmias and tissue
ischemia.
Renal dose adjustment necessary.
Monitor procainamide and NAPA
metabolite levels
May cause hypotension and increased

triglycerides. Contains 1.1 kcal/mL. Use
sedation scale to titrate.
Suggested dose 0.01-0.03 units/min.
***Mesenteric ischemia possible with
doses >0.04 units/min*** Serum lactate
monitoring may be indicated in doses
>0.04 units/min.
Train of four monitoring required. Goal
1-2 twitches.
Code Cart and Common Intensive Care Unit IV Push Medications

Drug
Suggested Dose
Comments
Adenosine
6 mg initial dose; after 1-2 min 12 mg

(May repeat 12 mg dose x1)
Due to short half-life, must administer by rapid IV push (1-3 seconds) followed by 10- 20 mL saline
or sterile water flush.
Amiodarone
Pulseless VT/VF:
300 mg
Pulseless VT/VF: 300 mg IV push unfiltered/undiluted-may repeat with 150 mg if needed.

Stable VT: 150 mg diluted in 25-50 mL NS or D5W infused over 10 minutes. Max 2.2g/24h
Aminophylline
Asystole:
250 mg
AV Block/bradycardia: Blocks adenosine receptors. Give 250mg IV push for atropine resistant asystole or 6 mg/kg IV over
6 mg/kg over 30 min
30 minutes (Max infusion rate 25 mg/min) for atropine resistant bradycardia.
Atropine
0.5-1.0 mg
Can be administered every 3-5 minutes to a maximum dose of 0.04 mg/kg.
Calcium Chloride
1 gm/ 10 mL
(1 amp=10mL)
Given for known hyperkalemia, hypocalcemia, hypermagnesemia, or toxic effects of calcium

channel blockers. May repeat as needed. Vesicant, use extreme caution when administering;
incompatible with phosphate solutions. Central line preferred.
Calcium Gluconate
1 gm/10 mL
(1 amp = 10 mL)
50 mg
1 mg (repeated every 3-5 minutes during
arrest)
Preferred over calcium chloride for non-emergent calcium supplementation. Dilute in 50 mL of NS

or D5W and administer over 1 hour.
Administer over 1-2 minutes.
Available in 1:10,000 (1mg in 10 mL abbojet) or 1:1,000 (1 mg/mL 30 cc vials).
Hydrocortisone
100 mg
IV push over 30 seconds to 1 minute.
Isoproterenol
Bradycardia:
1-20mcg
Lidocaine
1-1.5 mg/kg. (May repeat dose in 3-5

min)
Typical dose is 100 mg. Total maximum dose is 3 mg/kg.
Magnesium Sulfate
1-2 gms
Methylprednisolone
125 mg
Dilute to 10 mL with D5W or NS; administer over 1-2 minutes. For general magnesium
supplementation administer each 2 grams over 1 hr. Given for known hypomagnesemia and/or
Torsade de Pointes.
IV push over 30 seconds to 1 minute.
Metoprolol
Naloxone (Narcan)
5 mg slow IV push
0.4-2 mg every 2-3 min
May repeat every 5 minutes to total of 15 mg.

Dilute to 10 mL with NS or sterile water.
Phenytoin
15-20 mg/kg
(loading dose)
Careful when administering IV Push (max rate 50 mg/min). Max concentration 10 mg/mL. Must
be mixed in NS. Watch vital signs carefully.
Sodium Bicarbonate
1 mEq/kg (may repeat dose every 10

min or per ABGs)
Typical dose is 50 mEq. Incompatible with epinephrine and other sympathomimetic drugs.
Vasopressin
40 Units IV push
May Repeat in 10-20 min
Use in Pulseless VT/VF or asystole.

May resume epinephrine dosing in 5-10 minutes.
Diphenhydramine
Epinephrine
Stable VT:
150 mg
Torsades de Pointes: Given for atropine resistant bradycardia or torsade de Pointes. May repeat or start continuous
20-60mcg
infusion. May induce tachycardia and worsen cardiac ischemia.
NAVVEL: Narcan, atropine, valium, vasopressin, epinephrine and lidocaine may be administered via the ETT (endotracheal tube) if an IV is not available.
Dose is usually doubled and given in at least 10 mL of NS or sterile water (vasopressin dose is 40 Units via the ETT same as the IV dose). Patient is
ventilated aggressively after administration to facilitate absorption.
(University of Colorado Hospital. Updated January 2008. Ty Kiser, Pharm.D., BCPS)
- 134 -
Rheumatology
Indications: Arthrocentesis is both diagnostic and therapeutic. Any new mono- or polyarthritis
unrelated to trauma should be tapped for diagnosis, especially when considering the possibility of a
bacterial arthritis. Irreversible damage to cartilage occurs within the first day of infection, so timely
diagnosis is critical.
Contraindications: Relative contraindications include anticoagulation, bleeding diathesis, overlying
cellulitis, and active bacteremia. Discuss with ortho prior to tapping a joint with known hardware in it.
Differential:
1. Noninflammatory: OA, RA, trauma, osteochondritis dissecans, sickle cell, lupus, scleroderma,
amyloidosis, hypothyroid, Milwaukee shoulder
2. Inflammatory: RA, CPPD, gout, psoriatic arthritis, arthritis of IBD, ankylosing spondylitis,
viral arthritis, rheumatic fever, Behcets, vasculitis, Lyme dx, infection
3. Septic: Bacteria, Fungus, Mycobacterium
4. Hemorrhagic: trauma, bleeding disorder, crystalline arthropathy, tumor, prosthetic joint, sickle
cell, Charcots arthropathy
Synovial Fluid Examination: Normal fluid is clear/colorless to straw colored. Fluid is cloudy
because of the presence of increased cells/fibrin/lipids/crystals/etc. Off-white fluid is often PMNs
while very white fluid is usually gout (monosodium urate crystals). Greenish fluid is often RA.
Orange-brown fluid is associated with pigmented villonodular synovitis, a rare disorder.
Labs: Send the fluid gram stain, culture, cell count and microscopic examination under polarized
filter. Monosodium urate crystals (gout) are needle shaped and yellow when the filter is parallel with
the crystal=negative birefringence. Calcium pyrophosphate dehydrate (CPPD) crystals are rhomboid
shaped and blue when the filter is parallel with the crystal=positive birefringence. Pneumonic:
ABC=align, blue, calcium pyrophosphate. Unfortunately, the presence of crystals does not exclude
infection: the two can co-exist. Gram stain and culture are very helpful in this situation.
Type of Fluid
Normal
Inflammatory
Septic
Special Features
Clear, colorless, viscous
Clear, yellow, viscous
Purulent
Leukocytes
<200(<25%PMNS)
200-100,000 can be<50% PMNs
>50,000 (>75%PMNS) although
33% will be lower than 50,000
If WBC >50,000, strong suspicion for septic joint, but Reiters, gout and RA pseudosepsis can all look
like this. When in doubt, treat but trust your gram stain and cx. Gram stain is + in 80-85% of staph
infections. Its 50% positive in gram negative infections. Culture is 100% specific for all infections
except gonococcus, TB and fungal.
The NEJM website has a helpful PDF and video on arthrocentesis of the knee. Use it through the
website hslibrary.ucdenver.edu for all arthrocentesis. A great picture of crystals is found there. A
video on approach to the shoulder is at
http://webmedia.unmc.edu/intmed/general/demo/Arthro/shov1001.htm
-Use ultrasound!
- 135 -
Toxicology
Medical Toxicology/Poison Center Consults
Both Denver Health and UCH have active inpatient Medical Toxicology Consulting services.
We are here to assist you with the evaluation and management of poisoned patients or patients who
have symptoms that may be due to poisoning. Our service provides real-time bedside consultation and
we hope to be consulted on all admitted overdose patients. As poisoning is a dynamic process, please
contact us as soon as possible so we can provide any assistance early. We are particularly interested in
patients who have undifferentiated presentations that may be due to poisoning (such as altered mental
status, hypotension or metabolic acidosis without other explanations). Please call the Poison Center
at 1-800-222-1222 and ask to speak with the Medical Toxicology Fellow on call for all suspected
ingestions.
General Hint: The recognition of all toxicities requires a high level of suspicion. Look for
them in all patients with unexplained symptoms, those with active or historical depression (especially
in young, otherwise healthy patients) and in those with access to certain meds.
Aspirin Overdose
What to look for:
Early/mild: nausea, vomiting, hyperventilation, tinnitus, lethargy, delirium
Severe: coma, seizures, fever, hypoglycemia, unexplained pulm edema
Lab Abnormalities:
mixed respiratory alkalosis with metabolic acidosis
toxic levels generally greater than 30-40 (though levels are very inexact)
Therapy:
fluids to euvolemia as overcorrection will cause pulmonary edema; forced diuresis not helpful
bicarbonate (via boluses with ABG to follow serum pH, goal 7.45-7.5) to help with urinary
excretion, keep CNS penetration to a minimum
check labs including lactate, lytes, salicylate levels, ABGs q4h till stable
dialysis if renal failure, pulm edema, coma, seizures, levels greater than 100 or failure of
conservative techniques with worsening clinical course
(Adapted from Goldfranks Toxicologic Emergencies, 7th ed., 2002)
Tylenol Overdose
What to look for:
Stage I (1-24h): asymptomatic or nausea/vomiting, anorexia
Stage II (24-72h): all of the above + RUQ pain, LFT rise
Stage III (72-96h): jaundice, renal failure, coagulopathy, encephalopathy
Lab abnormalities:
initially will be normal but look for LFT, INR, PTT, creatinine changes
ABG may show metabolic acidosis although this can be variable
- 136 -
Tylenol levels need to be drawn at 4h after ingestion then every four hours till < 10; if time
cannot be established or patient shows up after 4 hours then the Rumack-Matthews nomogram
not helpful (otherwise very sensitive)
Remember: Chronic toxicity occurs at much lower APAP levels!
Therapy:
When in doubt, treat
N-acetyl cysteine 140 mg/kg PO load followed by 70 mg/kg every 4 hours x 17 doses or until
INR < 2 and encephalopathy resolved (whichever comes last)
Rumack-Matthews Nomogram (APAP Overdose)

500
200
200
150
Acetaminophen Level
100
50
Severe Tox Probable
10
Severe Tox Unlikely
12
16
20
24
Time Since Ingestion (hours)
Lithium Overdose
What to look for:
Mild/moderate: asymptomatic, tremor, slurred speech, weakness, ataxia lightheadedness,
hyperreflexia, nausea/vomiting, dry mouth, TWI on EKG
Severe: confusion, clonus, coma, seizures, renal failure
Lab abnormalities:
look or renal insufficiency, unexplained leukocytosis, hypothyroidism
Li+ levels for mild/moderate toxicity occur at 1.5 3.5 mEq/L, severe toxicity occurs at levels
greater than 3.5 mEq/L
Therapy:
- 137 -
aggressive volume replacement (watch for diabetes insipidus complicating this) with lytes
replacement as needed; forced diuresis not helpful
dialysis indicated for all ingestions with a level above 4.0, when level 2.5 with moderate
neurologic symptoms or if renal failure
TCA Overdose
What to look for:
ECG: sinus tach at 120-160 BPM, prolonged QRS duration; R-wave in aVr 3mm a good early
predictor of ingestion
altered mental status, hyperthermia, ileus, delirium, coma, seizures, unexplained hypotension,
ventricular arrhythmias
Expect a variable, very unpredictable course for about 24 hours
70% of cases will have a co-ingestion complicating thingslook for this!!
Lab abnormalities:
TCA levels take a long time to come back and are very unreliable when used to predict toxicity,
unlikely to help your management of the patient
check ABGs q4h if giving bicarb
Therapy:
most patients will require supportive care only (fluids, lytes, monitoring) which they should
receive in a step down or ICU
any ECG changes, hypotension or neurologic signs should get sodium bicarb:
o bolus 1-2 mEq/kg x 1 followed by NaBicarb drip (3 amps in 1L D5W) at 150 cc/hr till
symptoms resolve (goal pH 7.5 7.55)
intubation and hyperventilation (with same goal pH) for all critically unstable patients
treat seizures as above plus aggressive benzos to stop seizing
treat hypotension with aggressive fluids, norepinephrine if a pressor is needed
no role for dialysis
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Withdrawal Syndromes
Alcohol Withdrawal
What to look for:
consider this diagnosis in all patients who admit to consuming alcohol in any significant
quantity or are known to historically do so
mild withdrawal: irritability, agitation, hypervigilance, sleep disturbance, tremor, elevated HR,
elevated BP, elevated temperature without other known cause
hallucinosis: sensorium intact with above symptoms + auditory or visual hallucinations
seizures: always generalized tonic/clonic, often with a history of this during times of alcohol
abstinence
DTs: all the above + delirium and clouded consciousness, very hyperadrenergic; approx. 5%
of these patients will die as a result so treat this as a medical emergency
Lab abnormalities:
alcohol levels not helpful as these patients are always chronic, heavy drinkers and can
withdraw at high what would be a high BAL for a non-drinker
follow lytes carefully as malnutrition with resultant hypoK, hypoMg, hypoPhos can
complicate; hyponatremia is common and must be considered prior to aggressive fluid
resuscitation
Therapy:
most mild withdrawal can be treated as an outpatient with PO benzos and abstinence
more severe cases can be treated on the floor with careful observation; any patients with a
history of seizures or DTs or those requiring hourly benzo doses in the ER should be admitted
to the step down or ICU services for at least the first 48-72 hours
the mainstay of treatment is benzodiazepines, either via PO or IV depending on the severity of
symptoms and doses required; early symptom-based therapy (using a CIWA scale,
downloadable from UpToDate) has been proven to be the most effective method of keeping
people from entering full-on DTs
when benzodiazepine doses reach 15-20 mg lorazepam IV per hour it is good to consider
adjunctive therapy with clonidine 0.3 mg po q6h or haldol 0.5 1.0 mg IV q4h if delirium and
psychotic features are present
severe cases will often be associated with respiratory compromise and mechanical ventilation
should be considered as symptoms worsen and benzodiazepine needs increase
all patients admitted with an alcohol history must receive thiamine 100 mg/day, folate 1
mg/day and MVI 1 tab/day either PO or IV starting immediately on admission and
continuing for the length of their stay
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How To Think About Differential Diagnoses

The approach to a differential diagnosis is where it all comes together for the internist. It is the
blending of the art and the science of medicine. The art comes from your pretest probabilities and
the science from the tests you choose to discern which of your possible diagnoses is the actual culprit.
When you are approaching an unknown condition, it is best to think of the top 5 things it is
most likely to be in your mindthe art. How you come to these five possible conclusions comes from
your history taking, physical exam and clinical sense. While five is a random number, it is workable
(and you have to start somewhere). Once you have your most likely causative conditions, you can
apply the science in the form of tests, imaging and other studies. Here is the approach to the art and
science of medicine using chest pain as an example:
1) Select your five possible diagnoses and assign them a probability of being the correct one.
Make sure that all of the probabilities, when taken together add up to 100% (because it has to be
something). This is the art, in that the skills you will acquire over the next few years will refine your
ability to make this list accurately every timeyoull see why this is so important as tests are ordered
and therapies considered.
myocardial infarction 35%
GERD 20%
pneumonia 10%
anxiety 15%
pulmonary embolus 20%
2) Perform a series of tests to rule in or rule out each diagnosis. Evaluate one condition at a
time. Take your pre-test probablitiy and convert them to odds. This is done in order to make use of
the likelihood ratio associated with every test that you can order which will tell you if your condition is
more or less likely based on either a positive or negative test result. (Ex. for pneumonia with positive
CXR).
Pre-test Prob
10%
Pre Test Odds

10/90
x Pos LR
(5.5) or 5.5/1
Post Test Odds

55/90
Post test Prob

55/145 or 38%
3) Now that you have a new post-test probability, your list of five will no longer add up to
100%. You have to reassign probabilities to make sure that it does (more art). If a test has made
something so low on your list as to no longer be worthy of consideration, drop it from the list. Now
you are down to the four most likely things and are making progress. If new information has come to
light and something needs to be added to the list, feel free to do so, making sure to keep everything
adding up to 100%.
myocardial infarction 27%
GERD 15%
pneumonia 38%
anxiety 0% (drop from list)
pulmonary embolus 20%
4) Once something has become the dominant diagnosis, you have to decide if you are going to
treat or not. A treatment threshold (the percent probably something needs to be for you to feel justified
and correct in treating it) must then be considered. If you came up with GERD as your most likely
explanation of the chest pain but it was still only at 20% probability, you will feel OK treating it as the
therapy is very non-toxic and non-invasive (TUMS). If however your highest probability on your list
is myocardial infarction at 35%, you will need to do more testing to raise it above your treatment
threshold (likely more like 80-90% to perform cardiac catheterization). Pneumonia, as in the example
above, likely falls somewhere in between as antibiotic therapy is more toxic than TUMS but not nearly
- 140 -
as risky and invasive as a catheterization. 38% probable may be enough to start antibiotics; if not,
getting an negative ECG and negative d-dimer may lower other possibilities, allowing you to add their
probabilities to the diagnosis of pneumonia in order to raise it above your treatment threshold.
5) Continue this process until you have successfully diagnosed and treated the offending
condition. Usually there will still be other diagnoses on your list that you do not think are likely
enough to treat but you also cannot entirely rule outthis is OK. These are the things you are going to
keep in the back of your mind as other possible causes in case the treatment for your first
consideration does not produce the therapeutic results you had hoped for.
It sounds complicated but gets much easier with time. Its what good doctors do in their heads
every time they see a patient and it will become second nature for you, too.
- 141 -
The Patient-Centered Approach

The patient must always be at the forefront of our thoughts. Without patients there would be no
doctors, and caring for our patients in a compassionate, professional and intelligent manner is our
ultimate goal. While the rest of this book has been about this implicitly, we wanted to take one last
opportunity to mention it explicitly.
Your patients will come to you scared and looking for answers. Your mission over the next
three years is to learn to help with this fear and uncertainty. Diagnosis and treatment can be tricky and
time-consuming, without always being fruitful. Sometimes you will find the diagnosis and realize there
is no adequate treatment you can offer your patient. This is why the most important thing you can do
for your patients is to help alleviate the fear that comes with being ill. When approached correctly, this
goal can be accomplished almost every single time, in almost every single patient.
Make an effort to see your patients for who they really are: People, just like you, with families,
goals, dreams and desires who see all those things being thrown into disarray and peril by a gnawing
pain in the gut or a sudden flash of pain across the chest. Every interesting or cool case for you is a
potential threat to their existence. While we have come to residency to learn and expand our
knowledge, it is only because of the patients and their ordeals that this experience is possible.
So please be respectful of patients and their families. Understand that anger or irritation on their
part is not directed at you, and do your best not to take it personally. When you take the time to
understand that a patients anger might actually just be one of the stages of loss or dying, this becomes
much easier to accept. Learning to step outside of yourself and think from the patients point of view
will help bring all these things into perspective.
As we have said before, your time in the hospital over the next few years is going to be an
incredible, life-changing time for you. Understanding that it is the same for your patients will make it
all the richer, and will make you a better doctor.
- 142 -
Chiefs Pagers
There is always a CMR who can be reached, 24 hours a day, 7 days a week. During the day it
is best to call or page the chief assigned to the hospital you are working at that month, though all of us
will have our pagers on during the day if there is someone specifically with whom you would like to
address an issue or question.
At night there is a CMR on call. The call schedule is posted on the message board of the main
medical floor on which you are working or can be found on amion.com (logon: UCO). Feel free to
call with any question at any time.
Bryan Brimhall
Julia Clemons
Elsbeth Jensen-Otsu
Adrienne Mann
Allison Nitsch
303-266-3912
303-266-3914
303-266-3936
303-266-3951
303-266-3958
Housestaff Office Contact Info

Your housestaff office is a central resource for all your questions about the program. It is
staffed by some of the hardest working people in the department: Jennifer Weber is the Program
Administrator, and Allison Claybrook, Heidi Eckhoff and Melanie Murray are the administrative
assistants. Make it a point to introduce yourself to Jennifer, Alli, Heidi and Melanie early in the year;
they are fantastic and will be an incredible resource for you across your three years. They work very
hard for you, so be especially nice to them always. Danaa Kennedy is the Med/Peds Coordinator and
Akemi Iwanabe is the Primary Care contact. You can contact them at:
Alli Claybrook
Heidi Eckhoff
Akemi Iwanabe
Danaa Kennedy
Melanie Murray
Jennifer Weber
303-724-1792
303-724-1791
303-724-2264
303-724-6595
303-724-1784 (main number)
303-724-1788
- 143 -
Library information:
This comes from the pocket librarian guide that the medical librarians at Anschutz Medical Campus
put out.
POCKET LIBRARIAN, 2008
Health Sciences Library
University of Colorado
Anschutz Medical Campus
(303) 724-2152
http://hslibrary.ucdenver.edu/
Find these resources with a keyword search on the Librarys webpage
Residents Guide Keyword search: resident
Ask a Librarian http://hslibrary.ucdenver.edu/aal/
Online Journals Type the journal title into the search box and click on Journal Titles
Patient Education Keyword search: patient education
Handouts and Tutorials Keyword search: handouts or tutorials
PDA Resources Keyword: pda
Databases Page http://hslibrary.ucdenver.edu/databases/ (Choose Clinical Medicine or Find Databases
by Title or type the resource name into the webpage search box)
Differential Diagnosis: First Consult or Micromedex
Disease Reviews, Dx & Tx: ACP PIER, Dynamed, or FirstConsult
Calculators, Rules, Labs, Tables:
Micromedex - Main tab/Calculators & Labs
Essential Evidence Plus - Clinical Rules and Calculators
ACP PIER - disease chapters include dx & tx tables
Tests and Procedures - ACP PIER & FirstConsult-Procedures
Herbs and Supplements - Natural Medicines Comprehensive Database
PubMed TIPS http://hslibrary.ucdenver.edu/education/pubmed-tips.php
Use the URL from the Librarys webpage to connect to our online journals from PubMed
http://www.ncbi.nlm.nih.gov/pubmed
Click My NCBI (upper right) to register OR login: curesident pw: resident
Set up automatic email updates
Set up customized filters to group search results
Save results in a personalized collection of citations
Setup instructions at:
http://hslibrary.ucdenver.edu/handouts/#database
Not happy with your search results? Click the Details tab to see your complete search strategy, find out
what went wrong.
Quick Evidence Based Results Click Clinical Queries - lower left of PubMed homepage
- 144 -
Use the Related Articles link to quickly find more relevant results
Limit Your Results (use the Limits tab) to find:
Dates, age groups, authors, journals, publication type, languages, gender, humans
Find Articles Quickly Click Single Citation Matcher lower left of PubMed homepage
Focus Search Results Using Medical Subject Headings
http://www.ncbi.nlm.nih.gov/mesh
Question: How does exercise affect type 2 diabetes?
Enter type 2 diabetes into the search box
The MeSH database suggests the preferred term:
Diabetes Mellitus, Type 2
Click the checkbox next to the term & click the Send to menu, then click Search Box with AND
Type exercise into the search box
The MeSH database provides a list of possible matches
Click the checkbox next to Exercise and click the Send to menu, then click
Search Box with AND
Click the Search PubMed button
Display Abstracts Plus Change from summary to abstract plus, & click the ARTICLE LINKER (green
& white) button for full text
Each morning sees some task begun, each evening sees it close;
Something attempted, something done, Has earned a nights repose
Henry Wadsworth Longfellow
- 145 -

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What is the purpose of this guide?

What is the purpose of this guide?

What hospitals are covered in the hospital breakdown section?

What hospitals are covered in the hospital breakdown section?

Internal Medicine

University of Colorado Guide to Internal Medicine

The Experienced Approach to: Common Subspecialty Issues ............................................. 45

How to think about Differential Diagnoses ........................................................................... 138

A Message From The Chiefs

The Chief Medical Residents

The Eightfold Path Through Internship

Resident Mentoring Program

Associate Program Director;

Associate Program Director

Director, Hospitalist Program

Associate Program Director

Assistant Program Director

Assistant Program Director

Mentoring Areas of Interest/ Focus

CPHP (Colorado Physician Health Program) - 303-860-0122

BasketballFall and Winter

CMR office: x84246

Denver Health Medical Center

Cafeteria: M-F 6:30A-6:30 P; Holidays and weekends: 11:00A -2:00P.

Important Numbers and Codes:

9th Floor: 303-602-8700

Denver VA Medical Center

Cafeteria/Canteen, prosthetics dept., path to the nursing home

Inpt pharmacy 303-613-0404

Rose Medical Center

Radiology dictation line: 303-320-7421 or ext 7421

Basement cafeteria, grand rounds room

ER door code: 6789 (subject to change) ED back line: 5400

Breakfast: 6:30AM-10:30AM, 7 days a week

Conducting Yourself On The Wards

General Order Writing

An Ideal Admission Note (H+P)

An Ideal Progress Note

An Ideal Procedure Note

Operator: Your name, name of supervising resident

An Ideal Death Note

The Bane of Residency Discharge Summaries

The Experienced Approach to: Night Float/Cross Cover Issues

Low Urine Output (UOP) defined as less than 0.5 cc/kg/hr

Ca gluconate 500-1000 mg PO TID is a standard PO dosing (as is the use of

Heparin Drip Adjustment

Rising Creatinine/Acute Renal Failure see the renal section

Hypoglycemia/Hyperglycemia see the endocrinology section

The Experienced Approach to: Procedures

The Experienced Approach To:

Weiss), candidiasis, herpes zoster, costochondritis (Tietzes syndrome), anxiety

Who gets stress testing?

Works by causing vasodilation, and a coronary steal phenomenon

Cold and Dry

Cold and Wet

Heart Transplant Basics

The Immunosuppression Scheme:

Anti-lymphocyte Agents: used in induction and steroid resistant rejection

Anti-cytokine Receptor Antibodies: bind to subunit of IL-2 receptor, preventing

Advanced ECG reading