NORMAL FLUID AND ELECTROLYTE REQUIREMENTS

The body loses fluids through urine, insensible loses (respiration, skin, stools) and
intrinsic losses (by-product of metabolism).

Maintenance therapy is the fluid and electrolyte requirements needed by the average
child with normal renal function over a 24-hour period.

Calculating maintenance fluids: Holliday-Segar method.

Fluid per day Rate per hour

1st 10kg 100 mL/kg/day 4 mL/kg/hr

Next 10kg 50 mL/kg/day 2 mL/kg/hr
For every additional kg 20 mL/kg/day 1 mL/kg/hr

Maintenance electrolyte requirements in children are

 2-3 mmol/kg/day of sodium,
 1-2 mmol/kg/day of potassium
 3-5 mmol/kg/day of chloride

HYPONATRAEMIA

Hyponatraemia is serum sodium (Na) concentration of less than 135 mmol/L.

Causes

 Hypotonic fluid hydration

 Diarrhoea & vomiting
 Acute & chronic renal failure
 Hypothyroidism; adrenal insufficiency; SIADH
 Cirrhosis; congestive cardiac failure; nephrotic syndrome
 Ascites; effusions; pancreatitis
 Drugs - diuretics

Clinical features

Symptoms occur when serum Na levels fall below 125 mmol/L. If the changes are
chronic, the patient may be asymptomatic.

 Early signs: anorexia, headache, nausea & vomiting

 Hypo/hypertension, muscle weakness & cramps,
 Bizarre behaviour, hallucinations, seizures, decorticate/decerebrate posture, coma

Investigations

1
  Serum Na+; serum osmolality; Urea & creatinine; Urine osmolality & Na+
 Aldosterone, cortisol, free T4 & TSH, ACTH & ADH levels
 Imaging studies for underlying cause – U/S & CT scans (head, abdomen)

Management

Correction of hyponatraemia should be slow, not exceeding 8 mmol/L/day.

 With neurologic symptoms, raise the serum Na concentration by giving doses of

1-2 ml/Kg of 3% saline until symptoms resolve. Symptoms typically resolve with
a rise in sodium of 3-7 mmol/L
 Hypovolaemic hyponatraemia - correct volume depletion with normal saline,
then restriction of fluids to two-thirds (or less) of the volume needed for
maintenance
 Normovolemic hyponatremia due to SIADH include fluid restriction to two-
thirds (or less) of the volume needed for maintenance using normal saline; or the
use of 3% NaCl, and IV administration of furosemide
 Hypervolemic hyponatremia - restrict fluids and administer 3% NaCl to stop the
symptoms
 Treat the underlying cause

HYPERNATRAEMIA

Hypernatraemia is a serum sodium level greater than 145 mmol/L.

Causes

1. Excessive Sodium
 Improperly mixed formula
 Cow’s milk (UHT, Fresh milk)
 Excess sodium bicarbonate
 IV hypertonic saline
 Hyperaldosteromism

2. Water Deficit
 Nephrogenic diabetes insipidus
 Central diabetes insipidus
 Increased insensible losses
 Inadequate intake

3. Water and Sodium Deficit

2
  Diarrhoea
 Emesis
 Burns
 Excessive sweating
 Osmotic diuresis
 Chronic kidney disease
 Polyuric phase of acute tubular necrosis
 Post-obstructive diuresis

Clinical Features

 Irritability
 Restlessness
 Lethargy
 High pitched cry
 Hyperpnoea
 Cerebral haemorrhage
 Seizures
 Coma
 Stroke

Complications

 Dural sinus thrombosis

 Peripheral thrombosis
 Renal vein thrombosis

Management

 Priority is restoration of intravascular volume with isotonic fluid (slow infusion

of normal saline).
Firstly the water deficit is calculated as follows:

Water deficit (in Litres): = Body weight × 0.6 (1-145/[current sodium])

Replacement fluid is then calculated as follows:

• Replacement volume (in L) =

TBW deficit X [1 ÷ 1 - (Na concentration in replacement fluid in

mmol/L ÷ 154 mmol/L)]

 The volume calculated has to be replaced slowly over 48 -72 hours.

For example:

A 10kg child arrives with a history of dehydration. His labs reveal a Sodium 160 mmol/l.

3
Water Deficit: 10 x 0.6 x (1-145/160) = 0.6 litres

Fluid available is ½ strengh Darrows: Sodium content in Darrows = 61 mmol/L.

Therefore, Replacement Volume: 0.6 litres x [1/1- (61/154)] =1 litre

This volume of fluid should be given over 48 -72 hours.

Other measures

 Severe cases require dialysis with a fluid containing a high glucose concentration
and a low sodium concentration
 Hyperglycaemia resulting from hypernatremia is not usually treated with glucose.
The glucose concentration of IV fluid should be reduced
 The underlying cause should be treated whenever possible
 Central diabetes insipidus should be treated with desmopressin

HYPERKALAEMIA

Hyperkalaemia is defined as serum potassium (K) level of more than 5mmol/L.

Causes

1. Increased Intake
 Intravenous or oral
 Blood transfusions

2. Decreased Excretion
 Renal failure
 Urinary tract obstruction
 Sickle cell disease cellular leak
 Kidney transplant
 Renal tubular disease

3. Drugs
 Angiotensin converting enzyme inhibitors
 Angiotensin II blockers
 Potassium sparing diuretics
 Nonsteroidal anti-inflammatory drugs
 Trimethoprim
 Heparin

Clinical Features

 Paresthesias

4
  Weakness
 Tingling
 ECG changes peaked T waves, wide P-R interval, flattening p wave, widening
QRS complex
 Ventricular fibrillation
 Asystole

MANAGEMENT

Aims

- Stabilise the heart to prevent life threatening arrhythmias

- Remove potassium from the body

Drug Onset Mechanism

10% calcium gluconate Immediate Stabilises the heart

Salbutamol (nebulised or Few min Shifts potassium into cells

IV)

8.4% NaHCO3 (IV) Few min Shifts potassium into cells

Fluid bolus with frusemide Minutes Renal excretion of

(IV) potassium

Glucose (±insulin) 30 min Shifts potassium into cells

Calcium resonium (oral or 30 min (rectal) Potassium excretion

rectal) through gut
2h (oral)

Dialysis Rapid (haemodialysis) Removes potassium

Slower (peritoneal)

HYPOKALAEMIA

This a serum potassium level < 3mmol/L.

5
Causes

1. Decreased intake

 Anorexia nervosa

2. Extra-renal losses
 Diarrhoea
 Laxative abuse
 Sweating

3. Renal losses
 Renal tubular acidosis
 Diabetic ketoacidosis
 Interstitial nephritis
 Uretero-sigmoidostomy
 Cystic fibrosis
 Renin secreting tumour
 Adrenal adenoma or hyperplasia
 Cushing syndrome
 Gitelman syndrome
 Bartter syndrome
 Liddle syndrome
 Hypomagnesaemia

4. Drugs
 Amphotericin
 Cisplatin
 Aminoglycosides
 Loop and thiazide diuretics

Clinical features

 Muscle weakness and cramps

 Paralysis
 Heart block
 Paralytic ileus
 Polyuria
 Polydipsia
 ECG features: Flattened T waves, depressed ST segment, U wave
 Supraventricular tachycardia
 Ventricular tachycardia

6
Management

Potassium chloride is preferred.

Dose of intravenous potassium is 0.5-1mmol/Kg usually given over one hour.

Intravenous potassium should be used cautiously because of the risk of hyperkalaemia.

References

1. FRIEDMAN A L, Pediatric hydration therapy: Historical review and a new

approach. Kidney International (2005) 67, 380–388; doi:10.1111/j.1523-
1755.2005.00092.x

2. Vellaichamy M. eMedicine. University of Kansas School of Medicine, Wesley

Medical Centre, Updated April 16, 2009

3. Rachel S. Pediatric fluids and electrolytes, Rutgers University, Saint Barnabas

Medical Centre, Sept 27, 2007

4. Kleigman, Behrman, Jenson, Stanton: Nelson Textbook of Paediatrics. Volume

1. 18th Edition, 2007

5. Sidwell R and Thompson M. Concise Paediatrics. Concise Paediatrics. 2nd

Edition.

6. eMedicine. Hypernatremia. Paediatrics Cardiac Care and Critical Care Medicine

MANAGEMENT OF SHOCK

Immediate goals [ABCDE]

 Stabilize the airway

7
  Provide oxygen by mask or nasal catheter

 Establishment of vascular access

Two large bore peripheral intravenous catheters should be established.

If peripheral access is not readily available, intra-osseous access should

be established.

 Disability [neurological examination]

 Exposure

SEE SUMMARY OF TYPES, SIGNS AND SYMPTOMS AND TREATMENT OF

SHOCK ON NEXT PAGE

TYPE OF SHOCK SIGNS AND SYMPTOMS TREATMENT

Hypovolaemic Increased HR, reduced pulses, delayed Repeat boluses of 20 ml/kg crystalloid
CRT, hyperpnoea, dry skin, sunken as indicated up to 60 ml/kg in first
(reduced CO, eyes, oliguria hour
increased SVR)
Blood product as indicated for acute

8
 blood loss

Septic Increased HR, normal to reduced BP, Repeat boluses of 20 ml/kg crystalloid;
reduced pulses, delayed capillary refill may need up to 60ml/kg in first hour.
(increased CO, time, hyperpnoea, mental state Consider colloid if poor response to
increased SVR) changes, third spacing, oedema crystalloid

Pharmacologic support of BP with

dopamine or norepinephrine

Distributive Angioedema, rapid third spacing of Repeat boluses of 20 ml/kg crystalloid

fluids, reduced BP, respiratory distress as indicated
Anaphylaxis
(increased CO, Pharmacologic support of SVR with
reduced SVR) norepinephrine or phenylephrine

Distributive Reduced BP with normal HR, paralysis Pharmacologic support of SVR with
with loss of vascular tone norepenephrine or phenylephrine
Spinal cord injury
(normal CO, Fluid resuscitation as indicated by
reduced SVR) clinical status and associated injuries

Cardiogenic Normal to increased HR, reduced Pharmacologic support of CO with

pulses, delayed CRT, oliguria, JVD, dobutamine and dopamine
(reduced CO, hepatomegaly
normal to increased Judicious fluid replacement as
SVR) BP normal until late in course indicated clinically

CO = cardiac output, SVR = systemic vascular resistance, HR = heart rate, BP = blood

pressure, CRT = capillary refill time, MS = mental status, JVD = jugular venous
distension

VASOACTIVE MEDICATIONS

Agent (dose range)

9
Dopamine (3 to 20 mcg/kg/min)

Dobutamine (1 to 20 mcg/kg/min)

Epinephrine (0.01 to 1.0 mcg/kg/min)

Norepinephrine (0.01 to 1.0 mcg/kg/min

FORMULAE FOR ADMINISTRATION OF VASOACTIVE MEDICATIONS

Drug Infusion Preparation Infusion rate

Dopamine Body weight in kg x 6 = Amount 1 ml/h = 1 mcg/kg per minute

of drug (mg)
Dobutamine (Example: to deliver 10 mcg/kg per minute,
to be added to total volume of 100 run infusion at 10 ml/h)
ml IV fluid

Epinephrine Body weight in kg x 0.6 = 1 ml/h = 0.1 mcg/kg per minute

Amount of drug (mg)
Norepinephrine (Example: to deliver 0.3 mcg/kg per minute,
to be added to total volume of 100 run infusion at 3ml/h)
Milrinone ml IV fluid

References

1. Christian A McKeirnan and Stephen A leiberman. Circulatory shock in children:

An overview. Pediatr. Rev 2005

10
 2. Stephen M .Schexnayder. Pediatric septic shock; Pediatr.Rev.1999

POISONING IN CHILDREN

1. History

o When did the event happen?

11
 o The drug/substance ingested?

o The quantity of drug/substance ingested?

o Mode of poisoning e.g. ingestion/inhalation?

o Has any treatment been given?

2. Initial assessment and treatment

 A,B,C,D,E - Manage airway, breathing and circulation, disability [quick

neurological exam],exposure

 Place in left lateral position

 physical examination, including full neurological exam

3. Supportive care:

 Oxygen by nasal catheter/prongs [1-2 L/min]

 Intravenous fluids
Shock: check shock protocol
Maintenance fluids two thirds of normal [half-strength
Darrows in 10% dextrose]

 Do not use emetics

 Consider Gastric lavage EXCEPT in paraffin/alkaline/acid poisoning as well as

unconscious children.

 Give activated charcoal for enhanced elimination of most toxins [1g/kg by

mouth or via nasogastric tube]. Activated charcoal is contraindicated in a
unconscious child or in suspected GI haemorrhage or perforation.

4. Investigations

 Urine, vomitus for toxicology

 Blood levels

 Clotting profile, blood glucose, liver function tests, electrolytes, urea and
creatinine as and when indicated.

5. Specific poisons

5.1 Paracetamol

Clinical signs

12
In the first 24 to 48 hours, the child may appear well. However, nausea and vomiting
may occur.
In the next 48 to 72 hours, anorexia, nausea, vomiting, right subcostal pain
If there is severe liver damage, there will be repeated vomiting, jaundice,
hypoglycaemia, coagulopathy, encephalopathy, ALT > 2000 iu/L.
Death occurs about 4-18 days later, usually from cerebral oedema and sepsis.

Volume and concentration of the formulation should be established from the package
and volume/amount of tablets remaining

Management

If single dose of < 150 mg/kg or cumulative dose of < 90 mg/kg/day then no action
needed.

Estimate paracetamol levels

If staggered doses taken, start on N-acetylcysteine [NAC] without waiting for

paracetamol levels.

Take bloods for INR, LFTs, U/Es after NAC regimen.

Those presenting 8 hrs post ingestion should also start treatment immediately.
Abnormal blood results should prompt a further 16 hr NAC infusion.
NAC is given by IV route and should be administered when indicated using the
normograms or situations indicated above.
Dose: 150 mg/kg infused over 60 minutes, followed by a 4 hour infusion of 50 mg/kg,
followed by a 16 hour infusion of 100 mg/kg
NAC side effects include bronchospasm, nausea, vomiting, flushing and urticarial rash
which resolve after infusion is stopped and antihistamine is given.

NB: If bronchospasm occurs, stop NAC.

13
5.2 Aspirin

Clinical signs

Tinnitus, rapid breathing, vomiting, dehydration, fever, double vision, feeling faint.
Later signs include drowsiness, confusion, bizarre behaviour, unsteady walking and
coma
Rhabdomyolysis (dark urine), acute renal failure and respiratory failure may occur.

Management

Measure salicylate concentration if thought to have taken > 120 mg/kg.

Take sample at 2 hours [symptomatic patient] or 4 hours [asymptomatic patient].

14
Poisoning Mild moderate Severe

Plasma salicylate < 350 mg/l > 350 mg/l > 700 mg/l

Fluids Encourage oral fluids Intravenous Intravenous

fluids[two thirds fluids[two thirds
normal requirement] normal requirement]
Sodium bicarbonate Yes Yes
mEq {84 -840 mg}
/kg/day] in divided
doses
Consider repeated Yes Yes
doses of activated
charcoal
Urgent referral for Yes
haemodialysis

Bicarbonate 4.2% [42 mg/ml]

Bicarbonate

8.4% [84 mg/ml]

5.3 Organophosphate poisoning

Source

Insecticides, rat poison, etc...

Clinical manifestations

Suspect in a patient with miosis, excessive salivation.

Muscarinic signs and symptoms:

Diaphoresis, emesis, urinary and faecal incontinence, excessive lacrimation, drooling,

bronchorrhoea and bronchospasm, miosis, hypotension and bradycardia

Nicotinic signs and symptoms:

Muscle weakness, fasciculations, tremors, hypoventilation, hypertension , tachycardia,
and dysrythmias

15
CNS effects:

Malaise, confusion, delirium, seizures and coma.

Management

Decontaminate (remove all clothing if necessary)

Fluid and electrolyte support

Atropine 0.02-0.05 mg/kg (max dose = 2 mg) every 10-20 mins

[Effects of atropine: dry flush skin, tachycardia, mydriasis, fever]

Give atropine until heart rate and blood pressure are normal for age, chest is clear,
sweating stops and pupils are dilated.

Pralidoxime [in combination with atropine] at 20-50 mg/kg/dose. Repeat in 1-2 hours if
muscle weakness has not been relieved, then 10 to 12 hours intervals if cholinergic signs
recur.

5.4 Hydrocarbons poisoning [e.g. paraffin]

Clinical signs

Transient mild CNS depression, aspiration is characterized by coughing. Respiratory

symptoms may remain mild or may rapidly progress to respiratory failure. Fever occurs
and may persist for as long as 10 days after aspiration.

Management
Emesis is contraindicated because of the risk of aspiration.
GASTRIC LAVAGE IS ALSO CONTRAINDICATED.
If hydrocarbon-induced pneumonitis develops respiratory treatment is supportive.
Corticosteroids should be avoided, because they are not effective and may be harmful
Do CXR after 24 hrs if signs and respiratory distress and if severe respiratory distress,
add antibiotics.

References
1. Fiona Jepsen, Mary Ryan. Poisoning in children; Current Paediatrics, 2005; 15: 563-
568.

2. Carol K taketomo, Jane H Hodding, Donna M Kraus. Paediatric Dosage Handbook.

3. Kliegman, Berhman, Jenson and Stanton. Nelson Textbook of Pediatrics, 18th edition,

16
COMA

Definition
A state of deep unarousable unconsciousness with total loss of awareness of self and
environment. Consciousness is awareness of oneself and surroundings in a state of
wakefulness, altered by disease, poisoning or trauma.

Causes

Coma with fever Coma without fever

Meningitis/Sepsis Metabolic disorder
Cerebral malaria Hypertensive encephalopathy
Viral meningo-encephalitis Post-ictal state
Cerebro-vascular accident

Focused clinical history

 Child’s health and activity in the last 24 hrs

 Any history of fever
 Any chronic condition (DM, SCA, epilepsy,…)
 Time of last meal
 Pre-existing neurological disability
 Recent trauma

General physical examination

 Skin – Rash, trauma, haemorrhage

 Head – Full AF
 Neck – Rigidity
 Odour – Metabolic disorders, poisoning
 Eyes – Pupillary size and reaction to light
 Abdomen – Enlarged liver associated with hypoglycaemia

Degree of coma

17
This can be measured using:

Glasgow Coma Scale (GCS) in children > 5 yrs. Blantyre Coma Scale (BCS) in < 5
yrs

Eye opening Eye movement

Spontaneous 4 Focusing 1
To verbal stimuli 3 None 0
To pain 2
None 1

Best motor response Best motor response

Obeys verbal command 6 Localises 2
Localises pain 5 Flexes/extends 1
Withdraws from pain 4 None 0
Flexion to pain 3
Extension to pain 2
None 1

Best verbal response Best verbal response

Oriented 5 Appropriate 2
Confused 4 Inappropriate 1
Inappropriate words 3 None 0
Incomprehensible sounds 2
None 1

Total score 15 Total score 5

Primary assessment/resuscitation

A Airway
B Effort of breathing: Recessions, RR, grunting, flaring, use of accessory muscles
Effect of breathing: HR, skin colour, mental state, cyanosis
C Circulation: Pulse volume, pulse rate, capillary refill time, BP
D Disability: Degree of coma, posture, pupils, seizures
E Exposure: Temperature, rash, evidence of poison

Investigations

18
  Blood glucose
 Malaria parasite slide
 FBC, U/Es, blood culture, calcium, phosphate
 LFTs
 Blood/Urine toxicology
 CSF studies
 EEG
 Imaging studies (X-rays, CT scan,…)

Management

 Pay meticulous attention to Airway, Breathing and Circulation

 Further treatment depends on the provisional diagnosis
 Treat for raised ICP
 Nursing care (Skin care, oral hygiene, eye care, feeds, fluid balance)

References

1. Behrman RE et al. Nelson Textbook of Pediatrics, 18 th edition, 2007, Saunders,

Elsevier
2. James HE. Emergency of acute coma in children, Pubmed, 1993 Sep 1;
48(3):473-8
3. Donald AT. Coma in the Pediatric Patient: Evaluation and Management. Indian
Journal of Pediatrics, Volume 61, Number 1, 13-26

DIABETIC KETOACIDOSIS (DKA)

19
Definition

Diabetic ketoacidosis (DKA) is the state of uncontrolled catabolism associated with

insulin deficiency, resulting in hyperglycaemia, osmotic diuresis, and dehydration. It is
the commonest endocrine emergency usually encountered in previously diagnosed
diabetics.

Causes

It is caused by increased fatty acid metabolism and the accumulation of fatty acids due
to reduced insulin activity or deficiency of insulin, an intercurrent illness or it could just
be a new presentation.

Clinical features

 Dehydration
 Abdominal pain
 Ketone smell in the breath
 Acidosis
 Acidotic breathing/hyperventilation
 Unexplained coma
 Nausea
 vomiting

In DKA, a child may die from hypokalaemia or cerebral oedema. Cerebral oedema is
unpredictable, occurs more frequently in younger children and new diabetics, and has
mortality of around 80%.

These guidelines are intended for the management of children who are more than 5%
dehydrated and/or vomiting, drowsy or clinically acidotic.

Investigations

 Random glucose
 U/E, Creatinine, LFTs
 FBC
 Malaria parasite
 Urinalysis
 Urine m/c/s
 Arterial blood gases
Treatment

General resuscitation: A, B, C.

20
Airway: Ensure that airway is patent. If comatose, insert an airway. If comatose and has
recently vomited, insert a NGT, aspirate and leave on open drainage.

Breathing: Give 100% oxygen. Bag and mask ventilation if apnoeic.

Circulation: Insert two large bore IV cannulae and take blood samples.

If shocked (Tachycardia with poor capillary refill time or hypotension) give 20 ml/kg 0.9
saline as quickly as possible, and repeat if necessary up to a max of 60mls/kg.

Confirm the diagnosis:

 History: Polydypsia, polyuria
 Clinical: Acidotic respiration; dehydration; drowsiness; abdominal pain/vomiting
 Biochemical: High glucose, ketones or glycosuria, ketonuria

Conscious Level

 GCS or BCS
 Cerebral oedema: Irritability, slow pulse, high BP. Fundal examination.
Look for the focus of infection.
Observation to be carried out:
 Strict fluid balance chart
 Hourly blood glucose
 Daily weights
 GCS or BCS
 ECG
Fluids
Requirement = maintenance + deficit
Deficit = % dehydration x body weight
Maintenance= 100mls/kg-1st 10kgs,50mls/kg- next 10kgs, 20mls/kg for every kg
thereafter.
Add deficit and maintenance and give over the next 36 – 48 hrs

For example, for a 25kg diabetic patient, fluid is calculated as follows:

Deficit= 25x 10%=2.5L =2500mls, to be given over 48 hrs, therefore 1250mls to be
given over 24hrs

Maintenance = 1000mls+500mls+100mls= 1600mls/24hrs

Therefore total amount of fluid to be given over 24hrs is 1600mls+1250mls
=2850mls
This may be divided by 3 or 4 to be given at 950mls 8hrly or ~710mls 6hrly
respectively.

Type of fluid is 0.9% normal saline. Change to DNS once RBS has fallen to 12 mmol/l.
In the presence of Hypernatraemia, then half Normal Saline must be used (PLEASE
CONSULT)

21
Potassium
Commence potassium immediately unless anuria is suspected or there are peaked T
waves on ECG or the serum potassium is > 7 mmol/l.
Add 20 mmol KCl to every 500 ml intravenous fluids given for the first 24 hrs.

Insulin
Soluble insulin e.g. 0.1 IU/kg/hour continuous intravenous infusion.
Average rate of fall of blood glucose must not exceed 5mmol/l.

REFERENCES

1. David Southall International Child HealthCare. A practical Manual for

Hospitals Worldwide. First Edition, Book power 2003. Pages 213- 216. UK.

2. Richard E. Behrman, Nelson Textbook Of Paediatrics, 17th Edition, 2004.

Pages 1954 – 1959. USA.

3. Sharma S, Kochar GS, Sankhyan N, Gulati S. Approach to the Child with

Coma.
Department of Pediatrics, Child Neurology Division, All India Institute of
Medical Sciences, New Delhi, 110029, India. Indian J Pediatric. 2010 Sep 10.
[Epub ahead of print]

CRITERIA FOR ADMISSION TO PICU

 Cardiovascular system
a. Severe congestive cardiac failure with pulmonary oedema

22
 b. Hypertensive crisis/severe hypertension due to any cause
c. Cardiac tamponade or constriction with hemodynamic instability
d. Tetralogy of Fallot in hypoxic spell

 Pulmonary system
a. Acute respiratory failure requiring ventilator support – when ventilation
possible.
b. Status asthmaticus
c. Severe bronchiolitis
d. Apnoea in a neonate (> 7days) if < 7 days, refer to NICU

 Neurological disorders
a. Acute stroke with altered mental status
b. Coma (metabolic, toxic, septic or anoxic)
c. Meningitis with deteriorating GCS
d. Status epilepticus
e. CNS or neuromuscular disorders with deteriorating neurologic or pulmonary
function or potentially so, e.g. GBS

 Renal system
a. Acute renal failure
b. Chronic renal failure with acute complications (hypertension/anaemia/anuria)
c. Acute glomerulonephritis with hypertension
d. Nephrotic syndrome with
Hypertension
Spontaneous peritonitis or
CVA

 Metabolic

a. Diabetic ketoacidosis
b. Thyroid storm
c. Adrenal crisis
d. Hypernatraemia with seizures/altered consciousness
e. Hypo/Hyperkalaemia with dysrhythmias

 Miscellaneous
a. Haemodynamic monitoring
b. Environmental injuries ( e.g. drowning)

23
 c. Poisoning
d. Meningococcaemia (requiring hemodynamic support)
e. Any patient who has just undergone successful resuscitation

Discharge criteria

The status of patients admitted to PICU will be continuously monitored to identify

patients who may no longer need ICU care.

a. When a patient’s physiological status has stabilised and the need for ICU
monitoring and care is no longer necessary.

b. When a patient’s physiological status has deteriorated and active interventions

are no longer deemed to be of any benefit to the patient.

Patients admitted to PICU must be handed over by the senior most person available in
the unit, either physically or by verbal communication to ensure nothing is missed out on
the patient’s condition. Further, registrars must physically hand-over patients to the
PICU registrar either immediately or as soon as this is possible.

CONGESTIVE CARDIAC FAILURE (CCF)

Definition
CCF is a clinical syndrome in which the heart is unable to pump enough blood to the
body to meet its needs, to dispose of venous return adequately, or a combination of the

24
two. This is also defined as the inability of the heart to deliver oxygen to the tissues
at a rate commensurate with the metabolic demands.
Chronic heart failure syndrome is a condition of cardiac pump dysfunction with
activation of compensatory responses that ultimately contribute to silent and progressive
deterioration of myocardial function.

Aetiology
CCF may result from congenital or acquired heart diseases with volume and/ pressure
overload or from myocardial insufficiency.

Mechanical  Pressure overload

abnormalities

 Volume overload – Primary

– Ventricular dilatation

 Pericardial diseases

 Restrictive diseases

Arrhythmias  Bradyarrhythmias

 Tachyarrhythmias

Myocardial failure  Primary

 Secondary

Diagnosis

The diagnosis is based on several clinical findings and CXR. Cardiomegaly on CXR is
nearly a perquisite sign for CCF.

No single test is specific for CCF

The symptoms in cardiac failure are almost entirely as a consequence of poor cardiac
output and fluid retention.

History
1. Poor feeding of recent onset, tachypnoea that worsens during feeding, poor
weight gain, sudden weight gain, cold sweat of forehead suggest CCF in infants
2. Older children may complain of shortness of breath especially on exertion, easy
fatigability, puffy eyelids or swollen feet.

25
Physical Examination

Physical findings of CCF may be classified depending on their pathophysiologic

mechanisms as follows:
1. Compensatory response to impaired cardiac function
2. Pulmonary venous congestion( left-sided failure)
3. Systemic venous congestion (right-sided failure)
4. X-ray study
5. Electrocardiography
6. Echocardiography

Treatment

What are the aims of treatment?

1. To relieve symptoms and enhance quality of life

2. Elimination of the underlying cause is most desirable approach whenever
possible
3. Elimination of the precipitating causes ( e.g. infection, arrhythmias, fever)
4. Control heart failure
5. To stop progression of the maladaptive process that has been set into motion
6. If possible, to reverse the negative effects of the process.
7. Improve survival

General measures
1. Position to relieve respiratory distress ( prop up, cardiac chair, infant seat)
2. Humidified oxygen
3. Sedation with morphine sulfate ( 0.1 to 0.2 mg /kg/dose sc every 4 hours as
needed) or Phenobarbital 2 to 3 mg /kg/dose by mouth or IM
4. Salt and fluid restriction in older children
5. Daily weight in hospitalized patients
6. Predisposing factors such fever, anemia and infection should be treated.
7. Underlying causes such as hypertension are treated

Drug therapy

The cornerstones of management are:

 Diuretics
 Oral inotropes – digoxin
 Afterload reducing agents

26
 Drugs
1. Patients with CCF may improve rapidly after a dose of furosemide a fast acting
loop diuretic even before digitalization. Furosemide is a drug of choice.

2. Spironolactone, an aldosterone antagonist, is useful in the treatment of the

hyperaldosteronism component of CCF.

3. Digoxin is the most commonly used digitalis preparation in paediatric patients.

4. Afterload reducing agents tend to augment stroke volume without changing the
contractile state of the heart and without increasing myocardial oxygen
consumption. The agents are used with diuretics and digoxin.

5. Other inotopes, dobutamine and dopamine may used in severe CCF with distress,
renal dysfunction and in post-operative patients.

Dosages
DRUG ROUTE DOSAGE

Hydrochlorothiazide Oral 2-4 mg/kg/day in 2-3 divided doses

Furosemide IV 1-2 mg/kg/day in 2-3 divided doses

Oral
2-5 mg/kg/day in 2-3 divided doses
Spironolactone Oral
2-3 mg/kg/day in 2-3 divided doses

27
Digoxin Maintenance (mg/kg/day)
Oral TDD( mg/kg)

Age 0.02
0.005
Premature 0.03
0.008
Newborn 0.04-5
0.01-0.012
Under 2 yrs 0.03-4
0.008-0.01
Over 2 yrs

Dobutamine IV 2-4 µg/kg/min

Dopamine IV: Effects are dose 1. 2-5 µg/kg/min ↑RBF and urine output
dependant 2. 5-15 µg/kg/min ↑RBF,HR, inotropic, ↑CO
3. >20 µg/kg/min α-adrenegic effects with ↓RBF

Captopril Oral

Newborn 0.1- 0.4 mg/kg/dose, 1-4 times a day

Infants
0.5-6.0 mg/kg/day, 1-4 times/day
Child
12.5 mg/dose 12 to 8 hourly

Increase to 2mg/kg if maximum doses needed

Enalapril

Oral
0.1 mg/kg once or twice daily

Beta blockade – How does it work?

– Allows up-regulation of beta I receptors & regeneration of endogenous
catecholamines
– Heart becomes more receptive to “normal” sympathetic stimuli
– Reduces apoptosis
– Reduces catecholamine myocyte toxicity
– Blocks noradrenaline mediated fibrosis

28
Beta blockade - do’s and don’ts!
• Avoid in NYHA Class IV
• Must be introduced cautiously in hospital at a low dose – gradually increasing
over months
• Symptomatic improvement seen only in months
• New generation have alpha blockade as well making introduction easier

Drugs
These have not been used in paediatric patients in Zambia. These may be helpful in end
stage disease in patients who require heart transplant

Carvedilol

Indication: Dilated cardiomyopathy (DCM)

Doses: 0.08 mg/kg 12 hrly, if tolerated increase by 0.08 mg/kg every 1-2 wks to a
maximum 0.50 - 0.75 mg/kg 12 hrly.

ACUTE RHEUMATIC FEVER

Diagnosis

ARF can be confirmed if certain signs and symptoms are present from the Revised Jones
criteria
MAJOR CRITERIA MINOR CRITERIA

Carditis Fever

Polyarthritis Arthralgia

29
Sydenham’s chorea ↑ PR interval on ECG

Erythema marginatum ↑ ESR ≥ 30 mm/hr or CRP ≥ 30 mg/l

Subcutaneous nodules

Revised Jones Criteria

WHO guidelines set the international standard for diagnosis of ARF:
TWO MAJOR manifestations PLUS evidence of preceding streptococcal infection OR
ONE MAJOR and TWO MINOR manifestations PLUS evidence of preceding
streptococcal infection.
Management

Treat the illness

1. Benzathine penicillin injection stat or oral penicillin for ten days
2. Relieve symptoms
 Bed rest
 Relief of arthritis, pain and fever
 Treat chorea (if severe)
 Anti- heart failure medication ( see CCF protocol)

General Guidelines for Bed Rest and Ambulation

Arthritis Alone Minimal Carditis Moderate Carditis Severe Carditis
Bed rest

1-2 wk 2-3 wk 4-6 wk 2-4 mo

Indoor
ambulation
1-2 wk 2-3 wk 4-6 wk 2-3 mo
Outdoor activity
(school)
2 wk 2-4 wk 1-3 mo 2-3 mo
Full activity

After 4-6 wk After 6-10 wk After 3-6 mo Variable

Minimal carditis : Questionable cardiomegaly

Moderate carditis: Definite but mild cardiomegaly
Severe carditis: marked cardiomegaly or CCF

Recommended Anti-inflammatory Agents

Arthritis alone Minimal Moderate Severe Carditis
Carditis Carditis

Prednisolone nil nil 2-4 wks 2-6 wks

30
Aspirin 1-2 wks 2-4 wks 2-8 wks 2-4 mo

Dosages: Prednisolone 2 mg/kg/day in four divided doses

Aspirin 100 mg/kg/day in four to six divided doses

The dose of prednisolone should be tapered and aspirin started during the final
week.

Aspirin may be reduced by 60 mg/kg/day after two weeks of therapy.

Management of Sydenham’s chorea

1. Reduce physical and emotional stress and use protective measures as indicated
2. Eradicate GAS and then 2° prophylaxis with a penicillin
3. Anti-inflammatory agents not indicated
4. For severe chorea, any of the following drugs may be used :
 Phenobarbitone 15 to 30 mg every 6-8 hours po
 Haloperidol 0.5-2.0 mg every 8 hours po
 Chlorpromazine 0.5-2 mg/kg 6-8 hourly po or prn
 Diazepam 0.3 mg/kg prn po
 Steroids

Further management plan

 First dose of benzathine penicillin 2° prophylaxis
 Baseline echo
 ARF register (cardiac clinic), issue ARF prophylaxis card
 Education of patient and family
 Dental examination
 Long term 2° prophylaxis plan

Secondary prophylaxis to prevent recurrent ARF is a long term, regular

administration of antibiotics to

 Prevent GAS
 Prevent repeated development of ARF
 Prevent development of RHD

31
  Reduce severity of RHD
 Help reduce the risk of death from severe RHD

Secondary prophylaxis is considered in

 ARF confirmed by the Revised Jones Criteria
 ARF/RHD confirmed on Echo
 ARF/RHD NOT CONFIRMED but regarded as ‘highly probable’

Drugs for secondary prophylaxis

Benzathine penicillin every four weeks : 1,200,000 iu ALL people ≥ 20 Kg
600,000 iu < 20 Kg
Penicillin V 250 mg twice a day

Erythromycin 250 mg twice a day in those with penicillin allergy

SYSTEMIC HYPERTENSION

Definition

Hypertension in children may be defined statistically as systolic and/or diastolic pressure

levels greater than the 95th percentile for age and gender on at least three occasions. High
normal blood pressure is defined as an average systolic and/or diastolic blood pressure
between the 90th and 95th percentiles for age and gender. Values slightly above the 95 th
percentile may be considered significant hypertension, and values greater than the 95 th
percentile by 8 to10 mm Hg may be considered severe hypertension. A pre-requisite for
these definitions is the availability of reliable normative blood pressure values.

AGE BLOOD

PRESSURE

3-6 years 110/70

32
 6-9 120/75

10-13 130/80

14-19 140/85

AGE WEIGHT(approx. wt in kg) MEAN BP

95% RANGE

Term 3.0 40-60

3 mo 6.0 45-75

6 mo 7.5 50-90

1 yr 10 50-100

3 yr 14 50-100

7 yr 22 60-90

10 yr 30 60-90

12 yr 38 65-95

14 yr 50 65-95

21 yr 60 65-105

21 yr 70 70-110

Aetiology

Hypertension is classified into two general types; Essential or primary hypertension, in

which a specific etiology cannot be identified, and secondary hypertension in which a
cause can be identified.

Renal

 Glomerulonephritis, acute and chronic

 Pyelonephritis, acute and chronic

 Congenital anomalies [polycystic or dysplastic kidneys]

 Obstructive uropathies [hydronephrosis]

 Haemolytic-uremic syndrome

33
  Collagen diseases [periarteritis, lupus]

 Renal damage from nephrotoxic medications, trauma or radiation

Renovascular diseases

 Renal artery disorders [e.g. stenosis, polyarteritis, thrombosis]

 Renal vein thrombosis

Cardiovascular

 Coarctation of the aorta

 Conditions with large stroke volume [PDA, aortic insufficiency, system A-V
fistula, complete heart block]. These conditions cause only systolic hypertension.

Endocrine
 Hyperthyroidism [systolic hypertension]
 Excessive catecholamine levels
 Pheochromocytoma
 Neuroblastoma
 Adrenal dysfunction
Congenital adrenal hyperplasia
11-B-hydroxylase deficiency
17-hydroxylase deficiency
 Cushings syndrome

 Hyperaldosteronism
Primary

 Conn’s syndrome

 Idiopathic nodular hyperplasia

 Dexamethasone-suppressible hyperaldosteronism

Secondary

 Renovascular hyperplasia

 Renin-producing tumor or juxtaglomerular cell tumor

34
  Hyperparathyroidism [and hypercalcaemia]

Neurogenic

 Increased intracranial pressure[any cause, especially tumors, infections, trauma]

 Poliomyelitis

 Guillain-Barre syndrome

 Dysautonomia [Riley-Day syndrome]

Drugs and chemicals

Sympathomimetic drugs [nose drops, cough medications, cold preparations]

Amphetamines

Steroids

Oral contraceptives

Heavy-metal poisoning [mercury, lead]

Cocaine [acute or chronic use]

Miscellaneous

Hypervolaemia and hypernatraemia

Stevens-Johnson syndrome
Bronchopulmonary dysplasia [newborns]

Most Common Causes of Chronic Sustained Hypertension

Age Causes

Newborns Renal artery thrombosis, renal artery

stenosis, congenital renal malformation,
Coarctation of the aorta, bronchopulmonary dysplasia

< 6 yr Renal parenchymal disease, Coarctation of the aorta

35
 Renal artery stenosis

6 -10 yr Renal artery stenosis, renal parenchymal

disease, primary hypertension

>10 yr Primary hypertension, renal parenchymal

disease

Diagnosis and work-up

Many children with mild hypertension are asymptomatic, and hypertension is diagnosed
by routine BP measurement. Children with severe hypertension may be symptomatic
(headache, dizziness, nausea and vomiting, irritability, personality changes).
Occasionally neurologic manifestation, CCF, renal dysfunction, and stroke may be the
presenting symptoms.

Careful evaluation of history, physical findings and laboratory tests usually point to the
cause of hypertension.

Routine and special laboratory tests and their significance

Routine Laboratory Tests Significance of Abnormal Results

Urinalysis, urine culture, urea Renal parenchymal disease

Creatinine, uric acid

Serum electrolyte (hypokalaemia) Hyperaldosteronism 1° or 2°, Adrenogenital

syndrome, renin producing tumours

ECG,CXR, ECHO Cardiac cause of ↑BP, also baseline function

Specialised tests

IVU, US KIDNEY, CT scan Renal parenchymal disease, renovascular

36
 disease, tumours ( neuroblastoma, Wilms)

Plasma renin activity High-renin hypertension

 Renovascular disease
 Renin-producing tumours
 Some Cushing’s syndrome
 Some essential hypertension
Low-renin hypertension

 Adrenogenital syndrome
 Primary hyperaldosteronism
24-hr urine collection for 17- Cushing’s syndrome, adrenogenital syndrome
ketosteroids and 17-
hydroxycorticosteroids

24-hr urine collection for Pheochromocytoma, neuroblastoma

catecholamine levels and VMA

Aldosterone Hyperaldostreronism, primary or secondary

renovascular disease, renin-production tumours

Renal vein plasma renin activity Unilateral renal parenchymal disease,

renovascular hypertension

Abdominal aortogram Renovascular hypertension, abdominal CoA,

unilateral renal parenchymal disease,
pheochromocytoma.

Routine Laboratory Test

Initial laboratory test should be directed towards detecting renal parenchymal disease,
renovascular disease, and COA and therefore should include urinalysis; urine culture;
serum electrolyte, blood urea nitrogen, and uric acid levels; ECG; chest x-ray studies,
and possibly echo.

Specialized Studies

More specialized studies may be indicated for rare causes of secondary hypertension:
excretory urography, plasma renin activity, aldosterone levels in serum and urine, 24-
hour urine collection for catecholamine levels [norepinephrine, epinephrine] and their
metabolites [vanillymandelic acid levels], renal vein, and abdominal aortogram

37
The decision to undertake specialized tests and procures depends on availability and
familiarity with the procedure, severity of hypertension, age of the patient, and history
and physical findings suggestive of a certain aetiology, for example children under 10
years of the age with sustained hypertension require extensive evaluation, because
identifiable and potential curable causes are likely to be found. Adolescents with mild
hypertension and a positive family history of essential hypertension are more likely to
have essential hypertension, and extensive studies are not indicated.

Management

Essential hypertension

Non-pharmacologic intervention should be started as an initial treatment. Counseling

should encourage weight reduction if indicated; low-salt[and potassium-rich] foods; and
avoidance of smoking and oral contraceptives.

Drug therapy although there no clear guidelines for identifying those who should be
treated with antihypertensive drugs, a family history of early complications of
hypertension, the presence of target organ damage [e.g., ocular, cardiac, renal, central
nervous system], and the presence of other coronary artery risk factors favour drug
therapy. However, the possible adverse effects of long-term drug therapy on growing
children have not been evaluated adequately.

The stepped-care approach, using three classes of drugs: diuretics, B-blockers, and
vasodilators, is popular.

Step 1 is initiated with a small dose of a single antihypertensive drug, either thiazide
diuretic or an adrenergic inhibitor, then proceed to full dose if necessary.[B-Adrenergic
blockers may be contraindicated in diabetic patients and asthmatic patient; the diuretic
work well in adult black patients. In adolescents with hyperdynamic-type hypertension
(with a rapid pulse) or those associated with hyperthyroidism a β-Blocker is preferable.

Step 2 If the first drug is not effective, a second drug may be added to, or substituted for,
the first drug, starting with a small dose and proceeding to full dose.

38
Step 3 If the blood pressure still remains elevated, a third drug, such as a vasodilator,
may be added to the regimen. At this point, the possibility of secondary hypertension
should be reconsidered.

*Diuretics are the cornerstone of antihypertensive drug therapy, except in patients with
renal failure. Their action is related to a decrease in extracellular and plasma volume.

Recommended oral dosage of selected antihypertensive drugs for children

Drugs Dose[mg/kg] Times/day

Diuretics

Hydrochlorothiazide 1-2 2

Furosemide [lasix], 0.5-2 2

Spironolactone [aldactone] 1-2 2

Adrenergic inhibitors 1-3 3

5-10 2

Propranolol [inderal], 1-2 1

Methyldopa [aldomet],

Atenolol[tenormin]

Vasodilators

Hydralazine [Apresoline] 1-5 2-3

Nifedipine [Ca antagonist] 0.5-1 2

ACE inhibitors

39
Captopril [capoten]

<6 mo 0.05-0.05 3

>6 mo 0.5-0.2 3

HYPERTENSIVE CRISIS

A hypertensive Emergency is defined as any of the following features:

1. The patient has severe hypertension [>180 mm Hg systolic or 110 mm Hg

diastolic] or rapidly increasing blood pressure.

2. The patient has neurologic signs [hypertensive encephalopathy] with severe

headache, vomiting, irritability, apathy, papilloedema, retinal haemorrhage,
or exudates.

3. The patient has CHF or pulmonary oedema.

Aggressive parenteral administration of antihypertensive drugs is indicated to lower

blood pressure:

 Hydralazine [Apresoline], 0.15 mg/kg intravenously or intramuscularly may be

used. The onset of action is 10 minutes after an intravenous dose and 20 to 30
minutes after an intramuscular dose .The dose may be repeated at 4-6 to 6-hours
interval.
 A rapid-acting diuretic, such as furosemide [1 mg/kg], is given intravenously to
initiate diuresis.
 Sublingual Nifedipine 0.25-0.5 mg/kg stat. This may be repeated after 30
minutes
 Fluid balance must be controlled carefully, so intake is limited to urine output
plus insensible loss.
 Seizures may be treated with slow intravenous infusion of diazepam [Valium],
0.2 mg/kg or another anticonvulsant medication.
 When a hypertensive crisis is under control, oral medications replace the
parenteral medications.

40
NB. If Diazoxide (3-5 mg/kg as IV drip) or sodium nitroprusside (1-3ɱg/kg/min as IV
drip) are available is the treatment of choice.

CYANOTIC SPELL

Definition

Also called hypoxic spell or “tet” spell occurs in young infants with Tetralogy of Fallot
(TOF). It consists of hyperpnoea (i.e. rapid and deep respiration) worsening cyanosis and
the disappearance of the heart murmur. This occasionally results in complication of the
central nervous system and even death. Any event such as crying, defecation or
increased physical activity that suddenly lower the SVR or produce a large right-to left
ventricular shunt may initiate the spell by establishing a vicious cycle of hypoxic spell.
The sudden onset of tachycardia or hypovolaemia can also cause the spell. The resulting
fall in arterial PO2 in addition to an increase in Pco2 and a fall in pH stimulates the
respiratory center and produce hyperpnoea. In turn this makes the negative thoracic
pump more efficient and results in an increase in the systemic venous return. In the
presence of a fixed opening or fixed resistance at the RV outflow tract (i.e. pulmonary
resistance) the increased systemic venous return to the RV must go out the aorta. This
leads to a further decrease in the arterial oxygen saturation which establishes a vicious
cycle of hypoxic spell.

41
Treatment

It is aimed at breaking this cycle by using one or more of the following maneuvers:

1. Using the knee-chest position and holding the baby traps systemic venous blood in
the leg thereby decreasing the systemic venous return and helping to calm the baby.
The knee-chest position may also increase SVR by reducing arterial blood flow
through the femoral arteries.

2. Morphine sulfate, at 0.2 mg/kg administered sc, IM or IV suppresses the respiratory

center and abolishes hyperpnoea.

3. Sodium bicarbonate (NaHCO3) at 1 mmol/l IV .corrects acidosis and eliminates the

respiratory center–stimulating effect of acidosis. The same dose can be repeated in
10 to 15 minutes

4. Administration of oxygen may improve arterial oxygen saturation a little.

5. Vasoconstrictors such as phenylephrine at 0.02 mg/kg IV raise SVR.

6. Ketamine at 1 to 3 mg/kg given over 1 minute is a good drug to use since it

simultaneously increases the SVR and sedates the patient. Both effects are known to
terminate the spell.
7. Propranolol at 0.01 to 0.25 mg IV slowly has been used successfully in some cases
both acute or chronic. Its mechanism of action is not entirely clear. When
administered for acute cases propranolol may reduce the spam of the RV outflow
tract and slow the heart rate. The successful use of propranolol in the prevention of
hypoxic spell is more likely the result of the drugs peripheral action. It may stabilize
vascular reactivity of the systemic arteries thereby preventing a sudden decrease in
the SVR.

8. Oral propranolol therapy at 2 to 6 mg/kg/day in three to four divided doses may be

used to prevent recurrence of hypoxic spell and delay corrective surgical procedures
in high risk patients.

 Physicians should recognize and treat hypoxic spells. It is important to

educate parents to recognize the spell and what to do.
 Maintenance of good dental hygiene and antibiotic prophylaxis against
SBE are important
 Relative iron-deficiency anemia should be detected and treated. Anemic
children are more susceptible to CVA. Normal Hb or HCT or decreased
RBC indices indicate iron- deficiency anemia in cyanotic patients.

42
REFERENCES:

1. Guest lecture by Dr. John starling Red Cross Children’s Hospital

2. Paediatric cardiology for practitioners by Myung K Park, Third edition

3. World Heart Federation training manual for RF/RHD

4. Management of polycythaemia in adults with congenital cyanotic heart disease. S A

Thorne; Heart 1998; 79; 315-316

5. Cardiology by Neil R Grubb David E Newby; second edition

6. Essence of Paediatrics; Third edition

7. Standard treatment guidelines, essential medicines list and laboratory supplies list for
Zambia. 1st edition 2004.

8. Advanced paediatric life support the practical approach 4th edition.

9. Drugs doses by Frank Shann; Intensive Care Uinit; Royal children’s hospital
Parkville, Victoria 3052; Australia, 13th edition 2005.

10. Echo made easy; Sam Kaddoura

11. Clinical wizard, pocket clinical reference Guide; Mennen medical

12. Nelson test book of paediatrics 16th edidtion

43
VIRAL CROUP

Introduction

 Croup (laryngotracheobronchitis) is a common cause of upper airway

obstruction in toddlers (1-3 years old)
 It is characterised by varying degrees of inspiratory stridor, barking cough, and
hoarseness due to inflammation and oedema in the laryngeal region

Clinical Presentation

 Low grade fever and coryzal symptoms are followed over 12–24 h by a harsh,
barking cough
 Stridor is most evident when the child is upset or agitated

 Respiratory distress of varying degrees

44
  Usually, resolves spontaneously over a 3–4 day period

Diagnosis

 Croup is a clinical diagnosis

 Neck x-rays unnecessary unless the diagnosis is in doubt

 Important differential diagnoses

o Acute epiglottitis

o Bacterial tracheitis

o Foreign body inhalation

o Anaphylaxis

o Retropharyngeal abscess
Assessment of severity

Sign Mild croup Moderate croup Severe croup

Stridor Only when agitated At rest Severe , biphasic

Recession Mild subcostal Moderate tracheal tug Use of accessory

muscles

Level of Restless when Anxious, agitated Lethargic,

consciousness disturbed drowsy

Management

 Keep the child on the mother’s lap and handle gently

 Do not attempt to examine the oropharynx

 See flow chart below

Assess level of severity

45
 Mild croup Moderate croup Severe croup

Dexamethasone Dexamethasone 0.6 mg/kg Dexamethasone 0.6

PO/IM stat (max 12 mg) mg/kg PO/IM stat (max
0.6 mg/kg PO/IM stat 12 mg)
(max 12 mg) or prednisolone 2 mg/kg
PO stat Start nebulised
or prednisolone 2 mg/kg adrenaline immediately
PO stat Nebulised adrenaline 1:1000
(1-5 mls) diluted in 0.9% Give oxygen 1-3
or nebulised budesonide normal saline litres/min
2 mg stat
Can be repeated every 30 Admit PICU
Observe for 4 hours min (2 to 3 times)
Contact ENT
Discharge after 4 hours if Admit acute area surgeon/anaesthetist for
child stable and well possible tracheostomy
improving ifnot improving

Cautions

 Do not use antibiotics or bronchodilators unless diagnosis is in doubt

 Do not give adrenaline nebulisations if baseline heart rate >200/min

References

1. Cherry J.A. Croup. NEMJ 2008, January, 358; 4: 385-391

2. Fitzgerald D.A & Kilham H.A. Croup: Assement and Evidence-based Management. MJA 2003;
179: 372-377

3. Malhotra M & Krilov L.R. Viral croup. Pediatric Reviews. 2001; 22: 5-12

4. Forfar and Aneil. Textbook of Paediatrics. 6th edition

ACUTE BRONCHIOLITIS

Introduction

 Bronchiolitis is a seasonal viral illness, characterised by fever, nasal discharge

and dry, wheezy cough
 Respiratory syncytial virus (RSV) is responsible for the majority of the cases

46
  Infants are at the highest risk of severe bronchiolitis including infants born
prematurely, those with cardiac disease, chronic respiratory illness and the
severely immunosuppressed

Presentation and diagnosis

 The diagnosis is clinical

 Typically affected infants show worsening respiratory symptoms after a 2-3 days
of coryzal symptoms
 Tachypnoea with recession and fine crepitations all over the chest
 Wheezing may be present but it is not a prerequisite for the diagnosis
 Infants rarely systemically toxic
 May present with apnoea in ex-prems
 Most but not all infants febrile. But temperature >40o C is rare and should
prompt the
search for an alternative diagnosis

Treatment

 No specific therapy, treatment largely supportive

 Supplemental oxygen, 2-3 litres via nasal cannula
 Tube feeding if infant not sucking, IV fluids if dehydrated. Give 2/3 of normal
requirements as the risk of syndrome of inappropriate ADH secretion is high in
hypoxic infants
 No studies have shown any benefit of antibiotic therapy in uncomplicated
bronchiolitis
 Bronchodilators may produce short term clinical benefits, give a trial of
salbutamol or ipratopium bromide via inhaler with spacer or a nebuliser
 If condition deteriorates, consider ventilation
 No evidence of benefit for use of systemic corticosteroids

References

1. Bush A, Thomson A.H. Acute Bronchiolitis. BMJ 2007; 335:1037-1041

2. Smyth R.L, Openshaw P.J.M. Bronchiolitis. Lancet 2006; 368 : 312-22
3. Cornelli H.M, et al. A multicentre, randomised, controlled trial of
dexamethasone for bronchiolitis. N Eng J Med; 2007; 357 (4): 355-359

ACUTE EXACERBATION OF ASTHMA

Definition and clinical presentation

Asthma is a chronic inflammatory disorder of the airways, associated with airway

hyperresponsiveness leading to recurrent wheezy episodes, breathlessness, chest
tightness and persistent cough.

47
Pathogenesis

Environment Biological and

. Allergens Genetic risk

. Infections . Immune

. Pollutants . Lung

. Microbes . Repair

. Stress

Innate and Adaptive immune development (Atopy)

Lower . Respiratory viral infections

Airways . Aerollergens
Injury . Environmental tobacco smoke
. Pollutants/toxicants

. Persistent inflammation
Aberrant . Airway hyperresponsiveness
Repair . Remodelling
. Airways growth and differentiation

ASTHMA

Diagnostic criteria

 Episodes of breathlessness
 Chest tightness
 Wheezing
 Persistent cough
 Airflow obstruction, variability and reversibility by peak flow
measurement

48
Assessment of Asthma Severity

Sign Moderate Severe Life-

exacerbation exacerbation threatening
exacerbation

Sa02 > 92% < 92% < 92%

RR
2-5 years < 50/min > 50/ min > 50/ min
> 5 years < 30/min > 30/ min > 30/ min

HR
2-5 years < 130/min > 130/min > 130/min
> 5 years <120/min > 120/min > 120/min

Effort of Normal Use of accessory Poor respiratory

breathing neck muscles effort

Wheeze Expiratory Expiratory and Silent chest

inspiratory
Speech Normal Speaking with Unable to speak
difficulty
Level of Fully conscious Altered Altered
consciousness

Management
Moderate exacerbation Severe exacerbation Life-threatening asthma

 Salbutamol  High flow Oxygen  Admit to PICU and treat

inhalations as for severe
5-10 L/min exacerbation
up to 1 gram
 Salbutamol as for
(10 puffs) moderate

49
 3 doses back to back, exacerbation  In addition,

then every 30 minutes Do FBC, ESR, U&Es

to 4 hourly,  Add ipratropium blood culture,

bromide
Or portable CXR and blood
via spacer or
 Salbutamol gases if available
nebulisations nebuliser

2.5 mg < 2 years 125 mcg < 1 year

 IV 50% magnesium
5 mg > 2 years 250 mcg if 1-5 years sulphate 40 mg/kg over
20 min (Max 2 grams)
500 mcg >5 years
Diluted 1:5 in 0.9%
4-6 hourly
saline
 Start prednisolone
early
 Give prednisolone PO
2 mg/kg (Max 40 mg)  SC adrenaline 1:1000
If not improving or
PO OD for 3 days 0.01 mg/kg (Max 0.5
vomiting, mg)

 IV hydrocortisone  If not improving,

 Discharge if
improving, 4 mg/kg 6 hourly Prepare for intubation

and
 IV aminophyilline mechanical ventilation

 Otherwise admit and 5 mg/kg stat over 20

continue with regular min,
salbutamol
then infusion at

1 mg/kg/hour

 Admit to PICU

 Regular reviews

Discharge plan

50
  Patient can be discharge when stable on 4 hourly salbutamol inhalations.
 To complete 3 days course of prednisolone.
 Patient/parent education to be done on the ward.
 Patients with mild exacerbation of asthma can be reviewed at the local clinic.
 Those with moderate, severe or life-threatening exacerbations should be
booked for review in the asthma clinic.

References

1. British Thoracic Society. Management of Asthma Guidelines, April 2004

2. Standard Treatment Guidelines and Essential Drugs List for South Africa.
Paediatric Hospital Level. 1st Edition 1998.

3. Papadopoulos NG and Kalobatson A. Respiratory viruses in childhood asthma.

Curr Opin Allergy Clin Immunol,2007;7(1) 91-95

4. Tomlinson R. Postcard from Africa: Hospital management of asthma.

Arch dis child, 2002;87:356

5. AL-Hajjaj MS. Bronchial asthma in developing countries: A major social and

and economic burden. Annals of Thoracic Medicine, April-June 2008, vol 3,
2:39

6. Fischer GB and Camargos PAM. Paediatric asthma management in developing

Countries. Paediatric respiratory reviews, 2002, 3: 285-291

7. Busse VW and Lemanske RF. Asthma. New Engl Jour of Med, February 2001,
Number 5, vol 344:350-362

8. GINA. Global strategy for asthma management and prevention 2006 report.

PNEUMONIA

 Pneumonia is an important cause of morbidity and mortality in developing

countries
 Both bacteria and viruses are important causes of pneumonia
 Bacteria are the most common cause of pneumonia in HIV-infected children

Community-acquired pneumonia

51
  Pneumonia acquired outside the hospital settings
 In younger children, viral organisms are the common causative agents
 Streptococcal pneumoniae is the most likely cause in older children
 Mycoplasma pneumoniae should be considered in school going children
and adolescents

Clinical presentation
Cut-offs for fast
Age
 Fever >38.5 C0
breathing
 Tachypnoea, tachycardia
 Subcostal and intercostal < 2 months 60 breaths/min or more
recession
2-12 months 50 breaths/min or more
 Crackles
12 months-5 yrs 40 breaths/min or more

Indications for admission

 Infants
o Cyanosis, Sp O2 < 92%
o Increased respiratory rate
o Subcostal recession
o Intermittent apnoea, grunting
o Poor feeding
 Older children
o cyanosis, Sp O2 < 92%
o Increased respiratory rate
o Subcostal recession
o Restlessness or agitation
o signs of dehydration

Investigations

 Chest x-ray
 FBC, ESR
 U/E & creatinine
 Blood culture
 Arterial blood gases (if available)

Management

 General measures
o Oxygen by nasal cannula or mask
o IV fluids if required should be < 2/3 of requirements (risk of
SIADH in hypoxic children)

52
 o Antipyretic and analgesia as indicated
o Monitor vital signs

 Antibiotics therapy
o 0-3 months
 Benzyl penicillin 50,000 IU/kg/dose every 6 hours and
gentamicin 7.5 mg OD or BD (in divided doses)
o More than 3 months
 Benzyl penicillin 50,000 IU/kg/dose every 6 hours
o Ceftriaxone (50 mg/kg/dose OD) or cefotaxime (50 mg/kg QDS)
should be considered if no improvement within 48 hours
o In infants with HIV infection or exposure, PCP therapy with high
dose IV/PO cotrimoxazole (20 mg/kg/day of trimethoprim) should
be included
o Macrolides should be considered in school-going children and
adolescents who do not improve on 1st line treatment
 Erythromycin
 1 month – 2 years: 125 mg QID
 2-8 years: 250 mg QID
 8 – 18 years: 250-500 mg QID
 Azithromycin
 6 months-2years: 10 mg/kg OD
 3-7 years: 200 mg
 8-11 years: 300 mg
 12-14 years: 400 mg
 >14 years: 500 mg
References
1. British Thoracic Society Guidelines on the management of community-
acquired pneumonia in childhood. Thorax 2002; 57:i1-i24
2. WHO. Management of children with pneumonia and HIV in low resource
settings. Report on consultative meeting Harare, Zimbabwe, 30-31 January
2003. Geneva
3. WHO. Hospital care for children. Guidelines for the management of common
illnesses in low resource settings. 2005. Geneva

TUBERCULOSIS IN CHILDREN

Recommended approach to diagnose TB in children

1. History (TB contact, symptoms consistent with TB)

2. Clinical examination (including growth assessment)

53
 3. Tuberculin skin testing
4. Bacteriological confirmation whenever possible
5. Investigations relevant for suspected (a) PTB and (b) Extrapulmonary TB
6. HIV testing

Key risk factors for TB in children

 Household contact with a newly diagnosed smear positive case

 Age < 5 years
 HIV infection
 Severe malnutrition

Key features suggestive of TB

The presence of three or more of the following should strongly suggest a diagnosis of
TB:

 Chronic symptoms suggestive of TB

 Physical signs highly suggestive of TB
 A positive tuberculin skin test
 Chest X-ray suggestive of TB

Treatment of TB in children

 Recommended dosages
o Rifampicin (R) – 15 mg/kg (range 10 – 20 mg/kg); maximum dose
600 mg/kg
o Isoniazid (H) –10 mg/kg (range 10 – 15 mg/kg); maximum dose 300
mg/kg
o Pyrazinamide (Z) – 35 mg/kg (30 – 40 mg/kg)
o Ethambutol a (E) – 20 mg/kg (15 – 25 mg/kg)
o Streptomycin (S) – 15 mg/kg (12 – 18 mg/kg

 TB treatment categories:
o Paediatric category I
 New uncomplicated TB cases (2RHZ, 4RH)b
 PTB, Lymph node TB
o Paediatric category II
 Retreatment, Severe and complicated cases (2RHZS, 10RH)c
 TB meningitis, TB spine, Milliary TB, disseminated
TB.

54
 a. Although the Zambia National TB/HIV Programme has not endorsed the
use of Ethambutol in children, the WHO has recommended that
ethambutol used at this dosage is safe in children.
b. WHO recommends a four-drug regimen intensive phase with
ethambutol for children living in high HIV prevalence settings
c. WHO has recommended Ethambutol in place of Streptomycin for the
treatment of TB meningitis and other severe forms of TB

 Corticosteroids
Corticosteroids may be used for the management of some complicated forms of
TB, e.g. TB meningitis, complications of airway obstruction by TB lymph
glands, and pericardial TB. Prednisolone is recommended in a dosage of 2 mg/kg
daily, increased up to 4 mg/kg daily in the case of the most seriously ill children,
with a maximum dosage of 60 mg/day for 4 weeks. The dose should then be
gradually reduced (tapered) over 1–2 weeks before stopping.

References
1. Zambia National TB/HIV Manual.

2. Guidance for national tuberculosis programmes on the management of

tuberculosis in children. WHO 2006

3. Rapid advice; treatment of tuberculosis in children. WHO 2010

4. Ethambutol efficacy and toxicity; literature review and

recommendations for daily and intermittent dosage in children. WHO
2006

SEIZURES

1. First unprovoked seizure

Definitions (ILAE)

An epileptic seizure is a transient occurrence of signs and/or symptoms due to abnormal

excessive or synchronous neuronal activity in the brain

55
 Epilepsy is defined as a chronic disorder of the brain characterized by an enduring
predisposition to generate epileptic seizures, and by the neurobiological, cognitive,
psychological, and social consequences of this condition. The definition of epilepsy
requires the occurrence of at least one epileptic seizure.

The definition of epilepsy is usually practically applied as having two unprovoked

seizures >24 h apart. A patient with a first unprovoked seizure after a remote brain
insults (such as a stroke, CNS infection, trauma) has a risk of a second unprovoked
seizure that is comparable to the risk for further seizures after two unprovoked seizures.

First unprovoked seizure: occurrence of a seizure for the first time without a
provocative temporary or reversible factor lowering the seizure threshold and producing
a seizure at that point in time, such as high fever, head trauma or infection.

Etiology should not be confused with provocative factors, as some etiologies will
produce an enduring tendency to have seizures (i.e. brain tumor)

Careful history is warranted to rule out possible provocative factors and to ascertain
potential family history of epilepsy, prior neurological insults, neurological disorders,
history of seizure without a fever.

General examination (inclusive of skin lesions) and complete neurological

examination plus fundus oculi

Investigations

 The following should be chosen based on individual clinical circumstances rather

than on routine basis: FBC + DC, serum electrolytes (Ca++, Na+, and Mg++), AST,
ALT, urea, creatinine serum glucose, toxicology, lactate, ammonium, and urine
exam. Laboratory tests should be done in patients less than 2 years old, with
persistent alteration of level of consciousness, history suggestive of possible
intoxication or gluco-electrolytes imbalance.

 EEG – aids in diagnosis and management of epilepsy and in the identification of

specific focal anomalies. A negative EEG does not exclude epilepsy.

 Neuro-imaging – MRI preferred over CT scan, especially in focal neurologic

deficit
Urgent neuro-imaging to be requested in case of:
- prolonged postictal deficit
- persistent alteration of level of consciousness
- abnormal neurological exam
- suspect of potentially evolving brain lesion.

Treatment

56
Treatment with AED is not advised in absence of signs and symptom suggestive of CNS
pathology, negative history for CNS insults and/or negative EEG.

Treatment with AED to be evaluated, possibly in consultation with epileptologist, in

case of signs and symptom suggestive of CNS pathology, positive history for CNS
insults and/or positive EEG.

Diazepam 0, 5 mg/kg rectal (to be administer at home) or 0, 2-0, 5 mg/kg IV (hospital

setting) to abort prolonged seizures. (>3-5 min)

2. Status epilepticus

Classical Definition:

Continuous convulsion lasting longer than 20 to 30 mins or the occurrence of serial

convulsions between which there is no return of consciousness.

Operational Definition

Seizure lasting more than 5 min or recurrence of two or more seizures, between which
there is incomplete recovery of consciousness

Every child who arrives in ER while having a seizure must be treated as status
epilepticus.

Causes
 Febrile seizures
 Known epileptic who is non-compliant to treatment, is on erratic supply of drugs,
had sudden withdrawal of anticonvulsants, is sleep deprived or has an
intercurrent infection
 Initial presentation of epilepsy
 Encephalitis
 Meningitis
 Congenital malformations of the brain (lissencephaly, shizencephaly)
 IEMs especially in neonates
 Electrolyte abnormalities – hypocalcaemia, hypoglycaemia
 Drug intoxication – amphetamines, cocaine, phenothiazines, theophylline, TCAs
 Others – Reye’s syndrome, lead intoxication, extreme hyperpyrexia, brain tumor.

Investigations

 FBC and DC
 Random Blood Sugar

57
  Electrolytes & creatinine
 LFTs
 Calcium, magnesium, phosphate
 Gas analysis
 Lactate
 CSF studies (after brain CT)

Treatment

There are 4 goals of therapy

 Ensure adequate vital signs, systemic and cerebral oxygenation
 Terminate seizure activity
 Prevent seizure recurrence
 Establish the diagnosis and treat the underlying cause if possible

a) ABCDE
b) Give 10% dextrose – 5 ml/kg IV stat, then 10% dextrose infusion over 4-6 hours
c) Diazepam IV 0.2 – 0.5 mg/kg stat; Lorazepam 0.1 mg/kg IV is better as it does
not depress respiration as much as diazepam does and is longer acting.
Midazolan 0,2 mg/kg IV or IM may also be used,
d) If seizure continues, phenytoin IV loading dose of 15 to 20 mg/kg; infusion in 20
min (no faster than 1.0 mg/kg/min, max 50 mg/min) in Saline. Dextrose
solutions precipitate phenytoin and so should not be used. Maximum dose 1 gr.
Use a cannula minimum G22. Decrease the speed of infusion if bradycardia
and/or hypotension. Use carefully in cardiopathic patients. Cardiac and blood
pressure monitoring
e) In case of poor response to benzodiazepines and phenytoin, phenobarbitone IV
is administered at loading dose of 20 mg/kg; infusion in 10 min at rate of 2
mg/kg/min (max 100 mg/min) Maximum dose 1 gr. Maintenance is 5 mg/kg OD
or in 2 divided doses. Caution must to be exercised in patients who have already
received a benzodiazepine because respiratory depression may be exacerbated.
Phenobarbitone is the drug of choice in neonatal seizures, cardiac conduction
abnormalities and in hypersensitivity to phenytoin.
f) Paraldehyde can be administered rectally (0.3 ml/kg diluted 1:3) or
intramuscularly. It should be given in a glass syringe as it dissolves plastic or
rubber.
g) For refractory status epilepticus: Modalities include barbiturate coma,
diazepam or midazolam infusion, IV sodium valproate, thiopental and inhalation
anaesthesia. This is done in PICU where facilities for artificial ventilation exist.
h) Treat the underlying cause if possible.

FEBRILE SEIZURES

58
Definition

Febrile seizures are seizures that occur in febrile children between the ages of 6 and 60
months who do not have an intracranial infection, metabolic disturbance, or history of
afebrile seizures

Usually, there is rapidly rising core temperature to ≥ 38⁰C.

 Simple febrile seizure – usually generalized tonic-clonic, lasting for a maximum

of 15 min, and not recurrent within a 24-hour period.
 Complex febrile seizure is more prolonged (>15 min), is focal, and/or recurs
within 24 hours.

Febrile seizures frequently occur in the contest of:

 Viral URTIs
 HHV6 infection
 Acute otitis media
 Malaria

 Genetic predisposition, e.g. autosomal inheritance pattern in some families

Clinical features

 Core temperature to ≥ 38⁰c

 Generalized tonic- clonic, lasting up to 15 min
 Occurs once in 24 hrs (usually on first day of fever)
 For complex type – see above
 Recurrence is possible
 The vast majority are harmless, prognosis is good

Complete general and neurological examination

- check for focus of infections

- check for possible signs and symptoms of meningitis (see protocol for
meningitis).
NB: In infant less than 1 year old the AAP recommend LP as other signs and
symptoms of meningitis might not be present or be very subtle.

Investigations

- Investigation should be done on individual basis to determine the cause of fever -

MPS, FBC, nasopharyngeal swab, urine m/c/s, if no obvious focus is found.

59
 - EEG and Neuroimaging are not required for simple febrile seizures.
- The work-up of children with complex febrile seizures needs to be
individualized. This can include EEG and neuroimaging, particularly if the child
is neurologically abnormal.

Treatment

 Antipyretic should be used at the same dose and intervals used for lowering fever
during a febrile illness at optimal dosing:
- Paracetamol at 10 to 15 mg/ kg/dose every 4-6 hours (max 5 doses/day)
- Ibuprofen: 20-30 mg/kg/day in 3 doses.

 Abort seizure - Diazepam IV 0.2 – 0.5 mg/kg slowly (can also be given rectally 0.5
mg/kg) if duration more than 3-5 min.
 Supportive therapy – tepid sponging, nurse in semi-prone position, ensure adequate
airway.
 Assess for the cause of fever and treat appropriately - Coartem, amoxyl,…

References

1. Kliegman R, Berhman R et al; Nelson Textbook of Pediatrics; Saunders Elsevier;

18th ed, 2007
2. Ghai OP, Paul V & Bagga A; Ghai Essential Paediatrics; CBS Publishers; 7th ed,
2009
3. Oxford Handbook of Paediatrics; Oxford University Press; First ed; 2008.
4. British National Formulary for Children, Bmj Publishers; 2007
5. R.S. Fisher at al. Epilepsia. 2005;46:470-2)
6. R.S. Fisher at al. Epilepsia:1–8, 2014
7. Lowestein et al. Epilepsia. 1999;40 Suppl 1:S3-8

ACUTE BACTERIAL MENINGITIS (BEYOND THE NEONATAL PERIOD)

Definition

A life-threatening illness that results from bacterial infection of the meninges.

Aetiology

Streptococcus pneumoniae, Haemophilus influenzae type b,Neisseria meningitidis are

common causes.

60
Staphylococcus aureus, coagulase-negative staphylococci, salmonella species,
Pseudomonas aeruginosa may cause meningitis in patients with anatomic defects or are
immune deficient.

Clinical features

Non-specific findings

 Fever accompanied by URTI or GI symptoms

 Increasing lethargy and irritability
 Anorexia and poor feeding
 Tachycardia and hypotension
 Various cutaneous signs like petechiae, purpura, or an erythemaatous macular
rash

Specific findings

 Kernig’s and brudzinski’s sign

 Focal neurological signs e.g. facial nerve palsy
 Seizures
 Alteration of mental status (may be due to increased ICP, cerebritis or
hypotension). Manifestations include irritability, lethargy, stupor, obtundation
and coma.

Increased intracranial pressure is suggested by

 Headache
 Emesis
 Bulging anterior fontanel or widening of the sutures – in infants and toddlers
 Hypertension with bradycardia
 Apnoea with hyperventilation
 Decorticate or decerebrate posturing
 Stupor, coma.

Diagnosis

Pyogenic meningitis is confirmed by analysis of CSF. It typically reveals micro-

organisms on Gram stain and culture, a neutrophilic pleocytosis, elevated protein and
reduced glucose.

Contraindications for an immediate LP

 Seizures
 Evidence of increased ICP (other than a bulging fontanel), such as 3rd or 6th
cranial nerve palsy with a depressed level of consciousness, or hypertension and
bradycardia with respiratory abnormalities

61
  Severe cardiopulmonary compromise requiring prompt resuscitative measures for
shock or in patients in whom positioning for LP would further compromise
cardiopulmonary function
 Infection of the skin overlying the site of the LP

Other investigations

 Blood cultures may reveal the responsible bacteria in up to 80-90 % of cases of

meningitis
 LFTs, U&Es
 FBC & ESR
 Cranial Ultra Sound (in children with open anterior fontanel)
 CT or MRI scan

Treatment

 ABC
 Glucose – RBS and treat hypoglycaemia
 Immediate antibiotics 1st line IV Crystalline Penicillin 100,000 iu/kg/dose 6 hrly
AND IV Chloramphenicol 25 mg/kg/dose 6 hrly (Maximum dose 500 mg)
 2nd line – IV Cefotaxime 50 mg/kg/dose 6 hrly or IV Ceftriaxone 80 mg/kg in
two divided doses

 Intravenous Dexamethasone 0.15 mg/kg/dose 6 hrly started before or

simultaneously with antibiotics and given for 4 days (Note: of proven benefit in
high income countries, no benefit demonstrated in low income countries.
Contra-indicated in neonates.)

Duration of Treatment – 14 days, may be up to 21 days depending on organism isolated.

Treat increased ICP if present, MOF, shock,...

Supportive care

 Repeated medical and neurological assessments to identify early signs of CVS,

CNS and metabolic complications.
 Monitor pulse, BP, RR, pupillary reflexes, level of consciousness ( in those with
a GCS of less than 9, a nasogastric tube and urinary catheter may be needed)
 Urine output and specific gravity
 Keep nil by mouth initially and give 2/3rds of fluid requirement until there is no
evidence of SIADH
 Feeding – NGT feeds, 2 to3 hrly
 Serial Head Circumference in children less than 2 years

62
  Treat hypotension with intravenous fluids – e.g. normal saline. Reduced blood
pressure may result in reduced cerebral perfusion and CNS ischaemia. Treat
shock aggressively to prevent brain and other organ dysfunction. Patients with
septic shock may require fluid resuscitation and therapy with vasoactive agents
e.g. dopamine
 Antipyretic - paracetomal
 Care of the comatose patient, if unconscious

Treatment of seizures

 Diazepam 0.2-05 mg/kg/dose IV or 0.5 mg/kg PR

 Phenobarbitone 20 mg/kg IV stat, then 5 mg/kg/day for intractable seizures

Note that phenytoin 18 mg/kg stat is preferred as it causes less CNS depression
and permits a patient’s level of consciousness to be assessed)

Treatment of increased intracranial pressure

 Keep patient’s head in the midline and elevated to 30° C

 Endotracheal intubation with mild hyperventilation
 20% Mannitol 0.5-1 g/kg/dose
 IV Furosemide 1 mg/kg is a less effective but safer alternative to mannitol

Differential diagnosis of bacterial meningitis

 Cerebral malaria
 Acute viral meningoencephalitis
 Tuberculous Meningitis
 Cryptococcal meningitis
 Brain abscess
 Parameningeal abscess
 Malignancy
 Collagen vascular syndromes
 Exposure to toxins
References

 [Guideline] Tunkel AR, Hartman BJ, Kaplan SL, et al. Practice guidelines for the
management of bacterial meningitis. Clin Infect Dis. Nov 1 2004; 39 (9):1267-
84. [Medline].
 Beek, D., Gans, J., McIntyre, P. and Prasad, K. (2008), Cochrane review:
Corticosteroids for acute bacterial meningitis. Evidence-Based Child Health: A
Cochrane Review Journal, 3: 405–450. doi: 10.1002/ebch.240
 Kliegman, Behrman, Jenson, Stanton, Nelson Textbook of Paediatrics, 18th
Edition, 2007
 Robert C Tasker, Robert J McClure, Carlo Acerini, Oxford Handbook of
Paediatrics

63
ACUTE STROKE
Definition
A focal neurological deficit with an underlying vascular pathology is defined as:
Stroke - lasting > 24h
Transient ischaemic attack (TIA) - lasting < 24h
Reversible ischaemic neurological deficit (RIND) - lasting> 24 h but with full
recovery
“Stroke-like episode” - focal neurological deficit
lasting >24 hr with no obvious vascular pathology, e.g. Brain tumour, brain abscess
Rare in childhood (1-3/100,000 per year)

64
The cause can be ischaemic (vessel spasm, stenosis, dissection or vessel occlusion by
thrombosis or embolism) or haemorrhagic.
Note that SCD is the most common cause of stroke in Zambian children.

Ischaemia
 Embolism Cyanotic CHD, endocarditis
 Large vessel stenosis
Sickle cell disease, varicella, AIDS, homocystinuria
 Vessel spasm Meningitis
 Thrombosis Sickle cell disease, severe dehydration (venous sinus
thrombosis), homocystinuria, leukaemia, thrombocytosis,
meningitis, clotting disorder, e.g. protein S or C
deficiency, antithrombin III deficiency, lupus antibodies,
factor V laiden
 Vessel dissection Trauma ( e.g. fall on a pencil in child’s mouth), congenital
Heart disease
 Moya Moya disease Basal artery occlusion with telangiectasia
 Syndromes Williams syndrome, Down syndrome

Haemorrhage
 Low platelets Idiopathic thrombocytopaenic purpura
 Bleeding disorder Haemophilia
 Vessel disorder A-V malformation, cerebral aneurysm
 Trauma

Clinical features
 Hemiparesis
 Hemisensory signs
 Visual field defects
 Seizures (common in neonates)
 Deterioration in level of consciousness (seen in progression of bleed)

Investigations
 FBC, differential count, ESR, random blood sugar, sickling test, clotting defects
(e.g. protein C & S deficiencies, antithrombin III deficiency)
 Clotting Profile
 Electrolytes initially, then daily until stable
 Blood, urine and CSF cultures if febrile (remember to withhold LP if evidence of
↑ICP)
 Once stable, brain imaging (preferably MRI) and angiography

65
 MRI brain scan Outline area affected (thrombosis, bleed, abscess,
tumour, etc)
CT scan If MRI unavailable (to exclude haemorrhage)
MRA scan vascular outline
ECG and Echo cardiac anomaly or arrhythmia

Investigate for a possible thrombophilia even with an obvious cause like trauma as these
two conditions may co-exist.
Management
 Initial attention to ABCDE
 Consider admission to PICU for 1st 24 hours or until stable
 Monitor vital signs (BP, Pulse, Respiratory rate), input & output, level of
consciousness
 Maintain normoglycaemia
 Control fever
 Treat seizures and ↑ICP if present
 Fluid management
 Control systemic hypertension
 O₂ to by face mask to keep Spo2 greater than 92%
 Cefotaxime 100 mg/kg q 6 hr or ceftriaxone 100 mg/kg per day if febrile
 Other management is dependent on cause, e.g. exchange transfusion in SCD,
anticoagulants in prothrombotic coagulopathy and surgery in A-V malformation
and cerebral aneurysm
In neonates, treatment for prevention of a 2nd stroke is often not required because the risk
of recurrence is low. In children however, the recurrence risk is higher and long term
therapy with low dose aspirin is often needed.
Regular BT therapy in patients with SCD.
Immunosuppressant therapy for vasculitis.
Rehabilitation
Speech, occupational and physical therapies, psychological services, special education.
References
1. Recognition and Treatment of Stroke in Children, Child Neurology Ad Hoc
committee on Stroke in children Rachel U Sidwell, Mike Thomson, Concise
Paediatrics, 1st edition

2. Kliegman, Behrman, Jenson, Stanton, Nelson Textbook of Paediatrics, 18th

Edition

66
 3. Robert C Tasker, Robert J McClure, Carlo Acerini, Oxford Handbook of
Paediatrics

NEPHROTIC SYNDROME

Nephrotic syndrome is characterised by:

 Heavy proteinuria > 40 mg/m²/hr or urine protein 3+ to 4+ on a dipstick test
 Hypoalbuminaemia (serum albumin < 25g/L)
 Hyperlipidaemia
 Oedema

Causes
 Idiopathic (primary) nephrotic syndrome (Minimal change, Focal segmental
glomerulosclerosis)
 Secondary nephrotic syndrome (HSP, SLE, MPGN)
 Congenital nephrotic syndrome

Clinical features
 Oedema with or without ascites, pleural effusions, and genital oedema
 Hypertension and haematuria are atypical especially in minimal change
 Anorexia, irritability, abdominal pain and diarrhoea are common

Investigations

67
  Blood: FBC/ESR; U&Es; Creatinine; LFTs ; C3/C4 ; Triglycerides and
cholesterol levels
 Urine: Dipstick urinalysis. Spot urine protein/creatinine ratio ≥2.0.
 Renal biopsy if indicated i.e if steroid resistant.
 Other investigations as dictated by underlying cause, i.e. HB surface antigen,
RPR,...
.

Treatment

General measures
 No added salt diet
 20% albumin with frusemide cover if indicated in severe, symptomatic ascites
 Antibiotic cover against peritonitis in the presence of ascites

Specific treatment

68
 Dose of prednisolone in m2
60mg/m2 in the first 6 weeks and reduced to 40mg/m2 when taking alternate day
therapy.

 Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II blockers

may be helpful as an adjunct therapy to reduce proteinuria in steroid-resistant
patients.

Definitions

Remission Urine albumin nil or trace (or proteinuria <4

mg/m2 /h) for 3 consecutive days

Relapse Urine albumin 3+ or 4+ (or proteinuria >40

mg/m2 /h) for 3 consecutive days, having been
in remission previously

Frequent relapses Two or more relapses in six months of initial

response, or more than three relapses in any
twelve months

Steroid dependence Two consecutive relapses when on alternate

day steroids or within 14 days of its

69
 discontinuation

Steroid resistance Absence of remission despite therapy with 4

weeks of daily prednisolone at a dose of 2
mg/kg per day

Monitoring Recommendations for Children with Nephrotic Syndrome

 Urinalysis - Urine Protein

 Weight, Growth, BMI
 Blood pressure
 Creatinine, electrolytes
 FBC
 Lipid profile ( if indicated)

Complications

 Increased susceptibility to bacterial infections.

 Spontaneous bacterial peritonitis is
 Hypovolaemia and thromboembolism.
 Complications related to chronic steroid administration include hypertension,
obesity, and linear growth retardation.

References:

 Consensus statement on management of steroid responsive nephrotic

syndrome. Compiled by Arvind Bagga, M. Kanitkar, R.N. Srivastava on behalf
of Indian Pediatric Nephrology Group. Indian academy of Pediatrics 2001 38:
975-986
 Debbie S. Gipson, Susan F. Massengill, Lynne Yao, Shashi Nagaraj.
Management of Childhood Onset Nephrotic Syndrome. Pediatrics Vol. 124
No. 2 August 2009
 Richard E., Md. Behrman (Editor), Robert M., Md. Kliegman (Editor), Hal B.,
Md. Jenson (Editor) By W B Saunders. Nelson’s textbook of Pediatrics (18th
Edition), 2007

ACUTE GLOMERULONEPHRITIS

70
Definition: Glomerulonephritis is an immunologically mediated damage to the kidneys
characterised by acute onset of oedema, haematuria, and hypertension, which is usually
accompanied by oliguria.

Causes

Causes of acute glomerulonephritis include post-infectious, renal, and systemic

aetiologies.

1. Post-infectious aetiologies
 Bacterial: Streptococcus species (i.e. group A beta-haemolytic), the
commonest cause.
 Viral: Hepatitis B and C, HIV
 Parasitic: Malaria

2. Systemic causes

 Collagen vascular diseases (e.g. SLE)

 Vasculitis
 Drug-induced (i.e. gold, penicillamine)

Clinical Features

History

 Sudden development of puffiness of the eyelids and facial oedema in the

setting of a post-streptococcal infection.
 The urine may be dark and scanty.
 Non-specific symptoms include weakness, fever, abdominal pain, and
malaise

Physical examination
 Most frequently patients present with a combination of oedema,
hypertension, haematuria and oliguria.
 Other signs depend on the underlying cause.

Investigations


Urine microscopy – RBC’s, RBC casts, proteinuria, leukocytes

Blood – FBC, U/E and creatinine, ESR

Cultures – throat swab

Other (as indicated) - CXR, U/S-renal, ECHO, ASOT, antinuclear antibody,
anti-DNA antibodies.
 Complement levels (C3, C4)
Treatment
 Antibiotic, i.e. penicillin if indicated
 Antihypertensive, i.e. ACE inhibitors, diuretics, calcium channel
blockers

71
  Sodium restriction
 Treat underlying cause
 If patient progresses to acute renal failure, refer to acute renal failure
protocol.

Monitoring

 Blood pressure monitoring during each visit and urinalysis at 2, 4, and 6

weeks and then at 4, 6, and 12 months after discharge
Note – haematuria may persist for up to one year.
 Serum creatinine level monitoring at 2, 6, and 12 months
 Check serum complement by 6-8 weeks. If complement still low, then
refer.

References

Vinen CS and Oliveira DBG. Acute glomerulonephritis, Postgrad Med J 2003;

79:206–213

Derakhshan A, MD, Pediatric Nephrologist and Hekmat VR, Medical Student. Acute
Glomerulonephritis in Southern Iran; Iran J Pediatrics, Vol 18 (No 2); Jun 2008

Richard E., Md. Behrman (Editor), Robert M., Md. Kliegman (Editor), Hal B., Md.
Jenson (Editor). Nelson Textbook of Pediatrics, 18th edition, W B Saunders

ACUTE KIDNEY INJURY

Definition

72
An acute deterioration in kidney function resulting in failure to maintain normal
physiological homeostasis, characterized by an increase in blood urea and serum
creatinine values, often accompanied by hyperkalaemia, metabolic acidosis, and
hypertension. A urine output of 300 ml/m 2/24hrs or 1.0 ml/kg/day on average is required
to excrete the daily solute output.

Causes

 Pre-renal - Prerenal failure refers to hypoperfusion of the kidneys. This can be

due to dehydration, haemorrhage, sepsis, cardiac failure, hypoalbuminaenia
(nephrotic syndrome, liver disease)
 Renal (intrinsic) – Renal parenchymal damage, e.g. Acute glomerulonephritis,
Intrarenal vascular disease (Haemolytic-uremic syndrome, Vasculiditis), Acute
interstitial nephritis, Acute tubular necrosis, Nephrotoxins,...
 Post-renal
Congenital - Posterior urethral valves, pelvi-ureteric junction, vesico-
ureteric junction obstruction,...
Acquired (rare) – Urolithiasis, clots, tumours,...

Clinical features
These will reflect the cause and the consequent abnormalities.

 Signs of ARF include hypertension oedema, anaemia, and signs of congestive

cardiac failure (CCF), such as hepatomegaly, gallop rhythm, and pulmonary
oedema.

 Signs of intravascular volume depletion include tachycardia, hypotension,

decreased skin turgor, dry mucous membranes, and changes in sensorium.

 Although oliguria is a criterion used to diagnose and stage acute renal failure
(ARF), ARF can be present without oliguria, especially in patients with
nephrotoxic kidney injury, interstitial nephritis, or perinatal asphyxia. Oliguria
may be defined as urine output less than 0.5 ml/kg/h in neonates and children.

 Rash and arthritis(e.g. SLE and Henoch-Schonlein purpura nephritis), flank

masses (renal vein thrombosis, tumours, cystic diseases, urinary tract obstruction)

Investigations

 Dipstick urinalysis – leucocytes (UTI), Proteinuria & Haematuria

(Glomerulonephritis, nephrotic/nephritic syndrome), specific gravity
 Urine microscopy - red blood cell casts, granular casts, and red blood cells,
findings seen in glomerulonephritis
 Urine sodium and urine osmolality
 Electrolytes - K+, Na+, Ca++, Phosphate, Uric acid and urea, creatinine
 Full blood count, peripheral smear as indicated
 Other blood tests as dictated by underlying cause
 CXR – pulmonary congestion (fluid overload)
 Renal ultrasound (urinary tract obstruction)

73
  Renal biopsy ultimately if no clearly defined prerenal or postrenal ARF

Treatment

 Pass urinary catheter e.g. in neonates with suspected posterior valves, or for
urine output monitoring in non-ambulatory children/adolescents during ARF

 Fluids – if hypovolaemic will require volume expansion with isotonic saline at

20 ml/kg over 30 min. This may be repeated one or two more times at most
depending on the response.
Those with relatively normal intravascular volume – give insensible losses at 400
ml/m2/day plus urine output &extrarenal losses as appropriate. Use glucose
containing fluids without electrolytes (e.g. 5% or10% dextrose.).

Daily monitor urine & stool output, fluid intake, body weight, blood
chemistries.

 Complications

Hyperkalaemia > 6 mmol/l (indicated by the following ECG changes: peaked T-

waves, widening QRS complex, ST segment depression, ventricular arrhythmias
and cardiac arrest).
Eliminate exogenous potassium (IVF, diet) sources, oral or enema K +-binding
resin (Na polystyrene sulfonate) at 1g/kg single dose.
If K+ >7 mmol/l, + ECG changes, give the following:
Nebulised salbutamol 2.5 mg if weight < 25kg or 5 mg if weight >25 kg or IV
salbutamol 4µg/kg in 10 ml of water over 10 min
10% calcium gluconate (cardio-protective) at 1ml/kg IV over 3-5 min
8.4% sodium bicarbonate 1-2 mmol/kg IV over 5-10 min
Regular insulin 0.1 u/kg with 50% glucose 1 ml/kg over 1hr

Hypocalcaemia
Calcium carbonate orally 45 to 65 mg/kg per day. If tetany, IV 10% calcium
gluconate 0.5 to1 ml/kg (up to 10 ml), with low phosphorus diet or phosphorus
binders.

Hyponatraemia (dilutional usually)

Treat if < 120 mmol/l or symptomatic (seizures, lethargy). Correct to 125 mmol/l
using the following formula:
Required NaCl (mmol) = 0.6×weight×deficit (125 mmol/l – serum Na)

Metabolic acidosis

74
 Mild acidosis is common and requires not treatment. However, severe acidosis
(pH = 7.15, serum bicarbonate ˂ 8 mmol/l) should be corrected partially with IV
sodium bicarbonate to pH = 7.20, serum HCO 3- = 12 mmol/l, then the remainder
corrected by oral sodium bicarbonate. Rapid metabolic acidosis correction with
IV NaHCO3 may reduce ionised serum calcium leading to tetany!

Hypertension and Anaemia treat as per appropriate protocol.

Nutrition

Nutritional requirements should be addressed accordingly in consultation with

the dietician.

Renal replacement therapy

Dialysis (peritoneal dialysis or haemodialysis)
Dialysis indications: -
(i). Fluid overload/hypertension
(ii). Severe acidosis not responding to medical management
(iii). Persistent hyperkalaemia or other above uncontrollable electrolyte
imbalance (iv). Symptomatic uraemia or urea > 35.7 - 53.6 mmol/l
(v). Dialysable toxin
(vi). Established anuria

References

1. Behrman R. E, Kliegman R. M., Jenson H. B. Nelson textbook of paediatrics,17th

edition, Philadelphia, WB Saunders, 2004, pp1767-1770

2. McIntosh N, Helms J. P, Smyth L. R, Logan S. Forfar & Arneil’s textbook of

paediatrics, 7th edition, Edinburgh, Churchill Livingstone, 2008, pp587-589

3. Dilys A. Whyte and Richard N. Fine, Acute renal failure in children, Paediatrics
in Review 2008;29;299-307

ACUTE DIARRHOEAL DISEASE

1. Definition:

75
  Passage of three or more loose/watery stool or one voluminous
loose/watery stool per day.

2. Causes:

Infectious

 Bacterial infections: Commonly, Vibrio cholerae, Salmonella species,

Shigella, and Escherichia coli (E. coli), Campylobacter pylori

 Viral infections: rotavirus, adenovirus, Norwalk virus, astrovirus

 Parasites: Giardia lamblia, Entamoeba histolytica, Cryptosporidium

N.B. Diarrhoea may be watery or bloody (dysentery)

Non-infectious causes

 Drugs: Antibiotics, anti-hypertensives, cancer drugs, and antacids

containing magnesium
 Intestinal diseases: Inflammatory bowel disease and coeliac disease
 Food intolerance: Lactose
 Food allergy: Cows milk, Soya

N.B. Some of the above causes may lead to persistent/chronic diarrhoea

3. Clinical features:

 Watery or loose stools ± bloody stools

 Abdominal cramps
 Tenesmus
 Urgency
 Abdominal pain
 May be associated with vomiting and fever
 Dehydration

Signs of dehydration include

 Dry mucous membranes

 Rapid thready pulse, low blood pressure, capillary refill > 2sec

76
  No tears when crying
 No wet diapers for 3 hours or more
 Sunken eyes/anterior fontanelle
 High /low temperature
 Listlessness or irritability
 Reduced skin turgor

Classification of levels of dehydration

No dehydration Some dehydration Severe dehydration

General Well, alert Restless, irritable Lethargic or
condition unconscious
Eyes Normal Sunken Very sunken
Thirst Drinks normally, not Thirsty, drinks Drinks poorly, or not
thirsty eagerly able to drink at all
Skin pinch Goes back quickly Goes back slowly Goes back very slowly
(>2sec)

4. Investigations

 Stool m/c/s and virology

 U&E, Creatinine
 FBC, ESR
 Abdominal x-ray
 Barium enema/meal

5. Principles of management

 Fluids
 Zinc supplements
 Continued feeding

Fluid management

77
  Assess hydration and vital signs
 If in shock, refer to protocol on shock
 Depending on level dehydration, give fluids as outlined below

PLAN C – Severe dehydration: Rapid intravenous rehydration, 100 ml/kg

RL or

½ strength darrows

Age First give 30 ml/kg in Then give 70 ml/kg in

Infants 1 hour * 5 hours
Older children 30 min * 2½ hours
 Repeat once if pulses are weak or not detectable.
 Reassess patient every 1-2 hours. If hydration is not improving, give the
IV drip more rapidly.
 After completion of IV fluids, reassess the patient and choose the
appropriate treatment Plan (A, B or C).
 If IV therapy is not available, then ORS by nasogastric tube or orally at
20 ml/kg/hour for 6 hours (total of 120ml/kg) should be given. If
abdomen becomes distended or the child vomits repeatedly, then ORS
should be given more slowly.

Note: Dehydration may be hypotonic, isotonic or hypertonic. Hypertonic

dehydration is common in infants fed on cow’s milk .

PLAN B – Some dehydration:

75mls of ORS x patient’s weight (kg) to be given in 4 hours

 After 4 hours, reassess the child and decide what treatment to be given
next as per level of dehydration.
 Children who continue to have some dehydration even after 4 hours
should receive ORS by nasogastric tube or ½ strength darrows
intravenously (75 ml/kg in 4 hours).
 If abdominal distension occurs, oral rehydration should be withheld and
only IV rehydration should be given.

PLAN A – No dehydration: Amount of ORS to be given per loose stool dependent on

specific age as listed below.

78
 Age (years) <2 2-5 Older children
ORS (mls) 50-100 100-200 As much as they want

Zinc supplementation

Give zinc supplement (10-20 mg/day for 10 to 14 days)

3. CONTINUED FEEDING

Give appropriate feeds. Avoid juices and carbonated drinks

References

 Southall D, Coulter B, Ronald C, International Child Health Care, A practical

manual for hospitals worldwide. 1st Edition, Book Power, BMJ Publishing
Group, 2003

ACUTE UPPER GI BLEEDING

1. Definition

79
 Upper gastrointestinal (GI) bleeding refers to haemorrhage from any level above
the ligament of Treitz.

2. Causes:

Age Group Cause

Neonates -Haemorrhagic disease of the newborn
-Swallowed maternal blood
-Stress ulceration
-Coagulopathy
Infants (1 month – 1 year) Oesophagitis
Gastric ulceration
Infants (1 -2 years) Peptic ulcer disease
Gastritis
Children older than 2 years Oesophageal varices
Gastric varices
Adolescents Duodenal ulcers

3. Clinical features
Presentation of bleeding depends on the amount and location of haemorrhage.

 Haematemesis
 Coffee ground vomiting
 Melaena
 Haematochezia- if the haemorrhage is severe
 May also present with complications of anaemia/shock

4. Investigations

 FBC, ESR
 U/E’s, Creatinine, LFTs
 Barium swallow/meal
 Clotting profile
 Endoscopy

5. Treatment

 ABCDE
 Brief history as to possible cause of the bleeding
 Consider gastric wash out
 Consider antidote for bleeding due to poisoning
Iron – Desferrioxamine

80
 Warfarin – Vitamin K
 Monitor vital signs
 Replacement of volume with intravenous solutions and blood products if
required
 Endoscopy (electrocautery, clipping or banding)
 Pharmacotherapy including the following:

1. Proton pump inhibitors (PPIs) – Omeprazole IV

2. H2 receptor inhibitors - Cimetidine/ranitidine IV

3. Octreotide is a somatostatin analog believed to shunt blood away

from the splanchnic circulation

4. Terlipressin is a vasopressin analog used for variceal upper GI

haemorrhage

5. Propranolol

References.

1. Kliegman R, Berhman R et al; Nelson Textbook of Pediatrics; Saunders Elsevier;

18th ed, 2007

2. McIntosh N, Helms J. P, Smyth L. R, Logan S. Forfar & Arneil’s textbook of

paediatrics, 7th edition, Edinburgh, Churchill Livingstone, 2008

ACUTE HEPATIC FAILURE

Definition

81
Fulminant hepatic failure (FHF) is usually defined as the severe impairment of hepatic
functions in the absence of preexisting liver disease.

Causes

 Infective
 Viral - Hepatitis A, B, C and D, HIV, Parvovirus, Herpesvirus, Enterovirus,
Adenovirus, Varicella, Echovirus, CMV
 Drugs - Paracetamol, antituberculous drugs, carbamazepine, sodium valproate,
halothane
 Toxins - Mushroom, particularly amanita phalloides, herbs and traditional
medicines
 Infiltrative - Leukaemias, lymphomas
 Metabolic - Wilson’s, galactosemia, tyrosinaemia

Clinical Features

The child may present within hours or weeks with

 Protracted vomiting
 Jaundice
 Tender hepatomegaly
 Coagulopathy (bruising, petechiae, bleeding)
 Hypoglycaemia
 Electrolyte disturbance
 Encephalopathy (early signs of encephalopathy include alternate periods of
irritability, confusion and drowsiness. Older children may be aggressive or show
unusual behaviour)

Investigations

o Liver Function tests:

 Prothrombin time (PT) or International normalised ratio (INR)

 Serum albumin
 Transaminases
 Bilirubin total and direct
 Alkaline Phosphatase
 Blood Glucose levels

o Full Blood Count

o Urea, creatinine and electrolytes

82
 o CRP/ESR

o Imaging

o Investigate for underlying cause

Treatment

 ABCDE
 Oxygen by nasal cannulae or face mask
 Vitamin K, stat dose IV or IM (300 micrograms/kg for age 1 month to 12
years and 10 mg if >12 years to attempt correction of prolonged clotting time
 If frank bleeding (GI or other), fresh frozen plasma at 10 ml/kg IV
 Maintain blood glucose between 4 and 9 mmol/litre using 2/3 of maintenance
fluid volume consisting of 10% dextrose IV or orally
 Strictly monitor urine output and fluid balance, aim for a urine output of not
less than 0.5 ml/kg/hr
 Correct hypokalaemia if present as it can worsen encephalopathy
 Broad spectrum antibiotics for example cephalosporin to treat sepsis
 Systemic fungal infection may require IV amphotericin or oral fluconazole
 Maintain normothermia by environmental measures, DO NOT give
paracetamol
 Lactulose 5-10 mls 2-3 times daily to produce two to four soft and acid stools
per day, to be omitted if diarrhoea occurs
 Neomycin 20-30 mg/kg/day 6 hrly orally, maximum dose 2 gm/day

References.

3. Kliegman R, Berhman R et al; Nelson Textbook of Pediatrics; Saunders Elsevier;

18th ed, 2007

4. McIntosh N, Helms J. P, Smyth L. R, Logan S. Forfar & Arneil’s textbook of

paediatrics, 7th edition, Edinburgh, Churchill Livingstone, 2008

INTESTINAL OBSTRUCTION

83
This is the most common condition requiring emergency surgery in infants and children.
Most causes result from complications of congenital anomalies or from inflammatory
conditions that affect the bowel.

Causes

Small Bowel Obstruction

 Duodenal stenosis or atresia – One third of patients with Down’s syndrome and it
is also associated with other congenital malformations
 Atresia or stenosis of the jejunum or ileum
 Malrotation with volvulus
 Meconium ileus
 Meconium plug

Large Bowel Obstruction

Mainly caused by peristaltic dysfunction as in Hirschsprung’s disease and
congenital anomalies (rectal atresia).

Inflammatory lesions like tuberculosis and Crohn’s disease and worm infestation may
cause either small or large bowel obstruction.

Other extrinsic causes include incarcerated hernia, vascular bands and intussusception.

Symptoms and Signs

Patients present with vomiting which progresses to become bowel stained and cramping
abdominal pain with anorexia. Constipation and abdominal distension occur with the
degree of the distension being directly related to the site of the obstruction in the
gastrointestinal tract and being greater the more distal the obstruction. In neonates,
meconium may initially be passed, but subsequently its passage is usually delayed or
absent. High lesions will present soon after birth, but lower lesions may not present for
some days.

On examination, the patient may have tachycardia and signs of dehydration. Tenderness
and hyperactive or silent bowel sounds are present on abdominal examination.

Investigations

 Full blood count

 Urea, creatinine and electrolytes
 Group and save
 Abdominal x-rays, supine and erect
 Chest x-ray
 Barium meal is needed for bilious vomiting and for incomplete obstruction
 Barium enema may be required for distal obstruction

Treatment

The goal of treatment is to relieve the obstruction before ischemic bowel injury occurs.

84
  Resuscitate the patient
 IV access and collect blood for investigations
 Rehydrate
 Give maintainance fluids if patient is not dehydrated
 If patient is hypokalaemic, add potassium chloride to fluids
 Naso-gastric tube for gastric decompression
 Give IV 10% dextrose if patient is hypoglycemic
 Fluid input and Output balance chart
 Broad spectrum antibiotics (triple antibiotic therapy)

Once the patient is adequately resuscitated and fluid and electrolyte imbalances
corrected, laparotomy is performed and the cause treated.
At all times, adequate analgesia should be given.

References.

1. Kliegman R, Berhman R et al; Nelson Textbook of Pediatrics; Saunders

Elsevier; 18th ed, 2007

2. McIntosh N, Helms J. P, Smyth L. R, Logan S. Forfar & Arneil’s textbook of

paediatrics, 7th edition, Edinburgh, Churchill Livingstone, 2008

ANAEMIA
Definition
Haemoglobin (Hb) concentration or haematocrit two or more standard deviations below
the mean value for age and sex.

85
Causes

Decreased red cell production

 Deficiency of haematopoietic precursors ( Iron, Folate, vitamin B12)
 Bone marrow failure ( Malignant infiltration, Aplastic, Congenital
defects)

Increased red cell destruction

 Haemolytic disease
a) Extracorpuscular defects ( immune mediated )
b) Intracorpuscular defects ( Enzyme defect, membrane defect,
Globin defects)

Blood loss
 Acute
 Chronic

Clinical features

Symptoms associated with anaemia include

 Pica
 Headache
 Palpitations
 Easy fatigability
 Poor concentration
 Bleeding episodes
 Poor weight gain or weight loss
 Fever
 Bruising episodes
 jaundice

Signs associated with anaemia include

 Pallor
 Tachycardia
 Oedema

86
  Hepatosplenomegaly
 Lymphadenopathy
 Petechiae
 Purpura
 Wasting
 Fever

Investigations

 Full blood count

 Peripheral blood smear
 Reticulocyte count
 Total and direct serum bilirubin levels
These above first four tests are key in characterisation of the type of anaemia and possible cause
Other tests
 ESR – (erythrocyte sedimentation rate)
 Coombs – direct and indirect - tests
 Sickling test
 Bone marrow aspiration and bone marrow biopsy
 Coagulation studies ( APTT, PT/ INR, D-dimers, FDPs)
 Stool for occult blood and parasites and ova
 Urinalysis – dipstick, microscopy

Principles of management

 Establish the underlying pathology

 Replace the appropriate blood product deficiency

Blood replacement formulae when a transfusion is indicated:

 Packed red blood cells in mL = body weight x deficit Hb x 4

 Whole blood in mL = Body weight x deficit Hb x 6

References

1. Nelson Textbook of Pediatrics, 18th edition, 2007

2. Blueprints Pediatrics, 4th edition, 2007
3. WHO/ UNICEF. Anaemia statement. 2004
4. Essential Revision Notes in Paediatrics, 2nd edition, 2006
APPROACH TO DIAGNOSIS AND INVESTIGATION OF COMMON
MALIGNANCIES

87
Causes of malignancy
Risk factors for cancer can be broadly classified as:
 Genetic causes
 Environmental causes
Clinical features
In the first two years of life, embryonic tumours tend to be common. Examples include
Nephroblastoma, Retinoblastoma, Neuroblastoma, Teratoma, Rhabdomyosarcoma,
Medulloblastoma.
From 2-5 years of age, the embryonic tumours combine with Acute Lymphoblastic
Leukaemia, Non-Hodgkin’s Lymphoma, and Glioma.
In adolescents Hodgkin’s disease, Bone, Gonadal and Connective tissue tumours
predominate

Common signs and symptoms of cancer in children

 Abdominal mass
 Persistent generalized lymphadenopathy
 More than one abnormal hematopoietic lineage
 Specific neurologic deficit
 Increased intracranial pressure
 Proptosis
 White pupillary reflex
 Vaginal bleeding or mass
 Joint or bone swelling or pain
Uncommon signs and symptoms of cancer in children
 Superior vena cava syndrome
 Subcutaneous nodules
 Chronic diarrhoea
 Failure to thrive
 Skin lesions
History
General: a single symptom might cause patient to seek medical

88
 Attention (e.g. Pain, mass, Bleeding, recurrent fevers, weakness)
Specific: symptoms to look for in the history
CNS R/S MSS

Headache Cough Swelling

Fits Difficulties breathing Wasting

Blindness Haemoptysis Bone/joint pain

Vomiting Neck Non healing ulcer
Stiff neck Swelling Skin lesion
Confusion Engorgement Bleeding spots

GIT GUT OTHERS

Abdominal mass Pelvic/suprapubic mass Malaise

Diarrhoea Dysuria Anorexia
Easy satiety Haematuria Nights sweats
Dysphagia Urinary retention Fever
Poor appetite
Melaena

Physical examination
CNS R/S MSS

89
Mentation Tachypnoea Skin lesion

Cranial palsy Reduced breath sounds Wasting

Paraplegia/Paraparesis Stridor Oedema

Meningismus Haemoptysis

Vomiting NECK

Lymphadenopathy

Confusion Engorged vessels

GIT GUT

Abdominal mass Proteinuria

Hepatomegaly/splenomegaly Haematuria

Visible distension of vessels

Common cancers on the Haematology-Oncology Unit

1. Non-Hodgkin’s lymphoma
2. Nephroblastoma
3. Retinoblastoma
4. Leukaemia
5. Kaposi’s sarcoma

INVESTIGATIONS
Imaging Studies

Chest radiography: Postero-anterior and lateral views to

 Assess mediastinal masses

 Evaluate the airway
 Exclude pulmonary parenchymal lesions

Ultrasonography: Abdomen, Pelvis, Eye, Cranial to identify site and disease extent

Computed tomography

90
  CT scans of the chest, abdomen, and pelvis can be used to stage lesions
 Chest CT scan is indicated to assess for the degree of tracheal compression
 Head CT scans assist in excluding mass lesions and possible meningeal
involvement among individuals with CNS disease.

Bone scanning and skeletal surveys

When additional symptoms are present, these tests help in identifying additional sites
of disease.

Echocardiography can be obtained as baseline findings before patients are given

chemotherapy with anthracyclines, which can cause cardiomyopathy.

Other Tests

 Complete Blood count

 Peripheral Smear
 Erythrocyte sedimentation rate
 Liver and Kidney Test
 Retroviral test

Procedures
Bone marrow aspiration/biopsy
 Biopsy is necessary to assess for evidence of bone marrow involvement in
patients with lymphomas.

Biopsy

 For patients with a mass, tissue is generally available from resection or intra-
operative biopsy.
 As an alternative, a diagnosis may be made by using pleural fluid or ascetic fluid

Lumbar puncture

 To determine the CSF cell count and differential: This test is done to assess CNS
involvement, the presence of which alters therapy.

Management

91
Once diagnosis is made either histologically of clinically, stage the patient according to
the staging used for that particular tumour. Consult the protocol to determine treatment
modality which could be either one or a combination of two or all three:
1. Surgery
2. Chemotherapy
3. Radiation

Treatment should aim at either:

1. Cure or
2. Palliation

92
MALARIA

Malaria is one of the top five diseases causing morbidity and mortality in Zambian
children. Malaria is a febrile illness caused by infection with the plasmodium falciparum
parasite which is transmitted from person to person by mosquitoes. Malaria is diagnosed
by examining a patient’s stained blood slide through a microscope (MPS). Recently, a
rapid malaria diagnostic test (RDT) for malaria antigen can be done in the examination
room and results are available within 15 minutes. It is also important to also do a full
blood count (FBC).

Uncomplicated malaria symptoms and signs are as follows

 Fever

 Headache

 Abdominal pain

 Nausea

 Vomiting

 General body pains

 Weakness

Simple malaria is treated with Artemether 20 mg and Lumefantrine 120 mg (AL-

COARTEM) given with food (preferably containing fatty foods) as follows: stat, after 8
hrs, then 12 hourly doses on day 2 and day 3. If the drug is spat out or vomited within 30
minutes, the dose should be repeated. If more than two consecutive episodes of vomiting
occur, parenteral Artesunate should be administered.

WEIGHT(Kg) AGE (approx. in yrs.) DOSE (number of tabs of

AL, Artemether 20,
Lumefantrine 120mg)
5-<15 2months -3yrs 1 tab
15-25 3-8yrs 2 tab
25-35 9-12yrs 3 tab
>35 >12yrs 4 tab

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SEVERE MALARIA

Severe forms of malaria, may involve the brain (cerebral malaria), kidney (black water
fever) and lungs (pulmonary oedema). Severe forms may lead to death.

The symptoms and signs of severe malaria include

 Convulsions

 Changes in behaviour

 Reduced level of consciousness

 Coma

 Severe pallor

 Respiratory distress

 Jaundice

 Shock

 Black tea coloured urine

In endemic areas if a high quality blood slide is negative then only children with
severe disease or those with severe anaemia should get presumptive treatment.

Investigations for severe malaria

 Thick and thin malaria parasite smear or RDT

 FBC

 Blood glucose

 U&Es

 LFTs

 Blood gases

 CXR

 Urinalysis

 Do LP to exclude meningitis if indicated

Severe malaria = fever + any of the following

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 1) Impaired level of consciousness (AVPU= V, P, U or low GCS)
2) Unable to drink/feed
3) Respiratory distress with acidotic breathing
4) Severe anaemia Hb < 5 g/dl
5) Hypoglycaemia blood glucose < 2.2 mmol/L
6) 3 or more convulsions

If yes, treat with Artesunate 2.4mg/kg of body weight IV or IM given on admission

(time=0), then at 12hrs and 24hrs, then once a day.

After initial parenteral treatment for a minimum of 24hrs, once the patient regains
consciousness and can take medications orally, discontinue parenteral therapy and
commence full course of Artemether Lumefantrine

There should be an interval of at least 8hrs between the last dose of artesunate and the
first dose of artemether lumefantrine.

OR Alternative 2nd line drug for severe malaria is QUININE IV

1) Loading dose 20 mg/kg body weight(maximum 1200mg) diluted in 10 ml/kg (or

equal volume with Quinine) in 5% or 10% dextrose over 4 hrs)
Then after 8 hours, give a maintenance dose 10 mg/kg in 10 ml/kg of 10%
dextrose over 4 hours)
2) Treat hypoglycaemia with 5 ml/kg 10% dextrose IV infusion
3) Maintenance fluids/feeds and supportive oxygen by mask
4) If weak pulse and CRT > 3 sec, give 20 mls/kg normal saline until pulse is
restored ( use blood for resuscitation if Hb < 5g/dl at 20 ml/kg whole blood)
5) Treat convulsions with phenobarbitone

Once patient is able to swallow, oral quinine at 10mg/kg body weight every 8 hrs to
complete a 7-day course of treatment..

REFERENCES

1) Guidelines for the diagnosis and treatment of Malaria in Zambia, Fourth edition,
2014

2) Artesunate versus quinine for treating severe Malaria (review). The Cochrane
Collaboration. Published by John Wiley &Sons, Ltd.

TYPHOID (ENTERIC FEVER)

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Causes

Salmonella typhi, Salmonella paratyphi

Clinical features

High grade fever, coated tongue, anorexia, vomiting, hepatomegaly, diarrhoea, toxicity,
abdominal pain, pallor, splenomegaly, constipation, headache, jaundice, obtundation,
ileus, intestinal perforation.

Diagnosis

1. Blood culture

 Ideally 1st week of symptoms - Blood culture

2nd week of symptoms - Urine culture
3rd week of symptoms - Stool culture

NOTE: As most patients present late, all three cultures should be taken on
admission.

2. Widal test

 A single Widal test may be positive in only 50% cases in endemic areas
 Serial tests may be required

3. Mainstay of diagnosis remains CLINICAL

 Any high fever of >72 hours duration (with aforementioned features), especially
with no localizing upper respiratory signs or signs of meningitis or malaria must
be suspected of typhoid and managed accordingly.

4. Full Blood count (White cell count)

Leucopenia (WCC < 4 x109/litre) with a left shift in neutrophils may be seen in a
third of children; young infants may also commonly present with leukocytosis.

5. Other serological tests (expensive)

 Dot-Elisa
 Coagglutination
 TubexR

Management

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  Early diagnosis and instituting appropriate supportive measures and specific
antibiotic therapy is the key to appropriate management
 Adequate rest, hydration and correction of fluid-electrolytes
 Anti-pyretic therapy (paracetamol) as required if fever > 39oC
 Antibiotic therapy
o 1st line therapy- CIPROFLOXACIN( while awaiting culture results)
o 2nd line (drug resistant) – IMIPENEM

References

 Southall D, Coulter B, Ronald C, International Child Health Care, A practical

manual for hospitals worldwide pg 426-428

 Kliegman, Behrman, Jenson, Stanton, Nelson Textbook of Paediatrics, 18th

Edition, 2007

HYPOGLYCAEMIA IN CHILDREN AND ADOLESCENTS

97
Definition

Hypoglycaemia is defined as plasma glucose of less than 2.6 mmol/l. However, of note
is that in preterm neonates in the 1 st three days of life, glucose maybe as low as 1.1
mmol/l without any underlying abnormality. In term neonates, it may be as low as 1.7
mmol/L in the first three days and 2.2 mmol/l in the remainder of the week. Thereafter, a
glucose of 2.6 mmol/L or lower requires investigations.

Causes

 Intrauterine growth retardation and prematurity

 Perinatal asphyxia
 Infant of a diabetic mother
 Intrauterine infections and sepsis
 Rhesus incompatibility
 Inborn errors of metabolism
 Amino acids and organic acids
 Disorders of carbohydrate metabolism e.g. glycogen storage
disease, fructose intolerance, lactosaemia
 Fatty acid oxidation defects
 Urea cycle defects
 Endocrine causes
 Hypopituitarism
 Growth hormone or adrenal insufficiency
 Persistent hyperinsulinaemic hypoglycaemia of infancy
 Beckwith-wiedemann syndrome
 Insulinoma
 Ketotic hypoglycaemia
 Drugs including alcohol, aspirin, beta blockers
 Sepsis especially due to gram negative organisms

Signs and symptoms

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Hypoglycaemia is often accompanied by signs and symptoms of autonomic (adrenergic)
activation and/ or neurological dysfunction (neuroglycopenia)

 Autonomic signs and symptoms

 Tremors
 Pounding heart
 Cold sweatiness
 Pallor

 Neuroglycopenic signs and symptoms

 Difficulty concentrating
 Blurred vision
 Disturbed colour vision
 Difficulty hearing
 Slurred speech
 Poor judgment and confusion
 Problems with short-term memory
 Dizziness and unsteady gait
 Loss of consciousness
 Seizure
 Death
 Behavioral signs and symptoms
 Irritability
 Erratic behavior
 Nightmares
 Inconsolable crying
 Non-specific symptoms (associated with low, high or normal blood
glucose)
 Hunger
 Headache
 Nausea
 Tiredness

Investigation of Hypoglycaemia

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Blood taken for a diagnostic screen is only useful if taken when the patient is
hypoglycaemic (glucose < 2.6 mmol) and should include the following:

 Glucose
 Insulin
 Cortisol
 Growth hormone
 Lactate
 Free fatty acids
 Amino acids
 Ketone bodies ( hydroxyl butyrate and acetoacetate)
 Urine
 Organic acids

 Note

In hypoglycaemic states and in the absence of ketones, it is important to look at

free fatty acids (FFA). Normal FFA suggests hyperinsulinism and raised FFA
suggests a fatty acid oxidation defect. Hypoglycaemia in the presence of urinary
ketones suggests either a counter regulatory hormone deficiency or an enzyme
defect in the glycogenolysis or gluconeogenesis pathways.

Treatment

Hypoglycaemia should be treated promptly after obtaining the critical intravenous

samples by intravenous infusion of 5 ml/kg of 10% dextrose followed by adequate
glucose infusion to maintain euglycaemia.

Severe hypoglycemia can be reversed by the injection of glucagon: glucagon 0.5 mg <
12yr, 1.0 mg for ages >12yr or 10-30 mcg/kg body weight. Glucagon is given
intramuscularly or subcutaneously.

Treatment should also be aimed at the underlying cause of hypoglycaemia.

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 Fig 1 shows flow chart for the emergency management of Hypoglycaemia

References

1. Clarke W et al. Assessment and management of hypoglycemia in children and

adolescents with diabetes. Pediatric diabetes 2008: 9:165-174

2. Cox DJ et al. Perceived symptoms in the recognition of hypoglycemia. Diabetes

care 1993:16:519-527

3. Krishna MG, Gupta DK. Hutchison Paediatrics: Pages 437-438

4. Kliegman RM et al. Nelson Textbook of Pediatrics: Pages 655-668

ADRENAL CRISIS

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Definition

Severe adrenocortical insufficiency resulting in peripheral shutdown, cyanosis,

tachycardia, tachypnoea, hypotension, drowsiness and coma. It can be fatal if not
urgently treated.

Causes

It may be due to several processes e.g.

CONGENITAL

a) Congenital adrenal hyperplasia

b) Congenital adrenal hypoplasia
c) Adrenoleukodystrophy

ACQUIRED

a) Acute haemorrhagic destruction of both adrenal glands in previously

well children due to sepsis
b) Rapid withdrawal of steroids
c) Autoimmune process (Addison’s disease)
d) Tuberculosis
e) Birth Asphyxia

Clinical Features

 Vomiting/diarrhoea
 Weight loss
 Nausea
 Dehydration
 Acidosis
 Convulsions
 Signs of shock
 Hypotension

Investigations

 Random glucose (hypoglycaemia)

 Urinalysis (ketosis)
 ECG (Hyperkalaemia)
 Serum Cortisol - often low
 ACTH- often high
 U/Es (Hyponatraemia, Hyperkalaemia), Creatinine – (GFR decreases)

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  Aldosterone - levels are often normal
 Urinary Na and Cl increased, K is decreased
 Abdominal U/S, CT scan, MRI - size of adrenal glands
Treatment

 Airway
 Breathing
 Circulation – correct shock with normal saline at 20 mls/kg, then
correct dehydration
 Treat hypoglycaemia
 Normal saline to correct salt deficit.
 Hydrocortisone 4 hourly
 Daily maintenance hydrocortisone

References

1. David Southall, International Child Health Care, A practical Manual for

Hospitals worldwide. First edition, Book Power, Page 219. 2003, UK.

2. Behrman, Nelson Textbook of Paediatrics, 17th Edition, Page 1904,

Saunders 2004. USA.

3. PJ Simm, CM McDonnell and MR Zacharin.16th April 2004

Department of Endocrinology and Diabetes, Royal Children’s Hospital,
Melbourne, Victoria, Australia .Review of Primary Adrenal insufficiency
In Childhood And Adolescence. Advances In Diagnosis and
Management.

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