Clinical Protocol

in Pediatrics
Jaydeep Choudhury
Assistant Professor
Department of Pediatrics
Institute of Child Health
Kolkata, West Bengal, India

Jayanta Bandyopadhyay
Senior Consultant (Pediatrician)
Durgapur, West Bengal, India
Former Fellow, Pediatric Cardiac Critical Care
Madras Medical Mission
Chennai, Tamil Nadu, India
Senior Registrar, Pediatric Emergency Medicine
Mater Childrens Hospital
Brisbane, Australia

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Clinical Protocol in Pediatrics
First Edition : 2012
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PREFACE
Pediatric emergency is a demanding situation which requires immediate decisionmaking. Clinical Protocol in Pediatrics is an endeavor towards building up such an
interesting field of pediatrics wherein the first few golden moments at
presentation to emergency department, a rational, stepwise and correct approach
can not only save the child but also reduce the morbidity to a minimal.
Working in a busy emergency is often stressful and tiresome even for a skilled
doctor with sound knowledge. Going through textbook and descriptive text
may be time-consuming and mind-boggling too. We need at-a-glance format
which can be accessed by emergency physicians, emergency fellows, trainees,
pediatric postgraduates and even practicing pediatricians. This book focuses on
a stepwise approach to common pediatric emergency situations which are
presented in a ready-to-use format.
The book deals with ideas which can be practised in any reasonably good
hospital set-up. It also covers all emergency situations that can be dealt with
both by emergency physicians and pediatricians.
It was an absolute pleasure for us writing this book. We are indebted to our
alma mater The Child Trust Hospital, Chennai, Tamil Nadu, India, where during
our postgraduation, we used to encounter innumerable cases during our long
hours in the emergency room. Perhaps, it was the driving force for this venture.
We are also indebted Dr Robyn Brady, Deputy Director, Pediatric Emergency
Department, Mater Childrens Hospital, Brisbane, Australia, for his impetus
and support.
A supportive family is the backbone of any work. We are fortunate to have
understanding parents, wives and children.
We express our sincere gratitude to Mr Tarun Duneja (Director-Publishing),
Mr Tarun Vij (Director-Pharma), Ms Samina Khan, Mr KK Raman (Production
Manager), and their team in New Delhi, India and Mr Sabyasachi Hazra (Kolkata
Branch), M/s Jaypee Brothers Medical Publisher Pvt Ltd, New Delhi, India, for
their whole-hearted effort and cooperation.
We are open to suggestions and criticisms. Feel free to mail us at
drjaydeep_choudhury@yahoo.co.in and sendjayanta@yahoo.com.

Kolkata, West Bengal, India

Jaydeep Choudhury
Jayanta Bandyopadhyay

CONTENTS
1. Approach to a Child in Pediatric Emergency Department _ 1
2. Cardiopulmonary Resuscitation ______________________ 3
3. Shock ___________________________________________ 5
4. Coma ___________________________________________ 6
5. Anaphylaxis ______________________________________ 9
6. Oxygen Administration ___________________________ 11
7. Fluid and Electrolyte Balance _______________________ 12
8. Blood Component Transfusion _____________________ 14
9. Chest Tube Drainage and Needle Thoracocentesis ______ 19
10. Prolonged Neonatal Jaundice _______________________ 20
11. Neonatal Collapse ________________________________ 21
12. Respiratory Distress and Noisy Breathing _____________ 22
13. Croup _________________________________________ 23
14. Acute Epiglottitis ________________________________ 25
15. Bronchiolitis ____________________________________ 26
16. Acute Severe Asthma _____________________________ 27
17. Cyanotic Spell ___________________________________ 28
18. Heart Failure ____________________________________ 29

vi

Clinical Protocol in Pediatrics

19. Abnormal Pulse Rate or Rhythm ____________________ 31

20. Acute Abdominal Pain ____________________________ 35
21. Upper Gastrointestinal Bleeding ____________________ 37
22. Fulminant Hepatic Failure _________________________ 41
23. Acute Renal Failure ______________________________ 42
24. Hypertensive Crisis _______________________________ 46
25. Hematuria ______________________________________ 51
26. Status Epilepticus ________________________________ 52
27. Rapid Onset Limb Weakness _______________________ 54
28. Hypoglycemia in Neonates and Children ______________ 56
29. Adrenal Insufficiency and Addisonian Crisis ___________ 59
30. Animal Bites ____________________________________ 60
31. Snake Bite ______________________________________ 61
32. Near Drowning __________________________________ 62
33. Various Poisonings _______________________________ 63
34. Airway Foreign Body _____________________________ 66
35. Button Battery Ingestion __________________________ 68
36. Psychiatric Assessment for Nonpsychiatrists ___________ 70
37. Head Trauma ___________________________________ 71
38. Acute Neck Stiffness ______________________________ 77

Contents

vii

39. Acute Painful Hip ________________________________ 73

40. Spinal Cord Injury and Spinal Cord Injury without
Radiographic Abnormality (SCIWORA) ______________ 74
41. Ophthalmological Issues ___________________________ 76
42. Otolaryngological Issues ___________________________ 77
43. Fever with Rash __________________________________ 79
44. Urticaria and Angioedema _________________________ 80
45. Fever without Focus ______________________________ 81
46. Severe and Complicated Malaria ____________________ 84
47. Dengue ________________________________________ 85
48. Community Acquired Pneumonia ___________________ 87
49. Acute Meningitis _________________________________ 88
50. Urinary Tract Infection ___________________________ 89

Approach to a Child in
Pediatric Emergency
Department

TABLE 1.1: Warning symptoms in history

1.

Child with persistent lethargy, not smiled over a few hours.

2.

Child with prolonged irritability or inconsolable child.

3.

Child taking less than 50 percent of normal fluids.

4.

No urine output for six hours.

5.

Seizure, cyanosis, pallor or apnea.

6.

Parental concern out of proportion to childs illness.

TABLE 1.2: Warning signs in examination

1. Respiratory distress, grunting
2. Tired or looks sicker than usual illness
3. High pitched cry
4. Drowsy
5. Floppy
6. Pale
7. Alteration in vital signs
8. Low saturation
9. Signs of shock
10. Full or bulging fontanelle
11. Nonblanching petechiae or purpura
12. Bilious vomiting.

Clinical Protocol in Pediatrics

TABLE 1.3: Normal weight, respiratory and heart rate in children of different age groups
Age
Birth
3 months
6 months
1 year
2 years
4 years
6 years
8 years
10 years
12 years
14 years

Weight (kg)

RR / min

HR / min

2.5-3.5
6
8
10
12
15
20
25
30
40
50

40-60
30-50
30-50
30-40
20-30
20
16
16
16
16
16

100-160
100-160
100-160
100-160
100-150
80-130
70-120
70-110
60-100
60-100
60-100

TABLE 1.4: Differences between sick and well children

General behavior
Mood
Wakefulness
Tone
Vital signs

Well child

Sick child

Plays with toys

Interacts with parents
Normal
Alert, smiles
Consolable if cries
Awake
Normal sleep pattern
Normal
Afebrile
RR and HR normal

Not playful
Not much interaction
Irritable
Unhappy
Cries more than usual, inconsolable
Sleepy
Difficult to waken
Floppy
Fever
Tachypnea
Tachycardia

Cardiopulmonary
Resuscitation

TABLE 2.1: Method of chest compression in infants and children

Cardiac compressions

Infants

Children

Rate/min
Depth
Site

100
1/3 of AP chest diameter
Lower half of the sternum not
over the xiphoid (below
intermammary line)
2 fingers technique. OR
2 thumb-encircling hands
technique (preferred).

100
1/3 to 1/2 of AP chest diameter
Lower half of the sternum not
over the xiphoid

Technique

Heel of one hand or two hands

technique

TABLE 2.2: Medications to maintain cardiac output and for post-resuscitation stabilization
Medication

Dose

Comment

Dobutamine
Dopamine

2-20 g/kg/min IV/IO

2-20 g/kg/min IV/IO

Epinephrine

0.1-1 g/kg/min IV/IO*

Norepinephrine
Sodium nitroprusside

0.1-2 g/kg/min*
1-8 g/kg/min

Inotrope, vasodilator
Inotrope, chronotrope; renal and splanchnic vasodilator in low doses; pressor in
high dose
Inotrope, chronotrope, vasodilator in low
doses; pressor in higher doses
Inotrope, vasopressor
Vasodilator; prepare only in D5W

6 body weight (in kg) = mg of drug to add to 100 ml D5W then, an IV rate of 1 ml/h delivers 1 g/
kg/min of drug.
*0.6 body weight (in kg) = mg of drug to add to 100 ml D5W, then, an IV rate of 1 ml/h delivers 0.1
g/kg/min of drug.
IO = Intraosseous.

* flush with 5 ml of normal saline and follow-up with 5 ventilations

IO = Intraosseous.

Sodium bicarbonate

Procainamide

Naloxone

Magnesium sulfate

Lidocaine

Glucose

Calcium chloride (10%)

Epinephrine

Atropine

Bolus 1 mg/kg IV/IO

Maximum dose 100 mg
Infusion 20-50 g/kg/min ET* 2-3 mg
25-40 mg/kg IV/IO over 30 min, may be given faster in
Torsades pointes
Maximum dose 2 g
<5 y or 20 kg 0.1 mg/kg IV/IO/ET*
5 y or >20 kg 2 mg IV/IO/ET*
15 mg/kg IV/IO over 30-60 min adult dose 20 mg/min IV infusion
up to total maximum dose 17 mg/kg
1 mEq/kg/dose IV/IO slowly

0.1 mg/kg (max 6 mg)

Repeat dose 0.2 mg/kg (max 12 mg)
In pulse less VT or VF 5 mg/kg IV/IO
Repeat up to 15 mg/kg, maximum 300 mg
Infusion 25 mcg/kg/min for 4 hrs followed by
5-15 mcg/kg/min continuous
0.02 mg/kg IV/IO 0.03 mg/kg ET* repeat once if needed
minimum dose 0.1 mg maximum single dose in child 0.5 mg,
in adolescent 1 mg
20 mg/kg IV/IO (0.2 ml/kg)
0.01 mg/kg (0.1 ml/kg 1:10 000) IV/IO 0.1 mg/kg
(0.1 ml/kg 1:1000) ET* maximum dose 1 mg IV/IO; 10 mg ET*
0.5-1 g/kg IV/IO

Adenosine

Amiodarone

Dose

Medication

Use lower doses to reverse respiratory depression associated with

therapeutic opioid use (1-15 g/kg)
Monitor ECG and BP use caution when administering with other
drugs that prolong QT
After adequate ventilation

10% dextrose diluted with 5-10 ml/kg

25% dextrose diluted with 2-4 ml/kg
50% dextrose diluted with 1-2 ml/kg

Slowly
May repeat every 3-5 min

Higher doses may be used with organophosphate poisoning

Monitor ECG
Rapid IV/IO bolus
Monitor ECG and BP
Be cautious when administering with
other drugs that prolong QT

Remarks

TABLE 2.3: Medications for pediatric resuscitation and arrhythmias

4
Clinical Protocol in Pediatrics

Shock

Flow chart 3.1: Treatment priorities and stepwise assessment of shock

Coma

TABLE 4.1: Modified Glasgow Coma Scale (GCS)

Response
Eye opening
(i)
Spontaneous
(ii) To speech
(iii) To pain
(iv) None
Best verbal response
(i)
Smiles, oriented to sound, follows object, interacts
(ii) Consolable cry
(iii) Inconsistently consolable cry
(iv) Inconsolable cry, restless, agitated, unaware of environment or parents
(v) No response
Best motor response
(i)
Spontaneous movement/obeys verbal command
(ii) Localizes to supraocular pain
(iii) Withdraws
(iv) Abnormal flexion to pain
(v) Abnormal extension to pain
(vi) None
Grading 13-14 Mild, 9-12 Moderate, <8 severe

Score
4
3
2
1
5
4
3
2
1
6
5
4
3
2
1

Coma

TABLE 4.2: Methods of testing oculocephalic and oculovestibular reflexes

Oculocephalic reflex

Oculovestibular reflex

- Eyes move conjugately to the opposite

direction to head movement: Normal
- Lateral gaze palsy: Brainstem lesion
- No movement: Pontine lesion

- Nystagmus with fast component away

from site of stimulation: Normal
- No nystagmus or dysconjugate response:
Brainstem lesion
- Full deviation towards the stimulated side:
Cerebral hemispheric lesion with intact
brainstem

TABLE 4.3: Differences between metabolic and structural coma

Toxic/metabolic/infectious

Supratentorial lesions

Infratentorial lesions

i. Confusion precedes motor signs

ii. Pupillary reactions
preserved
iii. Symmetrical motor responses
iv. Asterixis, myoclonus
v. Hyper/hypoventilation

i. Initial focal signs

ii. Rostral to caudal
progression

i. Preceding brainstem
dysfunction
ii. Sudden onset
iii. Cranial nerve palsies
iv. Early respiratory
disturbances

Clinical Protocol in Pediatrics

Flow chart 4.1: Algorithm for the diagnosis

and management of coma in children

Anaphylaxis

TABLE 5.1: Clinical features of anaphylaxis

System

Features

Cutaneous
Upper respiratory

Urticaria and angioedema.

Hoarseness, dysphonia, feeling of lump in throat( features of laryngeal edema and upper airway obstruction).
Wheezing, dyspnea.
Hypotension, shock, cardiovascular collapse and arrhythmia.
Sneeze, itch, rhinorrhea, nasal and palatal pruritis, watery eyes diaphoresis.

Lower respiratory
Cardiovascular
General

TABLE 5.2: Pharmacotherapy of anaphylaxis

Medication

Dose

Epinephrine (1: 1000)

Norepinephrine
Hydrocortisone
Dopamine
Diphenhydramine

10 gm /kg IM and 0.1-1 g/kg/min IV as infusion

0.1-1 g/kg/min
4 mg/kg
2-20 g/kg/min IV
5 mg/kg/day PO in 3-4 divided doses

10

Clinical Protocol in Pediatrics

Flow chart 5.1: Algorithm for anaphylaxis treatment

Oxygen Administration

TABLE 6.1: Oxygen percentage with different systems

Lt/min

Simple mask

5
6
8
10
12
15

Partial rebreathing mask

<40%
45-50%

35%
45-50%
60%
60%
60%

Nonrebreathing mask
55-60%
60-80%
80-90%
90%
90-100%

TABLE 6.2: Administration of oxygen

Low flow devices

High flow devices

Nasal canula: It will provide low FiO2

between 30 to 40 percent. Fitting a nasal
canula in a neonate will give almost
90 percent FiO2 at 1 L/min.

Nonrebreathing mask: It has a valve at the

exhalation port that allows only exhaled
gases to enter the reservoir. A well fitting
mask can provide up to 100 percent oxygen.

Simple mask: Should not to be used

for conditions of hypoxemia.

Venturi masks: These are dilutional masks

where oxygen is delivered through a narrow
orifice at a high flow. There are openings near
the nozzle that allows room air to be sucked
in, diluting the oxygen. Changing the size of
the nozzle, the flow rates, as well as ports,
allows control of the amount of oxygen.

Partial rebreathing mask: This is a simple

mask with an additional reservoir that
allows accumulation of oxygen enriched
gas for rebreathing. Up to 60 percent
FiO2 can be delivered.

Oxyhood: Adequate flow of humidified

oxygen allows mixing of delivered gases
and flushing out of CO2. O2 gradient can
vary as 20 percent from top to bottom and
continuous flow of 6 L/min avoids this
problem. Cold airs causes heat stress and
condense on babys head, which is
mistaken as perspiration.

Nonrebreathing mask: It is similar but

has a valve which allows only oxygen from
the source to enter the reservoir and not
allowing the exhaled air. Hence, 80 to
100 percent O2 can be provided.

Fluid and Electrolyte

Balance

TABLE 7.1: Composition of commonly used rehydration solutions and plasma

Normal saline (NS)
0.45 NS 5% D
0.22% NS
8.4% NaHCO3
Human plasma
WHO-ORS

Content

Osmolality

Na = 150 mmol/L
Cl = 150 mmol/L
Na = 75 mmol/L
Cl = 75 mmol/L
Glucose = 50 g/L
Na = 37 mmol/L
Cl = 37 mmol/L
HCO3 = 1 mmol/ml
Na = 1 mmol/ml
Na = 145 mmol/L
K = 4.5 mmol/L
Na = 90 mmol/L
K = 20 mmol/L
Citrate = 30 mmol/L
Glucose = 110 mmol/L

300 mOsmol/kg
428 mOsmol/kg

290 mOsmol/kg
320 mOsmol/kg

TABLE 7.2: Volume replacement in dehydration

Mild
Moderate
Severe

Younger children

Older children

50 ml/kg
75 ml/kg
100 ml/kg

30 ml/kg
50-60 ml/kg
70-90 ml/kg

Fluid and Electrolyte Balance

13

TABLE 7.3: Sodium loss in various states of dehydration

Status

Approximate sodium loss

Isonatremia (Acute)
Isonatremia (Chronic)
Hyponatremia
Hypernatremia

100 mmol/L
70-80 mmol/L
120 mmol/L
40-60 mmol/L

TABLE 7.4: Water or calorie requirement

Weight

Water (or calorie) requirements

Birth-10 kg
11-20 kg
21-30 kg

100/kg
1000 + 50 /kg above 10
1500 + 20 /kg above 20

TABLE 7.5: Etiology and management of hyponatremia

Status
Etiology

Hypovolemic
hyponatremia
i. Renal loss
ii. Extrarenal loss
(Gastrointestinal,
sweat, third space)
Isotonic saline

Initial
management
Further
5% Dextrose with
management 0.45% saline

Euvolemic
hyponatremia

Hypervolemic
hyponatremia

i. Syndrome of
i. Renal loss
Inappropriate
Antidiuretic Hormone
ii. Water intoxication
ii. Edematous state
iii. Drugs
(Mineralocorticoids)
Water restriction
Salt and water restriction
Frusemide, hypertonic
saline

Hypertonic saline,
dialysis

Blood Component
Transfusion

TABLE 8.1: Blood components available

Products available
1. Red blood cells (RBC)
Homologous packed RBC
Leukocyte-poor RBC

Irradiated RBC
Washed RBC

Frozen RBC
Neocytes

Directed donor RBC

Autologous RBC

2. Platelets
Random donor platelets (RDP)
Platelet pheresis
Leukocyte-poor platelets

Preparations
Prepared from potential donors, are transfused most often.
Promote oxygen delivery for patients with active bleeding or
severe anemia.
Prepared by a variety of techniques to remove more than 99%
of leukocytes. Reduce febrile reactions; Prevent HLA
alloimmunization and CMV infection in potential transplant
recipients or those requiring chronic platelet transfusions.
Reduces transfusion associated graft-versus-host disease
(TAGVHD).
Washing red blood cells in saline removes most plasma
proteins and some leukocytes and platelets. Substitute for
homologous RBC in patients sensitive to a plasma component;
Avoid transfusion of anti-A and anti-B antibodies when
O-negative blood is used in patients who are type A, B, or AB.
Not often used today.
RBCs frozen in liquid nitrogen with glycerol as a cryoprotective
agent, can be stored for up to 10 years. Preserve autologous
RBC; maintain store of rare blood types.
Prepared by differential centrifugation or cell separators and
have a longer circulating life span than standard red cells, but
they are rarely used. Increase efficacy of individual transfusion
for patients with transfusion-dependent anemia, thalassemia,
etc.
After screening and informed consent, may be substituted for
volunteer RBC at patient request. Reduces multiple donor
exposure in chronically transfused patients.
May be collected preoperatively, by perioperative blood
salvage, or by acute normovolemic hemodilution to decrease
homologous red blood cell use.
Obtained from whole blood.
Obtained by apheresis technology. Also known as single donor
platelet (SDP). It has advantages over RDP.
Various techniques to prepare are available. It can remove
>99% of leukocytes. It reduces febrile reactions and HLA
alloimmunization and CMV transmission.
Contd...

Blood Component Transfusion

15

Contd...
Irradiated platelets
HLA matched platelets

3. Plasma and derivatives

Fresh frozen plasma (FFP)

Fresh plasma (liquid plasma)

Cryoprecipitate-poor plasma

Cryoprecipitate

4. Granulocytes
Leukapheresis

Reduces transfusion associated graft-versus-host disease.

Treat bleeding associated with thrombocytopenia in patients
who are refractory to platelet transfusions due to HLA
alloimmunization.
Prepared by separating plasma from whole blood and freezing
it within 6 hours after collection at 18C or colder. It can be
stored for up to 1 year and is thawed prior to administration.
It is very effective in coagulopathies.
Same as FFP, except does not contain factors V and VIII. Used
for preparation of plasma derivatives (e.g. immunoglobulin,
cryoprecipitate, albumin, coagulation factor concentrates).
Supernatant plasma remaining after preparation of
cryoprecipitate and contains adequate quantities of all
coagulation factors except Fibrinogen, factors VIII and XIII,
and vwf. Correct coagulation factor deficiencies other than
VIII, XIII, fibrinogen, vwF; may be indicated for treatment of
refractory TTP.
Formed by thawing FFP at 4C. This cryoprecipitate is separated
from the supernatant plasma and resuspended in a small
volume of plasma. It is then refrozen at 18C and kept for up
to 1 year.
Granulocyte concentrates are prepared by automated
leukopheresis from ABO-compatible donors stimulated several
hours before collection with corticosteroids, G-CSF or both.

16

Clinical Protocol in Pediatrics

TABLE 8.2: Therapeutic products derived from plasma

Plasma derivative

Therapeutic use

Albumin (heat-treated)
Plasma-derived factor VIII concentrate
Humate-P
Prothrombin complex concentrate

Hypoalbuminemia in nephrotic syndrome

Hemophilia A
Von Willebrands disease
Coaugulation inhibitors, factor X and prothrombin deficiencies
Factor VIII inhibitors
Hemophilia B*
Hypofibrinogenemia
Factor VII,XI,XIII deficiency
Thrombosis in antithrombin III deficiency
Angioedema
Prevent lung damage in 1-AT deficiency
Severe protein C or S deficiency
Immunodeficiency states; immune cytopenias,
Kawasaki syndrome, Guillain-Barr syndrome,
dermatomyositis
Passive immunization against hepatitis A
measles, poliomyelitis, varicella, rubella

Activated factor IX concentrates

Plasma-derived factor IX concentrate
Fibrinogen concentrate
Factor VII,XI,XIII concentrate
Antithrombin III concentrate
C1 esterase inhibitor concentrate
1-Antitrypsin concentrate
Protein C and S concentrate
Intravenous immunoglobulin
Immune serum globulin

TABLE 8.3: Infectious complications of transfusion therapy

Viruses

Bacteria

Spirochetes

Parasites

Prion

Hepatitis A, B, C
Parvovirus B 19
Cytomegalovirus
Epstein-Barr virus
HTLV 1 and 2
HIV
West Nile virus

Environmental
contaminants
Donor transmitted:
Yersinia, Salmonella,
Klebsiella
Serratia
Staphylococcus

Syphilis
Lyme disease

Malaria
Babesiosis
Chagas disease
Toxoplasmosis

Variant
CreutzfeldtJakob
disease

Blood Component Transfusion

17

TABLE 8.4: Nonhemolytic, noninfectious complications

Complication

Clinical manifestations, pathogenesis, prevention, and

treatment strategies

Febrile-nonhemolytic
transfusion reaction (FNHTR)

Occurs in 0.5-3% of transfusion. Rigors or chills followed by

fever during or shortly after transfusion due to prior
sensitization to WBC or platelet antigens, or to pyrogenic
cytokines released during storage. Prevent with antipyretics
or leukocyte depletion of blood components before storage.

Transfusion-related acute
lung injury (TRALI)

Noncardiogenic pulmonary edema with fevers, chills, tachycardia, and diffuse pulmonary infiltrates shortly after transfusion,
due to leukocyte incompatibility. Resolves in 1-4 days; rarely
results in respiratory failure. Occurs in approximately 1:5000
transfusions.

Allergic reactions

Occurs in 1-3% of transfusions. Urticaria, pruritus,

bronchospasm, or frank anaphylaxis due to recipient
sensitization to a cellular or plasma element. If severe, evaluate
recipient for IgA deficiency. Leukocyte depletion or washed
red cells may be necessary for subsequent transfusions.

Transfusion-associated
circulatory overload (TACO)

Common following transfusion for chronic anemia or when

patient has impaired cardiovascular reserve. Prevent by
transfusing only when clearly indicated, using the minimum
amount of blood required to reverse symptoms. Treat with
oxygen, diuretics, and, rarely, phlebotomy (save units for
reinfusion if necessary).

Dilutional effects

Transfusing with more than one blood volume or red blood

cells with dilute platelets and coagulation factors. Replacement
indicated only for clinical bleeding.

Hypocalcemia

Due to citrate intoxication following massive transfusion. Treat

only if symptomatic.

Hyperkalemia

May occur in patients with pre-existing renal insufficiency and

hyperkalemia or in neonates. Use of fresh blood or washed red
cells decreases potassium load for these patients.

Hypothermia

After massive transfusion of refrigerated blood, hypothermia

may cause cardiac arrhythmias. Refrigerated blood may
accelerate hemolysis in patients with cold agglutinin disease.
Prevent by warming blood.

Transfusion associated
Graft-versus-host disease

Immunocompetent donor T lymphocyctes may engraft if the

recipient is markedly immunosuppressed or if closely HLArelated. Symptoms and signs include high fever, maculopapular
erythematous rash, hepatocellular damage, and pancytopenia,
2-30 days after transfusion. Usually fatal despite treatment with
immunosuppressives. Prevent by irradiating all blood
components with 2500 cGy for immunocompromised
recipients or when donor is first-degree relative.
Contd...

18

Clinical Protocol in Pediatrics

Contd...
Iron overload

Multiple transfusions in the absence of blood loss lead to excess

accumulation of body iron with cirrhosis, heart failure, and
endocrine organ failure. Prevent by decreasing total amount
of red cells given, using alternatives whenever possible, using
neocytes, and modifying diet to decrease iron absorption. Iron
chelation indicated for patients with chronic transfusion
dependence if prognosis is otherwise good.

Post-transfusion purpura

Acute severe thrombocytopenia about 1 week after transfusion

due to alloantibodies to donor platelet antigen, usually human
platelet antigen 1A (HPA 1A). Self-limited, but treatment with
steroids, high-dose IgG, plasmapheresis, or exchange
transfusion recommended to prevent CNS hemorrhage. Platelet
transfusions are ineffective even with compatible platelets.

Miscellaneous

Increased supply of complement may accelerate hemolysis in

paroxysmal nocturnal hemoglobinuria or make angioedema
worse in patient with C1 esterase inhibitor deficiency. Increased
blood viscosity may occur in patients with Waldenstrms
macroglobulinemia, polycythemia, or leukemia with high WBC
count.

Chest Tube Drainage and

Needle Thoracocentesis

TABLE 9.1: Common causes and criteria for differentiation

between transudative and exudative pleural effusion
Variable
Common causes

Pleural fluid protein/

serum protein
Pleural fluid LDH/serum
LDH
Pleural fluid LDH

Transudate
i.
ii.
iii.
iv.

Congestive heart failure

Cirrhosis
Nephrotic Syndrome
Pulmonary embolism

Exudate
i.
ii.
iii.
iv.
v.
vi.

<0.5

Pneumonia
Trauma
Tuberculosis
Rheumatoid arthritis
SLE
Malignancy
>0.5

<0.6
<2/3 upper limit of serum
LDH

>0.6
>2/3 upper limit of serum
LDH

TABLE 9.2: Analysis of pleural fluid

Containers

Primary study

Plain red top tube

Protein, LDH, amylase, glucose and triglycerides if

needed
Cell count, differential
Fluid pH
Gram staining and culturing (for aerobic and anaerobic
organisms, mycobacteria, fungi)
Cytologic analysis

EDTA, lavender top tube

Heparin treated blood gas syringe
Sterile container
Green top tube, heparinized

Prolonged Neonatal
Jaundice

10

TABLE 10.1: Management of unconjugated hyperbilirubinemia in healthy term babies

(Total serum bilirubin in mg/dL)
Age in hours

Consider phototherapy

Institute phototherapy

Exchange transfusion if
phototherapy fails

12
15
17

15
18
20

20
25
25

24
25-28
49-72
72

TABLE 10.2: Indications for exchange transfusion and phototherapy in preterm babies
(Total serum bilirubin in mg/dL)
Birth weight (gram)
Upto 1000
1000-1250
1251-1500
1501-2000
2001-2500
>2500

Normal neonates
10-12
12-14
14-16
16-18
18-20
20-22

High risk neonates

8-10
10-12
12-14
14-16
16-18
18-20

11

Neonatal Collapse

Flow chart 11.1: Neonatal collapse algorithm

12

Respiratory Distress and

Noisy Breathing

TABLE 12.1: Differences between croup, epiglottitis and foreign body aspiration
Parameters

Croup

Epiglottitis

Foreign body

Age
Onset
Prodromal features
Temperature
Stridor

6-18 months
Gradual, over 24-48 hours
Present
May be mildly elevated
High pitched loud

2-5 years
Sudden
Nil
High
Low pitched soft

Barking cough
Hoarse voice
General appearance

Present
Present
Noisy and playful

No cough
Voiceless
Anxious, sits still

>6 months
Sudden
Nil
Normal
Variable, depends on
location of foreign
body
Variable
Variable
Depends on degree
of obstruction

Approach to Noisy Breathing

Diagnosis and management of various emergency situations of noisy breathing in children is
discussed in other sections. Few important points for noisy breathing are as follows:
1. Focused and detailed history.
2. Examination of noseSeptum, adenoid, foreign body.
3. Throat and larynxTonsils, diphtheritic patch, foreign body.
4. Pharynx and epiglottis.
5. Lymphadenopathy.
6. ENT consultation at the earliest.
Differentiating features between croup, epiglottitis and foreign body aspiration.

13

Croup

TABLE 13.1: Clinical Scoring System. By Westley CR, Cotton EK, Brooks JG
Level of consciousness
Cyanosis
Stridor
Air entry
Retraction

Normal (including sleep)

Disoriented
None
Cyanosis at agitation
Cyanosis at rest
None
When agitated
At rest
Normal
Decreased
Markedly decreased
None
Mild
Moderate
Severe

0
5
0
4
5
0
1
2
0
1
2
0
1
2
3

24

Clinical Protocol in Pediatrics

Flow chart 13.1: Croup management plan

14

Acute Epiglottitis

Flow chart 14.1: Management of acute epiglottitis

Bronchiolitis

15

TABLE 15.1: Bronchiolitis assessment tool (BAT)

Mild

Moderate

Severe

Wheeze
Feeding

None or end expiratory

Normal

Entire expiration
Less than usual

Oxygen
Chest indrawing

No oxygen requirement
Nil/mild

Behavior

Normal

May require oxygen

Intercostal and/or
tracheosternal
Irritability/lethargy

Inspiratory and expiratory

Not interested, gasping/
coughing
Requires oxygen
Severe with nasal flaring
Irritability/lethargy

Flow chart 15.1: Management of bronchiolitis

16

Acute Severe Asthma

Flow chart 16.1: Management of severe asthma

17

Cyanotic Spell

Flow chart 17.1: Algorithm for management of cyanotic spell

18

Heart Failure

Flow chart 18.1: Management of heart failure due to acute myocarditis

30

Clinical Protocol in Pediatrics

Flow chart 18.2: Management of heart failure due

to shunt lesions (VSD, PDA, AVSD)

19

Abnormal Pulse Rate

or Rhythm

TABLE 19.1: Normal respiratory and heart rate in children of different age groups
Age

RR / min

HR/ min

Birth
3 months
6 months
1 year
2 years
4 years
6 years
8 years
10 years
12 years
14 years

40-60
30-50
30-50
30-40
20-30
20
16
16
16
16
16

100-160
100-160
100-160
100-160
100-150
80-130
70-120
70-110
60-100
60-100
60-100

TABLE 19.2: Characteristics to distinguish between sinus tachycardia and SVT

Sinus tachycardia

Supraventricular tachycardia

Infants and children usually have a

HR <220/min
P waves if visible usually upright in
leads I and AVF
Beat-to-beat variability of HR present,
which is often responsive to stimulation
HR slows gradually in response to treatment.
Clinical scenario of shock with preceding
history of AGE, blood loss, septicemia, etc.

Usually HR >220/min
P waves if visible are usually negative in leads
II, III and AVF in SVT
No beat-to-beat variability of HR in SVT
Termination is abrupt
Clinical scenario usually points towards some
pre-existent or co-existent cardiac disorders.

32

Clinical Protocol in Pediatrics

Flow chart 19.1: PALS bradycardia protocol

Abnormal Pulse Rate or Rhythm

Flow chart 19.2: PALS Pulseless arrest protocol

33

34

Clinical Protocol in Pediatrics

Flow chart 19.3: PALS tachycardia algorithm

Acute Abdominal Pain

20

TABLE 20.1: Differentiation of non-organic from organic pain

Organic
Nature of pain
History

Examination

Any time in day and night

i.
ii.
iii.
iv.
v.
vi.
vii.

Weight loss
Lack of energy
Fever
Change in bowel habit
Urinary symptoms
Intestinal symptoms
Vomiting: continuous,
bile stained, hematemesis
viii. Rectal bleeding
Various manifestations

Non-organic
Periodic, usually in day, good
in-between. Often periumbilical.
i. Migraine
ii. School and family problem
iii. Isolated vomiting, not bile stained

Usually normal and thriving

36

Clinical Protocol in Pediatrics

Flow chart 20.1: Approach to acute abdominal pain

21

Upper Gastrointestinal
Bleeding

TABLE 21.1: Etiology according to age

Neonates
i. Swallowed maternal
blood
ii. Hemorrhagic
disease of newborn
iii. Gastritis
iv. Stress ulcer
v. Esophagitis
vi. Congenital blood
dyscrasias
vii. Vascular
malformation
viii. Idiopathic

1 month to 1 year

1 year to 12 years

Adolescents

i. Gastritis

i. Esophageal varices

i. Esophageal varices

ii. Stress ulcer

ii. Gastritis

ii. Gastritis

iii. Esophagitis
iv. Mallory-Weiss
syndrome
v. Vascular
malformation
vi. GIT duplication

iii. Stress ulcer

iv. Esophagitis

iii. Stress ulcer

iv. Esophagitis

v. Mallory-Weiss
syndrome
vi. Peptic ulcer

v. Mallory-Weiss
syndrome
vi. Peptic ulcer
vii. Foreign body

38

Clinical Protocol in Pediatrics

Flow chart 21.1: Management plan according to severity and bleeding

Upper Gastrointestinal Bleeding

Flow chart 21.2: Endoscopic evaluation of GI bleed

39

40

Clinical Protocol in Pediatrics

Flow chart 21.3: Management plan for acute variceal bleeding

Fulminant Hepatic Failure

22

TABLE 22.1: Clinical staging of hepatic encephalopathy

Stage

Asterixis

EEG changes

Clinical manifestations

Stage 1 Prodrome

Slight

Minimal

Stage 2 Impending
coma

Easily elicited

Generalized slowing
of rhythm

Stage 3 Stupor

Present if patient
is cooperative

Grossly abnormal
slowing

Stage 4 Coma

Usually absent

Appearance of delta
waves, decreased
amplitudes

Mild intellectual impairment, disturbed sleep

wake cycle
Drowsiness, confusion,
inappropriate behavior,
mood swing
Drowsy, unresponsive
to verbal commands,
markedly confused,
delirious
Hyperreflexia, extensor
plantar response,
unconscious, decerebrate
or decorticate response to
pain (4a) or absent (4b)

23

Acute Renal Failure

TABLE 23.1: Typical signs and symptoms of ARF in different situations

History/Symptoms

Signs

Diagnosis

Vomiting, diarrhea, hemorrhage

Falciparum malaria, G6PD
deficiency, snake bite, mismatched
blood transfusion
Fever
Recent H/O diarrhea. Melena/
sudden pallor/seizure
High fever
Sore throat / pyoderma
H/O nephrotoxic drugs
Variable urine output

Dehydration, shock
Variable, depending on
individual condition

Gastroenteritis, hypovolemia

Petechiae, bleeding

Sepsis, DIC
Suspect HUS, confirm with
laboratory results
Pyelonephritis
Acute glomerulonephritis
Drug induced ARF
Obstructive uropathy

Flank tenderness
Hypertension/edema
Suprapubic mass

Acute tubular necrosis

TABLE 23.2: Differentiating features of renal and prerenal causes of ARF

Prerenal

Renal

History/clinical features
Dehydration, hypovolemia

Yes

No. may be normal or over

hydration

Renal indices
Specific gravity
Urinary sodium
Urine/plasma osmolality
FENa
Diuretics and fluid challenge

>1020
<20 mEq/L.
>1:3
<1(< 2 in newborn)
Positive response

normal
>20 mEq/L
<1:3
>1(>2 in newborn)
No response

Anemia

Hypertension

Metabolic acidosis

Hyponatremia (Na <120 mEq/L)

Hypocalcemia (Total Ca <8 mg%

or ionized Ca <0.8 mmol%)

10% Ca gluconate 1-2 ml over 10 minutes with cardiac monitor

i. Fluid restriction (dilutional hyponatremia)
ii. 3% NaCl correct upto 125 mEq/L over 30-60 min (1ml = 0.5 mEq)
If pH <7.2 then, bolus NaHCO3 may be administered
(base excess weight 0.3 ) over 30 minutes
nifedepine, Nitroprusside, diazoxide (avoid betablocker in fluid
retention and ACE inhibitor causes potassium retention)
Packed cell transfusion

vi.

iv.
v.

i.
ii.
iii.

5% Dextrose for insensible water loss (400 ml/mt square/day)

+ 0.45% saline for previous days urine output
O2, frusemide, consider intubation and ventilation
K containing fluid to be avoided
Kayexalate (Sodium polysterene sulfate) 1 gm/kg enema or oral
10% Ca gluconate 0.5-1 ml/kg over 5-10 min, to be discontinued
if heart rate falls by 20
Salbutamol 5-10 mg nebulization
7.5% Sodium bicarbonate 1-3 mEq/kg
IV over 30 minutes
Dextrose (0.5-1 mg/kg) + Insulin 0.1 unit/kg over 1 hour

Fluid overload (Intrinsic renal failure)

Pulmonary edema
Hyperkalemia (K>5.5 mEq/L)

Treatment

Complication

TABLE 23.3: Complications of ARF and their management

Remarks

Should be lowered gradually

Latter binds phosphate so that serum

Ca Premains <70 mmol

Other losses to be monitored and replaced

accordingly
CVP to be monitored
Calcium stabilizes cell membrane and
salbutamol facilitates K entry into cells

Acute Renal Failure

43

44

Clinical Protocol in Pediatrics

Flow chart 23.1: Stepwise management of ARF

Acute Renal Failure

Flow chart 23.2: Fluid management of ARF

45

Hypertensive Crisis

24

TABLE 24.1: Common causes of hypertension in children

Age Group

Cause

Newborn

Renal vessel thrombosis

Renal artery stenosis
Congenital renal anomalies
Coarctation of the aorta
Renal parenchymal disease
Renovascular disease
Coarctation of the aorta
Renal parenchymal disease
Renovascular disease
Essential hypertension
Essential hypertension
Renal parenchymal disease
Renovascular disease

Early childhood (infancy to 6 years)

School age (6-10 years)

Adolescence

TABLE 24.2: Drugs to treat severe hypertension

Drug

Class

Dose

Route

Comments

Esmolol

blocker

100-500 g/kg/min

IV infusion

Hydralazine

Vasodilator

0.2-0.6 g/kg/min

IV/IM

Labetalol

and blocker Bolus: 0.2-1.0

mg/kg/dose
up to 40 mg/dose
infusion: 0.25-3.0
mg/kg/hr
Calcium channel 1-3 mcg/kg/min
blocker
Vasodilator
0.53-10 mcg/kg/min

Very short acting.

Constant infusion
preferred. May cause
profound bradycardia
Should be given every
4 hours when given IV
bolus.
Recommended dose is
lower than FDA label.
Asthma and overt heart
failure are relative
contradiction

Nicardipine
Sodium
Nitroprusside

IV bolus or
infusion

IV infusion
IV infusion

May cause reflex

tachycardia
Monitor cyanide levels
with prolonged (>72
hr) use or in renal
failure; or coadminister
with sodium thiosulfate

Hypertensive Crisis

TABLE 24.3: Common causes of pediatric hypertensive emergencies

Renal disease: (80%)
i. Nephritides:

ii. Vascular:

iii. Congenital malformations:

Miscellaneous:

Endocrine:
Cardiovascular:

Drugs:

Henoch-Schnlein purpura
Postinfectious glomerulonephritis
Systemic lupus nephritis
Rapidly progressive glomerulonephritis
Hemolytic-uremic syndrome
Renal artery stenosis and thrombosis
Renal vein thrombosis
Sickle cell nephropathy
Polycystic kidney disease
Tuberous sclerosis
Hydronephrosis
Renal hypoplasia
Obstructive uropathy
Iatrogenic fluid overload
Renal failure with fluid overload
Reflux nephropathy
Renal tumors
Pheochromocytoma
Congenital adrenal hyperplasia
Aortic thrombosis
Aortic coarctation
Aortic insufficiency
Subacute bacterial endocarditis
Corticosteroids
NSAIDs
Oral contraceptive pills
Theophylline
Phenylephrine

47

48

Clinical Protocol in Pediatrics

Flow chart 24.1: Step-wise management of hypertension

Hypertensive Crisis

Flow chart 24.2: Management of hypertensive emergency

49

50

Clinical Protocol in Pediatrics

Flow chart 24.3: Management of hypertensive urgency

25

Hematuria

Flow chart 25.1: Algorithm for approach to macroscopic hematuria

26

Status Epilepticus

Stage I
Lorazepam0.05 to 0.1 mg/kg IV (maximum 4 mg) or
Diazepam0.3 mg/kg IV (maximum 10 mg) undiluted over 2 minutes.
If IV access could not be established
Diazepam rectal 0.5 mg/kg or
MidazolamIM 0.2 mg/kg.

If seizure does not stop within 5 to 10 minutes

Go to stage II
If seizure stops:
Adjust previous antiepileptic medications or start oral anticonvulsants if required. (The decision
depends on the likelihood for seizure recurrence).
If patient is shocked or cyanosed with dilated pupils at any stage of management or has
been convulsing an hour or more, go straight to stage IV.

Stage II
Repeat lorazepam0.05 to 0.1 mg/kg IV (maximum 4 mg) or
Diazepam0.3 mg/kg IV (maximum 10 mg) undiluted over 2 minutes.
Then start
Phenytoin15 to 20 mg/kg (maximum dose 1000 mg) IV infusion at the rate 1 mg/kg/min
under ECG monitor. Prepare infusion as 10 mg phenyton/ml NS or
Fosphenytoin30 mg/kg IV infusion at the rate 3 mg/kg/min.
Consider pyridoxine100 mg IV for children <2 years of age.
Start 20 percent mannitol5 ml/kg over 20 minutes.
If still convulsing 10 minutes after starting phenyton a 3rd dose of diazepam may be given.

If there is response; continue phenytoin 5 mg/kg/day qevery 12 hours

Follow blood level
If no response 5 minutes after the end of phenytoin infusion.

Status Epilepticus

53

Stage III
PhenobarbitoneLoading dose 15 to 20 mg/kg IV, slowly over 10 minutes.
Be prepared for ventilation and if there is response continue maintenance
Phenobarbitone5 mg/kg/day every 12 hours.
If no response in 5 to 10 minutes after end of infusion or seizure already more than 60 minutes
or unstable vital signs.

Stage IV (ICU)
Intubation and ventilation muscle relaxant (use short acting muscle relaxant in repeated doses
to monitor seizure when EEG monitoring is not available).
Midazolam0.2 mg/kg IV bolus.
Then infusion 1 to 2 mcg/kg/minute titrated up to10 mcg/kg/min
(During infusion maintain phenytoin and phenobarbitone at high therapeutic level) or propofol
1 to 2 mg/kg followed by 2 to 10 mg/kg/hour. If seizure is not controlled in 1 to 2 hours induce
barbiturate coma.
Thiopentone2 to 8 mg/kg loading then reduce infusion to 1 to 10 mg/kg/hour when needed,
titrating for best control.
Monitor for BP, hypoglycemia, electrolytes imbalance, hypocalcemia, acidosis consumptive
coagulopathy (PT, APTT) and hyperpyrexia.
Restrict fluid to 60 percent maintenance (Unless low BP) and continue treatment for brain
edema with mannitol every 6 hours dexamethasone (With IV ranitidine).
After stabilization consider CT scan brain and work-up for possible causes.
Treat for CNS infection if indicated (LP after brain CT scan).

27

Rapid Onset
Limb Weakness

Flow chart 27.1: Management of acute onset limb weakness

Poliomyelitis
Less than 4 days, max. 7 days
Present
Proximal, asymmetrical
Diminished
Decreased or absent
Myalgia, back ache
Only when bulbar or bulbospinal
Only when bulbar or bulbospinal
Transient retention
Severe asymmetric atrophy
High
Normal or slight increase
Normal then slight decrease
Abnormal

Signs and symptoms

Progression of paralysis
Fever at onset
Flaccidity
Muscle tone
DTRs
Sensation
Cranial nerve
Decreased respiration
Bladder dysfunction
Sequele
CSF: WBC
CSF: Protein
NCV (3 wks)
EMG (3 wks)

From hours to 20 days

Absent
Distal, symmetrical
Diminished
Absent
Cramps, tingling, hyposthesia
Often present
In ascending paralysis
Sometimes
Absent or minimal
Less than 10
High
Abnormal demyelination
Normal

GBS

From hours to 4 days

Absent
Lower limbs, symmetrical
Diminished in lower limbs
Absent in lower limbs
Anesthesia of lower limbs, root pain
Absent
Absent
Present
Moderate atrophy
Normal
Normal or slight increase
Normal
Normal

Transverse myelitis

TABLE 27.1: Approach to rapid onset weakness of lower limbs

From hours to 4 days
Variable
Asymmetric limb
Diminished in limb
Decreased or absent
Pain in gluteal region
Absent
Absent
Absent
Peroneal atrophy
Normal
Normal
Abnormal in sciatic nerve
Normal

Traumatic neuritis

Rapid Onset Limb Weakness

55

1. Small for gestational age

2. Premature infant
3. Neonatal asphyxia or fetal
distress
4. Hypothermia
5. Fetal-alcohol syndrome
6. Mother taking hypoglycemia-inducing drugs
7. Diabetic or pre-eclamptic
mother
8. Congenital heart disease
9. Beckwith-Wiedemann syndrome
10. Erythroblastosis fetalis
11. Infection
12. Adrenal hemorrhage and
adrenal insufficiency

Perinatal

14.
15.
16.

13.

12.

9.
10.
11.

1.
2.
3.
4.
5.
6.
7.
8.

Starvation
Idiopathic ketotic hypoglycemia
Hypopituatrism
Hypoadrenalism
Hypothyroidism
Growth hormone deficiency
Inborn error of metabolism
Amino acid metabolic abnormality
Islet cell adenoma
Islet cell hyperplasia
Functional beta cell secretory
defect
Factitious insulin use or sulfonylurea use
Beckwith-Wiedemann syndrome
Infection
Hypothermia
Congenital heart disease

Infancy
1. Idiopathic ketotic hypoglycemia
2. Drug-induced (salicylate, alcohol)
3. Islet cell adenoma
4. Islet cell hyperplasia
5. Factitious insulin or sulfonylurea
use
6. Beckwith-Wiedemann syndrome
7. Infection
8. Hypothermia
9. Large non-beta cell tumors
10. Fulminant hepatic disease

Childhood

TABLE 28.1: Causes of pediatric hypoglycemia based on age

28
Hypoglycemia in Neonates
and Children

Hypoglycemia in Neonates and Children

Flow chart 28.1: Approach to hypoglycemia in neonates

57

58

Clinical Protocol in Pediatrics

Flow chart 28.2: Diagnostic approach to hypoglycemia in children

29

Adrenal Insufficiency and

Addisonian Crisis

TABLE 29.1: Features of adrenocortical failure caused by adrenal or CNS disease

Adrenalcortical
Disease

HypothalamicPituitary Disease

Biosynthetic Defect
(CAH 21-O Hase)

Deficient hormone(s)

Cortisol
Aldosterone

Cortisol Aldosterone
(Salt wasting variant)

Hyperpigmentation
Serum Na+

Yes
Low (salt wasting)

Serum K+
Serum ACTH
Cortisol response
to IV ACTH
17-OH progesterone
response to IV ACTH

High
High
None

ACTH/CRF Cortisol
(Aldosterone pathway
intact)
No
Mildly low when
patient well (unable
to excrete free water
load)
Normal
Low
Increase

High if salt waster

High
Increase

None

Increase

Exaggerated

Yes
Low if salt waster

Animal Bites

30

TABLE 30.1: Clinical features in furious and paralytic type of rabies

Furious Type (80%)

Paralytic Type (20%)

Tingling/numbness at bite site

Nonspecific symptoms
(Fever, malaise, headache, etc.)
Hydrophobia, Aerophobia
Photophobia
Death in 3-5 days
(Cardiac and respiratory failure)

Tingling/numbness at bite site

Nonspecific symptoms
(Fever, malaise, headache, etc.)
Ascending paralysis
Coma
Death in 7-21 days
(Cardiac and respiratory failure)

TABLE 30.2: Type of contact, exposure and recommended postexposure prophylaxis

Category

Type of contact

Type of
exposure

Recommended postexposure
prophylaxis

Touching or feeding of animals

Licks on intact skin
Nibbling of uncovered skin
Minor scratches or abrasions
without bleeding
Single or multiple transdermal
bites or scratches, licks on
broken skin
Contamination of mucous
membrane with saliva (i.e. licks)

None

None, if reliable case history

is available
Wound management
+
Antirabies vaccine
Wound management
+
Rabies immunoglobulin
+
Antirabies vaccine

II
III

Minor

Severe

Note: After carefully assessing the category of exposure, the treating doctor should evaluate the course of
action to be taken, based on the following general considerations. He should also keep in the mind that with
the presently available safe cell culture rabies vaccines (CCRV), it is always safe to offer treatment rather
than withhold in doubtful situations.

31

Snake Bite

Flow chart 31.1: Snake bite management plan

32

Near Drowning

Flow chart 32.1: Specific management of near

drowing in emergency department

33

Various Poisonings

Flow chart 33.1: Management plan of paracetamol overdose

64

Clinical Protocol in Pediatrics

TABLE 33.1: Elemental iron content of different iron salts

Iron salts

Ferrous sulfate

Elemental iron (%)

Ferrous gluconate Ferrous fumerate Ferrous succinate

20

12

33

35

TABLE 33.2: Toxic doses of iron

Toxicity

Elemental iron
mg/kg of body weight

Serum iron at
4 hours (gm/dL)

Serum iron at 4
hours (mol/L)

Mild
Moderate
Severe
Lethal

<30
>30
>60
>150

110-300
300-500
500
1000

20-55
55-90
>90
>180

TABLE 33.3: Clinical course of iron poisoning in various phases

Phase

Onset and duration

Clinical features

I.

0.5-6 hours

II.

6-24 hours

III.

12-48 hours

IV.

2-4 days

V.

2-8 weeks

Nausea, vomiting, abdominal cramps, dark red vomitus

and stool. Leukocytosis and hyperglycemia. Drowsy, lethargic, comatosed, convulsive, in shock and metabolic
acidosis in severe cases.
Latency. Apparent recovery and false sense of security.
May not be so in severe toxicity.
Severe lethargy, coma, convulsions, shock, GI hemorrhage,
metabolic acidosis, cardiovascular collapse, hepatic and
renal failure, pulmonary edema.
Hepatic failure, encephalopathy, acute lung injury. Monitor liver functions and bilirubin closely.
Stricture formation, gastric and pyloric scarring. Small intestinal necrosis and obstruction in sustained release
preparations. Evaluate with barium contrast studies.

TABLE 33.4: Severity of intoxication as per blood salicylate level

Blood salicylate level (mg/dL) at 6 hours
<50
50-100
>100

Level of severity
Mild
Moderate
Severe

Various Poisonings

Flow chart 33.2: Iron ingestion management plan

65

34

Airway Foreign Body

Flow chart 34.1: Management of airway foreign body

Airway Foreign Body

Flow chart 34.2: Management of complete airway obstruction

67

Zinc metal 32%

24.8%

Manganese dioxide

Zinc/Air

16%

Manganese dioxide

AlkalineManganese
LithiumManganese

0.3%

5%
3%

Mercuric oxide 40%

Silver oxide 39%

Mercury
Silver

Manganese
dioxide

Main constituent

Types

10%

12%

7%
8%

Potassium
hydroxide

7%

14%
13%

Zinc powder
amalgum

1.8%

3%

1.5%

Graphite

TABLE 35.1: Battery types and composition

0.5%

0.5%
0.15%

Zinc
oxide

Propylene
carbonate 6%,
Lithium
perchlorate 1%,
Lithium metal
anode 2%,
Ethylene
glycoldimethyl
ether 4.3%
Carbon black 2%,
Mercury metal 1%

Sodium aluminate
0.05%
Cement 1.5%

Others

35
Button Battery Ingestion

Button Battery Ingestion

Flow chart 35.1: Management plan for button battery ingestion

69

Usually suggests
Croup
Anxiety
Many potential medical and surgical causes
Idiopathic abdominal pain of later childhood
Gastroenteritis, other medical or surgical conditions
Wide variety of medical problems
Epilepsy
Gynecological cause
Systemic disease
Acute neurological problem
Drug overdose, acute neurological condition
Hypocalcemia
Epilepsy variant
Glue ear, congenital deafness
Organic cause
Major systemic illness

Symptom / sign

Acute stridor

Hyperventilation

Acute abdominal pain

Recurrent abdominal pain
(older child)
Acute vomiting

Chronic pain
Seizures

Amenorrhea
Diffuse muscle pain

Limb paralysis
Confusional state
Carpopedal spasm
Complex partial seizure

Deafness
Mutism
Inanition, inability to walk, speak

Hysterical stridor (in a child of 7

years or older)
Asthma. Could be due to either
or both in a child or adolescent
with asthma
Aerophagy due to anxiety
Peptic ulceration, renal
disease, gallstones
Somatization of psychological
symptoms
Underlying depression
Pseudoseizures, associated
with psychological problems
Anorexia nervosa
Hyperventilation due to long
standing anxiety
Conversion disorder
Hysterical fugue
Hyperventilation from anxiety
Masturbatory habit disorder, in
3-5 year olds
Autism spectrum disorders
Selective mutism
Pervasive refusal disorder

May be an indication of

TABLE 36.1: Symptoms and signs which may indicate both medical and psychiatric conditions

36
Psychiatric Assessment
for Nonpsychiatrists

37

Head Trauma

Flow chart 37.1: Head trauma management plan

38

Acute Neck Stiffness

Flow chart 38.1: Diagnostic approach to stiff neck

39

Acute Painful Hip

Flow chart 39.1: Management plan of acute painful hip

40

Spinal Cord Injury and Spinal

Cord Injury without
Radiographic Abnormality
(SCIWORA)

TABLE 40.1: Classification of cervical spine injuries

Mechanisms of injury
1. Flexion
i. Flexion tear drop fracture
ii. Bilateral facet joint dislocation
iii. Atlanto-occipital dislocation
iv. Displaced odontoid fracture
v. Anterior subluxation
vi. Anterior wedge fracture
vii. Clay Shovelers fracture
2. Extension
i. Atlantoaxial dislocation
ii. Hangmans fracture C2
iii. Extension tear drop fracture
3. Rotation
i. Rotary atlantoaxial dislocation
ii. Unilateral facet dislocation
4. Vertical compression
i. Jefferson fracture (burst fracture C1)
ii. Burst fracture vertebral body

Stability
Very unstable
Unstable
Unstable
Unstable
Unstable
Stable
Very stable
Very unstable
Unstable
Unstable (in extension)
Unstable
Stable
Very unstable
Stable

SCIWORA

Flow chart 40.1: Guideline to management

of the potentially injured cervical spine

75

41

Ophthalmological Issues

Flow chart 41.1: Approach to a child with red eye

Otolaryngological Issues

42

TABLE 42.1: Common causes of ear pain in children

Source of pain

Causes

Intrinsic to external ear

Otitis externa
Foreign body
Trauma
Perichondritis infected preauricular cyst or sinus
Acute otitis media
Middle ear effusion
Barotrauma
Mastoiditis
Via trigeminal nerve:
i. Dental
ii. Temporomandibular joint
iii. Jaw
iv. Oral cavity
Via facial nerve:
i. Herpes zoster
ii. Bells palsy
Via glossopharyngeal nerve:
i. Tonsil
ii. Oropharynx
iii. Nasopharynx
Via vagus nerve:
i. Laryngopharynx
ii. Esophagus
iii. Thyroid
Via cervical nerves:
i. Lymphnodes
ii. Cervical spine
iii. Neuralgia
Others:
i. Migraine
ii. Sinuses
iii. Salivary gland
iv. CNS

Intrinsic middle ear and mastoid

Referred

78

Clinical Protocol in Pediatrics

Flow chart 42.1: Treatment of acute otitis media

Fever with Rash

43

TABLE 43.1: Conditions associated with fever and rashes

Cause

Conditions

Viral

Varicella, measles, rubella, roseola, erythema infectiosum, HFM

(Hand, foot and mouth disease usually due to coxsackie B virus),
enteroviral exanthem, HSV infection, infectious mononucleosis, viral
hemorrhagic fever (like dengue), hepatitis B
Scarlet fever, scalded skin syndrome, toxic shock syndrome,
meningococcemia, infective endocarditis, spirochetal infections
(syphilis), leptospirosis, Lyme disease
Systemic lupus erythematosus, systemic onset juvenile rheumatoid
arthritis, vasculitis syndrome (Kawasaki disease, Henoch-Schnlein
purpura), inflammatory bowel disease
Leukemia, lymphoma
Rickettsial, fungal, helminthic and protozoal infections. StevensJohnson syndrome, toxic epidermal necrolysis, histiocytosis
syndrome

Bacterial
Inflammatory diseases
Malignancy
Miscellaneous

TABLE 43.2: Differential diagnosis of rashes

Erythematous

Maculopapular

Petechiae or Purpura

Vesico-bullous

Staphylococcal SSS
Toxic shock syndrome
Anaphylaxis
TEN
Scarlet fever

Viral exanthem
(measles, roseola,
rubella)
Urticaria
Lyme disease
Pityriasis
Drug reaction
Erythema multiforme
Stevens-Johnson
syndrome
Meningococcemia
Rocky Mountain
spotted fever
Eczema, Psoriasis

Meningococcemia
ALL
HSP
TTP
ITP
Vasculitis

Varicella Zoster
HSV
DIC
Pemphigus vulgaris
Bullous pemphigus
Necrotizing fascitis
Contact dermatitis
HFM disease
Stevens-Johnson
syndrome

44

Urticaria and Angioedema

TABLE 44.1: Antihistaminics used in children for urticaria and angioedema

Drug
Sedative
1. Promethazine
2. Chlorpheniramine
3. Hydroxyzine
4. Cyproheptadine
Mild sedative Cetrizine
Nonsedative
1. Fexofenadine
2. Loratadine
3. Levocetrizine

Dose
0.5 mg/kg/dose every 8 hourly
0.35 mg/kg/day
1-2 mg/kg/day
0.2 mg/kg/day
0.25 mg/kg/day
30 mg 12 hourly (6-12 years)
5 mg/day (used above 2 years)
2.5 mg (used above 6 years)

Fever without Focus

45

TABLE 45.1: Observation items to identify a child with SBI

Item

Unwell

Appearance

Sick looking (lethargy, reduced activity) Absent eye contact, does not
recognize parents, no activity
Whimpering
Weak cry, high pitched cry
Slow response, unwilling
Too weak to respond
Drowsy
Frequently falls sleep, difficult
to wake
Slightly dry mouth
Dry mouth, sunken fontanelle,
doughy skin
Peripheral cyanosis or pallor
Mottled pale face or ashen
Briefly smiles and responds
Not smiling, anxious face,
expressionless

Quality of cry
Response to cuddling
Alertness
Hydration
Color
Sociability/stimulation

Very unwell

82

Clinical Protocol in Pediatrics

Flow chart 45.1: Approach to fever with no focus in 0 to 3 months

Fever without Focus

Flow chart 45.2: Approach to a child with fever

without focus 3 to 36 months

83

Severe and
Complicated Malaria

46

TABLE 46.1: Features of severe malaria

a

Frequencya

Prognostic value

Clinical manifestation
+
Prostration
+++
Impaired consciousness
+++
Respiratory distress (acidotic breathing)
+
Multiple convulsions
+++
Circulatory collapse
+++
Pulmonary edema (radiological)
+++
Abnormal bleeding
++
Jaundice
+
Hemoglobinuria
Laboratory findings
+
Severe anemia
+++
Hypoglycemia
+++
Acidosis
+++
Hyperlactatemia
+/Hyperparasitemia
++
Renal impairment
a

+++
+++
+++
+++
+
+/+/+
+/+++
+++
+++
+++
++
+

On a scale from + to +++; +/- indicate infrequent occurrence.

TABLE 46.2: Arteminsinin based combination therapy (ACT)

Body weight

Dose of artemether + lumefantine

5-15 kg
>15-25 kg
>25-35 kg
above 35 kg

20 mg + 120 mg
40 mg + 240 mg
60 mg + 360 mg
80 mg + 480 mg

Dengue

47

TABLE 47.1: Interpretation of dengue IgM and IgG

IgM

IgG

Interpretation

Negative
Negative
Negative
Positive
Positive
Positive

Negative
Positive (Low titer)
Positive (High titer)
Negative
Positive (Low titer)
Positive (High titer)

Early sample
Postdengue infection
Secondary dengue infection
Primary dengue infection
Current or recent dengue infection
Secondary dengue infection

86

Clinical Protocol in Pediatrics

Flow chart 47.1: Volume replacement flow chart of

dengue fever and dengue hemorrhagic fever

Community Acquired
Pneumonia

48

TABLE 48.1: Antibiotics for outpatient treatment of CAP

Age

First line

Second line

3-5 months
>5 months

Amoxicillin
Amoxicillin

Co-amoxyclav
Macrolides / co-amoxyclav

TABLE 48.2: Injectable antibiotics for inpatient treatment of CAP

Age

First line

Second line

<3 months
3 months - 5 years

Cefotaxime/ceftriaxone
Co-amoxyclav/ampicillin

>5 years

Ampicillin/co-amoxyclav/macrolide

Suspected staphylococcus

Cefuroxime/co-amoxyclav/3rd
generation cephalosporin

Add aminoglycoside
Co-amoxyclav/cefotaxim/
ceftriaxone
Cefotaxime/ceftriaxone/
macrolide
Ceftriaxone/cefotaxime/
vancomycin/linezolid

Normal child

20-45 mg/dL

Protein

84 45 mg/dL

46 10 mg/dL

>50

Glucose

viral
10-500

TB

Normal

Partially treated

Low or normal

Polymorphs or
lymphocytes

5-10000

Very high,
High,
100-3000 mg/dL 100-500 mg/dL

Low

Early: Polymorphs Lymphocytes

then lymphocytes

Increased
rarely >1000

100-500 mg/dL 50-200 mg/dL

Low, <50%
of serum

Polymorphs

300-2000

Normal neonate Bacterial

<22
Polymorphs +
lymphocytes

<5

Predominant >75%
cells
lymphocytes

WBC

TABLE 49.1: Interpretation of CSF result

49
Acute Meningitis

50

Urinary Tract Infection

TABLE 50.1: Antimicrobial for oral treatment of UTI

Antimicrobial

Dosage

Trimethoprim-sulfamethoxazole
Amoxicillin/co-amoxyclav
Cephalexin
Cefixime
Cefuroxime axetil
Cefpodoxime

4-6 mg TMP, 20-30 mg SMX/kg/day q12 hours

20-40 mg of amoxicillin/kg/day in 3 doses
50-100 mg/kg/day in 4 doses
8 mg/kg/day in 2 doses
10 mg/kg/day in 2 doses
10 mg/kg/day in 2 doses

TABLE 50.2: Antibiotics for parenteral treatment of UTI

Antibiotic

Daily Dosage

Ceftriaxone
Cefotaxime
Ceftazidime
Gentamicim
Amikacin
Ampicillin

75 mg/ kg/day every 12 hours

150 mg/kg/day divided every 6 hours
150 mg/kg/day divided every 6 hours
7.5 mg/kg/day every 12-24 hours
15 mg/kg/day divided every 12 hours
100 mg/kg/day divided by every 6 hours

Indication

Rationale

Advantage: Less radiation Disadvantage:

Not as sensitive as MCUG does not show
urethral or bladder abnormalities

Rule out renal scarring

To rule out major urinary tract structural pathology

To rule out vesicoureteric reflux
Posterior urethral valve in boys
Anatomical or functional bladder abnormalities

Dosage
2 mg TMP once daily
1 mg/kg dose once daily
25 mg/kg dose once daily

Trimethoprim-sulfamethoxazole
Nitrofurantoin
Cephalexin

TABLE 50.4: Prophylactic antibiotics for prevention of UTI

All children following UTI

i. Acute pyelonephritis
ii. First UTI in a boy or girl <2 years age
iii. First UTI in a child of any age with family
history of UTI, urinary tract abnormalities or
abnormal voiding pattern
Suspected pyelonephritis at young age
Recurrent UTI evidence of vesicoureteric reflux
Used to follow-up vesicoureteric reflux after
initial traditional MCUG

Prophylactic antibiotics

Radionuclide cystogram

DMSA Scan

Ultrasound abdomen
MCUG

Investigation

TABLE 50.3: Follow-up investigations of UTI

90
Clinical Protocol in Pediatrics