Paediatrics Patients’

Management Guidelines
Bugando Medical Centre
Preface

The Department of Paediatrics in Bugando Medical Centre is always striving to

provide the best care possible to all children with whatever illness.
The aim is to reach a standard of care above the minimum standard provided so far.
To reach this goal, a simple, straight forward and a user friendly to use paediatric
protocol has been prepared for use by all, Paediatricians, Residents, Registrars,
Interns, Medical Students and Assistant Medical Officer students while attending
to paediatric patients.
This protocol contains, in summary, the management of the most common
childhood diseases seen in the hospital. Some of these are the most common
causes of death. Diseases like Pneumonia, Malaria, Acute watery diarrhaea, Severe
malnutrition, (Anaemia) and Paediatric HIV/AIDS. The manual is straight
forward and addresses the practical solutions applicable in developing countries
with limited resources.
The Management of some diseases in this book includes the Tanzania National
guidelines - for example, Malaria, Tuberculosis - which may be different from
regimes used in other countries. Every user of this book should find it a very good
quick reference manual and a very good guide for daily practical work.
It is expected that this book will stimulate a steady and progressive improvement
in children’s care and will be a useful tool for practicing doctors and students.

Dr Charles R. Majinge – MD, MMED (Obs/Gynae)

DIRECTOR GENERAL
 4 Paediatrics Patients’ Management Guidelines 5

ADMISSION GUIDELINES
Criteria for Admission to different Wards 06

MALNUTRITION 10

NEONATOLOGY
Neonatal Resuscitation 23
Neonatal Sepsis 30
Prematurity 35

INFECTIOUS DISEASE
Gastroenteritis/Worms/Parasites 53

HIV/AIDS 57
Malaria 64
Introduction Meningitis 70
Pneumonia 74
Tuberculosis 76
Urinary Tract Infection 79
Children constitute more than 45% of the population of most African countries
and mortality and morbidity rates in this population are dramatically high. There CARDIOLOGY
is nothing more to be said to explain why we consider Pediatrics as one of the most Congenital Heart Disease 82
sensitive medical fields in Africa. Heart Failure 88
The lack of healthcare personnel, such as physicians, nurses and midwives, has been Shock 94
reported by the WHO as one serious problem affecting all sub-Saharan countries.
This is particularly true for Tanzania, where the number of medical doctors is about ENDOCRINOLOGY
one in 25,000 inhabitants, and Pediatricians are virtually absent. Diabetes mellitus 99
This is why in 2009, the Bambino Gesù Children’s Hospital decided to start a Diabetes Ketoacidosis 101
partnership with the Bugando Medical Center, and to set-up the postgraduate
Master of Medicine in Pediatrics of the Catholic University of Health and Allied HAEMATOLOGY
Sciences of Mwanza, Tanzania. Anaemia 105
Sickle Cell Anaemia 108
Since then, the cooperation between the two Institutions has been growing steadily,
NEPHROTIC SYNDROME 111
and by now the two partners are working side by side in several pediatric areas, as
it is shown by this handbook of practical protocols and guidelines, which represent
SEIZURES AND EPILEPSY 116
one of the most tangible outcomes of the joint efforts of physicians and scholars
from the two Institutions. PULMONARY
“Teaching together, learning together” is the motto of our medical joint-venture in Asthma 122
Mwanza. Neonatal RDS 124
There is a lot of work to be done, but I am sure we are on the right track for the
success of this joint project. BURKITT’S LYMPHOMA 127

I thank all those who are working in this project for their commitment and PROCEDURES
dedication. Insertion of a Chest Tube 130
Insertion of an Intraosseous Line 132
Lumbar Puncture 134
Prof. Giuseppe Profiti
President of the Bambino Gesù Children’s hospital Rome - Italy TABLES 136
Child’s weight-for-age WHO tables
Hearth and Respiratory rate
Blood pressure
 6 Admission Paediatrics Patients’ Management Guidelines 7

Admission Guidelines inquire if any family members had problems after taking certain medications or
eating certain foods...)

Social History:
TRIAGE: • who does the patient live with, how many siblings, the health of the siblings,
and environmental risk factors
Look for emergency sign: if present MANAGE
Admission history and physical, required work-up for all patients, required Allergies:
admission orders, and criteria for admission to different wards • any known food or drug allergies and what the reaction is

History: Physical:
Chief complaint: stated in patient or parent’s own words General Condition: comment on comfort, any obvious distress. AVPU: Alert;
Voice; Pain; Unconsciousness
History of Present Illness:
• the first sentence should include the sex and AGE of the patient as well as any Vital Signs: temperature, heart rate, respiratory rate, blood pressure, oxygen
pertinent medical problems (i.e. This is a 4 yo male with sickle cell disease who saturation if available.
presents with...)
• include symptoms, duration, quality, alleviating or aggravating features, if it Anthropometric Measurements: weight, height, head circumference if <2 years
has happened before old or concern for macrocephaly, weight for height
• also include any pertinent positive and/or negative review of systems (ask
everyone about fever, weight loss, fatigue, night sweats) HEENT:
• head: size, shape
Past Medical History: • eyes: pupillary reflex, any discharge or conjunctivitis, color of sclera
• birth hystory includes gestational age, mode of delivery (if c-section, know • ears: any obvious deformities
why!), any resuscitation needed, any complications during pregnancy, any • nose: any discharge or other abnormalities
known maternal illnesses, any maternal medications • throat: any oral lesions or erythema, dry or moist mucous membranes?
• medical hystory include all known medical conditions (i.e. Sickle cell, IDS, Tb);
all past admissions commenting on date, length of admission, reason for and Skin: comment on color, any rashes, any abnormalities
diagnosis during admission, and any treatment given during admission
• surgical hystory include all surgeries if any, why they were done, and when they Lymph nodes: comment on any lymphadenopathy, location, quality
were done - GU: comment on external genitalia (normal or not), in males comment if
circumcised or not, if testes are descended
Medication: - Rectal: must be done in any patient with suspected constipation!!
• include all current medications and doses including any natural or home remedies
SISTEMIC EXAMINATION:
Diet:
• in young infant must specify if breastfeeding or bottle feeding, the quantity and Cardiac: regular or irregular heartbeat, any abnormal heart sounds (S3, S4),
frequency of feeds, when the patient was weaned murmur? If murmur, specify if systolic, diastolic, or both, where it is best heard,
• in older patients ask details about diet – well balanced? what the quality is (harsh, soft, musical, etc.
Developmental History: Respiratory: observe first for any obvious signs of resp distress – recessions,
• comment of developmental milestones, it is NOT enough to state the patient grunting, nasal flaring, then listen – comment on location of any crepitations or
is developmentally appropriate, must include what is appropriate and not wheezes.
appropriate.
Abdominal: observe first for any obvious abnormalities, auscultate, palpate, feel for
Immunizations: organomegaly
• include all immunizations received and proof of documentation - GU: comment on external genitalia (normal or not), in males comment if
circumcised or not, if testes are descended
Family History: - Rectal: must be done in any patient with suspected constipation!!
• include any pertinent family history (i.e. in a patient with suspected hemolysis
 8 Admission Paediatrics Patients’ Management Guidelines 9

Extremities: comment if warm or cool, any edema, pulses present, length of

capillary refill. Criteria for Admission
Neuro: include cranial nerves, motor (strength and tone), sensory, reflexes, and
to different Wards
cerebellar exam
Neonatal ICU:
Required Investigations: All neonates with emergency signs.
ALL patients MUST have a FBP and ESR!! Birth Weight less than 1.2 kg
ALL patients with any respiratory distress and/or abnormal lung findings MUST Any very sick neonate referred from peripheral hospital
have a CXR!! Neonate requiring close care / observation following surgery.
Any neonate that needs more frequent monitoring or speciality care that cannot be
Impression: state your working diagnosis and any other diagnoses provided in premature unit, related with resolvable diseases.
Plan: include investigations and any treatment ordered PICU / Adult ICU:
Any child older than 1-month-old with acute emergency signs.
Any child older than 1-month-old requiring close observation following surgery.
Admission Orders: Any ill child requiring more frequent monitoring or speciality care that cannot be
provided on paediatrics wards, related with acute or resolvable diseases.

Premature Unit:
Admit to which ward, date and time of admission, who should the nurses call if Any child born older than 1.2 kg with no emergency cares but requires observation
they have questions with the patient. due to fever, low birth weight, or other clinical sign or symptoms.
Working Diagnosis For care, if mother had complications during delivery and cannot take care of her
Condition at Admission (good, fair, serious, critical) child immediately after birth, and if mother is unable to breastfeed immediately
Vital signs parameters (how often vitals need to be taken, and what vital signs then child can be fed properly in premature unit.
nurses should call the intern with, depends on age of patient such as call if Neonates that were born at home or referred from outside facility without
respiratory rate > 60, temp greater 38C, etc.) emergency signs (only priority signs or non-urgent signs).
Activity: either as tolerated or specify such as left lateral position, knee chest
position, elevate head of bed, or frequent rotations to prevent ulcers. Paediatric Wards:
Nursing Orders: Record Ins and Outs accurately and call intern if decreased urine Any sick child older than 1 month of age that does not require ICU care.
output, change dressing every how often, etc. If patients condition changes, then patient must be transferred to ICU immediately.
Diet: NPO or specify type of feeding and how often (ex. Breastfeeding, EBM, high
protein diet, ORS-which plan?) Malnutrition Ward: for children presenting with features.
Allergies: which medications or foods in the patient allergic to and what allergic
reaction has the patient had in the past? EMERGENCY SIGNS: PRIORITY SIGNS:
IVF: Type of IVF (ex. RL, Normal saline, Dextrose 5%, etc), volume that should be • Central Cyanosis • Signs of malnutrition such as
infused per hour. • Severe Respiratory Distress wasting, Kwashiorkor dermatitis, etc
Medications: name of medications to be given in hospital, route of administration • Obstructed Breathing • Respiratory distress (mild)
(IV, oral, IM, per rectum), dosage and dosing interval, duration (PRN vs. number • Hypoxia • Pallor
days to give medications). • Signs of Shock (poor perfusion, • Mild dehydration
Labs: All patients need a FBP and ESR. Any specific investigations that the cool extremities, decreased pulses) • Persistent fever
patient being admitted requires such as a renal function panel, liver function tests, • Change in Mental Status: lethargy, • Oedema
etc. How often the labs should be drawn? (ex. Once on admission, daily, every unconsciousness, Coma • Any sick young infant less
monday, etc) • Severe Dehydration 2 months of age
Studies: Perform a chest X-ray in any patient with respiratory symptoms on • Bradycardia
history or an abnormal lung exam or increased work of breathing. Other studies to • Signs of sepsis: hypotension,
consider: echocardiogram, ultrasound, head CT, etc.) petechia, high fever, sign of shock
Consultations: Which services should be consulted on admission such as ENT,
pediatric surgery, etc and reason for consultation. Sign and fill out consultation form.
 10 Paediatrics Patients’ Management Guidelines 11

INVESTIGATIONS

1) Weight and height (document weight for height % on ALL patients)

2) Random blood glucose

Malnutrition
3) FBP
4) Blood slide for malaria parasites
5) Stool for ova and parasites
6) Urine analysis
7) Specific labs or imaging studies based on the history and physical exam

Treatment of Malnutrition
DEFINITION
PHASE ONE
Malnutrition is a clinical syndrome, due to a deficiency of protein, micronutrients,
or calories. Goal - To identify and treat major problems and to initiate re-feeding
It is a major cause of mortality and morbidity worldwide. 52% of under fives
deaths are attributable to malnutrition. 1) FEEDING
• 8 feeds per day (see appendix for ml for each feed), including feeds at night
• Breastfed children should be offered breast-milk before the diet and
ADMISSION CRITERIA FOR INFANTS MORE THAN on demand
6MONTHS TO 18YEARS • Diet: F75 (130ml = 100kcal) for all ages except < 6 month old infant
• A naso-gastric tube (NGT) should be inserted for feeding if the child: is
1. Children with severe acute malnutrition (SAM) taking < 75kcal/kg/day by mouth, is tachypneic, has painful mouth ulcers,
2. Children with moderate acute malnutrition(MAM) with complications has a disturbed level on consciousness

• Severe acute malnutrition (severe wasting) is defined as: 2) ROUTINE MEDICATIONS

• Weight for height/length <70% or <-3SDs of the median reference value. • Vitamin A (on day 1, and if the child present with sign of Vitamin A
• Mid-Upper Arm Circumference (MUAC) <11.5 cm deficiency repeat the dose on day 2 and day 14)
• Oedema of both feet - 6-11 months: 100,000 IU
• Moderate acute malnutrition (moderate wasting) is defined as: - > 12 months (or > 8kg): 200,000IU
• Weight for height/length from 70 to 79.9% or from -3SD to <-2SD or 2) Folic acid
• MUAC is from 11.5 to < 12.5cm • 5mg as a single dose
• With no oedema • Antibiotics: given to every patient for the entire length of Phase 1 + 4 days;
• Complications in malnutrition is defined as: to be given
• Vomiting - If the child has no complications and is not seriously ill - Amoxicillin 15 mg
• Hypothermia: axillary’s temperature < 35°C or rectal < 35.5°C per kg 8 hourly .
• Fever > 38°C - If the child is severely ill (apathetic, lethargic) or has complications, - IV/IM
• Respiratory distress - Ampicillin AND Gentamicin. The doses are:
• Extensive skin lesions/ infection - Ampicillin: 50mg/kg body weight IV/IM 6-hourly per dose
• Very weak, lethargic, unconscious - Gentamicin: 7.5mg/kg body weight IV/IM once daily
• Fitting/convulsions - In addition, give Metronidazole orally 7.5mg/kg body weight 8-hourly
• Severe dehydration based on history & clinical signs for 7 days to all children with persistent diarrhoea (diarrhoea lasting 14
• Any condition that requires an infusion or NG tube feeding. days or more).
• Very pale (severe anemia) - If child improves after 48 hours continue with oral Ampicilin and IM
• Jaundice Gentamicin in the same doses as above to complete the course of treatment.
• Other general signs the clinician thinks warrants transfer to the - If child fails to improve after 48 hours: Continue IV/IM Ampicillin
in-patent facility. and Gentamicin as above and ADD Chloramphenicol 25mg/kg
body weight 8 hourly IV/IM for 5 days, OR

 12 Malnutrition Paediatrics Patients’ Management Guidelines 13

- Stop Ampicillin and Gentamicin and start any third-generation intakes and IV fluids. Give a diuretic (Frusomide 1mg/kg IV
cephalosporin for a duration of 10 – 14 days. slowly) to make room for the blood. Transfuse whole blood
• Malaria treatment: see malaria guidelines for medication dosing. 10 ml/Kg slowly over 3 hours
Use IV quinine with caution. c. If there are signs of heart failure, give packed red cells 5 mls/kg
• Give measles vaccine for children > 6 months who have not been vaccinated.
On admission, and for those more than nine months at discharge give • CONGESTIVE HEART FAILURE
a second dose, if first dose was before nine months. - The onset of respiratory distress in a child with malnutrition should be
presumed to be due to heart failure!! (not simply pneumonia)
3) SURVEILLANCE - Treatment:
• Follow daily weights 1) Stop all oral and IV fluid even if this takes 24-48hours.
• Assess degree of edema daily as well as standard clinical exam 2) Give Small amounts of sugar-water can be given orally to prevent
• Body temperature twice daily hypoglycaemia.
• Measure height after 21 days 3) Give furosemide SINGLE dose (1mg/kg).
4) Digoxin can be given in SINGLE dose (5 micrograms/kg)
4) TREATMENT AND PREVENTION OF COMPLICATIONS
• HYPOGLYCAEMIA (blood sugar less than 3mmol/l or 54mg/Dl) • SEVERE ANAEMIA
- Signs of hypoglycaemia in malnourished child: hypothermia, lethargy, - If Hb < 40 g/l, give 10ml/kg packed RBC or whole blood over 3 hours
limpness, loss of consciousness - Fast for 3 hours after BT
- Treat: 50ml of 10% dextrose by mouth of via NGT (if unconscious, give - If signs of heart failure are present, DO NOT give blood transfusion
via NGT and give 5ml/kg 10% dextrose IV solution) - Do not give iron during Phase 1
- If no improvement in clinical condition in 10 minutes, consider other cause
• HYPOTHEMIA (rectal temp < 35.5°C, arm temp < 35°C) • SKIN LESIONS
- Do not bathe on admission (later, wash quickly during the warmest part - Keep open and dry
of the day) or allow to lie in wet clothes/blanket - Zinc paste + oral zinc supplementation
- Place hat on child, sleep in bed with caretaker
- “Kangaroo method”: place on caretaker’s bare chest and cover with Criteria to pass to Transition Phase
blankets, have caretaker drink hot water/tea • Return of appetite
• DEHYDRATION AND SEPTIC SHOCK • beginning of loss of edema
- Give oral rehydration for Malnourished children(ReSoMal, not ORS) • NEVER pass a child to the transition phase with an NGT, IV fluids or ReSoMal
1. 50-100ml/kg of ReSoMal over 10 hours (start with 5ml/kg every
30 minutes x 2 hours then 5-10ml/kg/hr)
2. Reassess the patient EVERY HOUR and document weight, TRANSITION PHASE
respiratory rate and pulse rate.
3. If signs of dehydration resolve or the weight increases to the goal Goal: to slowly introduce feeds that have a higher sodium content while avoiding
weight, stop rehydration fluid sodium retention and heart failure
- IV fluids NOT recommended UNLESS: severe shock with loss of Feeds are continued in the same frequency and volume as in Phase 1 (8 feeds/24
consciousness from confirmed dehydration hours) but increased from F75 to F100
1. 15ml/kg Ringer-Lactate with 5% Dextrose IV over 1 hour then Calories: ~130kcal/kg/day
reassess (and document weight and exam) Marasmic children should gain 5-7g/kg/day in the transition phase
2. If improvement, repeat the 15ml/kg IV of the same solution over the
next hour Criteria to move back to Phase 1:
3. As soon as the child regains consciousness of the HR normalizes, stop • Need for IV fluids, oral rehydration solution, or an NG tube
IV fluids and begin NG rehydration • Weight gain > 10g/kg/day in kwashiorkor children
4. Measure and record pulse and respirations every 10 minutes; (concern for fluid retention)
for 1 hour; • Development of tense abdominal distension, edema, increased liver size,
5. Then switch to oral or NG rehydration with ReSoMal diarrhea with associated weight loss
(Give 5-10 ml/kg in alternate hours with F75 for up to 10 hours)
6. If no improvement, presume septic shock ; Continue giving Criteria to pass to Phase 2:
IV antibiotics to cover both gram positive and gram negative • Good appetite
a. Give maintenance IV fluids (4ml/kg/h) while waiting for blood • Minimum of 2 days in Transition Phase for marasmic patients
b. Order fresh whole blood .When blood is available, stop all oral • Resolution of edema in kwashiorkor patients
 14 Malnutrition Paediatrics Patients’ Management Guidelines 15

PHASE TWO Stimulate breastfeeding

• Breastfeed every 3 hours for at least 20 minutes
Goal: Promote rapid catch-up weight gain and restore normal weight as quickly as (more often if child wants more/cries)
possible • About 1 hour after breast feeding, give maintenance amounts of
Intake is not limited, gain weight rapidly (~20g/kg/day), should not have edema F100 diluted—130kcal/kg/day (or if has edema, F75) using the
Calories: ~ 200kcal/kg/day supplementary suckling technique for 8 feeds/day (see appendix)

Criteria to move back to Phase 1 or Transition Phase: Supplementary suckling technique

• Edema • Supplementation given using a 5-8 French NGT placed beside the nipple
• Major illness (especially during the 1st week) • Infant suckles normally but receives nutrition from end of NGT
• Diarrhoea with weight loss (though simulates breastfeeding)

Steps to be taken during Phase 2 Monitor daily weights

• Give the correct amount of food • If the infant looses weight over 3 consecutive days yet seems hungry,
- F100 (100ml = 100kcal) add 5mls to each feed
- 6 feeds/day if < 8kg, no porridge • If the infant is gaining weight at 20g per day, decreased the quantity of
- 6 feeds/day + 1 porridge (100ml = 100kcal) if > 8kg (approx 24 months) diluted F100 to ½ maintenance. If maintains weight gain, stop
- See appendix for amount to be offered at each feed (NOT force-fed) supplementing (if not maintained, increase to ¾ of maintenance).
• Give routine medications
- `Iron: 1 crushed tablet ferrous sulphate (200mg)/package F100 used Give routine medications:
- Mebendazole if > 1 year (1-2 years 250mg; >2 years 200mg x3 days) • Vitamin A : 50,000 IU at admission
• Maintain good surveillance • Folic acid: 2.5mg as a single dose on admission
- Measure weight, document edema every other day or 3x/week • Iron: when the child suckles well and starts to grow
- Measure height every 3 weeks • Antibiotics: orally Amoxicillin 60mg/kg/day in 3 divided doses
- Measure body temperature each morning Continue until 4 days after the infant has started to gain weight
- Involve and counsel the family in care
• Identify any failure to respond to treatment Ensure appropriate care of mother
• Provide emotional/psychosocial support and encouragement
Criteria to progress to Discharge • Needs to drink at least 2 liters per day
• If > 6 months: weight for length ≥ 85% for 2 consecutive weights and • Needs to eat at least 2500kcal/day
no edema for 10 days • Administer Vitamin A to the mother (200,000 IU if the mother’s infant is < 2
• Give 2nd measles vaccine prior to discharge if > 9 months old months, 25,000 IU weekly if the infant is > 2 months)
Keep the infant for 5 days on breast milk alone to make sure they continue to gain
weight then discharge (regardless of weight for length)

Infants < 6 months INFANTS WITHOUT ANY PROSPECTIVE OF BEING

with severe Malnutrition BREAST FED

Criteria for Admission:

Weight for height < 70% or presence of bilateral edema
INFANTS WITH PROSPECTS OF BEING BREAST FED
Treatment according to the standard protocol for managing children with
Goal: Re-establish full and exclusive breast feeding of a quality that allows for
malnutrition with the following changes:
catch-up growth on breast milk alone
• Phase 1: give diluted F100 unless edema present, then give F75
The goal is NOT to have infants regain weight to over 85% of weight for height
• Transition Phase: give diluted F100
• Phase 2: offer twice the volume of diluted F100 than was given during Phase 1
Criteria for admission:
• Infant is too weak to suck effectively (any weight for height)
Discharge Criteria:
• Mother reports she does not have enough milk to feed her child
• Switch to infant formula(or animal milk) when weight for height > 85%
• Infant is not gaining weight at home
• Stable and gaining weight on infant formula(or animal milk) for 2 days
• Infant shows signs of malnutrition (weight for length < 70%, bilateral edema)
• Follow up plan in place (monthly)
 16 Malnutrition Paediatrics Patients’ Management Guidelines 17

FOLLOW-UP Weight for Height Reference Card

• Need close follow-up and nutritional support for at least 4 months
after recovery Boys’ weight (kg) Girls’ weight (kg)
-4SD -3SD -2SD -1SD Median Length Median -1SD -2SD -3SD -4SD
• Outpatient visits at least every 14 days for the 1st two months then monthly 60% 70% 80% 90% (cm) 90% 80% 70% 60%
for the next two months. 7.6 8.5 9.4 10.2 11.1 81 10.8 9.9 9 8.1 7.2
7.8 8.7 9.6 10.4 11.3 82 11 10.1 9.2 8.3 7.4
References: 7.9 8.8 9.7 10.6 11.5 83 11.2 10.3 9.4 8.5 7.6
1. Management of Acute Malnutrition as Health facility: Tanzanian National 8.1 9 9.9 10.8 11.7 84 11.4 10.5 9.6 8.7 7.7
Guidelines. The United Republic of Tanzania, Ministry of Health and Social 7.8 8.9 9.9 11 12.1 85 11.8 10.8 9.7 8.6 7.6
Welfare: 2009. 7.9 9 10.1 11.2 12.3 86 12 11 9.9 8.8 7.7
2. World Health Organisation: Management of severe malnutrition: A Manual for 8.1 9.2 10.3 11.5 12.6 87 12.3 11.2 10.1 9 7.9
8.3 9.4 10.5 11.7 12.8 88 12.5 11.4 10.3 9.2 8.1
Physicians and other Senior Health workers. WHO. Geneva: 1999. 8.4 9.6 10.7 11.9 13 89 12.7 11.6 10.5 9.3 8.2
8.6 9.8 10.9 12.1 13.3 90 12.9 11.8 10.7 9.5 8.4
8.8 9.9 11.1 12..3 13.5 91 13.2 12 10.8 9.7 8.5
Weight for Height Reference Card 8.9 10.1 11.3 12.5 13.7 92 13.4 12.2 11 9.9 8.7
9.1 10.3 11.5 12.8 14 93 13.6 12.4 11.2 10 8.8
Boys’ weight (kg) Girls’ weight (kg) 9.2 10.5 11.7 13 14.2 94 13.9 12.6 11.4 10.2 9
-4SD -3SD -2SD -1SD Median Length Median -1SD -2SD -3SD -4SD 9.4 10.7 11.9 13.2 14.5 95 14.1 12.9 11.6 10.4 9.1
60% 70% 80% 90% (cm) 90% 80% 70% 60% 9.6 10.9 12.1 13.4 14.7 96 14.3 13.1 11.8 10.6 9.3
1.8 2.1 2.5 2.8 3.1 49 3.3 2.9 2.6 2.2 1.8 9.7 11 12.4 13.7 15 97 14.6 13.3 12 10.7 9.5
1.8 2.2 2.5 2.9 3.3 50 3.4 3 2.6 2.3 1.9 9.9 11.2 12.6 13.9 15.2 98 14.9 13.5 12.2 10.9 9.6
1.8 2.2 2.6 3.1 3.5 51 3.5 3.1 2.7 2.3 1.9
10.1 11.4 12.8 14.1 15.5 99 15.1 13.8 12.4 11.1 9.8
1.9 2.3 2.8 3.2 3.7 52 3.7 3.3 2.8 2.4 2
10.3 11.6 13 14.4 15.7 100 15.4 14 12.7 11.3 9.9
1.9 2.4 2.9 3.4 3.9 53 3.9 3.4 3 2.5 2.1
2 2.6 3.1 3.6 4.1 54 4.1 3.6 3.1 2.7 2.2 10.4 11.8 13.2 14.6 16 101 15.6 14.3 12.9 11.5 10.1
2.2 2.7 3.3 3.8 4.3 55 4.3 3.8 3.3 2.8 2.3 10.6 12 13.4 14.9 16.3 102 15.9 14.5 13.1 11.7 10.3
2.3 2.9 3.5 4 4.6 56 4.5 4 3.5 3 2.4 10.8 12.2 13.7 15.1 16.6 103 16.2 14.7 13.3 11.9 10.5
2.5 3.1 3.7 4.3 4.8 57 4.8 4.2 3.7 3.1 2.6 11 12.4 13.9 15.4 16.9 104 16.5 15 13.5 12.1 10.6
2.7 3.3 3.9 4.5 5.1 58 5 4.4 3.9 3.3 2.7 11.2 12.7 14.2 15.6 17.1 105 16.7 15.3 13.8 12.3 10.8
2.9 3.5 4.1 4.8 5.4 59 5.3 4.7 4.1 3.5 2.9 11.4 12.9 14.4 15.9 17.4 106 17 15.5 14 12.5 11
3.1 3.7 4.4 5 5.7 60 5.5 4.9 4.3 3.7 3.1 11.6 13.1 14.7 16.2 17.7 107 17.3 15.8 14.3 12.7 11.2
3.3 4 4.6 5.3 5.9 61 5.8 5.2 4.6 3.9 3.3 11.8 13.4 14.9 16.5 18 108 17.6 16.1 14.5 13 11.4
3.5 4.2 4.9 5.6 6.2 62 6.1 5.4 4.8 4.1 3.5 12 13.6 15.2 16.8 18.3 109 17.9 16.4 14.8 13.2 11.6
3.8 4.5 5.2 5.8 6.5 63 6.4 5.7 5 4.4 3.7 12.2 13.8 15.4 17.1 18.7 110 18.2 16.6 15 13.4 11.9
4 4.7 5.4 6.1 6.8 64 6.7 6 5.3 4.6 3.9
4.3 5 5.7 6.4 7.1 65 7 6.3 5.5 4.8 4.1 SD = standard deviation score or Z-score; although the interpretation of a fixed percent-of-median value
4.5 5.3 6 6.7 7.4 66 7.3 6.5 5.8 5.1 4.3 varies across age and height, and generally the two scales cannot be compared; the approximate percent-
of-the median values for -1 and -2SD are 90% and 80% of median respectively (Bulletin of the World
4.8 5.5 6.2 7 7.7 67 7.5 6.8 6 5.3 4.5 Health Organization, 1994, 72: 273–283).
5.1 5.8 6.5 7.3 8 68 7.8 7.1 6.3 5.5 4.8 Length is measured below 85 cm; height is measured 85 cm and above. Recumbent length is on average
5.3 6 6.8 7.5 8.3 69 8.1 7.3 6.5 5.8 5 0.5 cm greater than standing height, although the difference is of no importance to the individual child.
A correction
5.5 6.3 7 7.8 8.5 70 8.4 7.6 6.8 6 5.2 may be made by deducting 0.5 cm from all lengths above 84.9 cm if standing height cannot be
5.8 6.5 7.3 8.1 8.8 71 8.6 7.8 7 6.2 5.4 measured.
6 6.8 7.5 8.3 9.1 72 8.9 8.1 7.2 6.4 5.6
6.2 7 7.8 8.6 9.3 73 9.1 8.3 7.5 6.6 5.8
6.4 7.2 8 8.8 9.6 74 9.4 8.5 7.7 6.8 6
6.6 7.4 8.2 9 9.8 75 9.6 8.7 7.9 7 6.2
6.8 7.6 8.4 9.2 10 76 9.8 8.9 8.1 7.2 6.4
7 7.8 8.6 9.4 10.3 77 10 9.1 8.3 7.4 6.6
7.1 8 8.8 9.7 10.5 78 10.2 9.3 8.5 7.6 6.7
7.3 8.2 9 9.9 10.7 79 10.4 9.5 8.7 7.8 6.9
7.5 8.3 9.2 10.1 10.9 80 10.6 9.7 8.8 8 7.1

SD = standard deviation score or Z-score; although the interpretation of a fixed percent-of-median value
varies across age and height, and generally the two scales cannot be compared; the approximate percent-
of-the median values for -1 and -2SD are 90% and 80% of median respectively (Bulletin of the World
Health Organization, 1994, 72: 273–283).
Length is measured below 85 cm; height is measured 85 cm and above. Recumbent length is on average
0.5 cm greater than standing height, although the difference is of no importance to the individual
child. A correction may be made by deducting 0.5 cm from all lengths above 84.9 cm if standing height
cannot be measured.
 18 Malnutrition Paediatrics Patients’ Management Guidelines 19

F-75 Reference Card − Volume to give for F-75 Reference Card for children with Severe
different weights (No oedema) (+++) Oedema

Weight of Volume of F-75 per feed (ml)* Daily total 80% of daily Weight with Volume of F-75 per feed (ml)
Daily total 80% of daily
child (kg) (130 ml/kg) total +++ oedema (100 ml/kg) total
Every 2 hours** Every 3 hours Every 4 hours (minimum) (kg) Every 2 hours
Every 3 hours Every 4 hours (minimum)
(12 feeds) (8 feeds) (6 feeds) (12 feeds)
(8 feeds) (6 feeds)
2.0 20 30 45 260 210 3.0 25 40 50 300 240
2.2 25 35 50 286 230 3.2 25 40 55 320 255
2.4 25 40 55 312 250 3.4 30 45 60 340 270
2.6 30 45 55 338 265 3.6 30 45 60 360 290
2.8 30 45 60 364 290 3.8 30 50 65 380 305
3.0 35 50 65 390 310 4.0 35 50 65 400 320
3.2 35 55 70 416 335 4.2 35 55 70 420 335
3.4 35 55 75 442 355 4.4 35 55 75 440 350
3.6 40 60 80 468 375 4.6 40 60 75 460 370
3.8 40 60 85 494 395 4.8 40 60 80 480 385
4.0 45 65 90 520 415 5.0 40 65 85 500 400
4.2 45 70 90 546 435 5.2 45 65 85 520 415
4.4 50 70 95 572 460 5.4 45 70 90 540 430
4.6 50 75 100 598 480 5.6 45 70 95 560 450
4.8 55 80 105 624 500 5.8 50 75 95 580 465
5.0 55 80 110 650 520 6.0 50 75 100 600 480
5.2 55 85 115 676 540 6.2 50 80 105 620 495
5.4 60 90 120 702 560 6.4 55 80 105 640 510
5.6 60 90 125 728 580 6.6 55 85 110 660 530
5.8 65 95 130 754 605 6.8 55 85 115 680 545
6.0 65 100 130 780 625 7.0 60 90 115 700 560
6.2 70 100 135 806 645 7.2 60 90 120 720 575
6.4 70 105 140 832 665 7.4 60 95 125 740 590
6.6 75 110 145 858 685 7.6 65 95 125 760 610
6.8 75 110 150 884 705 7.8 65 100 130 780 625
7.0 75 115 155 910 730 8.0 65 100 135 800 640
7.2 80 120 160 936 750 8.2 70 105 135 820 655
7.4 80 120 160 962 770 8.4 70 105 140 840 670
7.6 85 125 165 988 790 8.6 70 110 145 860 690
7.8 85 130 170 1014 810 8.8 75 110 145 880 705
8.0 90 130 175 1040 830 9.0 75 115 150 900 720
8.2 90 135 180 1066 855 9.2 75 115 155 920 735
8.4 90 140 185 1092 875 9.4 80 120 155 940 750
8.6 95 140 190 1118 895 9.6 80 120 160 960 770
8.8 95 145 195 1144 915 9.8 80 125 165 980 785
9.0 100 145 200 1170 935 10.0 85 125 165 1000 800
9.2 100 150 200 1196 960 10.2 85 130 170 1020 815
9.4 105 155 205 1222 980 10.4 85 130 175 1040 830
9.6 105 155 210 1248 1000 10.6 90 135 175 1060 850
9.8 110 160 215 1274 1020 10.8 90 135 180 1080 865
10.0 110 160 220 1300 1040 11.0 90 140 185 1100 880
11.2 95 140 185 1120 895
11.4 95 145 190 1140 910
*Volumes in these columns are rounded to the nearest 5 ml. **Feed 2-hourly for at least the first day. 11.6 95 145 195 1160 930
Then, when little or no vomiting, modest diarrhoea (<5 watery stools per day), and finishing most
feeds, change to 3-hourly feeds. 11.8 100 150 195 1180 945
12.0 100 150 200 1200 960
 20 Malnutrition Paediatrics Patients’ Management Guidelines 21

F-100 Reference Card: Preparation of F100-Diluted

Volume ranges for F100 feeding F100-Diluted is used to treated infants aged <6 months who are severely acutely
malnourished and have no oedema. The preparation is as follows:
Weight of Range of volumes per Range of volumes per Range of daily volumes
child (kg) 3-hourly feed of F-100 4-hourly feed of F-100 of F-100 For large number of children
(8 feeds daily) * (6 feeds daily) * • Add packet of F100 to 2.7 litres of water, instead of 2 litres. This is referred to as
Minimum Maximum Minimum Maximum Minimum Maximum “F100-Diluted”
ml ml ml ml ml (150 ml/ ml (220 ml/ For small number of children
kg/day) kg/day) • Add 35ml of water to 100ml of F100 already prepared, and that will give 135ml
2.0 40 55 50 75 300 440 of F100-Diluted. Discard any excess milk after use. Do not make smaller quantities.
2.2 40 60 55 80 330 484 • If you need more than 135ml, use 200ml of F100 and add 70ml of water, to
2.4 45 65 60 90 360 528 make 270ml of F100-Diluted and discard any excess milk after use.
2.6 50 70 65 95 390 572
2.8 55 75 70 105 420 616
3.0 55 85 75 110 450 660
3.2 60 90 80 115 480 704 MAINTANANCE AMOUNT OF DILUTED F100 FOR INFANTS
3.4 65 95 85 125 510 748 LESS
3.6 70 100 90 130 540 792 THAN 6 MONTHS WHO ARE BREASTFED
3.8 70 105 95 140 570 836
4.0 75 110 100 145 600 880 Weight (kg) Volume per feed Daily total
4.2 80 115 105 155 630 924
4.4 85 120 110 160 660 968 (8 feed per day)
4.6 85 125 115 170 690 1012 <1.2kg 25 200
4.8 90 130 120 175 720 1056
5.0 95 140 125 185 750 1100
1.3-1.5 30 240
5.2 100 145 130 190 780 1144 1.6-1.7 35 280
5.4 100 150 135 200 810 1188 1.8-2.1 40 320
5.6 105 155 140 205 840 1232
5.8 110 160 145 215 870 1276 2.2 – 2.4 45 360
6.0 115 165 150 220 900 1320 2.5 – 2.7 50 400
6.2 115 170 155 230 930 1364
6.4 120 175 160 235 960 1408 2.8 – 2.9 55 440
6.6 125 180 165 240 990 1452 3.0 – 3.4 60 480
6.8 130 180 170 250 1020 1496
7.0 130 195 175 255 1050 1540 3.5 – 3.9 65 520
7.2 135 200 180 265 1080 1588 4.0 – 4.4 70 560
7.4 140 205 185 270 1110 1628
7.6 145 210 190 280 1140 1672
7.8 145 215 195 285 1170 1716
8.0 150 220 200 295 1200 1760
8.2 155 225 205 300 1230 1804
8.4 158 230 210 310 1260 1848
8.6 160 235 215 315 1290 1892
8.8 165 240 220 325 1320 1936
9.0 170 250 225 330 1350 1980
9.2 175 255 230 335 1380 2024
9.4 175 260 235 345 1410 2068
9.6 145 265 240 350 1140 2112
9.8 185 270 245 360 1470 2156

10.0 190 275 250 365 1500 2200
 22 Malnutrition 23

Amounts of F100-Diluted or F75 to give to an

infant aged <6 months who is not breastfed

Phase 1: Stabilization Phase

Bodyweight (kg)

≤ 1.5
Volume of F100-Diluted or
F75 if 8 feeds per day* (ml)
30
Daily volume (ml)

240
Neonatology
1.6 – 1.8 35 280
1.9 – 2.1 40 320
2.2 – 2.4 45 360
2.5 – 2.7 50 400
2.8 – 2.9 55 440
3.0 – 3.4 60 480 · Neonatal Resuscitation
3.5 – 3.9 65 520 · Neonatal Sepsis
4.0 – 4.4 70 560
· Prematurity
Transition Phase

Bodyweight (kg) Volume of F100-Diluted or Daily volume (ml)

F75 if 8 feeds per day* (ml)
≤ 1.5 45 360 Newborn Resuscitation
1.6 – 1.8 53 424
1.9 – 2.1 60 480
Background
2.2 – 2.4 68 544 Neonatal resuscitation is most effective when performed by a designated team.
2.5 – 2.7 75 600
2.8 – 2.9 83 664
3.0 – 3.4 90 720 1- Precaution
3.5 – 3.9 96 768
4.0 – 4.4 105 840 a) All fluid products from patients (blood urine, stool, saliva, vomitus etc) has to
be treated as potentially infectious, mainly in the delivery rooms.
b) Gloves, gowns, aprons and masks (during procedures that generate droplets)
Phase 2: Rehabilitation Phase should be worn when resuscitating a newborn.
c) The operator should not use the mouth to apply suction via a suction device
Bodyweight (kg) Volume of F100-Diluted or Daily volume (ml)
F75 if 8 feeds per day* (ml) 2- Equipment and personnel
≤ 1.5 60 480
1.6 – 1.8 70 560 a) Every birth should be attended by someone who has been trained in initiating
1.9 – 2.1 80 640 neonatal resuscitation
2.2 – 2.4 90 720 b) Delivery rooms must be equipped with resuscitation bags, masks, laryngoscopes,
2.5 – 2.7 100 800 endothracheal tubes, mechanical suction machine.
c) When a high risk baby is expected appropriate equipment should be ready
2.8 – 2.9 110 880
to use.
3.0 – 3.4 120 960 d) Establish exactly the neonatal responsibility of team members before
3.5 – 3.9 130 1040 the birth
4.0 – 4.4 140 1120
 24 Neonatology Paediatrics Patients’ Management Guidelines 25

3- Resuscitation - 8F feeding tube and 20 ml syringe

- Meconium aspirator
• Which babies require resuscitation? 2) Bag and mask equipment
Risk Factors associated with the need for neonatal resuscitation - Device for PPV ventilation, capable of delivering 90 – 100% oxygen
(A copy of the list of these factors should be readly available in the delivery - Neonatal face masks ( newborn and premature size, cushioned – rim
rooms as a poster on the walls) masks) - (size 1 for newborn, size 0 for premature)
- Oxygen source with flowmeter (flow rate up to 10 L/min) and tubing
Antepartum factors 3) Intubation equipment
- age <16 or >35 years - Laryngoscope with straight blades N°0 (preterm), N° 1 (at term) and
- no prenatal care N° 00 (optional for extremely preterm neonates). Straight rather
- previous fetal or neonatal death than curve blades are preferred.
- bleeding in second or third trimester - Extra bulbs and batteries for laryngoscope
- maternal infection (TORCH infections, UTI)
- maternal cardiac, renal, pulmonary, thyroid, neurologic disease Endotracheal tubes (2.5, 3.0, 3.5, 4.0 mm e.g. for meconium aspiration),
- maternal diabetes chosing the size of the ET tube, in relation to the baby’s weight
- polyhydramnios, oligohydramnios
- pregnancy-induced hypertension, pre-eclampsia, chronic hypertension Tube size (in mm) Weight (g) Gestational age (w)
- premature rupture of membranes (inside diameter)
- pre-/post-term gestation 2.5 < 1000 < 28
- multiple gestation 3 1,000 – 2,000 28 - 34
- fetal hydrops 3.5 2,000 – 3,000 35 - 38
- size-dates discrepancy, anatomic misproportion (e.g. small stature of the mother) 4 > 3,000 > 38
- drug therapy (e.g. magnesium),
- maternal substance abuse (It may be helpful to post this table in the delivery room or near the radiant
- diminished fetal activity warmers).
Stylet (optional) that fits into the endotracheal tubes
Intrapartum factors Carbon dioxide (CO2) monitor or detector
- emergency caesarean section Suction setup (as in b1)
- forceps or vacuum-assisted delivery Roll of tape, ½ - ¾ inch, or endotracheal tube securing device
- breech or other abnormal presentation Scissors
- macrosomia Oral airway (Mayo tube)
- rupture of membranes (>18 hours before delivery) Meconium aspirator
- labor: premature Neonatal stethoscope (with neonatal head)
precipitous
prolonged (>24 hours) Positive pressure device, pressure gauge (optional for self inflating bags) and oxygen
prolonged second stage (>2 hours) tubes. Self inflating bag must have oxygen reservoir.
- uterine hyperstimulation
- persistent fetal bradycardia Intubation equipment should be stored in a clean, well marked container and
- use of general anesthesia placed in readily accessible location.
use of narcotics administered to mother within 4 hrs of delivery (e.g. morphine)
- placenta previa Intubation should be performed as a clean procedure. The endotracheal tubes and
- prolapsed cord stylets should be clean and protected from contamination. The laryngoscope blades
- significant intrapartum bleeding (e.g. abruptio placentae) and handle should be cleaned after each use.
- amniotic fluid: meconium-stained Endotracheal tubes are supplied in a sterile packages and should be handled with
foulsmelling (with fever of the mother: chorioamnionitis) sterile technique. They should be of uniform diameter to avoid damages or trauma
to the vocal cords.
• Neonatal resuscitation supplies and equipment
1) Suction equipment Consider to cutting the tube before the intubation. The extra length will increase
- Bulb syringe resistance to airflow. The tube may be shortened to 13 to 15 cm to make it easier to
- Mechanical suction and tubes handle during intubation and to lessen the chance of inserting the tube too far. For
- Suction catheters (5F,6F,8F,10F,12F,14F) make shorter the tube, remove the connector, then cut the tube diagonally to make
 26 Neonatology Paediatrics Patients’ Management Guidelines 27

it easier to reinsert the connector. Considerations

Remember: the correct position of the tip of the endotracheal tube is above the General
bifurcation of the Trachea (Carina). - a good teamwork is essential for a successful outcome of the resuscitation,
therefore say in advance who is doing what and do communicate with each
Before to perform endotracheal intubation: other while resuscitating.
- Endotracheal intubation may be performed at various points during
Prepare suction equipment: resuscitation, as indicated in the flow diagram.
- The timing of intubation is determined by many factors, one of them is the
Adjust the suction source ( if possible to 100 mmHg by increasing or decreasing the intubation skill of the resuscitator. People who are not adept at intubation
level of suction while occluding the end of the suction tubing); should call for help and focus on providing effective ventilation with a positive-
pressure device and mask, rather than spending valuable time tryng to intubate.
Connect a 10 F or larger suction catheter to the suction tubing so that it is
available to suction secretion from mouth and nose; Stimulation
- do not stimulate right after birth if meconium aspiration is suspected and the
Smaller suction tubes (5F, 6F or 8F ) should be available. newborn is not crying and floppy until the airways are cleared

Endotracheal tube size Catheter size Warmth

2.5 5F – 6F - very important therefore:
3 6F – 8F remove wet linen
3.5 8F provide dry and warm linen
4 8F – 10F cover the newborn´s head
place the newborn under a radiant warmer
Prepare device for administering positive pressure (bag and mask, T piece
resuscitator)
Turn on Oxygen (The flow should be set to 5 – 10 Lt/min) Steps in resuscitation
Get Stethoscope.
A: airways
- be aware of the correct position of the newborn´s head (neutral position, lifting
Other equipment the chin, jaw thrust, using a blanket under the newborn´s shoulders)
- radiant warmer - do not suction routinely but only if necessary (e.g. meconium stained amniotic
- oxygen source fluids and non vigorous newborn) as suctioning may cause bradycardia or
- dry (and warm) blankets damage the airways
- gloves
- NGT
- clock
- pulse oximeter
- stethoscope
- syringes, syringe needles

- drugs: 10% dextrose, 0,9% NaCl, Epinephrine (1:10,000) solution (

= 1ml epinephrine 1:1000 + 9 ml 0,9% NaCl)
 28 Neonatology Paediatrics Patients’ Management Guidelines 29

B: breathing Neonatal Resuscitation Guidelines

- the ambu bag should be compressed enough to visualize the chest rise -
do not overinflate the chest
- check the bilateral lung aeration by placing the stethoscope in the axilla on Newborn Resuscitation Algorithm
both sides Birth Term gestation? • Routine care
Breathing or crying? • Provide warmth
C: circulation Good tone? Yes, stay
• Clear airway if necessary
with mother
- cord pulsation is only reliable if found to be more than 100 beats min. • Dry
No
Cord pulsation below 100 beats/min does not necessarily mean that the heart • Ongoing evaluation
rate is below 100 beats/min. If in doubt check heart rate by listening to the Warm, clear airway
apical beat with a stethoscope if necessary,
dry, stimulate No
colour
- a healthy baby is born blue but becomes pink within 30 s of the onset of
effective breathing HR below 100, No Labored breathing
30 sec
gasping, or apnea? or persistent cyanosis?
- observe whether the baby is centrally pink, cyanosed or pale
- peripheral cyanosis is common and does not, by itself, indicate hypoxaemia. Yes Yes

success of resuscitation PPV, No Clear airway

Sp02 monitoring. SP02 monitoring
- following conditions indicate a successful resuscitation: raising heart rate, 60 sec Consider CPAP
improving skin colour, improving muscle tone and spontaneous breathing
No
cessation of resuscitation HR below 100?
- if after 20 min of resuscitation the baby is not breathing and pulse is absent
Yes

care after resuscitation Take ventilation Postresuscitation care

No
- keep the baby dry and warm with the mother (skin to skin contact) corrective steps
- give Vit. K according to National guidelines
- keep umbilical cord clean and dry
- special evaluation and ongoing assessment for infants with risk factors (prenatal HR below 60?
or intrapartum risk factors, ambu bag ventilation, extensive resuscitation)
Yes

Consider intubation
References Chest compressions
1. World Health Organization, Pocket Book of Hospital Care for Children: Coordinate with PPV
Guidelines for the Management of Common Illnesses with Limited Resources, Take ventilation No
Geneva, 2005 corrective steps
2. European Resuscitation Council Guidelines for Resuscitation 2005 Section 6. Intubate if HR below 60?
Paediatric life support. Resuscitation (2005) 67S1, S97-S133 no chest rise!
3. International Liaison Committee on Resuscitation. Neonatal resuscitation.
Resuscitation (2005) 67, 293-303 Yes Targeted Productal Spo2
Consider:
4. Circulation 2005;112;IV-188-IV-195: Neonatal Resuscitation Guidelines • Hypovolemìa After Birth
(American Heart Association) • Pneumetnorax IV epinephrine
1 min 60%-65%
Special Report—Neonatal Resuscitation:2010 International Consensus on 2 min 65%-70%
Cardiopulmonary Resuscitation and Emergency Cardiovascular Care 3 min 70%-75%
Science With Treatment Recommendations 4 min 75%-80%
PEDIATRICS Volume 126, Number 5, November 2010 5 min 80%-85%
10 min 85%-95%
Special Report—Neonatal Resuscitation:2010 American Heart Association
Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care American heart association 2010
PEDIATRICS 2010, volume 126 October 18.
 30 Neonatology Paediatrics Patients’ Management Guidelines 31

Neonatal Sepsis Infants within each group have specific causative organisms and risk factors.
• Less than 7 days of life an organism is usually acquired during passage through
the birth canal
• Greater than 7 days of life the organism is acquired via a nosocomial source or
via household contacts.
BACKGROUND AND DEFINITION
• Nosocomial sepsis should be considered if the neonates is admitted to Hospital
“Sepsis” is a systemic response to a physiologic insult – including infectious and and the onset of laboratory signs and clinical symptoms of infection is after 48
other etiologies – that lead to the development of further organ injury, ultimately hours from the admission.
culminating in multiple organ dysfunction syndrome.
Neonatal sepsis refers to a group of physical and laboratory findings that occur
in response to invasive infection within the first 30 days of life. There are various CAUSATIVE AGENTS of sepsis
infectious causes of neonatal sepsis; however, the pattern of presentation is quite
similar in all cases, as is the approach to treatment. Early onset :
Early onset infection is thought to occur during passage of the fetus through the
The importance of neonatal sepsis as a diagnosis is found in the fact that this birth canal. The principal organisms that account for early-onset infection include
diagnosis occurs in between 1 to 8 children per 1000 live births in the United predominantly group B streptococcus (GBS), as well as Escherichia coli (E. coli) in
States, and may be associated with a fatality rate of up to 30%. Moreover sepsis the remainder. Since early-onset infection is thought to occur during parturition,
can affect up to 30 per 1000 live births in the preterm population. The high it is not surprising that the major risk factor for this phase of neonatal sepsis is the
rate of neonatal infections in developing countries and the types of infections asymptomatic colonization of the maternal gastrointestinal or genitourinary tracts.
commonly identified (infections of the bloodstream with gram-negative rods) The maternal gastrointestinal or genitourinary tracts are colonized by GBS in up to
strongly suggest that lack of appropriate hygiene during labour and delivery, 30% of pregnant women. Additional risk factors for early-onset infection include
postnatal care, and feeding are major contributors in the developement of prolonged rupture of membranes, prematurity, male gender, low birth weight,
infections in the newborn. maternal infection, and poor prenatal care.
As such, it is essential that caregivers that are involved with the management of
neonates have a reliable approach to the diagnosis and treatment of infants with In summary the principal organisms that account for early-onset infection
sepsis, and that appropriate intervention be instituted in a timely manner. include:
In brief : Group B Streptococcus (GBS), Escherichia coli , coagulase-negative
• Sepsis is a term to indicate a severe infection in a newly born infant Staphylococcus, Haemophilus influenzae and Listeria monocytogenes
• Bacteria are disseminated in the blood
• Sepsis can cause death if not recognized and treated properly Late onset :
Late-onset infection occurs beyond the early delivery phase, and reflects organism
that may be acquired in the hospital setting or at home. Infants with late-onset
AGE OF INFANTS neonatal sepsis develop infections from hospital pathogens, including bacteria
(coagulase negative staphylococcal species), viruses, and fungi (candida species).
The causes of neonatal sepsis are best classified into three time periods: Patients that are on antibiotics for any length of time are at increased risk for the
1) infections that occur during pregnancy (so called “congenital infection”); development of late-onset infection, as are those infants that have any centrally
2) infections that occur early after delivery (“early-onset infection”); placed intravenous catheter. Such lines may include a Broviac or percutaneously-
3) infections that occur later on, such as after the infant is discharged from inserted central catheter (PICC-line), an umbilical arterial line, or an umbilical
the hospital (“late-onset infection”). venous line.
The division between early- and late- onset infection is thought to be between 2 to Late-onset neonatal sepsis can also occur in infants after they leave the hospital. In
5 days, although a longer period of time has also been suggested**. these cases, organisms that are similar to those causing early-onset sepsis i.e., GBS,
E. coli and other Gram-negative species predominate.
In brief:
• Septic neonates may be classified into three groups: In summary infants with late-onset neonatal sepsis develop infections from
• congenital, common hospital pathogens:
• early-onset, Coagulase-negative staphylococci, Staphylococcus aureus , E coli, Klebsiella,
• and late-onset. Pseudomonas, Enterobacter, Candida, GBS, Serratia, Acinetobacter, and anaerobes.
 32 Neonatology Paediatrics Patients’ Management Guidelines 33

RISK FACTORS skin water–marks,

convulsions,
• Prematurity and low birth weight and hypotonia.
• Maternal GBS, maternal peripheral infection
• Prolonged rupture of membranes (PROM) Laboratory findings
• Maternal fever, maternal chorioamnionitis Leukopenia (WBC count <5,000 mm3) or leukocytosis (WBC count >20,000 mm3),
• Sibling with sepsis low platelet count (platelets <100,000 mm3),
• Meconium at delivery blood C-reactive protein level >1.5 mg/dL,
• Need for resuscitation, fetal distress, Hypoxia fibrinogen >150 mg/dL,
• Male child Neutrophils immature/total ratio >0.2,
• Multiple gestation metabolic acidosis (base excess <-7 mmol/L)

In particular, maternal risk factors are: The diagnosis of sepsis requires careful clinical suspicion, detailed physical
Maternal GBS colonization (especially if untreated during labour) examination, and a combination of lab tests and x-rays because the clinical signs
Maternal rupture of membranes more than 18 - 24 hours before delivery and symptoms are really unspecific. Although there isn’t one single test that can
(pPROM, PROM) reliably diagnose sepsis in all neonates, the above combination will establish the
Maternal intrapartum fever (more than 37.5C) diagnosis in most.
Chorioamnionitis

And INVESTIGATIONS
Foetal risk factors are:
Prematurity and very low birth weight The laboratory work-up of septic neonates begins with a complete blood count,
Birth asphyxia (<6 at 1st or 5th min) including leukocyte count with differential, and platelet count. Evidence of
Male sex decreased circulating white blood cells may be noted (leucopenia), as may signs
Developmental or congenital immune defects of increased white blood cells (leukocytosis). Leucopenia is more common than
Congenital anomaly (urinary tract, asplenia, myelomeningocele, sinus tracts) leukocytosis in cases of neonatal sepsis. Neonatal sepsis may also be associated
Omphalitis with an increase in the release of immature white blood cells into the circulation,
Twinning (especially the second twin of an infected twin) as manifest by an increase in circulating band forms. A decrease in platelet count
may also be noted, a manifestation of the formation of small blood clots within
Definitions: the tissue or impaired production in the bone marrow. Additional tests of note
Neonatal infections are defined as confirmed if the neonate has clinical symptoms, include abnormalities in serum electrolytes, including increased or decreased
laboratory findings suggestive of infection and positive microbiological cultures, sodium concentrations, both of which are evidence of the free water imbalance that
and as suspected if microbiological cultures are negative. Sepsis are defined as accompanies sepsis. Septic infants may also manifest hyper- or hypo-glycemia.
confirmed or clinically suspected. Confirmed sepsis are those in which the neonate
manifests at least two clinical signs or two laboratory findings with positive Obtaining accurate cultures of all body fluids is the most important step in
blood culture and suspected if blood cultures are negative. In case of suspected establishing the diagnosis of sepsis. This includes a blood culture, as well as a
contamination, a diagnosis of confirmed sepsis required two consecutive blood culture of the urine and the cerebrospinal fluid. When obtaining a blood culture,
cultures positive for the same bacteria unless the neonate had no indwelling it is important to avoid drawing blood from intravenous catheters or central
intravascular catheter when blood was been drawn. lines. It is particularly important to be able to recognize the presence of common
contaminants in blood cultures, especially coagulase-negative staphylococcus
or viridans streptococci. The practice of obtaining cultures from two clean sites
SIGNS & SYMPTOMS facilitates this task.

Clinical symptoms: In summary neonatal sepsis work up includes:

Fever (rectal temperature >38°C), • Microbiological Cultures of blood, CSF, urine, gastric aspirate, stool
tachycardia (heart rate >180 beats per minute) or bradycardia (heart rate<100 beats • Random Blood Glucose (RBG)
per minute),
apnea lasting >20 seconds,
lethargy,
feeding problems,
gastric biliary stasis,
 34 Neonatology Paediatrics Patients’ Management Guidelines 35

TREATMENT References:
1. Nelson text book of pediatrics by Behran, Kliegman, Arvin 15th edition
Neonatal sepsis is associated with a high risk for morbidity and mortality. 2. Pocket book of hospital care for children; Guidelines for the mnagement of
Treatment should be directed towards maintaining blood pressure and perfusion common illnesses with limited resources World health Organization
to organ systems, while treating the specific infective agent. In addition to the 2005,reprinted 2007
maintenance of systemic vital signs, treatment of neonatal sepsis requires specific 3. www.emedicine.com, paediatrics neonatology
antimicrobial therapy. 4. American College of Chest Physicians/Society of Critical Care Medicine
Consensus Conference: definitions for sepsis and organ failure and guidelines
The specific antimicrobial agent is influenced by the type of neonatal sepsis. for the use of innovative therapies in sepsis. . Crit Care Med 1992;20:864-74.
Early-onset neonatal sepsis is treated with a combination of agents that treat group 5. Baltimore R. Neonatal sepsis: epidemiology and management. Paediatr Drugs
B streptococcus as well as Gram-negative species ( ampicillin and gentamicin, or 2003;5:723.
ampicillin plus cefotaxime). These agents in combination cover a broad spectrum of
the most common pathogens in early-onset sepsis, and have excellent penetration
into the central nervous system.
When gentamicin is used, close monitoring of renal function is required.
Problems of Pre-Maturity
For late-onset sepsis, the choice of antibiotic therapy should be based, in part, on
the prevailing flora of the individual NICU.
and their Management
In general, the same empiric treatment as for early-onset sepsis may be used
(ampicillin and gentamicin), unless micro-organisms with resistance to these agents Definition
are identified. In instances in which a central line is present, treatment should be
instituted to cover S. aureus and coagulase-negative staphylococci. - A premature baby is a baby or newborn that is delivered before the 37th week
There is increasing incidence of methicillin-resistant S. aureus or MRSA in infants from the day of the last menstrual period.
with line infections. In view of this, a first-line antimicrobial choice is vancomycin, - Premature means also delivered before maturity.
in addition to an aminoglycoside such as gentamicin, for empiric coverage of - Prematurity by body weight is defined by weight of 2,500gms or less
Gram-negative bacilli while awaiting the results of cultures.
The presence of fungemia in the setting of an infected central line necessitates line But babies born with a weight of 2,500gm or less are also known as Lowbirth
removal. weight infants (LBW).
In neonates who are admitted to the NICU from the community, antibiotic
selection should include treatment of meningitis. Empiric choices include a third- LBW
generation cephalosporin (i.e., cefotaxime or ceftriaxone) plus ampicillin. - Can be premature babies born immaturely with a shortened
gestational age.
In summary: - Can be intrauterine growth retarded for their gestational age. They are also
The antibiotic therapy should be initiated AFTER obtaining a culture samples and referred to as small for Gestational Age – SGA. OR have Intrauterine growth
it includes double therapy (Ampicillin and Gentamycin) for at least 10 days in the retardation (IUGR).
most serious cases; if not improving in 2 – 3 days, consider change of antibiotics.
For late-onset sepsis, the choice of antibiotic therapy should be based, in part, on • Very Low Birth weight infant
the prevailing flora of the individual NICU. These are infants that weigh less than 1.500gms.
Supportive treatment: • Extreme Low Birth weight infants.
Vitamin K These are infants weighing less than 1000gms.
Keep neonate warm, dry and well wrapped
‘Kangaroo’ mother care method Factors Related to Premature and low Birth weight.
Fluid Management - Low socioeconomic status
- in families with low SE status there are incidences of:-
Fluid Management: - Maternal under nutrition
Encourage mother to breastfeed - Anemia
Give more fluid if under radiant heater (1.2 – 1.5x more) - Illnesses
O2 Therapy - Inadequate ANC Care
- Drug addition
- Obstetric complications
 36 Neonatology Paediatrics Patients’ Management Guidelines 37

- Single parenting The more immature the baby the more likely are the following common
- Teenage pregnancy complications /problems:
- Close spacing pregnancies
- High parity Poor temperature control, hypothermia.
- Infections Normal temperature can be maintained by
- Drying the baby as soon as possible at birth.
- Put the baby against the mother’s chest inside her clothes.
General Problems of Preterm Babies - Cover baby’s exposed head with a cap (the head of a newborn constitute a
significant part of the body surface areas)
Gestational Age • Skin : Skin nursing known as the Kangaroo Mother Care (KMC)is associated
Sometimes a mother is unaware of a her last menstrual period. Then the baby’s with increased prevalence of breast.
gestational age must be assessed by using a clinical scoring system to estimate the • Mother method is associated with increased prevalence of breast
age of the newborn. Assessment can be done based on morphological criteria feeding, reduced incidence of apnoea, and reduced risk of infection apart
related to SKIN, NIPPLES, EARS, and FOOT CREASES. The method used to from keeping the temperature of the baby normal.
assess gestational age at B.M.C is the Firistrom score. See appendix
Difficulties in establishing feeding
• Babies born after 34 weeks are generally mature enough to suck
SCORE (Firistrom) and swallow but may be less demanding of feeds than term babies.
• Preterm babies can be helped to establish breast feeding in the
1 2 3 4 following way.
- Encourage early and prolonged skin contact.
Breast tissue 5 mm 5-10 mm 10 mm
- Encourage small, frequent feeds by waking the baby every three to four
Brest nipples Hardly visible Well defined Edge of aerola hours and putting to the breast.
lifted
- If the baby will not latch on and suck encourage the mother to express her
Skin vessels Big vessel visible Some veins and A few vessels No vessels visible breast milk after attempting a feed. The expressed milk can be given to the
over abdomen braches visible visible baby by gavages (or gastric nasogastric or cup).
Hair Thin and wooly Thick - Avoid giving formula or breast milk by bottle as small feeding cup (about
silk-like hair the size of a medicine measuring cup with a smooth rim) or a syringe can be
Finger nails Do not reach the Reaching finger- Reaches or passes Start to be carti- used. Give 20ml/kg of expressed breast milk every 3 hours.
fingertip tip but distal and finger-tip distal lage in the whole - If too unwell to suck or drink from a cup, give expressed breast milk via
not district an distinct nails ear also in helix nasogastric tube.
hard - As the baby becomes more vigorous, encourage a transition to demand
Ear cartilage No cartilage in Cartilage in Cartilage in The whole sole breast-feeding.
(see next page) antitragus antitragus antihelix has lines
Skin lines in sole No lines visible No lines the back Some lines over
of foot 2/3 of the foot the force 2/3 of
the foot Table of feeding

Points Gestational age Weeks DAY 1 2 3 4 10 14-

7 27 Per kg 60 ml 80ml 100 ml 120 ml 160 ml 180-
8 28 200ml/kg
9 29 BW Number Ml/meal Ml/meal Ml/meal Ml/ meal Ml/meal
10 30 of meals
11 31 Actual
12 32 1000g 12x 2*-5 -7 -9 - 11 13 weight
13 33
14 33 1200g 3*-6 -8 -10 - 12 14
15 34 (or 8x20) (or 8x20)
16 35 SFD: try +
17 36 1400g 4*-7 -9 - 11 -13 15 10-25%
18 37 (or 8x20) (or 8x20)
19 38
20 39 1500- 8x 5*-10 15 20 25 30
21 40 2000g
22 41
23 42
 38 Neonatology Paediatrics Patients’ Management Guidelines 39

Laboratory plasma glucose measurements.

HYPOGLYCAEMIA Reagent strips may show a glucose level as much as 15% lower than plasma
levels since whole blood is used.
Definition – Hypoglycemia is blood sugar level below
2.5mmol/litr (40mg/dl). • Laboratory plasma glucose determinations.
- Infants at risk of developing hypoglycemia - Useful for confirming hypoglycemia detected by reagent strips.
- Infants of Diabetic mothers - But blood samples must be processed promptly for accurate values since
- Preterm Babies glycolysis occurs in standing whole blood samples.
- Small –for-gestational age babies
- Large for gestational age babies NB: Do no wait for laboratory confirmation, start treatment immediately.
- Post-term babies
- Sick babies with infections and Respiratory failure. Management of Hypoglycaemia
- Fasted babies. • Infants at risk for hypoglycemia, appearing to be well.
- Initiate early feeding within 1 hour after birth with breast
Causes of Hypoglycaemia milk or formula, repeated every 2-3 hrs.
• Icreased utilization of glucose- Hyperinsulinism. - Feeding with 5% glucose in not recommended in infants
- Infants of diabetic mothers with hyperinsulinism because milk provides more energy.
- Erythroblastosis fetalis - Infants of diabetic mothers are unlikely to develop
- Insulin producing tumours hypoglycemia on the second day of life if tests in the first 24 hrs .
- Islet cell hyperplasia • Infants with symptomatic hypoglycemic or unable to feed or who failed
• Decreased production /stores correction of glucose levels with enterable feeding.
- Prematurity - Start Intravenous glucose boluses 200mg/kg over 5 min. (2ml/kg
- Small for gestational age of 10% glucose in water).
- Inadequate caloric intake
• Increased utilization and /or decreased production or other causes. NB: Remember giving high concentration of glucose solutions by
- Perinatal stress (asphysia, sepsis, shock, hypothermia, bolus injections can itself be dangerous, particularly form effects on the brain
- Pohylythoemia
- Defects in carbohydrate metabolism (galatosoemia fructose intolerance, - Follow with maintenance infusion of 10% glucose at a rate of 5-
glycogen storage disease. 8 mg/kg/min.

Investigations for Diagnosis. - If further episodes of hypoglycemia occur bolus should be

- Blood glucose concentration in the first 6 hours of life is very often low repeated and the infusion rate increased by 10-15%.
(<1.5-2.0mmol/litre). No evidence that this is harmful healthy infants adapt by
mobilizing other fuels. Therefore early testing (,6hrs of age) is not necessary – - Exclude infection. A baby who seems drowsy may be infected
pointless. Unless neurological sings are present. and a low blood glucose may be associated but not the main cause of
the problem.
WHEN TO TEST
• Symptomatic infants – with –Lethargy, poor feeding, temperature instability, - When administering boluses, never use high concentrations of
Respiratory distress, new- onset apnoea/bradycardia, jitteriness, seizures. Test to Glucose >10% because risk of intravascular hoemonhage and
be done immediately-Random Blood sugar test –RBG. /or cerebral oedema.
• Infants Risk. Soon after birth (within 6 hrs). then 3 hourly until stable at
2.5 mmol/litre (45mg/dl) or higher continue to monitor until feeds are well - Most infants will correct hypoglycoemia with infusion of 5-
established. 8mg/kg/min. it is not infrequent growth retardation and those
• Infants with Hypoglycemia. with hyperinsulinism may require infusion rates up to 12-15mg/kg/min.
- Check blood glucose -20-30 min. from beginning of treatment
than hourly until stable at 2.5mmol/litre (45mg/bl) or higher. - When normal blood glucose levels have been stable for 12-
Continue to monitor frequently (every 4-8 hrs) during treatment 24hours and the infant is tolerating enterable feeding –decrease the
and while decreasing supplemental I.V. glucose infusions. intravenous glucose infusion by 10 - 20% each time levels are greater
than 2.5mmol/l(45mg/dl).
Laboratory Diagnosis
• Reagent strips – are useful and rapid but in general are less reliable than - Always decrease intravenous infusion gradually because of the
 40 Neonatology Paediatrics Patients’ Management Guidelines 41

risk of precipitating hypoglycemia - Pulmonary Oedema due to a persistent PDA)

- If unable to gain intravenous access. - Pneumonia and acute or chronic pulmonary parenchymal disease
HYPOSTOPGEL-an oral glucose mixture containing 500 (Bronchopulmonary Dysplasia- BPD)
micrograms of glucose /ml can be helpful. Give 1-2 ml to the oral mucosa. - Hypovolemia
- Anemia
- If hypoglycemia persists beyond the first week of life- requiring
large (.8mg/kg/min) infusions of glucose – send child for Endocrine or • Secondary apnoea
metabolic disorders evaluation Apnoeic spells may also be secondary to clinical conditions that do non involve
the respiratory system. In this situation they are a clinical sign associated with
- Intraventricular Haemorrhage.
E. APNOEIC ATTACKS - Hypoglycaemia
- Hypocalcaemia
Definition – Apnoea can be defined as a cessation of respiration for 20 seconds - Temperature Instability
or more, associated or not with bradycardia and cyanosis. These signs of cardio - Sepsis or other infections This should always be suspected and ruled
respiratory failure are usually present when the apnoeic episode lasts more than 20 out by doing all the necessary Laboratory investigations.
seconds. After 30 to 45 seconds pallor and hypotonia occur and the infant may be - CBC, ESR, CXR, Blood for Bact culture and Antibiotics
unresponsive to tactile stimulation. should be given accordingly.
So an episode of apnoea lasting longer than 20 seconds is associated with - Convulsions
- Bradycardia In neonates repeated crisis of apnoea may be episodes of seizures.
- Cyanosis
- Pallor • AIRWAY OBSTRUCTION
- Hypotonia. Spontaneously occurring airway obstruction is when a preterm baby assumes a
The repeated and frequent crises of apnoea lead to hypoxia. position of neck flexion. Congenital malformations of the airway-may present as
apnoea eg. Tracheal oesophageal fistula. In these situations proper head positioning
Apnoeic attacks are common in preterm babies, more frequently in babies with a and correction of congenital anomalies should be attended to promptly.
gestational age lower than 35 weeks (apnoea of prematurity).
• Maternal Medication
Causes of APNOEA - Intrapartum maternal narcotic administration for maternal pain /sedation.
• Apnoea of Prematurity - Condition can be reversed by the use of Naloxone hydrochloride 100 μgm/kg i.m.
The occurrence of apnoea of prematurity is often a mixture of - High dose of Magnesium sulphate – Self limiting – no medication required
- Impaired central of brainstem neural function (central apnoea)
- Impaired chemoreceptor response (less response to increased levels of carbon
dioxide)
- Reflexes ( stimulation of the posterior pharynx, fluids in larynx) Neonatal Infections
- Ineffective ventilation from impaired coordination of the inspiratory muscles
- Sleep state (REM sleep)
- Intrapulmonary shunting • Early onset sepsis (First week)
- Upper airway obstruction (upper pharynx ) (obstructive apnoea). - Occurs during the first week of life.
The more frequently observed type of apnoea is mixed apnoea (central and - As a result of bacteria acquired by vertical transmission from mother to infant.
obstructive). Or during delivery.
- Escherichia coli-which are commonest.
Frequency and severity of apnoeic spells may be eliminated by treatment with- - Group B Bhoemolytic streptococcus.
Aminophylline, Theophylline or caffeine that stimulate the respiratory - Staphylococcus
centre. Caffeine is now more preferred because it has a long half life (daily dosing ) - Enterococcus
and serum levels do not have to be monitored.
Maternal Risk factors for early onset sepsis
(2) Other causes of Apnoea • Maternal chorioamnionitis
The hypoxemia may be involved in the pathogenesis of apnoeic spells. • Intrapartum maternal fever (esp. 38°C or greater).
Hypoxia makes the preterm babies less responsive to increased levels of carbon • Premature rupture of membranes
dioxide. Therefore clinical conditions associated with hypoxia may be involved • Prolonged rupture membranes (18hours or greater)
in the pathogenesis of apnoea: • Preterm Labour.
- Respiratory distress (Respiratory Distress Syndrome from HMD) • Maternal bacteriuria during pregnancy (esp. with group B haemolytic streptococcus).
 42 Neonatology Paediatrics Patients’ Management Guidelines 43

• Prior infected infant (group B haemolytic steptococcus). Neonatal Tetanus- You remember.
Main features of the disease.
Infection is acquired from mother at or shortly before delivery. - In this time/era of HIV Infection-Well vaccinated.
- Mothers who are at the same time HIV infected may fail to pass enough
anti Tetanus.
LABORATORY EVALUATION OF THE INFANT - Antibodies to their growing foetuses to prevent them from getting Tetanus
after birth. At the same time placental malaria reduce the transplacental transfer
• Blood Culture of antitetanus antibobies in utero.
Blood culture is the gold standard for neonatal sepsis but is is not 100%
sensitive. This sensitivity may further be reduced if intrapartum antibiotics were Meningtis
administered to the mother. Preseting features- Include – Lethargy, Irritability, hypotonia, Seizures, bulging or
• White blood cell count (WBC) with differential cell count. tense anterior fontanelle.
• Chest-X-ray. It should be obtained if there are any respiratory symptoms.
• Lumbar puncture Investigations
• Suprapubic aspirate of urine for culture. This is more useful after the first – Do LP and send CSF for investigations for gramstain, chemistries and
week or life. cell count.
• Blood glucose concentration. – CSF for preterm infants with intraventricular haemorrhage is different
• Serum Bilirubin concentration if baby appears jaundiced. and can be confusing.
– But in this case it should be treated as bacterial meningitis until cultures are
NB: Infants in whom sepsis is suspected priority should be given to stabilizing known to be negative.
cardiovascular and Respiratory problems while simultaneously obtaining a – If CSF is bloody treat baby as though infected and repeat LP after 24hrs.
blood culture followed by prompt administration of antibiotics. Other test can – If a CSF pleocytosis is present but no organism is identified consider to
be obtained once the infant is stable and antibiotics have been given. do computed tomography of the head to rule out brain abscess.

Antibiotics Treatment Treatment for Meningits: for 14 days if due to uncomplicated gram positive
• Most frequently used agents are Ampicillin and Gentamicin. bacteria; for 21 days if gram negative.
• Third- generation cephalosporius such as Cefotaxime, Ceftazidime,
or Ceftriaxone may by used but some gram-positive bacteria may not be covered
if a penicillin derivative is not included (eg. Entorococcus and Listeria). SKIN, Eye and mucous membrane infections

But disadvantage of these drugs is that may contribute to the development of Conjuctivitis.
strains of multiple drug resistant bacteria. - Most conjunctivitis presents as “STICKY EYES” but this may not always
Ceftriaxone should be avoided in infants with hyperbilirubinoemia. be of bacterial origin. Especially if it occurs in the first few days. (i.e. chemical
conjunctivitis from ophthalmologic pnophylaxis with topical antibiotic).
• Fludoxacillin (intravenous or oral) is preferable for paronychia or septic spots as - Rapidly progressive purulent conjunctivitis occurring within the first few days
these are usually caused by coagulase- positive staphylococci. must always be assumed to be to neisseria gonorrhoeae. Which with
must be promptly identified and aggressively treated with parenteral antibiotics
• Ciprofloxacin-may help in infections of resistant organisms. high rate of sexually transmitted diseases.
- Do swab for microscopy for culture and sensitivity.

LATE-ONSET SEPSIS Treatment should be for 7 days.

Most common infections are infected - drugs-Penicillin – I.V. –much resistance reported 3rd generation cephalosporin
- Umbilicus preferred as first line. Ceftriaxone 50mg/kg per day I.V or I.M. for 2 days
- Skin or Kanamycin 25mg/kg in a single does.
- Nails or Spectinomycin 25/kg I.M in a single dose.
- In hospital setting Nosocomial Root of infection is more common.
Pathogens include – Coagulase negative staphylococci, Gramnegative enterics Eyes should be frequently irrigated with starile normal saline or boiled and cooked
like (Klebsiella oxytoca, K. Pneumoniae, Enterobuter cloacae) Staphylococcus clean water.
aureus, Pseudomonas Species. Fungi sepsis must also be considered. Remember to wash your hand before and after the procedure.
 44 Neonatology Paediatrics Patients’ Management Guidelines 45

CHLAMYDIAL CONJUCTIVITS - Polycythemia

- Hypertonic milk feeds or medicines.
Clamydia Trachomatis is the most common cause of infectious conjunctivitis in the - Too rapid feeds
neonate. - All above may contribute to mucosal injury and subsequent infection leading to
Presents between 5 and 14 days. bowel necrosis.
Sometimes there may be purulent discharge. - Eg. Escherichia Coli, staphylococcus efidermids rotarirus, clostridium perfingens.

A giemsa stain of a conjuctival scraping may show basophilic intracytoplasmic Presenting Features
inclusion bodies. - Peripheral circulatory failure
Other test include – culture or rapid antigen detection. - Abdominal distension
- Bile stained emesis or gastric aspirates.
Treatment with Erythromycin for 3 weeks is effective. - Blood and mucus in the stools.

Pustules Features of coagulopathy- petechial hemorrhage.

Mostly coused by staphylococcus aurous. Most often these occur in small cdustes in Oliguria and haematuria may be present.
an otherwise healthy infant.
Investigations
Treatment. Topical therapy may be enough. Oral antibiotic such as • X-ray abdomen: Look for abnormal gas pattern, free intraperitoneal air . This is
- Flucloxacillin. best seen with a left side down (Lateral decubitus X-ray) where free air may be
- Or first generation cephalosporin- Cephalexin. For 7 days. easily seen overhying the dense hepatic tissue- Intramural gas
Should distinguish from-Erythematoxicum- Bening non infections new born rash. (Pneumatosis intestinalis) or gas in the portal tracts of the liver.
Careful examination of the contents of a pustule by Wright stain reveals numerous • WBC and Differential cell count. Platelet count.
eosinophyls in erythenatoxicumcompared to neutrophils and cocci bacteria with • Blood culture.
staphylococcus. • Serum Electrolytes
• Continuous heart and Respiratory rate monitoring should be done.
Umbilical Infection.
- Umbilicus disdarging pus. Treatment
• STOP ALL ENTERAL FEEDS. Provide I.V fluids at 120ml/kg/day of
Clean area with soap and warm water and remove /drain pus and crust. Dry 10% glucose with added electrolytes.
and paint the area with antiseptic. Eg. Gentian violet, povidone-iodine or • Put an NG tube and aspirate 4 hrly to keep the intestines decompressed.
chlorhexedine. • Start parenteral broad spectrum antibiotics: Ampicillin & gentamicin.
Metronidazole may be added to cover anaerobic bacteria- especially if
pneumatosis, perforation or evidence of peritonitis are present.
• Treat shock with 0.9% saline.
Necrotizing Enterocolitis (NEC) • If there is bleeding give 1 mg of vit K I.V. and fresh frozen plasma 20ml/kg.
• Antibiotics are given usually for 10-21 days depending on the severity of
the process.
During therapy parenteral nutrition if available should be given in place of
- Usually occurs in Premature babies. simple 10% glucose & electrolytes.
- After the first week of life.
- Common in ill infants Eternal feeds (breast milk) are reintroduced slowly at the end of antibiotics therapy-
- Affects – 15-20% of babies who have never been fed. with careful monitoring for abdominal distension or other signs of obstruction.
- Less common in babies exclusively fed with human milk.
- It is characterized by varying degrees of mucosal or TRANSMURAL
NECROSIS of the intestine. Jaundice and HyperbilirubianAemia
- (Preterm infants is particularly susceptible).
- Jaundice is observed in 80% of preterm infants during the 1st week of life.
Parts of Intestine Involved - The yellow colour in the skin is usually due to the accumulation of
- Distal ileum and proximal colon are envolved most frequently. unconjugated bilirubin, pigment (indirect –reacting)
- Gas accumulation in the submucosa of the bowel wall (pneumatosis, intestinatis). - It may also be due in part to the deposition of conjugated bilurudin
- Factors leading to necrosis. (direct-reacting).
 46 Neonatology Paediatrics Patients’ Management Guidelines 47

- The less mature the infants the greater the susceptibility to kernicterus.
Causes in Connection with Prematurity Clinical Features
In general for all infants-the metabolism of bilirubin is in transition from the fetal Symptoms and signs appear from 7th day in preterm infants.
stage during which the placenta is the principal route of elimination of the lipid- - Lethargy, poor feeding, loss of mororeflex.
soluble bilirubin to the adult stage –during which the water-soluble conjugated - Later infant may appear very ill with respiratory distress.
form is excreted from the hepatic cell into the biliary system and then into the - Opsisthotonos, Buldging of anterior fontanel.
gastrointestinal tract. - Twitching of face, or limbs.
- High pitched cry.
Unconjugated hyperbilirubinoemia may be cuased or increased in the premature - Later convulsions may appear and spasms with infants stiffly extending the arms
baby by an absence of or decreased amount of the enzyme or to reduction of in inward rotation with fist clenched. If child services – may develop cerebrolpasly.
bilirubin uptake by the liver cell.
Treatment of Hyperbilirubinaemia.
Toxicity of bilirubin to different cells is influenced by many factors – that increase. - Goal is to lowe concentration of indirect bilirubin in the blood to levels which
The permeability of the blood-brain barrier or nerve cell membranes to bilirubin. do not cause Neurotoxicity.
Or to the susceptibility of brain cells to its toxicity such as asphyxia, prematurity. - Phototherapy.
Jaundice – Physioligical. - Exchange Blood transfusion can be done.
Begins on face as serum level increases progress to the abdomen and then feet. Phototherapy- Jaundice & indirect hyper Bilirubinoemia may be reduced on
Patient infants with a rising level of jaundice must be investigated-serum level of exposure to a high intensity of light in visible spectrum.
bilirubin estimated. Bilirubin absorbs maximally in the blue range from 420 ot 470 nm.
Jaundice resulting from deposition of indirect bilirubin in the skin tends to appear
bright yellow or orange. Jaundice of the direct bilirubin in the skin tends to Absorbs light energy which converts toxin native unconjugated bilirubin into the
appear greens or muddy yellow. form which is excreted in bile.
Together with phototherapy – the basis cause or causes of the jaundice should be
Physiologic jaundice (icterus neonatorum) treated.
Normal situation-level indirect –reacting bilirubin is 1-3 mg/dl. And rises at a rate Under phototherapy in premature infants without significant hemolysis bilirubin
of less than 5mg/dl/24hrs. – jaundice becomes visible on the 2nd -3rd day. Usually levels are reduced within 2 days.
peaking between the 2nd and 4th day at 5-6mg/dl and decreases to below 2mg/ - Turn infant frequently for maximal skin exposure
dl between 5th and 7th days of life. All this occurs due from increased bilirubin - Monitor serum levels of bilirubin 8hrly in infants with hemolytic disease of
production following breakdown of red blood cells combined with transient new born.
limitation in the conjugation of bilirubin by the liver. - Eyes should be shielded.
- Body temperature should be monitored.
- Premature babies have indirect –reacting bilirubin greater than 15mg/dl.
Complications of phototherapy include.
Among premature infants. - Loose stools
- Rise in serum bilirubin tends to be a little slower or the same as that in - Erythematous macular rashes
term infants. - Overheating.
- Is of longer duration. - Dehydration (due to increased insensible water loss, diarrhea).
- Resulting in higher levels - Chilling from exposure.
- Peak reached between the 4th and 7th days. - Bronze baby syndrome+ a dark grayish brown discoloration of the skin – noted
- Peak levels of 8- 12mg/dl are reached by the 5th – 7th day. at times on infants under phototherapy. Infants with this syndrome have been seen
Jaundice is unfrequently observed after the 10th day. to have a mixed type of hyperbilirunaemia with significant elevation of direct –
reacting bilirubin and often with other evidence of obstructive liver disease.
KERNICTERRUS
- Neurological syndrome resulting from the deposition of unconjugated bilirubin
in brain cells. PHENOBARBITAL
Unconjugated-bilirubin may cross the blood-brain barrier and enter the brain Phenolarbitone enhances the conjugation and excretion of bilirubin.
by diffusion. Can not be used in the management of hyperbilirunaemia because its effect
Or Bilirubin may enter the brain following damage to the blood- brain barrier on bilirubin metabolism is usually not manifest until after several days of
by asphyxia. administration.
Or hyperosmolality. - It is less effective than phototherapy in lowering serum bilirubin concentrations.
- Kernicterus is rare in healthy term infants. - It may have an untoward sedative effect and does not add to the response
 48 Neonatology Paediatrics Patients’ Management Guidelines 49

to phototherapy
PATENT DUCTUS ARTERIOSUS P.D.A Other manifestations include
- Periods of apnoea
P.D.A –Is vascular connection between the Aorta (descending) and the pulmonary - Pallor
artery. - Cyanosis
After birth in full term babies this blood vessel should close. But it may fail to close - Failure to suck well.
and remain patent. - Abnormal eye signs.
- A high pitched cry.
In premature babies it often remains open. Patency is the result of hypoxia and - Muscular twitching.
immaturity. In premature infants therefore spontaneous closure can occur in most - Convulsions.
infants with PDA. Where as in the full term baby a PDA persisting after the first - Decreased muscular tone
weeks of life will never close. - Paralyses.
PDA is also common in infants born at high altitudes. - Metabolic acidosis.
- Shock.
Clinical Features - Decreased haematocrit or failure to increase after BT.
Depending on the size of the PDA. - Fontanel may be tense and bulging.
- Small PDA –no associated symptoms. - In severe cases – may progress to coma.
- Large PDA – there will be a systolic thrill classic continuous also called
humming top, or rolling thunder in quality will be maximally heard at 2nd left Diagnosis
intercostal space or radiate down the left sternal boarder or to the left clavide. To diagnose IVH-have to consider.
- With large PDA may develop –Congestive cardiac failure. History.
- Retardation of physical growth. Clinical manifestations.
Knowledge of Birth weight.
Management – Treat CCF if present do possible investigations like CXR, ECG& Then do
ECHO And Refer for surgery at referral Hospital. - Transfontanel ultrasonography.
- Computed tomography.

INTRACTRANIAL HAEMORRAGE. - Some surviving infants may later develop hydrocephalus, cerebral palsy.

May result from trauma or asphyxia and rarely from a primary hemorragic Treatment
disturbance or congenital vascular anomaly. If there are convulsions –give anticonvulsant.
Anoemia – shock – give –packed red blood cells.
In premature infants ICH often involve the ventricles (intraventricular hemorrhage. - metabolic acidosis – give 1-2 mEq/kg solution of Sodiumubicarbonate
Such infants are usually delivered spontaneously without apparent trauma.
If a permanent ventricular- peritoneal shunt- consult surgeon for the operation.
Predisposing factors to IVH
Prematurity, Respiratory distress syndrome, increased or decreased cerebral Birth Asphyxia
blood flow, reduced vascular integrity, increased venous pressure, pneumothorax, If an asphyxiated by is received in either NU or NICU who is not well resuscitated
hypervolemia and hypertension, hypoxic-ischoemic. – continue Resuscitation until baby is well resuscitated and stable.

All above lead to rupture of blood vessels.

Clincal Features
The lower the birth weight the higher the probability of IVH. Infants with weight
below 1kg. have a more than 5 times dangers of developing IVH than children of
weight above 1kg.
Most of cases occur between the 1st & 3rd day after birth. Delayed cases may
develop after the 1st week of life.
Manifestations –Diminished or absent moro reflex, muscular tone, poor lethargy,
apnoea, somnolence.
 50 Neonatology Paediatrics Patients’ Management Guidelines 51

The fetus and the Neonatal Infant

External Score Neurologic Score
Signs 0 1 2 3 4 Signs 0 1 2 3 4 5
edema obvious no obvious no edema posture wrists arms wrists bent elbows hips elbows hips elbows &
edema of edema of hips and and legs and legs and legs legs drawn
hands and hands & feet legs straight slightly bent but do bent to 90° close to
feet pitting pitting over bent not reach body
over tibia tibia 90°
skin texture very thin thin and smooth slight thick & square 90° 60° 45° 30° 0°
gelatinous smooth medium thick-ening parchment- window
thick-ness; super-ficial like superficial (wrist)
rash or crack-ing & ordeep
superficial peeling cracking ankle dorsi- 90° 75° 45° 20° 0°
peeling especially of flexion
hands & feet arm recoil 180° 90-180° < 90°
skin color dark red uniformly pale pink; pale; only leg recoil 180° 90-180° < 90°
pink variable over pink over
body ears lips popliteal 180° 160° 130° 110° 90° < 90°
palms or soles angle
skin opacity numerous veins & a few large a few large no blood heel to ear leg straight leg straight knee slightly knee bent knee bent
veins & tibutaries seen vessels seen vessels seen vessels seen toes reach toes reach bent heel heel reaches to 90° heel
venules seen over the indistinctly ear chin reaches 140° 120° from reaches 90°
especially over abdomen over the from prone prone from prone
abdomen abdomen
scarf sign elbow to elbow to elbow to elbow to
lanugo none abundant; hair thinning small at least half of opposite opposite midline axillary line
long & thick especially over amount of back devoid of axillary line midclavicu-
over whole lower back lanugo & bald lanugo lar line
back areas
plantar no skin faint red definite red indentations definite dee-
head lag head lags head head in line head bent
creases creases marks over marks over > over more pindentations
without slightly with body forward
for-ward forward but axis beyond
anterior half anterior 1/3; than anterior over more move-ment does not body axis
of sole indentations 1/3 than anterior at 90° to reach body
over < anterior 1/3 body axis axis
1/3
ventral heads heads head raised ead in line head raised
nipple nipple barely nipple well- areola stippled areola stippled suspension droops slightly but not to with body above body
formation visible no defined are- edge not raised edge raised down and raised and body axis axis back axis back
areola ola smooth & diameter diameter back greatly back less back slightly straight straight
flat diameter < 0.75 cm > 0.75 cm arched arms curved curved
< 0.75 cm & legs
no breast tis- breast tissue breast tissue breast tissue straight
breast size
sue palpable on one or on both sides both sides one
both sides 1 or both 0.5 - or both
< 0.5 cm 1.0 cm > 1.0 cm
diameter
ear form pinna flat incurving of partial well-defined
and shapeless part of edge incurving incurving
little or no of pinna whole whole of
incurving of of upper upper pinna
edge pinna
ear firmness pinna soft pinna soft cartilage to pinna firm
easily folded easily folded edge of pinna cartilage to
no recoil slow recoil but soft in edge instant
places ready recoil
recoil
genitals female labia labia majora labia majora
majora widely almost cover completely
separated labia minora cover labia
labia minora minora
protruding
genitals male
neither testis at least one at least one
in scrotum testis high in testis right
scrotum down
The score proposed by Dubowitz et al assesses an infant for the apparent gestational age by considering
both neurologic and external signs of development. Dubowitz score = SUM (points for each parameter)
Interpretation: • minimum score: 0 • maximum score: 72 (neurological sign 35 external sign 37)
estimated gestational age = (0.2642 * (total score)) + 24.595
 52 Neonatology Paediatrics Patients’ Management Guidelines 53

Gestational Age in weeks

Infectious
y=0.2642x + 24.595

44

disease
43
42
41
40
39
38
37
36
35
– Gastroenteritis/Worms/Parasit
34
33 – HIV/AIDS
32 – Malaria
31 – Meningitis
30 – Pneumonia
29 – Tuberculosis
28 – Urinary Tract Infection
27
26
10 20 30 40 50 60 70
Gastroenteritis
Definition

Gastroenteritis: Inflammation of the gastrointestinal tract. Usually secondary to an

infection (most often viral) that results in vomiting and diarrohea.

Classification of Diarrhoea Disease

1. Acute watery Diarrhoea is diarrhoea which develops abruptly and lasts
for less than 14 days.
2. Persistent Diarrhoea. This is diarrohea which develops abruptly but lasts f
or longer than 14 days.
3. Dysentery. This is Bloody Diarrhoea.

Causes / Etiology
Diarrohea is caused by Viruses, Bacteria, Parasites and fungi.
Viruses Bacteria Parasites Fungal
Rotavirus E.coli E. hystolitica Candida spp
Adenovirus C. defficile G. lamblia
Parvovirus Salmonella Cryptosporidium
Norwalk virus Shigella spp Strongyloides
S. aureus Trichuris trichiura
Vibrio cholerae
Y. enterocollitis
 54 Infectious Disease Paediatrics Patients’ Management Guidelines 55

RISK FACTORS TREATMENT

• Failing to breastfeed exclusively for the first 4 – 6 months. SEVERE DEHYDRATION

• Poor weaning practices Ringer’s Lactate solution
• Use of infant feeding bottles
• Storing cooked food at room temperature Age First give Then give
• Using contaminated drinking water 30ml/kg in: 70ml/kg in:
• Lack of immunizations.
Infants
• Poor hygiene. (under year 12months) 1hr 5hrs
• Malnutrition
• Immunosuppression Older children 30 minutes 2.5hrs
• Infections
Reassess the patient every 1-2 hrs. if hydration is not improving give the
intravenous drip more rapidly.
CLINICAL FEATURES Give ORS – when child can drink in an amount of 5ml/kg/hr.
Assess child for state dehydration after 6hrs for infants below 12 months and 3hrs
Diarrhoea with or without blood for older children and choose the appropriate treatment plan – Treatment plan
Vomiting A,B,or C to continue.
Fever
States of Dehydration SOME DEHYDRATION
Hypotension Treatment plan B for children with some Dehydration.
Tachycardia
Lethargy Approximate amount of ors solution to be given in 4 hours.
Unconsciousness
Age < 4mon 4-11mon 12-23mn 2-4yrs 5-14 ≥ 15yrs
Clinical Assessment of Dehydration. Weight < 5kg 5-7.9kg 8-10.9kg 11-15kg 16-29.9kg 30+kg
Volume
200- 400- 600- 800- 1200- 2200-
Features Severe Some dehydration No dehydration 400ml 600ml 800ml 1200ml 2200ml 4000ml
dehydration
General condition Very lethargic/ Restless/irritable Normal
unconscious Use the patient’s age ONLY when you do not know the weight, the approximate
Eyes Sunken Sunken Normal amount of ORS required (in ml) can also be calculated by multipeying the patients
Thirsty Drinks poorly/ Thirsty/drinks Drinks normally/ weight in kg by 75 (75 x kg).
unable to drink eagerly not thirsty If patient wants more ORS than shown give more.
Skin pinch Goes back very Goes back slowly Goes back quickly Encourage mother to continue Breast feeding her child.
slowly Infants under 6 months who are not Breastfed give 100 – 200ml of boiled / clean
Treatment Plan C Plan B Plan A water during this period.

Treatment Plan A
Investigations. Aim is to prevent Dehydration and Malnutrition.
• After proper History and physical examination.
• Blood for serum Electrolytes in sense cases. Mothers should be taught how to:
• Stool analysis microscopy and C/S • Give the child more fluids than usual to prevent dehydration. Fluids like.
Na > 150 mmol/L hypertonic dehydration - ORS
Na < 120 mml/L hypotonic dehydration - Rice water
• Rule out other serious illness eg meningitis, Malaria, Bacterial Sepsis, - Yoghurt drink
Pneumonia, Otitis Media and Urinary tract lafection. - Vegetable soup
- Plain water
- Black tea
 56 Infectious Disease Paediatrics Patients’ Management Guidelines 57

• Continue to feed the child to prevent Malnutrition. Continue Breast feeding Common Parasitic Diseases and their treatment
if child is still on Breast feeding.
• Take the child back to hospital if there are signs of dehydration and also if Parasite Treatment
child develops: fever, has blood in stool and can not drink. Amoebiasis Metronidazole
Medication and Diarrhea Giardiasis Metronidazole
Generally antibiotics can damage the bowel, prolong fecal excretion of a pathogen Ascariasis Mebendazole or Albendazole
or destroy many of the useful normal flora. Enterobius vermicularis Mebendazole or Albendazole
Hookworm Mebendazole or Albendazole
Give antibiotics only in: Trichuris trichiura Mebendazole or Albendazole
Dysentery Strongyloides stercolaris Thiabendazole
Vibrio cholera
Schistosoma mansoni Praziquantel
Salmonella typhi
Cryptosporidium Azithromycin
Entamoeba histolytica
Giardia lamblia Isospora belli Cotrimoxazole or Azithromycin

USE OF ZINC
– Zinc is used to replenish the lost amount during diarrohea, it is given in form of References:
a table together with rehydrating fluids. 1.) David Southall, Brian Coulter et al.: Diarrhoea Diseases, International
– DOSAGE - Infants below 6 months 10mg once daily for 10days older children Childhealth Care. A practical manual for hospitals worldwide, 2006
20mg daily for 10 days. 2.) Nelson Textbook of Paediatrics, 17th Edition
World Health Organization, Pocket Book of Hospital Care for Children:
ANTIMOTILITY DRUGS Guidelines for the Management of Common Illnesses with Limited Resources,
Use of antimotility drugs e.g lomotil and loperamide is NOT recommended Geneva, 2005

ANTISECRETORY AGENTS.
Not recommended.

COMPLICATIONS Pediatric HIV Infection

Dehydration
Electrolyte imbalance DEFINITION
Metabolic acidosis
Paralytic ileus Human Immunodeficiency Virus (HIV) is a retrovirus belonging to the lentivirus
Acute renal failure family. The virus attacks CD4+ cells causing destruction of the infected cells.
Haemolytic uraemic syndrome This breakdown of the immune system leads to vulnerability to a wide variety of
Malnutrition infections and the eventual development of AIDS (Acquired Immune Deficiency
Malabsorption Syndrome).
Anemia
Shock
Intussusception MODE OF TRANSMISSION
Convulsion
Death There are three main body fluids through which HIV can be transmitted:
• Blood
• Breast milk
PREVENTION • Genital secretions

Immunization More than 95% of HIV-infected children acquire HIV from their mothers
Good hygiene (mother-to-child-transmission: MTCT) during pregnancy, at the time of delivery,
Good nutrition status or postnatally through breast feeding. Without intervention, approximately 20
Breastfeeding (not bottle feeding). to 40% of HIV positive mothers transmit the virus to their newborns. Maternal
treatment can reduce MTCT to less than 2%.
 58 Infectious Disease Paediatrics Patients’ Management Guidelines 59

WHO CLINICAL STAGING FOR INFANTS AND CHILDREN <15

The majority of HIV-infected children (50-60%) develop symptoms in early life YEARS OF AGE
with disease progression and death by 3-5 years old.
Most HIV-infected children, in low resurces countries, die from common PRIMARY HIV INFECTION
childhood illness, rather than AIDS, which is why every child in clinic or in the • Asymptomatic
ward should be screened for HIV infection. • Acute Retroviral Syndrome

CLINICAL STAGE 1
DIAGNOSIS • Asymptomatic
• Persistent generalized lymphoadenopathy (PGL)
Depending on available resources in a given setting, diagnosis may be initially
made clinically but lab confirmation MUST follow as quickly as possible. Ideally, CLINICAL STAGE 2
diagnosis is made through early screening (Rapid test, PCR) before clinical • Hepatosplenomegaly (unexplained, persistent)
manifestations of HIV disease. • Papular pruritic eruptions
• Extensive human papilloma (wart) virus infection (facial, >5% of body area
or disfiguring)
PRESUMPTIVE DIAGNOSIS OF SEVERE HIV DISEASE • Extensive molluscum contagiosum (facial, >5% of body area or disfiguring)
• Recurrent oral ulcerations (2 or more episodes in 6 months)
A presumptive diagnosis may be made, and treatment initiated, in infants <18 • Lineal gingival erythema (LGE)
months of age who are HIV-antibody positive and either have a WHO clinical • Angular cheilitis
stage 3 or 4 (see below) or have two or more of the following: thrush, severe • Seborrheic dermatitis
pneumonia, or severe sepsis. • Parotid enlargement (unexplained, persistent)
Recent maternal death, advanced maternal HIV disease, and CD4 < 25% in the • Herpes zoster (current or past episode in last 2 years)
infant supporting the diagnosis. Confirmation of HIV infection is needed in • Recurrent or chronic upper RTIs (otitis media, otorrhea, sinusitis, tonsillitis)
children < 18 months. with 2 or more episodes in 6 months
• Fungal nail infections

SPECIFICITY OF MEDICAL DIAGNOSIS FOR HIV CLINICAL STAGE 3

Conditions where a presumptive diagnosis can be made on the basis of clinical signs
Specificity for HIV Signs/symptoms or simple investigations
• Moderate (< 2 SD or Z score) unexplained malnutrition not adequately
Signs/conditions very specific * As listed in WHO Clinical Stage 4 responding to standard therapy
to HIV infection • Unexplained persistent diarrhea (14 days or more)
• Unexplained persistent fever (> 37.5°, intermittent or constant, for longer
Signs/conditions common to HIV * Severe bacterial infections, than 1 month)
infected children and uncommon in particularly if recurrent
uninfected children • Oral candidiasis (persistent or recurring; outside first 6-8wks of life)
* Persistent or recurrent oral thrush
• Oral hairy leukoplakia
* Bilateral painless parotid enlargement • Acute necrotizing ulcerative gingivitis/ periodontitis
* Generalized persistent non-inguinal • Lymph node TB
lymphadenopathy • Pulmonary TB
* Hepatosplenomegaly • Severe recurrent presumed bacterial pneumonia (2 or more episodes
(unexplained by malaria) in 6 months)
* Persistent and/or recurrent • Conditions where confirmatory diagnostic testing is necessary
(unexplained) fevers
* Neurological dysfunction Symptomatic lymphoid interstitial pneumonitis (LIP)
* Herpes zoster, single dermatome • Chronic HIV-associated lung disease including bronchiectasis
* Persistent generalized dermatitis • Unexplained anaemia (<8gr/dl), neutropenia (<1000/mm3) or chronic
thrombocytopenia (<50,000/ mm3) >1 month
Signs/conditions frequently related to * Persistent or recurrent diarrhea
HIV infection * Tuberculosis CLINICAL STAGE 4
Conditions where a presumptive diagnosis can be made using clinical signs or
* Marasmus/Kwashiorkor
 60 Infectious Disease Paediatrics Patients’ Management Guidelines 61

simple investigations: with good adherence and a CD4 count > 350 cells/mm3.
• Unexplained severe (< -3 SD or Z score) wasting, stunting, or severe TREATMENT OF HIV
malnutrition not adequately responding to standard therapy
• Pneumocystis carinii (jiroveci) pneumonia As in adults, treatment of HIV infection in children requires life-long
• Recurrent severe presumed bacterial infections (eg. empyema, pyomyositis, administration of antiretroviral medications to achieve viral suppression. Viral
bone or joint infection, meningitis, but excluding pneumonia) (2 or more suppression leads to preservation or restoration of the immune system, improved
episodes in 6 months) growth and development, and reduced morbidity and mortality. Effective
• Chronic orolabial or cutaneous Herpes simplex infection (> 1 month duration), treatment is always composed of at least three antiretroviral medications and is
or visceral at any site known as combination therapy or highly-active antiretroviral therapy (HAART).
• Extrapulmonary tuberculosis To achieve and maintain viral suppression, excellent adherence to HAART is
• Kaposi’s sarcoma necessary. Medication adherence >95% is associated with long-term success.
• Oesophageal candidiasis (or candida of trachea, bronchi, or lungs) Even moderate or temporary lapses in adherence can lead to viral resistance and
• CNS toxoplasmosis (outside the neonatal period) treatment failure.
• HIV encephalopathy
• Conditions where confirmatory diagnostic testing is necessary: WHO immune criteria for ART initiation in infants and children

CMV infection (retinitis or of another organ; onset at age one month or older) <12 months 12-35 months 36-59 months ≥ 5 years
• Extrapulmonary Cryptococcsis (including meningitis) CD4 % ALL < 20% < 15%
• Any disseminated endemic mycosis (e.g. extrapulmonary Histoplasmosis,
CD4 absolute < 750 cells/mm3 < 350 cells/mm3 < 200 cells/mm3
Coccidiomycosis, Penicilliosis) value
• HIV-associated cardiomyopathy or HIV-associated nephropathy

LABORATORY DIAGNOSIS Algorithm for ART Initiation in Infants and Children

Serologic Tests (detect antibody to HIV)
• Rapid tests (ELISA): Tests of choice to diagnose HIV infection in adults and
Hiv infected
children ≥ 18 months of age. Due to passive transfer of maternal antibodies, a
positive test < 18 months of age indicates exposure and possible infection only.
Age < 1 yr Yes Start ART regardless
Virology Testing (directly detects virus) of CD4% or stage
• DNA PCR: Qualitative test that detects HIV DNA. Collected using “dried No
blood spot” (DBS)
• RNA PCR: Quantitative test (viral load) that detects HIV RNA.
Perform WHO Clinical Staging
Whom and when to test
• According to the national guidelines of PICT (provider initiated counseling
and testing) ALL patients should be tested at presentation to OPD or pediatric
ward. The goal is to diagnose asymptomatic patients as early as possible. WHO Stage 1 WHO Stage 2 WHO Stage 3 WHO Stage 4
• Appropriate pre- and post-test counseling must be provided.

PCP PROPHYLAXIS Perform CD4% Start ART Start ART

Cotrimoxazole (trimethoprim-sulfomethoxazole) is a broad-spectrum antimicrobial regardless of regardless of
used for prophylaxis against opportunistic infections. It is primarily used for PCP CD4% CD4%
(Pneumocystic jiroveci pneumonia) prophylaxis, but it is also useful in preventing
toxoplasmosis, malaria, various diarrheal infections and serious bacterial infections. CD4 > 20% CD4 < 20%
Cotrimoxazole prophylaxis (Dose: trimethoprim 4mg / kg /day OD) should be
given to all exposed infants, beginning at one month of age and continued until No ART
definitive negative diagnosis. All infected children less than five years of age should Monitor Start ART
also receive prophylaxis, even if they are on ART. patient
Older children, adolescents and adults require cotrimoxazole for symptomatic
infection (WHO Clinical Stage 2, 3 or 4) or for CD4 counts < 350 cells/mm.
Prophylaxis can be discontinued once a patient has been on ART for six-months
 62 Infectious Disease Paediatrics Patients’ Management Guidelines 63

ART REGIMENS <90%) is common and often out-of-proportion to the respiratory distress. Lung
sounds may be normal or have diffuse crepitations. Patients with undiagnosed
First-line ART regimen are Zidovudine (AZT) + Lamivudine (3TC) + Nevirapine PCP will have poor response to standard antibiotic therapy (consider this diagnosis
(NVP) for children less than 3 years and / or less than 10 kg BW and Zidovudine in any child whose HIV status is unknown and is not responding to antibiotics).
(AZT) + Lamivudine (3TC) + Efavirenz (EFV) for children 3 years and older and / Chest X-ray can be normal or may show diffuse, bilateral hazy infiltrates (classic)
or more than 10 kg BW. or focal findings. Promptly give HIGH DOSE cotrimoxazole (trimethroprim 15-
Stavudine (d4T) may be substituted for Zidovudine (AZT) in patients with 20mg/kg/day) 4 times a day for 3 weeks as treatment. Consider steroids (1-2 mg/
anemia (Hb < 7.5 g/dL). However, due to long-term side effects associated with kg/day) especially if child requires oxygen. Patients with PCP pneumonia should
Stavudine, it is not recommended for patients with other ART options. Initiation receive secondary prophylaxis with cotrimoxazole.
with Nevirapine requires a two-week induction dose to limit development of side
effects, particularly rash. Doses of medications should be reviewed at each visit Oral and Oesophageal Candidiasis
and adjusted as needed with weight gain. Use of a dosing card is recommended to For oral thrush: treat with Nystatin (100,000 units/ml) 1-2 ml into mouth 4 times
reduce dosing errors. a day for 7 days OR gentian violet solution 0.25-0.5%. If not responding, give
3mg/kg daily fluconazole.
Medication side effects and toxicities are generally uncommon and mild. However,
careful monitoring is needed to identify and treat more serious complications. Suspect Oesophageal candidiasis if there is: difficulty or pain while vomiting or
When evaluating for medication toxicity, the most important consideration is swallowing; reluctance to take food; excessive salivation; or crying during feeding.
the severity of the toxicity. Concurrent medications and other disease processes It may occur with or without evidence of oral thrush. Treatment is with oral
should also be evaluated when managing potential ART toxicity. Mild toxicities fluconazole 6mg/kg once daily for 7 days.
do not require a change in therapy. Moderate reactions generally do not require a
change in therapy and can be managed with symptomatic therapy. Severe reactions Lymphoid Interstitial Pneumonitis (LIP)
require substitution of the offending drug only. The offending drug should be Suspect LIP if chest X-ray shows bilateral reticuloendothelial pattern. This may be
replaced with another drug from the same class that does not have the same difficult to differentiate from PCP or military TB. Suspect this if the child does not
adverse effects. Life-threatening reactions require immediate discontinuation of all have fever or failure to thrive but has isolated respiratory symptoms including: Fast
ARV medications and administration of symptomatic and supportive care. Once or labored breathing; Cyanosis; Finger clubbing; Pulse oximetry reading <90%.
patient is stabilized, a modified ART regimen can be restarted. The most common Incidence is most common is children aged 3 – 8 years. Often, patients have been
life-threatening reaction seen in patients on ART is Stevens Johnson Syndrome. treated for pulmonary tuberculosis without improvement. Symptomatic treatment
Nevirapine is the medication most commonly implicated. If a patient has (SJS) on includes oral prednisolone 1-2mg/kg daily for 4 weeks, then every other day for
(NVP), it is recommended that ART be restarted on a protease inhibitor-containing 2-3 months with review. Provide oxygen during episodes of hypoxia and give
regimen. There is structural similarity between Efavirenz and Nevirapine that salbutamol if wheezing at presentation. Most children improve with ART.
can lead to cross-reactivity, therefore, it is safest not to reintroduce an NNRTI
(Efavirenz and Nevirapine) in patients with SJS. (Appropriate induction dosing of References:
Nevirapine reduces the incidence of SJS.) 1. Kourtis AP, Lee FK, Abrams EJ, Jamieson DJ, Bulterys M. Mother-to-child
transmission of HIV-1: timing and implications for prevention. Lancet Infect
Consult an HIV specialist for medication assistance for patients with prior exposure Dis 2006; 6: 726-732.
to ART and for patients with treatment failure. 2. National Guidelines for the management of HIV and AIDS, 3rd Edition.
National AIDS Control Programme (NACP), United Republic of Tanzania,
Ministry of Health and Social Welfare. Revised February 2009.
TREATMENT OF SELECTED HIV-RELATED CONDITIONS 3. Violari A, Cotton M, Gibb D, Babiker A, Steyn J, et al, on behalf of the
CHER (Children with HIV Early Antiretroviral Therapy) Study Team. Early
Tuberculosis Antiretroviral Therapy and Mortality among HIV-Infected Infants. N Engl J
Tuberculosis remains the primary cause of mortality in HIV-infected people. It is Med 2008;359:2233-44.
crucial to adequately screen for and treat tuberculosis. Treatment tuberculosis in 4. Scale up of HIV prevention, diagnosis, care and treatment for Infants and
HIV infected children the same as in non-infected children. NOTE: Have a high children: A Programming Framework, WHO and UNICEF 2008
index of suspicion for TB in any child on ARVs who is not gaining weight. For 5. HIV Early Infant Diagnosis Guidelines in Tanzania.
further management: see TB-guideline 6. The Sanford Guide to Antimicrobial Therapy 2009
7. The Harriet Lane Handbook, 18th Edition. 2009
Pneumocystis Jiroveci (formerly carinii) Pneumonia (PCP) 8. Hospital Care for Children. World Health Organization. 2007
PCP pneumonia is the leading cause of HIV-related deaths in infants, with a peak
incidence in the first six months of life. It presents similarly to other types of
pneumonia with tachypnea, cough, and shortness of breath. Hypoxia (saturation
 64 Infectious Disease Paediatrics Patients’ Management Guidelines 65

Malaria Dosage schedule of Artemether 20mg & Lumefantrine 120mg (ALU)

Day 1 Day 2 Day 3

DEFINITION Kg Dose h 1st 2nd 3rd 4th 5th 6th Colour
code
Malaria is an acute and chronic illness characterized by paroxysms of fever, chills, Hours 0 8 24 36 48 60 Coartem
sweats, fatigue, anemia, and splenomegaly, due by Plasmodium (P. falciparum, P.
malariae, P. ovale, P. Vivax, P. kwnolesi). There are uncomplicated forms and severe Age Tablets Tablets Tablets Tablets Tablets Tablets
forms.
Any child who presents with fever or unexplained systemic illness in a malaria- 3
months
endemic area should be assumed to have life-threatening malaria until proven 5-15 up to 1 1 1 1 1 1 Yellow
otherwise. 3 years
Malaria is caused by intracellular Plasmodium protozoa transmitted to humans by
female Anopheles mosquitoes (incubation period 5-12 days). 3 years
15-25 up to 2 2 2 2 2 2 Blue
8 years
CLINICAL FEATURES OF UNCOMPLICATED MALARIA 8 years
25-35 up to 3 3 3 3 3 3 Red
• Fever 12 years
• Headache
• Joint pain 35 and 12 years
• Malaise above and 4 4 4 4 4 4 Green
above
• Body weakness
• Vomiting
• Diarrhoea 0 hours means time of starting medication.
• Chest pain
• Anaemia (mild to moderate) Non response to ALU may be due to:
• Hepato-splenomegaly especially in children • Vomiting the drug
• Poor quality of the drug
• Inadequate dosage
TREATMENT OF UNCOMPLICATED MALARIA • Fever/symptoms from a cause other than malaria
• Parasite resistance to the drug (rare)
The first line treatment of uncomplicated malaria is the combination Artemether –
Lumefantrine Treatment of uncomplicated malaria with second line drug: Quinine
Available formulations: Available formulations
• Tablets: Combined tablets of Artemether 20 mg and Lumefantrine 120 mg • Tablets 300mg
(ALU). • Injection 600mg in 2mls
Contraindications: • Quinine hydrochloride syrup 100mg/5ml
• Hypersensitivity to either Artemether or Lumefantrine
Not recommended: Indications:
• Children below 5kg body weight • Treatment of uncomplicated malaria where ALU is contraindicated or has failed.
• First trimester of pregnancy Contraindications
• Lactating mother with child below 5kg of body weight • Hypersensitivity to quinine
Dosage regimes • Optic neuritis
The dose of Artemether – Lumefantrine is 1.5/12mg/kg body weight twice a day • Myasthenia gravis
for three days.
For convenience purposes, the dosing schedule for ALU (strength 20/120mg) is Dosage regimen
reported in table. Treatment with quinine tablets (salt) should be given for 7-10 days at a dose of
10mg/kg every 8 hours.
 66 Infectious Disease Paediatrics Patients’ Management Guidelines 67

SEVERE MALARIA MANAGEMENT OF SEVERE MALARIA

Severe Plasmodium falciparum malaria is a medical emergency. Delay in diagnosis

Investigations
and provision of appropriate treatment may lead to serious complications and
even death. The commonest presentations of severe malaria are severe anaemia and
Essential If indicated
cerebral malaria.
Blood glucose estimation Blood culture and sensitivity
Features of severe malaria Blood film for malaria parasites/RDT Chest radiograph
One or more of the following features indicates severe malaria
Full blood picture Cerebral spinal fluid analysis
Urinalysis (including detection of Hb) Urine culture and sensitivity
Clinical features Description / criteria
Biochemical tests: serum creatinine,
Prostration/ extreme weakness Unable to stand or sit without support liver function tests (bilirubin,
Impaired consciousness Altered level of consciousness AST, ALP) Arterial Ph and serum
Acute confusion state, coma electrolytes.
Change of behaviour Hallucinations, delusions, agitation
Convulsions Repetitive abnormal muscular Assessment and resuscitation
movements • ABCs of life
Nursing care and monitoring
Respiratory distress (due to lactic Acidotic breathing: deep and laboured
acidosis and/or pulmonary oedema breathing • Fluid input and output chart
Pulmonary oedema: laboured • Level of consciousness
breathing, restlessness, • Temperature, PR, RR, and BP
Blood stained frothy sputum especially
in adults Administration of intravenous quinine
Bleeding tendency/DIC Easy/prolonged bleeding Dose
• Quinine 10mg/kg body weight of salt diluted in 5-10 ml/kg body weight in
Jaundice Yellow coloration of mucus membranes
5% dextrose or dextrose saline
Circulatory collapse/shock Low systolic BP and fast pulse rate • Should be infused over 4 hours and repeated every 8 hours until patient is
(according to age limits) able to take orally.
Vomiting everything Throwing up after every feed/drink • The total volume given will depend on the patient’s overall fluid balance.
• The drop rate is calculated as follows:
Inability to drink or breast feed Not able to swallow
Drop rate per minute= amount of fluid to be infused (in ml) * 20 (drop factor)
Condition Corresponding indices Time period to be infused (in minutes)
Severe malarial anaemia Hb <7g/dl or haematocrit <21% • Continue with quinine for 7-10 days or ALU when patient can take orally.
Haemoglobinuria Dark brown or positive Hb on dipstick Non response to quinine therapy could be due to:
urine
• Persistence of clinical features of severe malaria
Pulmonary edema CXR: enlarged cardiac silhouette& • Failure of clearance of parasites after 5 days of treatment
azygous vein, peribronchial cuffing. • Other possible causes of illness which have not been investigated
Hyperparasitemia >5000 asexual parasites per 200 WBC
(>200,000 asexual parasites per micro Patients with malaria who have not responded to quinine therapy should be given
litre) parenteral artemether.
Metabolic acidosis Arterial pH < 7.3, Bicarbonate < Dose: 3.2mg/kg (loading dose) I.M. followed by 1.6mg/kg I.M. daily for 6 days
15mmol/L
Acute renal failure Oliguria urine output < 0.3ml/kg/hr
in children and < 17ml/hr in adults.
Raised serum creatinine >130mmol/L
and BUN >6.7mmol/L
Hypoglycaemia Glucose < 2.5mmol/L
 68 Infectious Disease Paediatrics Patients’ Management Guidelines 69

ADDITIONAL ASPECTS OF CLINICAL MANAGEMENT • Seizures

• Jaundice
Convulsions • Pallor
• Convulsions are common in children with severe P. falciparum malaria but are • Hepatosplenomegaly
relatively rare in adults. • Laboratory findings will include the presence of malaria parasites,
The general principles for the care of patient with convulsions should be followed hyperbilirubinemia, anaemia (Hb<13.5g/dl), hypoglycaemia and acidosis
(see seizures & epilepsy)
Management of neonatal malaria
Hypoglycaemia (refer guidelines) Neonates with suspected malaria should be admitted to the hospital immediately as
they can deteriorate quickly and die at home.
Hypotension (refer shock)
Assessment and resuscitation - ABCs
Pulmonary oedema (refer heart failure)
Investigations
Metabolic acidosis • The following investigations should be done:
In malaria patients metabolic acidosis is attributed to lactic acidosis, patient may • FBP, blood sugar, blood culture and sensitivity, urgent blood slide for malaria
present with deep laboured breathing, give oxygen and correct hypovolemia parasite, serum electrolytes.

Treatment
OTHER ANTIMALARIAL DRUGS AVAILABLE IN TANZANIA Broad spectrum antibiotic as provided in the Standard Treatment Guidelines (STG)
Parenteral quinine 10mg/kg 8-12 hourly till the baby is able to breast-feed,
Other artemisinin based combination drugs then oral quinine is given to complete 7 days treatment. (Beware of ventricular
• Artesunate and Amodiaquine combination tachycardia)
• Artesunate and Mefloquine combination If a neonate is not able to breast-feed, give 10%glucose IV 60ml/kg/24hrs
Antimalarial mono-therapies or single component combination therapies Give blood transfusion if Hb is <10g/dl
• Sulfadoxine/Pyrimethamine
• Sulfalene/Pyrimethamine (Metakelfin) Nursing care and monitoring
• Amodiaquine • Admit to neonatal ICU for monitoring
• Mefloquine • Monitor vital signs (PR,RR & Temperature)
• Halofantrine • Monitor input/output
• Proguanil Hydrochloride • Check BS for malaria parasite daily
• Doxycycline • Ensure feeding
• Advise on use of ITNs

MANAGEMENT OF MALARIA IN THE NEONATE AND Reference:

INFANTS BELOW 5KG 1. National Guidelines for malaria diagnosis and treatment (2006)

Introduction
Malaria in the neonate (first four weeks of life) is very rare: in Muhimbili Neonatal
Unit the incidence of congenital malaria in hospitalised newborns is 3/100,000.
Congenital or acquired malaria in this age group is life threatening and requires
immediate treatment. Quinine remains the drug of choice for treatment.

Clinical features
The signs and symptoms resemble those seen in the newborn with septicaemia,
including: Fever
• Lethargy
• Unable to breastfeed
• Vomiting
• Irritability
• Respiratory distress
 70 Infectious Disease Paediatrics Patients’ Management Guidelines 71

Meningitis • A drop of CSF placed on urine dip stick that shows low glucose, high protein
and high leucocytes may indicate bacterial meningitis
• CSF should be sent to microbiology in 2 sterile tubes/Bottles for
- gram stain and culture
DEFINITION - Cell count and differential
- Proteins
Meningitis is an infection of the meninges and cerebral spinal fluid (CSF). It - Z-N stain
results in meningeal inflammation, obstruction of the flow of the CSF (due to - Indian Ink for cryptococcus in immunosuppressed
purulent exudates), cerebral oedema, and local necrosis of nerve fibers and cerebral
vessels. • Sugar – CSF Specimen should be sent to biochemistry in fluoride bottle

CAUSES CSF values for common conditions

Most cases of meningitis are caused by bacteria (including TB), viruses, or fungi Organism Pressure WBC/ml Protein(Mg/dl) Glucose(Mg/dl)
• Neonates: S. pneumoniae, Group A and B streptococcus and enteric gram
negative bacilli (mainly E.coli) normal Normal Lymphocytes 0-5 10-50 >50% of serum
glucose
• 3 months to adolescence: H. influenzae, S. pneumoniae, N. meningitides and
Salmonella (esp. in association with diarrhoea, HIV/AIDS and malnutrition) bacteria Elevated >1000 100-500 40
• M. Tuberculosis is most common in young children, but can affect children polymophonucleates
of any age Viral Elevated <1000 50-200 Normal
• Cryptococcal neoformans, mostly in immunocompromised lymphocytes
• Viral (aseptic meningitis): Hepers simplex, mumps, enterovirus, adenovirus etc.
TB Elevated 50-500 lymphocytes 100- 3000 <50
in Immunocomproised patients
Fungal Elevated 5-500 monocytes 25- 500 50

CLINICAL PRESENTATION

Infants – Features non-specific, many signs may be absent Absolute Contraindications to lumbar puncture
Fever
Focal or generalized seizures • Deep coma – GCS<8, BCS<3 – or any FALLING coma score
Failure to breast feed - vomiting • Any new focal neurological sign – pupil dilatation, cranial nerve palsies
Irritability - high pitched cry • Papilloedema
Full/bulging fontanelle. • Protacted seizure
Apnoea • Severe vomiting

Older Children If there are contraindications to LP start treatment.

Fever CSF analysis will still give useful diagnostic information for up to 72 hours
Convulsions
Change in mental status/ altered level of consciousness Other important work up procedures
Headache • Malaria slide to rule out cerebral malaria
Photophobia • Full blood picture
Irritability • Blood and urine cultures may be supportive if they are positive with an
Stiff/retracted neck abnormal CSF. Other tests to be considered: nose or throat swab cultures,
Positive Kernig/Brudinsky signs culture of middle ear effusions or skin lesions.
• Blood Sugar
• serum Electrolytes
INVESTIGATIONS • Fundoscopy
• Brain ultrasound if anterior fontanel is still open-when hydrocephalous is
Lumbar puncture (LP) and CSF examination is the main diagnostic tool. Check suspected (increasing head circumference)
for signs of increased intracranial pressure before tap. • Neuroimaging [CT scan and/or MRI] have no role in diagnosis, but may be
• Bacterial meningitis should be presumed if the CSF appears cloudy/turbid in a used when complications are suspected
clean tube
 72 Infectious Disease Paediatrics Patients’ Management Guidelines 73

MANAGEMENT GENTAMICIN DOSING IN NEONATES

Antibiotic Combinations should be guided by culture and sensitivity results, Gestational Age Age (Postnatal) Dose Interval
however
≤ 29 weeks
Unknown aetiology beyond the Ampicillin + Chloramphenicol (first- (or if severe asphyxia) 0-28 days 2.5mg/kg/dose Every 24 hours
neonatal period: (empiric therapy) line treatment) > 28 days 3mg/kg/dose Every 24 hours
OR 30-36 weeks 0-14 days 3mg/kg/dose Every 24 hours
Benzyl penicillin + Chloromphenicol > 14 days 2.5mg/kg/dose Every 12 hours
OR ≥ 37 weeks 0-7 days 2.5mg/kg/dose Every 12 hours
Ceftriaxone (2nd line treatment)
> 7 days 2.5mg/kg/dose Every 8 hours
Unknown aetiology during the neonatal Ampicillin + Gentamicin- 1st line
period: (empiric therapy) OR Duration of Treatment
Ampicillin + Ceftriaxone- 2nd line
If aetiology unknown and as a general rule: 14 days
Haemophilus influenzae Ampicillin + Chloramphenicol Gram negative: 3 weeks
Pnemococci Benzyl penicillin + Chloromphenicol
If therapy is failing, consider adding
Rifampicin 20 mg/kg/day in 2 doses SUPPORTIVE TREATMENT
orally or switching to a 3rd generation
Cephalosporin
• Monitor vital signs temperature, pulse and respiration frequently, every hour
Meningococci Benzyl penicillin at first and every 4 hours when stable.
Tuberculosis Refer to the tuberculosis guidelines • Monitor neurological status using modified Glasgow coma score for children at
least twice a day. More frequent assessment may be necessary initially.
Cryptocococcal neoformans Amphotericin B for 2 weeks till • If the child is in coma manage as per recommendations for the unconscious
clinically stable then Fluconazole for 8 patient.
weeks then maintenance for life • Treat hypoglycaemia and electrolyte imbalance as indicated.
or Fluconazole alone for 6 to 10 weeks • Fluids at 2/3 (75%) maintenance
then maintenance • Monitor input and output (remember to watch for SIADH secretion)
• N/G tube for feeding if unconscious, vomiting or unable to take orally.
DRUGS ROUTE AND DOSING IN MENINGITIS • Control seizures if present. See management of convulsions.
• Antipyretics, paracetamol (15 mg/kg) 4-6 hourly, tepid sponging is needed if
febrile.
Dexamethasone IV 0.6mg/kg divided into 4 doses (max 40mg/day)
Mannitol IV 0.5 gr/kg x 4-6 doses/day FOLLOW-UP
Benzyl penicillin IV 0.25MU/kg/day divided into 4 doses The most frequent long-term consequence of meningitis is hearing loss. Refer to
ENT specialist after discharge.
Ampicillin IV 200–400 mg/kg/day in 3-4 doses (max 12g/day) Outpatient follow-up is important to monitor head circumference, developmental
Chloramphenicol IV 100 mg/kg/day in 4 doses (max dose 4g/day) milestones, and evaluate the need for community based rehabilitation.
Gentamicin IV 7.5mg/kg/day in 3 divided doses in children
(max 120mg x3) (see below for neonates) References
1. Standard Treatment Guidelines Tanzania Mainland, 2007, MOH
Cefotaxime IV 200-300 mg/kg/day in 4 doses (max 12g/day)
2. Hospital care for children 2007, WHO
Ceftriaxone IV 100 mg/kg/day in 2 doses (max dose 4g/day) 3. Forfar and Arneil’s Textbook of Paediatrics, Ed Campbell AGM, McIntosh N;
Ceftazidime Churchill Livingstone 1992
(for Pseudomonas) IV 150 mg/kg/day in 3 doses (max dose 6g/day) 4. Manual of International Child Health Ed Southall D, BMJ 2000
(Vancomicine) IV 40 mg/kg/day divided into 4 doses (max 2gr/d)
Amphotericin B IV 07 -1.0mg/kg/day
Fluconazole IV/OS 10-20 mg/kg/day for treatment 5mg/kg/day
maintenance
 74 Infectious Disease Paediatrics Patients’ Management Guidelines 75

Pneumonia CLINICAL SIGNS AND CLASSIFICATION OF PNEUMONIA

ACCORDING TO WHO
Type of Signs and symptoms TREATMENT
pneumonia
DEFINITION Amoxicillin or
Pneumonia Cough or difficulty in breathing
Pneumonia is an infection of the lung, usually caused by bacteria or viruses. and fast breathing* Cotrimoxazole (in HIV negative
Fast breathing: children)
age <2months 60/min
CAUSATIVE ORGANISMS BY AGE GROUPS age 2-12months 50/min
age 12months – 5yrs >40/min.
Neonates Infants Other children All the above plus
Bacteria Group B Streptococcus Streptococcus Severe Decreased breath sounds, X-pen for 72hrs, when improves
streptococcus pneumoniae pneumoniae pneumonia bronchial breath sounds, switch to oral amoxicillin to
E. coli Staphylococcus Haemophilus crackles complete 5 days.
Listeria aureus influenzae Abnormal vocal resonance Ampicillin and Gentamycin for
monocytogens Haemophilus Pertussis (decreased over the p/ 5 days. If improves complete
influenzae effusion and increased over Rx with oral amoxicillin and
Listeria consolidation) gentamycin for another 5 days.
monocytogens Pleural rub.
Viruses RSV, Measles, influenzae, parainfluenza, adenovirus, metap- Very severe All the above plus Alternative, chloramphenicol
neumoviruses, CMV pneumonia Central cyanosis, inability to or Ceftriaxone IV until child
breastfeed or drink, convulsions, improves then gives oral for a
Fungi H. capsulutum, B. dermatitis, C. neoformas, Pneumocystis lethargy or unconsciousness, total of 10 days.
jirovecii severe RDS (head nodding),
Atypical Chlamydia trachomatis, Ureoplasma ureolyticum, Mycopla- nasal flaring, grunting
organisms sma pneumoniae.
*Respiratory rate: always consider fluid overload and cardiac failure causing increased respiratory rate!

STAPHYLOCOCCAL PNEUMONIA
DIAGNOSIS OF PNEUMONIA This is suspected if there is rapid clinical deterioration despite treatment, by a
pneumatocoele or pneumothorax with effusion on chest CXR, numerous Gram
• Proper history and physical examination –positive in a smear of sputum or heavy growth of S. aureus in cultured sputum or
• Chest X-Ray empyema fluid.
• Full blood picture and ESR
• Saturation partial pressure of oxygen • If staphylococcus is suspected (e.g empyema) add Cloxacillin
• Arterial blood gases. • If Mycoplasma suspected (high ESR and not responding to treatment) treat
• Sputum for gram stain and Ziehl–Neelsen -stain and culture. with Erythromycin
• Blood culture • If PCP is suspected treat as very severe pneumonia plus high dose cotrimoxazole

SUPPORTIVE CARE
• Oxygen therapy if having difficulty in breathing/low saturation of oxygen.
• If the child has fever give paracetamol
• If wheezes are present give rapid acting bronchodilator e.g. salbutamol puff
• Remove any thick secretions which the child can’t clear by gentle suction
• Fluid maintenance
• Encourage the child to eat as soon as food can be eaten.
 76 Infectious Disease Paediatrics Patients’ Management Guidelines 77

Tuberculosis based on clinical findings (especially failure to thrive or weight loss), family history
of contact with smear positive case, X-ray examination and tuberculin skin testing,
culture (if available) and non response to broad spectrum antibiotic treatment. The
score chart below can help to reach the diagnosis of tuberculosis. Older children
who are able to cough up sputum should go through the same assessment as adults
OVERVIEW using smear microscopy as the ‘gold standard’, for younger children early morning
gastric aspirates should be obtained for microscopy.
• Tuberculosis is infection by mycobacterium tuberculosis
• Many children are infected but most do not develop tuberculosis disease Chest X-Ray
• Tuberculosis is most severe when the disease is located in the lungs or meninges • Cavitary lesions may be seen in pulmonary TB
• Other areas which can be involved include: bones, joints, abdominal viscera, • Diffuse, small nodular opacities seen in miliary TB
cervical lymph nodes, ear, eye, skin, pericardium, genital urinary tract CSF
• Low glucose
Risk factors for disease progression are • Lymphocytosis, elevated protein
• immune suppression e.g. HIV, steroids Biopsy
• age (weakened immunity at the extremes of age ) • Done to support diagnosis of TB adenitis
• malnutrition Microscopy:
• inter-current infection e.g. malaria, worms, measles, whooping cough • Ziehl–Neelsen stained smear (sputum, gastric aspirates & CSF)
• toxic factors e.g. alcohol and smoking • Sputum smear positive in 65-70% pulmonary TB in adult, 20 % in children,
• poverty (overcrowding, increased exposure to tubercle bacilli) • Sputum often negative in miliary TB
Culture
• More sensitive than microscopy, but not available for routine use
SIGNS AND SYMPTOMS (takes 6-8 weeks)
Non-specific symptoms (common): weight loss, anorexia, fever, night sweats, Scoring System to Aid Diagnosis of TB in children
malaise
Specific symptoms due to particular organ involved: FIRST, calculate the score based on the following criteria:
Pulmonary TB Score 0 1 3
• Productive cough, haemoptysis, chest pain, breathlessness
Length of illness < 2 weeks 2-4 weeks > 4 weeks
• Fine crepitations in the lung apices, bronchial breathing, localized wheeze, signs
of pleural effusions Nutrition (wt/age) > 80% 60-80% < 60%
FHx TB
Miliary TB (past or present) None Reported by family Positive sputum
• Most commonly affects infants and the immunosuppressed patients
• May have hepatomegaly, splenomegaly, choroidal tubercles
THEN, calculate the score based on the following possible features:
TB Adenitis
• Most common site: cervical lymph nodes (though any lymph node can Possible Features Score
be involved) Unexplained fever, night sweats with no response to malaria treatment 2
• Initially, nodes are rubbery and non-tender Large, painless lymph nodes: neck, axils, groin, firm, soft, sinus 3
• Later in disease, nodes become harder and matted
Malnutrition, not improving after 4 weeks of treatment 3
• Nodes can become suppurative and form sinuses and fistulas
Joint swelling, bone swelling, or sinus involvement 3
TB Meningitis Unexplained abdominal mass or ascites 3
• More common in children CNS symptoms: change in temperament, convulsions, coma 3
• Headache, irritability, vomiting, decreased consciousness, any unusual
Positive tuberculin test 3
progressive neurological symptoms
Angle deformity of the spine 4
The diagnosis of Tuberculosis in children
The diagnosis of TB in children can be very difficult owing to the wide range of
symptoms. Symptoms in children are not typical. The diagnosis should therefore be
 78 Infectious Disease Paediatrics Patients’ Management Guidelines 79

FINALLY, add the TWO above scores together to calculate the TOTAL SCORE CATEGORIZATION OF TB PATIENTS
• If the total score is ≥ 7, treat for TB
• Children with a total score of < 7, should be treated if:
• The CXR is characteristic of TB infection Category Patients
• The child does not respond to two 7-day courses of two different antibiotics Category I New sputum smear positive, PTB (pulmonary TB) and new
patients with severe forms EPTB (extra pulmonary TB)
TREATMENT REGIMENS WITH FIXED DOSE COMBINATION Category II Relapse: Treatment failure and sputum smear positive return
DRUGS FOR CHILDREN after default and others
Category III New sputum smear negative and EPTB (less severe forms)
CATEGORY I and III treatment regimens according to the dose and body
weight Category IV Chronic cases

Duration of Drugs 5-10kg 11-20kg 21-30kg 31-50kg >50kg Note: R=Rifampicin, H=Isoniazid, Z=Pyrazinamide, E=Ethambutol, EPTB= extra
treatment pulmonaryTB
2 months RHZ ½ tablet 1 2 3 4 Total duration of treatment for category I and III patients is 6 months
intensive 150/75/400mg Total duration of treatment for category II patients is 8 months
Phase, daily Direct observation of treatment (DOT) should be done daily for entire duration of
observed
treatment
4 months RH ½ tablet 1 2 3 4 Streptomycin (S) should not be given to pregnant women.
continuation 150/75
Phase, daily FOLLOW-UP
observed Close follow-up is needed for children with TB (including directly observed
therapy)
Efforts should be made to identify other family members with signs and symptoms
CATEGORY II treatment regimens according to the dose and body weight of TB; they should seek medical treatment to avoid re-exposure of the child and
others in the community
Duration of Drugs 5-10kg 11-20kg 21-30kg 31-50kg >50kg
treatment Reference:
Manual of the National Tuberculosis and Leprosy programme in Tanzania 2009
2 months S (IM) 15mg/kg 15mg/kg 500mg 750mg 1g
intensive RHZE
Phase, daily 150/75/ ½ tablet 1 2 3 4
observed 400/275mg

1 month RHZE ½ tablet 1 2 3 4

Urinary Tract Infection
intensive 150/75/
phase 400/275mg
DEFINITION
5 months RH ¼ tablet ½ 2 3 4
continua- 150/150 An infection of the urinary collecting system. Simple urinary tract infections
tion phase, E 400mg ¼ tablet ½ 1½ 3 4 (UTIs) are generally contained within the bladder and urethra. UTIs may progress
3 weekly to include the ureters and kidneys (pyelonephritis). Urinary tract infections are
observed common, particularly in young female infants. The diagnosis is based on clinical
signs and urine microscopy.

SIGNS AND SYMPTOMS

The classis signs/ symptoms of urinary tract infections are:

• Dysuria (Pain with urination)
• Increased urinary frequency
• Urgency
 80 Infectious Disease Paediatrics Patients’ Management Guidelines 81

The clinical presentation of a UTI can vary based on age. UTI should be Empiric UTI treatment (poor response to 1st line antibiotic, deterioration in
considered in neonates and infants with fever and all children who are symptomatic condition): Gentamicin 2.5-5mg /kg IV once daily) + Ampicillin (50mg / kg IV
with or without fever. every 6 hrs) OR a Cephalosporine (eg. Ceftriaxone 80 – 100mg/kg iv once daily)

Neonates Infants Older children Supportive care

The child should be encouraged to drink or breastfeed regularly in order to
Failure to thrive Fever Frequency maintain a good fluid intake, which will assist in clearing the infection and
Loss of weight >10% Vomiting Urgency prevent dehydration.
Prolonged jaundice Irritability Dysuria
Follow-up
Cyanotic spells Diarrhoea Incontinence Investigate all episodes of UTI in >1-year-old males and in all children with
Apathy Sepsis Haematuria more than one episode of UTI in order to identify the cause. This may require
Septicaemia Failure to thrive referral to a larger hospital with facilities for appropriate X-ray or ultrasound
investigations.
Progression to infection within the kidney (pyclonephritis) should be considered in
patients with high fever and flank pain (pain along the posterior costo – vertebral References:
angle). 1. Anthony D. Miller, David Hull, Hospital Paediatrics, 1999
2. Nelson Textbook of Paediatrics, 17th Edition

INVESTIGATIONS

Urine Dipstick (immediately available on the floor)

• Presence of nitrites, leukocytes suggests infection.
Urine Microscopy
• Clean, fresh, uncentrifuged specimen
• > 5 WBC / HPF suggests possible infection

Urine Culture and Sensitivity. Only one type of BACTERIA and not two must be
grown and its sensitivity identified.
• “Clean catch” or catch specimen.
• In very sick infants supra-public aspiration may be required
Ultrasound urinary tract: if history of recurrent UTIs to rule out structural
abnormalities and micturiting Cystorethrogram are important further in the
investigations in cases of recurrent U.T.Is in children.

CAUSATIVE ORGANISMS

Classic organisms causing UTIs include gram-negative organisms (intestinal

bacteria).
U.T.I mainly caused by Escherichia coli followed by Klebsiella and Proteus

TREATMENT

May be treated as an outpatient UNLESS any of the following are present:

• High grade fever and systemic symptoms (vomiting, in ability to drink).
• Flank pain (pyelonephritis)
• Young infants

Empiric treatment: Oral cotrimoxazole (4 mg trimethoprim/20mg

sulphamethoxazole) per kg every 12hrs for 7days.
Alternative: Cephalexin or Amoxycillin 10mg/kg/dose TDS.
Nitrofuration 3 – 5mg.kg in 3 divided doses.
 82 Infectious Disease Paediatrics Patients’ Management Guidelines 83

A special referral form for treatment outside the country is available which has to
be signed by a panel of three specialists and to be sent to the Ministry of Health in
Dar Es Salaam.
In the following some of the more common congenital heart diseases are presented.

Cardiology VENTRICULAR SEPTAL DEFECT (VSD)

More than twenty per cent of all CHD. Most frequent congenital heart disease and
most common associated malformation in complex CHD.
Incomplete closure of embryonal septal components leads to an interventricular
connection.
VSDs are divided into groups based on the location of the defect—muscular vs
perimembranous. The location can give some idea about the potential clinical
– Congenital Heart Disease outcome and surgical practicability. Muscular VSDs are more likely than
membranous VSDs to close spontaneously. The amount of shunting across the
– Heart Failure VSD determines the severity of clinical symptoms. The risk of developing a
– Shock pulmonary hypertension usually determines the prognosis.

Clinical features: Tachydyspnoea, failure to thrive, failure to suck, sweating,

recurrent chest infections

Congenital Heart Disease (CHD) Drugs:

Digoxine, Lasix, Captopril
Endocarditis prophylaxis (only in specific circumstances)

Repair: VSD-closure with open heart surgery (Dacron-patch), large

DEFINITION VSDs have to be closed earlier (6-12 months of life),
moderate sized VSDs might still be done later in childhood
Congenital heart disease (CHD) includes a variety of malformations of the heart or (depending on the echocardiographic findings of PHT)
its major blood vessels that are present at birth.

COMMON CLINICAL FEATURES

• Cyanosis
• Sweating (especially with feeds)
• Tachypnea
• Dyspnoea
• Failure to thrive
• Poor sucking

Note that these may not be detected by parents (especially with 1st born children).
A precise history should be taken to avoid missing these details on history. You may
need to describe these symptoms to some parents to help them recognize them.
The number of available drugs in Tanzania for children with CHD is limited.
Commonly used medications for the treatment of heart failure include digoxin,
lasix, aldactone, and captopril (see Heart failure).

Following investigations have to be done to prepare surgery abroad:

Basic cardiologic diagnostics: ECHO, ECG, Chest X-ray, SaO2, BP
Lab. investigations: HIV, Hepatitis B and C, Sickling test, Blood Group,
FBP, Liver and Renal Function
 84 Cardiology Paediatrics Patients’ Management Guidelines 85

TETRALOGY OF FALLOT (TOF) PATENT DUCTUS ARTERIOSUS (PDA)

Ten per cent of all CHD Ten per cent of all CHD (excluded Preterm infants below 1.500 g, in this group the
Consists of: risk is up to 30/100).
1) Ventricular Septal Defect (VSD), subaortal Failure of the prenatal physiologic aortopulmonal connection to close. Birth
2) Infundibular (and valvular) pulmonary stenosis asphyxia increases the risk of a PDA.
3) Overriding aorta
4) Right ventricular hypertrophy Clinical features: Frequently no symptoms. In preterm: respiratory distress and
failure to wean from mechanical ventilation. After reduction of
The TOF has many clinical and structural variations (much like VSDs). When pulmonary resistance, risk of severe heart failure. Increased risk
the aorta is overriding > 50% of the aortic diameter, the term Double Outlet Right of necrotizing enterocolitis (NEC) because of ischaemia.
Ventricle (DORV) is used. The extent of obstruction of the right ventricular Drugs: Consider Indomethacin (or Ibuprofene) IV in preterm if
outflow tract determines the clinical symptoms. available.

Indomethacin Therapy in Preterm Infants

Age Initial dose 2nd, 3rd dose after 12, 24 hrs

< 48 hrs 0.2 mg/kg BW 0.1 mg/kg BW
2 – 7 days 0.2 mg/kg BW 0.2 mg/kg BW
> 7 days 0.2 mg/kg BW 0.25 mg/kg BW

Monitor renal output! Temporary oliguria (< 0.7 ml/kg BW/h) is common.
ECHO control after completion of therapy.

Repair: Closure interventionally or with surgery. Comparatively simple

procedure. No open heart surgery. In preterm only if drug
closure fails.

Clinical features: Cyanosis, tachydyspnoea, recurrent chest infections, hypoxaemic

attacks (depending on the extent of the obstruction of the right
ventricular outflow tract).
Drugs: As heart failure is not common, there is normally no need for
antifailure treatment. No digoxine. Consider Propanolol PO
0.5-1.5 mg/kg every 6 hours for the prevention of hypoxic spells
Endocarditis prophylaxis
Hypoxic spell: Pull knees to chest to increase afterload. Oxygen. Sedation
(Diazepam, Ketamine or Morphine). Propanolol IV
(0.05-0.1 mg/kg slowly! Monitoring!
Repair: Repair with open heart surgery. If possible, elective repair
between 6-10 months of life.
 86 Cardiology Paediatrics Patients’ Management Guidelines 87

ATRIAL SEPTAL DEFECTS (ASD) VALVULAR AORTIC STENOSIS

ASD is one of the most common congenital cardiac anomaly. The anatomical sites of Congenital valvular aortic stenosis is a relatively common anomaly, estimated
ASD are shown in the figure below. to occurr in 3 to 6% of patients with congenital heart disease. Associated
cardiovascular anomalies are present in 20 % of the cases, mainly patent ductus
arteriosus and coarctation of the aorta.
The basic malformation consist s of the thickening of valve tissue with various
degrees of commissural fusion. The valve is commonly bicuspid.
When the magnitude of obstruction is significant a left ventricular lift ususally is
palpable and a precordial systolic thrill is palpated over the base of the heart with
transmission to the jugular notch and along the carotid arteries.

Clinical features: isolated aortic valcular stenosis seldom causes symptoms in

infancy. . In seriously ill newborns, administration of
prostaglandin is necessary in order to maintein a patency of the
ductus arteriosus that ensure the cardiac output.
In children symptoms are undue fatigue, exertional dyspnea,
angina pectoris and syncope.
Drugs: No drugs in asymptomatic patients. Heart failure drugs in
presence of left ventricular dysfunction.
Repair: ballon valvulopalsty or surgery in presence of severe aortic
stenosis (systolic gradiente exceeding 75 mmHg in association
ASD causes a left to right shunt with a volume overload of the right ventricle. with a normal cardiac output or an effective aortic orifice less
The pulmonary vascular resistance commonly is normal or low in older infants or than 0.5 cm2/m2).
children with ASD and the volume load is well tolerated, even though pulmonary
blood flow may be two to five times greater than systemic.
PULMONIC STENOSIS
Clinical features: Frequently no symptoms. Small defects, less than 4 to 8 mm,
Valvular pulmonic stenosis, resulting from fusion of the valve cusps during mid
have a modest probability of spontaneous closure. The ECG usually shows a right
to late intrauterine development is the most common form of isolated right
axis deviation, right ventricular hypertrophy and rSR’ or rsR’ pattern in the right
ventricular obstruction and occurs in about 7% of patients with congenital heart
precordial leads.
disease.
Drugs: No drugs.
Repair: Closure interventionally or with surgery. Comparatively simple
Clinical features: Severe pulmonic stenosis is characterized in neonates and
procedure.
infants by cyanosis caused by right to left shunting through the
foramen ovale, cardiomegaly and reduced pulmonary blood
flow. The main clinical disturbances in symptomatic neonates
COMPLETE AV CANAL
can be alleviated temporarily by infusion of Prostaglandin E1
to dilate the ductus arteriosus and ensure the pulmonary
The complete AV canal includes:
blood flow
1) ostium primum atrial septal defect
In children commonly pulmonic stenosis is asymptomatic and
2) a VSD in the posterior basal inlet portion
is discovered during routine examination. Symptoms when
3) a common AV orifice
present vary from mild exertional dyspnea and mild cyanosis to
signs and symptoms of heart failure, depending on the degree
Clinical features: patients with complete AV canal present clinically before age
of obstruction.
1 year with a history of frequent respiratory infections and poor
Drugs: No drugs in asymptomatic patients.
weight gain. Heart failure in infancy is extremely common.
Repair: Balloon valvuloplasty or surgery in presence of severe pulmonic
Drugs: cardiac decompensation shoul be controlled initially.
stenosis (a peak systolic transvalvular gradient > 80 mmHg or a
Repair: surgical repair before age 6 months even with adequate
peak systolic right ventricular pressure > 100 mmHg)
response to medical therapy because infants with AV canal are
at high risk of obstructive pulmonary vascular disease.
 88 Cardiology Paediatrics Patients’ Management Guidelines 89

COARCTATION OF THE AORTA Typically, the heart can respond to increased demands by means of one of the
following:
This lesion consists of a localized shelf-like thickening and infolding of the media • Increasing the heart rate, which is controlled by neural and humoral input
of the postero-lateral aortic wall opposite the ductus arteriosus. It is often associated • Increasing the contractility of the ventricles, secondary to both circulating
with muscular VSDs and bicuspid aortic valve. catecholamines and autonomic input
• Augmenting the preload, medicated by constriction of the venous capacitance
Clinical features: the manifestation of coarctation of the aorta depend on the vessels and the renal preservation of intravascular volume
prominence of the postero-lateral aortic shelf, which determines
the intensity of obstruction. Rapid severe obstruction in As the demands on the heart outstrip the normal range of physiologic
infancy is a cause of left ventricular failure and systemic compensatory mechanisms, signs of congestive heart failure occur. These signs
hypoperfusion. At the closure of the ductus arteriosus infants include tachycardia; venous congestion; high catecholamine levels; and, ultimately,
with severe aortic coarctation develop shock with severe left insufficient cardiac output with poor perfusion and end-organ compromise.
ventricular dysfunction.
Most children with isolated coarctation are asymptomatic.
Complaints of headache, systemic hypertension, cold CAUSES
extremities may be noted. Typical is a difference between the
pressure relevated at the high and low extremities. The causes of heart failure in children differ substantially from those found in adult
Drugs: no drugs in asymptomatic children. In presence of severely ill population and compromise cardiac and non cardiac causes.
neonates PGE infusion and inotropic support with urgent Cardiac causes can be associated with cardiac congenital malformations or
surgical repair. structurally normal heart.
Repair: surgery in neonates and infants. Stenting of the coarcation site
in children with a weight > 20 Kg. Congenital cardiac malformations
- Volume overload
• Left to right shunting
References: • Atrioventricular or semilunar valvular insufficiency
1. J. Robertson, N. Shilkofski, The Harriet Lane Handbook, 7th Edition, 2002 - Pressure overload
2. www.kumc.edu/.../pedcardio/tetralogydiagram.gif • Left sided obstruction
3. http://allhearts.blogspot.com/2007/02/patent-ductus-arteriosus-pda.html • Right sided obstruction
4. www.koeln.netsurf.de/.../Herzprojekt/vsd.gif - Complex congenital heart disease
5. http://emedicine.medscape.com/article/892980-overview and - treatment • Single ventricle
• Systemic right ventricle
Strcturally normal heart
- Primary cardiomyopathy
• Dilated
Heart Failure • Hypertrophic
• Retrictive
- Secondary cardiomyopathy
DEFINITION • Arrhythmogenic
• Ischemic
A precise definiton of heart failure is difficult to achieve in children. There is • Toxic
general agreement that heart failure is a progressive clinical syndrome with • Infiltrative
numerous etiologies d characteristis signs and symptoms, although the causes and • Infectious
clincal presentations may differ considerably among children of different age and
between children and adults.
The clinical syndrome is a manifestation of the pathophysiological syndrome of DEVELOPMENTAL CONSIDERATIONS
heart failure which includes complex interplay among circulatory, neurohormonal
and molecular anormalities associated with the important role of genetic The heart is the first organ to develop and becomes a fully formed organ at 10
characteristcs and predisposition highlighted recently. weeks of gestations. Even if the appearance is very similar to that of adult heart the
Congestive heart failure (CHF) occurs when the heart can no longer meet the physiology is very different. During the fetal life the ventricles pump in parallel
metabolic demands of the body at normal physiologic venous pressures. rather than in series, with the left ventricle pumping to the head and upper body
and the right ventricle pumping to the ductus arteriosus, lower body and placenta.
 90 Cardiology Paediatrics Patients’ Management Guidelines 91

As a result of the compensatory features of the parallel circulation, most congenital because of abnormal functioning of the subpulmonary ventricleor poor filling
malformations are well tolerated during the fetal life. of the systemic ventricle, conduction disturbances or arrhythmias, or increased
The fetal myocardium continues to develop shortly after birth. Myocyte numbers hypoxemia.
increase until 6 months postnatally but the fetal myocytes are smaller than its adult
counterpart and have a lower number of myofibrils and mitochondria. There is less
intracellular calcium and greater dependence on transsarcolemmal calcium flux. DIAGNOSIS
The result is a greater stiffness of the fetal herat with a limitation in preload and
contractile reserve. Thus the principal means of increasing fetal and cardiac output Echocardiography is the primary imaging modality in pediatric cardiology and
is through increased heart rate. provides excellent structural and functional detail in children.
Therefore data from several animal models demonstrate that myocardial contracility In adults measurement of maximal oxygen consumption is useful for risk
matures during the postnatal period, mediated by changes in signal transduction stratification, including the need of heart transplantation. In children exercise
and calcium homeostasis. For examples in the fetal and newborn heart stimulation testing could not be easely performed and the measurement are complicated by
of the beta-adrenergic receptor adenylyl cyclase- cAMP pathway has less effect the high variability of oxygen consumption with age and underlying pathology.
on contractility than in adult myocardium. Similarly the contractile response to In infants feeding is an informal exercise testing and growth failure is often an
phosphodiesterase inibition is generally less robust than in the adult heart. indicator that an intervention is necessary.
All these considerations have clear implications for the therapeutic approaches to The role of the dosage of neurohormonal activation in the diagnosis and
pediatric heart failure. management of heart failure in children is yet controversial. BNP levels can
distinguish between cardiac and pulmonary causes of respiratory distress and, in
acute decompensated heart failure due to cardiomyopathy are increased and related
CLASSIFICATION to the severity of symptoms. A BNP level > 300 pg/mL has been shown to predict
death, transplantation or heart failure hospitalization and correlates more strongly
Part of defining heart failure is defining a spectrum of severity. Being the NYHA with poor outcome than symproms or echocardiographic findings.
heart failure classification not applicable to children, the ROSS heart failure
classification was developed to provide a global assessment of heart failure severity
in infants and subsequentely been modified to apply to all pediatric patients. TREATMENT

Modified Ross Heart Classification in Children There are no agreed guidelines for the treatment of heart failure in children and
Class I asymptomatic limited specific research. Treatment goals are similar of those of adults: correct
Class II mild tachypnea or diaphoresis with feeding in infants underlying problems, minimize morbidity and mortality and improve functional
Dyspnea on exertion in older children status and quality of life. The treatment in children depends on the underlying
Class III marked tachypnea or diaphoresis with feeding in infants cause and child’s age.
Marked dyspnea on exertion
Prolonged feeding times with growth failure Digitalis
Class IV symptoms such as tachypnea, retractions, grunting Although only few pediatric data are available, digoxin is widely used to treat HF in
or diaphoresis at rest children. Although it has not been shown to improve survival, digoxin can improve
symptoms and prevent further episodes of HF.
A direct correlation between the Ross class and plasma norepinephrine • Digoxin Dosing Table
concentrations and an inverse relationship between the Ross class and beta-receptor
density support the validity of the Ross classification system. Age Total Digitalizing Dose Maintenance Dose
(µg/kg) (µg/kg/day)
Prematures 20 5
SIGNS AND SYMPTOMS Newborns 30 8
The characteristic signs and symptoms of heart failure include growth failure, < 2 years 40-50 10-12
respiratory distress and exercise intolerance and are present in children with heart >2 years 30-40 8 -10
failure regardless the aetiology.
Unfortunately Ross class at presentation is a poor predictor of worsening clinical Diuretics
outcome. No published data ara available concerning the effectiveness of diuretics in reducing
In patients with right heart dysfunction, as may occur in tetralogy of fallot or mortality or improving symptoms in pediatric patients, but their use is widespread.
ebstein anomaly, or in patients with single ventricle physiology the predominant Current guidelines in adult population recommend the use of diuretics in all
clinical findings are those of systemic venous congestion, decrased exercise capacity patients with fluid retention.
 92 Cardiology Paediatrics Patients’ Management Guidelines 93

In particular Spironolactone has been shown to improve survival in adults with institutional experience Shaddy et al. reviewed the results with metoprolol in 15
advanced HF. This does not appear to correlate to the diuretic effect but rather children with cardiomyopathy of differente etiologies. The patients treated with
to the blockade of aldosterone and to the interruption of the rennin-aldosterone- metoprolol showed a clinically important increase of ejection fraction over a period
angiotensin system. of 23 months. In another study of Azeka et al low doses of carvedilol in 22 children
• Furosemide (Lasix): 1-2 mg / kg / day IV or PO in 2-3 divided doses with DCM was responsible of an increase not only of the EF but also of the clinical
• Spironolactone: 2 (-3) mg / kg / day PO in 1 or 2 doses status.
The risks associated with the use of beta-blockers include hypotension and
Angiotensin Converting Enzyme Inhibitors and Angiotensin Receptor worsening HF. Bradycardia is seen but is usually asymptomatic, requiring
Blockers sometimes a dose reduction if there is associated hypotension.
Multiple large clinical trials have shown that therapy with ACE inhibitors improves Beta-blockers are controindicated in patients with bradycardia, or heart block,
symptoms and survival in adult patients. unless a pacemaker is in place and in patients with bronchial asthma or with
HF is associated with chronic activation of the RAAS and increased sympathetic cardiogenic shock.
drive. These alterations, which may be beneficial acutely, contribute to the • Carvedilol: 0,08 – 0,75 mg/ Kg / dose PO BD
progression of HF over time. Increased adrenergic tone increases afterload and • Metoprolol: 1- 2 mg / Kg /dose PO BD or TD
myocardial oxygen demand. Angiotensin II is a vasoconstrictor which causes
myocyte hypertrophy and fibrosis as well as aldosetrone secretion. Increased
concentrations of both aldosetrone and angiotensin II are associated to poor TREATMENT OF ACUTE PULMONARY EDEMA
outcome in HF pts. The efficacy of ACE inhibitors is related to disruption of the
activation of the rennin-angiotensin axis and to decreased cardiac adrenergic drive. Check for
Few studies concerning the administration of ACE-inhibitors to children with HF • Restlessness
are available., although ACE-inhibitors have been used in the pediatric population • Frothy sputum
for more than two decades with beneficial effect. • Basal crepitations
Effects on mortality have not been described, with the exception of one • Low oxygen saturation (<95%)
retrospective report, in which survival was improved by administration of ACE
inhibitors during the first year of treatment but not subsequently. Give
The use of ACE-inhibitors in patients with structural heart disease such as left to • Oxygen
right shunt or valvular insufficiency is less understood. However a controlled study • IV furosemide
in this population with preserved left ventricular function and volume overloaded • Mechanical ventilation may be needed
ventricles from valvar insufficiency showed a reduction in both LV volume overload
and hypertrophy over a follow up of 3 years. References:
In majority of patients ACE-inhibitors are well tolerated, symptomatic hypotension 1. MK Park, Pediatric Cardiology for Practitioners, 4th edition, 2002
can occurr and a careful uptritation is necesary. Particular care must be taken in the 2. N. James, N. Smith, Treatment of Heart failure in children, Current Paediatrics,
treatment with ACE-inhibitors in patients with renal insufficiency. Volume 15, Issue 7, Pages 539-548 (December 2005)
No safety or efficacy data regarding the use of ARB in children with HF are 3. G. Satou, Congestive Heart failure, Mar 19, 2009
available. http://emedicine.medscape.com/article/901307-overview
• Captopril: Infants 0.1 – 0.3 mg / kg / dose PO BD or TID 4. J Robertson, N. Shilkofski, The Harriet Lane Handbook, 7th Edition, 2002
Children 0.3 – 0.5 mg / kg / dose PO BD or TID 5. Rosenthal D et al. Iternational Society for heart and Lung Transplantation :
• Enalapril: 0,1-0,5 mg/ Kg /dose PO BD Practice Guidelines for Management of Heart Failure in Children. J Heart Lung
Transplant 2004;; 23: 1313-33
Beta-adrenergic blockers
In adult population several placebo-controlled studies have shown that beta-
blockers decrase the risk of clinical progression of HF and decrase all-cause
mortality.
Initial compensatory mechanisms in the failing heart include activation of the
sympathetic nervous system and increased levels of circulating catecholamines. In
the long term the increased levels of catecholamines, particularly norepinephrine,
contribute to the progression of HF through multiple mechanisms, including
myocardial fibrosis and apoptosis. The rationale for the use of adrenergic
antagonists in HF is to antagonize the deleterious effects of sympathetic activation
on the myocardium.
The reported use of beta-blockers in children with HF is very limited. In a muli-
 94 Cardiology Paediatrics Patients’ Management Guidelines 95

Shock CLINICAL MANIFESTATION

• Affected by the type of shock and the child’s compensatory responses

(eg: heart rate, systemic vascular resistance).
DEFINITION Compensated: If systolic BP is within normal range, but signs of inadequate
tissue perfusion are present. Duration can be possibly hours to progress to
• Inadequate delivery of oxygen and nutrients to the tissues relative to tissue decompensated.
metabolic demand Decompensated: If systolic hypotension and signs of inadequate tissue
• A normal blood pressure does not rule out shock! perfusion are present. Duration is potentially minutes to cardiac arrest.
PHYSIOLOGY OF SHOCK
Compensated Decompensated
• Adequate delivery of oxygen to tissue depends on: Heart Rate Tachycardia Tachycardia/Bradycarida
- Sufficient oxygen content in the blood Blood Pressure Normal Tensive Hypotensive
- Adequate flow of blood to tissues (cardiac output)
Pulses Bounding/weak pulses Weak/absent pulses
- Adequate matching of blood flow to local tissue metabolic demand
Skin Delayed cap refills (>2 sec.) Very delayed cap refills (>3 sec.)
Preload Warm/cool skin Cold Skin
Contractility > Stroke Volume x Heart Rate > Cardiac Output x O2 content > O2 Kidney Oliguria Oliguria/Anuria
Delivery
Brain Irritable, Restless Lethargic, Unresponsive
Afterload
Hypotension by Systolic Blood Pressure and Age
CAUSES
Age Systolic BP (mm Hg)
• Shock can result from: Term Neonates (0-28 days) < 60
Hypovolemic Shock: Inadequate blood volume or inadequate O2 carrying Infants (1-12 months) < 70
capacity Children (1-10 years) < 70 + (Age in years x 2)
• Diarrhea
• Inadequate fluid intake Children > 10 years < 90
• Vomiting
• Osmotic Diuresis (DKA) • Hypotension is a late ominous finding.
• Hemorrhage (internal and external) • Early recognition and timely intervention are critical to halting the progression
• Third-Space losses (eg: Pleural eff., Ascites) from compensated to decompensated shock to cardiopulmonary failure
• Burns and arrest.
Distributive Shock: Inappropriately distributed blood volume with inadequate
tissue perfusion
• Septic Shock LABORATORY INVESTIGATIONS
• Anaphylactic Shock
• Neurogenic Shock (eg: head injury, spinal injury) • Shock is a clinical diagnosis. Do not wait for labs to treat.
Cardiogenic Shock: Impairment of heart contractility • Emergency investigations (while putting the cannula): RBG, Hb and cross
• Congenital heart disease matching, BS for MPS
• Arrhythmias • Other Lab investigations will follow after resolution and stabilization of the
• Myocarditis child.
• Poisoning or drug toxicity
• Cardiomyopathy
• Myocardial injury (eg: trauma) TREATMENT
Obstructive Shock: Impaired cardiac output caused by obstruction of blood flow
• Cardiac tamponade (In child without severe malnutrition)
• Tension pneumothorax • Goals of treatment are to reverse perfusion abnormalities, improve the balance
• Ductal-dependent cong. Heart lesion between perfusion and tissue metabolic demand, restore organ function, and
• Massive pulmonary embolism prevent cardiac arrest.
 96 Cardiology Paediatrics Patients’ Management Guidelines 97

• Assess the effectiveness of treatment (fluid resuscitation and pharmacologic Class Drug Indications
support) by continuous monitoring of the following:
- Oxygen saturation - Mental status Inotropes Dopamine 2 to 20 Cardiogenic or distributive
- Heart Rate - Temperature (β-adrenergic receptors) µg/kg/min* Hypotensive
- Blood pressure - Urine output Epinephrine 0.1 to CHF or cardiogenic shock
- Capillary refill 1 µg/kg/min**
Dobutamine 2 to
START WITH ABC’S 20 µg/kg/min
Airway: Establish upper airway patency and evaluate the mental status Vasopressors Dopamine 2 to 20 Cardiogenic or distributive
Breathing: Evaluate respiratory rate and effort. Administer oxygen. (β-adrenergic receptors) µg/kg/min* Hypotensive
Circulation: Epinephrine 0.1 to Distributive shock
1. Establish peripheral vascular access with an intravenous line (and draw blood 1 µg/kg/min**
for emergency laboratory investigations). If peripheral access cannot be readily Norepinephrine 0.1 to
achieved in children with shock, intraosseous access is the second preferred 2 µg/kg/min
route of vascular access.
2. Attach Ringer’s Lactate or Normal Saline and give bolus according to suspected
type of shock. * Dopamine: Low infusion (1 to 5 µg/kg/min) stimulate dopaminergic and
β-adrenergic receptors; α-adrenergic effects become more prominent as infusion
Type of Shock Vol. of Fluid bolus Rate of Delivery rate is increased.
Hypovolemic Shock 20 ml/kg bolus Deliver rapidly ** Epinephrine: Low infusion (≤ 0.3 µg/kg/min) stimulates mostly β-adrenergic
(non-DKA) (over 5 to 10 min) receptors, higher infusion (> 0.3 µg/kg/min) stimulate α-adrenergic receptors.
Distributive Shock
Obstructive Shock
TREATMENT
Cardiogenic Shock 5 -10 ml/kg bolus Deliver more slowly (In child with severe malnutrition)
(over 10 to 20 min)
Diabetic Ketoacidosis 10-20 ml/kg bolus Deliver over 1 hr Give treatment only if severely malnourished child has signs of shock and is
(DKA) lethargic or has lost consciousness.

START WITH ABC’S

3. Reassess child after first infusion. If no improvement, repeat bolus. Airway: Establish upper airway patency and evaluate mental status
Breathing: Evaluate respiratory rate and effort. Administer oxygen.
4. Reassess child after second infusion. If no improvement, repeat bolus. Circulation:
If you are suspecting septic shock, administer first-dose antibiotics STAT. 1. Establish peripheral vascular access with an intravenous line (and draw blood
for emergency laboratory investigations). If peripheral access cannot be readily
5. Reassess child after third infusion. If no improvement, give blood 20ml/kg over achieved in children with shock, the intraosseous access is the second preferred
30 minutes (if shock is not caused by profuse diarrhea, in this case repeat RL route of vascular access.
or NS).
2. Give IV fluid 15 ml/kg over 1 hour. Use one of the following solutions (in
6. Reassess child after fourth infusion. If no improvement, see disease-specific order of preference), according to availability:
treatment guidelines. You should have established a provisional diagnosis by now. • Ringer’s Lactate with 5% Glucose (dextrose); or
• half-Normal Saline with 5% Glucose (dextrose); or
7. Vasoactive agents are indicated when shock persists after adequate volume • half-strength Darrow’s solution with 5% Glucose (dextrose); or, if unavailable
resuscitation (60ml – 100ml/kg). Common classes of pharmacologic agents • Ringer’s Lactate
used in shock are inotropes and vasopressors. Titrate to desired effect.
If there are signs of improvement (HR and RR rates fall):
• give repeat IV 15ml/kg over 1 hour; then
• switch to oral or NGT rehydration with ReSoMal 10ml/kg/hr up to 10 hours
• initiate refeeding with starter F-75
 98 Cardiology Paediatrics Patients’ Management Guidelines 99

If the child fails to improve after the first 15ml/kg IV, assume the child has septic
shock:
• give maintenance IV fluid while waiting for blood;
• when blood is available, transfuse fresh whole blood at 10ml/kg slowly over

Endocrinology
3 hours (use packed cells if in cardiac failure); then
• initiate refeeding with starter F-75
• start antibiotic treatment

If the child deteriorates during the IV rehydration (breathing increases by 5 breaths/

min or pulse by 15 beats/min), stop the infusion because IV fluid can worsen the
child’s condition.

References:
1. Pocket Book of Hospital Care for Children – Guidelines for the management
of common illnesses with Limited Resources. World Health Organization. 2006. – Diabetes Mellitus
2. American Heart Association: Pediatric advanced life support. Circulation. 2006.
– Diabetes Ketoacidosis

Diabetes Mellitus
DEFINITION

Diabetes mellitus (DM) is a chronic metabolic disorder, caused by absolute or

relative deficiency of insulin, resulting in hyperglycaemia and other metabolic
derangements.

CLASSIFICATION

Diabetes mellitus can be divided into two main subclasses:

• Type 1 or insulin-dependent diabetes mellitus (T1D)
• Type 2 or non-insulin-dependent diabetes mellitus (T2D)

SIGN AND SYMPTOMS

DM appears over days or weeks in previously healthy children or young adults.

Symptoms may include:
• polyuria
• polydipsia
• weight loss
• acidotic breathing (Kussmaul respiration), with smell of ketones in breathing
• severe dehydration, shock or coma
 100 Endocrinology Paediatrics Patients’ Management Guidelines 101

INVESTIGATIONS F/U IN THE DIABETES CLINIC

• RBG> 11mmol (it is diagnostic if in combination with symptoms of DM) RBG, glycosilated Hemoglobin every 3 months.
• URINALYSIS (glucose, ketones)
• SERUM Electrolytes and Blood gas analysis (if signs of DKA) References
• GLYCOSILATED HEMOGLOBIN 1.) The Harriet Lane Handbook, 18th edition
2.) Handbook of Paediatrics for developing countries 6th edition Oxford/Southern
Africa. Vicent C. Harrison
DIAGNOSTIC CRITERIA

Symptoms of DM (polyuria, polydipsia, weight loss) plus one of the following

criteria:
• RBG> 11mmol and/or Diabetic Ketoacidosis (dka)
• FBG > 7mmol

TREATMENT OF DM DEFINITION

Exogenous insulin therapy, diet, education, blood glucose monitoring DKA is a complication occurring in children with Diabetes Mellitus
(goal: 4.5-11 mmol/l) presenting with a combination of HYPERGLYCAEMIA (>11mmol/L),
HYPERKETONAEMIA (increased serum ketones-acetone or betahydroxybutyrate)
or large ketonuria with acidosis (venous PH<7.3 and/or serum bicarbonate
INSULIN INJECTION REGIME (S.C. INSULIN) <15mmol/L)

2:1 Mixture of Insulin prepared by the patient/parents mixing regular and Note: Blood glucose in mg/dl = mmol/L x 18
intermediate insulin just before the injection in the same syringe: The biochemical criteria for the diagnosis of DKA are as follows:
• 2/3 of the dose: intermediate-acting (cloudy) Insulin (Lente) • hyperglycaemia (blood glucose > 11 mmol litre−1)
• 1/3 of the dose: regular (soluble, clear) Insulin (Actrapid) • venous pH < 7.3 and/or bicarbonate < 15 mmol litre−1
Calculate the total daily dose of Insulin: approximately 0.6-1 units / kg BW / • ketonaemia or gross ketonuria
24 hours, considering that the dose is higher in adolescents and lower in infants,
toddlers and children. Causes of DKA
Divide the total daily dose in 2 doses: 2/3 of the dose 15-30 min before breakfast Insulin deficiency
1/3 of the dose 15-30 min before supper • absolute insulin deficiency as in type 1 diabetes at onset, or in recurrent
omission of the insulin therapy in patients with known diabetes.
BMC MWANZA Sliding Scale for Preprandial • relative insulin deficiency as in already known type 1 diabetes during stresses
Hyperglycemia in Children such as infections or accidents
Diabetic ketoacidosis may be rarely present at the onset of type 2 diabetes in
Preprandial RBG (mmol/L) Dose Adjustment of Soluble Insulin (IU) children and adolescents with gross obesity. The cause, in these cases, is the extreme
insulin resistance, usually the need of insulin therapy is transient, after the first few
> 25 give 3 additional units
days or weeks, the patients can go on with oral drugs (usually metformin) and an
20-25 give 2 additional units appropriate diet.
15-20 give 1 additional unit
10-15. no change
SYMPTOMS AND SIGNS OF DKA
5-10 (Goal) give as prescribed • Classic symptoms of hyperglycemia
- Thirst
2.5-5 no change, give carbohydrates - Polyuria, polydipsia
- Nicturia
< 2.5 give carbohydrates, wait for 30-60 minutes • Other symptoms
and then give the insulin injection - Generalized weakness
reducing the dose (1-2 units less)
 102 Endocrinology Paediatrics Patients’ Management Guidelines 103

- Malaise/lethargy FLOW CHART FOR MANAGEMENT OF DKA

- Nausea/vomiting BMC MWANZA Treatment of Diabetic Ketoacidosis in Children
- Decreased perspiration
- Fatigue
- Anorexia or increased appetite
- Confusion Name:
• Specific DKA signs Date:
- Ketotic breath (fruity, with acetone smell)
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20
Time (hours)
- Confusion
- Coma
RBG (mmol/L)
- Abdominal tenderness > 25
20-25
15-20
INVESTIGATIONS 10-15
5-10 (Goal)
Biochemistry: blood gas analyses, serum glucose, electrolyte, BUN, creatinine, CRP, 0-5
pH, ABE, HCO3. Urinalysis for ketones, sugar and casts. 0
ECG: to look for cardiac events, complications and to monitor potassium. Monitor RBG hourly
(CRP is important to exclude a concomitant infection that is often present and can
contribute to the worsening of the clinical condition) Monitor ketones in urine
at starting therapy, and
then at every urination,
TREATMENT until negative

Using the treatment flow sheet available for management of DKA, the following Monitor pH, ABE,
points need to be considered when managing DKA: HCO3, Na+ and K+
• Treatment of ketoacidosis should aim at correcting dehydration at starting therapy and
(replenishing electrolyte and volume losses), reversing the acidosis and ketosis, after 4 and 8 hrs
reducing plasma glucose concentration to normal and identifying the
underlying cause. NS 0.9%:
- 10-20 ml/kg in 1 h
• Patients undergoing continuous intravenous insulin infusion require frequent
(max. x 2) in shocked
monitoring, which is best completed in the ICU.
patients
• Check weight, urine output, consciousness and blood pressure at admission. - 6-8 ml/kg/h for 2 hh
• Start rehydration with normosaline solution (20 ml/kg in 1-2 hours in shocked if no shock
patients - 7-8 ml/kg per hour for two hours if no signs of shock are evident).
• Insulin must be given once glucose determination has been made. Insulin must Fluid replacement/
be diluted in normosaline solution and administered at the starting dose of infusion ml/h
0.1 U/ kg/ h by a pump for continuous intravenous infusion. (4 - 6 ml/kg/h)
• Always look for precipitating causes (especially infections, if CPR is positive
start antibiotics). NS 0.9%
Be alert to headache and altered mental status (eg, decreased alertness) since (RBG > 14 mmol/L)
these are signs of impending cerebral edema.
D5/NS 0.45%
(if RBG < 14 mmol/L
TRANSITION or if RBG is
decreasing too quickly
IV fluids can be stopped once acidosis is resolved and the patient is able to take (> 5.5 mmol/L/h))
substantial amounts of oral fluids without vomiting with RBG <12mmol/L.
S/C insulin injections can be started when the patient no longer needs IV fluids. Insulin infusion
Do not stop the insulin infusion until 1 to 2 hrs after the first s/c dose. rate (ml/h)
Consult diabetic specialist for further management of the patients.
Treat the precipitating causes of DKA (infections)
 104 Endocrinology Paediatrics Patients’ Management Guidelines 105

Start IV insulin drip at Potassium in infusion Transition

0.1 ml/ kg/ h to s.c. insulin
RBG < 14 mmol/L, no
acidosis (small amounts

Haematology
of ketones may be still
(50 ml NS 0.9% + 50 present in the urine),
IU soluble insulin) patient able to eat
K < 5.5: 40 meq/L

K initially > 5.5:

no potassium in IVF,
check again K after 4
hours, and start infusion
(KPO4: 40 mEq/l) Subcutaneous insulin: – Anaemia
when K becomes < 5.5 Give s.c. injection,
Decrease to 0.05 discontinue IV insulin /
– Sickle Cell Anaemia
units/kg/hr if RBG IV fluids after 1 hr, feed
decreasing too quickly child
(> 5.5 mmol/L/h)
Insulin dose: use the
previous dosing in
patients with known
diabetes.

Diabetes at onset Anaemia

(new patients):
0.7 – 1.0 its/kg/day

DEFINITION

• A decrease in red blood cell (RBC) mass.

References • Anemia is usually discovered and quantified by measurement of the RBC count,
1. International Society for Pediatric and Adolescent Diabetes (ISPAD), Haemoglobin (Hb) concentration, and hematocrit (Hct).
Pediatric Diabetes, 2009; 10 (suppl 12): 118-133
2. The Harriet Lane Hand book of pediatric, 17th Edition. WHO defines anaemia as having Hb below the following at sea level among
3. Nelson textbook of Pediatrics, 17th Edition. different age categories:

Category Anaemia is defined as:

Preterms and VLBW babies Hb <14g/dl
Neonates Hb <14g/dl
Children aged 6 months to 6 years Hb <11 g/dl
6 years to 14 years Hb <12 g/dl

Common causes of anaemia in our settings:

LOW BIRTH WEIGHT
- due to low iron stores (0 – 2 years age group)
DIETARY
- diets tend to be low in iron
 106 Haematology Paediatrics Patients’ Management Guidelines 107

INFECTIONS blood film. The latter two can get iron when Malaria parasites have cleared or in
Parasites - Malaria (haemolysis), Hookworm, Trichiuris (blood loss) etc. rehabilitation phase or when they have started gaining weight for those with severe
Bacteria - Tuberculosis, Clostridia, gram-negative sepsis, malnutrition.
Viral - HIV, Parvovirus B19, Hepatitis, EBV and CMV infections
GENETIC
- Haemoglobinopathies (HbSS, Thalasaemia and others) MANAGEMENT OF SEVERE ANAEMIA
- Glucose 6 phosphate dehydrogenase deficiency
MALIGNANCIES Blood transfusion followed by oral haematenics as described in management of
- Leukaemia, lymphomas, mild to moderate anaemia
DRUGS Indications for blood transfusion :
- Cytotoxic drugs, ARVs (AZT/d4T), Cotrimoxazole, Chloramphenicol, • Severe anaemia (Hb < 5g/dl)
• Cardiac failure due to severe anaemia even with Hb is above 5 g/dl
• Hyperparasitaemia in malaria if Hb < 6 g/dl
CLINICAL FEATURES • In severely malnourished Children;
- Hb below 4g/dl
Symptoms - Cardiac Failure due to severe anaemia
• May be asymptomatic until Hb 6 - 8 g/dl • Neonates if Hb < 10
• Fatigue Consider BT also if:
• Shortness of breath or Breathless on exertion when Hb < 5 g/dl - Hb ≤ 12 g/dL in a neonate requiring intensive care
• Failure to thrive - Hb ≤ 11 g/dL in a neonate with chronic O2 dependency
• Symptoms related to underlying disease pathology - Hb ≤ 7 g/dL in a stable infant (4 to 6 wk) with late anemia
Signs of Anaemia • Sickle cell disease a) if Hb < 5 g/dl or severe infection present
• Pallor of nail beds (the best site), palms and mucous membranes and eye lids - CVA (regardless of Hb)
• Splenomegaly - this occurs in chronic haemolysis and malignancy - Priapism (regardless of Hb)
• Jaundice - this may be present in haemolytic anaemias. • acute severe blood loss- remember that the Hb can initially be normal !

INVESTIGATIONS VOLUME OF TRANSFUSION

The tests should always be done before a transfusion! WHOLE BLOOD: 20 ml/kg OR PACKED RED CELLS: 10 –15 ml/kg
• Haemoglobin concentration (Hb) and cross matching • In both cases, rate = 3 ml/kg/hour (except in severely Malnourished Children)
• Peripheral Blood film • Furosemide 1mg/kg is given prior blood transfusion in cases of
• Full blood picture (FBP) plus reticulocyte count cardiac failure
• Thin and thick film for malaria parasites • It is particularly important that the volume of 10 ml/kg is not exceeded
• Stool test for Parasitic ova, cysts or trophozoites, occult blood in severely malnourished children. If the severely anaemic malnourished child
• Bone marrow aspirate and eventually bone marrow biopsy has signs of cardiac failure, transfuse packed cells (5-7 ml/kg) rather than whole
blood.
For Recurrent Anaemia
• Sickling test Haemoglobin electrophoresis: References:
• Red cell enzyme studies - G-6-PD. 1. Pocket book of Hospital care for children, WHO, 2007.
• Coombs test - identifies autoimmune haemolytic anaemia 2. Standard Treatment and Guidelines Tanzania Mainland, 3rd ed., MOHSW, 2007
• Bone marrow biopsy 3. O’Callaghan C, Stephenson T: Pocket Paediatrics, p.241, Churchill
Livingstone, 1992
4. Mulago Hospital paediatric guidelines, © Child Advocacy International, 2006.
MANAGEMENT OF MILD-MODERATE ANAEMIA 5. WHO - Focusing on anaemia Joint statement by the WHO and UNICEF 2004.
ORAL HAEMATINICS 6. Managing Anemia in Pediatric Office Practice: Part 1 &2. Pediatrics in
Review. 2002; 23:75-84.
• Iron 6mg of elemental iron /kg/day
• Folic acid 5 mg once daily
Iron should not be given to children with Sickle cell anaemia, severely
malnourished in the initial stages, and children who have Malaria parasites on the
 108 Haematology Paediatrics Patients’ Management Guidelines 109

decreased MCV normal MCV increased MCV (for max of 2dys, max daily dose 150mg).OR
• Ibuprofen by mouth 10mg/kg 3-4 times daily. OR
• Morphine in severe pain (with no difficulty in breathing) IM, IV, SC 0.1-
microcytic normocytic macrocytic
0.2mg/kg repeated every 2-4hrs.
- Hydration
• Initial bolus of 20mg/kg Ringer’s Lactate.
serum folate • Then 1.5 x MIVF* with 5% Dextrose + Ringer’s Lactate 1:1.
RBC folate - Blood transfusion as per anaemia guideline.
serum ferritin reticulocyte count vitamin B12 level - Oxygen if needed.
- Antimalarial + Antibiotic (Ceftriaxone IV 50-75mg/Kg/day) if complicated
Normal not
by fever(blood slide and blood culture should be taken/drawn before giving
Low Increased
increased medications)
or
abnormalities

Hb
of other • Acute chest syndrome →Due to clots in lung blood vessels can be precipitated
parameters
electrophoresis by pulmonary infections.
- presentation: fever, dyspnea, hypoxemia, chest pain, infiltrate on CXR
Iron Thalassaemia Haemolysis Marrow Folate B12 - Treatment: antibiotics (ceftriaxone + macrolide), oxygen, hydration (1xMIVF*),
deficiency minor or hypoplasia, deficiency deficiency blood transfusion, encourage deep breathing.
blood loss leukaemia,
infiltration • Aplastic crisis →arrest of RBC production. Usually caused by a virus—eg.
Parvovirus B19
- Lasts 2-14 days
- Treatment: Blood transfusion(as per anaemia guidelines)

Sickle Cell Anaemia • Splenic sequestration →pooling of RBC in spleen: Hb drops quickly. May
follow acute febrile illness.
- Presentation: Rapidly enlarging spleen. Can lead to hypovolemic shock.
- Treatment: urgent blood transfusion, parental education on spleen palpation
ETIOLOGY: • Priapism : → Mechanism is yet to be elucidated
- Presentation: painful erection >3 hrs.
• Genetic defect due to substitution of valine for glutamic acid in the 6th position - Treatment: hydration and pain meds. May need blood transfusion.
of β globulin chain • Gallstones: due to chronic hemolysis.
• Problems - Presentation: colicky RUQ pain, jaundice, nausea/vomiting, fever
- Cells are normal when they carry oxygen. They sickle when they don’t - Diagnosis: abdominal sonogram
- Sickle cells have a shorter lifespan→ chronic anemia (average Hb 6-8g/dL) - Treatment: surgery
- Sickle cells stick to the vascular wall more→causing clots • Osteomyelitis: due to infection of infarcted bone. Commonly by (Staph
Aureus, Salmonella, Strep Pneumonia)
- Diagnosis: bone x-rays, cultures from bone, blood cultures.
COMPLICATIONS - Treament: antibiotics start with IM/IV chloramphenicol (25 mg/kg every 8
hours) .Once the child’s temperature returns to normal, change to oral
• Hyper Haemolytic crisis treatment with the same antibiotic for a total of 5 weeks. Once you
- Breaking up sickle cells→leads to jaundice, severe anaemia have culture results, treat according to the causative organism and the results
- May need to transfuse of antibiotic sensitivity tests.
• Vaso-occlusive crisis - can be precipitated by infection, hypoxia, shock, - May need surgical treatment
exposure to cold usually lasts 2-7 days • Stroke: commonly Ischaemic but haemorragic also occurs. Typical age is
- <2 yrs of age: dactylitis between 2-10years.
- >2 yrs of age: pain crisis. Can be anywhere(often extremities, back, abdomen) - Symptoms: headache, change in neurologic exam (weakness and
- Treatment hypereflexia),aphasia(when dominant hemisphere is involved).
- Pain relief - Diagnosis. CT scan if indicated
• Paracetamol by mouth 60mg/kg/day in 3-4 doses. OR - Treatment: urgent blood transfusion
• Diclofenac by mouth 2-3mg/kg/24hrs in 2-4 divided • Infection: increased risk especially meningitis, bacteremia, pneumonia from
(max.total dose 150mg daily) for IV/IM 0.3-1mg/kg once or twice daily encapsulated organism: (S.pneumoniae, H. influenzae, N. meningitis)
 110 Haematology Paediatrics Patients’ Management Guidelines 111

- Spleen is infracted secondary to sickling, usually the spleen is lost by ~4 yrs

Nephrotic
of age
- Diagnosis: Should suspect infection if fever: do FBP,blood and urine culture,
LP if meningitis suspected. Blood slide for malaria parasite if fever and

Syndrome
anaemia
- Treatment: (ceftriaxone)- if etiology known change antibiotics to cover
appropriate organisms.

Blood Transfusion: In patients with sickle cell disease blood transfusion is

indicated but not limited to:
• Hb < 5 g/dl
• CVA (regardless of Hb)
• Priapism (regardless of Hb)
• Acute chest syndrome (regardless of Hb)
DEFINITION
Post Transfusion Haemoglobin Should Not Exceed 11grams
Nephrotic syndrome (NS), also known as nephrosis, is defined by the presence of
ROUTINE MEDICATION: nephrotic-range proteinuria, eodema, hyperlipidemia, and hypoalbuminemia.
• Folic acid supplementation give 5mg daily Nephrotic-range proteinuria in children is protein excretion of more than 40 mg/
• Consider Penicillin prophylaxis (Penicillin V p to 3yrs 125mg BD above 3 m2/h. (50mg/kg/24hrs).
years 250mg BD) until age 5.
• weekly malaria prophylaxis chloroquine 5mg/kg weekly until age 5
• Teach parents/patients to palpate spleen, use of ITNs, drinking plenty of water UNDERLYING ETIOLOGY
and prompt health seeking in events of fever, pain and acute anaemia.
• Prophylaxis with aspirin 5mg/kg (max 100 mg) The glomerular diseases that cause nephrotic syndrome generally can be divided
into Primary and Secondary etiologies.
*MIVFs = Maintenance IV Fluids 1. Primary nephrotic syndrome, also known as idiopathic nephrotic syndrome
Maintenance IVF fluids are calculated based on the patient’s body weight as (INS), is associated with glomerular diseases intrinsic to the kidney and not related
follows: to systemic causes. The subcategories based on histological descriptions include;
- Minimal Change Nephrotic Syndrome (MCNS)
Body Weight ml/kg/day ml/kg/hr - Focal Segmental Glomerulosclerosis (FSGS)
- Membranous Nephropathy (MN)
First 10kg (0-10kg) 100 4
- Membranoproliferative Glomerulonephritis (MPGN)
Second 10kg (11-20kg) 50 2 - Diffuse Mesangial Proliferation
Each additional kg (>20kg) 20 1
2. Secondary nephrotic syndrome refers to an etiology extrinsic to the kidney.
Secondary causes of nephrotic syndrome include;
References: - Infectious - Syphilis, Toxoplama, CMV, HIV, Hepatitis (B and C), Rubella,
1) Standard Treatment Guidelines (STG) and the National Essential Medicines Malaria.
List For Mainland Tanzania. Third edition (2007). - Drugs - NSAIDs, Interferon,Gold, Mercury, Lithium, Heroin,Penicillamine,
2) The management of sickle cell disease. National Institute of Health. National etc.
Heart, Lung and Blood Institute division of blood disease and resource. NIH - Systemic Disease - Diabetes melitus, sickle cell disease, Malignancy
publications.no.022117. fouth edition. (june 2002). (lymphoma and leukemia),vasculitis, immune complex mediated
3) Pocket book of Hospital care for children, WHO 2007 (Poststreptococcal glomerulonephritis) etc.

Idiopathic Nephrotic Syndrome is divided into steroid-sensitive (SSNS) and

steroid-resistant nephrotic syndrome (SRNS).90% of children with MCNS
responded to corticosteroid treatment with remission of their nephrotic syndrome,
only 20% of children with FSGS responded to steroids.
Nephrotic syndrome may also be caused by genetic abnormalities.eg. Infantile
Nephrotic Syndrome and congenital Nephrotic Syndrome.
 112 Nephrotic Syndrome Paediatrics Patients’ Management Guidelines 113

CLINICAL FEATURES INVESTIGATIONS

Typical features for steroid responsive nephritic syndrome include: INVESTIGATIONS AT INITIAL DURING IN –
PRESENTATION PATIENT STAY
Typical features Atypical features
Height •
Age 1-10 years Age <1year, >10 years
Normotensive Hypertensive Weight • Once daily
Normal Creatinine levels Elevated Creatinine Blood Pressure • Twice daily or more often
+/- microscopic haematuria Macroscopic haematuria
Blood tests Urea and electrolyte Blood tests do not
Total serum protein normally need to be
Children with atypical features are less likely to respond to steroid therapy and may
Serum Albumin repeated
need renal biopsy.
Cholesterol
Creatinine
FBP
ONSET AND OUTCOME
Urine tests Urine dipstick Dip stick for protein daily
As a general indication, consider that NS time onset is frequently associated with Urine analysis(sediments,
outcome. Albumin, casts)
• Congenital or Early onset < 1year: Urine for culture and
- Genetically determined sensitivity
- Infection during pregnancy (Syphilis-CMV-Toxo-Rubeola-HIV)
- Mythochondrial diseases Other investigations to HIV
- Majority is steroid resistant consider Hepatitis B and C
• Onset 2 -12 years: Idiopathic NS Majority is steroid sensitive Sickle cell
• Late onset > 12 years: Autoimmune disases (SLE), MPGN, MGN Kidney ultrasonography
Chest radiography

COMPLICATIONS OF NEPHROTIC SYNDROME You should monitor daily for main complications (hypovolemia, thrombosis and
infections)
Main complications with nephrotic syndrome include:
• Hypovolaemia
- looks for cold extremities, poor capillary refill, tachycardia, TREATMENT
hypovolaemia, watch for paradoxical hypertention.
• Infection • Steroids
- consider antibiotic prophylaxis whilst patient has significant - Induction therapy: Prednisolone at 60 mg/m2/d (2 mg/kg/d), with a
protenuria and /or grossly oedematous. maximum of 80 mg, daily for 6 weeks.
• Thrombosis - Maintenance therapy (following above induction therapy)
- risk for pulmonary embolism, celebral thrombosis, and renal • Prednisolone at 40 mg/m2 (or 1.5 mg/kg), with a maximum of 60 mg, given
vein thrombosis, might be exacerbated by hypovolaemia, as a single dose on alternate days for 6 weeks
patient should be encourage to move around. • After 6 weeks maintance therapy prednisolone should be tapered slowly over
Other complications are: acute renal failure, chronic renal failure and progression a period of time.
to end stage renal failure, increased risk of cardiovascular disease and drug - To minimize side effect prednisolone should be taken as a single dose in the
complications. morning with food.
- For up to 1 yr after completing prednisone therapy, the child will require
corticosteroid supplementation for severe illness or surgery
- Hydrocortisone 100mg/m2 IV start, prior to surgery or with onset of severe
illness. If remains seriously ill, give 100mg/m2/day in 4 divided doses. Wean
hydrocortisone as the child improves.
• Diuretics
Diuretic therapy may be beneficial, particularly in children with symptomatic
 114 Nephrotic Syndrome Paediatrics Patients’ Management Guidelines 115

edema. Loop diuretics, such as furosemide (starting at 1-2 mg/kg/d) may weeks. FBP should be monitored for the first few weeks of treatment.
improve edema; their administration, however, should be handled with care • After initiation of CYP, if patient is in remission of proteinuria, prednisone
because plasma volume contraction may already be present, and hypovolemic is reduced to 40mg/m2 (1.5 mg/kg) on alternate days for 4 weeks, then slowly
shock has been observed with overly aggressive therapy. tapered over 4 weeks.
• Antihypertensive • Patients must have weekly CBC counts to monitor for leukopenia.
Antihypertensive therapy should be given when hypertension is present and • Patients must also maintain adequate hydration and take CYP in the morning
particularly if it persists, but caution should be exercised. In some patients, (not at bedtime) to limit the risk of hemorrhagic cystitis. Families must be
the hypertension will respond to diuretics. ACE inhibitors or angiotensin II counseled to report gross hematuria, fever, or severe illness
receptor blocker (ARB) agents may also contribute to reducing proteinuria but • Always consider cumulative toxicity of CYP. A total dose > 120 mg/kg exposes
should be used cautiously in the presence of acute kidney failure or volume the patient to risk of permanent gonadal dysfunction (amenorrhea, testicular
depletion because their use can worse kidney function in these settings. atrophy, and sterility), cardiac accidents (heart necrosis), interstitial pneumonia,
• Salt/Fluid Restriction pulmonary fibrosis.
A low salt diet is used to try to prevent further fluid retention and oedema.
Fluid restriction may also be helpful. These restrictions are lifted once the child References:
goes into remission. 1. Malcom M. Heather L. et.al. Nephrotic Syndrome guidelines. Newcastle upon
• Penicillin Prophylaxis Tyre Hospitals (NHS Trust Foundation). Department of Paediatric Nephrology.
Whilst nephrotic, children are at increased risk of infection, particularly with January 2008.
encapsulated organisms such as pneumococcus. Penicillin V can be given while 2. Jerome C. Lane. Nephrotic Syndrome in Children. Department of Paediatric.
there is proteinuria and discontinued when the child goes into remission. Division of Kidney diseases. Children’s Memorial Hospital. Chicago. May
Grossly oedematous children are at risk of cellulitis and may benefit from 12.2010.
antibiotic prophylaxis. 3. Standard Treatment Guidelines (STG) and the National Essential Medicines
Dose: Under 5 yrs 125 mg bid List For Mainland Tanzania. Third edition (2007).
5yrs or above 250 mg bid
• Ranitidine
Ranitidine is not routinely used but if a child complains of dyspeptic symptoms
give 2mg/kg per dose bd po. (maximum dose = 150mg twice daily).

RESPONSE TO TREATMENT
Most children with nephrotic syndrome will respond to steroid treatment within
2-4 weeks. A remission is defined as 3 or more days of trace or negative proteins on
dipstick testing. Treatment is continued as outlined above. If proteinuria persists
beyond the first 4 weeks of steroid treatment, then children should be referred for
renal biopsy. In our setting consider for cyclophosphamide.

RELAPSE
Relapse is defined as proteinuria, ++ for 7 consecutive days or +++ for 3 consecutive
days. Frequent relapsers (FRNS) are diagnosed if there is: 2 or more relapses within
the first 6 months of presentation and 4 or more relapses within any 12 month
period. This becomes steroid dependency (SDNS) if the relapses are occurring
during steroid tapering.

TREATMENT OF RELAPSE
Treatment is started with predinisolone. Duration of treatment is different from
treatment of an initial presentation.
Give prednisolone 60 mg/m2 po daily (maximum daily dose = 80mg) as a single
morning dose until urine is protein-free for 3 days. After this daily regimen, give
prednisolone 40mg/m2 po on alternate days (maximum dose = 60mg on alternate
days) for a further 4 weeks, then stop.
Cyclophosphamide
• For children with frequent relapses, steroid resistant or those who are steroid
dependent consider a course of Cyclophosphamide 2-3 mg/kg/day for 8-12
 116 Nephrotic Syndrome Paediatrics Patients’ Management Guidelines 117

Categories of generalized seizures:

Seizures and
• grand mal
- starting with a warning (aura)- sound, light, abdominal pain etc
- usually tonic clonic (see description below)

Epilepsy
- there may be urinary incontinence, frothing and tongue biting
- a period of deep sleep follows
- episodes of mental confusion may follow(post ictal psychosis)

• Absence (petit mal)- mainly disorder of children

- Brief staring spells, blinking, short lapse in consciousness
- No memory of incident
- Recovery is usually as soon as seizure stops (no pronounced post-ictal phase)
- May be mistaken as a behavioural problem
- Usually begin between 6-12 years old
DEFINITIONS
• Myoclonic
Seizures: as a transient occurrence of signs and or symptoms due to abnormal - Quick muscle jerks
electrical discharge in the brain. - Consciousness generally not impaired
Epilepsy: a disorder resulting in recurrent seizures. A single seizure does NOT result - May occur alone, but generally occur in specific epileptic syndromes
in a diagnosis of epilepsy. A patient must have two or more unprovoked seizures to be
diagnosed with epilepsy. • Clonic
Status Epilepticus: continuous seizure lasting > 30 minutes or several seizures - Rapid, repetitive and rhythmic jerking of muscles (most noticeable in extremities)
occurring in succession without recovery of consciousness in between. - Consciousness impaired

• Tonic
CAUSES - Stiffening of muscles (often involves rigid extension of extremities)
- Consciousness impaired
• Infections
• Metabolic disorders • Tonic-Clonic (grand mal)
• Ingestion of drugs of abuse and other toxins. - Tonic phase usually begins first (stiffening of extremities)
• Medications - Clonic phase following (rhythmic jerking)
• Brain/cranial abnormalities - May have loss of bowel or bladder control, tongue biting, injury on falling
• Head trauma /intracranial bleeding - Followed by distinct post-ictal phase (may last hours) where the patient is in
• idiopathic a deep sleep and appears confused

• Atonic
Classification of Seizures - Sudden loss of muscle tone causing child to suddenly drop to the floor
(“drop attacks”)
CLINICAL FEATURES- depends on the type of seizures - Generally lasts only seconds
- May or may not have loss of consciousness
Partial (Focal) Seizures - High rate of injury due to falling
Abnormal electrical activity confined to a localized part of one cerebral hemisphere.
Categories of partial (focal) seizures: Febrile Seizure
• Without impairment of consciousness, symptoms vary based on area of origin • Brief, generalized tonic-clonic seizure associated with a FEBRILE illness
- Motor: hand jerking, facial twitching, lip smacking but WITHOUT any CNS infection or other known neurological cause.
- Sensory: odd taste or smell, seeing flashing lights, hearing buzzing noise • Occurs children aged 6 months-6 years (VERY uncommon outside this
- Autonomic: nausea, sweating age group).
- Emotional: anger, visual or auditory hallucinations, sense of fear • Risk of recurrence: 30% after 1st febrile seizure, 50% after 2nd, declines
• With impairment of consciousness to zero by age 5 years.
• Partial seizures that become secondarily generalized • No anticonvulsant is needed, only sponging and antipyretic agents are
Generalized Seizures recommended
Abnormal activity affecting the entire brain at the onset.
 118 Seizures and Epilepsy Paediatrics Patients’ Management Guidelines 119

• Further evaluation is needed if: seizure occurs > 24 hours after the onset of fever, Acute Management of Seizures
lasts > 15 minutes, appears focal (not generalized), more than one seizure occurs
during an illness, or there are ANY abnormalities on the neurological exam. MEDICATION DOSE COMMENTS
Diazepam IV: 0.25-0.5mg/kg per Immediate onset
dose (may give every 15
INVESTIGATIONS minutes x 2-3 doses if May cause severe
seizures persist) respiratory depression
• The diagnosis of seizures and epilepsy is based on history and physical exam Max total dose < 5 years
thorough neurological exam is mandatory. The diagnosis would be supported by 5mg, > 5years 10mg Avoid IM administration,
Rectally: this slower than rectal
an EEG if that were available. Rectal gel or IV form administration
used rectally:
• Laboratory studies - 0.5mg/kg/dose then
- blood film, culture for urine and blood – if patient has fever or irritability - 0.25mg/kg/dose in
- full blood picture, 10 minutes if seizure
continues
- random blood glucose,
- electrolytes (Na, Mg, K) Phenobarbitone Loading dose: 15-20mg/ Frequently used to treat
- renal function tests (creatinine, urea,) kg IV/IM. If seizures neonatal seizures and
- liver function tests, urine analysis, persist, may give may be the initial drug
- CSF studies (glucose, protein, RBC, WBC, gram stain and culture), additional 5mg/kg doses used in young children
- Blood gases every 15-30 minutes to May cause drowsiness
a maximum of 30mg/kg Repeated large doses
total. may cause respiratory
• Imaging studies Maintenance dose depression
- head CT/MR. These should be based on history and not simply ordered on every (oral/IV):
child with seizures. 3-5mg/kg/day in 1-2
- CXR to exclude aspiration in children with status epilepticus divided doses
Phenytoin Loading dose: 15-18 mg/ Fast administration may
kg/IV cause bradycardia
TREATMENT Maintenance dose (oral/
IV);
GENERAL RULES (see below for medications) 5-10 mg/kg/day in 1-2
- ABC divided doses
- acute management of the ongoing seizure activity Thiopental drip Loading dose: 4-7mg/kg In status epilepticus if no
- determine and treat the underlying cause. (to induce coma) — Maintenance: 2-5mg/kg/ response to other drugs
- If seizures last > 5 minutes or if 3 or more occur in one hour, treat aggressively with ICU ONLY hr (start at 2mg/kg/hr) Mechanical ventilation
medications to avoid progression to status Epilepticus (which can result in needed
permanent damage and death)

Management of Status Epilepticus (Seizure > 30 minutes) in children

Aggressive treatment is necessary. The longer a patient remains in status epilepticus,
the more difficult it will be to control stop the episode. The order of medications
based on the amount of time since the start of the event is listed below. As seizures
persist, continue down the pathway until seizures are halted.

0-5 minutes
Stabilize patient (airway, oxygen, IV access, check RBG, history/physical, labs if
needed/possible)
↓
5-15 minutes
Diazepam (rectal or IV, doses listed above)
If seizures persist, repeat Diazepam 5-10 minutes after initial dose
↓
 120 Seizures and Epilepsy Paediatrics Patients’ Management Guidelines 121

15-35 minutes DRUGS DOSE COMMENTS

If seizures persist, give loading dose of Phenobarbital
↓ Ethosuximide ≤ 6 years - Useful for absence
45 minutes - Initial 15mg/kg/day seizures
If seizures persist, give loading doses of Phenytoin in 2 divided doses (max
500mg/day)
Be prepared to support respirations - Increase every 4-7 days
↓ - Usual maintenance
60 minutes 15-40mg/kd/day in
If seizures persist, consider Thiopental drip (call anesthesia, transfer to ICU, prepare 2 divided doses
for mechanical ventilation) > 6 years
- Initial 250mg twice daily
- Increase every 4-7 days
Management of Epilepsy by 250mg/day
- Usual maintenance 20-
DRUGS DOSE COMMENTS 40mg/kg/day in 2 divided
doses (max 1500mg/day)
Phenobarbitone Generally given once - Long–acting barbiturate
daily at night but may be - Effective in generalized Levetiracetam Initial 10 mg/kg/day Useful in partial and
divided into two doses tonic-clonic and simple (KEPPRA) divided in 2 doses generalized seizures
- 3-5mg/kg/day partial seizures Increase weekly by 5-10 (tonic-clonic and absence
- First choice in neonates mg/kg/day in 2-3 divided seizures)
doses
Phenytoin Start with 5mg/kg/day - Useful in generalized Maintenance is usually
(divided into 2-3 doses) tonic-clonic, simple and 30-40 mg/kg/day in 2-3
may Increase to 7-10mg/ complex partial seizures divided doses
kg/day (divided into 2-3 - Ineffective in absence,
doses) if needed myoclonic, atonic seizures
- Prescribe only drugs with a secure and consistent supply
Carbamazepine - Initial 5-10mg/kg/day - Useful in partial seizures - Start at low end of dosing range and increase until seizure free
(Tegretol, Carbatrol) in 2-3 divided doses (especially complex partial (unless limited by side effects)
- Increase every weekly seizures) - Explain to parents/patient that the drugs must be taken regularly and for a long
by 5 mg/kg up to - May be useful in time (lifelong?)
25-30mg/kg/day. generalized tonic-clonic
Usual dose is 400- seizures BUT may worsen
800mg some types of generalized When to Stop Long-term Anticonvulsant Therapy
seizures Anti-epileptic medications should NOT be stopped abruptly
- Ineffective in absence, For neonates: - Taper then stop medication if seizure free for 3 months
myoclonic, atonic seizures Older children:- Taper then stop medication if seizure free for 1- 2 years
- Less effect on cognition
and behaviour than
phenobarbitone FOLLOW-UP
• Children with epilepsy must always have adult supervision when swimming,
Valproic Acid Initial 5-10mg/kg/day in - Useful for generalized crossing streets, around fire, and in any other situation in which the child could be
(Depakene, Depacon, 1-3 divided doses tonic-clonic, tonic, injured if a seizure were to occur
Depakote) Increase weekly by myoclonic, and absence • Counsel families to obtain a new supply of medications before they run out of
5-10mg/kd/day to a max seizures. medicine
of 40mg/kg/day)
Maintenance is usually • Children with epilepsy should go to school and lead regular lives, this should be
20-40mg/kg/day in 2-3 routinely discussed at follow-up visits and a letter should be written to the school
divided doses (may need allowing the child to participate in all activities.
higher doses if used
with other anti-epileptic References
drugs due to increased
metabolism) 1. MNH Guidelines for paediatric acute patients care 2nd edition 2005.
doses if used with other 2. standard treatment guidelines Tanzania mainland 3rd edition 2007
anti-epileptic drugs due to 3. Scottish clinical guidelines on Diagnosis and management of epilepsies in children
increased metabolism) and young people 2005
4. Nelsons textbook of pediatrics 18th edition
5. up to date 2009 Epilepsy syndromes in children Barry R Tharp, MD
 122 Seizures
Nephrotic
and
Syndrome
Epilepsy Paediatrics Patients’ Management Guidelines 123

Asthma severity Symptoms Daily controller

medication
Severe persistent Continual/persistent inhaled corticosteroids e.g
>800µg Budesonide

Pulmonary
plus:
long-acting ß2 Agonist
or
oralglucocorticosteroid
Moderate/persistent Daily inhaled corticosteroids e.g.
>1night /week 400-800µg Budesonide
(plus:
Long-acting inhaled ß2
Agonist)
– Asthma Mild persistence >2/week but <1x/day inhaled corticosteroids e.g.
>2night/month 100-400µg Budesonide
– Neonatal RDS
Mild Intermittent ≤2days/week No daily medication
≤2night/month needed

Review treatment every 3-6months, a gradual stepwise reduction in treatment may be

possible

Asthma THE ACUTE ASTHMATIC ATTACK

It is characterized by dyspnoea, anxiety, restlessness, tachycardia and usually intense
audible wheezes. Sometimes expiratory wheezes is heard on auscultation. Whispering
and pulsus paradoxus indicate significant airway obstruction.
Is a chronic inflammatory disorder of the airway resulting in recurrent episodes of
wheeze, breathlessness, chest tightness and cough particular at night and in early
Treatment
morning.
Beta 2 agonist bronchodilator by inhalation
Salbutamol(ventolin) or fenoterol (berotec) dose 200µg(2 puffs in MDI)
IMPORTANT FACTORS IN PATHOPHYSIOLOGY
If good response: repeat the dose 2-3 hourly
• Airway inflammation
If no response: repeat the dose within 30 minutes
• Bronchospasm
If still no response: treat for acute severe asthma
• Airway hyper-reactivity to physical or environmental stimuli eg cold air, exercise
and allergen
ACUTE SEVERE ASTHMA (STATUS ASTHMATICUS)
CLASSIFICATION
• Infrequent or episodic
Characterized by anxiety, laboured breathing, audible wheezes and tachypnoea. These
These asthmatic children experience mild and occasional wheeze or cough in
interfere with speech and feeding. The chest is markedly hyperinflated and accessory
the course of the year. Sleep is not disturbed and admission to hospital is not
muscles are used during breathing. Breath sounds are diminished and wheezing is
necessary. Symptoms are easy controlled by inhaled ß2 agonists. The PEFR is
intense.
more than 80% of the predicted rate.
• Mild persistent
TREATMENT
Approximately 20% of asthmatic children have more than six annual episodes
Use the four Hs: Hospitalize, treat Hypoxaemia, Hydrate adequately, give
of cough and wheeze. Sleep and schooling are occasionally disturbed and an
Hydrocortisone.
admission to hospital is sometimes necessary. The PEFR is 60-80% of the
predicted rate.
• Admit in ICU
• Severe
• Give oxygen
A minority of asthmatic children have severe symptoms. Wheeze and cough occur
• Hydration, DNS 60-80ml/kg/day
more than once a week, sleep is disturbed, and several admissions to hospital are
• Hydrocortisone 2mg/kg IV. Repeat 6 hourly until improvement. Then use oral
required annually. The PEFR is less than 60% of the predicted rate.
 124 Pulmonary Paediatrics Patients’ Management Guidelines 125

prednisolone for 5days. Methylprednisolone or dexamethasone may also be used. As the disease progresses, the baby may develop ventilatory failure (rising carbon
• Salbutamol puffs. Repeat 2-3 hourly dioxide concentrations in the blood), and prolonged cessations of breathing (apnea).
• Aminophylline
• Use this only if other therapy has failed. If theophylline has not been given
in previous 24 hours, loading dose 6mg/kg/IV over 10 minutes DIAGNOSIS
• If theophylline has been given in previous 24 hours: IV infusion 0.5mg/kg/hour
• Monitor vital signs throughout iv therapy The diagnosis is made by the clinical picture and the Chest xray which demonstrates:
• If respiratory failure: intubation and mechanical ventilation • decreased lung volumes (“bell-shaped chest”)
• absence of the thymus (after about 6 hrs)
• small, discrete and uniform infiltrate (“ground glass appearance”) that involves
References all lobes of the lungs
1. Handbook of Paediatrics for developing countries 6th edition Oxford/Southern • air-bronchograms
Africa. Vicent C. harrison
2. Jason Robertson and Nicole Shilkolski, The Harriet lane handbook, 17th Edition in severe cases, the infiltrate becomes exaggerated until the cardiac borders become in
apparent (a “white-out” appearance).
In arterial blood gases, blood oxygen levels fall and carbon dioxide rises,
resulting in rising blood acid level and hypoxia.

Neonatal respiratory distress In some patients, FBP and Blood for culture and sensitivity are necessary to rule out
infections (sepsis), and echocardiography is suggested to rule out congenital heart
syndrome (RDS) disease.

TREATMENT FOR RDS

DEFINITION
• Resuscitation (as needed immediately after birth)
RDS is a syndrome in premature infants caused by a developmental insufficiency of • Dry and keep the baby warm. Prevent hypoxia with warm and humidified O2
surfactant production and structural immaturity in the lungs. It can also result from a • IV fluids to stabilize the blood pressure, blood salt and blood sugar
genetic problem with production of surfactant associated proteins. • Attentive nursing care (temperature control, minimal handling etc)
RDS affects about 1% of newborn infants and is the leading cause of death in • Early use of nasal CPAP is mandatory to reduce the respiratory effort and to
preterm infants. maintain the Functional Residual Capacity.
Its occurrence is inversely related to gestation age and birth weight. Its incidence is • If available Surfactant (Natural or Synthetic) should be given by endotracheal
high between 24 to 34 weeks of pregnancy and most in infants below 1kg. intubation and then extubation to Nasal CPAP.
Also referred to as Hyaline Membrane Disease (HMD). • If respiratory failure ensues (Pco2 >60 mm Hg, pH <7.20, and Pao2 <50 mm Hg
with 100% oxygen), mechanical ventilation is indicated.
• Breast milk by nasogastric tube (if IV fliud are given, reduce this rate as the
RISK FACTORS FOR RDS volume of milk increases)
• Antibiotic therapy (Penicillin or Ampicillin and Gentamycin) until you have the
• Prematurity / Low birth weight blood culture results
• Maternal diabetes • Consider steroids in the severe and poorly responding patients. (Not routinely
• Birth asphyxia recommended)
• Male sex, white race, second twin. Note: Avoid high concentration/pressure O2 as these may cause more harm than
• Delivery of a previous preterm infant with RDS good i.e. Oxygen toxicity and barotraumas.

RDS begins shortly after the birth and is manifested by:

• Tachypnea, tachycardia COMPLICATIONS OF RDS
• Chest wall retractions (recession)
• Expiratory grunting Immediate complications
• Nasal flaring • Intraventicurlar hemorrhage or periventicular leucomalacia
• Cyanosis • Pulmonary hypertension
• Patent Ductus Arteriosus
 126 Pulmonary Paediatrics Patients’ Management Guidelines 127

• Pulmonary emphysema/Pneumothorax

Burkitt’s
• Pulmonary haemorrhage
• NEC
• Septicaemia

Long-term complications
• Bronchopulmonary Dysplasia (Chronic Lung Disease)
• Retinopathy of prematurity
• Neuro developmental and audiovisual handicaps
Lymphoma
• Failure to thrive

Prevention of RDS
• Antenatal steroid therapy with betamethasone/dexametahsone at least 48 hours
before delivery for foetal lung maturation
• Avoidance of unnecessary or poorly timed caesarean section INTRODUCTION
• Appropriate management of high-risk pregnancy and labour
• Prediction and possible in utero acceleration of pulmonary immaturity are Burkitt’s lymphoma (BL) is an undifferentiated B-cell cancer of the lymphoid
important preventive strategies tissue characterized by neoplastic proliferation of immature lymphoid cells that are
• Determination of the lecithin concentration in amniotic fluid by the lecithin: primarily accumulated outside the bone marrow. It is the fastest growing cancer
sphingomyelin ratio decrease the likelihood of delivering a premature infant. known by medical science with good response to chemotherapy and only in few
• Antenatal and intrapartum foetal monitoring may similarly decrease the risk of cases, surgery and radiotherapy may be needed.
foetal asphyxia. Asphyxia is associated with an increased incidence and severity of The age range is generally 2 –13 years of age in a male patient: female of 2:1.
RDS Burkitt’s lymphoma primarily occurs in the tropics especially in areas with high
prevalence of P.falciparum malaria, EBV and HIV.

References
1. Nelson text book of Pediatrics 18th edition CLASSIFICATION
2. Current Pediatric Diagnosis and Treatment 16th edition.
3. British association of Perinatal Medicine guideline for management of RDS. 2005. Three subtypes of BL have been reported;
• Endemic/African type – common in equatorial Africa and mainly involves
the jaw
• Sporadic/Non-African type – common outside Africa and the abdomen is the
main site of involvement (ileocecal region).
• Immunodeficiency associated BL – occurs in patients with congenital or
acquired immunodeficiency syndrome and post-transplant patients who are
on immunosuppressive treatment (post-transplant lymphoproliferative disorder
- PTLD)

SYMPTOMS & SIGNS: depends on the site involved, commonly jaw and
abdomen.
• Progressive jaw or abdominal mass of 2-8 weeks which is initially painless.
• Gingival (gum) swelling with occasional gum bleeding not following tooth
extraction.
• Dental anarchy (loose or disarranged teeth).
• Swelling of the orbit (with strabismus or blindness) or palate on one or both
sides of the face.
• Ascites and marked weight loss in advanced disease.
• Liver, spleen and kidney infiltration may occur.
• Enlarged ovaries (in girls) or enlarged testicles in boys may occur.
• Convulsions, paralysis of the lower limbs, urine and faecal incontinence in case
of CNS involvement.
 128 Burkitt’s Lymphoma Paediatrics Patients’ Management Guidelines 129

DIAGNOSTIC WORK-UP Gastritis – Omeprazole or Lansoprazole.

• FBP & ESR – baseline and before every cycle of IV chemotherapy. Constipation – osmotic laxatives e.g. laevolac/Normase
• RFT & LFT – baseline and before every cycle of IV chemotherapy. Cystitis – oral hydration, if severe flashing with low dose lasix.
• HIV rapid test – baseline.
• Serum uric acid and lactate dehydrogenase (LDH) – baseline and before every TUMOUR LYSIS SYNDROME
cycle of IV chemotherapy. Tumor lysis syndrome results from massive lysis of rapidly proliferating malignant
• Serum electrolytes (chloride, potassium, phosphorus) – elevated in tumour lysis cells and it usually occurs within the first 72 hrs of chemotherapy.
syndrome (sodium and calcium: normal or low). It is characterized by hyperuricemia, hyperkalemia, and hyperphosphatemia &
• X-rays AP and lateral views (chest, jaw) – baseline hypocalcemia.
• Abdominal Ultrasound scan – baseline, after third cycle and after last cycle. Risk Factors: dehydration, bulky tumours, use of effective chemotherapy,
• CSF for cytology – baseline and repeat until negative X 2 preexisting renal insufficiency.
• Bone marrow aspiration – baseline. Investigation: BUN, creatinine, uric acid, electrolytes, ECG, Glucose .
• FNAC/Biopsy – baseline. Management: Allopurinol and vigorous hydration prior to chemotherapy (twice
maintenance)
STAGING
Stage I – Single tumour excluding mediastinum & abdomen Reference
Stage II – Two or more tumours/LN on same side of diaphragm 1. Mary Avery & Lewis First: Pediatric Medicine, 2nd edition
Stage III – Tumours/LN on both sides of diaphragm 2. Behrman, Kliegman, Jenson: Nelson textbook of Pediatrics 16th edition
Stage IV – Tumour with primary CNS/bone marrow involvement at Dx 3. Cotran, Kumar & Collins: Robbin’s Pathologic basis of Disease, 6th edition.
4. MOHSW, Burkitt’s Lymphoma National treatment guidelines.
5. Mutalima N et al, Associations between BL among children in Malawi and
TREATMENT infections with HIV, EBV and malaria
6. Ferry JA, BL: Clinicopathologic features and differential diagnosis. The
All patients MUST be well hydrated with RL/NS and given Allopurinol (10mg/kg oncologist 2006;11:375-383.
OD for 7 days) to prevent tumour lysis syndrome.
Metochlopramide should be prescribed as a stat dose.

BSA = √ [height (cm) * weight (kg) / 3600]

Chemotherapy should include:

• Intravenous – vincristine (1.4 mg/m2), cyclophosphamide (1.2mg/m2) and
methotrexate (75mg/m2) to be given after every two weeks for 6 cycles.
• Intrathecal Methotrexate to be given every week for six cycles.
<3years – 10 mg
3 – 10 years – 12 mg
>10 years – 15 mg

TOXICITIES AND SIDE EFFECTS OF CHEMOTHERAPY

Nausea, vomiting, diarrhoea and bone marrow depression can happen with all
chemotherapy.
Cyclophosphamide – hemorrhagic cystitis, cytopenia.
Methotrexate – megaloblastic anaemia, pancytopenia, intestinal ulcers, alopecia,
liver damage, dermatitis, mucositis.
Vincristine – constipation, alopecia, neurotoxicity – peripheral neuropathy.

MANAGEMENT OF COMMON SIDE EFFECTS

Myelotoxicity – transfusional support including packed red blood cells (PRBC)
and platelet concentrates (Plts) – haematological growth factors (G-CSF)
Vomiting – Metochlopramide
Mucositis – Nystatin/ Miconazole
Diarrhoea – Fluid hydration +/- Loperamide
 130 Seizures
Nephrotic
and
Syndrome
Epilepsy Paediatrics Patients’ Management Guidelines 131

puncture site. Consider a differential diagnosis of tuberculosis.

• If the fluid is thin pus or cloudy (like milk), leave the catheter in place so that you
can draw out more pus several times a day. Make sure you seal the end of the
catheter so that no air can get in.

Procedures If the fluid is thick pus which cannot pass easily through the needle or catheter, insert
a chest tube.
• Select and prepare the site as described above.

- Make a 2–3 cm skin incision along the line of the intercostal space, just above the
rib below (to avoid damaging the vessels which lie under the lower edge of
each rib).

- Use sterile forceps to push through the subcutaneous tissue just above the upper
– Chest Tube edge of the rib and puncture the pleura.
– Intraosseous Line - Pass a gloved finger into the incision and clear a path to the pleura (this is not
Lumbar Puncture possible in infants).

- Use the forceps to hold the drainage catheter (16 gauge) and introduce it into the
chest for several centimetres, pointing upwards. Ensure that all drainage holes of
the catheter are inside the chest.

- Connect the catheter to a collection bottle with an underwater seal.

Asthma - Suture the catheter in place, secure with tape, and apply a gauze dressing

INSERTION OF A CHEST DRAIN

Pleural effusions should be drained, except when small. It is sometimes necessary to

drain both sides of the chest. You may have to drain the chest 2 or 3 times if the fluid
keeps coming back.

DIAGNOSTIC PROCEDURE

• Consider giving the child sedation or light anaesthesia with ketamine.

• Wash the hands and put on sterile gloves.
• Lay the child on the back.
• Clean the skin over the chest for at least 2 minutes with an antiseptic solution
(for example, 70% alcohol).
• Select a point in the mid-axillary line (at the side of the chest) just below the
level of the nipple (fifth intercostal space).
• Inject about 1ml of 1% lignocaine into the skin and subcutaneous tissue at this
point.
• Insert a needle or catheter through the skin and pleura and aspirate to confirm the
presence of pleural fluid. Withdraw a sample for microscopy and other tests and
place in a container. Insertion of a chest tube: the site is selected in the mid-axillary line in the 5th intercostal space
• If the fluid is clear (straw-coloured or brownish), pull out the needle or catheter (at the level of the nipple) on the superior aspect of the 6th rib.
after withdrawing enough fluid to relieve distress and put a dressing over the
 132 Procedures Paediatrics Patients’ Management Guidelines 133

by grasping the thigh and knee above and lateral to the cannulation site, with
the fingers and thumb wrapped around the knee but not directly behind the
insertion site.
• Palpate the landmarks again with the sterile glove (right hand).
• Insert the needle at a 90° angle with the bevel pointing towards the foot.
• Advance the needle slowly using a gentle but firm, twisting or drilling motion.
• Stop advancing the needle when you feel a sudden decrease in resistance
or when you can aspirate blood. The needle should now be fixed in the bone.
• Remove the stylet.
• Aspirate 1 ml of the marrow contents (looks like blood), using the 5-ml syringe,
to confirm that the needle is in the marrow cavity.
• Attach the second 5-ml syringe filled with normal saline. Stabilize the needle
and slowly inject 3 ml while palpating the area for any leakage under the skin. If
no infiltration is seen, start the infusion.
• Apply dressings and secure the needle in its place.
Note: Failure to aspirate marrow contents does not mean that the needle is not
correctly placed.
• Monitor the infusion by the ease with which the fluid flows and by the clinical
response of the patient.
• Check that the calf does not swell during the infusion.

Stop the intraosseous infusion as soon as venous access is available. In any case, it
Intraosseous infusion should not continue for more than 8 hours.

Complications include:
When carried out by a well trained and experienced health worker, intraosseous • Incomplete penetration of the bony cortex
infusion is a safe, simple and reliable method of giving fluid and drugs in an • Signs: The needle is not well fixed; infiltration occurs under the skin.
emergency. • Penetration of the posterior bone cortex (more common)
• Sign: Infiltration occurs, calf becomes tense.
The first choice for the puncture is the proximal tibia. The site for needle insertion • Infection
is in the middle of the antero-medial surface of the tibia, at the junction of the • Signs: Cellulitis at the site of the infusion.
upper and middle third to avoid damaging the epiphyseal plate (which is higher in
the tibia). An alternative site for needle insertion is the distal femur, 2 cm above the
lateral condyle.

Prepare the necessary equipment, i.e.:

— bone marrow aspiration or intraosseous needles (15–18 gauge or, if not
available, 21 gauge).
If these are not available, large-bore hypodermic or butterfly needles can be used in
young children
• antiseptic solution and sterile gauze to clean the site
• a sterile 5-ml syringe filled with normal saline
• a second sterile 5-ml syringe
• IV infusion equipment
• sterile gloves.
• Place padding under the child’s knee so that it is bent 30°from the straight
(180°) position, with the heel resting on the table.
• Locate the correct position (described above and shown in the illustration).
• Wash the hands and put on sterile gloves.
• Clean the skin over and surrounding the site with an antiseptic solution.
• Stabilize the proximal tibia with the left hand (this hand is now not sterile)
References: WHO Pocket book of Hospital Care for Children, 2005
 134 Paediatrics Patients’ Management Guidelines 135

Lumbar Puncture In young infants this decrease in resistance is not always felt, so advance the
needle very carefully.
- Withdraw the stylet, and drops of cerebrospinal fluid will pass out of the
The following are contraindications: needle. If no CSF is obtained, the stylet can be reinserted and the needle
• signs of raised intracranial pressure (unequal pupils, rigid posture or paralysis in advanced slightly.
any of the limbs or trunk, irregular breathing) - Obtain a sample of 0.5–1 ml CSF and place in a sterile container.
• skin infection in the area through which the needle will have to pass. - Withdraw the needle and stylet completely and put pressure over the site for
a few seconds.
If contraindications are present, the potential value of the information gained from
a lumbar puncture should be carefully weighed against the risk of the procedure. If Put a sterile dressing over the needle puncture site.
in doubt, If the needle is introduced too far, a lumbar vein may be punctured. This will
it might be better to start treatment for suspected meningitis, and delay performing result in a “traumatic tap” and the spinal fluid will be bloody. The needle should be
a lumbar puncture. withdrawn and the procedure repeated in another disc space.
• Position the child

There are two possible positions:

— the child lying down on the left side (particularly for young infants)
— in the sitting position (particularly for older children).

Lumbar puncture when the child is lying on the side:

• A hard surface should be used. Place the child on the side so that the vertebral
column is parallel to this surface and the transverse axis of the back is vertical.
• The assistant should flex the back of the child, pull up the knees towards
the chest, and hold the child at the upper back between the shoulders and
buttocks so that the back is bent. Hold the child firmly in this position.
Make sure that the airway is not obstructed and the child can breathe normally.
Take particular care in holding young infants. The assistant should
not hold a young infant by the neck nor flex the neck to avoid airway
obstruction.

• Check anatomical landmarks

- Locate the space between the third and fourth or between the fourth and
fifth lumbar vertebrae. (The third lumbar vertebra is at the junction of the line
between the iliac crests and the vertebral column).

• Prepare the site

- Use aseptic technique. Scrub the hands and wear sterile gloves.
- Prepare the skin around the site with an antiseptic solution.
- Sterile towels may be used.
- In older children who are alert, give a local anaesthetic (1% lignocaine)
infiltrated in the skin over the site.

• Perform the lumbar puncture

- Use an LP needle with stylet (22 gauge for a young infant, 20 gauge for an
older infant and child;
if these are not available, hypodermic needles may be used). Insert the
needle into the middle of the intervertebral space and aim the needle
towards the umbilicus.
- Advance the needle slowly. The needle will pass easily until it encounters
References: WHO Pocket
the ligament between the vertebral processes. More pressure is needed to book of Hospital Care
penetrate this ligament, less resistance is felt as the dura is penetrated. for Children, 2005
 136 Nephrotic Syndrome Paediatrics Patients’ Management Guidelines 137

Boys’ weight (kg) Age Girls’ weight (kg)

-4SD -3SD -2SD -1SD Median (months) Median -1SD -2SD -3SD -4SD
7.85 9.03 10.20 11.37 12.54 25 12.01 10.81 9.61 8.40 7.20

Tables
7.87 9.09 10.30 11.52 12.74 26 12.23 10.99 9.76 8.53 7.29
7.89 9.15 10.41 11.68 12.94 27 12.43 11.17 9.91 8.65 7.39
7.91 9.22 10.52 11.83 13.13 28 12.63 11.35 10.06 8.77 7.48
7.94 9.28 10.63 11.98 13.33 29 12.83 11.52 10.21 8.89 7.58
7.97 9.36 10.74 12.13 13.52 30 13.03 11.69 10.35 9.01 7.67
8.00 9.43 10.85 12.28 13.71 31 13.22 11.85 10.49 9.13 7.76
8.04 9.51 10.97 12.43 13.89 32 13.40 12.01 10.63 9.24 7.85
8.09 9.58 11.08 12.58 14.08 33 13.58 12.17 10.76 9.35 7.94
WHO tables to calculate the child’s 8.13 9.66 11.20 12.73 14.26 34 13.76 12.33 10.90 9.46 8.03
weight-for-age 8.18 9.75 11.31 12.88 14.44 35 13.93 12.48 11.03 9.57 8.12
8.24 9.83 11.43 13.03 14.62 36 14.10 12.63 11.15 9.68 8.21
Boys’ weight (kg) Age Girls’ weight (kg) 8.29 9.92 11.55 13.18 14.80 37 14.27 12.78 11.28 9.79 8.29
-4SD -3SD -2SD -1SD Median (months) Median -1SD -2SD -3SD -4SD 8.35 10.01 11.67 13.32 14.98 38 14.44 12.92 11.41 9.89 8.38
1.63 2.04 2.45 2.86 3.27 0 3.23 2.74 2.24 1.75 1.26 8.42 10.10 11.79 13.47 15.16 39 14.60 13.06 11.53 9.99 8.46
1.55 2.24 2.92 3.61 4.29 1 3.98 3.39 2.79 2.19 1.59 8.48 10.19 11.91 13.62 15.33 40 14.76 13.20 11.65 10.10 8.54
1.76 2.62 3.47 4.33 5.19 2 4.71 4.03 3.35 2.67 1.99 8.55 10.29 12.03 13.77 15.51 41 14.91 13.34 11.77 10.20 8.62
2.18 3.13 4.08 5.03 5.98 3 5.40 4.65 3.91 3.16 2.42 8.62 10.39 12.15 13.91 15.68 42 15.07 13.48 11.89 10.29 8.70
2.73 3.72 4.70 5.69 6.68 4 6.05 5.25 4.46 3.66 2.87 8.70 10.48 12.27 14.06 15.85 43 15.22 13.61 12.00 10.39 8.78
3.34 4.33 5.32 6.31 7.30 5 6.65 5.82 4.98 4.15 3.31 8.77 10.58 12.40 14.21 16.02 44 15.37 13.74 12.12 10.49 8.86
3.94 4.92 5.89 6.87 7.85 6 7.21 6.34 5.47 4.60 3.73 8.85 10.68 12.52 14.35 16.19 45 15.52 13.88 12.23 10.58 8.94
4.47 5.44 6.41 7.37 8.34 7 7.71 6.80 5.90 5.00 4.09 8.93 10.79 12.64 14.50 16.36 46 15.67 14.00 12.34 10.68 9.01
4.92 5.89 6.85 7.82 8.78 8 8.16 7.22 6.29 5.35 4.42 9.01 10.89 12.77 14.65 16.53 47 15.81 14.13 12.45 10.77 9.09
5.30 6.27 7.24 8.21 9.18 9 8.56 7.59 6.63 5.66 4.70 9.10 11.00 12.90 14.79 16.69 48 15.96 14.26 12.56 10.86 9.16
5.62 6.60 7.58 8.56 9.54 10 8.92 7.92 6.93 5.93 4.94 9.18 11.10 13.02 14.94 16.86 49 16.10 14.39 12.67 10.95 9.23
5.88 6.88 7.87 8.87 9.86 11 9.24 8.22 7.20 6.17 5.15 9.27 11.21 13.15 15.09 17.03 50 16.25 14.51 12.77 11.04 9.30
6.09 7.11 8.12 9.14 10.15 12 9.53 8.48 7.43 6.39 5.34 9.36 11.32 13.28 15.23 17.19 51 16.39 14.63 12.88 11.13 9.37
6.26 7.30 8.34 9.38 10.41 13 9.79 8.72 7.65 6.57 5.50 9.45 11.43 13.40 15.38 17.36 52 16.53 14.76 12.98 11.21 9.44
6.40 7.46 8.53 9.59 10.65 14 10.03 8.93 7.84 6.74 5.64 9.54 11.54 13.53 15.53 17.52 53 16.67 14.88 13.09 11.30 9.51
6.51 7.60 8.69 9.78 10.87 15 10.25 9.13 8.01 6.89 5.78 9.64 11.65 13.66 15.67 17.69 54 16.81 15.00 13.19 11.38 9.57
6.60 7.72 8.84 9.96 11.08 16 10.45 9.31 8.17 7.04 5.90 9.73 11.76 13.79 15.82 17.85 55 16.95 15.12 13.29 11.46 9.64
6.68 7.83 8.98 10.13 11.28 17 10.64 9.49 8.33 7.18 6.02 9.82 11.87 13.92 15.97 18.02 56 17.09 15.25 13.40 11.55 9.70
6.76 7.93 9.11 10.29 11.47 18 10.83 9.65 8.48 7.31 6.14 9.92 11.99 14.05 16.12 18.18 57 17.24 15.37 13.50 11.63 9.76
6.83 8.04 9.25 10.45 11.66 19 11.01 9.82 8.64 7.46 6.27 10.02 12.10 14.18 16.26 18.34 58 17.38 15.49 13.60 11.71 9.82
6.91 8.15 9.38 10.61 11.85 20 11.19 9.99 8.80 7.60 6.41 10.11 12.21 14.31 16.41 18.51 59 17.52 15.61 13.70 11.79 9.88
7.00 8.26 9.52 10.78 12.04 21 11.37 10.16 8.96 7.75 6.54 10.21 12.33 14.44 16.56 18.67 60 17.66 15.73 13.80 11.87 9.94
7.08 8.37 9.65 10.94 12.22 22 11.55 10.33 9.12 7.90 6.68 10.31 12.44 14.57 16.71 18.84 61 17.81 15.85 13.90 11.95 9.99
7.17 8.48 9.79 11.10 12.41 23 11.73 10.50 9.28 8.05 6.82 10.41 12.56 14.70 16.85 19.00 62 17.96 15.98 14.00 12.02 10.04
7.84 8.97 10.09 11.22 12.34 24 11.80 10.62 9.45 8.28 7.10 10.50 12.67 14.84 17.00 19.17 63 18.10 16.10 14.10 12.10 10.10
 138 Tables Paediatrics Patients’ Management Guidelines 139

Boys’ weight (kg) Age Girls’ weight (kg) Boys’ weight (kg) Age Girls’ weight (kg)
-4SD -3SD -2SD -1SD Median (months) Median -1SD -2SD -3SD -4SD -4SD -3SD -2SD -1SD Median (months) Median -1SD -2SD -3SD -4SD
10.60 12.78 14.97 17.15 19.33 64 18.25 16.23 14.20 12.17 10.15 12.99 16.46 19.94 23.42 26.90 103 26.89 22.91 18.93 14.95 10.97
10.70 12.90 15.10 17.30 19.50 65 18.40 16.35 14.30 12.25 10.20 12.99 16.52 20.06 23.60 27.14 104 27.20 23.14 19.08 15.03 10.97
10.79 13.01 15.23 17.45 19.67 66 18.56 16.48 14.40 12.32 10.25 12.98 16.58 20.18 23.78 27.38 105 27.51 23.38 19.24 15.11 10.98
10.89 13.13 15.36 17.60 19.84 67 18.71 16.61 14.50 12.40 10.29 12.98 16.64 20.30 23.97 27.63 106 27.82 23.61 19.40 15.20 10.99
10.99 13.24 15.49 17.75 20.00 68 18.87 16.74 14.60 12.47 10.34 12.97 16.70 20.43 24.15 27.88 107 28.14 23.85 19.57 15.28 11.00
11.08 13.35 15.63 17.90 20.17 69 19.03 16.87 14.70 12.54 10.38 12.97 16.76 20.55 24.34 28.13 108 28.46 24.10 19.73 15.37 11.01
11.18 13.47 15.76 18.05 20.34 70 19.19 17.00 14.81 12.62 10.42 12.96 16.82 20.67 24.53 28.39 109 28.79 24.34 19.90 15.46 11.02
11.27 13.58 15.89 18.20 20.51 71 19.36 17.13 14.91 12.69 10.46 12.95 16.87 20.80 24.72 28.65 110 29.11 24.59 20.07 15.55 11.03
11.36 13.69 16.02 18.35 20.69 72 19.52 17.27 15.01 12.76 10.50 12.94 16.93 20.93 24.92 28.91 111 29.44 24.84 20.24 15.65 11.05
11.45 13.80 16.15 18.51 20.86 73 19.70 17.41 15.12 12.83 10.54 12.93 16.99 21.05 25.12 29.18 112 29.78 25.10 20.42 15.74 11.06
11.54 13.91 16.29 18.66 21.03 74 19.87 17.55 15.22 12.90 10.57 12.91 17.05 21.18 25.32 29.45 113 30.12 25.36 20.60 15.84 11.08
11.63 14.02 16.42 18.81 21.21 75 20.05 17.69 15.33 12.97 10.61 12.90 17.11 21.31 25.52 29.72 114 30.45 25.62 20.78 15.94 11.10
11.71 14.13 16.55 18.97 21.38 76 20.23 17.83 15.43 13.04 10.64 12.89 17.17 21.45 25.72 30.00 115 30.80 25.88 20.96 16.04 11.12
11.80 14.24 16.68 19.12 21.56 77 20.42 17.98 15.54 13.11 10.67 12.88 17.23 21.58 25.93 30.28 116 31.14 26.14 21.15 16.15 11.15
11.88 14.35 16.81 19.28 21.74 78 20.61 18.13 15.65 13.18 10.70 12.87 17.30 21.72 26.14 30.57 117 31.49 26.41 21.33 16.25 11.18
11.96 14.45 16.94 19.43 21.92 79 20.80 18.28 15.76 13.24 10.72 12.86 17.36 21.86 26.36 30.86 118 31.84 26.68 21.52 16.36 11.21
12.04 14.56 17.07 19.59 22.10 80 21.00 18.44 15.87 13.31 10.75 12.86 17.43 22.00 26.57 31.15 119 32.19 26.95 21.72 16.48 11.24
12.12 14.66 17.20 19.75 22.29 81 21.20 18.59 15.99 13.38 10.77 12.98 16.64 20.30 23.97 27.63 106 27.82 23.61 19.40 15.20 10.99
12.19 14.76 17.33 19.90 22.47 82 21.41 18.76 16.10 13.45 10.79 12.97 16.70 20.43 24.15 27.88 107 28.14 23.85 19.57 15.28 11.00
12.26 14.86 17.46 20.06 22.66 83 21.62 18.92 16.22 13.52 10.81 12.97 16.76 20.55 24.34 28.13 108 28.46 24.10 19.73 15.37 11.01
12.33 14.96 17.59 20.22 22.85 84 21.84 19.09 16.34 13.58 10.83 12.96 16.82 20.67 24.53 28.39 109 28.79 24.34 19.90 15.46 11.02
12.39 15.06 17.72 20.38 23.04 85 22.06 19.26 16.46 13.65 10.85 12.95 16.87 20.80 24.72 28.65 110 29.11 24.59 20.07 15.55 11.03
12.46 15.15 17.85 20.54 23.24 86 22.29 19.43 16.58 13.72 10.86 12.94 16.93 20.93 24.92 28.91 111 29.44 24.84 20.24 15.65 11.05
12.52 15.25 17.97 20.70 23.43 87 22.53 19.61 16.70 13.79 10.87 12.93 16.99 21.05 25.12 29.18 112 29.78 25.10 20.42 15.74 11.06
12.57 15.34 18.10 20.87 23.63 88 22.76 19.79 16.82 13.85 10.88 12.91 17.05 21.18 25.32 29.45 113 30.12 25.36 20.60 15.84 11.08
12.63 15.43 18.23 21.03 23.83 89 23.01 19.98 16.95 13.92 10.89 12.90 17.11 21.31 25.52 29.72 114 30.45 25.62 20.78 15.94 11.10
12.68 15.52 18.35 21.19 24.03 90 23.26 20.17 17.08 13.99 10.90 12.89 17.17 21.45 25.72 30.00 115 30.80 25.88 20.96 16.04 11.12
12.72 15.60 18.48 21.36 24.24 91 23.51 20.36 17.21 14.06 10.91 12.88 17.23 21.58 25.93 30.28 116 31.14 26.14 21.15 16.15 11.15
12.77 15.69 18.61 21.52 24.44 92 23.77 20.55 17.34 14.13 10.92 12.87 17.30 21.72 26.14 30.57 117 31.49 26.41 21.33 16.25 11.18
12.81 15.77 18.73 21.69 24.65 93 24.03 20.75 17.48 14.20 10.92 12.86 17.36 21.86 26.36 30.86 118 31.84 26.68 21.52 16.36 11.21
12.84 15.85 18.85 21.86 24.86 94 24.30 20.95 17.61 14.27 10.93 12.86 17.43 22.00 26.57 31.15 119 32.19 26.95 21.72 16.48 11.24
12.87 15.92 18.98 22.03 25.08 95 24.57 21.16 17.75 14.34 10.93
12.90 16.00 19.10 22.20 25.30 96 24.84 21.37 17.89 14.41 10.94
12.92 16.07 19.22 22.37 25.52 97 25.12 21.58 18.03 14.49 10.94
12.94 16.14 19.34 22.54 25.74 98 25.41 21.79 18.18 14.56 10.94
12.96 16.21 19.46 22.71 25.97 99 25.70 22.01 18.32 14.63 10.95
12.97 16.28 19.58 22.89 26.19 100 25.99 22.23 18.47 14.71 10.95
12.98 16.34 19.70 23.06 26.43 101 26.29 22.45 18.62 14.79 10.96
12.98 16.40 19.82 23.24 26.66 102 26.59 22.68 18.77 14.87 10.96
 140 Tables Paediatrics Patients’ Management Guidelines 141

HEART RATE RESPIRATORY RATE

Age Lower range values Medium values Upper range values Age (yrs) Female Male
Newborn 70 125 190 0-1 30+/-6 31+/-8
1-11 mo 80 120 160 1-2 27+/-4 26+/-4
2 yrs 80 110 130 2-3 25+/-3 25+/-4
4 yrs 80 100 120 3-4 24+/-3 24+/-3
6 yrs 75 100 115 4-5 22+/-2 23+/-2
8 yrs 70 90 110 5-6 21+/-2 22+/-2
10 yrs 70 90 110 6-7 21+/-3 21+/-3
12 yrs F 65 85 105 7-8 20+/-2 20+/-3
M 70 90 110 8-9 20+/-2 20+/-2
14 yrs F 80 80 100 9-10 19+/-2 19+/-2
M 65 85 105 10-11 19+/-2 19+/-2
16 yrs F 55 75 95 11-12 19+/-3 19+/-3
M 60 80 100 12-13 19+/-2 19+/-3
18 yrs F 50 70 90 13-14 18+/-2 19+/-2
M 55 75 95 14-15 18+/-3 18+/-2
15-16 18+/-3 17+/-3
16-17 17+/-3 17+/-2
17-18 17+/-3 16+/-3

Age Systolic Pressure (Mmhg)

0-1 mo 60
1 mo-1 yr 70
>1 yr 70+ (2 x age in yrs)

DYASTOLIC PRESSURE=more or less 2/3 of systolic pressure

 142

Acknowledgements

This publication has been possible thanks to the contribution of the Doctors and
Students of Bugando Medical Centre of Mwanza and Ospedale Bambino Gesù of
Rome.
I want to express my personal gratitude to all the people who have supported, in
different ways, the realization of this most useful working tool.

Prof. Guido Castelli Gattinara

Director of Master of Medicine in Paediatrics
Catholic University of Health and Allied Sciences

Editorial board
Antke Züchner – Pediatric Cardiologist – Bugando Medical Center
Guido Castelli Gattinara – Pediatrician and Infectivologist – Bambino Gesù Hospital

Contributors Reviewers
Alexander Christopher Cinzia Auriti
Duncan Hau Carla Bizzarri
Adolfine Hokororo Marco Cappa
Shakilu Jumanne Guido Castelli
Rogatus Kabyemera Beatrice Chiarini
Neema Kayange Andrea Dotta
Tumaini Mada Salvatore Giannico
Godfrey Mbawala Alessandro Jenkner
Mercy Minde Laura Lancella
Naiz Mnong’one Matteo Luciani
Stella Mongella Valerio Nobili
Bahati Msaki Stefano Picca
Damas Mwizamholya Daniela Perrotta
Neema Orgenes Giacomo Pongiglione
Jill Sanders Federico Vigevano
Antke Zuechner Alberto Villani

BCV associati (Rome), design and lay-out

Tipografia Ograro (Rome), printing