DCH: P1; Q1
1a)
The characteristics of an innocent
murmur (10)
·
Common
·
Asymptomatic
·
Normal pulses and normal heart
sounds
·
Short ejection systolic
·
Never diastolic
·
Usually at the left sternal border
·
May change with posture
·
Soft (not more than 3/ 6)
·
Normal ECG
·
Normal CXR
·
Not associated with cyanosis
·
Not associated with heart failure
·
Accentuated by fever and exercise
·
No chest pain
·
Not associated with clubbing
·
Examples: Still’s vibratory murmur,
venous hum, pulmonary flow murmur, functional murmur
·
No other syndromic
features which may be associated with cardiac abnormalities
1 b)
Clinical features of poliomyelitis and polio eradication strategies Poliomyelitis (10)
·
An enteroviral
infection serotypes 1, 2, and 3. Fecorally spread.
Human reservoir
·
Viral infection that multiplies in
the GIT and Peyer’s patches leading to a viraemia. There are 4 clinical manifestations:
·
Inapparent
disease: > 95% of individuals infected remain asymptomatic
or have-
·
Abortive disease: Initially fever,
headache and vomiting and get minor non CNS illness- sore throat, nausea,
vomiting, diarrhoea, constipation, non specific abdominal pain lasting 5-7
days.
·
Non-paralytic disease:
<5% develop aseptic meningitis. Can also get neck stiffness and myalgias, backache. Meningitis with lymphocytic
pleocytosis. This phase lasts 1-2 weeks.
·
Paralytic disease:
<1% get asymmetrical flaccid paralysis. Can invade
the CNS along nerve routes with destruction of the motor neurons in the anterior horn and brainstem
·
Localised or widespread muscle pain,
spasms leading to weakness. Asymmetric loss of muscle function. Lower limbs
more than upper limbs.
·
There may be complete, partial or no
recovery in this phase
·
Death occurs by respiratory muscle
paralysis, bulbar involvement, vasomotor instability and rarely an encephalitic
illness.
·
virus is shed in the stool for
several weeks
Eradication
Strategies
Specific
measures:
·
Diagnosis is made by having a high index
of suspicion especially when dealing with a patient with acute flaccid
paralysis who particularly is not / or incompletely vaccinated. Travel history
is also important. The virus can be isolated from stool, (as well as throat
swabs). Treatment is mainly supportive with full infection control measures
·
Urgent telephonic notification
to the provincial EPI coordinator for the Department of Health should occur.
·
Containment of cases and spread
·
Immunisation of contacts should be
effected.
·
Avoidance of unnecessary visiting
areas reporting outbreaks
General
Measures:
·
WHO global initiative to eradicate
and eliminate polio
·
Prevention is by vaccination: EPI-SA
as part of the immunisation programme live oral polio drops(OPV) given at
birth; 6, 10, 14 weeks; 18 months and 5 years.
·
Inactivated polio vaccine (IPV) can
also be used for selected cases
·
National Coverage Immunisation
campaigns to mop up and increase herd immunity
·
Public awareness campaigns
·
Health Education, Promotion and
Training at community and health facility levels
·
Political Commitment and Department
of Health guidelines, updates and surveillance programmes
·
Provision of safe water and
sanitation to all
1c) List the features that would lead you to refer
a child with a ventricular septal defect for early
evaluation by a Cardiologist. (10)
Clinical:
·
Persistent tachypnoea
and dyspnoea
·
Poor feeding
·
Growth restriction and failure
·
Recurrent pneumonias
·
CCF
·
Pulmonary hypertension
·
Left praecordial
bulge
·
Cyanosis
·
Suspected endocarditis
Investigation:
·
Abnormal ECG
·
Abnormal CXR
Other:
·
Suspected complex lesion
·
Syndromic
e.g. Down Syndrome
1d) Causes and clinical features of erythema
nodosum (10)
Discreet painful nodules on
the shins, calves, thighs, buttocks and upper extremities representing a form
of delayed hypersensitivity to variety of stimuli. Often felt better than seen;
may be associated with fever and arthralgia. Usually self limiting. Resolution in a few
weeks. Progression through the colour changes of a bruise. Should look for a cause because it is not the erythema nodosum
itself that is the important illness. In many cases, there is an
underlying illness, often an infection that is thought to trigger this
inflammatory reaction.
·
Infections:
-
streptococcal infection
-
primary tuberculosis
-
·
Drugs -any
-
sulphonamides
-
penicillins
-
phenytoin
-
barbiturates
·
Other
-
inflammatory bowel disease
-
sarcoidosis
-
lymphoproliferative
disorders
-
Idiopathic
DCH: P1; Q2
1) Causes of apnoea in the first week of life.
Standard
Treatment Guidelines and Essential Drug List for
2) Pharmacological management of neonatal convulsions.
Standard
Treatment Guidelines and Essential Drug List for
Note that intravenous Phenobarbitone is available again and is regarded as first line drug of choice with loading dose of 20 mg/kg which can be repeated if no response. Diazepam is not recommended for neonates.
3) Principles of management of hypovolaemiac shock in a child.
Standard Treatment Guidelines and Essential Drug List for South Africa Hospital Level Paediatrics 2006 p. 8-11
APLS or PALS guidelines
4) Notifiable diseases affecting children.
Standard
Treatment Guidelines and Essential Drug List for
Standard Treatment
Guidelines and Essential Drug List for South Africa Hospital Level Paediatrics 2006 will be available in January 2007
DCH: P1; Q3
A. Vaccine
schedule, adverse effects and contra-indication
Use Coovadia textbook for
answers.
Tabulate which vaccines are given, their adverse
effects and contra-indications if any.
B. A 2 year
old who presents with a wheeze for the first time
C. Child
headed households
Problems that these children face can be psychological
and socio-economic. The majority of them have been orphaned by HIV/AIDS. They
have problems with the following issues:
i.
Stealing
ii.
prostitution
Possible Interventions
D. Thirteen
year old with PV bleeding
DCH: P1; Q4
Advice to parents who complain that “My 3-year old child
won’t eat.”
·
This
pattern is quite common: Children can start refusing food at any age but it
tends to start between the ages of one and two years.
·
Typically,
a child will take well to solid food, even eating a wide variety of foods but
the novelty of this can wear off, often around the time she becomes more
active.
·
Food
refusal can have different implications depending on the extent: many children,
for instance, point-blank refuse to eat anything green, having tried and
disliked strong-tasting vegetables such as broccoli or cabbage.
·
The
only situation which gives rise to real concern is when there is evidence of
failure to thrive (on a Road to Health Card), which is rarely the case.
·
There
is no link between refusing food as a toddler and eating disorders later in
life. Eating disorders are more to do with emotional problems and less to do
with food.
·
Parents
who have or in the past had an eating disorder are more likely to be anxious
about food refusal in their children.
·
Parents
should try not to give children lots
of attention when they refuse to eat, as they are more likely to continue with
any behaviour that gets attention. Instead, try
praising them when they do show interest in food, but making no comment
otherwise.
·
As
well as being common, food refusal often just goes away by itself.
Tips to encourage eating
·
Sit
and eat with your child – even if you are only having a sliced-up apple. She
will enjoy the company.
·
Introduce
a few action rhymes and songs which are just for mealtimes.
·
Keep
choices few and simple as too much variety can be confusing
·
Serve
small portions, so she doesn't feel over-faced with food: she can always
request a second helping.
·
If
your child is a poor eater, offer her foods that are high in calories and
nutritious, such as cheese and full-fat milk, to make up any shortfall.
·
Avoid
letting your child eat whatever she chooses, on the grounds that at least he's
eating something, as this will perpetuate the problem. Cut down gradually on
her favourites, introducing some variety.
·
The
occasional packet of sweets or plate of biscuits will do no harm once your
child has established better eating habits. However, you could make a rule that
they are limited to weekends or after meals.
·
Don't
put too much emphasis on eating only 'healthy' foods. Fats and sugar are
important sources of energy at this age.
·
Avoid
distractions such as TV or toys at mealtimes.
·
If
she is hungry, encourage her to eat freely from whatever foods you have
prepared. If not, don't force her but be clear there will be nothing else until
her next snack or mealtime, and stick to your guns.
·
You're
more likely to tempt your child to eat something new when she is at her
hungriest: offer her child-friendly portions of healthy snack foods.
·
Don't
allow her to fill up on juice and squash; instead, offer her a small cup of
water at mealtimes, and limit her fluid intake in the run-up to each meal.
·
Children
are influenced by their peer group and will often start to eat new foods when
visiting their friends for meals.
A comparison
of major causes of under 5 mortality globally, in Africa and in South Africa
Infectious
and parasitic diseases remain the major killers of children globally,
accounting for more than half of all deaths in children younger than five years
of age (Figure 1). The toll is even higher in sub-Saharan
In
high-income countries, perinatal causes have replaced
infectious diseases as the leading cause of death and are now responsible for
up a third of deaths. Such a shift in the cause of death pattern has not
occurred in Sub-Saharan Africa, where malaria, lower respiratory infections and
diarrhoeal diseases, in that order, are the leading causes of death.
In
Figure 1

Source: Global Burden of Disease and Risk Factors,
2006.
Figure 2 Main causes of death among children under-5
years, sub-Saharan

Source: Global Burden of Disease and Risk Factors,
2006.
Figure 3 Main causes of death among children under-5
years,
Source: SA MRC Burden of Disease study
Risk factors
for, and the prevention of, dental caries
Risk factors:

Preventative Measures
Fluoride
Foods, toothpastes, mouthwashes, and even tap water are fluoridated. Water
fluoridation is particularly important in dental prevention because it is an
effective, safe, and low-cost way to prevent and protect against the occurrence
of tooth decay. Using topical fluoride applications, such as fluoride
toothpastes, fluoride varnishes, or fluoride rinses, can also aid in remineralization.
Dental Sealants
The chewing surfaces at the back of the teeth, the molars, are where decay
often occurs. A dental sealant or a pit and fissure sealant is a
professionally-applied, safe plastic material that is placed on the chewing
surfaces of back teeth to protect and prevent against caries.
Behavioral Component
Dietary Practices
Unquestionably, sugar plays a huge role in the development
and progression of caries. Feeding children sweetened beverages coupled with
poor hygiene habits are detrimental to the health of children’s teeth.
Discontinuing the use of baby bottles, replacing sugary liquids, and using
fluoride gels all assist in reducing risk.
Parental
Education and Dental Knowledge
Both education and knowledge of dental caries are vital in prevention of
caries. Whether a parent or caretaker has the ability to read and thus,
understand and learn about the dangers of sugar intake, general facts about ECC
and its prevention methods can affect what practices a parent implements on the
dental health of her children. Training parents and caretakers to determine
decay or decalcification in children’s teeth can be important in secondary
prevention.
Access to Dental Care
Dental care is the most prevalent unmet health need in children.
The role of
the various team members in the management of a child with a cleft lip and
palate
A
collection of medical and social service providers speak to the needs of the
child born with a cleft and that child's family. The following persons may or
may not be on the team.
SURGEON
The Surgeon is often considered the "Captain" of the team. He/she
provides the plastic, reconstructive surgery on the cleft. This person will
close the lip and the palate and provide for any scar revision and rhinoplasty. The plastic surgery to repair and reconstruct
the cleft is often done by a Plastic Surgeon. Other persons who may do the
plastic surgery include Oral Maxillofacial surgeons, Otolaryngologists,
etc. PAEDIATRICIAN
The pediatrician looks at the overall well-being of the child. The pediatrician
checks the normal growth and development of the child and makes certain that
the child is physically fit for upcoming surgical procedures.
PAEDIATRIC DENTIST
The role of the pediatric dentist is to ensure that the child's teeth are
healthy and strong. Many times children with clefts have teeth in unlikely
positions in the mouth. It is sometimes very difficult to keep those teeth
clean and therefore healthy. The pediatric dentist helps to maintain a healthy
and cavity-free mouth.
ORTHODONTIST
The orthodontist, on the other hand, helps to establish a good shape to the
dental arches. A child with cleft may need the services of an orthodontist even
before she has teeth! The orthodontist will work to achieve a normal dental
arch prior to bone graft surgery, and then follow-up to maintain the integrity
of that arch once achieved.
PROSTHODONTIST
There are times when a child with a cleft needs a prosthetic device to meet her
specific needs. Such prosthetic devices may be an obturator,
a bridge, a retainer, an implant, or any one of a number of other devices. The prosthodontist works very closely with the orthodontist and
the surgeon to provide the cleft-affected child with necessary appliances.
OTOLARYNGOLOGIST
Children with clefts typically suffer from poorly functioning Eustachian Tubes
and therefore experience a larger than normal number of ear infections. The Otolaryngologist serves to keep those infections at a
minimum, and to minimize any damage done subsequent to such infections.
AUDIOLOGIST
The audiologist checks the child's hearing regularly. Recurring ear infections,
waxy build-up and fluid behind the ear drum (all common among children with
clefts) can rob a child of the ability to hear effectively. The Audiologist
measures how well a child is hearing and makes recommendations if a child's
hearing is compromised.
SPEECH AND LANGUAGE THERAPIST
The Speech and Language Therapist assists the child in producing intelligible
language. The Speech and Language Therapist will provide therapy in areas of
articulation and language development, depending upon the child's unique need.
It may be likely, due to the nature of speech therapy, that the child may see
more of the Speech and Language Therapist, and on a more regular basis, than
any other member of the team.
COMMUNITY HEALTH NURSE
The Community Health Nurse assesses the health needs of the entire family and
makes recommendations concerning resources that might aid in maintaining the
overall health of the household. The Community Health Nurse may also help by
instructing the parents on how to feed and otherwise care for the child.
GENETICIST
The Geneticist studies various aspects of the family, the family history, etc.
and assists the family in determining a recurrence risk when choosing whether
or not to have more children. The Geneticist helps the family gain an
understanding concerning the factors that contribute to clefting
conditions. The geneticist will also help persons of child-bearing age who were
born with clefts to determine the probability of producing a cleft child
themselves.
SOCIAL WORKER
The Social Worker helps the family to deal with all the issues that touch them
concerning the cleft. Issues of grief, finance, emotional and moral support,
feelings of anger and guilt, and so forth, are non-medical topics that affect
the over-all treatment of the child and the family. The Social Worker will help
the family to access appropriate resources and to network for support.
PSYCHOLOGIST
The Psychologist works with the child alone, the parents alone, or the family
as a group to ensure normal functioning. Many times parents find a child's
disability or deformity difficult to adjust to. Often, a child with a cleft has
self-esteem issues that limit his/her potential. The Psychologist will provide
intervention that speaks directly to those needs.
DCH: P1; Q5
a. Treatment of a child with severe anaphylactic
shock.
Initial assessment with particular attention to shock
& bronchospasm
Lie patient down
IVI with
Ringers Lactate /
with
20 ml/kg bolus if shocked
Adrenaline
1:1 000 0,3ml IM stat
1: 10 000 0,1 ml/kg IV
stat
Repeat in 20 minutes if
needed
Oxygen
Antihistamine Promethazine
Hydrocortisone stat & 4 – 6 hourly
Salbutamol : saline (1ml each) nebs if bronchospasm
present
Try to
identify allergen
Counsel and educate child and
caretaker
Arrange for
medic alert bracelet
Make a note
of sensitivity in patient’s medical record and RTHC
b. Intraosseous infusion
Aseptic
technique
Select
needle – intraosseous / short yellow spinal needle
Prepare
equipment
Set up
infusion – fluid, buretrol, giving set
Identify
infusion site - 2 – 3 cm below tibial tuberosity on flat antero-medial surface
Clean site
Push with
screwing motion till needle “gives” as it enters marrow cavity
Assess patency of needle
Connect
infusion
Secure and
protect needle and infusion site
c.
Causes for and immediate treatment of fractured femur in 6 year
old
Causes:
Normal bone accidental trauma
Non accidental injury
Abnormal bone rickets
Malignancies
Osteopaenia – variable causes
Osteogenesis imperfecta
Immediate
treatment:
Assess
fracture - clinically & with X-rays of both limbs including hips &
knees
open / closed
Isolated or
multiple
Associated
problems – dislocations
Assess haemodynamic status
Treat shock
Analgesia
Immobilisation – skin traction (too old for Gallows, too young for Thomas splint)
d. What
is a clinical audit?
Quality assurance activity that compares routine standards of care for a
clinical condition with a recognised gold standard
for care for that condition.
Select
topic for audit based on the burden of that condition on the health services
Very common
High morbidity or mortality
Expensive management
Identify
gold standard for comparison: International, national or local guidelines
Establish
indicators for comparison
12 – 15 in total
Include history, examination, investigations, treatment
Identify
clinical records
Collect and
review records
Analyse
performance against the ideal management
Identify
strengths and weaknesses / gaps in management
Plan
corrective measures to improve standard of care
Implement
corrective measures
Review
effect of corrective measures
DCH: P2;
Q1
Paper 2 Question 1
Thabo, a four-year old boy, is brought to
the paediatric casualty at the hospital by his
mother, Letitia. She says that he suffered a generalised tonic-clonic seizure
lasting 35 minutes about one hour ago. He is on phenobarbitone,
but has not been given his medication for the past 6 weeks as his mother “did
not have transport money” to get to the clinic. He has had frequent seizures
since stopping the medications, but this episode was particularly long.
Thabo was born at term at the local
midwife obstetric unit. He weighed 4.3kg at birth. He did not cry well at birth
and was referred to the district hospital, where he stayed for three weeks. Letitia remembers that Thabo was
very floppy in the first week of life and was fed via a nasogastric
tube for about two weeks. He also had seizures after birth that persisted after
discharge.
Letitia says that Thabo
has Cerebral Palsy (CP). He is still unable to sit, crawl or walk. He is unable
to talk and only makes sounds. He is attending CP Clinic for physiotherapy and
occupational therapy.
Thabo is microcephalic.
Both his weight and height are below the 3rd centiles
for age. He has contractures in his elbows and Achilles tendons. He has increased
muscle tone with his arms more affected than his legs. There are no signs of
meningitis. Thabo does not respond to auditory or
visual stimuli.
1. Define
cerebral palsy. (2)
Cerebral
palsy is a disability of motor (1/2) function due to a non-progressive
(1/2) insult or damage (1/2) to a developing brain (1/2)
2. What is the most likely cause for Thabo’s
cerebral palsy? Provide at least 4 facts that support your conclusion. (4)
Had hypoxic ischaemic encephalopathy after
birth (accept perinatal asphyxia) (1 mark)
Did not cry at birth, big baby, floppy, nasogastric
feeds, seizures (1 mark each)
3. How would you classify Thabo’s cerebral
palsy? (3)
Spastic (1) quadriplegic (1).
- with possible sensory deficits (vision, hearing)- 1 mark
4. Provide
a brief (one line) pathophysiological explanation for
each of the following signs: (8)
a) Clonus
Increased
reflexes (1/2) are a sign of a upper motor neuron
lesion (1/2)
b) Seizures
Indicates
damage to some part of the brain
c) Poor
response to visual stimuli
Accept
either that:
i) May be
blind- because of damage to the optic cortex or some part of the vision pathway
ii) Post-ictal and therefore non-responsive to stimuli
d)
Contractures
Related to
increased muscle tone with inadequate movement of relevant muscles and joints
5. Thabo has another generalised
(tonic-clonic) fit soon after arriving at the
hospital. List the critical steps in your management of the seizure. (5)
Secure
airway
Turn to
side
Administer
oxygen
Monitor
vital signs
Perform
appropriate investigations, e.g. Glucose
Manage
underlying problems, e.g. fever if present (no history of fever in this case)
Rectal
diazepam or buccal midazolam
Still
convulsing after 10 minutes- IV/IM Lorazepam (Rivotril) or IV Clonazepam
Still
convulsing after 10 minutes- IV Phenytoin over 30
minutes
6. What
grant is Thabo eligible for that could help provide
the “transport money” to allow him to attend the clinic regularly? Why does Thabo qualify for this grant (3)
Child dependency grant (1 mark). No marks for disability grant
Qualifies
because he has a disability (1) that requires full-time care (1)
7. List TWO primary and TWO secondary
prevention measures that could have prevented Thabo
from developing cerebral palsy. (4)
Primary:- Achieving
highest possible standard of maternal and child health.
Early antenatal booking ( pick up
high risk mothers ie. diabetic /mutiparous)
High risk deliveries
done in specialised centres.
Earlier
recognition and referral for Caesarean section for large baby.
Intrapartum monitoring,
CTG, Foetal scalp electrode etc.
Secondary:- Good
resuscitation at birth
Hypothermia
? high
dose phenobarbitone
8. How
would you optimise Thabo’s
anti-convulsant therapy to ensure adequate control of
his seizures? (5)
Monotherapy
is preferred to combination therapy. Combination therapy should be specialist
initiated
Drugs
levels are not indicated as there is a clear history of non-compliance.
Preferred
drug would be sodium valproate (rather than phenobarbitone).
2nd
line – carbamazepine
3rd
line- refer to specialist decision about need for lamotrigine
Counsel
parents on need for compliance
9. Thabo
continues to fit at the hospital despite appropriate anti-convulsant
treatment. He requires admission to the regional hospital’s ICU for a thiopentone infusion (general anaesthesia)
to control his seizures but is refused admission on the grounds that he has
cerebral palsy and is mentally retarded. Is this ethically justifiable? Briefly
discuss the principles involved. (6)
Need to
provide key principles, either for or against this
DCH: P2; Q2
a. Key
components of care over next 24 hours
Premature
Routine observation
Maintain
Warmth
Blood sugar with feeds
and fluids
Oxygenation
HIV exposed
no history of maternal nevirapine
Baby requires nevirapine
asap
b.
Feeding choices.
Exclusive
breast milk
Formula
feeds
Pasteurised
expressed breast milk
Pasteurised
pooled breast milk
HIV+ mother
with suspicion of progression to AIDS - risk of HIV infection from breast milk
Premature
baby with risk of NEC and other complications from formula feeds
Presumably
poor socio-economic circumstances with risk of increased infant mortality from
GE and ARI associated with formula feeding
The choice
should be made by the mother with support of health care workers
Ideally
this baby should have pasteurised EBM whilst in
hospital with the definitive choice being made prior to discharge, recognising the specific circumstances of this family
c.
Criteria for discharge.
Well baby
Well mother
Decision re
infant feeding
Established
source of infant feed
Baby
feeding well
Baby
gaining weight
Maintaining
temperature
Vaccinated
– BCG & Polio 0
Follow up
details arranged
d. Long
term care
Family care
– adoption
Foster care
Institutional
care – children’s home
|
|
|
Pros |
Cons |
|
Family |
Physical
care |
Secure |
|
|
|
|
Basic
needs provided |
|
|
|
Emotional |
One-on-one
care |
|
|
|
|
Supportive |
|
|
|
Social |
Part of a
family |
No
contact with biological family |
|
|
|
Permanent
- adoption |
Temporary
– foster care |
|
|
|
|
Risk of
abuse/exploitation |
|
|
Intellectual |
Stimulating |
|
|
|
|
|
|
|
Institutional |
Physical
care |
Secure |
|
|
|
|
Basic
needs address |
|
|
|
Emotional |
|
No
intimacy/family |
|
|
|
|
Temporary
placement |
|
|
Social |
Company |
Lack of
permanence |
|
|
|
|
Behavioural problems |
|
|
|
|
Risk of
abuse/exploitation |
|
|
Intellectual |
Good - fair |
|
e. Legal
processes.
All
placements into surrogate in this sort of circumstance require the same legal
process.
Children’s
court enquiry:
Social worker to:
present case to court
satisfy the court that adequate attempts
have been made to trace the family
recommend option for surrogate care
Presiding officer to:
declare
baby a child in need and a ward of the state
authorise surrogate care placement
Surrogate
parents to fulfil necessary criteria as adoption or
foster parents
f.
Medical assessment.
Full
physical assessment
Full
neurodevelopment assessment
Basic
screening tests – WR, HBV, Thyroid functions, urine
HIV
specific blood tests – ideally p24 Ag or more realistically PCR at 6 weeks
g.
Management of HIV status.
Confirm
diagnosis
with PCR at 6 weeks, if available
or Eliza test at 15 – 18 months if no
PCR available
Monitor
growth, development and wellbeing at routine IMCI visits
Early
treatment of intercurrent illnesses
Nutritional
support
Support for infant feeding choice
Micro-nutrient supplements especially Vit
A from 6 months
Immunizations
– routine EPI schedule
Cotrimoxazole prophylaxis from 6 weeks
h.
Long-term health risks.
Related to
Surrogate care Malnutrition
Abuse
or exploitation
Behavioural problems
Poor
immunisation status
Increased
general morbidity & mortality
Related to
HIV status Growth failure
Development delay
Increased frequency of infections
Opportunistic infections
Related to prematurity Development
delay
Interventions:
Supervised placement
Active monitoring of health status
in line with IMCI protocols
Active management of HIV status
DCH: P2;
Q3
Colette, a previously healthy three-year- old girl presents at the
hospital casualty with a four day history of coughing and fever. On examination
you note a respiratory rate of 53 breaths/min and chest wall indrawing (retraction). The left side of the chest is dull
to percussion with bronchial breathing heard posteriorly.
a.
What is
the most likely diagnosis using the IMCI classification. (1)
Severe pneumonia
b.
List
THREE organisms that commonly cause this presentation. (3)
Most likely bacterial or mixed cause. S.
pneumonia, H influenzae.
Less
likely in previously healthy child of this age: S. aureus,
M pneumoniae
c.
List
FOUR investigations that you think are necessary. Motivate the need for each. (8)
CXR – to confirm diagnosis, may help to establish
etiology (S aureus), look for complications like
effusion/empyema
Blood
culture -5% chance of culturing responsible organism
ESR. CRP – May support diagnosis of bacterial cause
WBC and
differential count - May support diagnosis of bacterial cause
NPA for viruses. – unnecessary
Induced
sputum – not helpful in this case
Mantoux – no supporting facts
Gastric
aspirates for acid-fast bacilli no supporting facts
Student
may motivate to do no special investigations – give marks if adequately
motivated
d. Describe the rational empirical use of antibiotics in community acquired pneumonia in South-African
children. (12)
|
|
Ambulant |
Hospitalised |
|
0-2mo |
Hospitalise all children < 2 mo |
Ampicillin/Penicillin + AG iv or Ceftriaxone/Cefotaxime iv |
|
3mo-5yr |
Amoxicillin po high dose |
Ampicillin iv/ Amoxicillin po high dose or Cefuroxime iv/Amoxi-Clav
po/iv Ceftriaxone/Cefotaxime iv Add Cloxa if S. aureus suspected |
|
>5yr |
Amoxicillin po high dose Or Macrolide po – if
suspected M. pneumoniae or Chlamydia spp. |
Ampicillin iv/ Amoxicillin po high dose or Cefuroxime iv/Amoxi-Clav
po/iv Ceftriaxone/Cefotaxime iv Add: Cloxa if S. aureus suspected Add: Macrolide po – if syuspected M. pneumoniae or Chalmydia spp |
If
description of reasons given:
Marks given for:
· Epidemiology of infecting organisms
· Prevalence of drug resistance
· HIV prevalence
· Available resources
· Aetiology in age groups
· Aetiology in HIV
· Specific organisms – treatment (more than 1 mark)
· Route of antibiotic administration
· Duration of treatment
e.
Discuss
the prevention of childhood community acquired pneumonia under the headings:
i.
General
preventative strategies (8)
ii.
Specific
preventative strategies (8)
i.
General preventative strategies
a.
Nutrition
1. Malnutrition predisposes to pneumonia
2. Breastfeeding decrease incidence of pneumonia up to 32%
3. Encourage breastfeeding up to 6 months
b.
Micronutrient supplementation
4. As routine care in HIV or malnourished
5. Vit A
a. Measles
6. Zinc
a. Particularly NB in malnourished children
c. Reduction in
7. Passive smoke
8. Indoor fuel exposure
ii.
Specific preventative strategies
i.
Immunisation
1. Routine
a. Measles
b. BCG
c. Pertussis
d. Hib
2. Pneumococcal
3. Influenza
4. Varicella
ii.
Prophylaxis
1. Pneumocystis jiroveci
prevention
2. TB prophylaxis where household contact
3. Palivizumab
4. HAART
Complete memo: SAMJ Dec 2005.
Diagnosis and Management of Community-Acquired Pneumonia in Childhood – SATS
Guidelines
DCH: P2; Q4
Johnny is 15 months old and his weight of 12
kilograms places him on the 75th percentile) He is brought to the
outpatient clinic because has been playing less and tiring easily. His mother
thinks he is pale. You do a full blood count. The results are: Hb 4g%, MCV 54fl, MCH 16pg. White cell and platelet counts
are normal
Hypochromic microcytic
anaemia
Iron deficiency, probably dietary
Sideroblastic, chronic disease, thalassaemia, blood loss, marrow diseases etc
Diet, promotors
and inhibitors of iron absorption, milk intake, vegetables, pica, family
history, ethnicity, other symptoms, medical history
On
examination, Johnny has a tachycardia and a gallop rhythm.
Incipient
failure
Yes, he is symptomatic and in
incipient failure
10
to 15 ml/kg/transfusion = 120 ml over 4 to 6 hours (30 to 20ml/hr)
Lasix 0,5mg IVI at end of or half way through the blood to
prevent further cardiac failure.
Observe
for any reactions to the blood, ie monitor pulse, RR,
BP, and temp as well as skin rashes.
Stop
infusion is any reaction and notify doctor on call
Compat to be done, forms filled in correctly
and checked before blood given
Lasix ,digoxin
( want what other drugs during transfusion not what others on discharge)
Johnny is stabilised and
ready for discharge in three days.
Ferrous sulfate 6mg of elemental
iron per kg per day
ie 72 mg elemental iron per day 2 or 3
divided doses until the Hb is normal and then half
the dose for another 2 to 3 months to replenish the stores.
May give Vit
C and folic acid
Do FBC after 3 to 4 weeks to check
response, the 4 to 6 weekly until normal. Repeat 2 to 3 months after all
treatment completed to check that he is not anaemic
again and that you did not miss diagnose the child
Make sure diet is adjusted, decrease
cows milk intake, make sure of meat and green leafy vegetables. Check for pica,
de worm
Poor neurodevelopment, poor growth,
poor school performance, immune abnormalities
Breast feed, supplement with iron at 3 to 4 months.
Formulae, are all fortified, should be enough iron
Use iron fortified cereals
De worm when appropriate
Mixed diet when able
Careful of amount of cow’s milk ingested
DCH: P2; Q5
Busisiwe, a 5-year-old female
presents to the local clinic with a six-week history of abdominal pain. The pain is not
associated with other symptoms. She is growing and gaining weight appropriately
a)
What
questions on history –taking may assist in establishing the significance of the
abdominal pain.
Questions
related to:
Location, intensity, character and duration of pain, time of day or
night that pain occurs
Appetite, diet, satiety, nausea, reflux, emesis
Stool pattern, consistency, completeness of evacuation
Review of systems: weight loss, growth or pubertal delay, fever, rash B
Medications and nutritional interventions
Family history, travel
Interference with school, play
b)
Provide TWO likely differential diagnoses for the abdominal
pain
Constipation, Functional pain, Giardiasis,
Parasites, Peptic ulcer disease,
Tumour/masses
Busisiwe’s blood
pressure is 140/100 mmHg. She has a smooth, firm, 8 cm by 7 cm mass palpated in the right upper
quadrant of her abdomen that does not cross the midline. The right side of her
body appears large than the left.
c)
Provide FOUR differential diagnoses for the abdominal mass.
Gastrointestinal - fecal mass, duplication, Meckel’s diverticulum
Liver – hepatomegly, hepatic cyst (hydatid) hydrops of gall
bladder.
Renal - hydronephrosis, megaureter,
polycystic kidney disease.
Tumors - neuroblastoma, Wilms’ tumour, lymphoma, hepatoblastoma,
rhabdomyosarcoma, ovarian cyst, teratomas.
d) What is the most likely diagnosis?
Nephroblastoma (Wilms’ tumour)
e) Provide a pathophysiological
explanation for Busisiwe’s
i) Blood pressure
Up
to a third of patients with Wilms’ tumour can present with hypertension secondary to
rennin-secreting tumour or production of renin in response to renovascular
insufficiency casued by tumour
mass.
ii) Body asymmetry
Wilms’ Tumour may arise in 3 clinical settings: (1) sporadic, (2) in
association with genetic syndromes, (3) familial. Genetic syndromes that
predispose to Wilms’ tumour include Hemihyperthrophy.
f) List the
investigations you would undertake, and suggest a likely
positive findings(s)
for each
test: at a
i) district hospital
FBC – anemia, neutropaenia, low
platelet count – suggest bone marrow infiltrate
U&E: High urea, creatinine –
kidney involvement or tumour lysis,
High LDH, high uric acid – suggests rapid cell turnover in
malignancy
IINR high, PTT prolonged – coagulation problem
Urinalysis – haematuria, proteinuria – lesions involving urinary system
CXR – lung metastases
Plain abdominal radiograph – intestinal
obstruction, calcifications.
Ultrasound – renal mass
ii) regional or tertiary hospital
g) How would you manage Busisiwe
at a:
i)
district hospital
Reduce high blood pressure, improve renal
function, give fluids and electrolytes , treat infection, transfuse if severe anemia and/or thrombocythopaenia.
Refer the patient as soon as possible to the regional/tertiary hospital.
ii)
regional or
tertiary hospital
Multimodality treatment: chemotherapy,
radiotherapy and surgery. The goal of current clinical trials is to reduce
therapy for children with low-risk tumours, thereby avoiding acute and
long-term toxicities.
Medical/Surgical therapy: The main agents include vincristine, dactinomycin,
and doxorubicin. Chemotherapy is
administered up front to reduce tumor volume, thereby
decreasing the risk of surgical spillage of tumor.
Radiation therapy is restricted for treatment of higher-stage (III and IV)
disease.
The aim of long follow up is to:
·
Monitor renal function
·
Evaluation of Anthcycline related cardiotoxicity
·
Assessment of growth and sexual development
·
Assessment of musculo-skeletal
development in irradiated patients
·
Assessment of fertility
·
Watch out for second malignant neoplasia
Support & Education Programs
When a child is diagnosed with cancer, it has a significant impact not only on
the child, but parents, siblings and extended family as well.
Psychological support
Cancer support group
Social worker involvement
Genetic counseling if required