Paeds Flashcards
Acute lymphoblastic leukaemia
Acute lymphoblastic leukaemia (ALL) is the most common malignancy affecting children and accounts for 80% of childhood leukaemias. The peak incidence is at around 2-5 years of age and boys are affected slightly more commonly than girls
Features may be divided into those predictable by bone marrow failure:
anaemia: lethargy and pallor
neutropaenia: frequent or severe infections
thrombocytopenia: easy bruising, petechiae
And other features
bone pain (secondary to bone marrow infiltration)
splenomegaly
hepatomegaly
fever is present in up to 50% of new cases (representing infection or constitutional symptom)
testicular swelling
Types
common ALL (75%), CD10 present, pre-B phenotype
T-cell ALL (20%)
B-cell ALL (5%)
Poor prognostic factors age < 2 years or > 10 years WBC > 20 * 109/l at diagnosis T or B cell surface markers non-Caucasian male sex
traffic light’ system for risk stratification of children under the age of 5 years presenting with a fever
Assessment
The following should be recorded in all febrile children: temperature heart rate respiratory rate capillary refill time
Signs of dehydration (reduced skin turgor, cool extremities etc) should also be looked for
Measuring temperature should be done with an electronic thermometer in the axilla if the child is < 4 weeks or with an electronic/chemical dot thermometer in the axilla or an infra-red tympanic thermometer.
Duchenne muscular dystrophy
- X-linked recessive inherited disorder in the dystrophin genes required for normal muscular function
Features
progressive proximal muscle weakness from 5 years
calf pseudohypertrophy
Gower’s sign: child uses arms to stand up from a squatted position
30% of patients have intellectual impairment
Investigation
raised creatinine kinase
genetic testing has now replaced muscle biopsy as the way to obtain a definitive diagnosis
Management
is largely supportive as unfortunately there is currently no effective treatment
Prognosis
most children cannot walk by the age of 12 years
patients typically survive to around the age of 25-30 years
associated with dilated cardiomyopathy
Diarrhoea in children
Gastroenteritis
- main risk dehydration
- most common cause - rota virus
- treatment rehydration
Chronic diarrheas
Infants
most common cause in the developed world is cows’ milk intolerance
toddler diarrhoea: stools vary in consistency, often contain undigested food
coeliac disease
post-gastroenteritis lactose intolerance
Pyloric stenosis
M>F
5-10% Family history in parents
Projectile non bile stained vomiting at 4-6 weeks of life
Diagnosis is made by test feed or USS
Treatment: Ramstedt pyloromyotomy (open or laparoscopic)
Acute appendicitis
Uncommon under 3 years
When occurs may present atypically
Mesenteric adenitis
Central abdominal pain and URTI
Conservative management
Mesenteric adenitis is a condition that more often affects children and teenagers. It causes inflammation and swelling in the lymph nodes inside the abdomen.
Intussusception
Telescoping bowel
Proximal to or at the level of, ileocaecal valve
6-9 months of age
Colicky pain, diarrhoea and vomiting, sausage-shaped mass, red jelly stool.
Treatment: reduction with air insufflation
Malrotation
High caecum at the midline
Feature in exomphalos, congenital diaphragmatic hernia, intrinsic duodenal atresia
May be complicated by the development of volvulus, an infant with volvulus may have bile stained vomiting
Diagnosis is made by upper GI contrast study and USS
Treatment is by laparotomy, if volvulus is present (or at high risk of occurring then a Ladd’s procedure is performed
exompthalos
an abdominal wall (tummy wall) defect. It happens when a baby’s abdominal wall does not develop fully while in the womb.
congenital diaphragmatic hernia
Congenital diaphragmatic hernia (CDH) is a defect in an unborn baby’s diaphragm, the muscle that divides the chest cavity and abdominal cavity. CDH occurs when the diaphragm does not close the right way during the baby’s development and abdominal organs push (“herniate”) through the defect into the chest cavity.
intrinsic duodenal atresia
Duodenal atresia is a disease of newborn infants. Absence or complete closure (atresia) of a portion of the channel (lumen)
Hirschsprung’s disease
Absence of ganglion cells from myenteric and submucosal plexuses
Occurs in 1/5000 births
Full-thickness rectal biopsy for diagnosis
Delayed passage of meconium and abdominal distension
Treatment is with rectal washouts initially, after that an anorectal pull through procedure
Oesophageal atresia
ssociated with tracheo-oesophageal fistula and polyhydramnios
May present with choking and cyanotic spells following aspiration
VACTERL associations
Meconium ileus
Usually delayed passage of meconium and abdominal distension
The majority have cystic fibrosis
X-Rays will not show a fluid level as the meconium is viscid, PR contrast studies may dislodge meconium plugs and be therapeutic
Infants who do not respond to PR contrast and NG N-acetyl cysteine will require surgery to remove the plugs
Biliary atresia
Jaundice > 14 days
Increased conjugated bilirubin
Urgent Kasai procedure
Necrotising enterocolitis
Prematurity is the main risk factor
Early features include abdominal distension and passage of bloody stools
X-Rays may show pneumatosis intestinalis and evidence of free air
Increased risk when empirical antibiotics are given to infants beyond 5 days
Treatment is with total gut rest and TPN, babies with perforations will require laparotomy
Nocturnal enuresis
The majority of children achieve day and night time continence by 3 or 4 years of age. Enuresis may be defined as the ‘involuntary discharge of urine by day or night or both, in a child aged 5 years or older, in the absence of congenital or acquired defects of the nervous system or urinary tract’
Nocturnal enuresis can be defined as either primary (the child has never achieved continence) or secondary (the child has been dry for at least 6 months before)
Management look for possible underlying causes/triggers constipation diabetes mellitus UTI if recent onset general advice fluid intake toileting patterns: encourage to empty bladder regularly during the day and before sleep lifting and waking reward systems (e.g. Star charts) NICE recommend these 'should be given for agreed behaviour rather than dry nights' e.g. Using the toilet to pass urine before sleep enuresis alarm generally first-line for children have sensor pads that sense wetness high success rate desmopressin particularly if short-term control is needed (e.g. for sleepovers) or an enuresis alarm has been ineffective/is not acceptable to the family
Necrotising enterocolitis
Abdominal x-rays are useful when diagnosing necrotising enterocolitis, as they can show:
dilated bowel loops (often asymmetrical in distribution)
bowel wall oedema
pneumatosis intestinalis (intramural gas)
portal venous gas
pneumoperitoneum resulting from perforation
air both inside and outside of the bowel wall (Rigler sign)
air outlining the falciform ligament (football sign)
Fallot’s tetralogy
-cyanotic congenital heart disease and presents with ventricular septal defect, right ventricular hypertrophy, overriding aorta, and pulmonary stenosis.
Coarctation of the aorta
This is a congenital narrowing of the aorta and would present with absent/weak femoral pulses; hypertension in arms but hypotension in legs.
Transposition of the great arteries
Transposition of the great arteries is where the aorta arises from the right ventricle and the pulmonary artery arises from the left ventricle. It presents mainly as cyanosis in children.
Ebstein’s anomaly
Ebstein’s anomaly results in low insertion of the tricuspid valve resulting in a large right atrium and small right ventricle causing tricuspid incompetence.
Patent ductus arteriosus
failure of the ductus arteriosus to close after birth causing a left-right shunting and would present as a loud continuous murmur with bounding pulses and a wide pulse pressure.
ebstein anomaly
Ebstein’s anomaly is a congenital heart defect characterised by low insertion of the tricuspid valve resulting in a large atrium and small ventricle. It is sometimes referred to as ‘atrialisation’ of the right ventricle.
Ebstein’s anomaly may be caused by exposure to lithium in-utero.
Associations
patent foramen ovale (PFO) or atrial septal defect (ASD) is seen in at least 80% of patients, resulting in a shunt between the right and left atria
Wolff-Parkinson White syndrome
Clinical features
cyanosis
prominent ‘a’ wave in the distended jugular venous pulse,
hepatomegaly
tricuspid regurgitation
pansystolic murmur, worse on inspiration
right bundle branch block → widely split S1 and S2
Jaundice <24h of birth
is always pathological and your differentials are:
rhesus haemolytic disease (RHD)
ABO incompatibility
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
hereditary spherocytosis
A blood film will show bite and blister cells in G6PD deficiency or spherocytes in hereditary spherocytosis. It would be correct to say that an osmotic fragility test would also be useful in the diagnosis but that option is not provided. Another useful test would be a Coomb’s test (this would be positive in RHD).
An exchange transfusion might be necessary but it is pertinent to understand the underlying cause; phototherapy is the first line management option.
A urine sample and thyroid function tests would be useful in prolonged jaundice (>14 days in term / >21 days in premature infants) because urinary tract infection or hypothyroidism may be the underlying cause.
Jaundice in the neonate from 2-14 days
Jaundice in the neonate from 2-14 days is common (up to 40%) and usually physiological. It is due to a combination of factors, including more red blood cells, more fragile red blood cells and less developed liver function.
It is more commonly seen in breastfed babies
Jaundice after 14 days (prolonged)
If there are still signs of jaundice after 14 days (21 days if premature) a prolonged jaundice screen is performed, including:
conjugated and unconjugated bilirubin: the most important test as a raised conjugated bilirubin could indicate biliary atresia which requires urgent surgical intervention
direct antiglobulin test (Coombs’ test)
TFTs
FBC and blood film
urine for MC&S and reducing sugars
U&Es and LFTs
Causes of prolonged jaundice
biliary atresia
hypothyroidism
galactosaemia
urinary tract infection
breast milk jaundice
jaundice is more common in breastfed babies
mechanism is not fully understood but thought to be due to high concentrations of beta-glucuronidase → increase in intestinal absorption of unconjugated bilirubin
prematurity
due to immature liver function
increased risk of kernicterus
congenital infections e.g. CMV, toxoplasmosis
Kawasaki disease medium vessel vasculitis
Kawasaki disease is a type of vasculitis which is predominately seen in children. Whilst Kawasaki disease is uncommon it is important to recognise as it may cause potentially serious complications, including coronary artery aneurysms.
Features
high-grade fever which lasts for > 5 days. Fever is characteristically resistant to antipyretics
conjunctival injection
bright red, cracked lips
strawberry tongue
cervical lymphadenopathy
red palms of the hands and the soles of the feet which later peel
Kawasaki disease is a clinical diagnosis as there is no specific diagnostic test.
Management
high-dose aspirin
Kawasaki disease is one of the few indications for the use of aspirin in children. Due to the risk of Reye’s syndrome aspirin is normally contraindicated in children
intravenous immunoglobulin
echocardiogram (rather than angiography) is used as the initial screening test for coronary artery aneurysms
Complications
coronary artery aneurysm
Dyskinetic cerebral palsy
Athetosis is a symptom characterized by slow, involuntary, convoluted, writhing movements of the fingers, hands, toes, and feet
Dyskinetic cerebral palsy is correct. This child is presenting with general symptoms of cerebral palsy - namely being slow to meet developmental milestones and feeding difficulties. This child is displaying symptoms of dyskinetic cerebral palsy, a subtype of cerebral palsy. Key symptoms that differentiate dyskinetic cerebral palsy from other subtypes are athetoid movements and oro-motor problems. The athetoid movements are shown in this stem by the slow writhing movements of his hands and feet and also the difficulty of holding onto objects. Patients with dyskinetic cerebral palsy experience difficulty in holding objects due to fluctuating muscle tone. The oro-motor problems are evidenced by this child’s drooling.
Cerebral palsy
Cerebral palsy may be defined as a disorder of movement and posture due to a non-progressive lesion of the motor pathways in the developing brain. It affects 2 in 1,000 live births and is the most common cause of major motor impairment.
Causes
antenatal (80%): e.g. cerebral malformation and congenital infection (rubella, toxoplasmosis, CMV)
intrapartum (10%): birth asphyxia/trauma
postnatal (10%): intraventricular haemorrhage, meningitis, head-trauma
Possible manifestations include: abnormal tone early infancy delayed motor milestones abnormal gait feeding difficulties.
Children with cerebral palsy often have associated non-motor problems such as: learning difficulties (60%) epilepsy (30%) squints (30%) hearing impairment (20%)
Classification
spastic (70%)
subtypes include hemiplegia, diplegia or quadriplegia
increased tone resulting from damage to upper motor neurons
dyskinetic
caused by damage to the basal ganglia and the substantia nigra
athetoid movements and oro-motor problems
ataxic
caused by damage to the cerebellum with typical cerebellar signs
mixed
Management
as with any child with a chronic condition a multidisciplinary approach is needed
treatments for spasticity include oral diazepam, oral and intrathecal baclofen, botulinum toxin type A, orthopaedic surgery and selective dorsal rhizotomy
anticonvulsants, analgesia as required
Turner’s syndrome
Turner’s syndrome is a chromosomal disorder affecting around 1 in 2,500 females. It is caused by either the presence of only one sex chromosome (X) or a deletion of the short arm of one of the X chromosomes.
Turner’s syndrome is denoted as 45,XO or 45,X.
Features
short stature
shield chest, widely spaced nipples
webbed neck
bicuspid aortic valve (15%), coarctation of the aorta (5-10%)
primary amenorrhoea
cystic hygroma (often diagnosed prenatally)
high-arched palate
short fourth metacarpal
multiple pigmented naevi
lymphoedema in neonates (especially feet)
gonadotrophin levels will be elevated
hypothyroidism is much more common in Turner’s
horseshoe kidney: the most common renal abnormality in Turner’s syndrome
There is also an increased incidence of autoimmune disease (especially autoimmune thyroiditis) and Crohn’s disease
Scarlet fever
Scarlet fever is a reaction to erythrogenic toxins produced by Group A haemolytic streptococci (usually Streptococcus pyogenes). It is more common in children aged 2 - 6 years with the peak incidence being at 4 years.
Scarlet fever is spread via the respiratory route by inhaling or ingesting respiratory droplets or by direct contact with nose and throat discharges, (especially during sneezing and coughing).
Scarlet fever has an incubation period of 2-4 days and typically presents with:
fever: typically lasts 24 to 48 hours
malaise, headache, nausea/vomiting
sore throat
‘strawberry’ tongue
rash
fine punctate erythema (‘pinhead’) which generally appears first on the torso and spares the palms and soles
children often have a flushed appearance with circumoral pallor. The rash is often more obvious in the flexures
it is often described as having a rough ‘sandpaper’ texture
desquamination occurs later in the course of the illness, particularly around the fingers and toes
Diagnosis
a throat swab is normally taken but antibiotic treatment should be commenced immediately, rather than waiting for the results
Management
oral penicillin V for 10 days
patients who have a penicillin allergy should be given azithromycin
children can return to school 24 hours after commencing antibiotics
scarlet fever is a notifiable disease
Scarlet fever is usually a mild illness but may be complicated by:
otitis media: the most common complication
rheumatic fever: typically occurs 20 days after infection
acute glomerulonephritis: typically occurs 10 days after infection
invasive complications (e.g. bacteraemia, meningitis, necrotizing fasciitis) are rare but may present acutely with life-threatening illness
Apgar score
A score of 0-3 is very low score, between 4-6 is moderate low and between 7 - 10 means the baby is in a good state
Pulse resp rate colour muscle tone reflex irratibillity
Croup
Croup is a form of upper respiratory tract infection seen in infants and toddlers. It is characterised by stridor which is caused by a combination of laryngeal oedema and secretions. Parainfluenza viruses account for the majority of cases.
Epidemiology
peak incidence at 6 months - 3 years
more common in autumn
Features stridor barking cough (worse at night) fever coryzal symptoms
CKS suggest admitting any child with moderate or severe croup. Other features which should prompt admission include:
< 6 months of age
known upper airway abnormalities (e.g. Laryngomalacia, Down’s syndrome)
uncertainty about diagnosis (important differentials include acute epiglottitis, bacterial tracheitis, peritonsillar abscess and foreign body inhalation)
Investigations
the vast majority of children are diagnosed clinically
however, if a chest x-ray is done:
a posterior-anterior view will show subglottic narrowing, commonly called the ‘steeple sign’
in contrast, a lateral view in acute epiglottis will show swelling of the epiglottis - the ‘thumb sign’
Management
CKS recommend giving a single dose of oral dexamethasone (0.15mg/kg) to all children regardless of severity
prednisolone is an alternative if dexamethasone is not available
Emergency treatment
high-flow oxygen
nebulised adrenaline
apnoa
transient cessation of respiration whether normal
Neonatal resuscitation guidelines
Birth: Dry the baby, remove any wet towels and cover and start the clock or note the time.
Within 30 seconds: Assess tone, breathing and heart rate.
Within 60 seconds: If gasping or not breathing - open the airway and give 5 inflation breaths
Re-assess: If no increase in heart rate look for chest movement
If chest not moving: Recheck head position, consider 2-person airway control and other airway manoeuvres, repeat inflation breaths and look for a response.
If no increase in heart rate look for chest movement
When the chest is moving: If heart rate is not detectable or slow (< 60 min-1) - start chest compressions with 3 compressions to each breath.
Reassess heart rate every 30 seconds. If heart rate is not detectable or slow (<60 beats per minute) consider venous access and drugs
basic life support (BLS) guidelines, infants (children under 1 year)
femoral and brachial pulse assessed
2015 Resuscitation Council guidelines made the following changes to paediatric basic life support
compression:ventilation ratio: lay rescuers should use a ratio of 30:2. If there are two or more rescuers with a duty to respond then a ratio of 15:2 should be used
age definitions: an infant is a child under 1 year, a child is between 1 year and puberty
Key points of algorithm (please see link attached for more details)
unresponsive?
shout for help
open airway
look, listen, feel for breathing
give 5 rescue breaths
check for signs of circulation
infants use brachial or femoral pulse, children use femoral pulse
15 chest compressions:2 rescue breaths (see above)
chest compressions should be 100-120/min for both infants and children
depth: depress the lower half of the sternum by at least one-third of the anterior–posterior dimension of the chest (which is approximately 4 cm for an infant and 5 cm for a child)
in children: compress the lower half of the sternum
in infants: use a two-thumb encircling technique for chest compression
Intussusception
Intussusception describes the invagination of one portion of bowel into the lumen of the adjacent bowel, most commonly around the ileo-caecal region.
Intussusception usually affects infants between 6-18 months old. Boys are affected twice as often as girls
Features
paroxysmal abdominal colic pain
during paroxysm the infant will characteristically draw their knees up and turn pale
vomiting
bloodstained stool - ‘red-currant jelly’ - is a late sign
sausage-shaped mass in the right upper quadrant
Investigation
ultrasound is now the investigation of choice and may show a target-like mass
Management
the majority of children can be treated with reduction by air insufflation under radiological control, which is now widely used first-line compared to the traditional barium enema
if this fails, or the child has signs of peritonitis, surgery is performed
Developmental dysplasia of the hip
Developmental dysplasia of the hip (DDH) is gradually replacing the old term ‘congenital dislocation of the hip’ (CDH). It affects around 1-3% of newborns.
Risk factors female sex: 6 times greater risk breech presentation positive family history firstborn children oligohydramnios birth weight > 5 kg congenital calcaneovalgus foot deformity
DDH is slightly more common in the left hip. Around 20% of cases are bilateral.
Screening for DDH
the following infants require a routine ultrasound examination
first-degree family history of hip problems in early life
breech presentation at or after 36 weeks gestation, irrespective of presentation at birth or mode of delivery
multiple pregnancy
all infants are screened at both the newborn check and also the six-week baby check using the Barlow and Ortolani tests
Clinical examination
Barlow test: attempts to dislocate an articulated femoral head
Ortolani test: attempts to relocate a dislocated femoral head
other important factors include:
symmetry of leg length
level of knees when hips and knees are bilaterally flexed
restricted abduction of the hip in flexion
Imaging
ultrasound is generally used to confirm the diagnosis if clinically suspected
however, if the infant is > 4.5 months then x-ray is the first line investigation
Management
most unstable hips will spontaneously stabilise by 3-6 weeks of age
Pavlik harness (dynamic flexion-abduction orthosis) in children younger than 4-5 months
older children may require surgery
Napkin rashes
General management points
disposable nappies are preferable to towel nappies
expose napkin area to air when possible
apply barrier cream (e.g. Zinc and castor oil)
mild steroid cream (e.g. 1% hydrocortisone) in severe cases
management of suspected candidal nappy rash is with a topical imidazole. Cease the use of a barrier cream until the candida has settled
Vesicoureteric reflux
Vesicoureteric reflux (VUR) is the abnormal backflow of urine from the bladder into the ureter and kidney. It is a relatively common abnormality of the urinary tract in children and predisposes to urinary tract infection (UTI), being found in around 30% of children who present with a UTI. As around 35% of children develop renal scarring it is important to investigate for VUR in children following a UTI
Pathophysiology of VUR
ureters are displaced laterally, entering the bladder in a more perpendicular fashion than at an angle
therefore shortened intramural course of the ureter
vesicoureteric junction cannot, therefore, function adequately
Possible presentations
antenatal period: hydronephrosis on ultrasound
recurrent childhood urinary tract infections
reflux nephropathy
term used to describe chronic pyelonephritis secondary to VUR
commonest cause of chronic pyelonephritis
renal scar may produce increased quantities of renin causing hypertension
Investigation
VUR is normally diagnosed following a micturating cystourethrogram
a DMSA scan may also be performed to look for renal scarring
The table below summarises the grading of VUR
Febrile convulsions
Febrile convulsions are seizures provoked by fever in otherwise normal children. They typically occur between the ages of 6 months and 5 years and are seen in 3% of children.
Clinical features
usually occur early in a viral infection as the temperature rises rapidly
seizures are usually brief, lasting less than 5 minutes
are most commonly tonic-clonic
Management following a seizure
children who have had a first seizure OR any features of a complex seizure should be admitted to paediatrics
Prognosis
the overall risk of further febrile convulsion = 1 in 3. However, this varies widely depending on risk factors for further seizure. These include: age of onset < 18 months, fever < 39ºC, shorter duration of fever before seizure and a family history of febrile convulsions
if recurrences, try teaching parents how to use rectal diazepam or buccal midazolam. Parents should be advised to phone for an ambulance if the seizure lasts > 5 minutes
regular antipyretics have not been shown to reduce the chance of a febrile seizure occurring
Link to epilepsy
risk factors for developing epilepsy include a family history of epilepsy, having complex febrile seizures and a background of neurodevelopmental disorder
children with no risk factors have 2.5% risk of developing epilepsy
if children have all 3 features the risk of developing epilepsy is much higher (e.g. 50%)
Cleft lip and palate
Cleft lip and palate affect around 1 in every 1,000 babies. They are the most common congenital deformity affecting the orofacial structures. Whilst they may be an isolated developmental malformation they are also a recognised component of more than 200 birth defects.
The commonest variants are:
isolated cleft lip (15%)
isolated cleft palate (40%)
combined cleft lip and palate (45%)
Pathophysiology
polygenic inheritance
maternal antiepileptic use increases risk
cleft lip results from failure of the fronto-nasal and maxillary processes to fuse
cleft palate results from failure of the palatine processes and the nasal septum to fuse
Problems
feeding: orthodontic devices may be helpful
speech: with speech therapy 75% of children develop normal speech
increased risk of otitis media for cleft palate babies
Management
cleft lip is repaired earlier than cleft palate, with practices varying from repair in the first week of life to three months
cleft palates are typically repaired between 6-12 months of age
Transient tachypnoea of the newborn
Transient tachypnoea of the newborn (TTN) is the commonest cause of respiratory distress in the newborn period. It is caused by delayed resorption of fluid in the lungs
It is more common following caesarean sections, possibly due to the lung fluid not being ‘squeezed out’ during the passage through the birth canal
Chest x-ray may show hyperinflation of the lungs and fluid in the horizontal fissure.
Management
observation, supportive care
supplementary oxygen may be required to maintain oxygen saturations
Transient tachypnoea of the newborn usually settles within 1-2 days
Williams syndrome
William’s syndrome is an inherited neurodevelopmental disorder caused by a microdeletion on chromosome 7
Features elfin-like facies characteristic like affect - very friendly and social learning difficulties short stature transient neonatal hypercalcaemia supravalvular aortic stenosis
Diagnosis is made by FISH studies
elfin facies
strabismus
broad forehead
short stature
Duchenne muscular dystrophy
dilated cardiomyopathy
Transient tachypnoea of the newborn
Transient tachypnoea of the newborn (TTN) is the commonest cause of respiratory distress in the newborn period. It is caused by delayed resorption of fluid in the lungs
It is more common following caesarean sections, possibly due to the lung fluid not being ‘squeezed out’ during the passage through the birth canal
Chest x-ray may show hyperinflation of the lungs and fluid in the horizontal fissure.
Management
observation, supportive care
supplementary oxygen may be required to maintain oxygen saturations
Transient tachypnoea of the newborn usually settles within 1-2 days
Acute Lymphoblastic Leukaemia
peak incidence of 2-5 years
affects slightly more boys than girls and accounts for 80% of childhood leukaemias. It is the most common malignancy affecting children. There is not a strong family correlation, although some genetic disorders, such as Down’s syndrome, increase the likelihood of developing the disease.
consent
The GMC guidance on consent in children is extensive. In short, when a child lacks capacity, consent from one parent is sufficient to administer treatment as long as it is in the best interests of the child. Additionally, though Dawn may lack capacity, encouraging her involvement in the decision-making process is important.
Meningitis in children - investigations
Investigations
Contraindication to lumbar puncture (any signs of raised ICP) focal neurological signs papilloedema significant bulging of the fontanelle disseminated intravascular coagulation signs of cerebral herniation
For patients with meningococcal septicaemia a lumbar puncture is contraindicated - blood cultures and PCR for meningococcus should be obtained.
Contraindications to lumbar puncture
(any signs of raised ICP)
focal neurological signs papilloedema significant bulging of the fontanelle disseminated intravascular coagulation signs of cerebral herniation
For patients with meningococcal septicaemia a lumbar puncture is contraindicated - blood cultures and PCR for meningococcus should be obtained.
Management of meningitis in children
- Antibiotics
< 3 months: IV amoxicillin (or ampicillin) + IV cefotaxime
> 3 months: IV cefotaxime (or ceftriaxone) - Steroids
NICE advise against giving corticosteroids in children younger than 3 months
dexamethsone should be considered if the lumbar puncture reveals any of the following:
frankly purulent CSF
CSF white blood cell count greater than 1000/microlitre
raised CSF white blood cell count with protein concentration greater than 1 g/litre
bacteria on Gram stain - Fluids
treat any shock, e.g. with colloid - Cerebral monitoring
mechanical ventilation if respiratory impairment - Public health notification and antibiotic prophylaxis of contacts
ciprofloxacin is now preferred over rifampicin
Threadworms
- extremely common helminths in children
- infection occurs via the ingestion of eggs present in the environment
- asymptomatic but it can cause perianal itching, particularly at night
- Most patients are treated empirically without having to confirm the diagnosis, with hygiene suggestions and mebendazole.
Infestation with threadworms (Enterobius vermicularis, sometimes called pinworms) is extremely common amongst children in the UK. Infestation occurs after swallowing eggs that are present in the environment.
Threadworm infestation is asymptomatic in around 90% of cases, possible features include:
perianal itching, particularly at night
girls may have vulval symptoms
Diagnosis may be made by the applying Sellotape to the perianal area and sending it to the laboratory for microscopy to see the eggs. However, most patients are treated empirically and this approach is supported in the CKS guidelines.
Management
CKS recommend a combination of anthelmintic with hygiene measures for all members of the household
mebendazole is used first-line for children > 6 months old. A single dose is given unless infestation persists
Capacity
Capacity is time and decision dependent. If in the past the patient has not had capacity to make a decision, but today for this decision you feel she has, the only consent you need is from her.
Kawasaki disease
- medium vessel vasculitis
Features:
- high-grade fever last >5days (resistant to antipyretics)
- conjunctival infection
- bright red, cracked lips
- strawberry tongue
cervical lymphadenopathy
- red palms of the hand and the soles of the fee which later peels
Management
high-dose aspirin
Kawasaki disease is one of the few indications for the use of aspirin in children. Due to the risk of Reye’s syndrome aspirin is normally contraindicated in children
intravenous immunoglobulin
echocardiogram (rather than angiography) is used as the initial screening test for coronary artery aneurysms
UTI in childhood
Urinary tract infections (UTI) are more common in boys until 3 months of age (due to more congenital abnormalities) after which the incidence is substantially higher in girls.
At least 8% of girls and 2% of boys will have a UTI in childhood
Presentation of UTI based on age
Presentation in childhood depends on age:
infants: poor feeding, vomiting, irritability
younger children: abdominal pain, fever, dysuria
older children: dysuria, frequency, haematuria
features which may suggest an upper UTI include: temperature > 38ºC, loin pain/tenderness
NICE guidelines for checking urine sample in a child
If there are any symptoms or signs suggestive or a UTI
with unexplained fever of 38°C or higher (test urine after 24 hours at the latest)
with an alternative site of infection but who remain unwell (consider urine test after 24 hours at the latest)
Urine collection method
clean catch is preferable
if not possible then urine collection pads should be used
cotton wool balls, gauze and sanitary towels are not suitable
invasive methods such as suprapubic aspiration should only be used if non-invasive methods are not possible
Management of UTI
infants less than 3 months old should be referred immediately to a paediatrician
children aged more than 3 months old with an upper UTI should be considered for admission to hospital. If not admitted oral antibiotics such as cephalosporin or co-amoxiclav should be given for 7-10 days
children aged more than 3 months old with a lower UTI should be treated with oral antibiotics for 3 days according to local guidelines, usually trimethoprim, nitrofurantoin, cephalosporin or amoxicillin. Parents should be asked to bring the children back if they remain unwell after 24-48 hours
antibiotic prophylaxis is not given after the first UTI but should be considered with recurrent UTIs
Intraventricular haemorrhage
haemorrhage that occurs into the ventricular system of the brain. It is relatively rare in adult surgical practice and when it does occur, it is typically associated with severe head injuries. In premature neonates it may occur spontaneously. The blood may clot and occlude CSF flow, hydrocephalus may result.
In neonatal practice the vast majority of IVH occur in the first 72 hours after birth, the aetiology is not well understood and it is suggested to occur as a result of birth trauma combined with cellular hypoxia, together the with the delicate neonatal CNS.
Caput succedaneum
caused by pressure on the fetal scalp during the birthing process. It results in a large oedematous swelling and bruising over the scalp. Treatment is not required as the swelling reduces over a few days.
cephalohaematoma
occur after a spontaneous vaginal delivery or following a trauma from the obstetric forceps or the ventouse. A haemorrhage results after the presidium is sheared from the parietal bone. The tense swelling is limited to the outline of the bone. It reduces over a few weeks - months.
Subaponeurotic haemorrhage
subgaleal haemorrhage is rare and is due to a traumatic birth. It may result in the infant losing large amounts of blood
intracranial haemorrhage
subarachnoid, subdural or intraventricular haemorrhages
Subarachnoid haemorrhages are common and may cause irritability and even convulsions over the first 2 days of life
Subdural can following the use of forceps.
Intraventricular haemorrhage mostly affects pre-term infants and can be diagnosed by ultrasound examinations.
