Paediatrics Flashcards
When can jaundice in a neonate be aetiologically normal
After 24 hours
How does rhesus haemolytic disease occur
Mum = rhesus negative
Baby = rhesus positive
Sensitising event eg trauma/abruption (baby’s blood exposed to mothers)
Mother develops antibodies against the baby’s blood = haemolytic anaemia
Unconjugated bilirubin is produced
How is rhesus haemolytic disease prevented
With anti-D immunoglobulin:
At 28 weeks
After sensitising events
One dose after birth if the mother is known to be rhesus negative
When does ABO incompatibility occur
Mother = type O = can develop anti-B or anti-A antibodies
Baby = type A or B
How is ABO incompatibility diagnosed
Coomb’s test
Which infections are included in TORCH
Toxoplasmosis
Other (syphilis, parvovirus, varicella zoster)
Rubella
CMV
Herpes; Hepatitis
Genetics of G6PD deficiency
X linked recessive
Genetics of hereditary spherocytosis
Autosomal dominant
Causes of jaundice under 24 hours
Rhesus haemolytic disease
ABO incompatibility
TORCH infections
G6PD deficiency
Hereditary spherocytosis
Causes of jaundice in the first 2-14 days (normal)
Physiological jaundice
Breast milk jaundice
Exacerbation by bruising and polycythaemia
Infection
Two main reasons for physiological jaundice
Increased bilirubin production as fetal haemoglobin has a lifespan of 70 days (compared to adult 120)
Decreased conjugated bilirubin due to liver immaturity (why premature babies have a higher incidence)
Why can breast milk feeding difficulties or infection cause jaundice in neonates
Feeding difficulties and infection cause dehydration which impairs bilirubin elimination
Why can polycythaemia occur in neonates
Gestational diabetes
Why can bruising occur in neonates
Caput
Cephalohaematoma
What is neonatal biliary atresia
Rare condition with failure of the biliary tree to develop
NB: Important to detect early as early surgery improves outcomes
Pathophysiology of kernicterus
Acute bilirubin encephalopathy: brain damage due to unconjugated bilirubin deposition in the basal ganglia and brain stem after it exceeds albumin binding capacity
Complications of kernicterus
Seizures, hypotonia, opisthotonos
Without treatment: cerebral palsy, learning disabilities, sensorineural deafness
Investigations of neonatal jaundice
Transcutaneous bilirubin levels
Bloods: coombs, kleihauer, U&Es (both conjugated and unconjugated bilirubin), FBC + blood film, blood cultures, TFTs
USS if there is a suspicion of biliary atresia
Treatment of neonatal jaundice
First line phototherapy: converts unconjugated bilirubin into harmless substances
Exchange transfusion: if bilirubin levels are very high
Clinical features of bronchiolitis
LRTI
Coryzal symptoms preceding a dry wheezy cough
Fever + poor feeding
Tachypnoea, tachycardia
Symptoms of RDS e.g. intercostal/subcostal recessions, tracheal tug, grunting, nasal flaring
When should you suspect pneumonia in a differential diagnosis of bronchiolitis
High fever
Localised signs (consolidation)
High risk children for bronchiolitis
congenital heart disease
BPD (bronchopulmonary dysplasia)
CF
prematurity
Prevention of bronchiolitis in high risk children
IM palivizumab (RSV monoclonal antibody)
Most common causal organism of croup/laryngotracheobronchitis
Parainfluenza virus
Clinical features of croup
URTI
Barking cough
Inspiratory stridor
Hoarse voice
Respiratory distress
Differential diagnosis of croup
Bacterial tracheitis – more toxic appearance
Laryngomalacia – no chest signs
Treatment of croup
Reassurance
One of dose of oral or nebulised steroids e.g. dexamethasone 150mcg/kg
Treatment of severe croup unresponsive to steroids
Hospital for nebulized adrenaline
Careful monitoring
Most common causal organism of epiglottis
Haemophilus influenzae
rare now due to the Hib vaccine
Clinical features of epiglottis
Toxic looking child - miserable fever
3 Ds: drooling, dysphagia, distress
Tripod position
Muffled voice
Inspiratory stridor
Epiglottis treatment
IV cefotaxime
Do not distress the child or examine the airway
Causes of meningitis/encephalitis under 3 months of age
Group B strep
Causes of meningitis over 3 months of age
Meningococcus, pneumococcus (haemophilus influenza b)
Mumps virus
RNA paramyoxovirus
Clinical features of mumps
Coryzal symptoms followed by parotid swelling
Ear ache
Trismus – spasm of the muscles of mastication when chewing
Complications of mumps
Meningitis
Encephalitis
Orchitis
Pancreatitis
Measles virus
RNA paramyxovirus: morbillivirus
Clinical features of measles
Catarrhal stage:
- 4 Cs – Cough, Cranky, coryza, conjunctivitis
Exanthematous stage:
- maculopapular rash with cephalocaudal progression
Complications: - most common is otitis media
Diagnosis of measles
Clinical diagnosis
Saliva swab for measles IgM to confirm since it is a notifiable disease
Rubella virus
RNA paramyxovirus – rubivirus
Clinical features of rubella
Coryzal prodrome
Pink maculopapular rash
Lymphadenopathy – sub occipital or posterior auricular
Arthralgia is common
Diagnosis of rubella
Clinical
Saliva swab for rubella IgM since it is a notifiable disease
Main risk group for rubella
Pregnant women:
<13 weeks: transmission to fetus is 80% (TOP can be offered)
>16 weeks: 25% risk of transmission/unlikely to cause defects
Clinical features of congenital rubella
Triad:
sensorineural deafness
cardiac abnormalities
eye abnormalities e.g. cataracts
Clinical features of parvovirus B19/fifth disease
Coryzal prodrome, fever
Malar rash
Glove and stocking erythema is also common
Arthropathy is common in older children
Once the rash appears they are no longer infectious
Complications of parvovirus B19
Pure red cell aplasia (high risk - sickle cell, thalassaemia)
Transient aplastic crisis (high risk - HIV, organ transplant patients)
Hydrops fetalis (> 70% transmission rate to the fetus if > 16 weeks - may require fetal blood transfusions in utero)
Causal organism of hand, foot and mouth
enteroviruses - mostly coxsackie A16
Are most sore throats viral or bacterial
viral
Causal organism of bacterial tonsilitis
group A beta haemolytic strep (GABHS) – strep. Pyogenes
Tonsilitis ‘Fever PAIN’ score
Fever
Purulent tonsils
Attended rapidly (within 3 days)
Inflamed tonsils
No cough or coryza
Score 2/3 = 30 – 40% chance of strep
Score 4/5 = 60% chance of strep
Treatment of tonsilitis
Bacterial:
Phenoxymethylpenicillin (pen V) for 7 – 10 days
Clarithromycin if penicillin allergic
Causal organism of scarlet fever
GABHS (group A B-haem strep) - release endotoxins that cause scarlet fever
clinical features of scarlet fever
Rash 12 – 48 hours after the onset of a sore throat
Red pin prick blanching red
Sandpaper feel to the rash
Strawberry tongue
Circumoral pallor
Treatment of scarlet fever
phenoxymethylpenicillin
(same as tonsilitis)
Causal organism of chickenpox
varicella zoster virus
Description of chickenpox rash
Macular – papular – vesicles (fluid filled)
Treatment of chickenpox
Supportive
Signs of infection (staph. Aureus) – flucloxacillin
Immunocompromised – acyclovir
Pregnant women contacts – VZIG or acyclovir if they develop a rash
3 complications of chickenpox
bacterial infection
pneumonia
encephalitis
causal organism of impetigo
staph aureus
peak ages of impetigo
2-5 years old
clinical features of impetigo
Pustules + blisters on an erythematous base
Blisters leave a brown ‘honey crust’ when they burst
treatment of impetigo
First line – topical hydrogen peroxide 1% or topical fusidic acid (both are just as effective)
If severe/widespread – oral flucloxacillin
school exclusion in impetigo
48 hours after antibiotics or until lesions have crusted over
school exclusion in mumps
7 days
school exclusion in measles
5 days after rash onset
school exclusion in rubella
5 days after rash onset
school exclusion in hand, foot and mouth
no school exclusion
Transient synovitis/irritable hip clinical features
Pain mostly on movement, improves throughout the day - will move it if persuaded!
2-12 years old
aetiology of transient synovitis/irritable hip
viral infection
management of any suspicion of septic arthritis or hip pain in a child < 3 years old
A&E
Perthe’s disease clinical features
Constant pain
Restricted ROM
Leg length discrepancy = late sign
5-10 years old
Dx + Ix Perthe’s disease
X ray – joint space widening/irregularity
- crescent sign (late sign)
SCFE clinical features
Vague pain
Drehmann’s sign
5-10 years old
overweight
pubertal
Dx + Ix SCFE/SUFE
X ray = diagnostic
Tx SCFE
Surgical fixation
Septic arthritis causal organism in children (most commonly <2 yrs old)
Staph aureus
Clinical features septic arthritis
Look for scratches/infected chicken pox
Acutely swollen tender joint
Pseudoparesis
Dx + Ix septic arthritis
blood cultures, CRP
joint aspiration
Tx septic arthritis
surgical debridement + IV ABx
Oesophageal atresia (OA)
Clinical features of OA +/- TOF
Prenatal:
polyhydramnios (cannot swallow the amniotic fluid)
Postnatal:
- blowing bubbles
- salivation + drooling
- cyanotic episodes on feeding
- respiratory distress + aspiration
Dx + Ix OA +/- TOF
NG tube > X-ray will show NG coiled in the oesophagus
Abdo X-ray: no bubbles = isolated OA
Gastroschisis
Paraumbilical defect, always to the right of the cord
gastroschisis Ix
Typically found on antenatal scans
AFP raised
Treatment of gastroschisis
Lower segment C section
Staged corrective surgery
TPN slowly introduced
Omphalocele
Ventral defect in the umbilical ring with herniation of abdominal contents covered by peritoneum
Kawasaki crash and burn
Conjunctivitis
Rash
Adenopathy
Strawberry tongue
Hand (swelling or erythema)
And burn
Kawasaki Tx
IgG a
ITP
What is caput succedaneum
Boggy superficial scalp swelling that can cross the suture line
(CS = Crosses Sutures)
What is caput succedaneum commonly caused by
pressure against the cervix during birth or ventouse delivery (Chignon)
What is cephalohaematoma
Subperiosteal haemorrhage
(periosteum is stuck tightly to the skull and so does NOT cross the suture lines)
Causes of omphalocele
Small defects (ie no liver) are associated with beckwith-Wiedemann syndrome (BWS)
Larger defects are caused by pulmonary hypoplasia
Omphalocele Ix
Antenatal scans
Raised AFP
Omphalocele Tx
Protect the herniated contents
Prevent hypothermia
Gastric decompression
Staged surgical repair
Signs of congenital diaphragmatic hernia (CDH)
- Resuscitation at birth
- Displaced apex beat
- Bowel sounds in hemithorax
- If small defect – may just have respiratory distress after feeding
- Scaphoid abdomen
Duodenal atresia associated genetic condition
Down syndrome
Duodenal atresia presentation
Small bowel obstruction symptoms with or without bilious vomiting
Duodenal atresia X ray finding
Double bubble sign
volvulus sign on X ray
Coffee bean sign
Why can small bowel obstruction occur in cystic fibrosis
Delayed passage of meconium due to it being thicker - some meconium gets stuck in the distal ileum
What treatment can help meconium pass in CF
Therapeutic contrast enema (gastrografin)
Hirschsprung’s disease pathogenesis
Congenital absence of ganglia (both myenteric and submucosal plexus) in a segment of the colon
NB: 75% rectosigmoid
Clinical features of Hirschsprung’s disease
Functional LBO with failure to pass meconium within 24 – 48 hours
abdominal distention + late bilious vomiting
PR would reveal a contracted distal segment
followed by a rush of liquid stool and temporary relief of symptoms
Diagnosis Ix Hirschsprung’s disease
Undescended testes / cryptorchidism treatment
Most will spontaneously descend by 6 months - 1 year
Orchidopexy at 1 year if still undescended
Indirect vs direct inguinal hernia
NB: ring occlusion test can differentiate between a direct and indirect hernia
What are neonatal inguinal hernias due to
Patent processus vaginalis (failure to become the tunica vaginalis)
Inguinal hernias clinical features
Indirect – bulge lateral to the pubic tubercle
more prominent on crying
Look for signs of incarceration e.g. tender
lump, irritable, vomiting
6/2 rule in the surgical treatment of Inguinal hernias
< 6 weeks operate within 2 days
< 6 months operate within 2 weeks
< 6 years operate within 2 months
Any signs of incarceration = emergency surgery
Hypospadias definition
Presence of the urethral meatus on the ventral aspect of the penile shaft
(Testosterone is needed for the meatus to move distally during development)
Zero to finals
Which deficiency should you investigate in hypospadias and undescended testes
Low testosterone
Clinical features of hypospadias
Meatus on the ventral surface
Hooded foreskin
Spraying on urination
Testicular torsion pathogenesis
Twisting of the spermatic cord cutting off blood supply to the testicle
Aetiology of testicular torsion
Peaks at times of high testosterone – larger
testes = more chance of twisting
Peak times are in neonates and pubertal teenagers
Neonates with undescended testes are at
higher risk because there is less secure attachment within the scrotum
Bell clapper deformity
Clinical presentation of testicular torsion
Testicle displaced higher, more horizontal
Acutely swollen, tender testicle
Vomiting due to pain
Absent cremasteric reflex
Negative Prehn’s sign
Negative prehns sign interpretation
differentiates between torsion and epididymitis - lift the testicle – if pain is relieved this is suggestive of epididymitis - if pain is not relieved – torsion
Surgical emergency chances of survival for testicular torsion
< 6 hours – 90% chance of testicular survival
24 hours – 10% chance of testicular survival
Intussusception definition
Condition where one section of bowel telescopes into the other, usually the ileum into the caecum
Presents 3 months – 2 years
Aetiology intussusception
Classically preceded by viral infection
Meckel’s diverticulum
CF
Lymphoma
Clinical features of intussusception
Episodes of colicky abdominal pain,
legs draw up
May be fine but lethargic in between episodes
Signs of SBO
Sausage shaped mass in the abdomen
Late sign – red current jelly stool due
to bowel ischaemia
Diagnosis/Ix intussusception
USS – target/donut sign
AXR – dilated proximal bowel loops
Treatment intussusception
Rectal air insufflation
- 75% success rate
- only perform if there are no signs of peritonism
Surgical correction if air insufflation fails or signs of ischaemia
Pyloric stenosis definition
Hypertrophy of the pylorus muscle leading to gastric outlet obstruction causing projectile vomiting
Incidence peaks at 2-8 weeks
4 x more common in boys
Clinical features of pyloric stenosis
Projectile vomiting very shortly after feeds
Non bilious
Hungry after vomiting
Dehydration
Weight loss is a late sign
Diagnosis/Ix pyloric stenosis
Test feed – feel for an olive size mass in the RUQ
USS – thickened pylorus
Hypochloraemic hypokalaemic metabolic
alkalosis
Treatment pyloric stenosis
Non urgent outpatient pyloromyotomy
Pathogenesis of anaemia
Blood loss e.g. acute haemorrhage
Decreased production e.g. nutritional deficiency
Increased consumption e.g. acquired (e.g. immune) or inherited (e.g. enzyme)
Blood parameters to check for
Hb (always check normal range for age and sex)
Is the abnormality isolated to a single cell line or part of multiple cell
lines (BM failure, infiltration, immune, hypersplenism)
MCV (microcytic, normocytic, macrocytic)
Microcytic (MCV low) anaemias
Iron deficiency Thalassaemia
Sideroblastic Anaemia Chronic disease
Lead toxicity
Macrocytic (MCV high) anaemias
Normal newborn
Aplastic anaemia Hypothyroidism Megaloblastic anaemia Early iron deficiency Increased erythropoiesis
Normocytic (MCV normal) anaemias
Acute blood loss
Infection
Renal failure
Early iron deficiency
Bone marrow infiltration
Most common causes of anaemia in childhood
Low birth weight
Dietary - excessive cows milk intake
Occult GI bleeding (E.g hookworm)
Cows milk intolerance
Presentation of anaemia in childhood
pallor, irritability, anorexia
when Hb<50, tachycardia,
cardiac dilatation, murmur,
poss. splenomegaly
Treatment of iron deficiency anaemia
Oral therapy for 3-6 months
Intra corpuscular causes of haemolysis
Haemoglobin
Enzyme
Membrane
Extra corpuscular causes of anaemia
Autoimmune
Fragmentation
Hyper splenism
Plasma factors
Presentation of haemolytic anaemia
Hydrops fetalis
Neonatal hyperbilirubinaemia (jaundice)
Neonatal ascites
Anaemia/failure to thrive
Splenomegaly
Cholecystitis/gall stones
Hyperbilirubinaemia
Leg ulcers
Aplastic crisis
Thromboembolism
Haemolysis screen
FBC
Retics
Blood film
LDH
Haptoglobin
Bilirubin
Direct Coombs test
Three main presentations of G6PD
Neonatal jaundice
Chronic non-spherocytic haemolytic anaemia
Intermittent episodes of intravascular haemolysis
Pathophysiology of sickle cell
Substitution of valine for
glutamic acid on β chain (HbS)
HbS polymerises when
deoxygenated leading to sickle shape
Occlusion of the microvascular
circulation producing vascular damage, infarcts, pain
Shortened survival of red cells leading to haemolysis
Sickle cell genetics
Autosomal recessive
NB: most common serious genetic disorder in England
Common presentations of sickle cell disease
Dactylitis
Acute chest syndrome
Splenomegaly (splenic sequestration)
Diagnosis sickle cell
Blood film
Screening: sickle solubility test
Thalassaemia
Reduced rate of one or more of the globin chains
Autosomal recessive
A Thalassaemia
4 a globin chains per cell (aa/aa)
B Thalassaemia
2 globin genes per cell
Necrotising enterocolitis (NEC) definition
Disorder affecting premature neonates where part of the bowel becomes necrotic which can lead to bowel perforation
Why is NEC a life threatening emergency
Bowel perforation can lead to peritonitis and shock
Risk factors for developing NEC
Very low BW or very premature
Formula feeds
Respiratory distress and assisted ventilation (hypoxia)
Sepsis
Patient ductus arteriosus / other congenital heart disease
Presentation of NEC
Intolerance to feeds
Vomiting, particularly with green bile
Generally unwell
Distended, tender abdomen (taught shiny skin)
Absent bowel sounds
PR fresh blood + mucus in stools (due to necrosis)
Blood test Ix for NEC
Full blood count: thrombocytopenia and neutropenia (low platelets = worse prognosis)
CRP: inflammation
Capillary blood gas: metabolic acidosis
Blood culture for sepsis
Clotting screen (NEC can lead to DIC)
Ix of choice for NEC
Abdominal X-ray
X-ray signs NEC
Dilated loops of bowel
Pneumotasis intestinalis (gas in the bowel wall) - PATHOGNOMONIC of NEC
Pneumoperitoneum (free gas in the peritoneal cavity = perforation)
NEC Tx
NBM with IV fluids + total parenteral nutrition (TPN)
Antibiotics (cefotaxime + vancomycin)
Nasogastric tube can be inserted to drain fluid and gas from the stomach and intestines
Some neonates will require surgery - laparotomy if rapid distention + signs of perforation
Why can treatment for patent ductus arteriosus cause NEC
Indomethacin (NSAID) causes vasoconstriction of mesenteric arteries
🚩 Red flag 🚩
Not keeping down any feed
Pyloric stenosis or intestinal obstruction
🚩 Red flag 🚩
Projectile or forceful vomiting
Pyloric stenosis or intestinal obstruction
🚩 Red flag 🚩
Bile stained vomit
Intestinal obstruction
🚩 Red flag 🚩
Haematemesis or melaena
Peptic ulcer, oesophagitis or varices
🚩 Red flag 🚩
Abdominal distention
Intestinal obstruction
🚩 Red flag 🚩
Reduced consciousness, bulging fontanelle or neurological signs
Meningitis or raised ICP
🚩 Red flag 🚩
Respiratory symptoms
Aspiration or infection
🚩 Red flag 🚩
Blood in the stools
Gastroenteritis or cows milk protein allergy
🚩 Red flag 🚩
Signs of infection
Pneumonia, UTI, tonsillitis, otitis or meningitis
🚩 Red flag 🚩
Rash, angioedema and other signs of allergy
Cows milk protein allergy
Signs of problematic reflux in GORD
Chronic cough
Hoarse cry
Distress, crying or unsettled after feeding
Reluctance to feed
Pneumonia
Poor weight gain/faltering growth
Disturbed sleep
Oesophagitis (can cause anaemia)
Why do most babies have gastro oesophageal reflux
The lower oesophageal sphincter is immature
(90% of babies stop having reflux by 1 year)
GORD Tx
Minor: reassurance; smaller and more frequent feds; sit up right after feeding
Severe: PPI e.g. omeprazole
Very severe: unresponsive to treatment and >1 year old: Nissen fundoplication
IgE mediated CMPA symptom onset
Type 1 hypersensitivity
Immediate symptom onset after only small amounts
Non IgE mediated symptom onset
Symptoms occur around 72 hours after ingestion
Clinical features IgE mediated CMPA
Derm: urticaria (hives), pruritus
GI: colicky abdo pain, vomiting, bloody stool
Resp: rhinorrhea (runny nose), itchy nose
Clinical features non IgE mediated CMPA
Loose frequent stool with blood + mucus
Colicky abdominal pain
Diagnosis/Ix CMPA
IgE mediated suspicion: skin prick weal = 4mm is positive
Non IgE: temporary removal from diet and then reintroduction to see if symptoms return
Tx CMPA
Breastfed - mum removes milk from her diet
Bottle fed - extensively hydrolysed formula
Sandifer’s syndrome (GORD)
Brief episodes of abnormal movements:
Torticollis (twisting of neck)
Dystonia (arching of back)
Aetiology acute otitis externa
Bacterial - mostly pseudomonas or staph aureus
Risk factors acute otitis externa
Humidity
Swimming
Scratching from eczema/psoriasis
Clinical features acute otitis externa
Pain (pulling at the ear)
Scaly skin + discharge
Conductive hearing loss on the affected side
Treatment of mild acute otitis externa
Topical antibiotics + steroid drops e.g. sofradex (aminoglycoside + steroid
Treatment of severe acute otitis externa (occluded ear canal)
Send to ENT for ear wicking (impregnated w/ antibiotics)
Treatment for spreading erythema around the ear in acute otitis externa
Flucloxacillin or ciprofloxacin (good against pseudomonas)
Aetiology acute otitis media
Mostly viral
Clinical feature of acute otitis media
Tympanic membrane bulges and becomes erythematous
Treatment acute otitis media
Watchful waiting - 60% resolve within 24 hours, 80% within 4 days
Indication for antibiotics: amoxicillin 5-7 days or erythromycin if penicillin allergic
— 4 days of symptoms
— Bilateral AOM in a child <2 years old
— Discharger = perforation
— Immunocompromised
Complications of acute otitis media
Tympanic membrane perforation
Mastoiditis
Glue ear definition
Otitis media with a collection of fluid behind the TM
Aetiology glue ear
Eustachian tube dysfunction - children have shorter and more horizontal eustachian tubes
URTI often causes adenoid hypertrophy which blocks the eustachian tubes
Children at increased risk - down syndrome, cleft palate
Diagnosis and investigation
Otoscopy - opaque + retracted TM, fluid level + bubbles
Glue ear treatment
Active observation for 3 months/otovent for symptomatic relief to improve conductive hearing loss
3 month: consider ENT referral for grommets
