Paediatric History Taking and Management Flashcards

1
Q

How can you structure a paediatric history?

A

Confirm full name and DOB
Presenting Complaint
How long have they been in hospital for? What brought them in? How have they been progressing? What treatment are they receiving – is it helping?

PDF BINDS
Past medical and surgical hx
Drug hx
Family hx
Birth history – how was the pregnancy? How many weeks were they born at? Mode of delivery? Birth weight? Complications after birth? SCBU stay?
Immunisations
Nutrition- how much do they eat and drink? Wet/dirty nappies?
Development
Social and sexual hx – including any previous social services input

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2
Q

How could you explore a presenting complaint of a child with a seizure?

A

Is there anything the parent thinks might have triggered it?

How were they leading up to the seizure? Any temperature? Complaining of a headache? Stiff neck? Any new rashes? N+V? Change in waterworks/bowel habit?

How did they look when they were seizing? One part of their body shaking or all of it? Was the child aware of what was happening? Tongue biting? Incontinence?

Eye rolling during the seizure?

How long did it last? How did it stop? How were they afterwards?

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3
Q

How would you investigate a child with a seizure?

A

measure their glucose and oxygen sats immediately

bloods for reversible causes e.g. electrolyte derangement

suspecting meningitis / encephalitis: inflammatory markers, viral PCR/ nasopharyngeal aspirates, blood cultures, LP, neuroimaging

ECG for arrythmia

EEG

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4
Q

DDx for a child with a seizure?

A

Febrile convulsions
Roseola infantum (can cause febrile convulsions)
Hypoglycaemia / hypoxia
Epilepsy
Meningitis
Encephalitis (e.g. herpes simplex)
SOL

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5
Q

How would you explain febrile convulsions and their management to a parent?

A

Explain that when some children run a temperature that their brain isn’t used to it and it may cause a seizure, occurs commonly in children from 6 months - 5 years

If they have had one febrile convulsion they are more likely to have another, but most children grow out of it by 5/6 years

Can give paracetomol to bring down the temperature but this doesn’t reduce the risk of them occuring

Safety netting advice: if seizing, clear obstacles, put cushion under head, call ambulance if lasting more than 5 mins

Explain that they don’t increase risk of epilepsy unless they are complicated / prolonged

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6
Q

How can non-blanching rashes be described?

A

Petechiae : < 5mm diameter
Purpura: 5-10mm diameter
Ecchymoses: >1cm diameter

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7
Q

What can cause non- blanching rashes in kids?

A

Meningococcal sepsis
Henoch-Schönlein purpura
Haemolytic uraemic syndrome
Idiopathic thrombocytopaenic purpura
Leukaemia
Forceful coughing/vomiting
Non-accidental injury

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8
Q

What features would you expect in the history and examination for a child with menigococcal sepsis?

A

Fever
Neck stiffness
Headache
Photophobia
Confusion and/or seizures

OE:
Kernig’s sign (pain and resistance on passive knee extension with hips fully flexed)
Brudzinski’s sign (knees and hips flex on bending the head forward)
Non-blanching rash

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9
Q

How could you investigate meningococcal sepsis?

A

MUST NOT DELAY TX

Baseline bloods (FBC, WCC CRP, U&E, clotting): inflammatory markers may be raised
Blood cultures
Pharyngeal swab: to screen for Neisseria meningitides in the pharynx

do not do lumbar puncture if signs of sepsis or rapidly evolving rash

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10
Q

How would you manage meningococcal sepsis?

A

GP: IM Benzylpenicillin

Hospital:
Intravenous cefotaxime and amoxicillin in patients under 3 months.
Intravenous ceftriaxone (and consider steroids) in patients over 3 months old.

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11
Q

What are the 5 key components of meningitis management in children?

A

Antibiotics

Steroids

Fluids
treat any shock, e.g. with colloid

Cerebral monitoring
mechanical ventilation if respiratory impairment

Public health notification and antibiotic prophylaxis of contacts - ciprofloxacin

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12
Q

Complications of untreated meningococcal sepsis?

A

Seizures
Raised intracranial pressure and hydrocephalus
Disseminated intravascular coagulation

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13
Q

What is Henoch-Schönlein purpura (HSP)?

A

IgA mediated vasculitis usually triggered by group A strep

peaks at 4-6 years

A prodromal URTI or GI infection
Generalised abdominal pain
N+V, sometimes bloody diarrhoea
Joint pain
IgA nephropathy - haematuria

Symmetrical rash on the back of the legs, buttocks and arms

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14
Q

What is an important differential for HSP?

A

intussusception : also presents as bloody diarrhoea and abdominal pain

Intussusception can also be a complication secondary to HSP

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15
Q

How can HSP be investigated?

A

Urinalysis: to test for the presence of haematuria or proteinuria

monitor blood pressure (renal involvement)

Baseline blood tests :FBC, clotting profile, (bc bleeding) U&Es, LFTs (bc diarrohea) CRP

Skin biopsy: can be considered if there is doubt surrounding the origin of the rash

Can do USS if worried about intussuception

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16
Q

How can HSP be managed?
Complications?

A

supportive care, analgesia, excellent prognosis (usually gone in a few weeks)

Complications:
recurs in 1/3 of patients
Nephrotic or nephritic syndrome
Renal failure
Intussusception

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17
Q

What is ITP? How does it present?

A

development of a purpuric rash in those with low circulating platelets with the absence of any clear cause

viral illness
followed by epistaxis / new rash

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18
Q

How could you investigate ITP?

A

Baseline blood tests (FBC) and blood film: thrombocytopenia

Bloodborne virus screen (HIV, hepatitis C): to exclude secondary cause of ITP

Bone marrow biopsy: only required if there are atypical features e.g.
lymph node enlargement/splenomegaly, high/low white cells, failure to resolve/respond to treatment

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19
Q

How can ITP be managed?

A

self limiting, ITP resolves in around 80% of children with 6 months

medical management:
avoid contact sports
if very low platelets or significant bleeding can consider steroids and platelet transfusion

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20
Q

What is Haemolytic Uraemic Syndrome?

A

follows infection with the Shiga toxin, commonly associated with E.coli 0157

peaks at 6 months to 5 years

Triad of:
Microangiopathic haemolytic uraemia
Acute kidney injury
Thrombocytopaenia

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21
Q

How will HUS present in the history?

A

Diarrhoea, which typically turns bloody around day three
Abdominal pain
Fever
Vomiting

make sure you ask about recent exposure to farm animals

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22
Q

What examination findings might there be for HUS?

A

Abdominal tenderness
Hypertension secondary to acute kidney injury
Small petechiae on the skin can occur due to low platelet count

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23
Q

How may you investigate HUS?

A

FBC, U&E, CRP, clotting: may show thrombocytopenia, raised WCC, anaemia and acute kidney injury

Urinalysis: to screen for haematuria and proteinuria

Stool cultures: to screen for the presence of E.Coli O157

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24
Q

How can HUS be managed?

A

supportive care, consider fluids

notifiable disease

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25
Q

How can you differentiate clinically between HSP and HUS?

A

both present with fever, abdo pain, bloody diarrhoea and a non blanching rash

purpuric rash over extensor surfaces and buttocks in HSP V widespread small petechial rash in HUS

joint pain and haematuria in HSP V not present in HUS

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26
Q

How could you explore a non-blanching rash in a history?

A

Rash - when did it come on, has it changed over time, is it itchy or sore?

triggers? have they been poorly recently?

high temperature, headache, photophobia, neck stiffness?

abdominal pain, N+V, diarrhoea (bloody? from onset or did it turn bloody?), joint pain? blood in urine?

nose bleeds? (ITP)

any recent exposure to farm animals? (HUS)

B symptoms - ALL!!!

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27
Q

Biliary atresia presents in the first few weeks of life with what symptoms and signs ?

A

Jaundice extending beyond the physiological two weeks
Dark urine and pale stools
Appetite and growth disturbance, (however, may be normal in some cases)
Hepatomegaly with splenomegaly
Cardiac murmurs if associated cardiac abnormalities present

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28
Q

How should biliary atresia be investigated?

A

Serum bilirubin : Total bilirubin may be normal, whereas conjugated bilirubin is abnormally high

LFTs including serum bile acids and aminotransferases : usually raised but cannot differentiate causes of neonatal cholestasis

Serum alpha 1-antitrypsin: Deficiency may be a cause of neonatal cholestasis

Sweat chloride test: check for CF

Ultrasound of the biliary tree and liver: May show distension and tract abnormalities

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29
Q

How can biliary atresia be managed? Complications?

A

Surgical intervention is only definitive tx

Medical intervention includes antibiotic coverage and bile acid enhancers following surgery

Complications :
Unsuccessful anastomosis formation
Progressive liver disease
Cirrhosis with eventual hepatocellular carcinoma

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30
Q

What is Bronchiolitis? Offending pathogen? Presenting features?

A

acute bronchiolar inflammation

Usually RSV (respiratory syncytial virus)
other causes: mycoplasma, adenoviruses
may be secondary bacterial infection

coryzal symptoms (including mild fever) precede:
dry cough
increasing breathlessness
wheezing, fine inspiratory crackles
feeding difficulties

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31
Q

In which patients is bronchiolitis more likely to be severe?

A

bronchopulmonary dysplasia (e.g. Premature), congenital heart disease or cystic fibrosis

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32
Q

How can bronchiolitis be investigated and managed?

A

immunofluorescence of nasopharyngeal secretions may show RSV

Management is largely supportive:
humidified oxygen is given via a head box
nasogastric feeding may be needed if children cannot take enough fluid/feed by mouth
suction is sometimes used for excessive upper airway secretions

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33
Q

Chickenpox is caused by primary infection with varicella zoster virus. How does it present?

A

fever initially
itchy rash starting on head/trunk before spreading - macular then papular then vesicular
systemic upset is usually mild

infectivity = 4 days before rash, until 5 days after the rash first appeared

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34
Q

How can chickenpox be managed?

A

keep cool, trim nails
calamine lotion
school exclusion: until lesions have crusted over (usually about 5 days after the onset of the rash)

immunocompromised patients and newborns with peripartum exposure should receive varicella zoster immunoglobulin (VZIG)
If chickenpox develops then IV aciclovir should be considered

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35
Q

Complications of chickenpox?

A

Secondary bacterial infection of the lesions - NSAIDs may increase risk, group A strep may cause necrotising fasciitis

pneumonia
encephalitis (cerebellar involvement may be seen)
disseminated haemorrhagic chickenpox

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36
Q

What are the causes of constipation in children?

A

Idiopathic - most common
dehydration
low-fibre diet
medications: e.g. Opiates
anal fissure
over-enthusiastic potty training
hypothyroidism
Hirschsprung’s disease
hypercalcaemia
learning disabilities

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37
Q

What red flags might suggest an underlying condition as opposed to idiopathic constipation?

A

Reported from birth or first few weeks of life

Passage of meconium > 48 hours

‘Ribbon’ stools

Abdominal distension

Faltering growth is an amber flag

Previously unknown or undiagnosed weakness in legs, locomotor delay

Signs of maltreatment

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38
Q

Prior to starting treatment for constipation, the child needs to be assessed for faecal impaction. Factors which suggest faecal impaction include:

A

symptoms of severe constipation
overflow soiling
faecal mass palpable in the abdomen (digital rectal examination should only be carried out by a specialist)

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39
Q

How can children with constipation be managed?

A

If faecal impaction is present
polyethylene glycol 3350 + electrolytes (Movicol Paediatric Plain) using an escalating dose regimen as the first-line treatment

Can add a stimulant laxative after 2 weeks if needed

consider regular toileting and non-punitive behavioural interventions

consider asking the Health Visitor or Paediatric Continence Advisor to help support the parents

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40
Q

How can constipation in an infant be managed?

A

Infants not yet weaned (usually < 6 months)
bottle-fed infants: give extra water in between feeds. Try gentle abdominal massage and bicycling the infant’s legs
breast-fed infants: constipation is unusual and organic causes should be considered

Infants who have or are being weaned
offer extra water, diluted fruit juice and fruits
if not effective consider adding lactulose

41
Q

Give some features of Cow’s milk protein intolerance/allergy (CMPI/CMPA)

A

regurgitation and vomiting
diarrhoea
urticaria, atopic eczema
‘colic’ symptoms: irritability, crying
wheeze, chronic cough
rarely angioedema and anaphylaxis

42
Q

How can cows milk allergy be investigated and managed?

A

Diagnosis is often clinical (e.g. improvement with cow’s milk protein elimination)

Ix:
skin prick/patch testing
total IgE and specific IgE (RAST) for cow’s milk protein

Mx:

Management if formula-fed =
extensive hydrolysed formula (eHF) milk is the first-line replacement formula

Management if breastfed =
continue breastfeeding
eliminate cow’s milk protein from maternal diet. Consider prescribing calcium supplements for breastfeeding mothers

43
Q

What is Croup? What is the causative organism? What age group is most commonly affected?

A

also known as laryngotracheitis

URTI characterised by stridor which is caused by a combination of laryngeal oedema and secretions

Usually caused by parainfluenza virus

typically affects children aged 6 months to 2 years

44
Q

Presenting features of croup?

A

stridor
barking cough (worse at night)
fever
coryzal symptoms

45
Q

How can croup be managed?

A

single dose of oral dexamethasone (0.15mg/kg) to all children regardless of severity
high-flow oxygen
nebulised adrenaline

46
Q

Coeliac disease is caused by sensitivity to gluten, with repeated exposure leading to villous atrophy which in turn causes malabsorption. Children normally present before the age of 3 years.

What features may the present with?

A

Features may coincide with the introduction of cereals (i.e. gluten)
failure to thrive
diarrhoea
abdominal distension
older children may present with anaemia
many cases are not diagnosed to adulthood

47
Q

How is coeliac diagnosed?

A

jejunal biopsy showing subtotal villous atrophy and crypt hyperplasia

First line blood tests:
Total IgA levels (to exclude IgA deficiency)
Anti-tissue transglutaminase antibodies (anti-TTG)
(anti-endomysial and anti-gliadin antibodies are also useful)

48
Q

What other conditions are associated with coealic disease?

A

Down’s syndrome
autoimmune thyroid disease
IDDM

49
Q

Complications of coeliac disease?

A

Nutritional deficiencies
Anaemia
Osteoporosis
Hyposplenism
Ulcerative jejunitis
Enteropathy-associated T-cell lymphoma (EATL)
Non-Hodgkin lymphoma
Small bowel adenocarcinoma

50
Q

Give some signs of respiratory distress in a child

A

Raised respiratory rate
Use of accessory muscles of breathing, such as the sternocleidomastoid, abdominal and intercostal muscles
Intercostal and subcostal recessions
Nasal flaring
Head bobbing
Tracheal tugging
Cyanosis (due to low oxygen saturation)
Abnormal airway noises

51
Q

What is palivizumab?

A

a monoclonal antibody that targets the respiratory syncytial virus

A monthly injection is given as prevention against bronchiolitis caused by RSV to high risk babies, such as ex-premature and those with congenital heart disease

52
Q

Most common cause of gastroenteritis in the UK?

A

rotavirus

53
Q

What is the usual course of D&V in kids?

A

diarrhoea usually lasts for 5-7 days and stops within 2 weeks
vomiting usually lasts for 1-2 days and stops within 3 days

54
Q

What are signs of clinical dehydration in children who have had prolonged D&V?

A

Appears to be unwell or deteriorating
Decreased urine output
Altered responsiveness (for example, irritable, lethargic)
Sunken eyes
Dry mucous membranes
Tachycardia
Tachypnoea
Reduced skin turgor

Normal peripheral pulses, cap refill and bp

55
Q

What are signs of shock in children who have had prolonged D&V?

A

Decreased level of consciousness
Cold extremities
Pale or mottled skin
Tachycardia
Tachypnoea
Weak peripheral pulses
Prolonged capillary refill time
Hypotension

56
Q

Features suggestive of hypernatraemic dehydration:

A

jittery movements
increased muscle tone
hyperreflexia
convulsions
drowsiness or coma

57
Q

When should you do a stool culture in children with diarrhoea?

A

you suspect septicaemia or
there is blood and/or mucus in the stool or
the child is immunocompromised

consider when:
the child has recently been abroad or
the diarrhoea has not improved by day 7 or
you are uncertain about the diagnosis of gastroenteritis

58
Q

How should you manage children with D&V who are becoming dehydrated?

A

give 50 ml/kg low osmolarity oral rehydration solution (ORS) solution over 4 hours, plus ORS solution for maintenance, often and in small amounts

continue breastfeeding

consider supplementing with usual fluids (including milk feeds or water, but not fruit juices or carbonated drinks)

59
Q

Causes of chronic diarrhoea in infants?

A

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

60
Q

How can you explain toddler’s diarrhoea to a parent? What management would you suggest?

A

It is thought that some children may have a fast gut transit time (the time it takes for the food to move through the bowel). As part of the role of the bowel is to absorb water, if things more through too quickly, a lot of the fluid
remains in the poo.

avoid sugary drinks and fruit squashes as they can irritate the gut

need enough fat in their diet - slows down movement in the gut, things like rice pudding and full fat milk

61
Q

What is the commonest cause of vomiting in infancy?

A

Gastro-oesophageal reflux

62
Q

Infant < 8 weeks, presents with milky vomits after feeds, often after being laid flat, excessive crying –>

A

?GORD

63
Q

How should GORD be managed in infants?

A

advise regarding position during feeds - 30 degree head-up

ensure infant is not being overfed (as per their weight) and consider a trial of smaller and more frequent feeds

a trial of thickened formula

a trial of alginate therapy e.g. Gaviscon. Alginates should not be used at the same time as thickening agents

64
Q

Complications of GORD in infants?

A

distress
failure to thrive
aspiration
frequent otitis media
in older children dental erosion may occur

65
Q

What organism causes Hand Foot and Mouth Disease? Clinical features? Mx?

A

coxsackie A16 and enterovirus

mild systemic upset: sore throat, fever
oral ulcers
followed later by vesicles on the palms and soles of the feet

symptomatic mx
reassurance no link to disease in cattle
children do not need to be excluded from school

66
Q

Most common cause of primary headache in children?

A

Migraine without aura

67
Q

Mx of paediatric migraine?

A

ibuprofen

triptans may be used in children >= 12 years but follow-up is required

68
Q

What is Intussusception? What features does it present with?

A

invagination of one portion of the bowel into the lumen of the adjacent bowel, most commonly around the ileo-caecal region

Features:
intermittent, crampy, progressive abdominal pain
inconsolable crying
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

69
Q

How should intussuception be investigated and managed?

A

Ix: USS: target like mass
Mx: reduction by air insufflation under radiological control , peritonitis = surgery

70
Q

What should be done if there are still signs of neonatal jaundice after 14 days ?

A

a prolonged jaundice screen is performed:

urine for MC&S

FBC, U&Es and LFTs
TFTs
conjugated and unconjugated bilirubin: look for biliary atresia
Direct antiglobulin test (Coombs’ test)

Blood film

71
Q

What can cause prolonged jaundice (over 14 days)?

A

prematurity ( immature liver function)

congenital infections e.g. CMV, toxoplasmosis

biliary atresia

breast milk jaundice (jaundice is more common in breastfed babies)

galactosaemia

hypothyroidism

UTI

72
Q

How can neonatal jaundice be managed?

A

Phototherapy is usually adequate to correct neonatal jaundice. Extremely high levels may require an exchange transfusion.

73
Q

Kawasaki disease is a type of vasculitis which is predominately seen in children.

How does it present?
Major complication?

A

high-grade fever which lasts for > 5 days
conjunctival injection
bright red, cracked lips
strawberry tongue
cervical lymphadenopathy
red palms of the hands and the soles of the feet which later peel

complication : coronary artery aneurysm

74
Q

How can Kawasaki disease be investigated?

A

FBC: anaemia, leukocytosis and thrombocytosis
LFTs: hypoalbuminemia and elevated liver enzymes
Inflammatory markers (particularly ESR) are raised
Urinalysis can show raised WCC
Echocardiogram can demonstrate coronary artery pathology

75
Q

How can Kawasaki disease be managed?

A

High dose aspirin to reduce the risk of thrombosis
IV immunoglobulins to reduce the risk of coronary artery aneurysms

76
Q

What is Laryngomalacia?

A

seen in infants - the supraglottic larynx is structured in a way that allows it to cause partial airway obstruction. This leads to a chronic stridor on inhalation, when the larynx flops across the airway as the infant breathes in

may resolve on its own or rarely requires tracheostomy

77
Q

How should nappy rash be managed?

A

disposable nappies are preferable to towel nappies
expose 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

78
Q

Necrotising enterocolitis is one of the leading causes of death in premature infants. Initial symptoms can include feeding intolerance, abdominal distension and bloody stools.

How can it be investigated?

A

abdo x-ray

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)

79
Q

How does neonatal sepsis present?
What causes it?

A

Grunting and other signs of respiratory distress are the most common presentation

Early-onset neonatal sepsis is most commonly caused by group B streptococcus

Late- onset can be caused by Staphylococcus epidermidis, Pseudomonas aeruginosa, Klebsiella and Enterobacter

80
Q

How should neonatal sepsis be investigated and managed?

A

Ix:

  • Urine MCS
  • FBC, CRP
  • Blood culture
  • Blood gases: metabolic acidosis is particularly concerning for neonatal sepsis, particularly a base deficit of ≥10 mmol/L
  • LP

Mx:
IV benzylpenicillin with gentamicin

81
Q

How does pyloric stenosis present?
Ix? Mx?

A

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)

82
Q

How does intestinal malrotation present? Ix? Mx?

A

High caecum at the midline
bilious vomiting and obstruction (volvulus)

Ix: upper GI contrast study and USS
Mx: laparotomy, if volvulus is present (or at high risk of occurring) then a Ladd’s procedure is performed

83
Q

How does Slipped upper femoral epiphysis present? Mx?

A

typically obese male adolescents
pain is often referred to the knee
limitation to internal rotation

Bed rest and non-weight bearing
internal fixation: typically a single cannulated screw placed in the centre of the epiphysis

84
Q

What is Perthe’s disease? Presenting features?

A

degenerative condition affecting the hip joints of children (typically 4-8 years) , due to avascular necrosis of the femoral head

hip pain: develops progressively over a few weeks
limp
stiffness and reduced range of hip movement
x-ray: early changes include widening of joint space, later changes include decreased femoral head size/flattening

85
Q

Complications of Perthe’s disease?

A

osteoarthritis
premature fusion of the growth plates

86
Q

How should Perthe’s disease be managed ?

A

To keep the femoral head within the acetabulum: cast, braces
If less than 6 years: observation
Older: surgical management with moderate results
Operate on severe deformities

87
Q

Spot diagnosis:
Softening of the cartilage of the patella
Common in teenage girls
Characteristically anterior knee pain on walking up and down stairs and rising from prolonged sitting
Usually responds to physiotherapy

A

Chondromalacia patellae

88
Q

Spot diagnosis:
Pain, tenderness and swelling over the tibial tubercle
Seen in sporty teenagers

A

Osgood-Schlatter disease
(tibial apophysitis)

89
Q

What can cause a napkin (nappy) rash?

A

Irritant dermatitis
most common cause, irritant effect of urinary ammonia and faeces, creases are characteristically spared

Candida dermatitis
erythematous rash which involve the flexures and has characteristic satellite lesions

Seborrhoeic dermatitis
erythematous rash with flakes, may be coexistent scalp rash

Psoriasis
erythematous scaly rash also present elsewhere on the skin

Atopic eczema
Other areas of the skin will also be affected

90
Q

Complications of measles?

A

otitis media: the most common complication
pneumonia: the most common cause of death
encephalitis: typically occurs 1-2 weeks following the onset of the illness)

91
Q

How can measles be investigated and managed?

A

Ix: IgM antibodies
Mx: mainly supportive
notifiable disease → inform public health

92
Q

What features does measles present with?

A

prodromal phase:
irritable, conjunctivitis, fever

Koplik spots:
typically develop before the rash
white spots (‘grain of salt’) on the buccal mucosa

rash:
starts behind ears then to the whole body
discrete maculopapular rash becoming blotchy & confluent
desquamation that spares the palms and soles may occur after a week

93
Q

What organism causes measles? What is the incubation period?

A

RNA paramyxovirus

infective from prodrome until 4 days after rash starts
incubation period = 10-14 days

94
Q

How should a non-immunised child be managed if they come into contact with measles?

A

MMR within 72 hours

95
Q

Contraindications to lumbar puncture in children with suspected meningitis?

A

Any signs of raised ICP:
focal neurological signs
papilloedema
significant bulging of the fontanelle
DIC
signs of cerebral herniation

meningococcal septicaemia:blood cultures and PCR for meningococcus instead

96
Q

What are the potential complications of mumps?

A

orchitis - occurs four or five days after the start of parotitis
hearing loss - usually unilateral and transient
meningoencephalitis
pancreatitis

97
Q

How can mumps be investigated and managed?

A

Ix:
PCR testing on a saliva swab. The blood or saliva can also be tested for antibodies to the mumps virus

Mx:
rest
paracetamol for high fever/discomfort
notifiable disease

98
Q

What clinical features does mumps typically present with?

A

fever
malaise, muscular pain
parotitis (‘earache’, ‘pain on eating’): unilateral initially then becomes bilateral in 70%

99
Q

Mumps is a caused by RNA paramyxovirus and tends to occur in winter and spring. What is the incubation period?

A

14-21 days