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
How can you differentiate clinically between HSP and HUS?
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
26
How could you explore a non-blanching rash in a history?
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!!!
27
Biliary atresia presents in the first few weeks of life with what symptoms and signs ?
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
28
How should biliary atresia be investigated?
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
29
How can biliary atresia be managed? Complications?
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
30
What is Bronchiolitis? Offending pathogen? Presenting features?
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
31
In which patients is bronchiolitis more likely to be severe?
bronchopulmonary dysplasia (e.g. Premature), congenital heart disease or cystic fibrosis
32
How can bronchiolitis be investigated and managed?
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
33
Chickenpox is caused by primary infection with varicella zoster virus. How does it present?
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
34
How can chickenpox be managed?
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
35
Complications of chickenpox?
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
36
What are the causes of constipation in children?
Idiopathic - most common dehydration low-fibre diet medications: e.g. Opiates anal fissure over-enthusiastic potty training hypothyroidism Hirschsprung's disease hypercalcaemia learning disabilities
37
What red flags might suggest an underlying condition as opposed to idiopathic constipation?
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
38
Prior to starting treatment for constipation, the child needs to be assessed for faecal impaction. Factors which suggest faecal impaction include:
symptoms of severe constipation overflow soiling faecal mass palpable in the abdomen (digital rectal examination should only be carried out by a specialist)
39
How can children with constipation be managed?
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
40
How can constipation in an infant be managed?
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
Give some features of Cow's milk protein intolerance/allergy (CMPI/CMPA)
regurgitation and vomiting diarrhoea urticaria, atopic eczema 'colic' symptoms: irritability, crying wheeze, chronic cough rarely angioedema and anaphylaxis
42
How can cows milk allergy be investigated and managed?
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
What is Croup? What is the causative organism? What age group is most commonly affected?
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
Presenting features of croup?
stridor barking cough (worse at night) fever coryzal symptoms
45
How can croup be managed?
single dose of oral dexamethasone (0.15mg/kg) to all children regardless of severity high-flow oxygen nebulised adrenaline
46
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?
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
How is coeliac diagnosed?
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
What other conditions are associated with coealic disease?
Down's syndrome autoimmune thyroid disease IDDM
49
Complications of coeliac disease?
Nutritional deficiencies Anaemia Osteoporosis Hyposplenism Ulcerative jejunitis Enteropathy-associated T-cell lymphoma (EATL) Non-Hodgkin lymphoma Small bowel adenocarcinoma
50
Give some signs of respiratory distress in a child
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
What is palivizumab?
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
Most common cause of gastroenteritis in the UK?
rotavirus
53
What is the usual course of D&V in kids?
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
What are signs of clinical dehydration in children who have had prolonged D&V?
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
What are signs of shock in children who have had prolonged D&V?
Decreased level of consciousness Cold extremities Pale or mottled skin Tachycardia Tachypnoea Weak peripheral pulses Prolonged capillary refill time Hypotension
56
Features suggestive of hypernatraemic dehydration:
jittery movements increased muscle tone hyperreflexia convulsions drowsiness or coma
57
When should you do a stool culture in children with diarrhoea?
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
How should you manage children with D&V who are becoming dehydrated?
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
Causes of chronic diarrhoea in 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
60
How can you explain toddler's diarrhoea to a parent? What management would you suggest?
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
What is the commonest cause of vomiting in infancy?
Gastro-oesophageal reflux
62
Infant < 8 weeks, presents with milky vomits after feeds, often after being laid flat, excessive crying -->
?GORD
63
How should GORD be managed in infants?
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
Complications of GORD in infants?
distress failure to thrive aspiration frequent otitis media in older children dental erosion may occur
65
What organism causes Hand Foot and Mouth Disease? Clinical features? Mx?
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
Most common cause of primary headache in children?
Migraine without aura
67
Mx of paediatric migraine?
ibuprofen triptans may be used in children >= 12 years but follow-up is required
68
What is Intussusception? What features does it present with?
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
How should intussuception be investigated and managed?
Ix: USS: target like mass Mx: reduction by air insufflation under radiological control , peritonitis = surgery
70
What should be done if there are still signs of neonatal jaundice after 14 days ?
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
What can cause prolonged jaundice (over 14 days)?
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
How can neonatal jaundice be managed?
Phototherapy is usually adequate to correct neonatal jaundice. Extremely high levels may require an exchange transfusion.
73
Kawasaki disease is a type of vasculitis which is predominately seen in children. How does it present? Major complication?
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
How can Kawasaki disease be investigated?
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
How can Kawasaki disease be managed?
High dose aspirin to reduce the risk of thrombosis IV immunoglobulins to reduce the risk of coronary artery aneurysms
76
What is Laryngomalacia?
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
How should nappy rash be managed?
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
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?
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
How does neonatal sepsis present? What causes it?
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
How should neonatal sepsis be investigated and managed?
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
How does pyloric stenosis present? Ix? Mx?
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
How does intestinal malrotation present? Ix? Mx?
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
How does Slipped upper femoral epiphysis present? Mx?
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
What is Perthe's disease? Presenting features?
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
Complications of Perthe's disease?
osteoarthritis premature fusion of the growth plates
86
How should Perthe's disease be managed ?
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
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
Chondromalacia patellae
88
Spot diagnosis: Pain, tenderness and swelling over the tibial tubercle Seen in sporty teenagers
Osgood-Schlatter disease (tibial apophysitis)
89
What can cause a napkin (nappy) rash?
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
Complications of measles?
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
How can measles be investigated and managed?
Ix: IgM antibodies Mx: mainly supportive notifiable disease → inform public health
92
What features does measles present with?
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
What organism causes measles? What is the incubation period?
RNA paramyxovirus infective from prodrome until 4 days after rash starts incubation period = 10-14 days
94
How should a non-immunised child be managed if they come into contact with measles?
MMR within 72 hours
95
Contraindications to lumbar puncture in children with suspected meningitis?
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
What are the potential complications of mumps?
orchitis - occurs four or five days after the start of parotitis hearing loss - usually unilateral and transient meningoencephalitis pancreatitis
97
How can mumps be investigated and managed?
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
What clinical features does mumps typically present with?
fever malaise, muscular pain parotitis ('earache', 'pain on eating'): unilateral initially then becomes bilateral in 70%
99
Mumps is a caused by RNA paramyxovirus and tends to occur in winter and spring. What is the incubation period?
14-21 days