Paediatrics (1) Flashcards
Aetiology of pneumonia in children
<5YO = viruses (most common = RSV)
>5YO = Mycoplasma pneumoniae/ Strep. pneumoniae/ Chlamydia pneumoniae
Clinical presentation on pneumonia in children
Fever, cough, rapid breathing (usually preceded by URTI)
Other: nasal flaring, chest indrawing, poor feeding, ‘unwell’ child
Management of pneumonia children
Supportive - oxygen, analgesia, IV fluids
Admission criteria: O2<92%, recurrent apnoea, inability to maintain to adequate fluid/ feed
Medical - oral amoxicillin (consider erythromycin if >5YO)
Why might you admit a child with pneumonia to hospital?
Admission criteria: O2<92%, recurrent apnoea, inability to maintain to adequate fluid/ feed
What is croup?
viral laryngotracheal infection characterised by barking cough + acute stridor, most common in infants (6 months - 3YO) in winter
Most common age for croup in children
6 months to 3YO
Most common aetiology of croup
Parainfluenzae = most common
Clinical presentation of croup
Upper resp symptoms (e.g. runny nose), fever, hoarseness, barking cough, inspiratory stridor
Mild = no stridor at rest, barking cough, mild work of breathing
Moderate = stridor at rest, mild work of breathing, no agitation
Severe = significant stridor at rest, severe respiratory distress, child = anxious/ pale/ tired
Investigations of suspected croup
Clinical Dx - Upper resp symptoms (e.g. runny nose), fever, hoarseness, barking cough, inspiratory stridor
CXR if unclear (steeple sign = indicative, subglottic tracheal narrowing)
What does the steeple sign on a CXR indicate?
Croup
Management of croup
Mild: oral dexamethasone (0.15mg/kg) + discharge with advice
Moderate: oral dexamethasone (0.15-0.3mg/kg) + observe for improvement/ discharge when stable
Severe: nebulised adrenaline, oxygen, oral OR IV/IM dexamethasone (0.3-0.6mg/kg) + monitoring
Assessing the severity of croup
Mild = no stridor at rest, barking cough, mild work of breathing
Moderate = stridor at rest, mild work of breathing, no agitation
Severe = significant stridor at rest, severe respiratory distress, child = anxious/ pale/ tired
Define asthma
chronic respiratory condition associated with airway inflammation + hyperresponsiveness, presents with multiple trigger wheeze
List potential triggers for asthma
Dust, excercise, cold, emotional upset, animal dander
Pathophysiology of asthma
Environmental triggers (e.g. cold air, dust, exercise, animal dander, emotional upset) + genetic predisposition + atopy → bronchial inflammation → bronchial hyperresponsiveness to inhaled stimuli → airway narrowing (reversible airflow obstruction) → symptoms
Clinical presentation of asthma
Multiple episodic wheeze associated with cough/ SOB/ chest tightness
Personal/ family Hx of atopic diseases
Diurnal variation (worse at night/ early in morning)
Positive response to asthma therapy
Diagnosis of asthma
Usually clinical.
Spirometry - reversible obstructive pattern (FEV1:FVC <70%)
Improvement of FEV1 by 12% or 200ml w/ bronchodilator
Improvement of FEV1 by 400ml w/ bronchodilator
PEFR - diurnal variation + reversible airflow obstruction
Other - skin prick test (suggest atopy), FeNo (>= 35ppb eosinophilic inflammation
Spirometry findings that are indicative of asthma
reversible obstructive pattern (FEV1:FVC <70%)
Improvement of FEV1 by 12% or 200ml w/ bronchodilator
Improvement of FEV1 by 400ml w/ bronchodilator
Management of chronic asthma
PRN SABA (salbutamol OR ipratropium bromide) → + ICS (e.g. beclomethasone/ budesonide) → + LABA (salmeterol)/ LTRA (Montelukast)
Severity of asthma attacks
Moderate - able to talk, O2 sat>92%, peak flow >50% [best]
Severe - too SOB to talk, O2 sat <92% (if <12YO), peak flow 33-50% [best]
Life-threatening - silent chest, cyanosis, poor respiratory effort, exhaustion, altered consciousness, peak flow <33% [best], O2 sat <92% (all ages)
Features of a life-threatening asthma attack
silent chest, cyanosis, poor respiratory effort, exhaustion, altered consciousness, peak flow <33% [best], O2 sat <92% (all ages)
Management of a life-threatening asthma attack
high flow oxygen + SABA nebulised + oral prednisolone/ IV hydrocortisone + nebulised ipratropium
Management of a moderate asthma attack
Moderate: SABA via spacer (2-4 puffs, increase by 2 puffs every 2 mins until 10 puffs) +/- oral prednisolone (1-2mg/kg, max 40mg)
Define bronchiolitis
mucosal inflammation + swelling of bronchioles, usually caused by an acute viral illness (RSV = 80%), peak incidence at 3-6 months in winter
Most common cause of bronchiolitis
Acute viral illness - RSV = 80%
Risk factors for bronchiolitis
Chronic lung disease, congenital heart disease, prematurity, Down’s syndrome, CF, neuromuscular disease
Clinical presentation of Bronchiolitis
Coryzal symptoms → dry wheezy cough + increased SOB (often associated with feeding)
Clinical signs: hyperinflation of the chest, subcostal + intercostal recession, fine-end inspiratory crackles, prolonged expiratory/ wheeze (expiratory»_space; inspiratory)
Diagnoses of bronchiolitis
Clinical. Coryzal symptoms for 3 days followed by cough/ tachypnoea/ wheeze/ crackles.
Management of bronchiolitis
Supportive (majority): monitor for apnoea, fluid support (oral/ NG/ IV), high flow oxygen/ CPAP
Admission criteria: O2<92%, poor feeding, persistent respiratory distress, social concern
Why might a child with bronchiolitis be admitted to hospital?
Admission criteria: O2<92%, poor feeding, persistent respiratory distress, social concern
What is cystic fibrosis?
autosomal recessive condition caused by a defective protein (CFTR) leading to a multisystem disorder characterised by thickened secretion + recurrent respiratory infections
Clinical presentation of CF
Neonatal screening - heel prick test + confirm w/ sweat test
Neonate w/ meconium ileus - in utero bowel obstruction (CP = vomiting, distent Abdomen, failure to pass meconium
Child w/ persistent ‘wet’ cough + recurrent respiratory infections
Other: pancreatic insufficiency (malabsorption, faltering growth, steatorrhoea, DM), nasal polyps, sinusitis, rectal prolapse, finger clubbing
Abnormal sweat test results
Cl concentration = 60-125mmol/L
Indicative of CF
Diagnoses of CF
2 +ve sweat tests + suggestive clinical assessment
How does heel prick screening test identify CF?
detects raised immunoreactive trypsinogen in neonates, +ve screening → screened for common CF gene mutations, 2 mutation → sweat test to confirm Dx
Management of CF
Rep: physiotherapy, mucolytics (hypertonic saline/ dornase alfa), prophylactic abx/ abx for for acute exacerbations
Nutrition: pancreatic enzyme supplementation (Creon)
Lung/ liver transplant: end stage organ failure
What is acute epiglottitis?
intense swelling of the epiglottis and surrounding tissues associated with septicaemia, life-threatening due to the risk of respiratory obstruction
Most common causative organism of acute epiglottitis
Haemophilus influenzae type b (Hib)
Clinical presentation of acute epiglottitis
Acute onset: high-grade fever, very ill child, drooling, muffled voice, inspiratory stridor, respiratory distress
TRIPOD POSITION
Cough minimal/ absent
Caution for investigating epiglottitis
Avoid assessment unless the airway is stable
First-line = laryngoscopy in controlled setting (second line = lateral neck radiograph)
Management of acute epiglottitis
Priority = secure airway
Other: nebulised adrenaline, high-flow oxygen, IV antibiotics (ceftriaxone), corticosteroids (dexamethasone), fluid replacement, analgesia
What is acute otitis media (AOM)?
infection of the middle ear that presents over days to weeks and is characterised by severe ear pain + visible inflammation of the tympanic membrane, peak incidence at 6-15 months
Aetiology of acute otitis media
S. pneumoniae = most common. Other bacterial = H. influenzae. Other viral = RSV.
Clinical presentation of otitis media
Ear pain, malaise, fever, coryzal symptoms lasting a few days
Otoscopy: erythematous tympanic membrane, potentially bulging/ perforated (small tear w/ purulent discharge in auditory canal)
Otoscopy findings for acute otitis media
Otoscopy: erythematous tympanic membrane, potentially bulging/ perforated (small tear w/ purulent discharge in auditory canal)
Management of acute otitis media
Majority resolve spontaneously within 24hrs - simple analgesia
Abx = systemically unwell, unwell for 4 days, discharge from ear, <2YO w/ bilateral infection
Complication of acute otitis media
Mastoiditis - infection spreads from middle ear to mastoid air cells → sub-periostal abscess behind ear → tenderness/ swelling behind + pushing forward of pinna AND neurological complications
Mx - IV abx (high-dose co-amoxiclav/ ceftriaxone)
Can lead to facial nerve palsy/ hearing loss
What is glue ear?
Otitis Media Effusion (OME) - build up of viscous inflammatory fluid within the middle ear → conductive hearing loss
Risk factors for glue ear
Bottle fed, paternal smoking, atopy, genetic disorders (Down’s syndrome, CF)
Clinical presentation + examination findings of glue ear
Difficulty hearing, pressure sensation, popping/ crackling in era
O/E: dull tympanic membrane, lost light reflexes
Management of glue ear
Monitoring (50% resolve within 3 months)
Non-surgical: hearing aids
Surgical: myringotomy + grommet insertion
What is a grommet?
tiny tubes inserted into tympanic membrane to allow fluid from the middle ear to drain out through membrane into ear canal, fall out within a year, ⅓ of patients require further grommet insertion
Insert if (NICE guidelines): > 3 months bilateral OME + hearing level in better ear <25-30dB
Criteria for inserting a grommet (NICE guidelines)
> 3 months bilateral OME + hearing level in better ear <25-30dB
Types of hearing loss
Sensorineural: caused by lesion on cochlear/ auditory nerve, usually present at birth and doesn’t improve, Mx: amplification/ cochlear implant
Conductive: caused by abnormalities in ear canal/ middle ear, intermittent/ may resolve, Mx: conservative/ amplification/ surgery
Aetiology of sensorineural hearing loss
genetic (majority), congenital infection, preterm baby, postnatal meningitis/ encephalitis
Aetiology of conductive hearing loss
OME (60%), eustachian tube defect (Down’s syndrome, cleft palate), wax (rare)
Investigating hearing loss
Objective (neonates/ infants) - e.g. otoacoustic emission (OAE) - part of newborn screening programme, identify moderate-profound deafness at birth (>40dB), misses mild losses
Subjective (behavioural) - e.g. Distraction Test - performed at 6-18 months, tests whether infant tries to turn/ find sound
What is moderate hearing loss?
Mild (20-40-dB) - may use hearing aids, struggle with background noise/ whispered conversation
Moderate (41-70-dB) - hearing aids, difficulty in a group/ background noise even with hearing aids
Severe (71-95-dB) - hearing aids w/ communication aids, without unable to hear speech
Profound (>95-dB) - hearing aids/ cochlear implant, without unable to hear speech/ most environmental sound
What is profound hearing loss?
Mild (20-40-dB) - may use hearing aids, struggle with background noise/ whispered conversation
Moderate (41-70-dB) - hearing aids, difficulty in a group/ background noise even with hearing aids
Severe (71-95-dB) - hearing aids w/ communication aids, without unable to hear speech
Profound (>95-dB) - hearing aids/ cochlear implant, without unable to hear speech/ most environmental sound
What is periorbital cellulitis?
infection of the periorbital soft tissue characterised by erythema + oedema, can lead to vision loss + life-threatening consequences
Staphylococcus aureus = most common (prev. Hib before immunisation)
Clinical presentation of periorbital cellulitis
Acute onset pain + swelling in the periorbital region +/- Hx of recent URTI/ trauma
Features of meningism on examination indicates intracranial spread of infection
Imaging for periorbital cellulitis
CT head - assess complications (e.g. abscess formation/ cavernous sinus thrombosis)
Management of periorbital cellulitis
IV abx + appropriate analgesia
Surgical drainage of subperiosteal + orbital abscesses
What is Starbismus?
Squint. When the eyes misaligned when focusing on an object can be occasional (phoria) or constant (tropia), often onset in childhood
Aetiology of squint
Primary - idiopathic/ congenital
Secondary - cranial nerve palsies, intracranial infection, intracranial/ intraorbital/ intraocular masses
Sequelae of squint
amblyopia (lazy eye) - brain unable to process input from one eye so favours the other leading to structural changes in visual pathway and cortex → decreased vision in an eye that’s otherwise normal
What is amblyopia?
Lazy eye.
brain unable to process input from one eye so favours the other leading to structural changes in visual pathway and cortex → decreased vision in an eye that’s otherwise normal
Why is it important to assess and treat squints early in life?
Need to start treatment <8YO (visual fields still developing). Delay = increased risk of permanent squint.
Occlusive patch - cover good eye and force weaker eye to develop
Types of squint
Esotropia/ phoria - inward deviation
Exotropia/ phoria - outward deviation
Hypertropia/ phoria - upward deviation
Hypotropia/ phoria - downward deviation
Clinical examination of potential squint
light reflex test (Hirschberg test), Bruckner test, cover test, cover-uncover test
What is Kawasaki’s disease?
Small/ medium vessel vasculitis, most common in children < 5YO, characterised by fever > 5 days + CREAM presentation
Clinical presentation of Kawasaki’s
Fever > 5 days + CREAM: conjunctivitis, rash (erythematous, maculopapular), edema (hands/ feet), adenopathy (cervical lymphadenopathy), mucous membrane changes (strawberry tongue, cracked/ red lips)
Investigations for Kawasaki’s
Echocardiogram/ ECG - identify/ monitor cardiovascular complications that often arise from 3rd week to 2nd month post-infection
Complications of Kawasaki disease
Gallop rhythm, myocarditis/ pericarditis, coronary artery aneurysms
Management of Kawasaki disease
IV immunoglobulins
High-dose aspirin
Why is aspirin usually avoided in children?
Reye’s syndrome - severe progressive encephalopathy affecting children that is accompanied by fatty infiltration of liver/ kidneys/ pancreas. Mx = supportive.
Causative organism of measles
RNA paramyxovirus
Clinical presentation of measles
Fever, cough, runny nose, conjunctivitis, marked malaise with specific features:
Koplik’s spots (white spots on buccal mucosa)
Rash (spreads downwards from behind ears to whole of body, initially maculopapular → blotchy + confluent)
What are Koplik spots?
White spots on buccal mucosa that are associated with measles.
Epidemiology of Kawasaki’s disease
Children (<5YO) of Japanese or black-Caribbean ethnicity
Management of measles
Advice (drink water, rest, simple analgesia) - usually self-limiting within a week
Stay away from at risk groups for 4 days after initially developing rash (at risk = pregnant women, immunocompromised, infants, un-vaccinated)I
Isolation of children with measles
4 days after onset of rash
Isolation of children with chicken pox
Until all lesions have crusted over (usually 5 days from onset of rash)
Isolation of children with Rubella
5 days from onset of rash
Complications of Measles
Resp - pneumonia 2ry bacterial infection/ otitis media, tracheitis
Neuro - febrile convulsions, EEG abnormalities, encephalitis
Other - diarrhoea, hepatitis, appendicitis, corneal ulceration, myocarditis
Chicken pox vs. shingles
Chicken pox = primary infection caused by varicella zoster virus + characterised by a very itch vesicular rash
Shingles = reactivation of dormant virus in dorsal root ganglia
Causative organism of chickenpox
Varicella zoster virus
Clinical presentation of chicken pox
Advice (fluid intake, smooth/ cotton fabrics)
Symptomatic Mx - paracetamol, topical calamine lotion (alleviate itch), chlorphenamine (avoid in pregnant/ breastfeeding women)
Complications of chicken pox
Secondary bacterial infection of the lesions
Disseminated disease in immunocompromised: give high-risk individuals Human varicella zoster immunoglobulin (VZIG) following contact
(If chickenpox develops, consider IV acyclovir)
Why might human varicella zoster immunoglobulins (VZIGs) be given to someone?
High-risk immunosuppressed individual following contact with chickenpox.
When is chickenpox the most infective?
1-2 days before onset of rash
Chickenpox rash description
Very itchy vesicular rash
Starts on head (check scalp) + trunk, progress to peripheries
What is rubella?
Viral infection caused by togavirus + spread via direct contact, maternal infection in non-immune women can cause some serious complications
Clinical presentation of rubella
Mild - fever, maculopapular rash initially on face then spread to whole of body (fades in 3-5 days)
Suboccipital and postauricular lymphadenopathy
NOT ITCHY
Complications of rubella
Arthritis, thrombocytopenia, encephalitis, myocarditis
What is congenital rubella syndrome?
Complications of rubella caused when a non-immune women is infected during her 1st trimester
Teratogenesis, sensorineural deafness, congenital cataracts, congenital heart disease, cerebral palsy, microcephaly
Features of congenital rubella syndrome
Teratogenesis, sensorineural deafness, congenital cataracts, congenital heart disease, cerebral palsy, microcephaly
Is Rubella a notifiable disease?
Yes. Alter local health protection unit
Why should pregnant women not be offered the MMR vaccine?
Risk of congenital rubella syndrome
Wait until they are post natal
Management of rubella
Supportive. Notifiable disease (alert local health protection team, HPT)
5YO boy. Unsure about immunisations. 2wks ago had cough, coryza, conjunctivitis and fever. Now developed a maculopapular rash that’s started down from his hairline and spread downwards. What’s your top differential?
Measles
6YO boy. Unsure of immunisation Hx. Come to paeds A&E in winter time. Had mild fever 1wk ago. Now has maculopapular rash, starting on face and spread down whole body. You spot Forchheimer spots + posauricular lymphadenopathy. Top differential?
Rubella
A 3-year-old girl is brought into A&E following a 1 week history of fever, lethargy and irritability. Her symptoms came on suddenly and despite being given paracetamol and ibuprofen she remains pyrexic. She has a reduced appetite and earlier this morning a widespread red rash appeared on her trunk. Examination reveals a widespread maculopapular rash, cervical lymph node enlargement, a swollen, bright red tongue and conjunctivitis. She is tachycardic and has a temperature of 39.2ºC.
Given the likely diagnosis, what is the most important investigation in this child?
Echocardiogram - coronary artery aneurysms are a complication of Kawasaki disease. This should be screened for with an echocardiogram.
A 6-year-old boy presents with a 3-day history of fever, sore throat, rash and enlarged lymph nodes behind his ears and back of his neck. He has an red, maculopapular rash on his face and neck that has started spreading down his body. He has not received any routine childhood immunisations.
Given the most likely diagnosis, what is the most appropriate school exclusion criteria?
Top differential = rubella - fever, mild coryzal, characteristic rash + lymphadenopathy
Exclusion criteria = children do not return to school for 5 days from the onset of the rash.
What is diptheria?
Infection caused by Corynebacterium. Part of 1 in 5 vaccine giiven at 2, 3, 4 months.
Eradicated in the UK
Clinical presentation of Diptheria
CP: thick white membrane over posterior pharynx in an unvaccinated child
Causes local disease (membrane formation affecting nose/ pharynx/ larynx) OR systemic disease (e.g. myocarditis/ neurological manifestations)
What is scalded skin syndrome
staphylococcal toxin causes areas of epidermis to separate on gentle pressure (Nikolsky sign) leaving denuded areas of skin, rare but serious
Clinical presentation of Scalded skin syndrome
Fever, malaise followed by… generalised patches of erythema → bullae (fluid-filled blisters) → bullae burst leaving tender erythematous skin similar to burn
Most fully recover with no scarring
Management of scalded skin syndrome
IV anti-staphylococcal antibiotics + analgesia + monitor fluid balance (prone to dehydration)
Causative organism of whooping cough
bordatella pertussis (gram -ve bacteria)
What is whooping cough
respiratory infection caused by bordatella pertussis (gram -ve bacteria), characterised by paroxysmal cough followed by inspiratory whoop + vomiting, notifiable disease
Clinical presentation of whooping cough
Catarrhal phase: wk of coryza (runny dose, sore throat, conjunctivitis, malaise)
Paroxysmal phase: severe dry cough followed by an inspiratory whoop, often culminates in vomiting
Management of whooping cough
Vaccination @ 8,12,16wks
Low threshold for hospital admission + macrolide abx (erythromycin/ azithromycin/ clarithromycin) if cough onset < 21 days + supportive care (rest, hydration, analgesics, antipyretics)
Stay at home until 48hrs after abxs started (or 21 days after symptoms started)
Diagnosis of whooping cough
Culture of per-nasal swab
Marked lymphocytosis on blood film
Exclusion period for whooping cough
Stay at home until 48hrs after abxs started (or 21 days after symptoms started)
Complications of whooping cough
Secondary pneumonia, apnoea, cerebral hypoxia, dehydration, weight loss, rectal prolapse, hernias, rib #s, pneumonthorax
Less serious: epistaxis, subconjunctival haemorrhage, otitis media
What is polio?
vaccination given as part of ‘5 in 1’ vaccine at 2,3, and 4 months of age, almost eradicated worldwide, complication = paralytic polio
Clinical presentation of polio
Children <5YO, most cases asymptomatic/ mild
Paralytic polio - CP: headache, vomiting, stiffness of neck, pain in limbs, paralysis within hrs, fatal when respiratory muscles become immobilised
CXR changes seen in tuberculosis
Ghon complex
Lung collapse
Pleural effusion
Investigations for diagnosing TB
Sputum culture = gold-standard
Sputum smear
Mantoux test - 0.1 ml of 1:1,000 purified protein derivative (PPD) injected intradermally, result read 2-3 days later
CXR
Clinical features
Why might you not use Mantoux testing for suspected TB in children < 6 months?
Young age (< 6 months) can cause false negatives
Clinical presentation of TB
Primary infection (fever, anorexia, weight loss, CXR changes) → Dormancy → Reactivation (most commonly = tuberculosis meningitis)
Management of TB
RIPE - rifampicin, isoniazid, pyrazinamide, ethambutol
What is the main route of HIV infection for children?
Mother-to-child transmission during pregnancy/ breastfeeding
(<1% MTCT w/ antenatal + labour/ delivery management)
Clinical presentation of HIV in children
Child asymptomatic for years before progressing to clinical disease:
persistent lymphadenopathy
Hepatosplenomegaly
recurrent fever
parotid swelling
SPUR infections
Diagnosis of HIV in children
<18 months - transplacental maternal IgG HIV antibodies (confirm exposure not infection)/ HIV DNA PCR (evidence of infection)
> 18 months - antibody tests
Management of HIV
Antiretroviral therapy (ART) + prophylaxis against Pneumocystis jiroveci pneumonia (PCP)
What is meningitis?
inflammation of the meninges covering the brain, confirm by finding WBCs in CSF, viral causes = most common (self-resolving)
Bacterial aetiology of meningitis in neonates/ up to 3 months
Group B Strep. = most common
Other = E. coli, Listeria monocytogenes
Bacterial aetiology of meningitis in children 1 month = 6YO
Neisseria meningitidis, Strep. pneumoniae, Haemophilus influenzae
Bacterial aetiology of meningitis in children > 6YO
Neisseria meningitidis, Strep. pneumoniae
Clinical presentation of Meningitis
Febrile children w/ non-blanching purpuric rash + features:
Brudzinski sign (flexion of neck w/ child supine causes flexion of knees + hips)
Kernig sign (child supine with knees + hips flexed. Back pain on extension of the knee)
Altered mental state
< 12 months: non-specific (fever, poor feeding, vomiting, irritability, lethargy, drowsiness, seizures, reduced consciousness)
later signs: bulging fontanelle, neck stiffness, arched back
What is the Brudzinski sign? What disease is it associated with?
Seen in meningitis
(flexion of neck w/ child supine causes flexion of knees + hips)
What is the Kernig sign? What disease is it associated with?
Seen in meningitis
(child supine with knees + hips flexed. Back pain on extension of the knee)
Later signs of meningitis in children < 12 months
Bulging fontanelle, neck stiffness, arched back
Management of viral meningitis
mostly self-limiting + improve over 7-14 days, consider acyclovir if meningitis secondary to HSV
Changes in CSF in meningitis
Bacterial: turbid appearance, raised polymorphs/ protein, low glucocse
Viral: clear appearance, raised lymphocytes, normal/ raised protein, normal/ low glucose
Tuberculosis: turbid/ clear/ viscous, raised lymphocytes, raised protein, low glucose
Management of meningitis
Abx + steroids if > 3 months (dexamethasone) + fluids + cerebral monitoring + public health notification
< 3 months = IV amoxicillin + IV cefotaxime
> 3 months = IV cefotaxime
Abx prophylaxis for contacts (ciprofloxacin/ rifampicin)
Abx for bacterial meningitis in children < 3 months
IV amoxicillin + IV cefotaxime
Abx for bacterial meningitis in children > 3 months
IV cefotaxime
Abx for meningitis prophylaxis in contact
Ciprofloxacin + rifampicin
What is encephalitis
Inflammation of the brain substance, most commonly caused by invasion by neurotoxic virus e.g. HSV/ enteroviruses/ resp viruses (e.g. influenza)
Aetiologies of encephalitis
Direct invasion of the brain by a neurotoxic virus (e.g. HSV)
Delayed brain swelling following a dysregulated neuroimmunology response to an antigen, usually a virus (e.g. Post-chickenpox)
Slow virus infection e.g. HIV/ SSPE
Most common causes: enteroviruses, respiratory viruses (e.g. Influenza), and herpesviruses (e.g. HSV/ VSV)
Clinical presentation of encephalitis
fever, altered consciousness, seizures
((HSV encephalitis = headache, psychiatric symptoms, vomiting, focal features e.g. aphasia))
Management of encephalitis
High-dose IV acyclovir until HSV encephalitis can be ruled out
What is HSV encephalitis?
Encephalitis caused by HSV characteristically affects the temporal lobes, high mortality rate if untreated (80%)
CP = fever, headache, psychiatric symptoms, seizures, vomiting, focal features (e.g. aphasia)
Ix = CT (medial temporal + inferior frontal changes, normal in ⅓ of cases)
Mx = IV acyclovir
Management of HSV encephalitis
IV acyclovir
CT findings in HSV encephalitis
medial temporal + inferior frontal changes
normal in 1/3 of changes
7 YO boy presents to A&E and is feeling unwell + lethargic, non-blanching rash on torso, responsive to pain. Chest clear, HS normal, abdo SNT. Temp 39, RR 38, HR 142, Sp02 88% OA, CRT 5s.
What is the most likely diagnosis?
Child in a febrile state w/ purpric rash = meningococcal septicaemia
Meningococcal septicaemia clinical presentation
Child in a febrile state (inadequacy of circulation to meet tissue demands leading to end-organ damage)
W/ purpuric rash
What is slapped cheek syndrome?
most common presentation of Parvovirus B18 infection, characteristic erythematous rash on cheek, can cause aplastic crisis in high-risk groups
What causes slapped cheek syndrome?
Parvovirus B18 infection
Clinical presentation of Parvovirus B18 infections
Viraemic phase of fever, malaise, headache → rash 1wk later (maculopapular, lace-like, trunk/ limbs/ cheek) - Slapped cheek syndrome
Other presentations: asymptomatic, aplastic crisis (in immunocompromised/ ppl with thalassemias + sickle cell), foetal hydrops
What infection can cause an aplastic crisis in immunocompromised people/ people with haemolytic anaemias + sickle cell disease?
Parvovirus B18
Management of slapped cheek syndrome
Supportive (fluid/ analgesia) as symptoms fade over 1-2wks
Further investigations in high-risk groups
What is impetigo?
localised + highly contagious staph/ strep infections, most common in infants/ young children (associated w/ pre-existing eczema)
Aetiology of impetigo
Staph/ strep infection
Clinical presentation of impetigo
Erythematous macules (face/neck/hands) → rupture → honey coloured crusting.
Rapidly spread to other parts of body (auto-inoculate, nasal carriage common)
Itching/ mild discomfort. No systemic features.
Management of impetigo
Systemically well = hydrogen peroxide 1% cream
Topical abx = fusidic acid 2% cream (Mupirocin if MRSA/ resistance to fusidic acid)
Widespread = oral flucloxacillin (clarithromycin/ azithromycin if penicillin allergy)
Exclude from school until lesions crusted OR 48hrs after commencing abx
Exclusion criteria for impetigo
Exclude from school until lesions crusted OR 48hrs after commencing abx
What is toxic shock syndrome?
triad = high fever/ hypotension/ diffuse erythematous maculopapular rash caused by toxins from Staph. aureus/ group A strep, medical emergency
Aetiology of Toxic Shock Syndrome
toxins from Staph. aureus/ group A strep
Clinical presentation of toxic shock syndrome
Triad = high fever, hypotension, diffuse erythematous maculopapular rash (desquamation after 1-2wks)
Organ dysfunction = liver/ renal impairment, vomiting + diarrhoea, mucositis, altered consciousness
Management of toxic shock syndrome
IV fluids + IV abx (ceftriaxone + clindamycin for 10 days)
What is scarlet fever?
notifiable disease, caused by a reaction to erythrogenic toxins produced by Group A haemolytic streptococci, peak incidence 2-6YO
Aetiology of scarlet fever
Reaction to erythrogenic toxins produced by Group A haemolytic streptococci
Clinical presentation of scarlet fever
Distinct ‘sandpaper’ like rash, fever, vomiting, abdo pain, strawberry tongue.
Appears on torso, spreads onto palms/ soles
Management of scarlet fever
Oral penicillin V for 10 days (azithromycin if allergic)
Return to school 24hrs after abx
Exclusion policy for scarlet fever
Return to school 24hrs after abx
Complications of scarlet fever
Otitis media = most common, rheumatic fever, acute glomerulonephritis
4YO girl presents with 3 days Hx of fever, vomiting, abdominal pain. Diffuse rash in neck/ chest areas with pallor around the lips. Rash has spread to flexor creases. Mum notes its very rough to touch. Exudate on tonsils. Strawberry tongue.
What is the most likely diagnosis?
Scarlet fever
Clinical presentation of candida infection
Skin - erythematous w/ large macules, ooze clear fluid, itching/ burning in skin folds
Oral - white coating on tongue/ top of mouth
Management of candida infection
Skin - topical clotrimazole/ miconazole (+ hydrocortisone cream for inflammation/ itch)
Oral - topical miconazole gel = first-line, oral nystatin = alternative
Difference between candida infection + nappy rash
Candida infection: large red macules + rash extending beyond areas of exposure to skin creases + groin
What is Coxsackie’s?
acute viral infection caused by Coxsackie A16 or Enterovirus 71 viruses, characterised by blister-like vesicular eruptions on hands/ feet/ mouth, usually mild + self-limiting
Clinical presentation of Coxsackie’s
Mild systemic upset (sore throat, fever, malaise, cough, abdo pain)
Oral ulcers
Macules/ papules of hands + feet develop soon after oral lesions
Management of Coxsackie’s
Symptomatic (advice RE: hydration analgesia), no exclusion from school
Exclusion of policy for Coxsackies’
no exclusion from school
When should immunodeficiency be considered in children?
SPUR infections - extensive candidiasis, severe/ long-lasting warts, atypical infections (opportunistic pathogens, unusually severe/ chronic, fail regular Tx)
Most common cause of primary immunodeficiency in children
selective IgA deficiency
CP = asymptomatic w/ recurrent ear/ sinus/ pulmonary infections, Mx = immunoglobulin therapy, long-term = stem cell transplant
What is selective IgA deficiency?
most common cause of primary immunodeficiency in children
CP = asymptomatic w/ recurrent ear/ sinus/ pulmonary infections
Mx = immunoglobulin therapy, long-term = stem cell transplant
Secondary causes of immunodeficiency
malignancy, malnutrition, HIV infection, immunosuppressive therapy, splenectomy
