Paediatrics Pt. 2

Question 1

How do you measure body temperature when assessing a febrile child?

Answer 1

• < 4 weeks of age: electronic thermometer in the axilla
• 4+ weeks to 5 years: electronic or chemical dot thermometer in the axilla OR infrared tympanic thermometer
• A fever in a child is considered a temperature > 37.5 degrees
• NOTE: axillary measurements tend to underestimate body temperatures by around 0.5 degrees

Question 2

What are clinical features of neonatal sepsis?

Answer 2

• Fever or temperature instability
• Poor feeding
• Vomiting
• Apnoea and bradycardia
• Abdominal distension
• Respiratory distress
• Jaundice

Question 3

How does age affect when assessing a febrile child?

Answer 3

• They may be suffering from a bacterial infection that is not possible to identify on clinical examination
• During the first few months of life, infants are relatively protected from viral infection because of passive immunity
• Unless a clear cause of the fever is identified, neonates should undergo urgent investigation with a septic screen and broad-spectrum antibiotics given IMMEDIATELY

Question 4

What is a septic screen?

Answer 4

• Blood culture
• FBC including differential WCC
• Acute phase proteins (e.g. CRP)
• Urine sample
• If indicated:
  
  • CXR
  • LP
  • Rapid antigen screen on blood/CSF/urine
  • Meningococcal and pneumococcal PCR on blood/CSF
  • PCR for viruses in CSF (especially HSV and enteroviruses)

Question 5

What to consider when assessing a febrile child?

Answer 5

• Body temperature
• Age
• Septic Screen
• Risk factors for infection
• Red Flag Features
• Rash
• Focus for infection

Question 6

What are risk factors for infection in child?

Answer 6

• Fever > 38 degrees if < 3 months old
• Fever > 39 degrees if 3-6 months
• Colour - pale, mottled or cyanosed
• Reduced consciousness, neck stiffness, bulging fontanelle, status epilepticus, focal neurological signs, seizures
• Significant respiratory distress
• Bile-stained vomiting
• Severe dehydration or shock

Question 7

How should a febrile child be managed?

Answer 7

• Children who are NOT seriously ill can be managed at home with regular review by the parents as long as they are given clear instructions
• Children who are very unwell require admission to the paediatric assessment unit, A&E or children’s ward
• A septic screen should be requested
• Parenteral antibiotics should be given to seriously unwell children
  
  • < 1 month who has been discharged from hospital: 3rd generation cephalosporin (e.g. cefotaxime)
    
    • Often ampicillin is added to cover Listeria infection
  • 1+ months: high dose ceftriaxone
  • Aciclovir may be given is herpes simplex encephalitis is suspected

Question 8

What is the management of a febrile child? (NICE Guidelines)

Answer 8

• Assess for risk of serious underlying cause
• Paracetamol or ibuprofen if temperature > 38 degrees who are distressed or unwell
  
  • NOTE: do NOT give antipyretics if they are well or if you are trying to prevent a febrile convulsion
  • IMPORTANT: do NOT give both drugs simultaneously. You may switch from one to the other if the first is ineffective
• Advice for Parents
  
  • Look for signs of dehydration (poor urine output, dry mouth, sunken anterior fontanelle)
  • Offer regular fluids
  • Dress the child appropriately for their surroundings
  • Check the child regularly
  • Keep the child away from nursery or school whilst the fever persists and notify the nursery or school of the illness
  • SAFETYNET - seek help if:
    
    • Signs of dehydration
    • Seizure
    • Non-blanching rash
    • Fever lasts > 5 days
    • Child becoming generally unwell
    • Distressed or concerned that they cannot look after the child

Question 9

What is the pathophysiology of bacterial meningitis?

Answer 9

• Bacterial infection of the meninges usually follows bacteraemia
• Host response to the infection rather than the organism itself mainly damages meninges
• Release of inflammatory mediators, recruitment of inflammatory cells and endothelial damage leads to cerebral oedema, raised ICP and decreased cerebral blood flow
• Inflammatory responses below the meninges leads to a vasculopathy resulting in cerebral cortical infarction
• Fibrin deposits may block the resorption of CSF by the arachnoid villi leading to hydrocephalus

Question 10

How do children with bacterial meningitis present?

Answer 10

• The early signs and symptoms of meningitis are non-specific, especially in infants and young children
• NOTE: neck stiffness may be seen in some children with tonsillitis and cervical lymphadenopathy
• As children with meningitis may also has sepsis, signs like tachycardia, tachypnoea and hypotension should be explored
• IMPORTANT: purpura in a febrile child of ANY AGE should be assumed to be due to meningococcal sepsis, even if the child does not seem particularly ill at the time

Question 11

What investigations are done for bacterial meningitis?

Answer 11

• Blood tests
  
  • CRP
  • WCC
  • Blood culture
  • PCR to check for N. meningitidis
• Lumbar puncture is performed to obtain CSF to confirm the diagnosis, identify the causative organism and antibiotic sensitivities
  
  • IMPORTANT: check for clinical signs of raised ICP before LP
• NOTE: there are exceptions to the CSF pattern shown in the diagram above
• Lymphocytes can predominate in bacterial meningitis (e.g. Lyme disease)
  
  • Glucose can be low in viral meningitis (e.g. enterovirus meningitis)
  • If a lumbar puncture is contraindicated (see above), it should be postponed until the child’s condition has stabilised
• In addition, rapid antigen screens can be carried out on urine and blood samples
• Throat swabs should also be obtained for culture and PCR
• A serological diagnosis can be made 4-6 weeks after the presenting illness if necessary

Question 12

What is the management of bacterial meningitis? (NICE Guidelines)

Answer 12

• Admit to hospital as EMERGENCY
• IM/IV benzylpenicillin
  
  • NOTE: if penicillin allergy, consider chloamphenicol and vancomycin
• IV ceftriaxone
  
  • Haemophilus influenzae - 10 days
  • Streptococcus pneumoniae - 14 days
  • Neisseria meningitidis - 7 days
• Dexamethasone if there is on CSF analysis:
  
  • Frankly purulent CSF
  • CSF WBC > 1000/µL
  • Raised CSF WBC + protein concentration > 1 g/L
  • Bacteria on Gram stain
  • NOTE: steroids should NOT be used in meningococcal septicaemia
• IV 0.9% saline if shock/dehydration (monitor fluid administration and urinary output)
• Discharge and follow up
  
  • Discuss potential long term effects and patterns of recovery
    
    • Complications: hearing loss, orthopaedic complications, skin complications, psychosocial problems, neurological and developmental problems, renal failure
  • Offer formal audiological assessment
  • Consider testing for complement deficiency if they have had more than one episode of meningococcal disease or an episode caused by a serogroup other than the common ones

Question 13

What are cerebral complications of bacterial meningitis?

Answer 13

• Hearing impairment
  
  • Due to inflammatory damage to cochlear hair cells
  • ALL CHILDREN who have had meningitis should have an audiological assessment done promptly
  • Children with hearing impairment may benefit from hearing amplification or a cochlear implant
• Local vasculitis
  
  • May lead to cranial nerve palsies and other focal neurological signs
• Local Cerebral Infarction
  
  • May result in focal or multifocal seizures, which may result in epilepsy
• Subdural Effusion
  
  • Particularly associated with H. influenzae and pneumococcal meningitis
  • Confirmed by CT or MRI
  • Most resolve spontaneously
• Hydrocephalus
  
  • May result from impaired resorption of CSF (communicating) or blockage of CSF flow (non-communicating)
  • Ventricular shunt may be required
• Cerebral Abscess
  
  • Will result in the child’s clinical condition deteriorating with or without the emergence of signs of space-occupying lesion
  • Temperature will continue to fluctuate
  • Confirmed by cranial CT or MRI
  • Drainage of abscess is required

Question 14

What is bacterial meningitis prophylaxis?

Answer 14

• Rifampicin or ciprofloxacin to eradicate nasopharyngeal carriage is given to ALL household contacts for meningococcal meningitis and H. influenzae infection
• It is NOT given to the patient as the 3rd generation cephalosporin will eradicate nasopharyngeal carriage anyway
• Household contacts of patients with group C meningococcal meningitis should be vaccinated with the meningococcal group C vaccine

Question 15

Describe partially treated bacterial meningitis

Answer 15

• Children are often given oral antibiotics for non-specific febrile illness
• If they have early meningitis, this treatment may lead to diagnostic problems
• CSF will show markedly elevated white cells, but cultures will usually be negative
• Rapid antigen screens and PCR are helpful

Question 16

What are the causes of viral meningitis?

Answer 16

• Enteroviruses
• EBV
• Adenoviruses
• Mumps
• NOTE: mumps meningitis is now rare in the UK thanks to the MMR vaccine
• Viral meningitis is usually a lot LESS SEVERE than bacterial meningitis and most cases make a full recovery

Question 17

How is viral meningitis diagnosed?

Answer 17

• Culture or PCR of CSF/stool/urine/nasopharyngeal aspirate/throat swabs
• Serology

Question 18

What are uncommon pathogens and other causes of viral meningitis?

Answer 18

• If the clinical course is atypical or there is a failure to respond to antibiotics or supportive therapy, unusual organisms should be considered
• Examples:
  
  • Mycoplasma
  • Borellia burgdorferi (Lyme disease)
  • TB
  • Fungal infections
• These uncommon organisms are particularly likely in children who are immunocompromised (e.g. immunodeficiency, chemotherapy)

Recurrent bacterial infections may occur in immunodeficient children or in those with structural abnormalities of the skull or meninges

Aseptic meningitis can occur in malignancy or autoimmune diseases

Question 19

How can encephalitis be caused?

Answer 19

• Direct invasion of the brain by neurotoxic virus (e.g. HSV)
• Delayed brain swelling following a dysregulated neuroimmunologial response to an antigen, usually a virus (post-infectious encephalopathy) e.g. following chickenpox
• Slow virus infection, such as HIV or subacute sclerosing pan-encephalitis following measles
• NOTE: encephalopathy due to a non-infectious cause (e.g. metabolic abnormality) may have clinical features that are similar to infectious encephalitis

Question 20

How does encephalitis present?

Answer 20

• Most children with encephalitis will present with fever, altered consciousness and often seizures
• Initially, it may be impossible to distinguish clinically between encephalitis and meningitis, so treatment for both should be started

Question 21

What are the most common causes of encephalitis in the UK?

Answer 21

• Enteroviruses
• Respiratory viruses (influenza viruses)
• Herpes viruses (HSV, VZV, HHV-6)

Question 22

What are the most common causes of encephalitis in the world?

Answer 22

• Mycoplama
• Borellia burgdorferi (Lyme disease)
• Bartonella henselae (cat scratch disease)
• Rickettsial infections (e.g. Rocky Mountain spotted fever)
• Arboviruses

Question 23

What should all children with encephalitis be treated with initially?

Answer 23

• high-dose IV aciclovir until herpes simplex encephalitis has been ruled out
• NOTE: most affected children will NOT have obvious signs of herpes infection such as cold sores or skin lesions

Question 24

How can HSV be detected?

Answer 24

• PCR is used to detect HSV in the CSF

- EEG and CT/MRI may show focal changes

Question 25

How is encephalitis managed?

Answer 25

• Proven/suspected HSV encephalitis should be treated with IV aciclovir for 3 weeks, as relapses may occur after shorter courses
• If untreated, the mortality rate is > 70% and survivors usually have serious neurological sequelae

Question 26

What is toxic shock syndrome?

Answer 26

• This syndrome can be caused by:
  
  • Toxin-producing S. aureus
  • Group A streptococci
• It is characterised by
  
  • Fever > 39 degrees
  • Hypotension
  • Diffuse erythematous, macular rash
• The toxin can be released from an infection at any site (including small abrasions and burns which look minor)
• The toxin acts as a SUPERANTIGEN and can cause organ dysfunction
  
  • Mucositis (conjunctiva, oral mucosa, genital mucosa)
  • Gastrointestinal dysfunction (vomiting/diarrhoea)
  • Renal impairment
  • Liver impairment
  • Clotting abnormalities and thrombocytopaenia
  • CNS (altered consciousness)
• Intensive care support is required to manage patients in shock
• Areas of infection should be surgically debrided

Question 27

What antibiotics are used for toxic shock syndrome?

Answer 27

• 3rd generation cephalosporin (e.g. ceftriaxone)
• Clindamycin
  
  • This acts on the bacterial ribosome to switch off toxin production
• IVIG
  
  • May be given to neutralise the circulating toxin

Question 28

What is Panton-Valentine Leukocidin?

Answer 28

• This is produced by < 2% of S. aureus strains
• PVL-producing S. aureus causes recurrent skin and soft tissue infections
• They can also cause necrotising fasciitis and a necrotising haemorrhagic pneumonia following an influenza-like illness
• These both carry a high mortality rate
• In children, the procoagulant state induced by the toxin can cause venous thrombosis

Question 29

What is necrotising fasciitis/cellulitis?

Answer 29

• This is a RARE, severe subcutaneous infection
• The area involved may enlarge rapidly, leaving poorly perfused necrotic areas of tissue at the centre
• It is accompanied by severe pain and systemic illness and usually required intensive care
• Invading organisms:
  
  • Staphylococcus aureus
  • Group A streptococcus
  • NOTE: these can exist with or without a synergistic anaerobic organism (i.e. it can be a mixed infection)

Question 30

What is the management of necrotising fasciitis/cellulitis?

Answer 30

• SURGICAL EMERGENCY
• Debridement of necrotic tissue
• IV fluids
• Empirical IV antibiotics (vancomycin, linezolid, daptomycin, tedizolid phosphate, tazocin, meropenem, imipenem/cilastatin, ertapenem)
• Any clinical suspicion of necrotising fasciitis requires urgent surgical consultation
• IVIG may also be given

Question 31

Describe meningococcal septicaemia

How should suspected meningococcal septicaemia be managed?

Answer 31

• This is a particularly DANGEROUS infection because it can potentially kill previously healthy children within hours
• Meningococcal infection has the lowest risk of long-term neurological sequelae with most survivors recovering fully
• PURPURIC RASH in meningococcal septicaemia
• The rash is characteristically non-blanching on palpation, irregular in size and outline, and may have a necrotic centre
• ANY FEBRILE CHILD with a purpuric rash should be treated IMMEDIATELY with IM penicillin or IV 3rd generation cephalosporin before urgent admission to hospital
• NOTE: after the inclusion of the meningococcus C vaccine in the UK, most cases of meningococcal septicaemia are caused by group B meningococci
• FUTURE: polysaccharide conjugate vaccines have been developed against group A, B and C meningococci so the incidence of meningococcal disease should continue to decline

Question 32

Where is S. pneumoniae in healthy children?
How is it transmitted?
What can S. pneumoniae cause?

Answer 32

• Streptococcus pneumoniae in the nasopharynx of healthy children
• This can be transmitted to other individuals via respiratory droplets
• Streptococcus pneumoniae can cause:
  
  • Pharyngitis
  • Otitis media
  • Conjunctivitis
  • Sinusitis
  • Invasive disease (pneumonia, bacterial sepsis, meningitis)
    
    • This mainly occurs in young infants as their immune system is weak against encapsulated pathogens
    • It carries a high morbidity and mortality
• NOTE: following the inclusion of the 13-valent pneumococcal vaccine in the UK, the incidence of invasive pneumococcal disease has declined
• Children who are at risk (e.g. due to hyposplenism) should be given daily prophylactic penicillin to prevent infection

Question 33

Why does haemophilus influnzae rarely cause systemic disease?

Answer 33

• Hib used to be an important cause of systemic illness in children (e.g. otitis media, pneumonia, meningitis)
• However, immunisation has been highly effective and Hib now rarely causes systemic disease

Question 34

How are staphylococcus and group A streptococcal infections caused?
What can follow streptococcal infections?
What is impetigo?

Answer 34

• Usually caused by direct invasion of the organisms
• Can release toxins which act as superantigens
  
  • Normal antigens will stimulate only a small subset of T cells, which have a specific antigen receptor
  • Whereas, superantigens bind to part of the TCR which is shared by many T cells
  • This results in massive T cell proliferation and cytokine release
• Some disease that follow streptococcal infections (e.g. post-streptococcal glomerulonephritis and rheumatic fever) are immune-mediated
• Impetigo
  
  • Highly contagious, staphylococcal or streptococcal skin infection
  • It most commonly occurs in infants and young children
  • More common in children with pre-existing skin disease (e.g. eczema)
  • Lesions are usually found on the face, neck and hands
  • They begin as erythematous macules which becomes vesicular/pustular or even bullous
  • Rupture of the vesicles with exudation of fluid leads to the honey-coloured crusted lesions
  • Infection readily spreads to adjacent areas and other parts of the body by autoinoculation of the infected exudate

Question 35

What is the management of Staphylococcal and Group A Streptococcal infections?

Answer 35

• Advice
  
  • Leaflets from British Association of Dermatologists (BAD)
  • Reassure that impetigo usually heals without any scarring
  • Hygiene is important: wash areas with soapy water, wash hands after touching lesions, avoid scratching affected areas and keep nails short, avoid sharing towels/bathwater etc.
  • Children should avoid school until the lesions are dry and scabbed over
  • Follow-up if no improvement after 7 days
• Medical Treatment
  
  • Localised Infection = topical fusidic acid (3-4/day for 7 days)
  • Extensive Infection = oral flucloxacillin (4/day for 7 days)
    
    • Clarithromycin can be used if penicillin allergy
  • Bullous Infection = oral flucloxacillin or clarithromycin/erythromycin
• Review diagnosis
  
  • Check compliance with treatment and hygiene measures
  • Take a swab
  • Consider oral antibiotics if fusidic acid was initially used

Question 36

What are boils?

How are they treated?

Answer 36

• S. aureus infections of hair follicles or sweat glands
• TREATMENT: systemic antibiotics and (occasionally) surgical incision
• Recurrent boils may occur due to persistent nasal carriage in the child or the family acting as a reservoir for reinfection
• RARELY, recurrent boils can be a feature of underlying immunodeficiency

Question 37

What are features of periorbital cellulitis?

Answer 37

• Fever with erythema, tenderness and oedema of the eyelid or other skin adjacent to the eye
• Almost always unilateral
• May follow trauma to the skin
• In older children, it can spread from a paranasal sinus infection or dental abscess

Question 38

What is the management of periorbital cellulitis?

Answer 38

• PROMPTLY IV antibiotics (e.g. high-dose ceftriaxone)
  
  • To prevent orbital cellulitis
• Incision and drainage of peri-ocular abscess may be required

Question 39

What are features of orbital cellulitis?

Answer 39

• Proptosis
• Painful or limited ocular movement with/without reduced visual acuity
• Can be complicated by abscess formation, meningitis or cavernous sinus thrombosis

Question 40

What is staphylococcal scalded skin syndrome?

Answer 40

• Caused by an exfoliative staphylococcal toxin
• It causes the separation of the epidermal skin through the granular cell layers
• It mainly affects infants and young children

Question 41

What are clinical features of staphylococcal skin scalded skin syndrome?

Answer 41

• Fever
• Malaise
• Purulent, crusting and localised infection around the eyes, nose and mouth
• Erythema and tenderness of the skin
• Nikolsky Sign: areas of epidermis will separate on gentle pressure, leaving denuded areas of skin
• NOTE: these areas of skin tend to heal without scarring

Question 42

What is the management of staphylococcal skin scalded skin syndrome?

Answer 42

• IV antibiotics (flucloxacillin)
• Analgesia
• Monitoring hydration and fluid balance

Question 43

How do common viral infections in children present?

What are the incubation periods?

Answer 43

• A fever and a rash
• Incubation periods of viral infections can vary from 24-48 hours for viral gastroenteritis, to about 2 weeks for chickenpox
• For some diseases, like HIV, the time between exposure and the development of symptomatic illness can be many years
• The infectious period characteristically begins 1-2 days before the rash appears and (for the purposes of nursery/school exclusion) lasts until the rash has resolved and the lesions have dried up

Question 44

What are the eight known types of herpes simplex viruses?

Answer 44

• HSV1
• HSV2
• VZV
• CMV
• EBV
• HHV-6
• HHV-7
• HHV-8

Question 45

What is the hallmark of herpes viruses?

Answer 45

• After primary infection, latency is established
• Virus stays in the host for a long time
• This can be reactivated after certain stimuli

Question 46

What lesions are associated with HSV infections?

Answer 46

• HSV1 = lip and skin lesions
• HSV2 = genital lesions
• NOTE: both viruses an cause both types of disease

Question 47

What is the general management of HSV infection?

Answer 47

• Paracetamol or ibuprofen for pain and fever
• Aciclovir (DNA polymerase inhibitor) may be considered
• IMPORTANT: most herpes simplex infections are asymptomatic

Question 48

What is gingivostomatitis?
What ages does it normally occur?
Presentation?

Answer 48

• MOST COMMON form of primary HSV in children
• Usually occurs in 10 months to 3 years of age
• Presents with vesicular lesions on the lips, gums and anterior surfaces of the tongue and hard palate
• They usually progress to extensive, painful ulceration and bleeding
• It is often accompanied by a high fever
• The illness can persist for up to 2 weeks
• Eating and drinking becomes painful, resulting in dehydration

Question 49

What is the management of gingivostomatitis?

Answer 49

• Symptomatic

- Severe cases may require IV fluids and aciclovir

Question 50

What are skin manifestations of herpes?

Answer 50

• Mucocutaneous junctions and damaged skin are particularly prone to HSV infection
• Cold sores are recurrent HSV lesions on the gingival/lip margin
• Eczema herpeticum
  
  • Widespread vesicular lesions develop on eczematous skin
  • This can be complicated by secondary bacterial infection, which can then, in turn, result in septicaemia
• Herpetic Whitlows
  
  • Painful, erythematous and oedematous white pustules on the site of broken skin (usually on fingers)
  • It is spread by autoinoculation from gingivostomatitis

Question 51

Describe HSV eye disease

Answer 51

• Blepharitis or conjunctivitis
• It an involve the cornea and cause dendritic ulceration
• This can result in corneal scarring and loss of vision
• ANY herpetic lesions near or in the eye require urgent ophthalmic assessment

Question 52

What are features of neonatal HSV infection?

Answer 52

• May be focal (e.g. affecting the skin, eyes or encephalitis)
• May be disseminated
• High morbidity and mortality

Question 53

Describe HSV infection in an immunocompromised host

Answer 53

• May be severe
• Cutaneous lesions can spread to involve adjacent sites (e.g. oesophagitis, proctitis)
• Pneumonia and disseminated infections involving multiple organs are major complications

Question 54

What are major complications of chickenpox (Primary HSV infection)?
What is Purpura Fulminans?

Answer 54

• Secondary Bacterial Infection
  
  • Mainly with staphylococci and group A streptococci
  • Can lead to toxic shock syndrome and necrotising fasciitis
  • Should be considered when there is onset of a new fever or persistent high fever after the first few days
• Encephalitis
  
  • May be generalised
  • Usually occurs early in the illness
  • GOOD prognosis (as opposed to HSV encephalitis)
  • Characteristically causes a VZV-associated cerebellitis
    
    • The child becomes ataxic with cerebellar signs
  • This usually occurs around 1 week after the onset of the rash
  • Usually resolves within a month
• Purpura Fulminans
  
  • Consequence of vasculitis in the skin and subcutaneous tissues
  • Best known in relation to meningococcal disease (purpuric rash)
  • Can lead to the loss of large areas of skin by necrosis
  • Rarely, after VZV infection, antiviral antibodies can cross-react and inactivate inhibitory coagulation factors (protein S and protein C), resulting in increased risk of clotting, which often manifests as a purpuric rash
• If the patient is immunocompromised, primary VZV infection could result in severe progressive disseminated disease (up to 20% mortality)
• Vesicular eruptions may become haemorrhagic

Question 55

What is the management of chickenpox? (NICE Guidelines)

Answer 55

• Admit if serious complications (e.g. pneumonia, encephalitis, dehydration)
• In immunocompetent adolescents and adults, consider oral aciclovir 800 mg 5/day for 7 days if they present within 24 hours of the onset of the rash of if the chickenpox is severe
• ADVICE
  
  • Encourage adequate fluid intake
  • Dress appropriately to avoid overheating or shivering
  • Wear smooth, cotton fabrics
  • Keep nails short
  • Explain that the most infectious period is 1-2 days before the rash appears
  • Infectivity continues until all the lesions are dry and crusted over (usually ~5 days after onset of the rash)
  • During this time, patients should AVOID contact with:
    
    • People who are immunocompromised
    • Pregnant women
    • Infants < 4 weeks
  • Children should be kept away from school until the vesicles have crusted over
  • Seek urgent medical advice if the condition deteriorates or they develop complications:
    
    • Bacterial superinfection - sudden high-grade pyrexia with erythema and tenderness around the original chickenpox lesions
    • Dehydration - e.g. reduced urine output, lethargy, cool peripheries
• Immunocompromised children
  
  • Should be treated with IV aciclovir
  • Oral valaciclovir may be substituted later on
• Prevention in immunocompromised patients
  
  • Human varicella zoster immunoglobulin for high-risk individuals with deficient T cell function following contact with chickenpox
  • NOTE: this protection is NOT absolute

Question 56

Describe shingles
What is it caused by?
Where does it commonly affect?

Answer 56

• UNCOMMON in children
• Caused by reactivation of latent VZV
• Characteristically causes a vesicular eruption in the dermatomal distribution of the sensory nerves
• Most commonly affects the thoracic region
• Recurrent or multi-dermatomal shingles is strongly associated with underlying immunocompromise (e.g. HIV infection)
• NOTE: in immunocompromised patients, reactivation of the infection can also disseminate and cause severe disease

Question 57

What is EBV?

Which diseases is it implicated?

Answer 57

• EBV causes infectious mononucleosis
• It is also involved in the pathogenesis of:
  
  • Burkitt lymphoma
  • Lymphoproliferative disease
  • Nasopharyngeal carcinoma
• EBV has a tropism for B lymphocytes and epithelial cells of the oropharynx
• It is transmitted by oral contact
• Most infections are subclinical

Question 58

What are features of EBV?

Answer 58

• Older children (and sometimes younger children) may develop a syndrome with:
  
  • Fever
  • Malaise
  • Tonsillitis/pharyngitis
    
    • Often severe enough to limit fluid and food intake
  • Lymphadenopathy
    
    • Prominent cervical lymph nodes, often with diffuse lymphadenopathy elsewhere
  • Other features
    
    • Petechiae of the soft palate
    • Splenomegaly (50%)
    • Hepatomegaly (10%)
    • Maculopapular rash
    • Jaundice

Question 59

How is EBV infection diagnosed?

Answer 59

• Very clinical but can be supported by certain laboratory findings
• Atypical lymphocytes (numerous large T cells)
• Positive monospot test
  
  • Detects the presence of heterophile antibodies
  • NOTE: this test is often negative in young children with EBV
• Seroconversion with production of THREE antibodies:
  
  • Viral capsid antigen antibodies (VCA) IgG and IgM
  • EB nuclear antigen (EBNA) antibodies
• Symptoms of infectious mononucleosis may persist for 1-3 months but will ultimately resolve

Question 60

What is the management of EBV infection?

Answer 60

• Paracetamol or ibuprofen to relieve pain and fever
• Explain the expected course of the illness (2-3 week duration)
• They don’t need to avoid work or school but should do it depending on how they feel
• Limit the spread of disease
• Avoid collision/contact sport
• Corticosteroids may be considered if the airway is severely compromised (RARE)
• Seek medical help if:
  
  • Stridor or respiratory difficulty
  • Difficulty swallowing fluids or signs of dehydration
  • Systemically very unwell
  • Abdominal pain (e.g. due to splenic rupture)
• WARNING: ampicillin and amoxicillin can cause a florid maculopapular rash in children infected with EBV so should be AVOIDED

Question 61

How is CMV transmitted?

What does it cause?

Answer 61

• Usually transmitted via saliva, genital secretion or breastmilk
• Causes mild or subclinical infection in normal paediatric and adult hosts
• About 50% of adults show serological evidence of past infection
• In the immuncompromised host and the developing foetus (transmitted from the mother), CMV is an important pathogen that can cause considerable morbidi

Question 62

What are features of CMV mononucleosis-like syndrome?

Answer 62

• Pharyngitis and lymphadenopathy are NOT as prominent as in EBV
• Atypical lymphocytes on the blood film
• They will be heterophile antibody negative

Question 63

What can CMV cause in an immunocompromised host?

Answer 63

• Retinitis
• Pneumonitis
• Bone marrow failure
• Encephalitis
• Hepatitis
• Oesophagitis
• Enterocolitis

Question 64

Why is CMV particularly important to monitor following bone marrow and organ transplantation?

Answer 64

• Transplant recipients are closely monitored for evidence of CMV reactivation by blood PCR
• This is why CMV-negative blood is used for transfusions
• Antiviral prophylaxis may also be used

Question 65

What is the management for CMV?

Answer 65

• CMV is self-limiting
• If necessary, CMV can be treated with:
  • IV ganciclovir
  • Oral valganciclovir
  • Foscarnet
  • NOTE: these all have serious side-effects

Question 66

What is HHV-6 and HHV-7?

Answer 66

• These two viruses are closely related and have similar presentations
• HHV6 is more prevalent
• MOST CHILDREN are infected by HHV6 o HHV7 by the age of 2 years, usually from the oral secretions of a family member
• These viruses classically cause exanthema subitum (aka roseola infantum)
  
  • This is characterised by a high fever and malaise lasting a few days
  • This is followed by a generalised macular rash, which appears at the fever wanes
  • Many children will have the fever without the rash and many will have a subclinical infection
  • NOTE: this is often misdiagnosed as measles or rubella
  • NOTE: infants seen in the febrile stage may be given antibiotics, and when the exanthema subitum rash appears, they can be misdiagnosed with an allergy to antibiotic

Question 67

What is the management of HHV-6 and HHV-7?

Answer 67

• The condition will resolve over a few days/week
• Paracetamol or ibuprofen for symptomatic relief
• Advise to maintain adequate hydration
• Explain risk of febrile seizures

Question 68

What does Human Parvovirus B19 cause?

How is it transmitted?

Answer 68

• Causes erythema infectiosum (aka fifth disease)
• It is commonly known as slapped-cheek syndrome
• Outbreaks are most common during the spring
• Transmitted via respiratory secretions or by vertical transmission from mother to foetus
• It can also be transmitted via infected blood products
• HPV-B19 infects the erythroblastoid red cell precursors in the bone marrow
• It is mild and self-limiting
• Advice on adequate rest and fluid intake
• It is NOT necessary to stay away from school, but they may need to avoid contact with pregnant women

Question 69

What clinical syndromes can Human Parvovirus B19 cause?

Answer 69

• Asymptomatic infection
  
  • About 65% of adults have antibodies against HPV-B19
• Erythema Infectiosum
  
  • MOST COMMON
  • It has a viraemic phase of fever, malaise, headache and myalgia
  • This is followed by a characteristic rash on the face (slapped-cheek), roughly a week later
  • This progresses into a maculopapular, ‘lace-like’ rash on the trunk and limbs
  • Complications are rare in children
  • In adults, it can cause arthralgia and arthritis
• Aplastic Crisis
  
  • MOST SERIOUS
  • Occurs in children with chronic haemolytic anaemias (e.g. sickle cell disease, thalassemia)
• Foetal Disease
  
  • Can lead to foetal hydrops and DEATH due to severe anaemia
  • Most infected foetuses will recover

Question 70

What is the management of erythema infectiosum? (BMJ Best Practice)

Answer 70

• Paracetamol or ibuprofen
• Adequate fluid intake
• Secondary arthritis may be treated with ibuprofen

Question 71

What are different types of enteroviruses?

How is it transmitted?

Answer 71

• There are many enteroviruses including
  
  • Coxsackie virus
  • Echoviruses
  • Polioviruse
• Transmitted via the faecal-oral and respiratory droplet routes
• Mainly occur in the summer and autumn
• Over 90% of infections are ASYMPTOMATIC or cause non-specific febrile illness
• Sometimes cause a blanching rash on the trunk and consists of fine petechiae
• Some children may have loose stools or vomiting
• The child is NOT usually systemically unwell

Question 72

What is hand, foot and mouth disease?

Answer 72

(Enterovirus)
- Painful vesicular lesions on the hands, feet, mouth and tongue

• Systemic features are generally mild
• Disease subsides within days

Question 73

What is herpangina?

Answer 73

(Enterovirus)
- Vesicular and ulcerated lesions on the soft palate and uvula leads to anorexia, painful swallowing and fever

• Severe cases may require IV fluids and analgesia

Question 74

How does enterovirus relate meningitis/encephalitis?

Answer 74

• In developed countries, enteroviruses are the MOST COMMON cause of viral meningitis
• Most cases make a full recovery

Question 75

What is Pleurodynia (Bornholm disease)?

Answer 75

(Enterovirus)

• An acute illness with
  
  • fever
  • pleuritic chest pain
  • muscle tenderness
• Recover within days

Question 76

How does enterovirus relate to myocarditis/pericarditis

Answer 76

• RARE
• Children may present with chest pain and/or heart failure associated with a febrile illness and evidence of myocarditis on ECG

Question 77

What is Enterovirus Neonatal Sepsis Syndrome?

Answer 77

• RARE
• Occurs in the first few weeks of life
• Results from transplacental/intrapartum infection of the infant
• The symptoms are often SEVERE, mimicking bacterial sepsis
• Affected infants may present with hypotension and multiorgan failure
• Intensive care support is required
• IMPORTANT: there are NO antiviral drugs that are effective against enteroviruses and the use of IVIG remains controversial

Question 78

What are the clinical features of measles?

Answer 78

• Encephalitis
  
  • RARE
  • Initial symptoms are headache, lethargy and irritability
  • This proceeds to seizures and coma
  • Up to 15% mortality
  • Serious long-term sequelae include: seizures, deafness, hemiplegia, severe learning difficulties
• Subacute Sclerosing Panencephalitis (SSPE)
  
  • RARE but devastating
  • Occurs, on average, 7 years after measles infection
  • Caused by a variant of the measles virus that persists in the CNS
  • Presents with loss of neurological function
  • This progresses, over several years, to dementia and death
• Older children and adults tend to have MORE SEVERE disease
• NOTE: in low-income countries, where malnutrition and vitamin A deficiency leads to impaired cell-mediated immunity, measles often follows a protracted course with severe complications

Question 79

What is the management of measles? (NICE Guidelines)

Answer 79

• Immediately notify the local Health Protection Team (HPT)
• Self-limiting disease but it is likely to cause unpleasant symptoms such as rash, fever, cough and conjunctivitis
• Rest and drink plenty
• Paracetamol or ibuprofen can be used for symptomatic relief
• Stay away from school for at least 4 days after the development of the rash
• Seek urgent medical advice if they develop complications such as:
  
  • Shortness of breath
  • Uncontrolled fever
  • Convulsions or altered consciousness
• Encourage vaccinations once the acute episode has subsided
• Find out the immunisation status of close contacts
• Children should be isolated in hospital
• In immunocompromised patients, ribavirin may be of use
• Vitamin A is given in low-income countries

Question 80

How is mumps spread?

Answer 80

• Spread by droplet infection to the respiratory tract where the virus replicates within epithelial cells
• The virus gains access to the parotid glands before further dissemination to other tissues

Question 81

What are the clinical features of mumps?

Answer 81

• Incubation period: 15-24 days
• The disease begins with a fever, malaise and parotitis
  
  • This may initially be unilateral, but it will eventually become bilateral after a few days
• In up to 30% of cases, the infection will be subclinical
• Parotitis is uncomfortable, and children may complain of earache or pain when eating/drinking
• Examination of the parotid duct may show redness and swelling
• The fever usually subsides after 3-4 days
• Plasma amylase levels are usually elevated due to parotid inflammation
• When associated with abdominal pain, consider pancreatic involvement
• Infectivity lasts for up to 7 days after the onset of parotid swelling
• The illness is usually mild and self-limiting
• Hearing loss can rarely follow mumps, but it is usually unilateral and transient

Question 82

What is the management of mumps? (NICE Guidelines)

Answer 82

• Notify the local Health Protection Unit (HPU)
• Oral swab to confirm diagnosis
• Self-limiting condition
• Rest and take in adequate fluids
• Paracetamol and ibuprofen for symptomatic relief
• Stay away from school for 5 days after parotitis develops
• Consider follow-up 1 week after the onset of parotitis
• Seek help if they experience symptoms suggestive of meningitis or epididymo-orchitis
• Find out the immunisation status of close contacts and tell them to watch out for symptoms of mumps

Question 83

What is seen in the CSF of mumps meningitis and encephalitis?
What percentage of cases have typical meningeal signs?

Answer 83

• Lymphocytes will be seen in the CSF in about 50% of cases
• Typical meningeal signs are only seen in 10%

Question 84

What is mumps orchitis?

Answer 84

• MOST FEARED complication
• Usually unilateral
• Infertility is unusual after mumps orchitis

Question 85

What is rubella?

Answer 85

• Mild disease in childhood
• Can cause severe damage to the foetus
• Incubation period: 15-20 days
• Spread by the respiratory route
• May have a prodrome of low-grade fever or no symptoms at all
• A maculopapular rash is often the first sign of infection
  
  • It tends to initially appear on the face and spread centrifugally to cover the whole body
  • Fades in 3-5 days
• Lymphadenopathy, particularly suboccipital and postauricular nodes, is prominent
• Complications are RARE in children (but include arthritis, encephalitis, thrombocytopaeina and myocarditis)
• Diagnosis is confirmed by serology
• There is NO effective antiviral treatment
• Prevention is dependent on immunisation

Question 86

What is the management of rubella? (NICE Guidelines)

Answer 86

• Contact the local Health Protection Unit (HPU)
• Diagnosed using an oral fluid sample
• Advise that it is a self-limiting disease
• Rest and take in adequate fluids
• Consider admitting if there is a serious complication such as haemorrhagic complications (caused by thrombocytopaenia) or encephalitis

Question 87

What are infective causes of a prolonged fever in a child?

Answer 87

• Bacterial infections e.g. typhoid, Bartonella henselae (cat scratch disease), Brucella
• Deep abscesses e.g. intra-abdominal, retroperitoneal, pelvic
• Infective endocarditis
• Tuberculosis
• Viral infections: HIV, CMV, EBV

Question 88

What are non-infective causes of a prolonged fever in a child?

Answer 88

• Systemic juvenile idiopathic arthritis (SJIA)
• Systemic Lupus Erythematosus (SLE)
• Vasculitis (Kawasaki disease)
• IBD
• Sarcoidosis
• Malignancy e.g. leukaemia, lymphoma, neuroblastoma

Question 89

What is Kawasaki disease?

Why is it important to recognise?

Answer 89

• Systemic vasculitis
• RARE, but important to recognise because aneurysms of coronary arteries are potentially devastating
• It mainly affects children aged 6 months to 4 years
• More common in Japanese children
• Young infants tend to be more severely affected and are more likely to have incomplete symptoms (i.e. not the full list of cardinal features)
• The diagnosis is clinical
• Patients will have high inflammatory markers (CRP, ESR, WCC) with a platelet count that rises in the 2nd week of the illness
• Coronary arteries are affected in about 1/3 of children within the first 6 weeks of the illness
• This can lead to aneurysms which can be detected on echocardiography
• Subsequence narrowing of the vessels due to scarring can lead to myocardial ischaemia and sudden death

Question 90

What are cardinal features of Kawasaki disease?

Answer 90

• CRASH and Burn
• Conjunctivitis
• Rash
• Adenopathy (usually cervical)
• Strawberry tongue
• Hand - swelling or erythema on the hands and feet
• Burn - fever
  
  • This fever is usually difficult to control

Question 91

What is the management of Kawasaki disease? (NICE Guidelines)

Answer 91

• IVIG
• High-dose aspirin (reduce thrombosis risk)
• Other treatment options include corticosteroids, infliximab and plasma exchange
• Children with giant coronary artery aneurysms may require long-term warfarin and close follow-up
• Patients should, therefore, have a cardiovascular risk assessment
• Children with persistent inflammation and fever may require corticosteroids, infliximab or ciclosporin

Question 92

Why is TB becoming more of a public health burden?

How is it transmitted?

Answer 92

• Emergence of multi-drug resistance strains
• Transmitted by the respiratory route
• NOTE: latent TB is more likely to transform into active TB in infants and young children

Question 93

How is TB diagnosed?

Answer 93

• Diagnosis in children is particularly difficult
• Clinical features are often non-specific
  
  • Prolonged fever
  • Malaise
  • Anorexia
  • Weight loss
  • Focal signs of infection (e.g. lymph node swelling)
  • NOTE: extra-pulmonary disease is relatively uncommon (e.g. TB lymphadenitis, osteoarticular TB, genitourinary TB, TB meningitis)
• Sputum samples are unobtainable in children < 8 years old
• Gastric washings on 3 consecutive mornings can be used to identify M. tuberculosis using Ziehl-Neelsen stains or auramine stains and mycobacterial cultures
  
  • This is obtained by passing an NG tube and washing out secretions in the stomach with saline
• TB is difficult to culture but it should still be attempted because it is important to identify the antibiotic sensitivities
• PCR-based methods are increasingly being used in parallel with mycobacterial cultures but these methods provide limited information about drug resistance
• Tuberculin Skin Test (TST)
• IGRAs
• IMPORTANT: neither the IGRA or the TST can reliably distinguish between latent TB and active TB
• NOTE: with advanced immunocompromise (e.g. HIV) both TST and IGRA can produce false negatives
• BEWARE: do NOT attempt to diagnose TB based on CXR alone in HIV patients because lymphoid interstitial pneumonitis can have a similar appearance and occur in 20% of HIV-infected children
• IMPORTANT: ALL individuals with TB should be tested for HIV and vice versa

Question 94

What is the Tuberculin Skin Test?

Answer 94

• Injecting purified protein derivative intradermally into the forearm and observing 48-72 hours later and measuring the induration in millimetres
• NOTE: PPD is a mixture of proteins, some of which are expressed by M. tuberculosis and the BCG, so a positive test result may be because of past BCG vaccination rather than latent TB
• Originally, previous vaccination was taken into account when interpreting the TST result
• NEW GUIDELINES: state that an induration of > 5 mm should be considered to be POSITIVE regardless of prior BCG vaccination

Question 95

What is IGRA?

Answer 95

• Interferon Gamma Release Assay
• New blood-based test
• Assesses the response of T cells to in vitro stimulation with a small number of antigens that are expressed by M. tuberculosis but NOT BCG
• Therefore, a positive result will indicate TB infection rather than BCG
• HOWEVER, a negative result does NOT reliably rule out TB infection

Question 96

What is the management of children with TB? (NICE Guidelines)

Answer 96

• Admit if the patient has suspected active TB and is unwell
• If hospital admission is not needed, urgent referral to specialist TB service to confirm diagnosis
• It is a notifiable disease
• Medical Management
  
  • Rifampicin + Isoniazid - 6 months
  • Pyrazinamide + Ethambutol - first 2 months
  • In adolescents, pyridoxine (vitamin B6) is given weekly to prevent peripheral neuropathy due to isoniazid
  • Dexamethasone in tuberculous meningitis to reduce the risk of long-term sequelae
  • IMPORTANT: asymptomatic children who are Mantoux or IGRA positive (i.e. latently infected) should also be treated as it will decrease the risk of reactivation later in life
• Risk assessment for drug-resistant TB
• A multidisciplinary approach should be taken including a key worker who should monitor the patient’s adherence to treatment, clinical response and any adverse effects
• Do contact tracing
• TB Alert is a good website with information about TB

Question 97

Describe Prevention and Contact Tracing in TB

Answer 97

• BCG does reduce incidence of TB but its protective effect is incomplete
• UK RECOMMENDATION: BCG is given at birth for high-risk groups
• IMPORTANT: BCG should NOT be given to HIV-positive or other immunocompromised children
• As most children are infected by a household contact, it is important to screen other family members
• NICE GUIDELINES: children < 2 years who had close contact with a sputum smear positive pulmonary TB person should be started on prophylactic isoniazid
  
  • If TST and IGRA are negative at 6 weeks, isoniazid should be discontinued and BCG should be given

Question 98

Describe nontuberculous mycobacterial infections

Answer 98

• There are several in the environment
• Immunocompetent individuals rarely get affected by these organisms
• May occasionally cause persistent lymphadenitis in young children
  
  • TREATMENT: complete lymph node excision or watchful waiting (in most cases, spontaneous resolution occurs)
• NOTE: these organisms are transmitted by soil and water so NO contact tracing is needed
• It can cause disseminated infection in immunocompromised individuals
• Mycobacterium avium intracellulare infections are particularly common in patients with advanced HIV
• These infections do NOT respond to conventional anti-TB treatment
• Patients with cystic fibrosis are particularly susceptible to these infections

Question 99

What are clinical features of tropical infections in children?
What are some examples of tropical infections?

Answer 99

• Fever and a recent history of foreign travel
• However, some tropical infections to consider are:
  • Malaria
  • Typhoid
  • Viral infections transmitted by mosquitoes (e.g. dengue fever, chikungunya, Zika virus)
  • Gastroenteritis and dysentery
  • Viral haemorrhagic fevers (e.g. Lassa, Marburg, Ebola, Crimean-Congo viruses

Question 100

What are routes of HIV transmission?

Answer 100

• Most affected children are in Sub-Saharan Africa
• The main route of transmission in children is mother-to-child transmission which can occur:
  
  • Intrauterine (during pregnancy)
  • Intrapartum (at delivery)
  • Postpartum (through breastfeeding)
• Uncommon routes of transmission to children include infected blood products, contaminated needles and sexual abuse

Question 101

How is HIV diagnosed?

Answer 101

• Children > 18 months: detect antibodies against the virus
• Children < 18 months who are born to infected mothers will have transplacental maternal IgG HIV antibodies, so a positive antibody test will confirm HIV exposure but not infection
  • The most sensitive test in this age group is HIV RNA PCR
  • ALL babies born to HIV-infected mothers should be tested, irrespective of whether they are symptomatic or not

Question 102

What are the clinical features of HIV?

Answer 102

• Some infants will progress rapidly to symptomatic disease and AIDS within the first year of life
• Others are asymptomatic for months or years
• Presentation depends on the degree of immunocompromise
  
  • Mild: lymphadenopathy or parotid enlargement
  • Moderate: recurrent bacterial infections, candidiasis, chronic diarrhoea, lymphocytic interstitial pneumonitis
  • SEVERE: Pneumocystic jirovecii pneumonia, severe growth faltering, encephalopathy, malignancy (RARE)
• IMPORTANT: an unusual constellation of symptoms (especially infectious) should make you consider HIV

Question 103

What is the management of HIV?

Answer 103

• Decision to start is based on a combination of clinical status, HIV viral load and CD4 count
• IMPORTANT: infants should start ART shortly after diagnosis because they are at higher risk of disease progression
• PCP prophylaxis with co-trimoxazole is given to infants who are HIV-infected, and for older patients with low CD4 counts
• Other aspects of management:
  
  • Immunisation (except BCG)
  • MDT approach
  • Regular follow-up with particular attention to weight and developmental progress
• Advise on risk reduction strategies
• Reducing Vertical Transmission

Question 104

How is vertical transmission in HIV reduced?

Answer 104

• Mothers with a high viral load are more likely to transmit HIV to their infant
• Avoidance of breastfeeding also reduces transmission
• In high-income countries, perinatal transmission of HIV is < 1% due to:
  
  • Use of effective ART during pregnancy and intrapartum to achieve an undetectable maternal viral load at delivery
  • Post-exposure prophylaxis given to infant
  • Avoidance of breastfeeding
  • Active management of labour/delivery to avoid prolonged rupture of the membranes and unnecessary instrumentation
  • Pre-labour caesarean section if the mother’s viral load is detectable close to the due date

Question 105

What causes Lyme Disease?
How is it transmitted?
When does infection occur?

Answer 105

• Caused by spirochaete Borrelia burgdorferi
• Transmitted by hard ticks
• History of tick bite is only elicited in about half of cases
• Infections most commonly occur in the summer months in rural settings

Question 106

What are clinical features of Lyme Disease?

Answer 106

• Incubation period: 4-20 days
• Erythematous macule at the site of the tick bite enlarges to cause erythema migrans
• Erythema migrans is described as a painless, red, expanding lesion with a bright red outer spreading edge
• Early Features
  
  • Fever (fluctuate over several weeks and resolve)
  • Headache
  • Malaise
  • Myalgia
  • Arthralgia
  • Lymphadenopathy
• NOTE: dissemination of infection early is RARE but can lead to cranial nerve palsies, meningitis, arthritis or carditis
• Late Features (weeks or months after initial infection)
  
  • Neurological (meningoencephalitis, cranial and peripheral neuropathies)
  • Cardiac (myocarditis, heart block)
  • Joint (varies from brief migratory arthralgia to acute asymmetric monoarthritis and oligoarthritis of the large joints)
    
    • Occurs in 50% of patients
    • Recurrent attacks of arthritis are common
    • Chronic erosive joint disease can occur months/years after the initial attack in 10% of cases

Question 107

How is Lyme Disease diagnosed?

Answer 107

• Based on clinical and epidemiological features and serology
• Isolation of the organism is difficult
• If Lyme disease is suspected without erythema migrans, offer an ELISA for Lyme disease
• If the ELISA is positive, perform an immunoblot test
• If immunoblot is positive, start treatment with oral antibiotics

Question 108

How is Lyme Disease managed? (NICE Guidelines)

Answer 108

• 1st line: DOXYCYCLINE
• 2nd line: AMOXICILLIN
• 3rd line: AZITHROMYCIN
• IV ceftriaxone is needed for carditis or neurological disease
• ADVICE
  
  • Explain that it is a bacterial infection treated with antibiotics but it can take some time (around a month) to get better
  • Some people can have a Jarish-Herxheimer reaction (antibiotics cause lysis of bacterial membranes leading to the release of toxins causing symptoms to worsen)
  • Lyme disease does NOT give lifelong immunity

Question 109

What does the 6 in 1 vaccine contain?

Answer 109

• Diphtheria
• Tetanus
• Pertussis
• Polio
• Hib
• Hepatitis B

Question 110

When is the 6 in 1 vaccine given?

Answer 110

• 2 months
• 3 months
• 4 months

Question 111

When is the pnemococcal conjugate vaccine (PVC13) given?

Answer 111

• 2 months
• 4 months
• 12 months

Question 112

When is the meningococcal B vaccine given?

Answer 112

• 2 months
• 4 months
• 12 months

Question 113

When is the Rotavirus vaccine given?

Answer 113

• 2 months

- 3 months

Question 114

When are the Booster Hib, MenC, MMR, HPV and Meningococcal ACWY conjugate vaccines given?

Answer 114

• Booster Hib and MenC is given at:
  
  • 1 year
• MMR is given at :
  
  • 1 year
  • 3 years 4 months
• HPV is given to girls at:
  
  • 12-13 years
• Meningococcal ACWY conjugate vaccine is given at :
  
  • 14 years

Question 115

What are complication of vaccinations?

Answer 115

• Swelling and discomfort at the injection site with mild fever and malaise
• Anaphylaxis can occur but is very rare
• Live vaccines should NOT be given to immunocompromised children (except HIV-positive children on ART)
• Vaccination should be postponed if the child has an acute illnes

Question 116

How is immunodeficiency classified?

Answer 116

• Primary (RARE): genetically determined defect of the immune system
• Secondary: caused by another disease or treatment such as malignancy, chemotherapy, malnutrition, HIV, immunosuppressive therapy, splenectomy or nephrotic syndrome

Question 117

What are features of primary immunodeficiency?

Answer 117

• Most are X-linked recessive or autosomal recessive
• May be a family history of consanguinity or unexplained death
• Primary immunodeficiency should be considered in children presenting with Severe, Prolonged, Unusual or Recurrent infections

Question 118

What are presenting features of immunodeficiency?

Answer 118

• Recurrent (proven) bacterial infections
• Severe infections (e.g. meningitis, osteomyelitis, pneumonia)
• Infections that present atypically, are unusually severe or chronic or fail to respond to regular treatment
• Infections caused by an unexpected or opportunistic pathogen or a pathogen the child has been immunised against
• Severe or long-lasting warts, generalised molluscum contagiosum
• Extensive candidiasis
• Complications following live vaccinations (e.g. disseminated BCG)
• Abscesses of internal organs; recurrent skin abscesses
• Prolonged or recurrent diarrhoea (often combined with faltering growth)

Question 119

What is the management of immunodeficiency?

Answer 119

• Antimicrobial prophylaxis
  
  • For T-cell and neutrophil defects:
    
    • Co-trimoxazole to prevent PCP
    • Itraconazole or fluconazole to prevent other fungal infections
• For B-cell defects:
  
  • Antibiotic prophylaxis (e.g. azithromycin) to prevent recurrent bacterial infection
• Antibiotic treatment
  
  • Prompt treatment of infections
  • Longer courses
  • Low threshold for IV therapy
• Screening for end-organ disease
  
  • E.g. CT scan in children with antibody deficiency to detect bronchiectasis
• Immunoglobulin replacement therapy
  
  • For children with antibody deficiency
• Bone marrow transplantation
  
  • E.g. for SCID, chronic granulomatous disease
• Gene therapy

Question 120

What is a food allergy?

What is food intolerance?

Answer 120

• Pathological immune response occurs against a specific food protein
• Usually IgE mediated
• A non-immunological hypersensitivity reaction to a specific food is called food intolerance

Question 121

What is secondary food allergy?

Answer 121

• This is usually due to cross-reactivity between proteins present in fresh fruits/vegetables/nuts and those present in pollens
• E.g. a child who can eat apples may develop an allergy to apples when they are older if they develop an allergy to birch tree pollen, which has a very similar protein
• This is called pollen food allergy syndrome
• It can cause mild allergic reactions (e.g. itchy mouth)

Question 122

What are common causes of food allergy in infants and other children?

Answer 122

• Infants: most common causes are milk, eggs and peanut

- Older Children: peanut, tree nut, fish, shellfish

Question 123

What are the clinical features of food allergy/intolerance?

Answer 123

• History of allergic symptoms varying from urticaria to facial swelling to anaphylaxis
• Allergy occurs 10-15 mins after ingestion of a food
• Non-IgE mediated food allergy usually presents with diarrhoea, vomiting, abdominal pain and sometimes faltering growth
  
  • Colic or eczema may also be present
  • It may present with blood in the stools due to proctitis in the first few weeks of life or severe repetitive vomiting which can result in shock (food protein-induced enterocolitis syndrome)

Question 124

When does Non-IgE mediated allergy occur?

Answer 124

• typically occurs hours after ingestion and usually involves the GI tract

Question 125

How is food allergy diagnosed?

Answer 125

• Clinical history
• For IgE mediated food allergy, skin-prick tests are the most useful
• Patch testing - identify allergens that cause reactions through delayed contact hypersensitivity where T cells play a major role
  
  • The allergenic extract is held against the skin for 48 hours
• Measurement of specific IgE antibodies in the blood is also useful
• The greater the result, in both tests, the more likely the child is to be allergic
• Non-IgE mediated food allergies more reliant on clinical history and examination
• Endoscopy and intestinal biopsy are sometimes performed
• The diagnosis of non-IgE mediated food allergy is supported by the presence of eosinophilic infiltrates
• IMPORTANT: for both IgE and non-IgE mediated food allergies, the GOLD STANDARD investigation in cases of doubt is EXCLUSION of the relevant food under the dietician’s supervision
  
  • This is followed by a double-blind placebo-controlled food challenge
  • This involves the child being subject to increasing amounts of the food or placebo
  • It should be performed at hospital with full resuscitation facilities available

Question 126

What is the management of food allergy?

Answer 126

• Avoidance of the relevant food
• Educating the child and family about how to manage an allergic attack (allergy action plan)
• Provide written self-management plans and training
• Mild reactions (no cardiorespiratory symptoms) are treated with non-sedating antihistamines
• Severe reactions (with cardiovascular, laryngeal or bronchial involvement) require IM adrenaline (may be given by autoinjector (EpiPen))
• Food allergy to cow’s milk and egg often resolves in early childhood, so gradual reintroduction may be possible
• Food allergy to nuts and seafood usually persist through to adulthood

Question 127

What is cow’s milk protein allergy?

How is it classified?

Answer 127

• Abnormal reaction by the body’s immune system to a protein found in cows’ milk
• Classification
  • IgE-mediated = immediate reaction
  • Non-IgE Mediated = delayed reaction

Question 128

How does cow’s milk protein allergy present?

Answer 128

• GI symptoms: vomiting, abdominal pain, blood in stools, diarrhoea
• Skin symptoms: hives, eczema
• Babies: wheezing, irritability, facial swelling, poor growth

Question 129

How is cow’s milk protein allergy diagnosed?

Answer 129

• History and examination

- Consider referral to secondary care for a skin prick and/or specific IgE antibody blood test

Question 130

How is cow’s milk protein allergy managed? (NICE Guidelines)

Answer 130

• Eliminate cow’s milk for at least 6 months or until the child is 9-12 months
  
  • Breastfed Babies: advise mother to exclude cows’ milk protein from her diet. Consider prescribing daily supplement of 1000 mg of calcium and 10 mcg of vitamin D
  • Formula-fed Babies: advise replacement of cows’ milk-based formula with hypoallergenic infant formula (e.g. extensively hydrolysed formula or amino acid formula)
  • Weaned infants/older children: exclude cows’ milk protein from their diet
• Offer nutritional counselling with a paediatric dietician
• Regularly monitor growth
• Re-evaluate the child to assess for tolerance to cows’ milk protein (every 6-12 months) - this involves re-introducing cows’ milk protein into the diet
  
  • If tolerance is established, greater exposure of less processed milk is advised following a ‘Milk Ladder’
• SUPPORT: British Dietetic Association (BDA) has produced a useful fact sheet

Question 131

What is allergic rhinitis and conjunctivitis?

Answer 131

• This can be atopic or non-atopic
• It is classified based on pattern and severity of symptoms
  
  • Pattern: intermittent or persistent
  • Severity: mild, moderate or severe
• It can also be classified as seasonal or perennial
• It can also present with a cough due to post-nasal drip or chronically blocked nose leading to sleep disturbance

Question 132

How is allergic rhinitis and conjunctivitis managed?

Answer 132

• Assess for symptoms of asthma
• Try to identify the most likely causative allergen
• Look for signs of chronic nasal congestion (e.g. mouth breathing, cough, halitosis)
• Examine the nose for nasal polyps, deviated nasal septum, mucosal swelling or depressed or widened nasal bridge
• For those who want ‘as required’ treatment for occasional symptoms
  
  • If aged 2-5 or preference for oral treatment = oral antihistamine (e.g. cetirizine)
  • All others = intranasal azelastine (antihistamine)
• For those who want preventative treatment for frequent symptoms
  
  • Avoid the causative agent
  • If main issue is nasal blockage or nasal polyps = intranasal corticosteroid (e.g. beclometasone)
  • If main issue is sneezing or nasal discharge = oral antihistamine or intranasal corticosteroid
• For people requiring rapid relief whilst waiting for preventive treatment to take effect
  
  • Intranasal corticosteroids for up to 7 days
  • Consider adding oral antihistamine
  • If symptoms are severe and/or impairing quality of life, prescribe a 5-10 day course of prednisolone

Question 133

What are the causes of acute urticaria?

Answer 133

• Viral infection (rash lasts for days)

- Allergen exposure (rash lasts for hours)

Question 134

How is angioedema caused?

Answer 134

• Urticaria can involve deeper tissues to produce swelling (angioedema), especially of the lips and soft tissues around the eyes

Question 135

What are the presenting features of urticaria and angioedema?

Answer 135

• Hives or redness and results from local vasodilation and increased permeability of capillaries and venules
• This is dependent on activation of skin mast cells, leading to the release of various mediators including histamines
• Itchy
• When allergy has caused urticaria, there is a risk of anaphylaxis
• Chronic urticaria (> 6 weeks) is usually non-allergic

Question 136

What is the management of urticaria and angioedema?

Answer 136

• Identify and manage underlying triggers
• Symptom diaries can be useful
• Consider assessing severity using a tool such as Urticaria Activity Score (UAS7)
• Advise that urticaria is likely to be self-limiting
• If symptomatic:
  
  • Offer non-sedating antihistamine (e.g. cetirizine) for up to 6 weeks
  • If severe, offer oral corticosteroid
  • If symptoms improve, consider giving treatment to take as required (if there were to be future episodes) or daily antihistamines for 3-6 months if symptoms are likely to be persistent
• Consider referral to the dermatologists
• In refractory cases, leukotriene receptor antagonists or anti-IgE antibody (omalizumab) may be used

Question 137

Describe drug allergy

Answer 137

• Antibiotics allergy is common in children
• A lot of children who have been labelled as ‘drug allergic’ are NOT truly allergic
• This is because viral illnesses may cause a delayed rash, before which antibiotics are often erroneously given to the child

Question 138

Describe insect sting hypersensitivity

Answer 138

• Arises mainly from bee and wasp stings
• Severity may be:
  
  • Mild: local swelling
  • Moderate: generalised urticaria
  • Severe: systemic symptoms with wheeze or shock
• Those who have suffered from a severe reaction should be offered an EpiPen and allergen immunotherapy

Question 139

What is acute appendicitis?

Answer 139

• Acute inflammation of the vermiform appendix

Question 140

What is the aetiology of acute appendicitis?

Answer 140

• Obstruction of the appendiceal lumen, causing a cycle of progressive inflammation and bacterial outgrowth

Question 141

What is the epidemiology of appendicitis

Answer 141

• Most common cause of an acute abdomen in children
• Incidence: 4/100
• Any age, most common >5 years of age, uncommon <2 years

Question 142

What are presenting symptoms of appendicitis?

Answer 142

• Large variation in clinical picture
• Periumbilical colicky pain then localises to the right iliac fossa. Constant with peritoneal inflammation and increased with movement
• Anorexia (vague abdominal pain and won’t eat their favourite food)
• Vomiting (young children)
• Constipation or diarrhoea (less common)
• Low grade pyrexia

Question 143

What are signs of appendicitis on examination?

Answer 143

• General: Tachycardia, pyrexia, reluctance to move
• Abdominal examination: Percussion tenderness signifies inflammation of the peritoneum . Guarding may be present in RIF (McBurney’s point). Rovsing’s sign (LIF palpation causing RIF pain). There may also be pain on expansion and recession of the abdomen. Cough may exacerbate pain. Peritoneal irritation signs may be absent with a retrocaecal appendicitis
• Rectal examination: Should be performed by the most senor doctor only when diagnosis is in doubt. There is marked tenderness against rectal wall, especially with a retrocaecal appendix

Question 144

What are the investigations for appendicitis?

Answer 144

• General: Appendicitis is a clinical diagnosis: investigations may aid diagnosis in difficult cases.
• Bloods: Increased WCC (normal WCC doesn’t exclude appendicitis), increased CRP, U&Es (especially if vomiting), clotting (raised neutrophil count is the most sensitive serological investigation for appendicitis)
• Urine: MC&S to exclude UTI, leucocytes may be present with an inflamed appendix against bladder wall (nitrite -ve)
• Radiology: Plain AXR not indicated; if performed, may show dilated loops of bowel and a fluid level in the RIF. USS may show the inflamed appendix as a non-compressible tubular structure, presence of free fluid or appendiceal mass

Question 145

What is the management of appendicitis?

Answer 145

• Surgical: once diagnosed is confirmed clinically. May be performed via the traditional open approach (Lanz incision) or laparoscopically. Washout essential with complicated appendicitis
• Conservative: With a confirmed appendiceal abscess that responds to intravenous antibiotics. If this management fails then surgical intervention (+/- drain insertion) is indicated. If conservative management succeeds then the patient is offered an interval appendicectomy

Question 146

What are complications of appendicitis?

Answer 146

• Perforation: <3 years old = 80-100%; >10 years old = 10-20%. Complicated appendicitis (perforated/presence of pus); wound infection/intra-abdominal abscess formation.
• Decreased fertility in girls after complicated appendicitis (ovarian/fallopian tube involvement), small bowel obstruction, adhesions

Question 147

What is the prognosis of appendicitis?

Answer 147

• Usually excellent

Question 148

What is asthma?

Answer 148

• Chronic inflammatory airways disease characterised by
  
  • variable reversible airway obstruction
  • airway hyper-responsiveness
  • bronchial inflammation

Question 149

What is viral induced wheeze?

Answer 149

• Result from small airways obstructing and becoming narrow due to inflammation and aberrant immune responses to viral infection
• MOST wheezy preschool children have viral episodic wheeze
• Viral episodic wheezing usually resolves after about 5 years (probably due to an increase in airway size)

Question 150

What is the aetiology of asthma?

Answer 150

• Genetic factors: Positive family history of asthma or atopy.
• Environmental triggers: Passive or active smoking, URTIs, exercise, cold weather, inhalant
  allergies (house dust mite/pollens/moulds/pets) and food allergens

Question 151

What is the aetiology of viral induced wheeze?

Answer 151

• RISK FACTORS: maternal smoking during and/or after pregnancy and prematurity

Question 152

What is the epidemiology of asthma and viral induced wheeze?

Answer 152

• Prevalence: 10–15%. Age: 80% of asthmatic children are symptomatic by the age of 5. M:
  F, 2:1; equalises in adulthood.
• Distribution: Viral-associated wheeze/recurrent wheezy
  bronchitis “ in urban areas and in children of low socio-economic status families.

Question 153

What are the presenting symptoms of asthma and viral induced wheeze?

Answer 153

• Age-related symptoms
  
  • <1 year: Persistent or recurrent nocturnal cough, wheezing with URTIs.
  • 2–3 years: Nocturnal cough, wheezing during exercise with URTIs.
  • <5 years: Non-productive cough may be the only symptom, often worse at night and in
    the morning.
• Assess severity: Frequency of attacks (mild: <1 attack in 2 months; moderate: >1 attack
  in 2 months; severe: persistent symptoms, decreased exercise tolerance), effect on school
  attendance, hospital attendances and admissions to PICU.

Question 154

What are the signs of asthma and viral induced wheeze?

Answer 154

• Respiratory: End-expiratory wheeze, recession, use of accessory muscles, tachypnoea,
  hyper-resonant percussion note, diminished air entry, hyperexpansion, Harrison sulcus
  (anterolateral depression of thorax at insertion of diaphragm).
• Peak flow: Peak flow: Useful in >5 years of age; use as baseline (predicted best) and as determinant for
  efficacy of treatment

Question 155

What are the BTS guidelines for severe asthma?

Answer 155

• Too breathless to speak
• Tachycardia
  
  • > 120 bpm in 2-5 years
  • > 130 bpm in <2 years
• Tachypnoea
  
  • > 30 breaths in 2-5 years
  • > 50 breaths in <2 years
• Peak flow: <50% predicted > 5 years

Question 156

What are the BTS guidelines for life threatening asthma?

Answer 156

• Silent chest
• Cyanosis
• Poor respiratory effort
• Hypotension
• Exhaustion
• Confusion
• Coma
• Peak Flow: <33% predicted in >5 years

Question 157

What are the investigations for asthma and viral induced wheeze?

Answer 157

• CXR: In acute severe cases to exclude pneumothorax or first presentation to exclude
  congenital anomaly.
• Lung function (spirometry): Can be performed in >5 years. Obstructive airways disease:
  FEV1 <80%, FVC normal or reduced, FEV1/FVC <70%. Assess reversibility after 400 mg
  salbutamol inhalation.

Question 158

How is an asthma attack managed?

Answer 158

• High-flow oxygen via reservoir bag.
• Salbutamol and ipratropium bromide via volumatic spacer or nebulised.
• Oral prednisolone 20 mg (2–5 years), 30–40 mg (>5 years) or IV hydrocortisone if unable
  to retain oral medication.
• Commence IV salbutamol (bolus then infusion) or aminophylline infusion.
• Magnesium sulphate (40 mg/kg) IV.
• If not responding (<92% O2 saturations) or any life-threatening features present, discuss
  with PICU for ventilatory support.
• Discharge criteria: Patients can be discharged when stable on 3–4-hourly inhaled
  bronchodilators. Peak flow 75% of predicted best, and O2 saturations >94%.
• Education: On adherence to medication, recognition of acute attacks, emergency protocol,
  maintaining normal activities

Question 159

What are key principles when managing chronic asthma?

Answer 159

1. Avoid obvious precipitants, e.g. passive smoking, allergen avoidance.
2. Ensure good inhaler technique þ / volumatic spacer.
3. Check compliance.
4. Review treatment every 3–6 months.
5. ‘Rescue’ prednisolone in acute deterioration.
6. If obese advise weight reduction.

Question 160

When should a preventer inhaler be started?

Answer 160

1. Symptomatic/use b2-agonist inhalers 3 times/week.
2. Waking one night/week.
3. Frequent exacerbations

Question 161

How should chronic asthma in children <5 years be managed?

Answer 161

Step 1, mild intermittent asthma: Short-acting b2-agonist inhalers (e.g. salbutamol)
as necessary.

Step 2, regular preventer control: Add low-dose inhaled steroid (200–400 mg/day
budesonide equivalent) or leukotriene receptor antagonist if steroid cannot be used.

Step 3, add-on therapy: Trial of leukotriene receptor antagonist.

Step 4, persistent poor control: Refer to respiratory paediatrician.

Question 162

How should chronic asthma in children 5-12 years be managed?

Answer 162

• STEP 1: offer a SABA (e.g. salbutamol) as reliever therapy
• STEP 2: consider an 8-week trial of paediatric moderate dose ICS in children with:
  
  • Symptoms at presentation that clearly indicate the need for maintenance therapy (e.g. asthma-related symptoms > 3 times per week)
  • Suspected asthma that is uncontrolled by SABA alone
• STEP 3: Consider an LTRA in addition to the ICS and review in 4-8 weeks
• STEP 4: Consider stopping the LTRA and starting a LABA
• STEP 5: Consider changing the ICS and LABA maintenance therapy to a MART regimen, with paediatric low maintenance ICS dose
• STEP 6: Consider increasing ICS to a paediatric moderate maintenance dose
• STEP 7: refer to specialist care (they may consider using paediatric high dose ICS or a trial of an addition drug (e.g. theophylline))

Question 163

What are possible complications from asthma?

Answer 163

• Decreased linear growth rate due to poorly controlled asthma more
  usual than from overprescription of inhaled steroids, chest wall deformity, recurrent infections, status asthmaticus can be fatal.
• One-third of deaths occur under the age of 5 years

Question 164

What is the prognosis of asthma?

Answer 164

• Asthma often remits during puberty and many children are symptom free as
  adults, especially those who have mild asthma and are asymptomatic between attacks, or
  who develop asthma at >6 years.
• Rates of admission and mortality in asthma have decreased since the early 1990s.

Question 165

What are breath-holding attacks?

Answer 165

• A developmental condition in which the child experiences a brief episode
  of apnoea.

Question 166

What is the aetiology of breath-holding attacks?

Answer 166

• Pallid (or white) breath-holding attacks: Abnormally sensitive response to carotid sinus or ocular compression with the production of temporary asystole or marked bradycardia.
• Cyanotic (or blue) breath-holding attacks: Mechanism unclear; however, includes centrally mediated reduced respiratory effort and altered lung mechanics, which may inappropriately stimulate pulmonary reflexes, thus resulting in apnoea and hypoxia.

Question 167

What is the epidemiology of breath-holding attacks?

Answer 167

• Occurs in 1–2% of children between the ages of 6 months and 5 years, 75% of which occur between 6 and 18 months. M = F.
• Breath-holding spells usually occur from 1–2/day to 1–2/month. 60% have cyanotic type, 20% pallid type and 20% a combination.

Question 168

What are presenting symptoms of breath-holding attacks?

Answer 168

Pallid breath-holding attack
- Triggered by fear or a painful stimulus such as a knock to the head or falling
>
- Child stops breathing and rapidly loses consciousness
>
- Child becomes pale and hypotonic
>
- May experience a tonic seizure as a result of cerebral underperfusion (reflex anoxic seizure)

Cyanotic breath-holding attack
- Triggered by anger, frustration, upsetting event or scolding
>
- Child cries and subsequently holds breath in expiration
>
- Rapid onset of cyanosis that may progress to loss of consciousness
>
- Brief tonic-clonic jerks, opisthotonos (rigidity and arching of the back, with head thrown
backwards)
>
- Bradycardia may follow

Attacks last less than a minute. There is usually full resumption of normal activity within
minutes. Some children may remain lethargic and drowsy for some time after an attack.

Question 169

What are signs of a breath-holding attack?

Answer 169

• Neurological examination to exclude focal signs suggestive of an underlying structural abnormality if unusual features in history.

Question 170

What are investigations of a breath-holding attack?

Answer 170

• Not usually required.
• EEG: Generalised slow waves with flattening during the attack (a pattern characteristic of cerebral hypoxia). Interictally the EEG is normal.
• ECG: If cardiac arrhythmia is suspected.

Question 171

How are breath-holding attacks managed?

Answer 171

• Parental education: Reassurance and emphasis on consistency and not reinforcing the child’s behaviour pattern after the attack.
• Child should lie flat during attack for cerebral perfusion.
• Atropine sulphate may be considered in refractory pallid attacks to block the vagus nerve.

Question 172

What are complications from breath-holding attacks?

Answer 172

• No immediate complications except if the child collapses in an
  unsafe environment

Question 173

What is the prognosis of breath-holding attacks?

Answer 173

• Stop having the attacks after the age of 5 or 6 years.
• Children who have pallid attacks have an “ incidence of syncope in adulthood.
• There is no increased incidence of epilepsy in either type.

Question 174

What is bronchiolitis?

Answer 174

• Respiratory condition characterised by coryza followed by a ‘bronchiolitic’ dry, wheezy cough, breathlessness, poor feeding, hyperinflation of the chest and expiratory wheeze in infants

Question 175

What is the aetiology of bronchiolitis?

Answer 175

• RSV (75%)

- There may be multiple causative agents (rhinovirus, parainfluenza, influenza or adenovirus).

Question 176

What is the epidemiology of bronchiolitis?

Answer 176

• Most common LRTI in infants, especially 3–6 months. Winter epidemics: <=3% infants are admitted to hospital.

Question 177

What are presenting symptoms of bronchiolitis?

Answer 177

• Cough
• Breathlessness
• Wheeze.
• In more severe cases infants may become too breathless to feed, have apnoeic spells or become lethargic

Question 178

What are the signs of bronchiolitis?

Answer 178

• General: Mild pyrexia, tachycardia, irritability.
• Respiratory distress: Tachypnoea, subcostal/intercostal recession, nasal flaring, grunting, widespread expiratory wheeze +/- fine crepitations.
• Severe disease: Cyanosis, lethargy.

Question 179

What are the investigations for bronchiolitis?

Answer 179

• Bloods: Not indicated in mild disease. May find increased WCC, decreased Na (2˚ to SIADH), capillary gas (decreased pO2 and increased pCO2 if child is becoming exhausted)
• CXR: Not indicated in mild disease; will show hyperinflation due to small airways obstruction and air trapping. Collapse (classically of the right upper lobe) and/or consolidation in secondary bacterial infection may also be seen.
• Serology: RSV may be identified by immunofluorescent staining of nasopharyngeal aspirations (NPA) using specific viral antisera.

Question 180

How is bronchioloitis managed?

Answer 180

• Humidified oxygen supplementation if saturation is persistently < 92%
• Consider CPAP if impending respiratory failure
• Consider upper airway suction if there is evidence of increased airway secretions (this should definitely be performed if they are presenting with apnoea)
• Give fluids by nasogastric or orogastric tube if they cannot take enough fluid by mouth
• Supportive
• IMPORTANT: RSV is highly infectious, so infection control measures are needed to prevent cross-infection
• Most infants will recover within 2 weeks
• RARELY, the illness may cause permanent damage to the airways (bronchiolitis obliterans)

Question 181

How is bronchiolitis prevented?

Answer 181

• Humidified oxygen supplementation if saturation is persistently < 92%

Consider CPAP if impending respiratory failure

Consider upper airway suction if there is evidence of increased airway secretions (this should definitely be performed if they are presenting with apnoea)

Give fluids by nasogastric or orogastric tube if they cannot take enough fluid by mouth

Supportive

IMPORTANT: RSV is highly infectious, so infection control measures are needed to prevent cross-infection

Most infants will recover within 2 weeks

RARELY, the illness may cause permanent damage to the airways (bronchiolitis obliterans)

Question 182

What are complications of bronchiolitis?

Answer 182

• Mortality 0.2%, intensive care unit admission 2.7% and need for ventilatory assistance 1.5%.
• Cardiac failure may occur, predominantly in infants with underlying CHD.

Question 183

What is the prognosis of bronchiolitis?

Answer 183

• Difficulty breathing, wheeze and poor feeding: 6–7 days, cough: 12 days.
• Diarrhoea may complicate the recovery phase.
• Persistent cough and recurrent viral-induced
  wheeze recur in 20% of infants (up to 60% of infants hospitalised).
• Recurrent wheeze is more common in the first 5 years after RSV bronchiolitis, but there is conflicting evidence as to whether RSV bronchiolitis predisposes to asthma.

Question 184

What is heart failure?

Answer 184

• Results when the heart can no longer meet the metabolic demands of the body.

Question 185

What is congestive cardiac failure?

Answer 185

• Refers to increased venous congestion in the pulmonary (left heart failure) or systemic (right heart failure) veins.
• This occurs when the compensatory mechanisms used to improve cardiac output are no longer adequate, and heart failure becomes uncompensated

Question 186

What is the aetiology of heart failure?

Answer 186

• Overcirculation: Normal forward blood flow is disrupted and the heart becomes an
  inefficient pump.
  
  1. Congenital heart disease (CHD): hypoplastic left heart (HLH), severe aortic stenosis,
     interrupted aortic arch, coarctation of the aorta (COA), patent ductus arteriosus (PDA),
     total anomalous pulmonary venous drainage (TAPVD), large VSD, transposition of the
     great arteries (TGA), truncus arteriosus.
  2. Postoperative repair of CHD.
  3. Arteriovenous malformation, e.g. hepatic.
  4. Severe anaemia, e.g. hydrops fetalis.
• Pump failure: Heart muscle is damaged and no longer contracts normally
  
  1. Viral myocarditis/cardiomyopathy
  2. Metabolic cardiomyopathy (e.g. Pompe disease)
  3. Arrhythmias: SVT, VT or congenital heart block (CHB)
  4. Ischaemia (post Kawasaki disease)
  5. Duchenne muscular dystrophy
  6. Medications e.g. chemotherapy

Question 187

What is the epidemiology of heart failure?

Answer 187

• Rare in children; more common in infants with CHD.

Question 188

What are the presenting symptoms of heart failure?

Answer 188

• Infants: Breathlessness, wheeze (cardiac asthma), grunting, feeding difficulties, sweating, failure to thrive, recurrent chest infections.
• Older children: Fatigue, exercise intolerance, dizziness or syncope.

Question 189

What are the signs of heart failure?

Answer 189

• General: Tachycardia (not in CHB); absence of a heart murmur does not exclude heart disease (TGA, HLH, COA).
• Left CHF: Tachypnoea, respiratory distress (recession), gallop rhythm, displaced apex.
• Right CHF: Hepatosplenomegaly +/- oedema or ascites. Jugular venous distension is not a
  reliable indicator in infants and young children.
• Uncompensated CHF: Hypotension, cool peripheries, prolonged capillary refill time, thready pulse, decreased urine output, signs of renal and hepatic failure in severe cases

Question 190

What are investigations for heart failure?

Answer 190

• Bloods: Acid/base balance, electrolytes and osmolality (likely SIADH), liver and renal function.
• CXR: Cardiomegaly, increased pulmonary vascular markings and fluid collection in the horizontal fissure/pleural effusions may be detected
• ECG: Rate, rhythm, atrial/ventricular hypertrophy or hypoplasia. Evidence of myocarditis/cardiac ischaemia or ventricular strain.
• ECHO: Diagnostic for CHD.
• Cardiac catheterisation: Measures intracardiac pressures and shunts.

Question 191

What is the management of cardiac failure?

Answer 191

• Aims
  
  • Reduce preload
    
    • Using diuretics (e.g. furosemide) or, more rarely, venous dilators (e.g. nitroglycerin)
  • Enhance cardiac contractility
    
    • Using IV agents (e.g. dopamine)
    • Other options: digoxin, dobutamine, adrenaline, milrinone
  • Reduce afterload
    
    • Oral ACE inhibitors
    • IV agents (e.g. hydralazine, nitroprusside, alprostadil)
  • Improving oxygen delivery
    
    • Beta-blockers (e.g. carvedilol)
  • Enhancing nutrition
• If there is heart failure due to a cardiac malformation
  
  • If cyanotic –> Prostaglandin infusion
    
    • This maintains a PDA in duct-dependent cyanotic heart disease and buys time before surgical correction can be performed
  • Echocardiography to identify the underlying structural defect is necessary

Question 192

What are complications of heart failure?

Answer 192

• Arrhythmias
• SVT
• VT
• CHB
• cardiogenic shock

Question 193

What is the prognosis of heart failure?

Answer 193

• Poor in children in the absence of correctable CHD

Question 194

What is cerebral palsy?

Answer 194

• Non-progressive disorder of movement and posture.

Question 195

What is the aetiology of cerebral palsy?

Answer 195

• Antenatal (80%): Cerebral dysgenesis/malformation, congenital infections (rubella, toxoplasmosis, CMV).
• Perinatal (10%): Hypoxic ischaemic encephalopathy, birth trauma.
• Postnatal (10%): Meningitis, encephalitis, extradural haemorrhage, IVH, head injury, NAI, hyperbilirubinaemia (kernicterus), prolonged hypoglycaemia.

Question 196

What is the epidemiology of cerebral palsy?

Answer 196

• 2/1000 live births. Usually presents in infancy

Question 197

What are symptoms and signs of cerebral palsy?

What are the different types?

Answer 197

• General: Delayed milestones, poor feeding,
  abnormalities of tone, posture, gait, difficulties with language, impaired social skills

Clinical Types
- Spastic (70%): Affected limbs show increased tone (clasp-knife), brisk reflexes, extensor plantar
responses:
- Hemiplegia: unilateral, arm > leg, fisting and early hand preference <1 year, characteristic posture of abduction of shoulder, flexion at elbow and wrist, pronation of forearm, and extension of fingers
- Diplegia: legs > arms, hypertonicity of hip adductors ! leg ‘scissoring’
- Quadriplegia: all 4 limbs affected – arms > legs, poor head control, paucity of movement.
Abnormal primitive reflexes and fisting in the first few months.

• Dyskinetic (10%): Normal progress until 6–9 months, followed by progressive dystonia of lower limbs, trunk, and mouth exaggerated by involuntary movements; athetoid (writhing) and choreographic movements (jerking).
• Ataxic (10%): Hypotonia, ataxia of trunk and limbs, postural imbalance, intention tremor.
• Mixed (10%).

Question 198

What are the investigations for cerebral palsy?

Answer 198

• Assessment of hearing and vision.

- EEG if seizure prone

Question 199

What is the management of cerebral palsy?

Answer 199

• Education: mainstream school + extra support (liaison with (SENCO)) or special needs school
• Physiotherapy: early to maintain full ROM, function, normal development and prevent contractures.
• Occupational therapy: splints, crutches, walking frames, wheelchairs.
• SALT: including control of drooling (oral training).
• Feeding: may be unable to suck, chew or swallow, therefore requiring gastrostomy feeds.
• Orthopaedic: surgery to correct deformity and improve function.
• Neurosurgical intervention: considered to reduce muscle spasticity or for disabling dystonic movements.
• Medical: baclofen or botulinum toxin injections to
  relieve spasticity. Genetic counselling

Question 200

What are the complications of cerebral palsy?

Answer 200

• Aspiration pneumonia
• Failure to thrive
• Scoliosis
• Dislocated hips.

Question 201

What is the prognosis of cerebral palsy?

Answer 201

• Spastic hemiplegia: Delayed but eventually normal gait.
• Spastic diplegia: Characteristic gait (knees flexed, toe walking, and adducted hips).
• Spastic quadriplegia: Poor prognosis related to feeding disability and immobility. Sufferers
  are often totally dependent and life expectancy is significantly reduced. Usually die from
  chest infections 2 to muscular weakness and poor chest dynamics 2 to kyphoscoliosis.
• Dyskinetic: Usually unable to walk independently, quality of life can often be poor.
• Ataxic: Most children walk (though often delayed) with the aid of crutches