Kawasaki, near drowning, scabies, conjunctivitis, VZV

Question 1

What is Kawasaki disease?

Answer 1

An uncommon (8/100,000) systemic large/ medium vessel vasculitis with unknown aetiology

Question 2

What are the consequences of Kawasaki disease?

Answer 2

Coronary artery aneurysm
Sudden death (1-2%)

Question 3

Who does Kawasaki affect?

Answer 3

Children 6mnth-4ys
M>F
Japanese/ Black-Caribbean > White

Question 4

What are the main symptoms of Kawasaki disease?

Answer 4

Conjunctivitis
Rash (hands/ feet, maculopapular erythmatous)
Adenopathy (cervical LN)
Strawberry tongue
Hands/feet swollen

and

Burn: fever, >5 days, difficult to treat

Question 5

What investigations do you do for Kawasaki?

Answer 5

Clinical Dx
Bloods- FBC (anaemia, WCC raised, PLT high wk2, high CRP, ESR, LFTs)
Echo- Aneurysms

Question 6

What is the initial management of Kawasaki?

Answer 6

IVIG within 10 days

High dose aspirin then low dose aspirin (6wks)

Question 7

What are the alternative management options for kawasaki?

Answer 7

Corticosteroids
Infliximab
Ciclosporin
Plasmapheresis

Long term warfarin if cornary artery aneurysm

Question 8

What is near drowning?

Answer 8

Drowning: death from asphyxia <24h after submersion in water.

Near drowning: Survival of submersion episode.

Question 9

What is the background of near drowning?

Answer 9

Second or third larges COD in UK in children.

Secondary: seizures hypoglycaemia, intoxication, suicide attempt, arrhythmias, syncope, trauma of head or spine.

· <1y: bathtubs
· 1-5y: swmming pools
· 5+ y: lakes and oceans, sea.

Question 10

What do you establish from the history and exam from near drowning?

Answer 10

Discer: time submerged, temperature of water, ingestion of substances, trauma, water contamination, resuscitation attempts.

Hypothermia, high RR, low or high HR, low GCS. May have caridorespiratory arrest.

Question 11

What is the pathophysiology of near drowning?

Answer 11

90% aspirate and 10% go into shock and laryhgospasm. à hypoxia and acidosis.

· CNS: hypoxic neuronal injury, cerebral odema.

· CVS: cardiogenic shock, dysrythmias, hypovolaemia due to massive capillary exudation.

· Respiratory: aspiration dilutes surfactant, therefore ARDS.

Mammalina diving reflex: aopnea, bradycardia, vasoconstriction.

Question 12

What investigations do you do for near drowning?

Answer 12

Blood: ABG, WCC, drug screen.

Bronchoalveolar lavage: BAL

Monitor caridac, pulse oxymetry, RR, O2.

Trauma series (Chest, Cspine, Pelvis XR)

CT head if deteriorating GCS or neurology.

Question 13

What is the management of near drowning?

Answer 13

BLS, C spine immobilisaiton, consider ET intubaiton and NG tube to prevent vomit and aspiration. 100% O2 via reservior bag. Consider mechanical ventilation if intubated. Fluid resuscitate and ionotropes if BP not restoerd.

Disability: AVPU score (alert, berbal, pain, unersponsive) GCS. May require IV mannitol to rescue ICP.

Consider spinal incidents in all driving accidents. Correct hypothermia as exacerbates bradycardia, acidosis, remove cold clothing, rewarming, ensure core temperature >32.

Prophylactic Abx and steroids for sepsis (if BAL positive

Question 14

What are the complications and prognosis of near drowning?

Answer 14

Cerebral odema and raised ICP causing II injury, pulmonary infection, rhabdomyolysis, ARDS. Acute organ failure, DIC, cardiac arrhythmias.

70% survival if BLS provided, however very dependent on submersion circumstance. Better prognosis if higher GCS, lower time submerged, warmer water, CPR <35min at the scene.

Question 15

What is Scabies?

Answer 15

Human scabies is an intensely pruritic skin infestation caused by the host-specific mite Sarcoptes scabiei hominis.

Question 16

What is the background of scabies?

Answer 16

Infective: Sarcoptes scabiei hominis. Transmitted by contact.

Approximately 300 million cases of scabies/yr

Question 17

What do you look for in the history and exam for scabies?

Answer 17

Classic presentations: Burrowing lesions, greyish elevation of epidermis

Nodular scabies: pink brown nodules, 2-20mm in diameter

Crusted scabies: lesions are heperkeratotic and crusted, over large areas.

Secondary lesions: from infection and scratching

Burrows are a pathognomonic sign and represent the intraepidermal tunnel created by the moving female mite. They appear as serpiginous, grayish, threadlike elevations in the superficial epidermis, ranging from 2-10 mm long. High-yield locations for burrows include the following:

· Webbed spaces of the fingers

· Flexor surfaces of the wrists, Elbows, Axillae

· Belt line, Feet, Scrotum (men) / Areolae (women)

Question 18

What investigations do you do for scabies?

Answer 18

Clinical if characteristic appearance with burrows

Confirmation by light microscopic identification of mites, laevae, ovum etc in skin scrape

?biopsy specimens, serum IgE (usually raised)

Question 19

What is the management of scabies?

Answer 19

Scabicidal agent (eg, permethrin, lindane, or ivermectin)

Pruritus may be partially alleviated with an oral antihistamine, such as hydroxyzine hydrochloride (Atarax). Severe = predinisolone.

Crusted scabies: topical scabicides or oral scabicide.

Question 20

What are the complications and prognosis of scabies?

Answer 20

Allergic dermatitis to topical medicine

Infection due to rubbing and scratching (strep pyogenes, staph areous)

Exacerbation of underlying eczema, psoriasis, and Grover disease

Question 21

What is the prognosis of scabies?

Answer 21

Excellent with treatment, resoves in 2-4wk. Residual pruritus may last longer.

Immunocompromised – more often becomes crusted.

Question 22

What is conjunctivitis?

Answer 22

Mucoid/purulent discharge from eye.

Question 23

What is the background of conjunctivitis?

Answer 23

· Newborn: blocked lacrimal duct.

· Infectious: Staph areus, chlamidia trichomiasis, N. ghonorreae, viral adeno/HSV.

· Allergic: vernal keratoconjinctivitis (VKC), chornic allergic inflammation.

Associate dwiht maternal genital infection, atopy in family, FHx allergy.

1% live births.

Question 24

What are you looking for in the history and exam of conjunctivitis?

Answer 24

Newborn: first week mild mucoid discharge with no overt conjunctival inflammation, Non canalised lacrimaml duct may persist 1y.

Infectious:

· Staph/strep: Mild, lid odema, conjunctival injection, chemosis, discharge.

· Gonococcal: day 1, bilateral purulent, lip odema and chemosis. Rhinitis, stomatitis, arthritis or meningitis.

· Chlamydial: 5014d. Mild hyperaemia with scan discharge or lid swelling chemosis with pseudomembrane formation. Can have ENT infection too.

· Viral: with unilarteral red watery eye.

· VKC: Stringy white discharge, in spring. Pereniall, itchy, giant papillae in the upper tarsal conjunctiva.

Question 25

What is the management of conjunctivitis?

Answer 25

Regular saline cleaning.

Empirical chloramphenicol eye drops. After culture: Ghonorreal needs IV benzylpenicillin. Chlamydia oral erythromycin. HSV topical or IV acyclovir.

Prevent by screening mother and treating. Opthalmia neonatorium (Ghonorreal) is a notifiable disease.

Question 26

What are the complications and prognosis of conjunctivitis?

Answer 26

HSV causes corneal ulceration. Gonococcal causes abscess and perforation. Chlamydia: reversion of eyelids, infeciton and scarring à blindness.

Question 27

What are the investigations for conjunctivitis?

Answer 27

Not usually required in the newborn. If cleaned for >4h screen for infection and visual acuity.

· MCS of discharge, chamydia culture, viral swab for PCR

· Skin prick test or specific Iga for VKC. IOP measurement.

Question 28

What is VZV?

Answer 28

Contageous infectious disease caused by the DNA herpesvirus VZV.

Question 29

What is the background of VZV?

Answer 29

Antenatal: varicella embryopathy (VE) transplacental transmission of maternal infection.

Postnatal: varicella in the newborn VON. Severity dependso n time of infection

· 21-5d pre deliver apears in the first 4 days, good prognosis.

· 5 days pre delivery: presents d6-26 post eliver, poor prognosis. 30% mortality.

Postnatal: resipratory transmission

Childhood: Virus enters RT, at 4-6 days infeciton spreads to reticuloendothelial cells, spleen and liver. 11-24 days II viraemia to viscera and skin, which elicits skin lesions.

Household transmisison rates 80-90%.

Question 30

What is in the history/ exam of VZV?

Answer 30

VE:

· CNS: microcephaly, paralysis, developmental delay, seizures

· Ocular: cataracts, chorioenteritis, micropthalmia, nystagmnus.

· MSKL dermatiodal skin lesions and scarring, unilateral atrophy of limb.

VON

· Prodrome of poor feeding, mild pyrexia and malaise.

· Rash: morbilliform rask in prodrome developms into generalised purpuric vescicular rash.

Childhood

· Prodrome of mild pyrexia before skin 1-2d.

· Rash: crops at different times, papule, vescicle, pustule and crust. Hallmark is simulatenous presence of lesions at different stages.

· Systemic: abdominal pain, malaise, naorexia, cough, coryza.

Question 31

What investigations do you use for VZV?

Answer 31

Usually clinical diagnosis. Specific serology, VZV specific IgM, detect antigens by ELISa, vierology from vescicular fluis.

Question 32

What is the management for VZV?

Answer 32

Conservative: cool compress, lotion, discourage scratching. Sedating antihistamines may be required.

VZIG indicated in infants born to mothers who hadi nfection 5d pre partum, in at risk infants (<28wk or <1kg birth) and exposed seronegative pregnant women.

Prevention by routine VZ immunisation in some countries.

Question 33

What are the complications and prognosis for VZV?

Answer 33

Neurological: meningoecephalitis, acute cerebellar ataxia, Reye syndrome.

Skin: impetigo from scratchin g(II bacterial infection) scarring, nec fasciitis.

Other: pneumonia, GN, myocarditis, pancreatitis, HSP.

Mortaltiy 1/199k in otherwise healthy children. Higher in those with maternal infection <5d from birth.