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Ebola persistence and recrudescence

General paediatrics, Infectious disease

Now documented that Ebola can recur, or else persist (and therefore be transmissible) from survivors.

Only 2 documented cases of recurrence.  Must be v low risk.

Where blood/urine PCR positive, always ill. Detectable in urine, sweat for up to 40 days.

Circulating neutralizing antibody would reduce risk from blood, but “immune protected” sites different eg Eyes, Pregnancy / breast milk, semen, Central nervous system.

Only 2 cases of sexually transmitted ebola.

So far no evidence of persistence beyond 1yr.

 

Lymphoedema

General paediatrics, Surgical

In adults, usually after surgery or radiotherapy.  But can be primary, appearing in childhood (but not necessarily in early childhood).  Secondary causes include Klippel-Tranaunay, Noonans, Turners, other venous malformation.

The incidence of primary lymphoedema is approximately 1 in 6,000 births. Approximately 10 children are born each year with primary lymphoedema in Scotland.

Lymphoedema, particularly if not well controlled, “carries significant human, personal, financial and societal costs”. Apart from cosmetic issues, pain is often a significant problem (underestimated), plus risk of cellulitis.  Inadequate treatment increases risk of complications:

  • fibrosis,
  • papillomatosis (warty growths consisting of dilated lymphatics and fibrous tissue)
  • lymphorrhoea (leakage of lymph fluid through the skin),
  • functional limitations
  • psychological morbidity, social isolation and limitation of life choices, including employment opportunities

So early diagnosis and control important.

Examination

Deep pressure for at least 30 seconds! If pits, then lymphatics ok.

Positive Stemmer sign= the inability to pick up a fold of skin at the base of the second toe, indicating thickening of the skin. This is useful in differentiating lymphoedema from other forms of oedema. [http://www.woundsinternational.com/ Journal of Lymphoedema, 2009, Vol 4, No 2]

Investigations

Consider secondary causes, as above.

Consider LFTs, thyroid function (impaired lymphatic drainage seen in hypothyroidism, hence oedema and even effusions).

Imaging to assess venous blood flow eg USS with dopplers.

MRI can show hypertrophy of fat, as in lipoedema (see below), or other tissues (viz Klippel Trenaunay).

Lymphoscintigraphy is gold standard but not readily available.

Differential is Lipoedema – almost exclusively females, presents at or after puberty, symmetrical lower limb enlargement.  Often a history of easy bruising and tenderness in the affected limbs. Lymphoedema can later develop as a secondary complication.

Further advice from http://www.thebls.com/patients/index.php?bls_user=9f0a85c93b84f4e36a2629f6d17c38e7

Patient support from http://www.lymphoedema.org/

[SMASAC Short Life Working Group on Lymphoedema – Lymphoedema Care in Scotland, Achieving Equity and Quality, 2013]

 

Pharyngitis treatment

Common, General paediatrics, Infectious disease,

Pencillin is generally recommended, as resistance in group A streptococcus is unheard of, and risk of rash with amoxicillin if actually Epstein-Barr.  For group A streptococcus a 10 day course has better microbiological clearance but probably no benefit clinically to 5 days.

For scarlet fever, treat for 10 days with any antibiotic except azithromycin (5 days).

Comparative efficacy of antibiotics vs gp A strep pharyngitis – Seventeen trials (5352 participants) were included; mixed adults and kids?

  • no difference in symptom resolution between cephalosporins and penicillin (intention-to-treat (ITT) analysis; N = 5; n = 2018; odds ratio for absence of resolution of symptoms (OR) 0.79, 95% confidence interval (CI) 0.55 to 1.12).
  • Clinical relapse was lower with cephalosporins (N = 4; n = 1386; OR 0.55, 95% CI 0.31 to 0.99; overall number needed to treat to benefit (NNTB) 50), but found only in adults (OR 0.42, 95% CI 0.20 to 0.88; NNTB 33).
  • There were no differences between macrolides and penicillin. Children experienced more adverse events with macrolides (N = 1, n = 489; OR 2.33; 95% CI 1.06 to 5.15).

Evidence is insufficient to show clinically meaningful differences between antibiotics for GABHS tonsillopharyngitis. Based on these results and considering the low cost and absence of resistance, penicillin can still be recommended as first choice.  But not much logic in replacing any other antibiotic with penicillin! [Cochrane Database of Systematic Reviews. 4:CD004406, 2013. UI: 23633318]

Short courses (3-6 days) of amox, co-amox, cefuroxime/cefixime (cefalexin not studied), macrolides etc are actually better than standard 10 day course of penicillin, but more expensive.  [ Cochrane Database of Systematic Reviews 2012, Issue 8. Art. No.: CD004872.]

SAPG 2022 recommends penicillin but if shortage amoxicillin then flucloxacillin. For penicillin allergy, clarithromycin preferred, then erythromycin, then azithromycin. Third line cefalexin, then co-amoxiclav, then co-trimoxazole.

Diabetic Ketoacidosis

Emergency medicine, Endocrinology, General paediatrics

DKA – BSPED guidance 2021.

The potentially serious acute complication of diabetes.  In the absence of adequate insulin, glucose levels start to rise in the blood, spilling over the threshold for kidney resorption and causing a diuresis.  Metabolism switches to ketone bodies, causing acidosis.

Presents with weight loss, tiredness, vomiting, heavy breathing (Kussmaul), reduced consciousness.  Diabetes symptoms of course, if first presentation, which might just be new wetting, or unusually heavy nappies.  Can be confused with pneumonia, or appendicitis! Often missed diagnosis.  In 2020 Lanarkshire audit, half had seen GPs at least once before diagnosis, with many having had bloods done rather than BM, or being asked to hand in urine the next day… 40% had BM done by family member!

Traditionally 15-17% of new presentations of diabetes are DKA, but with pandemic went up to 66%

ISPAD def DKA = Bicarbonate pH under 7.3 (H+50) PLUS ketones 3+ (blood or urine).

Beware can develop with normal glucose levels IN THOSE TAKING INSULIN.  Suspect if blood ketones above 3 in known diabetic, refer to hospital.  Between 0.5 and 3, follow sick day rules.

Mild (over 7.2 or 63) vs moderate (7.1-7.2 or 79) vs severe (79+) categories.  Treat as 5 vs 7 vs 10% dehydrated respectively.

All get 10ml/kg over 30 mins (assuming you start IV fluids) unless shocked (10/kg over 15 mins, repeat up to 40 then inotropes).

Maintenance fluids (0.9% NaCl with 20mmol KCl per 500ml bag) as per traditional formula (Holliday-Segar method) – 100ml/kg/d for under 10kg; 50ml/kg/d additionally for each kilo between 10-20kg; 20ml/kg/d for each kilo above that.

  • Calculate deficit as above. Subtract initial 10/kg bolus (but not shock boluses) and correct over 48hrs
  • ONLINE CALCULATOR (dka-calculator.co.uk) comes with disclaimer, gives fluid calculations but then prints out 16 pages which you don’t need! [KB]
  • Note SCOTSTAR has separate DKASupportDocument for those likely to need transfer

See graphic in BMJ 2016.

Complications

If acidosis not correcting, check cannula, check fluid calculations, consider sepsis.  Replace insulin syringe! Acidosis can also be caused by hyperchloraemia (hence Plasmalyte preferred at RHC – less chloride).

Risk of thromboembolism due to dehydration and immobility during recovery.

Cerebral oedema

25% mortality from cerebral oedema, 34% long term neurodisability.  Headache, irritability, agitation.  Posturing, focal neurology eg eye movements, pupil asymmetry.  Cushings triad – bradycardia, hypertension, breathing irregularity.

Hypertonic saline (2.7 or 3%, 2.5-5ml/kg over 10-15 mins) or mannitol (20%, 0.5-1g/kg over 15 mins), no preference.  

Switching

Stay on DKA pathway (and not transfer to subcutaneous insulin) until:

  • The patient has been reviewed by a Consultant, or paediatric diabetes team medical staff and
  • The patient has no evidence of dehydration has no nausea or vomiting for 6 hours, and
  • Has blood glucose less than 10mmol/l, and
  • The blood ketones have fallen below 0.9mmol/l

Panton Valentine Leucocidin

General paediatrics, Infectious disease

PVL for short.

Cytotoxin associated with Staph SCCmec type IV (this is the cassette that contains mecA), which is the one sensitive to most non-beta lactam antibiotics, but in the US many MRSA too.

Causes lysis of neutrophils and macrophages.  But clinical effects probably through immune dysregulation.

Associated with higher virulence eg necrotizing, multifocal disease eg osteomyelitis, sepsis, multiorgan failure.

Should be treated with combination of beta lactam and protein synthesis blocking antibiotic (clindamycin, linezolid, rifampicin or gentamycin).  Some evidence to support addition of daptomycin.

Surgery often required to remove foci of infection in necrotic tissue.

Decolonisation therapy with chlorhexidine body wash and mupirocin nasal cream recommended.

Chronic Recurrent Multifocal Osteomyelitis

General paediatrics, Infectious disease, Orthopaedic

Adolescents, longbones, probably 1% of all osteomyelitis. ?mech – biopsies usually negative on culture! Pain, ?arthritis if adjacent to focus. Associated with:

  • pyoderma gangrenosum
  • uveitis
  • palmar plantar pustulosis (as in psoriasis)
  • IBD (may come later)

ie inflammatory, autoimmune sounding. Osteolytic & sclerotic lesions on XR, hotspots on bone scan. Histology not characteristic. Differential diagnosis is Langerhans cell histiocytosis.

Rx NSAIDs, steroids if severe/recurrent, ?pamidronate, ?infliximab.

Self limiting but relapsing over 2-4 yrs. 1 case series showed high rate of deformity, but the largest found no long term complications at all!

Osteomyelitis

General paediatrics, Infectious disease, Orthopaedic

Bone infection.  Caused either by haematogenous spread (from distant site), direct innoculation (trauma) or spread from adjacent focus (eg otitis media).

Can be acute or more indolent eg 2/52+ symptoms (Brodie abcess). Mostly femur, tibia, humerus but can be anywhere. Up to 20% multifocal. Pelvic disease often presents with abdo/lumbar pain!

Septic arthritis – similar to OM, usually due to bacteraemia, same organisms. Potential for growth plate or joint consequences. Can lead to OM and vice versa.

Discitis – same bugs (probably), generally under 3-5yrs only, due to persistence of blood vessels in cartilage that subsequently atrophy – can mimic vertebral OM. Well, blood culture neg (cf vertebral osteomyelitis – >3yr, toxic, blood culture pos). Rx clindamycin for 2/52 but no evidence! Likely that some of these would resolve spontaneously if untreated.

Note also Chronic recurrent multifocal Osteomyelitis (CRMO) – clue is in the name! Sterile. Treat with NSAIDS.

Neonatal

Neonatal cases have wider range of organisms and generally involve both bone and joint.  Approx 50% have no systemic features, present with pseudoparalysis alone.

Bugs

Epidemiology varies. MRSA predominant in US etc.

Staph aureus is the main cause, plus:

  • Neonates – GBS, candida, enterobacteriae
  • Infant – kingella, rarely pneumococc, GAS, haemophilus (type B and others), MRSA.
  • Penetrating injuries – risk of contamination, so odd organisms

Kingella, incidentally, is often resistant to vanc and clinda!

Beware salmonella (sickle cell), meningococcal (gonococcal too), TB and non tuberculous mycobateria.  But unknown in up to half, PCR vs culture…

Panton Valentine Leucocidin toxin positive associated with higher fever, higher inflammatory markers, multiple sites, chronic/recurrent.

Radiology

X-ray shows mixture of fast (cortical breach, lysis) and slow (sclerosis, periosteal reaction) changes – but non-specific.

Abscess with sinus extending into soft tissue is indicative of infection.

Fistula and sequestrum (isolated bit of dead bone) more suggestive but take 1-2 weeks to develop.

“Onion skin appearance” suggests chronic infection but is also seen in normal infants, malignancy and in retinoid therapy.

USS may show sub-periosteal oedema early on.

MRI standard for defining collections and guiding surgery: 92-97% sens cf 64-71% for bone scan (latter is also operator dependent).

Investigations

CRP better than ESR.  But can (like WBC) be normal.

Bone biopsy rarely done unless cancer suspected. Joint/pus aspiration can be useful, but generally diagnosis relies on blood culture, hence low identification rates. New PCR technique for Kingella from conventional culture media.

Treatment

Surgical drainage if collection identified or poor response after 48-72hrs in absence of resistance. But still not well defined – over 1 yr and delayed presentation seems to have worse prognosis but will also depend on virulence and resistance.

A septic hip should always be drained promptly, but less clear for other sites – some still advocate early intervention given potential for rapid joint destruction. Aspiration and irrigation probably adequate for most, with second line open arthrotomy (laparoscopic view is limited)

Immobilization +/- traction are considered good practice. For SA, window of 4hrs considered acceptable to get samples before starting antibiotics.

Poor evidence for antibiotic treatment.  Current recommendations:

Cefuroxime under <6yrs (non-neonatal) else Fluclox  or clinda. Beware PVL staph, Hib unimmunized and risk factors for MRSA.  Broad spectrum if neonate, immuncompromised or sickle cell disease.

For all antibiotics use the maximum dose. Never give rifampicin monotherapy as resistance quickly induced. Beware erythromycin resistant MRSA and clinda (inducible resistance). Teico good for bone (keep level>10).

Switch to oral when clinically improved +/- CRP response (eg<20 or down more than 2/3 of peak), median 4 days.  Under 3 months, give full 4/52 treatment course IV.

Failure to improve –

  • consider metastatic infection, DVT, unusual organism eg Fusobacterium. PVL pos
  • IV for 21 days minimum, total 6/52 minimum (even SA)
  • HPA recommend max dose clinda, rifamp AND linezolid. Max 4/52 linez – neuropathy.

Total duration 4-6 weeks for OM, in textbooks, 3 weeks for SA.

Recent HPA guidelines suggest initial therapy for deep seated PVL positive Staphylococcus aureus infections in children as intravenous clindamycin plus rifampicin and linezolid (linezolid maximum of 4 weeks due to the risk of development of peripheral neuropathy), followed by clindamycin plus rifampicin.  Beware thrombosis.

Shorter courses eg 10 days? Peltola’s Finnish studies of shorter courses may not be applicable, as possibly selected for milder infection, exclude culture negative but have high rates of positive diagnosis (staph). [Current Opinion in Pediatrics. 25(1):58-63, 2013 Feb. UI: 23283291] Howard-Jones & Isaacs in JPedsCH however feel evidence for 3/52 courses (grade 2B), emphasize QDS dosing. 1 small old study suggested nafcillin/methicillin inferior to cefuroxime, so Clinda preferable to Fluclox. [Jourrnal of Paediatrics and Child Health 49 (2013) 760–76 UI: 23745943]

[Saul Faust Arch Dis Child 2012;97:545–553. doi:10.1136/archdischild-2011-301089]

Codeine

General paediatrics,

A European review of the safety of codeine-containing medicines licensed for pain relief in children (age 0–18 years) began in October 2012. This review was triggered by concerns of an increased risk of morphine toxicity when susceptible children receive codeine for pain after surgery. These concerns follow the reporting of three fatalities and one life-threatening case of respiratory depression in children given codeine after tonsillectomy or adenoidectomy in the treatment of obstructive sleep apnoea.

Recommendation

Do not use codeine-containing medicines in children under 12 as it is associated with a risk of respiratory side effects related to opiate toxicity. Codeine is not recommended for adolescents (12 to 18) who have problems with breathing eg neurorespiratory problems.

Contraindicated in all patients of any age known to be CYP2D6 ultra-rapid metabolisers (esp common in Africans, else 1-2%) who convert codeine into morphine.

CYP2D6 substrates include tricyclics, SSRIs, opioids, antipsychotics, beta-blockers, Chlorphenamine (!) among others. Rifampicin and dexamethasone are the only inducers, inhibitors include SSRIs. Effect depends on whether a drug needs cytochrome P450 to activate it in the first place, and whether oxidation products are more or less active than original form.

[MHRA]

Post streptococcal acute glomerulonephritis

General paediatrics, Renal

PSAGN for short.  Develops 7-14 days post streptococcal pharyngitis, longer if pyoderma.

Classic presentation is with acute nephritis viz

  • Oliguria
  • Hypertension
  • Haematuria

which leads to fluid overload.  But can be milder eg microscopic haematuria without oliguria.

Microscopic haematuria may persist 1yr+. Acute severe hypertension can present with symptoms of visual impairment, headache, encephalopathy.  Treat with labetolol or nitroprusside infusion.

Insensible losses = 400ml/m2/d.

Less than 2% have long term haematuria or hypertension.

IgA nephropathy

General paediatrics, Renal

Various presentations – usually presents as episode frank haematuria in otherwise well individual.

Can be microscopic haematuria post URTI but within 2-3 days, not delayed as in PSAGN.

Diagnosis requires biopsy – looks like HSP. IgA is found in kidney, no abnormality in blood levels!

Up to 20% progressive renal disease so not quite benign.