Usually worse abdominal pain than usually seen in gastroenteritis, can also be high fever. If severe, shigella/campylobacter can be treated with antibiotics.
If chronic, consider
constipation (stools might be soft but would expect them then to be massive)
An added sound heard when listening with a stethoscope, distinct from heart sounds or other clicks or snaps.
Can indicate a structural abnormality. But can be heard in normal hearts too, esp kids.
Still’s murmur
Or “innocent” murmur. Characteristic vibratory, low pitched, crescendo-decrescendo sound – “like an Aeolian harp” – loudest along left sternal border. Never louder than grade 3. Typically gets quieter when child sits or stands up (reduced venous return?) – you would not expect a murmur caused by a structural abnormality to change much.
Present at any age. Usually goes away by adolescence.
Venous hum
Another innocent one, a rumble heard in the upper chest, disappears when lying down, or when neck turned or neck veins occluded gently.
Pulmonary flow murmur
Pulmonary valve closest to anterior chest wall, which might explain why you sometimes hear this. Might be confused with pulmonary stenosis or subaortic membrane.
A viral rash, sometimes dramatic, can last for months! Typically young adults. Some characteristic features:
Viral illness itself can be trivial
Usually not itchy
Herald patch – starts with an oval scaly macule, can grow up to 5cm in diameter. Looks like ringworm, but then:
Then multiple smaller scaly oval macules or plaques, typically chest and back – up to 20 days after appearance of herald patch. Classically “pine tree” distribution – think drooping branches extending out from midline.
Older infants who otherwise appear well and have a positive urine dipstick or microscopy to suggest UTI, do not routinely require a lumbar puncture to exclude bacterial meningitis – PECARN study of 697 febrile infants aged 28-60 days with suspected UTI found no cases of bacterial meningitis.
In bronchiolitis, wide variation in practice – NICE bronchiolitis guidelines do not comment, and NICE suspected sepsis guidelines do not say that bronchiolitis exempts you from “suspected sepsis”.
Traumatic tap
Increasing RBC counts were statistically associated with increasing WBC counts (P < .001). But in febrile babies under 90 days,where RBC < 10 000/mm3 no real impact and reference range for WBC in uninfected infants with traumatic lumbar punctures was still 0 to 16/mm3.
CSF protein increased linearly with increasing CSF RBCs (up 1.1 mg/dL for every 1000 RBC).
Correct 500:1? Sounds good in theory, but not in practice. Predicted leukocytes matched observed leukocytes poorly for 682 CSF specimens. Adjusted blood counts in CSF have no advantage over uncorrected counts for predicting bacterial meningitis. [PIDJ 2006;25(1):8-11DOI: 10.1097/01.inf.0000195624.34981.36 · ]
Rare in developed world now, still common in underdeveloped world, or at least in underdeveloped communities eg Aboriginal Australians. Prob also genetic susceptibility.
Autoimmune, multisystem disease triggered by Group A streptococcus infection. Important cause of acquired heart valve disease.
Can recur.
Probably cross reactivity between specific Group A strep M proteins and human tissues.
Erythema marginatum
Diagnosis
Jones criteria:
Major
Carditis eg new murmur. Mitral most commonly, classically apical blowing pan-systolic. Aortic next most common.
Arthritis esp large joints. Migratory.
Subcutaneous nodules – these are the most uncommon major criterium (in Turkish study of over 1000 cases there were none with nodules). Typically over extensor surfaces of joints, 0.5-2cm, symmetrical.
Erythema marginatum – not specific to rheumatic fever. Seen in 0.4% of Turkish study patients. Serpiginous or annual eruption, can look similar to erythema multiforme. Provoked by warmth eg bath. Non pruritic.
Minor
Fever
Arthralgia
Prolonged PR interval on ECG
Elevated CRP/ESR
2 major or 1 major plus 2 minor, plus confirmation of group A streptococcal infection eg positive culture, high ASO titre sufficient for diagnosis. Modified Jones takes into account background incidence.
Note that initial infection may be subclinical eg pharyngitis, erysipelas. Symptoms of rheumatic fever develop 10 days to several weeks later. Chorea can appear months later. Low threshold for echo as carditis can also be subclinical.
Established criteria for rheumatic valvulitis – Gewitz 2015
Treatment
Antibiotics – Treat with penicillin, this does not however affect clinical course but hopefully prevents further spread of that particular bug. Traditionally single dose intramuscular Penicillin G Benzathine.
NSAIDs for joint pain. Usually dramatic response, if not then reconsider diagnosis!
Valproate for chorea, possibly steroids – see Sydenham’s.
Aspirin and/or Steroids for carditis, but not much evidence. Diuretics, ACE inhibitors for cardiac failure.
Long term treatment
Recurrence with progression of valve damage is the main concern, and well recognized. Subclinical carditis improves in about 50% but definite risk of progression (mild definite and borderline RHD showed 26% and 9.8% echocardiographic progression respectively).
Regular intramuscular penicillin (benzathine pencillin G) every 2-3 weeks has the lowest recurrence rates but oral penicillin V more acceptable. Erythromycin or cephalexin if allergic.
WHO recommendations:
Rheumatic fever without carditis: 5 years after last attack or until age 18 (whichever is longer)
Rheumatic fever with carditis but without residual disease: 10 years after last attack or until age 25 (whichever is longer)
Residual valve disease or valve replacement: lifelong
American and Australian heart association guidelines vary slightly:
Seizures, fits, funny turns, convulsions, attacks… None of these really has a medical meaning. Convulsion suggests rhythmic motor activity, but that’s about it. The implication of most of these is that there is excessive abnormal, involuntary muscle contraction, usually bilateral. But more broadly, some involuntary, usually sudden and self terminating episode of abnormal (or at least non-purposeful) activity and/or impaired awareness. Can be sustained or interrupted.
Neonate or young infant? Some additional possibilities eg hypoxic ischaemic encephalopathy (HIE), Fifth day fits, drug withdrawal (neonatal abstinence syndrome), pyridoxine dependent epilepsy.
Most commonly Febrile convulsions ie age related, benign. Beware complex (multiple seizures in same illness, focal features, prolonged >15 mins) and any abnormal findings eg neck stiffness, bulging fontanelle, prolonged illness, abnormal cognition before/after.
The foreskin cannot, and should not, be retracted in newborn babies. It should gradually begin to separate in the first few years of life. Sometimes it takes until puberty.
Retraction should lead to a pouting appearance of the foreskin. Technically this is not phimosis, which implies an abnormality. Some ballooning with micturition is seen, and is not an indication for surgery.
Can try application of topical steroid cream to speed up separation eg 0.025% betamethasone (1 in 4, or RD) cream twice daily for 2 to 4 weeks. Gently retract foreskin without causing any discomfort and apply a thick layer of cream to the tightest part of the foreskin. Steroid creams of higher potency may be tried if this fails.
Inflammation of the foreskin (posthitis), glans (balanitis) responds usually just to hygiene measures – bathing, cleaning, drying. Antibiotics might be needed if spreads on to shaft. Topical steroids can help.
Circumcision if significant phimosis and steroid creams fail.
Smegma pearls
Retained smegma can accumulate into substantial but painless lumps down the shaft of the penis. Can be ignored.
Balanitis Xerotica Obliterans
A form of lichen sclerosus affecting the tip of the penis. No pouting of foreskin seen on retraction. Can be white, crinkly thickening. Can be bleeding, discomfort. No good evidence for topical steroids, usually surgical treatment.