Bilirubin needs to be around 60 to see visible jaundice.
AST is less specific than ALT – also produced in kidney, brain etc. But perhaps changes more quickly than ALT. Most important other source of AST and ALT is muscle – so check CK too, especially if bilirubin normal. Myopathies, viral myositis, muscular dystrophy can all present with “abnormal LFTs”.
Gamma GT is also found in other tissues so not 100% specific but typically suggests cholestasis or other biliary problem (together with alkaline phosphatase).
Alkaline phosphatase also produced in bone, so look at calcium, phosphate and vitamin D as well as signs of rickets or renal disease. Most common cause of isolated high alkaline phosphatase is benign transient hyperphosphatasaemia. There is a rare inherited disease of bone/tooth mineralisation, hypophosphatasia, where levels of ALP are abnormally low.
Falling transaminases can be ominous in situation of bilirubin, albumin, coagulation deteriorating…
The Uvea is the term for the whole eye (uvea=peeled grape). Whereas conjunctivitis looks like a red eye, it’s only really the surface that is inflamed. With uveitis, all the different tissues of the eye are inflamed. Acutely, might not look that different to conjunctivitis but painful, whereas latter usually just itchy. Anterior chamber starts to fill up with inflammatory cells so vision starts to deteriorate. An irregular pupil due to synechiae can eventually be seen, with hypopyon. Cataracts and scarring can follow.
Chronic on the other hand can be subclinical but potential for visual loss so screening important in associated conditions.
Usually idiopathic, otherwise:
Juvenile idiopathic arthritis – about 10% of patients with non-oligoarthritis, and 30% of ANA positive oligo so pretty common
HLA-B27 – with or without other B27 conditions such as Ankylosing spondylitis
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.
Or “innocent” murmur. Characteristic vibratory, crescendo-decrescendo sound, loudest along left sternal border. Never louder than grade 3. Typically gets quieter when child stands up (you would not expect a murmur caused by a structural abnormality to change).
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.
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 · ]
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.
Prolonged PR interval on ECG
2 major or 1 major plus 2 minor, plus confirmation of group A streptococcal infection eg positive culture, high ASO titre sufficient for diagnosis.
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.
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. 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.
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: