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.
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
- Behcet’s disease (so do HLA B51)
- Crohns disease and other IBD
- Granulomatosis with polyangitis (ex-Wegeners)
- Sarcoidosis (so do chitotriosidase)
- Tubulointerstitial nephritis and uveitis (TINU) syndrome
Some infections can cause it:
- Start outside, work in – soft tissues, then bones, then lungs/heart, finally neck/infradiaphragmatic.
- Safety check – position of lines/tunes, check apices for pneumothorax, any foreign bodies?
- Rotation – look at symmetry of clavicles and anterior rib ends.
- If clavicles high, then lordotic film. May obscure apices.
- Penetration – should just be able to make out intravertebral spaces, without lung fields being too dark.
- Inspiration – hila become artificially prominent if underinflated.
Pesky thing! Can look like pneumonia. Latter more likely if air bronchograms, volume loss (displaced fissure/trachea/mediastinum), effusion. Classically:
- indentations where ribs overlie.
- Pointy outside edge (“sail sign”).
- No mass effect
- Lowish density – should still be able to see vascular markings of lung behind
Spinnaker sign is where pneumomediastinum around thymus creates long curving line.
Other normal things
Azygos lobe – normal variant where RUL has near vertical line extending up and out, giving impression of mediastinal mass.
Mach effect – a line parallel to heart border, looks like pneumocardium but actually optical illusion where your eye “detects” border where there isn’t one…
One diaphragm usually higher than other – both ok, as long as no more than 2cm (one rib space).
Hilum – rings or tram lines suggest bronchitis. Round opacity adjacent to and larger than ring suggests vascular prominence due to left to right shunt.
Silhouette sign – where heart border and/or diaphragm obscured in lower zone due to consolidation in lower lobe (left or right).
Effusion – vertical line at costophrenic angle.
Round pneumonia – will have air bronchograms, compare mass.
Collapse vs consolidation – sharp lower border is the fissure so if deviated then collapse.
Pneumothorax – lucency without clear edge may suggest lung hyperinflation eg bronchial atresia.
If edge projects below diaphragm then likely to be skin fold!
Foreign body – get expiratory film, which will enhance air trapping.
According to NICE, 3 or more loose or liquid stools in a day (or more frequently than is normal for the individual) counts as diarrhoea.
Persisting for more than 14 days makes it chronic.
Acute typically gastroenteritis. Presence of blood and/or mucus suggests more invasive inflammation, viz colitis.
In kids, can occur with pretty much any illness!
Vomiting with diarrhoea makes a primary gut cause more likely, but still not specific.
Bloody stools, think VTEC rules!
Acute bloody diarrhoea usually infective –
- Shigella/salmonella (non typhoid strains)
- E coli (some, eg EHEC)
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
Some serious causes:
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.
Or erythema subitum. Dramatic viral rash. Caused by Herpesvirus 6 and 7.
Classically high fever, URTI symptoms or no focus, potentially febrile convulsion! Then rash appears as fever subsides, day 2-4.
Rash is widespread fine maculopapular, can be pale haloes around spots, mostly on trunk. Can be in mouth! Not itchy.
A viral rash, sometimes dramatic, can last for months! 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
- Then multiple smaller oval macules or plaques, typically chest and back – up to 20 days after appearance of herald patch
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 ;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.
Caused by Group A streptococcus. Important cause of acquired heart valve disease. Can recur.
Probably cross reactivity between specific Group A strep M proteins and human tissues.
- 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. Typically over extensor surfaces of joints, 0.5-2cm, symmetrical.
- Sydenhams chorea
- Erythema marginatum – not specific to rheumatic fever. Serpiginous or annual eruption, can look similar to erythema multiforme. Provoked by warmth eg bath. Non pruritic.
- 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.
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.
UFMG rating scale for assessing function.
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: