The PMJ blog has been running for 2 and a half years, and in that time I have looked at many aspects of medical practice and education that have been thrown up by papers published in the PMJ.
As time has gone on, we have had several submissions to the journal which seem to fit better within the blog format than as ‘fillers’ within the published journal, but do not necessarily link directly to manuscripts that are due for publication. However, they stand in their own right as pieces of interest to the PMJ readership, and cover experiences wider than my own.
As such, you will see different ‘voices’ within the blog, and I hope that these voices will also challenge and inform about subjects that have struck them as important in their clinical lives. In contrast to the ever increasing enforcement of reflection in clinical practice, here are vignettes and observations that demonstrate reflection, but are submitted for wider circulation, and not hidden away on the servers of an eportfolio, or appraisal folder.
So over to Dr Welsby who has submitted the following ‘jaundiced view of jaundice’:
A confused young man and had been admitted with “?Hepatitis.” He was febrile and deeply jaundiced (patients with Hepatitis A or B, once jaundice is obvious, are usually afebrile and, barring complications, often feel better).
Obviously ”liver function tests” were in order. The first liver function test was to observe that his underwear was bile stained. The usual liver function tests were mandatory but predictable. His bilirubin was obviously high, too high to be caused by haemolysis alone (because haemolytic jaundice is lemon coloured and mild whereas obstructive or hepatitic jaundice tends to be deep and greenish). His ALT was moderately raised – unsurprising because his liver was tender on palpation and his alkaline phosphatase was raised in keeping with anatomical or physiological obstructive jaundice.
Obviously a clotting screen should be undertaken but what two tests that are rarely considered to be liver function tests should be performed. Firstly, the blood urea was high. This is unusual in hepatitis because the inflamed liver tends not to make urea (in formal hepatic failure the urea is characteristically low) and his raised urea suggested a degree of renal failure. Secondly, the glucose level (it is mostly liver glycogen that keeps up the blood glucose. In formal liver failure the glucose is characteristically low and intravenous glucose is often required. Hypoglycaemia is the only liver function test that can be immediately normalised.
One investigation that should not be omitted was the most important. A phone call to get a full history. He had recently been in Africa and his blood was full of falciparum malaria that would not have shown up on a routine blood count.
His parasitaemia demanded an exchange transfusion because parasitized red blood corpuscles cannot transport oxygen. Accordingly his blood was venesected and replaced by donated blood. Now, here is a question to which I have never received a sensible answer “How long does it take for stored blood, once administered, to start to transport oxygen?” Answers range between “a few hours” to “about 24 hours.” For stored blood duration of storage would obviously be relevant (someone should do an MD to investigate this). If he were given non-oxygen transporting blood there is a prospect of doing him a disservice by making him more hypoxic. This is why fresh blood is often used for such exchange transfusions.