A 36 year old soldier developed a flu-like illness (fever, chills, headache, myalgia) 4 days after returning to Jakarta, Indonesia, from a 1 year posting to Papua New Guinea. He was known to have chronic hepatitis B infection, with chronically mildly abnormal liver function tests, but was not on any treatment for this, and had otherwise been well. 3 days later he developed nausea and vomiting and abdominal pain, and jaundice was noted. After a week of this illness he was admitted to hospital where he was thought to have obstructive jaundice, so on the 10th day of his illness he was transferred to a tertiary centre.
From the UK Kidney Association’s international case presentation series. This case contributed by Dr Jonny and colleagues from Jakarta, Indonesia.
On transfer he was initially alert, deeply jaundiced, apyrexial, BP 107/53, but becoming obtunded. Some upper abdominal tenderness was noted. Ultrasound showed normal liver oultline no obstruction, thickened gallbladder wall with sludge. Elastography suggested severe liver fibrosis. Blood test results are shown (click to enlarge). The urea converts to 117 mmol/l, Creat 1160 micromol/l. High enough for uraemic encephalopathy. He was also oliguric. He was anaemic, Hb 7.6 g/dl, wbc 19.9 (neutrophilia), plats 462.
The initial suspicion was that he had an acute exacerbation of chronic HBV hepatitis, possibly with acute cholecystitis, complicated by AKI.
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What happened next
There are interesting lists of simultaneous jaundice and renal disease
- infective (e.g. Leptospirosis)
- toxic (many, including paracetamol)
- just secondary to severe hepatic disease – hepatorenal syndrome and (perhaps controversially, is it just an epiphenomenon?) bilirubin cast nephropathy.
The key result here was a blood smear.
A revealing test
A blood smear showed Plasmodium falciparum gametocytes, 63 per 500 erythrocytes, 1008 parasites per microlitre. The patient therefore has severe falciparum malaria, with ‘blackwater fever’ and possibly cerebral manifestations (though this could have been just uraemia). The urine did indeed look very dark, which you can also see in rhabdomyolysis, but you can sometimes see similar in severe ATN. Especially perhaps if a patient is jaundiced.
Outcome and further information
He developed multi-organ failure and despite anti-malarial therapy and CVVH (continuous haemofiltration) he deteriorated, developing secondary sepsis, and unfortunately died of septic shock.
Malaria is endemic in Papua New Guinea, but not in Jakarta. He had not been taking prophylaxis while away. The lack of substantial fever probably hindered recognition, and he was treated too late. Simple things.