Acute surgical abdomen—an atypical presentation of Plasmodium vivax malaria

A search of the existing literature did not identify any previously reported cases of acute abdomen as atypical features of vivax malaria. The case presented here illustrates the ubiquitous nature of this disease with its unusual clinical manifestations in the UK.

A 51‐year‐old Asian man presented to the acute surgical admissions unit with a 1 week history of left iliac fossa pain, malaise and non‐bilious vomiting. No other bowel or urinary symptoms were present. His medical history included asthma, which was well controlled with inhalers. He had no history of any previous abdominal surgery.

On examination, he was found to be clammy and to have dry mucosal surfaces. Initial observations recorded a temperature of 40.1°C and a regular pulse of 133 beats/min, with a blood pressure of 108/51 mm Hg and a respiratory rate of 20 breaths/min. Pulse oximetry showed an oxygen saturation of 97% in room air. Cardiorespiratory examination was normal. Abdominal examination showed marked left iliac fossa tenderness with signs of peritonism. No evidence of hepatosplenomegaly was seen. Per rectal examination was normal. Chest and abdominal x rays were unremarkable, with no evidence of perforation. Urine analysis was negative. Blood tests gave 13.1 g/dl haemoglobin, 2.97×10/l leucocytes, 115×10/l platelets, 9.8 mmol/l urea, and 128 mmol/l creatinine. All other blood tests including serum amylase were normal. The initial clinical impression was sepsis secondary to diverticulitis with localised diverticulum perforation.

The patient was resuscitated with crystalloid, with a lack of response to resuscitation or deterioration in the clinical condition indicating an emergency laparotomy. However, over a period of observation with aggressive fluid resuscitation, he stabilised haemodynamically (pulse 80 beats/min and blood pressure 92/57 mm Hg). An abdominal/pelvic computed tomogram showed no evidence of diverticulitis or perforation. No focal small or large bowel abnormality was detected. A cardiac echo excluded infective endocarditis. Interestingly, blood films taken for haematology were reported to show Plasmodium vivax infestation. Further questioning revealed that the patient had returned from Pakistan 8 months before. He also admitted to not taking prophylaxis. Treatment for malaria was initiated with a 600 mg chloroquine stat dose, 300 mg once daily for 2 days. This was followed with primaquine, 30 mg once daily for 14 days. The patient was discharged 4 days later, having remained pain‐free and apyrexial.

This case report shows that increased global travel results in infections in non‐endemic areas.¹ Therefore, doctors in non‐endemic areas need to be familiar with the clinical features of this disease (fever, chills,² headache, myalgia, nausea, vomitting, cough,³ malarial paroxysm, migraine, urticarial rashes, bradycardia, postural hypotension,⁴ jaundice, cerebral involvement, anaemia, thrombocytopenia, pancytopenia,⁴ splenic rupture due to splenomegaly⁵), as diagnosis may not be straightforward and malaria presents in many atypical ways. Firstly, it is important to take a travel history. Secondly, symptoms and illness from vivax malaria may present many months after travel and exposure, possibly as a relapse from an earlier mild infection.⁶ Thirdly, malaria may cause abdominal pain.⁷ This patient presented with all the clinical features of localised peritonitis with concomitant dehydration and hypotension, and was being considered for an exploratory laparotomy. The diagnosis was made on the smear obtained for full blood count. The patient recovered rapidly with malaria treatment, and all symptoms and signs resolved within days. The hypothesis behind this case report is that prolonged incubation period, relapse after months or years after the primary infection, coexistence of P vivax and P falciparum with P vivax suppressing P falciparum, and sequestration in gut and visceral ischaemia may cause intense abdominal pain.