A 46-year-old man, previously well, presented at Kapit Hospital, Sarawak, Malaysian Borneo with fever, chills and rigors for 2 days. It was associated with severe epigastric and left hypochondrium pain and loose stool. There was no preceding history of trauma. Upon arrival to the emergency unit, his general condition was stable. Physical examination revealed blood pressure of 123/86 mmHg, pulse rate of 114 beats/min and temperature of 39 °C. His respiratory rate was 23 breath/min and the oxygen saturation on room air measured by pulse oximetry was 97%. The abdomen was generally tender and guarded, maximal at the epigastric region. Bedside focused abdominal ultrasonography revealed free fluid in the abdomen. Chest radiograph did not reveal any obvious sign of pneumoperitoneum.\nHaematological analysis showed haemoglobin of 11.5 g/dL, white blood cell count of 8.2 × 103/μL and platelet count of 77 × 103/μL. His creatinine level was 89 μmol/L and electrolytes were within the normal range. The results of the liver function tests were as follows: aspartate aminotransferase 15 U/L, alanine aminotransferase 11.8 U/L and total bilirubin 22.9 μmol/L. Serum amylase was normal. The arterial blood gas revealed good oxygenation and absence of metabolic disturbance (pH 7.44, PaO2 87 mmHg, PaCO2 34 mmHg, bicarbonate of 22.3 mmol/L and base excess − 1.8 mmol/L). The serum lactate measured was 0.8 mmol/L.\nPlasmodium knowlesi was identified by examination of a Giemsa-stained blood film and the parasitaemia was estimated to be 240 parasites/μL blood. Finger prick blood samples from the patient were spotted on filter paper and sent to the Malaria Research Centre at Universiti Malaysia Sarawak where DNA was extracted as described previously []. The DNA was examined by nested PCR assays specific for P. knowlesi, P. falciparum, P. vivax, P. malariae and P. ovale, which indicated the patient was infected with P. knowlesi [].\nThere was no formal radiological imaging done, such as abdominal ultrasonography or computed tomography, since this service is unavailable at Kapit hospital. Four tablets of artemether–lumefantrine were given upon laboratory diagnosis of P. knowlesi malaria.\nThe patient later developed hypotension despite fluid resuscitation and required single inotropic support, noradrenaline at a dose of 0.2 mcg/kg/min. He simultaneously experienced worsening peritonism. The surgical team was consulted, and he was posted for emergency exploratory laparotomy after stabilization. The anti-malarial was changed to intravenous artesunate in view that the patient was vomiting.\nIntraoperatively, haemoperitoneum was observed upon entering the abdomen, with blood clots seen overlying the splenic region. Gross examination of the spleen revealed tear of splenic capsule and subcapsular haematoma at the superior pole (Fig. ). Otherwise, the spleen was of average size, measuring 12 cm. Total splenectomy was performed and no visceral perforation was seen. The estimated blood loss was 7 L. During the operation, he required high dose of inotrope infusion: noradrenaline up to 2 mcg/kg/min, adrenaline up to 1 mcg/kg/min and dobutamine constant at 5 mcg/kg/min, fluid resuscitation (2 L of crystalloid and 1.5 L of colloid solution) and disseminated intravascular coagulation (DIC) regime transfusion due to massive blood loss. Postoperatively, the patient was managed in the high dependency ward of Kapit Hospital. There, he remained stable, inotrope was weaned off and he was extubated on the next day after the operation. He was administered with intravenous artesunate for 4 days. It was later switched to oral artemether–lumefantrine which he completed following a total of 6 doses. Subsequent blood films were negative for malaria parasites.\nHistopathological examination revealed splenic tissue with focal breaching of the capsule with areas of haemorrhage, consistent with splenic haemorrhage. There were a few brownish pigments within the spleen indicative of malarial pigment. The patient recovered well after the operation and was discharged after 9 days of hospital stay. He was given routine follow up post-malaria treatment and later administered with the routine post-splenectomy vaccinations against Streptococcus pneumoniae, Neisseria meningitidis and Haemophilus influenzae. One month later, he was well upon review at the surgical outpatient clinic.
A 63-year-old Caucasian woman without medical history stayed for several weeks in Cameroun, without taking any antimalarial chemoprophylaxis. She developed severe gastrointestinal symptoms and, after three days, due to her suspicion of a malaria attack, she took at once four pills of Coartem (each containing 20 mg artemether and 120 mg lumefantrine). After that, the patient became unable to ingest any food or drug and a transfer to Europe was rapidly decided. She became seriously ill during the flight back. On arrival at the airport, she was found stuporous and hypotensive and was rapidly transferred to the intensive care unit (ICU) of the nearest hospital. The diagnosis of Plasmodium falciparum malaria was rapidly made on the blood smear and treatment was started with intravenous quinine and doxycycline (as artesunate was not available). Parasitemia was estimated less than 1%. Admission coagulation tests revealed activated partial thromboplastin time 37 sec, international normalized ratio 1.2, fibrinogen 299 mg/dL, D-dimers >8000 ng/mL (normal, <500), ADAMTS13 activity undetectable (reference range, 50–150%), von Willebrand factor (VWF) antigen 340% (reference range, 50–150%), and platelet count 21,000/mm³. Early complications included refractory hypotension and hypoxemia and neurological worsening. Intubation was required for mechanical ventilation; norepinephrine infusion was progressively increased to the maximal infusion rate of 46 μg/min. An acute left ventricular dysfunction could be demonstrated at echocardiography. Continuous venovenous hemofiltration was initiated for acute renal failure. Due to the evidence of multiple organ failure and despite relatively low parasitemia, exchange transfusion therapy was performed. Only one session of 87 minutes was performed. The patient's theoretical total blood volume was 4407 mL; on the whole, 1409 mL of red blood cells was removed and replaced by 1277 mL of packed red blood cells. Blood coagulation tests remained disturbed, with epistaxis and rectal bleeding. The nadir of platelet count (5,000/mm³) and plasma fibrinogen (66 mg/dL) was noted on day 4, but there was only a mild increase in activated partial thromboplastin time and prothrombin time. The activity of ADAMTS13 slightly increased to 32%; no inhibitor or ADAMTS13 autoantibodies were found. From day 2, blackish discoloration of both hands and feet was noted and by the following days a definite line of demarcation was observed between gangrenous and normal skin (). Ultrasound-Doppler examination confirmed the absence of distal perfusion. Plastic surgeon suggested postponing the extensive surgery. Further clinical course was characterized by repeated candidemia (days 4, 7, 9, 10, and 11) and bacteraemia (Pseudomonas aeruginosa on day 7 and Enterococcus faecalis on days 12, 13, and 18), despite appropriate antifungal and antimicrobial therapy. The abdomen computed tomography (CT) failed to reveal bowel ischemia, but diffuse thickening of the jejunal wall was found. Endoscopy on day 11 disclosed multiple duodenal ulcerations from ischemic origin (); colonoscopy performed on day 28 was also consistent with ischemic injury disseminated in the sigmoid colon (). Norepinephrine infusion had been definitely stopped on day 14. The patient regained consciousness progressively from day 22 and extubation was possible on day 32.\nThe decision to perform quadriamputation was discussed after recovery from the critical period, when she became able to give her consent. Surgery was performed two months after the first signs of peripheral gangrene. Renal function recovered and the patient was further transferred for rehabilitation.