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.
A 42-year-old Cameroonian (black African) man with no relevant past medical history presented to our hospital with a 1-week history of fever and a 4-day history of no bowel movements. The fever was intermittent and worse in the evenings, and associated with headache, joint pains, and anorexia. He self-medicated an undocumented orally administered antimalarial medication but symptoms persisted. Three days later, he developed generalized abdominal pain, colicky in character, with a severity of 5/10 on a visual analogue scale. This was associated with progressive abdominal distension and an altered bowel pattern initially characterized by an inability to pass stool and flatus over 4 days but he denied any vomiting. A worsening of his symptoms prompted his visit to our hospital.\nOn examination, his mucous membranes were dry, his conjunctivae were pink, and his vital signs were normal. His abdomen was mildly distended with mild diffuse tenderness. There was neither guarding nor rebound tenderness. Percussion note was tympanic and bowel sounds were hyperactive. His rectum was empty per digital rectal examination and his prostate was not enlarged. The rest of the physical examination was unremarkable.\nA rapid diagnostic (Alere™ Malaria Ag P.f, Abbott Rapid Diagnostics, USA) test for malaria was positive. Also, his complete blood count values were within normal ranges: white blood cell count of 6200 cells/uL, hemoglobin of 12.5 g/dL, and platelet count of 222,000 cells/uL. His metabolic panel was within normal range: serum sodium ion (Na+) of 140 mmol/L, serum potassium ion (K+) of 4.0 mmol/L, serum chloride ion (Cl−) of 98 mmol/L, serum creatinine of 0.9 mg/dL, alanine aminotransferase was 41.2 U/L, aspartate aminotransferase was 33.0 U/L, total bilirubin was 0.81 mg/dL, and alkaline phosphatase was 55.9 U/L. His human immunodeficiency virus serology was non-reactive. His rapid antibody test for typhoid fever was also non-reactive. There was no significant air fluid level or increased bowel gas on a plain abdominal radiograph and an abdominal ultrasound revealed mild free intra-abdominal fluid in all four quadrants.\nWe concluded on a working diagnosis of functional bowel obstruction secondary to malaria. He received three doses of intravenously administered quinine base infusion (600 mg in 500 ml of dextrose 5% to flow for 4 hours every 8 hours for 24 hours) and intravenously administered crystalloids (0.9% normal saline at rate of 1 liter 8 hourly for 48 hours) and was placed on “nothing by mouth.” He passed a small quantity of feces 48 hours after initiation of antimalarial medication, with complete resolution of the abdominal pain, distension, and bowel movements on the fourth day of hospital stay. A stool examination was done with no organisms identified. We then concluded on a final diagnosis of sub-acute intestinal obstruction secondary to malaria. He was then discharged on an orally administered artemisinin-based antimalarial combination (artemether/lumefantrine 20/120 mg, 4 tablets 12 hourly for 3 days). His 2-week follow up was unremarkable.