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.
A 29-year-old male peacekeeper, deployed in the Democratic Republic of Congo (DRC) for 2 months, presented with a history of 3-day fever, headache, fatigue and 1-day jaundice. There was no past medical history. He was taking compound dihydroartemisinin tablets (dihydroartemisinin + piperaquine phosphate + trimethoprim) weekly as chemoprophylaxis since entering the mission area. Physical examination showed fever (39.4 °C), acute sick looking, poor spirit, yellow staining of skin and sclera.\nPulse oxygen saturation was 96%. Glasgow coma scale (GCS) was 15. Ultrasonic examination of the abdomen showed splenomegaly. The blood smear revealed 8% parasitemia. The laboratory results after admission were summarized in . Of note were hyperbilirubinemia (total bilirubin 81.3 µmol/L), electrolyte disturbance, and thrombocytopenia. Hepatitis series tests were negative. A rapid diagnostic test was positive for Plasmodium falciparum. A diagnosis of severe falciparum malaria was made.\nWe carried out antimalaria therapy with intramuscular artemether 240 mg at admission and 160 mg at 12, 24 h later (artesunate was temporarily unavailable), correcting dehydration and the electrolyte disturbance, and protecting liver function. The patient did not sweat and the body temperature did not drop after antimalarial treatment. It was above 39.0 °C. Thirty-six hours after admission, he felt left upper quadrant pain, combined by nausea, vomiting, and diarrhea, all of which occurred for three times. The pain was so severe that he could not take a deep breath or cough, resulting in shallow and fast breathing, and a pulse oxygen saturation of 92%. And this was followed with progressive abdominal distension and an inability to pass stool and flatus. On examination, the patient was extremely weak and tired. Without abdominal guarding and rigidity, tenderness was obvious in the left. There was no rebound tenderness. Bowel sounds disappeared. In addition, the blood smear revealed 5% parasitemia. Liver function deteriorated (total bilirubin 189.5 µmol/L), and platelets decreased further (52 × 109/L). Fifty-five hours after admission, his abdominal pain was significantly worse. The consciousness was gradually indifferent, and GCS was 13. Breath rate was 45/min, and pulse oxygen saturation was 89%. X-ray of the chest showed lung texture thickening and upright abdominal plain film indicating that the colon was dilated and gas accumulation in the splenic flexure (). Ultrasound of the abdomen showed hepatomegaly and splenomegaly. So we considered the patient was complicated by ACPO. At this time artesunate was available and 2.4 mg/kg body weight administered intravenously (time = 0), then at 12 h and 24 h. At the same time, fasting, no retention enema, rectal decompression tubes and oral 30 mL paraffin oil were taken. One day after these measures, he passed a small quantity of feces; and abdominal pain and distension were relieved. Body temperature also gradually decreased. Blood test showed bilirubin level dropped than before (total bilirubin 165.7 µmol/L), platelets level rose to a certain extent (81 × 109/L), and the blood smear revealed 1% parasitemia. X-ray of the abdomen revealed that dilation of the left colon disappeared, and intestinal gas accumulation decreased (). Five days after admission, the patient could tolerate oral therapy, so he completed a treatment of 3-day artemisinin-based combination therapies.\nWe concluded that ACPO was secondary to malaria. Ten days later, all symptoms disappeared and the patient was discharged. His 1-month follow-up was unremarkable.