A 54 years old male Ugandan presented to Kenyatta National Hospital, a major referral tertiary hospital, in Kenya. He had initially reported with headache and joint pain to a local health facility in Uganda and was diagnosed to have severe Plasmodium falciparum malaria infection, and thereafter treatment with intravenous quinine commenced.\nTreatment at the facility had been responsive; however two days after the onset, the patient started experiencing episodes of headache, pain, numbness, coldness, and swelling of the extremities. This was followed by darkening of the digits of his toes and hands, which gradually progressed proximally.\nOn presentation at out institution, he was conscious, alert, oriented, but lethargic and unable to walk. He was a non-smoker and non-alcoholic, and had no history of diabetes, hypertension or any angiopathies. He however had a history of numerous episodes of malaria bouts and a family history of hypertension with his father having succumbed to a stroke.\nOn physical examination, apart from fever, abdominal, cardiovascular, respiratory, and neurological systems were normal. Jaundice, pallor and cyanosis were absent. A right low paramedian scar was noted secondary to appendicectomy conducted in the year 1995. On local examination, the overlying skin cold, dry, wrinkled, and was darkened with a clear line of proximal demarcation (). Pain was present in the regions proximal to the discolouration, and absent in the distal regions.\nInvestigations tested negative for HIV, HBV, HCV, and VDRL on ELISA. Urea, Electrolyte and creatinine tests were normal. Clotting profile showed a prolonged Prothrombin time of 19sec, Prothrombin time index of 74%, and an INR of 1.36. A haemogram showed macrocytic normochromic anaemia (Hb 9.03 g/dL, MCV 89.9fL, MCH 29.5pg, MCHC 27.2g/dL), Hct 33.2%, RBC 3.69x1012/L. WBC 4.39x109, Neutrophils 2.11x109 (48.2%), Lymphocytes 1.73x109 (39.5%), Monocytes 0.314x109 (7.16%), Eosinophils 0.193x109 (4.4%), Basophils 0.035x109 (0.796%).\nAn echocardiogram was normal except for type 1 left ventricular dysfunction and mild tricuspid regurgitation. The Dorsalis pedis pulses showed absence of blood flow, and a diagnosis of Symmetrical peripheral gangrene was made. Management was initiated with clopidogrel, Acetylsalicylic Acid, and Atorvastatin, and quad-amputation recommended. Time was allowed for marginalization of the gangrene, which was noted two months later. Meanwhile fresh frozen plasma was regularly administered to counter suspected thrombophilia.\nFollowing satisfactory marginalization of the gangrene, the patient underwent surgical excision of the necrotic tissue. This involved transmetatarsal amputation of both feet and ray amputation of the hands. The wounds healed well thereafter facilitated by vacuum dressing at -7.5mmHg over one month. He was then referred to plastic surgeons for prosthesis.
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.