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 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.