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 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.