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 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.