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 50-year-old uneducated male of low socioeconomic status was scheduled for amputation of toes. To start with, he had complaint of fever associated with chills and rigors for 3 weeks. He consulted a local practitioner who prescribed some tablets about which patient could not give the details. He noticed blackening of toes of both the feet, which was slow and progressive over 1 week. As he was not responding to the treatment, he was rushed to our medical college. There was no history of trauma, significant drug ingestion particularly ergot, alcohol consumption or smoking. On physical examination, he was febrile, dehydrated, and had pallor; there was no icterus, cyanosis, edema, or significant lymphadenopathy. A pulse rate of 120/min, respiratory rate of 24/min, and blood pressure of 90/70 mmHg was recorded. All peripheral pulses were palpable. On systemic examination, mild hepatosplenomegaly was present and rest of the systemic examination was normal. On local examination, there was blackish discoloration of all toes, extending up to malleoli [Figures and ]. Intavenous line was secured. Ringer lactate was started and investigations were sent for. Reports were as follows [].\nPeripheral blood smear showed ring forms of P. falciparum with occasional gametocytes. Three consecutive blood cultures for bacteria were negative. Color Doppler study of the lower limbs revealed normal flow in both the femorals and the popliteal, with slightly reduced flow in tibial and dorsalis pedis artery with hypoechogenic shadow in its lumen.\nThe patient was given i.v. quinine, loading dose of 20 mg/kg followed by a maintenance dose of 10 mg/kg thrice a day for 2 days. Then, the patient was shifted to oral quinine (dose 10 mg/kg) thrice a day and oral paracetamol 500 mg thrice a day for 5 days. Two units of packed cell transfusion were also given. Fever subsided within 5 days of treatment. His peripheral smear for malarial parasite became negative after 7 days of quinine course. Line of demarcation did not progress any further. For management of gangrene, amputation was planned. All repeated blood investigations were within normal limits except prothrombin time 16.5 s, fibrinogen level 2.9 g/L (normal value 1.5-4 g/L), and D-dimer 1.7. The surgery was done under total i.v. anesthesia.