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 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.