Hantaviruses are a large family of enveloped viruses with two medically important families Cricetidae and Muridae which are known to cause rodent-borne diseases worldwide. Some strains cause clinical syndromes with multiorgan involvement in humans such as hantavirus haemorrhagic fever with renal syndrome (HFRS) and hantavirus cardiopulmonary syndrome (HCPS), which is also known as hantavirus pulmonary syndrome. Clinical differentiation of this infection from other endemic infections in Sri Lanka such as leptospirosis and rickettsial infections is extremely difficult due to overlapping clinical and epidemiologic features such as exposure to rodents and farming. Here, we report two serologically confirmed cases of hantavirus infection from Sri Lanka with different presentation. The first patient had a combination of HCPS and HFRS. The second patient was treated for HPS complicated with acute respiratory distress syndrome (ARDS). Both had a significant clinical, biochemical, and radiological response with early initiation of corticosteroids. However, further studies are required to assess whether steroids hasten the recovery of severe hantavirus infections. We believe that hantavirus infection is an important emerging disease in the country and should be considered as a differential diagnosis in patients presenting with an acute febrile illness as well as in patients presenting with ARDS. Early diagnosis and prompt treatment improve prognosis.

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Green pit viper (Trimeresurus trigonocephalus) is considered a potentially highly venomous arboreal endemic pit viper which inhabits Sri Lanka. Green pit viper bites usually result in local envenoming and systemic envenoming features like coagulopathy are rare. We report an authenticated case of green pit viper envenoming which resulted in severe local inflammation which was associated with mild coagulopathy.

Abrus precatarius is a tropical climber, whose seeds contain abrin, which is known to cause toxicity in humans. We report a case of a young girl, who presented with haemorrhagic enterocolitis, bilateral septal vein thrombosis, and basal ganglia haemorrhage leading to seizures and coma, following ingestion of toxic A. precatarius seeds. To the best of our knowledge, this is the first ever case to describe such an intracranial complication of abrin poisoning.

Introduction Cardio-cerebral infarction (CCI), the simultaneous occurrence of acute ischemic stroke (AIS) and acute myocardial infarction (AMI), is infrequent and poses a management challenge for physicians. There is a paucity of available evidence for the best management approach of this rare clinical entity. Case Presentation A 59-year-old female with uncontrolled type 2 diabetes mellitus, hypertension, hyperlipidemia presented 6 ½ hours following sudden right-sided hemiparesis, hemisensory loss, right upper motor neuron facial nerve palsy, aphasia, vertigo, and vomiting. She also had complained of vague anterior chest pain since 12 hours earlier and had worsened to a sudden agonizing chest tightness with autonomic symptoms within a few minutes following the acute neurological event. On admission to the tertiary care center, she had vitals of; pulse rate 79/ minute, blood pressure – 182/100 mmHg, respiratory rate – 22/ minute, SpaO2 – 95%, was confused with GCS of 14/15, and had right-sided long tract signs with aphasia. NIHSS was calculated to be 12. Urgent electrocardiogram (ECG) revealed acute inferior-posterior and right ventricular ST-elevation myocardial infarction (STEMI), a non-contrast CT (NCCT) of the brain revealed acute ischemic stroke in the right centrum semiovale with multiple lacunar infarctions in the right temporoparietal region. With the patient presenting out of the thrombolytic window for AIS and in the absence of facilities for thrombectomy for AIS in the hospital, the patient’s subsequent management was taken with discussions involving the cardiology and neurology teams. The risk of secondary cerebral hemorrhage was presumed to be high from peri-PCI antithrombotic therapy or thrombolysis for AMI. Hence patient was managed conservatively, initially with a single antiplatelet (aspirin), a statin, meticulous multiparameter monitoring, oxygen supplementation, anti-anginal, blood pressure, and diabetic control. With a subsequent NCCT brain taken at 48 hours showing small extension of the size of the infarct, and with an improvement of the level of consciousness, dual antiplatelets (addition of clopidogrel) and LMWH therapy sequentially started and continued while actively monitoring for cerebral complications. The disease was later complicated with hypotension due to right ventricular infarct, which was fluid responsive, and ischemic hepatitis requiring N-acetyl cysteine therapy. Though the patient did not receive the ideal management and was offered the best possible management at that point, she showed a favorable outcome. 2D echocardiogram showed moderate systolic dysfunction without ventricular clots, and modified Rankin score was 3 on discharge. Early outpatient secondary PCI and passive physiotherapy-based neurorehabilitation were arranged. Conclusion CCI management should be individualized according to the clinical circumstances and the vascular territories involved in each organ. The selection of treatment is limited by the safety of antithrombotic therapy against the extent of cardio cerebral injury and the availability of choices for endovascular interventions. Further evidence on management needs to build up for a better clinical outcome.