Background
Hump-nosed viper (Hypnale species) bites are an important cause of mortality and morbidity in southern India and Sri Lanka, accounting for 27 and 77% of venomous snake bites, respectively (1). Previously, they were known to be moderately venomous snakes with predominant local envenomation, but since recently, severe systemic envenomation incidents have been reported, including hemostatic dysfunction, microangiopathic hemolysis, kidney injury, myocardial toxicity, and death.
Here we report a case of hump-nosed viper bite complicated with type 2 myocardial infarction and acute pulmonary oedema secondary to acute heart failure in a Sri Lankan female presented to the National Hospital of Colombo, Sri Lanka.
Case presentation
A 39-year-old previously healthy female from Kegalle was transferred to our hospital for further management of her condition from a local hospital. She gave a history of snake bites three days ago, and the offending snake was identified as a hump-nosed viper. She complained of chest tightness on day 3 of the illness and progressive shortness of breath with associated orthopnea and paroxysmal nocturnal dyspnea. She had bilateral lower-limb edema. She denied having a past history of similar episodes, and her past medical history was insignificant. Her conscious level was stable, but she was tachypneic and tachycardic, with a respiratory rate of 32/min and a pulse rate of 120 bpm, respectively. She was hemodynamically stable, with a blood pressure of 100/60 mmHg. She had bilateral lower zone fine crepitations in the lungs with elevated jugular venous pressure, and her heart sounds were normal. She had an oxygen dependency with an air saturation of ~85%. Upon monitoring, her urine output was adequate. Her ECG showed lateral lead ST segment depressions (I, avL, V2-V6 leads) and T wave inversions. Her cardiac troponin I titer was elevated, with a value of 5.9 ng/mL. Her renal functions were normal (0.8 mg/dL). A chest X-ray showed evidence of pulmonary edema, and a 2D echocardiogram showed an ejection fraction of 60% with mild lateral wall hypokinesia. CT coronary angiography was carried out with the metabolic screening, which revealed normal coronary arteries and a negative metabolic screening. She was managed with supportive therapy with loop diuretics and oxygen, and a follow-up 2D echocardiogram showed complete recovery of the cardiac function. She was asymptomatic at 3 months into the follow-up. Therefore, since the CT coronary angiogram showed normal coronary arteries, the case was concluded to be a case of venom-induced type 2 myocardial infarction leading to heart failure with acute pulmonary oedema.