Endocrine and Metabolic Manifestations of Snakebite Envenoming

Abstract

Snakebite envenoming is a neglected, public health problem in tropical and subtropical regions. Local tissue necrosis, neurotoxic, and hemo-vasculotoxic effects are well-recognized features, whereas the endocrine and metabolic derangements are not as well known. In addition to contributing to morbidity, some of these manifestations can be potentially life-threatening if not recognized early. The most prominent endocrine manifestation is hypopituitarism (HP), which can manifest acutely or remain asymptomatic and present years later. Unexplained recurrent hypoglycemia and refractory hypotension are early clinical clues to suspect corticotroph axis involvement in acute settings. Chronic pituitary failure may present, like Sheehan's syndrome, several years after the bite. The occurrence of acute kidney injury, capillary leak syndrome, and disseminated intravascular coagulation are predictors of HP. Adrenal hemorrhages are documented in autopsy series; however, primary adrenal insufficiency is very rare and confounded by the presence of HP. Hyponatremia, hypokalemia or hyperkalemia, and dysglycemia can occur, but the mechanisms involved are only partially understood. Awareness, a high index of suspicion, correct interpretation of hormonal parameters, and timely treatment of these abnormalities can be lifesaving.

Cerebral Complications of Snakebite Envenoming: Case Studies

“…Although treated with AV, the misidentification of the snake species at the beginning causes irreversible damage, leading to a fatality [ 12 ]. Such iatrogenic causes of snakebite, either by a mistake in diagnosis [ 12 ] or by mistreatments [ 109 , 110 ], make the cases worse. Neostigmine, a cholinesterase inhibitor for overcoming paralysis of skeletal muscle, is commonly used to cotreat with AV when patients have neural disorders such as ptosis and muscle weakness [ 26 , 29 , 30 , 31 , 38 , 40 ].…”

A simple mortality risk prediction score for viper envenoming in India (VENOMS): A model development and validation study

“…CLS presents with manifestations of parotid swelling, conjunctival-chemosis, periorbital edema, hypotension, albuminuria and hemo-concentration. Other organ-systems including kidneys, heart, presynaptic neuromuscular junction and hypothalamo-pituitary axis are also affected in Russell's viper envenoming resulting in acute kidney injury (AKI), early neuromuscular paralysis, acute adrenal insufficiency and long-term consequences like chronic kidney disease and Sheehan like syndrome [20][21][22][23][24].…”

Panhypopituitarism and Central Diabetes Insipidus Almost Three Decades After Russell's Viper Envenomation: A Remarkable Case Report and Literature Review

“…Amid these endocrine disorders, anterior pituitary insufficiency has been the most commonly detected manifestation following Russell's viper envenomation (Daboia russelii in India; and Daboia siamensis in Burma). 3 Russell's viper envenomationtriggered hypopituitarism can manifest acutely (even during the initial admission for management of envenomation) or have a chronic or surprisingly delayed appearance, making the diagnosis further enigmatic. 3,4 Neurohypophysis, in contrast to adenohypophysis, is resistant to vascular events (because it receives direct arterial supply from an inferior hypophyseal artery; and it tends to remain unaffected by intrasellar pressure changes during capillary leak syndrome and disseminated microthrombi formation).…”

“…3 Russell's viper envenomationtriggered hypopituitarism can manifest acutely (even during the initial admission for management of envenomation) or have a chronic or surprisingly delayed appearance, making the diagnosis further enigmatic. 3,4 Neurohypophysis, in contrast to adenohypophysis, is resistant to vascular events (because it receives direct arterial supply from an inferior hypophyseal artery; and it tends to remain unaffected by intrasellar pressure changes during capillary leak syndrome and disseminated microthrombi formation). Therefore, Russell's viper envenomation-mediated damage to neurohypophysis and resultant central diabetes insipidus is remarkably infrequent.…”