Key words : Antivenom administration, Graft injury, Immunosuppression regimen, Liver transplant recipients, Snake envenomation

Introduction

Snake envenomation presents a substantial health challenge in various regions worldwide and contributes to significant levels of morbidity and mortality.^1,2 Although liver transplant recipients represent a susceptible group due to altered immune responses, literature on snakebite envenomation in this population remains scarce. This report aims to shed light on this infrequent encounter and its potential effect on posttransplant management.

We present the case of a 52-year-old female patient with a significant medical history of decompensated nonalcoholic steatohepatitis cirrhosis for which she had received a deceased donor liver transplant 5 years prior to the presentation we describe here. She presently remains under monotherapy with tacrolimus at a dose of 2 mg twice daily, with stable liver graft function, and is under regular follow-up by a transplant hepatologist.

The patient was admitted due to rattlesnake envenomation at the dorsal aspect of the third digit of her right hand, which had resulted in marked swelling and severe pain during the initial evaluation (Figure 1). Her laboratory panel results were unremarkable. She received 4 vials of CroFab Crotalidae polyvalent immune Fab (ovine) antivenom and was closely monitored. On the first day after admission, her liver enzyme levels were elevated in a mixed pattern of hepatocellular and cholestatic injury (Table 1). Her tacrolimus levels upon admission were 2.3 ng/mL. Her transplant hepatologist was consulted and decided to admit the patient for further observation and to monitor liver function and maintain her standard immunosuppression regimen.

Throughout her hospital stay, the patient expe-rienced a substantial reduction in swelling and pain, but her elevated liver enzyme levels persisted. The results of abdominal Doppler ultrasonography were notable for hyperechoic hepatic echogenicity consistent with fatty infiltration, with patent appropriately directed vascular structures. Consequently, the patient was discharged after a 5-day hospitalization, with plans for close follow-up by her hepatologist and continued monitoring of her liver enzyme levels. Approximately 1 week later, her liver function tests had nearly returned to baseline, and follow-up laboratory results at 1 month showed complete restoration of graft function (Table 1).

Snakebite envenomation induces significant disturbances in hepatic function that are primarily attributed to venom-mediated effects on liver mitochondria and hepatocytes. This process triggers the release of interleukin 6, which results in systemic activation of Kupffer cells. Furthermore, various venom constituents, including phospholipase A2, metalloproteinases, 3-finger toxins, and L-amino acid oxidase, contribute to oxidative damage.³ Histopathological evaluation of affected livers reveals a diverse spectrum of changes, including hepatocyte architectural distortion, pyknosis, karyorrhexis, cytoplasmic vacuolation, necrosis accompanied by amyloid deposition, fatty degeneration, portal vein thrombosis, and hepatocyte atrophy.⁴ Microscopic analysis consistently demonstrates evidence of sinusoidal and Kupffer cell activation, as well as mitochondrial injury and glycogen depletion.⁵

The clinical presentations following snake enve-nomation are notably heterogeneous and contingent upon various factors, including the snake species, the quantity of venom administered, and the accessibility of antivenom treatment. The various bioactive molecules in the venom can cause diverse clinical effects, including local tissue injuries and systemic manifestations (neurotoxicity, cardiotoxicity, bleeding, acute kidney injury, and rhabdomyolysis).^6,7 For example, in cases of Bothrops envenomation in South America, patients have exhibited patterns of injury characterized by hepatic hematoma and shock,^8,9 whereas Russell’s viper bites have manifested as severe fatty changes and hepatocellular necrosis.¹⁰ Furthermore, cerebral hemorrhages and ischemic infarcts have been documented as consequences of Russell’s viper envenomation, alongside ventricular tachycardia, all of which demonstrate the wide array of clinical presentations associated with snakebite envenomation.^11-13

Our case report emphasizes the significant risk of snake envenomation to contribute to graft injury and potential graft loss in liver transplant recipients. This vulnerable population requires heightened vigilance, including close monitoring of graft function and timely administration of antivenom when necessary. However, it is crucial to note that the management of snake envenomation in this specific patient group lacks well-established guidelines, and there remains an urgent need for further research and the development of evidence-based protocols to facilitate optimal care from health care providers for these patients. This case is a compelling reminder of these clinical challenges and the importance of future collaborative efforts to improve outcomes for liver transplant recipients who may encounter snake envenomation.

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