From Bite to Bleed-out: Managing Vasculotoxic Snakebite Induced Catastrophic Complications in Resource Constrained Settings

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From Bite to Bleed-out: Managing Vasculotoxic Snakebite Induced Catastrophic Complications in Resource Constrained Settings

   

Hayatu Umar1*, Faruk Bello1, Femi Akindotun Akintomide1, Abdulaziz Aminu1, Shamsuddeen Ahmad Aliyu2, Farouk Kabir Umar3, Ibrahim Anka Abubakar4

1Department of Internal Medicine, Usmanu  Danfodiyo University Teaching Hospital, Sokoto. Nigeria
2Department of Radiology, Usmanu Danfodiyo University, Sokoto. Nigeria
3Department of Radiology, Usmanu Danfodiyo University Teaching Hospital, Sokoto. Nigeria
4Department of Veterinary Parasitology and Entomology, Faculty of Veterinary Medicine, Usmanu Danfodiyo University, Sokoto, Nigeria

*Corresponding author:  Hayatu Umar, Department of Internal Medicine, Usmanu  Danfodiyo University Teaching Hospital, Sokoto. Nigeria

Citation: Umar H, Bello F, Akintomide FA, Aminu A,
Aliyu SA, et al. From bite to Bleed-out: Managing
Vasculotoxic Snakebite Induced Catastrophic 
Complications in Resource Constrained Settings. J
Clin Pract Med Case Rep. 1(2):1-12.

Received: October 03, 2024  | Published: December 26, 2024

Copyright© 2024 genesis pub by Umar H, et al. CC BY-NC-ND 4.0 DEED. This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives 4.0 International License. This allows others distribute, remix, tweak, and build upon the work, even commercially, as long as they credit the authors for the original creation.

DOI: https://doi.org/10.52793/JCPMCR.2024.1(2)-19

Abstract

Snake bite envenomation is a serious but under-reported disease in sub-Saharan Africa, especially among the rural population who frequently experience catastrophic complications. The management of these complications can be challenging for the attending physician in resource constrained settings. Herein, is a case of a 27-year-old farmer referred to our hospital with two weeks history of snakebite on his left thumb. Three days after the bite, he presented to a rural hospital with spontaneous bleeding from the gum and at the site of a previous traumatic foot ulcer which resulted in a transfusion of seven pints of blood but no anti-snake venom therapy. Nine days after spontaneous gum bleeding, he developed progressive abdominal swelling and passage of melena at the local hospital which necessitated his referral.

At the presentation, his bedside whole blood clotting time was more than 20 minutes. Abdominal paracentesis yielded non-clotted hemorrhagic aspirate, pack cell volume was 18% and abdominopelvic ultrasound revealed moderate to severe intra-abdominal hemorrhage. Coagulopathy was not reversed despite therapy with the only available 200 mls of polyvalent anti-snake venom and five days later, he received one vial (10mls) of EchiTab-plus, the only available specific anti-snake venom procured far away at an outrageous cost. Besides, he got three pints of blood, prophylactic antibiotics, close monitoring, and reassurance. He archived the reversal of coagulopathy with a favorable clinical outcome. In sub-Saharan Africa, without, access to appropriate anti-snake venom in our health facilities, severe complications may result in rapid death.

Keywords

Vasculotoxic snake-bite; Catastrophic complications; Coagulopathy; Intra-abdominal hemorrhage; Gastrointestinal bleeding; EchiTab-plus

 

Abbreviations

  • MOD: Multiple organ dysfunction
  • WBCT: Whole blood clotting time
  • FDP: Fibrin degradation products
  • ED: Emergency department
  • PCV: Pack cell volume
  • GI: Gastrointestinal bleeding

Introduction

Snakebite envenoming in sub-Saharan Africa is a neglected and poverty-related disease with significant loss of productivity, health care cost, catastrophic complications, morbidity and mortality [1-5]. Venomous snakebite appears to be a double tragedy in sub-Saharan Africa because it is related to poverty and it occurs in a region with extreme poverty and limited resources, making the prognosis dismal. The main factors contributing to poor clinical outcomes in snakebite envenomation in sub-Saharan Africa are delayed hospital presentation, unavailability and high cost of anti-snake venom, health care costs, poor health care and storage facilities, counterfeit anti-snake venom, poverty, illiteracy, limited health care access in remote areas of the region and poor public awareness (were most affected patient always resort to trade-medicine before presentation to hospital) and the false public believes in snake charmers [1,4-6]. Snakebite envenoming in sub-Saharan Africa is mainly a rural problem and most people at risk are subsistent farmers, herdsmen, hunters, snake charmers, and plantation workers with most bites occurring before the rainy season and during heavy rain [1,4,5]. In view of the aforementioned observations, management of snake bite envenomation in sub-Saharan Africa is challenging.  

Clinico-pathologically, snakebite envenoming is categorized into three on the basis of the body system involved into myotoxic, neurotoxic, and vasculotoxic (hematoxic). The vasculotoxic snakebite envenoming in sub-Saharan Africa is commonly caused by the Viperidae family of snakes which include Echis ocellatus [2,4,5]. The venom is a complex secretion that contains high molecular weight enzymes ranging with molecular weight ranging between 13-150 Kilo Daltons (KDa) which form 80-90 percent of the viper’s venom, polypeptide toxins with a molecular weight of 5-10kDa, and low molecular weight compounds with a molecular weight of less than 1.5kDa [5]. The enzymes include serine proteases (procoagulants of viper venoms, zinc metalloproteinases) and hemorrhagins, while Echis venom contains activators of factor X and prothrombin hemorrhagins, a prothrombin-activating procoagulant, phospholipase A2, and hyaluronidase [4,5,7,8]. In vasculotoxic snakebite envenoming, incoagulable blood and hemorrhage arise from venom anticoagulants, consumptive coagulopathy, thrombocytopenia, platelets dysfunction, primary fibrinolysis, vascular wall damage by hemorrhagins and rupture or necrosis of intra-abdominal organ such as the intestine, liver, and spleen [4,5,7-9,10]. All these combines to cause life-threatening hemorrhage, whereas biogenic amines and phospholipase A2 induce local swelling [4,5].

Clinically, the initial manifestation of vasculotoxic snakebite envenoming is local pain and progressive swelling, followed by coagulopathy which presents as continuous bleeding (>20 minutes) from the fangs puncture wound, venipuncture sites, and previously partially healed wounds. These are the first clinical evidence of coagulopathy followed by spontaneous systemic hemorrhage which manifests as gingival bleeding, most often detected in the gingival sulci, epistaxis, and hematuria (asymptomatic or total) detected a few hours after the bite [4,5]. Other forms of spontaneous bleeding are subconjunctival hemorrhage, intracranial hemorrhage in the form of intracerebral or subarachnoid hemorrhage (manifesting with restlessness, irritability, loss of consciousness, meningism, cerebral thrombosis, hemiplegia or hemiparesis), bleeding into the floor of the mouth and tympanic membrane, gastrointestinal bleeding presenting as (melena or hematochezia), ecchymoses, petechiae, discoid/follicular hemorrhage and the anterior pituitary hemorrhage (which mimic Sheehan’s syndrome) [4,5,7,8,11].

A rare and life-threatening intra-abdominal hemorrhage in the form of hemo-retro-peritoneum, hemoperitoneum, or both, and gastrointestinal bleeding from vasculotoxic snakebite has been reported in the literature [2,3,9,10]. Other rare complications associated with vasculotoxic snakebite envenoming include hemoptysis, endocrinopathies such as stress-induced hyperglycemia, hypoglycemia and Sheehan’s syndrome, shock, cardiotoxicity, multiple organ dysfunction (MOD), acute kidney injury and severe anemia [4,5,7,8,11]. In spite of the aforementioned complications associated with vasculotoxic snakebite envenoming, the clinical severity is determined by the type of snake, the nature, quantity, and degree of toxicity of the snake venom administered, the location of the wound, timing of first-aids and therapies provided, and underlying medical comorbidities [12,13].

We present a case of vasculotoxic snakebite-induced catastrophic complications; coagulopathy, intra-abdominal hemorrhage, gastrointestinal bleeding, and anemia in a subsistent farmer with financial constraints, who have multiple risk factors for snakebite, indices of clinical severity, and predictors of mortality. Despite these and management challenges, the clinical outcome was favorable.          

Case report 

A 27-year-old subsistent farmer presented to our emergency department (ED) with 2 weeks history of snake bite to his left thumb while clearing the farm. The snake was identified as a carpet viper (Echis ocellatus) by the patient and coworkers. Immediately after the bite, severe pain and fang marks with minimal hemorrhage occurred at the site, which he overlooked without seeking for trado-medicine or medical attention. However, over time, progressive swelling that involved two-thirds of his left forearm was noted. Three days after the bite, he developed spontaneous gum bleeding at the site of a prior traumatic left foot ulcer. Nine days after spontaneous gum bleeding, the patient started passing melena and developed progressive abdominal swelling with associated mild lower abdominal pain. However, no hematuria, hematochezia, petechial hemorrhages, ecchymosis, and differential limb weakness. No history of chronic liver disease, bleeding disorders, diabetes mellitus, acid peptic disease, and chronic kidney disease. On account of the severe gum bleeding, he presented to a nearby general hospital where he was admitted for about 11 days and was transfused 7 pints of blood, but no anti-snake venom therapy prior to referral to our hospital because of unavailability. 

General physical examination was unremarkable except for tachypnea, pallor, dehydration, significant peripheral (left axillary) lymphadenopathy, and the site of the bite in the dorsolateral aspect of the left thumb (Figure 1). Cardiovascular examination revealed a pulse rate of 92/minute, Blood pressure of 140/80 mmHg, and heart sounds were loud S1 and S2 only. Respiratory rate was 28 breath/minute with normal breath sound. The abdomen was grossly distended with a girth of 116 cm (Figure 2), moved with respiration, no areas of tenderness and organomegaly difficult to appreciate, and bowel sound was reduced. Diagnostic abdominal paracentesis yielded hemorrhagic non-clotted aspirate (Figure 3) and per rectal examining finger was stained with a black stool. Neurological examination was unremarkable. Bedside whole blood clotting time (WBCT) was more than 20 minutes and random blood sugar was 6.5 mmol/L.

Figure 1: Dorsolateral surface of the left thumb showing the site of bite.