Arsenical Toxicosis in Animals
Arsenic, a ubiquitous toxic element derived from industrial activities, wields a profound impact on animal health. Recognizing its multifaceted repercussions is indispensable in delivering optimal care. From hemorrhagic diarrhea to aberrant behavior and neurological manifestations, this discourse delves into the diverse clinical presentations and underlying mechanisms. The subsequent sections delve deeper, illuminating the distinctive facets of arsenic toxicosis, elucidating diagnostic and therapeutic approaches, all while emphasizing the crucial role of vigilant veterinary management.
Arsenic toxicosis, stemming from industrial activities and prevalent in soil and water, is a critical concern for veterinary professionals. Arsenic, existing in diverse forms, binds readily with other elements like oxygen, sulfur, and copper. In cattle, sporadic acute arsenic toxicosis can arise from ingesting treated wood ashes or contaminated environments, often exacerbated by chromium or lead. Differing toxicities of trivalent and pentavalent arsenic forms, with LD50 values ranging from 1-25 mg/kg to 30-100 mg/kg respectively, reflect its complex nature.
Clinical manifestations encompass subtle signs leading to sudden mortality, primarily affecting high ATP-demanding organs. Gastrointestinal mucosal inflammation and vascular compromise underpin pathogenesis, resulting in hallmark symptoms like hemorrhagic diarrhea and ataxia. Microvascular impairment and plasma transudation contribute to hypovolemic shock. Swift symptom onset, typically within hours, underscores urgency, with cases ranging from rapid death to sudden mortality without apparent lesions.
Diagnosis challenges arise due to limited antemortem data, prompting postmortem assessments. Heightened liver enzymes and azotemia coincide with energy-demanding organ damage. Antemortem arsenic quantification in blood and urine facilitates diagnosis. Gastrointestinal lesions manifest as mucosal inflammation, vascular rupture, and subepithelial tissue necrosis. Hyperemic lesions on ruminants' serosal omasum surface and abomasal mucosa highlight gastrointestinal effects, potentially leading to perforation. Concurrent liver and kidney inflammation with necrosis and fatty degeneration are evident, along with cutaneous exposure-related skin necrosis.
Effective treatment strategies depend on the presence of clinical signs. Recent exposure and absent clinical signs warrant emesis induction, followed by activated charcoal administration and subsequent gastrointestinal protectant administration. For symptomatic animals, intensive fluid therapy, blood transfusion if necessary, and dimercaprol at 4-7 mg/kg IM, thrice daily for 2-3 days, are recommended.
Larger animals benefit from thioctic acid, alone or with dimercaprol, or sodium thiosulfate treatment. Supportive care, including intravenous fluids for cardiovascular stability and monitoring kidney and liver function, is crucial.
Promising outcomes involve higher sodium thiosulfate dosages and fluid administration. Adequate fluid support emerges as pivotal in mitigating acute arsenic toxicosis, underscoring its significance for successful outcomes. Veterinary professionals must comprehend these multifaceted approaches for optimal management of affected animals. Awareness of diverse clinical presentations, diagnostic modalities, and tailored treatments is essential for addressing this intricate condition effectively.
REFERENCES:
Bertin, FR. Arsenic Toxicosis in Cattle: Meta-Analysis of 156 Cases. J Vet Intern Med 2013; 27: 977-981.
