Page 194 - Cote clinical veterinary advisor dogs and cats 4th

79.e2 Arsenic Toxicosis

Arsenic Toxicosis Client Education
Sheet
VetBooks.ir

○ Hepatic and renal damage from direct
BASIC INFORMATION
for arsenic.
effect of arsenic or secondary to hypovo- • Suspected baits, soil, or water can be tested
Definition lemia and hypoperfusion
Condition resulting from exposure to damaging • Toxicity varies with form and valence state TREATMENT
amounts of arsenic of arsenic
○ Inorganic arsenic (arsenic trioxide) is more Treatment Overview
Epidemiology toxic than organic forms (melarsomine, Treatment goals include early decontamination
SPECIES, AGE, SEX arsanilic acid). if possible. Intravenous fluid therapy to hydrate
Cats and immature animals are more sensitive. ○ Trivalent arsenic (arsenite) is more toxic and support blood pressure, control of GI signs,
than pentavalent forms (arsenate). and chelation if indicated
RISK FACTORS ○ Highly soluble forms (arsenous acid,
• Availability of arsenic-containing insecticides, arsenic acid) are more toxic than insoluble Acute General Treatment
herbicides, animal feed additives, or wood forms. • Control life-threatening signs.
preservatives • Single lethal dose of sodium arsenite: ○ Intravenous fluids for hypovolemia, shock,
• Living environment near certain types of 1-25 mg/kg body weight in most species dehydration
mining, manufacturing, or naturally occur- • Arsenic trioxide 3-10 times less toxic than ○ Blood transfusion if needed for GI blood
ring arsenic-contaminated groundwater sodium arsenite loss
• Iatrogenic exposure can also occur with use ○ Correct acid-base and electrolyte
of arsenic-containing heartworm adulticides. DIAGNOSIS imbalances
○ Thermoregulation
CONTAGION AND ZOONOSIS Diagnostic Overview • Prevent systemic absorption.
Some sources of environmental arsenic are Diagnosis is based on known or suspected ○ Emesis in asymptomatic patients and if
common to people and animals living in the exposure with typical acute signs such as < 60 minutes after exposure (p. 1188)
same area (e.g., well water with arsenic in it). vomiting, watery diarrhea with mucosal shreds, ○ Gastric lavage should be considered
If an animal is diagnosed with arsenic poison- and progressive weakness or shock. The diag- if recent large ingestion and if emesis
ing, there also may be a risk to humans, nosis can be confirmed by analyzing arsenic unsuccessful.
depending on source. levels in the urine, feces, or vomitus. ○ Activated charcoal adsorbs arsenic poorly;
most sources suggest using it, but efficacy
Clinical Presentation Differential Diagnosis is limited at best. Do not give activated
DISEASE FORMS/SUBTYPES • Enteritis (viral, or other) charcoal if vomiting or bleeding.
• Peracute or acute toxicosis occurs after • Hemorrhagic gastroenteritis • Chelation
exposure to a single high dose. • Pancreatitis ○ Recommended if large exposure or signs
• Subacute or chronic arsenic toxicosis occurs • Zinc phosphide toxicosis are progressive
after multiple low-dose exposures; rare in ○ Succimer (meso-2,3-dimercaptosuccinic
animals. Initial Database acid [DMSA]) is chelator of choice because
Changes are not specific for arsenic poisoning. it has less adverse effects than other chelat-
HISTORY, CHIEF COMPLAINT • CBC ing agents.
• Exposure to arsenic-containing compound ○ Initial evidence of hemoconcentration ■ 10 mg/kg PO or PR q 8h for 10 days
• Peracute death ○ Mild anemia possible later in clinical ■ Use with caution in animals with renal
• Acute: severe gastrointestinal (GI) signs, weak- course insufficiency; maintain hydration.
ness, ataxia, recumbency, shock, and death • Serum chemistry • Manage GI effects.
• Subacute/chronic: watery diarrhea, renal ○ Azotemia if subacute ○ Antiemetics
failure ○ Acidosis if subacute ■ Maropitant citrate 1 mg/kg SQ q 24h
• Urinalysis or 2 mg/kg PO q 24h
PHYSICAL EXAM FINDINGS ○ Proteinuria ■ Chlorpromazine 0.2-0.5 mg/kg IM or
Vomiting and diarrhea, abdominal pain on ○ Cellular casts SQ q 6-8h; do not use if hypotensive
palpation, weakness, ataxia, poor pulse quality, ○ Urine-specific gravity (USG) of 1.008- ○ Consider antibiotics effective against
shock, dehydration 1.012 with azotemia consistent with renal gram-negative and anaerobic organisms
disease to prevent sepsis from GI translocation
Etiology and Pathophysiology ○ Acute kidney injury may produce oliguria • Manage renal damage (p. 23)
• Arsenic binds sulfhydryl groups on enzymes • Blood pressure: hypotension is common and
and other proteins, impairing cellular respira- requires treatment. Chronic Treatment
tion and depleting energy stores. Some forms • Manage ongoing diarrhea and kidney injury
of arsenic can also uncouple oxidative Advanced or Confirmatory Testing as needed.
phosphorylation. • Arsenic levels can be measured in urine, feces, • Consider starting hepatoprotective agents
• Tissues most affected are those rich in oxida- or vomitus. Levels in urine of < 1 ppm are ○ SAMe (Denosyl), 18 mg/kg PO for 1-3
tive enzymes (GI tract, endothelium, lung, considered normal. months
kidney, liver, epidermis). • Arsenic levels can also be measured in liver
○ GI inflammation and necrosis cause or kidney tissue; > 10 ppm wet weight is Nutrition/Diet
hemorrhagic gastroenteritis. consistent with arsenic poisoning. Bland diet while GI signs are present
○ Endothelial damage results in fluid loss into • Hair is not useful diagnostically.
interstitium, hypovolemia, hypotension, • Blood is not reliable for confirming arsenic Possible Complications
and noncardiogenic pulmonary edema. exposure. Possibly chronic kidney disease

www.ExpertConsult.com