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127.e2 Boric Acid Toxicosis

Boric Acid Toxicosis Client Education
Sheet
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Mechanism of toxicosis:
BASIC INFORMATION
• The exact mechanism is unknown. Boric acid TREATMENT
Definition is considered cytotoxic to all cells. Treatment Overview
Toxicosis results from ingestion of inorganic • Rapidly absorbed after oral ingestion through Treatment is aimed at inducing emesis in large
compounds of boron used in ant or roach baits, mucous membranes, as well as through exposures and providing supportive care as
flea products for dogs and cats, cleaning abraded skin needed. Most cases are self-limited (signs resolve
compounds, buffering agents, eye washes, and • Concentrated in the kidneys before excretion; within a few hours).
as an anticaking agent. Although ingestions excreted unchanged in the urine
are common, serious toxicosis is rare because • Half-life in dogs is 12 hours, but total Acute General Treatment
of the large amount of product that needs to elimination may take up to 7 days. Decontamination of patient:
be ingested. However, clinically significant • No death or serious systemic toxicosis • Emesis: induce vomiting in cases involving
ingestions are characterized by vomiting, diar- is reported in dogs given 1.54-6.51 g/ large ingestions.
rhea, anorexia, lethargy, and (rarely) kidney kg of borax or 1-3 g/kg of boric acid. • Activated charcoal is not useful in binding
injury. Examples: boric acid.
○ 20 ounces (570 g) of a 5.4% boric acid • Bathe the animal for dermal exposures, using
Synonyms ant bait would have to be ingested by a diluted liquid dishwashing detergent.
Borax, boric acid, orthoboric acid, sodium 20-kg dog to reach a dose of 1.5 g/kg. Supportive care:
borate ○ Similarly, 1.1 ounces (31 g) of a 99% boric • Control excessive vomiting with maropitant
acid agent would need to be ingested by 1 mg/kg SQ q 24h, up to 5 days or meto-
Epidemiology a 20-kg dog to reach a dose of 1.5 g/kg. clopramide 0.022-0.044 mg/kg PO, SQ, or
SPECIES, AGE, SEX ○ In either case, systemic signs are not IM after ruling out GI obstruction.
• All cats and dogs are susceptible. likely, except possibly for vomiting and • GI protectants
• Cats may be exposed after walking through diarrhea. ○ Sucralfate 0.5-1 g q 8h PO and
the agent when it is placed in cupboards or ○ Famotidine 0.5 mg/kg PO, SQ, or IM q
closets or when flea powders containing boric DIAGNOSIS 12-24h or
acid are used topically. ○ Omeprazole 0.7 mg/kg PO q 24h for 5-7
Diagnostic Overview days
RISK FACTORS Diagnosis rests on history and physical exam: • IV crystalloid fluid diuresis for 24-48 hours
Pre-existing kidney disease may increase the suspected or witnessed exposure and presence in cases involving large ingestions
risk of nephrotoxicosis from large ingestions. of gastrointestinal (GI) signs (vomiting, diar- • Treat acute kidney injury if it occurs.
rhea) that are typically self-limited • Control seizures with diazepam 0.5-2 mg/
Clinical Presentation kg IV unless underlying cause is metabolic
HISTORY, CHIEF COMPLAINT Differential Diagnosis (e.g., hypoglycemia, hypocalcemia, hepatic
• History of using a boric acid–containing Toxicologic: encephalopathy).
product on the animal or in the house (for • Garbage toxicosis
fleas or control of other insects) • Dietary indiscretion Chronic Treatment
• Vomiting • Nephrotoxic agents (ethylene glycol, phar- Kidney injury or other systemic effects (seizures)
• Hypersalivation maceuticals, lilies [cats], grapes and raisins are rare.
• Anorexia [dogs])
• Lethargy Non-toxicologic, spontaneous: Possible Complications
• Infectious enteritis (e.g., parvoviral, corona- May exacerbate pre-existing kidney disease
PHYSICAL EXAM FINDINGS viral, bacterial)
Findings tend to be nonspecific. • GI obstruction (e.g., foreign body, Recommended Monitoring
• Common intussusception) • Recheck renal parameters (blood urea
○ Hypersalivation • Any disorder causing acute GI signs nitrogen, creatinine, urinalysis) at 24 and
○ Lethargy 48 hours after exposure if more than mild
○ Vomiting, diarrhea Initial Database GI signs occur.
• Possible • CBC: microcytic hypochromic anemia • If renal parameters are within reference
○ Oliguria/anuria (rare) possible ranges at that time, further problems not
○ Ataxia (rare) • Serum biochemistry panel: azotemia, expected.
○ Seizures (rare) hyperchloremia, hypernatremia, hyperkale-
mia, and metabolic acidosis may be noted PROGNOSIS & OUTCOME
Etiology and Pathophysiology in severe cases; rarely, elevated liver enzymes
Source: • Urinalysis: in severe cases causing oliguria Excellent in animals with signs limited to
• Some ant baits may contain < 5% boric or anuria with tubular necrosis, albuminuria, vomiting/diarrhea
acid, whereas some roach products can hematuria, proteinuria, and epithelial casts
contain 100% boric acid. (acute kidney injury), or isosthenuria concur- PEARLS & CONSIDERATIONS
• Boric acid–containing formulations are rently with azotemia (chronic kidney disease)
available as powders, liquids, or gels. may be noted. Comments
• Borates have been used in pharmaceutical • Activated charcoal adsorbs boric acid poorly
preparations (mouthwash, toothpastes, Advanced or Confirmatory Testing (boron compounds do not adhere well to
cosmetics), toiletries, cleaning compounds, Boric acid may be detected in the urine, charcoal). A 30 : 1 ratio of activated charcoal
and as insecticides. cerebrospinal fluid, blood, and plasma. to boric acid was needed to absorb 38% of

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