Human Medication Toxicity

Antidepressants (SSRIs and others)

Medications that cause GI signs, CNS changes (stimulation or depression), seizures, mydriasis, heart rate ($HR$) and blood pressure ($BP$) changes, respiratory depression, and arrhythmias.

Barbiturates

Medications that lead to sedation, respiratory depression, and coma during toxicosis.

Sleep aids

Medications that present with ataxia, tremors, and CNS stimulation or depression; treatment should specifically avoid the use of diazepam.

Cardiac medications (ACE inhibitors, $Ca^{2+}$ channel blockers, beta-blockers)

Drugs that cause hypotension, bradycardia, and arrhythmias; high doses can lead to respiratory depression, pulmonary edema, hyperkalemia, and seizures.

Amphetamines

Medications found in ADHD and illegal forms that cause GI signs, CNS stimulation, tachycardia, hypertension, and hyperthermia.

Cyproheptadine

A serotonin antagonist used as a specific treatment for $SSRI$ (selective serotonin reuptake inhibitor) toxicity.

External cooling

A specific treatment measure often required for amphetamine toxicity to manage hyperthermia.

Acute Kidney Injury (AKI)

A clinical risk associated with severe or lasting hypotension during medication toxicity.

Extended release formulas

Medication formulations that can delay the onset of clinical signs of toxicity by a few hours.

Diazepam

A sedative/anticonvulsant that is contraindicated (must not be used) in the treatment of sleep aid toxicity.

Colloids/Vasopressors

Agents used symptomatically to manage cardiovascular instability during prescription medication toxicity.

Salicylic acid

The major active metabolite of aspirin that inhibits platelet function for the life of the exposed platelets.

Low-dose Aspirin Toxicity

Exposure causing GI ulcers and signs of GI upset typically within $1-4\,d$.

High-dose Aspirin Toxicity (Acute)

Exposure resulting in metabolic acidosis, hyperthermia, seizures, and coma within a few $h$.

High-dose Aspirin Toxicity (Delayed)

Exposure leading to hepatic dysfunction within $1-3\,d$.

Hematochezia and Melena

Clinical signs of ongoing bleeding at any aspirin dose resulting from the inhibition of platelet function.

Buccal mucosal bleeding time

A lab measurement that increases in aspirin toxicity, indicating platelet dysfunction despite a normal platelet count.

Aspirin CNS Effects Mechanism

Neurological signs resulting from low brain glucose levels despite normal peripheral glucose levels.

GI Protectants

Therapeutic agents such as misoprostol, sucralfate, and antacids used to treat aspirin-induced GI ulcers.

IV dextrose CRI

A treatment indicated for aspirin toxicity when neurological signs are present, addressing low cerebral glucose.

Aspirin vs. Other NSAIDs

A clinical distinction where kidney damage is rare in aspirin toxicity compared to other nonsteroidal anti-inflammatory drugs.

Poor Prognosis Indicator

The clinical outcome is generally poor if neurological (CNS) signs are present following aspirin exposure.

COX enzymes

Enzymes blocked by NSAIDS to inhibit prostaglandins, which are necessary for normal kidney blood flow and generating GI mucosal barriers.

Species most sensitive to Ibuprofen

Cats and ferrets, which are highly toxic at lower doses than those seen in dogs.

Low-dose Ibuprofen signs ($6$-$12\,h$)

Vomiting and GI upset.

Low-dose Ibuprofen signs ($12$-$24\,h$)

Hematemesis and melena due to GI ulcers.

Higher-dose Ibuprofen signs

Renal failure (following GI signs in $1$-$2\,d$) and PU/PD.

Very high-dose Ibuprofen signs

CNS effects including depression, seizure, and coma.

Ibuprofen toxicity labwork findings

Anemia and low protein (from GI ulcers).

Urinalysis monitoring for NSAID toxicity

Baseline and daily monitoring for tubular casts and proteinuria.

Kidney value monitoring protocol

Baseline kidney values and recheck $q24h \times 3d$.

Ibuprofen decontamination (first $24\,h$)

Emesis within $4\,h$ and Activated Charcoal ($AC$) with repeated dosing in the first $24\,h$.

GI protectant duration

Antacids (H2 and/or proton pump inhibitors) and sucralfate for $14\,d$; prostaglandin analogs for $2$-$3\,d$.

IV fluid diuresis protocol

IV fluid diuresis for $48\,h$ with normal renal values, or longer with azotemia.

Symptomatic neuro support for NSAIDs

The use of Diazepam for seizures.

Surgery for NSAID toxicity

Indicated for GI perforation.

Ibuprofen use in dogs

Do not use ibuprofen in dogs even though there are published doses.

Ibuprofen toxicosis prognosis

Good with prompt Tx; worsening with delayed care or large doses; may lead to chronic kidney Dz.

Methemoglobinemia

A condition occurring 1-12 hours after acetaminophen ingestion, characterized by muddy/brown mucous membranes, dyspnea, weakness, tachycardia, facial/paw edema, and cyanosis.

Hemolytic anemia

A condition that follows methemoglobinemia within 72 hours, often presenting as Heinz body anemia and hemolysis.

Hepatotoxicity

Signs of liver failure, including hyperbilirubinemia and increased liver enzymes, occurring 24-48 hours after acetaminophen ingestion.

White filter paper test

A diagnostic test where affected patient's blood appears brown compared with normal patient blood.

N-acetylcystine (NAC)

A treatment administered as an IV bolus followed by repeated doses that binds toxic metabolites and supports the liver.

Glucuronidation

The elimination pathway cats lack, leading to an alternate pathway that breaks down acetaminophen into a toxic metabolite.

Cat toxic dose (Acetaminophen)

$$10-40\,mg/kg$$

Dog toxic dose (Acetaminophen)

$$>100\,mg/kg$$

Keratoconjunctivitis sicca (KCS)

An acute condition involving dry eyes that dogs rarely develop following acetaminophen ingestion.

Ascorbic acid and SAM-e

Specific supportive medications used in the treatment of acetaminophen toxicity.

Enterohepatic circulation

The reason why repeated doses of activated charcoal (AC) are required during treatment.

Acetaminophen (Classic Case)

Toxicity that affects cats significantly more severely than dogs.