9 Anticoagulant rodenticides

Although rodent baits are all similar in appearance, do not confuse anticoagulant rodenticides with bromethalin (a neurotoxin) or cholecalciferol (a vitamin D analogue). Small doses of anticoagulants can cause coagulopathy by inhibiting the recycling of vitamin K₁ and blocking the synthesis of clotting factors II, VII, IX, and X. Clinical signs generally occur three to seven days after exposure when circulating clotting factors are depleted. Bleeding may occur in any location, so signs may be nonspecific and include weakness, lethargy, and dyspnea.¹³ Hemorrhage is most common in the lungs, so cough or respiratory difficulty is a common finding.¹⁴ Frank hemorrhage or ecchymoses may be seen. Lameness may occur if bleeding occurs in a joint, and various neurologic signs may be noted if bleeding occurs in the brain or spinal cord.¹³

Anticoagulant rodenticide poisoning can be diagnosed by measuring the prothrombin time (PT). PIVKA (proteins induced by vitamin K₁ absence or antagonism) and Thrombotest (Axis-Shield) time are other screening tests for anticoagulant toxicosis. PT and PIVKA tests are most sensitive to depletions of factor VII because it has the shortest half-life.¹⁴

Also test the PT or PIVKA about 48 hours after cessation of vitamin K₁ treatment to determine whether the patient was treated long enough. If an animal presents in hemorrhagic crisis, treatment is generally supportive and should consist of whole blood or plasma transfusions and stabilization as needed as well as vitamin K₁.¹³ If treatment is started before coagulopathy, the prognosis is excellent. The prognosis is guarded if the patient is already bleeding.

10 Amphetamines

In people, amphetamines in prescription medications are used for appetite suppression, attention deficit disorder, and narcolepsy. Another source of amphetamine exposure is illicit preparations of amphetamine, methamphetamine, and 3,4-methylenedioxymethamphetamine (MDMA), also known as Ecstasy. Amphetamines act as CNS stimulants by increasing catecholamine release, inhibiting catecholamine reuptake, and increasing release of serotonin.¹⁵ Almost any exposure in a cat can result in clinical signs such as agitation, hyperthermia, tremors, seizures, tachycardia, hypertension, cardiac arrhythmias, and coma (ASPCA APCC Database: Unpublished data, 2002-2005).

Treatment should include gastric decontamination if the animal is asymptomatic, but a rapidity in the onset of clinical signs may limit the possibility for this. Monitor cardiovascular and CNS signs closely. Also monitor body temperature, and maintain it in a normal range. Administer acepromazine or chlorpromazine for agitation, and barbiturates may be used to control seizures.¹⁶ Cyproheptadine may be used as a serotonin antagonist. Treat cardiac arrhythmias as needed (e.g. propranolol if tachycardia is present). Intravenous fluids will help promote elimination. Consider administering ammonium chloride or ascorbic acid to acidify the urine and promote elimination if acid-base balance can be monitored. The half-life of the drug and the duration of signs depend on the urinary pH, and signs may be seen for 12 to 48 hours or more.¹⁶ The prognosis with aggressive supportive care is good in most cases.

"Toxicology Brief" was contributed by Valentina Merola, DVM, DABT, and Eric Dunayer, MS, VMD, DABT, ASPCA Animal Poison Control Center, 1717 S. Philo Road, Suite 36, Urbana, IL 61802. The department editor is Petra A. Volmer, DVM, MS, DABVT, DABT, College of Veterinary Medicine, University of Illinois, Urbana, IL 61802.