Ethylene Glycol (Antifreeze) Poisoning

Ethylene Glycol (Antifreeze) Poisoning – An Overview

  • Results from ingesting substances containing ethylene glycol (such as antifreeze)
  • Common in small animals (such as dogs)
  • Highest fatality rate of all poisons
  • Higher likelihood of pet having ethylene glycol (antifreeze) poisoning in colder areas, where antifreeze use is more common

Signalment/Description of Pet

Mean Age and Range

  • Any age is susceptible
  • Mean—3 years of age

Signs/Observed Changes in Pet

  • Signs are dependent on the amount of ethylene glycol (antifreeze) ingested
  • Almost always sudden (acute)
  • Signs caused by ethylene glycol itself and its toxic metabolites (frequently fatal); “metabolites” are substances produced by the body’s chemical processes as it breaks down the ethylene glycol
  • Early signs—seen from 30 minutes to 12 hours after ingestion of ethylene glycol in dogs; nausea and vomiting; mild to severe depression; wobbly, incoordinated or “drunken” appearing gait or movement (known as “ataxia”) and knuckling; twitching muscles; short, rapid movements of the eyeball (known as “nystagmus”); head tremors; decreased withdrawal reflexes and righting ability; increased urination (known as “polyuria”) and increased thirst (known as “polydipsia”)
  • Dogs—with increasing depression, the pet drinks less but increased urination (polyuria) continues, resulting in dehydration; central nervous system signs lessen transiently after approximately 12 hours, but return later
  • Production of only small amounts of urine (known as “oliguria”) often develop in dogs 36–72 hours after ingestion of ethylene glycol (antifreeze);lack of production of urine (known as “anuria”) is seen 72–96 hours after ingestion of ethylene glycol—if untreated
  • May note severely low body temperature (known as “severe hypothermia”)
  • Severe sluggishness (lethargy) or coma
  • Seizures
  • Lack of appetite (known as “anorexia”)
  • Vomiting
  • Oral ulcers
  • Salivation or drooling
  • Kidneys—often swollen and painful

Causes

  • Ingestion of ethylene glycol, the principal component (95%) of most antifreeze solutions

Risk Factors

  • Access to ethylene glycol—widespread availability; somewhat pleasant taste; small minimum lethal dose (in other words, ingestion of a small amount can kill a pet); lack of public awareness of toxicity of ethylene glycol–containing antifreeze

Treatment

Health Care

  • Dogs—usually outpatient if presented to veterinarian under 5 hours from the time of ingestion and treated with fomepizole; inpatient if presented to veterinarian more than 5 hours after the time of ingestion for intravenous fluids to correct dehydration, increase blood flow to the tissues, and promote production of urine (known as “diuresis”)
  • Goals—prevent absorption of ethylene glycol into the body; increase excretion or removal of ethylene glycol from the body; prevent chemical processing (metabolism) of ethylene glycol by the body to toxic compounds
  • Induction of vomiting and flushing of the stomach (known as “gastric lavage”) with administration of activated charcoal are not recommended, unless they can be performed in the first 30 minutes following ingestion, due to the rapid absorption of ethylene glycol
  • Intravenous fluids—correct dehydration, increase blood flow to the tissues, and promote production of urine (diuresis); accompanied by administration of bicarbonate (given slowly intravenously) to correct metabolic acidosis (condition in which the pH of the body is too low)
  • If the pet develops excess levels of urea and other nitrogenous waste products in the blood (known as “uremia” or “azotemia”) and kidney failure characterized by production of small amounts of urine (oliguria) in dogs—most of the ethylene glycol has been metabolized; little benefit from treatment specifically designed for ethylene glycol poisoning; correct fluid, electrolyte, and acid–base disorders; promote production of urine (diuresis); medications to induce production and elimination of urine (known as “diuretics”; particularly mannitol) may help; peritoneal dialysis (a type of dialysis in which fluids are put into the abdomen and the lining of the abdomen [known as the “peritoneum”] acts as a filter to remove waste products from the blood; after a certain amount of time, the fluids and waste products are removed from the abdomen) may be useful; may need extended treatment (several weeks) before kidney function is reestablished

Activity

  • Avoid stress and excitement as these could make nervous system signs (hyperreflexia or seizures) worse

Diet

  • Suddenly (acutely) affected pet—do not feed
  • Recovering or convalescent pet—bland diet for several days to allow recovery from gastrointestinal problems

Medications

Medications presented in this section are intended to provide general information about possible treatment. The treatment for a particular condition may evolve as medical advances are made; therefore, the medications should not be considered as all inclusive.

  • Fomepizole (4-methyl pyrazole; Antizol-Vet®)
  • Ethanol, propylene glycol, and 1,3-butanediol—effectively inhibit ethylene glycol metabolism; may cause central nervous system depression; even in early stages of ethylene glycol (antifreeze) poisoning, requires hospitalization for approximately 3 days; constant intravenous (IV) infusion (ethanol and fluids); continuous monitoring for breathing and acid–base status

Follow-Up Care

Patient Monitoring

  • Bloodwork to monitor the kidneys (such as blood urea nitrogen [BUN]), acid–base status, and urine output—monitored daily for the first few days
  • Monitor urine pH to determine response to treatment

Preventions and Avoidance

  • Increasing awareness of the toxicity of ethylene glycol (found in most brands of antifreeze)—help prevent exposure; earlier treatment of pets
  • Use new antifreeze products, containing propylene glycol (relatively non-toxic)

Possible Complications

  • Without excess levels of urea and other nitrogenous waste products in the blood (azotemia)—usually no complications
  • Urine concentrating ability—may be impaired with excess levels of urea and other nitrogenous waste products in the blood (azotemia); pets recover
  • Death

Expected Course and Prognosis

  • Untreated—kidney failure characterized by the production of only small amounts of urine (oliguria) is seen in dogs at 36–72 hours after ingestion of ethylene glycol; lack of production of urine (anuria) is seen by 72–96 hours following ingestion
  • Dogs treated less than 5 hours following ingestion of ethylene glycol—prognosis is excellent with fomepizole treatment
  • Dogs treated up to 8 hours following ingestion of ethylene glycol—most recover
  • Dogs treated up to 36 hours following ingestion of ethylene glycol—may benefit from prevention of the body’s chemical processing (metabolizing) of any remaining ethylene glycol
  • If a large quantity of ethylene glycol is ingested, prognosis is poor, unless treated within 4 hours of ingestion
  • Pets with excess levels of urea and other nitrogenous waste products in the blood (azotemia) and kidney failure characterized by the production of only small amounts of urine (oliguria)—prognosis poor; almost all of the ethylene glycol will have been chemically processed by the body (metabolized) to toxic metabolites

Key Points

  • Ethylene glycol poisoning results from ingesting substances containing ethylene glycol (such as antifreeze)
  • Signs are dependent on the amount of ethylene glycol ingested
  • Ethylene glycol is readily available in many brands of antifreeze; it has a somewhat pleasant taste that attracts pets to ingest it; ethylene glycol has a small minimum lethal dose (in other words, ingestion of a small amount can kill a pet)
  • The public needs to be aware of toxicity of ethylene glycol–containing antifreeze; people should take precautions to safeguard their pets and other pets from potential sources of ethylene glycol

Chocolate Poisoning

Chocolate Poisoning – An Overview

  • Sudden (acute) gastrointestinal, nervous system, and heart problems caused by excessive intake of chemicals (known as methylxanthine alkaloids, such as theobromine and caffeine) present in chocolate and cocoa bean hulls, used for mulch
  • Dogs are poisoned most frequently based on their non-selective appetite, their access to chocolate or chocolate-containing products, and their ability to consume large amounts of chocolate
  • Other species may be affected, but they have a more limited access to chocolate and cocoa bean hull mulch than dogs; cocoa bean hulls may be a source of poisoning in horses and poultry
  • Theobromine is the chemical that is in the highest concentration of methylxanthines in chocolate products and in cocoa bean hull mulch; caffeine is in a much lower concentration in these products
  • Theobromine has a longer half-life in dogs than in people, meaning that it stays in the dog’s body for a longer time period than it does in people
  • Cocoa bean hull mulch is an increasingly popular product for using around gardens; it is composed of the shells (or hulls) of the cocoa bean and is produced during processing of the bean for chocolate

Signalment/Description of Pet

  • Small dogs—may be more at risk (amount of chocolate available compared to dog’s body weight)
  • Puppies and young dogs—may be more likely to ingest large amounts of unusual foods, such as chocolate or chocolate-containing foods, or cocoa bean hull mulch

Signs/Observed Changes in Pet

  • Signs are seen after recent chocolate or cocoa bean hull ingestion (family may find evidence of chewed containers or remnants of packaging from chocolate or chocolate-containing products
  • Vomiting and diarrhea—often the first reported signs; occur 2–4 hours after ingestion
  • Early restlessness and increased activity or nervousness
  • Frequent urination (known as “polyuria”)—may result from diuretic action of chemicals in chocolate
  • Blood in the urine (known as “hematuria”)—occasional sign
  • Advanced signs—stiffness; excitement; seizures
  • Increased body temperature (known as “hyperthermia”)
  • Exaggerated reflexes (known as “hyperreflexia”)
  • Muscle rigidity
  • Dilated pupils (known as “mydriasis”)
  • Rapid breathing (known as “tachypnea”)
  • Rapid heart rate (known as “tachycardia”)—heart rate may reach 200 beats per minute or more
  • Irregular heartbeats (known as “arrhythmias”)
  • High blood pressure (known as “hypertension”)
  • Increased thirst (known as “polydipsia”)
  • Death—12–48 hours after ingestion

Causes

  • Usually some form of processed chocolate (used for baking and candies, such as milk chocolate)—contain high concentrations of theobromine and caffeine
  • Dogs—eating cocoa bean hulls used as garden mulch

Risk Factors

  • Dogs—most commonly affected because they consume large amounts of many foods quickly
  • Chocolate—highly palatable or tasty and attractive; often readily available and unprotected in homes and kitchens, especially around the holidays when chocolate products and candies are common
  • Use of cocoa bean hull mulch in the garden

Treatment

Health Care

  • Describe the type of chocolate and amount of exposure to your veterinarian; take your pet to a veterinary hospital as a potential poisoning emergency
  • Fluid therapy—prevent dehydration and promote production of urine; correct electrolyte disturbances caused by vomiting, as necessary
  • Control seizures
  • Detoxification (if not having seizures or seizures are controlled)—your veterinarian may induce vomiting (known as “emesis”), flush the stomach with fluids (known as “gastric lavage”), and administer activated charcoal
  • Control overheating (hyperthermia)
  • Treat rapid heart rate (tachycardia)
  • Allow pet to urinate frequently or catheterize the bladder to remove urine to reduce the possibility of the methylxanthines being reabsorbed into the body from the urine

Activity

  • Avoid stress and excitement as these could make nervous system signs (hyperreflexia or seizures) worse

Diet

  • Suddenly (acutely) affected pet—do not feed
  • Recovering or convalescent pet—bland diet for several days to allow recovery from gastrointestinal problems

Surgery

  • Rarely, a solid mass or hard lump of chocolate could form, which must be removed surgically

Medications

Medications presented in this section are intended to provide general information about possible treatment. The treatment for a particular condition may evolve as medical advances are made; therefore, the medications should not be considered as all inclusive.

  • Induce vomiting (emesis)—only if the pet is not having seizures—apomorphine, syrup of ipecac, or 3% hydrogen peroxide
  • Flush the stomach (gastric lavage)—only before onset of vomiting and other clinical signs or vomiting has been controlled, if drugs to induce vomiting are not effective, seizures are controlled, and an endotracheal tube is in place
  • Once vomiting is controlled—activated charcoal to attract and keep the remaining alkaloids in the gastrointestinal tract
  • Osmotic cathartic—sodium sulfate or sorbitol 70% promotes gastrointestinal elimination of chocolate
  • Hyperactivity and seizures—controlled with diazepam
  • Ventricular rapid heart rate (known as “tachycardia”) in dogs—lidocaine (without epinephrine)
  • Serious abnormal heart rhythms (arrhythmias) that persist after medical treatment—metoprolol or propranolol; metoprolol preferred but may be difficult to obtain; may use oral therapy once the pet is stable; monitor electrocardiogram (ECG) and watch for hypotension (a possible complication to this treatment)
  • In rare cases of slow heart rate (known as “bradycardia”)—atropine
  • Control may be obtained with methocarbamol
  • If response to diazepam inadequate—consider phenobarbital
  • For refractory seizures—pentobarbital; “refractory seizures” are seizures that do not respond or are not controlled with treatment

Follow-Up Care

Patient Monitoring

  • Electrocardiogram (ECG) to evaluate and monitor abnormal heart rhythms or irregular heartbeats (arrhythmias)
  • Watch for mild to moderate kidney disease (known as “nephrosis”) in recovering pets

Preventions and Avoidance

  • Chocolate is among the 20 most common poisonings reported in recent literature, by small animal veterinary practices, animal poison control centers, and human poison control centersKeep chocolate in a secure location, out of reach of pets
  • Do not use cocoa bean hull mulch in areas accessible to pets

Possible Complications

  • Pregnant pet—risk for abnormal development of fetus leading to birth defects of newborns
  • Nursing pets—overstimulation of nervous system in nursing newborns

Expected Course and Prognosis

  • Expected course—12–36 hours, depending on dosage of chocolate and effectiveness of decontamination and treatment
  • Successfully treated pets—usually recover completely
  • Prognosis—good if oral decontamination occurs within 2–4 hours of ingestion; guarded with advanced signs of seizures and irregular heartbeats (arrhythmias)

Key Points

  • Chocolate ingestion is hazardous to pets; if you suspect your pet has eaten chocolate, chocolate-containing products, or cocoa bean hull mulch, contact your veterinarian immediately
  • Describe the type of chocolate and amount of exposure to your veterinarian; take your pet to a veterinary hospital as a potential poisoning emergency
  • Chocolate is among the 20 most common poisonings reported in recent literature by small animal veterinary practices, animal poison control centers, and human poison control centers
  • Keep chocolate in a secure location, out of reach of pets
  • Be especially careful around holidays when chocolate products and candies are readily available
  • Do not use cocoa bean hull mulch in areas accessible to pets

Anticoagulant Rodenticide Poisoning

Anticoagulant Rodenticide Poisoning – An Overview

  • An “anticoagulant” is something that prevents blood from clotting; a “rodenticide” is a product that kills rodents (such as mice and rats)—commonly known as “rat bait”
  • Blood-clotting disorder (known as a “coagulopathy”) caused by reduced vitamin K1–dependent clotting factors in the circulation after exposure to anticoagulant rodenticides
  • “Clotting factors” are components in the blood involved in the clotting process—the clotting factors are identified by Roman numerals I through XIII

Signalment/Description of Pet

Mean Age and Range

  • Younger pets may be more likely to ingest rat bait than older pets

Signs/Observed Changes in Pet

  • Difficulty breathing (known as “dyspnea”) and exercise intolerance
  • Bleeding
  • Localized mass of blood in a tissue or organ (known as a “hematoma”)—often along the lower areas of the body (known as the “ventrum”) and at sites where intravenous catheters were placed or blood was drawn (known as “venipuncture sites”); may have multiple hematomas
  • Muffled heart or lung sounds
  • Pale gums and moist tissues of the body (known as “mucous membranes”)
  • Sluggishness (lethargy)
  • >Depression

Causes

  • Exposure to anticoagulant rodenticide products (rat bait)
  • First-generation coumarin anticoagulants (such as warfarin, pindone)—have been largely replaced by more potent second-generation anticoagulants
  • Second-generation anticoagulants (such as brodifacoum, bromadiolone, diphacinone, and chlorophacinone)—are generally more toxic and some persist longer in the animal’s body than first-generation agents
  • Difenthialone (D-Cease Mouse and Rat Bait Pellets)—highly toxic to mice and rats; less toxic to dogs than are brodifacoum, bromadiolone, chlorophacinone, and warfarin

Risk Factors

  • Use of anticoagulant rodenticides
  • Anticoagulant rodenticide poisoning may be slightly more likely in the spring and fall, when rodenticide products are used
  • Small doses over several days more dangerous than a single large dose; either type of exposure may cause bleeding problems
  • Secondary poisoning by consumption of poisoned rodents—unlikely

Treatment

Health Care

  • Inpatient—sudden (acute) crisis
  • Outpatient—consider once the blood-clotting disorder (coagulopathy) is stabilized
  • Fresh whole blood or plasma transfusion—may be required if pet is bleeding; provides immediate access to vitamin K1–dependent clotting factors; whole blood may be preferred with severely low red blood cell count (known as “severe anemia”) from sudden (acute) or long-term (chronic) blood loss

Activity

  • Confine the pet during the early stages; activity enhances blood loss/li>

Diet

  • No recognized effect

Surgery

  • Procedure to tap the chest (known as “thoracocentesis”)—may be important for removing free blood in the space between the chest wall and lungs (known as the “pleural space”), which causes difficulty breathing (dyspnea) and breathing failure
  • Must correct blood-clotting disorder (coagulopathy) before surgery

Medications

Medications presented in this section are intended to provide general information about possible treatment. The treatment for a particular condition may evolve as medical advances are made; therefore, the medications should not be considered as all inclusive

  • Vitamin K1—administered by mouth, as directed by your pet’s veterinarian; length of treatment depends on the specific anticoagulant rodenticide product to which the pet was exposed; feeding of a small amount of fat, such as canned dog food, helps absorption of vitamin K1

Follow-Up Care

Patient Monitoring

  • Blood tests (activated clotting time [ACT] and prothrombin time [PT]) to evaluate clotting status—assess effectiveness of therapy; monitoring continued 3–5 days after discontinuation of vitamin K1 treatment

Preventions and Avoidance

  • Do not allow pets to have access to anticoagulant rodenticides (rat bait)

Possible Complications

  • Secondary bacterial pneumonia after bleeding into the lungs
  • Bleeding into or around the brain (known as “intracranial hemorrhage”), leading to nervous system signs (such as stupor or coma)
  • Bleeding into the joints (known as “intra-articular hemorrhage”), leading to lameness
  • Death

Expected Course and Prognosis

  • If the pet survives the first 48 hours of sudden (acute) blood-clotting disorder (coagulopathy)—prognosis improves

Key Points

  • Anticoagulant rodenticide (rat bait) poisoning is a common problem—many rodent baits are sold over the counter and widely used in homes
  • Reexposure of the pet to anticoagulant rodenticides could be a serious problem
  • Do not allow pets to have access to anticoagulant rodenticides

Acetaminophen Toxicity

Acetaminophen Toxicity – An Overview

  • Results from owners overdosing the pet with over-the-counter medications containing acetaminophen, a medication intended to control pain or fever in humans

Signalment/Description of Pet

  • Young and small dogs – greater risk from owner-given single-dose acetaminophen medications

Signs/Observed Changes in Pet

  • May develop 1–4 hours after dosing
  • Progressive depression
  • Rapid breathing
  • Darkened mucous membranes (moist tissues of body, such as gums)
  • Drooling (salivation)
  • Vomiting
  • Abdominal pain
  • Rapid breathing (known as “tachypnea”) and bluish discoloration of skin and moist tissues of body (known as “cyanosis”) due to a abnormal compound (methemoglobin) in the blood (condition known as “methemoglobinemia”) that disrupts the ability of the red blood cells to carry oxygen to the body
  • Fluid buildup (edema)—face, paws, and possibly forelimbs; after several hours
  • Chocolate-colored urine due to the presence of blood in the urine (known as “hematuria”) and the presence of methemoglobin in the urine (known as “methemoglobinuria”);
  • Death

Causes

  • Acetaminophen overdosing

Risk Factors

  • Nutritional deficiencies of glucose and/or sulfate
  • Simultaneous administration of other glutathione-depressing drugs

Treatment

Health Care

  • With methemoglobinemia (abnormal compound [methemoglobin] in the blood that disrupts the ability of the red blood cells to carry oxygen to the body)—must evaluate promptly; inpatient care
  • With dark or bloody urine or yellowish discoloration of skin and moist tissues of the body (known as “jaundice” or “icterus”)—inpatient care
  • Gentle handling—imperative for clinically affected pets
  • The veterinarian will induce vomiting (known as “emesis”) and may perform flushing of the stomach (known as “gastric lavage”)—useful within 4–6 hours of ingestion of acetaminophen
  • Low red blood cell count (known as “anemia”), blood in the urine (hematuria), or presence of hemoglobin in the urine (known as “hemoglobinuria”)—may require whole blood transfusion
  • Fluid therapy to maintain hydration and electrolyte balance
  • Drinking water should be available at all times

Activity

  • Restricted

Diet

  • Food—offered 24 hours after initiation of treatment

Medications

Medications presented in this section are intended to provide general information about possible treatment. The treatment for a particular condition may evolve as medical advances are made; therefore, the medications should not be considered as all inclusive

  • Activated charcoal—administered immediately after the veterinarian has induced vomiting or flushed the stomach (gastric lavage) and after vomiting is controlled; activated charcoal is used to attract and keep the remaining acetaminophen in the gastrointestinal tract
  • N-acetylcysteine (Mucomyst®) is administered; considered to be an antidote for acetaminophen toxicity
  • Other sulfur donor drugs—if N-acetylcysteine not available; sodium sulfate
  • 1% methylene blue solution—combats methemoglobinemia without inducing red blood cell destruction (known as a “hemolytic crisis”)
  • Ascorbic acid—slowly reduces methemoglobinemia

Follow-Up Care

Patient Monitoring

  • Continual clinical monitoring of methemoglobinemia (abnormal compound [methemoglobin] in the blood that disrupts the ability of the red blood cells to carry oxygen to the body)
  • Serum liver enzyme activities to monitor liver damage
  • Blood glutathione level—provide evidence of the effectiveness of therapy

Preventions and Avoidance

  • Give careful attention to acetaminophen dose; acetaminophen should only be given to dogs under a veterinarian’s supervision

Possible Complications

  • Liver damage and resulting scarring (fibrosis)—may compromise long-term liver function in recovered pets

Expected Course and Prognosis

  • Rapidly progressive methemoglobinemia (abnormal compound [methemoglobin] in the blood that disrupts the ability of the red blood cells to carry oxygen to the body)—serious sign
  • Methemoglobin concentrations greater than 50%—grave prognosis
  • Progressively rising serum liver enzymes 12–24 hours after ingestion—serious concern
  • Expect clinical signs to persist 12–48 hours; death owing to methemoglobinemia possible at any time
  • Receiving prompt treatment that reverses methemoglobinemia and prevents excessive liver damage may recover fully
  • Death as a result of liver damage may occur in a few days

Key Points

  • Acetaminophen should only be given to dogs under a veterinarian’s supervision
  • Considerably less frequent in dogs
  • Treatment in clinically affected pets may be prolonged and expensive
  • Pets with liver injury may require prolonged and costly management