Poisons and Toxins

The first aid section covers what basic steps should be taken if you suspect your pet has been poisoned. The basic steps in helping your pet should always include:

2. Thoroughly flush skin or eyes with large quantities of water. Wear gloves while handling the animal to prevent contact with
offending or dangerous substance.

3. Provide plenty of fresh air for the the cat to breathe.

4. Induce emesis (vomiting) unless a.) it has been over 2 hours since the suspected poison was ingested or b.) if the cat is very depressed or unconscious, or c.) if you suspect the animal of having ingested a petroleum product, acids, alkali, tranquilizers or other drugs, which cause vomiting.

Emesis can be induced by giving the cat a tablespoon of syrup of ipecac (less to small cats), OR a tablespoon of hydrogen peroxide. The ipecac is the most reliable emetic drug.

6. Bring the pet to a veterinary care center quickly, and try to bring a sample of the vomit, and/or any boxes or cans which you suspect the toxins may have come in.

For specific, detailed information contact a Poison Control Center. A Poison Reference has also been included below to help match the specific poisoning to the exact chemical(s) responsible and move you directly to the appropriate section. Read carefully any labels or information available on the material(s) you believe poisoned your pet. This information will speed your search herein and be important to your veterinarian as well.

Sources Many prescription and over-the-counter brands of analgesic and antipyretic drugs contain acetaminophen or its ethyl ether, phenacetin. Examples are Tylenol, SineAid, SineOff, Anacin-3, Comtrex, Daytril, Nyquil, Allerest, and Vanquish.

Mechanism of action Phenacetin is metabolized to acetaminophen. Acetammophen is metabolized by enzymes of the cytochrome P-450 series to intermediate products: nonreactive glucuronides and sulfates (which are conjugated and eliminated in the urine), and reactive metabolites, which are metabolized with glutathione to nontoxic mercapturic acid (which is eliminated). If the toxic metabolites accumulate as a result of insufficient glucuronide or sulfate metabolism or insufficient glutathione, they are converted to toxic macromolecules that directly cause cellular death. Cats lack glucuronyl transferase and inefficiently form glucuronic acid and sulfate conjugates, leaving more acetaminophen or phenacetin to be metabolized to toxic metabolites. The glutathione stores are rapidly depleted in cats, leaving a large amount of toxic metabolites. Methemoglobinernia occurs.

Clinical signs Acute signs in cats are related to methemoglobin formation, whereas acute signs in the dog are related to hepatic damage. Toxicity is mainly seen in cats when even a small amount of acetarninophen is ingested (half of a 325 mg tablet for a 3.5 kg cat); dogs can usually tolerate dosages up to 100 mg/kg. Signs include cyanosis (which is caused by methemoglobinemia), dyspnea, facial edema (a hallmark of acetaminophen poisoning mechanism unknown), depression, hypothermia, vomiting. Signs may progress to weakness, coma, and subsequently death. Increased ALT from hepatic damage may be seen.

Treatment Since the toxic metabolites bind preferentially with glutathione rather than cell macromolecules, supplying a glutathione precursor is an important part of treatment. N-Acetylcysteine provides the cysteine needed for glutathione synthesis and also increases serum sulfate levels, which supplies sulfate for conjugation. Ascorbic acid is used to change methemoglobin to reduced hemoglobin. Acetarninophen is rapidly absorbed and reaches peak blood levels within 30 to 60 minutes; emesis is performed immediately after ingestion (if possible), and a saline cathartic is given. Steroids should not be given because they have been reported to cause a dose-dependent increase in mortality. Antihistamines have been reported to be contraindicated.

Signs

Cyanosis
Dyspnea
Facial edema
Depression
Hypothermia
Vomiting
Increased ALT
Weakness
Coma
Death

EMERGENCY TREATMENT

Procedures

I .    Secure the airway and ventilate as necessary.
2.    Administer supplemental oxygen.
3.    Secure venous access. Collect blood for laboratory testing. Administer fluids as needed to support blood pressure and
       perfusion.
4.    Control seizures.

Decontaminate

I .    Induce emesis if sate to do so or perform gastric lavage .

2.    Administer activated charcoal. Repeat dose every 3 to 4 hours. If N-acetylcysteine is to be given orally, activated
       charcoal administration should be delayed for 30 to 60 minutes.

3.    Administer saline or osmotic cathartics.

Administer antidotes or other indicated supportive care

1. N-Acetylcysteine (Mucomyst) 280 mg/kg PO loading dose (dogs) or 140 to 240 mg/kg PO loading dose (cats), followed
     by 140 mg/kg PO q4h for 3 days (dogs) or 70 mg/kg q6h for 3 days of treatments (cats). Mucomyst, although not labeled
     for IV use, can be administered intravenously (either directly from the bottle or diluted in D 5W) by infusion through a 0.2
     pin filter. The oral route is preferred because Mucomyst is rapidly absorbed from the GI tract where it enters the portal
     circulation. This is believed to increase the amount of drug presented to the liver, the site of utilization.

2. Administer fluids to maintain hydration and urine output.

3. Treat increased intracranial pressure if suspected.

4. Ascorbic acid at 30 mg/kg PO, SC, or 20 mg/kg IV may be given as an attempt to convert methemoglobin to
     oxyhemoglobin If severe acidosis (pH <7. 1, rare), sodium bicarbonate can be used. Cimetidine reduces metabolism of
     acetaminophen by the cytochrome P-450 system. Metabolism of acetaminophen by this system results in the production
     of a hepatotoxic metabolite. Therefore the administration of cimetidine is warranted.

Enhancement of elimination

Hemoperfusion has been shown to enhance elimination of acetaminophen.

Avoid

Excessive handling and stress.

References

Aronson LR, Drobatz KJ Acetaminophen toxicosis in 17 cats, J Vet Emerg Crit Care 6(2):65-69, 1996. Cullison R: Acetarninophen toxicosis in small animals: clinical signs, mode of action, and treatment, Compend Cont Ed Pract Vet 6(4):315-320, 1984.

Hjelle J: Acetaminophen-induced toxicosis in dogs and cats, J Am Vet Med Assoc 188(7):742-745, 1986.

0ehme F: Aspirin and acetaminophen. In Kirk RW, editor: Current veterinary therapy, Philadelphia, 1986, Saunders.

ACETONE    (Organic Solvents and Fuels)

Sources This section includes many chemicals that are found in solvents, degreasing agents, dry cleaning agents, and fuels for camp stoves, warmers, etc. Acetone, benzene, benzol, methanol, methylene chloride, naphtha, trichloroethane, trichloroethylene, toluene, toluol, xylene, and xylol are examples included in this category.

Mechanism of action Nearly all these compounds cause pulmonary injury from direct effects with inhalation or systemic effects from ingestion and inhalation. Pulmonary aspiration is one of the greatest concerns in patients exposed to these compounds. Aspiration of very small amounts will likely induce chemical pneumonia. Most of these agents also have direct CNS-depressant effects. They are reported to be irritating to the skin, eyes, and mucous membranes. Further, they are known to sensitize the myocardiurn to catecholamines, thus increasing cardiac dysrhythmias. Hypoxemia may be seen if the patient was exposed to the compound in an enclosed space. Hepatic and renal injury may occur by undefined mechanisms.

Signs Inhalation or exposure to fumes causes conjunctivitis, nausea, vomiting, depression, wheezing, cyanosis, weak pulse, convulsions, and collapse. Signs noted after ingestion include nausea, vomiting, diarrhea (hemorrhagic at times), fixed pupils, ataxia, depression, and coma. Hemolysis and methemoglobinemia have been reorted with exposure to naphthalene and toluene.

Treatment Treating poisoning by inhalation requires removing the patient from the source, administering oxygen (when available), and washing the eyes copiously with water. Treating poisoning by ingestion involves oxygen therapy, treatment for aspiration or chemical pneumonia (see discussions of bronchospasm, and pulmonary edema, cautious gastric lavage, activated charcoal, and a cathartic. Epinephrine and other catecholamines should be avoided if possible because of the possible sensitization of the myocardium by these agents.

Signs

INHALATION
    Conjunctivitis
    Nausea
    Vomiting
    Depression
    Cyanosis
    Weak pulse
    Convulsions
    Collapse

INGESTION
   Nausea
   Vomiting
   Diarrhea (possibly bloody)
   Fixed pupils
   Ataxia
   Depression
   Methemoblobinemia
   Hemolysis
. Coma

EMERGENCY TREATMENT

Procedures

I      Secure the airway and ventilate as necessary.

2.    Administer supplemental oxygen.

3.    Secure venous access. Collect blood and urine for laboratory testing.

4.    Administer isotonic crystalloids as needed to support blood pressure and perfusion.

5.    Control seizures.

6.    Treat bronchospasm, pulmonary edema, methemoglobin.

Decontaminate

If exposure is by inhalation, remove the source or move the patient to a well-ventilated environment. Do not induce emesis. Perform cautious gastric lavage if the ingestion was within the last I to 2 hours. Take care not to allow aspiration of gastric contents during procedure. Give activated charcoal. Administer saline or sorbitol cathartic. Magnesium-containing solutions should be avoided.

If exposure is dermal, bathe the patient in warm, soapy water or mild dishwashing detergent (Dawn) and rinse well with warm water. Perform this in a well-ventilated room. Avoid inducing hypothermia.

Administer antidotes or other indicated supportive care

1.   There are no known antidotes.

2.   Treat chemical pneumonia with oxygen, ventilation, nebulization, and coupage ('percussion of the thorax to aid in the
      removal of secretions). Broad-spectrum antibiotics are not indicated prophylactically but may become necessary if the
      chemical pneumonia initiates bacterial infection. Monitor blood counts, sputum, and pulmonary washings as necessary to
      determine the need for antibiotics.

3.    Monitor ECG and treat cardiac dysrhythmias. CAUTION: These agents cause increased myocardial sensitivity. Use of
       epinephrine or other sympathomimetic amines may induce or aggravate cardiac dysrhythmias.

4.    Monitor urine output and renal parameters to observe for onset of acute renal failure.

5.    Monitor for evidence of hepatic injury and treat accordingly.

6.    Treat methemoglobinernia if present.

Enhancement of elimination

There are no techniques that are effective.

Avoid

Catecholamines

References

Kirk RW, Bistner SI, Ford RB: Handbook of veterinary procedures and emergency treatment, ed 5, Philadelphia, 1990, Saunders.

Osweiler GD, Carson TL, Buck WB, Van Gelder GA: Clinical and diagnostic veterinary toxicology, ed 3, Dubuque, Iowa, 1985, Kendall/Hunt.

Sources Household cleaning products, toilet bowl and drain cleaners, dishwasher detergents, cleaners, antirust compounds, alkaline batteries.

Mechanism of action Acids produce corrosive burns, resulting in coagulation necrosis, which limits their penetration into deeper tissues. Visible lesions (necrotic eschars) are seen on mucous membranes; laryngeal spasm and edema may occur. Alkalis produce liquefaction necrosis, allowing deep tissue penetration that continues until the alkali is neutralized by the tissues.

Clinical signs Irritation of the oral mucous membranes is prominent; ptyalism is common. Oral ulcers and burns may be present but, when absent, do not indicate a lack of esophageal involvement. Gray, yellow, or..black lesions most commonly result from acids. Pain, vocaCization, dysphagia, panting, laryngeal edema with upper airway obstruction, abdominal pain, hematemesis, and shock have been reported. In cases of severe injury, perforation of the esophagus or stomach (especially in the region of the pylorus) may be seen. Signs include ptyalism, pain, pneumothorax, peritonitis, pleuritis, sepsis, shock, collapse, and death.

Treatment

GENERAL

Emesis and lavage are contraindicated. Activated charcoal is ineffective. Both acids and alkalis can induce pain upon exposure to mucous membranes; this usually limits the amount of concentrated poison ingested, which minimizes esophageal injury. Diluted agents produce less pain and potentially more severe esophageal burns. injury to the pharynx, larynx, or glottis may cause loss of airway requiring immediate endotracheal tube placement or tracheostomy tube placement.

In general, caustic substances such as acids or alkalis cause local injury, mostly to the mouth, esophagus, and stomach. The degree of oral injury does not correlate well with deeper injuries. For this reason, endoscopic examination of the esophagus and stomach is indicated in patients who have ingested a caustic substance. The procedure should be performed 12 to 24 hours after the incident based on clinical signs.

Treatment of ingestions usually is limited to administration of diluents such as water or milk. Systemic supportive measures must be instituted on a case-by-case basis. Some patients will require intensive shock therapy, whereas others may require only minimal treatment for oral burns.

Pain control is almost always indicated. Corticosteroids may minimize scar formation and thus limit the degree of stricture in cases of esophageal burns. They should be started within 48 hours of injury. Broad-spectrum antibiotics are indicated when steroid therapy is used.

ALKALI INGESTION

Emesis and lavage are contraindicated in alkali ingestion. Gastric secretions are usually sufficient to neutralize the alkali. Activated charcoal is ineffective in alkali ingestion. Since the clinical signs rarely correlate to the degree of esophageal or gastric injury, endoscopic exam should be performed in patients with alkali burns. The procedure should be delayed until the patient has been evaluated for at least 12 hours, and then the procedure should be performed carefully. The procedure should be halted at the first sign of esophageal necrosis.

Ingested alkaline batteries should be removed from the esophagus endoscopically as soon as possible to prevent perforation. If the battery is in the stomach, the probability of perforation is greatly reduced, but the battery should be retrieved in a timely manner. Consider induction of emesis, whole bowel irrigation, or endoscopic retrieval. Serial radiographs to monitor the position of the battery are indicated.

ACID INGESTION

When acids contact mucous membranes, intense pain results. For this reason, most animals will not ingest very much. Emesis is contraindicated. The patient should be given copious quantities of diluents such as water or milk. Activated charcoal is ineffective. Supportive care is advised. With severe esophageal injury, food and water are withheld until endoscopic evidence of healing is available; the animal is maintained on parenteral food and water or with a feeding tube (as with a jejunostomy, gastrostomy).

TOPICAL EXPOSURE

Topical exposure to acids or alkalis should be treated with extensive irrigation with running water. The area should be flushed for at least 30 minutes. If the eye was exposed, it should be flushed with water or saline (strongly advise sterile saline if available) for 30 minutes.

Signs

Irritation of oral mucous membranes
Salivation
Oral ulcers or burns
Oral lesions colored gray, yellow, or black (acids)
Hematemesis
Panting, dyspnea (especially upper airway although pulmonary edema has been reported)
Pain
Vocalization
Dysphagia
Shock
Perforation of the esophagus (stomach or intestines may perforate but are less likely to do so)
Pneumothorax
Peritonitis
Pleuritis
Sepsis
Shock, collapse, and death

EMERGENCY TREATMENT

Procedures

1.    Secure the airway and ventilate as necessary
2.    Administer supplemental oxygen.
3.    Secure venous access. Collect blood and urine for laboratory testing.
4.    Administer large volumes of water (preferable) or milk orally.

Decontaminate

1.    GI exposure (ingestion). Emesis and gastric lavage are contraindicated in alkali and acid injuries. Rarely the use of gastric
        lavage with aluminum hydroxide at 30 to 90 mg/kg for acid injury if esophageal injury is minimal has been recommended.

2.    Dermal exposure. Wash thoroughly with warm water (with or without soap) for a minimum of 30 minutes. Wear rubber
       gloves when bathing the patient; avoid inducing hypothermia.

3.    Exposure of the eyes. Flush the eyes with water or sterile saline (preferable) for 30 minutes.

4.    Administer crystalloid fluids to maintain blood pressure or hydration and urine output.

Enhancement of elimination

There are no known effective techniques

Avoid

Do riot give "neutralizing agents." These are usually heat-producing reactions, which may cause additional injury.

ISOPROPANOL (ISOPROPYL ALCOHOL)

Sources Isopropanol (2-propanol, secondary propyl alcohol, dimethylcarbinol and petrohol) is used as an antiseptic and disinfectant and in skin lotions, hair tonics, after-shave lotions, perfumes and colognes, cleaning solvents, and sanitizers.

Mechanism of action Isopropanol is a potent CNS depressant. It is twice as toxic as ethanol; intoxication can be seen after ingestion of less than 3.0 mL/kg. It is a gastrointestinal irritant when ingested. Isopropanol is readily absorbed from the GI tract; the rate of biotransformation is generally slower than that for ethanol. Inhalation can produce chemical pneumonia, pulmonary edema, and coma.

Clinical signs The pet will appear drunk and often has an alcohol odor. Emesis, including hematemesis, retching, and cranial abdominal tenderness may be seen. Rapid CNS depression characterized by respiratory depression and coma occur. CNS stimulation may be observed preceding the depression if the product contains camphor, methyl salicylates, or naphthalenes. Shock can occur, as can ketonemia with uria (usually without glucosuria) and high anion-gap acidosis. Signs are similar to methanol, ethanol, and ethylene glycol intoxication.

Treatment   Although gastric lavage will probably not remove much isopropanol from the gut (because of alcohol's rapid absorption from the stomach), lavage is advised if large amounts were ingested within the past 2 hours. Emesis is not recommended because of the potential for rapid onset of CNS depression, which increases risk of aspiration. Dialysis is used in people.

Signs

Drunkenness
Alcohol odor
Emesis, hematemesis
Retching
Cranial abdominal tenderness
CNS depression (may follow CNS stimulation)
Respiratory depression
Coma
Shock
Ketonemia, ketonuria
High anion-gap acidosis
Increased osmolar gap

EMERGENCY TREATMENT

Procedures

1.    Secure the airway and ventilate as necessary.

2.    Administer supplemental oxygen.

3.    Secure venous access. Collect blood and urine for laboratory testing.

Decontaminate

INGESTION

1.    Perform gastric lavage if large ingestions within the past 2 hours.

2.    Although isopropanol is not adsorbed well by activated charcoal, current literature recommends activated charcoal be
       administered.

3.    Administer saline or osmotic cathartic. Cathartics containing magnesium should be avoided because of the potential for
       additional CNS depression from magnesium.

Administer antidotes and other supportive care

1.    There are no known antidotes.

2.    Blood gas determinations are important. CNS depression may induce respiratory acidosis. lsopropanol induces a wide
       anion-gap metabolic acidosis as well. The combination may cause profound acidernia.

3.    Administer crystalloid or colloid fluids to support blood pressure, hydration, and urine output as needed.

Enhancement of elimination

1.    Hemodialysis is helpful in removing the alcohol from the body, though this is rarely necessary because most patients can
       be treated successfully with supportive care alone.

2.    Peritoneal dialysis is effective, but, because most patients can be treated successfully with supportive care alone, it is
       not likely to be worth the risks associated with it.

3.    Heinoperfusion, inultiple-dose activated charcoal, and forced diuresis are not helpful.

ALKALI

Emesis and lavage are contraindicated in alkali ingestion. Gastric secretions are usually sufficient to neutralize the alkali. Activated charcoal is ineffective in alkali ingestion. Olive oil or egg whites can be given early as a protectant Since the clinical signs rarely correlate to the degree of esophageal or gastric injury, endoscopic exam should be performed in patients with alkali burns. The procedure should be delayed until the patient has been evaluated for at least 12 hours, and then the procedure should be performed carefully. The procedure should be halted at the first sign of esophageal necrosis.

Ingested alkaline batteries should be removed from the esophagus endoscopically as soon as possible to prevent perforation. If the battery is in the stomach, the probability of perforation is greatly reduced, but the battery should be retrieved in a timely manner. Consider induction of emesis, whole bowel irrigation, or endoscopic retrieval. Serial radiographs to monitor the position of the battery are indicated.

Sources Amitraz is found in external lotions and dip used in treatment of demodectic mange. Products known to contain amitraz include Mitaban (Upjohn) and Preventic flea and tick collars. (Mitaban also contains xylene [see Organic solvents and fuels). Dogs and cats have been poisoned by dermal absorption after application of amitraz. Ingestion of the dip or accidental ingestion of a portion of a collar are most commonly reported as the source of poisoning.

Mechanism of action Amitraz acts at alpha 2- adrenergic receptor sites in the CNS and at both alphal and alpha 2-adrenergic receptor sites in the periphery.

Clinical signs Vomiting, ataxia, staggering, and CNS depression or sedation are noted. This may progress to coma. Central alpha 2- stimulation results in bradycardia and hypotension. Peripheral vasoconstriction (and possibly hypotension) contribute to pallor of the mucous membranes. Gastrointestinal hypornotility, hypothermia, and hyperglycemia are often noted. Polyuria is noted within 2 to 3 hours of poisoning. Seizures have been reported as a sign of amitraz intoxication. (It has been suggested that sedation, ataxia, and even coma may additionally be signs of xylene toxicosis if intoxication was caused by Mitaban [see Organic solvents and fuels]

Treatment Treatment of amitraz poisoning is best accomplished by decontamination of the patient and administration of antidotes (yohimbine or atiparnizole).

Signs

Vomiting
Ataxia, incoordination, staggering
Sedation
Gastrointestinal hypornotility
Hyperglycemia
Pallor of mucous membranes
Hypotension
Bradycardia
Polyuria
Sedation or coma
Seizures(?)

EMERGENCY TREATMENT

Procedures

1.   Secure the airway and ventilate as necessary.

2.   Administer supplemental oxygen
.
3.   Secure venous access, Collect blood for laboratory testing.

4.   Administer fluids as needed to support blood pressure and perfusion.

5.   Control seizures if necessary.

Decontaminate

1.    Induce emesis if safe to do so or perform gastric lavage. In cases of Mitaban intoxication, induction of emesis is not
       advisable because of the presence of xylene, an organic solvent that is known to cause aspiration pneumonia.

2.    Administer activated charcoal. Repeat dose every 3 to 4 hours.

3.    Administer saline or osmotic cathartics.

DERMAL EXPOSURE

Wash thoroughly with warm, soapy water. Wear rubber gloves when bathing the patient; avoid chilling the patient.

Administer antidotes or other indicated supportive care

1.   Alpha-adrenergic receptor antagonists are antidotal.

•    Atiparnizole administered at 50 mcg/kg IM reverses signs within 10 minutes. Doses may be repeated every 3 to 4 hours if
      necessary.

•    Yohimbine
      Dogs 0.11 mg/kg IV slowly
      Cats 0.5 mg/kg IV slowly

      Or 50 mcg/kg atiparnezole given IM followed by 0. 1 mg/kg yohimbine IM q6h.

2. Administer fluids to maintain hydration and urine output.

Enhancement of elimination

Because of the effective nature of the antidotes, there is no reason to consider enhanced elimination techniques.

Avoid

Avoid treating bradycardia with anticholinergic drugs such as atropine

References

Duncan KL: Treatment of amitraz toxicosis, J Am Vet Med Assoc 203(8):1115-1116, 1993.

Hugnet C, Buronfosse F, Pineau X, et al: Toxicity and kinetics of armtraz in dogs, AmJVetRes 57(10):1506-1510, 1996.

Sources Diet pills, drugs used in the treatment of narcolepsy and hyperactivity, illegal drugs ("uppers," "speed," and "bennies"). Sustained-release preparations are available.

Mechanism of action Amphetamines are CNS stimulants with some adrenergic properties. They are believed to stimulate the release of norepinephrine and act directly on both alpha-1 and beta 1 -adrenergic receptor sites as well as inhibiting monoamine oxidase. Amphetamines are rapidly absorbed from the GI tract; high concentrations develop in the brain and CNS.

Clinical signs Signs in amphetamine poisoning include flushing or pallor followed by restlessness, hyperactivity, tachypnea, tachycardia, tremors, hypertension or hypotension, dysrhythmias, heart block, circulatory collapse, mydriasis, hyperthermia, ptyalism, hypoglycemia, and lactic acidosis. Life -threatening toxicosis is rare because of the large margin of safety between therapeutic and lethal doses (in people) though deaths have been reported after ingestion of low dosages (1.3 mg/kg) of methamphetamine.

Treatment Sedatives are used, and external stimuli are minimized. Fluids and perhaps steroids are used if shock develops. Urinary acidification with oral ammonium chloride will enhance renal elimination (but use only if the pet is not acidemic). Repeated doses of charcoal and cathartics are needed if sustainedrelease products were ingested. Chlorpromazine or haloperidol are used to combat drug-induced hyperthermia, convulsions, and hypertension. Diazepam is used for seizures; increased intracranial pressure (ICP) should be treated with furosemide and mannitol or corticosteroids (though no scientific data could be found to prove that corticosteroids improve morbidity and mortality in treatment of increased ICP). The electrocardiogram should be monitored for dysrhythmias.

Clinical findings

Flushing or pallor
Restlessness
Hyperactivity
Tachypnea
Tremors
Hypertension or hypotension
Dysrhythmias or heart block
Circulatory collapse
Mydriasis
Hyperthermia

EMERGENCY TREATMENT

Procedures

1. Secure the airway and ventilate as necessary.

2. Administer supplemental oxygen .

3. Secure venous access. Collect blood and urine for laboratory testing.

4. Control seizures.

5. Treat hyperthermia if present.

Decontaminate

I .    Remove toxins by induction of emesis or gastric lavage if ingestion was within the last 60 minutes.

2.    Administer activated charcoal. Repeat dose every 3 to 4 hours.

3.    Administer saline cathartics.

Administer antidotes or other indicated supportive care

I .    Chlorpromazine at I to 2 mg/kg IV, IM q12h PRN or haloperidol at I mg/kg IV. Chlorpromazine in higher doses
       (10 to 18 mg/kg IV) have been reported to be beneficial in dogs that have consumed large quantities of an amphetamine.

2.    Furosemide, mannitol, and corticosteroids may be indicated for treatment of increased intracranial pressure

3.    Administer fluids to maintain hydration and urine output.

Enhancement of elimination

Amphetamines are suitable for ion trapping by urinary acidification.

Ammonium chloride 100 to 200 mg/kg/day PO divided dose q8-12h (dog) or 20 mg/kg PO ql2h (cat).
Contraindicated if rhabdomyolysis (myoglobinuria), renal failure, or acidemia is present.

References

Kisseberth WC, Trammel HL: Illicit and abused drugs, Vet Clin North Am Small Anim Pract 20(2) : 405-418, 1990.

Sources Arsenic and arsenates are found in nature (pyrites and sulfides) and are common ingredients in herbicides, defoliants, insecticides, ant baits, and rodent baits. They may be found in insulation and some forms of vermiculite or may be a by-product of metal ore refining. Several forms of arsenic are used as wood preservatives. The ashes of treated wood may remain toxic.

Mechanism of action   Soluble forms of arsenic are readily absorbed through skin, mucous membranes, and the respiratory system and from the gastrointestinal tract. Toxicity is influenced by the route of exposure, rate of absorption, metabolic rate and excretion rate, and most important the type of arsenical present. Arsenic maybe present as the trivalent form (arsenite) or the pentavalent form (arsenate). Trivalent forms are 4 to 10 times more toxic than the pentavalent form. The mechanism of action of the trivalent form is believed to be its ability to disrupt cellular respiration by binding to sulfhydryl groups on several important enzymes. Vasodilatation and loss of capillary integrity result in fluid losses and hypovolemia. This occurs in all tissues rich in oxidative enzymes (such as lungs, kidney, liver) but is most pronounced in the gastrointestinal tract. The mechanism of action of the pentavalent forms has not been fully elucidated but may involve interference with vitamin B , and B 6 metabolism.

Clinical findings

ACUTE

    Acute onset of gastroenteritis with severe abdominal pain
    Staggering, weakness, and perhaps tremors
    Salivation, vomiting
    Odontoprisis
    Diarrhea, perhaps bloody
    Possible hematuria
    Shock, thready pulses
    Oliguria, dehydration
    Death in hours to 2 or 3 days

SUBACUTE

Depression, anorexia Watery diarrhea, which may contain blood and shreds or pieces of intestinal mucosa Polydipsia with polyuria initially followed by anuria Dehydration Possible hematuria Rear limb weakness, paresis, paralysis Seizures may occur Death in 4 or 5 days

CHRONIC

    Rarely diagnosed in veterinary medicine
    Lackluster appearance with rough, dry hair coat
    Skin may become paper thin and crack, secondary pyoderma

    If respiratory system is affected, the animal may have tachypnea and dyspnea, especially when excited.

   Brick red oral mucous membranes may be seen.

   Polydipsia

Laboratory findings

Results of biochemical profiles will reveal the systems involved, but results are nonspecific.

Liver, kidney, stomach, and intestinal contents may be analyzed for arsenic. Urine may also be analyzed for presence of arsenicals.


EMERGENCY TREATMENT

Procedures

Stabilize the patient:

1.    Secure the airway and ventilate if necessary.

2.    Administer crystalloid fluids to treat hypovolemia and shock and to maintain hydration.

3.    Monitor and treat electrolyte imbalances caused by diarrhea.

4.    Monitor blood gases (venous blood gas determination will be appropriate if the patient has no respiratory signs) and treat
       acidemia with sodium bicarbonate as needed.

Decontaminate

1.    If ingested within the last I to 2 hours and no other contraindications exist, induce vomiting.

2    If contraindication to emesis exists and the exposure has been within the last 2 to 4 hours, gastric lavage is indicated. if
      signs are pronounced, there is a relative contraindication to performing a gastric lavage because of increased likelihood
      of perforation.

3.    Gastric lavage should be followed by administration of activated charcoal. Cathartics are not indicated because diarrhea
       usually results from poisoning.

4.    Dermal exposure may require that the offending substance be brushed or vacuumed off or removed by bathing. Care must
       be taken to avoid contamination and exposure of the caregivers to the offending substance. Masks, face shields, and other
       precautions are advisable.

Administer antidotes or other indicated supportive care

I    Administer dimercaprol (BAL) 3 to 4 mg/kg IM q8h until recovery. in severe exposures, dose may be increased to 6 to 7
      mg/kg IM q8h on the first day.

2    A new chelator that is more effective than dimercaprol has recently been used in children. Succimer (meso-
      dimercaptosuccinic acid, also listed as DMSA) is available as Chemet (from McNeil Consumer Products, a division
      of McNeil-PPC, Inc., Fort Washington, PA 19034). This chelator has shown promise in the treatment of heavy
      metal toxicosis in children and adults. It is known to have greater specificity for arsenic and lead than calcium EDTA or
      penicillarnme. Studies have shown succimer to be effective in treating lead poisoning in dogs. The dose used in the study
      was 10 mg/kg PO every 8 hours for 10 days. It has a wide margin of safety.

3    Administer acetyleysteine. A study of the toxicity of sodium arsenite in rats showed that administration of acetylcysteine
      reduced the toxicity, It has the advantage that it can be administered IV for acute arsenic poisoning.

    DOSE:

          Cat    140 to 240 mg/kg PO; then 70 mg/kg PO q6h for 3 days

          Dog    280 mg/kg PO loading dose; then 140 mg/kg PO q4h for 3 days

      Acetylcysteine may be given intravenously if the patient is vomitiing. It is recommended that the solution be
      administered at the lower dose, diluted with D5W, and given through a 0.2 mcm filter over 15 to 30 minutes.

4.    Blood (whole blood, packed red blood cells, plasma) may be necessary.

5.    Dopamine may be required to support blood pressure or urine production.

6.    B vitamins in the fluids have been recommended.

Murphy MJ: Toxin exposures in dogs and cats: pesticides and biotoxins, J Am Vet Med Assoc 205 (3):414-421, 1994.

Ramsey DT, Casteel SW, Fagella AM, et at: Use of orally administered succimer (meso-2,3-dimercaptosuccinic acid) for treatment of lead poisoning in dogs, J Am Vet Med Assoc 208 (3) :371-375, 1996.

ASPIRIN (ACETYLSALICYLIC ACID, SALICYLATE) Pepto-Bismol

Sources Many analgesic, antiinflammatory, antipyretic, and anticliartheal (Pepto-Bismol) agents that contain salicylates are sold as OTC preparations. Some keratolytic products contain salicylates.

Mechanism of action Acetylsalicylic acid inhibits cyclooxygenase, which then inhibits production of certain prostaglandins, including protective prostaglandins of the E series. High levels are known to directly stimulate the respiratory center (early) to cause an initial respiratory alkalosis. High doses are also known to uncouple' oxidative phosphorylation and may cause hyperglycemia and glycosuria.

Clinical signs The biologic half-life of aspirin is 7.5 to 8 hours in dogs and 38 to 45 hours in cats at a dose of 25 mg/kg/day. The toxic dose in cats is >25 mg/kg/day in cats and >50 mg/kg/day in dogs. Signs are noted within 4 to 6 hours after ingestion of a toxic dose and include depression, vorniting, anorexia and lethargy, tachypnea (caused by initial respiratory alkalosis), and hyperthermia. The vomitus may be blood-tinged from GI ulceration. CNS depression leads to muscle weakness and ataxia; coma and death can occur within I or more days. Gastrointestinal ulceration or perforation may be seen after the administration of repeated doses over several days' duration. Anemia, bone marrow depression, Heinz body formation (cats), and toxic hepatitis may occur.

Toxic signs may be seen at doses of Pepto-Bismol >7 mL/kg/day in dogs and cats. Two tablespoons of PeptoBismol contain the salicylate equivalent of one 5-grain aspirin tablet.

Treatment There is no specific antidote. The stomach should be emptied by induction of emesis or lavage if within <2 hours of ingestion though there are literature reports that gastric evacuation may be of value up to 12 hours after ingestion of enteric-coated aspirin preparations. Multiple-dose activated charcoal is warranted. Acid-base balance is corrected as needed; diuresis is instituted. Alkalinization of the urine with sodium bicarbonate can be done to hasten urinary excretion, though this requires intense monitoring and is difficult to achieve safely. Peritoneal dialysis allows direct removal of salicylic acid from serum. Gastric ulceration or perforation is treated as needed.

Clinical findings

Depression
Vomiting (possibly blood tinged)
Anorexia or lethargy
Tachypnea
Pulmonary edema (infrequent)
Hyperthermia or hypothermia (late)
Anemia
Bone marrow depression
Heinz body formation (cats)
Toxic hepatitis
Muscle weakness
Ataxia
Seizures
Cerebral edema
Coma
Death

Laboratory findings

Hyperglycemia or hypoglycemia are possible.

Respiratory alkalernia with metabolic acidosis early. Metabolic acidemia later.

Electrolyte abnormalities are common
    Wide anion gap acidosis
    Hypokalemia
    Hypernatremia
Increased bleeding time
Anemia, possibly with Heinz body formation
Increased liver enzyme levels

Alkaline phosphatase (ALK-P)
AST
ALT
GGT

EMERGENCY TREATMENT

Procedures

1.    Secure the airway and ventilate as necessary.

2.    Administer supplemental oxygen
.
3.    Secure venous access. Collect blood for laboratory testing. Administer fluids as needed to support blood pressure and
       perfusion..

4.    Control seizures.

5.    Treat hyperthermia if present.

6.    Treat pulmonary edema.

Decontaminate

1.    Induce emesis or perform gastric lavage.

2.    Administer activated charcoal. Repeat dose every 3 to 4 hours.

3.    Administer saline or osmotic cathartics. Enemas may also be indicated.

Administer antidotes or other indicated supportive care

1.    There are no known antidotes.

2.    Administer fluids carefully to initiate brisk diuresis.

       Closely observe for onset of pulmonary edema.

       a. Furosemide
       b. Dopamine drip (I to 3 mcg/kg/min)
       c. Mannitol is not usually recommended.

3. Treat increased intracranial pressure if suspected

4. Correct acid-base and electrolyte imbalances.

       a. Sodium bicarbonate should be administered to combat metabolic acidemia as well as induce renal elimination of
           salicylates. Blood gases and urine pH should be monitored carefully to guide dosage and avoid complications caused
           by therapy. When blood gases are not available, sodium bicarbonate may be administered at I to 2 mEq/kg IV very
           slowly.

       b.Hypokalemia must be corrected because potassium depletion inhibits alkalinization of the urine.

5. Optional glucose

6. Protect the GI tract:

       a. Administer sucralfate at 250 to 1000 mg for dog q6-8h PO and 250 mg for cat q6-12h PO.

       b. Administer misoprostol (Cytotec) at I to 5 mcg/kg q8-12h PO (dog only) for ulcer prophylaxis. Administer
            omeprazole at 0.7 mg/kg q24h PO for dog only. H 2-receptor antagonists have not been shown to be of benefit as a
            prophylactic therapy against NSAID-induced GI ulcers. Their use in aspirin intoxication is also questionable.

Enhancement of elimination

1 . Urinary alkalinization enhances urinary excretion

2. Hemodialysis is effective.

3. Hernoperfusion.

4. Peritoneal dialysis is effective.

References

Murphy NIJ: Toxin exposures in dogs and cats: drugs and household products, JAmVet Med Assoc 205(4):557-560, 1994.

Oehme F: Aspirin and acetarninophen. In Kirk RW, editor: Current veterinary therapy, ed 9, Philadelphia, 1986, Saunders.

B

Sources Sleeping pills, anticonvulsants, tissues of animals that were euthanatized, and illicit drugs.

Mechanism of action Barbiturates are known to cause global depression of neuronal activity in the brain. These effects are apparently mediated through enhancement of gamma - aminobutyric acid (GABA)-mediated synaptic inhibition (by opening membrane chloride channels). Barbiturates do not act directly on the chloride channel or GABA receptors but affect an allosteric site that prolongs the increase in chloride -channel conductance and facilitates GABA action. Different mechanisms of action may be seen in different areas of the CNS by different doses of different barbiturates.

Clinical findings

SEVERE INTOXICATIONS

    Coma, anesthesia
    Hypothermia
    Miosis or mydriasis
    Respiratory depression, hypoxemia, hypercapnia, respiratory acidosis
    Hypotension, reflex tachycardia
    Depression of cardiac contractility
    Splenornegaly
    Death

MODERATE INTOXICATIONS

•    Hypothermia

•    Ataxia

•    Lethargy

•    Sleepiness

•    Nystagmus may be seen

•    Splenornegaly

•    Possible hypotension

•    Possible hypothermia

Laboratory findings

Barbiturates are easily detected with routine toxicologic screens.

EMERGENCY TREATMENT

Support the patient. Secure the airway and ventilate the patient if necessary. Treat coma, hypotension, and hypothermia if they exist.

Decontamination

1.     Induce emesis only if the ingestion was within the last 60 minutes and the patient shows no clinical signs.

2.     Perform gastric lavage if the ingestion was within the last 2 to 4 hours.

3.     Give repeated doses of activated charcoal.

4.     Administer saline cathartic. Magnesium- containing solutions should be avoided.

5.     Consider whole bowel irrigation using CoLyte or GoLYTELY.

Enhanced elimination

Alkalinization of the urine has been shown to increase the elimination of phenobarbital but none of the other barbiturates. Its value in acute overdose has not been proved, and it may contribute to fluid overload and pulmonary edema.

Hemoperfusion is indicated for the severely overdosed patient.

Avoid

•    Lactate, glucose, and epinephrine if used improperly (at very high doses) may cause prolonged effects of some of the
      barbiturates. if these solutions are used properly, there is no clinical significance.

•    Chloramphenicol will potentiate the effects of many of the barbiturates and is contraindicated.

References

Dayrell-Hart B, Steinberg SA, VanWinkle TJ, Farnbach GC: Flepatotoxicity of phenobarbital in dogs: 18 cases (1985-1989), J Am Vet Assoc 199(8):1060-1066, 1991.

Dumonceaux GA, Beasley VR: Emergency treatments for police dogs used for illicit drug detection, JAm Vet Assoc 197(2):185-187, 1990.

Owens JG, Dorman DC: Drug poisoning in small animals, Vet Med 92(2):149-156, 1997.

Sources   Household laundry bleaches most commonly contain sodium hypochlorite at concentrations of 3% to 6%. Industrial-strength bleaches and swimming pool supplies may contain 50% sodium hypochlorite. other common ingredients in (nonchlorine or colorfast) bleaches include trichloroisocyanuric acid and sodium perborate.

Mechanism of action Sodium hypochlorite is corrosive and usually has local effects on the mucous membranes and esophageal tissues. Animals rarely ingest enough bleach to cause systemic signs. Further, ingestion of a bleach solution usually re sults in vomiting, limiting the quantity of toxic principal absorbed. The hypochlorite bleaches are alkaline, and tissues exposed to it will suffer alkali burns. Trichloroisocyanuric acid is corrosive but of low toxicity. Sodium perborate degrades to hydrogen peroxide (which may cause gastritis and emesis) and borate (which may cause systemic signs of boric acid poisoning,.

Clinical signs Most pets have a "bleach" odor and may show bleaching of the hair. Ptyalism, emesis, and rebound tenderness of the cranial side of the abdomen may occur. Hernaternesis and pharyngeal edema may be seen.

Treatment   Although induction of emesis within 3 hours of ingestion has been recommended by at least one reference, we ad vise against this. Bleaches are alkalis, and the rules of alkali exposure should be followed (pp. 70 to 72). Although most patients will vomit within minutes after ingestion of common bleaches, vomiting should not be the goal of the veterinarian presented with a case of bleach ingestion. Current advice for ingestion of bleaches includes administering large volumes of water or milk.

Past recommendations included administering milk of magnesia, egg whites, or powdered milk slurry. Baking soda (sodium bicarbonate) causes carbon dioxide formation and gastric distension as well as formation of hypochlorous acid and should not be given.

Signs

Bleach odor
Bleaching of hair
Salivation
Emesis, hematernesis
Rebound tenderness of cranial abdomen
Pharyngeal edema

EMERGENCY TREATMENT

Procedures

I . Secure the airway and ventilate as necessary.
2. Administer supplemental oxygen.
3. Secure venous access. Collect blood and urine for laboratory testing.
4. Administer large volumes of water or milk.
5. Administer analgesics.
6. Administer antidotes.
    a. There are no known antidotes.
    b. Milk of magnesia has been recommended at 2 to 3 mL/kg PO.

Decontaminate

GI EXPOSURE (INGESTION)

See step 4 above.

DERMAL EXPOSURE

Wash thoroughly with warm, soapy water. Wear rubber gloves when bathing the patient. Avoid chilling the patient.

Enhancement of elimination

Administer fluids to maintain blood pressure or hydration and urine output.

Sources    Borates and boric acid are contained in many products including roach killers, flea products, fertilizers, herbicides, antiseptics, disinfectants, and contact lens solutions. Sodium perborate is found in mouthwashes and denture cleansers. Other boron-containing compounds include sodium borate, sodium biborate, sodium pyroborate, sodium tetraborate, boric anhydride, boron oxide, boron trioxide, boric oxide, boron sesquioxide, borax, sodium metaborate, and magnesium perborate.

Mechanism of action    The lethal oral dose for boric acid for small mammals is 0.20 to 0.50 g/kg of body weight. Emesis usually occurs only after substantial amounts of borate have been ingested. Borates are readily absorbed from the GI tract. They are absorbed through abraded skin, but do not easily penetrate intact skin. Borates are excreted in the urine, with 40% to 60% of the dose excreted within 12 to 24 hours. Blood concentrations of borate above 50 mcg/mL are diagnostic for borate poisoning. The exact mechanism of action is not understood. Borates are generally cytotoxic to all cells. Because borates are concentrated by the kidney and excreted in the urine, the kidneys are often damaged more than other systems. The brain and liver are also known to be damaged by borates.

Clinical signs   Signs include ptyalism, diarrhea, abdominal pain, rebound cranial abdominal tenderness, ataxia, hyperesthesia, tremors, muscle weakness, metabolic acidosis, seizures, coma, and death. Mild hyperthermia, shock, disseminated intravascular coagulation, and Cheyne-Stokes respiration occur.

Treatment Emesis or gastric lavage should be induced if ingestion occurred within 2 hours. Although borates are poorly adsorbed by activated charcoal, it is commonly recommended (in addition to adminstration of a cathartic). To be effective in removing borates from a patient, activated charcoal would have to be administered in dosages 5 to 10 times normal recommendations. This clinically impractical. The use of activated charcoal in patients known to have ingested borates is therefore not recommended. Persistent vomiting and seizures are controlled as needed. Hemodialysis is known to be effective in humans and should be considered in pets.

Signs

Salivation
Diarrhea, possibly bloody
Abdominal pain
Rebound cranial abdominal tenderness
Ataxia
Hyperesthesia
Tremors
Muscle weakness
Seizures
Coma
Mild hyperthermia
Shock
Disseminated intravascular coagulation
Cheyne-Stokes respiration
Death

EMERGENCY TREATMENT

Procedures

1.   Secure the airway and ventilate as necessary.
2.   Administer supplemental oxygen.
3.   Secure venous access. Collect blood and urine for laboratory testing.
4.   Control seizures.
5.   Treat hyperthermia if present.
6.   Administer crystalloids fluids to maintain perfusion and blood pressure.

Decontaminate

GI EXPOSURE (INGESTION)

Induce emesis if recent ingestion and if signs are not present.

Gastric lavage if signs are present after ingestion (p. 52).

Administcr saline cathartic unless diarrhea already present.

DERMAL EXPOSURE

1. Wash thoroughly with warm, soapy water. Wear rubber gloves when bathing the patient; avoid chilling the patient.

2. Administer antidotes and other supportive care

3. Induce a brisk diuresis Administer fluids at 2 or 3 times maintenance dose. Monitor for signs of overhydration.

4. Administer furosemide if the patient has normal renal function and is adequately hydrated.

Enhancement of elimination

Hemodialysis is effective. Peritoneal dialysis. Exchange transfusions.

Mechanism of action   Bromethalin is a potent diphenylamine neurotoxin that acts by uncoupling oxidative phosphorylation leading to decreased Na+/K+-ATPase activity. Without normal Na+/K+-ATPase activity, the ability to maintain normal cellular membrane potential and osmotic gradient is lost, Sodium flows into the cell following its electrochemical gradient, and fluid follows resulting in swelling and loss of function. Signs are related to CNS dysfunction. Death is usually caused by respiratory paralysis.

Clinical signs Clinical signs are extremely variable depending on amount of toxin ingested. High doses may result in onset of signs within hours, whereas lower doses may not have noticeable effects for several days. High doses in dogs have produced signs of hyperexcitability, tremors, hyperreflexia of the hindlimbs, running fits, focal or generalized seizures, and death. Low doses produced depression, anorexia, vomiting, tremors, paresis (of one or more limbs), paralysis, and death. Animals poisoned with bromethalin have been noted to assume Schiff - Sherington posture or to have extensor rigidity. Miosis and anisocoria have been noted. Cats have similar signs including depression, ataxia, progressive motor dysfunction to paralysis, abdominal swelling, convulsions, and death. Death is seen with low doses as well as with high doses.

Brornethalin poisoning should be suspected whenever acute signs of cerebral edema or posterior paresis or paralysis are seen. Differential diagnosis includes alcohol intoxication, ethylene glycol intoxication, salt poisoning, rabies, polyradiculoneuritis, tick paralysis, and botulism.

Treatment Treatment mainly supportive because no antidote exists. Treatment is aimed at decreasing absorption of the toxin and decreasing cerebral edema. Fluids should be used carefully to prevent aggravation of the cerebral edema. Mannitol and corticosteroids may be ineffective in treating bromethalin toxicity though they are currently recommended in reducing cerebral edema from other causes. Activated charcoal improves survivability when given early.

Signs

ACUTE EXPOSURE
    Hyperexcitability
    Severe muscle tremors
    Running tits
    Grand mal seizures
    Hindlimb hyperreflexia
    Depression
    Death

CHRONIC EXPOSURE
    Tremors
    Depression
    Ataxia
    Vomiting
    Lateral recumbency

EMERGENCY TREATMENT

Procedures

I .    Secure the airway and ventilate as necessary.
2.    Administer supplemental oxygen .
3.    Secure venous access. Collect blood and urine for laboratory testing.
4.    Administer isotonic crystalloids as needed to support blood pressure and perfusion.
5.    Control seizures.
6.    Treat hyperthermia if present.

Decontaminate

Induce emesis only if the ingestion was within the last 60 minutes and the patient shows no clinical signs.

Perform gastric lavage if the ingestion was within the last 2 to 4 hours.

Give repeated doses of activated charcoal.

Administer saline cathartic. Magnesium-containing solutions should be avoided.

Consider whole bowel irrigation using CoLyte or GoLYTELY.

Administer antidotes or other indicated supportive care

There are no known antidotes.

Treat cerebral edema. (Treatment may not be effective in cases of edema known to be caused by bromethalin.)

I .    Furosemide

2.    Mannitol administered at 0.1 to 0.5 g/kg IV slowly qI-6h PRN

3.    Methylprednisolone sodium succinate at 25 to 30 mg/kg IV initially followed by 12.5 to 15 mg/kg IV at 2 and 6 hours
       later and then 2.5 mg/kg/hour IV continuous infusion for 8 to 42 hours.

4.    Dexamethasone sodium phosphate at 2 to 3 mg/kg IV followed by I mg/kg SC q6-8h in doses tapering off.

Enhancement of elimination

There are no reported techniques (other than repeated doses of activated charcoal) that are effective in enhancing the elimination of bromethalin from the body.

Avoid Drugs that might induce hypoventilation (such as high doses of narcotics or tranquilizers).

References

Carson T: Bromethalin poisoning. In Kirk RW, Bonagura JD, editors: Current veterinary therapy, ed 10, Philadelphia, 1989, Saunders.

Osweiler GD: Toxicology, Philadelphia, 1996, Williams & Wilkins, pp 286-288.

BUILDERS

See also Detergents, Soaps

Mechanism of action Builders, which bind elements in detergents and are responsible for water hardness, act by inflicting caustic burns and inducing hypocalcemia by binding calcium (oxalates). Common compounds in descending order of toxicity include metasilicate, sodium carbonate or sesquicarbonate, polyphosphates, silicates, and bicarbonates.

Clinical signs   Similar to acids in causing highly corrosive coagulation necrosis. Hypocalcemia may also be seen.

Treatment   Treatment is aimed at flushing the mucous membranes and other exposed areas with copious amounts of water. Calcium and diuresis with intravenous fluids and furosemide may be needed in oxalate ingestions.

Signs

Highly corrosive coagulation necrosis
Hypocalcemia

EMERGENCY TREATMENT

Procedures

I .    Secure the airway and ventilate as necessary.

2.    Administer supplemental oxygen.

3.    Secure venous access. Collect blood for laboratory testing. Administer fluids as needed to support blood pressure and
       perfusion.

4.    Treat hyperthermia if present.

Decontaminate

1.    Induce emesis or perform gastric lavage if exposure was by ingestion.

2.    Administer activated charcoal. Repeat close every 3 to 4 hours.

3.    Administer saline or osmotic cathartics. Enemas may also be indicated.

Administer antidotes or other indicated supportive care

1.    Pulverized chalk, slurry of powdered milk (100 mL PO), lime water (150 to 200 mL) may be given orally to precipitate
       oxalates in the GI tract.

2.    If signs of hypocalcemia are present, administer calcium gluconate 0.25 to 1.5 mL/kg IV slowly over 20 to 30 minutes
       observing for bradycardia to effect if serum calcium decreases.

3.    Osmotic diuresis with mannitol 20% at 0. 1 to 0. 5 g/kg IV q1 -6h PRN or furosemide at I to 5 mg/kg IV PRN qI-4h.

       CAUTION: Furosemide may promote calciuresis, thus enhancing hypocalcemia.

Enhancement of elimination

There are no known effective techniques.

C

CARBAMATES

Sources   Combustion, fires, patients suffering smoke inhalation, vehicles (automobiles, airplanes) with faulty exhaust systems, improperly vented heaters.

Mechanism of action Carbon monoxide has an affinity for hemoglobin that is 240 times greater than that of oxygen. When carbon monoxide is combined With hemoglobin, it is known as carboxyhemoglobin. Carboxyhemoglobin causes a leftward shift of the oxygen dissociation curve; that is, the oxygen is bound more tightly and is not released to the tissues so readily.

Clinical findings The most characteristic finding in the patient suffering carbon monoxide poisoning is cherry red blood (similar to cyanide) and red or dark pink mucous membranes, skin, and other tissues. Blood gases may reveal hypoxemia or acidosis; however they do not reveal the presence or absence of carbon monoxide. Blood gas measurements are for the most part unaffected by the presence of carboxyhemoglobin. Oxygen saturation levels are falsely normal when determined by pulse oximetry because carboxyhemoglobin is "invisible" to this technologic method. Carboxyhemoglobin may be detected using direct oximetry or co-oximetry, technologic methods not widely available in veterinary medicine.

Signs

Signs noted depend on the level of carboxyhemoglogin. Carboxyhemoglobin levels of 10% or higher will cause confusion and dyspnea. Additional signs include ataxia, lethargy, deafness, seizures, psychornotor disturbances, and coma. Levels >60% (or sometimes less) are fatal.

•    Tachypnea, dyspnea, hyperpnea

•    Signs of shock

•    Bright red mucous membranes
    Collapse

Hypoxemia -induced mentation changes including confusion, dizziness (staggering), seizures, and coma.

Agonal respirations followed by respiratory paralysis.

Cyanosis may be noticed soon after onset of hypoventilation. Classic finding is the cherry red blood.

EMERGENCY TREATMENT

Procedures

I .    Secure the airway and ventilate as necessary.

2.    Administer supplemental oxygen. Administer 80% to 100% oxygen for at least 30 minutes. The half-life of
       carboxyhemoglobin approaches 300 minutes in room air but is decreased to about 30 minutes in 100 % oxygen.

3.    Secure venous access. Collect blood for laboratory testing. Administer fluids as needed to support blood pressure and
       perfusion.

4.    Control seizures.

Decontaminate

Remove the patient from the source of carbon monoxide.

Administer antidotes or other indicated supportive care

There are no known effective antidotes.

Enhancement of elimination

There are no known effective techniques other than administration of high levels of oxygen.

Taken internally, this chemical causes nausea and vomiting, diarrhea, collapse and death. Liver failure can also result from ingestion..

External: Flush skin and remove any chemical as soon as possible, provide fresh air, remove cat from fumes, induce emesis or lavage followed by repeated doses of activated charcoal. Laxatives to clean out the GI tract. IV dextrose and calcium may also be given along with antidotes and medications to maintain kidney function. Immediate emergency treatment is necessary.

CHOCOLATE (THEOBROMINE) AND CAFFEINE POISONING

Sources Cooking, baking, candy, landscaping (with cacao shells), white chocolate (negligible amounts of theobromine), sweetened milk chocolate (1/10 the amount of theobromine as found in unsweetened chocolate, approximately 45 to 60 mg/oz), semisweet or dark chocolate contains 130 to 185 mg/oz. Unsweetened (baking) chocolate (450 mg/oz), cocoa powder (150 to 600 mg/oz); coffee, tea, soft drinks.

Mechanism of action Theobromine inhibits phosphodiesterase, which results in increased cAMP and release of catecholamines. Caffeine directly stimulates the myocardium and central nervous system. It also causes a competitive antagonism of cellular adenosine receptors. Increased muscle contractility is caused by increased entry of calcium and inhibition of sequestration by the sarcoplasmic reticulum (mechanism unknown). Benzodiazepine receptors in the brain are competitively antagonized.

Clinical signs

THEOBROMINE

A slight increase in blood pressure is seen. Bradycardia or more commonly tachycardia occurs, and myocardial dysrhythmias, especially ventricular premature beats, are possible. Central nervous system excitability, manifested as nervousness, excitement, tremors, seizures, and ultimately coma, are seen. Panting and urinary incontinence are also possible. Death occurs within 6 to 24 hours with acute exposure. With chronic ingestion (over several days), death may result from cardiac failure.

CAFFEINE

Tachycardia, tachypnea, hyperexcitability, tremors, seizures, premature ventricular beats. Dilatation of coronary, pulmonary, and systemic vessels may cause congestion or hemorrhage. The lethal dose for caffeine is 150 mg/kg for dogs, cats, and people.

Treatment   No antidote exists; treatment is supportive. Emesis is used and may be effective even after several (4 to 6) hours have passed since ingestion; gastric lavage is useful if emesis is only partially productive or contraindicated. Activated charcoal is useful and can significantly decrease the half-life of theobromine. Diazepam is used to control tremors, anxiety, or seizures. Bradycardia is treated with atropine; tachycardias are treated with lidocaine, metoprolol, or propranolol. The urinary bladder should be catheterized to prevent reabsorption of theobromine through bladder mucosa. Fluids are given as part of supportive treatment.

Signs

THEOBROMINE
    Mild hypertension
    Bradycardia or tachycardia
    Dysrhythmias (especially PVCs)
    Nervousness
    Excitement
    Tremors
    Seizures
    Panting
    Urinary incontinence
    Coma
    Death

CAFFEINE

Tachycardia Tachypnea Hyperexcitability Tremors Seizures Dysrhythmias (especially PVCs) Generalized congestion or hemorrhage.

EMERGENCY TREATMENT

Procedures

I .    Secure the airway and ventilate as necessary.

2.    Administer supplemental oxygen.

3.    Secure venous access. Collect blood and urine for laboratory testing.

4.    Control seizures. Diazepam is indicated as first choice in controlling seizures but is often ineffective because of the
       antagonism of the benzodiazepine receptors. If diazepam is ineffective, use phenobarbital followed by pentobarbital if
       necessary.

5.    Treat hyperthermia, if present.

6.    Monitor ECG for cardiac dysrhythmias. Treat dysrhythmias when noticed with generally accepted treatment options.
       (See notes below.)

Decontamination

I .    Although chocolate is not very effectively removed during vomiting because of its "sticky" composition when melted, it is
        still most commonly recommended to induce emesis if ingestion was recent.

2.    Gastric lavage with warm water will help to remove the melted chocolate from the stomach. Cool or cold water may
       actually worsen retrieval of chocolate.

3.    Administer activated charcoal and a saline cathartic; repeat PRN q4-6h

.
Administer antidotes or other supportive care

1.    There are no effective antidotes.

2.    Atropine (for bradycardia) at 0.02 mg/kg IV PRN.

3.    Metoprolol. Dog: 0.5 to 1.0 mg/kg PO q8h; cat: 12.5 to 25 mg/cat PO q8-12b (an IV dose has been published as 0.04
       to 0.06 mglkg given slowly IV q8h; we have not used this route of administration and would advise caution) or
       propranolol (acute dysrhythmias: 0.02 to 0.06 mg/kg IV over several minutes; nonacute: dogs: 2.5 to 10 mg/dog PO
       q8-12h; cats: 2.5 to 5.0 mg/cat PO q8-12h) for atrial or ventricular tachycardias. NOTE: Metoprolol is the beta-blocker
       of choice because propranolol is known to slow renal excretion of xanthines (in humans).

4.    Lidocaine (in place of metoprolol or propranolol for ventricular tachycardias) at I to 2 mg/kg IV bolus followed by 25 to
       75 mcg/kg/min IV infusion (dogs) or 0.25 to 1.0 mg/kg IV bolus followed by 5 to 40 mcg/kg/min IV infusion (cats)
.
5.    Administer fluids to support blood pressure and to maintain hydration and urine output.

Enhancement of elimination

1.    Fluid diuresis may enhance excretion.

2.    Dialysis and ion trapping are not effective.

Avoid

1.    Erythromycin and corticosteroids are known to interfere with excretion of methylxanthines.

2.    Hypoventilation

References

Hooser S, Beasley V: Methylxanthine poisoning (chocolate and caffeine toxicosis), in Kirk RW, editor: Current veterinary therapy, ed 9, Philadelphia, 1986, Saunders.

Murphy MJ: Toxin exposures in dogs and cats: drugs and household products, J Am Vet Med Assoc205(4):557-560, 1994.

Owens JG, Dorman DC: Drug poisoning in small animals, Vet Med 92(2):149-156, 1997.

Ingestion of these chemicals cause stiffness, weakness, staggering, paralysis, coma and death.

Flush and wash skin and mouth. Pump and flush the stomach. IV fluids to flush the kidneys and good general supportive care are important.

Clinical signs of poisoning in cats will not often show for 2-4 days after ingestion. Vomiting, depression, anorexia, diarrhea, Polydipsia (greater than normal water consumption) and Polyuria (greater than normal urine production) and frequent urination, and increased body temperature have all been reported. Death usually occurs 4-7 days after exposure.

Induce emisis if early (within 3 hours). Administer activated charcoal. IV fluids including calcium, cortisone, diuretics, and calcitonin can all be used. Most cats survive with proper care. Feeding milk may also be helpful.

COCAINE

Sources Commercial preparations include topical and local anesthetics. Free-based cocaine is called "crack," "rock," or "flake." illicit cocaine may contain impurities including other ,came" anesthetics, caffeine, amphetamine, or quinine.

Mechanism of action Cocaine is rapidly absorbed from mucous membranes, whereas there is a slight delay of absorption from the GI tract. Cocaine causes an initial sympathetic discharge by interfering with reuptake of endogenous catecholamines. It also is known to interfere with reuptake of doparnine resulting in an increase in dopaminergic neurotransmission. Direct cardiotoxicity is seen with large doses.

Clinical signs Cocaine causes CNS excitement, peripheral vasoconstriction, increased muscle activity, and secondary hyperthermia. Depression may follow stimulation. Death is caused by the effects of hyperthermia, respiratory arrest, or cardiac arrest.

Treatment Emesis followed by charcoal and a cathartic. Because cocaine is rapidly absorbed from the GI tract (which may make emesis ineffective), gastric lavage maybe preferable. Surgery is needed if bags of cocaine are ingested. if surgery is not an option, consider whole bowel irrigation using polyethylene glycol solutions such as CoLyte or GoLYTELY. Chlorpromazine may antagonize many of cocaine's effects and may control hyperthermia, though it should not be used if seizures are present because phenothiazines are known to aggravate seizures. Seizures are controlled with diazepam or barbiturates; hyperthermia is treated as needed (see Hyperthermia, p. 30). Respiratory support should be assisted as needed.

Sources Fires, cyanogenic plants (apricot pits, Prunus spp., Sambucus spp., cassava, etc.), photographic chemicals, plastic manufacture, laboratories, drugs (nitroprusside). it has been used as a rodent fumigant and in baits to kill wild animal pests such as the coyote. Hydrogen cyanide gas is a by-product of combustion of many substances found in homes; thus cyanide toxicity is common in animals trapped in burning buildings.

Hemodialysis may be of value in patients who have developed high thiocyanate (a less toxic compound from cyanide metabolism) levels.

2. Do not use atropine to treat bradycardia or AV block associated with hypertension. The bradycardia is a protective
reflex and, if removed, may worsen the hypertension.

DEET   (N,N-diethyl-m-toluamide)

Sources Insect repellants such as Off, Deep Woods Off, and Cutters are examples of pure DEET (or deet) products. Hartz Blockade is a repellent and insecticide product containing DEET and fenvalerate (a pyrethroid).

Mechanism of action Has not been fully elucidated.

Clinical signs Vomiting, tremors, excitation, ataxia and seizures have been reported in dogs and cats where deet was suspected as the toxic product. Irritation of the skin is also a possibility.

-
EMERGENCY TREATMENT

Procedures

I . Secure the airway and ventilate as necessary.

2.    Administer supplemental oxygen .

3.    Secure vt!nous access. Collect blood and urine for laboratory testing.

4.    Administer isotonic crystalloids as needed to support blood pressm~ and perfusion.

5.    Control seizures.

6.    Treat hyperthermia if present
.

Decontaminate

•    induction of emesis is relatively contraindicated.

•    Perform gastric lavage if the ingestion was within the last 2 hours.

•    Give repeated doses of activated charcoal.

•    Administer saline cathartic. Cathartics containing magnesium should be avoided.

•    Consider whole bowel irrigation using CoLyte or GoLYTELY.

•    Bathe the patient in liquid dishwashing detergent or mild shampoo. Continue for at least 15 minutes or until the odor is
      gone.

Administer antidotes or other indicated supportive care

There are no known antidotes.

Enhancement of elimination

There are no reported techniques that have been effective.

Reference:

Dorman DC: Diethyltoluamide (DEET) insect repellent toxicosis, Vet Clin North Am Small Anim Pract 20 (2):387- 391, 1990.

Often found dead. Occasionally terminal seizures are observed. Vary from mild gastrointestinal upset (anorexia, vomiting, diarrhea) to terminal arrythmias. Slowed atrioventricular conduction will progress to AV block followed by ventricular rhythms.

The gastrointestinal tract should be decontaminated. induction of emesis or gastric ravage should be performed as needed, followed by administration of activated charcoal. Cathartics should also be used if necessary. Treat as for digitalis overdose.

6. Support hydration to maintain blood pressure or hydration and urine output with fluid therapy.

Murphy M: Toxin exposures in dogs and cats: pesticides and biotoxins,
J Am Vet Med Assoc 205 (3):414-421, 1994

Mild fever, rapid breathing,, restlessness, seizures and death from respiratory failure.

Reducing body temperature, administration of IV dextrose, oxygen and pumping the stomach.

Mechanism of action Ethylene glycol is metabolized by the liver using alcohol dehydrogenase in the first step of the pathway. Metabolites that are produced include glycoaldehyde (which causes CNS depression, including respiratory depression), glycolate (which causes metabolic acidosis), and oxalate (which combines with calcium to form calcium oxalate crystals, which precipitate in the renal tubules causing renal damage; oxalate also contributes to metabolic acidosis).

Many brands of antifreeze' contain phosphorus rust inhibitors; monitor phosphorus and treat hype rphosphaternia if needed.

Clinical signs The minimum lethal dose of undiluted ethylene glycol is 4.2 to 6.6 mL/kg for dogs (4.5 oz for a 20 lb dog) and 1.5 mL/kg for cats (I tablespoon of ethylene glycol diluted 50:50 with water in radiator fluid in the average-sized cat). There are three stages of poisoning, the first two are often not noticed by owners (and may not be present if the animal is brought for treatment immediately after it has consumed the product).

Stage I occurs 30 minutes to 12 hours after ingestion and includes nausea, vomiting, depression, ataxia, seizures, and rarely coma and death. These signs are similar to acute alcohol intoxication and resemble drunkenness. Polyuria and polydipsia often occur within I hour after ingestion.

Stage 2 occurs 12 to 24 hours after ingestion and includes tachycardia and tachypnea.

Stage 3 occurs 24 to 72 hours after ingestion in dogs and 12 to 24 hours after ingestion in cats. This stage is characterized by oliguric renal failure; signs include severe depression, vomiting, diarrhea, azotemia, and oliguria.

Increased osmolality, increased osmol gap, and high anion gap metabolic acidosis (which is seen within 3 hours after ingestion) occur. Low urine specific gravity (<1.020) is also seen within 3 hours after ingestion. Calcium oxalate or hippuric acid crystals, or both, are occasionally but not always seen in the urine. The oxalate crystals can be the more common monohydrate form or the dihydrate form. Calcium oxalate crystals are occasionally seen in normal pets.

There is a test for ethylene glycol intoxication (PRN, Pharmacol Inc., Pensacola, Fla.) that can be used to support a diagnosis. This test will detect only ethylene glycol but not the toxic metabolites. Therefore the test must be run soon after ingestion to detect the ethylene glycol before metabolism. The test is not sensitive enough for cats. A positive test on cat blood means the cat has ingested a lethal dose and must be treated aggressively. A negative test on a cat is meaningless; cats are so sensitive to ethylene glycol that the color control used in the test has more than a feline lethal dose in it. A negative test on a dog indicates that the dog does not have lethal amounts of ethylene glycol in the circulation at the time of testing. it does not mean that the patient did not ingest antifreeze; it is possible that metabolism has reduced ethylene glycol levels lower than detectable by the test. The test cross-reacts with propylene glycol and other chemicals, and so it must be run on blood drawn before any medications are given (including activated charcoal). Antifreezes containing propylene glycol (Sierra, ARCO) are "safe" and are unpleasantly flavored to prevent ingestion. These "safer" compounds will not be metabolized to oxalate but could possibly cause problems related to the propylene glycol (Heinz body anemia).

Treatment The toxin is removed from the GI tract if recently ingested. Intravenous fluids are used to correct dehydration and metabolic acidosis. Ethanol, which is preferentially metabolized by alcohol dehydrogenase, is the mainstay of treatment. 4-Methylpyrazole is antidotal in dogs. Sodium bicarbonate is used to correct metabolic acidosis.

Polyuria, polyclipsia Nausea Vomiting Depression Ataxia Seizures increased osmolality, increased osmol gap, and high aniongap metabolic acidosis Hyperglycemia Low urine specific gravity (<1.20) Calcium oxalate crystals (occasionally) Coma or death (rare in stage 1).

4. Administer isotonic crystalloids as needed to support blood pressure and perfusion. Monitor urine output, being especially
vigilant for oliguria or anuria.

Induce emesis only if the ingestion was within the last 60 minutes and the patient shows no clinical signs. Perform gastric lavage if the ingestion was within the last 2 to 4 hours. Give repeated doses of activated charcoal. Consider appropriate use of saline cathartic.

Fornepizole (4-methylpyrazole) has recently been approved for use in dogs (Antizol-Vet, Orphan Medical, Minnetonka, MN 55305). This synthetic alcohol dehydrogenase inhibitor is considered to be as effective as ethanol (possibly more effective) but has fewer side effects; thus it is the recommended antidote for ethylene glycol ingestion in dogs. The 1. 5 mL vial of fomepizole is diluted with 30 ml, of 0.9% sodium chloride to be used as an injection (provided with the kit). A loading dose of 20 mg/kg is administered IV. At 12, 24, and 36 hours after the initial loading dose of Antizol-Vet, doses of 15, 15, and 5 mg/kg should be administered respectively. If ethylene glycol is still detected in the bloodstream of the dog after this, the clinician should continue to dose the dog with 5 mg/kg IV every 12 hours until ethylene glycol does not remain in the bloodstream or the animal has visibly recovered. 4-MP should not be used in cats.

The preferred method of administration of ethanol is by constant IV infusion. For continuous IV infusion:

Administer a loading dose of 600 mg/kg, followed by a continuous maintenance infusion of 100 mg/kg/hour. Administer this in fluids such as lactated Ringer's solution or half-strength saline at a rate suitable to provide one and one half times the maintenance needs.

Pure ethanol contains 754 mg/mL, and so 190 proof contains approximately 715 mg/mL.

Using a 20% solution is recommended in some texts. It is given at 5.5 mL/kg IV q4h for 5 treatments and then q6h (dogs) for 4 treatments. Cats are treated with 5 mL/kg q6h for 5 treatments and then q8h for 4 treatments. IV ethanol is usually 100% effective if started within I hour after ingestion. By 4 hours after ingestion, therapy is less effective because of the rapid metabolism of ethylene glycol.

Sodium bicarbonate is used to correct metabolic acidosis. The amount to give is based on the bicarbonate deficit.

Replace '/4 to '/2 of the calculated bicarbonate deficit slowly IV (over I hour); monitor the bicarbonate q4-6h and administer more as needed. If bicarbonate monitoring is not available, an alternative schedule of sodium bicarbonate administration has been recommended:

Dogs Sodium bicarbonate (5%) IP at 8 mL/kg q4h X 5 and then q6h for 4 additional treatments.

Cats Sodium bicarbonate (5%) IP at 6 mL/kg q6h X 5 and then q8h for 4 additional treatments.

Peritoneal dialysis is known to be highly effective in removing ethylene glycol if used early. The dose of IV alcohol should be doubled during peritoneal dialysis.

The effect of the fertilizer depends on the type of constituents found in the product. Increased salivation, ulcers in the mouth, vomiting, abdominal pain, fever, rapid heart rate, tremors, weakness and seizures are all possible from the ingestion of fertilizers.

Flush and pump the stomach as early as possible and give activated charcoal. Giving milk THEN inducing vomiting is another option. IV fluids and electrolytes are also important.

Cats are extremely susceptible to this poison. Cats will vomit, defecate and urinate, frequently straining, trouble breathing, followed by bursts of wild activity mostly characterized as running fits, which are characteristic for poisoning by Compound 1080 and Compound 1081. Other symptoms of poisoning by these compounds are howling and/or crying, tremors, seizures and death unless treated immediately. Compound 1080 is the sodium salt, and compound 1081 is fluoroacetamide..

Induce emesis. Gastric lavage if within 2 hours of ingestion. IV fluids, dextrose, calcium, and anesthesia are all used but the prognosis is very poor if moderate or large amounts of poison have been ingested. Antidotal medication is available. Early treatment will be needed to save the life of the cat.

When eaten, fluoride will cause salivation, vomiting blood, abdominal pain, decreased heart rate with weak respiration, convulsions and blood in the urine.

The stomach should be flushed with certain calcium containing medications, IV fluids and calcium, and generalized cardiac and respiratory support is all needed.

G

GARBAGE AND FOOD INTOXICATIONS

Sources Food-related poisonings are more prevalent in the warmer months and during the holidays than at other times. Poisoning occurs as a result of ingestion of food contaminated by microorganisms or their toxins. Common organisms and toxins implicated in food poisoning include Escherichia coli, Staphylococcus, Streptococcus, and Salmonella spp.; Clostridium perfringensand Clostridium botulinum (see Botulism); and Bacillus spp.

Mechanism of action Enterotoxemia causes altered gastrointestinal biochemical pathways and activation of autocoids (prostaglandins, kinins, etc.) that leads to altered motility, permeability, and CNS interactions.

Endotoxemia, which results from absorption of endotoxin released in the GI tract, may be seen as life - threatening endotoxic shock. Endotoxin is a lipopolysaccharide released from the cell wall of dead bacteria (mostly gram negative). Upon absorption from the gastrointestinal tract, the endotoxin acts through numerous mechanisms to initiate cascades or events that cause deleterious effects throughout the body. There are many texts that cover the syndrome quite well; the full syndrome is not covered in this text. Suffice to say that, untreated, endoloxemia is a severe, life-threatening disease that leads to shock, disseminated intravascular coagulopathy, pulmonary thromboembolism, acute respiratory distress syndrome, systemic inflammatory response syndrome (SIRS), multiple organ dysfunction syndrome (MODS), and death.

Clinical signs Pets suffering enterotoxemia often vomit, usually within 3 hours after eating the contaminated or spoiled substance. Vomiting may remove the offending substance or substances, effecting a cure. Diarrhea, often bloody, may be seen if signs progress, and it develops 2 to 48 hours after food ingestion. Recovery normally occurs within 48 hours.

Protracted vomiting and diarrhea, along with permeability changes in the gastrointestinal tract caused by the toxin, may result in significant fluid losses and electrolyte imbalances. Early in the course of enterotoxicosis, hypermotility of the gastrointestinal tract may be noted. This may be followed in 12 to 72 hours by ileus and gas accumulation in the gut lumen. Gut stasis favors the growth of gram-negative bacteria, which may lead to enclotoxemia.

Signs of endotoxemia are seen 5 to 48 hours after ingestion and include fever, vomiting, and possibly diarrhea. in severe intoxications, signs of endotoxic shock including depression, collapse, rapid-to-slow capillary refill time, hypotension, hypothermia or hyperthermia, early leukopenia and neutropenia followed by leukocytosis and neutrophilia with toxic neutrophils, hyperglycemia (early), or hypoglycemia (late), and oliguria may be seen.

Treatment Food intoxications can mimic serious problems such as gastric or intestinal torsions and foreign bodies. A thorough work-up including radiographs is warranted to ensure proper diagnosis and treatment!

In cases where vomiting has occurred, the patient may have purged himself, thus requiring only supportive care (fluids, activated charcoal with a cathartic). If vomiting has failed to purge the stomach, treatment is by gastric lavage, repeated doses of activated charcoal, and perhaps use of a cathartic. Antiernetics may be necessary if vomiting continues after decontamination of the GI tract. Kaopectate can be used as an adsorbent or gastrointestinal protectant. Fluids are given as needed to treat hypovolemia, shock, or dehydration. Broad-spectrum antibiotics are given at the doctor's discretion. Enterotoxemia cases may appear to go well only to relapse. If relapse occurs, it usually does so within 48 hours. This may be related to onset of gut stasis and endotoxemia.

External contact can cause skin irritation and vapors can be inhaled or fluid ingested by licking.

Inhalation can cause mild to moderate respiratory irritation, muscular twitching, dilated pupils and convulsions leading to death.

Ingestion leads to salivation, vomiting, diarrhea, muscle twitching and seizures.

Fresh air should be provided to decrease the inhalation of more fumes. Skin should be flushed well with water, and washed with soap and water. Oxygen therapy, IV fluids, pumping the stomach followed by giving olive oil to coat the stomach are useful. With good care most cats do quite well.

GINSENG

Sources Dried roots of plants of the genus Panax are touted as a tonic for increasing strength and alleviating fatigue.

Mechanism of action Saponins called ginsengosides are believed to be the active ingredients. The saponins decrease blood glucose and liver cholesterol, increase erythropoiesis, hemoglobin production, and iron absorption from the G1 tract, stimulate the CNS, and increase blood pressure, heart rate, and GI motility. Toxicity is unlikely and has occurred only at extremely high levels. Supportive treatment (fluid therapy, seizure control) may be needed but is unlikely.

-
EMERGENCY TREATMENT

Procedures

I .    Secure the airway and ventilate as necessary.
2.    Administer supplemental oxygen.
3.    Secure venous access. Collect blood and urine for laboratory testing.
4.    Control seizures. Check for hypoglycemia and treat if necessary.
5.    Treat hypertension if necessary.

Most glues cause local dermatitis and occasionally will ulcerate lips or gums if eaten. Vomiting can occur if swallowed.

Remove any material using water and gentle pressure. Avoid solvents as these too may be toxic. Supportive care is important if vomiting occurs. Most cats recover well.

HERBICIDES

See also Dinoseb, Diquat and Poraquat

Sources Preernergent and postemergent products for weed control including Betasan (bensulide), Round-up (glyphosate), Aatrex (atrazine), Banvel (dicamba), OrthoParaquat/Gramoxone/Surefire/Cyclone/Prelude (paraqUat). Herbicides are rarely responsible for severe toxicosis in pets, although G1 signs may be seen. Most pets could not consume enough toxin from eating treated lawns. Rather, toxicity is more likely caused by ingestion of the product directly. The risk of canine lymphoma was reportedly increased (doubled) when owners applied 2,4-D ([2,4-dichlorophenoxy I acetic acid) several times per year, though the Conclusions reached in this epiderniologic survey have been questioned. oral and dermal exposure to lawn where diluted liquids or granules are properly applied are generally of neglible risk.

Mechanism Of action 2,4-D causes anorexia, lethargy, myotonia, and metabolic acidosis when an acute lethal dose is ingested Concentrated formulations are irritating and may produce gastroenteritis. The LD,() (mediurn lethal dose) for dogs is approximately 100 mg/kg; a 20 kg dog could consume this dose by ingesting only 10 mL of a liquid formulation containing 23% of the acid equivalent of 2,4-D; however, it is unlikely that an animal Could consume a lethal dose after application of a properly diluted formulation. Mecoprop (MMCP) is toxicologically similar to 2,4-D. Atrazine and dicamba are not likely to be toxic unless chronic exposure occurs. Monosodium methane arsenals (MSMA), disodiurn methane arsenate (DSMA), and octyldodecyl ammonium salts of methyl arsenic acid are used as postemergents and do not have a high acute toxicity. Signs and treatment of acute arsenic poisoning are discussed elsewhere .

Paraquat intoxication (1). 208) causes seizures, hyperexcitability, and incoordination. Surviving pets may die 3 to 5 days later from severe pulmonary congestion (pulmonary edema may develop within I to 3 days) or may develop pulmonary fibrosis in 7 to 10 days. Concentrated solutions are corrosive to the eyes and skin. Oxygen increases the toxicity and Should be used sparingly as necessary. Forced diuresis is important because paraquat is a renal tubular toxin.

Glyphosatc, simazine (similar to atrazine), and amitrole are believed to have low to neglible acute toxicity. Glyphosate has caused transient signs of ocular and dermal irritation after exposure to recently treated grass; signs resolve quickly when the product is rinsed from the pet.

Treatment Treatment of 2,4-D poisoning includes activated charcoal and alkaline diuresis. Paraquat treatment is discussed on 1). 209. Treatment of glyphosate poisoning would be necessary only in the event the pet drank directly from a concentrated formulation. Treatment would necessitate gastrointestinal decontamination and activated charcoal administration. Further treatment would be symptomatic and supportive.

HOUSEHOLD CLEANING PRODUCTS

See also Adds and alkalis, Bleaches, Builders Phenolics, Soaps

General information

Many brands of cleaners are available, and many of these cleaners contain multiple poisons. Therefore the decision regarding treatment may become complex. In general, treat the poison that is most toxic.

Surfactants and alkalis may dissolve mucous membranes and cause liquefaction necrosis; intravascular hemolysis can be seen as well. Alkalis continue to penetrate tissue until removed or inactivated by deeper tissues. Acids, formaldehyde, phenols, and other corrosives produce a coagulation necrosis; the coagulum acts as a barrier to further penetration, making acid injuries less serious than alkali injuries. Phenols may also produce a penetrating lesion and are .hepato-, neuro-, and nephrotoxi . xalates bind calciurn. A toxic mechanism has not been discovered for some products, including borates.

Antidote information is commonly found on many household cleaning products. The Poisindex (Micromedex, Inc., Denver, CO 80204-4506) and Clinical Toxicolqgy of Commercial Products are handy references.

No attempt should be made to neutralize acids or alkalis by any of the commonly mentioned "antidotes," such as lenion juice, vinegar, antacids, or bicarbonate; these are ineffective and may cause further injury by the heat generated by the exothermic reactions. Water is generally sufficient in attempting to remove or dilute the poison.

HYDROGEN SULFIDE

Sources Hydrogen sulfide is a highly toxic gas that is heavier than air. It is found in oil wells, refineries, tanneries, sulfur hot springs, hot asphalt fumes, mines, manure-holding pits, septic tanks, and sludge pools.

Mechanism of action Hydrogen sulfide ions bind to cytochrome oxiclase within mitochondria, thus blocking electron transport. This blockade results in cellular asphyxia similar to (but different from) the action of cyanide. It is also capable of causing direct irritation to mucous membranes.

NONSTEROIDAL ANTI INFLAMMATORY DRUGS (NSAIDS)

See also Acetaminophen, Aspirin

Sources Many analgesics, antipyrerics, antiinflammatory drugs belong to this class of drug. txamples include indomethacin, piroxicam (Feldene), ibuprofen (Motrin, Advil Nuprin, Vick's DayQuil), phenylbutazone (Bute, Butazoliclin): naproxen (Naprosyn, Aleve).

Mechanism of action NSAIDS inactivate cyclooxygenase and therefore inhibit production of protective prostaglandins of the E-series. Reduced prostaglandin production results in reduced blood flow to the Gi tract, reduced secretion of gastric mucus, and G1 tract ischemia and ulceration (which may perforate). Prostaglandin inhibition also reduces blood flow to the kidneys resulting in renal papillary necrosis and acute renal failure. Newer NSAIDS such as carprofcn are touted to have fewer toxic side effects because of decreased inhibition of prostaglandin synthesis and yet offer effective antiinflammatory action.

Clinical signs Abdominal pain, lethargy, anemia, melena, and hematemesis are most commonly seen with G1 irritation and ulceration. if perforation has occurred, clinical signs may include abdominal pain, perhaps a fluid wave, shock, injected sclera, brick-red mucous membranes, and tachycardia. Temperature may be elevated or depressed. Pulses may be bounding or weak and thready.

Clinical signs associated with acute renal failure include hyposthenuria or isosthenuria, renal tubular cell casts in the urine sediment, or glucosuria without hyperglycemia. Urine gammaglutamyltransferase erase (GGT) will be elevated. These early signs of acute renal failure will be followed by increasing BUN and creatinine, electrolyte disturbances, and possibly oliguria or more rarely polyuria. Occasionally, increased alanine aminotransferase (ALT) and alkaline phosphatase (ALP) may be seen.

Signs

Abdominal pain Lethargy Anemia Melena, hematochezia Hematemesis Increased BUN and creatinine Hyposthenuria or isosthenuria Renal tubular casts Glucosuria without hyperglycernia Increased ALT and ALP Hypoventilation or apnea in some cases Acid-base disorders (sometimes initial alkalemia with later metabolic acidemia) Signs of peritonitis if perforation Coma, rarely seizures

Treatment Treatment involves preventing or correcting GI ulceration, perforation, and acute renal failure. There is no specific antidote for NSAIDs.

EMERGENCY TREATMENT

Procedures

I .    Secure the airway and ventilate as necessary.
2.    Administer supplemental oxygen .
3.    Secure venous access. Treat shock if needed. Collect blood and urine for laboratory testing. Obtain data base including
   &nb