a) Chronic ethanol abusers may present with alcoholic ketoacidosis after a sudden reduction of caloric intake. Patients with alcoholic ketoacidosis and isopropyl alcohol intoxication may be misdiagnosed with ethanol, methanol, or ethylene glycol intoxication.

a) Subjects exposed to isopropyl alcohol vapors developed a sense of irritation at 800 ppm. Brief splash contact to human eyes has resulted in transient burning, stinging, and tearing (Grant & Schuman, 1993).

a) CASE REPORT: A 2.5-year-old boy with fever developed eye irritation and pain due to a splash injury after his parents used isopropanol sponge-bathing as a home remedy to reduce his fever. The examination of the eyes revealed a large left corneal abrasion. His corneal abrasion resolved after symptomatic treatment, including antibiotic ointment and patching for 5 days (Osborn & Rosales, 1981a).

a) Hypotension occurs in severe poisonings and may result from peripheral vasodilation (DeBellonia et al, 2008; Emadi & Coberly, 2007; Natowicz et al, 1985; Visudhiphan & Kaufman, 1971; Vivier et al, 1994; King et al, 1970; Pappas et al, 1991).
b) CASE REPORT: A 37-year-old man developed deep coma (Glasgow coma scale 6) and hypotension (BP 77/40 mmHg) after drinking 200 to 250 mL of a "fat solvent for engines" containing 100% isopropanol. On admission, his isopropanol blood level was 5 g/L. His condition did not improve following flumazenil and naloxone therapy. However, he was treated successfully with a 4-hour hemodialysis (Trullas et al, 2004).

a) Tachycardia is common (DeBellonia et al, 2008; Kelner & Bailey, 1983).

a) CASE REPORT: A 45-year-old female chronic ethanol abuser, presented with confusion, agitation, and chest pain after drinking a large amount of alcohol during the previous 2 weeks. Laboratory results revealed a wide plasma osmolal gap (44 mmol/kg) and anion gap metabolic acidosis (15 mmol/L) with elevated serum beta-hydroxybutyric acid levels (3620 mcmol/L), normal serum lactate levels, negligible levels of salicylate and ethanol, and elevated acetone concentration (at least 80 mg/L). Because of a suspicion of ethanol or ethylene glycol intoxication, she was treated with a loading dose of 15 mg/kg of fomepizole; however, she remained confused. Further laboratory analysis revealed elevated isopropyl alcohol concentrations (1.69 mmol/L) and acetone (38 mmol/L). At this time, she admitted to drinking rubbing alcohol and eating little food for several days. Following the discontinuation of fomepizole and continued supportive therapy, including treatment for alcohol withdrawal symptoms, her condition gradually improved and returned to baseline mental and functional status after 3 days (Meng et al, 2015).

a) In patients with severe intoxication, respiratory depression or failure may occur (Vujasinovic et al, 2007; Adelson, 1962; Pappas et al, 1991; Lewis, 2000a; Visudhiphan & Kaufman, 1971; Manring et al, 1997). Death from respiratory paralysis may occur in 24 to 36 hours following ingestion (Proctor et al, 1989).
b) CASE REPORT: Respiratory depression and coma occurred rapidly following an accidental intravenous infusion of 35% isopropyl alcohol (800 mL) in saline in a 19-year-old previously healthy man. Mechanical ventilation was required. Serum isopropyl alcohol level was 142 mg/dL 5 hours after infusion and acetone level was 117 mg/dL. The patient's recovery was uneventful following hemodialysis (Manring et al, 1997).

a) Hemorrhagic tracheobronchitis may be present (Goldfrank, 2002).

a) CHRONIC INHALATION: A 63-year-old woman presented with bilateral lung infiltrates, hemoptysis, and acute respiratory failure after chronically abusing isopropyl alcohol by inhalation multiple times daily for 3 years. On presentation, her oxygen saturation was 88% on room air, blood pressure was 121/72 mmHg, heart rate was 88 beats/min, and temperature was 98 degrees F. An echocardiogram revealed a left ventricular ejection fraction of more than 70%, no valvular or wall motion abnormalities, and a small pericardial effusion. A video-assisted thoracotomy (VATS) showed significant and diffuse pleural adhesions involving the entire pleural cavity with the entire lung adhered to the pleural wall. Bronchoscopy revealed unremarkable mucosa with some bloody secretions throughout the subsegmental bronchi. A lung biopsy showed an airway centric pattern of fibrosis and chronic inflammation with scattered lymphoid aggregates. Following aggressive supportive care, including steroids, antibiotics, and albuterol therapies, her symptoms gradually improved. On follow-up, 5 months later, computed tomography of the chest revealed significant improvement in lung infiltrates and ground glass opacities with the presence of residual subpleural ground glass opacities (Blow et al, 2012).

a) PREEXISTING RESPIRATORY CONDITIONS: In persons with impaired pulmonary function, especially those with obstructive airway diseases, inhalation of isopropanol might cause exacerbation of symptoms, due to its irritant properties (HSDB, 2003).

a) The stimulatory phase seen with ethyl alcohol is generally absent following isopropyl alcohol ingestion, which may result in apparent inebriation, headache, weakness, hypothermia, lethargy, sleepiness, hypotonia, and coma. Deep coma and areflexia are common following severe intoxication (Vujasinovic et al, 2007).
b) Infants and adults have developed hypotonia and coma following prolonged topical application of isopropyl alcohol for fever relief (McFadden & Haddow, 1969; Senz & Goldfarb, 1958; Garrison, 1953; Martinez et al, 1986; Visudhiphan & Kaufman, 1971) Vivier et al, 1991).
c) Lethargy or unresponsiveness was reported in 20% of 35 pediatric patients who had ingested isopropyl alcohol accidentally. The patients recovered without sequelae (Stephan et al, 1997).
d) CASE REPORT: A 43-year-old man with alcoholism became hypotensive and delirious after drinking an unknown amount of a hand sanitizer containing isopropanol (63% v/v). His isopropanol and acetone levels were 13.6 mg/dL and 269.4 mg/dL (normal range, 0 to 1.9 for both), respectively. Following supportive therapy, he recovered completely (Emadi & Coberly, 2007).
e) Somnolence and coma have been reported following acute isopropanol intoxication (Vujasinovic et al, 2007).
f) CASE REPORT: A 45-year-old female chronic ethanol abuser, presented with confusion, agitation, and chest pain after drinking a large amount of alcohol during the previous 2 weeks. Laboratory results revealed a wide plasma osmolal gap (44 mmol/kg) and anion gap metabolic acidosis (15 mmol/L) with elevated serum beta-hydroxybutyric acid levels (3620 mcmol/L), normal serum lactate levels, negligible levels of salicylate and ethanol, and elevated acetone concentration (at least 80 mg/L). Because of a suspicion of ethanol or ethylene glycol intoxication, she was treated with a loading dose of 15 mg/kg of fomepizole; however she remained confused. Further laboratory analysis revealed elevated isopropyl alcohol concentrations (1.69 mmol/L) and acetone (38 mmol/L). At this time, she admitted to drinking rubbing alcohol and eating little food for several days. Following the discontinuation of fomepizole and continued supportive therapy, including treatment for alcohol withdrawal symptoms, her condition gradually improved and returned to baseline mental and functional status after 3 days (Meng et al, 2015).

a) CASE REPORT: A 38-year-old woman developed an acute sensori-motor axonal polyneuropathy (confirmed by nerve conduction studies) and erythromelalgia after walking barefooted for several hours on carpets soaked by a disinfectant containing isopropanol (Microban(R)). She experienced burning paresthesia in both feet and legs temporarily relieved by immersion in cold water. Neurological examination showed dysesthesia to light touch from the knees down and distal hyperesthesia to pin prick. In addition, vibration sense and proprioception were impaired distally, and symmetrical exclusively distal weakness was present. Although high-dose oral corticosteroid therapy was not effective, amitriptyline and gabapentin partially relieved her symptoms (Rajabally & Mortimer, 2004).

a) Ataxia, dysarthria, and nystagmus are reported less commonly than with ethanol exposure (Kelner & Bailey, 1983; Rich et al, 1990).
b) Wernicke's encephalopathy should be considered in patients with the above symptoms (Wrenn, 1991).
c) Ataxia and combativeness occurred in 20% of 35 pediatric patients who accidentally ingested isopropyl alcohol (Stephan et al, 1997).

a) Hyporeflexia and areflexia usually accompany significant CNS depression (Kelner & Bailey, 1983; Pappas et al, 1991; Mydler et al, 1993).

a) RARE EFFECT: CSF PROTEIN: Marked elevation in CSF protein (peak 200 mg/mL) was reported in a 2-year-old child with a serum isopropanol level of 520 mg/dL (Visudhiphan & Kaufman, 1971).

a) RARE EFFECT: Seizures were reported in a 21-day-old infant after the child's mother repeatedly applied cotton soaked with 70% isopropyl alcohol to the umbilicus with every diaper change for 3 weeks (Vivier et al, 1994).
b) CASE REPORT: A 4-year-old girl became unresponsive and developed generalized tonic-clonic motor seizures (lasting 2 to 3 minutes) approximately 3 hours after bathing in a preparation of chamomile and isopropyl alcohol during a Mexican folk healing ritual (curanderismo, to treat evil spirits). Following supportive therapy, she recovered over the next 2 days (DeBellonia et al, 2008).

a) Somnolence and coma have been reported following acute isopropanol intoxication (DeBellonia et al, 2008; Vujasinovic et al, 2007).
b) Coma and respiratory depression occurred rapidly following an accidental intravenous infusion of 35% isopropyl alcohol (800 mL) in saline in a 19-year-old, previously healthy man. The patient was awake and alert and extubated following hemodialysis; recovery was uneventful (Manring et al, 1997).
c) CASE REPORT: A 37-year-old man developed deep coma (Glasgow coma scale 6) and hypotension (BP 77/40 mmHg) after drinking 200 to 250 mL of a "fat solvent for engines" containing 100% isopropanol. On admission, his isopropanol blood level was 5 g/L. His condition did not improve following flumazenil and naloxone therapy. However, he was treated successfully with a 4-hour hemodialysis (Trullas et al, 2004).
d) CASE REPORT: After ingesting rubbing alcohol, a 38-year-old man with a history of paranoid schizophrenia and suicide attempts developed coma and the presence of skew eye deviation (left eye lower than right) mimicking basilar artery thrombosis. Motor examination revealed flaccid tetraplegia with no response to noxious stimuli. Deep tendon reflexes were hypoactive in the upper and absent in the lower extremities without response to plantar stimulation. Brain CT angiography revealed a patent basilar artery. Gas chromatography revealed an isopropanol level of 287 mg/dL with an acetone level of 123 mg/dL. Following supportive therapy, he recovered over the next 48 hours (Mueller-Kronast et al, 2003).

a) CASE REPORT: A 45-year-old female chronic ethanol abuser, presented with confusion, agitation, and chest pain after drinking a large amount of alcohol during the previous 2 weeks. Laboratory results revealed a wide plasma osmolal gap (44 mmol/kg) and anion gap metabolic acidosis (15 mmol/L) with elevated serum beta-hydroxybutyric acid levels (3620 mcmol/L), normal serum lactate levels, negligible levels of salicylate and ethanol, and elevated acetone concentration (at least 80 mg/L). Because of a suspicion of ethanol or ethylene glycol intoxication, she was treated with a loading dose of 15 mg/kg of fomepizole; however, she remained confused. Further laboratory analysis revealed elevated isopropyl alcohol concentrations (1.69 mmol/L) and acetone (38 mmol/L). At this time, she admitted to drinking rubbing alcohol and eating little food for several days. Following the discontinuation of fomepizole and continued supportive therapy, including treatment for alcohol withdrawal symptoms, her condition gradually improved and returned to baseline mental and functional status after 3 days (Meng et al, 2015).

a) Patients often vomit following isopropyl alcohol ingestion (Stremski & Hennes, 2000).

a) GI hemorrhage and hematemesis have been reported (Lehman & Chase, 1944; Zaman et al, 2002).
b) CASE REPORT: A 2-year-old boy developed hemorrhagic gastritis after topical isopropanol exposure. His grandmother used isopropanol (half of a 240 mL bottle of isopropanol 70%) sponge-bathing as a home remedy to reduce his fever. Following supportive therapy, he recovered without further sequelae. Laboratory results were serum isopropanol 92 mg/dL (normal 0), acetone 181 mg/dL (normal 0), and serum osmolality 341 mOsm/kg (osmolal gap 55 mOsm/L) (Dyer et al, 2002).

a) Abdominal pain and cramping, along with gastritis, nausea, and vomiting have been reported (Zaman et al, 2002).

a) RECTAL ABSORPTION

a) Mild hepatic injury has been reported (Chapin, 1949).
b) Isopropyl alcohol appears to greatly accentuate the hepatic injury caused by carbon tetrachloride.

a) INTERACTION

a) Renal insufficiency including anuria, followed by oliguria, nitrogen retention, and edema may be a complication of isopropyl poisoning (Hathaway et al, 1996a).

a) CASE REPORT: A 54–year-old man with a history of alcohol abuse, diabetes mellitus, and hypertension presented to the emergency department on 3 occasions in a 5-month period after ingestion of isopropyl alcohol. On each occasion, the patient was found to have elevated serum creatinines up to 3.6 mg/dL over his baseline serum creatinine of 1.0 mg/dL. He was treated conservatively with intravenous fluids, and on each occasion his serum creatinine levels returned to baseline (Zaman et al, 2002).

a) Acute renal tubular necrosis has been reported in a few cases of isopropanol ingestion with associated prolonged hypotension or rhabdomyolysis (Adelson, 1962; Chapin, 1949; Juncos & Taguchi, 1968).

a) Myoglobinuria may occur in comatose patients and was reported in 1 patient with rhabdomyolysis (Juncos & Taguchi, 1968).

a) Ataxia and microscopic hyaline droplets in the kidneys were seen in male rats exposed to isopropanol at concentrations up to 5000 ppm for 6 hours per day, 5 days per week, for 13 weeks (Burleigh-Flayer et al, 1994b).

a) Ketosis and ketonuria without acidosis is common (Vujasinovic et al, 2007). Normoglycemic ketoacidosis is rare but may occur (Alexander et al, 1982).

a) Metabolites of methanol and ethylene glycol can cause metabolic acidosis. Although isopropyl alcohol is metabolized to acetone and does not usually cause metabolic acidosis, it can occur in patients who drink isopropyl alcohol and have decreased caloric intake. Chronic ethanol abusers may present with alcoholic ketoacidosis after a sudden reduction in calorie ntake. Patients with alcoholic ketoacidosis and isopropyl alcohol intoxication may be misdiagnosed with ethanol, methanol, or ethylene glycol intoxication. Fomepizole reduces the clearance of isopropyl alcohol and prolongs its effects; therefore, it is contraindicated in patients with isopropyl alcohol intoxication (Meng et al, 2015).

a) Possible red blood cell hemolysis (hematocrit 31.9% and urine red) developed in an adult following accidental infusion of 35% isopropyl alcohol (800 mL) in saline. Complete recovery occurred following hemodialysis without sequelae (Manring et al, 1997).

a) Chemical burns have occurred in premature infants following topical application of isopropyl alcohol (Schick & Milstein, 1981; Watkins & Keogh, 1992).
b) SUSCEPTIBLE POPULATIONS: Persons with preexisting skin disorders may be more susceptible (HSDB, 2003). Premature infants may be at greater risk of developing chemical burns (Schick & Milstein, 1981).

a) ABSORPTION: Isopropyl alcohol intoxication occurred following dermal absorption in a 21-day-old infant, resulting in seizures, hypotension, lethargy, and CNS depression. The child's mother repeatedly applied cotton soaked with 70% isopropyl alcohol to the umbilicus with every diaper change for 3 weeks (Vivier et al, 1994).

a) DERMAL ABSORPTION: Significant dermal absorption of isopropyl alcohol has been demonstrated in rabbits when inhalational absorption was shown to be negligible (Martinez et al, 1986). Blood levels of isopropyl alcohol after 4 hours of dermal exposure to 70% solution were greater than 100 mg/dL (Martinez et al, 1986).

a) Possible rhabdomyolysis (CK 772 U/L) developed in a 19-year-old man following accidental infusion of 35% isopropyl alcohol (800 mL) in saline. The patient recovered without sequelae following hemodialysis (Manring et al, 1997).

a) Mild hyperglycemia is often reported in exposed adults (Lacouture et al, 1983; McCord et al, 1948).

a) Isopropyl alcohol interferes with gluconeogenesis and may result in hypoglycemia (Zaman et al, 2002).
b) Hypoglycemia might be expected to occur in children.

a) No teratogenic effects were observed in rats inhaling 3500 parts per million (ppm) for 7 hours/day during organogenesis. Exposure to higher concentrations (7000 and 10,000 ppm) produced maternal toxicity and resulted in dose-related decreased fetal weight and increased skeletal malformations. The blood isopropanol levels in nonpregnant rats were shown to be undetectable after exposure to 3500 ppm, 680 mg/dL after exposure to 7000 ppm, and 790 mg/dL after exposure to 10,000 ppm (Nelson et al, 1988).
b) A 2-generation reproductive study with oral isopropyl alcohol at doses of up to 1000 mg/kg/day revealed effects on neonatal survival and birthweight at maternally toxic doses. No increase in malformations was observed (Bevan et al, 1995).
c) Skeletal malformations in the offspring of rats have been reported following maternal inhalation exposure to isopropyl alcohol at levels which produced maternal toxicity. Developmental toxicity was not reported in offspring of rats and rabbits in the absence of maternal toxicity (Nelson et al, 1988; Tyl et al, 1994).

a) Listed as: Isopropanol
b) Carcinogen Rating: 3

a) Listed as: Isopropanol manufacture (strong-acid process)
b) Carcinogen Rating: 1

a) Acetone may be detectable in the urine by 3 hours after ingestion, and in the blood by one-half to 1 hour after isopropyl alcohol ingestion. A presumptive diagnosis can be made with Acetest tablets (Lacouture et al, 1989). As the level of isopropyl alcohol decreases, the concentration of acetone increases and then decreases following elimination.
b) A high serum or urinary acetone without metabolic acidosis is strongly suggestive of isopropyl alcohol intoxication (Zaman et al, 2002).
c) DISEASE STATE: Detection of isopropyl alcohol in the blood of a patient with diabetic ketoacidosis was reported, despite denial of any exposure to isopropyl alcohol prior to presentation. It has been suggested that the detection of isopropyl alcohol may be a result of endogenous biotransformation of acetone to isopropyl alcohol in certain disease states, and not due to an acute isopropyl alcohol ingestion (Jones & Summers, 2000).

a) A falsely elevated serum creatinine concentration may occur in the presence of acetonemia when colorimetric methods of analysis are used (Rich et al, 1990) but the BUN measurement is not affected (Linden, 1996).

a) The absence of hyperglycemia or glucosuria when acetone is present helps differentiate between alcohol intoxication or diabetic ketoacidosis versus isopropyl alcohol intoxication (Zaman et al, 2002).

a) NORMAL OSMOLAL GAP: There are wide variations in what is defined as a normal osmolal gap, depending on the formula used. An individual's osmolal gap may fall within the defined normal range and still be distinctly elevated. Thus, an apparent normal osmolal gap cannot be reliably used to exclude the possibility of isopropanol ingestion (Hoffman et al, 1992).
b) INCREASED OSMOLAL GAP: The presence of an increased osmolal gap suggests the possibility of a toxic alcohol (including isopropanol) ingestion.
c) DETERMINATION OF OSMOLAL GAP: Measure the serum osmolality (using the freezing point depression method).
d) Correct for coingested ethanol (if present) by dividing the measured blood ethanol concentration (in mg/dL) by 4.6 and adding the result to the calculated osmolality before determining the osmolal gap.
e) Subtract the calculated serum osmolality from the measured serum osmolality to determine the osmolal gap. This difference can be accounted for by the presence of osmotically active substances (including isopropanol).
f) Osmolal gap x 6 = predicted isopropanol level in mg/dL.
g) OTHER LIMITATIONS: Methanol, ethylene glycol, ethanol, and acetone can cause an osmolal gap (Cadnapaphornchai et al, 1981).

a) To convert traditional units (mg/dL) into SI units (mmol/L), multiply traditional units by 0.1664.
b) To convert SI units (mmol/L) into traditional units (mg/dL), divide SI units by 0.1664.

a) Treatment is symptomatic and supportive.

a) Treatment is symptomatic and supportive. Critically ill patients will need emergent management of airway, breathing, and circulation. CNS depression may require intubation, and alcohol-induced vasodilation and vomiting may lead to hypotension requiring fluid resuscitation, and rarely vasopressors.

a) CASE REPORT: A 45-year-old female chronic ethanol abuser, presented with confusion, agitation, and chest pain after drinking a large amount of alcohol during the previous 2 weeks. Laboratory results revealed a wide plasma osmolal gap (44 mmol/kg) and anion gap metabolic acidosis (15 mmol/L) with elevated serum beta-hydroxybutyric acid levels (3620 mcmol/L), normal serum lactate levels, negligible levels of salicylate and ethanol, and elevated acetone concentration (at least 80 mg/L). Because of a suspicion of ethanol or ethylene glycol intoxication, she was treated with a loading dose of 15 mg/kg of fomepizole; however, she remained confused. Further laboratory analysis revealed elevated isopropyl alcohol concentrations (1.69 mmol/L) and acetone (38 mmol/L). At this time, she admitted to drinking rubbing alcohol and eating little food for several days. Following the discontinuation of fomepizole and continued supportive therapy, including treatment for alcohol withdrawal symptoms, her condition gradually improved and returned to baseline mental and functional status after 3 days (Meng et al, 2015).

a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).

a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
b) DOSE

a) Isopropyl alcohol produces greater CNS depression than ethanol at comparable blood concentrations (Wallgren, 1960). Toxic effects generally occur with concentrations between 50 and 100 mg/dL. Death has been reported at 150 mg/dL, while levels to 440 mg/dL have survived following treatment with hemodialysis.
b) Blood concentrations of 150 mg/dL: coma likely (McCord et al, 1948)
c) Blood concentrations greater than 200 mg/dL: generally fatal if no medical treatment is provided.

a) ADULT
b) PEDIATRIC

1) Isopropanol

1) 2-Propanol

a) TWA: 400 ppm (980 mg/m(3))
b) STEL: 500 ppm (1225 mg/m(3))
c) Ceiling:
d) Carcinogen Listing: (Not Listed) Not Listed
e) Skin Designation: Not Listed
f) Note(s):

a) IDLH: 2000 ppm
b) Note(s): [10%LEL]

a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.

a) 3 : The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.

a) 1 : The agent (mixture) is carcinogenic to humans. The exposure circumstance entails exposures that are carcinogenic to humans. This category is used when there is sufficient evidence of carcinogenicity in humans. Exceptionally, an agent (mixture) may be placed in this category when evidence of carcinogenicity in humans is less than sufficient but there is sufficient evidence of carcinogenicity in experimental animals and strong evidence in exposed humans that the agent (mixture) acts through a relevant mechanism of carcinogenicity.

a) 8-hour TWA:

a) 4477 mg/kg

a) 3600 mg/kg

a) 2735 mg/kg

a) 5045 mg/kg

a) 10,000 ppm for 7H

a) Begin treatment immediately.
b) Keep animal warm and do not handle unnecessarily.
c) Remove the patient and other animals from the source of contamination or remove dietary sources.

a) ASPCA Animal Poison Control Center, 1717 S Philo Road, Suite 36 Urbana, IL 61802
b) It is an emergency telephone service which provides toxicology information to veterinarians, animal owners, universities, extension personnel and poison center staff for a fee. A veterinary toxicologist is available for consultation.
c) Contact information: (888) 426-4435 (hotline) or www.aspca.org (A fee may apply. Please inquire with the poison center). The agency will make follow-up calls as needed in critical cases at no extra charge.

a) EMESIS/GASTRIC LAVAGE -
b) ACTIVATED CHARCOAL/CATHARTIC -

a) Formula for bicarbonate addition when blood gases are available: milliequivalents bicarbonate added = base deficit x 0.5 x body weight in kilograms. Give one half of the determined dose slowly over 3 to 4 hours intravenously; titrate as needed.
b) Continue to dose based on blood gas determinations. When blood gases are not available and patient is symptomatic, administer 1 to 4 milliequivalents/kilogram intravenously slowly over 4 to 8 hours.

a) Peritoneal or hemodialysis for 5 hours or longer may be the most effective way to remove this toxin (Coppock et al, 1988).

a) Admit all symptomatic patients and begin treatment.
b) Unless life threatening signs develop, these patients may be kept in the primary care clinic (24 hour monitoring is not necessary).

a) Instruct the owner to return for a follow up appointment at which physical examination and appropriate laboratory tests will be repeated.

1) SUMMARY
2) Treatment should always be done on the advice and with the consultation of a veterinarian.
3) Additional information regarding treatment of poisoned animals may be obtained from a Veterinary Toxicologist or the National Animal Poison Control Center.
4) ASPCA ANIMAL POISON CONTROL CENTER
5) SMALL ANIMALS: Due to lack of reports of large animal intoxication with this substance, the following sections address small animals (dogs and cats) only.
6) In the case of a poisoning involving large animals, consult a veterinary poison control center.

1) GENERAL TREATMENT