a) Hypotension may occur after ingestion of concentrated oxalic acid secondary to corrosive injury to the gastrointestinal tract with hemorrhagic gastroenteritis (Gawarammana et al, 2009). Patients may develop a weak pulse, hypotension, cardiac dysrhythmias and asystole in severe cases (Dassanayake & Gnanathasan, 2012; Hamilton et al, 1999).

a) As serum calcium levels decline with hypovolemia and poor coronary perfusion, cardiac dysrhythmias may occur and can lead to asystole (Hamilton et al, 1999). Bradycardia developed in one patient (Dassanayake & Gnanathasan, 2012).

a) Chronic inhalation of vapors may cause inflammation of the respiratory tract.

a) Symptoms may include drowsiness, stupor, CNS depression and/or coma.
b) Drowsiness developed in one patient (Dassanayake & Gnanathasan, 2012).

a) Muscle twitching, cramps and exaggerated deep tendon reflexes may be noted.

a) HYPOCALCEMIA may lead to muscular fasciculation, tetany, and rapid onset of seizures (Hamilton et al, 1999).

a) The patient may experience epigastric pain and hematemesis because of hemorrhagic gastritis, which can develop due to the corrosive action of oxalic acid on mucous membranes. Severe vomiting and profuse diarrhea may develop early (Hamilton et al, 1999; Gosselin et al, 1984; Dassanayake & Gnanathasan, 2012). In patients who ingest dilute solutions, the onset of symptoms is delayed and gastroenteritis may be absent. Gastric perforation and stricture are uncommon.
b) CASE SERIES - In Sri Lanka, intentional ingestion of a laundry detergent containing a sachet each of 12.5 g of oxalic acid and potassium permanganate 1.2 g resulted in 115 cases of toxicity with 18 fatalities. Gastrointestinal symptoms developed within 24 hours of ingestion. Of the individuals that ingested oxalic acid only, a case fatality ratio of 25.4% was observed, while a case fatality ratio of 9.8% occurred in patients ingesting both oxalic acid and potassium permanganate. No deaths occurred in the potassium permanganate group. Most deaths occurred within one hour of ingestion. Postmortem exam revealed macroscopic evidence of superficial erosions of the esophagus, oropharynx and larynx in all cases (Gawarammana et al, 2009).
c) CASE REPORT: A 59-year-old man presented with a severe sore throat, tachypnea, nausea, and vomiting 4 hours after ingesting 30 mL of oolong tea mixed with oxalic acid. Arterial blood gases revealed anion gap high metabolic acidosis. On day 3, upper gastrointestinal tract endoscopy revealed erosive esophagitis from the midthoracic esophagus to lower esophagus, erosive gastritis and thickening of the gastric wall of the gastric body. Despite supportive care, he developed acute renal failure; however, following hemodialysis, he gradually improved and was discharged home on day 31 (Yamamoto et al, 2011).

a) Calcium oxalate crystals can be deposited in the liver resulting in hepatic necrosis and failure in severe cases. Milder cases may manifest as elevated serum liver enzymes (Hamilton et al, 1999).

a) SUMMARY: Oxalates are excreted via the kidney and the oxalic acid crystals may cause damage to renal tubules. Injury to the kidneys may result in oliguria, anuria, and hematuria. If injury is severe enough, the patient may develop uremia.
b) CASE REPORT: Acute tubular necrosis developed in a 47-year-old male following an intentional ingestion of 150 grams of sodium oxalate. Within 24 hours of the ingestion his serum creatinine had risen to 404 mcmol/L (normal 50 to 120 mcmol/L) and urea was 13.1 mmol/L (normal 2.5 to 6.7 mcmol/L), with oliguria. Hemodialysis was started, with 4 sessions over 5 days. Creatinine peaked on day 9 (1202 mcmol/L). By day 14 the patient was in the recovery stage. At his 2 month follow-up, recovery was complete with the exception of an elevated creatinine of 150 mcmol/L (Hamilton et al, 1999).
c) CASE SERIES: In Sri Lanka, intentional ingestion of a laundry detergent containing a sachet each of 12.5 g oxalic acid and 1.2 g potassium permanganate resulted in 115 cases of toxicity with 18 fatalities. Of the individuals that ingested a sublethal dose of oxalic acid and potassium permanganate (n=51), acute renal failure was observed 2 to 3 days after exposure. Median serum creatinine was 1.7 (Interquartile range: 0.91-4.4). Most recovered with supportive care (Gawarammana et al, 2009).
d) CASE REPORT: A 59-year-old man presented with a severe sore throat, tachypnea, nausea and vomiting 4 hours after ingesting 30 mL of oolong tea mixed with oxalic acid. Arterial blood gases revealed anion gap high metabolic acidosis with a pH of 7.329, PaCO2 32.5 torr, PaO2 80.2 torr, BE -7.9 mmol/L, HCO3 16.6 mmol/L, and an anion gap of 18 mEq/L. Laboratory analysis revealed elevated levels of white blood count (21,700/mcL), C-reactive protein (1.89 mg/dL), and lactate (50 mg/dL). Despite supportive care, his renal function deteriorated gradually and he developed acute renal failure on day 4 (serum creatinine: 4.7 mg/dL; BUN: 41 mg/dL; creatinine clearance: 6). On day 6, calcium oxalate was found in his urine. His serum creatinine increased to 9.4 mg/dL 3 days later, but decreased following hemodialysis. A renal biopsy at this time revealed calcium oxalate deposits in some renal tubules, and the renal tubular epithelial cells had swelling and necrosis. Following supportive care, including further hemodialysis, he gradually improved and he was discharged home on day 31 (Yamamoto et al, 2011).
e) CASE REPORT: A 32-year-old woman developed abdominal pain and profuse vomiting immediately after ingesting about 12.5 g of 70% oxalic acid mixed in a glass of water. She presented 4 hours postingestion with drowsiness, bradycardia (HR 50 beats/min), and a blood pressure of 80/60 mmHg. Despite supportive therapy, she continued to have vomiting with 2 episodes of blood stained vomitus, and worsening generalized edema with a reduction of urine output (about 20 mL/hr) by day 3. Laboratory results revealed elevated serum creatinine (up to 704 mcmol/dL) and BUN concentrations (up to 43.5 mmol/dL). At this time, she had fever (temperature 99.6 degrees C), nausea, and mild tachypnea, but stable vital signs. Arterial blood gases revealed a metabolic acidosis (pH 7.328, PaCO2 33.2 mmHg, PaO2 84.2 mmHg, BE -6.2, HCO3 18.9 mmol/L). Despite undergoing hemodialysis on day 3 and an initial symptomatic improvement, her urine output remained low and post dialysis arterial blood gases showed a respiratory alkalosis (pH 7.479, PaCO2 34.9 mmHg, PaO2 91.9 mmHg, BE 2.5, HCO3 26.2 mmol/L). On day 7, she underwent a second hemodialysis, resulting in increasing urine output, but serum creatinine concentration remained high. On day 8, renal biopsy showed acute tubulointerstitial nephritis associated with diffuse moderate acute tubular damage with refractile crystals seen in some tubules, suggesting oxalic acid poisoning. Following further supportive care, her condition gradually improved. Another laboratory analysis revealed a mild normochromic normocytic anemia (Hb: 9.1 g/dL) with normal WBC and platelets. On day 28, she was discharged home and a normal serum creatinine concentration was observed on follow-up day 28 (Dassanayake & Gnanathasan, 2012).

a) Oxalate complexes with calcium and calcium oxalate crystals are deposited in the kidney following acute overdoses. On urine examination, typical birefringent crystals of calcium oxalate, which exist in both the needle-like and envelope-shaped dimorphic forms, may be seen. Renal tubular damage may occur. Large renal calculi may require surgical removal or lithotripsy (Woolf, 1993).
b) Ascorbic acid (vitamin C) is metabolized to oxalates. Chronic ingestion of large amounts of ascorbic acid may result in the development of renal disease through the deposition of calcium oxalate in the kidneys. Ascorbic acid supplementation in dialysis patients results in hyperoxalemia (Ono, 1986). Therefore, patients with compromised renal function are at greater risk following oxalic acid or oxalate ingestion.
c) CASE SERIES: A study of railroad car cleaners in Norway who were heavily exposed to oxalic acid solutions and vapors revealed a 53.3% prevalence of urolithiasis, compared to a rate of 11.9% among unexposed workers from the same company (Laerum & Aarseth, 1985).

a) Metabolic acidosis may occur in severe cases (Hamilton et al, 1999).
b) CASE REPORT: A 59-year-old man presented with a severe sore throat, tachypnea, nausea and vomiting 4 hours after ingesting 30 mL of oolong tea mixed with oxalic acid. Arterial blood gases revealed anion gap high metabolic acidosis with a pH of 7.329, PaCO2 32.5 torr, PaO2 80.2 torr, BE -7.9 mmol/L, HCO3 16.6 mmol/L, and an anion gap of 18 mEq/L. Laboratory analysis revealed elevated levels of white blood count (21,700/mcL), C-reactive protein (1.89 mg/dL), and lactate (50 mg/dL). Despite supportive care, his renal function deteriorated gradually and he developed acute renal failure on day 4 (serum creatinine: 4.7 mg/dL; BUN: 41 mg/dL; creatinine clearance: 6). On day 6, calcium oxalate was found in his urine. His serum creatinine increased to 9.4 mg/dL 3 days later, but decreased following hemodialysis. A renal biopsy at this time revealed calcium oxalate deposits in some renal tubules, and the renal tubular epithelial cells had swelling and necrosis. Following supportive care, including further hemodialysis, he gradually improved and he was discharged home on day 31 (Yamamoto et al, 2011).
c) CASE REPORT: A 32-year-old woman developed abdominal pain and profuse vomiting immediately after ingesting about 12.5 g of 70% oxalic acid mixed in a glass of water. She presented 4 hours postingestion with drowsiness, bradycardia (HR 50 beats/min), and a blood pressure of 80/60 mmHg. Despite supportive therapy, she continued to have vomiting with 2 episodes of blood stained vomitus, and worsening generalized edema with a reduction of urine output (about 20 mL/hr) by day 3. Laboratory results revealed elevated serum creatinine (up to 704 mcmol/dL) and BUN concentrations (up to 43.5 mmol/dL). At this time, she had fever (temperature 99.6 degrees C), nausea, and mild tachypnea, but stable vital signs. Arterial blood gases revealed a metabolic acidosis (pH 7.328, PaCO2 33.2 mmHg, PaO2 84.2 mmHg, BE -6.2, HCO3 18.9 mmol/L). Despite undergoing hemodialysis on day 3 and an initial symptomatic improvement, her urine output remained low and post dialysis arterial blood gases showed a respiratory alkalosis (pH 7.479, PaCO2 34.9 mmHg, PaO2 91.9 mmHg, BE 2.5, HCO3 26.2 mmol/L). On day 7, she underwent a second hemodialysis, resulting in increasing urine output, but serum creatinine concentration remained high. On day 8, renal biopsy showed acute tubulointerstitial nephritis associated with diffuse moderate acute tubular damage with refractile crystals seen in some tubules, suggesting oxalic acid poisoning. Following further supportive care, her condition gradually improved. Another laboratory analysis revealed a mild normochromic normocytic anemia (Hb: 9.1 g/dL) with normal WBC and platelets. On day 28, she was discharged home and a normal serum creatinine concentration was observed on follow-up day 28 (Dassanayake & Gnanathasan, 2012).

a) Oxalate is an irritant, corrosive to the skin, and may cause dermatitis. Skin lesions begin with epithelial cracking and the formation of slow-healing ulcers. The fingers may appear cyanotic.

a) Rare chemical burns may occur from oxalic acid and may cause hypocalcemia (Saydjari et al, 1986).

a) Gangrene has occurred in the hands of people working with oxalic acid solutions without rubber gloves. The hands of one case were described as follows: mottled, cyanotic appearance, tense and immobile, cold, and with very little sensation (Grolnick, 1929).

a) Obtain an ECG, and institute continuous cardiac monitoring.

a) Treatment is symptomatic and supportive. Do not induce emesis. Following an ingestion, rinse mouth immediately and administer milk or water. Monitor for evidence of severe symptoms (ie, severe pain, drooling, or difficulty swallowing). Oral analgesics may be necessary for pain. Antihistamines, inhaled beta agonists, corticosteroids may be necessary to treat laryngeal swelling or edema. Administer intravenous fluids as necessary to maintain hydration. Monitor urine output. Early (within 12 hours) gastrointestinal endoscopy should be considered to evaluate for burns. Perform barium swallow or repeat endoscopy several weeks after ingestion (sooner if difficulty swallowing) to evaluate for stricture formation.

a) Treatment is symptomatic and supportive. Monitor respiratory effort; airway support may be needed in patients that develop difficulty swallowing, drooling or evidence of glossitis or laryngeal edema following exposure to oxalic acid. Early bronchoscopy should be considered in patients with respiratory distress or upper airway edema. Treat seizures with IV benzodiazepines; barbiturates or propofol may be needed if seizures persist or recur. Intravenous administration of calcium gluconate or calcium chloride may be required for significant hypocalcemia. Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia. Hemodialysis is indicated in renal failure. Early surgical consultation should be considered for patients with severe burns, large deliberate ingestions, or signs, symptoms or laboratory findings concerning for tissue necrosis or perforation.

a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).

a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .

a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).

a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2010; Chin et al, 2008).

a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).

a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):

a) REFERENCES: Gaudreault et al, 1983; Symbas et al, 1983; Crain et al, 1984; (Schild, 1985; Moazam et al, 1987; Sugawa & Lucas, 1989; Previtera et al, 1990; Zargar et al, 1991; Vergauwen et al, 1991; Gorman et al, 1992; Nuutinen et al, 1994)

a) Advancing across the cricopharynx under direct vision
b) Gently advancing with minimal air insufflation
c) Never retroverting or retroflexing the endoscope
d) Using a pediatric flexible endoscope
e) Using extreme caution in advancing beyond burn lesion areas
f) Most authors recommend endoscopy within the first 24 hours of injury, not advancing the endoscope beyond areas of severe esophageal burns, and avoiding endoscopy during the subacute phase of healing when tissue slough increases the risk of perforation (5 to 15 days after ingestion) (Zargar et al, 1991).

a) Several scales for grading caustic injury exist. The likelihood of complications such as strictures, obstruction, bleeding and perforation is related to the severity of the initial burn (Zargar et al, 1991):
b) Grade 0 - Normal examination
c) Grade 1 - Edema and hyperemia of the mucosa; strictures unlikely.
d) Grade 2A - Friability, hemorrhages, erosions, blisters, whitish membranes, exudates and superficial ulcerations; strictures unlikely.
e) Grade 2B - Grade 2A plus deep discreet or circumferential ulceration; strictures may develop.
f) Grade 3A - Multiple ulcerations and small scattered areas of necrosis; strictures are common, complications such as perforation, fistula formation, or gastrointestinal bleeding may occur.
g) Grade 3B - Extensive necrosis through visceral wall; strictures are common, complications such as perforation, fistula formation, or gastrointestinal bleeding are more likely than with 3A.

a) ANIMAL
b) HUMAN

a) STUDY - In a retrospective study of patients with extensive transmural gastroesophageal necrosis after caustic ingestion, all 4 patients treated in the conventional manner (endoscopy, steroids, antibiotics, and repeated evaluation for the occurrence of esophagogastric necrosis and perforation) died, while all 3 patients treated with early laparotomy and immediate esophagogastric resection survived (Estrera et al, 1986).
b) Wu & Lai (1993) reported the results of emergency surgical resection of the alimentary tract in 28 patients who had extensive corrosive injuries due to the ingestion of acids or other caustics. Operative mortality was most frequently associated with sepsis. Non-fatal bleeding, infections, biliary or bronchial fistulas were other noted complications. Morbidity and mortality were related to the severity of the damage and the extent of surgery required.

a) ASSESSMENT CAUSTIC EYE BURNS: It may take 48 to 72 hours after the burn to assess correctly the degree of ocular damage (Brodovsky et al, 2000a).
b) The 1965 Roper-Hall classification uses the size of the corneal epithelial defect, the degree of corneal opacification and extent of limbal ischemia to evaluate the extent of the chemical ocular injury (Brodovsky et al, 2000a; Singh et al, 2013):
c) A newer classification (Dua) is based on clock hour limbal involvement as well as a percentage of bulbar conjunctival involvement (Singh et al, 2013):

a) IRRIGATION: In a medical facility: Begin irrigation with copious amounts of water or sterile 0.9% saline, which ever is more rapidly available, immediately. Once irrigation has begun, instill a drop of local anesthetic for comfort; switching from water to slightly warmed sterile saline may also improve patient comfort (Ernst et al, 1998; Grant & Schuman, 1993a).
b) Continue irrigation for at least an hour or until the superior and inferior cul-de-sacs have returned to neutrality, pH of 7.0 to 8.0, and remain so for 30 minutes after irrigation is discontinued (Brodovsky et al, 2000).
c) Search the conjunctival sac for solid particles and remove them while continuing irrigation (Grant & Schuman, 1993a). Emergent ophthalmologic consultation is needed in these cases.

a) SUMMARY
b) ARTIFICIAL TEARS
c) TOPICAL CYCLOPLEGIC
d) TOPICAL ANTIBIOTICS
e) PAIN CONTROL

a) SUMMARY
b) ARTIFICIAL TEARS
c) PAIN CONTROL
d) CARBONIC ANHYDRASE INHIBITOR
e) TOPICAL STEROIDS
f) ASCORBATE
g) CITRATE
h) COLLAGENASE INHIBITORS
i) ANTIBIOTICS
j) TOPICAL CYCLOPLEGIC
k) SOFT CONTACT LENSES

a) SURGICAL THERAPY CAUSTIC EYE INJURY

a) 2.4 milligrams/liter is considered to be the upper limit of normal serum oxalate level. In 4 females who ingested an unknown amount of potassium hydrogen oxalate, the one survivor had a serum level of 3.7 milligrams/liter whereas the levels in the 3 fatalities ranged from 18 to 110 milligrams/liter (Houts et al, 1985).

1) Oxalic acid

a) TWA: 1 mg/m(3)
b) STEL: 2 mg/m(3)
c) Ceiling:
d) Carcinogen Listing: (Not Listed) Not Listed
e) Skin Designation: Not Listed
f) Note(s):

a) IDLH: 500 mg/m3
b) Note(s): Not Listed

a) 8-hour TWA:

a) 270 mg/kg

a) 7500 mg/kg
b) 9.5 mL/kg -- 5% solution (Budavari, 1996)
c) Male, 9.5 mL/kg -- 5% solution (Hathaway, 1996)
d) Male, 475 mg/kg -- 5% aqueous solution (Clayton & Clayton, 1994)
e) Female, 7.5 mL/kg -- 5% solution (Hathaway, 1996)
f) Female, 375 mg/kg -- 5% aqueous solution (Clayton & Clayton, 1994)

a) These recommendations may be used in the unlikely event of a primary exposure to oxalic acid.
b) EMESIS - Is not recommended, unless undertaken within minutes of ingestion, due to propensity for the agent to cause gastrointestinal burns and loss of consciousness.
c) ACTIVATED CHARCOAL - Administer activated charcoal. Dose: 2 grams/kilogram per os or via stomach tube. Avoid aspiration by proper restraint, careful technique, and if necessary tracheal intubation.
d) CATHARTIC - Administer a dose of a saline cathartic such as magnesium or sodium sulfate (sodium sulfate dose is 1 gram/kilogram). If access to these agents is limited, give 5 to 15 milliliters magnesium oxide (Milk of Magnesia) per os for dilution.
e) OCULAR - Rinse eyes with copious amounts of tepid water for 15 minutes. If irritation, pain or photophobia persist, see your veterinarian.
f) INHALATION - Move patient to fresh air. Monitor patient for respiratory distress. Emergency airway support and supplemental oxygen with assisted ventilation may be needed. If a cough or difficulty in breathing develops, evaluate for respiratory tract irritation or bronchitis.
g) DERMAL - Wash exposed animals with soap and water. If possible, shave or clip long hair to facilitate thorough cleaning. All handlers should wear gloves and protect themselves from exposure.

1) Begin treatment immediately.
2) Keep animal warm and do not handle unnecessarily.
3) Sample vomitus, blood, urine, and feces for analysis.

1) ASPCA Animal Poison Control Center, An Allied Agency of the University of Illinois, 1717 S. Philo Rd, Suite 36, Urbana, IL 61802, website www.aspca.org/apcc
2) 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.
3) The following 24-hour phone number is available: (888) 426-4435. 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.

1) GENERAL TREATMENT

1) Ongoing treatment is symptomatic and supportive.

1) GENERAL