a) Ammonia ingestion may produce burns to the oropharynx, upper airway, esophagus and occasionally stomach. Spontaneous vomiting may occur. The absence of visible oral burns does NOT reliably exclude the presence of esophageal burns. The presence of stridor, vomiting, drooling, and abdominal pain are associated with serious esophageal injury in most cases.
b) PREDICTIVE: The grade of mucosal injury at endoscopy is the strongest predictive factor for the occurrence of systemic and GI complications and mortality.

a) Remove contaminated clothes and any particulate matter adherent to skin. Irrigate exposed skin with copious amounts of water for at least 15 minutes or longer, depending on concentration, amount and duration of exposure to the chemical. A physician may need to examine the area if irritation or pain persist.

a) CASE SERIES: Three children who accidentally bit into capsule of aromatic ammonia (glass capsule containing a fiber mesh and 0.33 milliliters of 18% ammonia and 36% ethanol) developed burns of the lips and tongue without involvement of the esophagus (Wason et al, 1990). The small volume of liquid contained in these makes esophageal injury unlikely.

a) FIBROSIS: RATS continuously exposed to 470 mg/m(3) of ammonia for 90 days developed myocardial fibrosis (HSDB , 1992).

a) Ammonia exposure may cause bronchospasm, laryngitis, tracheitis, wheezing, dyspnea, cough, hemoptysis, chest pain, cyanosis, and laryngeal stridor (Boyd et al, 1944; Caplin, 1941; Helmers et al, 1971; Birken et al, 1981; Kocks & Scott, 1990).

a) MUCOSAL BURNS: Inhalation of (concentrated) ammonia vapors may cause mucosal burns to the tracheobronchial tree (Close et al, 1980; Millea et al, 1989).
b) CASE REPORT: A 28-year-old man developed pharyngeal and laryngeal edema and severe tracheobronchial burns after exposure to high concentrations of anhydrous ammonia (Leduc et al, 1992). He developed dyspnea, chest tightness and copious bronchial secretions and expectorated a large cast of burned tracheobronchial mucosa.

a) Inhalation of vapors from household ammonia (5% to 10% ammonia) is irritating to the eyes and upper respiratory tract (Ziarnik et al, 1986).
b) CASE SERIES: Volunteers exposed to ammonia vapor for 2 hours at concentrations of 50, 80, 110, and 140 ppm experienced no effects on ventilatory capacity or 1-second expiratory and inspiratory volumes. Half of the volunteers found irritation from 140 ppm so severe that they terminated exposure prematurely (Clayton & Clayton, 1993).
c) CASE SERIES: Volunteers exposed to 35 mg/m(3) for 5 minutes reported no irritation of the eyes, nose, throat, or chest (Clayton & Clayton, 1993).
d) CASE REPORT: A 5-minute exposure to 94 mg/m(3) caused chest irritation in 1 volunteer (Clayton & Clayton, 1993).

a) Pulmonary edema, bronchiectasis, and hypoxemia may occur following exposure to concentrated ammonia vapors (Boyd et al, 1944; Caplin, 1941; Hathaway et al, 1996; Levy et al, 1964; Kocks & Scott, 1990) (Sittig, 1991).
b) CASE REPORT: A 69-year-old woman developed aspiration pneumonitis and severe corrosive injury to the esophagus and upper airway after swallowing an unknown amount of household ammonia (Klein et al, 1985). She developed non-cardiogenic pulmonary edema and died several days after ingestion.

a) An initial phase of pulmonary edema, congestion, hemorrhage, and atelectasis may be followed by apparent clinical improvement after 48 to 72 hours, followed by gradual onset of airway obstruction and respiratory failure (Arwood et al, 1985).

a) CASE REPORT: A 41-year-old man, who was a Jehovah's Witness, developed severe respiratory distress following exposure to anhydrous ammonia after an explosion occurred at his job. He presented with second degree burns to his face, neck, and upper chest, and corneal damage. An initial bronchoscopy showed diffuse erythema of his airway and fibrinous exudates. During his hospital course, he developed bilateral deep venous thromboses and bilateral pulmonary emboli, despite prophylactic anticoagulation with warfarin. Following successful decannulation after a prolonged period of mechanical ventilation, dyspnea on exertion continued to persist, and pulmonary function tests determined the development of chronic obstructive pulmonary disease. Despite supportive care and intensive pulmonary rehabilitation, the patient's condition continued to deteriorate and a double-lung transplant was indicated. Due to his religious practices, he underwent a double-lung transplant without the use of blood products. His lung transplant appeared to be successful, with pulmonary function tests showing significant improvement, and an improvement in the patient's quality of life (Ortiz-Pujols et al, 2014).

a) VENTILATORY AND DIFFUSION ABNORMALITIES: Chronic exposure in workers may lead to initial complaints of chronic cough, dyspnea on effort, bilateral infiltrates on chest x-ray, and lung function indices reflecting ventilatory and diffusion abnormalities (Proctor et al, 1988). After three years away from ammonia exposure, some workers have had persistent evidence of pulmonary damage (Finkel, 1983; Proctor et al, 1988)

a) CHRONIC TOXICITY

a) CHRONIC TOXICITY
b) BRONCHOSPASM

a) CASE REPORT: Direct exposure to an ammonia solution caused chemical pneumonitis (Clayton & Clayton, 1993).
b) AMMONIA/HYPOCHLORITE: The mixture of ammonia and hypochlorite bleaches results in formation of chloramines, which produce a toxic pneumonitis following inhalation, and may produce residual pulmonary function abnormalities (Reisz & Gammon, 1986; Faigel, 1964; Gapany-Gapanavicius et al, 1982).

a) Death can result from exposure to 5000 ppm from laryngospasm, inflammation, or laryngeal edema.

a) During controlled human exposures at approximately 500 ppm for 30 minutes, irregular minute ventilation with a cyclic pattern of hyperpnea has been noted (HSDB , 2001).

a) OBSTRUCTIVE PULMONARY DISEASE has been reported.

a) Exposure of experimental animals to ammonia at 7000 mg/m(3) for 1 hour resulted in death in approximately 50% of the animals.

a) An altered mental status, including coma may occur and is probably secondary to hypoxia from ammonia-induced respiratory injury.

a) If there is extensive absorption, hypertonus and convulsions may occur (HSDB , 2001).

a) Encephalopathy was observed in 3 of 8 patients receiving glycine irrigation following transurethral prostatectomy (Shepard et al, 1987).

a) PIGS: One pig exposed to 280 ppm of ammonia had convulsions after 36 hours of exposure, which continued for 3 hours after exposure had ended (HSDB , 1992).

a) Irritant effects including nausea, vomiting, burning sensation. Swelling of the lips, mouth, and larynx have been reported.

a) Oral and esophageal burns may occur with swallowed household ammonia, particularly if ingestion is deliberate. Esophageal burns were reported in three adults who ingested household ammonia products (containing 3% to 3.6% ammonia at a pH of 11.5 to 11.8) in suicidal attempts (Klein et al, 1985).
b) CASE SERIES: Ingestion of milk contaminated with 530 to 1524 ppm ammonia (pH 9 to 10) in 20 children resulted in nausea and severe burning of the mouth and throat (Ziarnik et al, 1986).

a) Ingestion of concentrated ammonia may produce ulcerative esophagitis with late strictures (Gossot et al, 1990).
b) Gastric, duodenal, and jejunal stenosis have also resulted. Unrecognized late strictures may be confused with malignant growths (O'Donnell et al, 1949); (Cardona & Daly, 1964).

a) CASE REPORT: Severe gastritis has been reported following a sudden and massive inhalation of ammonia. Symptoms included abdominal pain, and nausea (Dupuy et al, 1968).

a) Oral and esophageal burns or esophageal and gastric perforation within 24 to 72 hours leading to mediastinitis have been reported.

a) CASE REPORT: Hyperamylasemia was reported in 2 fatal cases of industrial ammonia liquid inhalation (Arwood et al, 1985).

a) FOOD POISONING: An outbreak of gastrointestinal illness occurred after students were served chicken tenders that were contaminated with ammonia. Onset of illness was within 180 minutes of eating lunch. Symptoms included stomachache in 82%, headache in 61%, nausea in 41%, and vomiting in 23% of the children. A warehouse leak of ammonia refrigerant was the cause of the contamination. Levels as high as 2,468 ppm were detected in the uncooked chicken tenders (Dworkin et al, 2004).

a) Guinea pigs were exposed to approximately 170 ppm of ammonia for 6 hours/day, 5 days a week, for 18 weeks; congestion of the liver was seen at autopsy (HSDB , 1992).

a) Urinary retention may occur after acute inhalation exposure (HSDB , 2001).

a) Rats exposed to 470 mg/m(3) of ammonia for 90 days developed calcification and epithelial proliferation of the renal tubules (HSDB , 1992).

a) Guinea pigs were exposed to approximately 170 ppm of ammonia for 6 hours/day, 5 days a week, for 18 weeks; congestion of the kidneys and degenerative changes in the suprarenal glands were seen at autopsy (HSDB , 1992).

a) The effects of the addition of ammonia into tissue cultures in bovine blood during clinical and subclinical urea toxicosis were studied. Approximately 30% of the bovine lymphocytes were killed by ammonia during 72 hours of incubation (HSDB , 1992).

a) Skin and eye exposure cause vesiculation and corrosive burns which feel soapy due to saponification of fat in the tissue (Dalton & Bricker, 1978). Ammonia acts as an alkali, producing liquefaction necrosis, deep penetrating burns, and scarring (Cordona & Daly, 1964; (Chassin & Slattery, 1953).
b) Extensive burns of the face and mouth occurred following direct exposure to an ammonia solution (Clayton & Clayton, 1993).
c) Less severe skin injury may appear as grey-yellow, soft regions (Millea et al, 1989). More severe skin injury may appear as black, leathery tissue (Millea et al, 1989; Birken et al, 1981).

a) Hives and urticaria have been reported (HSDB , 1992).

a) Exposure to anhydrous ammonia stored at minus 28 degrees F may produce frostbite injury with thrombosis of surface vessels and subsequent ischemia and necrosis (Millea et al, 1989; AAR, 1987).

a) CHRONIC EXPOSURE: Dermatitis has been reported in chronically exposed workers (Andanson et al, 1976).

a) Adrenocortical system changes were investigated in an enclosed atmosphere; the most pronounced changes were noted when the ammonia content was 5 mg/m(3) (HSDB , 2001).

a) Results of a study in steers suggested that the hyperglycemia observed during hyperammonemia may result from an under-utilization of glucose by insulin-sensitive tissues (Fernandez et al, 1988).

a) A serum concentration of 1,000 to 10,000 mcg/dL is considered toxic.

a) Monitor pulse oximetry or arterial blood gases in patients with signs and symptoms suggestive of upper airway burns.
b) Endoscopy is recommended following ingestions in symptomatic patients or those swallowing large amounts or solutions with high concentrations of ammonia.

a) In a survey of the POISINDEX(R) editorial board (Consensus, 1988), 7 of 10 members routinely recommended dilution, provided that no airway compromise was present. Two other members expressed concern that dilution might precipitate vomiting, but this was not the experience of other members.

a) In a series of 22 cases of corrosive ingestions, 4 of 7 patients treated with dilution vomited. None of the 15 patients not given fluids vomited. One patient suffered severe consequences following vomiting after 6 ounces of milk. A 3-year-old child died after one glass of milk caused vomiting (Honcharak & Marcus, 1989).

a) Swallowed milk may obscure esophagoscopy (Howell, 1987), but is not a problem with equipment containing water irrigation attachments. Maull (1985) found water to be an ineffective diluent in vitro. Other in vitro work has demonstrated efficacy of milk or water (Rumack & Burrington, 1977).

a) The amount of diluent recommended by the POISINDEX(R) editorial board varied widely, ranging from 2 to 12 ounces in adults and 1 to 8 ounces in children. The majority recommended a maximum amount of 8 ounces in adults and 4 ounces in children (Consensus, 1988).

a) SEIZURE CONTROL: Is mandatory prior to gastric emptying.
b) AIRWAY PROTECTION: Alert patients - place in Trendelenburg and left lateral decubitus position, with suction available. Obtunded or unconscious patients - cuffed endotracheal intubation. COMPLICATIONS:

a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)

a) REFERENCES: (Dogan et al, 2006; Symbas et al, 1983; Crain et al, 1984a; Gaudreault et al, 1983a; 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)

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 study of 11 children with deep circumferential esophageal burns after caustic ingestion, insertion of a silicone rubber nasogastric tube for 5 to 6 weeks without steroids or antibiotics was associated with stricture formation in only one case (Wijburg et al, 1989).

a) STUDY - In a retrospective study of patients with extensive transmural esophageal necrosis after caustic ingestion, all 4 patients treated in the conventional manner (esophagoscopy, 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).

a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)

a) Corneal fluorescein staining and slit lamp examination are highly recommended after splash contact with household ammonia.

a) Topical antibiotics for minor damage and topical steroids for more serious epithelial damage may be required (Beare et al, 1988).

a) Cycloplegic or mydriatic agents may decrease the discomfort and help to prevent synechiae (Millea et al, 1989).
b) Topical steroids may be useful to reduce the inflammation (Levy et al, 1964).

a) Rewarming of a localized area should only be considered if the risk of refreezing is unlikely. Avoid rubbing the frozen area which may cause further damage to the area (Grieve et al, 2011; Hallam et al, 2010).

a) Do not institute rewarming unless complete rewarming can be assured; refreezing thawed tissue increases tissue damage. Place affected area in a water bath with a temperature of 40 to 42 degrees Celsius for 15 to 30 minutes until thawing is complete. The bath should be large enough to permit complete immersion of the injured part, avoiding contact with the sides of the bath. A whirlpool bath would be ideal. Some authors suggest a mild antibacterial (ie, chlorhexidine, hexachlorophene or povidone-iodine) be added to the bath water. Tissues should be thoroughly rewarmed and pliable; the skin will appear a red-purple color (Grieve et al, 2011; Hallam et al, 2010; Murphy et al, 2000).
b) Correct systemic hypothermia which can cause cold diuresis due to suppression of antidiuretic hormone; consider IV fluids (Grieve et al, 2011).
c) Rewarming may be associated with increasing acute pain, requiring narcotic analgesics.
d) For severe frostbite, clinical trials have shown that pentoxifylline, a phosphodiesterase inhibitor, can enhance tissue viability by increasing blood flow and reducing platelet activity (Hallam et al, 2010).

a) Digits should be separated by sterile absorbent cotton; no constrictive dressings should be used. Protective dressings should be changed twice per day.
b) Perform twice daily hydrotherapy for 30 to 45 minutes in warm water at 40 degrees Celsius. This helps debride devitalized tissue and maintain range of motion. Keep the area warm and dry between treatments (Hallam et al, 2010; Murphy et al, 2000).
c) The injured extremities should be elevated and should not be allowed to bear weight.
d) In patients at risk for infection of necrotic tissue, prophylactic antibiotics and tetanus toxoid have been recommended by some authors (Hallam et al, 2010; Murphy et al, 2000).
e) Non-tense clear blisters should be left intact due to the risk of infection; tense or hemorrhagic blisters may be carefully aspirated in a setting where aseptic technique is provided (Hallam et al, 2010).
f) Further surgical debridement should be delayed until mummification demarcation has occurred (60 to 90 days). Spontaneous amputation may occur.
g) Analgesics may be required during the rewarming phase; however, patients with severe pain should be evaluated for vasospasm.
h) IMAGING: Arteriography and noninvasive vascular techniques (e.g., plain radiography, laser Doppler studies, digital plethysmography, infrared thermography, isotope scanning), have been useful in evaluating the extent of vasospasm after thawing and assessing whether debridement is needed (Hallam et al, 2010). In cases of severe frostbite, Technetium 99 (triple phase scanning) and MRI angiography have been shown to be the most useful to assess injury and determine the extent or need for surgical debridement (Hallam et al, 2010).
i) TOPICAL THERAPY: Topical aloe vera may decrease tissue destruction and should be applied every 6 hours (Murphy et al, 2000).
j) IBUPROFEN THERAPY: Ibuprofen, a thromboxane inhibitor, may help limit inflammatory damage and reduce tissue loss (Grieve et al, 2011; Murphy et al, 2000). DOSE: 400 mg orally every 12 hours is recommended (Hallam et al, 2010).
k) THROMBOLYTIC THERAPY: Thrombolysis (intra-arterial or intravenous thrombolytic agents) may be beneficial in those patients at risk to lose a digit or a limb, if done within the first 24 hours of exposure. The use of tissue plasminogen activator (t-PA) to clear microvascular thromboses can restore arterial blood flow, but should be accompanied by close monitoring including angiography or technetium scanning to evaluate the injury and to evaluate the effects of t-PA administration. Potential risk of the procedure includes significant tissue edema that can lead to a rise in interstitial pressures resulting in compartment syndrome (Grieve et al, 2011).
l) CONTROVERSIAL: Adjunct pharmacological agents (ie, heparin, vasodilators, prostacyclins, prostaglandin synthetase inhibitors, dextran) are controversial and not routinely recommended. The role of hyperbaric oxygen therapy, sympathectomy remains unclear (Grieve et al, 2011).
m) CHRONIC PAIN: Vasomotor dysfunction can produce chronic pain. Amitriptyline has been used in some patients; some patients may need a referral for pain management. Inability to tolerate the cold (in the affected area) has been observed following a single episode of frostbite (Hallam et al, 2010).
n) MORBIDITIES: Frostbite can produce localized osteoporosis and possible bone loss following a severe case. These events may take a year or more to develop. Children may be at greater risk to develop more severe events (ie, early arthritis) (Hallam et al, 2010).

1) Ammonia

a) TWA: 25 ppm (18 mg/m(3))
b) STEL: 35 ppm (27 mg/m(3))
c) Ceiling:
d) Carcinogen Listing: (Not Listed) Not Listed
e) Skin Designation: Not Listed
f) Note(s):

a) IDLH: 300 ppm
b) Note(s): Not Listed

a) 8-hour TWA:

a) 4837 ppm for 1H (Lewis, 2000a)

a) 350 mg/kg (Lewis, 1992a)

a) 112,000 mg/m(3) for 15M (RTECS, 2005)
b) 71,900 mg/m(3) for 30M (RTECS, 2005)
c) 4840 mg/m(3) for 60M (RTECS, 2005)

a) 20 ppm -- ulcerated nasal septum, conjunctive irritation, change in trachea or bronchi (RTECS, 2005)
b) 40 mg/m(3) -- conjunctive irritation, cough, respiratory depression (RTECS, 2005)
c) 3 mg/m(3) for 8H -- change in heart rate, respiratory depression (RTECS, 2005)
d) 1200 mg/m(3) -- acute pulmonary edema, cough, dyspnea (RTECS, 2005)

a) 1000 mg/kg (ITI, 1995)

a) All mammalian species are susceptible to ammonia poisoning, and have similar susceptibility to poisoning by ammonium salts.

a) Ruminants are more susceptible to ammonia toxicosis from urea than other forms of NPN because the rumen contains the urolytic enzyme urease. The enzyme catalyzes the hydrolysis of urea, hastening the liberation of ammonia (Haliburton et al, 1989).
b) Non-protein-nitrogen toxicosis usually results from improper mixing of NPN into feed; error in calculations or formulations of rations; inadequate period of adaptation to NPN; NPN rations deficient in energy, low in protein and high in fiber; and unrestricted consumption of liquid NPN supplements (Haliburton et al, 1989).
c) Within 10 minutes to 4 hours following the ingestion of excess urea or other NPN sources, animals may exhibit frothy salivation, depression, hyperirritability, grinding of teeth, abdominal pain, increased defecation, and polyuria. Animals may appear blind. Muscle tremors, incoordination, increased respiratory rate and general weakness are commonly seen (Beasley et al, 1989).
d) Ruminants may show signs of mild toxicosis following ingestion of 0.3 to 0.5 gram of urea or ammonium salts/kg body weight (Beasley et al, 1989).
e) Signs appear when rumen ammonia and blood ammonia concentrations exceed 80 mg/100 mL and 2 mg/100 mL, respectively. Bloat and regurgitation of rumen contents may occur especially in sheep. Recumbency, hyperthermia, cyanosis, anuria and seizures are common terminal signs (Beasley et al, 1989).
f) The pathological changes associated with ammonium or ammonium salt poisoning include: pulmonary edema; large hemorrhagic patches on the mucous membranes of the stomach and intestines; edema and ulceration of the intestinal mucous membranes; enlarged, pale, friable liver; petechiae in the skin; hemorrhages on the surfaces of kidneys and epicardium; and degenerative changes in the central nervous system (Humphreys, 1988).
g) Some predisposing factors for ammonia toxicosis in ruminants include: fasting; high roughage diets; lack of adaptation to high NPN diets; high ruminal pH; high rumen and body temperature; dehydration or low water intake; and hepatic insufficiency (Osweiler et al, 1985).
h) The ruminant needs as much as several days to adapt fully to incorporation of additional ammonia into microbial protein (Osweiler et al, 1985).

a) Monogastric animals, such as the pig and baby calf, are unaffected by oral ingestion of urea except for a transient diuretic action (Osweiler et al, 1985).

a) Administration of 1 mole of acetic acid per mole of urea at 15 minutes, and 1 mole per mole 180 minutes after giving 0.44 gram/kilograms body weight of urea resulted in the survival of 28 of 29 pregnant cows (Humphreys, 1988).
b) LAVAGE - Rumen lavage via a rumenotomy incision or trochar is believed by some to be superior to cold water and acetic acid (Beasley et al, 1989).

a) As little as 50 grams can cause poisoning in cattle not accustomed to it. Slowly increasing the urea content of the feed can allow bullocks to tolerate as much as 400 grams/day without ill effects (Humphreys, 1988).

a) Feed tag states that the feed contains 70% crude protein with 10% from soybean meal and the remaining 60% as protein equivalent from NPN sources. 60% x 0.34 = 20.4% urea content.
b) One kilogram would contain 204 grams urea -- enough to poison a 200 to 400 kilogram animal if rapidly ingested (Beasley et al, 1989).

a) Horses are of intermediate susceptibility to poisoning by urea. Doses of 4 grams/kilogram of urea and 1.4 grams/kilogram of ammonium salts may cause death (Beasley et al, 1989).
b) Ammonia toxicosis was produced in ponies by feeding one pound of urea (Robinson, 1987).
c) Minimum lethal dose is greater than or equal to 4 grams/kilogram (Howard, 1986).

a) The concentration of ammonia in the atmosphere in poultry houses should not exceed 30 parts per million (Humphreys, 1988).

1) Treatment is only effective if given within 20 to 30 minutes after the appearance of clinical signs. Recumbent animals almost never respond. Treatment should involve the use of weak acid as a chemical antidote, demulcents, and stimulants.

1) Ongoing treatment is symptomatic and supportive.

1) GENERAL

a) CATTLE
b) HORSE
c) CAT

1) Clinical signs and history of acute illness after ingestion of urea or other NPN sources
2) Chemical analysis of suspect feed, rumen fluid, jugular whole blood or serum are necessary for a definitive diagnosis.
3) Blood ammonia values ranging from 1 to 4 mg/100 ml and rumen values greater than 80 mg/100 ml are compatible with a diagnosis of ammonia toxicosis.
4) Samples of blood and urine should be collected immediately after death and frozen if tests cannot be done in 1 hour.
5) Significant increases in hematocrit, blood ammonia, blood glucose, BUN, serum potassium and phosphorus, rumen pH, rumen ammonia, and SGPT are commonly seen. Blood pH and urine production are decreased (Beasley et al, 1989).

1) For ammonia analysis the following specimens are required: whole blood or serum - 5 mL; rumen contents (composite) - 100 gm; or urine - 5 mL. These samples should be frozen or have 1 to 2 drops of saturated HgCl2 added (Howard, 1986).
2) Analysis of free ammonia in whole blood, rumen fluid, vitreous fluid and cerebrospinal fluid can be used for confirmation of ammonia toxicosis when the specimens are collected and stored properly (Haliburton et al, 1989).
3) Normal blood and vitreous ammonia concentrations in cattle are less than 0.5 mg/dL. Clinical signs are seen at blood ammonia concentrations of 1 mg/dL while death is associated with blood and vitreous ammonia concentrations of 2 mg/dL or greater (Haliburton et al, 1989).

1) Toxicosis from organochlorine or organophosphorus insecticides, cyanide, protein or grain engorgement, enterotoxemia, meningitis and encephalitis
2) Rumen pH values should help differentiate these disorders.

1) Is a CNS syndrome reported in cattle after ingestion of higher quality ammoniated forages, ammoniated molasses and molasses-urea-protein blocks.
2) CLINICAL SIGNS - Cows and/or calves nursing affected cows exhibit a sudden onset of hyperexcitability, wild running, circling, seizures, and often death. The only lesions found are from trauma.
3) TREATMENT - None
4) DIAGNOSIS - History of ingestion of ammoniated feed, clinical signs, no lesions, identification of 4-MI in feedstuffs.