Toxicosis associated with ingestion of quick-dissolve granulated chlorine in a dog

Aaron S. Hofmeister Department of Veterinary Clinical Sciences, Center for Veterinary Health Sciences, Oklahoma State University, Stillwater, OK 74078

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Johanna C. Heseltine Department of Veterinary Clinical Sciences, Center for Veterinary Health Sciences, Oklahoma State University, Stillwater, OK 74078

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Claire R. Sharp Department of Veterinary Clinical Sciences, Center for Veterinary Health Sciences, Oklahoma State University, Stillwater, OK 74078

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Abstract

Case Description—A dog was referred for treatment after ingestion of quick-dissolve chlorine granules intended for use in a swimming pool.

Clinical Findings—At evaluation 18 hours after ingestion of the granules, the dog had tachypnea, signs of depression, approximately 5% dehydration, oral mucositis, and a productive cough. Increased respiratory tract sounds and wheezes were ausculted in all lung fields. Complete blood count revealed erythrocytosis and lymphopenia. Serum biochemical analyses revealed mildly high activities of hepatic enzymes and creatine kinase. Arterial blood gas concentrations were consistent with hypoxemia and hyperventilation. Thoracic radiography revealed widespread pulmonary alveolar infiltrates predominantly affecting the ventral portions of both lungs, consistent with noncardiogenic pulmonary edema secondary to aspiration of the granulated chlorine.

Treatment and Outcome—Initial treatment included IV administration of an electrolyte solution with supplemental KCl, ranitidine, furosemide, cefotaxime, buprenorphine, and supplemental oxygen. Subsequent treatment included administration of meloxicam and an endoscopically placed percutaneous gastrostomy tube. Endoscopic examination revealed esophagitis and mild gastritis; therefore, metoclopramide and sucralfate were also administered. Fifteen days later, the gastrostomy tube was removed prior to discharge; endoscopic examination revealed grossly normal esophageal and gastric mucosa, and thoracic radiography revealed complete resolution of the lung lesions.

Clinical Relevance—Although ingestion of granulated chlorine is rare in veterinary patients, the resulting disease processes are common and can be treated successfully.

Abstract

Case Description—A dog was referred for treatment after ingestion of quick-dissolve chlorine granules intended for use in a swimming pool.

Clinical Findings—At evaluation 18 hours after ingestion of the granules, the dog had tachypnea, signs of depression, approximately 5% dehydration, oral mucositis, and a productive cough. Increased respiratory tract sounds and wheezes were ausculted in all lung fields. Complete blood count revealed erythrocytosis and lymphopenia. Serum biochemical analyses revealed mildly high activities of hepatic enzymes and creatine kinase. Arterial blood gas concentrations were consistent with hypoxemia and hyperventilation. Thoracic radiography revealed widespread pulmonary alveolar infiltrates predominantly affecting the ventral portions of both lungs, consistent with noncardiogenic pulmonary edema secondary to aspiration of the granulated chlorine.

Treatment and Outcome—Initial treatment included IV administration of an electrolyte solution with supplemental KCl, ranitidine, furosemide, cefotaxime, buprenorphine, and supplemental oxygen. Subsequent treatment included administration of meloxicam and an endoscopically placed percutaneous gastrostomy tube. Endoscopic examination revealed esophagitis and mild gastritis; therefore, metoclopramide and sucralfate were also administered. Fifteen days later, the gastrostomy tube was removed prior to discharge; endoscopic examination revealed grossly normal esophageal and gastric mucosa, and thoracic radiography revealed complete resolution of the lung lesions.

Clinical Relevance—Although ingestion of granulated chlorine is rare in veterinary patients, the resulting disease processes are common and can be treated successfully.

An 11-month-old 7.57-kg (16.6-lb) sexually intact male Jack Russell Terrier was referred to OSUCVHS for treatment after ingestion of 1 mouthful of quick-dissolve chlorine granulesa intended for use in a swimming pool. The dog had ingested the granulated chlorine 18 hours previously, and the owners reported the dog appeared agitated and was coughing and vomiting shortly thereafter. The dog was taken to a local emergency center. Initial blood analyses revealed mild hyperchloremic metabolic acidosis (Cl concentration, 120 mmol/L [reference range, 105 to 115 mmol/L]; total CO2 concentration, 18.0 mmol/L [reference range, 23 to 29 mmol/L]; pH, 7.341 [reference range, 7.35 to 7.45]; HCO3 concentration, 16.9 mmol/L [reference range, 20 to 30 mmol/L]). Thoracic radiography revealed an alveolar pattern in the cranioventral portions of the lung lobes. Initial treatment included IV administration of an electrolyte solutionb (5.9 mL/kg/h [2.68 mL/lb/h] for 8 hours), butorphanol (0.32 mg/kg [0.145 mg/lb], IV, once), metoclopramide (0.43 mg/kg [0.195 mg/lb], IV, once), sucralfate (133 mg/kg [60.6 mg/lb], PO, once), enrofloxacin (3 mg/kg [1.36 mg/lb], IM, once), furosemide (5.3 mg/kg [2.41 mg/lb], IV, once), and supplemental oxygen via oxygen cage.

At evaluation at the OSUCVHS, the dog had signs of depression, tachypnea (72 breaths/min), and dehydration (approx 5%). Oral mucous membranes, tongue, and perioral tissues were hyperemic and appeared inflamed. A productive cough was evident. Increased respiratory sounds and wheezes were ausculted in all lung fields, most prominently over the right cranial and middle lung lobes.

Diagnostic evaluation included CBC, serum biochemical analyses, urinalysis, arterial blood gas measurements, and thoracic radiography. Complete blood count revealed moderate erythrocytosis (Hct, 65.3% [reference range, 33% to 55%]) and moderate lymphopenia (lymphocyte count, 0.36 × 103 cells/mL [reference range, 1.0 to 5.0 × 103 cells/mL]). Serum biochemical analyses revealed mildly high activities of hepatic enzymes (alanine aminotransferase concentration, 142 U/L [reference range, 3 to 69 U/L]; alkaline phosphatase concentration, 419 U/L [reference range, 20 to 157 U/L]) and creatine kinase (concentration, 809 U/L [reference range, 22 to 491 U/L]). Urinalysis revealed no abnormalities. Arterial blood gas concentrations were consistent with hypoxemia and hyperventilation (PaCO2, 31.4 mm Hg [reference range, 34 to 40 mm Hg]; PaO2, 77 mm Hg [reference range, 85 to 100 mmHg]). Blood pH was within reference range. Thoracic radiography revealed widespread pulmonary alveolar infiltrates predominantly affecting the ventral portion of the right and left lungs, normal pulmonary vasculature, and normal cardiac silhouette, consistent with noncardiogenic pulmonary edema secondary to aspiration of the chlorine (Figure 1).

Figure 1—
Figure 1—

Left lateral (A) and dorsoventral (B) radiographic views of the thorax of a dog with hypochlorite toxicosis caused by inhalation and ingestion of chlorine granules. Notice widespread pulmonary alveolar infiltrates that mostly involve the ventral portions of both lungs, consistent with noncardiogenic pulmonary edema.

Citation: Journal of the American Veterinary Medical Association 229, 8; 10.2460/javma.229.8.1266

Initial treatment included IV administration of an electrolyte solutionb with supplemental KClc (total K, 20 mEq/L), ranitidined (2 mg/kg [0.9 mg/lb], IV, q 8 h) to decrease gastric acidity for possible gastritis, furosemidee (2 mg/kg, IV, q 8 h) for pulmonary edema, cefotaximef (22 mg/kg [10 mg/lb], IV, q 8 h) to prevent secondary bacterial infection across eroded gastrointestinal mucosa, and buprenorphineg (0.01 mg/kg [0.005 mg/lb], IV, q 6 h) for analgesia. Supplemental oxygen (fraction of inspired O2, 40 to 60%) was also provided via oxygen cage. Food and water were with-held until the following day, when a baby food–water mixture was offered without success.

On day 3 of hospitalization, abnormal lung sounds were diminished and respiratory effort was markedly improved. Consequently, the furosemide dose was decreased (1 mg/kg [0.45 mg/lb], IV, q 8 h). Serum electrolyte analysis revealed mild hyponatremia and hypochloremia (Na concentration, 134 mmol/L [reference range, 138 to 153 mmol/L]; Cl concentration, 94 mmol/L [reference range, 105 to 117 mmol/L]). Intravenous administration of fluids was changed to 0.9% NaClh solution with supplemental KCl (total K, 20 mEq/L). The dog was still unwilling to eat. Because anorexia was attributed to pain and inflammation, administration of meloxicami (0.05 mg/kg [0.023 mg/lb], IV, once; 0.1 mg/kg [0.045 mg/lb], IV, q 24 h thereafter) was begun.

On day 4 of hospitalization, the dog remained anorexic and a PEG tube was placed. Endoscopic examination revealed mild pharyngeal erythema, inflammation and mild sloughing of ventral lingual mucosa, erythema and irregularity of the proximal one third of the esophagus consistent with esophagitis, and mild gastritis with occasional pinpoint mucosal hemorrhages in the body and pyloric regions. After recovery from anesthesia, oxygen supplementation was discontinued, and a constant rate infusion of metoclopramidej was initiated (1 mg/kg, IV, over 24 hours) to increase tone of the gastroesophageal sphincter and minimize the risk of acid reflux. The dog was not given food or water for 24 hours after PEG tube placement.

On day 5 of hospitalization, results of thoracic auscultation were normal and furosemide administration was discontinued. By use of a commercially available high-calorie diet,k PEG tube feeding was instituted. Water was offered PO. Sucralfatel (133 mg/kg [60.6 mg/lb], PO, q 8 h) was given.

On days 6 and 7, the medications were switched to orally administered formulations. Administrations of meloxicam and buprenorphine were discontinued along with IV administration of fluids. Cefpodoximem (13.5 mg/kg [6.14 mg/lb], via PEG tube, q 24 h) was given until day 10. Administrations of ranitidinen (2.54 mg/kg [1.15 mg/lb], via PEG tube, q 8 h) and metoclopramideo (0.2 mg/kg [0.09 mg/lb], via PEG tube, q 8 h) were continued until discharge on day 15.

On day 15, the dog was anesthetized and the PEG tube removed prior to discharge from the hospital. During endoscopic removal of the feeding tube, the esophageal and gastric mucosa appeared normal. Thoracic radiography on the day of discharge revealed complete resolution of the lung lesions.

Discussion

Hypochlorite salts are used as disinfectants, bleaches, and deodorizers and can be found in various forms in almost every home.1 Laundry bleach is a 5.25% sodium hypochlorite solution.2,3 Powdered formulations used in industry and as swimming pool disinfectants often contain > 50% hypochlorite, usually in the form of the calcium salt.1,4,5 The compound involved in this case contained from 60% to 80% calcium hypochlorite.6

In humans, bleach is the most commonly reported household toxicant, yet ranks tenth in fatalities among poisonings.3 Bleach is an uncommon poison in animals.7,8 To the authors' knowledge, there are no reports of bleach or hypochlorite ingestion in veterinary patients. Poisonings with chlorine gas and lithium toxicosis in dogs receiving water treated with lithium hypochlorite have been reported, but the circumstances and clinical findings in those reports9,10 were markedly different from those in the present report.

Bleaches and granulated hypochlorite salts are potent oxidizers and cause mostly local damage to skin, oral mucous membranes, and mucosal surfaces of the alimentary tract.1,2 Powdered or granulated forms are generally considered more toxic because of the higher concentration of hypochlorite and likelihood of prolonged contact with surfaces.3 However, because of hypochlorite's action as a potent emetic (5 times more potent than syrup of ipecac), much of the ingested substance may be vomited soon after ingestion.1 Therefore, lethality of hypochlorite poisoning is a function of concentration more than dose.1 Because of the quick-dissolve nature and powdered formulation of the product ingested in this case, substantial mucosal damage occurred, although the dog vomited within 10 minutes of ingestion. Although there are no specific clinical signs associated with hypochlorite ingestion, immediate signs include salivation, vomiting, and signs of abdominal pain.4,8 A bleach odor or discoloration of hair around the muzzle may also be detected.4 Chemical burns and erosions of the lips, tongue, and oral mucosa, as well as irritation to mucosal surfaces of the stomach and intestine, can be associated with ingestion of concentrated formulations.7 Mucositis and gastric ulceration were evident in the dog described in this report. Systemic consequences of hypochlorite poisoning such as toxemia, shock, gastrointestinal perforation, and hemorrhage are rare and are generally secondary to severe local injury.1,5 However, hypochlorite forms hypochlorous acid in low-pH environments such as the stomach, and this acidic form can penetrate mucosal surfaces deeply, causing local protein coagulation and increasing the likelihood of systemic effects.1,3,5 Human ingestion of 500 mL of 10% sodium hypochlorite may cause metabolic acidosis and hypernatremia, attributed to systemic absorption of hypochlorous acid and excess sodium.2,3 No systemic effects were seen in the dog of this report. Respiratory effects of hypochlorite toxicosis are generally associated with inhalation of fumes or powders.5 Chemical pneumonitis may cause coughing, retching, dyspnea, wheezing, or stridor, depending on the degree of involvement of the upper portions of the airways.3,5 In the dog reported here, noncardiogenic pulmonary edema secondary to aspiration of the granulated chlorine was evident.

Noncardiogenic pulmonary edema results from altered vascular endothelial permeability in the lungs and can be caused by pulmonary and extrapulmonary processes.11 Inhalation of smoke or toxic gases and aspiration of stomach contents are among the known causes of NPE.12 Noncardiogenic pulmonary edema is often evident radiographically in the caudodorsal region on lateral views and typically causes an interstitial pattern that progresses to mixed interstitial-alveolar or alveolar patterns as was seen in this case. Treatment of NPE involves removal of the inciting cause if possible, oxygen therapy, and fluid replacement to maintain cardiac output and tissue oxygenation. Furosemide given at 2 mg/kg IV or IM every 6 to 8 hours may also be helpful in decreasing NPE. Prognosis for NPE is primarily determined by the underlying cause and therefore can range from excellent to grave.11 In this dog, clinical signs of NPE resolved by day 5, and thoracic radiography revealed complete resolution on day 15.

Management of dogs with hypochlorite ingestion follows guidelines for other caustic agents. Prompt veterinary evaluation is warranted. Induction of emesis is contraindicated.4,7,13 Administration of acidic neutralizing solutions is contraindicated because this increases the generation of hypochlorous acid and may promote tissue penetration.5 Early administration of antacids or milk of magnesia may be beneficial.4,7 Sodium bicarbonate should not be used as an antacid because it causes carbon dioxide production with gastric distention and formation of hypochlorous acid.4 Large volumes of water or milk may be beneficial in diluting any hypochlorite still present in the gastrointestinal tract, and activated charcoal may be administered as an adsorbent.4,13 Because the patient in this case was not brought to the hospital until 18 hours after ingestion, these treatments were not used. Management of hypochlorite ingestion after the acute phase of the intoxication involves supportive or palliative care. Respiratory tract complications should be managed as described. Esophagitis and gastritis may be managed with histamine-2 receptor blockers or proton pump inhibitors.13,14 Sucralfate and metoclopramide may also be of benefit in the management of esophagitis. Sucralfate suspension coats ulcerated esophageal mucosa, and metoclopramide increases gastroesophageal sphincter tone, thereby reducing acid reflux.14 Antimicrobial treatment to prevent secondary bacterial infection may be prudent if erosion or severe irritation of the alimentary tract is suspected.7 Corticosteroids are recommended in the event of severe esophagitis, to prevent stricture formation.4 Because esophageal stricture is considered a very uncommon sequela, corticosteroids may not be necessary.1,3 Corticosteroids were not used in this dog because nonsteroidal anti-inflammatory treatment was begun prior to endoscopic examination.

ABBREVIATIONS

OSUCVHS

Oklahoma State University Center for Veterinary Health Sciences

PEG

Percutaneous endoscopic gastrostomy

NPE

Noncardiogenic pulmonary edema

a.

Arch Chemicals Inc, Stamford, Conn.

b.

Normosol R, Hospira Inc, Lake Forest, Ill.

c.

Abbott Laboratories, North Chicago, Ill.

d.

Zantac, GlaxoSmithKline, Research Triangle Park, NC.

e.

Furoject, Burns Veterinary Supply, Rockville Centre, NY.

f.

Claforan, Aventis Pharmaceuticals NJ, Bridgewater, NJ.

g.

Buprenex, Reckitt Benckiser Pharmaceuticals Inc, Richmond, Va.

h.

Hospira Inc, Lake Forest, Ill.

i.

Metacam, Boehringer Ingelheim Vetmedica Inc, St Joseph, Mo.

j.

Mayne Pharma (USA) Inc, Paramus, NJ.

k.

Eukanuba Maximum-Calorie/Canine & Feline Canned, The Iams Co, Dayton, Ohio.

l.

Carafate, Aventis Pharmaceutical Inc, Kansas City, Mo.

m.

Simlicef, Pharmacia & Upjohn Co, Division of Pfizer Inc, New York, NY.

n.

Zantac, Pfizer Consumer Healthcare, Morris Plains, NJ.

o.

Teva Pharmaceuticals USA, Sellersville, Pa.

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