Toxicology Brief: Sodium hypochlorite bleach ingestion in two dogs

Typically, sodium hypochlorite bleach ingestion causes caustic gastrointestinal tract injury in animals and people. In people, severe clinical illness and death are rare.1,2 To date, there have been no published case reports regarding sodium hypochlorite bleach ingestion in animals.

In this case report, two dogs ingested an unknown volume of Clorox Regular-Bleach (The Clorox Company) containing 6.15% sodium hypochlorite and subsequently developed marked hypernatremia and hyperchloremia as well as numerous other biochemical abnormalities. Ultimately, the dogs were euthanized because of the severity of their clinical signs from the toxicosis.

CASE HISTORY

A 13-year-old 35.2-lb (16-kg) spayed female Shar-Pei and a 5-year-old 39.6-lb (18-kg) castrated male mixed-breed dog were presented to the Texas Veterinary Medical Center at Texas A&M University for evaluation of an acute onset of vomiting, diarrhea, and ataxia. The dogs had been housed in a kitchen and laundry area for about six hours before the owner returned home and found both dogs in distress. Multiple areas of vomit and diarrhea and copious amounts of clear fluid were found on the floor along with a severely chewed and punctured empty bleach bottle near the dogs. The owner transported the dogs to the Texas Veterinary Medical Center shortly after she discovered the situation.

The owner reported that she frequently used empty plastic milk jugs as toys for the dogs, and they likely had mistaken the bleach bottle for a toy. The owner estimated that the 2.83-L bottle of bleach had been about 75% (2.12 L) full before being damaged. The owner stated that there was no evidence that the animals had been exposed to any other potentially toxic material.

Clinical and laboratory findings

On presentation, both dogs were poorly responsive and hypothermic (94 F [34.4 C]). The female dog was laterally recumbent, and the male dog was markedly ataxic. Both dogs vomited clear-yellow, foamy fluid during their physical examinations, and their skin and coats were damp and smelled of urine and bleach. The female was also salivating excessively and had a green, mucoid nasal discharge.

Both dogs had a respiratory rate of 16 to 20 breaths/min with shallow, labored breathing. The male dog had a heart rate of 150 beats/min with tacky mucous membranes and a slightly prolonged capillary refill time. The female dog had a heart rate of 100 beats/min with a normal capillary refill time. No obvious oral lesions were observed.

Venous blood samples were obtained for a complete blood count (CBC) and a serum chemistry profile in both dogs and a coagulation profile in the female dog. The CBC results revealed an elevated calculated hematocrit in the female and a high normal calculated hematocrit in the male (Table 1). There was a moderate discrepancy between the calculated hematocrit and spun hematocrit in the female and a mild discrepancy between the calculated hematocrit and spun hematocrit in the male. A decreased mean corpuscular hemoglobin concentration (MCHC) and a high or high normal mean corpuscular volume (MCV) were noted in both dogs.

Table 1: Selected Complete Blood Count Results

The coagulation profile in the female dog revealed a mild increase in prothrombin time and a marked increase in the D-dimer concentration (Table 2).

Table 2: Selected Coagulation Profile Results

The female dog had severely elevated sodium and chloride concentrations (Table 3). The anion gap was moderately elevated, with a marked decrease in the enzymatic carbon dioxide concentration. The blood urea nitrogen (BUN) concentration was mildly elevated, and the creatinine concentration was at the high end of the reference interval. The female dog's magnesium, phosphorus, glucose, and calcium concentrations were also elevated. A moderate hypocholesterolemia was also observed.

Table 3: Serum Chemistry Profile Results

In the male dog, the serum sodium, chloride, BUN, creatinine, and magnesium concentrations were elevated, as were the alanine transaminase and alkaline phosphatase activities and the anion gap (Table 3). Decreased calcium, total protein, and enzymatic carbon dioxide concentrations were also present.

Treatment, radiographic examination, and outcome

The dogs were admitted to the intensive care unit, and flow-by oxygen was administered. Initial intravenous fluid therapy consisted of boluses of warmed lactated Ringer's solution. The animals were dried and placed under warm-air circulating blankets to treat the hypothermia. Initial gastroprotectant therapy was limited to intravenous famotidine because of continued vomiting episodes.

Thoracic and abdominal radiographic examination of the female dog revealed interstitial and peribronchial infiltrates in the right middle and cranial lung lobes, with distention of the stomach and small intestines by a mixture of fluid and air. These findings were consistent with severe gastroenteritis and pneumonia. Since pulmonary complications resulting from bleach aspiration are reported to contribute to death in people,3 aspiration of bleach or vomitus was given primary consideration as a cause of the pulmonary radiographic abnormalities.

Despite continued treatment with fluid therapy and anti-inflammatory doses of intravenous dexamethasone in both dogs and intravenous calcium supplementation in the male dog, the animals continued to clinically deteriorate. The female dog remained hypothermic and developed profuse, watery diarrhea; its neurologic status declined to a borderline comatose state, and its breathing became progressively labored. The male dog also developed increased respiratory effort, and it remained severely ataxic, though its temperature did improve to 97 F (36.1 C). A marked decrease in urine production was noted in the male, and a urinary catheter was placed. The development of oliguria despite aggressive fluid therapy was concerning for acute renal failure.

Both animals were euthanized less than 12 hours after admission. The owner declined a request to perform necropsies on the dogs.

DISCUSSION

To our knowledge, this is the first report of sodium hypochlorite bleach ingestion in animals. Although no specific reports were found, most veterinary toxicology books associate bleach ingestion with varying degrees of caustic injury to the gastrointestinal tract and possibly secondary respiratory or ocular lesions due to irritation from chemical fumes.2 Death from ingestion of bleach or other hypochlorite-containing products also has not been reported in animals. A case involving calcium hypochlorite ingestion in a dog was recently reported, but severe systemic involvement was not observed and the dog survived.4

Toxic dose

The clinical outcome of sodium hypochlorite bleach toxicosis in people is often determined by the concentration of sodium hypochlorite in the product and the volume ingested.1,2 Sodium hypochlorite concentrations vary considerably depending on the type of product. For example, some household products may contain < 3%, while industrial products may contain up to 15%. Other related compounds containing hypochlorite salts, such as swimming pool products, may contain up to 50% hypochlorite.2

Clorox Regular-Bleach contains 6.15% (weight/volume) sodium hypochlorite and < 1% sodium hydroxide. The sodium hypochlorite concentration in this product is approximately 61.5 mg/ml. Sodium hypochlorite contains 31% sodium and 48% chloride by weight, equivalent to approximately 19.1 mg/ml of sodium and 30 mg/ml of chloride.

While fatalities in people are rare, they have occurred in adults who ingested as little as 250 to 500 ml of bleach at higher concentrations (e.g. 12.5% sodium hypochlorite).3 It should be noted that bleach ingestion in adults is often associated with intentional poisoning (suicide), and death may be hastened by the consumption of other toxins, chemicals, or pharmacologic agents.1,3 In children, death may occur with smaller doses, but the exact amount ingested is often unknown. Defining a lethal dose in people is difficult since there are few cases in the literature, sodium hypochlorite concentrations in bleach vary, and cases of intentional poisonings may involve multiple toxins.

In this case, the exact volume of bleach ingested by each animal was unknown since copious amounts of clear fluid were noted in multiple areas near the dogs on initial discovery. This fluid may have been bleach, urine, or a mixture of both. Also, the fluid on the skin and coat of both dogs smelled like urine and bleach. It was speculated that each dog ingested at least several hundred milliliters of the estimated 2.12 L in the bottle.

While a lethal dose of sodium hypochlorite in dogs is not established in the veterinary literature, extrapolation from a reported lethal dose of sodium chloride of 3.7 g/kg in dogs may be considered.5 For example, a 40-lb (18-kg) dog would have to ingest about 67 g of sodium chloride to attain this lethal dose. The consumption of 1 L of 6.15% sodium hypochlorite bleach containing 19.1 mg/ml of sodium and 30 mg/ml of chloride would equal the ingestion of 49.1 g of sodium chloride. Assuming the animals only ingested several hundred milliliters of bleach, this amount would not have been sufficient to attain the lethal dose of sodium chloride. However, corrosive injury to the gastrointestinal tract and the development of other metabolic derangements and secondary complications, such as aspiration pneumonia, likely contributed to the severity of the toxicosis. Therefore, it is reasonable to suspect that ingestion of at least several hundred milliliters of bleach resulted in the severe morbidity of these dogs, which led to their euthanasia.

Toxic effects

The severe metabolic derangements and complications noted in these two dogs are comparable to those that occur in fatal cases in people.

Increased serum osmolality. A common finding in fatal cases of sodium hypochlorite bleach ingestion in people is altered consciousness resulting from acute elevations of serum sodium concentrations and osmolality.1 These elevations may cause central nervous system lesions such as intracranial hemorrhage, cerebral edema, and cerebral or cerebellar herniation.1

The calculated serum osmolality for these dogs was approximately 391 mOsm/L in the female and 340 mOsm/L in the male (reference interval = 290 to 310 mOsm/L). Both animals were poorly responsive, which was attributed to the acute hypernatremia and elevated osmolality. In addition, the hypernatremia likely initiated the shifting of solutes within the erythrocytes in an attempt to equilibrate with the hypertonic plasma. When the erythrocytes were exposed to the isotonic diluent used by the hematology analyzer, cell swelling resulted in the detection of an increased MCV (macrocytosis), a decreased MCHC (hypochromasia), and a higher calculated hematocrit.

In dogs, macrocytosis and hypochromasia are most commonly associated with a regenerative anemia, which would be unexpected in this case since both dogs had either a high normal or an elevated hematocrit. Cell swelling may also explain the discrepancies noted between the calculated and spun hematocrit in our patients since the hematology analyzer calculates the hematocrit based on the measured MCV value and the red blood cell count. In this case, an artifactual elevation of the MCV due to in vitro red blood cell swelling would have led to an increase in the calculated hematocrit. The spun hematocrit for both animals was in the high normal range, which was attributed to dehydration.

Hemostatic abnormalities. The slight elevation of the prothrombin time and markedly elevated D-dimer concentration in the female may have indicated developing hemostatic abnormalities and fibrinolysis associated with disseminated intravascular coagulation, given the severity of the dog's clinical condition.

Hypernatremia and hyperchloremia. Hypernatremia is a biochemical abnormality classically associated with an increase in the ratio of total body sodium to total body water. Hypernatremia may develop in conditions resulting in inadequate water intake, pure water loss, or water loss in excess of sodium.6 Hypernatremia may also develop as the result of excessive intake of sodium (e.g. large amounts of sorbitol and glycol products such as paintball pellets, homemade play dough, salt water) or decreased renal excretion.5,7 The high concentrations of both sodium and chloride in the bleach coupled with dehydration likely resulted in the moderate to marked serum elevations of these electrolytes in our patients.

The elevated anion gap hyperchloremic metabolic acidosis identified in the dogs was likely caused by multiple factors. It was partially attributed to a developing lactic acidosis, which is also observed in people who have consumed large quantities of sodium hypochlorite bleach.1 The accumulation of uremic acids from developing renal insufficiency may also have contributed to the elevated anion gap metabolic acidosis in these dogs. In addition to supplying large amounts of sodium and chloride, ingested sodium hypochlorite initiates chemical reactions that result in the perpetuation of hyperchloremia, consumption of bicarbonate, and development of a hyperchloremic metabolic acidosis (Figure 1).1 Further, the high serum chloride concentrations may promote urinary excretion of bicarbonate through direct ion exchange mechanisms in the kidney.1,8 The high chloride content in the intestinal fluid may also interfere with exchange mechanisms at the intestinal luminal membrane, resulting in bicarbonate loss,1,9 which is further exacerbated by diarrhea.

Figure 1. Ingestion of sodium hypochlorite initiates chemical reactions that result in the perpetuation of hyperchloremia, consumption of bicarbonate, and development of a hyperchloremic metabolic acidosis.

Additional biochemical abnormalities. The dogs' elevated BUN, creatinine, phosphorus, and magnesium concentrations were all consistent with renal insufficiency, particularly given the development of oliguria in the male dog despite aggressive fluid therapy. However, urine was not obtained for a complete urinalysis, and a combination of renal azotemia with a prerenal component due to dehydration was likely. The elevated BUN concentrations may have also partially been the result of hemorrhage into the gastrointestinal tract since bleach ingestion has been associated with erosive lesions in the oropharynx, esophagus, and stomach from the product's caustic nature and alkalinity (pH of about 11.4).2

The female's hyperglycemia was attributed to a stress response. The alterations in the calcium concentrations in the dogs were particularly perplexing (i.e. hypercalcemia in the female and hypocalcemia in the male). The underlying cause for these abnormalities was not readily apparent, and alterations of calcium concentrations are not a consistent finding in people who have ingested bleach. Whether these animals had other disorders that may have caused or contributed to the calcium-related abnormalities is unknown. The clinical significance of the hypocholesterolemia in the female and the increases in alanine transaminase and alkaline phosphatase activities in the male was undetermined.

TREATING MILDER CASES OF BLEACH TOXICOSIS

Common recommendations for treating less serious cases of bleach ingestion include oral administration of milk or water to dilute the bleach solution.2 Inducing emesis is not advised. Dermal exposure should be treated by washing the affected areas with a mild soap and rinsing thoroughly with water. Evaluating the animal for corrosive injury to the gastrointestinal tract is also recommended.

CONCLUSION

This report describes a unique case of sodium hypochlorite bleach toxicosis, which resulted in the development of severe metabolic derangements and complications, including hypernatremia and hyperchloremia, metabolic acidosis, renal insufficiency, possible cerebral edema, aspiration pneumonia, and possibly a coagulation disorder, which led to the decision to euthanize the dogs. The marked biochemical abnormalities and complications noted in our patients are comparable to those seen in fatal cases in people. The major limitation of this report is the lack of gross and histologic findings that would have allowed further comparison of animal and human cases. Diagnostic tests were also limited because of owner monetary constraints and the rapid clinical deterioration of both dogs.

In conclusion, sodium hypochlorite bleach ingestion is a potentially fatal toxicosis, and affected animals may present with severe clinical signs and metabolic derangements.

"Toxicology Brief" was contributed by Seth Chapman, DVM; Jennifer Pittman, DVM; Mary Nabity, DVM, DACVP; and Mark Johnson, DVM, DACVP, Department of Veterinary Pathobiology, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843. Dr. Pittman's current address is Veterinary Teaching Hospital, College of Veterinary Medicine, University of Georgia, Athens, GA 30602. The department editor is Petra Volmer, DVM, MS, DABVT, DABT.

REFERENCES

1. Ross MP, Spiller HA. Fatal ingestion of sodium hypochlorite bleach with associated hypernatremia and hyperchloremic metabolic acidosis. Vet Hum Toxicol 1999;41(2):82-86.

2. Peterson ME, Talcott PA. Small animal toxicology. 2nd ed. St. Louis, Mo: Elsevier Saunders, 2006;233-234.

3. Racioppi F, Daskaleros PA, Besbelli N, et al. Household bleaches based on sodium hypochlorite: review of acute toxicology and poison control center experience. Food Chem Toxicol 1994;32(9):845-861.

4. Hofmeister AS, Heseltine JC, Sharp CR. Toxicosis associated with ingestion of quick-dissolve granulated chlorine in a dog. J Am Vet Med Assoc 2006;229(8):1266-1269.

5. Campbell A, Chapman M. Handbook of poisoning in dogs and cats. Oxford, Great Britain: Blackwell Science, 2000;238-239.

6. Stockham SL, Scott MA. Fundamentals of veterinary clinical pathology. Ames: Iowa State Press, 2002;340-349.

7. Donaldson CW. Paintball toxicosis in dogs. Vet Med 2003;98(12):995-998.

8. Rose BD, Post TW. Clinical physiology of acid-base and electrolyte disorders. 5th ed. New York: McGraw-Hill, 2001;338-339.

9. DiBartola SP. Fluid therapy in small animal practice. 2nd ed. Philadelphia, Pa: WB Saunders Co, 2000;330-335.