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.
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.