Necropsies were performed on 77 Alaskan sea otters (Enhydra lutis) from April 5 to May 8, 1989, affected by the Exxon Valdez oil spill in Prince William Sound, Alaska. Twelve of the animals were mortalities collected in the wild. The remaining 66 animals were captured live in the wild and transported to a rehabilitation center for cleaning and medical support prior to death in captivity. All animals had varying degrees of external contamination with oil. Thirty-seven were female (48%) and 18 were male (23%); sex was not recorded for the remaining animals. Ten females were pregnant, each with one fetus, and four were in lactation. Eight stillborn or neonatal pups that died shortly postpartum were also examined.

The clinical status and duration of survival in captivity was variable. Available hematological data indicated that most animals were anemic (HCT range 35-72%, n=18, normal range 50-62%; RBC = 3.2-4.2 x 10⁶/ µl, n=9, normal range 4.3-5.9 x 10⁶ /µl). The anemia may have been due to a direct toxic effect on erythrocytes. Heinz body anemia has been reported in some avian species exposed to crude oil, although there was no evidence of Heinz body formation in the erythrocytes of these otters. Gastrointestinal hemorrhage may have contributed to the anemia in these animals. Serum chemistries revealed an elevated blood urea nitrogen (range 86-449, n=17, normal range 42-92 mg/dl), alkaline phosphatase (range 62-288, n=15, normal range 25-93 IU/L), serum glutamic oxalacetic transferase (range 370-15,770, n=16, normal range 87-54 IU/L) lactate dehydrogenase (range 320-15,770, n=16, normal range 95-419 IU/L), total bilirubin (range 0.1-2.0, n=15, normal range=0.1-0.5 mg/dl) and creatine phosphokinase (>1800, n=8, normal range 170-490 IU/L). Total protein, albumin, glucose and serum electrolytes were generally within normal limits. The above data was suggestive of possible hepatic insult and myopathy.

Respiratory distress was a common clinical observation in animals prior to death and was of ten associated with subcutaneous emphysema. A few animals also exhibited convulsions or were comatose or in a state of narcosis prior to death. Hypothermia was a common clinical problem secondary to the loss of the insulating capacity of the pelage following contamination with oil.

Necropsy findings revealed a spectrum of lesions, although the majority of animals had a similar pattern of lesions. A majority (68%) had pulmonary interstitial emphysema often associated with pleural, pericardial, mediastinal and subcutaneous emphysema. Aspiration of stomach contents occurred in a few animals and most likely occurred agonally prior to death. The etiology and pathogenesis of the pulmonary interstitial emphysema was not determined, but may have been due to a direct toxic effect from the oil or an abnormal stimulation of the diving reflex with constriction of the terminal airways and disruption of the patency or integrity of the airways secondary to air trapping. Microscopic examination of tissues from selected animals confirmed the gross diagnosis of interstitial emphysema, although there was no conclusive evidence of lack of integrity of the airways. Preliminary radiographic studies with injection of radiopaque material into the airways of intact formalin-fixed lungs also did not support this conclusion. Humans with acute hydrocarbon toxicity exhibit similar lesions, but the pathogenesis of these lesions has also not been determined.

Gastrointestinal mucosal ulcerations, primarily involving the pylorus and the proximal intestine were also a common finding (35%). The consistency of the gastric and intestinal contents varied from a thin to viscous dark brownish-green to reddish-black fluid. A few animals had dark black, tarry intestinal contents suggesting melena or intestinal contents that were a pale yellowish-green and tenacious with increased amounts of mucous. Exposure of the peritoneal cavities and internal viscera in the animals that had thin to viscous dark greenish black to reddish-black intestinal contents was associated with the presence of a strong, dense, sweet odor suggestive of hydrocarbon ingestion and deposition in the internal organs. Intestinal parasitism primarily due to acanthocephalan infection was a common finding (40%). Cestode (8.0%) and nematode infections (7.0%) also occurred. These were considered background infections acquired in the wild. Microscopic examination confirmed the gross diagnosis of acute to subacute gastrointestinal ulceration. There was congestion and hemorrhage of the gastrointestinal mucosa. There was degeneration and necrosis of the intestinal mucosal epithelial cells and the intestinal mucosal lymphoid cell population was apparently depleted.

Three animals that were maintained in close proximity prior to death that had dark reddish-black intestinal contents with congestion and hemorrhage of the intestinal mucosa were examined for distemper virus using immunohistochemical techniques. The sections were negative for distemper virus in situ, although viral or other infectious etiologic agents could not be ruled out. Ulceration of the oropharyngeal mucosa, especially the gingival mucosa, was common (22%) and intestinal intussusception occurred in a few animals. The livers were of ten grossly pale reddish-brown to yellowish-brown with pale green mottling, enlarged with prominent rounded edges, and friable. Other animals had dark reddish-brown atrophic livers that were also often friable. Microscopically, the grossly atrophic livers had centrilobular congestion with atrophy and degeneration of the centrilobular and midzonal hepatocytes. Severely affected animals also had centrilobular necrosis and hemorrhage. These lesions may have been caused by hydrocarbon toxicity, but could also be explained by hypoxia, secondary to respiratory compromise caused by the pulmonary interstitial emphysema, and possibly anemia. The enlarged, pale, friable livers observed grossly were often associated with a vacuolar hepatopathy that may have been due to the hormonal, reproductive and/or nutritional status of the animal. The gallbladders were prominently thickened, often with pronounced folding of the gallbladder mucosa. A large number of animals (34%) had trematode infections of the gallbladder that were considered to have been acquired in the wild. The bile was often thick and pale brown-green.

There was an apparent mild degeneration of the myocardial fibers in a few animals or prominent cross striations of the myocardial fibers. Myocardial fiber degeneration may have been due to hypoxia. Prominent myocardial cross-striations may have been due to increased contraction of the myocardial fibers at the time of death, possibly also due to hypoxia. There was an apparent depletion of lymphocytes within lymph nodes with an associated reticuloendothelial cell or fixed monocyte/macrophage hyperplasia of the lymph nodes and spleen. The lymphoid depletion may have been secondary to an increased endogenous corticosteroid production. A few animals had an apparent adrenal gland hyperplasia with microscopic evidence of adrenocortical hemorrhage. Unfortunately, endogenous corticosteroids were not monitored clinically in these animals.

The kidneys and brain were grossly and microscopically normal in the majority of animals examined. A few had renal cysts that were considered background lesions. Thyroid follicular hyperplasia with coalescence and formation of microcysts was a common finding, although the significance was not known. Various other lesions also occurred, but are too numerous to list in this narrative.

The rapid clinical deterioration of these animals and the spectrum of lesions was considered to be the result of primary hydrocarbon toxicity in combination with the secondary effects of hypothermia, anemia, and respiratory compromise. Ingestion of hydrocarbons is of ten associated with symptoms of mucous membrane irritation, vomiting, and CNS depression. Chemical pneumonitis may also occur secondary to aspiration, although there was no evidence of pneumonia in these animals. Hepatic toxicity and cardiac arrhythmias have also been reported.

Microscopic examination of tissues from additional animals and further correlation of clinical pathology and hematology data with necropsy findings is presently in progress.