Abstract

In January of 2004, an 18-year-old, 58 kg, female harbor seal (Phoca vitulina) housed in an inland, marine water system was presented with a history of two days of anorexia and depression. Over the next few days, the animal did not improve. Blood work (CBC and serum chemistries) was within normal limits and the appetite stimulant megestrol acetate was used. After 10 days these methods did not significantly alter condition, and a more comprehensive work up under anesthesia was undertaken.

The animal was immobilized with isoflurane after pre-anesthetic administration of midazolam and atropine sulfate. Abdominal radiographs showed the animal to have metal foreign bodies in the stomach. Most gastric foreign bodies were removed via endoscopy, though several were left due to the length of anesthesia, periodic bouts of apnea, and difficulty grasping the remaining foreign bodies. Foreign bodies removed included several small rocks, 8 partially digested coins and two costume jewelry rings. The anesthesia lasted for a total of 115 minutes from injection of pre-anesthetic medication to recovery, indicated by coordinated voluntary movement and vocalization. The animal died 120 minutes post-operatively, in spite of the uneventful recovery.

A post mortem was performed. Grossly the stomach contained six 3x3 cm rocks and 15 coins. The lungs were moderately congested. There were no other significant gross findings. Histologically, the heart had scattered small clusters of necrotic myocardial cells, often with minimal accumulations of neutrophils. There was widespread congestion of the lungs and splanchnic organs indicative of cardiovascular collapse.

Serum chemistries and CBC from blood taken during the procedure revealed mild prerenal azotemia (dehydration), acidosis, elevated CPK and LDH, and mild anemia. Given the blood sample was taken during anesthesia, acidosis was likely due to inadequate ventilation during periodic apnea (e.g., respiratory acidosis). Very likely myocardial necrosis was a consequence of anoxia, possibly with some metabolic changes due to acidosis as CO2 levels climbed.

Mild anemia with elevated potassium, CPK and LDH suggested hemolysis: Coupled with coins in the stomach, zinc toxicosis was suspected as the cause of original clinical signs. Frozen liver and kidney were submitted for multi-element screen. Elevated zinc levels were not substantiated; however hepatic and renal lead levels were 38.4 and 4.92 ppm respectively, sufficient to warrant a diagnosis of lead toxicosis. Lead toxicosis was subsequently considered the source of clinical signs. Anemia and elevated CPK and LDH were attributed to low-grade hemolysis, though some level of enzyme elevations could have also been due to myocardial necrosis.

Samples of ingested rocks and the two rings were submitted for analysis of lead levels. One ring, which was heavily eroded prior to analysis, contained 34% lead. At analysis the ring was 6 g, thus total available lead was about 2 g, with an unknown quantity already lost to gastric acid digestion. The toxicologist estimated 0.5 g had to be available for absorption for toxicosis to occur in this seal, which was considered plausible. No other source of lead was found in review of the enclosure and to date no other animal has had evidence of lead intoxication. Interestingly, several months after the death of the seal, the U.S. government recalled a line of toy jewelry containing dangerous levels of lead.