Zinc is a metallic element found in many household objects. Pennies minted after 1982 contain a zinc wafer core that is coated in copper. Each penny contains approximately 2,440 mg of elemental zinc.1 Many carrying cages used to transport pets have galvanized nuts and bolts that are coated in zinc. Medicinal items such as zinc oxide ointment and zinc gluconate are commonplace in many households. Although the mere presence of these objects in the environment does not represent a danger, once ingested, erosion of material in the acidic environment of the stomach can release zinc and lead to subsequent toxicosis.1 Ingestion of zinc by dogs can result in hemolytic anemia, pancreatitis, acute renal failure, or signs of gastrointestinal dysfunction.2–6 Humans with zinc toxicosis develop sideroblastic anemia, pancytopenia, and acute pancreatitis.7–10 To the authors' knowledge, the first case of zinc toxicosis reported in a dog was published in 1984,11 and hemolytic anemia was first reported in 1986.6,12 Despite the fact that zinc toxicosis has been recognized, only a single case series characterizing the clinical course of toxicosis has been published that the authors are aware of.13 In that report, 3 of 5 dogs died or were euthanized. Clinical impressions derived from the outcome of dogs admitted to the authors' hospital and from other published individual case reports are that the prognosis is much better. The purpose of the present study was to describe clinical variables and outcome in animals with hemolytic anemia secondary to zinc ingestion.
Criteria for Selection of Cases
The medical records computer database of the Matthew J. Ryan Veterinary Hospital of the University of Pennsylvania was searched for records of animals with a diagnosis of zinc toxicosis from 1991 through 2003. Records were included if there was documentation of a zinc source, the animal was anemic, and clinical signs resolved with removal of the zinc source. Animals with concurrent disease, as determined from the medical history and diagnostic testing performed in the hospital, were excluded.
Procedures
Variables recorded included signalment, body weight, historical findings, initial owner complaints, physical examination findings, clinicopathologic findings, blood zinc concentrations, source of zinc, treatments given, duration of hospital stay, and outcome. Blood for measuring zinc concentrations was collected in glass tubes appropriate for assay of trace elements.a
Statistical analysis—Continuous variables were described with median and minimum and maximum values. Categoric variables were described by determination of frequencies, proportions, and percentages. All statistical evaluations were performed with a statistical software program.b
Results
Signalment—Twenty-seven cases of zinc intoxication were identified in the computerized search results. After the medical records were reviewed, those for 8 animals were excluded. Six were excluded as a result of incompleteness of the records and 2 were incorrectly coded, leaving 19 records for review, all of which involved dogs. Eleven breeds were represented, including 3 Shetland Sheep Dogs; 2 each of Beagle, Chihuahua, Cocker Spaniel, Pug, Shih-Tzu, and Toy Poodle; and 1 each of Bichon Frise, mix, Maltese, and Schipperke. Median age was 1.3 years (range, 0.33 to 7 years). The group included 12 females (6 sexually intact and 6 spayed) and 7 males (4 sexually intact and 3 castrated). Median body weight was 5.6 kg (12.3 lb; range, 2.6 to 11.5 kg [5.7 to 25.3 lb]).
Initial owner complaints—Mean duration of clinical signs prior to admission to the hospital was 2.3 ± 1.2 days. The most common owner complaint was vomiting (n = 14 dogs), followed by pigmenturia (12), lethargy (10), decreased appetite or inappetance (7), diarrhea (6), ingestion of screws (1), and weakness (1). Of the dogs that vomited, 2 expelled coins and in 1 of those instances, the coins were identified as pennies. Two dogs were referred after the referring veterinarian had removed metallic foreign bodies from the gastrointestinal tract during exploratory laparotomy; pennies were identified in 1 of those instances.
Physical examination findings—The most common physical examination abnormalities were pale mucous membranes (n = 13 dogs), tachycardia (11), icterus (10), and heart murmur (6). Other abnormalities noticed were tachypnea (n = 2 dogs), dehydration (2), fever (2), hepatomegaly (1), signs of abdominal pain (1), and hyphema (1). The dog with signs of abdominal pain had recently undergone abdominal surgery. Coagulation assays were not performed in the dog with hyphema, but the platelet count was within reference range. That dog was later determined to have anterior uveitis of unknown origin.
Clinicopathologic findings—Clinicopathologic data were summarized (Tables 1–4). Complete blood counts revealed moderate-to-severe anemia in all dogs and leukocytosis characterized by mature neutrophilia. Heinz bodies were detected in 5 of 10 dogs. The most consistent findings from serum biochemical analyses were high serum activities of certain liver-associated enzymes (eg, aspartate aminotransferase, alkaline phosphatase, and G-glutamyltransferase) and high total bilirubin concentration. Blood zinc concentrations were high in all 8 dogs in which it was measured (median, 30.6 ppm; range, 5.5 to 159 ppm [reference range, 0.7 to 2.0 ppm]).
Summary of hematologic data for 19 dogs with zinc toxicosis.
| Variable | No. of dogs tested | Median | Range | No. of dogs with values above reference | No. of dogs with values below reference range | Reference range |
|---|---|---|---|---|---|---|
| PCV(%) | 18 | 17 | 8–26 | 0 | 18 | 37–55 |
| TS(g/dL) | 18 | 6.8 | 5.2–9.5 | 8 | 1 | 5.7–7.1 |
| RBC(X106/μL) | 16 | 1.9 | 1.02–2.98 | 0 | 16 | 5.8–8.9 |
| MCV(fL) | 16 | 76 | 6–91 | 8 | 9 | 63–76 |
| MCHC(g/dL) | 15 | 33 | 28–54 | 2 | 4 | 32–36 |
| Reticulocytes(X 103/μL) | 10 | 374 | 57–535 | <60 | ||
| nRBC(/100 WBC) | 15 | 8 | 1–34 | 14 | 0 | 0–1 |
| WBC(X 103/μL) | 16 | 27.7 | 9.5–60.9 | 13 | 0 | 5.3–19.8 |
| Neutrophils(X 103/μL) | 16 | 20.2 | 5.8–51 | 11 | 0 | 3.1–14.4 |
| Band neutrophils(X 103/μL) | 15 | 0.6 | 0–2.4 | 13 | 0 | 0–0.2 |
| Lymphocytes(X 103/μL) | 15 | 2.8 | 0.9–6.4 | 1 | 1 | 0.9–5.5 |
| Monocytes(X 103/μL) | 15 | 1.4 | 0.3–6.5 | 6 | 0 | 0.1–1.4 |
| Eosinophils(X 103/μL) | 15 | 0 | 0–1.6 | 0 | 0 | 0–1.6 |
| Basophils(X 103/μL) | 15 | 0 | 0–0.3 | |||
| Platelets(X 103/μL) | 16 | 200 | 45.3–503 | 2 | 7 | 177–398 |
TS = Total solids. MCV = Mean corpuscular volume. MCHC = Mean corpuscular hemoglobin concentration. nRBC = Nucleated RBC.
Summary of venous blood gas data for the same dogs as in Table 1.
| Variable | No. of dogs tested | Median | Range | No. of dogs with values above reference | No. of dogs with values below reference range | Reference range |
|---|---|---|---|---|---|---|
| pH | 13 | 7.3 | 7.3–7.5 | 1 | 7 | 7.35–7.45 |
| PCO2(mm Hg) | 13 | 38 | 15–45 | 0 | 5 | 33–50 |
| Bicarbonate(mmol/L) | 13 | 19 | 11–25 | 0 | 4 | 18–26 |
| Chloride(mmol/L) | 13 | 115 | 106–129 | 10 | 1 | 107–113 |
Summary of coagulation variables for the same dogs as in Table 1.
| Variable | No. of dogs tested | Median | Range | No. of dogs with values above reference | No. of dogs with values below reference range | Reference range |
|---|---|---|---|---|---|---|
| PT(% difference from reference range) | 9 | 0 | −11–67 | 4 | 4 | 0 |
| PTT(% difference from reference range) | 9 | 65 | 29–364 | 9 | 0 | 0 |
PT = Prothrombin time. PTT = Partial thromboplastin time.
Summary of serum biochemical variables for the same dogs as in Table 1.
| Variable | No. of dogs tested | Median | Range | No. of dogs with values above reference | No. of dogs with values below reference range | Reference range |
|---|---|---|---|---|---|---|
| SUN(mg/dL) | 17 | 35 | 13–134 | 11 | 0 | 5–30 |
| Sodium(mmol/L) | 19 | 144 | 136–162 | 3 | 1 | 140–150 |
| Potassium(mmol/L) | 19 | 3.5 | 2.2–4.2 | 0 | 16 | 3.9–4.9 |
| Glucose(mg/dL) | 19 | 106 | 59–246 | 4 | 1 | 65–112 |
| Creatinine(mg/dL) | 16 | 0.8 | 0.4–3.2 | 1 | 7 | 0.7–1.8 |
| Total bilirubin(mg/dL) | 15 | 2.3 | 0.5–23 | 12 | 0 | 0.3–0.9 |
| Phosphorus(mg/dL) | 15 | 5.6 | 4.0–8.4 | 5 | 0 | 2.8–6.1 |
| AST(U/L) | 11 | 138 | 45–1,023 | 10 | 0 | 23–65 |
| ALK(U/L) | 13 | 437 | 107–1,422 | 12 | 0 | 20–155 |
| GGT(U/L) | 5 | 107 | 16–237 | 4 | 0 | 7–24 |
| ALT(U/L) | 14 | 19.5 | 3–92 | 1 | 3 | 16–91 |
AST = Aspartate aminotransferase. ALK = Alkaline phosphatase. GGT = γ-Glutamyltransferase. ALT = Alanine aminotransferase.
Urinalyses were performed in 6 dogs. Median urine specific gravity was 1.020 (range, 1.010 to 1.028). All dogs had proteinuria, ranging from trace to severe. One dog had trace ketones, but the rest were not ketonuric. Two dogs had trace glucosuria without hyperglycemia. All dogs had pigmenturia in the form of either bilirubinuria or hemoglobinuria, ranging from mild to severe. Hemoglobinuria was detected in 2 dogs, 1 of which had 8 to 12 RBCs/hpf and the other of which had 10 to 18 RBCs/hpf. Rare coarse granular casts were observed in the urine of 1 dog.
Methods of zinc source removal and metallic foreign bodies removed—Endoscopy was performed in 15 dogs, and laparotomy and gastrotomy were performed in 2 dogs (1 at the Matthew J. Ryan Hospital and 1 at the referring veterinarian's facility). One dog underwent both endoscopy and gastrotomy. Coins were detected in the vomitus of 2 dogs, and 1 dog was euthanized without treatment.
Metallic foreign bodies removed included pennies (from 8 dogs), quarters (4), unspecified coins (1), nickels (2), dimes (1), metallic objects (1), and a tack (1). Multiple metallic foreign bodies were removed from 14 dogs.
Treatments—A balanced electrolyte solution was administered IV in 18 dogs. Fifteen dogs received packed RBCs (median, 0.125 units/kg; range, 0.04 to 0.33 units/ kg). Six dogs received plasma (median, 0.25 units/kg; range, 0.1 to 0.8 units/kg). Other treatments included histamine-2 receptor blockers (n = 14 dogs), sucralfate (12), antimicrobials (5), metoclopramide (2), S-adenosylmethionine (1), dolasetron (1), ursodiol (1), vitamin K1 (1), ophthalmic atropine and bacitracin-neomycin-polymixin ointment (1), and opioids (1). Prior to hospitalization, 1 dog was being treated with prednisone for immune-mediated hemolytic anemia; treatment was continued in that dog during hospitalization. Two dogs received chelation treatment with Ca-EDTA (dosage, 26.8 mg/kg [12.2 mg/ lb] q 4 h for 2 days, or 24.5 mg/kg [11.1 mg/lb] q 8 h for 3 days).
Outcome—Seventeen dogs survived to discharge, and 2 dogs did not survive. One was euthanized without any treatment, presumably for financial reasons, and the other dog was discharged from the hospital but returned the next day in severe respiratory distress and died. No necropsy was performed in that dog. Thirteen dogs were discharged from the hospital after ≤ 3 days of hospitalization. Overall median duration of hospitalization was 2 days (range, 1 to 15 days). In the dog that was hospitalized for 15 days, severe pancreatitis was the primary reason for the prolonged hospital stay. Mean ± SD PCV at discharge (n = 16 dogs) was 38 ± 8%, with 9 of the dogs having a PCV within reference range (37% to 55%) and 7 dogs having a PCV less than reference range. Mean ± SD increase in PCV between admission and discharge was 21 ± 11%, representing a mean percent change in PCV from that at admission of 114% (range, 15% to 512%).
Discussion
In 8 of the 19 dogs with zinc-induced hemolysis, diagnosis was confirmed on the basis of high blood zinc concentrations. In the 11 dogs in which blood zinc concentration was not measured, the diagnosis of hemolysis secondary to zinc toxicosis was made presumptively. It is possible that there were other causes for the hemolysis, but the temporal sequence of resolution of hemolysis after metallic foreign body removal made the diagnosis of zinc-induced hemolysis likely. In the 8 dogs in which blood zinc concentration was measured, the median concentration was 30.55 ppm (range, 45 to 159 ppm). The reference range for zinc in dogs is 0.7 to 2.0 ppm, and most dogs in which toxicosis is confirmed have concentrations > 10 ppm.1 Blood collected for measurement of zinc concentration should be collected into tubes made for trace element assays (usually tubes with royal blue stoppers). Zinc contamination of blood samples can be derived from rubber stoppers and syringes. It is standard practice at the authors' hospital to submit blood for determination of zinc concentration in such tubes.
All animals with zinc toxicosis admitted to our hospital have been dogs. This may be because of the more indiscriminant eating behavior of dogs rather than an intrinsic resistance to zinc toxicosis in cats. To the authors' knowledge, there are no reports of anemia secondary to zinc toxicosis in cats, although in 1 experimental study,14 ferrets developed anemia secondary to gastrointestinal tract hemorrhage.
Dogs in the present study were young (median age, 1.2 years), a finding that was consistent with those in most other reports2,4–6,15 in the literature. This is likely because young dogs are more likely to ingest inappropriate objects than older dogs. Most dogs were small in size (mean weight, 5.9 kg [13 lb]), and the largest dog weighed 11.5 kg, reflecting the breed distribution. Although we did not compare the weights and breed distribution with those of the general hospital population, it appears that smaller dogs were overrepresented. We consider that there are 2 potential reasons for this: first, smaller dogs have smaller pylori, making it more difficult for objects to pass from the stomach. This allows more time for erosion of the metallic object by the gastric acid and frees more zinc for absorption. It is also possible that a dose-related effect is involved.
The most common owner complaints (eg, vomiting, pigmenturia, lethargy, decreased appetite or inappetance, and diarrhea) were nonspecific in nature, except for pigmenturia. Pigmenturia can be a result of hematuria, hemoglobinuria, myoglobinuria, or bilirubinuria. It is impossible to distinguish among those conditions solely on the basis of urine appearance; however, given the clinical diagnosis of hemolytic anemia, hemoglobinuria was the most likely cause of pigmenturia observed in study dogs. In addition, zinc toxicosis reportedly causes intravascular hemolysis,5 leading to hemoglobinemia and subsequent loss into the urine. The most common physical examination findings were consistent with hemolytic anemia.
Vomiting in affected dogs may result from various causes, including the physical presence of the metallic objects and subsequent gastric irritation, zinc-induced gastric irritation,2,6 pancreatitis,3 or intestinal hypoxia secondary to anemia. Vomiting is such a frequent clinical sign that its absence in an animal with hemolysis lowers the index of suspicion for zinc toxicosis; nevertheless, the possibility cannot be excluded. Abdominal radiography should be performed in any animal with hemolytic anemia. The source of zinc may be found anywhere in the gastrointestinal tract, from esophagus to rectum, and thoracic views may be necessary to find the zinc source. Lead objects are another cause of hemolytic anemia and can also be seen as radiographically opaque objects.
In humans, anemia that develops with zinc toxicosis appears to be chronic and caused by copper deficiency.7,16 In dogs of the present study, the duration of signs was short, with signs manifesting a mean of 2.2 days before a diagnosis was reached. This suggests that the appearance of gastrointestinal tract lesions and onset of anemia are related temporally.
Mean PCV at initial evaluation was 16%. Of the dogs in which reticulocyte counts were performed, most (10/11) had signs of RBC regeneration (mean reticulocyte count, 313 × 103 cells/μL), indicating that there was adequate time for bone marrow response. In general, a regenerative response takes 2 to 4 days after the onset of anemia to develop.17
The pathophysiology of zinc-induced hemolysis in dogs has not been fully elucidated, but may be partially related to inhibition of glutathione reductase and enzymes of the hexose-monophosphate-shunt pathway. Absence of these enzymes' function would make RBCs more susceptible to oxidative damage.5 In general, when RBCs undergo oxidative damage, they develop Heinz bodies.18 Only 33% of dogs in the present study had Heinz bodies, which have been inconsistently noticed in previous case reports.2,4–6 This indicates that although oxidative damage may be part of the pathogenesis of the hemolysis, it may not entirely account for the condition.
It can be difficult to differentiate immune-mediated hemolytic anemia from zinc-induced hemolytic anemia on the basis of laboratory data alone. Spherocytes are the hallmark of immune-mediated hemolytic anemia.17 Only 20% of the dogs in the present study had spherocytosis, and spherocytosis was considered to be mild in all of those instances. Spherocytes have been detected in association with zinc-induced hemolysis in dogs, but similar to findings in the dogs of our study, this has been an inconsistent finding.2,5,6,15 Animals with more severe spherocytosis should be suspected more strongly of having immune-mediated hemolytic anemia.
Heavy metal poisoning causes renal tubular injury, and acute renal failure has been reported in association with zinc toxicosis in dogs.5,6 The authors of those reports5,6 speculated that zinc could have caused tubular injury, but other causes, including dehydration, electrolyte abnormalities, concurrent sepsis, hemoglobinuria, and disseminated intravascular coagulation, could not be ruled out. Acute renal failure was not definitively diagnosed in any of the dogs in the present study. Only 1 dog had a serum creatinine concentration higher than reference range, and the median creatinine concentration for all dogs was 1.0 mg/dL. The BUN concentration was greater than reference range in 11 of 17 dogs, with a median concentration of 48 mg/dL. This pattern of a disproportionate increase in BUN concentration, compared with that of creatinine, has been reported in another dog with zinc intoxication.6 This was speculated to be caused by dehydration or, possibly, gastrointestinal tract hemorrhage. Melena was not reported in any of the dogs in the present study, but has been reported in other dogs with zinc toxicosis.6 Our findings and those of previous reports indicate that acute renal failure is not a common sequela of zinc toxicosis in dogs.
Serum bilirubin concentration was high in 12 of the 15 dogs in which it was measured, with an overall median concentration of 2.3 mg/dL. That finding is consistent with hemolysis, although the possibility of cholestatic abnormalities or liver dysfunction cannot be ruled out; however, those conditions seem unlikely in the absence of evidence of substantial acute liver injury. Only 1 dog had serum alanine aminotransferase activity greater than reference range. Twelve of 13 dogs had alkaline phosphatase activities greater than reference range, and most of those activities were mildly or moderately high. In addition, several dogs were puppies, which would skew the alkaline phosphate activities to high values.19 Serum aspartate aminotransferase activity was high in 10 of 11 dogs. Aspartate aminotransferase is an enzyme associated with hepatocellular leakage, but is also found in important quantities in RBCs and muscle cells.19 Given the near-normal serum alanine aminotransferase activities in dogs in the present study, the source of the high aspartate aminotransferase activity was likely a result of RBC hemolysis or muscle hypoxia.
The median prothrombin time was not prolonged, and the median partial thromboplastin time was prolonged by 65%. The latter finding has been reported in some dogs with zinc-induced hemolysis,6 and it was speculated in that report that zinc caused inhibition of coagulation factors, especially factors VIII, IX, XI, and XII, all of which are involved in the intrinsic pathway and, hence, are assessed by partial thromboplastin time. Median prothrombin time, which assesses function of the extrinsic pathway, was not as prolonged. Additionally, thrombocytopenia has been reported as a complication of zinc toxicosis in dogs, but there was no evidence of this in the present study. The cause for thrombocytopenia in previous reports was not elucidated, although disseminated intravascular coagulation was suggested as a possibility.6
The acidic environment in the stomach is important for absorption of zinc because it leads to formation of soluble zinc salts; therefore, zinc is more likely to be absorbed from objects in the stomach than from those that pass into the intestines.12 This is consistent with our finding that most (n = 17/19) of the metallic objects were removed endoscopically, indicating that the objects were still present in the proximal portion of the gastrointestinal tract despite a mean duration of clinical signs of 2.2 days. The reason why objects remained in the proximal portion of the gastrointestinal tract is unknown, but we speculate that most objects were too large to pass through the pylorus.
Zinc oxide is another form of zinc that may be ingested. It is typically associated with self-limiting gastritis.20 However, in 1 case report,6 ingestion of copious amounts of zinc oxide was associated with hemolytic anemia. In the present study, no dogs had hemolytic anemia associated with zinc oxide ingestion.
The duration of clinical signs does not definitively indicate when ingestion of the foreign body occurred, and information concerning time from ingestion to clinical signs was not available in the medical records reviewed. Ingestion of the metallic objects could have occurred at any time before the onset of clinical signs. The duration from ingestion to development of toxic blood concentrations varies and depends on multiple factors including the nature of the object itself, gastric pH, presence or absence of food, and length of time the object was in the stomach.1 The time from ingestion to clinical signs was not documented in most previous reports.
One dog developed clinically evident pancreatitis and was the basis of a published case report.3 The dog had a prolonged hospital stay but was discharged and reported as doing well on follow-up several months later. Zinc is excreted through the pancreas, but the mechanism by which it induces pancreatitis is not completely understood. Pancreatitis secondary to zinc ingestion has been well described in humans10,21 and was suspected in an earlier veterinary case report.6 Pancreatic fibrosis has also been associated with zinc toxicosis in a dog.22 Because of the difficulty of diagnosing pancreatitis on the basis of routine laboratory data and the fact that few of the dogs in this study underwent abdominal ultrasonography, it is difficult to comment on the frequency of this complication in this population. However, only 1 dog had signs that were consistent with clinically important pancreatitis that did not resolve with removal of the zinc source.
All dogs with zinc-induced hemolytic anemia in the present study received either packed RBCs or a commercially available oxygen-carrying solutionc as part of treatment. Dogs received a mean dose of 18 mL/ kg of packed RBCs, which is a moderately high dose. The blood products available in the authors' hospital are prepackaged in specific volumes. Patients typically receive an entire volume rather than a specific dose. Because most of the dogs with zinc-induced hemolytic anemia were small in size, they may have received a higher milliliter per killigram dose of blood than larger dogs. Higher doses of blood products have been associated with volume overload, which results in tachypnea, dyspnea, or tachycardia.22 Because nearly all dogs in the present study survived and did well clinically, it does not appear that this high dose of blood administered affected outcome. However, not enough dogs were analyzed to permit stratification according to dose of blood received or to draw valid conclusions.
The most common treatments (not including blood product administration or chelation therapy) instituted included IV fluid administration, gastrointestinal tract protectants, antimicrobials, and antiemetics. Unfortunately, treatment was not standardized, and meaningful conclusions could not be drawn regarding the treatments.
Chelation therapy as treatment for zinc toxicosis has been described.3 Most ingested sources of zinc are discrete objects that can be removed. Therefore, removal of the source of zinc is the recommended treatment. In addition, chelation treatment may cause increased intestinal absorption of zinc that has entered the gastrointestinal tract,1 making it a controversial treatment for zinc toxicosis. Two dogs in the present study received chelation treatment. Treatment consisted of administration of calcium EDTA at a dosage of 26.8 mg/kg (12.2 mg/lb) every 4 hours for 2 days in 1 dog and 24.5 mg/kg (11.1 mg/lb) every 8 hours for 3 days in the other. Although there were insufficient data on which to base any conclusions, those 2 dogs were hospitalized for 5 and 15 days (the latter dog had severe pancreatitis). This is considerably longer than the median hospital stay of 2 days. Chelation treatment with other substances such as succimer or D-penicillamine has not been reported, to the authors' knowledge. Without evidence to support their use and in light of the ease of zinc source removal, it is difficult to recommend the use of these agents.
Results of the present study revealed a good prognosis and a reasonably short hospital stay for affected dogs. Two dogs died, 1 was euthanized without treatment, and 1 was discharged from the hospital but returned the next day in severe respiratory distress and died. No necropsy was performed in that dog, but the cause of death was speculated as pulmonary thromboembolism or bronchopneumonia. Survival and hospital duration times were better in the present study, compared with those in earlier reports. This is most likely a result of earlier recognition of the association between zinc and hemolysis, compared with the situation in earlier reports, in which the association was still being characterized.
Dogs with zinc toxicosis appeared to do well after the source of zinc was removed. The mean hospital stay was short, and the outcome was favorable in all dogs except one. The source of zinc is usually in the stomach and can often be removed endoscopically. Owners of affected dogs should be warned about the potential complication of pancreatitis.
Vacutainer brand tubes, Becton-Dickinson, Franklin Lakes, NJ.
Stata, version 8.0 for Windows, Stata Corp, College Station, Tex.
Oxyglobin, Biopure Corp, Cambridge, Mass.
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