By Dr. Becker
Zinc is an essential trace mineral that plays a role in several important biologic processes. Zinc is abundant in nature and exists in many forms. Unfortunately, ingestion of some forms can lead to the creation of toxic zinc salts in the acidic environment of the GI tract.
Zinc poisoning occurs in humans and a wide variety of large and small animals. It is most often seen in family dogs, thanks to the availability of zinc-containing substances around the home, coupled with the canine tendency toward dietary indiscretion.
Common sources of zinc include:
Batteries Hardware used in pet carriers Automotive parts Coating on galvanized metals Paints Staples and tacks Zinc-oxide creams Nails Herbal supplements Jewelry Zippers Certain cold remedy lozenges Board-game pieces U.S. pennies produced after 1983
Another source of zinc not frequently mentioned is deliberate supplementation by pet owners who believe their dog or cat needs extra zinc in their diet. There is a rare skin condition called canine zinc-responsive dermatosis that occurs in some northern breed dogs. Some pet owners wrongly assume supplemental zinc will help with their pet’s dry, flakey or allergic skin and begin supplying zinc pills, which can cause fatal toxicosis in some cases.
Another way owners can accidently feed their pets too much zinc is in the form of additional multivitamins. Good quality, commercially available, balanced pet food contains adequate zinc. Some well-intentioned pet owners assume their pets will benefit from adding a multivitamin, and instead of buying one specifically for pets, they share their own vitamins with their pets, which can cause a toxic overdose of many nutrients.
According to dvm360, in 2010 there were over 4,600 cases of zinc exposure in dogs and 250 cases in cats. Most sources of zinc in these cases were metallic objects, multivitamins, and creams and ointments containing zinc oxide.
Case reports and retrospective studies indicate that ingestion of pennies is the primary source of zinc intoxication, and small-breed dogs are the most frequent victims.
How Zinc Turns Toxic, and Signs of Zinc Poisoning
Most of the toxic effects of zinc occur when free zinc is released by stomach acid. Free zinc forms soluble zinc salts that damage the intestinal mucosa and are absorbed and quickly distributed to the liver, kidneys, prostate, muscles, bones, and pancreas. Zinc salts have irritant and caustic effects on tissue, interfere with the metabolism of other minerals such as calcium, iron and copper, and inhibit the production and function of red blood cells.
The median lethal dose of zinc salts in cases of acute toxicity has been reported to be ∼100 mg/kg. Also, diets containing high levels of zinc (>2,000 ppm) have been reported to cause chronic zinc toxicosis in large animals. A toxic dose has not been established in dogs. However, normal zinc serum concentrations are between 0.7 and 2 μg/ml.
Symptoms of zinc toxicosis begin to appear within a few days of ingestion, and the severity depends on the amount ingested. Clinical signs can range from mild vomiting to death. Early symptoms include vomiting, diarrhea, black tarry stools, and loss of appetite. Additional symptoms include lethargy, depression, orange-colored feces, jaundice, shock, cardiac arrhythmias, and seizures.
Diagnosing Zinc Toxicosis
A physical examination of a dog with zinc toxicosis will often reveal pale mucous membranes, irregular heartbeat, heart murmur, dehydration, jaundice and abdominal pain. Neurologic signs can vary from mild lethargy to significant depression. There may be weakness, and in severe cases, seizures.
Routine laboratory tests should include a biochemistry profile, electrolytes, urinalysis and a complete blood count (CBC). The CBC may show anemia as the result of zinc-related destruction of red blood cells, granules in red blood cells (Heinz bodies), and/or variations in red blood cell coloration known as polychromasia.
The biochemistry profile may point to high levels of hemoglobin and bilirubin. If there are also high levels of blood urea nitrogen, creatinine, liver or pancreatic enzymes, it is indicative of multiple organ failure.
Another test called the packed cell volume (PCV) is necessary to calculate the number of viable red blood cells to determine whether a blood transfusion is warranted.
To confirm a diagnosis of zinc toxicosis, laboratory tests to measure the levels of zinc in the dog’s blood must be run. These tests can also provide information about blood clotting activity.
X-rays are also often taken to confirm ingestion of a zinc-containing material.
Treatment of Zinc Toxicosis
Treatment primarily involves supportive care and removing the source of the zinc. Initial efforts should be focused on treating dehydration, shock, and electrolyte imbalances, and increasing urine output.
If a zinc-containing foreign object is found in the animal’s GI tract, it must be removed once the patient’s condition is stabilized. If the object is in the stomach, it can be removed by endoscopy. If it has moved into the small intestine, a laparotomy must be performed to remove it.
Drugs to lower stomach acidity and promote the release of zinc will be given. These typically include proton-pump inhibitors like omeprazole, or H2 blockers to decrease production of stomach acid in order to limit systemic absorption of zinc salts from the GI tract. If there is gastric irritation or ulceration, gastroprotectants may be given, and anti-nausea drugs and painkillers may also be indicated.
If there has been severe red blood destruction, blood transfusions may be required.
Prompt treatment is necessary to save the life of a pet with zinc toxicity. Often, the levels of zinc in the blood drop quickly once the source is removed. Unfortunately, dogs with severe complications like multiple organ failure have much less chance of survival.