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Toxicology case: How to help dog owners manage zinc oxide toxicosis
An overview of the diagnosis and treatment of zinc oxide toxicosis due to ingestion of diaper rash cream.
A 6-month-old 42-lb (19.1-kg) Labrador retriever chewed on a tube of diaper rash ointment containing 10% zinc oxide. The dog punctured the tube and ingested about 3 oz of the ointment but did not ingest any of the plastic tube. The estimated dose of zinc oxide ingested by this dog was 448.8 mg/kg.
The owner called the ASPCA Animal Poison Control Center (APCC) about 15 minutes after the exposure. At that time, the dog, which was in good health, was not exhibiting clinical signs.
THINKSTOCK/JAROSLAW WOJCIK; GETTY IMAGES/VASILYPETKOV
Since the dog was asymptomatic, ASPCA APCC staff advised the owner to give the dog a small amount of milk to act as a demulcent (a coating agent that helps to reduce and relieve irritation to the oral cavity and stomach) and to monitor the dog at home for signs of mild gastrointestinal (GI) upset, including vomiting, anorexia, and diarrhea. The owner was also instructed to withhold food and water if the dog vomited.
The dog started vomiting about 75 minutes after the exposure and had intermittent vomiting for about 45 minutes. The vomitus contained clear liquid and evidence of the ointment. The dog was lethargic but was completely back to normal within seven hours.
Diaper rash creams contain 10% to 40% zinc oxide. Zinc oxide can also be found in sunscreens (1% to 25%), powders, ointments, medicated bandages, dental cements, and calamine products. When used in diaper rash ointments, zinc oxide is often combined with other ingredients such as vitamins A, D, and E; cod liver oil; lanolin; petrolatum; mineral oil; dimethicone; methylparaben; and butylated hydroxyanisole. When administered topically, zinc oxide acts as an astringent and also has bactericidal properties.1
Zinc is an essential trace mineral required in all species, and feed-grade zinc oxide is often found in premixed rations fed to poultry, livestock, and fish. Zinc oxide is also found in most commercial dog and cat foods. The absorption of zinc depends on many variables, including the form of zinc salt, how much calcium is in an animal's diet (high-calcium diets may reduce zinc absorption), the concentrations of other minerals ingested along with the zinc, and whether or not phytate (a plant protein that may bind to zinc, decreasing absorption) is present in the animal's diet. On average, about 10% of dietary zinc is absorbed systemically. In animals that eat diets containing high amounts of plant proteins, this amount may decrease. However, animals that eat diets containing high amounts of animal proteins, in the absence of high calcium concentrations, may increase their zinc absorption to 25%.2
Dogs and cats that ingest metallic zinc sources, such as U.S. pennies minted after 1982 (containing 97.5% metallic zinc) or galvanized metal objects, are at significant risk for developing systemic zinc intoxication. Clinical signs of systemic zinc toxicosis include vomiting, inappetence, and abdominal pain. Pale mucous membranes and tachycardia secondary to hemolytic anemia can be seen in addition to elevations in liver and renal values and pancreatic enzyme activities. Hemoglobinuria and bilirubinuria are also common in symptomatic patients.1
The exact mechanism of action for zinc toxicosis is unknown. The red blood cells, liver, kidneys, and pancreas are most commonly affected. It is thought that there may be oxidative damage and inhibition of red blood cell enzymes and direct injury to the red blood cell membrane, leading to intravascular hemolysis, but that has not been proven. Excess zinc will accumulate within the liver, kidneys, and pancreas in dogs and cats.3
Zinc oxide ointments are irritating to the GI mucosa, but absorption of zinc from the GI tract is poor. As a result, dogs and cats often vomit and self-decontaminate, decreasing the risk of systemic toxicosis. Prolonged or repeated exposure to zinc oxide ointments, such as when an owner applies zinc oxide topically and the animal repeatedly licks the ointment off its skin, may lead to systemic zinc toxicosis.4
The other ingredients in zinc oxide ointments, such as cod liver oil, petrolatum, and mineral oil, result in a laxative effect but do not cause systemic toxicosis. Occasionally, some dogs will develop facial swelling and hives after ingesting zinc oxide ointments. The cause of this hypersensitivity reaction is not clear, but it is speculated to be from the parabens that are used as preservatives in these products.1
There are numerous causes for GI upset. Other rule-outs may include foreign body obstruction, viral or bacterial gastroenteritis, dietary indiscretion, or any other condition that may cause vomiting.
Diagnosis and treatment
Diagnosing zinc oxide toxicosis can be difficult since the signs can be nondescript; however, often, there is evidence of the ointment in the vomitus or the exposure was witnessed. The owner may also find the chewed tube in the house if the exposure was not observed.
According to the ASPCA APCC database, the most common clinical sign is vomiting. Vomiting is often seen shortly after ingestion, and the vomitus may contain white, frothy material (ASPCA APCC, Urbana, Ill: Unpublished data, 2012). The ASPCA APCC database also suggests that if vomiting does not occur there is an increased risk that diarrhea will develop (ASPCA APCC, Urbana, Ill: Unpublished data, 2012).
If the ingestion occurred within the past two hours and vomiting has not occurred, advise owners to give the dog milk or a small meal to help demulsify the zinc oxide ointment. There is some evidence that calcium can decrease the absorption of zinc.2
Vomiting typically manifests within four hours of ingestion.5 If vomiting does occur, advise owners to withhold food and water for at least an hour, then gradually reintroduce water and then food. If pieces of the tube are ingested, monitor the patient for a foreign body obstruction (vomiting more than 24 hours after the ingestion, anorexia, depression, inability to hold down food or water) and consider bulking the diet with whole wheat or whole grain bread, plain canned pumpkin, or cooked brown rice to facilitate passage of the foreign material.
If vomiting persists, the owner should bring the pet in to the clinic for evaluation. If there are signs of an obstruction, the pet should be evaluated as well. Other signs could include depression if the vomiting has resulted in dehydration. Persistent vomiting can be treated with maropitant (Cerenia—Zoetis; 1 mg/kg subcutaneously once a day).6 Monitor for electrolyte abnormalities, and provide intravenous fluids if needed.
CONCLUSION AND CLINICAL RELEVANCE
Zinc oxide exposures are typically not life-threatening. Most owners are able to manage the signs at home, but veterinary care might be needed if clinical signs become persistent. The tube itself is generally not toxic; it is usually made of plastic or aluminum. However, the tube has the potential to cause an obstruction in the GI tract.
Treatment of acute zinc oxide toxicosis is usually limited to treating gastroenteritis and does not require treatment with chelating agents.
Samantha Wright and Brandy R. Sobczak, DVM, ASPCA Animal Poison Control Center, 1717 S. Philo Road, Suite 36, Urbana, IL 61802.
1. Zinc oxide—topical. In: POISINDEX System (electronic version). Truven Health Analytics, Greenwood Village, Colo. Available at: http://www.thomsonhc.com. Accessed Dec. 12, 2012.
2. Ozpinar H, Abas I, Bilal T, et al. Investigation of excretion and absorption of different zinc salts in puppies. Lab Anim 2001;35:282-287.
3. Dziwenka MM, Coppock R. Metals and minerals—zinc. In: Plumlee KH, ed. Clinical veterinary toxicology. St. Louis, Mo: Mosby, 2004;221-226.
4. Welch SL. Oral toxicity of topical preparations. Vet Clin North Am Small Anim Pract 2002;32(2):443-453.
5. Zinc oxide. The Merck veterinary manual (electronic version). Available at: http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/214015.htm. Accessed Aug. 12, 2013.
6. Plumb DC. Plumb's veterinary drug handbook. 7th ed. Stockholm, Wis: PharmaVet, 2011;624-626.