CVT, BS, ASPCA Animal Poison Control Center, Urbana, Illinois
Carrie has been working as a certified veterinary technician at the ASPCA Animal Poison Control Center (APCC) since 2007. She obtained her associate’s degree in veterinary technology from Parkland College in 2003 and her bachelor’s degree in natural resources and environmental science from the University of Illinois in 2006. She worked for 2.5 years at a small animal clinic while in college and has assisted with several research projects in fish and wildlife ecology.
During her 10 years at the APCC, Carrie has gained a wealth of knowledge in the field of toxicology. She has been published in several peer-reviewed journals and is currently studying to become a board-certified toxicologist.Read Articles Written by Carrie Lohmeyer-Mauzy
The winter holiday season holds an abundance of dangers for domestic pets that could result in toxicosis. This article will focus on exposures to chocolate, grapes and raisins, and homemade playdough in dogs. Plants that dogs and cats are commonly exposed to during the winter months will also be discussed.
The APCC received more calls about chocolate than any other agent in 2016, averaging over 41 cases per day. An influx of chocolate exposures is observed by APCC during the winter season because the agents are readily available to pets in the home. Examples of common forms of chocolate the APCC receives calls about are candy bars, snack mixes, chocolate desserts (brownies, cakes, and cookies), and baking goods such as chocolate chips and cocoa powder.
Chocolate contains 2 methylxanthines of toxicologic significance: theobromine and caffeine.1 The concentration of these methylxanthines differs between products (TABLE 1). White chocolate has a very low concentration of methylxanthines and has low toxicologic significance. Milk chocolate, dark chocolate (semi-sweet chocolate), baking chocolate (unsweetened chocolate), and cocoa powder have much higher concentrations of methylxanthines, and exposures to these more commonly result in toxicosis.
Methylxanthine toxicosis causes stimulation of the cardiovascular and central nervous systems. The degree of toxicity is dose dependent. With low doses of chocolate, only mild gastrointestinal (GI) upset is observed. At cardiotoxic doses, more severe signs such as tachycardia, tachypnea, hyperthermia, cardiac arrhythmias, tremors, and seizures can develop. If exposure to chocolate is suspected or observed, an estimated dose of methylxanthines should be calculated. In an asymptomatic patient, this dose will determine whether decontamination or treatment is necessary (BOX 1).
Decontamination and Treatment
Decontamination through emesis is recommended in patients that have ingested >35 mg/kg of methylxanthines. Doses lower than this are not expected to cause serious clinical signs. With large exposures to chocolate that do not yield a toxic dose, emesis is recommended to prevent severe GI upset and to decrease the risk of pancreatitis. Emesis should be considered if the exposure occurred within the past 2 to 6 hours.2
Activated charcoal can help in preventing absorption of methylxanthines from the GI tract. However, charcoal can cause electrolyte changes and therefore is only recommended when a risk of severe toxicosis exists.
There is no antidote for chocolate toxicosis; therefore, treatment consists largely of supportive and symptomatic care.2 Propranolol is recommended in treating moderate to severe tachycardia,2 whereas muscle tremors can be managed with methocarbamol or diazepam.2 Diazepam is also recommended for the management of seizure activity.2 IV fluids are recommended to help increase excretion of methylxanthines,2 and the bladder should be emptied regularly to prevent reabsorption of methylxanthines through the bladder wall.2
The prognosis for chocolate toxicosis is generally considered good with successful decontamination and veterinary intervention.1 However, pets that present with seizures or tachyarrhythmias have a more guarded prognosis.2
Grapes and Raisins
Exposures to grapes and raisins are especially common during the winter season because these items are used in many holiday recipes and meals.
Grapes, raisins, and zante currants belong to the genus Vitis, and ingestion can result in acute renal injury in dogs.3 The mechanism of action is unknown at this time. Although studies have evaluated these fruits for mycotoxins, pesticides, heavy metals, and vitamin D3,3 there have been no positive results for these nephrotoxins.
Not all dogs that ingest grapes or raisins develop acute renal injury. A dose-response relationship, common to other toxic agents, has not been observed with Vitis exposures.4 Therefore, the severity of toxicosis does not depend on the amount of grapes or raisins ingested. Also, grape seed extract, grape juice, grape jelly, and wine have not been shown to cause Vitis toxicosis.5
Clinical signs may be delayed by several hours after the ingestion of Vitis species. Vomiting is common within the first 24 hours,4,6 followed by diarrhea, anorexia, lethargy, and abdominal pain.1,6 Oliguria or anuria may be observed days to weeks after the exposure as renal injury progresses.1 Elevated creatinine, blood urea nitrogen, calcium, and phosphorus can be observed 24 hours after ingestion,6 whereas pathologic changes observed on blood chemistries may be delayed by several days.1,6
Decontamination and Treatment
Any exposure to grapes or raisins should be considered significant, and decontamination via emesis and activated charcoal is recommended. Grapes and raisins have a tendency to sit in the stomach for prolonged periods of time6; therefore, emesis can be induced in asymptomatic patients up to 6 hours after the exposure.5
Protection of the kidneys is critical with exposures to Vitis species. IV fluid diuresis is recommended for 48 to 72 hours.6 A baseline blood chemistry should be obtained and rechecked every 12 hours for 72 hours to monitor renal function, and electrolytes should be monitored along with urinalysis. Furosemide, dopamine, or mannitol can be used to treat oliguria, while hemodialysis or peritoneal dialysis may be helpful in treating uremia.1 The prognosis is considered poor for pets that develop weakness, ataxia, oliguria, or anuria.1,6
Exposures to homemade playdough are not as common as exposures to chocolate or grapes and raisins. The ingestion of playdough, however, can result in rapid onset of a life-threatening toxicosis called hypernatremia, an excessive amount of sodium in the blood.
Onset of Hypernatremia
Homemade playdough, used to make salt ornaments and other holiday crafts, is made from dough consisting of flour, table salt (sodium chloride), and water. Other ingredients such as vegetable oil, cornstarch, and cream of tartar are also used in some recipes. Homemade playdough contains a high concentration of salt. Some dough formulations contain 8 g of salt per tablespoon of dough.7 When the dough is ingested, an increase in sodium in the vasculature results in a fluid shift in the body, causing cellular dehydration and vascular expansion.7
Signs of salt toxicosis can be observed at a dose of 2 g of NaCl per kilogram of body weight, with the lethal dose at 4 g/kg.7 A dog is considered to be hypernatremic when the serum sodium concentration is >156 mEq/L.7 Clinical signs are commonly observed when the serum sodium concentration is >170 mEq/L.7 Vomiting develops within the first 2 hours of ingestion,5 followed by neurologic signs, including tremors and seizures.8 Signs most commonly observed by the APCC include vomiting, anorexia, diarrhea, ataxia, polydipsia, trembling, weakness, tremors, and seizures.5
Decontamination and Treatment
The treatment for acute salt toxicosis includes decontamination, management of clinical signs, and lowering serum sodium levels. With recent exposures (<2 hours) and in patients that are asymptomatic, emesis is recommended. Baseline electrolytes should be obtained and frequently monitored. Asymptomatic patients with a normal serum sodium concentration should be allowed free access to water after emesis has been managed and monitored closely for clinical signs.
Patients that have clinical signs or elevations in serum sodium concentration should be started on IV fluids using a low-sodium fluid (D5W, 0.4% NaCl).5 Warm-water enemas at a dose of 5 to 10 mL/kg can be used in addition to IV fluids.5 A loop diuretic, such as furosemide, can be administered to aid in sodium excretion and to help prevent pulmonary edema caused by fluid overload.5 Patients exhibiting mild to moderate clinical effects that receive timely and aggressive treatment generally have a favorable prognosis.5 The prognosis is guarded in patients that have developed severe neurologic signs.5
There are several popular holiday plants that dogs and cats may have the opportunity to ingest during the winter season that may remain in the home several months.
- Christmas cactus
- Evergreen trees
- Christmas kalanchoe
Exposures to Christmas cactus, evergreen trees, holly, mistletoe, and poinsettias commonly result in GI upset, but are unlikely to cause serious toxicosis. Amaryllis and Christmas kalanchoe can cause more serious signs, depending on the part of the plant the pet is exposed to and the amount of the plant ingested. TABLE 2 lists the clinical signs that can be expected after ingestion of these plants.
- Bough M. Food-associated intoxications. In: Poppenga RH, Gwaltney-Brant S, eds. Small Animal Toxicology Essentials. West Sussex: John Wiley and Sons; 2011:207-219.
- Dolder LK. Methylxanthines: caffeine, theobromine, theophylline. In: Peterson ME, Talcott PA, eds. Small Animal Toxicology. 3rd ed. St. Louis: Saunders; 2013:647-652.
- Gwaltney-Brant SM. Renal toxicity. In: Gupta RC, ed. Veterinary Toxicology: Basic and Clinical Principles. 2nd ed. Waltham: Academic Press; 2012:264-277.
- Eubig PA, Brady MS, Gwaltney-Brant SM, et al. Acute renal failure in dogs after the ingestion of grapes or raisins: a retrospective evaluation of 43 dogs (1992-2002). J Vet Intern Med 2005;19:663-674.
- ASPCA Animal Poison Control Center. Unpublished data 2017.
- Mostrom MS. Grapes and raisins. In: Peterson ME, Talcott PA, eds: Small Animal Toxicology. 3rd ed. St. Louis: Saunders; 2013:569-572.
- Tegzes JH. Sodium. In: Peterson ME, Talcott PA, eds. Small Animal Toxicology. 3rd ed. St. Louis: Saunders; 2013:807-810.
- Thompson LJ. Sodium chloride (salt). In: Gupta RC, ed: Veterinary Toxicology: Basic and Clinical Principles. 2nd ed. Waltham: Academic Press; 2012:558-561.
- Gwaltney-Brant SM. Christmastime plants. In: Peterson ME, Talcott PA, eds. Small Animal Toxicology. 3rd ed. St. Louis: Saunders; 2013:499-511.
- Delaporte J, Means C. Plants. In: Poppenga RH, Gwaltney-Brant S, eds. Small Animal Toxicology Essentials. West Sussex: John Wiley and Sons; 2011:147-160.