Digging Into Compost Intoxication
AN EXAMPLE OF COMPOST
The contents can vary significantly, potentially leading to a wide range of clinical signs.
Welcome to Practical Toxicology, brought to you in partnership between Today’s Veterinary Practice and the ASPCA Animal Poison Control Center (APCC) (aspcapro.org/poison). This column provides practical clinical information about diagnosing and treating pets that have been exposed to potentially harmful substances. If treating a patient that requires emergency care for poisoning, call the APCC at 888-426-4435.
Household compost is most commonly produced through the controlled decomposition of food waste and plant material. Once thoroughly decomposed, compost can be used as a fertilizer or soil amendment.1 Compost piles in pet owners’ backyards are often accessible to companion animals and may contain foodstuffs that make the compost very attractive for pets to ingest.
Animals presenting to veterinary hospitals with clinical signs after ingesting compost may not always have a history of ingesting compost, but it should be considered if compost is present in the animal’s environment and clinical signs are consistent. Even with a history of ingesting compost, the clinical signs and toxicity concerns will vary depending on the configuration of the compost and the degree of decomposition. Thorough history taking, careful monitoring, and symptomatic and supportive care based on the clinical signs are key to providing the best chance of a positive outcome in these cases.
Depending on what is in the compost pile, onset of clinical signs can be rapid. In addition, the toxic items found in a compost pile may have a synergistic effect, increasing the severity of the intoxication. The entire veterinary team can participate in triaging a compost exposure case, with one team member evaluating the patient and stabilizing if needed, while another team member obtains a brief initial history. As with any critical situation, vital signs should be obtained and the ABCs (airway, breathing, circulation) assessed. When clinical signs are present, remember to treat the pet and not the poison. Triaging may also include confining the patient to prevent injury, minimizing sensory stimuli, and promptly removing vomit or feces.
With a compost exposure, obtaining a history starts when the client service representative takes the call or when the patient arrives at the clinic (TABLE 1).2 Understanding the circumstances of a compost exposure can provide the veterinary team with valuable information. This team approach helps to determine what could be in the compost pile and confirms details on timing or circumstances of the ingestion. A good history will also provide important details about the patient that can affect the compost exposure, such as existing health concerns, drug interactions, or recent surgeries. Documentation is equally important. A compost pile can contain a variety of items, and good documentation allows referencing of this information, especially if signs persist or the clinical picture changes.
After triaging the patient and obtaining a detailed history, the next step is decontamination. Given the range of items that can be found in a compost pile, decontamination options can vary. When the patient is asymptomatic, we can start with inducing emesis. For additional information on at-home and in-clinic instructions and contraindications, see Freed et al.3 Depending on what was ingested, activated charcoal may be indicated to help bind to material and possibly decrease transit time. In some situations, hypersalivation can be seen because of a taste, and something as simple as wiping the mouth or offering something tasty will do the trick.3 As with many treatment recommendations, there are contraindications or limitations. These factors may include history of exposure, current clinical signs, or pre-existing clinical signs. Remember to tailor all treatments according to the complete picture of the compost exposure.
SPECIFIC TOXINS POTENTIALLY PRESENT IN COMPOST
The composition of compost varies greatly between households. Some of the most common concerning items in the compost pile are foods (including moldy and fermented foods) and toxic plants.
A variety of toxic foods can be present in compost piles. Grapes and raisins, for example, can cause acute kidney injury in some dogs.4 The mechanism is unknown. Macadamia nuts can cause gastrointestinal upset, tremors, and hind-end weakness.5 Garlic, onion, leeks, and chives can cause Heinz body anemia and hemolysis with secondary kidney injury.6 Chocolate and coffee and cause stimulatory signs, such as tachycardia, hyperactivity, tremors, and seizures.7 When cooked, bones can splinter, leading to gastrointestinal trauma and potential foreign-body obstruction. Finally, xylitol can cause hypoglycemia and liver injury.8
The list of potentially toxic plants is extensive. Many plants will remain toxic well into the composting process. A small sampling of common landscaping plants of concern are yew (Taxus species), rhododendrons and azaleas (Rhododendron species), oleander (Nerium oleander), foxglove (Digitalis species), and sago palm (Cycas revoluta).9,10 Ingested weeds can present an additional problem, most notably poison hemlock (Conium maculatum), castor bean (Ricinus communis), and water hemlock (Cicuta maculata).10 Tomatoes (Solanum lycopersicum) can be an issue, especially if the fruits are placed into the compost pile and then sprout. Additionally, with the increasing popularity of home brewing, hops (Humulus lupulus) can cause severe toxicosis if the spent hops are ingested from the compost pile.11
Decomposing material in the compost piles can start to form mold. Most molds cause only gastrointestinal upset. However, some molds can produce tremorogenic mycotoxins, which cause tremors and seizures in animals. Tremorogenic mycotoxins are more likely to grow on material that is rich in lipids and proteins, such as dairy, grains, shells, and husks, making compost piles an ideal environment for their growth. Clinical signs associated with tremorogenic mycotoxin toxicosis include gastrointestinal upset, tremors, seizures, hyperesthesia, and nystagmus. Changes in laboratory results (such as hypoglycemia and increased levels of liver enzymes, lactate, and creatine kinase) and disseminated intravascular coagulation secondary to hyperthermia can also occur.12
Some of the decomposing material may ferment as it breaks down, producing ethanol as a byproduct. Fruits, grains, and sources of sugar (such as honey) are most likely to produce ethanol. This is an anaerobic process, so even a well-maintained compost pile can contain ethanol. Clinical signs shown from a pet that ingests this fermented material include lethargy, ataxia, depression, hypothermia, recumbency, and acidosis. There is a risk of aspiration if the pet vomits while intoxicated, due to a decreased ability to protect their airway.13
Treatment is aimed at controlling the clinical signs that are being exhibited. Baseline laboratory testing should be considered for these patients and monitored as clinical signs and potential exposures indicate. If the patient is exhibiting generalized muscle tremors, a benzodiazepine could be considered, but often tremors will be refractory and treatment with methocarbamol will be necessary.10 Intravenous fluids should be considered for support in any patient showing clinical signs. Continued intravenous fluid diuresis may be indicated if the patient may have ingested grapes or raisins.4 Good nursing care and rapid identification of new or worsening clinical signs are key to successfully managing compost intoxication cases.
Compost intoxication can present multiple toxicologic risks. However, accurate and thorough history taking allows a complete understanding of all potential risks and facilitates subsequent treatment. Monitoring for all the toxicants present in the compost pile can maximize the chances of a full recovery.
- Composting for the homeowner. University of Illinois Extension. March 26, 2018. https://web.extension.illinois.edu/homecompost/benefits.cfm
- Lohmeyer C. Taking a toxicologic history. In: Poppenga R, Gwaltney-Brant S, eds. Small Animal Toxicology Essentials. Ames, IA: Wiley-Blackwell; 2011:27-30.
- Freed E. Oral decontamination in dogs and cats. Today’s Veterinary Nurse. 2016;1(6):30-34.
- Gwaltney-Brant S, Holding J, Donaldson C, Eubig P, Khan S. Renal failure associated with ingestion of grapes or raisins in dogs. JAVMA 2001;218(10)1555-1556.
- Hansen S, Buck WK. Weakness, tremors, and depression associated with macadamia nuts in dogs. Vet Hum Toxicol 2000;42(1)18-21.
- Freed E. A pungent poisoning: onion toxicosis in a cat. Vet Med August 1, 2015. http://veterinarymedicine.dvm360.com/pungent-poisoning-onion-toxicosis-cat. Accessed May 16, 2018.
- Gwaltney-Brant S. Chocolate intoxication. Vet Med 2001;96(3):108-110.
- Dunayer E. New findings on the effects of xylitol ingestion in dogs. Vet Med 2006;December:791-797.
- Barr AC. Household and garden plants. In: Peterson M, Talcott P, eds. Small Animal Toxicology, 3rd ed. St. Louis: Elsevier; 2013:357-400.
- Burrows G, Tyr R. Toxic Plants of North America. Ames, IA: Wiley-Blackwell; 2013.
- Duncan K, Hare W, Buck W. Malignant hyperthermia-like reaction secondary to ingestion of hops in five dogs. JAVMA 1998;210(1):51-54.
- Waratuke K. Practical toxicology: tremorgenic mycotoxin intoxication in dogs. Today’s Veterinary Practice 2017;May/June:85-88
- Richardson J. Ethanol. In: Peterson M, Talcott P, eds. Small Animal Toxicology. St. Louis: Elsevier; 2013:547-549.