A number of factors need to be considered in deciding the best approach to decontaminating a toxicant-exposed patient. In animals orally exposed to toxicants, these factors include consideration of the substance and amount ingested, whether multiple agents were ingested, the time since ingestion, whether attempts at decontamination have been undertaken prior to presentation, the species of animal involved, number of individuals exposed and whether there is any known underlying organ dysfunction, especially affecting the liver or kidneys.
A number of factors need to be considered in deciding the best approach to decontaminating a toxicant-exposed patient. In animals orally exposed to toxicants, these factors include consideration of the substance and amount ingested, whether multiple agents were ingested, the time since ingestion, whether attempts at decontamination have been undertaken prior to presentation, the species of animal involved, number of individuals exposed and whether there is any known underlying organ dysfunction, especially affecting the liver or kidneys. Obviously, the inherent toxicity of an ingested substance is important. If the substance is non-toxic or has relatively low toxicity, then extensive decontamination procedures are generally not necessary. An exposure assessment should always be attempted in order to estimate the dose ingested; this estimate should be compared to known toxicity information whenever possible. If the ingested dose approaches a toxic dose, then more vigorous decontamination procedures are warranted. For example, if a dog has recently ingested an amount of an anticoagulant rodenticide that is well below reported toxic doses (less than or equal to 1/10th of an LD50 as a general, but not absolute, rule), then close monitoring at home for several days may be sufficient. Ingestion of higher doses may warrant administration of an adsorbent such as activated charcoal (AC) with or without a cathartic followed by close monitoring in the hospital. Unfortunately, in many situations, toxicity information may not be available for the specific toxicant ingested or, if toxicity data is available, it may have been determined only in a laboratory species such as a rat or mouse. In the latter case, extrapolation of toxicity data to the affected species can be problematic. In such situations, it is probably better to be conservative and institute decontamination procedures as soon as possible.
The nature of the substance ingested should be considered. For example, if a volatile organic hydrocarbon has been ingested, the high risk of aspiration of material into the lungs following emesis precludes the routine administration of an emetic. If a product containing several potentially toxic substances was ingested, all ingredients in the formulation need to be considered in selecting an appropriate decontamination plan. Volatile petroleum hydrocarbons can be vehicles for a variety of pesticides. Therefore, the risks associated with aspiration of the hydrocarbons needs to be considered in comparison to the toxicity and amount of active ingredient ingested.
The time since ingestion is critical; numerous studies have shown that the amount of material retrieved from the stomach following induction of emesis or performance of gastric lavage (GL) declines dramatically with time. Therefore, in most situations, induction of emesis or performance of GL greater than one hour following ingestion may not retrieve a clinically significant amount of material and may delay the administration of an adsorbent such as activated charcoal (AC). If toxicant-induced emesis has occurred or owners have successfully induced emesis at home prior to presentation, there is little to be gained from further attempts to remove material from the stomach.
Exposure to potential toxicants other than via the oral route may necessitate specific decontamination procedures such as ocular irrigation or bathing. Large volumes of warm water and a mild detergent should be used to thoroughly wash hair and skin; multiple cycles of washing and rinsing may be necessary. Severely depressed or comatose patients require close monitoring to avoid hypothermia or aspiration of water and detergent. Whatever decontamination procedure is undertaken, it is important to protect oneself and others from toxicant exposure.
Once a determination is made that an animal has been exposed to a potentially toxic amount of a substance or is intoxicated, a general approach to case management should adhere to the following principles: (1) stabilize vital signs (this may include administration of an antidote if sufficient information concerning a specific toxicant exposure is immediately available), (2) obtain a history and clinically evaluate the patient, (3) prevent continued systemic absorption of the toxicant, (4) administer an antidote if indicated and available, (5) enhance elimination of absorbed toxicant, (6) provide symptomatic and supportive care, and (7) closely monitor the patient. Obviously, each situation is unique and one or more of the steps may be eliminated. For example, there may not be an antidote for a given toxicant or a way to significantly enhance its elimination once systemically absorbed.
Specific approaches to stabilization of vital signs are discussed more thoroughly elsewhere. Briefly, attention should be paid to maintaining a patent airway and providing adequate ventilation, maintaining cardiovascular function with attention to appropriate fluid and electrolyte administration, maintaining acid-base balance, controlling central nervous system signs such as seizures and maintaining body temperature. In some situations, it may be critical to administer an antidote quickly. For example, in suspected cholinesterase-inhibiting insecticide intoxication (organophosphates or carbamates), administration of atropine may be critical to control life-threatening muscarinic signs such as bronchospasm and bronchorrhea before proceeding with subsequent management steps.
Obtain a History and Clinically Evaluate the Patient
Once vital signs are stable, a thorough history should be obtained while the animal is being further evaluated. If blood or urine samples are obtained for clinical evaluation, appropriate portions should be set aside for possible toxicologic testing. A minimum database in suspected toxicologic cases includes: CBC, BUN, creatinine, serum electrolytes, glucose, liver enzymes, ECG, blood gases, pulse oximetry, urinalysis and body temperature. Abdominal radiographs should be considered to detect ingested metal objects.
Prevent Continued Absorption of Toxicant
Gastrointestinal decontamination (GID) is a critical component of case management. Appropriate and timely decontamination may prevent the onset of clinical signs or significantly decrease the severity or shorten the course of intoxication. GID consists of three components: 1) gastric evacuation, 2) administration of an adsorbent and 3) catharsis.
Gastric evacuation
Approaches to gastric evacuation include induction of emesis with emetics such as syrup of ipecac, 3% hydrogen peroxide, apomorphine or xylazine and GL. Syrup of ipecac and 3% hydrogen peroxide are often available in the home and should be considered for inducing emesis if there will be a delay in bringing an animal to the hospital. Owners may have difficulty administering syrup of ipecac to cats due to its objectionable taste. Three percent hydrogen peroxide can be administered relatively easily; if emesis does not occur within 10 minutes, the dose can be repeated once. Emesis is often more effectively induced when the stomach is full; therefore, instructing the owner to feed a small amount of food prior to induction can improve efficacy. Disadvantages of syrup of ipecac include prolonged emesis and adsorption by AC. The later is undesirable since the administration of AC may have to be delayed to allow the emetic action of syrup of ipecac to occur. The primary disadvantage of 3% hydrogen peroxide is its inconsistent efficacy.
In a clinical setting, apomorphine is the emetic of choice for dogs. Apomorphine stimulates dopaminergic receptors in the chemoreceptor trigger zone (CRTZ) and the emetic center. Stimulation of the CRTZ induces emesis while stimulation of the emetic center suppresses emesis. Therefore, it is important that apomorphine reaches the CRTZ before the emetic center. This is accomplished by rapidly administering apomorphine either IV, IM or via instillation in the conjunctival sac. Oral administration is less efficacious. Apomorphine is not recommended for use in cats. As an alternative, xylazine can be used. While apomorphine and xylazine induce emesis quickly, they also cause CNS depression and bradycardia, which are unwanted side effects. Naloxone can reverse the CNS and respiratory effects of apomorphine, while yohimbine can be used to reverse the respiratory depression and bradycardia associated with xylazine use. Table salt, liquid dish detergent and dry mustard should not be used as emetics due to their questionable efficacy and potential for side effects. In the case of repeated administration of table salt, iatrogenic hypernatremia can be a serious sequela.
GL can be employed in those cases in which gastric evacuation is indicated but administration of an emetic is contraindicated (presence of seizures, severe depression or coma, loss of normal gag reflex, hypoxia, species unable to vomit, and known, prior ingestion of corrosives or volatile petroleum products). In a conscious animal, GL requires anesthesia. Airway protection is necessary whenever GL is performed. As large a gastric tube as possible with terminal fenestrations is introduced into the stomach. Tube placement is confirmed by aspiration of gastric contents or air insufflation with a stethoscope placed over the stomach. After the tube is placed, the mouth should be kept lower than the chest. Tepid tap water or normal saline (5 to 10 ml/kg) is introduced into the stomach with minimal pressure application and is withdrawn by aspiration or allowed to return via gravity flow. The procedure is repeated until the last several washings are clear; numerous cycles may be required. AC (+/- cathartic) can be administered via the tube just before its removal. The initial lavage sample should be retained for possible toxicologic analysis.
Adsorbents
Realistically, the only adsorbent routinely used in veterinary medicine is AC. AC is available as a powder, an aqueous slurry or combined with cathartics such as sorbitol. It is formed from the pyrrolysis of various carbonaceous materials such as wood, coconut or peat. The material is treated with high temperatures and oxidizing agents to form a maze of pores to increase its surface area. Adsorption of chemicals occurs as a result of non-covalent binding (ion-ion, dipole and van der Waal's forces). Rate of adsorption is dependent on external surface area while the adsorptive capacity is dependent on internal surface area. In rare instances, other adsorbents such as Fuller's earth or bentonite may be suggested for specific toxicants such as paraquat. AC is an effective adsorbent for a number of toxicants with several notable exceptions. Substances not well adsorbed to AC include strongly ionized and dissociated salts such as sodium chloride and small, highly polar, hydrophilic compounds such as alcohols, strong acids, alkalis and bromide and metals such as lead, iron and lithium. In those situations in which there is a high suspicion of significant toxicant ingestion but a specific toxicant cannot be identified, AC should be administered.
AC given repeatedly (multiple dose AC or MDAC) is effective in interrupting enterohepatic recycling of a number of toxicants and the continued presence of AC in the gastrointestinal tract may allow the tract to serve as a sink for trapping toxicant passing from the circulation into the intestines. MDAC has reportedly increased the elimination of digitoxin, phenobarbital, carbamazepine, phenylbutazone, dapsone, methotrexate, nadolo, theophylline, salicylate, cyclosporine, propoxyphene, nortriptyline and amitriptyline. MDAC has theoretical benefits when large amounts of toxicant are ingested, where dissolution of toxicant is delayed (masses of capsules), when toxicant has a delayed or prolonged release phase or if the toxicant undergoes extensive enterohepatic recirculation. Empirically, a loading dose of 1 to 2 g/kg of AC is administered followed by 0.25 to 0.50 g/kg every 1 to 6 hours. The total dose administered may be more important than the actual dosage protocol. There is little hazard to repeated administration of AC, although cathartics should be given only once. On rare occasions, constipation or intestinal obstruction can occur with MDAC, particularly in dehydrated patient.8
Timing of AC administration is important. AC should be administered as soon as possible after toxicant ingestion. In a recent summary of reduction of drug absorption by a single dose of AC in a series of 115 human volunteer studies at various times after drug administration, the mean % reduction when AC was given within 60 minutes of drug ingestion was ~ 64% compared to only ~ 33% when AC was given greater than 60 minutes after drug administration.
Cathartics
Both saline (sodium sulfate or magnesium sulfate or citrate) and saccharide (sorbitol) cathartics are available for use. In theory, cathartics hasten the elimination of unabsorbed toxicant via the stools. In general, cathartics are safe, particularly if used only once. However, repeated administration of magnesium-containing cathartics can lead to hypermagnesemia manifested as hypotonia, altered mental status and respiratory failure. Also, repeated administration of sorbitol can cause fluid pooling in the gastrointestinal tract, excessive fluid losses via the stool and severe dehydration. Contraindications to the use of cathartics include: absence of bowel sounds, intestinal obstruction or perforation, recent bowel surgery, volume depletion, significant electrolyte imbalance or ingestion of a corrosive substance. Use of a cathartic is questionable in a patient that presents with toxicant-induced diarrhea. Additionally, cathartics should be used cautiously in very young or old animals. Bulk and lubricant laxatives such as methylcellulose and mineral oil, respectively, are not recommended for use due to their relatively slow onset of action. Irritant or stimulant laxatives such as castor oil or phenolphthalein are also not recommended. The efficacy of administering mineral oil to horses exposed to toxicants has not been demonstrated and its use in lieu of more accepted methods of gastrointestinal decontamination (AC + osmotic cathartic) is difficult to justify.
In recent years, a critical reappraisal of GID approaches in human intoxications has occurred that is relevant for the management of intoxicated animals. There has been a movement away from gastric evacuation (induction of emesis or GL) followed by the administration of an adsorbent toward the administration of only the adsorbent, especially in mild to moderate intoxications. Early administration of AC alone has been shown to be as efficacious as the combination of gastric evacuation followed by AC. The advantages to the administration of AC alone compared to gastric evacuation procedures followed by AC administration include the more rapid administration of AC and subsequent adsorption of toxicant, the rapid movement of an AC slurry through the pylorus to the small intestine where systemic absorption of the majority of toxicants occurs and the effectiveness of AC to adsorb most commonly ingested toxicants.
The case for or against the inclusion of a cathartic with AC is less clear-cut but the administration of a single dose of a cathartic along with the initial dose of AC is currently recommended. Those AC formulations that include a cathartic such as sorbitol should be administered only once followed by AC alone if repeated doses of AC are indicated.
One newer approach to human GID is whole bowel irrigation (WBI), which involves the oral administration of large volumes of an electrolyte-balanced solution until a clear rectal effluent is produced. A polyethylene glycol solution, routinely employed to cleanse the gastrointestinal tract for surgical or radiographic procedures in humans, is used. WBI has been shown to be efficacious in those situations in which an ingested toxicant is poorly adsorbed to AC or in which sustained-release medications have been ingested. Another potential use might be in those instances in which small metal objects or lead-based paint have been ingested. WBI has been well tolerated in human pediatric patients. The utility of WBI in veterinary medicine has not been determined, but the need to administer large volumes of liquid may limit its use.
Endoscopic removal of foreign objects can be a viable decontamination procedure. Removal of potentially toxic metallic objects such as zinc-containing pennies, galvanized metal or lead objects or button batteries from the stomach may prevent or minimize morbidity or mortality.
Additional Reading
1. American Academy of Clinical Toxicology and the European Association of Poison Centres and Clinical Toxicologists: Position statement: ipecac syrup. J Toxicol Clin Toxicol 35:699-709, 1997.
2. American Academy of Clinical Toxicology and the European Association of Poison Centres and Clinical Toxicologists: Position statement: gastric lavage. J Toxicol Clin Toxicol 35:711-719, 1997.
3. Beasley VR and Dorman DC, in Beasley VR: The Veterinary Clinics of North America: Toxicology of Selected Pesticides, Drugs, and Chemicals. Philadelphia, 1990, Saunders, pp 307-337.
4. Shannon MW and Haddad LM, in Haddad LM: Clinical Management of Poisoning and Drug Overdose, ed 3, Philadelphia, 1998, Saunders, pp 2-31.
5. Hackett T: Emergency approach to intoxications. Clin Tech Sm An Prac 15:82-87, 2000
6. Drellich S, Aldrich J, in Peterson ME, Talcott PA, Small Animal Toxicology. Philadelphia, 2001, Saunders, pp 33-47
7. American Academy of Clinical Toxicology and the European Association of Poison Centres and Clinical Toxicologists: Position statement: single dose activated charcoal. J Toxicol Clin Toxicol 35:721-741, 1997.
8. Oehme FW, Mannala S. In Peterson ME, Talcott PA: Small Animal Toxicology. Philadelphia, 2001, Saunders, pp 653-665.
9. Kulig K, in Ford MD et al.: Clinical Toxicology. Philadelphia, 2001, Saunders, pp 34-41.
10. American Academy of Clinical Toxicology and the European Association of Poison Centres and Clinical Toxicologists: Position statement: cathartics. J Toxicol Clin Toxicol 35:743-752, 1997.
11. Perry H, Shannon M: Emergency department gastrointestinal decontamination. Pediatric Annals 25:19-29. 1996.
12. American Academy of Clinical Toxicology and the European Association of Poison Centres and Clinical Toxicologists: Position statement: whole bowel irrigation. J Toxicol Clin Toxicol 35:753-762, 1997.
Podcast CE: A Surgeon’s Perspective on Current Trends for the Management of Osteoarthritis, Part 1
May 17th 2024David L. Dycus, DVM, MS, CCRP, DACVS joins Adam Christman, DVM, MBA, to discuss a proactive approach to the diagnosis of osteoarthritis and the best tools for general practice.
Listen