Initial Management of the Acutely Poisoned Patient

Chapter 5 Initial Management of the Acutely Poisoned Patient



Sharon Drellich, DVM, Janet Aldrich, DVM


According to the American Association of Poison Control Centers, 140,614 poison exposures were reported in animals in 1993-1994.1 These data do not include poisonings handled in veterinary hospitals and not reported, so the actual number of poisonings in animals in any one year is higher. The majority of reported poisonings (82%) occurred in dogs, whereas only 14% occurred in cats. More than 90% of canine and 75% of feline poisonings occurred by ingestion. Dermal exposure was the second most common route. Inhalation and ocular exposures comprised less than 2% of exposures in both species.1 Poisonings, real or suspected, are situations encountered often by emergency veterinarians. Treatment of poisonings can be very rewarding for the owner, pet, and veterinarian, but it is essential to have a plan in place for dealing with poisonings to ensure a successful outcome.


The aim of this chapter is to provide an overall approach to the acutely poisoned patient similar to the approach taken to any critically ill patient. When it is germane to the topic, antidotes will be mentioned. However, specific antidotal treatments for specific poisons are covered elsewhere in the text.



TELEPHONE TRIAGE


The first contact with the owner is often over the telephone. Species, size, age, and breed of animal should be determined. Historical information collected should include the length of time elapsed since the exposure and, if possible, the type and amount of compound the animal was exposed to. It is impossible to determine over the telephone the condition of the animal, but it is important to try to establish the level of consciousness. If the time before arrival at the hospital will bring the time elapsed since exposure to more than an hour, it may be of benefit to have the owner induce emesis. Induction of emesis should not be recommended if the animal is mentally compromised, if the level of consciousness cannot be determined, if there is any respiratory distress, or if there is a preexisting condition affecting the patient’s ability to protect its airway (i.e., laryngeal paralysis). Induction of emesis is also contraindicated in animals who have ingested caustic substances, such as acids or alkalis. Owners of animals that have ingested alkali or acid materials should be instructed to give the pet large amounts of water or milk to dilute the material and proceed as quickly as possible to the veterinary hospital for further care.


If it is determined that the animal is alert and not in respiratory distress, emesis may be indicated. Syrup of ipecac, table salt, and 3% hydrogen peroxide (H2O2) are most often used for inducing emesis at home. Salt and hydrogen peroxide appear to induce emesis by irritating the pharyngeal and gastric sensory neurons, which transmit impulses via the glossopharyngeal and vagus nerves, respectively, to the central nervous system. Excessive salt ingestion could potentiate hypernatremia and other metabolic derangements; therefore, its use as an emetic is strongly discouraged. Hydrogen peroxide has been associated with a few cases of fatal air emboli and mucosal erosions in humans.2


Syrup of ipecac is readily available over the counter. The recommended dose is 1 to 2 mL/lb PO in dogs and 3.3 mL/lb PO in cats.3 Ipecac directly stimulates the gastric mucosal receptors and indirectly stimulates the chemoreceptor trigger zone in the posterior medulla to induce emesis. Although ipecac syrup has a high margin of safety, many adverse side effects of its use have been reported, including prolonged vomiting and diarrhea, lethargy, fever, and irritability along with isolated cases of gastric rupture, intracranial hemorrhage, and diaphragmatic hernia in humans.4 After a review of the available scientific literature related to emesis induction in poisonings, the American Academy of Clinical Toxicology and the European Association of Poison Centres and Clinical Toxicologists published a position statement regarding ipecac syrup. They found that clinical studies in people have not confirmed that ipecac syrup improves the outcome of poisoned patients, and its routine use should be abandoned. Its use may delay further gastrointestinal decontamination and administration of activated charcoal and oral antidotes caused by prolonged emesis. The effectiveness of the activated charcoal and antidotes may be reduced as well.4 If vomiting is induced, it should be in cases of witnessed toxin ingestion and should be performed within 60 minutes of ingestion, and the gastric contents should always be saved and brought to the hospital with the pet for visual and toxicological examination. Although it is often recommended to repeat the emetic in 15 minutes if no vomiting has occurred, it may be more helpful in the long run if the owners are on their way to the veterinary hospital by that time.


If the animal is having seizures or is trembling, care should be taken to avoid self-induced trauma while en route to the hospital. Owners should be advised that a pet with an altered mental state, or one that is anxious and uncomfortable, may bite or react unexpectedly, so owners should protect themselves from possible injury as well. The animal should be kept warm if it is recumbent and/or unconscious.



AT THE VETERINARY HOSPITAL


Management of an acute case of intoxication can be organized into five areas: (1) ABCs of the critically ill patient: a irway, b reathing, c irculation; (2) gaining control of seizures or tremors; (3) assessment of metabolic and medical derangements and institution of a plan for their management; (4) gastrointestinal decontamination; and (5) supportive care. In this chapter we will discuss the first four areas; supportive care and further details on gastrointestinal decontamination are discussed in later chapters. To some extent, these first four areas should be dealt with at the same time; it is merely convenient for the sake of discussion to put them in order.


On arrival at the veterinary hospital, vital signs should be immediately assessed. The patency of the airway should be evaluated and reestablished with a cuffed endotracheal tube if necessary. Anticonvulsants should be administered as necessary (to be discussed in more detail later), and hydration and metabolic status should be assessed and addressed rapidly. Poisoned animals may have severely altered homeostatic mechanisms and therefore may be hypothermic or hyperthermic. It is necessary to treat the patient and not the toxicosis. This means that although gastric decontamination is integral to the long-term outcome, there may be more immediate life-threatening concerns in any individual case.



THE ABCS OF CRITICAL PATIENT CARE



Airway


Any animal that is unconscious, appears to have neuromuscular paralysis or paresis, or is in severe respiratory distress is a candidate for intubation. If there is no voluntary respiratory effort or if gastric lavage is planned, intubation is required. Anesthesia is required for intubation if the animal is conscious. These patients may or may not also require intermittent positive pressure ventilation. An appropriately sized cuffed endotracheal tube is placed, the cuff is inflated, and the tube is tied securely to the muzzle. When possible, a blood sample is collected for arterial blood gas determination; this helps in assessing the need for supplemental oxygen and assisted ventilation. Other methods available for monitoring ventilation include apnea alert monitors and end-tidal carbon dioxide (CO2) monitors.



Breathing


Hypoventilation indicates a need for assisted ventilation. Hypoventilation is identified by the presence of hypercapnia (PaCO2 >45 mm Hg) with acidosis (pH <7.35). If assisted ventilation is contraindicated or is unavailable, a degree of “permissive hypercapnia” may be well tolerated by the patient. Guidelines for permissive hypercapnia state that a PaCO2 of >50 mm Hg can be tolerated if the pH remains above 7.25 and cardiovascular function is adequate.5 Hypoventilation is usually secondary to central nervous system and neuromuscular abnormalities. If pulmonary function in dogs and cats is normal, ventilation at normal minute volumes (100 to 200 mL/kg) with room air or a slightly increased FiO2 should return the blood gases to normal. Permissive hypercapnia is contraindicated in patients with CNS disease or cerebral edema because the resulting cerebral acidosis will cause cerebral vasodilation and can increase cerebral morbidity.


Hypoxemia (PaO2 >65 mm Hg) should be treated with enriched oxygen of 40% or more as necessary to maintain the PaO2 at >65 mm Hg. If continued increases in the inspired oxygen concentration do not improve the PaO2, or if the effort required to maintain the PaO2 at that level is excessive and exhausting, assisted ventilation is required. If the toxin was not inhaled, a reason for the hypoxemia must be sought. Aspiration pneumonia or preexisting respiratory disease should be considered, and a work-up should be performed when the patient is stabilized. The management of patients on mechanical ventilation is beyond the scope of this chapter, and the reader is referred to the references at the end of the chapter.6,7



Circulation (oxygen delivery)


Adequate oxygen delivery (circulation) is dependent on the volume of blood in the vessels, the pumping function of the heart, the integrity of the blood vessels, and the oxygen content of the blood. An early assessment of the electrocardiogram (ECG) will aid in determining the function of the pump. Toxins such as oleander, foxglove, and other cardiotoxic plants, organophosphates, and overdoses of therapeutic drugs for cardiac disease directly affect the heart. Many hydrocarbons and industrial chemicals have arrhythmogenic properties as well.8


The vascular volume status of any intoxicated patient varies greatly among individuals. The presence of a deficit in interstitial or vascular volume depends on whether the animal has been able to eat and drink or has had vomiting or diarrhea, the type of toxin and whether it induces a diuresis, and the presence of preexisting medical conditions. As in any emergency situation, tachycardia, cold extremities, pale mucous membranes, and slow capillary refill time indicate a vascular volume deficit and perhaps hypovolemic shock. A patient with these signs should be resuscitated quickly with isotonic crystalloid solutions (60 to 90 mL/kg in dogs and 40 to 50 mL/kg in cats), colloid solutions (10 to 20 mL/kg in dogs and 5 to 10 mL/kg in cats), or a combination of these. If the poison was a vitamin K antagonist, the preferred fluid may be frozen plasma and packed red blood cells. The source of hemorrhage should be located and vitamin K1 therapy begun immediately.


Interstitial deficits are identified by decreased skin turgor, dry or tacky mucous membranes, and perhaps mild azotemia. The serum sodium concentration may be high if the patient has had free water losses, or low if the patient has had losses from vomiting and/or diarrhea, but is continuing to drink water. The percentage of deficit should be estimated and the deficit volume calculated. For example, a 10-kg dog who is estimated to be 7% dehydrated has a fluid volume deficit of 10 kg × 0.07 or 0.700 kg (700 mL). The deficit can be replaced over 8 to 12 hours using an isotonic crystalloid solution. A continuing maintenance fluid should be administered at the same time to keep up with insensible losses. Ongoing fluid losses (caused by diarrhea, vomiting, or polyuria) should also be assessed and a replacement fluid added to the fluid plan. Nonsteroidal antiinflammatory agents (NSAIDs) are known to be nephrotoxic.9 If a patient has ingested toxic amounts of NSAIDs, fluid therapy planning should maximize renal perfusion. Blood urea nitrogen and creatinine levels and urinalysis should be monitored closely.


If fluid therapy does not restore adequate circulation, the heart may be unable to provide adequate cardiac output because of intrinsic damage to or disease of the myocardium. Inotropic drugs, such as dobutamine, may be justified in this setting if adequate monitoring is available. Dobutamine is delivered as a continuous IV infusion at 5 to 15 μg/kg/minute. Dopamine is an effective first line vasopressor at an initial IV dose of 3 μg/kg/minute. The dose can be titrated up to 15 μg/kg/minute. Higher doses cause dangerous tachycardia and vasoconstriction with no further improvement in cardiac output and blood pressure. Epinephrine can be used if dopamine is unsuccessful at improving blood pressure. Epinephrine is a potent alpha and beta agonist that increases cardiac output and can improve blood pressure. Higher doses increase vasoconstriction and heart rate without leading to further improvement in cardiac output. The IV dosage of epinephrine is 0.05 to 0.30 μg/kg/minute. Higher dosages of epinephrine should be avoided because they predispose the patient to ventricular fibrillation. Norepinephrine is indicated if the previously mentioned agents do not improve blood pressure. Norepinephrine is an extremely potent vasoconstrictor and may impair perfusion to the viscera and periphery. The infusion is begun at a dosage of 0.5 μg/kg/minute and can be titrated up to 1 μg/kg/minute.


Toxins may affect the blood vessels by altering the function of the smooth muscle in the vessel walls or by poisoning the endothelial cells directly. Vascular endothelium is exposed to any blood-borne toxin, and accumulation of toxin in endothelial cells can occur. Toxins can also induce the activation of inflammatory mediators produced by the endothelium, which can greatly affect vascular tone and incite the cascades responsible for the systemic inflammatory response.8 Blood pressure should be measured and maintained above a mean of 60 mm Hg. Volume replacement is the initial means of restoring blood pressure. When maximum safe volumes have been administered without satisfactory effect, vasopressor medications may have to be given.


If the blood pressure stays persistently elevated (>140 mm Hg mean arterial pressure) after adequate fluid restoration and there is evidence of increased peripheral vascular resistance, hydralazine or nitroprusside can be used to reduce the blood pressure. The use of these agents requires adequate myocardial contractility. Hydralazine is primarily an arteriolar vasodilator. It works by decreasing cytosolic calcium. Hydralazine can be administered enterally or parenterally at a dose of 0.5 to 3 mg/kg every 8 to 12 hours. In the acute care setting, a test dose can be given intravenously. Onset of action occurs in 10 to 30 minutes, and the effect lasts up to a few hours. Because of the decrease in systemic vascular resistance induced by this drug, heart rate can increase significantly and should be monitored closely. Nitroprusside is a venous and arteriolar vasodilator. It is given intravenously and its onset of action is immediate. The dosage of nitroprusside is 0.5 to 1 μg/kg/minute. This drug should not be used in patients with preexisting renal or hepatic disease. Administration of any vasoactive agent requires close monitoring of the ECG, blood pressure, and volume status of the patient. These drugs are all potentially arrhythmogenic and can dangerously elevate or reduce systemic blood pressure. Their use should not be considered if adequate monitoring is not available.


The oxygen-carrying capability of the blood is affected by several toxins. The blood oxygen content is a product of oxygen bound to hemoglobin and oxygen dissolved in the blood. These can be maximized by instituting transfusions of red blood cells, when anemia is present, and by increasing the inspired oxygen concentration. Carbon monoxide (CO) and acetaminophen are two toxins that inhibit the ability of hemoglobin to transport oxygen. Initial management in poisoning with either of these toxins is to increase the inspired oxygen concentration and support ventilation if necessary. In CO poisoning, hyperbaric oxygen therapy may be required. Acetaminophen toxicosis is treated with acetylcysteine at an initial dose of 150 mg/kg PO or IV in dogs and cats followed by three to five additional treatments at 70 mg/kg every 4 hours. Blood transfusions may be indicated based on the clinical picture.


Parameters, such as heart rate, mucous membrane color, distal extremity temperature, and color and mentation, should be monitored along with clinical laboratory indicators to aid in adjustment of the fluid plan as the patient’s condition changes. Urine output is an important indicator of vascular volume and blood pressure adequacy. Monitoring urine output accurately requires placement of a urethral catheter and a closed collection system. A urine output of less than 1 mL/kg/hour suggests a volume deficit, decreased blood pressure, or a change in renal function and should be evaluated and treated promptly.

Related posts:

  1. Summary of Small Animal Poison Exposures
  2. Considerations in Pregnant or Lactating Patients
  3. Cyanide
  4. Grapes and Raisins

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Sep 11, 2016 | Posted by in SMALL ANIMAL | Comments Off on Initial Management of the Acutely Poisoned Patient

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