The poisoned or envenomated patient represents a unique challenge to the EMS medicine practitioner. In many cases the offending medication, toxin, plant, or animal is unknown to the rescuer. Even when the offending agent is known, treatment can vary significantly based on severity of symptoms. Management of a patient with tricyclic antidepressant ingestion, for example, can range from benzodiazepines to bicarbonate to intravenous intralipid emulsion therapy. Proper education and training, coupled with robust, updated protocols, is needed to care for this group of patients effectively.
Describe important toxidromes for the evaluation of prehospital patients.
Describe the initial prehospital evaluation and management of overdose on prescription medications.
List common toxic ingestions and their antidotes (Table 46-1), including whether or not charcoal is indicated.
Describe the initial prehospital evaluation and management of exposure to pesticides.
Describe the initial prehospital evaluation and management of exposure to dangerous inhalants.
Describe the initial prehospital evaluation and management of carbon monoxide poisoning.
Describe the initial prehospital evaluation and management of insect envenomations.
Describe the initial prehospital evaluation and management of reptile envenomations.
Describe the initial prehospital evaluation and management of marine envenomations.
Common Toxic Ingestions and Their Antidotes
Ingestion | Common Antidotes | Other Therapies | Charcoal Indicated |
---|---|---|---|
Narcotics | Naloxone | Sodium bicarbonate (for wide complex dysrhythmias with propoxyphene)1 | Not indicated |
Benzodiazepines | Flumazenil | Not indicated | |
β-Adrenergic antagonists (beta blockers) | Glucagon | Phosphodiesterase inhibitors2 | Indicated |
Calcium | Intravenous fat emulsion3 | ||
High-dose insulin maintaining euglycemia | Intra-aortic balloon pump | ||
Inotropes and vasopressors | Extracorporeal circulation | ||
Atropine | Cardiac pacing | ||
Calcium channel blockers | Atropine | Intravenous fat emulsion4 | Indicated |
Calcium | |||
Inotropes and vasopressors | Intra-aortic balloon pump | ||
Glucagon | Extracorporeal circulation | ||
High-dose insulin maintaining euglycemia | Cardiac pacing | ||
Phosphodiesterase inhibitors | |||
Alkali substances | None available | Dilutional therapy5,6 | Not indicated |
Ethylene glycol | Ethanol | Pyridoxine7 | Not indicated |
Fomepizole | Thiamine | ||
Iron | Deferoxamine | Continuous arteriovenous hemofiltration8 | Not indicated |
Tricyclic antidepressants | Sodium bicarbonate (for QRS prolongation) | Intravenous fat emulsion9 | Indicated |
Benzodiazepines (for seizures) | |||
Vasopressors and antidysrhythmics | |||
Acetaminophen | N-acetylcysteine | Indicated |
Prehospital patients who are exposed to toxins or a drug overdose frequently display a set of signs and symptoms known as a toxidrome. Table 46-2 describes the physiologic effects of several toxidromes. These effects are important clues to the exposure and can often guide management.
Toxidrome Drug Groups and Their Physiologic Characteristics
Anticholinergics |
|
Cholinergics |
|
Ethanol and other sedative-hypnotics |
|
Opioids |
|
Sympathomimetics |
|
Withdrawal from sedative-hypnotic |
|
Withdrawal from opioids |
|
Toxicological emergencies frequently present as a result of overdose on home prescription medications. Although it may appear obvious as to whether the overdose was accidental or intentional, the prehospital care provider should proceed with caution, and be very judicial with initial assumptions. In this sense, scene safety is a primary concern. A street-wise provider will enter the premises with caution, and law enforcement involvement should routinely be in place. While the patient who sustains accidental overdose on prescription medication may be of little threat, the patient who seeks to injure himself may be prepared to endanger the welfare of others. Finally, some patients who sustain an intentional overdose may have formulated a “backup” plan which may involve other means of self-harm. Beware the patient who has been medically resuscitated after an intentional overdose. They should not be left alone, and should be supervised so as to not ingest a secondary medication or produce another weapon of self-harm.
Medical priorities involve a rapid assessment of airway, breathing, circulation, and mental status. These elements will inform the building of a toxidrome, and guide further management. Any derangement of respiration or circulation should be managed accordingly. Further management should be in accordance with local and state protocols, and medical judgment. Refinement of any toxidromes should include integration of a full set of vital signs and 12-lead ECG with specific consideration of the QRS complex width and QTc interval length.
Mostly nontoxic metabolites of acetaminophen are formed when it is taken in therapeutic doses since the drug can be conjugated with glucuronide or sulfate in the liver. However, acetaminophen can also be oxidized by cytochrome P-450 to N-acetyl-p-benzoquinoneimine (NAPQI) which is hepatotoxic. In acetaminophen overdose, a large amount of NAPQI is formed since the normal glucuronide and sulfate conjugation pathway is overwhelmed.
N-acetylcysteine (NAC) is the antidote in acetaminophen toxicity. NAC has three roles in overdose: preventing toxicity by preventing the formation of NAPQI, increasing the ability to detoxify by serving as a glutathione precursor and substitute, and treating the toxicity itself through nonspecific mechanisms.10–12 NAC is very effective if given within the first 8 to 10 hours after an ingestion, but is still beneficial even if given late.13 There is both an oral (Mucomyst) and intravenous (Acetadote) route of administration of NAC.
Benzodiazepines can be used as sedatives, as an induction agent of anesthesia, or as an anticonvulsant. Benzodiazepines work through enhancement of the GABA receptors that lead to decreased neuronal firing. Decreased neuronal firing can lead to multiple CNS, respiratory, and cardiovascular issues, including lethargy, slurred speech, ataxia, coma, respiratory depression, and hypotension in overdose.
The treatment of a benzodiazepine overdose is supportive care; there is a reversal agent available, flumazenil, which may be used with extreme caution since acute GABA receptor antagonism in the setting of chronic GABA agonism can cause immediate withdrawal symptoms including seizure. Thus, the role of flumazenil is limited. In cases of mixed overdoses, flumazenil may lead to seizures or dysrhythmias since the benzodiazepine component may actually be protective of other agents’ effects. In patients who are benzodiazepine dependent, flumazenil will induce withdrawal symptoms, including seizures. In patients who have had intravenous benzodiazepines, flumazenil may not reverse the respiratory depression. The most useful indication for flumazenil is in a benzodiazepine-naïve patient who has only taken a benzodiazepine, usually after procedural sedation.14,15
When dealing with hazardous material incidents, scene safety and the safety of those around the incident are of upmost importance. When approaching the scene, approach cautiously, identify hazards, and secure the scene. When dealing with pesticide exposure, be aware that the exposure can be intentional self-harm (suicide attempt), accidental (farming incident), or an act of terrorism.
Part of securing the scene is the establishment of safety zones. In the hot or red (contamination) zone, contamination is actually present, personnel must wear the appropriate protective gear, limit the number of rescuers to those who are necessary, and bystanders are not allowed. In the warm or yellow (control) zone, life-saving emergency care and decontamination are performed and this is the area immediately surrounding the contamination zone. In the cold or green (safe) zone, normal triage, stabilization, and treatment are performed.
All patients in the hot zone are considered contaminated. As soon as the patient is contacted, and if conditions allow, airway, breathing, and circulatory support should begin. Cautious must be used if starting intravenous therapy as hazardous material may inadvertently be introduced into the patient. All clothing should be removed as soon as possible and skin should be washed with water and soap (triple wash: water, soap, water and rinsed again).
Organophosphates (OP) and nonorganophosphates (carbamates) are cholinesterase-inhibiting pesticides commonly used throughout the world. The toxicity is through the inhibition of cholinesterase, which increases the activity of all nicotinic and muscarinic receptors.16 Carbamates bind cholinesterase transiently (due to rapid hydroxylation of the carbamate-AChE bond) and last minutes to hours. Aging, which is the irreversible binding of the pesticide to cholinesterase, can occur with organophosphates and makes these patients particularly challenging to manage.17,18
Symptoms of OP exposure can occur within 5 minutes, depending on the dose of the exposure. Symptoms can be variable because acetylcholine receptors are found in both the sympathetic and parasympathetic nervous systems.19 There are several mnemonics associated with the cholinergic toxidrome, including SLUDGE (salivation, lacrimation, urination, miosis, defecation, GI distress, emesis) and DUMBBBELS (defecation, urination, miosis, bronchospasm, bronchorrhea, bradycardia, emesis, lacrimation, salivation).20
Death from OP is caused by respiratory failure and the subsequent hypoxemia. The antidotes for OP pesticide poisoning are atropine and pralidoxime. Atropine competitively antagonized acetylcholine at muscarinic receptors. Classically, atropine is given in doses high enough to cause “atropinization,” which is where the patient’s skin and mucous membranes are dry. These doses can be as 1 to 5 mg every 2 to 20 minutes.21,22 Atropine does not reverse nicotinic effects, and therefore, the patient must be monitored for possible respiratory failure from delayed neuromuscular junction dysfunction.23 There are several adverse effects of atropine; however, its benefit in pesticide poisoning usually outweighs the risks.24
Pralidoxime (2-PAM) is an oxime that can potentially reactivate inhibited cholinesterase.25 Side effects are minimal and may only include emesis, hypertension, and possibly mild cholinergic effects with rapid infusion.26 Due to the short activity of carbamates, the use of pralidoxime may not be indicated. If it is unknown which type of pesticide was used, giving pralidoxime will most likely not be detrimental if it was only a carbamate. Pralidoxime should not be given as the sole therapeutic agent and should be used only after a trial of atropine.
Diazepam may be considered an adjunctive therapy for OP poisonings as it may help with decreasing seizures and neuropathy. It is not recommended to be given routinely in all cases of exposure, but rather to be used with seizures and agitation as well as to aid intubation.19,27,28 Activated charcoal should be considered if there is an ingestion of an insecticide.29
Dangerous inhalants are important source of exposure that prehospital providers must consider and be prepared to manage. Of utmost concern in responding these incidents is the scene safety outlined above. Numerous emergency responders have been subject to morbidity and mortality resulting from exposure to inhalants. Principles of management include the establishment of scene safety and proper HAZMAT response when indicated. Principles of patient decontamination are important even when dealing with inhalants. Once patient care is initiated, the basics of airway, breathing, and circulation must be rigorously assessed and managed.