Many nurses—even experienced ER and ICU nurses—are uncomfortable caring for a patient who has taken an overdose. Toxicology is often more art than science, and there is often a limited amount of easily available information a busy nurse can use for practical advice. Also, poisoning emergencies are far less common than medical emergencies such as myocardial infarctions and cerebrovascular accidents, and without a background of hands-on experience, comprehensive care is difficult. This activity will provide nurses with the knowledge they need to provide comprehensive care for a patient with an overdose. This activity will stress that taking care of the poisoned patient requires specific knowledge, but also flexible and creative thinking.
This course is designed for nurses who may care for patients who have taken an overdose or who have unintentionally been poisoned.
NetCE is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's Commission on Accreditation. NetCE is accredited by the International Association for Continuing Education and Training (IACET). NetCE complies with the ANSI/IACET Standard, which is recognized internationally as a standard of excellence in instructional practices. As a result of this accreditation, NetCE is authorized to issue the IACET CEU.
NetCE designates this continuing education activity for 5 ANCC contact hour(s). NetCE designates this continuing education activity for 3 pharmacotherapeutic/pharmacology contact hour(s). NetCE designates this continuing education activity for 6 hours for Alabama nurses. NetCE is authorized by IACET to offer 0.5 CEU(s) for this program. AACN Synergy CERP Category A.
In addition to states that accept ANCC, NetCE is approved as a provider of continuing education in nursing by: Alabama, Provider #ABNP0353, (valid through December 12, 2017); California, BRN Provider #CEP9784; California, LVN Provider #V10662; California, PT Provider #V10842; Florida, Provider #50-2405; Iowa, Provider #295; Kentucky, Provider #7-0054 through 12/31/2017.
The purpose of this course is to provide information regarding the most common poisoning emergency and their treatments to ensure that these cases are identified and treated early, resulting in better outcomes and improved patient care.
Upon completion of this course, you should be able to:
- Evaluate indications for interventions to stabilize the poisoned patient, and describe the components of the coma cocktail.
- List drugs/toxins with unique properties, such as low toxic doses and delayed effects, that may affect patients' clinical presentation.
- Identify toxidromes and their associated signs and symptoms.
- Outline laboratory and other testing that may be useful when assessing the poisoned patient.
- Compare and contrast various gastric decontamination techniques.
- Compare antidotes and indications for their use.
- Analyze the care for common dermal, ocular, and inhalational exposures.
Dana Bartlett, RN, BSN, MSN, MA, CSPI, is a Certified Specialist in Poison Information. He worked at the Poison Control Center in Philadelphia as a hotline operator from 1993 until 2011. From 2011 to the present, he has been working as a hotline operator at the Connecticut Poison Control Center. Mr. Bartlett received his BSN from the University of Massachusetts, Amherst, in 1976; his MSN from Boston University in 1978; and his MA in journalism from Temple University in 1988. His clinical experience includes 6 years as an ICU nurse and 10 years as an ER nurse. He has authored more than 100 continuing education modules for RNs and allied health personnel, and he has been published in Nursing Magazine, OR Nurse, Journal of Emergency Nursing, Legal Nurse Consultant, American Nurse Today, Journal of Emergency Services, and Orthopedics Today. He has also authored textbook chapters and NCLEX material and has edited and reviewed for several major publishers.
Contributing faculty, Dana Bartlett, RN, BSN, MSN, MA, CSPI, has disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.
Jane C. Norman, RN, MSN, CNE, PhD
The division planner has disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.
The purpose of NetCE is to provide challenging curricula to assist healthcare professionals to raise their levels of expertise while fulfilling their continuing education requirements, thereby improving the quality of healthcare.
Our contributing faculty members have taken care to ensure that the information and recommendations are accurate and compatible with the standards generally accepted at the time of publication. The publisher disclaims any liability, loss or damage incurred as a consequence, directly or indirectly, of the use and application of any of the contents. Participants are cautioned about the potential risk of using limited knowledge when integrating new techniques into practice.
It is the policy of NetCE not to accept commercial support. Furthermore, commercial interests are prohibited from distributing or providing access to this activity to learners.
- AN OVERVIEW OF POISONING EMERGENCIES
- ASSESSMENT AND STABILIZATION
- USING THE LABORATORY AND OTHER DIAGNOSTIC TOOLS
- GASTRIC DECONTAMINATION
- ELIMINATION TECHNIQUES
- DERMAL, INHALATION, AND OCULAR POISONINGS
- CASE STUDIES
- Works Cited
- Evidence-Based Practice Recommendations Citations
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#34441: Caring for the Poisoned Patient
Many nurses, even experienced emergency and intensive care nurses, are uncomfortable caring for a patient who has taken an overdose. This is not surprising, as poisoning and overdose emergencies are far less common than medical emergencies such as myocardial infarctions (MIs), cerebrovascular accidents, or traumas. Toxicology is not covered extensively in basic or advanced nursing textbooks, and treatment recommendations for nursing care of poisoning emergencies are often based on a small number of anecdotal reports. Protocols can be frustratingly vague.
Lack of experience, lack of education, and lack of information make caring for the poisoned patient an unsettling challenge for many nurses. However, any experienced nurse has the skills to do it. Caring for a poisoned patient is no different than any other clinical situation; it is based on assessing the patient and making a plan of care. The difference is that these clinical challenges demand a slightly higher level of flexibility and adaptability. But it is important to remember that more poisoned patients have been saved by skilled attention to their basic needs than by the use of specialized procedures or antidotes.
In 2013, the American Association of Poison Control Centers reported almost 2.2 million calls to poison control centers that involved a human exposure; most cases did not result in serious harm, but there were 2,477 deaths . Although many poisonings are managed by emergency nurses, transport staff, and poisoning specialists, these events can occur in a wide variety of settings. Therefore, all nurses should have knowledge of the processes for identifying and treating poisonings or overdoses.
Nursing care of the poisoned patient should follow this process:
Assessment, including evaluation of airway, breathing, and circulation (the ABCs).
Stabilize the ABCs.
Use the coma cocktail, if indicated.
Obtain a history and perform a physical exam.
Determine what toxic effects may be caused by the particular drug, poison, or other toxin.
Perform gastric decontamination, if indicated.
Consider enhanced elimination techniques.
Obtain laboratory and diagnostic tests.
Use an antidote, if indicated, and/or deliver specific care or symptomatic/supportive care.
These steps are discussed individually but they can be, and many times are, essentially done at the same time. Also, aside from evaluating the ABCs, which is always the first step, the steps do not need to be performed in a specific order; the circumstances of each case will dictate what needs to be done and when. Simplified, the process is: assess and stabilize the ABCs, give an antidote if indicated, and increase the elimination of or remove the poison.
Begin the care of a poisoned patient by assessing the ABCs. In some cases of poisoning or overdose, there will not be significant and/or characteristic changes in the ABCs or the ABCs may be normal. However, there are drugs and toxins that can cause distinctive and serious derangements in the ABCs (Table 1) [2,3].
ABC CHANGES SEEN WITH OVERDOSE
|Sign||Possible Overdose Agent|
|Bradycardia||Beta blockers, calcium channel blockers, clonidine, digoxin|
|Bradypnea||Benzodiazepines, ethanol, opioids (e.g., heroin)|
|Hypothermia||Barbiturates, ethanol, opioids|
|Hyperthermia||Amphetamine, anticholinergics (e.g., antihistamines), monoamine oxidase (MAO) inhibitors (e.g., selegiline), 3,4-methylenedioxymethamphetamine (MDMA or Ecstasy), serotonergic drugs (e.g., fluoxetine, lithium)|
|Hypotension||Antihypertensives, beta blockers, calcium channel blockers, clonidine, tricyclic antidepressants (e.g., amitriptyline), opioids|
|Hypoxia||Barbiturates, benzodiazepines, carbon monoxide, ethanol, opioids|
|Tachycardia||Amphetamine, anticholinergics, cocaine|
|Tachypnea||Toxic alcohols, salicylates|
These changes in pulse, blood pressure, body temperature, and breathing can help confirm an ingestion or help identify what the patient has taken if the ingestion was not witnessed or if the patient is unconscious or incoherent. Many drugs and toxins can cause changes in the ABCs, but it is vital to remember no single change in one of the ABCs can be considered diagnostic.
A 12-lead electrocardiogram (ECG) should also be obtained while the ABCs are being assessed. ECG changes and poisoning will be discussed in detail later in this course.
If the poisoned patient has a significant derangement in her or his ABCs, the first step is to provide supportive care. In addition, treatment measures that are considered standard for any patient should be instituted. Secure the patient's airway if it is compromised or may become so, and administer supplemental oxygen if the patient is hypoxic or ventilation is inadequate. If the patient is hypotensive and her or his lungs are clear, an IV infusion of 0.9% sodium chloride or lactated Ringer's solution should be used. Hyperthermia or hypothermia can be treated with cooling or warming measures.
Some poisoned patients will require specific treatments or an antidote. For example, the patient who has taken an overdose of metoprolol and is hypotensive should be given an IV infusion of glucagon . The patient who has taken an overdose of heroin and has respiratory depression and inadequate ventilation requires naloxone along with oxygen . However, with very few exceptions, standard, supportive care is an appropriate first choice.
The coma cocktail is an informal term for four interventions that can be used to treat a poisoned patient who has an altered mental status. These interventions—dextrose, oxygen, naloxone, and thiamine—are often referred to by the mnemonic DONT.
The administration of dextrose, oxygen, naloxone, and thiamine was once considered to be routine care for poisoned patients with a depressed sensorium. However, although these drugs are comparatively safe, they should not be given if there is no indication for their use. It is also important to consider the possible side effects, the contraindications to the use of these drugs, and the correct dose and route of administration. There is also some concern regarding the risks of naloxone-induced withdrawal, and this should be considered when selecting treatment .
Hypertonic dextrose should be given to any patient who has an altered mental status, unless the serum glucose level is normal. The normal dose is 0.5–1 g of 50% dextrose in water given as an IV bolus . The most common side effect is irritation of the vein; serious side effects are rare. Hyperglycemia may worsen acute ischemic brain injury. However, this fact is not considered to be a contraindication for the administration of hypertonic dextrose to a poisoned patient who has an altered mental status [3,5].
When taken in overdose, many drugs can produce respiratory depression and/or a compromised airway. The resulting hypoxia can cause a depressed sensorium, and high-flow oxygen at 8–10 L/min can be used for a poisoned patient who has an altered mental status. There are no significant side effects with short-term use. Furthermore, short-term use of high-flow oxygen is safe for poisoned patients who have chronic obstructive pulmonary disease . The use of high-flow oxygen is contraindicated if a patient has ingested the herbicide bipyridylium (Paraquat) . High-flow oxygen given to someone who has ingested bipyridylium can initiate an oxidation-reduction reaction that causes permanent alveolar lung damage .
Naloxone prevents binding of opioids to receptors and is used to reverse respiratory depression caused by opioids. The dose is 0.4–2 mg, and the drug is usually given as an IV bolus; naloxone can also be given as a continuous IV infusion . The major side effect is precipitation of opioid withdrawal if large amounts of naloxone are given to an opioid-dependent patient. There are essentially no contraindications.
Chronic alcohol abusers may have a thiamine deficiency and develop Wernicke-Korsakoff syndrome, resulting in coma, confusion, or other neurological deficits . Thiamine can be given empirically to patients with a depressed sensorium. The dose is 100 mg IV over 5 minutes . Side effects are very rare, and there are no contraindications.
Flumazenil (Romazicon) prevents benzodiazepines from binding to benzodiazepine receptors, and it will reverse the central nervous system (CNS) depression and respiratory depression caused by these drugs. Overdoses with benzodiazepines are very common, and it is tempting to add flumazenil to the coma cocktail and administer it to poisoned patients who present with altered mental status. However, flumazenil should be used only in certain circumstances, and it should not be considered to be a routine part of the coma cocktail .
When the ABCs have been evaluated and stabilized and the poisoned patient with an altered mental status has received one or all of the components of the coma cocktail (if indicated), a history and physical exam should be completed. The importance of obtaining a good history cannot be overstated. Inexperienced nurses often focus on what the patient took, but the circumstances of an overdose are just as important or more important. Determining exactly what happened is the most overlooked part of caring for a poisoned patient.
The first step in taking a history is determining what the patient took or was exposed to and how the poisoning occurred. Remember, what can happen is determined by the pharmacology of the drug, but what is likely to happen depends upon the circumstances of the overdose. For example, an acute overdose of lithium carbonate can cause coma and seizures, but these effects are much more likely to occur if the patient has been taking the medication for several months, because the CNS tissues will be saturated with the drug. An overdose of a tricyclic antidepressant (TCA) (e.g., amitriptyline) can cause arrhythmias, hypotension, and seizures, but these effects always happen within 6 hours of the ingestion.
Most poisoned patients have taken an overdose of a medication, so it is essential that the history include:
What the patient took
How much the patient ingested
The strength and properties of the medication (e.g., extended-release formulation)
When the overdose occurred
If it was the patient's medication or someone else's
Length of history with the medication
Accuracy of the history (e.g., witnesses)
The patient's age, her or his pre-existing medical problems, body weight, and other medications currently being used can also strongly influence the clinical course of an overdose. Make sure that this information is obtained and documented. A patient may state that she or he has taken an overdose of aspirin, in which case serial salicylate levels should be obtained. But if this same patient has been diagnosed with bipolar disorder, determine if lithium has been prescribed and request serum lithium levels, if indicated.
Some drugs/toxins can be dangerous if the patient has been exposed to a very small amount, some can have a delayed onset of effects, and some may seem innocuous because the patient's signs and symptoms may initially be minor, or there may not initially be any signs or symptoms. A knowledge of these properties can be helpful when formulating a treatment plan.
Calcium channel blockers
Hydrofluoric acid in high concentrations
Monoamine oxidase (MAO) inhibitors (e.g., phenelzine, selegiline)
Calcium channel blockers
In addition, delayed effects commonly occur with the practice known as body packing or stuffing. This involves an individual ingesting or inserting sealed packets of illicit drugs (e.g., cocaine, heroin) for the purposes of trafficking. These packets can then rupture, causing acute overdose hours after ingestion.
Overdoses or exposures to the following drugs and toxins may initially present with minor signs and symptoms or with signs similar to other conditions :
Illicit drugs hidden in the body (e.g., body packers)
Button/disc battery ingestion
High-pressure injection injuries
Imidazoline decongestants that are often found in over-the-counter ophthalmic preparations, such as Visine
Obtaining a good history when caring for a poisoned patient can be difficult. The patient may be unable to provide information or may not accurately remember what she or he took. In some cases, patients may misrepresent the facts of the overdose or may only mention the parts of the situation that seem important to them. Every effort should be made to find out exactly what happened. Family members, friends, and emergency medical services (EMS) personnel can all be valuable resources when obtaining a history. The patient's medical records should be obtained as well.
Many drugs and toxins can produce similar clinical effects, and providing basic symptomatic and supportive care is one of the most important aspects of caring for a poisoned patient. However, obtaining information about the specific effects of any particular drug/toxin and guidance about specific treatments is often necessary.
While even a brief outline of the effects and treatment of all possible toxins is beyond the scope of this course, all nurses should know where to find this information. Clinical toxicology textbooks and online resources are useful, but the best source for fast and accurate delivery of the information for the care of a poisoned patient is a poison control center. Poison control centers are open 24 hours every day, and dialing 1-800-222-1222 will connect to the closest poison control center. The centers are staffed by certified specialists in poison information (CSPIs). Most CSPIs are nurses or pharmacists who have received special training in clinical toxicology. They use a computer database (Poisindex) that has millions of entries and the latest information about drugs, chemicals, natural toxins, and household and personal care products. CSPIs can provide information regarding effects a drug or toxin may produce and specific treatment guidelines. The CSPIs at a poison control center can also contact a physician toxicologist; she or he can provide another level of expertise and experience and can provide a telephone consultation to the treating physician. Poison control centers also provide services to the general public.
The patient's age, weight, past medical history, current vital signs, and present condition should be noted prior to contacting a poison control center. In addition, it is important to have information regarding the basics of the case (e.g., what was taken, when, how much, if the ingestion was witnessed). The CSPI will need this data in order to make an assessment and a treatment plan. As always, the circumstances of an overdose are just as important as what was taken.
When taken in an overdose, many drugs do not produce characteristic signs and symptoms, and the clinical picture will be indistinct. A patient who has taken an overdose of one of the commonly used psychotropics or sedative-hypnotics is likely to be drowsy and tachycardic, but there are many drugs that cause CNS depression and tachycardia.
But as noted, some drugs taken in an overdose will produce a distinct clinical picture. In toxicology, this is termed a toxidrome. A toxidrome is a set of characteristic signs and symptoms associated with overdose or poisoning from a particular drug or toxin. Toxidromes can be used to confirm an ingestion or exposure. They are also useful if a poisoning is suspected, but it is not clear what the patient has taken; in these situations, the presence of a toxidrome can narrow the number of possibilities.
Although not all medications or toxins produce a toxidrome, many of those that cause changes in the ABCs do. Knowing the toxidromes is an important part of the assessment of the poisoned patient. The most common toxidromes are categorized as anticholinergic, cholinergic, opioid, sedative-hypnotic, sympathomimetic, hallucinogenic, and serotonin .
The anticholinergic toxidrome is caused by drugs that block acetylcholine from binding to cholinergic receptors. The result is central and peripheral effects that include agitation, confusion, decreased bowels sounds, delirium, dilated pupils, dry and flushed skin, dry mucous membranes, hyperthermia, tachycardia, and urinary retention . In severe cases, arrhythmias, coma, and seizures are possible. Drugs that can cause anticholinergic toxidrome include antihistamines, antispasmodics (such as hyoscyamine), TCAs (less commonly), and psychoactive plants such as Amanita muscaria (fly agaric mushroom) and Datura stramonium (jimson weed). The duration of anticholinergic signs and symptoms after a poisoning can be several days.
The cholinergic toxidrome is caused by drugs and toxins that stimulate the cholinergic receptors. Patients with this syndrome present with bradycardia, bronchorrhea, diarrhea, emesis, lacrimation, miosis, salivation, and urinary incontinence . Organophosphate and carbamate insecticides can cause the cholinergic toxidrome. Donepezil, a commonly prescribed drug used to treat Alzheimer's disease, can cause cholinergic effects as well.
A mnemonic device may be helpful to remember the signs of cholinergic toxidrome. One such device is the acronym DUMBELS, which stands for diarrhea, urinary incontinence, miosis, bradycardia, emesis, lacrimation, and salivation. Some use the mnemonic SLUDGE, which is short for salivation, lacrimation, urination, defecation, and gastric emptying, but leaves out bradycardia and miosis. Note that in both cases salivation also refers to excess bronchial secretions.
The opioid toxidrome is caused by drugs that stimulate the opioid receptors. It is characterized by CNS depression, hypotension, miosis, and respiratory depression. Drugs that can cause the opioid toxidrome include codeine, heroin, methadone, morphine, oxycodone, and tramadol.
This toxidrome is caused by drugs such as barbiturates and benzodiazepines that act by increasing the activity of gamma-aminobutyric acid (GABA), one of the major inhibitory neurotransmitters. The sedative-hypnotic toxidrome is characterized by CNS depression, delirium, mydriasis, and respiratory depression . In addition to barbiturates and benzodiazepines, this toxidrome can develop with methaqualone (Quaalude) and anticonvulsants.
The sympathomimetic toxidrome results when one or a combination of the following occurs:
Adrenergic receptors are directly stimulated.
A drug or toxin stimulates the release of catecholamines.
Synaptic reuptake of catecholamines is decreased.
Catecholamine breakdown is decreased.
Signs and symptoms of this toxidrome include agitation, diaphoresis, fever, hypertension, mydriasis, and tachycardia . Severe cases can cause arrhythmias, MI, and seizures. Amphetamine and cocaine are two commonly used drugs that can cause the sympathomimetic toxidrome.
The hallucinogenic toxidrome is generally the result of ingestion of drugs or substances that result in an altered state of consciousness. The hallucinations associated with this toxidrome may be visual, auditory, or tactile . Although there are several categories of drugs/toxins that can result in hallucinations, the most commonly encountered are most likely lysergic acid diethylamide (LSD), psilocybin mushrooms, phencyclidine (PCP), ketamine, mescaline, and 3,4-methylenedioxymethamphetamine (MDMA or Ecstasy) .
Acute hallucinogen toxicity should be suspected in patients presenting with unexplained, acute psychotic behavior . Other presenting symptoms may include mydriasis, hypertension, tachycardia, tachypnea, and nausea and vomiting; however, the exact symptoms will depend on the substance ingested. Treatment is generally supportive, and care should be taken to ensure that the patient will not harm him/herself or others. A sedative may be used to decrease agitation or combativeness .
The serotonin toxidrome, more commonly referred to as the serotonin syndrome, is caused by excessive stimulation of serotonergic receptors. Medications involved in the development of the syndrome act by inhibiting the reuptake of serotonin, causing the release of serotonin into synapses, directly stimulating serotonin receptors, or decreasing the metabolism of serotonin. It can also occur when a drug-drug interaction inhibits the breakdown of a serotonergic drug. Mild cases of serotonin syndrome present with signs and symptoms such as anxiety, diaphoresis, and gastrointestinal complaints. Severe cases can present with confusion, hypertension, hyperthermia, hyperreflexia, and seizures. The serotonin toxidrome has a variable presentation and can be difficult to detect; the signs and symptoms are similar to those seen in the anticholinergic and sympathomimetic toxidromes. The most distinguishing features are clonus, fever, and hyperreflexia. Of course, the most important feature is a history of exposure to serotonergic drugs. Selective serotonin reuptake inhibitors (SSRIs) are a common cause of the serotonin toxidrome, and some analgesics, antiemetics, anti-migraine drugs, and illicit drugs may cause the toxidrome as well. Most cases of serotonin toxidrome are the result of two or more serotonergic drugs being ingested simultaneously .
When caring for a poisoned patient, drug levels or levels of toxins may be measured in blood or urine. These levels can be used to predict the possibility of toxic effects of an overdose, to assess the level of damage done by an overdose, and to determine the need for therapy. Drug/toxin levels should be obtained if a patient has ingested or been exposed to :
The levels of these drugs and toxins are (usually) quickly available and can be used assess damage, predict toxicity, or help determine the need for treatment. However, in many cases, drug levels or toxin levels are not useful because they are not reliable as indicators or predictors of toxicity. Many drug or toxin levels cannot be quickly obtained, so they are not useful for the management of an acutely ill patient. In addition, there is a risk of false positive and/or false negative results for certain drugs.
The urine drug screen that is often used as part of a diagnostic workup in cases of poisoning measures the levels of several common drugs of abuse, such as amphetamine, cocaine, cannabis, and opioids. These screens often detect the metabolite of the drug, so they confirm prior use but not necessarily current intoxication. The toxicology literature does not support the use of a urine drug screen for managing the poisoned patient .
The laboratory tests needed to assess and evaluate a poisoned patient will depend on what the patient has ingested or been exposed to and the patient's clinical condition. If the drug or toxin responsible for the poisoning is unknown, one or several of the following tests may help determine what the exposure might have been. A single laboratory test is rarely sufficient to identify an unknown drug or toxin.
Please note that the drugs and toxins associated with the laboratory abnormalities discussed in the following section are not the only ones that may cause changes. Rather, they are drugs and toxins that are commonly encountered and cause significant laboratory changes that would be a prominent part of the clinical presentation of a patient who has been poisoned.
An arterial blood gas test can be used to detect and diagnose acid-base disturbances and hypoxemia. Acetaminophen (in severe cases), aspirin, carbon monoxide, cyanide, ethanol (in alcoholic ketoacidosis), ethylene glycol, ibuprofen (in severe cases), iron, isoniazid, metformin, and methanol can all cause acidosis . Barbiturates, carbon monoxide, cyanide, opioids, and simple asphyxiants (e.g., methane) can cause hypoxemia .
Acetaminophen is one of the most commonly ingested drugs in cases of self-poisoning. The early signs and symptoms of acetaminophen poisoning are nonspecific and often mild in intensity. There may not be any signs or symptoms early in the course, and the longer the time between toxic ingestion of acetaminophen and treatment, the less effective the treatment will be. An acetaminophen level should always be obtained in cases of self-poisoning.
Blood urea nitrogen (BUN) and serum creatinine levels are used to evaluate renal function and detect renal damage. Acetaminophen poisoning can on occasion cause elevations in BUN and creatinine, as can a massive ingestion of ibuprofen. Ethylene glycol and methanol poisoning produce metabolites that are directly toxic to the kidney.
A complete blood count (CBC) can identify a variety of hemolytic and other blood abnormalities. Benzocaine, dapsone, naphthalene mothballs, and nitrites can cause hemolysis. Benzocaine, dapsone, lidocaine, nitrites, phenazopyridine, and prilocaine can cause methemoglobinemia . Anticoagulant rodenticides (e.g., d-CON) and warfarin can cause abnormal coagulation studies .
Measurement of blood glucose levels should be considered. Hypoglycemia can be caused by aspirin, sulfonylurea, and ethanol poisoning. Hyperglycemia can be caused by iron poisoning, beta blockers, and calcium channel blockers.
Poisoning with different drugs and toxins can result in specific electrolyte imbalances. For example, an elevated anion gap can be caused by acetaminophen (in very serious cases), aspirin, carbon monoxide, cyanide, ethanol (in alcoholic ketoacidosis), ethylene glycol, iron, isoniazid, metformin, and methanol. Changes in specific electrolytes associated with poisoning are too numerous to discuss. As examples, MDMA (Ecstasy) can cause hyponatremia, digoxin and hydrofluoric acid can cause hyperkalemia, and hydrofluoric acid poisoning can cause hypocalcemia and hypomagnesemia .
Ethanol (in alcoholic ketoacidosis), ethylene glycol, isopropyl alcohol, and methanol can increase serum osmolality and cause an osmolar gap. Acetaminophen, Amanita phalloides mushroom, and valproic acid poisoning can cause liver damage and elevation of hepatic transaminases. Urinalysis can be useful in assessing imbalances. In cases of isopropyl alcohol poisoning, ketonuria may be seen. One of the metabolites of ethylene glycol, oxalic acid, forms a complex with calcium, and the calcium oxalate crystals may be seen in the urine of patients who have ingested this toxin.
Both commonly prescribed and illicitly used drugs can affect ECG findings [15,16]. Antiarrhythmic drugs, digoxin, diphenhydramine, phenothiazines, propoxyphene, and TCAs can cause prolonged QRS. Amiodarone, chlorpromazine, droperidol, erythromycin, haloperidol, methadone, sotalol, and thioridazine are drugs that can cause a prolonged QT and possibly torsades de pointes. In addition, amphetamine, anticholinergic drugs, beta blockers, calcium channel blockers, cocaine, digoxin, and phenothiazines are associated with other conduction defects and arrhythmias.
Imaging studies can also be useful in assessing the poisoned patient. An x-ray can identify accidental ingestions of a simple hydrocarbon (to rule out aspiration), a disc battery, iron tablets, or lead paint chips.
Simple hydrocarbons are not dangerous unless they are aspirated into the lungs. If aspiration occurs, pneumonitis is possible. Disc batteries from hearing aids and other small electronic devices can cause perforation if they are lodged in the esophagus. This can happen relatively quickly, so localization of the battery with an x-ray is critically important. Lead paint chips are often visible by x-ray, and iron tablets can sometimes be seen. Other medications may be visible in the gut using x-ray, but this should not be depended on as a reliable method for determining if a patient has or has not swallowed a medication .
Imaging studies may also be helpful when patients are suspected of body stuffing or packing (usually for the purposes of drug trafficking) or a patient has ingested a transdermal drug patch. X-rays of the abdomen are often ordered in these cases. However, false negatives are possible, and computed tomography scanning is the best technique for this situation [18,19].
After the ABCs have been evaluated and stabilized and the history and physical exam have been completed, the use of gastric decontamination should be considered. Gastric decontamination refers to techniques used to either prevent the absorption of a poison or actively remove it; some techniques do both.
Gastric decontamination makes intuitive sense. If an individual has ingested a drug or a poison, the first instinct is to make an effort to remove it or prevent it from being absorbed. However, the effectiveness of gastric decontamination techniques has never been proven. It is clear that activated charcoal can adsorb ingested drugs and gastric lavage and whole bowel irrigation can remove ingested drugs, but it has not been shown that adsorbing or removing ingested drugs with gastric decontamination techniques improves clinical outcomes .
Due to this lack of evidence, some in the clinical toxicology community feel that gastric decontamination should not be used. The American Academy of Clinical Toxicology (AACT) and the European Association of Poison Centres and Clinical Toxicologists (EAPCCT) support the use of gastric decontamination by individuals with proper training and expertise, but they recommend that it be treated as any other therapeutic intervention—there must be an indication for its use and an awareness of the risks, benefits, and contraindications .
There is very little unequivocal data about gastric decontamination. The recommendations presented here, about which gastric decontamination technique to use, when to use them, and their risks and benefits, represent the opinions of clinical toxicology experts, but different recommendations have been made in toxicology texts and articles. Consider the information in this module to be a guideline, with the decision to use gastric decontamination made on an individual basis, as with any other therapy.
Activated charcoal is produced from carbonaceous substances such as peat or wood that have been pulverized and specially treated. Ingested drugs or toxins are adsorbed (not absorbed) by activated charcoal. Most drugs and toxins are well adsorbed by activated charcoal, but acids, alkalis, alcohols, iron, and lithium are not. The adsorption bond is very strong. The charcoal-drug complex is excreted in the stool, absorbed by macrophages, or dissociated slowly enough so the drug does not cause harm. Although it is clear that activated charcoal can adsorb toxins and drugs, it is unknown if this action improves clinical outcomes [21,22].
Decontamination with activated charcoal is indicated in cases of recent ingestion (within one hour of arrival to a healthcare facility) of a toxic dose of a medication [21,22]. However, the time limit of one hour is not universally accepted or always used. If a patient has ingested a large amount of a particularly dangerous drug (e.g., a calcium channel blocker), if there is no antidotal therapy, if supportive care may not be effective, or if the ingested drug by itself slows down absorption (e.g., an anticholinergic agent) or is slowly absorbed (e.g., a sustained-release product), this time limit may be extended [21,22].
Use of activated charcoal is contraindicated if the drug or the amount ingested is not considered toxic or if the drug is not adsorbed by activated charcoal. It is also avoided if the patient is uncooperative or cannot protect her or his airway (e.g., significant CNS depression). Charcoal will be ineffective in cases of foreign body ingestion, acid or alkali ingestion, and compromised bowel function.
The optimal dose of activated charcoal is not known. The conventional recommendations for dosing are a ratio of 10:1 charcoal to drug if the amount of drug ingested is known, or 1 g/kg of body weight if the amount ingested is not known. In either case, consider the patient's tolerance for charcoal and the risks involved of administering a large amount prior to initiating treatment .
Many patients vomit after being given charcoal. Aspiration of vomitus/charcoal is a concern, although it is not common unless the patient is seriously ill. Aspiration of charcoal and vomitus may be more dangerous than aspiration of gastric contents alone, and patients should be monitored closely .
Multi-dose activated charcoal involves administering doses several hours apart. The patient is given at least two doses with the hope that multi-dose activated charcoal will adsorb drugs/toxins that linger in the gut, interrupt enterohepatic recirculation, or act as a gut dialysis mechanism. It is a controversial technique. The last position paper on the subject, published in 1999, stated that this technique should only be used if a patient had ingested a life-threatening amount of carbamazepine, dapsone, phenobarbital, quinine, or theophylline . Studies published in 2009 and 2011 support the use of multi-dose activated charcoal for phenobarbital poisoning and valproic acid poisoning, but others state that there is no evidence that the multi-dose technique improves patient outcomes [2,31,32]. Absolute contraindications for this method are the same as those described for single-dose activated charcoal.
The initial dose of charcoal should be the same as for a single dose. Subsequent doses should be 0.25–0.5 g/kg given every 1 to 6 hours . The initial dose of activated charcoal can be premixed with sorbitol, but subsequent doses should be without sorbitol. Again, vomiting and aspiration are concerns, and patients should be monitored carefully.
Cathartics have been used to increase gastrointestinal transit time and decrease the absorption of ingested drugs. The osmotic cathartics magnesium citrate and sorbitol have been most commonly used to treat poisoned patients; however, cathartics, either alone or used with activated charcoal, are no longer generally recommended as a treatment for the poisoned patient . Some brands of activated charcoal are pre-mixed with a sorbitol cathartic, and a one-time dose can be given safely. Excessive use of cathartics can cause abdominal cramping, electrolyte imbalances, and fluid loss.
Gastric lavage removes drugs/toxins from the gut before they can be absorbed. It should be attempted only if the patient has ingested a life-threatening amount of a drug/toxin and presents within 60 minutes of the ingestion. The patient must be able to protect her or his airway or the airway must be protected with a cuffed endotracheal tube. The need for gastric lavage seldom occurs, and clinical studies generally support discontinuation of the practice based on a lack of beneficial effect [28,29].
In order to perform gastric lavage, the patient should be in the left lateral decubitus position and a 36–40F gastric tube inserted through the mouth or nose into the stomach. When the correct position of the tube has been confirmed, the stomach contents may be withdrawn. Next, activated charcoal is instilled, followed by tepid water or saline. Instill 250 mL of liquid, remove the liquid, and repeat this process until the return is clear or 2 L has been instilled.
Gastric lavage is associated with a risk of aspiration, vomiting, bleeding, dysrhythmias, hypoxia, tracheal intubation, and injury to the airway, esophagus, or stomach. Absolute contraindications include compromised airway, ingestion of an acid or alkali, ingestion of drug packets, ingestion of a hydrocarbon (e.g., gasoline), recent abdominal surgery, and risk for excessive bleeding.
Syrup of ipecac induces vomiting by stimulating receptors in the small intestine and chemoreceptor triggers in the CNS. The usual dose is 30 mL for adults or 15 mL for children younger than 5 years of age . The induced vomiting is meant to expel ingested medications or toxins that are still in the stomach. Although some ingested drugs may be retrieved with this approach, the amount is quite variable and very unpredictable.
Although common in the past, the AACT, the EAPCCT, and the American Academy of Pediatrics have recommended that syrup of ipecac not be used to treat poisoned patients [8,35]. It can be particularly damaging to patients who have, or may develop, a depressed sensorium or who have ingested an acid, alkali, or petroleum distillate (e.g., gasoline or kerosene). In addition, there is an increased risk for drowsiness, excessive and prolonged vomiting, and Mallory-Weiss tear. In cases of caustic toxins, such as gasoline, additional damage may result from repeated exposures of the oral mucosa and esophagus to the chemical.
Despite recommendations against its use, syrup of ipecac is discussed here because there are situations in which it might be helpful if it is used correctly. If a child has ingested a drug/toxin that may cause harm and will not cause excessive drowsiness, if vomiting would not add risk to the situation, and if transport time to a healthcare facility is unreasonably long, then syrup of ipecac may be of benefit. However, these circumstances would be very rare. Also, syrup of ipecac must be given within 30 minutes after an ingestion to have any positive effect, and few pharmacies and households stock it.
Whole bowel irrigation is a gastric decontamination technique that physically removes drugs/toxins from the gut . It is performed by giving the patient a non-absorbable polyethylene glycol solution orally or through a nasogastric tube. The flow and high volume of the irrigation mechanically flushes drugs/toxins out. The infusion is started at 250 mL per hour, and the rate is gradually increased to 1–2 L . The infusion is continued until the rectal effluent is clear of drugs/toxins. Because these solutions are non-absorbable and electrolyte balanced, fluid and electrolyte disorders do not occur. Unfortunately, no controlled trials have been performed to evaluate the effectiveness of whole bowel irrigation in treating poisoned patients, and there is no conclusive evidence that the intervention improves or changes clinical outcomes .
Whole bowel irrigation is indicated in cases of ingestion of drug packets (e.g., cocaine, heroin), iron tablets or lithium, or a sustained-release drug . Contraindications include compromised integrity of the gut, compromised airway or the possibility of developing a compromised airway, and gastrointestinal hemorrhage. Possible adverse effects include abdominal bloating, nausea, diarrhea, and vomiting.
In cases when antidotes are ineffective or unavailable, drugs and toxins can be removed by elimination techniques. This can be done by manipulating the pH of the urine (as with sodium bicarbonate) or by charcoal hemoperfusion, exchange transfusion, and hemodialysis. Extracorporeal removal by hemodialysis or other techniques has a limited role in treating poisoned patients because many drugs and toxins have a high volume of distribution and are tightly bound to proteins. Whether or not to use hemodialysis or any other extracorporeal removal technique will depend upon:
Characteristics of the drug or toxin
The patient's clinical condition
The availability and effectiveness of other treatments
The ability of the patient to eliminate/excrete the drug or toxin
Hemodialysis is a very useful and highly effective technique for treating aspirin poisoning, lithium poisoning, and toxic alcohol poisoning. It removes aspirin, ethylene glycol, and methanol (and the toxic metabolites) and also corrects the acid-base disturbances that are common to these exposures. Activated charcoal and lavage will not be helpful in treating lithium poisoning, but whole bowel irrigation has a limited role. Although fluid replacement helps lithium excretion, it may not be helpful for severely ill patients.
Most poisoned patients can be managed with supportive care. However, in some cases antidotal therapy is needed because the toxic effects of a particular drug or poison can only be interrupted or reversed by an antidote. In addition, some antidotes bind the drug after it has been absorbed. When use of an antidote is being incorporated in the management plan, the indications, contraindications, dose, risks, and benefits should be assessed. If a patient has taken an overdose but does not have signs or symptoms, consider what the patient has taken, how much, the effectiveness of supportive care, and other factors before using an antidote.
Bites from pit vipers, such as rattlesnakes, can cause significant tissue damage and serious systemic effects, with the exception of copperhead snake envenomations, which are generally mild and rarely require antivenin. Bites from venomous spiders can on occasion cause serious systemic effects, but these bites are relatively rare. Antivenin is seldom needed for spider bites, and the use of this antivenin will not be discussed in this course.
The snake antivenin crotalidae polyvalent immune FAB (CroFab) has largely replaced the crotalinae polyvalent antivenin, an older formulation. The older antivenin was derived from horse serum and the risk of anaphylactic reaction was much higher than the risk associated with CroFab, which is derived from sheep serum. The antivenin binds to the snake venom and inactivates it. Prompt use of antivenin can prevent tissue damage and systemic effects when supportive care alone cannot. Antivenin should be given to patients who have signs and symptoms of envenomation by a pit viper, including pain, swelling, coagulopathies, hypotension, and neurological signs/symptoms (e.g., fasciculations or paresthesias). CroFab is contraindicated in persons with sensitivity to sheep or sheep products or to papayas or papain. Anaphylaxis is a potential adverse effect, and drugs and equipment to treat anaphylaxis should be immediately available. Antivenin is administered via IV, and the initial dose is usually 4 to 6 vials . Each vial should be reconstituted with 10 mL of the provided diluent or sterile saline. Gently rotate/swirl the vials; do not shake. The reconstituted CroFab should be incorporated into 250 mL of normal saline solution and the infusion started at 20–60 mL per hour for the first 10 minutes . If the patient has no signs or symptoms of anaphylaxis, increase the rate to 250 mL per hour. One hour after the infusion is complete, assess the patient for a clinical response. If there is no response or the response is unsatisfactory, give 4 to 6 vials and repeat as needed. When a good response has been achieved, give 2 vials every 6 hours for 3 doses . Higher doses may be required for severe envenomations .
Atropine is a competitive antagonist of acetylcholine at parasympathetic and sympathetic synapses and at the neuromuscular junction. It also increases heart rate and cardiac conduction. Atropine is used to treat cases of organophosphate or carbamate insecticide poisoning . Patients with poisoning from ingestion of these chemicals die as a result of respiratory failure; atropine can be very effective in treating this. Atropine may also be administered to treat cases of beta blocker, calcium channel blocker, and digoxin poisoning, but it is seldom effective for these patients .
Use of atropine is contraindicated in the presence of angle-closure glaucoma, myasthenia gravis, bowel obstructions, and urinary tract obstruction. It should be used cautiously if the patient cannot tolerate a rapid heart rate. Anticholinergic effects are the main risk associated with use. Bradycardia can develop if low doses of atropine are used or if an IV bolus is given too slowly. Given that organophosphate (and to a lesser degree carbamate insecticide) poisoning can be very dangerous, the risks and benefits of using atropine in patients with these medical conditions must be carefully evaluated.
The initial dose of atropine in poisoning cases is 1–6 mg given rapidly as an IV bolus . Double the initial dose every 5 minutes until atropinization is achieved. This is evidenced by increased heart rate, stopped wheezing, and a decreased amount of bronchial secretions. Patients who have been severely poisoned by an organophosphate or a carbamate may require large doses of atropine (up to 1000 mg in 24 hours) or a continuous infusion .
Calcium flow across the cardiac membranes is needed for impulse formation and cardiac conduction and contraction. Calcium flow across cell membranes is also needed for maintaining smooth muscle vascular tone. Calcium channel blockers (e.g., amlodipine, diltiazem, verapamil) inhibit the movement of calcium through voltage-gated calcium channels, while high doses of calcium increase calcium flow across cell membranes and increase the release of calcium from intracellular stores. Patients who have been poisoned with a calcium channel blocker are unlikely to respond to atropine and the commonly used vasopressors. As such, IV calcium is the preferred treatment for these individuals .
Calcium replacement is indicated for symptomatic cases of calcium channel blocker poisoning and symptomatic cases of hydrofluoric acid burns and poisoning. Hydrofluoric acid is used in the home as a rust remover and aluminum cleaner, and it has many industrial uses as well. Hydrofluoric acid poisoning causes pain, burns, and possibly profound hypocalcemia. Calcium can also be used for beta blocker poisoning.
For treating calcium channel blocker poisoning, give 10–20 mL of calcium chloride or 30–60 mL of calcium gluconate IV over 5 minutes . Repeat every 10 to 20 minutes as needed or use a continuous infusion of 20–50 mg/kg/hour. Use the same dosing for beta blocker poisoning. The dosing recommendations for hydrofluoric acid burns and poisoning are lengthy and complex and will not be discussed; consult a poison control center for the latest recommendations.
Treatment with calcium has been associated with potential adverse effects, including bradycardia, dysrhythmias, and hypotension if calcium is rapidly infused. Tissue irritation is common. It is contraindicated in patients with digoxin toxicity or hypoglycemia.
Iron toxicity can cause CNS depression, hypotension, metabolic acidosis, and shock. Deferoxamine is used for treating iron poisoning; it binds free iron moving between iron storage sites . The deferoxamine-iron complex is then excreted in the urine, which will often cause the urine to turn pink or light red.
Deferoxamine is indicated if the serum iron level is greater than 450–500 mcg/L or if a patient with iron poisoning has symptoms (e.g., acidosis, CNS depression, hypotension, or shock). It should be used with caution in patients with poor renal function.
Deferoxamine is given as an IV infusion started slowly with a dose not to exceed 15 mg/kg per hour. The maximum dose is 6 grams per day. The endpoint of deferoxamine therapy is not clearly defined. However, it is reasonable to stop when signs and symptoms of iron poisoning have resolved, when the serum iron level is less than 350 mcg/dL, or when the urine color has returned to normal. If a patient requires deferoxamine therapy for more than 24 hours, use the lowest dose possible.
Deferoxamine can cause hypotension if it is infused too rapidly. Acute lung injury and Yersinia enterocolitica sepsis are possible complications if therapy continues for more than 24 hours.
The myocardium normally uses free fatty acids for energy, but when the myocardium is stressed, as with calcium channel blocker poisoning, it switches to glucose metabolism for fuel. However, calcium channel blocker toxicity also impairs insulin release and glucose uptake. The resultant lack of energy compounds the toxic effects of calcium channel blockers on the myocardium. Dextrose and insulin give the poisoned myocardium a source of energy and the means to use it. In addition, insulin has a positive inotropic effect [38,39]. Although dextrose and insulin are primarily used for calcium channel blocker poisoning, there is also evidence that this therapy may be helpful for treating beta blocker poisoning. Dextrose-insulin therapy appears to be effective for correcting hypotension and less effective for correcting bradycardia and conduction defects.
The first step when administering this therapy is giving a bolus dose of regular insulin at 1 Unit/kg followed by a continuous infusion of regular insulin. As the insulin is being given, the patient should receive an IV bolus of 25 g of 50% dextrose. Additional glucose should be given to maintain a serum glucose level of 100–200 mg/dL. Serum glucose and potassium levels should be checked frequently. It may take up to 30 to 45 minutes to see an effect on the cardiovascular system. Potential adverse effects include hypoglycemia and hypokalemia.
Digoxin-specific antibodies, also called Fab fragments, irreversibly bind to free digoxin to resolve symptoms of digoxin toxicity. The Fab-digoxin complex is then renally excreted. As the Fab-drug complex is excreted, an imbalance in the concentrations of digoxin between the tissues and the serum develops. As a result, more digoxin travels from the tissues into the serum and is bound to the Fab fragments and excreted. Fab fragments are recommended to treat patients with digoxin poisoning who have serious arrhythmias, serum digoxin levels ≥10 ng/mL at 6 hours or more after ingestion, serum potassium levels ≥5.0 mEq/L, or have ingested ≥10 mg. It is important to note that abnormally high serum potassium is a better predictor of potentially serious harm from digoxin poisoning than the serum digoxin level or ECG changes.
Fab fragments are dosed according to the number of vials. There are two methods for dosing: by the serum digoxin level or by the amount of digoxin ingested (Table 2). If the amount ingested is not known and a serum digoxin level cannot be quickly obtained, 10 to 20 vials can be given empirically . Fab fragments can be given as an IV bolus, but they are usually administered IV over 30 minutes. The response to Fab fragments should be seen within 30 minutes. Patients with atrial fibrillation or heart failure may experience an exacerbation. Hypokalemia is possible. Because Fab fragments are derived from the antisera of sheep, sensitivity to sheep-derived products is considered a contraindication.
CALCULATING DOSING FOR FAB FRAGMENTS
Digoxin-specific antibody therapy is very effective. One study showed that 80% of patients given Fab fragments had a resolution of the signs and symptoms of digoxin poisoning .
Flumazenil is a benzodiazepine antagonist that prevents benzodiazepines from binding to receptors. It will reverse the CNS and respiratory depression caused by these drugs, avoiding the need for endotracheal intubation. It is indicated in the treatment of benzodiazepine toxicity after it is has been determined there are no contraindications. Flumazenil should be avoided in patients who have a history of seizures or have ingested a TCA or any other medication that is likely to cause seizures. Patients who are addicted/habituated to benzodiazepines should not be administered flumazenil, as it may precipitate withdrawal.
When used to reverse the effects of benzodiazepine poisoning, flumazenil is given in gradually increasing doses until the patient responds, starting with a dose of 0.2 mg IV . If there is no response, give 0.3 mg; if this dose is ineffective, give doses of 0.5 mg every 30 seconds to a maximum of 3 mg.
Potential adverse effects include anxiety, headache, nausea, and vomiting. Seizures are possible in patients who have ingested a TCA or any other medication that is likely to cause seizures or who are experiencing benzodiazepine withdrawal.
Ethylene glycol and methanol are commonly called the toxic alcohols. These alcohols are metabolized by alcohol dehydrogenase to acids and other compounds that can cause profound acidosis, coma, permanent ocular damage, and renal failure. Fomepizole blocks the metabolism of ethylene glycol and methanol by inhibiting the activity of alcohol dehydrogenase . Fomepizole is much easier and less risky to use than hemodialysis or the traditional antidote for toxic alcohol poisoning, ethanol. Thus, it is indicated in cases of confirmed or suspected ethylene glycol or methanol poisoning.
Administer a loading dose of 15 mg/kg; this should be given IV over 30 minutes . The loading dose is followed by 4 doses of 10 mg/kg, each dose separated by 12 hours. After the fourth dose, the patient should receive doses of 15 mg/kg every 12 hours until the ethylene glycol or methanol level is <20 mg/dL. Possible adverse effects include dizziness, headache, and nausea. If hemodialysis is also being used, dosing fomepizole is complicated and beyond the scope of this course. This information is in the package insert or available from a poison control center.
Beta blocker poisoning causes bradycardia, cardiac conduction delays, and hypotension. Treatment with stimulants and vasopressors (e.g., epinephrine, dopamine) may not be effective because these drugs work by stimulating adrenergic receptors. In these cases, glucagon is the treatment of choice. Glucagon binds to specific cell membrane receptors, bypasses the adrenergic receptors, and increases the intracellular concentration of cyclic adenosine monophosphate (cAMP). cAMP is a second messenger, and it activates intracellular enzymes that affect myocardial activity. In cases of beta blocker poisoning, glucagon increases heart rate, improves cardiac conduction, and increases contractile force. It has also been used for treating calcium channel blocker poisoning.
In the treatment of beta blocker poisoning, administer 3–10 mg IV over 1 to 2 minutes . After the bolus dose, administer a continuous IV infusion of 1–5 mg/hour. Possible adverse effects include hyperglycemia, hypokalemia, nausea, and vomiting. Use of glucagon is contraindicated in patients with insulinoma or pheochromocytoma.
Levocarnitine is a naturally occurring amino acid derivative that is used by the mitochondria for fatty acid metabolism. Valproic acid poisoning prevents the synthesis of levocarnitine, so fatty acid metabolism is disrupted and patients can develop hyperammonemia. Hyperammonemia can cause profound CNS depression. Exogenous levocarnitine decreases serum ammonia levels and may be effective at improving the clinical course of valproic acid poisoning .
Levocarnitine is used to treat valproic acid poisoning that has caused encephalopathy, hepatotoxicity, and hyperammonemia. The initial dose is 100 mg/kg IV over 2 to 3 minutes . A 50 mg/kg dose may be repeated every 8 hours, if needed. The endpoint of therapy is not clear, but levocarnitine therapy can probably be stopped when serum ammonia levels are decreasing and the patient's clinical condition is improving. Treatment may be required for several days . Some patients will develop diarrhea, nausea, and vomiting.
Excessive oxidative stress can change hemoglobin to methemoglobin, a form of hemoglobin that cannot carry oxygen. Chemicals such as nitrates and some drugs—particularly dapsone, local anesthetics like benzocaine, and phenazopyridine—can cause the formation of methemoglobin and overwhelm the body's normal methemoglobin reducing mechanisms. Methemoglobinemia produces very distressing signs and symptoms, and for some patients, the hypoxemia can be dangerous. Waiting for methemoglobinemia to spontaneously resolve is not reasonable or safe.
Methylene blue increases the activity of the nicotinamide adenine dinucleotide phosphate-reducing system (normally a minor pathway) and changes methemoglobin to hemoglobin. Methylene blue should be used for patients who have a methemoglobin level greater than 30% or who have a higher than normal methemoglobin level and signs and symptoms of hypoxemia . However, methylene blue should be avoided in the presence of severe renal failure, glucose-6-phosphate dehydrogenase (G6PD) deficiency, or methemoglobin reductase deficiency. It should not be used to reverse methemoglobinemia that was induced during treatment for cyanide poisoning.
The recommended dose is 1–2 mg/kg IV over 5 minutes; this dose may be repeated after 60 minutes . The IV line should be flushed with normal saline, as methylene blue irritates the veins. Methylene blue produces maximal effects within 30 minutes of administration. Nonresponse after two doses could be a sign that the patient has G6PD deficiency or methemoglobin reductase deficiency, the doses have been too low, or the drug is still present in the gut. Dizziness, headache, and nausea may develop. High doses (greater than 7 mg/kg) may cause methemoglobinemia or hemolysis .
When doses of acetaminophen greater than 7.5 grams or 150 mg/kg are taken, the normal metabolic pathways for the drug are overwhelmed and a large amount of a toxic metabolite is produced. This metabolite can cause significant liver damage and occasionally kidney damage as well. By several complex mechanisms, N-acetylcysteine (NAC) counteracts the effects of acetaminophen poisoning.
NAC is indicated for serum acetaminophen levels 150 mcg/mL or greater at 4 hours or later after ingestion or laboratory signs of acetaminophen poisoning, such as elevation of serum transaminases, BUN, and creatinine. It may also be used for patients with clinical signs and symptoms of acetaminophen poisoning or ingestion of a toxic amount of acetaminophen. The oral form cannot be used if the patient has a malfunctioning gut, and the IV form should be used cautiously if the patient has asthma or bronchospasm.
If NAC is given within 8 hours of an ingestion of acetaminophen, it is highly effective at preventing liver damage, so therapy should be initiated as soon as it is decided upon. The dose for the oral preparation is 140 mg/kg, followed in 4 hours by 70 mg/kg given every 4 hours to a total of 17 doses . The dose for the IV preparation is 150 mg/kg mixed in 200 mL of diluent administered over 60 minutes, followed by 50 mg/kg in 500 mL of IV diluent administered over 4 hours then 100 mg/kg in 1000 mL of IV diluent administered over 16 hours. The oral and IV forms of NAC are equally effective .
Nausea and vomiting are very common in patients receiving oral NAC. This can be prevented, at times, by chilling the solution, diluting it, and covering the container with a lid to hide the noxious smell. The IV form can cause flushing, erythema, and an anaphylactoid response characterized by angioedema, bronchospasm, hypotension, and rash. This happens most often during the first infusion. This reaction can be handled by stopping the infusion, treating the patient, and then starting the infusion at a slower rate when the signs and symptoms have abated.
Opioids bind to specific mu and kappa receptors in the brain and spinal cord. When these receptors are stimulated, CNS activity in certain parts of the brain is decreased and the clinical effects of opioids (e.g., analgesia, respiratory depression, sedation) are produced. Naloxone is an opioid antagonist that prevents binding of opioids to receptors. As such, it can reverse respiratory depression and help avoid endotracheal intubation and prolonged hospital stays.
Naloxone is used to reverse respiratory depression caused by opioid poisoning. Although naloxone will reverse sedation, this should not be the primary goal of its use. There is some evidence that naloxone will reverse CNS and respiratory depression caused by clonidine poisoning and the toxic effects of other drugs, but the evidence for this is anecdotal and inconsistent .
Naloxone is administered at a dose of 0.4–2 mg as an IV bolus, repeated every 2 to 3 minutes as needed . Always start at the lower end of the dosing range. If a patient has not responded to a total dose of 10 mg of naloxone, it can be assumed that she or he is not opioid poisoned. Because the half-life of some drugs is long and the effects of naloxone diminish and are gone in 1 to 2 hours, some patients with opioid poisoning will require a continuous IV infusion. In these cases, give the patient two-thirds of the dose that was successful in reversing respiratory depression every hour, or 0.4–0.8 mg/hour . Naloxone can also be given intramuscularly, subcutaneously, intranasally, and via an endotracheal tube, but the IV route is preferred.
Naloxone can precipitate opioid withdrawal, and there are reports of arrhythmias and pulmonary edema . However, serious adverse effects occur very rarely, and if used judiciously, naloxone is considered safe.
Octreotide is a synthetic analog of somatostatin. It decreases the release of insulin by the pancreas. Patients with sulfonylurea poisoning often have profound hypoglycemia that lasts for days and is not easily treated with IV dextrose or food. Octreotide is indicated in these cases [42,43].
To reverse sulfonylurea poisoning, administer 50–100 mcg of octreotide every 6 hours as needed, subcutaneously (preferred) or IV . If given IV, dilute the drug and give the dose over 15 to 30 minutes. Patients should be observed for recurrent hypoglycemia for 24 hours after therapy has been stopped.
Octreotide is well tolerated and does not appear to cause any major adverse effects . Minor side effects of dizziness, headache, gastrointestinal effects, and pain at the injection site are possible.
Physostigmine is used to identify and/or treat patients who have severe anticholinergic poisoning who cannot be managed with supportive care. Physostigmine is a reversible inhibitor of acetylcholinesterase, increasing the activity and concentration of acetylcholine at cholinergic synapses.
Physostigmine should never be used to treat the anticholinergic effects of TCAs, and it should never be used concurrently with depolarizing neuromuscular blockers such as succinylcholine. Because physostigmine increases acetylcholine concentration at synapses, it should be used cautiously if the patient has a bladder or intestinal obstruction, cardiac conduction defects, peripheral vascular disease, or reactive airway disease.
Patients with anticholinergic poisoning should have a 12-lead ECG and cardiac monitoring prior to treatment. To initiate treatment, administer 0.5–2 mg IV slowly over 5 minutes . Rapid infusion may increase the risk of adverse effects. The dose can be repeated as needed every 10 to 30 minutes until response occurs; additional dosing may be required.
The major adverse effects possible with physostigmine are asystole, bradycardia, heart block, and seizures . Diarrhea, nausea, and vomiting are possible, and patients with reactive airway disease may develop bronchorrhea and bronchospasm.
Organophosphate and carbamate insecticides bond to acetylcholinesterase. If the bonding is not interrupted, it becomes irreversible and the enzyme is permanently damaged. This results in excess cholinergic stimulation. Pralidoxime, also known as 2-PAM, can break this bond, and when it is used with atropine, the two are synergistic.
2-PAM is approved for the treatment of organophosphate or carbamate insecticide poisoning with signs and symptoms of cholinergic toxicity. It may also be use for persons exposed to certain chemical warfare agents, such as sarin and tabun, which are essentially organophosphates.
It is important to give 2-PAM as soon as possible. The longer the period of time from exposure to treatment with 2-PAM, the less likely it is the drug will break the bond between acetylcholinesterase and the insecticide.
After a response to atropine is established, administer 1–2 g of 2-PAM in 100 mL of normal saline infused over 15 to 30 minutes; repeat bolus dose after 1 hour . This dose can be repeated every 10 to 12 hours until the patient is asymptomatic for 24 hours.
Diplopia, dizziness, drowsiness, headache, and nausea may occur. If 2-PAM is given too rapidly, laryngospasm and serious cardiac and neurological effects are possible . Use of this agent should be avoided in patients with myasthenia gravis.
Isoniazid is an antitubercular agent, but an overdose interferes with pyridoxine (vitamin B6) availability. Pyridoxine is essential in the production of GABA, a major inhibitory neurotransmitter. Because GABA production is decreased, patients with have taken an overdose of isoniazid are at risk for seizures. These seizures often do not respond to conventional therapy but can be ameliorated with pyridoxine supplementation.
The chemical monomethyl hydrazine has similar effects to those seen with isoniazid, and pyridoxine is used for patients with toxic exposures to this substance . Also referred to as MMH, monomethyl hydrazine is found in some mushrooms, most notably the false morels, and is part of the formulation for some types of rocket propellants. Because MMH is believed to have the same action as isoniazid, treatment is similar for both types of poisonings .
One gram of pyridoxine should be given for every gram of isoniazid or MMH ingested (maximum: 5 g); the dose should be given IV over 5 to 10 minutes . If the dose ingested is not known, give 5 g and repeat this dose every 5 to 10 minutes as needed. Although seizures caused by isoniazid or MMH usually do not respond to conventional therapy, benzodiazepines should be given in addition to pyridoxine, as the two drugs are synergistic. Massive doses of pyridoxine cause sensory neuropathy, but supplementation in cases of isoniazid or MMH poisoning should be a high priority.
Using sodium bicarbonate as an antidote is referred to as alkalinization, and sodium bicarbonate has three primary uses in toxicology. It is used in cases of aspirin poisoning, as sodium bicarbonate prevents aspirin from entering CNS tissue and increases excretion of aspirin in the urine. It may also be used for TCA poisoning (and possibly other drugs similar to TCAs). TCAs inhibit sodium ion channels, causing arrhythmias, conduction defects, and hypotension, and sodium bicarbonate will increase the sodium gradient at the ion channels and prevent TCA toxicity. In addition, it can prevent TCAs from binding to tissues by increasing the serum pH. Finally, sodium bicarbonate has been used to treat cases of phenobarbital poisoning because it increases urinary excretion of the drug, but this use is not supported by strong data .
Aspirin poisoning causes metabolic acidosis, and alkalinization can correct acidemia and increase excretion of the drug. Sodium bicarbonate should be used in patients with signs and symptoms of aspirin poisoning or serum salicylate levels of 30 mg/dL or greater. The serum pH and the patient's clinical status should be given equal importance when deciding whether or not to give sodium bicarbonate.
Severe metabolic or respiratory alkalemia and severe hypernatremia are contraindications to the use of sodium bicarbonate. Because using sodium bicarbonate to treat cases of aspirin poisoning requires administration of large volumes of IV fluids, this therapy should be cautiously used if a patient has pulmonary edema, congestive heart failure, or renal failure.
For administration, mix 100–150 mEq sodium bicarbonate and 20–40 mEq potassium in 1 L of IV solution; potassium is an essential aspect of effective therapy. The flow rate of the solution should be adjusted to achieve a urine pH of 7.5 to 8.0.
Alkalemia and fluid overload are the two primary adverse effects of alkalinization. Severe metabolic or respiratory alkalemia or severe hypernatremia are considered contraindications of sodium bicarbonate.
Because TCAs affect sodium ion channels in the myocardium, TCA toxicity is reflected in ECG abnormalities. Alkalinization should be used to treat cases of TCA poisoning if the duration of QRS is greater than 100 msec or if there are other signs of cardiovascular toxicity, such as arrhythmias, hypotension, a negative S wave and a positive R wave in lead aVR, or a terminal 40 msec axis of 120° to 270°.
The recommended dose for TCA toxicity is 1–2 mEq/kg IV over several minutes, and then by a continuous infusion. Add 2 to 3 ampules of sodium bicarbonate to 1 L of IV solution and infuse this at a rate that will maintain a serum pH of 7.45 to 7.55. The bolus dose can be repeated as needed, and the ECG should be monitored closely during treatment.
Sodium thiosulfate is the antidote for cyanide poisoning. It binds to cyanide to form a thiocyanate, and this compound, which is minimally toxic, is excreted renally. The result is a rapid reversal of the toxic effects of cyanide poisoning.
Sodium thiosulfate is administered at a dose of 12.5 g IV . It should be administered in conjunction with sodium nitrite, with sodium nitrite started first. The rate of infusion depends on the clinical condition of the patient; it can be given as a rapid IV bolus or infused over 10 to 30 minutes. Minor adverse effects are possible and include nausea and vomiting.
Dermal, inhalation, and ocular poisonings occur frequently. The two important questions to keep in mind when caring for a patient with skin, respiratory tract, or eye exposure are:
Will this exposure cause systemic effects?
Are there any special treatments that are needed?
For most cases of skin, respiratory tract, or ocular poisoning, toxicity is localized and standard care is sufficient to resolve any adverse effects. For dermal exposures, all contaminated clothing should be removed. The skin is flushed with tepid water for 15 minutes, and then the level of damage can be assessed. If there are burns, provide standard burn care.
Patients with inhalational exposures should be moved to fresh air. A thorough assessment will help identify injuries requiring immediate attention. Supportive care, such as bronchodilators and oxygen, is applied as needed. These patients often experience systemic effects, as entrance into the bloodstream is swift.
The first step in treating ocular exposures is to carefully remove contact lenses (if present) and flush the eyes for 15 minutes. The flushing can be done at home with tepid water or in a healthcare facility with sterile saline. Flushing as soon as possible after the exposure is much more important than which solution is used; flushing the eyes should not be delayed. If the patient has an ocular abrasion or burn, contact an ophthalmologist.
There are some situations in which dermal, inhalational, and ocular exposures may cause systemic toxicity and will require special care. The most common of these are hydrofluoric acid exposures to the skin, which can cause serious electrolyte abnormalities and arrhythmias. In these cases, treatment of the systemic effects should be initiated as soon as possible.
Patient A, a girl 14 years of age, is brought to a local emergency department by her parents at 9 p.m. The parents state that 45 minutes prior to arriving they found the patient in her room. She was very upset and stated that she had just taken "a whole bottle of pills." The parents are able to account for their daughter's actions and location since she returned from school at 3 p.m., and they state that she had been awake, alert, and acting normally. She had been alone for only 5 to 10 minutes. The father found an empty bottle of acetaminophen 500 mg tablets in the patient's room. The bottle contained 60 tablets when it was purchased, but neither parent can remember how many tablets were in the bottle before the exposure. They estimate that it might have been half full.
Patient A is awake, alert, and oriented to time, place, and person. Her speech is clear. Her vital signs are: temperature 98.3°F; pulse 80 beats per minute and regular; respiratory rate 16 breaths per minute; and blood pressure 112/60 mm Hg. Her skin is warm and dry, and no cyanosis is noted. Her pupils are 5 mm in diameter, and they are equal in size and normally reactive to light. Her chest is clear to auscultation, and her heart tones are normal. She has a normal gag reflex and bowel signs, and her bladder is not distended. She weighs 55 kg. Patient A has a past medical history of bipolar disorder, for which she takes lithium carbonate 300 mg, once in the morning and once in the evening; her last dose was at 9 a.m. today. The medication is given to the patient by the parents, and they are sure that she did not and could not have access to it. The patient has no other medical problems and takes no other medications. Neither parent takes any prescription medications. They state that the only other medication in the house is antacid tablets.
Patient A's ABCs are normal, and this is to be expected. Acetaminophen causes delayed onset liver and (occasionally) kidney damage, typically about 24 hours after ingestion. If a patient had taken a massive overdose of acetaminophen, other organ systems could be affected and there would be changes in the ABCs. However, these cases are rare, and even then it takes time for toxicity to develop. A dose of acetaminophen greater than 7.5 g or 150 mg/kg is considered potentially toxic. It is estimated that Patient A may have taken 15 g or 272 mg/kg. This is a large dose and potentially toxic, but she has presented to the emergency department soon after the ingestion. As such, the dose does not put her at risk for serious derangements of the ABCs. If the ABCs were abnormal, an exposure to another drug or toxin would need to be strongly considered. There is no indication that dextrose, oxygen, naloxone, or thiamine is needed.
It appears that the patient ingested only acetaminophen, had no access to any other medications, and the history seems accurate and reliable. The patient takes lithium carbonate, and it is very unlikely that an overdose of this medication was ingested. However, the possibility should be kept in mind. The patient does not have any signs or symptoms of a toxidrome, and the physical exam is normal.
As a part of the treatment plan, gastric decontamination is considered. The patient is awake and alert, has a normal gag reflex, and has a normally functioning gastrointestinal tract. It is very unlikely that Patient A's mental status or ability to maintain her airway will deteriorate. There are no contraindications to the use of activated charcoal and it binds very well to acetaminophen, so activated charcoal would be the gastric decontamination technique to use. Syrup of ipecac should never be used, lavage is reserved for patients who have ingested a life-threatening amount of a dangerous drug and/or drug for which there is no effective antidote, and whole bowel irrigation is reserved for drugs that are not adsorbed by activated charcoal or sustained-release preparations. One dose of plain charcoal should be given. Most activated charcoal is available in 50 g doses.
NAC is a highly effective antidote for acetaminophen poisoning. It is commonly available, easy to administer, and relatively safe. It can be given any time within 8 hours of an acetaminophen overdose and be equally effective; after 8 hours, the effectiveness begins to decrease. Patient A may need NAC depending on the amount of drug she took. However, the time of ingestion in this case is known and within 8 hours of arrival, so there is no need to give NAC immediately. NAC should be used for acetaminophen poisoning if the patient has ingested a toxic dose, there is evidence of liver damage, or the serum acetaminophen level is toxic. In this case, the dose is unknown and it is too early to see signs, symptoms, or laboratory evidence of liver damage, so the decision of whether or not to use NAC will depend on the serum acetaminophen level. Hospital laboratories can usually perform and report the results of serum acetaminophen level test within one hour of receiving the blood sample.
It is clear that a serum acetaminophen level should be obtained, but it must be done 4 hours or later after the ingestion. If the level is measured sooner, it cannot be reliably interpreted. Interpreting the level as toxic or nontoxic on the basis of the numerical value alone could lead to treatment errors. The level and associated risk for hepatotoxicity should be interpreted using the Rumack-Matthew nomogram (Figure 1). Serum hepatic transaminases, BUN, and serum creatinine should also be obtained. Although it is unlikely the patient had access to her lithium, it would be prudent to check a lithium level as well. There is no need for other laboratory tests, an ECG, or imaging studies.
In some cases, a serum aspirin level should be checked. It is not unusual for patients to use the terms acetaminophen and aspirin interchangeably. However, because of the particulars of this case study, an aspirin level would not be needed.
When an overdose of acetaminophen is taken, the two primary metabolic pathways for the drug become saturated and a third pathway is used. This metabolic pathway produces large amounts of a toxic metabolite, N-acetyl-p-benzoquinoneimine (NAPQI), and it is this metabolite that causes liver and kidney damage. Manipulating the pH of the urine or serum would not affect acetaminophen metabolism or the production of NAPQI, so these techniques are not used. Acetaminophen can be quickly and easily removed with hemodialysis, but hemodialysis has risks. Because there is a highly effective antidote available, hemodialysis or any other type of extracorporeal removal would not be needed.
At this point, care of Patient A focuses on monitoring vital signs, arranging a consultation with a mental health professional, maintaining patient safety, and treating with NAC if her acetaminophen level is greater than 150 mcg/mL.
Patient B, a man 56 years of age, is brought to the emergency department at 4:30 p.m. His wife called EMS because the patient had reportedly taken an overdose of his prescription medications. According to the EMS personnel, the ingestion was unwitnessed; Patient B had told the wife that he wanted to die and that some time that morning he had "taken all of his pills." The exact time of ingestion is not known, but a reasonable estimate is 10 a.m. The EMS personnel report that they found empty bottles of bupropion, metoprolol, and verapamil (all three sustained-release formulations), and the patient's name was on the bottles. The patient told EMS that he had been drinking vodka and when that ran out, he drank some antifreeze. The EMS personnel did not find any bottles of antifreeze. He has a past history of chronic alcohol abuse, depression, and hypertension.
Patient B is awake and alert, but drowsy. His vital signs are: temperature 97.8°F; pulse 44 beats per minute; respiratory rate 16 breaths per minute; and blood pressure 82/38 mm Hg. The cardiac monitor shows sinus bradycardia. His oxygen saturation is 93%, and his bedside serum glucose level is 148 mg/dL. His nail beds are cyanotic, there is no peripheral edema, and his skin is cool and clammy. His pupils are 5 mm and reactive, his lungs are clear, and his heart tones are normal. His abdomen is soft and nontender, and there is no bladder distention.
The most immediate need in this situation is to stabilize the ABCs. Supplemental oxygen is applied, and IV access is obtained. It is reasonable to assume that the bradycardia and hypotension are being caused by the metoprolol and verapamil. Atropine, fluids, and vasopressors are seldom effective for the cardiovascular toxicity caused by beta blockers and calcium channel blockers. Those drugs can be tried, but if they do not quickly reverse the bradycardia and hypotension, additional treatment should not be delayed. For Patient B, antidotal care is a top priority. Antidotal care may also be needed to treat ethylene glycol poisoning.
The physician administers 10% calcium chloride 10 mL IV over 5 minutes. The dose can be repeated every 10 to 20 minutes, or a continuous infusion can be used. Concurrently, an IV bolus dose of glucagon is given, 5 mg over 5 minutes. This can be followed (if needed) with a continuous IV infusion at 1–5 mg/hour. If these are unsuccessful, a dextrose-insulin infusion and cardiac pacing are the next steps. Give a bolus dose of regular insulin, 1 Unit/kg, followed by a continuous infusion of regular insulin at 1–10 Units/kg/hour. As the insulin is being given, the patient should receive an IV bolus of 25 g of 50% dextrose. Additional glucose should be given to maintain the serum glucose level of 100–200 mg/dL. Consider giving fomepizole. Antifreeze almost always contains ethylene glycol, but many hospital laboratories are not prepared to measure ethylene glycol levels. If a level cannot be obtained, the decision to use fomepizole will depend on how likely it is the patient ingested ethylene glycol, the patient's arterial blood gases, and if the patient has a large anion gap and/or a large osmolar gap. The risks of fomepizole are slight, and the benefit can be enormous.
Patient B's serum glucose is normal, so he does not require dextrose. Supplemental oxygen is started immediately. He does not have signs or symptoms of an opioid poisoning, so naloxone is not appropriate. Although he chronically abuses alcohol, the patient has no signs of Wernicke-Korsakoff syndrome, so thiamine should not be given.
The circumstances of the overdose are not very clear, but if Patient B did take the medications and the antifreeze, there is a high risk for serious morbidity and death. The time of ingestion is not known with certainty, but it appears that it happened approximately 6.5 hours prior to arrival. Given the patient's clinical condition and the empty bottles of metoprolol and verapamil, it seems reasonable to assume that he took an overdose of these medications and took an intoxicant that can cause CNS depression—in this case, ethanol and/or ethylene glycol.
Upon physical examination there is no evidence of a toxidrome, as would be expected. Because the patient has ingested a beta blocker, a calcium channel blocker, ethanol, and a toxic alcohol, the patient should be assessed for signs and symptoms of circulatory compromise, respiratory depression, intoxication, and metabolic acidosis. Circulatory compromise is evident. The patient is drowsy, and this may be due to the bupropion, the ethanol, the ethylene glycol, or a combination of the three. There is no respiratory depression, so Patient B may not have ingested sufficient quantities of the alcohols for this to develop. There are no signs of metabolic acidosis, but this could develop in the next few hours. Laboratory conformation is needed to detect and confirm an acid-base disturbance. If acidosis is present, it could, in part, explain the CNS depression.
Gastric decontamination should not be performed for Patient B. Although the patient has ingested medications and a toxin that can be very dangerous, it has been more than one hour since the ingestion. Also, it could cause the patient's CNS depression to worsen. Any method of gastric decontamination would put the patient at risk for aspiration and/or worsening of his cardiac status and would probably not be useful.
Measurement of Patient B's serum acetaminophen level, serum ethanol level, and serum ethylene glycol level should be attempted. Blood levels of bupropion, metoprolol, and verapamil can be done, but they cannot be obtained immediately and would not be useful in caring for the patient. Obtain electrolytes to look for an anion gap, assess arterial blood gases to check for an acid-base disturbance, and request a serum osmolarity to look for an osmolar gap. A 12-lead ECG should be done, and the patient should be on continuous cardiac monitoring. Urinalysis should also be ordered. Ethylene glycol metabolism produces oxalate crystals in the urine, which could help confirm the diagnosis.
Bupropion, metoprolol, and verapamil cannot be removed by dialysis or hemoperfusion nor can their elimination be enhanced by manipulating the pH of the urine. However, hemodialysis is very effective at removing ethylene glycol and the toxic aids produced by ethylene glycol metabolism. A nephrologist should be notified of the possible need for hemodialysis.
The number of patients who overdose each year is relatively small, but not insignificant. There are tens of thousands of overdose cases and toxic exposures in the United States annually. The experience of most poison control center personnel is that many nurses would benefit from a basic knowledge of toxicology and the information necessary to provide good care for the poisoned patient.
This course has provided an overview of the most common poisoning emergencies and their treatments. By applying this information to one's practice, these cases can be identified and treated early, resulting in better outcomes and improved patient care.
1. Mowry JB, Spyker DA, Cantilena LR Jr, McMillan N, Ford M. 2013 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 31st Annual Report. Clin Toxicol (Phila). 2014;52(10):1032-1283.
2. Olson KR. Comprehensive evaluation and treatment. In: Olson KR, Anderson IB, Benowitz NL, et al. (eds). Poisoning and Drug Overdose. 6th ed. New York, NY: McGraw-Hill; 2011: 1-68.
3. Nelson LS, Lewin NA, Howland MA, Hoffman RS, Goldfrank LR, Flomenbaum NE. Initial evaluation of the patient: vital signs and toxic syndromes. In: Nelson LS, Lewin NA, Howland MA, Hoffman RS, Goldfrank LR, Flomenbaum NE (eds). Goldfrank's Toxicologic Emergencies. 9th ed. New York, NY: McGraw-Hill; 2011: 33-36.
4. Salomone JA III. Hallucinogen Toxicity. Available at http://emedicine.medscape.com/article/814848-overview. Last accessed January 21, 2015.
5. Velez LI, Dealaney KA. Dextrose. In: Nelson LS, Lewin NA, Howland MA, Hoffman RS, Goldfrank LR, Flomenbaum NE (eds). Goldfrank's Toxicologic Emergencies. 9th ed. New York, NY: McGraw-Hill; 2011: 728-733.
6. Geller RJ. Paraquat and diquat. In: Olson KR, Anderson IB, Benowitz NL, et al. (eds). Poisoning and Drug Overdose. 6th ed. New York, NY: McGraw-Hill; 2011: 321-323.
7. Howland MA. Flumazenil. In: Nelson LS, Lewin NA, Howland MA, Hoffman RS, Goldfrank LR, Flomenbaum NE (eds). Goldfrank's Toxicologic Emergencies. 9th ed. New York, NY: McGraw-Hill; 2011: 1072-1077.
8. McGregor T, Parkar M, Rao S. Evaluation and management of common childhood poisonings. Am Fam Physician. 2009;79(5): 397-403.
9. Verive MJ. Pediatric Methemoglobinemia Treatment and Management. Available at http://emedicine.medscape.com/article/204178-treatment. Last accessed January 22, 2015.
11. Smith TW. Review of clinical experience with digoxin immune Fab (ovine). Am J Emerg Med. 1991;9(2 Suppl 1):1-6, 33-34.
12. Ables AZ, Naqubilli R. Prevention, recognition, and management of the serotonin syndrome. Am Fam Physician. 2010;81(9): 1139-1142.
13. Rainey PM. Laboratory principles. In: Nelson LS, Lewin NA, Howland MA, Hoffman RS, Goldfrank LR, Flomenbaum NE (eds). Goldfrank's Toxicologic Emergencies. 9th ed. New York, NY: McGraw-Hill; 2011: 70-89.
15. Clancy C. Electrocardiographic principles. In: Nelson LS, Lewin NA, Howland MA, Hoffman RS, Goldfrank LR, Flomenbaum NE (eds). Goldfrank's Toxicologic Emergencies. 9th ed. New York, NY: McGraw-Hill; 2011: 314-329.
16. Arizona Center for Education and Research on Therapeutics. Combined List of Drugs That Prolong QT and/or Cause Torsades de Pointes (TDP). Available at http://www.crediblemeds.org/pdftemp/pdf/CompositeList.pdf. Last accessed January 22, 2015.
18. Maurer MH, Niehues SM, Schnapauff D, et al. Low-dose computed tomography to detect body packing in an animal model.Eur J Radiol. 2011;78(2):302-306.
19. Yang RM, Li L, Feng J, et al. Heroin body packing: clearly discerning drug packets using CT. South Med J. 2009;102(5):470-475.
20. Eddleston M, Hagglla S, Reginald K, et al. The hazards of gastric lavage for intentional self-poisoning in a resource poor location. Clin Toxicol. 2007;45(2):136-143.
21. Olson KR. Activated charcoal for acute poisoning: one toxicologist's journey. J Med Toxicol. 2010;6(2):190-198.
22. American Academy of Clinical Toxicology. Position paper: single-dose activated charcoal. Clin Toxicol. 2005;43(2):61-87.
23. Frithsen IL, Simpson WM Jr. Recognition and management of acute medication poisoning. Am Fam Physician. 2010;81(3):316-323.
24. LexiComp Online. Available at http://online.lexi.com. Last accessed January 22, 2015.
25. Juckett G, Hancox JG. Venomous snakebites in the United States: management review and update. Am Fam Physician. 2002;65(7):1367-1374.
26. Mayo Clinic. Ipecac Syrup (Oral Route). Available at http://www.mayoclinic.org/drugs-supplements/ipecac-syrup-oral-route/proper-use/drg-20064363. Last accessed January 22, 2015.
27. American Academy of Clinical Toxicology. Position paper: cathartics. J Toxicol Clin Toxicol. 2004;42(7):243-253.
28. Benson BE, Hoppu K, Troutman WG, et al. Position paper update: gastric lavage for gastrointestinal decontamination. Clin Toxicol (Phila). 2013;51(3):140-146.
29. Li Y, Tse GL, Gawarammana I, Buckley N, Eddleston M. Systematic review of controlled clinical trials of gastric lavage in acute organophosphorus pesticide poisoning. Clin Toxicol. 2009;47(3):179-192.
30. American Academy of Clinical Toxicology. Position statement and practice guidelines on the use of multi-dose activated charcoal in the treatment of acute poisonings. J Toxicol Clin Toxicol. 1999;37(6):731-751.
31. Roberts DM, Buckley NA. Enhanced elimination in acute barbiturate poisoning: a systematic review. Clin Toxicol. 2011;49(1):2-12.
32. Vannaprasaht S, Tiamkao S, Sirivongs D, Piyavhatkul N. Acute valproic acid overdose: enhance elimination with multiple-doses activated charcoal. J Med Assoc Thai. 2009;92(8):1113-1115.
33. Benson BE, Hoppu K, Troutman WG, et al. Position paper update: gastric lavage for gastrointestinal decontamination. Clin Toxicol (Phila). 2013;51(3):140-146.
34. Day E, Bentham P, Callaghan R, Kuruvilla T, George S. Thiamine for Wernicke-Korsakoff syndrome in people at risk from alcohol abuse. Cochrane Database Syst Rev. 2008;(1):CD004033.
35. Lorett J. Ipecac syrup. In: Olson KR, Anderson IB, Benowitz NL, et al. (eds). Poisoning and Drug Overdose. 6th ed. New York, NY: McGraw-Hill; 2011: 244-246.
36. Gussow L. Yesterday's heresy, today's gospel: rethink use of naloxone. Emerg Med News. 2009;31(12):6.
37. American Academy of Clinical Toxicology. Position paper: whole bowel irrigation. J Toxicol Clin Toxicol. 2004;42(6):843-854.
38. Lheureux P, Zahir S, Gris M, Derry AS, Penaloza A. Bench-to-bedside review: hyperinsulinaemia/euglycaemia therapy in the management of overdose of calcium-channel blockers. Crit Care. 2006;10(3):212-217.
39. Engebretsen KM, Kaczmarek KM, Morgan J, Holder JS. High-dose insulin therapy in beta-blocker and calcium-channel blocker poisoning. Clin Toxicol. 2011;49(4):277-283.
40. Perrott J, Murphy NG, Zed PJ. L-carnitine for acute valproic acid overdose: a systematic review of published cases. Ann Pharmacother. 2010;44(7-8):1287-1293.
41. Bebarta VS, Kao L, Froberg B, et al. A multi-center comparison of the safety of oral versus intravenous acetylcysteine for treatment of acetaminophen overdose. Clin Toxicol. 2010;48(5):424-430.
42. Glatstein M, Garcia-Bournissen F, Scolnik D, Koren G. Sulfonylurea intoxication at a tertiary care paediatric hospital. Can J Clin Pharmacol. 2010;17(1):51-56.
43. Dougherty PP, Klein-Schwartz W. Octreotide's role in the management of sulfonylurea-induced hypoglycemia. J Med Toxicol. 2010;6(2):199-206.
44. Newton CR, Delgado JH, Gomez HF. Calcium and beta receptor antagonist overdose: a review and update of pharmacological principles and management. Semin Respir Crit Care Med. 2002;23(1):19-25.
45. Howland MA. Antidotes in depth: pyridoxine. In: Nelson LS, Lewin NA, Howland MA, Hoffman RS, Goldfrank LR, Flomenbaum NE (eds). Goldfrank's Toxicologic Emergencies. 9th ed. New York, NY: McGraw-Hill; 2011: 845-848.
1. Lee WM, Larson AM, Stravitz T. AASLD Position Paper: The Management of Acute Liver Failure: Update 2011. Baltimore, MD: American Association for the Study of Liver Diseases; 2011. Summary retrieved from National Guideline Clearinghouse at http://www.guideline.gov/content.aspx?id=36894. Last accessed February 9, 2015.
2. Assessment and Management of Risk for Suicide Working Group. VA/DoD Clinical Practice Guideline for Assessment and Management of Patients at Risk for Suicide. Washington, DC: Department of Veterans Affairs, Department of Defense; 2013. Summary retrieved from National Guideline Clearinghouse at http://www.guideline.gov/content.aspx?id=47023. Last accessed February 9, 2015.
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