4: Principles of Managing the Acutely Poisoned or Overdosed Patient

For over 5 decades, medical toxicologists and poison information specialists have used a clinical approach to poisoned or overdosed patients that emphasizes treating the patient rather than treating the poison.¹ Too often in the past, patients were initially all but neglected while attention was focused on the ingredients listed on the containers of the product(s) to which they presumably were exposed. Although the astute clinician must always be prepared to administer a specific antidote immediately in instances when nothing else will save a patient, such as cyanide poisoning, all poisoned or overdosed patients will benefit from an organized, rapid clinical management plan (Fig. 4–1).

Over the past 4 decades, some basic tenets and long-held beliefs regarding the initial therapeutic interventions in toxicologic management have been questioned and subjected to an “evidence-based” analysis. For example, in the mid-1970s, most medical toxicologists began to advocate a standardized approach to a comatose and possibly overdosed adult patient, typically calling for the intravenous (IV) administration of 50 mL of ­dextrose 50% in water (D₅₀W), 100 mg of thiamine, and 2 mg of naloxone along with 100% oxygen at high flow rates. The rationale for this approach was to compensate for the previously idiosyncratic style of overdose management encountered in different health care settings and for the unfortunate likelihood that omitting any one of these measures at the time that care was initiated in the emergency department (ED) would result in omitting it altogether. It was not unusual then to discover from a laboratory chemistry report more than one hour after a supposedly overdosed comatose patient had arrived in the ED that the initial blood glucose was 30 or 40 mg/dL—a critical delay in the management of unsuspected and consequently untreated hypoglycemic coma. Today, however, with the widespread availability of accurate rapid bedside testing for capillary glucose, pulse oximetry for ­oxygen saturation, and end-tidal CO₂ monitors coupled with a much greater appreciation by all physicians of what needs to be done for each suspected overdose patient, clinicians can safely provide a more rational, individualized approach to determine the need for, and in some instances more precise amounts of, dextrose, thiamine, naloxone, and oxygen.

A second major approach to providing more rational individualized early treatment for toxicologic emergencies involves a closer examination of the actual risks and benefits of various gastrointestinal (GI) emptying interventions. Appreciation of the potential for significant adverse effects associated with all types of GI emptying interventions and recognition of the absence of clear evidence-based support of efficacy have led to abandoning of syrup of ipecac-induced emesis, an almost complete elimination of orogastric lavage, and a significant reduction in the routine use of activated charcoal (AC). The value of whole-bowel irrigation (WBI) with polyethylene glycol electrolyte solution (PEG-ELS) appears to be much more specific and limited than originally thought, and some of the limitations and (uncommon) adverse effects of AC are now more widely recognized.

Similarly, interventions to eliminate absorbed xenobiotics from the body are now much more narrowly defined or, in some cases, abandoned. Multiple-dose activated charcoal (MDAC) is useful for select but not all xenobiotics. Ion trapping in the urine is only beneficial, achievable, and relatively safe when the urine can be maximally alkalinized after a significant salicylate or phenobarbital poisoning. Finally, the roles of hemodialysis, hemoperfusion, and other extracorporeal techniques are now much more specifically defined.² With the foregoing in mind, this chapter represents our current efforts to formulate a logical and effective approach to managing a patient with probable or actual toxic exposure.

Table 4–1 provides a recommended stock list of antidotes and therapeutics for the treatment of poisoned or overdosed patients.

Rarely, if ever, are all of the circumstances involving a poisoned patient known. The history may be incomplete, unreliable, or unobtainable; multiple xenobiotics may be involved; and even when a xenobiotic etiology is identified, it may not be easy to determine whether the problem is an overdose, an allergic or idiosyncratic reaction, or a drug–drug interaction. Similarly, it is sometimes difficult or impossible to differentiate between the adverse effects of a correct dose of medication and the consequences of a deliberate or unintentional overdose. The patient’s presenting signs and symptoms may force an intervention at a time when there is almost no information available about the etiology of the patient’s condition (Table 4–2), and as a result, therapeutics must be thoughtfully chosen empirically to treat or diagnose a condition without exacerbating the situation.

Initial Management of Patients with a Suspected Exposure

Similar to the management of any seriously compromised patient, the clinical approach to the patient potentially exposed to a xenobiotic begins with the recognition and treatment of life-threatening conditions, including airway compromise, breathing difficulties, and circulatory problems such as hemodynamic instability and serious dysrhythmias. After the “ABCs” (airway, breathing, and circulation) have been addressed, the patient’s level of consciousness should be assessed because this helps determine the techniques to be used for further management of the exposure.

Management of Patients with Altered Mental Status

Altered mental status (AMS) is defined as the deviation of a patient’s sensorium from normal. Although it is commonly construed as a depression in the patient’s level of consciousness, a patient with agitation, delirium, psychosis, and other deviations from normal is also considered to have an AMS. After airway patency is established or secured, an initial bedside assessment should be made regarding the adequacy of breathing. If it is not possible to assess the depth and rate of ventilation, then at least the presence or absence of regular breathing should be determined. In this setting, any irregular or slow breathing pattern should be considered a possible sign of the incipient apnea, requiring ventilation with 100% oxygen by bag–valve–mask followed as soon as possible by endotracheal intubation and mechanical ventilation. Endotracheal intubation may be indicated for some cases of coma resulting from a toxic exposure to ensure and maintain control of the airway and to enable safe performance of procedures to prevent GI absorption or eliminate previously absorbed xenobiotics.

Although in many instances, the widespread availability of pulse oximetry to determine O₂ saturation and end-tidal CO₂ monitors have made arterial blood gas (ABG) analysis less of an immediate priority, these technical advances have not entirely eliminated the importance of blood gas analysis. An ABG determination will more accurately define the adequacy not only of oxygenation (PO₂, O₂ saturation) and ventilation (PCO₂) but may also alert the physician to possible toxic-metabolic etiologies of coma characterized by acid–base disturbances (pH, PCO₂) (Chap. 19). In addition, carboxyhemoglobin determinations are now available by point-of-care testing, and both carboxyhemoglobin and methemoglobin may be determined on either venous or arterial blood specimens (Chaps. 125 and 127). In every patient with an AMS, a bedside rapid capillary glucose concentration should be obtained as soon as possible.

After the patient’s respiratory status has been assessed and managed appropriately, the strength, rate, and regularity of the pulse should be evaluated, the blood pressure determined, and a rectal temperature obtained. Both an initial 12-lead electrocardiogram (ECG) and continuous rhythm monitoring are essential. Monitoring will alert the clinician to dysrhythmias that are related to toxic exposures either directly or indirectly via hypoxemia or electrolyte imbalance. For example, a 12-lead ECG demonstrating QRS widening and a right axis deviation might indicate a life-threatening ­exposure to a cyclic antidepressant or another xenobiotic with sodium channel–blocking properties. In these cases, the physician can anticipate such serious sequelae as ventricular tachydysrhythmias, seizures, and cardiac arrest and consider both the early use of specific treatment (antidotes), such as IV sodium bicarbonate, and avoidance of medications, such as procainamide and other class IA and IC antidysrhythmics, which could exacerbate the situation.

Extremes of core body temperature must be addressed early in the evaluation and treatment of a comatose patient. Life-threatening hyperthermia (temperature >106°F; >41.1°C) is usually appreciated when the patient is touched (although the widespread use of gloves as part of universal precautions has made this less apparent than previously). Most individuals with severe hyperthermia, regardless of the etiology, should have their temperatures immediately reduced to about 101.5°F (38.7°C) by sedation if they are agitated or displaying muscle rigidity and by ice water immersion (Chap. 30). Hypothermia is probably easier to miss than hyperthermia, especially in northern regions during the winter months, when most arriving patients feel cold to the touch. Early recognition of hypothermia, however, helps to avoid administering a variety of medications that may be ineffective until the patient becomes relatively euthermic, which may cause iatrogenic toxicity as a result of a sudden response to xenobiotics previously administered.

For a hypotensive patient with clear lungs and an unknown overdose, a fluid challenge with IV 0.9% sodium chloride or lactated Ringer solution may be started. If the patient remains hypotensive or cannot tolerate fluids, an antidote, a vasopressor, or an inotropic agent may be indicated, as may more invasive monitoring.

At the time that the IV catheter is inserted, blood samples for glucose, electrolytes, blood urea nitrogen (BUN), a complete blood count (CBC), and any indicated toxicologic analyses can be obtained. A pregnancy test should be obtained in any woman with childbearing potential. If the patient has an AMS, there may be a temptation to send blood and urine specimens to identify any central nervous system (CNS) depressants or so-called drugs of abuse in addition to other medications. But the indiscriminate ordering of these tests rarely provides clinically useful information. For the potentially suicidal patient, an APAP concentration should be routinely requested along with tests affecting the management of any specific xenobiotic, such as carbon monoxide, lithium, theophylline, iron, salicylates, and digoxin (or other cardioactive steroids), as suggested by the patient’s history, physical examination, or bedside diagnostic tests. In the vast majority of cases, the blood tests that are most useful in diagnosing toxicologic emergencies are not the toxicologic assays but rather the “nontoxicologic” routine metabolic profile tests such as BUN, glucose, electrolytes, and blood gas analysis.

Xenobiotic-related seizures may broadly be divided into three categories: (1) those that respond to standard anticonvulsant treatment (typically using a benzodiazepine); (2) those that either require specific antidotes to control seizure activity or that do not respond consistently to standard anticonvulsant treatment, such as isoniazid-induced seizures requiring pyridoxine administration; and (3) those that may appear to respond to initial treatment with cessation of tonic–clonic activity but that leave the patient exposed to the underlying, unidentified xenobiotic or to continued electrical seizure activity, as is the case with carbon monoxide poisoning and hypoglycemia.

Within the first 5 minutes of managing a patient with an AMS, four therapeutic interventions should be considered, and if indicated, administered:

1. High-flow oxygen (8–10 L/min) to treat a variety of xenobiotic-induced hypoxic conditions

2. Hypertonic dextrose: 0.5–1.0 g/kg of D₅₀W for an adult or a more dilute dextrose solution (D₁₀W or D₂₅W) for a child; the dextrose is administered as an IV bolus to diagnose and treat or exclude hypoglycemia

3. Thiamine (100 mg IV for an adult; usually unnecessary for a child) to prevent or treat Wernicke encephalopathy

4. Naloxone (0.04 mg IV with upward titration) for an adult or child with opioid-induced respiratory compromise

The clinician must consider that hypoglycemia may be the sole or contributing cause of coma even when the patient manifests focal neurologic findings; therefore, dextrose administration should only be omitted when hypoglycemia can be definitely excluded by accurate rapid bedside testing. Also, while examining a patient for clues to the etiology of a presumably toxic-metabolic form of AMS, it is important to search for any indication that trauma may have caused, contributed to, or resulted from the patient’s condition. Conversely, the possibility of a concomitant drug ingestion or toxic metabolic disorder in a patient with obvious head trauma should also be considered.

The remainder of the physical examination should be performed rapidly but thoroughly. In addition to evaluating the patient’s level of consciousness, the physician should note abnormal posturing (decorticate or decerebrate), abnormal or unilateral withdrawal responses, and pupil size and reactivity. Pinpoint pupils suggest exposure to opioids or organic phosphorus insecticides, and widely dilated pupils suggest anticholinergic or sympathomimetic poisoning. The presence or absence of nystagmus, abnormal reflexes, and any other focal neurologic findings may provide important clues to a structural cause of AMS. For clinicians accustomed to applying the Glasgow Coma Scale (GCS) to all patients with AMS, assigning a score to the overdosed or poisoned patient may provide a useful measure for assessing changes in neurologic status. However, in this situation, the GCS should never be used for prognostic purposes because despite a low GCS score, complete recovery from properly managed toxic-metabolic coma is the rule rather than the exception (Chap. 24).

Characteristic breath or skin odors may identify the etiology of coma. The fruity odor of ketones on the breath suggests diabetic or alcoholic ketoacidosis but also the possible ingestion of acetone or isopropyl alcohol, which is metabolized to acetone. The pungent, minty odor of oil of wintergreen on the breath or skin suggests methyl salicylate poisoning. The odors of other substances such as cyanide (“bitter almonds”), hydrogen sulfide (“rotten eggs”), and organic phosphorus compounds (“garlic”) are described in detail in Chap. 26 and summarized in Table 26–1.

Further Evaluation of All Patients with Suspected Xenobiotic Exposures

Auscultation of breath sounds, particularly after a fluid challenge, helps to diagnose pulmonary edema, acute lung injury, or aspiration pneumonitis when present. Coupled with an abnormal breath odor of hydrocarbons or organic phosphorus compounds, for example, crackles and rhonchi may point to a toxic pulmonary etiology instead of a cardiac etiology; this is important because the administration of certain cardioactive medications may be inappropriate or dangerous in the former circumstances.

Heart murmurs in an injection drug user, especially when accompanied by fever, may indicate bacterial endocarditis. Dysrhythmias may suggest overdoses or inappropriate use of cardioactive xenobiotics, such as digoxin and other cardioactive steroids, β-adrenergic antagonists, calcium channel blockers, and cyclic antidepressants.

The abdominal examination may reveal signs of trauma or alcohol-related hepatic disease. The presence or absence of bowel sounds helps to exclude or to diagnose anticholinergic toxicity and is important in considering whether to manipulate the GI tract in an attempt to remove the toxin. A large palpable bladder may signal urinary retention as a further manifestation of anticholinergic toxicity.

Examination of the extremities might reveal clues to current or former drug use (track marks, skin-popping scars); metal poisoning (Mees lines, arsenical dermatitis); and the presence of cyanosis or edema suggesting ­preexisting cardiac, pulmonary, or kidney disease (Chap. 29).

Repeated evaluation of the patient suspected of an overdose is essential for identifying new or developing findings or toxic syndromes and for early identification and treatment of a deteriorating condition. Until the patient is completely recovered or considered no longer at risk for the consequences of a xenobiotic exposure, frequent reassessment must be provided even as the procedures described later are carried out. Toxicologic etiologies of abnormal vital signs and physical findings are summarized in Tables 3–1, 3–2,3–3,3–4,3–5, and 3–6. Toxic syndromes, sometimes called “toxidromes,” are summarized in Table 3–1.

Typically in the management of patients with toxicologic emergencies, there is both a necessity and an opportunity to obtain various diagnostic studies and ancillary tests interspersed with stabilizing the patient’s condition, obtaining the history, and performing the physical examination. ­Chapters 5, 6, and 16 discuss the timing and indications for diagnostic imaging procedures, qualitative and quantitative diagnostic laboratory studies,­ and the use and interpretation of the ECG in evaluating and managing poisoned or overdosed patients.

The Role of Gastrointestinal Evacuation

A series of highly individualized treatment decisions must now be made. As noted previously and as discussed in detail in Chap. 8, the decision to evacuate the GI tract or administer AC can no longer be considered standard or routine toxicologic care for most patients. Instead, the decision should be based on the type of ingestion, estimated quantity and size of pill or tablet, time since ingestion, concurrent ingestions, ancillary medical conditions, and age and size of the patient. The indications, contraindications, and procedures for performing orogastric lavage and for administering WBI, AC, MDAC, and cathartics are listed in Tables 8–1 through 8–7 and are discussed both in Chap. 8 and in the specific Antidotes in Depth sections immediately following Chap. 8.

Eliminating Absorbed Xenobiotics from the Body

After deciding whether or not an intervention to try to prevent absorption of a xenobiotic is indicated, the clinician must next consider the applicability of techniques available to eliminate xenobiotics already absorbed. Detailed discussions of the indications for and techniques of manipulating urinary pH (ion trapping), diuresis, hemodialysis, hemoperfusion, hemofiltration, and exchange transfusion are found in Chap. 10. Briefly, patients who may benefit from these procedures are those who have systemically absorbed xenobiotics amenable to one of these techniques and whose clinical conditions are both serious (or potentially serious) and unresponsive to supportive care or whose physiologic route of elimination (liver–feces, kidney–urine) is impaired.

Alkalinization of the urinary pH for acidic xenobiotics has only limited applicability. Commonly, sodium bicarbonate can be used to alkalinize the urine (as well as the blood) and enhance salicylate elimination (other xenobiotics are discussed in Chap. 10), and sodium bicarbonate also prevents toxicity from methotrexate (Antidotes in Depth: A5). Acidifying the urine to hasten the elimination of alkaline substances is difficult to accomplish, probably useless, and possibly dangerous and therefore has no role in poison management. Forced diuresis also has no indication and may endanger the patient by causing pulmonary or cerebral edema.

If extracorporeal elimination is contemplated, hemodialysis should be considered for overdoses of salicylates, methanol, ethylene glycol, lithium, valproic acid, and xenobiotics that are both dialyzable and cause fluid and electrolyte problems. If available, hemoperfusion or high-flux hemodialysis should be considered for overdoses of theophylline, phenobarbital, and carbamazepine (although rarely, if ever, for the last two). When hemoperfusion is the method of choice (as for a theophylline overdose) but not available, hemodialysis is a logical, effective alternative and certainly preferable to delaying treatment until hemoperfusion becomes available. Peritoneal dialysis is too ineffective to be of practical utility, and hemodiafiltration is not as efficacious as hemodialysis or hemoperfusion, although it may play a role between multiple runs of dialysis or in hemodynamically compromised patients who cannot tolerate hemodialysis. In theory, both hemodialysis and hemoperfusion in series may be useful for a very few life-threatening overdoses such as thallium or salicylates. Plasmapheresis and exchange transfusion are used to eliminate xenobiotics with large molecular weights that are not dialyzable (Chap. 10).

The history alone may not be a reliable indicator of which patients require naloxone, hypertonic dextrose, thiamine, and oxygen. Instead, these therapies should be considered (unless specifically contraindicated) only after a clinical assessment for all patients with AMS. The physical examination should be used to guide the use of naloxone. If dextrose or naloxone is indicated, sufficient amounts should be administered to exclude or treat hypoglycemia or opioid toxicity, respectively.

In a patient with a suspected but unknown overdose, the use of vasopressors should be avoided in the initial management of hypotension before administering fluids or assessing filling pressures.

Attributing an AMS to alcohol because of its odor on a patient’s breath is potentially dangerous and misleading. Small amounts of alcohol and its congeners generally produce the same breath odor as do intoxicating amounts. Conversely, even when an extremely high blood ethanol concentration is confirmed by the laboratory, it is dangerous to ignore other possible causes of an AMS. Because individuals with chronic alcoholism may be awake and seemingly alert with ethanol concentrations in excess of 500 mg/dL, a concentration that would result in coma and possibly apnea and death in a nontolerant person, finding a high ethanol concentration does not eliminate the need for further search into the cause of a depressed level of consciousness.

The metabolism of ethanol is fairly constant at 15 to 30 mg/dL/h. Therefore, as a general rule, regardless of the initial blood alcohol concentration, a presumably “inebriated” comatose patient who is still unarousable 3 to 4 hours after initial assessment should be considered to have head trauma, a cerebrovascular accident, CNS infection, or another toxic-metabolic ­etiology for the alteration in consciousness, until proven otherwise. Careful neurologic evaluation of the completely undressed patient supplemented by a head computed tomography scan or a lumbar puncture is ­frequently indicated in such cases. This is especially important in dealing with a seemingly “intoxicated” patient who appears to have only a minor bruise because the early treatment of a subdural or epidural hematoma or subarachnoid hemorrhage is critical to a successful outcome.

As in the case of the patient with AMS, vital signs must be obtained and recorded. Initially, an assumption may have been made that the patient was breathing adequately, and if the patient is alert, talking, and in no respiratory distress, all that remains to document are the respiratory rate and rhythm. Because the patient is alert, additional history should be obtained, keeping in mind that information regarding the number and types of xenobiotics ingested, time elapsed, prior vomiting, and other critical information may be unreliable, depending in part on whether the ingestion was intentional or unintentional.

When indicated for the potential benefit of the patient, another history should be privately and independently obtained from a friend or relative after the patient has been initially stabilized. Recent emphasis on compliance with the federal Health Insurance Portability and Accountability Act (HIPAA) may inappropriately discourage clinicians from attempting to obtain information necessary to evaluate and treat patients. Obtaining such information from a friend or relative without unnecessarily giving that person information about the patient may be the key to successfully helping such a patient without violating confidentiality.

Speaking to a friend or relative of the patient may provide an opportunity to learn useful and reliable information regarding the ingestion, the patient’s frame of mind, a history of previous ingestions, and the type of support that is available if the patient is discharged from the ED. At times, it may be essential to initially separate the patient from any relatives or friends to obtain greater cooperation from the patient and avoid violating confidentiality and because their anxiety may interfere with therapy. Even if the history obtained from a patient with an overdose proves to be unreliable, it may nevertheless provide clues to an overlooked possibility of a second ingestant or reveal the patient’s mental and emotional condition. As is often true of the history, physical examination, or laboratory assessment in other clinical situations, the information obtained may confirm but never exclude possible causes.

At this point in the management of a conscious patient, a focused physical examination should be performed, concentrating on the pulmonary, cardiac, and abdominal examinations. A neurologic survey should emphasize reflexes and any focal findings.

Initial efforts at establishing rapport with the patient by indicating to the patient concern about the problems that led to the ingestion and the availability of help after the xenobiotic is removed (if such procedures are planned) often facilitates management. If GI decontamination is deemed necessary, the reason for and nature of the procedure should be clearly explained to the patient together with reassurance that after the procedure is completed, there will be ample time to discuss related problems and provide additional care. These considerations are especially important in managing the patient with an intentional overdose who may be seeking psychiatric help or emotional support. In deciding on the necessity of GI decontamination, it is important to consider that a resistant patient may transform a procedure of only potential value into one with predictable adverse consequences.

In general, a successful outcome for both the mother and fetus depends on optimum management of the mother, and proven effective treatment for a potentially serious toxic exposure to the mother should never be withheld based on theoretical concerns regarding the fetus (Chap. 31).

Physiologic Factors

A pregnant woman’s total blood volume and cardiac output are elevated through the second trimester and into the later stages of the third trimester. This means that signs of hypoperfusion and hypotension manifest later than they would in a woman who is not pregnant, and when they do, uterine blood flow may already be compromised. For these reasons, the possibility of hypotension in a pregnant woman must be more aggressively sought and, if found, more rapidly treated. Maintaining the patient in the left-lateral decubitus position helps prevent supine hypotension resulting from impairment of systemic venous return by compression of the inferior vena cava. The left lateral decubitus position is also the preferred position for orogastric lavage if this procedure is deemed necessary.

Because the tidal volume is increased in pregnancy, the baseline PCO₂ will normally be lower by approximately 10 mm Hg. Appropriate adjustment for this effect should be made when interpreting blood gas results.

Use of Antidotes

Limited data are available on the use of antidotes in pregnancy. In general, antidotes should not be used if the indications for use are equivocal. On the other hand, antidotes should not be withheld if their use may reduce potential morbidity and mortality. Risks and benefits of either decision must be considered. For example, reversal of opioid-induced respiratory depression calls for the use of naloxone, but in an opioid-dependent woman, the naloxone can precipitate acute opioid withdrawal, including uterine contractions and possible induction of labor. Very slow, careful, IV titration starting with 0.04 mg naloxone may be indicated unless apnea is present, cessation of breathing appears imminent, or the PO₂ or O₂ saturation is already compromised. In these instances, naloxone may have to be administered in higher doses (ie, 0.4–2.0 mg) or assisted ventilation provided or a combination of assisted ventilation and small doses of naloxone used.

An APAP overdose is a serious maternal problem when it occurs at any stage of pregnancy, but the fetus is at greatest risk in the third trimester. Although APAP crosses the placenta easily, N-acetylcysteine has somewhat diminished transplacental passage. During the third trimester, when both the mother and the fetus may be at substantial risk from a significant APAP overdose with manifest hepatoxicity, immediate delivery of a mature or viable fetus may need to be considered.

In contrast to the situation with APAP, the fetal risk from iron poisoning is less than the maternal risk. Because deferoxamine is a large charged molecule with little transplacental transport, deferoxamine should never be withheld out of unwarranted concern for fetal toxicity when indicated to treat the mother.

Carbon monoxide (CO) poisoning is particularly threatening to fetal survival. The normal PO₂ of the fetal blood is approximately 15 to 20 mm Hg. Oxygen delivery to fetal tissues is impaired by the presence of carboxyhemoglobin, which shifts the oxyhemoglobin dissociation curve to the left, potentially compromising an already tenuous balance. For this reason, hyperbaric oxygen is recommended for much lower carboxyhemoglobin concentrations in a pregnant compared with a nonpregnant woman (Chap. 125 and Antidotes in Depth: A38). Early notification of the obstetrician and close cooperation among involved physicians are essential for the best results in all of these instances.

The xenobiotics that people are commonly exposed to externally include household cleaning materials; organic phosphorus or carbamate insecticides from crop dusting, gardening, or pest extermination; acids from leaking or exploding batteries; alkalis, such as lye; and lacrimating agents that are used in crowd control. In all of these cases, the principles of management are as follows:

1. Avoid secondary exposures by wearing protective (rubber or plastic) gowns, gloves, and shoe covers. Cases of serious secondary poisoning have occurred in emergency personnel after contact with xenobiotics such as organic phosphorus compounds on the victim’s skin or clothing.

2. Remove the patient’s clothing, place it in plastic bags, and then seal the bags.

3. Wash the patient with soap and copious amounts of water twice regardless of how much time has elapsed since the exposure.

4. Make no attempt to neutralize an acid with a base or a base with an acid. Further tissue damage may result from the heat generated by this reaction.

5. Avoid using any greases or creams because they will only keep the xenobiotic in close contact with the skin and ultimately make removal more difficult.

Chapter 18 discusses the principles of managing cutaneous exposures.

Although the vast majority of toxicologic emergencies result from ingestion, injection, or inhalation, the eyes are occasionally the routes of systemic absorption or are the organs at risk for ophthalmic exposures. The eyes should be irrigated with the eyelids fully retracted for no less than 20 minutes. To facilitate irrigation, a drop of an anesthetic (eg, proparacaine) in each eye should be used, and the eyelids should be kept open with an eyelid retractor. An adequate irrigation stream may be obtained by running 1 L of 0.9% sodium chloride through regular IV tubing held a few inches from the eye or by using an irrigating lens. Checking the eyelid fornices with pH paper strips is important to ensure adequate irrigation; the pH should normally be 6.5 to 7.6 if accurately tested, although when using paper test strips, the measurement will often be near 8.0. Chapter 25 describes the management of toxic ophthalmic exposures in more detail.

There is a risk of needlessly subjecting a patient to potential harm when a patient with a nontoxic exposure is treated aggressively with GI evacuation techniques and other forms of management indicated for serious exposures. More than 40% of exposures reported to poison centers annually are judged to be nontoxic or minimally toxic. The following general guidelines^3,4 for considering an exposure nontoxic or minimally toxic will assist clinical decision making:

1. Identification of the product and its ingredients is possible.

2. None of the US Consumer Product Safety Commission’s “signal words” (CAUTION, WARNING, or DANGER) appear on the product label.

3. The history permits the route(s) of exposure to be determined.

4. The history permits a reliable approximation of the maximum ­quantity involved with the exposure.

5. Based on the available medical literature and clinical experience, the potential effects related to the exposure are expected to be at most benign and self-limited and do not require referral to a clinician.^3,4

6. The patient is asymptomatic or has developed the expected benign self-limited toxicity.

The best way to ensure an optimal outcome for the patient with a suspected toxic exposure is to apply the principles of basic and advanced life support in conjunction with a planned and stepwise approach, always bearing in mind that a toxicologic etiology or co-etiology for any abnormal conditions necessitates modifying whatever standard approach is brought to the bedside of a severely ill patient. For example, it is extremely important to recognize that xenobiotic-induced dysrhythmias or cardiac instability require alterations in standard protocols that assume a primary cardiac or nontoxicologic ­etiology (Chaps. 16 and 17).

Typically, only some of the xenobiotics to which a patient is exposed will ever be confirmed by laboratory analysis. The thoughtful combination of stabilization, general management principles, and specific treatment when indicated will result in successful outcomes in the vast majority of patients with actual or suspected exposures.

• Patients with a suspected overdose or poisoning and an AMS present some of the most serious initial challenges.

• Conscious patients, asymptomatic patients, and pregnant patients with possible xenobiotic exposures raise additional management issues, as do the victims of toxic cutaneous or ophthalmic exposures.

• One of the most frequent toxicologic emergencies that clinicians must address is a patient with a suspected toxic exposure to an unidentified xenobiotic (medication or substance), sometimes referred to as an unknown overdose.

• Consider not only patients who have an AMS but also those who are suicidal, those who use illicit drugs, and those who are exposed to xenobiotics of which they are unaware.

Acknowledgment

Neal E. Flomenbaum contributed to this chapter in previous editions.

References