NAC therapy is generally indicated in 3 different

patient cohorts. Start NAC in patients with (1) acute

ingestions and 4-hour levels that lie above the nomogram

cutoff, (2) in patients who report significant ingestions if

obtaining a level will be significantly delayed, and (3) in

those with evidence of hepatoxicity presumed secondary

to APAP regardless of APAP level.

ACETAMINOPHEN TOXICITY

Seek early consultation with a liver transplant center if

the patient shows any signs of deterioration ( eg, altered

mental status, acidosis, worsening liver function) . I deally,

the patient should be transferred before meeting liver

transplantation criteria.

DISPOSITION

� Admission

Admit all patients who require treatment with NAC or

demonstrate any signs of hepatotoxicity. Patients with

hemodynamic instability, altered mental status, systemic

acid-base derangements, and evidence of end-organ

damage require admission to a critical care setting. Patients

with intentional overdoses require psychiatric assessment.

� Discharge

Patients with unintentional ingestions who exhibit no signs

of hepatotoxicity and have downtrending serum APAP levels

in the nontoxic range can be safely discharged home.

SUGGESTED READING

Dart RC, Rumack BH. Patient-tailored acetylcysteine adminis ­

tration. Ann Emerg Med. 2007;50:280-28 1.

Kanter MZ. Comparison of oral and IV acetylcysteine in the

treatment of acetaminophen poisoning. Am ] Health Syst

Pharm. 2006;63:1821-1827.

Rumack BH. Acetaminophen hepatotoxicity: the first 35 years.

J Toxicol Clin Toxicol. 2002;40:3-20

Salicylate Toxicity

Steven E. Aks, DO

Key Points

• Salicylate toxicity causes a mixed respiratory alkalosis,

metabolic alkalosis, and elevated anion gap metabolic

acidosis.

• Chronically intoxicated patients will be more seriously

ill at lower salicylate concentrations than their acutely

poisoned counterparts.

• Pursue hemodialysis in patients with refractory acidosis,

pulmonary edema, renal insufficiency, and altered

INTRODUCTION

Analgesics are among the most commonly ingested

substances in patient overdose. According to the National

Poison Data System, there were more than 300,000 cases of

analgesic overdose reported in the year 2009, with salicylates

accounting for the 1 3th most common cause of isolated

drug ingestion and 62 total fatalities. Aspirin is most often

ingested in some form of aspirin-containing combination

product such as over-the-counter cold remedies. It can also

be found as a component in various prescribed combination

products such as Fiorinal, Soma Compound, and Percodan.

Methyl salicylate, the major component of oil of wintergreen,

is commonly found as a rubefacient in various medical

products such as Ben Gay and in multiple household items,

including air fresheners and mouthwash. One teaspoon of

98o/o methyl salicylate can contain as much as 7 g of salicylate

(>20 tablets of 325 mg aspirin).

Aspirin absorption can be very erratic with peak

concentrations occurring > 20 hours after ingestion. That

said, levels obtained six hours after ingestion generally

reveal evidence of toxicity. Salicylate metabolism follows

Michaelis-Menten kinetics. At concentrations over

30 mg/dL, salicylates are metabolized by zero-order kinetics

due to enzyme saturation. This means that a constant

mental status or seizure, regardless of the actual serum

salicylate level.

• Match the ventilation rate in intubated patients with

severe sal icylate poisoning to their pre-intu bation

minute ventilation, as most req uire rema rkably high

rates for adequate respiratory compensation.

amount will be eliminated per unit of time. Below this

concentration, salicylate metabolism follows first-order

kinetics, with elimination rates proportional to serum

salicylate concentrations.

In overdose scenarios, salicylates induce a mixed acidbase disorder. They cause an initial respiratory alkalosis by

directly stimulating the medullary respiratory center. In

addition, excessive circulating salicylate induces lipolysis,

inhibits the Krebs cycle, and uncouples oxidative

phosphorylation. This process impairs normal cellular

respiration, resulting in the accumulation of organic acids and

a secondary elevation in the anion gap. Furthermore, volume

depletion secondary to excessive vomiting can lead to a

concurrent metabolic alkalosis. Therefore, the classic

(although far from uniformly present) acid-base disorder

with salicylate poisoning is a mixed respiratory alkalosis,

metabolic alkalosis, and elevated anion gap metabolic acidosis.

CLINICAL PRESENTATION

� History

It is very important to determine the amount ingested and

the timing of exposure. In addition, try to distinguish

between acute, chronic, and acute on chronic ingestions.

244

SALICYLATE TOXICITY

Patients with chronic intoxication often present with more

subtle signs of toxicity. For example, elderly patients may

present with isolated signs of altered mental status or tinnitus. Conversely, acutely poisoned patients typically present

with more dramatic findings, including nausea, vomiting,

tachypnea, diaphoresis, and altered mental status. Attempt

to identify the exact type of product ingested. Immediaterelease aspirin will produce much more rapid symptom

onsets and elevated salicylate concentrations compared to

the enteric-coated variety. Patients who ingest combination

products may exhibit toxic effects from the secondary agent

( eg, a concurrent opiate toxidrome from ingestion of a combined salicylate-opioid analgesic).

� Physical Examination

Pay very careful attention to patient vital signs. Patients are

frequently tachycardic due to significant volume loss.

Tachypnea is common secondary to stimulation of the

medullary respiratory center and as a compensation for

the metabolic acidosis. Fever can occur as a result of uncoupiing of the oxidative phosphorylation chain. Finally,

hypoxia may be present secondary to salicylate-induced

acute lung injury (ALI).

The remainder of the exam should focus on the skin,

abdomen, and neurologic systems. Diaphoresis is an

important sign in moderate to severe salicylate toxicity.

Abdominal tenderness can be present because of the

erosive effects of salicylate on the gastric mucosa. Patients

may display alterations in their mental status. This can be

a presenting sign in the chronically intoxicated patient or

may accompany significant acute poisonings. Seizures may

also be present in advanced cases.

DIAGNOSTIC STUDIES

� Laboratory

Obtain a complete blood count, chemistry panel, urinalysis, and bedside urinary pregnancy test. Calculate the

anion gap and follow it serially. Order a serum blood gas to

look for evidence of a mixed acid-base disorder. Check

salicylate concentrations every 2 hours until a peak concentration and subsequent decline has been observed, as

pharmacobezoar formation is not uncommon with sec ­

ondary erratic absorption. It is also wise to obtain a serum

acetaminophen concentration because of the prevalence of

readily available combination analgesics and their high

rates of use in patient overdoses.

� Imaging

Imaging studies are generally unrewarding to detect

ingested salicylates. A routine chest radiograph should be

obtained to assess for ALI.

PROCEDURES

Meticulous attention should be paid to the airway. The

decision to intubate a patient in the face of salicylate overdose is truly a life or death decision. Many patients with

severe salicylate poisoning have very high minute ventilations exhibited by both an increased depth of respiration

and a high respiratory rate. It is sometimes difficult, if not

impossible, to mechanically reproduce a salicylate-poisoned

patient's minute ventilation. If you are forced to intubate a

salicylate-poisoned patient, the ventilator rate needs to be

set very high to replicate the pre-intubation minute ventilation. Frequent post-intubation blood gases should be

obtained to be sure that the pH does not drop.

MEDICAL DECISION MAKING

Always obtain a thorough history from the patient, family,

and paramedics on what substances may be ingested.

Determine whether the patient's presentation is consistent

with an acute or chronic exposure.

 

 Be alert for the

co-ingestion of alternative analgesics including acetaminophen. Patients with the classic picture of salicylate

poisoning may mimic the systemic inflammatory response

syndrome, and one must consider alternative causes

including sepsis. Obtain salicylate concentrations every

2 hours until a peak value has been obtained. In patients

with salicylate levels <30 mgldL, follow until <20 mgldL

and treat supportively. Initiate urinary alkalinization for

patients with levels >30 mg/dL to facilitate urinary

clearance and limit central nervous system penetration.

One must observe vigilantly for any signs of clinical

deterioration and initiate early hemodialysis, as this may

be a life-saving intervention. Such findings include patients

with altered mental status, seizures, severe acid-base

derangements, pulmonary edema, and renal insufficiency.

Furthermore, patients with salicylate levels >90 mgldL

after an acute ingestion and those with levels >60 mg/dL

with chronic exposures warrant hemodialysis. These

thresholds should be lowered for patients with significant

comorbidities (Figures 57-1).

TREATMENT

As with all poisonings, the initial focus should be on

aggressive supportive care. Pay meticulous attention to the

patient's airway, breathing, and circulation. Intubate

patients only if absolutely necessary because of the

difficulty in attaining the required minute ventilation with

mechanical respiration. Because most patients are

significantly dehydrated, initiate aggressive volume

resuscitation with 1-2 L of normal saline to ensure an

adequate urine output ( 1-2 rnL/kg/hr).

There are several available modalities for patient

decontamination. Administer activated charcoal at a dose

of 1 g/kg to awake and alert patients with intact airway

reflexes and no concern for vomiting. This can be repeated

as needed to adsorb salicylates that form a concretion.

Urinary alkalinization is performed by injecting 3 ampules

of sodium bicarbonate into a 1 -L bag of So/o dextrose

solution to create an isotonic solution. Infuse this solution

CHAPTER 57

Suspect significant salicylate

ingestion or evidence of toxicity

Address ABC's, decontaminate with

activated charcoal at 1 gjkg with

intact airway and bowel motility

Figure 57-1. Salicylate toxicity diagnostic algorithm.

at 200 mL/hr. Pay careful attention to potassium levels and

replete as necessary, as hypokalemic patients will excrete

hydrogen ions into the distal renal tubules to retain

potassium, thereby impairing successful alkalinization of

the urine. The goal of alkalinization is to raise the urine

pH > 7 .S-8. Avoid alkalinization in patients with congestive

heart failure and renal failure, as they will be unable to

tolerate the necessary volume load.

DISPOSITION

� Admission

All symptomatic patients will require hospitalization.

Patients who require urinary alkalinization or hemodialysis

should be admitted to a critical care setting. All patients

with a suicidal ingestion will require psychiatric evaluation.

� Discharge

Patients with a detectable serum salicylate level require

serial testing to rule out continued absorption. An

asymptomatic patient with an undetectable salicylate con ­

centration at the 6-hour mark can be safely cleared from a

toxicologic perspective.

SUGGESTED READING

Bronstein AC, Spyker DA, Canti.lena LR, et al. 2010 Almual report

of the American Association of Poison Control Centers'

National Poison Data system (NPDS): 28th annual report.

Clin Toxicol. 20 11:49:910-941.

Chyka PA, Erdman AR, Christianson G , e t al. Salicylate poisoning: An evidence-base consensus guideline for out-of-hospital

management. Clin Toxicol. 2007;45:95-13 1.

O'Malley G. Emergency department management of the

salicylate-poisoned patient. Emerg Med Clin North Am.

2007;25:333-346.

Yip L. Aspirin and salicylates. In: Tintinalli JE, Stapczynski JS,

Ma OJ, Cline DM, Cydulka RK, Meckler GD. Tintinalli's

Emergency Medicine: A Comprehensive Study Guide. 7th ed.

New York, NY: McGraw-Hill, 201 1, pp. 1243-1245.

Carbon Monoxide

Poisoning

Vinodinee L. Dissa naya ke, MD

Key Points

• Consider carbon monoxide (CO) poisoning in all patients

with headaches, flu-like symptoms, altered mental

status, or an unexplained anion gap metabolic acidosis.

• Immediately administer supplemental 02 to all patients

with potential co poisoning before any confirmatory studies.

• Pulse oximetry values will be falsely elevated in patients

with CO poisoning as a result of the inabil ity of standard

INTRODUCTION

Carbon monoxide (CO) is an invisible killer; it is an odor ­

less, colorless, and nonirritating gas. It is generally encountered as a byproduct of the incomplete combustion of

carbon-based fuels (eg, coal, gasoline, natural gas). Faulty

furnaces and vehicle exhaust fumes are common sources for

clinical CO poisoning. Methylene chloride, a substance

found in paint stripper and bubbling holiday lights, is

metabolized in vivo into CO and may account for cases of

delayed poisoning. According to 20 10 US Poison Control

Center data, more than 13,000 cases of possible CO poisoning were reported. Approximately 5,000 of these cases were

treated in medical facilities, and CO is the leading cause of

toxin-related fatalities in children less than 5 years of age. In

survivors of CO poisoning, it is not uncommon to develop

delayed neurologic sequelae, including recurrent headaches,

cognitive deficits, and motor disorders.

CO exposure produces toxicity by 3 major pathways.

The first of these is an inhibition of systemic 0 2 delivery.

CO binds to hemoglobin (Hb) with an affinity roughly

240 times greater than 0 2• Systemic 0 2 delivery plummets

as the majority of circulating Hb binding sites are now

occupied by CO. In addition, Hb that has bound CO has an

increased affinity for concurrently bound 02, resulting in

oximetry to distinguish between oxyhemoglobin and

carboxyhemoglobin.

• Symptomatology is often more important than the

absol ute carboxyhemoglobin level when determining

treatment and disposition.

the impaired release of 0 2 as it reaches the target tissues.

This results in a leftward shift and altered shape of the oxyhemoglobin dissociation curve (Figure 58-1).

The ability o f C O t o inhibit normal cellular respiration

accounts for its second mechanism of toxicity. CO binds to

cytochrome aa3 and inhibits normal transit through the

electron transport chain. The resulting shutdown in the

oxidative phosphorylation pathway leads to a rapid decimation of stored ATP and secondary cellular death.

The binding of CO to myoglobin accounts for the third

mechanism of toxicity. Myoglobin binds to CO with an

affinity 40 times that of 02, impairing the adequate delivery of oxygen to muscle tissues. When myocardial cells are

affected, a global reduction in cardiac contractility occurs.

Of note, CO readily crosses the placenta and binds to fetal

hemoglobin (HbF) with a 10-15% higher affinity than

adult Hb, so fetal toxicity in cases of CO poisoning is often

more severe than is evident on examination of the mother.

CLINICAL PRESENTATION

� History

The symptoms of CO poisoning are notoriously nonspe ­

cific, but typically present with some degree of neurologic

and cardiovascular impairment. A vague headache is the

247

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CHAPTER 58

Asymptotic curve CO Hb02

Sigmoid curve Hb02

1 50 mm Hg

Oxygen tension

Figure 58-1. Carboxyhemoglobin "shift to the left"

reshaping of the oxyhemoglobin (Hb02) dissociation

curve. Reprinted with permission from Maloney G.

Chapter 217. Carbon monoxide. In: Tintinalli JE,

Stapczynski JS, Ma OJ, Cline OM, Cydulka RK, Meckler GO,

eds. Tintinalli's Emergency Medicine: A Comprehensive

Study Guide. 7th ed. New York: McGraw-Hill, 201 1.

most common complaint, followed by fatigue, malaise,

nausea, cognitive difficulties including memory impairment, paresthesias, weakness, altered mental status, and

lethargy. Cardiovascular symptoms include ischemic chest

pain, shortness of breath, and palpitations. Maintain a high

index of suspicion in patients with vague symptomatology,

 

CLINICAL PRESENTATION

..... History

Always attempt to identify the exact formulation, amount,

and timing of the ingestion. Ask about any coingestants

(eg, ethanol) that might impact the metabolism of APAP

and clarify the number and frequency of ingestions to rule

out chronic toxicity. Ask about risk factors for increased

toxicity, including chronically ill and alcoholic patients and

those taking medications that activate the cytochrome

P450 system (eg, anticonvulsants, antituberculosis).

The majority of symptoms are abdominal and

neurologic in nature. Ask about the presence of any

abdominal pain, nausea, and vomiting. Inquire about any

symptoms of altered mental status and decreased levels of

consciousness, as these portent a more serious clinical

course.

..... Physical Examination

Pay careful attention to the patient's vital signs.

Hemodynamic instability suggests a significant poisoning.

Significant tachypnea may indicate an attempt to

compensate for an ongoing metabolic acidosis.

Coingestions or combination products ( eg, APAP + opioid

or APAP + diphenhydramine) may cause marked

abnormalities due to concurrent opioid or anticholinergic

toxidromes.

Note the patient's general appearance, mental status,

and level of consciousness. Carefully examine the abdomen.

Diffuse abdominal tenderness is common after significant

overdose, and tender hepatomegaly may be evident

beginning in the latent stage. Finally, examine the skin and

sclera, looking for signs of jaundice.

DIAGNOSTIC STUDIES

..... Laboratory

Obtain an immediate serum APAP level in all patients and

follow with serial testing to establish an upward or

downtrending value. In patients with clearly timed acute

ingestions, order a second level at the 4-hour mark

postexposure. These values can be plotted on the RumackMatthew nomogram to help determine treatment

(Figure 56-1). Check a full panel of liver studies (aspartate

aminotransferase, alanine aminotransferase, albumin,

bilirubin) in all patients and follow serially, looking for

evidence of worsening hepatotoxicity. Order a coagulation

profile (prothrombin time [PT] , international normalized

ratio and partial thromboplastin time) to determine the

degree of liver synthetic dysfunction.

Check a baseline complete blood count and follow

serial hemoglobin levels in patients who develop

coagulopathies. Order a metabolic panel to assess for

electrolyte abnormalities and to calculate the anion gap, as

a significantly elevated anion gap metabolic acidosis may

be present. Confirm the degree of acidosis with blood gas

sampling. Finally, check the renal function in all patients,

as acute kidney injury is common secondary to intra-renal

NAPQI production.

..... Imaging

Consider a head computed tomography (CT) in patients

whose mental status does not correlate with an isolated

ingestion. Cerebral edema secondary to hyperammonemia

may occur in hepatic failure. Abdominal CT imaging is

usually of limited utility in APAP poisoning but should be

considered in patients with signs of peritonitis.

MEDICAL DECISION MAKING

Many exposures and overdoses have the potential for

significant hepatotoxicity. In most cases, a thorough history

will be sufficient to identify APAP as the culprit. In patients

presenting with elevated transaminases or signs of hepatic

failure and no obvious source, there is usually little

downside in empirically starting therapy with

N -acetylcysteine (NAC) until more information is o btained.

Draw baseline APAP and liver function tests and follow

serially to determine whether the levels are rising or falling.

In patients with acute ingestions of reliable timing,

plot their 4-hour APAP level on the Rumack-Matthew

nomogram to determine treatment. Of note, the

nomogram cannot be used if either the time of ingestion is

unknown or the ingestion is chronic (occurring over

hours/days). The nomogram may also be unreliable in

cases of coingestions with products that alter APAP

absorption and pharmacokinetics.

Use the King's College liver transplant criteria early to

estimate the severity of exposure and identify which

patients may require transfer for specialty care. Patients

with either a pH <7.3 after fluid resuscitation or a combination of PT > 100, creatinine >3.3 mg!dL, and grade 3 or

4 encephalopathy are considered to meet these criteria.

Consult your regional poison control center for all patients

with significant hepatotoxicity to help determine the ideal

treatment (Figure 56-2).

TREATMENT

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ACETAMINOPHEN TOXICITY

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Figure 56-1 . Rumack-Matthew nomogram. Reprinted with permission from

Tintinalli JE, Stapczynski JS, Ma OJ, Cline OM, Cydulka RK, Meckler GO. Chapter 1 84.

Acetaminophen. In: Tintinalli JE, Stapczynski JS, Ma OJ, Cline OM, Cydulka RK,

Meckler GO, eds. Tintinolli's Emergency Medicine: A Comprehensive Study Guide.

7th ed. New York: McGraw-Hill, 201 1.

26

As with all cases of acute poisoning, address the patient's

airway, breathing, and circulation. Gastric decontamination

is occasionally indicated and generally performed with

activated charcoal (AC). AC readily absorbs APAP and

should be given in cases with recent ingestions (within

8-12 hours of exposure) or those with evidence of ongoing

absorption, provided there are no contraindications. Give

a starting dose of 1 g/kg and consider repeated dosing in

patients with significantly large ingestions. Beware AC

products containing sorbitol with repeated dosing to

avoid significant fluid and electrolyte abnormalities.

Gastric lavage and whole-bowel irrigation are rarely

CHAPTER 56

.A. Figure 56-2. Acetaminophen toxicity diagnostic algorithm. ABCs, airway, breathing, and circulation; AC, activated

charcoal; ALT, alanine aminotransferase; APA� acetaminophen; AST, aspartate aminotransferase; CM� comprehensive

metabolic panel; ICU, intensive care un it; NAC, N-acetylcysteine.

utilized due to the effective binding qualities of AC and

the ready availability of an effective antidote.

NAC detoxifies NAPQI via multiple pathways, including

functioning as a glutathione precursor. It is given orally in

a loading dose of 140 mg/kg and subsequent doses of

70 mg/kg every 4 hours. NAC is adsorbed by charcoal, but

there is no evidence that there is less effectiveness when

NAC and charcoal are given together orally. Of note, oral

NAC can be given by the intravenous (N) route if passed

through a 0.22-micron filter, and multiple protocols exist

taking advantage of this. There is also a Food and Drug

Administration-approved IV NAC formulation, Acetadote,

that doesn't require the use of a filter and has a lower

likelihood of anaphylactoid reaction compared with giving

the oral compound intravenously. N NAC can be used in

all patients (including pregnancy) and is particularly

useful in patients who cannot tolerate anything by mouth

due to vomiting or altered mental status. Regardless of

route, current guidelines recommend to continue NAC

treatment until the liver function has normalized and

APAP levels are undetectable.

 

DISPOSITION

..... Admission

All patients with hemodynamic abnormalities, persistent

mental status changes, and metabolic or acid-base

irregularities should be admitted to an intensive care

setting. Additionally, those who ingested medications that

either require antidotal therapy or have prolonged or

delayed toxic effects ( eg, sulfonylureas, extended-release

calcium channel blockers, or beta-blockers) also require

admission to a critical care setting. All suicidal patients will

require psychiatric consultation for clearance.

CHAPTER 54

..... Discharge

Patients with accidental ingestions of innocuous substances,

those with no evidence of acute toxicity, and those who

have no potential for delayed detrimental effects can be

discharged.

SUGGESTED READING

Barry JD. Diagnosis and management of the poisoned child.

Pediatr Ann. 2005;34:937-946.

Erickson TB, Thompson TM, Lu JJ. The approach to the patient

with the unknown overdose. Emerg Med Clin North Am.

2007;25:249-28 1.

Hack JB, Hoffman RS. General management of poisoned

patients. In: Tintinalli JE, Cline DM, Cydukla RK, et al., eds.

Tintinalli's Emergency Medicine: A Comprehensive Study

Guide. 7th ed. New York, NY: McGraw Hill, 201 1:11 87-1 193.

Toxic Alcohols

Ma rk B. Mycyk, MD

Key Points

• Consider toxic alcohol poisoning in cases of an

unexplained anion gap acidosis or an elevated osmol

gap.

• Focus your initial treatment on the early inh ibition of

alcohol dehydrogenase (ADH) in cases of ethylene

glycol or metha nol poisoning to prevent the

accumulation of toxic metabol ites.

INTRODUCTION

With the exception of ethanol, no other alcohols are safe

for human consumption and are therefore considered

toxic alcohols. Ethylene glycol, methanol, and isopropanol

are the most common toxic alcohols associated with

human poisoning. Toxic alcohols are often ingested in 1 of

2 ways, either unintentionally if placed in an inappropriately labeled container, or intentionally by patients either

attempting suicide or trying to become intoxicated when

regular ethanol is not readily available. Of note, each of the

3 is capable of causing inebriation, with isopropanol being

twice as intoxicating as ethanol.

According to the National Poison Data System, more

than 35,000 toxic alcohol exposures are reported to the

American Association of Poison Control Centers yearly.

Isopropanol is the most frequently ingested but causes the

fewest number of deaths, whereas methanol is the least

commonly ingested toxic alcohol but associated with the

highest number of fatalities.

Although the parent compound is responsible for

inebriation, toxicity results from the metabolism of these

compounds via alcohol dehydrogenase (ADH) into toxic

organic acid byproducts with consequent end organ injury.

Ethylene glycol is metabolized to glycolic acid, glyoxylic

• Consult your local poison center (800-222-1 222) or local

toxicologist in all suspected cases for help initiating

antidota l therapy and obtaining confirmatory toxic

alcohol levels.

• Consult a nephrolog ist early to prepare for hemodia lysis

in cases involving large ingestions or severe metabolic

acidosis.

acid, and oxalic acid, all of which can produce systemic

acidosis and acute kidney injury. Methanol is converted to

formic acid which can produce systemic acidosis and

retinal toxicity. Isopropanol is not converted to an organic

acid but is rather metabolized into acetone, which can

produce hemorrhagic gastritis and systemic hypotension

in the absence of a concurrent acidosis. If either are

unrecognized or untreated, all toxic alcohol ingestions can

result in patient fatality.

CLINICAL PRESENTATION

..... History

Obtaining a history of toxic alcohol ingestion is often

challenging. Patients may be obtunded on arrival to the

emergency department (ED), not forthcoming with the

ingestion history, or too young to be appropriately

descriptive (children). Reading the ingredient lists on the

labels of any empty bottles found at the scene or brought

to the ED can be extremely helpful. If a bottle or label is not

available, ask the patient what kind of product was

ingested. For example, antifreeze usually contains ethylene

glycol, windshield-washing fluid usually contains methanol, and rubbing alcohol usually contains isopropanol.

235

CHAPTER 55

That said, remember that some products may contain different types of toxic alcohols ( eg, some gas-line antifreeze

products contain methanol). Beyond attempting to identify exactly what was ingested, it is critically important to

determine the time of ingestion, as this will affect the

interpretation of laboratory results and impact patient

management priorities.

..... Physical Examination

Most patients poisoned with a toxic alcohol will

demonstrate some level of central nervous system (CNS)

depression analogous to inebriation. Patients arriving

soon after an ingestion may appear well with unremarkable physical exams, whereas those who arrive many hours

after ingestion may be obtunded with unstable vital signs.

Of note, the peak serum level of a toxic alcohol correlates

poorly with the physical exam findings. As with all

overdoses, perform a careful neurologic examination

(mental status, cranial nerves, cerebellar findings, and

motor strength).