Do not use water warmed above 42°C to avoid

superimposed thermal injury. Never initiate rewarming in

the prehospital setting if there is any potential for refreezing,

as this can worsen tissue injury.

A rewarming period of between 15 and 60 minutes

is adequate for most patients. Use the appearance of the

affected tissues to guide the duration of therapy. Appropriately

rewarmed tissue should appear erythematous and pliable.

Encourage active movement of the affected extremity to

stimulate increased circulation. Rewarming can be exceptionally painful, and parental opioids are frequently required.

Numerous adjunctive therapies have been proposed, although

the evidence supporting their use is lacking ( Table 62- 1).

It may take many weeks for the full extent of the

patient's injuries to declare. That said, certain early findings

do suggest better or worse outcomes. Findings associated

with a better prognosis include the rapid re-establishment

of normal skin temperature and sensation and the

CHAPTER 62

Table 62-1. Adj unctive therapies for frostbite.

Debride clear bl isters.

Leave hemorrhagic blisters intact.

Apply aloe vera cream (Dermaide) every 6 hours to affected

tissue.

Dress affected areas in soft, dry bandages.

Elevate and splint affected extremity.

Administer tetanus prophylaxis.

Administer NSAID (ibuprofen 400 mg every 8 hours).

Administer penicillin orally or intravenously every 6 hours for

48-72 hours.

Admit to hospital for daily hydrotherapy at 40°C.

Strictly prohibit smoking.

development of large clear blisters. Persistent tissue

cyanosis, firm insensate skin, and the delayed formation of

small hemorrhagic blisters all portent a poor prognosis.

DISPOSITION

� Admission

Admit all patients with acute frostbite for a minimum of

24-48 hours, as the full extent of tissue injury may not be

evident on initial presentation. Transfer to a specialized

burn center may be required in severe cases where

significant tissue necrosis will necessitate surgical

debridement. Consider admission for all high-risk patients

(young children, elderly, and homeless) with NFCI and

most patients with significant immersion foot to limit

further progression of disease.

� Discharge

Most patients with frostnip, chilblains, and mild cases of

immersion foot can be safely discharged home provided

they have access to adequate cold-weather clothing and a

warm, dry environment. All discharged patients require

clear instructions on proper wound care and further injury

prevention. Ensure adequate outpatient analgesia and

arrange for close surgical follow-up as necessary.

SUGGESTED READING

Ikaheimo TM, Junila J, Hirvonen J, Hassi J. Frostbite and other

localized cold injuries. In: Tintinalli JE, Stapczynski JS, Cline

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

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

New York, NY: McGraw-Hill, 201 1.

Irnray C, Grieve A, Shillon S, Caudwell Xtreme Everest Research

Group. Cold damage to the extremities: Frostbite and nonfreezing cold injuries. Postgrad Med ]. 2009;85:48 1--488.

 

tive medications, and external conditions such as high altitude exposure. Mechanical risk factors compose the final

category and are the most easily correctable. Common

examples include constrictive clothing and jewelry,

prolonged contact with heat conductive materials, and

immobility.

Of the 3 types of NFCI, frostnip is the least severe. It

typically affects the distal extremities after prolonged

exposure to cold but nonfreezing temperatures. Ice crystal

formation and profound vasoconstriction are common in

the superficial tissues, and patients frequently complain of

a dull throbbing pain during rewarming. Essentially a

precursor to frostbite, overt tissue destruction is lacking.

Chilblains (pernio) involve the formation of inflammatory skin lesions after repeated intermittent exposure to a

nonfreezing but cold and wet environment. Although

chilblains can affect any area of the body, the face, dorsal

surfaces of the hands and feet, and pretibial tissues are the

most commonly involved. Permanent tissue damage

secondary to vascular inflammation and tissue bed hypoxia

may develop. Women, children, and patients with

underlying vasculitides are most commonly affected.

263

CHAPTER 62

Immersion foot develops after the prolonged exposure

to persistently wet conditions, both warm and cold,

although the latter typically results in more severe tissue

injury. The long-term exposure to moisture induces tissue

edema and inflammation, whereas the prolonged cold

exposure leads to direct tissue injury. The consequently

encountered vasospasm, intravascular thrombosis, and

neuronal destruction can lead to full-thickness tissue loss.

Immersion foot is most commonly seen in the homeless

population.

Frostbite involves the freezing of tissues and can

result in significant tissue loss and long-term disability.

Ice crystal formation within the extracellular space can

induce intracellular dehydration, enzymatic dysfunc ­

tion, and cellular death. Microvascular occlusion sec ­

ondary to profound vasospasm and intraluminal

thrombosis further the severity of tissue loss. Circulating

tissue inflammatory markers frequently exacerbate the

intensity of tissue injury and complicate the reperfusion

of warmed tissue.

CLINICAL PRESENTATION

� History

Taking an adequate history should never delay the removal

of a patient from a cold environment. Inquire about

previous medical or psychiatric illnesses, drug and alcohol

use, and housing status. Any history of trauma should be

documented. Try to identify the overall duration of cold

exposure and elicit any previous history of frostbite or a

thawing and refreezing pattern of tissue injury. The review

of symptoms should attempt to discover the presence of

altered sensitivity, numbness, or burning pain.

Frostnip generally presents with numbness, pain,

pallor, and paresthesias of the ears, nose, fmgers, and toes.

Patients with chilblains typically present with complaints

of erythema, edema, and an intense pruritus or burning

sensation. Immersion foot is usually associated with

significant pain and swelling and occasionally numbness

and/or the inability to ambulate. Frostbitten patients

generally complain of the inability to feel the affected

areas.

� Physical Examination

Remove all clothing and thoroughly examine the entire

body, focusing primarily on the face, hands, lower legs and

feet, and buttocks and genitalia. Patients with frostnip may

present with paleness of the affected areas, but a normal

exam does not rule out injury. Chilblains frequently present

with erythema and edema and occasionally with vesicles,

bullae, and even ulcerations. The characteristic lesions are

purple or bluish in hue and appear 12-24 hours after exposure. Extremities affected by immersion foot will be swollen

and erythematous. Tissue sloughing is common, and there

may be an associated malodor. Frostbite typically presents

with mottled or violaceous tissue that may have a waxy

Figure 62-1. Deep frostbite of the toes.

.A. Figure 62-2. Superficial frostbite. Note the tissue

edema and clear bl isters.

appearance. Although frostbite can be classified similar to

burns into superficial and deep tissue injuries, this distinction

often cannot be made until the tissue is properly rewarmed.

Secondary blister formation is common, with the early formation of large clear blisters generally imparting a better

prognosis than the delayed development of smaller hemorrhagic bullae (Figures 62-1 and 62-2). Significant tissue

necrosis can complicate cases of deep tissue freezing despite

minimal initial physical exam findings.

DIAGNOSTIC STUDIES

Diagnostic studies of any kind are of limited utility in the

initial evaluation of patients with cold inducted tissue

injuries. That said, pursue radiographic and laboratory

studies as dictated for the evaluation of concurrent medical

COLD-INDUCED TISSUE INJURIES

illness or traumatic injury. Radionuclide bone scanning

and magnetic resonance imaging may a prognostic role in

long-term management.

MEDICAL DECISION MAKING

Include cold-induced tissue injuries in the differential diagnosis of all patients exposed to freezing or near freezing

temperatures, but evaluate and treat for any life-threatening

conditions before dealing with these injuries. Check the c ore

body temperature of all cold exposed patients to rule out

hypothermia. Investigate for and address any concurrent

trauma or dehydration. Attempt to delineate between freezing and nonfreezing injuries, as the treatments will differ. If

unclear between the two, always err on the side of frostbite

and treat accordingly. Consider compartment syndrome in

frostbitten regions if the swelling does not resolve and pulses

do not return after adequate rewarming.

Keep in mind that other injuries or illnesses can both

mimic and contribute to cold-induced tissue injury.

For example, the erythema of rewarmed frostnip and

immersion foot can resemble cellulitis or deeper tissue

infections. Peripheral vascular disease and vasculitides not

only appear similar to both frostbite and chilblains but also

increase their likelihood secondary to impaired microvascular circulation. Finally, the color changes and blisters of

frostbite can be confused with both stasis dermatitis and

autoimmune bullous forming conditions (Figure 62-3 ).

Add ress hypothermia,

dehydration and life

threats

Ambient rewarming

Figure 62-3. Cold-ind uced tissue injuries

diag nostic algorithm.

TREATMENT

All clothing should be removed and replaced with warm

blankets. Wet clothing is especially problematic as it will

continue to cool the patient during treatment. Dehydration

is a common complicating condition and requires

aggressive volume resuscitation with intravenous (IV)

crystalloids to lessen blood hyperviscosity. All body parts

that have suffered cold-induced tissue injury will need

some type of rewarming, with the pattern of injury

sustained determining the appropriate modality.

Frostnip usually resolves spontaneously with dry

rewarming measures at room temperatures and requires

no further intervention. Rewarm chilblains affected skin at

room temperature and then wash, dry, and dress in a soft

sterile bandage. Initiate pain control as needed and elevate

the affected extremity to prevent excessive edema

formation, as this will predispose to subsequent infection.

Patients with recurrent episodes may benefit from

treatment with oral nifedipine (30-60 mg/day), and topical

and systemic corticosteroids have both shown promise in

certain patient cohorts.

Immersion foot requires slightly more detailed care.

Rewarm affected tissues at room temperature and allow

them to air dry. Restrict patients to bed rest and elevate the

affected extremities during the rewarming period. Certain

patients may achieve adequate pain relief with oral

nonsteroidal anti-inflammatory drugs, whereas others may

require parental opioid analgesia. The early use of t ricyclic

antidepressants may help limit the future development of

chronic neuropathic pain. Extreme cases of immersion

foot may be indistinguishable from frostbite and should be

treated as the latter until proven otherwise. Finally, all

patients with NFCI require clear instructions to limit their

potential for recurrent exposure and injury.

Frostbite requires more aggressive treatment to limit

progressive tissue damage. Rewarm all affected areas in a

warm water recirculating bath ( 40-42°C) with a mild antibacterial agent mixed in (eg, povidone-iodine or chlorhexidine).

 

erable variations in potency. The majority of clinical

• Cardiovascular toxicity (specifica lly refractory hypotension) is the leading cause of morbidity and morta lity in

cycl ic antidepressant overdose.

• Hypertonic sodium bicarbonate should be given in

1 -2 mEq/kg boluses to reverse the wide-complex

dysrhythmias commonly encountered with cyclic

antidepressant poison ing.

findings associated with CA poisoning can be attributed to

;:::1 of the following pharmacologic actions:

• Competitive inhibition of acetylcholine at central and

peripheral muscarinic (but not nicotinic) receptors

• Inhibition of a-adrenergic receptors

• Inhibition of norepinephrine and serotonin uptake

• Sodium channel blockade

• Antagonism of GABA-A receptors

Although it is the inhibition of norepinephrine and

serotonin uptake that is believed to account for the antidepressant effects of these agents, the alternative actions just

listed account for the significant toxicity associated with

CA overdose, with sodium channel blockade being the

most important factor contributing to patient mortality.

CLINICAL PRESENTATION

� History

Patients commonly present to the emergency department

with minimal clinical findings only to develop life-threatening cardiovascular and central nervous system (CNS)

manifestations within the timespan of a few hours.

255

CHAPTER 60

Co-ingestants are not uncommon in patients with CA

overdoses, and this possibility must always be investigated.

Attempt to determine the exact amount of drug

ingested, as the cyclic antidepressants have a rather narrow

therapeutic window, and small excursions beyond the

usual therapeutic range (2-4 mg/kg) may result in significant toxicity. Acute ingestions of more than 1 0-20 mg/kg

will cause significant cardiovascular and CNS disturbances

owing to the blockade of cardiac sodium channels and

inhibition of CNS GABA-A receptors, respectively. Toxicity

in children has been reported with ingestions as low as

5 mg/kg.

� Physical Examination

The clinical presentation of CA toxicity varies widely from

mild anti-muscarinic signs and symptoms to severe

Table 60-1 Clinical manifestations of toxicity

resulting from cyclic antidepressants.

Cardiovascular Toxicity

Conduction Delays

PR interval, QTc interval, and QRS complex prolongation

Terminal right access deviation (S in lead I and R in aVR)

Atrioventricular block

Dysrhythmias

Sinus tachycardia

Supraventricular tachycardia

Wide·complex tachycardia

Sinus tachycardia with rate·dependent aberrancy

Ventricular tachycardia

Torsades de pointes

Bradycardia

Ventricular fibril lation

Asystole

Hypotension

Central Nervous System Toxicity

Altered mental status

Delirium

Psychosis

Lethargy

Coma

Myoclonus

Seizures

Anticholinergic Toxicity

Altered mental status

Hyperthermia

Urinary retention

Paralytic ileus

Pulmonary Toxicity

Acute lung·injury aspiration

Repri nted with permission from Flomenbaum N, Goldfrank L,

 

 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

1 00%

Cii

[f)

�

N

0 .0

I

0

0

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,

 

 looking for radio-opaque ingestions (eg, leaded

paint chips or toys, batteries, selected drug packets) as

indicated to help complete the work-up.

MEDICAL DECISION MAKING

The first priority must always be supportive care in the management of the poisoned patient. Use all available historical

items to help identify the possible toxin. A thorough physical

exam including careful attention to the patient's mental

status, vital signs, pupillary size and responsiveness, the presence of seizures, or abnormal changes in skin color, tern ­

perature, and moisture may help classify the patient's

presentation into a specific toxidrome. Use the ancillary

studies described previously to help clarify the diagnosis and

guide further management (Figure 54-1).

TREATMENT

The treatment of poisoned patients can be broken down

into a very systematic approach outlined by the mnemonic

ABCDEFGH. First and foremost, initiate aggressive

supportive care. The airway and breathing must be secured

and addressed without delay. Intubation may be prevented

Toxic exposure or poisoning

Supportive care: Address ABC's, IV

ccess, supplemental 02- cardiac monitor

Lab studies, ECG, identify toxidromes,

contact poison control center

consider decontamination:

• Wash patient

• Activated charcoal

• Gastric lavage

• Whole bowel irrigation

Consider enhanced elimination:

• Mu lti-dose activated charcoal

• Urinary alkalinization

• Hemodialysis

Consider focused antidotal therapy

Figure 54-1 The poisoned patient

diag nostic algorithm. ABCs, airway,

breathing, and circu lation; ECG,

electrocard iogram; IV, intravenous.

with the successful use of a focused therapy such as

naloxone in opioid toxicity or supplemental dextrose in

hypoglycemic patients. Likewise, correct any circulatory

compromise in the form of hypotension or bradycardia

with standard fluid and/or vasopressor administration. Pay

careful attention to the core temperature. Aggressively and

expeditiously correct hyperpyrexia with active cooling measures and not systemic antipyretics. These measures, rather

than the early search for specific antidotes, are the cornerstone of the initial management of the poisoned patient.

The basic goal of decontamination is to remove the poison

from the patient and the patient from the poison. Attempt

decontamination as early as possible to achieve maximal

benefit. Washing a patient's skin with soap and water to

prevent further absorption and/or prevent harm to the

emergency staff (eg, a patient covered with an organophosphate) is the simplest form of decontamination. Activated

charcoal (1 g/kg or a 10:1 ratio of charcoal to toxin) can be

given orally to bind ingested poisons and limit further gastrointestinal (GI) absorption. Although most drugs are

THE POISONED PATIENT

amenable to this, lithium, iron and other metals, hydrocarbons, caustics, and toxic alcohols are not. Consider gastric

lavage in patients who present very early (within 1 hour)

after a potentially lethal ingestion. Additionally, any potentially fatal ingestions that don't have available antidotes may

warrant lavage regardless of the timing of ingestion (eg,

massive colchicine overdose). Contraindications to gastric

lavage include the ingestion of hydrocarbons or other caustic agents, and potential complications include increased

intracranial pressure, aspiration, and esophageal rupture.

Whole-bowel irrigation with polyethylene glycol

(GoLYTELY), given at a rate between 0.5 L/hr (pediatrics)

and 2 L/hr, may help to "flush" toxins that won't bind to

charcoal (eg, leaded paint chips) out of the GI tract and

therefore limit total absorption. Contraindications to

whole-bowel irrigation include hemodynamic instability

(hypotension = lack of GI perfusion) and decreased bowel

sounds (impaired GI motility). Of note, pulmonary aspira ­

tion is the most common adverse side effect for all forms of

GI decontamination, and patients must have an intact air ­

way for these procedures to be pursued.

There are several different modalities available to

enhance the elimination of poisons. Hemodialysis is ideal

for smaller-sized poisons with small volumes of distribution

( <1 L/kg) and low degrees of protein-binding. Ideal agents

for hemodialysis include aspirin, toxic alcohols, and lithium.

Hemodialysis should also be performed in all patients with

profound acidemia regardless of the etiology. Alkalinization

of the urine is commonly initiated for ingestions of weak

acids such as aspirin and phenobarbital. The proposed

mechanism depends on increasing the urinary pH by giving

doses of intravenous (IV) sodium bicarbonate. Circulating

toxins will be preferentially converted to their conjugate

bases in the alkaline environment and consequently trapped

in the renal tubules, where they will be excreted in the urine.

Alkalinization can also benefit patients in select cases ( eg,

salicylate overdose) by keeping the poison preferentially out

of the CNS, as the ionized form cannot enter through the

blood-brain barrier. Finally, multiple doses of oral activated

charcoal (MDAC) can be administered to patients poisoned

with select agents including theophylline, phenobarbital,

carbamazepine, dapsone, or quinine. The proposed mechanism relies on the use of the GI tract wall as a dialysis membrane. The intraluminal charcoal functions to pull

circulating toxins back into the GI tract where they are

bound to the charcoal and excreted. MDAC can also be

employed to further decontaminate the gut of agents that

have erratic and prolonged absorption ( eg, salicylates, val ­

proic acid). If MDAC is entertained, ensure that the charcoal is not premixed with sorbitol, as cathartics (unlike

polyethylene glycol) can cause marked fluid and electrolyte

shifts, resulting in significant morbidity and/or mortality.

Antidotal therapy is important and necessary when

managing the poisoned patient, but should never take

priority over the supportive measures already mentioned.

Examples of selected focused therapy along with general

indications are listed in Table 54-3. The final portion of the

Table 54-3. Specific antidotes for toxicologic agents.

Acetaminophen

Crotalidae bite

Poison

Hydrofluoric acid, calcium channel

antagonists

Cyanide

Iron

Digoxin

Ethylene glycol, methanol

Methanol, methotrexate

Calcium channel blocker, � blocker

Oxidizing chemicals (nitrites, benzocaine,

sulfonamides)

Refractory hypoglycemia after oral

hypoglycemic

Opioid, clonidine

Anticholinergic (not TCA)

Cholinergic

Heparin

Isoniazid

Anticoagulants

TCA, tricyclic antidepressant.

Antidote

N-acetylcysteine

Antivenom Fab

Calcium gluconate or

calcium chloride

Sodium nitrite, thiosulfate

Deferoxamine

Digoxin Fab

Fomepizole or ethanol

Folic acid/leucovorin

Glucagon

Methylene blue

Octreotide

Naloxone

Physostigmine

Pralidoxime (HAM)

Protamine

Pyridoxine

Vitamin K

management algorithm includes G and H. This is a

reminder for clinicians to never hesitate in calling their

regional poison center ( 1-800-222-1222) for assistance

during any point in the care of the poisoned patient.

Getting help early may facilitate a more focused work-up,

prevent unnecessary laboratory and/or diagnostic studies,

provide insight into potentially life-saving antidotal

therapy, and assist with appropriate disposition making.