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BURNS

747

this may represent a potentially beneficial active interven-

tion as opposed to supportive care and good pulmonary

toilet that represents the mainstay of current care of smoke

inhalation injury.

Infection

The immune dysfunction following burns, for which a specific

cause is unknown, also may be a potential site of pharmaco-

logic intervention. Granulocyte-macrophage colony-stimulat-

ing factor (GM-CSF; sargramostim), in addition to

stimulating proliferation of granulocyte and macrophage pro-

genitor cells, increases macrophage phagocytic and cytocidal

activity, granulocyte RNA and protein synthesis, granulocyte

oxidative metabolism, and antibody-dependent cytotoxic

killing in mature cells in vitro. In a small cohort of burn

patients, sargramostim therapy increased granulocyte counts

by 50%. Administration of sargramostim reduced granulocyte

cytosolic oxidative function and myeloperoxidase activity to

control levels without changing superoxide production.

However, following cessation of treatment, superoxide activity

was subsequently increased compared with untreated burn

patients. These findings caution against clinical extrapolation

of in vitro results. A reduction in myeloperoxidase activity

actually may be detrimental because bactericidal capability

may be compromised. Increased superoxide production could

potentiate endothelial cell damage leading to increased capil-

lary permeability. The inability of immunomodulatory drugs

to significantly alter the postburn changes in immune func-

tion simply may represent the inability of single agents to alter

the complex cascade of pathophysiologic events occurring in

extensively burned patients.

The concept that the gut plays a central role in mainte-

nance of a persistent catabolic state in severely injured

patients has gained substantial popularity. Many animal stud-

ies support this hypothesis; however, the lack of clinically sig-

nificant bacteremia and endotoxemia in humans makes the

meaning of these findings unclear. Intestinal permeability is

increased preceding and during episodes of sepsis in burn

patients. Whether alterations in intestinal permeability result

in infection or represent only an epiphenomenon remains to

be proved. In a recent clinical study, the administration of

prophylactic enteral polymyxin B to burn patients resulted in

a decrease in endotoxemia; however, no correlation with ill-

ness severity score or outcome was observed.

Wound Closure

Excision of the burn wound with subsequent split-thickness

skin grafting is now common practice in most institutions.

Some clinicians advocate complete excision of the burn

wound within the first several days of hospitalization. The

postulated benefits of this treatment include decreasing the

extent and duration of hypermetabolism and immunosup-

pression, shortening the length of the hospital stay, and

improving survival. Prompt excision and closure of the burn

wound has been shown to ameliorate the hypermetabolic

response in laboratory animals, provided that the entirety of

the excised wound is closed by grafting. Similar reversal of

the immunosuppressive effects of burning also has been

documented. Such findings have yet to be observed in

humans probably because the entirety of the full-thickness

wound is seldom removed, partial-thickness wounds are not

excised, and definitive closure of large wounds cannot be

accomplished in a single operation. In several reports dealing

exclusively with early wound excision in burned children, the

duration of hospital stay was clearly shortened, intraopera-

tive blood loss was decreased, and survival was reported to be

improved. The duration of hospitalization has decreased for

adult burn patients in many centers because excisional ther-

apy is employed routinely, but a favorable impact of early

complete excision of the burn wound on pathophysiologic

changes and outcome has not been documented. Moreover,

the deleterious hemodynamic and pulmonary effects of gen-

eral anesthesia during the early postburn period speak for

cautious use of such procedures during the resuscitation

period in the severely burned patient. Such excisions should

be performed on carefully selected patients and only by expe-

rienced operating teams and anesthesiologists.

The identification and availability of various growth fac-

tors have stimulated interest in the potential for accelerating

the healing of burns, skin grafts, and skin graft donor sites.

An effective agent could produce more rapid healing of

burns (hastening return to work), permit more frequent har-

vesting of donor sites in massive burns, and shorten healing

time of skin grafts (reducing periods of immobility). The

topical application of epidermal growth factor has been

shown to enhance healing of split-thickness skin graft donor

sites by reducing the time to complete healing by 1.5 days.

Although the decrease in healing time was statistically signif-

icant, the clinical benefit would be minimal. A 50% reduc-

tion in skin graft donor-site healing time would be required

to be clinically effective. The systemic administration of

human growth hormone also has been reported to decrease

the time of skin graft donor-site healing in children, but the

same effect was not observed routinely in adult patients. The

ability of growth factors to improve healing in burn patients

continues to be an area of active research and debate.

Hypermetabolism

The hypermetabolic response to thermal injury is well

described, and in addition to the classic hormonal mediators,

cytokines may play an important role in maintenance of the

hyperdynamic state. Circulating levels of tumor necrosis fac-

tor, IL-1, and IL-6 are increased at various times following

thermal injury and sepsis; however, the effect of pharmaco-

logic or immunologic blockade of these cytokines is not

clearly established following burn injury. In a series of exten-

sively burned patients, blood levels of TNF-α, IL-1, and IL-6,

although frequently elevated, had no correlation with the

patients’ clinical courses.

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748

The hypermetabolic response to thermal injury can be

attenuated by β-adrenergic blockade. Administration of pro-

pranolol has been effective in decreasing metabolic rate and

cardiac work in burned children and adults; however,

increased nitrogen loss was induced presumably from periph-

eral β-receptor blockade. Cardioselective β-adrenergic block-

ers are currently being studied that may circumvent the

nitrogen-wasting effects of nonselective agents. Attempts to

decrease catabolism and protein wasting also have been stud-

ied. The selective β

-adrenergic agonist clenbuterol increased

resting energy expenditure and normalized muscle protein

content, muscle mass, and body weight gain in burned rats.

Administration of insulin-like growth factor 1 (IGF-1) to

burn patients, decreased protein oxidation and protein break-

down only in patients in whom an insulin-like effect also

occurred. Similar responses in burn patients were demon-

strated with the administration of low-dose exogenous

insulin and glucose. Testosterone analogues also have been

used to reduce postinjury catabolism. Oxandrolone, a weakly

androgenic testosterone analogue, has been shown recently to

decrease net daily nitrogen loss and weight loss in seriously

burned patients. This study also described a decrease in heal-

ing time of standarized donor sites from 13 ± 3 days to 9 ± 2

days. Complications were similar between groups, and no side

effects directly attributed to the drug were identified.

Herndon and colleagues evaluated the effect of β-adrenergic

blockade using orally administered propranolol on resting

energy expenditure and muscle-protein catabolism in

severely burned children. After 2 weeks of treatment, a dose

sufficient to decrease the resting heart rate by 20% resulted in

a 24% decrease in resting energy expenditure in the propra-

nolol group compared with a 5% increase in a matched con-

trol group. The net muscle-protein balance increased by 82%

over baseline values in the propranolol group, whereas it

decreased by 27% in the control group.

Further studies are required to determine if the apparent

benefits of blockade of the hypermetabolic response result in

decreased morbidity and mortality for the severely burned

patient or whether they merely reflect short-term changes in

protein metabolism.

Basadre JO et al: The effect of leukocyte depletion on smoke

inhalation injury in sheep. Surgery 1988;104:208–15.

Baxter CR: Future perspectives in trauma and burn care. J Trauma

1990;30:S208–9.

Brown GL et al: Enhancement of wound healing by topical treat-

ment with epidermal growth factor. N Engl J Med 1989;321:

76–9. [PMID: 2659995]

Chance WT et al: Clenbuterol decreases catabolism and increases

hypermetabolism in burned rats. J Trauma 1991;31:365–70.

[PMID: 2002523]

Cioffi WG Jr et al: Effects of granulocyte-macrophage colony-

stimulating factor in burn patients. Arch Surg 1991;126:74–9.

[PMID: 1845929]

Davis CF et al: Neutrophil activation after burn injury:

Contributions of the classic complement pathway and of endo-

toxin. Surgery 1987;102:477–84.

Demling RH, Lalonde C: Early burn excision attenuates the post-

burn lung and systemic response to endotoxin. Surgery

1990;108:28–35. [PMID: 2360187]

Demling RH, Lalonde C: Effect of partial burn excision and clo-

sure on postburn oxygen consumption. Surgery 1988;104:

846–52. [PMID: 3187900]

Demling RH et al: Fluid resuscitation with deferoxamine prevents

systemic burn-induced oxidant injury. J Trauma 1991;31:

538–43. [PMID: 1708429]

Demling RH, Orgill DP: The anticatabolic and wound healing

effects of the testosterone analog oxandrolone after severe burn

injury. J Crit Care 2000;15:12–7. [PMID: 10757193]

Desai MH et al: Reduction in mortality in pediatric patients with

inhalation injury with aerosolized heparin/N-acetylcystine

therapy. J Burn Care Rehabil 1988;19:210–2. [PMID: 9622463]

Desai MH et al: Early burn wound excision significantly reduces

blood loss. Ann Surg 1990;211:753–9. [PMID: 2357138]

Gore DC et al: Effect of exogenous growth hormone on whole-

body and isolated-limb protein kinetics in burned patients.

Arch Surg 1991;126:38–43. [PMID: 1898697]

Herndon DN et al: Determinants of mortality in pediatric patients

with greater than 70% full-thickness total body surface area

thermal injury treated by early total excision and grafting.

J Trauma 1987;27:208–12. [PMID: 3546714]

Herndon DN et al: Effect of propranolol administration on hemo-

dynamic and metabolic responses of burned pediatric patients.

Ann Surg 1988;208:484–92. [PMID: 3052328]

Herndon DN et al: Effects of recombinant human growth hor-

mone on donor-site healing in severely burned children. Ann

Surg 1990;212:424–49. [PMID: 2121109]

Herndon DN et al: The pathophysiology of smoke inhalation injury

in a sheep model. J Trauma 1984;24;1044–51. [PMID: 6512897]

Herndon DN et al: Reversal of catabolism by beta-blockade after

severe burns. N Engl J Med 2001;345:1223–9. [PMID: 11680441]

Ireton-Jones CS, Turner WW Jr, Baxter CR: The effect of burn

wound excision on measured energy expenditure and urinary

nitrogen excretion. J Trauma 1987;27:217–20. [PMID: 3820355]

Lalonde C, Demling RH: The effect of complete burn wound exci-

sion and closure on postburn oxygen consumption. Surgery

1987;102:862–8. [PMID: 3672326]

Sartorelli KH, Silver GM, Gamelli RL: The effect of granulocyte

colony-stimulating factor (G-CSF) upon burn-induced defec-

tive neutrophil chemotaxis. J Trauma 1991;31:523–39. [PMID:

2020039]

Schirmer WJ et al: Complement-mediated hemodynamic depres-

sion in the early postburn period. J Trauma 1989;29:932–8.

[PMID: 2746703]

Strock LL et al: The effect of insulin-like growth factor I on post-

burn hypermetabolism. Surgery 1990;108:161–4.

Tanaka H et al: Reduction of resuscitation fluid volumes in severely

burned patients using ascorbic acid administration. Arch Surg

2000;135:326–31. [PMID: 10722036]

Tchervenkov JI et al: Early burn wound excision and skin grafting

postburn trauma restores in vivo neutrophil delivery to inflam-

matory lesions. Arch Surg 1988;123:1477–81. [PMID: 3056334]

Thompson P et al: Effect of early excision on patients with major

thermal injury. J Trauma 1987;27:205–7. [PMID: 3820353]

Waxman K et al: Hemodynamic and oxygen transport effects of

pentastarch in burn resuscitation. Ann Surg 1989;209:341–5.

[PMID: 2466449]

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II. CHEMICAL BURN INJURY

The severity of injury caused by chemical exposure is related

to the amount and concentration of the agent and the dura-

tion of contact with the tissues. Strong alkalis and acids

found in common household cleaners are responsible for

the majority of minor chemical injuries. More extensive

injuries often result from industrial and laboratory acci-

dents or from assaults. The amount of tissue damage

incurred also depends on the nature of the specific agent.

Strong alkalis react with tissues to produce saponification

and liquefaction necrosis. Acids are water-soluble and pene-

trate easily into subcutaneous tissue and cause coagulation

necrosis soon after contact. The exothermic reaction pro-

duced by contact with strong acids or bases also contributes

to the depth of injury. Organic solvents and petroleum

products, which are highly lipid-soluble, injure tissues by

delipidation. Cutaneous absorption of certain chemical

agents may cause systemic toxicity, which complicates sub-

sequent therapy and makes identification of the causative

agent imperative.



Initial Care of Chemical Burns

Chemical injuries, unlike other thermal injuries, require

immediate care of the burn wound. The caustic agent must

be washed from the skin surface as soon as possible. All

clothing, including shoes and gloves, must be removed and

the wounds copiously irrigated with water. If possible,

lavage of chemical injuries should continue for at least 30

minutes. In the case of alkali burns, this treatment should

continue for a minimum of 1 hour. If ocular injury is sus-

pected, prompt and prolonged irrigation with saline or

water should begin. A search for specific antidotes is unnec-

essary and may only delay the initiation of adequate water

lavage. Assessing the depth of injury in chemical burns is

difficult because many agents may produce a tanned or

bronzed appearance of the skin, which remains pliable to

the touch but may represent extensive full-thickness tissue

necrosis. With the exception of the initial attention given to

the burn wound, the resuscitation and later treatment of

skin injury follow that of thermal burns.



Specific Chemical Agents & Systemic

Toxicities

In general, the use of antidotes for specific chemicals is con-

demned, and copious water lavage is considered the appro-

priate form of initial therapy. However, several specific

chemical agents exist for which treatment with a specific

antidote has proved beneficial. Injury owing to hydrofluo-

ric acid exposure is an occupational hazard of petroleum

refinery workers, etchers, and those employed in the clean-

ing of air-conditioning equipment. Following contact with

this agent, there is usually a pain-free interval followed by

pallor in the area of contact in association with severe tis-

sue pain. Fluoride ion continues to penetrate the tissues

until inactivated by calcium salt formation. Immediately

after exposure, the area should be copiously irrigated with

water. Topical treatment with a calcium gluconate gel

should be instituted, and if the pain does not subside, local

injection of 10% calcium gluconate into the damaged tissue

may provide prompt pain relief. Intraarterial infusion of

calcium gluconate also has been used to limit tissue damage

and relieve pain, but surgical excision of the damaged tissue

may be necessary for complete pain control. Hypocalcemia

may occur following extensive hydrofluoric acid burns.

Phenol

Phenol is an aromatic acid alcohol with high lipid solubility.

Initial treatment consists of copious water lavage; however,

owing to the poor water solubility of phenol, a lipophilic sol-

vent such as polyethylene glycol (50% solution in water) may

be more effective at removing the residual agent. Sufficient

systemic absorption of phenol produces CNS depression,

hypothermia, hemolysis, renal failure, and hypotension.

Maximal ICU support may be required. No specific antidote

is available.

Hydrocarbons

Cutaneous injury from immersion in gasoline and other

hydrocarbons is often overlooked in victims of motor vehicle

accidents who sustain prolonged exposure during extrica-

tion. Skin necrosis results from lipid dissolution. Partial- and

full-thickness injuries have been described, and systemic tox-

icity, similar to that produced by ingestion or inhalation, may

occur. The pulmonary excretion of hydrocarbons may pro-

duce chemical pneumonitis and bronchitis. Systemic lead

poisoning from cutaneous absorption of leaded gasoline also

has been described.

Inhalation of Aerosolized Chemicals

Inhalation of aerosolized chemicals may produce pulmonary

injury and systemic toxicity, thus requiring accurate diagno-

sis and aggressive treatment. Varying degrees of pulmonary

insufficiency may be agent-specific and manifested by severe

airway edema formation, mucosal sloughing, and bron-

chospasm. Systemic toxicity through pulmonary absorption

may occur; thus the causative agents must be clearly identi-

fied to ensure appropriate diagnostic and treatment strate-

gies. The degree of pulmonary support required is

determined by the severity of pulmonary insufficiency.

Ocular Injury

If chemical eye injury is suspected, prompt and prolonged

irrigation of the eye with water or saline should ensue. A spe-

cially designed scleral contact lens with an irrigating sidearm

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750

is useful when prolonged irrigation is necessary. Epithelial

defects may be identified by fluorescein stain.

Ophthalmology consultation should be obtained on all sus-

pected chemical eye injuries.

Mozingo DW et al: Chemical burns. J Trauma 1988;28:642–7.

[PMID: 3367407]

III. ELECTRICAL BURN INJURY

Tissue damage from electrical injury results from heat gener-

ated by the passage of electric current through the body as

well as direct thermal injury caused by the ignition of cloth-

ing. The severity of the injury depends on the voltage, the

type of current (alternating or direct), the path of the current

through the body, and the duration of contact. High- and

low-voltage injuries are arbitrarily defined as those above

and below 1000 V.

Tissue damage from electrical injury may be obvious at

the cutaneous contact site or sites but also may involve

underlying tissues and organs along the path of the current.

The amount of heat generated is proportionate to tissue

resistance; however, the differences in tissue resistance (eg,

bone, fat, nerve, etc.) are so small that the body acts as a

volume conductor. Current density then predominates as

the main determinant of tissue damage, with severity of

injury being inversely proportional to the cross-sectional

area traversed by current. Thus severe injuries to the

extremities are often encountered, and significant injuries

to the torso are rare. Superficial tissues in a limb may be

normal, whereas tissues near bone may be nonviable owing

to longer duration of heating because of the slower heat

dissipation from bone. Alternating current injuries may ini-

tiate ventricular fibrillation, whereas high-voltage injury

and lightning injury are associated with asystolic cardiopul-

monary arrest.

Treatment

Cardiac arrest often occurs following an electrical contact

and requires immediate cardiopulmonary resuscitation.

Patients with electric injury are more likely to have associ-

ated injuries owing to falls or tetanic skeletal muscle con-

tractions from the electric current; therefore, the patient’s

spine should be immobilized until cervical, thoracic, and

lumbar radiographs exclude the presence of spinal frac-

tures. In patients not sustaining an initial cardiac arrest,

cardiac dysrhythmias occur in a small percentage of

patients. All patients should have continuous electrocar-

diographic monitoring for at least 24 hours, and function-

ally significant dysrhythmias should be treated promptly if

they occur.

The estimation of resuscitation fluid requirements in

patients sustaining electrical injury is difficult owing to

extensive subcutaneous or deep tissue involvement with only

limited areas of cutaneous injury. This “iceberg” effect may

require the performance of fasciotomy—rather than

escharotomy—to ensure adequate perfusion of the distal

extremity and to evaluate the viability of the underlying sub-

cutaneous tissue and muscle. With extensive muscle necrosis,

hemochromogens may be liberated, resulting in the appear-

ance of those pigments in the urine. Intravenous fluids are

administered to achieve a urine output of 100 mL/h in

adults. If the hemochromogenuria does not clear with an

adequate urine output, 50 meq sodium bicarbonate should

be added to each liter of intravenous fluid to promote alkalin-

ization of the urine and prevent pigment precipitation in the

renal tubules. If after aggressive fluid resuscitation the renal

output does not reach 100 mL/h, an osmotic diuretic such as

mannitol also may be administered (a bolus dose of 25 g with

12.5 g added to each liter of IV fluid until pigment clearing

occurs) to force an increased urine output. When urine pro-

duction is increased by the use of diuretics, invasive hemody-

namic monitoring with a pulmonary artery catheter should

be considered because urine output is no longer a reliable

measure of intravascular volume and organ perfusion.

Complications

Associated injuries are more common in patients sustaining

electrical injury than those injured by thermal burns. Owing

to the titanic contractions of the paraspinal musculature

induced by the electric current, compression fractures of the

lumbar and thoracic spine may occur. Furthermore, many

electrical injuries involve workers who fall from heights.

Blunt traumatic injuries should be suspected and appropri-

ate diagnostic measures initiated.

A complete neurologic examination must be performed

on admission and at scheduled intervals in all patients sus-

taining electrical injury. Neurologic changes may be of early

or late onset. Immediate peripheral deficits owing to the

damaging effects of electric current may be irreversible; how-

ever, early deficits in a distribution where there is no clear tis-

sue damage are likely to resolve. Neurologic symptoms of

delayed onset, often mimicking upper motor neuron disease,

tend to be progressive and permanent. Progressive thrombo-

sis of nutrient vessels of the spinal cord or nerve trunks may

play a role in the pathogenesis of the late-occurring upper

motor neuron deficits.

Direct electrical injury to the viscera is rare; however, liver

necrosis, intestinal perforation, focal pancreatic necrosis, and

gallbladder necrosis have been reported in patients with

high-voltage electric injury and truncal contact points. An

increased occurrence of cholelithiasis has been reported in

convalescent patients following electric injury.

Delayed hemorrhage from moderate-sized to large blood

vessels has been described following electrical injury and

attributed by some to an “arteritis” produced by the electric

current. The actual mechanism of this complication is unclear,

but inadequate initial wound debridement and subsequent

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751

exposure and desiccation of the involved vessel appear to be

causative factors.

In patients in whom the electrical contact point involved

the head or neck, the development of cataracts up to 3 years

or more following injury has been described.

Ophthalmologic slit-lamp examination should document

the presence or absence of cataracts during the initial hospi-

talization. Additional information on electrical injuries is

presented in Chapter 37.

Grube BJ et al: Neurologic consequences of electrical burns. J

Trauma 1990;30:254–8.

Pruitt BA Jr, Mason AD: Lightning and electric shock. In

Weatherall DJ, Ledinghan JGG, Warrell DA (eds), Oxford

Textbook of Medicine, 2nd ed. New York: Oxford University

Press, 1987.

REFERENCES

Advances in understanding trauma and burn injury. J Trauma

1990;30:S1–211.

Demling RH: Burns. In Wilmore DW et al (eds), Care of the Surgical

Patient, Vol 1: Critical Care. New York: Scientific American, 1991.

McManus WF, Pruitt BA Jr: Thermal injuries. In Mattox KL, Moore

EV, Feliciano DV (eds), Trauma. Stanford, CT: Appleton & Lange,

1988.

Pruitt BA Jr, Goodwin CW Jr: Burns: Including cold, chemical and

electrical injuries. In Sabiston DC Jr (ed), Textbook of Surger y,

13th ed. Philadelphia: Saunders, 1986.

Pruitt BA Jr, Goodwin CW: Burn injury. In Moore EE (ed), Early

Care of the Injured Patient. New York: BC Decker, 1990.

Pruitt BA Jr: The universal trauma model. Bull Am Coll Surg

1985;70:2.

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752

An integral part of the practice of critical care is treating the

patient who either intentionally or inadvertently ingests or is

exposed to a potentially toxic substance. The magnitude of this

problem is staggering. In 2002, the American Association of

Poison Control Centers documented 2,112,774 episodes of

toxin exposure resulting in poison center notification. This

number actually underrepresents the true number of poison-

ings because 70% are never reported to poison control centers.

Treating these patients requires a working understanding

of the principles of stabilization and supportive care, decon-

tamination, drug elimination, use of antidotes, and the

pathophysiologic features specific to the poisons or toxins

involved. This chapter will cover the general principles

involved in caring for these patients and will discuss the

details of treating the specific poisons typically encountered

in the practice of critical care.

EVALUATION OF POISONING IN THE ACUTE

CARE SETTING OR ICU

The pathophysiologic consequences following an exposure

are poison-specific, and adequate treatment requires an

understanding of these individual differences. However, there

are several general guidelines for the evaluation and treat-

ment of a patient with a potential ingestion or toxic exposure.



Diagnosis of Poisoning

History

Obtaining a history from a patient with a potential ingestion

or toxic exposure may be difficult if the patient is too young

to communicate, is obtunded, or is reluctant to cooperate. It

may be helpful to question the patient’s relatives, friends, or

coworkers to obtain additional historical information in

these cases. When getting the patient’s history, several points

require particular attention: the drugs or toxins involved, the

route of exposure (ie, oral, dermal, inhalation, etc.), and the

time of the exposure or ingestion. It is important to remem-

ber, however, that the history may be unreliable in patients

who intentionally ingest toxins. Careful physical examina-

tion is key, and laboratory evaluation and close observation

are frequently required.

Symptoms and Signs

The physical examination can provide a wealth of informa-

tion, even in patients unable to provide a useful history. An

abbreviated physical examination, which could be called the

toxidrome-oriented physical examination, focuses on the phys-

ical findings observed in patients exposed to particular types

of poisons and offers rapid assessment and guides testing and

treatment. This physical examination should include vital

signs, a brief neurologic examination emphasizing level of

consciousness and pupillary and motor responses, palpa-

tion of the skin for moisture and inspection for cyanosis

and rashes, auscultation and percussion of the lungs, and

auscultation of bowel sounds (Table 36–1). Table 36–2 sum-

marizes the physical findings associated with the major

groups of poisons and lists several examples of each.

Laboratory Studies

A rapid bedside serum glucose concentration should be checked

in all patients with altered mental status, and if it is found to be

low, intravenous glucose should be administered. Serum elec-

trolytes, blood urea nitrogen (BUN), serum creatinine, arterial

blood gas, serum osmolality, calculated osmolar gap, and a uri-

nalysis (ie, crystals, myoglobinuria or hemoglobinuria) are the

basic laboratory tests in the evaluation of patients with over-

doses (Table 36–3). Other tests (eg, drug levels, methemoglobin

level, and carboxyhemoglobin level) may be helpful in specific

patients and will be discussed later in this chapter.

As a general rule, toxicology screens are of limited value

in evaluation of these patients and are expensive and

Poisonings & Ingestions

∗

Diane Birnbaumer, MD

∗

Envenomation (snakebite, etc.) is discussed in Chapter 37.



POISONINGS & INGESTIONS

753

time-consuming. In some specific situations, however,

screening may be helpful. These tests can be useful in nar-

rowing the differential diagnosis in patients who present

with altered mental status or abnormal vital signs; in such

cases, a directed toxicology screen should be ordered that

tests for agents consistent with the patient’s presentation and

physical findings. A toxicology screen also may be helpful in

patients with mixed-drug ingestions or those who present

with signs of major toxicity. Finally, a sample of blood may

be saved for future toxicology evaluation in patients in whom

the diagnosis is unclear.

Serum concentrations of some drugs are helpful in guid-

ing management decisions (Table 36–4). Salicylate, aceta-

minophen, barbiturates, digoxin, ethanol, iron, lithium, and

theophylline serum levels are available in most hospital lab-

oratories on an urgent basis. (Methanol and ethylene glycol

levels often need to be sent out; positive tests are often used

to confirm a suspected case, but management must begin

before levels are available.) Salicylate serum drug levels are

not necessary in all ingestion cases, an acetaminophen level

should be sent in virtually all cases. This drug is found in

many prescription and over-the-counter medications, and

patients may ingest potentially lethal amounts but show

minimal or nonspecific signs of toxicity.

Physical Examination Sedative– Hypnotic Cholinergic Anticholinergic Sympathomimetic Sympatholytic

Temperature N/– N N/+ N/+/++ N/–

Respiratory rate N/–/– – +/– N/– +/– –

Heart rate N/– + or – +/++ ++ N/–

Blood pressure N/– + N/+ ++ N/–

Level of consciousness Normal

Obtunded

Comatose

Normal

Confusion

Coma

Delirium

Coma

Normal

Agitated

Paranoid, delusional

Normal

Lethargy, coma

Pupillary examination Miosis Miosis Mydriasis Mydriasis N or miosis

Motor responses N/– Weakness

Paralysis

Fasciculations

N N N

Skin, moisture N ++

Diaphoresis

Dry, hot Diaphoresis Dry

Lung examination N Bronchospasm

Bronchorrhea

N N N

Bowel sounds N/– ++

(SLUD)

–– N/– N/–

Examples Opioids

Benzodiazepines

Alcohols

Barbiturates

Organophosphates

Carbamates

Physostigmine

Edrophonium

Some mushrooms

Tricyclics

Phenothiazines

Antihistamines

Scopolamine

Amantadine

Cocaine

Amphetamine

Methamphetamines

Phenylpropanolamine

Ephedrine

Caffeine

Theophylline

Phencyclidine

Clonidine

SLUD = salivation, lacrimation, urination, defecation; N = no effect; + = increased; ++ = markedly increased; – = decreased; – – = markedly decreased.

Vital signs

Temperature

Blood pressure

Respiratory rate

Heart rate

Brief neurologic examination

Level of consciousness

Pupillary examination

Motor responses

Skin examination: moisture, rash, cyanosis

Lung examination

Auscultation for bowel sounds

Table 36–1. The toxidrome-oriented physical examination.

Table 36–2. Toxidromes.



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Electrocardiography

An ECG should be ordered in all patients with potential drug

ingestions. The heart rate, evidence of dysrhythmias, vector

axes, and interval measurements are helpful in determining

the presence or severity of several ingestions, and serial elec-

trocardiographic evaluation can, in some cases, help to fol-

low the progression of toxicity.

Imaging Studies

A plain abdominal film may be helpful in patients who ingest

radiopaque medications such as iron tablets or some enteric-

coated medications. These films also may be helpful in visu-

alizing drug packets in “body packers”—individuals who

ingest wrapped packets of illicit drugs to transport them.

Although the packages themselves are often not radiopaque,

they still may be visualized by the changes caused in bowel

gas patterns by their presence.



Differential Diagnosis of Poisoning

The differential diagnosis of the toxin-exposed patient is

extensive and varies with the agent involved. In general, how-

ever, infectious processes (eg, meningitis, encephalitis, and sep-

sis), metabolic disorders (eg, hypo- or hyperthyroidism, hypo-

or hyperglycemia, hypo- or hypercalcemia, and hypo- or

hypernatremia), and environmental disorders (eg, heat

stroke) are the most common other causes of the clinical

syndromes found in toxic exposures. Head trauma or hypox-

emia also may cause findings similar to those observed fol-

lowing toxin exposure.

Erickson TB et al: The approach to the patient with an unknown

overdose. Emerg Med Clin North Am 2007;25:249–81. [PMID:

17482020]

Mokhlesi B et al: Adult toxicology in critical care: I. General

approach to the intoxicated patient. Chest 2003;123:577–92.

[PMID: 12576382]

Lai MW et al: 2005 Annual Report of the American Association of

Poison Control Centers’ national poisoning and exposure data-

base. Clin Toxicol (Phila) 2006;44:803–932. [PMID: 17015284]

TREATMENT OF POISONING IN THE ICU

General Measures

The first priority in treating any patient with a toxic exposure

is resuscitation and stabilization; assessing the patient’s air-

way, breathing, and circulation are the initial goals. This may

require establishing an airway, ventilating and oxygenating

the patient, and supporting circulation by normalizing and

maintaining an adequate heart rate and blood pressure. These

measures should be taken regardless of the toxin involved;

more specific interventions can be made after stabilization is

completed. All overdose or toxin-exposed patients should be

placed on a cardiac monitor and given supplemental oxygen

if hypoxic. Intravenous access should be established.

Airway Management

Endotracheal or nasotracheal intubation is indicated in all

patients who are inadequately ventilating, those who have

significant hypoxemia, those who cannot protect their airway

because of obtundation or a poor gag reflex, or those with an

anticipated clinical course of deterioration. Intubation for

airway protection also should be considered in patients who

need gastric lavage, although this once frequently used prac-

tice is now indicated in only rare instances.

There are two potential situations where an obtunded

patient may not need intubation. Altered patients whose

rapid blood glucose is low may respond sufficiently to intra-

venous dextrose to obviate the need for intubation. (In

patients with suspected alcohol abuse or those who appear

significantly malnourished, administration of dextrose

should be preceded by a 100-mg dose of thiamine intra-

venously or intramuscularly.) Obtunded patients taking nar-

cotics or benzodiazepines may respond to administration of

naloxone or flumazenil (see “Antidotes” below).

Hemodynamic Support

Abnormal blood pressure, heart rate, and temperature should

be managed in the usual fashion; more specific interventions

Electrolytes

Serum glucose and rapid bedside glucose level

Blood urea nitrogen

Serum creatinine

Arterial blood gases

Serum osmolality

Calculated osmolal gap

Urinalysis

Electrocardiogram

Acetaminophen level

Other laboratory test (methemoglobin level, carboxyhemoglobin

level, etc) as indicated

Specific drug levels (as indicated)

Abdominal x-ray (as indicated)

Table 36–3. Screening evaluation of the poison-exposed

patient.

Salicylates Ethylene glycol

Acetaminophen Iron

Barbiturates Isopropyl alcohol

Digoxin Lithium

Ethanol Theophylline

Methanol

Table 36–4. Drug levels helpful in guiding management.

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755

or modifications of treatment can be addressed when more

information regarding the toxin involved is available.

Control of Seizures

Benzodiazepines should be used initially for the manage-

ment of seizures; phenytoin or barbiturates may be needed if

benzodiazepines are not effective. In cases of refractory

seizures, general anesthesia or the use of paralytic agents may

be required; in this case, electroencephalographic monitor-

ing should be instituted to determine if the patient continues

to have electrical seizure activity. It is important to note that

normalization of vital signs and control of seizures may

require interventions specific to the toxin involved (eg, pyri-

doxine for treating isoniazid ingestion).

Opioid and Benzodiazepine Antagonists

Comatose patients should receive naloxone, particularly if

they are hypoventilating and have miotic pupils. The usual

dose is 0.8 mg intravenously in both adults and children; if

there is a suspicion that the patient may be narcotic-

addicted, the dose should be titrated in increments of

0.2–0.4 mg to prevent abrupt withdrawal symptoms. Certain

opioid ingestions, particularly propoxyphene, may require

larger doses of naloxone to be effective. If this ingestion is

suspected, 2 mg naloxone should be administered.

Flumazenil—a benzodiazepine antagonist—may be indi-

cated in patients who present with obtundation or coma sus-

pected to be due to benzodiazepine ingestion. Since use of

this agent in the benzodiazepine-dependent patient may pre-

cipitate withdrawal seizures, this agent should be used with

extreme care in these patients if it is used at all. The initial

dose of flumazenil is 0.2 mg intravenously given over

30 seconds; if, after observation for 30 seconds, the patient

does not respond, an additional dose of 0.3 mg should be

given over 30 seconds. If additional doses are needed, 0.5 mg

should be given over 30 seconds at 1-minute intervals to a

total dose of 3–5 mg; if the patient does not respond to this

maximum dose, the primary cause of altered mental status is

unlikely to be due to benzodiazepines. Because the half-life of

flumazenil is approximately 1 hour (shorter than the half-life

of all currently available benzodiazepines), resedation occurs

in 50–65% of patients with benzodiazepine overdose. When

it occurs, the resedation is usually within 1–3 hours of

flumazenil administration; this necessitates close observation

of these patients.

Decontamination

After stabilization and initial basic therapeutic interventions

have been completed, decontamination should be addressed.

A. External Exposures—Patients who have dermal expo-

sure to a toxin should be undressed and copiously irrigated

with tepid water. Health care personnel must take appropri-

ate measures to ensure that they are not exposed to the agent

while caring for the patient. Irrigation also should be used in

patients with eye contamination, particularly with alkali or

acid substances.

B. Ingestions—Since the vast majority of poisonings occur

by ingestion, gastric emptying and gut decontamination have

been a mainstay of management. Studies have shown, how-

ever, that these interventions are of little benefit in most cases.

1. Syrup of ipecac—In the past, syrup of ipecac was used

extensively to induce gastric emptying in patients with toxic

ingestions, particularly children, but studies question the role

of ipecac in these situations. Ipecac is no longer recom-

mended for the treatment of most ingestions (see “Current

Controversies and Unresolved Issues” below).

2. Gastric lavage—Gastric lavage is a relatively effective

means of accomplishing gastric emptying, decreasing drug

absorption by as much as 50%. Studies of its impact on clin-

ical outcome in poisoned patients, however, have reported

conflicting results. Gastric lavage should not be used routinely

in all poisoned patients but may have a role in specific clini-

cal situations. Gastric lavage should be considered in patients

who present within 1 hour of ingesting a potentially lethal

amount of a toxin. Another possible indication is in poison-

ings with agents that decrease gastric motility (eg, anticholin-

ergic agents), although utility in these cases is questionable.

Gastric lavage may be useful when patients ingest agents that

bind poorly to activated charcoal and in life-threatening poi-

sonings with agents such as theophylline, tricyclic antidepres-

sants, and cyanide. Table 36–5 summarizes these indications.

When gastric lavage is performed, the patient should be

placed in the head-down lateral position. Owing to the risk

of aspiration, gastric lavage never should be performed with

the patient supine, particularly if the patient is in restraints

and cannot be turned quickly if emesis occurs. Suction

equipment should be available at all times. A large-bore gav-

age tube (ie, 36–42F in adults and 16–32F in children) should

be used to remove large pill fragments and whole pills. Some

authors recommend that extra holes be cut along the sides of

the distal end of the tube to facilitate pill removal. Since these

tubes are large, they should not be passed through the nose;

oral passage is better tolerated and has fewer complications.

Once gastric tube position is confirmed, aspiration of the

stomach should be performed to remove as much of the

Recent ingestion (<1 hour) of a potentially life-threatening poison

Ingestion of a substance that slows gastric emptying (eg, anticholinergic

medications)

Ingestion of a poison that is slowly absorbed from the gastrointestinal

tract

Ingestion of a substance that does not bind well to activated charcoal

(eg, iron, lithium)

Ingestion of specific life-threatening poisons (eg, tricyclic antidepres-

sants, theophylline, cyanide)

Table 36–5. Indications for gastric lavage.

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756

poison as possible before irrigation is instituted. Once aspi-

ration is complete, tepid tap water should be used for gastric

lavage. In patients under age 5, normal saline should be used

to prevent electrolyte disturbances. Using 150–300-mL

aliquots (50–150 mL in children), the fluid should be alter-

natively instilled down the tube and then allowed to efflux

from the stomach by gravity; amounts in excess of 300 mL

increase the risk of emesis and aspiration. Lavage should be

continued until the effluent fluid is clear of pill fragments. If

activated charcoal and a cathartic is to be used, it can be

placed down the lavage tube before it is withdrawn.

Several complications are associated with gastric lavage.

Aspiration and subsequent pneumonitis can occur; there-

fore, it is critical that patients who cannot protect their air-

ways be intubated prior to gastric lavage. Esophageal

perforation has been reported, as has inadvertent tracheal

tube placement (with subsequent instillation of lavage fluid

into the lungs). Children under the age of 5 years may

develop electrolyte imbalances if normal saline is not used as

the lavage fluid. Laryngospasm and cardiac dysrhythmias

also have been described.

Gastric lavage has only one absolute contraindication—it

should not be used in caustic ingestions because it may cause

the patient to vomit, leading to more extensive esophageal

and oral burns.

3. Charcoal—Activated charcoal is an odorless, tasteless

powder that is beneficial in many types of ingestions and is

the cornerstone of therapy for most cases. In the gut, it binds

the toxin and prevents its absorption. Although it binds

many compounds, there are several potentially life-

threatening poisons that do not bind well to charcoal

(Table 36–6). When used in repeated doses, activated char-

coal can both interrupt enterohepatic circulation and

enhance the elimination of some drugs that have already

been absorbed from the GI tract (Table 36–7); this is referred

to as gastrointestinal dialysis. When used in this fashion, the

dose of activated charcoal should be 25–50 g orally every 2–4

hours; in children, it is 0.25–1 g/kg every 2–4 hours.

Activated charcoal is administered as a slurry of water

and charcoal. Although the initial dose is 50–100 g orally in

adults and 1–2 g/kg in children, when the amount of ingested

agent is known, the optimal dosing of activated charcoal is in

a ratio of 10:1, charcoal to ingested agent.

The only relative contraindication to giving charcoal is in

patients with caustic ingestions; the charcoal accumulates in

burned areas of the GI tract and interferes with endoscopy.

The most common complication of charcoal administration

is constipation. This problem can be addressed by adding a

cathartic to the charcoal. If repeat-dose activated charcoal

therapy is to be used, the cathartic should be added only to

the first dose of charcoal because the every 2–4-hour dosing

of the repeat-dose activated charcoal regimen can lead to

excessive cathartic administration and possible electrolyte

imbalances from the resulting diarrhea. In addition, some

children have become hypermagnesemic when magnesium

citrate was used as the cathartic. The most common cathartics

used in this situation are 70% sorbitol (1 g/kg), magnesium

citrate (4 mL/kg), and 10% magnesium sulfate (250 mg/kg).

4. Bowel irrigation—Whole bowel irrigation is a method

of removing ingested toxins from the gut by forcing the toxin

rapidly through the GI tract. Indications for whole bowel

irrigation are limited; the most common use of this tech-

nique is in patients who intentionally ingest packets of illicit

compounds such as cocaine or heroin in order to transport

them without detection. The other indication for this ther-

apy is in patients who ingest potentially lethal toxins that are

difficult to remove from the stomach and do not bind well to

charcoal (eg, iron).

The technique for whole bowel irrigation involves admin-

istration of 1–2 L of polyethylene glycol electrolyte solution

per hour, either orally or via a nasogastric tube. In children

under the age of 5 years, the solution should be given at a rate

of 150–500 mL/h. The goal is to produce a rectal discharge

with the same appearance as the administered oral solution,

which indicates complete cleansing of the gut. Effective

whole bowel irrigation usually takes 6–12 hours. The patient

must be able to cooperate and sit either on a toilet or a bed-

side commode during the procedure.

The only contraindications to this procedure are the pres-

ence of ileus, GI perforation, and bleeding. It should not be

used in patients who are uncooperative or combative or in

those with CNS depression or respiratory distress. The compli-

cations associated with whole bowel irrigation are abdominal

Bromides

Caustics

Cyanide

Ethylene glycol

Heavy metals

Iron

Isopropyl alcohol

Lithium

Methanol

Table 36–6. Poisons not well bound by activated charcoal.

Carbamazepine

Diazepam

Digitalis

Phenobarbital

Phenytoin

Salicylates

Theophylline

Tricyclic antidepressants

Table 36–7. Some drugs amenable to repeat-dose

activated charcoal therapy.