Hydrocarbon aspiration in children and adolescents Patricia A Primm, MD Last literature review version 16.1: Janeiro 2008 | This topic last updated: Setembro 13, 2005 Modified by Jefferson P Piva (june2008)

INTRODUCTION — Hydrocarbons

are

organic

• Aliphatic hydrocarbons

substances that contain carbon and hydrogen;

Aromatic hydrocarbons are cyclic compounds

they are liquid at room temperature [1] . All petroleum distillates (eg,

kerosene,

containing a benzene ring (eg, benzene, toluene,

gasoline,

and xylene). They are used primarily in solvents,

mineral seal oils, and naphtha) are hydrocarbons;

glues, nail polish, paints, and paint removers [1] .

however, not all hydrocarbons are petroleum

Halogenated

distillates. Hydrocarbons also often are mixed with agents that have systemic toxicity such as camphor,

aniline

dyes,

heavy

metals,

hydrocarbons

chlorinated, chloride

and

or

brominated

chloroform,

trichloroethylene,

pesticides.

are

fluorinated,

(eg,

carbon

methylene

tetrachloride,

tetrachloroethylene).

The

terpenes include turpentine and pine oil. The

Ingestion of large quantities of hydrocarbons by

aliphatic hydrocarbons are petroleum distillates.

children is unusual because hydrocarbons are

They are found in furniture polish, lamp oil, and

foul-tasting. Aspiration of hydrocarbons by young

lighter fluid [1] .

children typically is an unintentional occurrence

HYDROCARBON

that can be prevented through safe packaging

TOXICITY — Hydrocarbons

also can be classified according to their toxicity

and storage. In contrast, hydrocarbon aspiration

[1] :

in teenagers usually occurs intentionally (eg,

• Nontoxic

during inhalant abuse, or when attempting to

(unless

complicated

by

gross

aspiration) — Examples include asphalt, tars,

siphon gasoline).

mineral oil, liquid petrolatum, motor oil, axle EPIDEMIOLOGY — Hydrocarbon accounted

for

approximately

ingestion 2

percent

grease, baby oil.

of

• Aspiration hazard — Clinical effects typically are

ingestions by children younger than six years of age in 2002 [2] . Between 1997 and 1999, an

limited

estimated 6400 children younger than five years

subsequent

of

turpentine, gasoline, kerosene, mineral seal oil

age

were

seen

in

hospital

emergency

to

direct

pulmonary

inflammation.

Examples

charcoal

and

include

departments for possible hydrocarbon aspiration

(furniture

after ingestion of household cleaning products [3]

cigarette lighter fluid, and mineral spirits.

. Gasoline, lubricating oils, motor oils, mineral

polish),

damage

lighter

fluid,

• Systemic toxicity — Halogenated and aromatic

spirits, lighter fluid, naphtha, and kerosene were

hydrocarbons are absorbed readily through the

the most common exposures [4] . In 1998,

gastrointestinal

unintentional ingestion of hydrocarbon resulted in

and/or

respiratory

systems.

Systemic effects include cardiac arrhythmia and

the deaths of four children younger than 13 years

central nervous system (CNS) depression. In

of age; an additional 14 deaths were caused by

addition

intentional ingestion. Death from hydrocarbon

to

halogenated

and

aromatic

hydrocarbons, hydrocarbons that are combined

aspiration usually is caused by respiratory failure.

with toxic additives (eg, organophosphates, CLASSES OF HYDROCARBONS — The structural classes of hydrocarbons are: • Aromatic hydrocarbons • Halogenated hydrocarbons • Terpene hydrocarbons

four

heavy metals, camphor) also have systemic toxicity. Determinants of toxicity — With the exception of aromatic and halogenated compounds, most

1

hydrocarbons cause clinical toxicity only when

the body and into the CNS [5,6] . Neurons, which

aspirated or inhaled because they are poorly

have

absorbed through the gastrointestinal tract. The

susceptible

aspiration

Manifestations in the CNS also occur secondary to

hazard

of

the

hydrocarbons

is

a

high

lipid

content,

the

solvent

to

are

particularly

properties

[7]

.

determined by three properties:

severe pulmonary injury and hypoxia.

• Volatility — The ability to vaporize or to exist in

The respiratory system also is affected by direct injury. Low viscosity, low surface tension, and

a gaseous form

• Surface

tension

cohesiveness) surface;

of

lower

—

The

adherence

molecules

along

surface

a

solvent

(or

of

aspirated

hydrocarbons

together determine a compound's ability to cause

liquid

tension

properties

chemical

allows

pneumonitis

pathologic

compounds to spread or "creep" over a larger

finding

pneumonia.

area

[1] is

Other

.

The

severe

findings

primary

necrotizing

include

direct

destruction of the airway epithelium, alveolar

• Viscosity — The resistance to flow through an

septae, and pulmonary capillaries, as well as

orifice or the tendency of a compound to resist

solubilization

"stirring;" lower

Secondary changes include atelectasis, interstitial

viscosity facilitates deeper

The systemic

toxicity

of

the

lipid

surfactant

layer.

inflammation, and hyaline membrane formation.

penetration into the tracheobronchial tree The

of

hydrocarbons

is

inflammatory

response

from

chemical

irritation generally causes temperature elevation,

determined by their volatility. Gases such as

usually within hours of exposure.

methane, ethane, propane, butane, and benzene CLINICAL MANIFESTATIONS

are the most volatile. They cause asphyxia by replacing alveolar gas, are readily absorbed into the

circulatory

depression.

system,

However,

and they

cause

Vital signs — Between 30 and 60 percent of

CNS

rarely

patients with hydrocarbon aspiration have fever

cause

at the time of presentation (38 to 40ºC) [8] .

pulmonary injury. Gasoline and naphtha also can cause direct CNS depression based upon their

Respiratory — Pulmonary manifestations result

high volatility.

from

any

degree

of

hydrocarbon

aspiration,

although their onset may be delayed for 12 to 24 The

aspiration

hazard

of

hydrocarbons

is

hours. Immediate signs of aspiration include

inversely related to viscosity and surface tension and

directly

hydrocarbons

related with

to

volatility.

decreased

coughing,

Thus,

viscosity,

resonance on percussion, suppressed or tubular breath sounds, and crackles. Displacement of

distal airways while the low surface tension

alveolar

facilitates spread over a greater area. As an are

gas

by

vaporized

hydrocarbon

may

aggravate hypoxemia caused by inflammation

example, simple petroleum distillates (kerosene, polish)

vomiting.

include tachypnea, dyspnea, cyanosis, diminished

low viscosity permits greater penetration into the

furniture

and

degree of pulmonary injury. Physical findings may

to be aspirated and cause pulmonary injury. The

liquid

gagging,

Respiratory examination findings vary with the

low

surface tension, and high volatility are more likely

gasoline,

choking,

and edema.

chiefly

aspiration hazards. They have high potential to

The

cause aspiration pneumonitis but rarely cause

hydrocarbon

major

systemic symptoms.

necrotizing

pulmonary aspiration chemical

complications include

of

asphyxia,

pneumonitis,

lipoid

pneumonia, and hemorrhagic pulmonary edema, PATHOPHYSIOLOGY — Hydrocarbon aspiration primarily

affects

the

central

nervous

which quickly progresses to shock and respiratory

and

arrest. Pneumothorax, subcutaneous emphysema

respiratory systems. Volatile hydrocarbons are

of the chest wall, and pleural effusion, including

highly lipid soluble. They enter the circulation

empyema, also may occur. Secondary infection

through the lungs and rapidly diffuse throughout

2

with

bacteria

or

viruses

may

occur.

Hematologic — Leukocytosis occurs early in the

Pneumatoceles may develop in areas of extensive

clinical

consolidation during the recovery period. (See

unrelated to pneumonitis and may last as long as

"Spontaneous pneumothorax in children").

one week [10] . Hemolysis, hemoglobinuria, and

Radiographic

findings — The

course

of

hydrocarbon

aspiration

consumptive coagulopathy also may occur with

radiographic

significant ingestion [11] .

findings of hydrocarbon aspiration often occur before the development of physical findings. They

MANAGEMENT — All children with hydrocarbon

may be seen within 20 minutes or as late as 24

aspiration should be observed for at least six to

hours after aspiration.

eight hours in an emergency department setting. Chest radiographs should be obtained in all

The initial findings are multiple, small, patchy

patients who have cough or any respiratory

densities with ill-defined margins. The lesions become

larger

and

coalesce

as

the

symptoms at presentation. Patients with normal

injury

initial radiographs should have them repeated

progresses. In some cases, the radiographic

four to six hours after ingestion.

findings may be minimal at a few hours and then rapidly

progress

Emphysema

or

Radiographic

to

extensive

pneumothorax

Decontamination — The child's clothing should

develop.

continued inhalation

peak

exposure. All patients should have their skin cleaned. The eyes should be flushed if any

resolution of radiographic changes is gradual and

evidence of redness, tearing, or lid swelling is

lags behind clinical improvement, which usually

present.

three

to

five

typically

be removed to prevent

between two and eight hours after aspiration. The

occurs

abnormalities

infiltrates.

may

days

after

aspiration.

As

Pneumatoceles may develop in this latent period.

a

general

rule,

decontamination

of

the

gastrointestinal tract in children with hydrocarbon

Cardiovascular — Cardiac arrhythmia may occur

ingestion should avoid gastric emptying or lavage

after

and induction of emesis because of the risk for

inhalation.

sensitize

the

Solvent

myocardium

hydrocarbons to

can

catecholamines,

aspiration during these procedures [12,13] .

leading to fatal arrhythmia ("sudden sniffing

Gastric

death"). Gastrointestinal — Ingestion

of

aliphatic

• Those

hydrocarbons causes direct local irritation to the pharynx,

lavage

may

be

esophagus,

stomach,

and

Orogastric

and

intestinal

irritation

small

may

toxic

effects

(eg,

(eg, heavy metals or insecticides)

be

• Large volume of ingestion (eg, a suicide attempt)

These effects usually are mild and rarely require

The following measures, taken before gastric

treatment.

emptying, can minimize the risk of aspiration: nervous

system — Hydrocarbon

• Endotracheal intubation with a balloon-cuffed

ingestion or inhalation may have direct CNS

endotracheal tube

effects, including somnolence, headache, ataxia, dizziness,

systemic

• Petroleum distillates that contain toxic additives

associated with nausea and hematemesis [1] .

Central

with

halogenated and aromatic hydrocarbons)

intestine, with edema and mucosal ulceration.

blurred

vision,

weakness,

• Lateral decubitus or Trendelenburg positioning

fatigue,

• Pinching off the nasogastric or orogastric tube

lethargy, stupor, seizures, and coma. In addition,

and withdrawing it quickly after the procedure

hypoxia caused by hydrocarbon aspiration may cause

emptying — Gastric

indicated for certain hydrocarbon ingestions [1] :

secondary

CNS

depression,

is complete

including

drowsiness, tremors, or convulsions [9] . (See

Pulmonary management — The treatment of

"Acute

hydrocarbon

toxic-metabolic

encephalopathy

in

pneumonitis

is

supportive.

Endotracheal intubation is indicated in patients

children").

3

with

CNS depression

or

impaired ventilation

• All children for whom close follow-up cannot be

[1,14] . Additional measures include oxygen,

established

physiotherapy, and continuous positive airway

Indications

pressure.

observation include:

Children

who

have

hydrocarbon

pneumonitis that is refractory to conventional supportive

therapy

may

be

candidates

for

discharge

after

six

hours

of

• Asymptomatic children with normal chest

for

radiograph

receiving extracorporeal membrane oxygenation

• Asymptomatic children with mildly abnormal

[15,16] .

chest

radiographs

who

do

not

develop

Bronchospasm should be treated with selective

symptoms during the observation period and

beta 2 agonists. Epinephrine and isoproterenol

who can receive adequate outpatient follow-up

should be avoided because they can cause fatal ventricular

dysrhythmia

in

the

PROGNOSIS — Although most children survive

hydrocarbon-

without complications or sequelae, some progress

sensitized myocardium (see above).

rapidly to respiratory failure and death. Systemic symptoms (eg, somnolence, convulsions, and

Corticosteroids have no beneficial effect on the course

of

hydrocarbon

aspiration

[17,18]

coma) may dominate the course.

.

Pneumatoceles rarely rupture and do not require treatment

[19]

.

Pneumonitis

caused

The prognosis is affected by the volume of

by

ingestion

hydrocarbon aspiration should not be treated routinely

with

antibiotics

unless

signs

or

aspiration,

the

specific

agent

involved, and the adequacy of medical care. The

of

typical clinical course averages two to five days.

secondary infection, including the following, are

The mild CNS depression that is seen soon after

present:

ingestion

seldom

produces

serious

morbidity

• Recurrence of fever after the first 48 hours [20]

provided that pulmonary involvement does not

• Increasing infiltrate in chest radiograph

occur.

• Leukocytosis Disposition — Indications

for

The small airways are at greatest risk for long-

immediate

term injury [23] . One study examined pulmonary

admission of children who have ingested or

function in 17 children eight to 14 years after

aspirated hydrocarbons include [21,22] :

hydrocarbon aspiration [24] . More than 80

• Symptomatic child with abnormal initial chest

percent had at least one pulmonary function

radiograph

abnormality. The clinical significance of these

• Patient with suicidal intent or massive ingestion

findings is uncertain.

• Hypoxic or obtunded patient regardless of chest

SUMMARY — Patients

radiograph findings

with

hydrocarbon

ingestion should be observed for at least six

• Patient with substantially abnormal chest

hours because the symptoms and radiographic

radiograph

findings may be delayed.

Indications for admission that become apparent

• Thorough washing of contaminated skin and

during up to six hours of observation include:

hair is an important part of therapy [13] .

• Child with mildly abnormal chest radiograph

• Children who are symptomatic on presentation,

who develops symptoms during the observation

who develop symptoms during the six-hour

period

observation period, or who have ingested a

• Child who develops symptoms related to toxic

particularly toxic agent (eg, furniture polish,

additives during the observation period (eg,

organophosphate,

heavy metal or organophosphate insecticide)

heavy

metal)

should

be

admitted to the hospital.

• Child with mild symptoms and normal chest

• Children who remain asymptomatic during six

radiograph who fails to improve during the

hours of observation should continue to be

observation period

4

observed at home. Parents should be instructed

• Corticosteroids have no beneficial effect on the

to return if any respiratory symptoms occur.

course of the illness as shown in double-blind

• Pulmonary therapy is initiated based upon the development

of

symptoms.

controlled human studies [17,18] .

Catacholamines

• Pneumatoceles rarely rupture and do not

(eg, epinephrine and isoproteronol) should not

require treatment.

be used to treat bronchospasm.

• Parents should be reminded to keep cleaning

• Antibiotics should be used if the patient

fluids and kerosene out of the reach of children

develops signs of secondary bacterial infection.

(eg, in locked cabinets, or out of the home).

REFERENCES 1.

2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24.

Osterhoudt, KC, Burns Ewald, M, Shannon, M, Henretig, FM. Toxicologic emergencies. In: Textbook of pediatric emergency medicine, 5th ed, Fleisher, GR, Ludwig, S, Henretig, FM (Eds), Lippincott, Williams & Wilkins, Philadelphia, 2006, p. 951. Watson, WA, Litovitz, TL, Rodgers, GC Jr, et al. 2002 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med 2003; 21:353. Barone, S. Child-resistant packaging. Consumer Product Safety Review. 2002; 6:3. (www.cpsc.gov/cpscpub/pubs/cpsr_nws23.pdf). Litovitz, TL, Klein-Schwartz, W, Caravati, EM, et al. 1998 Annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med 1999; 17:435. Dinwiddie, SH. Abuse of inhalants: A review. Addiction 1994; 89:925. McHugh, MJ. The abuse of volatile substances. Pediatr Clin North Am 1987; 34:333. Kurtzman, TL, Otsuka, KN, Wahl, RA. Inhalant abuse by adolescents. J Adolesc Health 2001; 28:170. Amoroso, K, Ginsburg, C. Hydrocarbon ingestions. In: Essentials of Pediatric Intensive Care, Levin, DL, Morriss, FC (Eds). Quality Medical Publishing Inc, St. Louis, 1990. p.639. Wolfsdorf, J, Paed, D. Kerosene intoxication: an experimental approach to the etiology of the CNS manifestations in primates. J Pediatr 1976; 88:1037. Food and Drug Administration. Poison control case report summary-calendar year 1982. Rockville, MD, 1984. Banner, W Jr, Walson, PD. Systemic toxicity following gasoline aspiration. Am J Emerg Med 1983; 1:292. Shannon, M. Ingestion of toxic substances by children. N Engl J Med 2000; 342:186. Arena, JM. Hydrocarbon poisoning--current management. Pediatr Ann 1987; 16:879. Zucker, AR, Berger, S, Wood, LD. Management of kerosene-induced pulmonary injury. Crit Care Med 1986; 14:303. Scalzo, AJ, Weber, TR, Jaeger, RW, et al. Extracorporeal membrane oxygenation for hydrocarbon aspiration. Am J Dis Child 1990; 144:867. Liebelt, EL, DeAngelis, CD. Evolving trends and treatment advances in pediatric poisoning. JAMA 1999; 282:1113. Marks, MI, Chicoine, L, Kegere, G, Hillman, E. Adrenocorticosteriod treatment of hydrocarbon pneumonia in children — A cooperative study. J Pediatr 1972; 81:366. Steele, RW, Conklin, RH, Mark, HM. Corticosteroids and antibiotics for the treatment of fulminant hydrocarbon aspiration. JAMA 1972; 219:1434. Bergeson, PS, Hales, SW, Lustgarten, MD, Lipow, HW. Pneumatoceles following hydrocarbon ingestion. Report of three cases and review of the literature. Am J Dis Child 1975; 129:49. Karlson, KH Jr. Hydrocarbon poisoning in children. South Med J 1982; 75:839. Shannon, M. Petroleum distillate poisoning. Harwood-Nuss, A (Ed), JP Lippincott, 1991. Anas, N, Namasonthi, V, Ginsburg, CM. Criteria for hospitalizing children who have ingested products containing hydrocarbons. JAMA 1981; 246:840. Klein, BL, Simon, JE. Hydrocarbon poisonings. Pediatr Clin North Am 1986; 33:411. Gurwitz, D, Kattan, M, Levison, H, Culham, JA. Pulmonary function abnormalities in asymptomatic children after hydrocarbon pneumonitis. Pediatrics 1978; 62:789

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