hydrocarbo (1)

8/12/2019 HYDROCARBO (1)

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HYDROCARBONS ANDVOLATILE

SUBSTANCES


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Dr.A.AMINI ; ASSISSTANT PROFESSOR OFE.M. 3

Most hydrocarbons are produced from

petroleum distillation: aliphatic (open-chain) mixtures of hydrocarbons

& Short-chain& Intemediate-chain The wood distillates

Aromatic hydrocarbons (containing a benzene ring)

halogenated hydrocarbons


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Epidemiology Exposures to hydrocarbons and volatiles most

commonly occur in one of two settings: #Ingestion#Inhalation.

3.5 to 10percent of young people have experimented

with volatile substance inhalationto produce inebriation

The most commonly implicated volatiles were:butane (39 percent),

aerosols (26 percent),

cleaners (16 percent),

glue (10 percent).


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CLINICAL FEATURES The toxic potential of hydrocarbons depends on:

physical characteristics(volatility, viscosity, and surface tension) chemical characteristics(aliphatic, aromatic, or halogenated), presence

of toxic additives (pesticidesor heavy metals),

route of exposure,

concentration,

dose.

Viscosity: the resistance to flow, and surface tension, ( a

major role in determining the aspiration potential.) substances with viscosities less than60 SUS(e.g.,

gasoline, kerosene, mineral seal oil, turpentine, andaromatic and

halogenated hydrocarbons) are at greater riskfor than arethose ingesting substances with viscosities

greater than 100 SUS(e.g., diesel oil, grease, mineral oil,

paraffin wax, and petroleum jelly)


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Low surface tensionalso increases the riskof aspiration.

Volatility:denotes the ability of a substance to vaporize. A compound with high volatilityevaporates easilyand usually has low

viscosity and low surface tension.

Inhalationof volatile agents, )such asaromatic hydrocarbons, halogenated

hydrocarbons, or gasoline(, resultsin systemic absorptionand the potential for

significant toxicity. Dermal exposureto hydrocarbons:causes local toxicity, and occasionally

leads to systemic absorption. Intravenousadministration of hydrocarbons:may cause pulmonary toxicity

by their first-pass exposure through the lungs (first capillary bedencountered).


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Characteristic presentations usually affect one or

more of thefollowing systems:pulmonary,Neurologic :central

peripheral,

GI,Cardiac,

Hepatic,

Renal,

Hematologic,

Dermal.


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Pulmonary Toxcity

Pulmonary complications, especially aspiration, are the

most frequentadverse effects of hydrocarbon exposure. Aliphatichydrocarbons have a limited GI absorption;

toxicity usually results from aspiration of the low-viscosity

compounds or inhalation (with resulting systemic

absorption) of compounds with high volatility. Ingestion ofaromaticor halogenatedhydrocarbons may

also result in aspiration, GI absorption is greater.

That results in the development of lipoid

pneumonia. Deaths from hydrocarbon lipoid

pneumonia have been reported.


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The risk and degree of aspiration is not dependenton volume

ingested. ( 0.2 mLinstilled intratracheally has caused pneumonitis.)

Pulmonary toxicitydoes not result from GI absorptionbutoccurs from direct aspirationof the hydrocarbon into thepulmonary tree.

There is no evidencethat hydrocarbons reflux from thestomach into the airway.

Spontaneousvomiting, however, does increasethe risk ofaspiration.

Pulmonary toxicity manifested as: acute bilateral pneumonitis( from the inhalation of an aerosolized aliphatic hydrocarbon such asgasoline)


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Hydrocarbon aspiration causes :

direct toxic injury to the pulmonary parenchyma

altered surfactant function.increased vascular permeability and edema.

clinical bronchospasm

ventilation/perfusion mismatch.

CNS manifestations

Pneumatoceles,

pneumothoraces,

pneumomediastinum

bacterial superinfection,

acute respiratory distress syndrome,death.

Long-term pulmonary dysfunction may occur.


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CNS manifestations seen after ingestion of a poorly GI-

absorbed aliphatic hydrocarbon are thought to be

from :hypox iasecondary to the hydrocarbon induced pneumonitis

and/or direct CNS toxici tyfollowing the pulmonary absorption

19 percenthad clinical or radiographic evidenceofpulmonary aspiration.

35 percenthave initial symptoms,

only 3 percenthave progressive pulmonary symptoms'


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The clinical manifestations of pulmonary aspiration areusually apparent almo st immediatelyon ingestion.

The early effectsresult from irritation of the oral mucosaand tracheobronchial tree.

Symptoms :

coughing,

choking,

gasping,

dyspnea,

burning of the mouth.

Patients with these symptoms should be assumed to have

aspirated until proven otherwise.


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Physical examination:

grunting respirations,

retractions,

tachypnea, tachycardia,

cyanosis.

An odor of the hydrocarbon may be noted on the

patient's breath. An elevated temperature of 39C (I 02.2F) or greater is

common ( may occur upon initial presentation or bedelayed for 6 to 8 h.)

Auscultation may be normal,or reveal wheezing and

decreased or absent breath sounds. Arterial blood gas analysis may demonstrate a widened

alveolar-arterial oxygen gradient or frank hypoxemia.


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Dr.A.AMINI ; ASSISSTANT PROFESSOR OF

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The development of a necrotizing pneumonitisand

hemorrhagic pulmonary edemausually occurs within

hoursin severe aspiration. Most fatalitiesfrom these complications occur within 24

to 48 h.

With less-severe damage, symptoms usually subsidewithin 2 to 5 days

pneumatocelesand lipoid, pneumonias

whose symptoms may persist for weeks to months.


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most patientswith clinically significant aspirationhave

abnormal chest x-rays,

radiographic changes varies and correlation with physical

examination may be poor.

Changes may be seen as early as 30 min after aspiration, butthe initial radiograph in the symptomatic patient may be

deceptively clear.

Radiographic changesusually appear by 2 to 6 hand arealmost always present by18 to 24 h, if they are to occur.


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Radiographic changes limited to bilateral perihilar

regionswith clear lung bases are also common,

mild radiographic changes do not automatically mean

the patient will become symptomatic.

right-sided involvement is more common than left-sided

involvement.

Multilobar involvement is more common than single-lobeinvolvement


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Central Nervous System Toxicity

Result from: a direct toxic response to the systemic absorption of the hydrocarbon,

indirect result of severe hypoxia secondary to aspiration,

a result of simple asphyxiation due to either loss of ventilatory drive,

the use of a plastic bag or other device during "bagging."

Through: GI absorption,

the inhalation of highly volatile petroleum distillates,

direct dermal penetration, usually by prolonged contact with

chlorinated hydrocarbons.


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Volatile solvent abuse most often occurs in teenagers

and younger adults,

These patients are described as "huffers" or "baggers"depending on whether they inhale through a rag soaked

with the hydrocarbon held to the mouth or rebreathe into

a plastic bag containing the hydrocarbon.

The act of rebreathing to facilitate inhalation may alsocontribute to toxicity by producing significant hypercarbia

and hypoxia.

They behave similarly to the inhalational anesthet ic agents.

Hydrocarbon intoxication may be confused with ethanolinebriation.


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CNS depressionranges in severity from : dizziness,

slurred speech,

ataxia, lethargy to obtundation,

coma and apnea.

These effects are usually dose-dependent.

Although hydrocarbons are CNS depressants, they often

have an initial excitatory effect manifested as : euphoria,

exhilaration,

giddiness,.

More severe excitatory featuresinclude:

tremor, agitation,

convulsions.

Perceptual changes, such as confusion, hallucinations,and psychosis, may occur.


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Chronic CNS sequelae: Recurrent headaches,

cerebellar ataxia,

chronic encephalopathy consisting of tremors,

emotional lability,

mental status changes,

cognitive impairment,

psychomotor impairment,

These effects may be transitory or permanent.

The development of encephalopathy, ataxia,

tremor, chorea, and myoclonus also isassociated with the habi tual sni f f ing of leaded

gasol ine.


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Peripheral Nervous System Toxicity

Exposure to aliphatic hydrocarbons is associated with

the development of a characteristic peripheralpolyneuropathycaused bydemyelinization and

retrograde axonal degeneration.

Onset of symptoms may bedelayedfor months toyearsafter initial exposure.

Toxicity is attributed to a metabolite,2,5-hexanedione,

produced by the cy tochrome P450-mediatedbiotransformation of the parent compounds.


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Long, distal nerves seem to be most vulnerable,

characteristically producing foot and wr is t dropwith

numbnessand paresthesias.

Unleaded gaso l ine sn if f inghas produced a similar

clinical picture as well.


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Gastrointestinal Toxicity

Most hydrocarbons act as intestinal irritants.

resulting in burning in the mouth and throat, abdominal pain,

belching,

nausea,

vomiting, diarrhea.

Vomiting, which occurs in approximately one-third of thepatients with aliphatic hydrocarbon ingestions, is

particularly trouble some because of the inc reased riskof pulm onary aspirat ion.

Corrosive GI injury, as well as pancreatitis, has been reported withingestion of some chlorinated hydrocarbons.


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Cardiac Toxicity

Li fe-threatening dysrhy thm ias, such as ventricular

tachycardiaand ventricular fibrillation, suddenDeathmay occur with systemic absorption

(gastrointestinal or inhalational) of a variety of

hydrocarbon compounds.

Most commonly, dysrhythmias occur after exposure tohalogenated hydrocarbons and aromatic hydrocarbons.

The term "sudden sniffing death"describes solvent

abusers who die suddenly after exertion, panic, or fright.(The sudden release of catecholamines,asphyxia, respiratory depression,

and vagal inhibition.)


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The use of exogenous catecholamines, such as

epinephrine, may p recipi tate sudden

dys rhythm ias and should be avoided except i frequired for cardiac resusci tat ion.

Decreases in myocardial contractilityandperipheral vascular

resistanceas well as bradycardia and atrioventricularconduction blocks have also been associated with volat i le

so lvent abuse.


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Hepatic Toxicity

Halogenated hyd rocarbonsis well described.

Carbon tetrachloridetoxicity has been used as a model

for toxin-induced hepatic dysfunction. As little as 3 mL

of carbon tetrachloride has been associated with the

development of fatal liver injury.

Chloroformand methylene chloride, are also associated

with liver dysfunction. (Free-radical metabolites)

Patholog ic exam inat ionreveals acute fatty

degenerat ion of th e liverwith areas of centr i lobular

necrosis.


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Liver funct ion testsmay be elevated within 24 hafter

ingestion,with the development of liver tenderness andjaundice in 48 to 96 h.

Chronic exposureto carbon tetrachloridemay be

associated with the development of cirrhosisandhepatomas.


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Renal and Metabolic Toxicity

Solvent abuse and occupational exposure to

hydrocarbons may result in renal dysfunction. Exposure to hepatotoxic halogenated hydrocarbons,

such as carbon tetrachloride, trichloroethylene, andchlorinated paraffins, have caused acute renal fai lur e,

Renal tubu lar acidosismay occur in patients whoabuse toluene containing substances.(Patients present witha non-anion gap metabolicacidosis, hypokalemia, and

hypophosphatemia.)

Significant rhabdomyolys ismay also result.

Toluene toxicitymay also cause a high anion gapmetabolic acidosisas a result of the accumulation ofhippuric acidand benzoic acidmetabolites.

Proteinuriaand renal insufficiency can occur in patientswho abuse toluene.


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Hematologic Toxicity

Chronic exposureto benzene, the prototypical aromatic

hydrocarbon,is associated with an increased incidence

of hematologic disorders including aplast ic anem ia,acute myelogenous leukemia, and mu l t ip le myeloma.

Although aplastic anemiais associated with glue sniffing,

this is most likely a result of the benzenefraction of the

glue, and not the toluene.


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Dermal Toxicity

Dermal exposure to hydrocarbons may also result in

toxicity. Cutaneous injury is most often associated with the

short-chain aliphatic,aromatic, and halogenated

hydrocarbons.

Clinically, skin findings can range from local erythema,papules, and vesicles to a generalized scarlatiniform

erupt ionand an exfol iat ive dermati t is.

A " huffer 's rash"may be noted over the face of patients

who chronically abuse the volatile hydrocarbons. Pruritusmay also be present.

Extensivepartial-thicknessandfull-thickness

bums following immersionin hydrocarbons may also occur.


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TREATMENT

Prehospital

Not all patientswho have ingested hydrocarbons

require emergency department evaluation.

patients who are asymptomaticor who quickly become

asymptomaticafter ingestion can be watched safely at

home. (reliable follow-up can be ensured.)


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All symptomaticpatients and intentionalexposuresshould be referred to the hospital forfurther evaluation.

Patients who ingest hydrocarbons that maycause significant systemic toxicity (e.g.,aromatic, halogenated hydrocarbons, or toxic

additives), whether or not symptomatic, shouldalso be referred to the hospital.

Volatile substance abusersand others exposed

to volatiles should have immediate cardiacmonitoringand advanced life support transport,if available,because of the potential for l i fe-threatening dysrhy thm ias.

All symptomaticpatients and intentionalexposuresshould be referred to the hospital forfurther evaluation.

Patients who ingest hydrocarbons that maycause significant systemic toxicity (e.g.,aromatic, halogenated hydrocarbons, or toxic

additives), whether or not symptomatic, shouldalso be referred to the hospital.

Volatile substance abusersand others exposed

to volatiles should have immediate cardiacmonitoringand advanced life support transport,if available,because of the potential for l i fe-threatening dysrhy thm ias.


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Emergency Department

Establishing theairwayand maintaining ventilationis the

cr i t ical f i rst maneuverin any patient who presents withresp iratory depressionand/or signif icant CNS

depression.

The detection of a sweet odor: Certain halogenated hydrocarbon exposures (especially chloroform

or trichloroethylene)

petrol odor suggests gasoline or some other petroleum derivative.

Continuous cardiac monitoringshould be initiated,and an electrocardiogramshould be obtained.

Hydrocarbon induced dysrhythmias, if present, would generally

occur sho rt ly after the expo sure, especially with inhalational use

Hypotension should be treated with aggressive fluid


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Hypotensionshould be treated with aggressive fluidresuscitation.

Catecholamines, such as dopamine,norepinephrine, or epinephrine, should be

avoided to prevent precipitating dysrhythmias,especially following exposure to halogenatedhydrocarbons and aromatic hydrocarbons.

The administration of glucose, thiamine, and naloxoneshould be considered in cases of altered mental status

The patient needs to be fully undressedto prevent

ongoing contamination from hydrocarbon-soakedclothes.

Dermal decontamination withsoap and water,

eye decontamination with salineirrigation,should be

performed.


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Prehospita ldecontamination is preferable.

It is important for staff to wear protective gloves and aprons to

prevent po ssib le secondary expos ure, especially for

organophosphate containing mixtures.

Useful diagnost ic testsinclude the chest x-rayand

arterial blood gasto detect pulmonary aspiration and

hypoxemia.

Abdominal radiographsmay show evidence of

chlorinated hydrocarboningestions,such as carbon

tetrachloride, because ofthe radiopaque nature of these

polyhalogenated substances

Tests of liver and renal functionshould be obtained for

the development of hepatic and renal injury.


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A carboxyhemoglobin levelis useful to evaluate the

extent of endogenous carbon monoxide production

following methylene ch lor ideexposure.

Pulse oximetry will not differentiate between oxyhemoglobin and

carboxyhemoglobin.

Routine drug screens are not useful for the detection of

hydrocarbons,

In al l intent ion al ingest ions, an acetaminophen

level, ethanol level, anion gap, and osmolality may be

helpful in assessing for the presence of other

coingestants.

G t i t ti l D t i ti


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Gastrointestinal Decontamination

For most hydrocarbon ingestions, gastrointestinal decontamination

would provide little benefit;

The necessity for GI decontamination depends on the type ofhydrocarbonandrouteof exposure.

supportive careand appropriate treatmentof coexisting ingestions

are all that is required.

The major i ty of hydrocarboningestions, which consist of aliphatic

hydrocarbons mixtures do not requireGI decontamination.

Gl decontamination may be warranted when the ingested

hydrocarbon is known to have good Gl absorpt ionand may causesignificant systemic toxicity (e.g.,toluene, chloroform,wood

distillates)or an add it ivein the toxic agent (e.g., organophosphate

pesticidesareoften mixed in petroleum distillates).


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If the patient presents to the ED shortly after theingestion of these toxic hydrocarbons, aspiration with asmal lnasogastr ic tube may be useful.

In patients who present with an altered mental status,the airway should be protectedwith a cuffed

endotracheal tu be,

In smaller children younger than 8 yearsof age, the cuff

should be kept inflated only during the period of lavagebecause of cuff-related injury from prolonged inflation.

Ipecac induced Emesis is contraindicated

Although activated charcoalmay adsorb

somehydrocarbon compounds, its use is notrecommendedfor most hydrocarbon ingestions


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Charcoalinstillation may distend the stomach increasing

the risk for vomiting and aspiration.

The use of charcoalshould only be considered i f one

of the CHAMP-type h ydro carbonshas been ingested,

and extreme cautionshould be exercised because of

aspirat ion r isk.

Many patients will already have diarrheafrom the

hydrocarbon, and further catharsisis not required.

Oil-based cathart ics, which had been used in the past

to thicken the ingested hydrocarbon to increase its

viscosity and decrease the subsequent risk of aspiration,

are con traindicated.

P l T t t


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Pulmonary Treatment Nebu l ized oxygenis helpful in the treatment of

pulmonary aspiration.

Inhaled B-agonistsmay also be useful, especially in thesetting ofbroncho spasm,( but their role in the treatment of

hydrocarbon pneumonitis has not been studied)

Positive end-expiratory pressure (PEEP)or continuous

positive-airway pressure (CPAP)may sometimes berequired, but because of the potential for further injury

from barotrauma,one should observe for the

development of pneumatocelesor pneumothorax.

In cases of severe pulmonary aspirationresulting inrefractory hypoxem ia, treatment with extracorporeal

membrane oxygenationand high-frequency jet

ventilationhas proved successful.


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Cort icosteroids are contra ind icatedbecause they

impair the cellular immune response and increase the

chance of bacterial superinfection remains.

An t ib iot ics have no p roven role in prophylaxisandare usually not required except in cases of continued

pulmonary deterioration because of the risk of a

superimposed bacterial pneumonitis.

Nacetyl cysteineand hyperbar ic oxygenmay have arole in preventing hepatic toxicityafter carbon

tetrachloride(and possibly chloroform)exposure, but

more studies are needed.

Hyperbar ic ox ygentherapy may be indicated forpatients who develop significant carbon monoxide

toxicity after exposure to methylene chloride,


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B-blockersmay be useful in the treatment of

hydrocarboninduced malignant dysrhythmias.

Although extracorporeal removal with hemodialysis,

hemoper fus ion, or peri toneal dialysishas beenattempted for severe intoxications, clinically controlled

evidence of eff icacy is lacking.

Specific antidotal treatmentdirected at the complications

of toxic additives, such as organophosphates, pyrethrinsor heavy metals, may also be needed.

DISPOSITION


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DISPOSITION Hospital izat ion is required for patients who have

ingested aliphatic hydrocarbons who are symptomatic at

the time of evaluation, and patients exposed tosignificant amounts of methemoglobinemia-producinghydrocarbons.

After a 6-h observat ion period, asymptomaticpatientswith a normal chest x-raymay be discharged

home, but follow up should be assured as delayedtox ici ty (18+ h)has been reported.

Similar disposition of asymptomaticpatients, withabnormal chest x-rayshas also been suggested if

reliable follow-up can be ensured. Some physicians,however, prefer to observe these patients for 24 hin thehospital.


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Hospital izat ionis recommended for those who

ingest hydrocarbons capable of producingdelayed complications (e.g., halogenated

hydrocarbonscausing hepatic toxicity) and

those with toxic additives(organophosphates

and organic metal compounds). All patients taking ingestions with suicidal intent

or presenting with complications of solvent

abuseshould have psychiatric evaluation.


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Dr.A.AMINI ; ASSISSTANT PROFESSOR OF 46

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