Transcript Hydrocarbons and Caustics

Hydrocarbons, Volatile
Substances and Caustics
David R. Fisher, D.O.
Tintinalli Chapters 180 & 181
February 23, 2006
1
Hydrocarbons and Volatile Substances
Exposure may cause life
threatening toxicity and in
some cases sudden death
2
Hydrocarbons
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Carbon and hydrogen atoms
– Aliphatic (open chain) and aromatic (benzene ring)
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Household and occupational settings
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Fuels
Lighter fluids
Lamp oil
Paints
Paint removers
Pesticides
Medications
Cleaning and polishing agents
Spot removers
Degreasers
Lubricants
Solvents
3
Volatile Substances

Liquid chemicals or gases
– May be abused for euphoric effects
 Hydrocarbons
– Glue (toluene)
– Propellants (butane, trichloroethylene, Freon)
– Gasoline
 Non-hydrocarbons
– Nitrites (isobutyl nitrite)
– Nitrous oxide
4
Classification

Most hydrocarbons result from petroleum distillation
– Aliphatic mixtures of hydrocarbons of different chain lengths
 Chain length and branching determines the phase of the hydrocarbon
at room temperature
– Short-chain (methane, propane or butane): gases
– Intermediate-chain: liquids
 Most hydrocarbon exposures seen in the ED
– Long-chain: waxes/solids
5
Classification
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Wood distillates
– Turpentine and pine oil
– GI absorption greater than petroleum distillates
– CNS depression
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Aromatics and halogenated aliphatic hydrocarbons
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Industrial solvents
Inhalation route of toxicity
Substance abusers and some jobs most often affected
CNS, cardiovascular, hepatic, renal and hematologic toxicity
Additives such as lead in gasoline and pesticides
– Toxic additive usually dictates the clinical approach
6
Epidemiology
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Most exposures ingestion or inhalation
– 3-10 % of all unintentional childhood poisonings in the US
– Most frequent:
 Gasoline, kerosene, lighter fluid, mineral seal oil and turpentine
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10% of youths inhale volatiles to get high
– Butane, aerosols, cleaners and glue
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Most exposures have a benign clinical course
– 80,000 hydrocarbon exposures
– 5% moderate to severe toxicity
– 12 died in 2001 in US
7
Determinants of Toxicity

Toxic potential of hydrocarbons depends on:
– Physical characteristics
 Volatility, viscosity, surface tension
– Chemical characteristics
 Aliphatic, aromatic, halogenated
– Presence of toxic additives
 Pesticides, heavy metals
– Route of exposure
– Concentration
– Dose
8
Aspiration Potential Depends On:
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Viscosity
– Lower viscosity, greater risk for aspiration
 Low
– Gasoline, kerosene, mineral seal oil, turpentine and aromatic and
halogenated hydrocarbons
 High
– Diesel oil, grease, mineral oil, paraffin wax and petroleum jelly
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Surface tension
– Lower increases risk of aspiration
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Volatility
– Higher, increased risk of systemic absorption and toxicity
 Aromatic hydrocarbons, halogenated hydrocarbons or gasoline
9
Determinants of Toxicity
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Dermal exposure
– Local toxicity
 Occasionally leads to systemic absorption
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Pulmonary toxicity
 First pass exposure through the lungs
10
Determinants of Toxicity

Toxicity characteristic of organ system affected
– Pulmonary
– Neurologic
– GI
– Cardiac
– Hepatic
– Renal
– Hematologic
– Dermal
11
Pulmonary Toxicity
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1° adverse affect of hydrocarbon exposure
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Typically unintentional childhood ingestion
– Small amounts of aliphatic hydrocarbons stored at home
– Limited GI absorption
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Ingestion of aromatics or halogenated less likely to
result in aspiration as GI absorption is greater
12
Pulmonary Toxicity
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Risk and degree of aspiration not volume
dependent
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Occurs from aspiration into pulmonary tree
– Occurs at time of ingestion
– Hydrocarbons do not reflux into airway
– Vomiting increases risk of aspiration
13
Pulmonary Toxicity

Aspiration chemical pneumonitis
– Altered surfactant function
– Destruction of alveoli & capillaries
– Bronchospasm and V/Q mismatch
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CNS manifestations
– Hypoxia 2° to pneumonitis
– Toxicity after pulmonary absorption of volatile
hydrocarbon
14
Pulmonary Toxicity
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Other
– Pneumatoceles
– Pneumothoraces
– Pneumomediastinum
– Bacterial superinfection
– ARDS
– Long-term pulmonary dysfunction
– Death
15
Pulmonary Toxicity

Irritation of oral mucosa and tracheobronchial
tree
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Symptoms:
– Coughing
– Choking
– Gasping
– Dyspnea
– Burning of the mouth
16
Pulmonary Toxicity
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If symptomatic, aspiration until proven otherwise
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Physical exam:
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Grunting respirations
Retractions
Tachypnea
Tachycardia
Cyanosis
Odor of hydrocarbons may be present
17
Pulmonary Toxicity
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Temp 39° C or > common
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Auscultation: normal, wheezing, decreased or absent
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ABG: widened A-a gradient or hypoxemia
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Necrotizing pneumonitis and hemorrhagic pulmonary
edema may occur within hours in severe aspiration
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Fatalities occur within 24-48 hours
18
Pulmonary Toxicity
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Most with significant aspiration have abnormal CXRs
– Time course of changes varies
 Correlation with physical examination may be poor
– Changes as early as 30 minutes after aspiration
 Initial radiograph in symptomatic patient may be deceptively clear
– Changes usually by 2-6 hours
 Almost always present by 18-24 hours if they are to occur
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Pulmonary Toxicity
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Infiltrates vary
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Usually dependent lobes
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Multilobar > single-lobe
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R>L
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Radiographic changes limited to bilateral perihilar regions with
clear lung bases are also common
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Mild radiographic changes does not guarantee sympoms
20
CNS Toxicity
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Direct response to systemic absorption of hydrocarbon
 GI, aspiration, dermal
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Indirect result of severe hypoxia 2° to aspiration
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Asphyxiation via:
– Loss of ventilatory drive
– Use of plastic bag or other device during bagging
21
CNS Toxicity

Exposure to volatile hydrocarbons
– Inadvertent vs. deliberate solvent abuse
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Volatile solvent abuse
– Teenagers and younger adults
– Low SES and Native Americans
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Huffers and baggers
– Huffers inhale through rag soaked with the hydrocarbon held to mouth
– Baggers rebreathe into a bag containing the hydrocarbon
 May result in significant hypercarbia and hypoxia
22
CNS Toxicity
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Hydrocarbon affinity for lipid-rich neural tissue, dose-dependant
effect:
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Dizziness
Slurred speech
Ataxia
Lethargy
Obtundation
Coma
Apnea
Exhilaration
Giddiness
Tremor
Agitation
Convulsions
Confusion
Hallucinations
Psychosis
Confused with alcohol intoxication
23
Chronic CNS sequelae

May result from recurrent inhalational exposure
– Common with house painters
– Intentional sniffing
 Solvent abuse
– Toluene
 Leaded gasoline
– Encephalopathy, ataxia, tremor, chorea and myoclonus
– Effects of tetraethyl lead and its toxic metabolites
24
Chronic CNS sequelae
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Other
– Recurrent headaches
– Cerebellar ataxia
– Chronic encephalopathy
 Tremors
 Emotional lability
 Mental status changes
 Cognitive impairment
 Psychomotor impairment
25
Peripheral Nervous System Toxicity
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Peripheral polyneuropathy
– Demyelinization and retrograde axonal degeneration
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Onset of symptoms may be delayed months to years
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Long distal nerves most vulnerable
– Foot and wrist drop
– Numbness and paresthesias
– Similar clinical picture in those who sniff unleaded gasoline
26
Gastrointestinal Toxicity
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Most act as intestinal irritants
– Burning in the mouth and throat
– Abdominal pain
– Belching
– Nausea
– Vomiting
– Diarrhea
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Corrosive GI injury and pancreatitis reported
27
Cardiac Toxicity
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V-tach and V-fib
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Halogenated and aromatic hydrocarbons
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Aliphatics
– Dysrhythmia and sudden death
– Heart sensitized to catecholamines
28
Cardiac Toxicity
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Sudden sniffing death
– Solvent abusers die suddenly after exertion, panic or fright
 Release of catecholamines induces fatal dysrhythmias
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Others deaths
– Asphyxia, respiratory depression, vagal inhibition
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Volatile abuse
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Decreased myocardial contractility
Decreased peripheral vascular resistance
Bradycardia
Atrioventricular conduction blocks
29
Renal and Metabolic Toxicity
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Halogenated hydrocarbons
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Carbon tetrachloride
Trichloroethylene
Chlorinated paraffins
Acute renal failure
Centrilobular hepatic necrosis
– Large ingestions
 Renal excretion of aliphatic hydrocarbons may occur
– Visible hydrocarbon droplets in urine
– Hemorrhagic cystitis reported
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Renal and Metabolic Toxicity
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Toluene Abuse
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Proteinuria
Renal insufficiency
Renal tubular acidosis
Non-anion gap metabolic acidosis
Hypokalemia
Hypophosphatemia
Rhabdomyolysis
High anion gap metabolic acidosis
 Accumulation of hippuric and benzoic acid metabolites
31
Hepatic Toxicity
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Halogenated hydrocarbons
– Carbon tetrachloride
 3 cc may be fatal
 Chronic exposure may result in cirrhosis
– Chloroform and methylene chloride
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Cell destruction via lipid peroxidation from free radicals
Acute fatty degeneration centrilobular necrosis
LFTs elevated 24 hours after ingestion
Development of liver tenderness and jaundice in 48-96 hours
32
Hematologic Toxicity
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Benzene
– Chronic exposure
 Aplastic anemia
– Glue sniffers
 Acute myelogenous leukemia
 Multiple myeloma
– Etiology of blood dyscrasias are the toxic metabolites
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Hematologic Toxicity
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Hemolysis
– Gasoline, kerosene, tetrachloroethylene and mineral spirits
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Consumptive coagulopathy reported
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Delayed methemoglobinemia
– Hydrocarbons with amines (aniline)
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Hemolytic anemia
– Naphthalene
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Hematologic Toxicity
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Methylene chloride exposure
– Endogenous production of carbon monoxide
– Carbon monoxide formation may continue after
cessation of exposure
– Consider CO production if present with CNS and
cardiac symptoms
35
Dermal Toxicity
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Hydrocarbons are irritants and sensitizers:
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Pruritis
Local erythema
Papules
Vessicles
Generalized scarlatiniform eruption
Exfoliative dermatitis
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Huffer’s rash on face in chronic volatile HC abuse
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Defatting dermatitis similar to chronic eczematoid
dermatitis
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Dermal Toxicity
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Frostbite with inhalational abuse of fluorinated agents
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Cellulitis and sterile abscesses with injection
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Partial and full-thickness burns with immersion
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Skin penetration may result in systemic toxicity
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Exposure to heated high-viscosity, long chain aliphatics
– Tar, asphalt or bitumen
– Associated with hyperthermia and difficult decontamination
37
Prehospital Treatment
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Not all ingestions require ED evaluation
– Fewer than 1% require physician intervention
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Asymptomatic after ingestion watched safely at home
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Decision supported when:
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Ingestion is accidental
Known ingredients
Ingredients not significantly systemically toxic when ingested
Reliable follow-up can be ensured
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Prehospital Treatment
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Symptomatic and intentional exposures should
be referred to hospital for further evaluation
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Accidental volatile exposure and abusers need
cardiac monitoring and ALS transport due to
potential of life-threatening dysrhythmias
39
ED Treatment
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ABCs
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Continuous cardiac monitoring
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ECG
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Odor:
– Sweet
 Halogenated hydrocarbons
– Especially chloroform or trichloroethylene
– Petroleum
 Gasoline or other petroleum derivative
40
ED Treatment
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Dysrhythmias
– If present occur shortly after exposure
 Especially with inhalational use
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Hypotension: aggressive fluid resuscitation
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Catecholamines
– Dopamine, norepinephrine or epinephrine
– Avoided to prevent precipitating dysrhythmias
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Glucose, thiamine and naloxone should be considered in cases
of altered mental status
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ED Treatment
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Staff protection
– Gloves, goggles and aprons
– Prevent possible 2° exposure
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Fully undress patient
– Prevents ongoing contamination from hydrocarbon-soaked clothes
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Decontamination
– Pre-hospital preferable
– Skin
 Soap and water
– Eyes
 Saline irrigation
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ED Treatment
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CXR and ABG
– Pulmonary aspiration and hypoxemia
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Abdominal X-ray
– Evidence of chlorinated HC ingestions like CCl4
 Polyhalogenated substances radiopaque
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LFTs and renal function
– Aromatic and halogenated hydrocarbon exposures
– Check for respective organ injury
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ED Treatment
Carboxyhemoglobin
– Extent of endogenous CO production post methylene chloride exposure
Pulse oximetry
– Doesn’t differentiate oxyhemoglobin from carboxyhemoglobin
Routine drug screens
– Not useful for hydrocarbons
All intentional ingestions: assess for coingestants
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Acetaminophen level
EtOH level
Anion gap
Osmolality
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GI Decontamination
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Need depends on type of hydrocarbon and route of exposure
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For most ingestions GI decontamination of little benefit
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Supportive care and treatment for coexisting ingestions
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Risk vs. benefits:
– Systemic toxicity by intestinal absorption
– Risks of aspiration associated with gastric emptying
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GI Decontamination
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Little data as to effectiveness of GI decontamination
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Most aliphatic HC ingestions do not require GI decontamination
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Poor GI absorption
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Toxicity limited primarily to pulmonary aspiration
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Childhood accidental ingestion volume usually a swallow or
about 5 cc
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Suicidal ingestions involve large amounts of HCs and associated
with spontaneous emesis
– Further decontamination not usually required
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GI Decontamination
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Warranted:
– Ingested HC with good GI absorption
– May cause significant systemic toxicity
 Toluene, chloroform, wood distillates
– Additive in the toxic agent
 Organophosphate pesticides often mixed with petroleum
distillates
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GI Decontamination
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CHAMP
– GI decontamination considered
 Camphor, halogenated hydrocarbons, aromatic
hydrocarbons, metals, pesticides
 If presents shortly after ingestion of these hydrocarbons,
aspiration with a small NG tube may be useful
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GI Decontamination
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Altered mental status
– Airway should be protected with a cuffed ET tube
– Especially during lavage
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Ipecac induced emesis contraindicated
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Charcoal not recommended for most hydrocarbon ingestions
– Distends the stomach increasing the risk for vomiting and aspiration
– Only use if a CHAMP hydrocarbon has been ingested
– Extreme caution due to aspiration risk
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GI Decontamination
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Cathartics no proven efficacy in hydrocarbons
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Many already have diarrhea
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Oil based cathartics contraindicated
– Increase GI absorption
– Risk of lipoid pneumonia when aspirated
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Pulmonary Treatment
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Nebulized oxygen helpful
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Inhaled β2 agonists for bronchospasm
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PEEP and CPAP
– Consider barotrauma
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ECMO and high-frequency jet ventilation:
– Severe aspiration resulting in refractory hypoxemia
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Steroids contraindicated
– Impairs cellular immune response
– Increased chance of bacterial superinfection
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Antibiotics
– No proven role except in superimposed bacterial pneumonitis
51
Other
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Few antidotes to counteract actions of HCs
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NAC and hyperbaric O2 may help prevent hepatic toxicity after CCl4 exposure
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Hyperbaric oxygen may be indicated in those with CO toxicity after exposure
to methylene chloride
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β blockers useful for HC induced malignant arrhythmias
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Little evidence for hemodialysis efficacy
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Specific antidotes for complications of toxic additives such as
organophosphates, pyrethrins or heavy metal
52
Tar and Asphalt injury
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Difficult to remove without causing further tissue injury
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Pre-hospital cooling with cold water to limit injury
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Debridement of blistered skin may aid removal of adherent
substances
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De-Solv-It
– Surface active petroleum based solvent
– Non-irritating and effective in removing these agents
– Should only apply briefly
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Others:
– Polyoxyethylene sorbitan-containing ointments
– Petroleum preparations such as neosporin and polysporin may work
53
Tar and Asphalt injury
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May apply all but De-Solv-It under an occlusive
dressing for 24 hours to solubilize the substance so it
may be washed off
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Not necessary to remove all the tar with first visit
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Close follow-up required
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Excision and skin grafting for severe hot tar burns
54
Disposition
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Toxicologist or poison control center consulted
– Symptomatic HC exposures
– Asymptomatic exposures with halogenated, aromatic and
hydrocarbon exposures with toxic additives
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Discharge after 6 hour observation period if:
– Asymptomatic with a normal chest X-ray or with abnormal
chest X-ray if reliable follow-up can be ensured
55
Hospitalization Required
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Aliphatic hydrocarbons and symptomatic at the time of evaluation
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Significant amounts of methemoglobinemia-producing hydrocarbons
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Hydrocarbons capable of producing delayed complications
– Halogenated hydrocarbons causing hepatic toxicity
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Hydrocarbons with toxic additives
– Organophosphates and organic metal compounds
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Suicidal
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Complications of solvent abuse
56
Caustics
57
Epidemiology
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100 K caustic exposures yearly
– Dermal, occular and oral ingestion
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Usually < 6 years old
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Most unintentional
– Suicidal intent results in more severe injury
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In 2000:
– 387 exposures resulted in severe morbidity
– 20 deaths
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Sources: Chemicals in industry
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Acids
– Cleaners
 HCl
 H2SO4
– Etching and metal cleaning
 HF
– Metal Plating
 Chromic acid
– Leather and Textile tanning
 Formic acid
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Alkali
– Cleaning fluids
 NaOH
 KOH
– Concrete
 CaOH
– Photography
 LiOH
– Fertilizer
 Ammonium hydroxide
59
Sources: Household
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Common
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Most less concentrated than industry
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Acids
– Sulfuric acid
 Drain cleaners
 Automobile batteries
– HCl
 Cleaners
– Formic acid
 Airplane glue
– HF
 Rust removers
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Alkali
– NaOH
 Drain cleaners, oven cleaners,
Clinitest tablets
– Sodium Hypochlorite
 Household bleach
 Most common alkali exposure
reported
 Most exposures benign
 3 deaths in 2000
– Ammonium
 Glass, tub and tile cleaners
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Alkali Pathophysiology
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May be deep due to liquefaction necrosis
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Proteins rapidly denatured
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Lipids undergo saponification
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Cellular destruction on contact
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Thrombosis of microvasculature
– Leads to further necrosis
61
Alkali Pathophysiology
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Solid alkali exposure
– Oropharynx and proximal esophagus
 Less distal esophageal injury
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Liquid ingestion
– Esophageal injuries
– Severe intentional ingestion
 May result in multisystem organ injury
– Gastric perforation
– Necrosis of abdominal viscera
– Pancreas, gallbladder and small intestine injury
62
Alkali Pathophysiology
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Household bleach
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3-6% sodium hypochlorite solution
pH of 11
Not corrosive to esophagus
Ingestion may cause emesis
 2° to gastric or pulmonary irritation
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Industrial bleach
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Higher concentrations of sodium hypochlorite
Esophageal necrosis with ingestion
Aspiration pneumonitis
Sight-limiting occular injuries
63
Acid Pathophysiology
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Strong acids produce coagulation necrosis
– Tissue destruction and cell death results in eschar formation
 Protects against deeper injury
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Not esophageal sparing
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May settle in stomach
– Gastric necrosis, perforation and hemorrhage
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Less tissue destruction than alkali
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Higher mortality than alkali ingestion
– May be due to complications of systemic absorption
 Metabolic acidosis
 Hemolysis
 Liver failure
64
Clinical Features
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Severe pain
Odynophagia
Dysphonia
Oral and facial burns
Respiratory distress
Abdominal pain
Drooling
Coughing
Vomiting
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Laryngotracheal injury
– Dysphonia
– Stridor
– Respiratory distress
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Esophageal and GI
injury
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Dysphagia
Odynophagia
Epigastric pain
Vomiting
65
Clinical Features

Conflicting data as to reliability of presence or
absence of signs and symptoms for predicting
upper GI injury
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No single symptom or group of symptoms has
100% positive or negative predictive value for
esophageal injury
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Management: Initial Assessment

ED staff should take precautions to prevent personal
injury 2° to exposure from patient

Initial step is airway evaluation
– May have oral, pharyngeal or larygnotracheal injury
– Ideally should have fiberoptic evaluation prior to intubation
to determine extent of damage
– Blind nasotracheal intubation is contraindicated due to risk
of further injury
67
Airway

Establish airway early
– Avoids 2° effects of injury such as edema

Oral intubation with direct visualization is the
first choice for definitive management

Surgical cricothyrotomy may be required
68
Initial Management

Directed history and physical exam
– Type and amount of caustic ingested
– Intentional or unintentional
– Hemodynamic instability
 Shock from:
– GI bleeding, perforation and volume depletion
– Peritoneal signs
 Hollow viscus perforation
– Chest discomfort
 Mediastinitis
– Eyes and skin for dermal and ocular exposure
69
Laboratory and Ancillary Tests

ABG
– Strong acids may cause acid-base disorders
– Arterial line if serial ABGs required

Electrolytes
– Calcium and magnesium after HF acid exposure

Hepatic profile

CBC
70
Laboratory and Ancillary Tests

Coagulation profile

Upright chest X-ray
– Detects peritoneal and mediastinal air

Intentional ingestion
– ECG, aspirin, acetaminophen for co-ingestions
71
Gastric Decontamination

Charcoal
– Does not bind caustics well
– Impedes visualization

Ipecac
– Do not give
– Vomiting
 Precipitates perforation
 Results in repeated exposure of airway and GI tract to caustic agent

NG tube
– Risks outweigh benefits
 High risk of perforation with alkali ingestion
 Endoscopist may insert with acid ingestion to aspirate residual
72
Neutralization and Dilution

Not recommended
– Should not be done in pre-hospital or ED setting

Risks outweigh benefits
– Risks
 Vomiting, airway injury, perforation
– Benefits
 Not clearly demonstrated in clinical setting
73
Endoscopy

Location and severity of injury post ingestion
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Endoscopist consult for all cases of caustic ingestion
for decision

Endoscopy within first several hours after ingestion

CT or US may be used and may screen for
intraabdominal necrosis outside the GI tract or in
areas not reachable with endoscopy
74
Steroids

Controversial

Might decrease stricture formation post caustic ingestion due to inhibition of
the inflammatory response

Benefit not established in studies

May increase risk of infection, perforation and hemorrhage

Never recommended in acid ingestions

If steroids used, may add penicillin that covers oral flora
– Otherwise, no support for prophylactic antibiotics
75
Systemic Toxicity

Alkali injury
– Direct tissue necrosis

Acid injury
– Absorption of acid in addition to local tissue destruction
– Acid-base disorders, hemolysis and renal failure may result
– Manipulation of pH with sodium bicarbonate may be
required if the pH is below 7.10 due to metabolic acidosis
76
Ocular Exposures

Devastating to vision

30% of corneal transplants for eye injuries due to
chemicals

Alkali worse than acid
– Penetrates deep into ocular tissue
 Destructive after superficial removal
– Acid causes superficial damage of coagulation necrosis
which limits penetration
77
Ocular Exposures

Treat immediately with copious irrigation
– At least 2 L of NS per affected eye
– Nitrazine paper to ensure acid or base has been eliminated
– pH after successful irrigation should be between 7.5-8.0
 Wait 10 minutes post irrigation for most accurate assessment
– Complete eye examination including fluorescein staining and
all except the most superficial exposures should have ED
ophthalmology consultation
78
Treatment of Dermal Exposures

Most injuries occur on the extremities

Most respond well to copious normal saline irrigation

Alkali exposures may appear superficial, but burn
deeply for extended periods
– Need irrigation for long periods
– Need to remove residual compound

For powders such as lime, need to brush off the dry
compound and remove clothes prior to irrigation
79
Treatment of Dermal Exposures

Portland/Ready-mix cement
– Alkali lime mixture
– CaOH, NaOH and KOH produced when water mixed with dry
compound
– May present with severe pain without obvious injury
– Eventually develop blisters and skin necrosis if not irrigated
early

All cutaneous caustic injuries require close follow-up
or early referral to a plastic surgeon to ensure the
injuries are not progressing
80
Surgery, Stents, Dilatation

Major ingestions may result in immediate perforation of the GI
tract and require surgery

Emergency laparotomy
– Peritoneal signs
– Free intraperitoneal air

Esophageal perforation diagnosed by mediastinal air on plain
films or endoscopy

Some require dilation or stenting within first three weeks post
injury vs. early surgical resection
81
Disposition

All patients with symptoms post ingestions
should be admitted

Mild to moderate dermal exposures may be
irrigated, aseptic dressings applied and
discharge with close follow-up
82
Disposition

Admit:
– Dermal injuries:
 Cross flexor or extensor surfaces
 Facial injuries
 Perineal injuries
 Partial thickness injuries greater than 10-15 % BSA
 All full thickness injuries
 Less severe injuries at extremes of age
83
Hydrofluoric Acid

Relatively weak

Glass etching, metal cleaning and petroleum
processing, chrome wheel cleaner, rust remover

Great potential for causing morbidity and death
84
Hydrofluoric Acid

Free Fl ion complexes with calcium and
magnesium resulting in cellular death
– Hypocalcemia, hypomagnesemia, hyperkalemia,
acidosis and ventricular dysrhythmias
– Ventricular fibrillation and death reported with
dermal exposure of only 2.5 % of body surface area
85
Hydrofluoric Acid

Most injuries to upper extremities
– Benign appearance
– Severe pain
– Slight white discoloration, may become black and
necrotic with cellular death progression
86
Hydrofluoric Acid: Treatment

Thoroughly irrigate with water

Next, place in a paste of calcium gluconate or
benzalkonium chloride solution
– Soaked until pain relief for end point of therapy

Other
– Intradermal injection of 5% Ca gluconate or Mg sulfate
around area
– For distal upper extremity injuries, IV calcium gluconate
87
Hydrofluoric Acid: Treatment

Oral ingestion has high mortality rate
– NG tube and NS gastric lavage recommended
– Oral magnesium or calcium should be given
– Hemodynamic monitoring for dysrhythmias
– Follow calcium and magnesium levels closely
 May require large dose supplementation of Ca or Mg
88
Airbag-Related Burns

Aerosolized NaOH and Na carbonate released with
airbag deployment

Burns skin
– Usually minor due to chemical or heat from melted clothing
– Requires basic burn care

Enters eyes with resulting chemical keratitis
– Copious irrigation, pH testing, ophthalmology consult
89
Long Term Morbidity

Most long-term sequelae are from injuries to GI tract

Acid scars the pylorus with resulting gastric outlet obstruction

Alkali may result in esophageal strictures
– Resulting dysphagia, odynophagia and malnutrition

Caustic esophageal injuries at risk for cancer
– 1000 X risk with ingestion
– Seen decades after initial ingestion
– May need prophylactic esophagectomy with grade 3 lesions
90
Questions

1. Toxic potential of hydrocarbons depends on:
A.
 B.
 C.
 D.
 E.

Physical characteristics
Chemical characteristics
Presence of toxic additives
Route of exposure
All of the above
91
Questions

2. Treatment of caustic exposures with steroids is
controversial because:

A. Benefit is not established in studies
B. May increase risk of infection, perforation and
hemorrhage
C. Never recommended in acid ingestions.
D. If steroids used add penicillin to cover oral flora
E. All of the above




92
Questions

3. The CHAMP pneumonic refers to when GI
decontamination is considered with exposure
to:
A.
 B.
 C.
 D.
 E.
 F.

Camphor
Halogenated hydrocarbons
Aromatic hydrocarbons
Metals
Pesticides
All of the above
93
Questions

4. With caustic exposures, you should admit all
patients with dermal injuries that:
A.
 B.
 C.
 D.
 E.

Cross flexor or extensor surfaces
Involve the face
Involve the perineal area
Are full thickness injuries
All of the above
94
Questions

5. With hydrofluoric acid exposure, which of the
following may occur?


A.
B.
C.
D.
E.

1-5: all of the above



Hypocalcemia
Hypomagnesemia
Hyperkalemia
Acidosis
All of the above
95