TOXICOLOGY: HYDROCARBONS, CORROSIVES, GLYCOLS, AND ALCOHOLS
Hydrocarbons: organic cmpds made of hydrogen and carbon
Background
-- 4 basic types: aliphatic, halogenated, aromatic, and terpenes
-- 67,000 hydrocarbon exposures in 1996; 23% req’d tx; 40% in children<6
Aliphatic
-- Straight chain cmpds produced from the fractional distillation of petroleum
-- Most common hydrocarbon poisoning
-- Majority of deaths are from inhalational abuse
-- Elimination mainly by pulm excretion and cyt P-450 metabolism
-- Major organs affected: lungs, CNS, GI
-- Pulmonary findings: major toxicity comes from aspiration
-- Potential for aspiration is determined by viscosity (most
impt), surface tension, and volatility
-- Low viscosity (<60 SSU) has incr risk of aspiration; high
viscosity (>100 SSU) has lower risk; more localized dz
-- Decreased surface tension incr aspiration risk
-- High volatility increases risk of pulm absorption
-- Upon aspiration: surfactant disrupted leading to alveolar
collapse, V/Q mismatching, bronchospasm, capillary damage
(hemorrhagic alveolitis), tissue necrosis, etc
-- Clinical features: after ingestion, can have burning sensation
in mouth, coughing, and gagging  may or may not have
vomiting  tachypnea (best early indicator of aspiration) and
resp distress; early cyanosis can develop from displacement of
alveolar gas by hydrocarbon gas
-- CXR findings (bilat basilar infiltrates, perihilar densities,
etc) correlate poorly with clinical sx
-- Resp sx should begin within the first 6 hours; may get fever
within 30 minutes of exposure
-- Most pts pulm dz recovering by 3rd to 8th day
-- CNS findings
--Usually sec to hypoxia and acidosis
-- These agents are highly lipid soluble; inhalational agents
are rapidly absorbed through the lungs and distribute within
the CNS and fatty tissues
-- Transient depression or excitation, lethargy, seizures,
coma
-- GI findings
-- Poorly absorbed by the GI system so sx are from local
irritation
-- N/V, abd pain, diarrhea, incr LFT’s (assoc with hepatic
damage from vapor inhalation)
-- Other findings
-- CV – arrhythmogenic sec to potentiation of endogenous
catecholamines
-- Dermal – pigment changes, local skin irritation, etc
-- Renal – ATN (rare), hemoglobinuria (sec to hemolysis)
-- Diagnosis- history (including hydrocarbons as carriers)
-- Labs: ABG, CXR, elytes, CBC, LFT’s, UA
-- Management:
-- Gastric decontamination NOT recommended unless airway
protected; charcoal only if toxic additive present
-- Supportive care
-- Selective bronchodilators
-- Abx if febrile or symptomatic >40 hours or documented
infxn
-- Long term px: no major sequelae (minor PFT changes)
-- Halogenated
-- Class of aliphatic and aromatic hydrocarbons that contain halogen
-- Account for 13% of hydrocarbon exposures
-- Well absorbed from GI tract, lungs, and skin
-- Metabolized by liver and kidney and excreted by lungs and kidneys
-- Carbon tetrachloride – seen in solvents and aerosol propellants
-- Main manifestations include CNS (drowsiness, lethargy),
hepatic (incr LFT’s on day#2), renal dysfx, cardiac
dysrhythmias
-- Diagnosis: history and radiographs
-- Treatment: supportive, gastric decontamination, wash skin;
+/- hyper baric O2, NAC
-- Prognosis: excellent if no renal or hepatic failure after 5
days
-- Methylene chloride – seen in degreasers and paint removers
-- Absorbed in GI tract and lungs
-- Main toxicity is to CNS (directly and secondary to incr
carboxyhgb levels)
-- Treatment: supportive, hyperbaric O2
-- Trichloroethane
-- Seen in hairsprays, furniture polishes, correction fluid, etc
-- Rapidly absorbed thru lungs and GI tract
-- Main toxicity on CNS and on CV system (assoc with
PVC’s, and ST depression)
-- Diagnosis: history
-- Treatment: supportive, decontamination
-- Aromatic
-- Contain one or more benzene rings
-- Seen in glues, paints, etc
-- Exposure mainly via inhalation
-- Toluene- colorless, volatile, sweet smelling; seen in model glue
-- Highly lipid soluble; metabolized by cyt P-450
-- Affects CNS (excitation, euphoria, then depression),
peripheral neuropathy, renal dysfx (chronic use leads to
tubulointerstitial damage that is reversible), hypokalemia and
hypocalcemia, acidosis, sudden cardiorespiratory arrest
(cardiac sensitization)
-- Diagnosis: history, chemistries, ABG, UA
-- Treatment: supportive; gastric decontamination
-- Terpines
-- Aliphatic cyclic hydrocarbons; seen in turpentine, pine oil, etc
-- Lower risk of aspiration because of low volatility
-- Lethal dose = 2 cc/kg
-- Well absorbed thru GI tract; distributes throughout entire body; excreted
thru kidney
-- Symptoms mainly related to GI and CNS; systemic toxicity will appear
within 3 hours of exposure
-- Diagnosis: history
-- Treatment: supportive, gastric decontamination if within 2 hours, pt is
alert, and large amount ingested
Alcohols and Glycols
-- Ethanol
-- Aliphatic alcohol; diffuses into all body tissues; rapidly absorbed via GI
tract
-- May affect multiple ion channels by influencing their structure
-- Potentiates GABA receptor
-- Metabolism occurs in the liver via 3 pathways by zero-order kinetics
(fig130-1)
-- Clinical presentation
-- CNS – depression of RAS, ataxia, disconjugate gaze (in
comatose pts), anaesthetic, etc
-- Pulmonary – aspiration risk
-- Hypoglycemia – children <10 yo and poorly nourished are most
susceptible; can cause seizures
-- In pts with impaired glycogen stores, ETOH impairs
gluconeogenesis by incr NADH:NAD+ ratio and shunting
pyruvate to lactate instead of leading to gluconeogenesis
-- Ketoacidosis – usu only occurs when ETOH levels low (fig.
130-2)
-- Arrhythmias (atrial fib and AV block) in pts with preexisting dz
-- Diagnosis: BAC, elytes, LFT’s, osmoles (if cannot get BAC), ECG
-- Management: supportive, protect airway, treat hypoglycemia, ketoacidosis
can be treated with glucose, thiamine (allows pyruvate into CAC), and
hydration, while watching phosphorous levels; gastric lavage indicated if
ingestion within 2 hours and >1g/kg or those who are comatose or seizing;
charcoal does not efficiently help; may do hemodialysis
Methanol
-- Seen in cleaning soln’s, sterno, antifreeze, gasoline, etc
-- Absorbed orally, dermally, and through resp tract; has large volume of
distribution
-- Elimination follows first-order mechanics at low doses; zero at high doses
-- Minimal lethal dose unknown; toxicity comes from its metabolites (fig
130-5)
-- Clinical symptoms: there is a latent period before toxicity develops
-- CNS – mania, lethargy coma, seizures,
-- GI – pancreatitis, N/V, hemorrhagic gastritis
-- Acidosis – formic acid inhibits mitochondrial cyt oxidase
lactic acidosis
-- Ophthomlogical – cyt oxidase inhibition leads to disruption of electron
transport and decr electrical conduction in the optic nerve
-- Diagnosis: history, methanol levels (if early), formic acid levels if later,
osmoles, elytes, etc
-- Treatment: supportive, lavage if early, bicarb for acidosis, folate
(necessary for metabolism of formate)
-- ETOH therapy – for peak methanol levels >20mg/dl, intake >0.4
ml/kg or 30cc, acidosis, or abnormalities of vision
-- 10% ETOH in D5W -- loading dose of 0.6cc/kg over
~30 minutes and infusion at ~1cc/kg/hr to get a level of 100
mg/dl
-- Hemodialysis for peak methanol level >50mg/dl, unremitting
acidosis, visual disturbances or renal failure
-- Fomepizole – inhibits alcohol dehydrogenase
Ethylene glycol
-- Colorless, odorless, sweet liquid found in antifreezes, detergents, paints, etc
-- Metabolites, specifically glycolic acid, are toxic (fig130-4)
-- Clinical presentation divided into 3 stages
1) 30 min-12 hours  ETOH-like CNS sx (lethargy, seizures, etc)
2) 12-24 hours CV and pulmonary effects
3) 48-72 hours renal failure, hypocalcemia, and acidosis
-- Diagnosis: blood levels, elytes, ECG, osmoles (if used early and
cautiously), ABG (will show anion gap acidosis later), UA (for crystals)
-- Treatment: same as for methanol; pyridoxine and thiamine convert
glycoxylic acid to nonoxalate cmpds
Propylene Glycol
-- Used as a solvent and as a diluent in IV meds including lorazepam,
phenytoin, procainamide, nitroglycerine, theophylline, sulfadiazene creams
-- Oral and dermal absorption poor, unless thru abraded/burned skin
-- ½ undergoes hepatic oxidation via alcohol dehydrogenase; ½ excreted
unchanged in urine
-- Clinical symptoms:
-- Rapid IV loads can cause prolonged PR and QRS duration,
cardioresp depression and arrest
-- Hyperosmolarity, hypoglycemia, lactic acidosis, seizures
-- Diagnosis: history, osmolar gap
-- Therapy: supportive, GI decontamination with lavage and charcoal, stop
infusion
Corrosives
-- Responsible for 2.5% of all deaths due to poisonings
-- Liquid lye drain cleaners responsible for most GI injuries but acidic toilet
bowl cleaners are responsible for most deaths
-- Cmpds, acids or bases, that cause tissue injury as a result of a chemical
reaction—they react with organic molecules and disrupt cell membranes
-- Can also cause thermal burns if heat is generated during this reaction
-- Pathophysiology
-- Alkali cause liquefaction necrosis and heat production by
breaking down proteins and cellular membranes  results in tissue
necrosis and thrombosis of small vessels  allows for further
penetration of the substance
-- Injury can progress over several hours
-- Days later can then have bacterial infxn and
inflammation
-- Collagen deposition ~2 weeks later strictures
-- Acids cause coagulation necrosis with eschar formation after
proteins are denatured
-- Titratable reserve (amt of acid or base needed to neutralize the pH) better
indicator of corrosive potential than pH
-- Clinical symptoms: mainly involve eyes, dermis, GI tract
-- Eyes – conjunctival hemorrhages, chemosis, corneal erosion,
incr intraocular pressure, etc.
-- Severity assessed by extent of vessel obliteration
-- Dermis – assessing level of burn difficult because chemical
burns rarely blister and affected skin will be discolored and will
not slough; healing takes longer than for thermal burns
-- GI -- can cause injury from mouth to jejunum; mostly in areas
of narrowing
-- Alkali assoc with worse esophageal lesions while acids
usu cause more stomach injury
-- Common sx: oropharyngeal pain, dysphagia, abd pain
-- Vomiting, drooling, stridor predictive of severe injury
-- Superficial burns (with membrane) heal without
complications
-- Full thickness burns assoc with perforation and fistula
formation  perforation can lead to
mediastinitis/peritonitis
-- 70% of burns with deep ulceration will lead to
esophageal stricture as early as 1 week later; strictures also
assoc with reflux
-- Alkali burns assoc with esophageal cancer
-- Airway
-- Burns to the trachea seen in 50% of pts with significant
exposure; edematous epiglottis and aryepiglottic folds
-- Systemic
-- Can be associated with acidosis and CV collapse (HCL),
hypocalcemia (phosphoric acid), pulm edema, liver dysfx,
coma (ammonia), hemolysis and cardioresp arrest (bleach)
-- Management
-- Medical staff should wear protective clothing
-- Resuscitation and decontamination take priority
-- Eye exposure
-- Irrigation; persistent pain indicates significant injury and
requires pH assessment, slit lamp eval, acuity check
-- Topical abx, steroids, eye patching
-- Dermal exposure
-- Removal of agent; irrigation unless substance reacts with
water like aluminum salt
--Assessment of location, size, color, neurovascular status
similar to thermal burns
-- Assessment of systemic toxicity
-- GI tract exposure
-- Assessment of airway and oropharynx; radiographs
-- Dilution with water or milk; can use NG if careful
-- Flexible endoscopy between 6-24 hours after exposure in
symptomatic pts or those with visible burns in mouth
-- Most impt findings are depth of ulceration and presence
of necrosis
-- +/- steroids with abx in those with alkali burns
--H2- blockers, analgesia
-- +/- stents to prevent strictures