TOXICOLOGY: HYDROCARBONS, CORROSIVES, GLYCOLS, …
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 children40 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 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. 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
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