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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