HYDROCARBONS AND VOLATILE SUBSTANCES

1. HYDROCARBONS AND VOLATILESUBSTANCES

2. Hydrocarbons are a diverse group of organic compounds consisting primarily of carbon and hydrogen atoms arranged in various aliphatic and aromatic configurations. • Products containing hydrocarbons are found in many household and occupational settings: fuels, lighter fluids, lamp oil, paints, paint removers, pesticides, medications,cleaning and polishing agents, spot removers, degreasers, lubricants,and solvents. • Hydrocarbon and volatile substance exposure may cause life-threatening toxicity and, in some cases, sudden death. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.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 Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

4. Epidemiology • Exposures to hydrocarbons and volatiles most commonly occur in one of two settings: # Ingestion #Inhalation. • 3.5 to 10 percent of young people have experimented with volatile substance inhalation to produce inebriation • The most commonly implicated volatiles were: butane (39 percent), aerosols (26 percent), cleaners (16 percent), glue (10 percent). Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

5. 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 risk for than are those ingesting substances with viscosities greater than 100 SUS (e.g., diesel oil, grease, mineral oil, paraffin wax, and petroleum jelly) Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

6. Low surface tension also increases the riskof aspiration. • Volatility:denotes the ability of a substance to vaporize. • A compound with high volatilityevaporates easily and usually has lowviscosity and low surface tension. • Inhalation of volatile agents, )such asaromatic hydrocarbons, halogenated hydrocarbons, or gasoline(, resultsin systemic absorption and the potential for significant toxicity. • Dermal exposure to 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). Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

7. Characteristic presentations usually affect one or more of thefollowing systems: pulmonary, Neurologic :central peripheral, GI, Cardiac, Hepatic, Renal, Hematologic, Dermal. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

8. Pulmonary Toxcity • Pulmonary complications, especially aspiration, are the most frequent adverse 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 ofaromatic or halogenated hydrocarbons 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. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

9. The risk and degree of aspiration is not dependent on volume ingested. ( 0.2 mL instilled intratracheally has caused pneumonitis.) • Pulmonary toxicitydoes not result from GI absorption but occurs from direct aspiration of the hydrocarbon into the pulmonary tree. • There is no evidence that hydrocarbons reflux from the stomach into the airway. • Spontaneous vomiting, however, does increase the risk of aspiration.‘ • Pulmonary toxicity manifested as: acute bilateral pneumonitis ( from the inhalation of an aerosolized aliphatic hydrocarbon such as gasoline) Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

10. 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. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

11. CNS manifestations seen after ingestion of a poorly GI-absorbed aliphatic hydrocarbon are thought to be from : hypoxia secondary to the hydrocarbon induced pneumonitis and/or direct CNS toxicity following the pulmonary absorption • 19 percent had clinical or radiographic evidence of pulmonary aspiration. • 35 percent have initial symptoms, • only 3 percent have progressive pulmonary symptoms' Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

12. The clinical manifestations of pulmonary aspiration are usually apparent almost immediately on ingestion. • The early effects result from irritation of the oral mucosa and tracheobronchial tree. Symptoms : • coughing, • choking, • gasping, • dyspnea, • burning of the mouth. Patients with these symptoms should be assumed to have aspirated until proven otherwise. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

13. 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 39°C (I 02.2°F) or greater is common ( may occur upon initial presentation or be delayed 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. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

14. The development of a necrotizing pneumonitis and hemorrhagic pulmonary edema usually occurs within hours in severe aspiration. • Most fatalities from these complications occur within 24 to 48 h. • With less-severe damage, symptoms usually subside within 2 to 5 days • pneumatoceles and lipoid, pneumonias whose symptoms may persist for weeks to months. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

15. most patients with clinically significant aspiration have 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, but the initial radiograph in the symptomatic patient may be deceptively clear. • Radiographic changes usually appear by 2 to 6 h and are almost always present by18 to 24 h, if they are to occur. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

16. Radiographic changes limited to bilateral perihilar regions with 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-lobe involvement Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

17. 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. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

18. 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 also contribute to toxicity by producing significant hypercarbia and hypoxia. • They behave similarly to the inhalational anesthetic agents. • Hydrocarbon intoxication may be confused with ethanol inebriation. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

19. CNS depression ranges 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 features include: • tremor, • agitation, • convulsions. • Perceptual changes, such as confusion, hallucinations, and psychosis, may occur. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

20. 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 is associated with the habitual sniffing of leaded gasoline. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

21. Peripheral Nervous System Toxicity • Exposure to aliphatic hydrocarbons is associated with the development of a characteristic peripheral polyneuropathy caused by demyelinization and retrograde axonal degeneration. • Onset of symptoms may be delayed for months to years after initial exposure. • Toxicity is attributed to a metabolite, 2,5-hexanedione, produced by the cytochrome P450-mediated biotransformation of the parent compounds. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

22. Long, distal nerves seem to be most vulnerable, characteristically producing foot and wrist drop with numbness and paresthesias. • Unleaded gasoline sniffing has produced a similar clinical picture as well. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

23. 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 the patients with aliphatic hydrocarbon ingestions, is particularly trouble some because of the increased risk of pulmonary aspiration. • Corrosive GI injury, as well as pancreatitis, has been reported with ingestion of some chlorinated hydrocarbons. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

24. Cardiac Toxicity • Life-threatening dysrhythmias, such as ventricular tachycardia and ventricular fibrillation, sudden Death may occur with systemic absorption (gastrointestinal or inhalational) of a variety of hydrocarbon compounds. • Most commonly, dysrhythmias occur after exposure to halogenated 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.) Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

25. The use of exogenous catecholamines, such as epinephrine, may precipitate sudden dysrhythmias and should be avoided except if required for cardiac resuscitation. • Decreases in myocardial contractility and peripheral vascular resistance as well as bradycardia and atrioventricularconduction blocks have also been associated with volatile solvent abuse. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

26. Hepatic Toxicity • Halogenated hydrocarbons is well described. • Carbon tetrachloride toxicity 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.“ • Chloroform and methylene chloride, are also associated with liver dysfunction. (Free-radical metabolites) • Pathologic examination reveals acute fatty degeneration of the liver with areas of centrilobular necrosis. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

27. Liver function tests may be elevated within 24 h after ingestion,with the development of liver tenderness and jaundice in 48 to 96 h. • Chronic exposure to carbon tetrachloride may be associated with the development of cirrhosis and hepatomas. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

28. 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, and chlorinated paraffins, have caused acute renal failure, • Renal tubular acidosis may occur in patients who abuse toluene containing substances.(Patients present with a non-anion gap metabolicacidosis,hypokalemia, and hypophosphatemia.) • Significant rhabdomyolysis may also result. • Toluene toxicity may also cause a high anion gapmetabolic acidosis as a result of the accumulation of hippuric acid and benzoic acid metabolites. • Proteinuria and renal insufficiency can occur in patients who abuse toluene. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

29. Hematologic Toxicity • Chronic exposure to benzene, the prototypical aromatic hydrocarbon,is associated with an increased incidence of hematologic disorders including aplastic anemia, acute myelogenous leukemia, and multiple myeloma. • Although aplastic anemia is associated with glue sniffing, this is most likely a result of the benzene fraction of the glue, and not the toluene. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

30. 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 eruption and an exfoliative dermatitis. • A "huffer's rash" may be noted over the face of patients who chronically abuse the volatile hydrocarbons. • Pruritus may also be present. • Extensive partial-thickness and full-thickness bums following immersion in hydrocarbons may also occur. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

31. TREATMENT Prehospital • Not all patients who have ingested hydrocarbons require emergency department evaluation. • patients who are asymptomatic or who quickly become asymptomatic after ingestion can be watched safely at home. (reliable follow-up can be ensured.) Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

32. All symptomatic patients and intentional exposuresshould be referred to the hospital for further evaluation. • Patients who ingest hydrocarbons that may cause significant systemic toxicity (e.g., aromatic, halogenated hydrocarbons, or toxic additives), whether or not symptomatic, should also be referred to the hospital. • Volatile substance abusers and others exposed to volatiles should have immediate cardiac monitoring and advanced life support transport, if available,because of the potential for life-threatening dysrhythmias. • All symptomatic patients and intentional exposuresshould be referred to the hospital for further evaluation. • Patients who ingest hydrocarbons that may cause significant systemic toxicity (e.g., aromatic, halogenated hydrocarbons, or toxic additives), whether or not symptomatic, should also be referred to the hospital. • Volatile substance abusers and others exposed to volatiles should have immediate cardiac monitoring and advanced life support transport, if available,because of the potential for life-threatening dysrhythmias. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

33. Emergency Department • Establishing the airway and maintaining ventilation is the critical first maneuver in any patient who presents with respiratory depression and/or significant 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 monitoring should be initiated, and an electrocardiogram should be obtained. • Hydrocarbon induced dysrhythmias, if present, would generally occur shortly after the exposure, especially with inhalational use Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

34. Hypotension should be treated with aggressive fluid resuscitation. Catecholamines, such as dopamine, norepinephrine, or epinephrine, should be avoided to prevent precipitating dysrhythmias, especially following exposure to halogenated hydrocarbons and aromatic hydrocarbons. • The administration of glucose, thiamine, and naloxone should be considered in cases of altered mental status • The patient needs to be fully undressed to prevent ongoing contamination from hydrocarbon-soaked clothes. • Dermal decontamination with soap and water, • eye decontamination with saline irrigation,should be performed. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

35. Prehospital decontamination is preferable. • It is important for staff to wear protective gloves and aprons to prevent possible secondary exposure, especially for organophosphate containing mixtures. • Useful diagnostic tests include the chest x-ray and arterial blood gas to detect pulmonary aspiration and hypoxemia. • Abdominal radiographs may show evidence of chlorinated hydrocarbon ingestions,such as carbon tetrachloride, because ofthe radiopaque nature of these polyhalogenated substances • Tests of liver and renal function should be obtained for the development of hepatic and renal injury. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

36. A carboxyhemoglobin level is useful to evaluate the extent of endogenous carbon monoxide production following methylene chloride exposure. • Pulse oximetry will not differentiate between oxyhemoglobin and carboxyhemoglobin. • Routine drug screens are not useful for the detection of hydrocarbons, • In all intentional ingestions, an acetaminophen level, ethanol level, anion gap, and osmolality may be helpful in assessing for the presence of other coingestants. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

37. Gastrointestinal Decontamination • For most hydrocarbon ingestions, gastrointestinal decontamination would provide little benefit; • The necessity for GI decontamination depends on the type of hydrocarbon and route of exposure. • supportive care and appropriate treatment of coexisting ingestions are all that is required. • The majority of hydrocarbon ingestions, which consist of aliphatic hydrocarbons mixtures do not require GI decontamination. • Gl decontamination may be warranted when the ingested hydrocarbon is known to have good Gl absorption and may cause significant systemic toxicity (e.g., toluene, chloroform, wood distillates)or an additive in the toxic agent (e.g., organophosphate pesticidesare often mixed in petroleum distillates). Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

38. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

39. If the patient presents to the ED shortly after the ingestion of these toxic hydrocarbons, aspiration with a small nasogastric tube may be useful. • In patients who present with an altered mental status, the airway should be protected with a cuffed endotracheal tube, • In smaller children younger than 8 years of age, the cuff should be kept inflated only during the period of lavage because of cuff-related injury from prolonged inflation. • Ipecac induced Emesis is contraindicated • Although activated charcoal may adsorb somehydrocarbon compounds, its use is not recommended for most hydrocarbon ingestions Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

40. Charcoal instillation may distend the stomachincreasing the risk for vomiting and aspiration. • The use of charcoal should only be considered if one of the CHAMP-type hydrocarbons has been ingested, and extreme caution should be exercised because of aspiration risk. • Many patients will already have diarrhea from the hydrocarbon, and further catharsis is not required. • Oil-based cathartics, which had been used in the past to thicken the ingested hydrocarbon to increase its viscosity and decrease the subsequent risk of aspiration, are contraindicated. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

41. Pulmonary Treatment • Nebulized oxygen is helpful in the treatment of pulmonary aspiration. • Inhaled B-agonists may also be useful, especially in the setting of bronchospasm,( 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 be required, but because of the potential for further injury from barotrauma,one should observe for the development of pneumatoceles or pneumothorax. • In cases of severe pulmonary aspiration resulting in refractory hypoxemia, treatment with extracorporeal membrane oxygenation and high-frequency jet ventilation has proved successful. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

42. Corticosteroids are contraindicated because they impair the cellular immune response and increase the chance of bacterial superinfection remains. • Antibiotics have no proven role in prophylaxis and are usually not required except in cases of continued pulmonary deterioration because of the risk of a superimposed bacterial pneumonitis. • Nacetyl cysteine and hyperbaric oxygen may have a role in preventing hepatic toxicity after carbon tetrachloride (and possibly chloroform)exposure, but more studies are needed. • Hyperbaric oxygen therapy may be indicated for patients who develop significant carbon monoxide toxicity after exposure to methylene chloride, Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

43. B-blockers may be useful in the treatment of hydrocarboninduced malignant dysrhythmias. • Although extracorporeal removal with hemodialysis, hemoperfusion, or peritoneal dialysis has been attempted for severe intoxications, clinically controlled evidence of efficacy is lacking. • Specific antidotal treatment directed at the complications of toxic additives, such as organophosphates, pyrethrins or heavy metals, may also be needed. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

44. DISPOSITION • Hospitalization is required for patients who have ingested aliphatic hydrocarbons who are symptomatic at the time of evaluation, and patients exposed to significant amounts of methemoglobinemia-producing hydrocarbons. • After a 6-h observation period, asymptomatic patients with a normal chest x-ray may be discharged home, but follow up should be assured as delayed toxicity (18+ h) has been reported. • Similar disposition of asymptomatic patients, with abnormal chest x-rays has also been suggested if reliable follow-up can be ensured. Some physicians, however, prefer to observe these patients for 24 h in the hospital. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

45. Hospitalization is recommended for those who ingest hydrocarbons capable of producing delayed complications (e.g., halogenated hydrocarbons causing 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 abuse should have psychiatric evaluation. Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.

46. شاد باشید Dr.A.AMINI ; ASSISSTANT PROFESSOR OF E.M.