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Chapter: Modern Medical Toxicology: Hydrocarbons and Pesticides: Hydrocarbon

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Aliphatic Hydrocarbons

Ingestion of aliphatic hydocarbons with high molecular weight such as paraffin wax, vaseline, grease, etc. is associated with little or no toxicity.

ALIPHATIC HYDROCARBONS

Uses

Listed in Table 27.1.


Mode of Action

■■   Ingestion of aliphatic hydocarbons with high molecular weight such as paraffin wax, vaseline, grease, etc. is associated with little or no toxicity.

■■   Liquid hydrocarbons are the most toxic, but symptoms gener-ally are the result of aspiration into the airways rather than absorption from the GI tract.

■■   The aspiration potential of a hydrocarbon depends on properties—viscocity, surface tension, and volatility. Viscocity is the tendency of a substance to resist flow (“the ability to resist stirring”) which is measured in Saybolt Seconds Universal (SSU). The lower the viscocity (i.e. below 60 SSU), the higher the tendency for aspira-tion. Surface tension refers to the adherence of a liquid compound along its surface (“the ability to creep”). It is the result of cohesive forces generated by the attraction between molecules (van der Waals forces). The lower the surface tension, the higher the tendency for aspira-tion. Volatility refers to the ability of a liquid to become a gas. The higher the volatility, the higher the tendency for aspiration.

■■  Aliphatic hydrocarbons possessing high aspiration potentialinclude gasoline, kerosene, mineral seal oil, and turpentine.

Clinical Features

RS: Respiratory distress from aspiration usually begins within 30 minutes of exposure, and is manifested mainly by gasping, coughing, and choking. There are 3 grades:

·              Mild : coughing, choking, tachypnoea, drowsiness,rales, rhonchi.

·              Moderate : grunting, lethargy, flaccidity, bronchospasm.

·              Severe : cyanosis, coma, seizures.

Moderate fever is often present but does not correlate with severity. Haemoptysis and pulmonary oedema may occur after significant aspiration or inhalation.

CNS: Lethargy with depressed sensorium. Coma and convulsions are rare. Aniline, heavy metals, camphor, pesti-cides and other additives or contaminants in hydrocarbon preparations may produce additional CNS toxicity. For instance, chronic cerebellar degeneration may be associated with lead additives of gasoline.

GIT: Burning of mouth, sore throat, nausea, and vomiting. Haematemesis may occur. Diarrhoea is rare.

CVS: Arrhythmias are seen in solvent abuse, but are rare in ingestions.

Skin: Acute exposure can cause dermatitis, and if this is prolonged it may result in full thickness burns. Chronic exposure to kerosene can cause severe acne. Contact with liquefied petroleum gases (e.g. propane, butane, propylene, isobutane, butenes, n-butane), ethane, etc. can result in frostbite or effects resembling frostbite.

Haematologic: Disseminated intravascular coagulation, haemolytic anaemia and pancytopenia have occasionally been reported following vapour inhalation, aspiration, or ingestion of hydrocarbons.

Other effects:

·              Elevated liver enzyme levels and hepatosplenomegaly can occur with petroleum distillate ingestion.

·              Renal effects (acute renal tubular necrosis, proteinuria, or haematuria) occur infrequently following acute expo-sure to petroleum distillates and other unsubstituted hydrocarbons.

·              Straight chain hydrocarbons with few carbon atoms (e.g. methane, ethane, propane gases) can cause asphyxiation if exposure occurs in poorly ventilated spaces.

·              Injection of kerosene, naphtha, turpentine, gasoline, or hydrocarbon insecticides has resulted in febrile reac-tions, local tissue inflammation and systemic effects, including pulmonary oedema, pneumonia and mild CNS depression. Injection of pressurised hydrocarbons has caused severe tissue damage. Subcutaneous injec-tion of paint, lacquer or other material via high pres-sure spray guns is a surgical emergency. High-pressure injection injuries can result in necrosis and thrombosis with amputation required in 60 to 80% of cases.

·              Exposure to hydrocarbons may result in the loss of colour vision, with the risk of impaired colour vision increasing with increasing exposure.

·              Poisoning due to inhalation of butane and other similar gaseous hydrocarbons is dealt with under “Glue sniffing”.

Diagnosis

·      X-Ray—Changes may be evident as early as 30 minutes after exposure and peak at about 72 hours, after which there is gradual resolution. Common radiologic findings include perihilar densities, bronchovascular markings, bibasilar infiltrates, and pneumonic consolidation. Early upright

·              X-rays may reveal two liquid densities in the stomach (double bubble sign) (Fig 27.1), which represents two interfaces: air-hydrocarbon, and hydrocarbon-fluid, since hydrocarbons are not miscible with water and are usually lighter. Two important points are to be noted in connection with radiographic changes in hydrocarbon ingestion—


o     They correlate poorly with clinical symptoms.

o     They lag behind clinical improvement.

·      Arterial blood gases—There is hypoxaemia.

·              Blood—Leucocytosis is common during the first 48 hours.

Treatment

·      The following signs and symptoms present upon initial examination of patients after hydrocarbon ingestion have 80% or better predictive value for pneumonitis:

o     Lethargy, rhonchi, rales, retractions, cyanosis, and the development of leukocytosis and fever within 4 hours.

o     The only parameter with an 80% or greater predictive value for NO toxicity was the absence of tachypnoea.

o     Early chest X-rays were not useful in predicting pneu-monitis in symptomatic or asymptomatic patients.

·      The immediate concern is the threat of respiratory failure. A chest X-ray should be taken after stabilisation to confirm or rule out aspiration. The following measures are necessary if respiration is compromised:

o     Endotracheal intubation.

o     Oxygen.

o     Continuous positive airway pressure or positive end-expiratory pressure. A recent innovation is high frequency jet ventilation (HFJV), utilising high respiratory rates (220 to 260) with small tidal volumes. Extracorporeal membrane oxygenaion (ECMO) is an effective option in severe pulmonary toxicity when all other meaures have failed.

o     Bronchodilators—preferably inhaled cardioselective drugs such as salbutamol.

·      Decontamination:

o     If there is suspicion of dermal exposure, all clothing should be removed and the skin washed with copious amounts of soap and water, since significant toxicity can result from cutaneous absorption.

o     Induction of vomiting is not recommended.

o     Stomach wash may be done cautiously after intuba-tion, especially in those cases where a large quantity of hydrocarbon has been ingested. However, several investigators are against this practice and assert that it only enhances the risk of pulmonary toxicity.

o     Activated charcoal is generally considered to be inef-fective in adsorbing petroleum distillates, though there are experimental studies suggesting the opposite.

·      While prophylactic administration of corticosteroids was advocated in the past, it is not advocated today, since studies have not demonstrated any beneficial effects. On the other hand it can increase the chances of bacterial superinfection.

·      Similarly, prophylactic administration of antibiotics which was the norm in the past is also discouraged today, since it can alter the bacterial flora and lead to subsequent infection by resistant gram-negative bacteria. Pulmonary cultures should be done to decide on antibiotic adminis-tration, though this may not be practicable in critically ill patients. In such cases, prophylactic antibiotic therapy may be justified.

·              Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general, the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output.

Treatment of frostbite:

Rewarming—

–– Do not institute rewarming unless complete rewarming can be assured; refreezing thawed tissue increases tissue damage. Place affected area in a water bath with a temperature of 40 to 420 Celsius for 15 to 30 minutes until thawing is complete. The bath should be large enough to permit complete immersion of the injured part, avoiding contact with the sides of the bath. A whirlpool bath would be ideal. Some authors suggest that an antibacterial (hexachlorophene or povidone-iodine) be added to the bath water.

––  Correct systemic hypothermia.

–– Rewarming may be associated with increasing pain, requiring narcotic analgesics.

Wound Care—

–– Digits should be separated by sterile absorbent cotton; no constrictive dressings should be used. Protective dressings should be changed twice per day.

–– Perform daily hydrotherapy for 30 to 45 minutes in warm water 400 Celsius. This helps debride devital-ised tissue and maintain range of motion.

–– The injured extremities should be elevated and should not be allowed to bear weight.

–– Clear blisters should be debrided but haemorrhagic blisters left intact.

–– Further surgical debridement should be delayed until mummification demarcation has occurred (60 to 90 days). Spontaneous amputation may occur.

–– Analgesics may be required during the rewarming phase; however, patients with severe pain should be evaluated for vasospasm. Arteriography and nonin-vasive vascular techniques (e.g. Doppler ultrasound, digital plethysmography, isotope scanning), have been useful in evaluating the extent of vasospasm after thawing.

––  Tetanus prophylaxis as indicated.

–– Topical aloe vera may decrease tissue destruction and should be applied every 6 hours.

–– Ibuprofen is a thromboxane inhibitor and may help reduce tissue loss. Adult dose of 200–400 mg every 12 hours is recommended.

The following treatment measures/drugs are contraindicated in hydrocarbon poisoning:

·              Emetics

·              Activated charcoal

·              Olive oil/mineral oil

·              Cathartics

Catecholamines (dopamine, adrenaline, noradrenaline, isoproterenol, etc.). 

Tar and asphalt can cause distressing problems of a different sort. These hot hydrocarbon mixtures can produce severe burns on dermal contact. The material hardens quickly and becomes extremely difficult to remove. Thermal injury can be minimised by immediate cooling with cold water. Removal of hardened tar can be attempted after application of mineral oil, petroleum jelly, or antibac-terial ointment. Recent reports suggest that surface-acting agents in combination with a hydrocarbon ointment may be more effective.

Autopsy Features

·              Pulmonary oedema and varying degree of lung pathology are prominent features.

·              There may also be evidence of gastrointestinal congestion and (rarely) corrosion.

·              There is often characteristic odour depending on the type of hydrocarbon ingested.

Forensic Issues

·              Most cases of poisoning result from accidental exposure. In India, accidental kerosene poisoning is quite common in the paediatric age group, since it is a popular household fuel and is often negligently left around in the kitchen in bottles or cans.

·              uncommon because of easy availability of many of these agents.

·              Experimental animal studies and some studies on cancer incidence and mortality in human occupational groups suggest that hydrocarbon exposure is associated with renal neoplasia.


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