HYDROCARBON poisoning. Clinical manifestation, Management

Hydrocarbon poisoning occurs when a person is exposed to hydrocarbons, which are organic compounds primarily made up of hydrogen and carbon. This can happen through ingestion, inhalation, or dermal exposure, often associated with accidental or intentional exposure to chemicals such as gasoline, kerosene, paints, solvents, or other petroleum products.
So, hydrocarbon poisoning happens when someone gets exposed to hydrocarbons, which are basically just chemicals made of hydrogen and carbon. You can get this stuff in your system by swallowing it, breathing it in, or even through your skin. It often comes from accidents or situations where people intentionally use things like gasoline, kerosene, paints, solvents, or other petroleum products. Just gotta be careful with that stuff, y'know?

1. HYDROCARBON POISONING Dr. SONOMA MARIA K.B Assistant Professor Department of Pharmacy Practice

2. HYDROCARBONS HYDROCARBONS: PETROLEUM PRODUCTS A hydrocarbon is an organic compounds primarily composed of carbon and hydrogen atoms. These compounds can exist as gases, liquids, or solids, depending on their molecular structure and size. The number of carbon molecules can vary from 1 to 60. In general, compounds which contain 1 to 4 carbon molecules are gaseous, while those which have 5 to 19 are liquids, and compounds with more than 20 are solids. These include a wide array of chemical substances found in thousands of commercial products.

3. CLASSIFICATION: 1. ALIPHATIC HYDROCARBONS ( PARAFFINS): These comprise compounds with saturated molecules (containing no carbon-carbon double or triple bonds) which have straight or branched-chain arrangements. Common examples include Gaseous: butane, ethane, methane and propane Liquids: gasoline or petrol, diesel oil, kerosene, mineral seal oil, lubricating oil or mineral oil, and turpentine Semi-liquids or solids : paraffin wax, petroleum jelly or Vaseline, grease

4. 2. AROMATIC HYDROCARBONS: They contain at least one benzene ring and are unsaturated compounds. Common examples include benzene, toluene, xylene, styrene and naphthalene. 3. HALOGENATED HYDROCARBONS: Most of these are clear, colourless liquids which have a chloroform – like odour. Common examples include carbon tetrachloride, ethylene dibromide, chloroform, methyl chloroform, organochlorine insecticides, fluorocarbons. 4. CYCLOPARAFFINS ( NAPHTHENES): They are saturated hydrogen compounds which are arranged in closed rings. Common examples include cyclohexane, methylcyclopentane .

5. 5. ALKENES ( OLEFINS): These compounds contain one carbon-carbon double bond in the molecule. They are mostly used in the manufacture of other hydrocarbon products such as halogenated hydrocarbons.

6. USES:

7. 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 generally are the result of aspiration into the airways rather than absorption from the GI tract. Aliphatic hydrocarbons possessing high aspiration potential include gasoline, kerosene, mineral seal oil, and turpentine.

8. The aspiration potential of a hydrocarbon depends on 3 properties: 1. Viscocity is the tendency of a substance to resist flow (“the ability to resist stirring”) SI unit- Saybolt Seconds Universal (SSU). The lower the viscocity (i.e. below 60 SSU), the higher the tendency for aspiration. 2. Surface tension refers to the adherence of a liquid compound along its surface (“the ability to creep”). The lower the surface tension, the higher the tendency for aspiration. 3. Volatility refers to the ability of a liquid to become a gas. The higher the volatility, the higher the tendency for aspiration.

9. CLINICAL MANIFESTATIONS: 1. 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: a. Mild : coughing, choking, tachypnoea, drowsiness, rales, rhonchi. b. Moderate : grunting, lethargy, flaccidity, bronchospasm. c. Severe : cyanosis, coma, seizures. Moderate fever is often present but does not correlate with severity. Hemoptysis and pulmonary oedema may occur after significant aspiration or inhalation

10. 2. CNS: Lethargy with depressed sensorium. Coma and convulsions are rare. Aniline, heavy metals, camphor, pesticides 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. 3. GIT: Burning of mouth, sore throat, nausea, and vomiting. Haematemesis may occur. Diarrhoea is rare. 4. CVS: Arrhythmias are seen in solvent abuse, but are rare in ingestions. 5. 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. 6. Haematologic : Disseminated intravascular coagulation, haemolytic anaemia and pancytopenia have occasionally been reported following vapour inhalation, aspiration, or ingestion of hydrocarbons

11. DIAGNOSIS: Chest X- Ray and oximetry done about 6 hours after ingestion. If patients are too obtunded to provide a history, hydrocarbon exposure may be suspected if their breath or clothing has an odour or if a container is found near them. Paint residue on the hands or around the mouth may suggest recent paint sniffing. Obtain baseline CBC, electrolytes, glucose -6-phosphate dehydrogenase level, liver enzymes and renal function tests, urine analysis and urine dipstick test for haemoglobinuria . Measurement of urinary metabolites may help to confirm the diagnosis Diagnosis of aspiration pneumonitis is by symptoms and signs as well as by chest X-ray and oximetry, which are done about 6h after ingestion or sooner if symptoms are severe. If respiratory failure is suspected, ABGs are measured. CNS toxicity is diagnosed by neurologic examination and MRI.

12. DIAGNOSIS: 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.

13. MANAGEMENT: The following signs and symptoms present upon initial examination of patients after hydrocarbon ingestion have 80% or better predictive value for pneumonitis: a. Lethargy, rhonchi, rales, retractions, cyanosis, and the development of leukocytosis and fever within 4 hours. b. The only parameter with an 80% or greater predictive value for NO toxicity was the absence of tachypnoea. c. Early chest X-rays were not useful in predicting pneumonitis in symptomatic or asymptomatic patients.

14. 2. If Respiratory Failure is a Concern: Initial Step: Stabilize the patient, then take a chest X-ray to confirm or rule out aspiration pneumonitis. Supportive Measures (if respiration is compromised): Airway Management: Endotracheal intubation Oxygen Therapy: Administer supplemental oxygen Ventilatory Support: CPAP (Continuous Positive Airway Pressure) PEEP (Positive End-Expiratory Pressure)

15. Bronchodilators: Use inhaled cardio-selective bronchodilators like salbutamol. Advanced Options: High Frequency Jet Ventilation (HFJV): High respiratory rates (220–260 breaths/min) Low tidal volumes ECMO (Extracorporeal Membrane Oxygenation): Used in severe pulmonary toxicity when other methods fail

16. 3 . Decontamination: a. 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. b. Induction of vomiting is not recommended. c. Stomach wash may be done cautiously after intubation, especially in those cases where a large quantity of hydrocarbon has been ingested. d. Activated charcoal is generally considered to be ineffective in adsorbing petroleum distillates, though there are experimental studies suggesting the opposite. 4. 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.

17. 5. Treatment of frostbite: a. 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 42 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 b. 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 devitalised tissue and maintain range of motion.

18. 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 non-invasive 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.

19. 6. The following treatment measures/drugs are contraindicated in hydrocarbon poisoning: Emetics Activated charcoal Olive oil/mineral oil Cathartics Catecholamines (dopamine, adrenaline, noradrenaline, isoproterenol, etc.).

20. HYDROCARBONS: POLYETHYLENE GLYCOL (PEG): PEG is a colourless, odourless, sweet – tasting chemical. It is poisonous if swallowed. PEG may be swallowed accidentally, or it may be taken deliberately in a suicide attempt. PEG has been widely applied in various medical fields due to its outstanding properties such as satisfactory safety, biocompatibility, hydrophilicity etc. Although PEG is normally considered as almost non- toxic, some unsafe problems of PEG with molecular weight have been noticed by researchers.

21. USES: PEG has pharmaceutical and industrial uses. Pharmaceutical uses include cleansing the colon prior to GI examination or surgery and for the treatment of constipation. Industrial uses include lubrication for textile fibers , rubber moulds, and metal- forming operations, as well as in water paints, paper coatings, and polishes, and in ceramics industry. LMWs PEG are used as reactive intermediates in the manufacture of fatty acid surfactants as solvents in gas processing and as diluents in pharmaceuticals Intermediate weight are used in pharmaceutical ointments and toothpaste formulations and as bases for cosmetic creams and lotions. Higher- molecular weight PEGs find use as binders, plasticizers, stiffening agents, moulding compounds and paper adhesives.

22. TOXICITY LEVELS: Acute toxicity increases with decreasing molecular weight of PEG. Liquid forms of PEG have a LMW and are used as vehicles for iv or topical medications. Toxicity has resulted in patients receiving prolonged, high dose infusions of Lorazepam containing PEG 400 and in burn patients receiving repeat dermal application of PEG 200 to 400.

23. CONT.. An intentional oral ingestion of 2 litres of PEG 400 by an adult resulted in serious toxicity. Solid forms of PEG have a higher molecular weight(MW GREATER THAN 3000) and are not readily absorbed with oral ingestion; therefore, these formulations rarely produce toxicity.

24. MECHANISM: PEG 3500 is an osmotic agent, which causes water to be retained in the stool, enhancing bowel movement through the colon. High and intermediate molecular wt PEG is generally considered non-toxic, as it is not absorbed following ingestion. Acute toxicity decreases with increasing mol.wt . Massive ingestion, prolonged iv infusion and prolonged application of low weight PEG products have been associated with metabolic acidosis and renal injury.

25. CONT.. Hypercalcaemia occurs and might be related to specific PEG diacid metabolites (3-oxapentane-1,5-dicarboxylic acid and 3,6-dioxaoctane-1,8-dicarboxylic acid), which are avid calcium binders. With binding of ionized calcium, parathyroid hormone is stimulated and total serum calcium increases. Toxicity is unlikely following ingestion of small amounts or from contact with intact skin.

26. CLINICAL (TOXIC) SYMPTOMS: Nausea, vomiting, abdominal fullness, delayed gastric emptying, diarrhea and taste disorders may develop after ingestion. Contact dermatitis and immediate urticarial reactions may develop after dermal exposures. Metabolic acidosis, increased serum osmolality, ARF, increased total serum calcium with normal or decreased ionized calcium, and ventricular dysrhythmias (PVCs, ventricular tachycardia) may develop. Aspiration causes severe pulmonary edema , that is usually reversible. Acute pancreatitis and angioedema have been reported rarely.

27. DIAGNOSIS: Monitor acid-base balance, osmolal gap, serum electrolytes, renal function and pulmonary function in symptomatic patients. Blood levels are not generally available or clinically useful. A tandem quadrupole mass spectrometry technique can identify PEG and its metabolites. Monitor pulmonary function and Chest X-ray in cases of suspected PEG aspiration or systemic fluid overload. Assess adequacy of oxygenation with pulse oximetry or ABGs.

28. MANAGEMENT: Treatment is symptomatic and supportive. Patients will generally recover with supportive care. Administer IV fluids to maintain adequate urine output. Acute anaphylactic reactions associated with PEG administration are managed as anaphylaxis from other causes. Aspiration may require supplemental oxygenation and mechanical ventilation with PEEP, bronchoalveolar lavage may be used for treatment. For patients with dermal exposure, irrigate the site of exposure and provide supportive care.

29. CONT… Decontamination: GI decontamination and activated charcoal is not required. Gastric aspiration soon after an acute ingestion of a large amount of LMW PEG solution may be beneficial. There is no specific antidote. Competitive antidiuretic hormone inhibitor therapy ( eg : Fomepizole , Ethanol) may inhibit PEG metabolism.However , efficacy on clinical outcomes after PEG intoxication is unknown and they are not generally recommended. Extracorporeal techniques may be helpful in managing patients with PEG toxicity, particularly with hepatic or renal dysfunction. Dialysis can correct acid base and electrolyte abnormalities, and reduce the osmolal gap. It is rarely necessary as most patients do well with supportive care.

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