Hydrocarbons

1.   Hydrocarbons

2. PERSPECTIVE: BACKGROUND AND EPIDEMIOLOGY • Human exposure to hydrocarbons (HCs) is a common problem. U.S. poison centers report 50,000 HC exposures annually, with the majority handled in an outpatient setting. HC exposures that present to the emergency department (ED) generally can be classified into four types. The first is accidental ingestion involving children younger than age 5 years.

3. This is the most common scenario causing fatality, and it usually involves significant pulmonary injury. Second is intentional inhalational abuse of volatile HCs. Recreational abuse has been a medical problem since solvent inhalation became popular during the late 1800s. Fatalities in this group will typically occur within distinct demographic groups (American Indians, homosexual males,and teenagers). Third is accidental inhalational or dermal exposure to HC in the household or workplace setting. The fourth type is massive oral ingestion of HC in a suicide attempt.

4. PRINCIPLES OF DISEASE Definitions and Terminology • HCs are a diverse group of organic compounds that contain hydrogen and carbon. Most HCs (e.g., gasoline) are by-products of crude oil and are therefore called petroleum distillates. Some products, such as turpentine, are derived from pine oil, not petroleum. HCs can also be classified by their structure.

5. The two main categories are straight chain HCs (aliphatic, such as propane) and those containing a benzene ring structure (aromatic, such as toluene). HCs can also have multiple nonorganic side chains. For example, halogenated HCs (e.g., carbon tetrachloride) usually will have one or more bromide, chloride, fluoride, or iodide moieties.

6. Finally, HCs are used as the solvent base for many toxic chemicals such as insecticides and metals that in turn can cause a separate type of poisoning. Although the range of toxicity of HCs can vary widely, the majority of human exposures are confined to petroleum distillates.

7. Spectrum of Hydrocarbon Toxicity

8. Pathophysiology • Acute HC toxicity usually affects three main target organs: the lungs, the central nervous system (CNS), and the heart. Although certain HCs can enter the body through the skin or gastrointestinal (GI) tract, HCs cause the most damage via the lungs. Despite the fact that there are thousands of different types of HCs, their potential for acute toxicity depends mainly on four characteristics:   

9. Viscosity is the capacity to resist flow or change. Low viscosity allows a substance to spread rapidly, and a low-viscosity HC spreads easily into the airway and lungs. Thus, the lower the viscosity, the higher the toxicity. Viscosity is measured in Saybolt Seconds Universal (SSU), and substances with an SSU of less than 60 have the highest potential risk of aspiration. Lubricants and mineral oil have high viscosity and low toxicity, whereas furniture polish has low viscosity and high toxicity.

10. 2. Volatility is the ease for a liquid to turn into a gas. High volatility gives an odor and enables a substance to displace alveolar oxygen. Butane and gasoline are types of HCs with high volatility. 3. Surface tension is the capacity for a substance to collect on a liquid surface. Low surface tension enables a substance (e.g., turpentine) to disperse easily.

11. 4. Chemical side chains often increase potential toxicity. These toxic side chains include metals (e.g., arsenic), halogens (e.g., carbon tetrachloride), and aromatic structures (e.g., toluene).

12. Pulmonary Pathophysiology • The primary organ of toxicity for HCs is the lung. Fatalities after ingestion usually occur with an accompanying aspiration. Studies have shown that pulmonary toxicity is caused by aspiration rather than by GI absorption and hematogenous spread. A small amount of an HC in the trachea can be devastating, whereas a much larger amount of the same compound in the stomach can be benign.

13. HCs affect the lungs through several mechanisms. HCs are usually poorly water soluble and are thereby able to penetrate into the lower airways, producing bronchospasm and an inflammatory response. Second, volatized HCs can displace oxygen in the alveolar space causing hypoxia. Third, HCs can cause direct injury to pulmonary alveoli and capillaries, producing distinct uniform lesions.

14. HCs affect the lungs through several mechanisms. HCs are usually poorly water soluble and are thereby able to penetrate into the lower airways, producing bronchospasm and an inflammatory response. Second, volatized HCs can displace oxygen in the alveolar space causing hypoxia. Third, HCs can cause direct injury to pulmonary alveoli and capillaries, producing distinct uniform lesions.

15. Autopsy findings of these lesions include hyperemia, diffuse hemorrhagic exudative alveolitis with granulocytic infiltration, and microabscesses. Finally, HCs can inhibit surfactant function leading to alveolar instability and collapse. These mechanisms lead to alveolar dysfunction, ventilation perfusion mismatch, hypoxemia, and respiratory failure.

16. Central Nervous System Pathophysiology • Certain HCs cause CNS depression (i.e., toluene, benzene, gasoline, butane, and chlorinated HCs). After respiratory exposure, most HCs passively diffuse through the pulmonary alveolus and are highly absorbed in blood and tissues. These HCs can cause euphoria, disinhibition, confusion, and obtundation. With an isolated single exposure, these effects usually have a rapid onset of intoxication and rapid recovery.

17. For these reasons, substance abusers seek these HCs for recreational use. Inhalation of these substances avoids hepatic first-pass metabolism and generates high concentrations in the CNS.

18. Chronic use of inhaled HCs can cause severe abnormalities in nervous system function, which include peripheral neuropathy, cerebellar degeneration, neuropsychiatric disorders, chronic encephalopathy, and dementia.

19. Cardiac Pathophysiology • HCs can cause sudden death, especially after intentional inhalation. These compounds are thought to produce myocardial sensitization of endogenous and exogenous catecholamines, which then precipitates ventricular dysrhythmias and myocardial dysfunction.

20. Other Pathophysiology • Various HCs have been reported to be toxic to other organ systems. Certain recognized syndromes include toluene-induced renal tubular acidosis, benzene-induced bone marrow toxicity and leukemia, methylene chloride–induced carbon monoxide poisoning, and chlorinated HC–induced centrilobular hepatic necrosis and renal failure. Direct skin exposure of certain HCs can cause extensive chemical burns. HCs are often used as solvents for other chemicals that may have their own significant inherent toxicity.

21. CLINICAL FEATURES: SYMPTOMS AND SIGNS • There are several typical life-threatening clinical presentations of acute HC exposures. The first scenario is a child who has ingested an unknown quantity of an HC. Significant life-threatening poisonings usually have early respiratory symptoms, including cyanosis, coughing, grunting, noisy respirations, or repeated bouts of vomiting.

22. These findings suggest aspiration. A patient may initially have mild symptoms and then develop tachypnea, dyspnea, bronchospasm, wheezing, rales, and fever within 6 hours. A change in mental status can be a manifestation of hypoxia or hypercapnia, but it is also a direct effect of HCs. In extreme cases, these patients may present with frank respiratory failure.

23. Additives or solutes in the HC base can produce varying symptoms (e.g., seizures from camphorated hydrocarbons or cyanosis from nitrite-induced methemoglobinemia). Pesticides are a classic example of such atoxic substance that is often placed in an HC base. With pesticide exposures, it can be very difficult to distinguish acute respiratory distress syndrome induced by HC aspiration from pulmonary edema induced by organophosphate exposures.

24. The second scenario is the solvent-abusing adolescent or adult. In the extreme case, these patients will be in cardiac arrest. Nonhospital medical personnel often describe an individual who has inhaled solvents, performed some type of physical activity, and then suddenly collapsed. This is thought to be due to cardiac sensitization by endogenous catecholamine and the ensuing development of dysrhythmias.

25. Various paraphernalia commonly include plastic bags used for “bagging” (a method of pouringHCs in a bag or container and then inhaling deeply) or an HC-soaked cloth used for “huffing” (a method in which abusers inhale through a saturated cloth). Other paraphernalia include gasoline containers, multiple butane lighters, and spray paint cans.

26. These patients often have a distinctive odor because almost all of these products are volatile. They may have paint or a rash over the mouth and nose (“glue-sniffer's rash”). These patients can also present to the ED with CNS intoxication comprising euphoria, agitation, hallucinations, confusion, and bizarre behavior.

27. This may progress to CNS depression and seizures. Drug abusers who chronically inhale HCs may not be brought to medical attention specifically for treatment of their drug abuse but, rather, for behavioral problems or nonspecific medical symptoms caused by their abuse.

28. Typical presentation of paint sniffer (“huffer”) with paint around the face and sedation

29. A third common scenario is the accidental dermal or inhaled (non aspiration) respiratory exposure to HCs in the workplace or home. Fortunately, this is rarely life-threatening. Most cases do not seek medical care or are handled primarily through local poison control centers. A very small percentage will seek treatment in the ED.

30. Most of these patients will either be asymptomatic or have transient nonspecific symptoms such as headache, dizziness, or nausea. Those with significant respiratory exposure may have persistent pulmonary complaints and physical findings such as coughing, wheezing, and cyanosis. Patients with significant acute dermal exposures may have pain and evidence of chemical burns consisting of erythema, swelling, blistering, and dermal destruction.

31. The patient who intentionally ingests or intravenously injects HCs in a suicide attempt is rare. However, these patients can be difficult to treat because HCs are often ingested in combination with other substances. In the absence of aspiration or co-ingestion of another toxic substance, the massive oral ingestion of most commonly available HCs is not associated with significant morbidity or mortality. These patients risk aspiration if they vomit.

32. DIAGNOSTIC STRATEGIES • The diagnosis of HC poisoning is made on clinical grounds.

33. History and examination should focus on possible aspiration. These symptoms include cough, difficulty breathing, or shortness of breath. Signs of a significant exposure include tachypnea, tachycardia, wheezing, and hypoxemia. Patients with a significant HC exposure should have a chest radiograph taken. Radiographic changes can occur within 30 minutes of ingestion and may identify pathology not recognized by auscultation in more than 50% of cases.

34. CBC, U&E, LFTs, ABG

35. DIFFERENTIAL CONSIDERATIONS • In the most common fatal scenario—the child who ingests and then aspirates HC—the physician should be sure that no other toxic substances are involved. Organophosphate, salicylate, and paraquat poisonings can mimic the symptoms of HC aspiration.

36. In the scenario of the recreationalabuser, multiple drugs ofabuse may be present. Behavioral disorders and confusion can be caused by hypoxia and respiratory compromise as well as from the drugs themselves. In the chronicabuser, it can be difficult to differentiate between a functional and an organic confusional state.

37. MANAGEMENT • Dermal exposures of HCs can cause extensive burns, and exposed patients should be decontaminated immediately. Contaminated clothing should be removed, and the skin should be washed with soap and copious lukewarm water. The GI decontamination of ingested HCs is controversial. The aphorism “the safest place in the body for hydrocarbons is the duodenum” holds true for most HCs regardless of the volume ingested. Routine gastric lavage or

38. emesis should be avoided because HCs are much more toxic to lungs than to the GI tract, where they also have a low potential for systemic absorption. Efforts at decontamination after the ingestion of a benign HC can result in aspiration, thereby converting a relatively nontoxic ingestion to a toxic aspiration.

39. Although the method of decontamination is controversial and there is scant literature to support the effectiveness of GI decontamination, use of a small-caliber nasogastric tube to evacuate stomach contents can be considered

40. Because HCs can cause sudden decompensation in a patient's pulmonary, cardiac, and CNS functions, all patients should be monitored with cardiac monitors and pulse oximeters in a well-observed area. In severe cases, early intubation for airway control and positive end-expiratory pressure have been advocated.

41. Corticosteroids and antibiotics have not been shown to be beneficial in HC aspiration.

42. Epinephrine and isoproterenol should be avoided unless required for cardiac resuscitation.

43. In most cases of HC ingestion or inhalation, supportive care and close observation and monitoring are the cornerstone of management. Currently, there are no specific antidotes for HCs.

44. DISPOSITION • Patients with exposures of known, relatively benign HCs should have a 4- to 6-hour period of observation. Patients who have ingested HCs and do not have symptoms should be monitored for a minimum of 6 hours with a reassessment that may include repeat physical examination, pulse oximetry, arterial blood gas measurements, and chest radiograph during the last hour of observation.

45. Any evidence of symptoms at this time mandates hospital admission and further observation. Asymptomatic patients with accidental exposures to HCs can be discharged after a period of observation with appropriate follow-up

46. Chest radiograph of a patient with hydrocarbon ingestion 6 hours after exposure

47. Patients who have ingested HCs and have symptoms suggestive of aspiration should be admitted for a minimum of 24 hours for observation. Patients who present after an episode of recreational HC use should also be observed for 4 to 6 hours. All patients in this category should be offered drug addiction counseling.

49. True/False HCs poisoning can cause 1- CNS depression 2- Pneumonitis 3- Cardiac dysrhythmias 4- Tachypnoea 5- Bradycardia

50. True/False Management of HCs poisoning, 1- Gastric lavage is beneficial if performed early 2- Desferioxamine is the antidote 3- Activated charcoal has been proved beneficial 4- Haemodialysis effectively removes the toxic compound 5- is mainly supportive.