Acute hydrocarbon exposure: Management

INTRODUCTION — This topic will discuss the management of acute hydrocarbon toxicity. Clinical toxicity, evaluation, and diagnosis of acute hydrocarbon exposure and inhalant abuse in children and adolescents are discussed separately. (See "Acute hydrocarbon exposure: Clinical toxicity, evaluation, and diagnosis" and "Inhalant misuse in children and adolescents".)

STABILIZATION — Most hydrocarbon exposures involve ingestion of a small amount of an aliphatic or terpene hydrocarbon and are stable at presentation. However, patients with large ingestions, asphyxial inhalation exposure, or exposure to aromatic or halogenated hydrocarbons may require emergency stabilization of the airway, breathing, and circulation as follows [1]:

●Severe respiratory distress or altered mental status – Patients with severe respiratory distress, those who are unresponsive to oxygen and beta-2 bronchodilators (eg, albuterol), or those with significant lethargy or coma that makes them unable to maintain their airway should undergo endotracheal intubation. (See "Rapid sequence intubation in adults for emergency medicine and critical care" and "Rapid sequence intubation (RSI) in children for emergency medicine: Approach".)

●Cardiac arrhythmias – All symptomatic patients and asymptomatic patients who have ingested aromatic or halogenated hydrocarbons warrant a 12-lead electrocardiogram and continuous cardiac monitoring for ventricular arrhythmias. Patients with ventricular arrhythmias should receive Pediatric or Advanced Cardiac Life Support that is modified by avoiding the use of epinephrine. (See 'Ventricular arrhythmias' below.)

●Seizures – Patients with seizures should receive benzodiazepines (eg, lorazepam or diazepam) in addition to support of airway and breathing to improve oxygenation. (See "Convulsive status epilepticus in adults: Classification, clinical features, and diagnosis" and "Management of convulsive status epilepticus in children".)

●Organophosphate exposure from co-ingestion – Patients with suspected organophosphate exposure indicated by muscarinic findings (eg, salivation, miosis, lacrimation, urination, bronchorrhea, vomiting, and/or diarrhea), seizures, and/or nicotinic findings (diaphoresis, muscle fasciculations, and weakness) warrant presumptive antidotal treatment with atropine and pralidoxime as described in the rapid overview table (table 1) and discussed in detail separately. (See "Organophosphate and carbamate poisoning", section on 'Management'.)

MANAGEMENT — Successful management of hydrocarbon exposure requires recognition of pulmonary, cardiac, and/or neurologic toxicity and rapid initiation of appropriate supportive care.

Regional poison control centers in the United States are available at all times for consultation on patients who are critically ill, require admission, or have clinical pictures that are unclear (1-800-222-1222). In addition, some hospitals have clinical and/or medical toxicologists available for bedside consultation and/or inpatient care. Whenever available, these are invaluable resources to help in the diagnosis and management of toxic exposures. Contact information for poison centers around the world is provided separately. (See "Society guideline links: Regional poison control centers".)

Staff protection — Prior to initiating decontamination of patients with external hydrocarbon exposure, the health care team should don personal protective equipment appropriate to the hazard posed by the specific chemical. (See "Topical chemical burns: Initial evaluation and management", section on 'Protection of clinicians'.)

External decontamination — Contaminated clothing should be removed from the patient to prevent continued inhalation exposure. Affected skin and hair should also be cleansed as many hydrocarbons cause irritation [2].

Certain hydrocarbon compounds (eg, gasoline, methylene chloride) cause cell membrane injury and dissolution of lipids, which may result in skin necrosis and burns with prolonged exposure. Treatment of dermal and ocular exposure initially consists of pain control and copious water irrigation.

External decontamination should not delay life-saving interventions (eg, endotracheal intubation for respiratory failure or coma, treatment of arrhythmias, or anticonvulsant therapy). (See "Topical chemical burns: Initial evaluation and management", section on 'Hydrocarbons'.)

Hydrocarbon ingestion

Gastrointestinal decontamination — The approach to gastrointestinal decontamination after hydrocarbon ingestion varies according to the type and amount of hydrocarbon ingestion:

●Isolated petroleum distillate or terpene hydrocarbon ingestion – Most patients with an isolated aliphatic or terpene hydrocarbon ingestion should not receive activated charcoal or undergo gastric emptying because of the risk of provoking vomiting and further pulmonary aspiration (algorithm 1) [1-4]. Furthermore, activated charcoal does not bind well to hydrocarbons and is unlikely to be beneficial.

Some experts suggest nasogastric aspiration in patients who ingest large amounts of aliphatic hydrocarbons (eg, suicide attempt in an adult patient) and present within 60 minutes because of the potential for systemic absorption with central nervous system (CNS) and pulmonary toxicity [3]. Consultation with a regional poison control center is strongly advised when determining the need to provide gastrointestinal decontamination procedures in such patients. (See 'Additional resources' below.)

●Aromatic or halogenated hydrocarbon ingestion – Consultation with a regional poison control center is strongly advised when determining the need to provide gastrointestinal decontamination procedures in patients who have ingested aromatic or halogenated hydrocarbons (see "Acute hydrocarbon exposure: Clinical toxicity, evaluation, and diagnosis", section on 'Additional resources'). For such patients who present for care within 60 minutes of ingestion, we suggest gastric emptying using nasogastric aspiration [3].

This recommendation is based on clinical experience regarding how to manage this uncommon scenario and randomized trials that indicate little benefit of gastric lavage more than 60 minutes after an ingestion [3,5,6]. Nasogastric lavage should only be performed when the risk of systemic toxicity from gastrointestinal absorption of the hydrocarbon is equal to or exceeds the increased risk of pulmonary aspiration associated with nasogastric lavage. Nasogastric lavage should be withheld in patients with a depressed mental status who may not be able to protect their airway, unless endotracheal intubation is performed first. The following measures, performed before nasogastric aspiration, may minimize the risk of pulmonary toxicity:

•Endotracheal intubation with a balloon-cuffed endotracheal tube

•Left lateral decubitus with mild Trendelenburg positioning (eg, head inclined 20 degrees below the feet)

•Pinching off the nasogastric tube and withdrawing it quickly after the procedure is complete

●Polysubstance ingestion – For patients who present within two hours of exposure and ingest hydrocarbons that are combined with an adsorbable toxic additive (eg, organophosphates or other pesticide/herbicide) or who co-ingest a life-threatening amount of prescription medicines or other adsorbable toxin, we suggest administration of a single dose of activated charcoal (1 g/kg) [3,7].

The recommendation of activated charcoal administration in this select group of patients who ingest hydrocarbons derives from indirect evidence of benefit in volunteers, animal studies, and evidence of benefit following ingestions of other substances. Because of adverse effects, such as vomiting and dehydration, the combination of a cathartic (eg, sorbitol) and activated charcoal should be used sparingly, if at all, and only a single dose of a cathartic should be given to any patient. (See "Gastrointestinal decontamination of the poisoned patient", section on 'Evidence of efficacy and adverse effects' and "Gastrointestinal decontamination of the poisoned patient", section on 'Cathartics'.)

Symptomatic patients — Common symptoms after acute hydrocarbon exposure reflect lung, CNS, and/or cardiac toxicity.

Chemical pneumonitis — Patients with mild to moderate respiratory symptoms on presentation are at risk for the development of significant chemical pneumonitis with progression to respiratory failure over the next 24 to 48 hours. In addition to supplemental oxygen, as needed, and close monitoring, they should have chest radiographs performed at the time of presentation (algorithm 1). These patients should also not have any oral intake (remain NPO) during the initial observation period and receive maintenance intravenous fluids.

The treatment of hydrocarbon pneumonitis is supportive and includes close monitoring of respiratory status [1]:

●Oxygen – Patients with hypoxemia (eg, pulse oximetry <90 percent) should receive oxygen therapy to maintain an oxygen saturation of at least 93 percent with a target of 96 percent. Patients who require oxygen concentrations of >60 percent for longer than six hours warrant measures to avoid oxygen toxicity. (See "Adverse effects of supplemental oxygen", section on 'Prevention'.)

●Bronchospasm – Bronchospasm should be treated with selective beta-2 agonists.

●Hypercarbic respiratory failure or CNS depression – Endotracheal intubation and conventional mechanical ventilation are indicated for hypercarbic respiratory failure or CNS depression with an inability to maintain the airway [7,8]. (See "Initiating mechanical ventilation in children" and "Mechanical ventilation of adults in the emergency department".)

●Respiratory failure with severe hypoxemia – Although evidence is lacking for the progressive management of severe hypoxemic respiratory failure in patients with chemical pneumonitis, it is reasonable to perform a trial of high-flow nasal cannula oxygen delivery and/or noninvasive ventilation in alert patients in an attempt to stabilize their condition and avoid endotracheal intubation and mechanical ventilation. (See "High-flow nasal cannula oxygen therapy in children" and "Heated and humidified high-flow nasal oxygen in adults: Practical considerations and potential applications" and "Noninvasive ventilation for acute and impending respiratory failure in children" and "Noninvasive ventilation in adults with acute respiratory failure: Practical aspects of initiation".)

For patients who receive mechanical ventilation, lung-sparing strategies are appropriate to reduce barotrauma. (See "Initiating mechanical ventilation in children", section on 'Inadequate oxygenation' and "Acute respiratory distress syndrome: Ventilator management strategies for adults".)

Therapeutic options for the small minority of children who have hydrocarbon pneumonitis and respiratory failure with severe hypoxemia unresponsive to conventional mechanical ventilation include:

•Exogenous surfactant – Exogenous surfactant has been proposed to enhance oxygenation based upon case reports and may be appropriate to try prior to more invasive therapy [9,10]. If used, a formulation that is resistant to inactivation (eg, calfactant) is preferred [9].

•High-frequency ventilation – Case reports in children also indicate that high-frequency ventilation (eg, jet ventilation, high-frequency oscillatory ventilation, or high-frequency percussion ventilation) may be lifesaving for selected patients [11-13].

•Extracorporeal membrane oxygenation (ECMO) – In a case series that evaluated survival after ECMO, 13 of 19 (68 percent) of children with hydrocarbon pneumonitis survived versus 52 percent of over 880 children with other respiratory disease [14]. This experience suggests that the pulmonary injury sustained by children with hydrocarbon pneumonitis is reversible in some patients and that ECMO may be lifesaving in selected patients with severe hydrocarbon pneumonitis.

Advanced ventilatory strategies and therapeutic options in adults are discussed separately. (See "Acute respiratory distress syndrome: Ventilator management strategies for adults", section on 'Refractory patients'.)

●Parenchymal lung disease (pneumonitis and pneumatoceles) – Patients with chemical pneumonitis should not receive antibiotics unless signs of secondary infection, including the following, are present:

•Recurrence of fever after the first 48 hours [15]

•Increasing infiltrate on chest radiograph

•Leukocytosis after the first 48 hours

•Sputum or tracheal aspirate positive for bacteria

Corticosteroids have shown no beneficial effect on the course of hydrocarbon aspiration pneumonitis in observational studies and may be harmful [16,17].

Pneumatoceles usually resolve spontaneously and do not require specific treatment [18,19].

Ventricular arrhythmias — Hydrocarbon ingestion and inhalation may sensitize the myocardium to catecholamine-induced ventricular arrhythmias, especially after inhalational exposure to halogenated hydrocarbons. Treatment depends upon the presentation:

●Ventricular arrhythmias with cardiac arrest – For patients who develop ventricular arrhythmias with cardiac arrest after inhaled hydrocarbon exposure or any exposure to halogenated hydrocarbons, we suggest modification of Advanced Cardiac Life Support or Pediatric Advanced Life Support (algorithm 2 and algorithm 3) treatment of ventricular fibrillation or pulseless ventricular tachycardia consisting of early administration of lidocaine in place of epinephrine [20]. Epinephrine should be avoided because it may further precipitate ventricular arrhythmias.

●Unstable ventricular tachycardia – Patients with unstable ventricular tachycardia after hydrocarbon exposure should undergo synchronized cardioversion (algorithm 4 and algorithm 5).

●Stable ventricular tachycardia – Patients with stable ventricular tachycardia warrant pharmacologic therapy in consultation with a cardiologist.

For patients who persist with ventricular arrhythmias after inhalant use despite the use of Advanced Life Support protocols, administration of propranolol or esmolol may be beneficial [20]. (See "Catecholaminergic polymorphic ventricular tachycardia".)

Lethargy or coma — In our experience, lethargy or coma typically resolves within 12 hours of exposure with supportive care alone, but patients who cannot maintain their airway require endotracheal intubation and mechanical ventilation for airway protection [7].

Seizures — Seizures should be treated with benzodiazepines (eg, diazepam or lorazepam) and aggressive treatment of hypoxemia. For patients with status epilepticus, arrhythmogenic anticonvulsants (eg, fosphenytoin and phenytoin) should be avoided. In such patients, the clinician may use levetiracetam or phenobarbital in consultation with a neurologist. (See "Management of convulsive status epilepticus in children", section on 'Emergency antiseizure treatment' and "Convulsive status epilepticus in adults: Management", section on 'Emergency antiseizure treatment'.)

Seizures occurring after a hydrocarbon exposure should also raise the concern for possible organophosphate poisoning, especially when associated with signs of cholinergic excess and/or muscle weakness (table 1). (See "Organophosphate and carbamate poisoning", section on 'Management'.)

Asymptomatic patients — Patients who are asymptomatic at presentation warrant serial examinations with monitoring of pulse oximetry. These patients should also not have any oral intake (remain NPO) during the initial observation period. Radiographic evaluation should occur at four to six hours after hydrocarbon ingestion or sooner if the patient becomes symptomatic (eg, increased respiratory distress or decreased oxygen saturation by pulse oximetry) or vomits (algorithm 1).

Disposition — The disposition after acute hydrocarbon exposure is determined by the specific hydrocarbon, presence of co-ingestants, and degree of toxicity:

●Ingestion of petroleum distillates, turpentine, and other aliphatic hydrocarbons – Clinical findings and radiographic results largely determine patient disposition after petroleum distillate, turpentine, or other aliphatic hydrocarbon ingestion (algorithm 1):

•Patients with early onset of respiratory distress are at significant risk of respiratory failure and warrant admission to an intensive care unit [21,22].

•Patients who develop mild signs of chemical pneumonitis during observation or have an abnormal chest radiograph warrant inpatient admission with the level of care determined by the degree of findings.

•Patients who may be discharged or medically cleared for mental health evaluation after an intentional exposure include:

-Asymptomatic patients with normal chest radiographs obtained four or more hours after exposure

-Asymptomatic patients with mildly abnormal chest radiographs who do not develop symptoms or hypoxemia during the observation period and can receive timely outpatient follow-up the next day

●Pine oil ingestion – Patients with persistent lethargy at four hours after ingestion or signs of chemical pneumonitis warrant hospital admission as described above.

Patients with rapid resolution of lethargy and without evidence of chemical pneumonitis at four to six hours after ingestion may be discharged home.

●Aromatic or halogenated hydrocarbon ingestion or inhalation – Patients with an abnormal electrocardiogram, arrhythmias, or lethargy that does not resolve after four hours of observation warrant admission to an intensive care or cardiac telemetry unit.

Patients with ingestion but without evidence of cardiac toxicity during a four- to six-hour observation period should have their disposition determined by signs of chemical pneumonitis, either respiratory symptoms or abnormal chest radiograph, as described above.

Patients with mild symptoms that quickly resolve warrant mental health screening for substance use disorder, depression, and suicidality but may be discharged with appropriate psychiatric and other medical follow-up. (See "Inhalant misuse in children and adolescents", section on 'Disposition'.)

Hydrocarbon inhalation or other exposure

Hydrocarbon inhalation — The management of hydrocarbon inhalation is discussed in detail separately. (See "Inhalant misuse in children and adolescents", section on 'Management'.)

Chemical burns — External decontamination as described above is typically sufficient for most patients with brief dermal exposure to hydrocarbons. (See 'External decontamination' above.)

Patients with prolonged exposure can develop partial and full thickness burns due to dermal absorption. These patients should receive emergency consultation with a burn specialist. Initial management of these chemical burns is described separately. (See "Topical chemical burns: Initial evaluation and management".)

In addition, patients with partial or full thickness burns can develop systemic toxicity that, depending upon the specific chemical compound and degree of exposure, can rarely cause severe pulmonary, neurologic, cardiac, hepatic, and/or renal toxicity [23].

The disposition for patients with hydrocarbon chemical burns is determined by the extent and depth of the burn as discussed separately. (See "Moderate and severe thermal burns in children: Emergency management" and "Emergency care of moderate and severe thermal burns in adults".)

Intentional parenteral injection — Parenteral injection of hydrocarbons can cause major tissue destruction including tissue necrosis and necrotizing fasciitis. These patients warrant emergency surgical consultation and hospital admission.

Initial treatment of subcutaneous or intramuscular injection consists of elevation and immobilization of the affected extremity [24]. These patients should be admitted to a surgical service for frequent assessment of neurovascular status and compartment syndrome.

Indications for surgical intervention include [24]:

●Neurovascular compromise

●Elevated compartment pressure

●Development of an abscess

●Persistent fever, increased leukocytosis, worsening pain, and signs of tissue ischemia

For patients who have injected radiopaque hydrocarbons (eg, chlorinated hydrocarbons) and have developed necrotizing fasciitis, radiographs of the extremity can help identify the surgical margins for debridement.

In addition to localized tissue effects, intravenous injection can cause thrombophlebitis and hemorrhagic pneumonitis with hypoxemic respiratory failure. These patients require supportive intensive care similar to patients with severe chemical pneumonitis. (See 'Chemical pneumonitis' above.)

High-pressure paint injection — High-pressure paint injection injuries are deceptive because the extent of chemical contamination is usually much greater than what is initially apparent on inspection [25]. They typically involve the nondominant hand or finger [26]. Hydrocarbon-based paints have the highest potential for tissue necrosis, but latex- and water-based paints can cause similar damage.

Initial treatment consists of tetanus prophylaxis, prophylactic antibiotics targeting skin pathogens (including methicillin-resistant Staphylococcus aureus in regions with high prevalence), and emergency consultation with a hand surgeon [26]. These injuries typically require emergency debridement under regional or general anesthesia. Hydrocarbon injection is associated with a higher risk for widespread tissue necrosis that requires amputation.

Co-ingestion of organophosphate pesticides — Treatment of organophosphate poisoning is provided in the table (table 1) and discussed in detail separately. (See "Organophosphate and carbamate poisoning".)

PROGNOSIS — Most patients have mild or no serious clinical toxicity after acute hydrocarbon exposure [27]. The typical clinical course of chemical pneumonitis ranges from two to five days. The mild central nervous system (CNS) depression that is seen soon after ingestion seldom produces serious morbidity provided that further pulmonary aspiration does not occur. Rarely, patients with chemical pneumonitis may progress rapidly to respiratory failure and death. CNS effects (eg, somnolence, convulsions, and coma) and/or pulmonary symptoms may dominate the course.

Evidence is lacking to suggest long-term clinically important pulmonary effects from hydrocarbon aspiration [28].

PREVENTION — Legislation that requires child-resistant packaging and education to keep hydrocarbons in their original containers have been the primary means of preventing hydrocarbon exposure [29]. By contrast, product engineering to adjust viscosity and surface tension of lamp oil in the European Union was unsuccessful in reducing the number or severity of hydrocarbon aspiration exposures [30].

The prevention of poisoning in children is discussed in detail separately. (See "Prevention of poisoning in children".)

ADDITIONAL RESOURCES

Regional poison control centers — Regional poison control centers in the United States are available at all times for consultation on patients with known or suspected poisoning, and who may be critically ill, require admission, or have clinical pictures that are unclear (1-800-222-1222). In addition, some hospitals have medical toxicologists available for bedside consultation. Whenever available, these are invaluable resources to help in the diagnosis and management of ingestions or overdoses. Contact information for poison centers around the world is provided separately. (See "Society guideline links: Regional poison control centers".)

Society guideline links — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: General measures for acute poisoning treatment" and "Society guideline links: Treatment of acute poisoning caused by specific agents other than drugs of abuse".)

SUMMARY AND RECOMMENDATIONS

●Regional poison control centers in the United States are available at all times for consultation on patients who are critically ill, require admission, or have clinical pictures that are unclear (1-800-222-1222). In addition, some hospitals have clinical and/or medical toxicologists available for bedside consultation and/or inpatient care. Whenever available, these are invaluable resources to help in the diagnosis and management of toxic exposures. Contact information for poison centers around the world is provided separately. (See 'Management' above and 'Additional resources' above.)

●Prior to initiating decontamination of patients with external hydrocarbon exposure, the health care team should don personal protective equipment appropriate to the hazard posed by the specific chemical. (See 'Staff protection' above.)

●Contaminated clothing should be removed from the patient to prevent continued inhalation exposure. Affected skin and hair should also be cleansed as many hydrocarbons cause irritation. Prolonged exposure to certain compounds (eg, gasoline or methylene chloride) may also cause skin necrosis and burns. Treatment of dermal and ocular exposure initially consists of pain control and copious water irrigation. (See 'External decontamination' above and "Topical chemical burns: Initial evaluation and management", section on 'Hydrocarbons'.)

●Most patients with an isolated aliphatic or terpene hydrocarbon ingestion should not receive activated charcoal or undergo gastric emptying because of the risk of provoking vomiting and further pulmonary aspiration. Consultation with a regional poison control center is advised to determine the benefit for nasogastric aspiration or administration of activated charcoal in selected patients (see 'Gastrointestinal decontamination' above):

•For patients with an ingestion of a large amount of an aliphatic hydrocarbon (eg, suicide attempt in an adult patient), aromatic hydrocarbon, or halogenated hydrocarbon who present within 60 minutes of ingestion, we suggest nasogastric aspiration (Grade 2C).

•For patients with hydrocarbon ingestion and co-ingestion of a life-threatening agent with potential for adsorption with activated charcoal who present within two hours of ingestion, we suggest a single dose of activated charcoal (Grade 2C).

●Supportive care is the primary treatment for symptomatic chemical pneumonitis (algorithm 1):

•Chemical pneumonitis is treated with supplemental oxygen as needed, selective beta-2 agonists (eg, albuterol) for bronchospasm, and high-flow nasal cannula oxygen delivery or noninvasive/invasive mechanical ventilation for respiratory failure with severe hypoxemia. Potential advanced therapies for children failing conventional mechanical ventilation include exogenous surfactant (eg, calfactant), high-frequency ventilation, and extracorporeal membrane oxygenation (ECMO). (See 'Chemical pneumonitis' above.)

•Patients with chemical pneumonitis should not receive antibiotics unless signs of secondary infection are present. Corticosteroids are potentially harmful and should be avoided. (See 'Chemical pneumonitis' above.)

●Hydrocarbon ingestion and inhalation sensitizes the myocardium to catecholamine-induced ventricular arrhythmias. We suggest that patients who develop ventricular arrhythmias with cardiac arrest after hydrocarbon exposure receive Advanced Cardiac Life Support or Pediatric Advanced Life Support modified to include early administration of lidocaine in place of epinephrine (Grade 2C). Epinephrine should be avoided because it may further precipitate ventricular arrhythmias (algorithm 2 and algorithm 3). For patients who persist with ventricular arrhythmias after inhalant use despite the use of Advanced Life Support protocols, administration of propranolol or esmolol may be beneficial. (See 'Ventricular arrhythmias' above.)

●Lethargy or coma typically resolves within 12 hours of exposure with supportive care alone, but patients who cannot maintain their airway require endotracheal intubation and mechanical ventilation for airway protection.

●Seizures should be treated with benzodiazepines (eg, diazepam or lorazepam) and aggressive treatment of hypoxemia. For patients with status epilepticus, arrhythmogenic anticonvulsants (eg, fosphenytoin and phenytoin) should be avoided. In such patients, the clinician may use levetiracetam or phenobarbital; consultation with a neurologist is warranted.

●Patients who are asymptomatic after hydrocarbon ingestion warrant serial examinations with monitoring of pulse oximetry. These patients should also not have any oral intake (remain NPO) during the initial observation period. Radiographic evaluation should occur at four to six hours (algorithm 1).

●Clinical findings and radiographic results largely determine patient disposition after petroleum distillate, turpentine, or other aliphatic hydrocarbon ingestion. (See 'Disposition' above.)

●Management of other types of hydrocarbon exposures include:

•External decontamination as described above is typically sufficient for most patients with brief dermal exposure to hydrocarbons (see 'External decontamination' above). Patients with prolonged exposure can develop partial and full thickness burns due to dermal absorption. These patients should receive emergency consultation with a burn specialist. Initial management of these chemical burns is described separately. (See "Topical chemical burns: Initial evaluation and management".)

•Parenteral injection of hydrocarbons can cause major tissue destruction including tissue necrosis and necrotizing fasciitis. These patients warrant emergency surgical consultation and hospital admission. (See 'Intentional parenteral injection' above.)

•High-pressure paint injection injuries are deceptive because the extent of chemical contamination is usually much greater than what is initially apparent on inspection. Initial treatment consists of tetanus prophylaxis, prophylactic antibiotics targeting skin pathogens (including methicillin-resistant S. aureus in regions with high prevalence), and emergency consultation with a hand surgeon. (See 'High-pressure paint injection' above.)

•Hydrocarbon inhalation is discussed in detail separately. (See "Inhalant misuse in children and adolescents", section on 'Management'.)

•Treatment of organophosphate poisoning is provided in the table (table 1) and discussed in detail separately. (See "Organophosphate and carbamate poisoning".)