Sajid Maqbool*
Dean & Professor of Pediatrics, The Children's Hospital & The Institute of Child Health, Lahore, Pakistan *
Toxicity of these hydrocarbons (HC) depends on the dose, route, volatility and viscosity of the HC product as well as the additives. Lungs are affected most commonly, but CNS, heart, GI tract, kidneys, skin or hematological involvement may also be seen. Causes of HC poisoning are accidental ingestion; intentional abuse (recreational purposes) and massive oral ingestions are associated with suicide attempts.

Compounds with less viscosity, low surface tension and high volatility are more toxic. Pulmonary toxicity is due to aspiration and resultant chemical pneumonitis. The resultant V/Q mismatch contributes to hypoxemia and ultimately respiratory failure. Direct mucosal irritation and quick absorption across tissue layers can also cause toxicity. Ingestions thus can cause chemical burns, with burning pain in the mouth, throat, abdominal pain, nausea and vomiting. Being lipophilic HC are attracted to lipid rich neural tissue. Systemic absorption can cause CNS & peripheral nervous system toxicity. Exposure to some HC's (n-hexane, methyl n-butyl ketone) may cause demyelinating peripheral neuropathy whereas chronic headaches, ataxia, cognitive and psychopathic impairment may be seen after long term workplace exposure to other volatile HC's.

About 0.23-3.3% of the poisonings are due to HC, with mortality of 0.64 to 11.6% and occurs below 5 years (peak age 2-3 years) with predominantly male affection. Uneducated parents, low socioeconomic status, frequent change or residence, large family size, anxiety or depression, and single parent are some of the risk factors for HC poisoning.
Clinical features:
  • Local - Mucous membrane burning, pruritis, or rash
  • RS - Respiratory distress may develop within 30 minutes

  • GIT - Nausea, vomiting, and sore throat (usually with furniture polish)
  • CNS - Transient euphoria (solvent abuse), lethargy, dizziness, ataxia and depressed sensorium usually associated with significant aspiration pneumonitis or caused by toxic additives from large intestinal ingestions.
  • CVS - Dyspnea, syncope and sudden cardiac death from arrhythmias (A relatively young healthy patient may present in full arrest after engaging in strenuous athletic events following solvent abuse).

Physical Examination:
  • Examination of airway, breathing and circulation (ABCs): Urgently triage patients with signs of respiratory distress and place them in a room where airway management equipment is readily available.
  • Odor on breath or clothes from HCs is a common finding.
  • Skin lesions, such as erythema, blistering, and pain, are common after dermal exposures. Chronic solvent abusers may have perioral and nasal irritant dermatitis or conjunctivitis from repeated contact with HCs. Patients may present with dermal irritation and destruction following injection of HC either subcutaneously or intravenously from suicide attempts or for recreational purposes.
  • Fever often is present but does not correlate with clinical symptoms.
  • Tachypnea, grunting respirations, accessory muscle use, rales, wheezing, or rhonchi indicate pulmonary toxicity. Hypoxia is observed with severe aspiration pneumonia and may lead to cardiac and CNS dysfunction.
  • Cardiac toxicity is rare with acute ingestion. Evidence of cardiac toxicity includes tachycardia, cardiac dysrhythmias, and hypotension.
  • Coma is uncommon. It is present in fewer than 3% of hospitalized patients. Depressed sensorium and lethargy are observed with serious aspiration pneumonia's.
Lab Studies:
Complete blood count: Leukocytosis is common within the first 48 hours, anemia and thrombocytopenia from (DIC), chronic exposure to benzene (aplastic anemia and acute myelogenous leukemia).

Electrolytes, blood urea nitrogen, creatinine:
Hypomagnesemia, hypophosphatemia potassium abnormalities, and anion gap acidosis (toluene exposure). Acute renal failure (rarely massive HC exposure).
Hepatic function:
Elevated aminotransferases may be observed with HC ingestions. The halogenated HCs are particularly hepatotoxic.

Renal failure is documented with HC exposure and a baseline urinalysis may be helpful for substantial exposures.

Arterial blood gases:
Abnormalities include hypoxemia and hypocarbia caused by V/Q mismatch. Methemoglobinemia may be observed following exposure to nitrite-containing HCs (e.g., aniline, nitrobenzene).

Creatine kinase:
Acute rhabdomyolysis reported in association with isolated HC exposure, particularly toluene exposures, is rare.

Chest X-ray:
Occur within 30 minutes of significant aspiration but may be delayed for up to 12 hours, do not correlate with clinical presentation, radiographic abnormalities progressively worsen for the first 72 hours and then resolve over several days.

Obtain an ECG on all substantial HC ingestions. Individuals with solvent abuse are particularly prone to arrhythmias. Observe patients on cardiac monitors.

  • Emergency Department Care: Management for HC ingestion is supportive. No specific antidotes are available. Observe asymptomatic patients for signs of toxicity. The primary and most immediate threat from HC ingestion is pulmonary toxicity.
  • Observe patients in a monitored setting for signs of respiratory distress. Cardiac monitor and pulse oximetry are recommended. Provide supplemental oxygen to all patients with significant HC exposures and obtain intravenous access.
  • For altered mental status, consider naloxone, thiamine and glucose (or check blood glucose level).
  • Patients who show signs of impending respiratory failure, despite supplemental oxygen, may require rapid sequence intubation for definitive airway management. Intubation and positive pressure ventilation may be required for evidence of ongoing respiratory distress. Indications for intubation include apnea, coma, hypoventilation (low tidal volumes), arterial blood gases with PO2 less than 50 or PCO2 more than 50 or evidence of impending respiratory failure.
  • Nebulized albuterol can be administered for bronchospasm. Avoid epinephrine because potential for cardiac arrhythmias exists.

    Patients with hypotension usually respond to IV crystalloid challenge to support intravascular volume. Avoid vasopressors and catecholamines if possible, because of the potential for inducing arrhythmias.
  • Decontamination of the GI tract generally is not recommended because of the risk of aspiration and the low GI toxicity of most HCs. Very large doses of charcoal have been shown to adsorb HCs in the GI tract; however, it is generally not recommended because of increased risk of emesis and subsequent aspiration with charcoal administration. Only attempt gastric lavage after securing the airway with endotracheal intubation. Aggressive gastric decontamination is indicated only for a few select situations in which the inherent toxicity of the HC or additives exceeds the risk of aspiration.
  • In patients with dermal exposure, decontaminate the skin with lipophilic soap and water to prevent further absorption and dermal injury.
  • Steroids, surfactant and prophylactic antibiotics have not demonstrated effectiveness in improving outcomes. Some authors advocate N-acetyl-cysteine for carbon tetrachloride and chloroform but more studies are needed to clarify efficacy.
  • Observe all patients for at least 6 hours post-exposure for signs of toxicity. Admit all symptomatic patients. Asymptomatic patients with a normal chest radiograph and normal oxygenation can be discharged. If reliable follow-up care can be established, patients who are asymptomatic, have a normal respiratory rate and do not require oxygen may be discharged despite mildly abnormal chest x-ray findings.
  • Admit symptomatic patients, those with grossly abnormal chest x-ray findings, abnormal respiratory rate or pulse oximetry and patients with suicidal intent. Admit patients who ingest agents with potential for delayed toxicity (e.g., halogenated HCs, organophosphates).

Inpatient Care:
Treatment is supportive. Most pulmonary symptoms resolve in 72 hours with standard pulmonary support. Patients with marked pulmonary toxicity may require positive end expiratory pressure or continuous positive airway pressure to prevent alveolar collapse. Monitor mechanically ventilated patients for signs of barotraumas. Follow CBC, liver function, and acid-base status. Replace fluids and electrolytes as needed, maintaining the fluid balance at zero, if possible, to avoid pulmonary edema. Consider antibiotics for patients with fever after the first 24-48 hours or with documented bacterial pneumonia from sputum or tracheal aspirate. Patients who fail to respond to conventional therapy may be candidates for extracorporeal membrane oxygenation (ECMO).

Follow up Outpatient Care:
Asymptomatic patients should be seen within 12-24 hours following discharge. Repeat chest x-ray document resolution of abnormalities. Establish baseline pulmonary function tests to detect obstructive pulmonary disease, particularly in children.

Controlling access, making environment safe, adequate parental supervision and safe packaging and storage are some of the ways of prevention.
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