Acute exposure

Inhalation

The victim should be removed from exposure and all contaminated clothing removed. The carboxyhaemoglobin concentration should be determined and 100% oxygen given. The ECG, renal function and liver function should be monitored in symptomatic patients. Symptomatic and supportive care. See below for management of systemic effects.

Dermal

Contaminated clothing should be removed and the skin thoroughly irrigated with water or saline. Further treatment is symptomatic and supportive. See below for management of systemic effects.

The eyes should be thoroughly irrigated with water or saline for 15 minutes and then stained with fluorescein. Referral to an ophthalmologist is recommended if there is any uptake of fluorescein.

Toxicology of Solvents Ingestion

Methylene chloride is radiopaque (Dally et al., 1987) and an X-ray may confirm ingestion. Emesis and gastric lavage are contraindicated due to the corrosive effects of methylene chloride. Nasogastric aspiration up to one hour post-ingestion may be considered if a large volume has been ingested. This is likely to be relevant only in deliberate ingestions. However, aspiration of the stomach contents may prove difficult. An 18 month old boy swallowed an unknown amount of paint stripper (methylene chloride 81%, methanol 14%) and when nasogastric aspiration of the stomach contents was attempted, the tip of the tube dissolved in the paint stripper. Aluminium hydroxide gel was passed down the tube and an hour later when the stomach contents were aspirated, gastric mucosa was found in the aspirate (Bates, 1997).

Oral fluids may be given unless perforation is suspected. In cases of suspected corrosive injury, gastro-oesophagoscopy should be undertaken within 12-24 hours of the event to assess the extent and severity of the injury. Prolonged follow up and treatment including surgical intervention may be required for patients with perforation or stricture. See below for management of systemic effects.

Systemic effects

Carboxyhaemoglobin concentrations should be measured in all cases where systemic effects are present (even in mild cases where headache or nausea are the only symptoms). 100% oxygen should be given. Carboxyhaemoglobin concentrations are thought to increase within two hours of inhalation exposure, but concentrations may continue to rise after exposure to methylene chloride has ceased. The half-life of carboxyhaemoglobin produced by methylene chloride exposure is about 2.5 times longer than after exposure to carbon monoxide, so oxygen therapy is likely to be more prolonged in methylene chloride exposure cases. Oxygen should be administered until the carboxyhaemoglobin is less than 5%. The ECG, arterial blood gases, liver and renal function should be monitored.

Despite the fact that hyperbaric oxygen therapy does not seem to significantly decrease the half-life of carboxyhaemoglobin after methylene chloride exposure, its use has improved the outcome in some cases (Rioux and Myers, 1989). Hyperbaric oxygen therapy may be considered for patients with prolonged CNS effects or persistently elevated concentrations of carboxyhaemoglobin despite normobaric oxygen therapy.

Antidotes Oxygen

Oxygen is administered following methylene chloride exposure to enhance the dissociation of carboxyhaemoglobin and thereby increase oxygen delivery to tissues. Normobaric oxygen therapy has been shown to decrease the half-life of carboxyhaemoglobin resulting from exposure to methylene chloride, and most cases of methylene chloride poisoning can be managed supportively with 100% oxygen (Tomaszewski and Thom, 1994).

The half-life of carboxyhaemoglobin subsequent to methylene chloride exposure varies as follows:

• 13 hours in a subject breathing normal air (Ratney et al., 1974),

• 5.8 hours in a subject breathing 100% oxygen (Rioux and Myers, 1989),

• 4.75-6.8 hours in a subject breathing hyperbaric oxygen (Rioux and Myers, 1989).

Hyperbaric oxygen

Hyperbaric oxygen involves inhalation of oxygen at a pressure greater than 1 atm (usually 2-3 atm). It is commonly used to treat cases of decompression sickness and air embolism, and is also used to treat carbon monoxide poisoning where it has been shown to decrease the half-life of carboxyhaemoglobin (Tomaszewski and Thom, 1994). In contrast, it has not been shown to significantly decrease the half-life of carboxyhaemoglobin following methylene chloride exposure and did not prevent elevations of carboxyhaemoglobin in two patients (Rioux and Myers, 1989). However, its use has improved clinical outcome in acutely poisoned patients (Rioux and Myers, 1989; Rudge, 1990) and should be considered in patients with prolonged CNS effects or persistently elevated concentrations despite normobaric oxygen therapy.

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