We present a 52-year-old woman who had serious symptoms of methanol intoxication. She was initially admitted to the emergency department with symptoms of fatigue, pain and lethargy to another centre. She had normal cranial tomography (CT) findings in that centre and had been discharged home. The following day her symptoms worsened, and she was admitted to our hospital. In the emergency room she had visual loss, deteriorating mental state and hyperventilation. She became unresponsive with a Glasgow Coma Scale score of 3. Other observations were as follows: blood pressure (BP) 90/60 mmHg, heart rate (HR) 110 beats min−1 and body temperature 38°C. The arterial blood gases were: pH 6.94, PCO2 13.3 mmHg, PO2 189.9 mmHg (breathing oxygen via a face mask at 6 L min−1) and HCO3 of 2.9 mmol L−1. The anion gap was 32 mmol L−1 with an osmolality of 316 mosm kg−1. She was intubated orally in the emergency room and admitted to the intensive care unit (ICU). It was subsequently learned from her relatives that the patient had suffered with chronic shoulder, back, knee and elbow pain and she had used cologne and spirit to massage her legs and arms. In the last 3 days she had more frequent massage because of aggravated pain. There was no known history of drinking such substances.
The patient was mechanically ventilated in the ICU. After correction of acidosis with intravenous (i.v.) NaHCO3 (150 mmol NaHCO3 bolus, 150 mmol NaHCO3 infusion for 24 h) her blood gases were: pH 7.37, PCO2 34.6 mmHg, PO2 61 mmHg (FiO2 0.3), HCO3 20.4 mmol L−1. Mechanical ventilation was terminated after 4 h in the ICU, and the patient was extubated after 8 h. Her vital signs were: BP 110/70 mmHg, HR 110 beats min−1 and body temperature 37°C. The patient's neurological status quickly improved. The blood chemistry was: Na 147 mmol L−1, K 3.2 mmol L−1, Cl 112 mmol L−1, urea 54 mg dL−1, creatinine 1.9 mg dL−1, glucose 214 mg dL−1. Her APACHE II score at 24 h was 23. Therapy included NaHCO3 infusion for correction of metabolic acidosis, haemodialysis (two periods, each lasted 4 h) for elimination of toxins, ethyl alcohol (1 g kg−1 bolus and 0.1 g kg−1 h−1 infusion via a nasogastric tube) and folate (1 mg kg−1, six times per day). After 3 days she was discharged from the ICU to a ward then to home on the 5th day. By the time of discharge, she had 3/5 right monoparesis, left hemihypoaesthesia and bilateral optical disc atrophy. CT findings were frontal subcortical necrosis and bilateral lentiform nuclei hypodensity.
Methanol intoxication usually occurs when taken orally but inhalational and dermal exposure to methanol can cause clinical intoxication. Although methanol is not toxic itself, more than 95% is metabolized to formaldehyde by alcohol dehydrogenase and then to formic acid by aldehyde dehydrogenase. The remainder, which is not metabolized, is excreted via the kidneys and lungs. Acidosis is mainly caused by formic acid. Methanol has poor affinity for alcohol dehydrogenase which can delay clinical toxicity by up to 24 h after ingestion. Ocular damage and acidosis may occur when blood levels reach 20 mg dL−1.
Of the reported alcohol poisonings from 1993 to 2002 in Izmir, Turkey, 11.3% were methanol induced. . Abuse ratio of methanol intoxication is 55.7% in Turkey and 8.3% in the USA . Of the reported cases, all had taken methanol as spirits, cologne or in anti-freeze form via the oral route . The diagnosis of methanol intoxication can be made by observing mental changes, anion gap, metabolic acidosis, visual disturbances and methanol ingestion history. Blood methanol levels or methanol concentration, which is calculated from osmolal gap, can make the diagnosis more accurate . In our hospital blood methanol levels cannot be measured so the diagnosis was based on the clinical history, anion gap, metabolic acidosis, high osmolality and the patients clinical condition. Almost all of the patients who need ICU treatment have taken methanol orally. Our patient has no history of oral ingestion but her history included extensive use of spirit and cologne topically. In the days before admission to hospital, she had increased the frequency and amount of methanol administration. Dermal methanol intoxication is reported to be rare . Our patient suffered more serious intoxication than has been previously reported. Cutaneous absorbtion of methanol may increase blood levels and methanol can enter the systemic circulation following 4 h of exposure . Methanol intoxication may cause liver damage. It has been demonstrated experimentally that N-acetyl cysteine may prevent liver damage in such conditions . We prescribe N-acetyl cysteine for our methanol intoxicated patients in the ICU (300 mg three times per day i.v.). The patient had normal liver function tests during her follow up in hospital.
Permanent visual loss may be seen in methanol intoxicated patients. Optic atrophy and blindness may occur according to the severity of intoxication. This patient also had some neurological deficit. CT and magnetic resonance imaging findings may include bilateral haemorrhagic necrosis in the putamen and caudate nuclei, diffuse subcortical white and grey matter necrosis, cerebellar and optic nerve necrosis, cerebral and intraventricular haemorrhage and diffuse cerebral oedema . Our patient had developed a frontal subcortical infarct and bilateral lentiform nuclei hypodensity.
It is important for the clinician to consider unusual routes of administration when investigating poisonings.
M. Y. Ozkalkanli
a1Izmir Ataturk Training and Research Hospital, Anesthesiology and Reanimation Clinic, Intensive Care Department, Izmir, Turkey
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