Acute Methyl Alcohol Poisoning: A Review Based on Experiences in an Outbreak of 323 Cases

Bennett, Ivan L.; Cary, Freeman H.; Mitchell, George L.; Cooper, Manuel N.

doi:10.1097/00005792-195312000-00002

Cited by 281 publications

(146 citation statements)

References 0 publications

Supporting

Mentioning

137

Contrasting

Unclassified

Order By: Relevance

Section: B Ocular Symptoms And/or Findingsmentioning

confidence: 84%

“…It appears that the absence of initial inebriation would be more likely to occur with methanol rather than ethylene glycol poisoning. Cases of methanol poisoning in which individuals were noted to be "rational and conversing, and …ambu-latory" who soon became comatose have been described [12]. Inference from a rat study suggests why inebriation may be less likely with methanol than with ethylene glycol [13].…”

Section: A Inebriationmentioning

confidence: 99%

“…A conscious patient may describe vision changes, and mydriasis with sluggishly responsive or unresponsive pupils may be identified in a patient with methanol toxicity [12]. However, the absence of either findings cannot reliably exclude methanol poisoning, and neither were present in this patient [12]. Blindness, in the setting of a severe acidosis, is also not specific for methanol, as it has been described in both alcoholic ketoacidosis and metformin-associated lactic acidosis (MALA) [17][18][19][20][21].…”

Section: B Ocular Symptoms And/or Findingsmentioning

confidence: 99%

See 2 more Smart Citations

Case Files from the University of California San Diego Health System Fellowship Coma and Severe Acidosis: Remember to Consider Acetaminophen

Villano

O'Connell

et al. 2015

J. Med. Toxicol.

View full text Add to dashboard Cite

A 28-year-old man was brought to the Emergency Department (ED) for evaluation of a depressed level of consciousness that developed while in jail. Sixteen hours previously, he had been arrested on charges of murder. The patient's mental status was reported as normal at the time of arrest, and it had remained so during several hours of interrogation and during the booking process at jail. Following interrogation, the patient was placed into a cell with no other inmates. During the jail intake process, the patient had not reported any history of medical problems nor was he prescribed with any medications. Paramedics arrived to find him unresponsive, but maintaining airway reflexes and hemodynamically stable. They measured a blood glucose of 300 mg/dL and noted one episode of blood-tinged emesis during transport to the ED. No seizure activity was witnessed.On arrival to the ED, vital signs were: heart rate 132/min, blood pressure 129/74 mmHg, temperature 35.3°C (95.5°F), respiratory rate 24/min, and 100 % oxygen saturation on 15 l/ min of oxygen delivered by non-rebreather face mask.Physical examination was notable for a depressed level of consciousness. His eyes remained closed to pain, he withdrew all extremities equally to pain, and he was non-verbal. He had no signs of trauma, and his pupils were normal in size and reactive. Rapid sequence tracheal intubation was performed for airway protection. An electrocardiogram was normal except for sinus tachycardia at a rate of 111/min. An initial peripherally drawn arterial blood gas obtained immediately after intubation revealed: pH 6.97, pCO 2 40 mmHg, pO 2 215 mmHg. A computed tomography scan of the brain was normal. Initial blood chemistry panel was significant for a serum bicarbonate of 7 mEq/L, glucose of 362 mg/dL, and a normal potassium, blood urea nitrogen (BUN), creatinine, and calcium. The initial serum anion gap was 34 mEq/L. Measured serum osmolality was 320 mOsm/kg, yielding an osmol gap of 9 mOsm/kg (using formula of [2(Na)+BUN/2.8+glu-cose/18] for calculated serum osmolarity). Initial lactate was 156.5 mg/dL (normal reference range 4.5-19.8 mg/dL) and beta-hydroxybutyrate (βHB) 2.9 mg/dL (normal reference range 0.0-2.8 mg/dL). Initial liver panel included an aspartate aminotransferase (AST) of 64 U/L, alanine aminotransferase (ALT) of 27 U/L, and bilirubin of 0.4 mg/dL. Prothrombin time was 13.1 s (reference range 9.7-12.5), and lipase was normal at 25 U/L. Initial creatinine phosphokinase (CK) was slightly elevated at 373 U/L (0-175). Urinalysis was positive for small ketones and crystals were not present. Measurements of acetone and acetoacetate were not performed. Serum ethanol and salicylate levels were undetectable, and a urine drug of abuse panel by immunoassay was negative for amphetamines as a class, barbiturates as a class, benzodiazepines as a class, benzoylecgonine (cocaine metabolite), methadone, opiates as class, oxycodone, phencyclidine, and tetrahydrocannabinoids. Iron concentration was normal at 87 mcg/dL.Over the first hour of management,...

show abstract

Section: B Ocular Symptoms And/or Findingsmentioning

confidence: 84%

Section: A Inebriationmentioning

confidence: 99%

Section: B Ocular Symptoms And/or Findingsmentioning

confidence: 99%

See 1 more Smart Citation

Case Files from the University of California San Diego Health System Fellowship Coma and Severe Acidosis: Remember to Consider Acetaminophen

Villano

O'Connell

et al. 2015

J. Med. Toxicol.

View full text Add to dashboard Cite

show abstract

“…Formic acid is responsible for the characteristic signs and symptoms of methanol toxicity such as coma, seizure, visual disturbances, and metabolic acidosis with a high plasma anion gap [1][2][3][4]. Also, due to inhibition of mitochondrial cytochrome oxidase by formate, lactic acid accumulation can occur [5][6][7][8][9][10][11]. Two antidotes for methanol intoxication include ethanol and fomepizole since they both are competitive inhibitors of ADH [1,12,13].…”

mentioning

confidence: 99%

“…None of the laboratory tests of the patient including arterial blood gases, measured osmolality, osmolal gap, and calculated anion gap was abnormal 5 and 11 h after the ingestion of methanol. Since methanol is rapidly absorbed after ingestion, its serum concentration usually reaches the peak level within 30 to 60 min [1], and the methanol-intoxicated patient generally becomes symptomatic within 6 to 30 h post-ingestion [8,9]. With this amount of pure methanol ingested, as the authors themselves suggested [17], their patient should have become symptomatic or at least have developed metabolic acidosis within this period of time (11 h).…”

mentioning

confidence: 99%