Methyl Alcohol Poisoning Research Articles

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Methyl alcohol intoxication is a global problem with high mortality and long-term visual sequelae and severe brain damage in survivors. The role of neuroinflammation in the mechanisms of methyl alcohol-induced toxic brain damage has not been well studied. We measured the acute concentrations and dynamics of lipoxins LxA4 and LxB4 and the interleukins IL-4, IL-5, IL-9, IL-10, and IL-13 in the serum of patients treated with methyl alcohol poisoning and the follow-up concentrations in survivors two years after discharge from the hospital. A series of acute measurements was performed in 28 hospitalized patients (mean age 54.2 ± 5.2 years, mean observation time 88 ± 20 h) and the follow-up measurements were performed in 36 subjects who survived poisoning (including 12/28 survivors from the acute group). Visual evoked potentials (VEP) and magnetic resonance imaging of the brain (MRI) were performed to detect long-term visual and brain sequelae of intoxication. The acute concentrations of inflammatory mediators were higher than the follow-up concentrations: LxA4, 62.0 ± 6.0 vs. 30.0 ± 5.0 pg/mL; LxB4, 64.0 ± 7.0 vs. 34.0 ± 4.0 pg/mL; IL-4, 29.0 ± 4.0 vs. 15.0 ± 1.0 pg/mL; IL-5, 30.0 ± 4.0 vs. 13.0 ± 1.0 pg/mL; IL-9, 30.0 ± 4.0 vs. 13.0 ± 1.0 pg/mL; IL-10, 38.0 ± 5.0 vs. 16.0 ± 1.0 pg/mL; IL-13, 35.0 ± 4.0 vs. 14.0 ± 1.0 pg/mL (all p < 0.001). The patients with higher follow-up IL-5 concentration had prolonged latency P1 (r = 0.413; p = 0.033) and lower amplitude N1P1 (r = −0.498; p = 0.010) of VEP. The higher follow-up IL-10 concentration was associated with MRI signs of brain necrotic damage (r = 0.533; p = 0.001) and brain hemorrhage (r = 0.396; p = 0.020). Our findings suggest that neuroinflammation plays an important role in the mechanisms of toxic brain damage in acute methyl alcohol intoxication.

Neuroinflammation markers and methyl alcohol induced toxic brain damage

Methyl alcohol intoxication is a global problem with high mortality and long-term visual sequelae and severe brain damage in survivors. The role of neuroinflammation in the mechanisms of methyl alcohol-induced toxic brain damage has not been well studied. We measured the acute concentrations and dynamics of lipoxins LxA4 and LxB4 and the interleukins IL-4, IL-5, IL-9, IL-10, and IL-13 in the serum of patients treated with methyl alcohol poisoning and the follow-up concentrations in survivors two years after discharge from the hospital. A series of acute measurements was performed in 28 hospitalized patients (mean age 54.2 ± 5.2 years, mean observation time 88 ± 20 h) and the follow-up measurements were performed in 36 subjects who survived poisoning (including 12/28 survivors from the acute group). Visual evoked potentials (VEP) and magnetic resonance imaging of the brain (MRI) were performed to detect long-term visual and brain sequelae of intoxication. The acute concentrations of inflammatory mediators were higher than the follow-up concentrations: LxA4, 62.0 ± 6.0 vs. 30.0 ± 5.0 pg/mL; LxB4, 64.0 ± 7.0 vs. 34.0 ± 4.0 pg/mL; IL-4, 29.0 ± 4.0 vs. 15.0 ± 1.0 pg/mL; IL-5, 30.0 ± 4.0 vs. 13.0 ± 1.0 pg/mL; IL-9, 30.0 ± 4.0 vs. 13.0 ± 1.0 pg/mL; IL-10, 38.0 ± 5.0 vs. 16.0 ± 1.0 pg/mL; IL-13, 35.0 ± 4.0 vs. 14.0 ± 1.0 pg/mL (all p < 0.001). The patients with higher follow-up IL-5 concentration had prolonged latency P1 (r = 0.413; p = 0.033) and lower amplitude N1P1 (r = −0.498; p = 0.010) of VEP. The higher follow-up IL-10 concentration was associated with MRI signs of brain necrotic damage (r = 0.533; p = 0.001) and brain hemorrhage (r = 0.396; p = 0.020). Our findings suggest that neuroinflammation plays an important role in the mechanisms of toxic brain damage in acute methyl alcohol intoxication.

Diagnostics of methyl alcohol intoxication: possibilities&#x0D; and prospects

Intake of toxic alcohols especially methyl alcohol posses a serious threat to health. Despite relatively low toxicity of methanol (hazard class III), its metabolite formic acid resulting from biotransformation of methyl alcohol by alcohol dehydrogenase is ranked among substances creating a high risk of toxic action. The long period of methanol toxification (~48 hr) makes difficult diagnostics of intoxication and therefore delays provision of emergency medical aid. It imposes high requirements on express diagnostics of methyl alcohol intoxication (Т51.1 ICD-10). The main diagnostic modality - routine evaluation of osmolar and anion gaps, has advantages and disadvantages. Drawbacks of emergency medical aid to the victims of methyl alcohol intoxication necessitates the search for new diagnostic options some of which sre discussed in the present article.

Neuromuscular Functions on Experimental Acute Methanol Intoxication.

The incidence of accidental or suicidal ingestion of methyl alcohol is high and methyl alcohol intoxication has high mortality. Methyl alcohol intoxication causes severe neurological sequelae and appears to be a significant problem. Methyl alcohol causes acute metabolic acidosis, optic neuropathy leading to permanent blindness, respiratory failure, circulatory failure and death. It is metabolised in the liver, and its metabolite formic acid has direct toxic effects, causing oxidative stress, mitochondrial damage and increased lipid peroxidation associated with the mechanism of neurotoxicity. Methanol is known to cause acute toxicity of the central nervous system; however, the effects on peripheral neuromuscular transmission are unknown. In our study, we aimed to investigate the electrophysiological effects of experimentally induced acute methanol intoxication on neuromuscular transmission in the early period (first 24 h). After approval by the Animal Experiment Ethics Committee of Ege University, the study was carried out on 10 Wistar rats, each weighing about 200 g. During electrophysiological recordings and orogastric tube insertion, the rats were anaesthetised using intra-peritoneal (IP) injection of ketamine 100 mg kg(-1) and IP injection of xylazine 10 mg kg(-1). The rats were given 3 g kg(-1) methyl alcohol by the orogastric tube. Electrophysiological measurements from the gastrocnemius muscle were compared with baseline. Latency measurements before and 24 h after methanol injection were 0.81±0.11 ms and 0.76±0.12 ms, respectively. CMAP amplitude measurements before and 24 h after methanol injection were 9.85±0.98 mV and 9.99±0.40 mV, respectively. CMAP duration measurements before and 24 h after methanol injection were 9.86±0.03 ms and 9.86±0.045 ms, respectively. It was concluded that experimental methanol intoxication in the acute phase (first 24 h) did not affect neuromuscular function.

Adaptation of international guidelines for management of methyl alcohol poisoning in patients admitted to the Poisoning Unit in Alexandria Main University Hospital

Background Methanol intoxication is one of the cases of toxicity seen in the Poison Unit in Alexandria Main University Hospital (AMUH). Well-planned evidence-based clinical practice guidelines are needed for the triage and management of these patients. Aim The aim of this study was to adapt the international guidelines on the management of acute methanol intoxication to local use to improve the quality of medical service provided at the AMUH Poison Unit. Patients and methods All patients with acute methanol toxicity admitted to the Poison Unit of AMUH between 1 December 2012 and 31 May 2013, a total of 19 patients, were included in the study. Their diagnosis and management were recorded for analysis. Results More than half of the studied cases (57.9%) of methanol toxicity were cases of severe toxicity. All cases received respiratory care, care for circulation, and fluid therapy. All of them suffered from acidosis. An overall 63.2% of patients recovered with good outcome and the most common complication was severe metabolic acidosis (68.4%). A high percentage of patients were not followed up (84.0%) and hence the dangerous effects of methanol toxicity on them could not be ascertained. Conclusion The management of methanol poisoning includes standard supportive care, correction of metabolic acidosis, no administration of antidotes, and selective hemodialysis to correct severe metabolic abnormalities and enhance methanol and formate elimination.

Muerte cerebral secundaria a intoxicación por metanol

Las intoxicaciones por alcohol metílico son raras, pueden ser secundarias a intentos suicidas, accidentes e incluso a envenenamientos endémicos, tienen consecuencias severas que incluyen la muerte, secundarias a productos de la degradación del alcohol metílico por la alcohol deshidrogenasa, a continuación, presentamos un caso de intoxicación por alcohol metílico que como secuelas presentó alteraciones neurológicas y muerte

Fatal ethyl and methyl alcohol-related poisoning in Ankara: A retrospective analysis of 10,720 cases between 2001 and 2011

Methyl and ethyl alcohol poisoning are still responsible for high morbidity and mortality rates. The purpose of this retrospective study was to examine ethyl and methyl alcohol poisoning related deaths in Ankara and surrounding cities between 2001 and 2011 and compare them with previous studied conducted in Turkey and other countries. For this purpose, 10,720 medico-legal autopsy cases performed in Ankara Branch of the Council of Forensic Medicine were reviewed in terms of alcohol poisonings.The deaths due to methanol and ethanol poisoning were 74 (0.69% of all medico-legal autopsies performed) and the distribution among them was 35 (47.3%) for methanol poisoning and 39 (52.7%) for ethanol poisoning. Overwhelming majority of the cases were male (n = 67, 90.5%). The mean age of the victims was 44.9 ± 10.9 years and ranging from 21 to 92 years. The age group of 35–49 years was the mostly affected. Most of the cases were seen in 2004 (n = 12, 16.2%). The levels of postmortem blood alcohol levels were available for all cases and the mean alcohol levels were 322.8 ± 155.5 mg/dL ranging from 74 to 602 mg/dL for methanol and 396.8 ± 87.1 mg/dL and ranging from 136 to 608 mg/dL for ethanol.Early diagnosis is essential for successful treatment in methanol and ethanol poisoning. Besides increased awareness, more sensitive/specific diagnostic tools, and the prompt approach to the poisoned individual should be implemented in the hospitals.

Methyl alcohol poisoning - a morphological study for 20-years period

The clinical manifestations of methanol poisoning have been the subject of several review articles over the past forty years (2, 11), though de tailed post mortem pathologic studies are relatively few. The earliest autopsy studies on methanol poisoning have emphasized the acute changes secondary to hypoxic or ischemic in jury to the gray matter, cerebral oedema and acute neuronal in jury. Post mortem studies of individuals, who survive intoxication several days or weeks have shown brain in jury characterized by bilateral putamen necrosis, particularly affecting the lateral portions of the nuclei (1, 10). In some of the cases there has also been a dramatic pattern of white matter hemorrhagic necrosis, involving the centrum semiovale, especially affecting subcortical regions /10/. The precise mechanism of methanol toxicity remains a matter of debate /2/. The observed lesions represent direct toxic effects of methanol and its metabolites and injury, secondary to anoxia and acidosis. In jury to the putamen likely represents a selective toxic effect, possibly potentiated by poor venous drain age. The pathogenesis of the white matter hemorrhagic necrosis remains unexplained /6/. Scripta Scientifica Medica 2008; 40(2): 175-176.

FATAL POISONINGS IN THE SOUTH MARMARA REGION OF TURKEY

Aim: The aim of this study is to describe the characteristics of medico-legal autopsies of fatal poisonings in the south Marmara region, Turkey, in the period of 1996-2003, in order to provide further data for the characterisation of fatal poisonings, because there is a scarcity of such information from Turkey. Methods: Of the 4242 autopsied cases, 415 (9.8%) deaths due to poisonings were examined; 26.8% females and 73.2% males. The mean age was 40.1±19.2 years old (range 0-88). Results: The three most common types of poison were carbon monoxide (43.5%), insecticides (24.6%), and alcohol (18.4%). The most frequent unnatural manner of death was accidents (67.5%), followed by suicidal (27.5%) deaths. Insecticides were the cause in 71.9% of suicidal poisonings, whereas the cause was carbon monoxide in 63.2%, and alcohol in %27.1% of the unintentional poisonings. The deaths due to carbon monoxide were associated with coal stoves (48.3%), water heaters in bath (31.1%), and fires (17.8%). Organophosphorus insecticides were responsible for 91.1% of total insecticide poisonings. 73.7% of the alcohol poisonings were observed in years 2000-2002, and of the methyl alcohol poisoning, 35.9% and 29.7% were seen in years 2001 and 2002, respectively. Therapeutic drugs were encountered most frequently (75%). Conclusion: In conclusion, in fatal poisoning cases who have undergone medico-legal autopsy in Bursa and province, CO is of great ratio.

Intravenous methylprednisolone could salvage vision in methyl alcohol poisoning

Intravenous methylprednisolone could salvage vision in methyl alcohol poisoning

Intoxicación por alcoholes

Alcohol intoxication is the principal drug addiction in many countries of the world. It affects all age groups, both sexes and almost all social groups. Mortality associated with acute alcohol poisoning on its own is exceptional, but it can be an important factor if it coexists with recreational drugs. It is directly responsible for more than half of traffic accidents. Diagnosis is easy by means of anamnesis and clinical examination, and can be confirmed by determining the level of ethanol in the bloodstream. Supportive care is the best therapy in order to protect the patient from secondary complications. Methanol, or alcohol fuel, is used as a solvent, and can also be found as an adulterant of alcoholic drinks. Poisoning by oral means is the most frequent. Oxidized in the liver through dehydrogenase enzyme alcohol, toxicity is due to its metabolites, formaldehyde and formic acid. The clinical picture basically consists of cephalea, nausea, vomiting, hypotension and depression of the central nervous system. The optic nerve is especially sensitive, with total and irreversible blindness as a possible result. Ethylenglicol is used as a solvent and as an antifreeze; toxicity is due to an accumulation of its metabolites. The clinical picture includes symptoms that are held in common with methylalcohol intoxication. Kidney failure due to tubular necrosis and the deposit of oxalate crystals can occur.

Fatalities due to methyl alcohol intoxication in Turkey: an 8-year study

The aim of this study is to examine methyl alcohol poisoning cases from the medico-legal point of view. The records of the Morgue Department of Council of the Forensic Medicine were reviewed retrospectively for all methyl alcohol poisonings for the period of 27.10.1992 and 30.05.2001. The victim’s age, sex, death year, death place, methyl alcohol blood levels, the source of methyl alcohol, accompanying laboratory results and histopathologic tissue changes were recorded. The number of deaths due to the methyl alcohol poisoning was 271 during that period of time. Two hundred and forty-two of the (89.3%) total 271 methyl alcohol fatalities were men and 29 (10.7%) of were women. The largest age group was 36–40 years old, followed by 41–45. The methyl alcohol blood concentrations ranged widely from 50 to 755 mg for per 100 ml. There were 222 cases (81.9%) with the methyl alcohol blood concentrations over 100 mg/dl. Twenty-nine (10.7%) victims were poisoned through the consumption of cologne and three of them with alcoholic beverage named “Raki”. Consumed products were not known in all other cases because of insufficient patient history and data. As a conclusion, regarding the distribution according to years, mortality due to methyl alcohol intoxication in our country have been proceeding on a certain level. In order to decrease the mortality due to methyl alcohol intoxication, some precautions should be developed that could prevent the production and consumption of alcoholic beverages illegally produced.

Recognition and treatment of methyl alcohol poisoning

Recognition and treatment of methyl alcohol poisoning

Hyperamylasemia Following Methyl Alcohol Intoxication

Methyl alcohol intoxication has been reported to cause hyperamylasemia and pancreatitis. We describe a patient with severe, nonfatal methyl alcohol intoxication who had a rise in serum amylase activity with the level peaked on the second hospital day at tenfold the upper limit of normal. However, isoamylase analysis showed that this striking hyperamylasemia was due to salivary-type amylase. Furthermore, the serum lipase activity remained entirely normal during the peak amylase elevation. Thus, in cases of methyl alcohol intoxication, as in other clinical situations, hyperamylasemia, even when striking, should not be equated with pancreatitis. More specific laboratory tests for pancreatitis should be used before embarking on extensive investigations of the pancreas.

Hyperamylasemia following methyl alcohol intoxication. Source and significance

Hyperamylasemia following methyl alcohol intoxication. Source and significance

Visual loss in methyl alcohol poisoning

Visual loss in methyl alcohol poisoning

Ethylene Glycol Poisoning

<h3>To the Editor.—</h3> We read the recent case reports of massive ethylene glycol ingestion by Stokes and Aueron (1980;243:2065) and by Peterson et al.¹Our own experience in a recent ethylene glycol poisoning, where the diagnosis was not evident from the patient's history and made only post mortem, caused us to review the clinical indications and available methods for ethylene glycol determination. A metabolic acidosis value with a high anion gap and a substantial discrepancy between the measured and calculated osmolality is suggestive of ethylene glycol or methyl alcohol intoxication. In either case, one must often start therapy with the infusion of ethyl alcohol, correction of the acidosis with sodium bicarbonate, and preparation for dialysis before there is laboratory confirmation. If a gas chromatograph is available for volatile toxins, a change in the usual screening conditions will include ethylene glycol among the identifiable poisons. As usually performed, volatile screens

Methyl alcohol poisoning in an 8-month-old boy: An unusual route of intoxication

Methyl alcohol poisoning in an 8-month-old boy: An unusual route of intoxication

An Outbreak of Acute Methyl Alcohol Intoxication

An outbreak of acute methyl alcohol intoxication occurred in Port Moresby, Papua New Guinea, in March 1977. Twenty-eight young men attended a drinking party and drank methyl alcohol. The amount consumed by each individual ranged from an equivalent of 60--600 ml of pure methanol. Three had prior ethanol ingestion. All 28 became ill 8--36 hours after drinking and were hospitalized. The most commonly observed clinical syndromes were: acute metabolic acidosis, severe visual impairment and acute pancreatitis. Four died within 72 hours after admission to the hospital. All had severe metabolic acidosis and visual impairment and three pancreatitis. Of 24 who recovered, 16 showed no residual complications, six had bi-lateral visual impairment and two had difficulty in speech as well as visual impairment. A three month follow-up examination showed no change in the findings. Coma, seizures and prolonged acidosis were poor prognostic signs. The estimated amount of consumed methanol and the rapidity of the appearance of signs of toxicity following methanol ingestion did not seem to influence the outcome of poisoning. The treatment of acute methyl alcohol intoxication in centres where dialysis is not available is discussed.

Ocular manifestations and complications of acute methyl alcohol intoxication.

The ocular manifestations of acute methyl alcohol intoxication were studied in 24 men during an outbreak in Port Moresby, Papua New Guinea. The visual acuity, pupillary reactions to light, fundal appearances and visual fields were recorded in all patients within 72 hours of ingestion of methanol and again three months later. Three groups were identified. Nine patients had no ocular abnormality (Group 1). Seven patients had only transient ocular abnormalities (Group 2). Eight patients had permanent ocular abnormalities (Group 3). Transient abnormalities included peripapillary oedema, optic disc hyperaemia, diminished pupillary reactions to light, and central scotomata. Permanent ocular abnormalities included optic disc pallor, attenuation of arterioles, sheathing of arterioles, diminished pupillary reaction to light, diminished visual acuity, central scotomata, and other nerve fibre bundle defects. Complete blindness occurred in two patients, while severe visula deficit resulted in four others. The incidence of permanent ocular abnormalities was found to correlate with the incidence of metabolic acidosis (P less than 0.01), and with the stated volume of methanol consumed (P less than 0.05). An inverse correlation was found between stated volume of methanol consumed and onset of blurred vision. The difficulties in management and rehabilitation of these patients are discussed.