|
1
|
Safari H, Ajudani R, Savaie M, Babadi AJ, Alizadeh P. Intracerebral hemorrhage in methanol toxicity patients during COVID-19 pandemic: case report and review of literature. Forensic Toxicol 2024; 42:242-247. [PMID: 38334843 DOI: 10.1007/s11419-023-00680-y] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/09/2023] [Accepted: 12/18/2023] [Indexed: 02/10/2024]
Abstract
PURPOSE The aim of this study is to examine the clinical and imaging manifestations of methanol toxicity during the COVID-19 pandemic, as well as to review existing studies on this topic. The most common cause of methanol intoxication is methanol-adulterated liquor. The primary metabolite of methanol, formic acid, is responsible for pathological changes. Symptoms typically present within 6-24 h of consumption and can include visual disturbances, acute neurological symptoms, and gastrointestinal issues. During the initial year of the COVID-19 pandemic, methanol poisoning cases increased significantly. METHODS In this study, We present six different patients with methanol intoxication and their clinical and imaging features. RESULTS In the literature review, the most common clinical presentation was loss of consciousness and obtundation and the other was vision loss. CT scan findings showed bilateral putaminal necrosis and hemorrhage in 55% of methanol toxicity patients. CONCLUSION Methanol intoxication, causing bilateral putaminal involvement and a 50% mortality rate in intracerebral hemorrhage patients, warrants urgent toxicological analysis due to potential putaminal hemorrhage.
Collapse
Affiliation(s)
- Hosein Safari
- Pain Research Center, Neurosurgery department, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
| | - Reza Ajudani
- Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
| | - Mohsen Savaie
- Ahvaz Anesthesiology and Pain Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
| | | | - Pooyan Alizadeh
- Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
| |
Collapse
|
|
2
|
Alhusain F, Alshalhoub M, Homaid MB, Esba LCA, Alghafees M, Al Deeb M. Clinical presentation and management of methanol poisoning outbreaks in Riyadh, Saudi Arabia: a retrospective analysis. BMC Emerg Med 2024; 24:64. [PMID: 38627622 PMCID: PMC11020920 DOI: 10.1186/s12873-024-00976-1] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/17/2023] [Accepted: 03/27/2024] [Indexed: 04/19/2024] Open
Abstract
BACKGROUND Acute methanol intoxication, whether unintentional or deliberate, necessitates prompt intervention to prevent severe morbidity and mortality. Homemade alcoholic beverages are a frequent source of such poisoning. This retrospective analysis examined two outbreaks of methanol intoxication in Saudi Arabia. It investigated the clinical presentation, implemented management strategies, and any lasting complications (sequelae) associated with these cases. The aim was to assess the potential impact of different treatment modalities and the timeliness of their initiation on patient outcomes. METHODS This was a retrospective case series of methanol poisoning cases which presented to the adult emergency department (ED) at King Abdulaziz Medical City (KAMC) in Riyadh, Saudi Arabia. There were two separate outbreaks in the city, the first one was from September 1 to September 10, 2020 and the second one was from May 14 to May 20, 2021. Electronic charts were reviewed, and data were extracted to previously prepared data extraction sheets. RESULT From the 22 patients who arrived in the ED alive, the most common complaints were nausea or vomiting followed by altered level of consciousness. About 9% from the patient were hypotensive, 36% were tachycardic, 41% were tachypneic and 4% were having SpO2 < 94%. Brain CT was abnormal in 6 patients. Vision impairment was the most common sequalae of methanol poisoning (7 out of 12 patients who were assessed by ophthalmologist, 58%). When the patients were divided based on severity (mild, moderate, severe), nausea or vomiting and loss of consciousness were the most common complaints among the moderate group while loss of consciousness predominated in the severe group. Two patients presented with low blood pressure and were in the sever group. The severe group had a mean Glasgow Coma Scale (GCS) of 8. Most of the patients in the severity groups underwent the same management apart from those who died or deposited. Eight patients in the severe group had to be intubated. CONCLUSION This study demonstrates the multifaceted clinical presentation of methanol poisoning, culminating in a 17.4% mortality rate. Notably, our findings emphasize the critical role of prompt diagnosis and swift initiation of combined fomepizole therapy and hemodialysis in mitigating mortality and minimizing the potential for chronic visual sequelae associated with methanol poisoning.
Collapse
Affiliation(s)
- Faisal Alhusain
- Emergency Medicine Department, Ministry of the National Guard - Health Affairs, Riyadh, Saudi Arabia.
- King Abdullah International Medical Research Center, Riyadh, Saudi Arabia.
| | - Mohammed Alshalhoub
- Emergency Medicine Department, Ministry of the National Guard - Health Affairs, Riyadh, Saudi Arabia
- King Abdullah International Medical Research Center, Riyadh, Saudi Arabia
| | - Moath Bin Homaid
- Emergency Medicine Department, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia
| | - Laila Carolina Abu Esba
- King Abdullah International Medical Research Center, Riyadh, Saudi Arabia
- Pharmaceutical Care Services, Ministry of the National Guard- Health Affairs, Riyadh, Saudi Arabia
| | - Mohammad Alghafees
- King Abdullah International Medical Research Center, Riyadh, Saudi Arabia
- Surgery Department, Ministry of the National Guard - Health Affairs, Riyadh, Saudi Arabia
| | - Mohammad Al Deeb
- Emergency Medicine Department, Ministry of the National Guard - Health Affairs, Riyadh, Saudi Arabia
- King Abdullah International Medical Research Center, Riyadh, Saudi Arabia
| |
Collapse
|
|
3
|
Takahashi M, Kondo T, Yamasaki G, Sugimoto M, Yoshida H, Harada K, Matsumoto H, Asano M, Ueno Y. An Autopsy Case Report of Homicide by Methanol Intoxication With Pinkish Bilateral Putamina. Am J Forensic Med Pathol 2023; 44:55-58. [PMID: 36037297 DOI: 10.1097/paf.0000000000000790] [Citation(s) in RCA: 2] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
ABSTRACT Many deaths caused by methanol occur as a result of intentional suicide attempts or accidental ingestion, and several investigators have quantified methanol and formic acid in blood and organs. However, to the best of our knowledge, no reports have described regional differences in the concentration of methanol in the brain. A man in his 50s drank alcohol that had been deliberately contaminated with methanol by his wife, and he died of multiple-organ failure after 4 days of intensive medical treatment including hemodialysis. On medicolegal autopsy, cross sections of the brain showed scattered petechial hemorrhage in the brain stem and microscopic hemorrhage with congestion in the bilateral putamina, which showed pinkish discoloration. The concentrations of methanol, formic acid, and ethanol in autopsy samples were measured by headspace gas chromatography, revealing relatively high concentrations of residual methanol and formic acid in the brain (especially in the basal ganglia), although methanol had been eliminated from the blood. Even after 4 days of medical treatment, postmortem toxicological analysis of the brain tissue indicated methanol ingestion. The accumulation of formic acid and the consequent local metabolic acidosis may cause brain lesions.
Collapse
Affiliation(s)
- Motonori Takahashi
- From the Division of Legal Medicine, Department of Community Medicine and Social Health Science, Kobe University Graduate School of Medicine, Hyogo
| | - Takeshi Kondo
- From the Division of Legal Medicine, Department of Community Medicine and Social Health Science, Kobe University Graduate School of Medicine, Hyogo
| | - Gentaro Yamasaki
- From the Division of Legal Medicine, Department of Community Medicine and Social Health Science, Kobe University Graduate School of Medicine, Hyogo
| | - Marie Sugimoto
- From the Division of Legal Medicine, Department of Community Medicine and Social Health Science, Kobe University Graduate School of Medicine, Hyogo
| | | | | | - Hiroshi Matsumoto
- Department of Legal Medicine, Osaka University Graduate School of Medicine
| | - Migiwa Asano
- Department of Legal Medicine, Ehime University Graduate School of Medicine, Ehime, Japan
| | - Yasuhiro Ueno
- From the Division of Legal Medicine, Department of Community Medicine and Social Health Science, Kobe University Graduate School of Medicine, Hyogo
| |
Collapse
|
|
4
|
Ebadi Z, Asadollahzade E, Ghadiri F, Naser Moghadasi A. The first MS attack after methanol toxicity in a young man: a case report. Neurol Sci 2023; 44:2185-2186. [PMID: 36809421 DOI: 10.1007/s10072-023-06689-w] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/08/2023] [Accepted: 02/13/2023] [Indexed: 02/23/2023]
Affiliation(s)
- Zahra Ebadi
- Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran
| | - Elnaz Asadollahzade
- Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran
| | - Fereshteh Ghadiri
- Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran
| | - Abdorreza Naser Moghadasi
- Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.
| |
Collapse
|
|
5
|
McEnery B, Scalzo A, Maliakkal J. Methanol toxicity in a pediatric patient treated with fomepizole and hemodialysis. CEN Case Rep 2022; 12:195-199. [PMID: 36307578 PMCID: PMC10151443 DOI: 10.1007/s13730-022-00744-9] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/18/2019] [Accepted: 10/03/2022] [Indexed: 11/07/2022] Open
Abstract
Methanol toxicity is an important cause of toxic alcohol exposure resulting in morbidity and mortality in both adult and pediatric populations. Methanol is metabolized into formaldehyde and formic acid: toxic metabolites that can cause altered mental status, visual disturbances, multisystem organ failure, and death. Recognition of methanol intoxication and rapid treatment are critical for the prevention of long-term sequelae. We present the case of a 16-year-old male with a past medical history of depression who intentionally ingested windshield wiper fluid containing methanol. Based on the patient's osmolal gap, he was estimated to have a serum methanol level of 374 mg/dL; a send-out laboratory measurement later revealed a serum methanol level of 436 mg/dL. Therapy included two hemodialysis treatments as well as fomepizole and supportive care. The patient recovered remarkably with no long-term sequelae. This case demonstrates the effectiveness of swift recognition and treatment of methanol ingestion. Optimization of methods of measuring serum methanol and evidence-based guidelines for therapy are needed to improve the care of patients with methanol intoxication.
Collapse
|
|
6
|
Yaşgüçlükal MA, Eyüpoğlu S, Kaya B. Late hemorrhagic transformation of brain lesions in case with methanol intoxication. Neuroradiol J 2022; 35:658-661. [PMID: 35487801 PMCID: PMC9513911 DOI: 10.1177/19714009221096822] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/15/2022] Open
Abstract
Methanol intoxication can be occurred as accidental or suicidal ingestion or intentional ingestion through abuse. Formic acid is the primary toxic metabolite which causes high anion gap metabolic acidosis and end-organ damage in the human body. Here we presented a 46-year-old man who loss of consciousness on the 23rd day of hospitalization and his cranial computed tomography revealed bilateral subcortical hemorrhages. This case indicates us an example of late appearance of hemorrhagic transformation in methanol intoxication.
Collapse
Affiliation(s)
- Miray A Yaşgüçlükal
- Giresun Training and Research
Hospital, Neurology Department, Giresun, Turkey
| | - Selin Eyüpoğlu
- Giresun Training and Research
Hospital, Department of Intensive Care, Turkey
| | - Bahar Kaya
- Giresun Training and Research
Hospital, Neurology Department, Giresun, Turkey
| |
Collapse
|
|
7
|
Li J, Feng ZJ, Liu L, Ma YJ. Acute methanol poisoning with bilateral diffuse cerebral hemorrhage: A case report. World J Clin Cases 2022; 10:6571-6579. [PMID: 35979299 PMCID: PMC9294890 DOI: 10.12998/wjcc.v10.i19.6571] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/29/2021] [Revised: 04/04/2022] [Accepted: 05/07/2022] [Indexed: 02/06/2023] Open
Abstract
BACKGROUND Acute methanol poisoning (AMP) is a systemic disease that mainly affects the central nervous system and is characterized by ocular damage and metabolic acidosis. If appropriate treatments are inadequate or delayed, the mortality can exceed 40%. As the most serious complication, cerebral hemorrhage is rare with reported prevalence of 7%-19%.
CASE SUMMARY A 62-year-old man drank liquor mixed with 45% methanol and 35% alcohol. His vision blurred 10 h later and he fell into coma in another 9 h. Serum toxicological tests were performed immediately, and continuous renal replacement therapy (CRRT) was carried out as the lactic acid exceeded 15 mmol/L and blood pH was 6.78. In addition, the toxicological report revealed 1300.5 μg/mL of methanol in serum and 1500.2 μg/mL in urine. After 59 h of CRRT, the methanol level decreased to 126.0 μg/mL in serum and 151.0 μg/mL in urine. However, the patient was still unconscious and his pupillary light reflex was slow. Computed tomography showed hemorrhage in the left putamen. After 16 d of life support treatment, putamen hemorrhage developed into diffuse symmetric intracerebral hemorrhage. In the end, his family gave up and the patient was discharged, and died in a local hospital.
CONCLUSION Cerebral hemorrhage requires constant vigilance during the full course of treatment for severe cases of AMP.
Collapse
Affiliation(s)
- Jin Li
- Department of Critical Care Medicine, Air Force Medical Center, PLA, Beijing 100142, China
| | - Zhi-Juan Feng
- Department of Critical Care Medicine, Air Force Medical Center, PLA, Beijing 100142, China
| | - Lei Liu
- Department of Critical Care Medicine, Air Force Medical Center, PLA, Beijing 100142, China
| | - Yu-Jie Ma
- Department of Critical Care Medicine, Air Force Medical Center, PLA, Beijing 100142, China
| |
Collapse
|
|
8
|
Tian M, He H, Liu Y, Li R, Zhu B, Cao Z. Fatal methanol poisoning with different clinical and autopsy findings: Case report and literature review. Leg Med (Tokyo) 2021; 54:101995. [PMID: 34844153 DOI: 10.1016/j.legalmed.2021.101995] [Citation(s) in RCA: 9] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/27/2020] [Revised: 11/12/2021] [Accepted: 11/14/2021] [Indexed: 12/24/2022]
Abstract
Methanol poisoning is responsible for high morbidity and mortality, and the elevated concentration of methanol in the body is the major criteria for forensic diagnosis of methanol poisoning. However, in cases with lower methanol concentrations, diagnosis is mainly dependent on highly variable postmortem manifestations.Herein, we report a fatal methanol poisoning cases that two subjects ingested the same amount of methanol simultaneously, yet the subject one presented only non-specific gastrointestinal and mild central nervous system symptoms, while the other subject exhibited typical toxic manifestations with the exception of visual compromise. In autopsy, subject number 1 did not show typical pathological changes caused by methanol poisoning, except for the elevated levels of methanol in body fluids. On the contrary, bilateral basal ganglia hemorrhage and necrosis caused by methanol-induced brain lesion was observed in case number 2. Due to the complex and multifactorial process of methanol intoxication, many factors, including comprehensive autopsy, quantitative detection of methanol and formic acid, and genotype analysis, participate in its metabolism and toxicity, and can impact the clinical symptoms, prognosis and postmortem manifestations. Therefore, a combination of multiple diagnosis methods may more accurately contribute to the forensic diagnosis of methanol poisoning and should be tailored on an individual basis. This case report also reviews forensic diagnosis literature on methanol poisoning to provide a reference for forensic pathologists.
Collapse
Affiliation(s)
- Meihui Tian
- School of Forensic Medicine, China Medical University, No.77 Puhe Road, Shenyang North New Area, Shenyang 110122, PR China
| | - Hongyu He
- The Department of Pathology, the General Hospital of Northern Theater Command of Chinese People's Liberation Army, No.83 Wenhua road, Shenhe Area, Shenyang 110016, PR China
| | - Ye Liu
- Forensic Science Service of the Yingkou Public Security Bureau, No.12 Riyue Road, Bayuquan District, Yingkou 115007, PR China
| | - Rubo Li
- School of Forensic Medicine, China Medical University, No.77 Puhe Road, Shenyang North New Area, Shenyang 110122, PR China
| | - Baoli Zhu
- School of Forensic Medicine, China Medical University, No.77 Puhe Road, Shenyang North New Area, Shenyang 110122, PR China.
| | - Zhipeng Cao
- School of Forensic Medicine, China Medical University, No.77 Puhe Road, Shenyang North New Area, Shenyang 110122, PR China.
| |
Collapse
|
|
9
|
Illescas AC, Argyropoulos CP, Combs SA, Shaffi SK, Xu ZQ, Aragon MA, Teixeira JP. Severe methanol poisoning treated with a novel hemodialysis system: a case report, analysis, and review. RENAL REPLACEMENT THERAPY 2021; 7:43. [PMID: 34367669 PMCID: PMC8330177 DOI: 10.1186/s41100-021-00362-8] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/18/2021] [Accepted: 07/15/2021] [Indexed: 11/10/2022] Open
Abstract
In May and June 2020, an outbreak of methanol poisoning arose in the southwest United States linked to ingestion of contaminated hand sanitizer imported during the coronavirus disease 2019 pandemic, ultimately resulting in over a dozen hospitalizations and at least four deaths in New Mexico and Arizona. In this report, we describe one of these cases in which profound methanol intoxication was successfully treated with the Tablo® Hemodialysis System, the first reported case of toxic alcohol poisoning treated with this novel device. We carry out a formal regression analysis of the serial methanol levels obtained in this case to conservatively estimate that intermittent hemodialysis with Tablo achieved a clearance of methanol of 239 mL/min (95% confidence interval, 173–305 mL/min), a clearance that is well within the previously published standard of care. We conclude by reviewing both the treatment of toxic alcohol poisoning and the determinants of small molecule clearance with hemodialysis, emphasizing the importance of optimizing the dialytic treatment of intoxications with extended treatment times and the use of high-efficiency dialyzers.
Collapse
Affiliation(s)
- Alisa C Illescas
- Department of Internal Medicine, University of New Mexico School of Medicine, MSC10-5550, 1 University of New Mexico, Albuquerque, NM 87131 USA
| | - Christos P Argyropoulos
- Department of Internal Medicine, University of New Mexico School of Medicine, MSC10-5550, 1 University of New Mexico, Albuquerque, NM 87131 USA.,Division of Nephrology, University of New Mexico School of Medicine, MSC10-5550, 1 University of New Mexico, Albuquerque, NM 87131 USA
| | - Sara A Combs
- Department of Internal Medicine, University of New Mexico School of Medicine, MSC10-5550, 1 University of New Mexico, Albuquerque, NM 87131 USA.,Division of Nephrology, University of New Mexico School of Medicine, MSC10-5550, 1 University of New Mexico, Albuquerque, NM 87131 USA
| | - Saeed K Shaffi
- Department of Internal Medicine, University of New Mexico School of Medicine, MSC10-5550, 1 University of New Mexico, Albuquerque, NM 87131 USA.,Division of Nephrology, University of New Mexico School of Medicine, MSC10-5550, 1 University of New Mexico, Albuquerque, NM 87131 USA
| | - Zhi Q Xu
- Department of Internal Medicine, University of New Mexico School of Medicine, MSC10-5550, 1 University of New Mexico, Albuquerque, NM 87131 USA.,Division of Nephrology, University of New Mexico School of Medicine, MSC10-5550, 1 University of New Mexico, Albuquerque, NM 87131 USA
| | | | - J Pedro Teixeira
- Department of Internal Medicine, University of New Mexico School of Medicine, MSC10-5550, 1 University of New Mexico, Albuquerque, NM 87131 USA.,Division of Nephrology, University of New Mexico School of Medicine, MSC10-5550, 1 University of New Mexico, Albuquerque, NM 87131 USA.,Division of Pulmonary, Critical Care, & Sleep Medicine, University of New Mexico School of Medicine, MSC10-5550, 1 University of New Mexico, Albuquerque, NM 87131 USA
| |
Collapse
|
|
10
|
Marumo M, Wakabayashi I. Effects of methanol and formic acid on human platelet aggregation. Environ Health Prev Med 2017; 22:81. [PMID: 29246106 PMCID: PMC5732411 DOI: 10.1186/s12199-017-0687-7] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/19/2017] [Accepted: 12/01/2017] [Indexed: 11/15/2022] Open
Abstract
Background Although ethanol is known to inhibit platelet aggregation, the effects of another variant of alcohol, methanol, have not been reported. The purpose of this study was to determine whether methanol and its metabolite, formic acid, affect Ca2+ entry into and subsequent aggregation of platelets in vitro. Methods Ca2+ entry into and aggregation of human platelets were measured by spectrofluorometry using Fura-2/AM as an indicator and the light transmission method, respectively. Results Thrombin-induced platelet aggregation was significantly augmented by methanol at pharmacological concentrations (0.5–2%) in a concentration-dependent manner. Methanol at 2% significantly attenuated thapsigargin-induced platelet aggregation, which was not significantly affected by lower concentrations (0.5 and 1%) of methanol. Methanol (0.5–2%) did not significantly affect platelet aggregation induced by 1-oleoyl-2-acetyl-sn-glycerol (OAG), or Ca2+ entry into platelets induced by thrombin, thapsigargin, or OAG. Platelet aggregation induced by thrombin, thapsigargin, or OAG was significantly inhibited by formic acid at toxic concentrations (0.01% or higher). Ca2+ entry into platelets induced by thrombin or thapsigargin was also significantly inhibited by formic acid at 0.01% or higher, while that induced by OAG was not affected by formic acid at 0.005 and 0.01% and augmented by that at 0.02%. Conclusions Methanol at pharmacological doses has diverse effects on platelet aggregation, depending on the aggregation stimuli, without affecting Ca2+ entry into platelets. Formic acid at toxic concentrations has an inhibitory action on platelets aggregation, which was partly explained by the reduction of Ca2+ entry into platelets.
Collapse
Affiliation(s)
- Mikio Marumo
- Department of Environmental and Preventive Medicine, Hyogo College of Medicine, Mukogawa-cho 1-1, Nishinomiya, Hyogo, 663-8501, Japan
| | - Ichiro Wakabayashi
- Department of Environmental and Preventive Medicine, Hyogo College of Medicine, Mukogawa-cho 1-1, Nishinomiya, Hyogo, 663-8501, Japan.
| |
Collapse
|
|
11
|
Affiliation(s)
- Tharwat M Aisa
- Department of Intensive Care Unit, King Fahad Hospital, Baha, Kingdom of Saudi Arabia. E-mail:
| | | |
Collapse
|
|
12
|
Hassanian-Moghaddam H, Bahrami-Motlagh H, Zamani N, Fazeli SA, Behnam B. Intracranial Hemorrhage in Methanol Toxicity: Challenging the Probable Heparin Effect during Hemodialysis. J Res Pharm Pract 2017; 6:186-189. [PMID: 29026846 PMCID: PMC5632941 DOI: 10.4103/jrpp.jrpp_17_39] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/30/2022] Open
Abstract
Brain hemorrhages are rare complications of acute methanol poisoning. There is a debate on association of brain hemorrhage in methanol toxicity and application of systemic anticoagulation during hemodialysis (HD). A 70-year-old male presented to us with severe metabolic acidosis and a methanol level of 7.6 mg/dL. Ethanol and folinic acid were administered, and HD was performed. Brain computed tomography (CT) scan which was normal on presentation showed extensive bilateral subcortical supratentorial hypodensities on the 3rd day after commencing the treatment. However, the next CT scan performed 2 weeks later revealed expanding hemorrhagic transformation in previous hypodensities. Hemorrhagic changes could not be explained by patient's coagulation profile on the 3rd day. Anticoagulation agents such as heparin are used routinely during a dialysis session to prevent clot formation in dialysis circuits. This case is possibly questioning the role of heparin in hemorrhagic brain lesions of methanol intoxication.
Collapse
Affiliation(s)
- Hossein Hassanian-Moghaddam
- Toxicological Research Center, Department of Clinical Toxicology, Loghman-Hakim Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran
| | - Hooman Bahrami-Motlagh
- Department of Radiology, Loghman-Hakim Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran
| | - Nasim Zamani
- Toxicological Research Center, Department of Clinical Toxicology, Loghman-Hakim Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran
| | | | - Behdad Behnam
- Brain Mapping Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
| |
Collapse
|
|
13
|
Zakharov S, Kotikova K, Vaneckova M, Seidl Z, Nurieva O, Navratil T, Caganova B, Pelclova D. Acute Methanol Poisoning: Prevalence and Predisposing Factors of Haemorrhagic and Non-Haemorrhagic Brain Lesions. Basic Clin Pharmacol Toxicol 2016; 119:228-38. [DOI: 10.1111/bcpt.12559] [Citation(s) in RCA: 39] [Impact Index Per Article: 4.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/13/2015] [Accepted: 01/14/2016] [Indexed: 01/06/2023]
Affiliation(s)
- Sergey Zakharov
- First Faculty of Medicine; Department of Occupational Medicine; Toxicological Information Center; Charles University in Prague and General University Hospital; Prague Czech Republic
| | - Katerina Kotikova
- First Faculty of Medicine; Department of Occupational Medicine; Toxicological Information Center; Charles University in Prague and General University Hospital; Prague Czech Republic
| | - Manuela Vaneckova
- First Faculty of Medicine; Department of Radiology; Charles University in Prague and General University Hospital; Prague Czech Republic
| | - Zdenek Seidl
- First Faculty of Medicine; Department of Radiology; Charles University in Prague and General University Hospital; Prague Czech Republic
| | - Olga Nurieva
- First Faculty of Medicine; Department of Occupational Medicine; Toxicological Information Center; Charles University in Prague and General University Hospital; Prague Czech Republic
| | - Tomas Navratil
- First Faculty of Medicine; Department of Occupational Medicine; Toxicological Information Center; Charles University in Prague and General University Hospital; Prague Czech Republic
- Department of Biomimetic Electrochemistry; J. Heyrovsky Institute of Physical Chemistry of AS CR; Prague Czech Republic
| | - Blazena Caganova
- National Toxicological Information Center; University Hospital Bratislava; Bratislava Slovakia
| | - Daniela Pelclova
- First Faculty of Medicine; Department of Occupational Medicine; Toxicological Information Center; Charles University in Prague and General University Hospital; Prague Czech Republic
| |
Collapse
|
|
14
|
Lee SM, Moon JM, Chun BJ, Song KH. Unusual intracranial hemorrhage in severe methanol intoxication. Am J Emerg Med 2015; 33:1717.e1-2. [DOI: 10.1016/j.ajem.2015.03.031] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/27/2015] [Accepted: 03/15/2015] [Indexed: 10/23/2022] Open
|
|
15
|
Recommendations for the role of extracorporeal treatments in the management of acute methanol poisoning: a systematic review and consensus statement. Crit Care Med 2015; 43:461-72. [PMID: 25493973 DOI: 10.1097/ccm.0000000000000708] [Citation(s) in RCA: 99] [Impact Index Per Article: 9.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/21/2022]
Abstract
OBJECTIVE Methanol poisoning can induce death and disability. Treatment includes the administration of antidotes (ethanol or fomepizole and folic/folinic acid) and consideration of extracorporeal treatment for correction of acidemia and/or enhanced elimination. The Extracorporeal Treatments in Poisoning workgroup aimed to develop evidence-based consensus recommendations for extracorporeal treatment in methanol poisoning. DESIGN AND METHODS Utilizing predetermined methods, we conducted a systematic review of the literature. Two hundred seventy-two relevant publications were identified but publication and selection biases were noted. Data on clinical outcomes and dialyzability were collated and a two-round modified Delphi process was used to reach a consensus. RESULTS Recommended indications for extracorporeal treatment: Severe methanol poisoning including any of the following being attributed to methanol: coma, seizures, new vision deficits, metabolic acidosis with blood pH ≤ 7.15, persistent metabolic acidosis despite adequate supportive measures and antidotes, serum anion gap higher than 24 mmol/L; or, serum methanol concentration 1) greater than 700 mg/L (21.8 mmol/L) in the context of fomepizole therapy, 2) greater than 600 mg/L or 18.7 mmol/L in the context of ethanol treatment, 3) greater than 500 mg/L or 15.6 mmol/L in the absence of an alcohol dehydrogenase blocker; in the absence of a methanol concentration, the osmolal/osmolar gap may be informative; or, in the context of impaired kidney function. Intermittent hemodialysis is the modality of choice and continuous modalities are acceptable alternatives. Extracorporeal treatment can be terminated when the methanol concentration is <200 mg/L or 6.2 mmol/L and a clinical improvement is observed. Extracorporeal Treatments in Poisoning inhibitors and folic/folinic acid should be continued during extracorporeal treatment. General considerations: Antidotes and extracorporeal treatment should be initiated urgently in the context of severe poisoning. The duration of extracorporeal treatment extracorporeal treatment depends on the type of extracorporeal treatment used and the methanol exposure. Indications for extracorporeal treatment are based on risk factors for poor outcomes. The relative importance of individual indications for the triaging of patients for extracorporeal treatment, in the context of an epidemic when need exceeds resources, is unknown. In the absence of severe poisoning but if the methanol concentration is elevated and there is adequate alcohol dehydrogenase blockade, extracorporeal treatment is not immediately required. Systemic anticoagulation should be avoided during extracorporeal treatment because it may increase the development or severity of intracerebral hemorrhage. CONCLUSION Extracorporeal treatment has a valuable role in the treatment of patients with methanol poisoning. A range of clinical indications for extracorporeal treatment is provided and duration of therapy can be guided through the careful monitoring of biomarkers of exposure and toxicity. In the absence of severe poisoning, the decision to use extracorporeal treatment is determined by balancing the cost and complications of extracorporeal treatment to that of fomepizole or ethanol. Given regional differences in cost and availability of fomepizole and extracorporeal treatment, these decisions must be made at a local level.
Collapse
|
|
16
|
|
|
17
|
Unusual cause of spontaneous unilateral intracerebral hematoma—acute methanol poisoning: case report. Am J Emerg Med 2014; 32:1154.e1-2. [DOI: 10.1016/j.ajem.2014.02.034] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/19/2014] [Accepted: 02/20/2014] [Indexed: 11/23/2022] Open
|
|
18
|
Grasso D, Borreggine C, Perfetto F, Bertozzi V, Trivisano M, Specchio LM, Grilli G, Macarini L. Lentiform fork sign: a magnetic resonance finding in a case of acute metabolic acidosis. Neuroradiol J 2014; 27:288-92. [PMID: 24976195 DOI: 10.15274/nrj-2014-10041] [Citation(s) in RCA: 23] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/14/2014] [Accepted: 04/05/2014] [Indexed: 11/12/2022] Open
Abstract
We report a 33 year-old woman addicted to chronic unspecified solvents abuse with stupor, respiratory disorders, tetraplegia and severe metabolic acidosis. On admission an unenhanced cranial CT scan showed symmetrical hypodensities of both lentiform nuclei. MR imaging performed 12 hours after stupor demonstrates bilateral putaminal hemorrhagic necrosis, bilateral external capsule, corona radiata and deep cerebellar hyperintensities with right cingulate cortex involvement. DWI reflected bilateral putaminal hyperintensities with restricted water diffusion as to citotoxic edema and development of vasogenic edema in the external capsule recalling a fork. On day twenty, after specific treatments MRI demonstrated a bilateral putaminal marginal enhancement. Bilateral putaminal necrosis is a characteristic but non-specific radiological finding of methanol poisoning. Lentiform Fork sign is a rare MRI finding reported in literature in 22 patients with various conditions characterized by metabolic acidosis. Vasogenic edema may be due to the differences in metabolic vulnerability between neurons and astrocytes. We postulate that metabolic acidosis could have an important role to generate this sign.
Collapse
Affiliation(s)
- Daniela Grasso
- Department of Imaging Diagnostics, University of Foggia; Foggia, Italy -
| | - Carmela Borreggine
- Specialisation School in Radiodiagnostics, University of Foggia; Foggia, Italy
| | - Francesco Perfetto
- Radiodiagnostic Unit, "Ospedali Riuniti" University Hospital; Foggia, Italy
| | - Vincenzo Bertozzi
- Radiodiagnostic Unit, "Ospedali Riuniti" University Hospital; Foggia, Italy
| | - Marina Trivisano
- Specialisation School in Neurology, University of Foggia; Foggia, Italy
| | | | - Gianpaolo Grilli
- Radiodiagnostic Unit, "Ospedali Riuniti" University Hospital; Foggia, Italy
| | - Luca Macarini
- Specialisation School in Radiodiagnostics, University of Foggia; Foggia, Italy
| |
Collapse
|
|
19
|
|
|
20
|
Sivrioğlu AK, Velioğlu M, İncedayı M, Arıbal S, Sönmez G, Başhekim Ç. Common Late-Onset Subcortical Cerebral Hemorrhage Following Excessive Alcohol Consumption. ELECTRONIC JOURNAL OF GENERAL MEDICINE 2013. [DOI: 10.29333/ejgm/82372] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/21/2022]
|
|
21
|
Reddy NJ, Sudini M, Lewis LD. Delayed neurological sequelae from ethylene glycol, diethylene glycol and methanol poisonings. Clin Toxicol (Phila) 2011; 48:967-73. [PMID: 21192754 DOI: 10.3109/15563650.2010.532803] [Citation(s) in RCA: 43] [Impact Index Per Article: 3.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/13/2022]
Abstract
INTRODUCTION Ethylene glycol, diethylene glycol and methanol are widely available chemicals and are found in a variety of common household products including antifreeze, windshield washer fluid, brake fluid and lubricants. Following ingestion of these glycols and methanol, patients frequently develop an early neurological syndrome consisting of inebriation, ataxia, and if severe, seizures and coma. Though uncommon, a neurological syndrome may also develop as a delayed complication. METHODS Using Pub Med 438 references were identified of which 45 were relevant. FEATURES Ethylene glycol poisoning has produced cranial nerve deficits (usually VII nerve dysfunction) after a delay of 5-20 days, Parkinsonism and cerebral edema. Diethylene glycol ingestion has been associated with the development of optic nerve injury, cranial nerve deficits, quadraparesis and peripheral neuropathy. Methanol poisoning has led to Parkinsonism and polyneuropathy. MECHANISMS OF TOXICITY Oxalate crystal deposition likely causes the cranial neuropathies related to ethylene glycol and 2-hydroxyethoxyacetic acid is thought to be the causal moiety in cranial neuropathies resulting from diethylene glycol toxicity. Formic acid is implicated in the optic nerve damage associated with methanol. CONCLUSIONS Uncommonly, delayed neurological syndromes may develop as complications of poisoning due to ethylene glycol, diethylene glycol and methanol; the onset of such neurological damage is often days or even weeks post-ingestion. Further research is required to explain why the facial nerve is the cranial nerve most commonly involved and why the basal ganglia are predisposed to injury.
Collapse
Affiliation(s)
- Nandi J Reddy
- Section of Clinical Pharmacology and Toxicology, Department of Medicine, Dartmouth Medical School & Dartmouth-Hitchcock Medical Center, Lebanon, NH 03756, USA
| | | | | |
Collapse
|
|
22
|
Casaletto JJ. Is salt, vitamin, or endocrinopathy causing this encephalopathy? A review of endocrine and metabolic causes of altered level of consciousness. Emerg Med Clin North Am 2010; 28:633-62. [PMID: 20709247 DOI: 10.1016/j.emc.2010.03.013] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/20/2022]
Abstract
Altered level of consciousness describes the reason for 3% of critical emergency department (ED) visits. Approximately 85% will be found to have a metabolic or systemic cause. Early laboratory studies such as a bedside glucose test, serum electrolytes, or a urine dipstick test often direct the ED provider toward endocrine or metabolic causes. This article examines common endocrine and metabolic causes of altered mentation in the ED via sections dedicated to endocrine-, electrolyte-, metabolic acidosis-, and metabolism-related causes.
Collapse
Affiliation(s)
- Jennifer J Casaletto
- Department of Emergency Medicine, Virginia Tech-Carilion School of Medicine, CRMH-Admin 1S, 1906 Belleview Avenue, Roanoke, VA 24014, USA.
| |
Collapse
|
|
23
|
Lin SH, Tseng GF, Liang CC, Hung YC. Methanol Intoxication With Bilateral Putaminal and Occipital Necrosis. Tzu Chi Med J 2010. [DOI: 10.1016/s1016-3190(10)60064-x] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/25/2022] Open
|
|
24
|
Abstract
Patients who ingest toxic substances may require extracorporeal removal of the poisons or their toxic metabolites if native renal clearance is not sufficient because of acute kidney injury, acuity of symptoms, or burden of toxin. Here, a case is presented, and the literature on renal replacement therapy in the event of acute intoxication is reviewed. Extracorporeal therapy efficacy is examined in terms of the characteristics of the toxin (molecular size, charge, protein, or lipid binding); the patient (body habitus and volume of distribution); and the process (membrane effects on extraction ratios and sieving, role of blood, and dialysate flow rates). The choice of extracorporeal therapy and hemodialysis prescriptions for specific poisonings are discussed.
Collapse
|
|
25
|
Geibprasert S, Gallucci M, Krings T. Alcohol-induced changes in the brain as assessed by MRI and CT. Eur Radiol 2009; 20:1492-501. [DOI: 10.1007/s00330-009-1668-z] [Citation(s) in RCA: 39] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/28/2009] [Revised: 10/21/2009] [Accepted: 10/23/2009] [Indexed: 11/25/2022]
|
|
26
|
Abstract
An unresponsive 30-year-old female with a history of anxiety and chronic alcohol abuse presented to an emergency department with altered mental status and a severe metabolic acidosis. The patient was intubated for airway protection, and she empirically received folic acid, bicarbonate, and 5% ethanol continuous infusion for suspected ingestion of toxic alcohol. Following transfer to our institution, the patient was minimally responsive to noxious stimuli. She received fomepizole at dosing corrected for hemodialysis(HD), and bicarbonate via multiple boluses and continuous infusion. The ethanol drip was stopped. The nephrology service had been alerted to this patient's arrival and condition; hemodialysis via a standard heparinized circuit was initiated immediately after her arrival, which produced a marked improvement in the patient's acid-base status. Her serum methanol concentration subsequently returned at > 200 mg/dL. After 12 hours and 2 sessions of hemodialysis, the patient remained unresponsive despite minimal sedation. Anisocoria was noted on exam. Computed tomography of the brain demonstrated a large hematoma in the left basal ganglia that extended into the left frontal and parietal white matter accompanied by intraventricular extension, midline shift, loss of grey-white differentiation throughout, suggesting tonsillar herniation (Figure 1). Forty-eight hours after presentation, radionuclide imaging of the brain revealed no intracranial blood flow; heart, lungs, liver, kidneys, and pancreas were subsequently harvested for transplantation.
Collapse
|
|
27
|
Taheri MS, Moghaddam HH, Moharamzad Y, Dadgari S, Nahvi V. The value of brain CT findings in acute methanol toxicity. Eur J Radiol 2008; 73:211-4. [PMID: 19101105 DOI: 10.1016/j.ejrad.2008.11.006] [Citation(s) in RCA: 39] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/24/2008] [Revised: 07/17/2008] [Accepted: 11/10/2008] [Indexed: 10/21/2022]
Abstract
OBJECTIVE Due to depressant effects of methanol on the central nervous system, brain computed tomography (CT) scan has been introduced as a diagnostic device in methanol intoxication. The authors aimed to present brain CT findings in patients with acute methanol intoxication and to determine signs associated with death. MATERIALS AND METHODS This cohort study involved 42 consecutive patients with acute methanol intoxication. Inclusion criteria were consisted of characteristic clinical presentation of methanol poisoning, and metabolic acidosis with increased anion and osmolar gaps. Brain CT scans without contrast medium were obtained. To determine the association between the CT findings and death, the chi-square test or the Fisher's exact test, odds ratio (OR) and its 95% confidence interval (95% CI) were calculated. RESULTS Twenty-eight patients (66.6%) had a total of 55 abnormal findings on brain CT, in which bilateral putaminal hypodense lesions was the most common manifestation (27 cases, 96.4%). Putaminal hemorrhage with varying degrees was observed in 7 patients (25%). Six patients (21.4%) had low attenuation lesions in the subcortical white matter of the insula. A significant association was observed between putaminal hemorrhage (OR=8, 95% CI=1.187-53.93, P=0.018) and subcortical necrosis of the insula (OR=11, 95% CI=1.504-80.426, P=0.007) with death. CONCLUSION In addition to clinical and laboratory findings, presence of putaminal hemorrhage and insular subcortex white matter necrosis are associated with a poor clinical outcome in patients with methanol poisoning.
Collapse
Affiliation(s)
- Morteza Sanei Taheri
- Department of Radiology, Shohada Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
| | | | | | | | | |
Collapse
|
|
28
|
Mostafazadeh B, Talaie H, Mahdavinejad A, Mesri M, Emanhadi M. Gastrointestinal and urinary tract bleeding in methanol toxicity. BMJ Case Rep 2008; 2008:bcr0820080619. [PMID: 21716826 DOI: 10.1136/bcr.08.2008.0619] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/04/2022] Open
Abstract
Methanol is a clear, colourless liquid with a smell and taste similar to ethanol. Intoxications with methanol are still frequent in large parts of the developing world. Haemodialysis should be done in cases of severe toxicity to eliminate toxic metabolites. In this case report, we describe a 37-year-old chronic alcohol abuser with methanol poisoning, who developed haematuria and upper gastrointestinal (GI) bleeding after haemodialysis. The upper GI endoscopic findings showed only low grade oesophageal ulceration. Haematuria and upper GI bleeding in our patient might also have cause by the effect of heparinisation during haemodialysis.
Collapse
Affiliation(s)
- Babak Mostafazadeh
- Shahid Beheshti University of Medical Sciences, Forensic Medicine and Clinical Toxicology, Loghman-Hakim Hospital Poison Center, Tehran 13334, Islamic Republic of Iran.
| | | | | | | | | |
Collapse
|
|
29
|
Mora-Ordóñez JM, Martín D, Curiel Balsera E, Muñoz Bono J. Intoxicación mortal por metanol: donante de órganos. Med Clin (Barc) 2008; 130:39. [DOI: 10.1157/13114548] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/21/2022]
|
|
30
|
Abstract
Methanol poisoning in Australia is now very rare as methanol has been removed from methylated spirits. In acute intoxication methanol may result in a wide range of damage to the central nervous system. Few cases have been imaged with MRI. We present two cases and their striking neuroimaging findings with a discussion of the published work on methanol poisoning.
Collapse
Affiliation(s)
- R J Bessell-Browne
- Department of Radiology, Sir Charles Gairdner Hospital, Perth, Western Australia, Australia.
| | | |
Collapse
|
|
31
|
Sefidbakht S, Rasekhi AR, Kamali K, Borhani Haghighi A, Salooti A, Meshksar A, Abbasi HR, Moghadami M, Nabavizadeh SA. Methanol poisoning: acute MR and CT findings in nine patients. Neuroradiology 2007; 49:427-35. [PMID: 17294234 DOI: 10.1007/s00234-007-0210-8] [Citation(s) in RCA: 59] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/03/2006] [Accepted: 01/07/2007] [Indexed: 10/23/2022]
Abstract
INTRODUCTION Methanol poisoning is an uncommon but potent central nervous system toxin. We describe here the CT and MR findings in nine patients following an outbreak of methanol poisoning. METHODS Five patients with a typical clinical presentation and elevated anion and osmolar gaps underwent conventional brain MRI with a 1.5-T Gyroscan Interna scanner. In addition nonenhanced CT was performed in another three patients with more severe toxicity. RESULTS Bilateral hemorrhagic or nonhemorrhagic necrosis of the putamina, diffuse white matter necrosis, and subarachnoid hemorrhage were among the radiological findings. Various patterns of enhancement of basal ganglial lesions were found including no enhancement, strong enhancement and rim enhancement. CONCLUSION A good knowledge of the radiological findings in methanol poisoning seems to be necessary for radiologists. The present study is unique in that it enables us to include in a single report most of the radiological findings that have been reported previously.
Collapse
Affiliation(s)
- S Sefidbakht
- Department of Radiology, Shiraz University of Medical Sciences, Shiraz, Iran
| | | | | | | | | | | | | | | | | |
Collapse
|
|
32
|
Reddy NJ, Lewis LD, Gardner TB, Osterling W, Eskey CJ, Nierenberg DW. Two cases of rapid onset Parkinson's syndrome following toxic ingestion of ethylene glycol and methanol. Clin Pharmacol Ther 2007; 81:114-21. [PMID: 17186009 DOI: 10.1038/sj.clpt.6100013] [Citation(s) in RCA: 32] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/21/2023]
Abstract
Ethylene glycol and methanol are toxic alcohols commonly found in a variety of commercial products. We report two cases, one associated with ethylene glycol and one with methanol poisoning, which both led to acute hemorrhagic necrosis of the basal ganglia and resulted in acute Parkinson's syndrome. It is unlikely that oxalate crystal deposition is the only mechanism for such basal ganglia necrosis, because similar findings were seen following methanol intoxication. We discuss other possible mechanisms that may contribute towards this unusual neurotoxicity. Both of our patients survived their toxic ingestions, but then developed acute Parkinson's syndrome within 10 days of the ingestion. However, the patient who ingested methanol developed respiratory muscle stiffness/weakness, which responded poorly to anti-Parkinsonian drug therapy. Treatment with carbidopa/levodopa improved cogwheel rigidity and bradykinesia in both patients. We conclude that acute Parkinsonism is one of the lesser-recognized devastating complications of both ethylene glycol and methanol poisoning.
Collapse
Affiliation(s)
- N J Reddy
- Section of Clinical Pharmacology and Toxicology, Dartmouth Medical School, Dartmouth Hitchcock Medical Center, Lebanon, New Hampshire, USA
| | | | | | | | | | | |
Collapse
|
|
33
|
Abstract
Metabolic acidosis is defined as an acidemia created by one of three mechanisms: increased production of acids, decreased excretion of acids, or loss of alkali. This article addresses the identification and correct diagnosis of metabolic acidosis by reviewing important historical factors, pathophysiological principles, clinical presentation,and laboratory findings accompanying common high and normal anion gap metabolic acidoses in emergency department patients.
Collapse
Affiliation(s)
- Jennifer J Casaletto
- Department of Emergency Medicine, Maricopa Medical Center, 2601 East Roosevelt Avenue, Phoenix, AZ 85007, USA.
| |
Collapse
|
|
34
|
En-nouali H, Mahi M, Akjouj S, Nassar I, El Quessar A, El Hassani MR, Chakir N, Benchaaboun N, Jiddane M. [What is your diagnosis? Methanol poisoning]. JOURNAL DE RADIOLOGIE 2005; 86:957-60. [PMID: 16342883 DOI: 10.1016/s0221-0363(05)81476-3] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 05/05/2023]
Affiliation(s)
- H En-nouali
- Service de Neuroradiologie, Hôpital des spécialités ONO, CHU Ibn Sina, Rabat, Maroc
| | | | | | | | | | | | | | | | | |
Collapse
|
|
35
|
Hernández MA, Holanda MS, Tejerina EE, González C, López M, Hernández JL. Methanol poisoning and heparin: A dangerous couple? Am J Emerg Med 2004; 22:620-1. [PMID: 15666275 DOI: 10.1016/j.ajem.2004.08.004] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/22/2022] Open
|
|
36
|
Server A, Hovda KE, Nakstad PH, Jacobsen D, Dullerud R, Haakonsen M. Conventional and diffusion-weighted MRI in the evaluation of methanol poisoning. Acta Radiol 2003. [PMID: 14616218 DOI: 10.1046/j.1600-0455.2003.00138.x] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/20/2022]
Abstract
Cerebral lesions were studied in 2 methanol-poisoned patients using conventional magnetic resonance imaging (MRI). In 1 patient, diffusion-weighted MRI (DWI) was also performed. In this patient, conventional MRI showed symmetrical, bilateral increased signal in the lentiform nuclei, involving predominantly putamina, but also extending into the corona radiata, centrum semiovale and subcortical white matter. DWI showed decreased diffusion, which most probably reflects cytotoxic edema. In the other patient, fluid attenuated-inversion recovery (FLAIR) and T2-weighted images showed hyperintensity in the putamina, characteristic of post-necrotic changes.
Collapse
Affiliation(s)
- A Server
- Departments of Neuroradiology, Division of Radiology, and Medicine, Ullevål University Hospital, Oslo, Norway.
| | | | | | | | | | | |
Collapse
|
|
37
|
Rojas vera J. Lesiones hemorrágicas cerebrales en intoxicación por metanol. Med Intensiva 2003. [DOI: 10.1016/s0210-5691(03)79923-9] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/26/2022]
|
|
38
|
Barceloux DG, Bond GR, Krenzelok EP, Cooper H, Vale JA. American Academy of Clinical Toxicology practice guidelines on the treatment of methanol poisoning. JOURNAL OF TOXICOLOGY. CLINICAL TOXICOLOGY 2002; 40:415-46. [PMID: 12216995 DOI: 10.1081/clt-120006745] [Citation(s) in RCA: 355] [Impact Index Per Article: 15.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/14/2022]
Abstract
EPIDEMIOLOGY Almost all cases of acute methanol toxicity result from ingestion, though rarely cases of poisoning have followed inhalation or dermal absorption. The absorption of methanol following oral administration is rapid and peak methanol concentrations occur within 30-60minutes. MECHANISMS OF TOXICITY Methanol has a relatively low toxicity and metabolism is responsible for the transformation of methanol to its toxic metabolites. Methanol is oxidized by alcohol dehydrogenase to formaldehyde. The oxidation of formaldehyde to formic acid is facilitated by formaldehyde dehydrogenase. Formic acid is converted by 10-formyl tetrahydrofolate synthetase to carbon dioxide and water. In cases of methanol poisoning, formic acid accumulates and there is a direct correlation between the formic acid concentration and increased morbidity and mortality. The acidosis observed in methanol poisoning appears to be caused directly or indirectly by formic acid production. Formic acid has also been shown to inhibit cytochrome oxidase and is the prime cause of ocular toxicity, though acidosis can increase toxicity further by enabling greater diffusion of formic acid into cells. FEATURES Methanol poisoning typically induces nausea, vomiting, abdominal pain, and mild central nervous system depression. There is then a latent period lasting approximately 12-24 hours, depending, in part, on the methanol dose ingested, following which an uncompensated metabolic acidosis develops and visualfunction becomes impaired, ranging from blurred vision and altered visual fields to complete blindness. MANAGEMENT For the patient presenting with ophthalmologic abnormalities or significant acidosis, the acidosis should be corrected with intravenous sodium bicarbonate, the further generation of toxic metabolite should be blocked by the administration of fomepizole or ethanol and formic acid metabolism should be enhanced by the administration of intravenous folinic acid. Hemodialysis may also be required to correct severe metabolic abnormalities and to enhance methanol and formate elimination. For the methanol poisoned patient without evidence of clinical toxicity, the first priority is to inhibit methanol metabolism with intravenous ethanol orfomepizole. Although there are no clinical outcome data confirming the superiority of either of these antidotes over the other, there are significant disadvantages associated with ethanol. These include complex dosing, difficulties with maintaining therapeutic concentrations, the need for more comprehensive clinical and laboratory monitoring, and more adverse effects. Thus fomepizole is very attractive, however, it has a relatively high acquisition cost. CONCLUSION The management of methanol poisoning includes standard supportive care, the correction of metabolic acidosis, the administration of folinic acid, the provision of an antidote to inhibit the metabolism of methanol to formate, and selective hemodialysis to correct severe metabolic abnormalities and to enhance methanol and formate elimination. Although both ethanol and fomepizole are effective, fomepizole is the preferred antidote for methanol poisoning.
Collapse
Affiliation(s)
- Donald G Barceloux
- American Academy of Clinical Toxicology, Harrisburg, Pennsylvania 17105-8820, USA
| | | | | | | | | |
Collapse
|
|
39
|
Davis LE, Hudson D, Benson BE, Jones Easom LA, Coleman JK. Methanol poisoning exposures in the United States: 1993-1998. JOURNAL OF TOXICOLOGY. CLINICAL TOXICOLOGY 2002; 40:499-505. [PMID: 12217003 DOI: 10.1081/clt-120006753] [Citation(s) in RCA: 25] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 11/03/2022]
Abstract
OBJECTIVES We investigated U.S. methanol-poisoning exposures since little recent information is available about the frequency, sources of methanol, or outcomes of individuals who consume methanol. METHODS We reviewed human methanol exposures reported to the American Association of Poison Control Centers Toxic Exposure Surveillance System 1993-1998. RESULTS The mean number of cases per year was 2254. Each year 167 cases had an outcome of moderate effect, major effect, or death. One death occurred in every 183 exposures to methanol. Symptomatic cases increased abruptly from 1.8 to 2.5% for infants and children, from 14.1 to 12.3% for adolescents and adults, while the intentional exposures increased from < 1 to 21% for adolescents, and 11% for adults. Cases occurred in every decade of life but toddlers had the highest number of exposures. In 68 methanol fatalities, confusion developedfollowed by coma, hypotension, respiratory depression, and cerebral edema. Blood methanol levels were above 100mg/dL (70%), metabolic acidoses (62%), and anion gaps > 25 (100%). Methanol products were recorded, showing windshield wiper fluids to be 60.8% of exposures. Other automotive sources were 23.7%. Commercial nonautomotive products were 12.2% and pure methanol products were 2.3%. Unintentional exposures were reported in 90.3% of all cases, while 8.3% were due to intentional exposures, and 1.4% wasfor unknown or mixed reasons. Intentional exposures resulted from suspected suicides (51.2%) and from abuse and misuse (38.8%). CONCLUSIONS Methanol poisonings continue to occur in the United States with toddlers at the highest risk for exposure, but adolescents and adults at the highest risk for life-threatening intoxications. Over half of product-identified cases were due to consumption of windshield wiperfluid. Efforts should be undertaken to minimize methanol exposures.
Collapse
Affiliation(s)
- Larry E Davis
- Neurology Service, New Mexico VA Health Care System, Albuquerque, New Mexico 87108, USA.
| | | | | | | | | |
Collapse
|
|
40
|
Affiliation(s)
- C A Robinson
- Saskatoon District Health and Royal University Hospital, SK, Saskatoon, Canada
| |
Collapse
|
|
41
|
Aziz MH, Agrawal AK, Adhami VM, Ali MM, Baig MA, Seth PK. Methanol-induced neurotoxicity in pups exposed during lactation through mother: role of folic acid. Neurotoxicol Teratol 2002; 24:519-27. [PMID: 12127898 DOI: 10.1016/s0892-0362(02)00231-3] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/27/2022]
Abstract
Role of folic acid on methanol-induced neurotoxicity was studied in pups at Postnatal Day (PND) 45 exposed to methanol (1%, 2% and 4%, v/v) during lactation through mothers maintained on folic acid-deficient (FD) and folic acid-sufficient (FS) diet. A gradual loss in the body weight gain was observed in the pups exposed to 2% and 4% methanol in the FD group, while FS group exhibited this alteration only at 4% exposure. The assessment of spontaneous locomotor activity (SLA) showing a significant increase in the distance travelled was observed in the 2% and 4% methanol-exposed groups in both the FS and FD animals when compared with their respective controls, but the effect was more marked in the FD group. A significant decrease in the conditioned avoidance response (CAR) was observed in pups exposed to 2% and 4% methanol in the FD group at PND 45. The results also suggest that disturbances in dopaminergic and cholinergic receptors were more pronounced in the FD group as compared to the FS group. A significant decrease in striatal dopamine levels was also observed in the FD group at 2% and 4% methanol exposure, while in the FS group, a significant decrease was exhibited only at 4% methanol exposure. An aberrant increase in the expression of Growth-Associated Protein (GAP-43), a neuron-specific growth-associated protein was observed in pups in the FD group exposed to 2% and 4% methanol, while an increase in the expression of GAP-43 in the FS group was found only at 4% methanol exposure in the hippocampal region as compared to their respective controls. Results suggests that methanol exposure during growth spurt period adversely affects the developing brain, the effect being more pronounced in FD rats as compared to FS rats, suggesting a possible role of folic acid in methanol-induced neurotoxicity.
Collapse
Affiliation(s)
- Moammir Hasan Aziz
- Predictive Toxicology Group, Developmental Toxicology Division, Industrial Toxicology Research Centre, Post Box No. 80, M.G. Marg, Lucknow, India
| | | | | | | | | | | |
Collapse
|
|
42
|
López-Navidad A, Caballero F, González-Segura C, Cabrer C, Frutos MA. Short- and long-term success of organs transplanted from acute methanol poisoned donors. Clin Transplant 2002; 16:151-62. [PMID: 12010136 DOI: 10.1034/j.1399-0012.2002.01109.x] [Citation(s) in RCA: 29] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/23/2022]
Abstract
BACKGROUND The shortage of organs for transplantation has made it necessary to extend the criteria for the selection of donors, among others including those patients who die because of toxic substances such as methanol. Methanol is a toxic which is distributed through all the systems and viscera of the organism and tends to cause a severe metabolic acidosis. It can specifically cause serious or irreversible lesions of the central nervous system (CNS) and retina, and ultimately brain death. We present our experience with 16 organ donors who died as a result of acute methanol intoxication in 10 Spanish hospitals over the last 14 yr. PATIENTS AND METHODS Between October 1985 and July 1999, 16 organ donors with brain death caused by acute methanol intoxication, 13 females and three males with a mean age of 38.4 +/- 7.6 yr (interval: 26-55 yr), allowed 37 elective transplants to be performed: 29 kidneys, four hearts and four livers for 37 recipients, and one urgent liver transplantation to a recipient with fulminant hepatitis. RESULTS The immediate postoperative period was favourable for the 38 graft recipients. None of the graft recipients presented gap anion metabolic acidosis in the immediate postoperative period, nor symptomatology or lesions of the CNS characteristic of methanol intoxication. Two patients died during the first month post-transplantation, a liver recipient and a heart recipient, at 16 and 24 days, respectively, because of acute rejection of the graft. At 1 month after transplantation 35 of the 36 recipients had been discharged from hospital with normal-functioning grafts. The last of the recipients, a kidney recipient, was discharged at 6 wk with normal-functioning graft. Actuarial survival of the graft and patient of kidney recipients at 1, 3 and 5 yr was 92.6, 77.8, and 75%, and 100, 88.9 and 83.3%, respectively; with average serum creatinines of 139.9 +/- 42.9, 150.4 +/- 42.8, and 164.4 +/- 82.5 micromol/L, respectively. At 1 yr after transplantation the three heart recipients and two of the three liver recipients had normal-functioning graft. CONCLUSIONS Methanol intoxication is not transferred from the donor to the recipient. The survival of the graft and kidney, heart and liver recipients using organs from donors who die because of methanol does not differ in the short- and long-term from the transplants performed with organs from donors who die from other causes.
Collapse
Affiliation(s)
- A López-Navidad
- Department of Organ & Tissue Procurement for Transplantation, Hospital de la Santa Creu i Sant Pau, Universitat Autónoma de Barcelona, Spain.
| | | | | | | | | |
Collapse
|
|
43
|
Abstract
Intoxications frequently perturb acid-base and electrolyte status, intravascular volume, and renal function. In selected cases, extracorporeal techniques effectively restore homeostasis and augment intoxicant removal. The use of 4-methylpyrazole, an inhibitor of alcohol dehydrogenase, is a new and effective treatment for patients exposed to toxic alcohols. In this section, practical approaches to commonly encountered intoxicants and the use of extracorporeal techniques are critically reviewed.
Collapse
Affiliation(s)
- Steven C Borkan
- Department of Medicine, Boston University, Boston Medical Center, Renal Section, Boston, MA, USA.
| |
Collapse
|
|
44
|
Comoğlu S, Ozen B, Ozbakir S. Methanol intoxication with bilateral basal ganglia infarct. AUSTRALASIAN RADIOLOGY 2001; 45:357-8. [PMID: 11531765 DOI: 10.1046/j.1440-1673.2001.00937.x] [Citation(s) in RCA: 14] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 11/20/2022]
Abstract
Methanol is a toxic agent that affects the central nervous system, especially the optic nerves and basal ganglia. Symmetrical hypodense lesions in the basal ganglia, which can be demonstrated by CT or MRI, is accepted as the most characteristic radiological feature of the disease. A case of a patient with bilateral putaminal hypodense infarcts due to methanol intoxication is presented.
Collapse
Affiliation(s)
- S Comoğlu
- Department of Neurology, Ankara Numune State Hospital, Ankara, Turkey
| | | | | |
Collapse
|
|
45
|
Girault C, Tamion F, Moritz F, Callonnec F, Droy JM, Bonmarchand G, Leroy J. Fomepizole (4-methylpyrazole) in fatal methanol poisoning with early CT scan cerebral lesions. JOURNAL OF TOXICOLOGY. CLINICAL TOXICOLOGY 1999; 37:777-80. [PMID: 10584591 DOI: 10.1081/clt-100102456] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 11/03/2022]
Abstract
BACKGROUND Methanol poisoning, potentially fatal, is generally treated with the combination of ethanol as antidote, and hemodialysis. Fomepizole, a competitive inhibitor of alcohol dehydrogenase, has more recently been used, and is capable of blocking the toxic metabolism of methanol. To our knowledge, its use has never been reported as an antidote in severe methanol poisoning requiring hemodialysis. CASE REPORT We report a case of fatal methanol poisoning (1.9 g/L on admission) suspected due to the combined presence of coma and severe metabolic acidosis with normokalaemia. CONCLUSION The fomepizole treatment protocol (10 mg/kg by i.v. infusion over 1 hour before dialysis, repeated 12 hours later in combination with 1.5 mg/kg/h during dialysis) was simple to use and appeared effective in eliminating methanol in combination with hemodialysis. The case is also unusual in terms of severity and the early onset of cerebral lesions demonstrated by computed tomography (CT) scan.
Collapse
Affiliation(s)
- C Girault
- Service de Reánimation Medicale, Hôpital Charles Nicolle, Centre Hospitalier Universitaire, Rouen, France.
| | | | | | | | | | | | | |
Collapse
|
|
46
|
|
|
47
|
Li W, Zheng T, Wang J, Altura BT, Altura BM. Methanol elevates cytosolic calcium ions in cultured canine cerebral vascular smooth muscle cells: possible relation to CNS toxicity. Alcohol 1999; 18:221-4. [PMID: 10456574 DOI: 10.1016/s0741-8329(99)00007-5] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/19/2022]
Abstract
Acute exposure of cultured canine cerebral vascular smooth muscle cells to methanol (10-400 mM) results in concentration-dependent elevation of the concentration of intracellular free calcium ion ([Ca2+]i) as measured with the fluorescent indicator, fura-2, and digital imaging microscopy. The resting level of [Ca2+]i in the cerebral vascular smooth muscle cells was 89.3+/-5.3 nM. Exposure of these cells to 10 mM methanol for only 5 min resulted in significant elevation in [Ca2+]i (i.e., to 105.7+/-4.6) (p < 0.05). Methanol (10 mM) is a concentration found in the blood of victims demonstrating early CNS toxicity. Other, higher concentrations of methanol rapidly raised [Ca2+]i upwards of 60% over basal resting levels. These result suggest that methanol-induced cerebral vasospasm is a consequence of large rises in intracellular Ca2+. These events could play a crucial role in methanol-induced cerebral edema, brain hemorrhage, and cerebral and retinal infarcts, eventuating in severe deficits in brain blood flow and the known, subsequent CNS disturbances.
Collapse
Affiliation(s)
- W Li
- Department of Physiology, State University of New York, Health Science Center at Brooklyn, 11203, USA
| | | | | | | | | |
Collapse
|
|
48
|
Affiliation(s)
- L E Davis
- Department of Neurology, Veterans Affairs Medical Center, University of New Mexico, School of Medicine, Albuquerque 87108, USA
| | | |
Collapse
|
|
49
|
Hantson P, Duprez T, Mahieu P. Neurotoxicity to the basal ganglia shown by magnetic resonance imaging (MRI) following poisoning by methanol and other substances. JOURNAL OF TOXICOLOGY. CLINICAL TOXICOLOGY 1997; 35:151-61. [PMID: 9120884 DOI: 10.3109/15563659709001186] [Citation(s) in RCA: 36] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 02/04/2023]
Abstract
OBJECTIVE To define specific brain magnetic resonance features in methanol intoxicated patients and to evaluate the clinical relevance of monitoring these features. BACKGROUND During the past decade magnetic resonance imaging has proven to be an exquisitely sensitive modality in depicting subtle water changes in diseased areas of the brain, allowing the definition of high-risk structures in numerous pathological conditions. METHOD Four patients admitted to our institution for acute methanol intoxication were repeatedly evaluated by brain magnetic resonance imaging or a combination of computed tomography and magnetic resonance imaging. Common features of initial brain status were shown in all four cases and compared to those of patients presenting with other intoxications or critical deprivation states. RESULTS Preferential localization of methanol-induced lesions within the putamina was observed in all four cases. This finding is specific compared to intoxication by other substances like carbon monoxide, or in the critical phase of metabolic disorders. The striking regression of the putaminal lesions on follow-up magnetic resonance examinations correlated with complete neurological recovery and the absence of extrapyramidal disturbance. Two patients exhibited discrete symmetric additional lesions in the medial areas of the parieto-occipital lobes. In a third one, the occipital lesions were severe. All three suffered from permanent visual impairment. The fourth patient, in whom magnetic resonance examinations failed to reveal any occipital lesion, never complained of visual disturbance though signs of optic neuropathy were detected in the visual evoked potentials. CONCLUSION Magnetic resonance imaging appeared as a well suited neuroimaging modality in methanol intoxicated patients both in revealing a specific pattern of brain lesions and in demonstrating valuable correlation between evolution of brain changes on magnetic resonance images and clinical outcome.
Collapse
Affiliation(s)
- P Hantson
- Department of Intensive Care, Cliniques Universitaires St-Luc, Brussels, Belgium
| | | | | |
Collapse
|
|
50
|
Giudicissi Filho M, Holanda CV, Nader NA, Gomes SR, Bertolucci PH. Bilateral putaminal hemorrhage related to methanol poisoning: a complication of hemodialysis? Case report. ARQUIVOS DE NEURO-PSIQUIATRIA 1995; 53:485-7. [PMID: 8540827 DOI: 10.1590/s0004-282x1995000300020] [Citation(s) in RCA: 14] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/31/2023]
Abstract
A case of acute methanol intoxication is presented, in which bilateral putaminal hemorrhage developed after hemodialysis. Even though the patient was initially comatose and profoundly acidotic, favorable outcome was achieved, with long-term neurologic impairments essentially restricted to mild crural paraparesis, retrograde amnesia, and marked visual deficit. A comparative literature review is evaluated.
Collapse
Affiliation(s)
- M Giudicissi Filho
- Division of Neurosurgery, Hospital Municipal Arthur Ribeiro de Saboya, São Paulo, Brasil
| | | | | | | | | |
Collapse
|