American Journal of Emergency Medicine xxx (2014) xxx–xxx
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Case Report
Unusual cause of spontaneous unilateral intracerebral hematoma—acute methanol poisoning: case report Abstract Brain hemorrhage is a rare but lethal complication in methanol poisoning. We report a case of massive unilateral intraparenchymatous insular hematoma in a 34-year-old woman with unintentional methanol poisoning. She was admitted to a territorial hospital 72 hours post-ingestion of an unknown dose of methanol for high anion gap metabolic acidosis and confusion. Computed tomographic (CT) scan showed lesions in putamen and cerebral deep white matter. Sixteen days after methanol exposure, she suddenly developed coma, followed by cardiorespiratory arrest. A second CT scan revealed massive unilateral intraparenchymatous insular hematoma which led to death. Emergency physicians should be aware of this unusual complication of a methanol exposure. A 34-year-old woman was brought to a territorial hospital by ambulance in a critical condition, with acidotic breathing, confusion, blood pressure of 80/60 mmHg, tachycardia 130 beats/minute. According to the husband's statement, 72 hours before admission she complained of abdominal pain, nausea, and repeated vomiting. Her arterial blood analysis showed severe high anion gap metabolic acidosis: pH of 6.98, PCO2 22 mmHg, PO2 78 mmHg, Na 143 mmol/L, K 3.8 mmol/L, Cl 101 mmol/L, HCO3 5 mmol/L, anion gap 41.8, lactate 4 mmol/L. ABCs were started—orotracheal intubation, IV line with crystalloid administration, and vasopressors, followed by repeated sodium bicarbonate administration. Forty-eight hours from admission, she was still intubated, was hemodinamically stable, and maintained confusional state. Her chest radiograph, electrocardiogram, blood glucose level, and renal function tests were normal. Metabolic acidosis has been corrected. Her abdominal echography and Computed tomographic (CT) scan were normal. Cerebral CT scan was performed and revealed hypodense areas in lenticular nucleus bilateral, that were interpreted as cerebral ischemic lesions. Fundoscopic examination showed toxic optic neuropathy. According to information from the patient's husband that she is a drinker, in the presence of severe high anion gap metabolic acidosis associated with optic neuropathy and ischemic brain CT scan lesions, methanol poisoning was suspected. Her husband was sent back home to search for a clue, and he found a 500-mL recipient with only 200 mL methanol left. The patient was transferred to the intensive care unit of our hospital toxicology department 5 days after methanol ingestion. At presentation she was intubated, with 8 Glasgow Coma Scale, 100/60 mmHg blood pressure, 120 beat/min heart rate. Arterial blood analysis and renal function tests were normal. Coagulation parameters were normal. Endotracheal intubation was suspended 48 hours after arrival in our hospital. The renal function was maintained normal
without renal replacement therapies. Neurological status was improved with persistence of confusion. Repeated fundoscopic examination revealed bilateral optic neuropathy with optic atrophy and bilateral blindness. The blood methanol level could not be measured in our hospital, because of technical limitations. Ten days after methanol ingestion she suddenly developed severe bradycardia, 40 beat/min, associated with collapse 60/40 mmHg, that responded to atropine administration. After this episode she developed fever 39 to 40 degrees and maintained a confusional state. We repeated brain CT scan that revealed hypodense areas both in basal nuclei and right thalamus, right cerebral peduncle, midbrain and pons, as well as in the right cerebellum hemisphere. Sixteen days after methanol exposure, she suddenly presented an abrupt deterioration of the consciousness, with profound coma (Glasgow Coma Scale 3), followed by cardiorespiratory arrest that was successfully resuscitated. A new cerebral CT scan showed an intraparenchymatous hematoma in the right insula and right internal capsule, with important perilesional edema which realized mass effect, displacing towards right with approximately 8 mm transtentorial and subtentorial the median line structures, compressing the third ventricle and right lateral ventricle, with important cerebral edema, and hypodensity in basal ganglia, pons and midbrain. She was transferred in neurosurgery department, where decompressive craniotomy was performed, followed by death in the next 24 hours. Cerebral toxicity in methanol poisoning is characterized by bilateral ischemic or necrotic lesions in basal ganglia and subcortical areas, or putaminal hemorrhage [1-3]. Hemorrhagic brain lesions are found in severe methanol poisoning, having almost always a bad prognosis, leading to a patient's death. Orthner was the first that describe lesions of hemorrhagic necrosis in putamen and white matter as a consequence of acute methanol poisoning. Then, Phang and his team communicated 6 cases of bilateral extensive hemorrhagic necrosis in basal ganglia, interesting also the ventricles, as a complication of methanol poisoning possibly favored by heparin administration during hemodialysis [4-6]. We presented this case because, to the extent of our knowledge, there is only one case reported in literature by Hernandez and colleagues, with methanol exposure and transformation of bilateral brain infarction into extensive unilateral intraparenchymal hematoma [6]. Another particularity of our case is represented by the presence of unilateral putaminal hemorrhage associated with insular subcortex white matter necrosis that is known to have a poor clinical outcome. The definite selective neurotoxicity mechanism explaining the lesions is still unclear. It is supposed that all of these are the consequence of a “histotoxic” hypoxia induced by methanol and its metabolites, especially formic acid, determined both by insufficient venous drainage from lenticular nuclei, and by inappropriate arterial
0735-6757/$ – see front matter © 2014 Elsevier Inc. All rights reserved.
Please cite this article as: Bologa C, et al, Unusual cause of spontaneous unilateral intracerebral hematoma—acute methanol poisoning: case report, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.02.034
2
C. Bologa et al. / American Journal of Emergency Medicine xxx (2014) xxx–xxx
flux at this level [7,8]. Another mechanism involved is the so called “metabolic vulnerability” of the putamen to the hypoxia produced by formic acid excess [1,7]. This region is known to have much higher oxygen and glucose demands, as compared to the white matter nearby or other areas in basal ganglia [1]. Recently, Li and colleagues described another possible mechanism for methanol-induced cerebral toxicity, represented by increased intracitosolic calcium leading to cerebral vasospasm, followed by ischemic brain lesions [9]. In our case, intraparenchymal hemorrhage appeared 16 days after methanol ingestion, a quite large interval. Delayed presentation to the hospital was determined by late development of symptoms, as a consequence of ethanol coingestion. Lack of history data about a toxic ingestion and circumstances of appearance, presentation to the hospital after 3 days evolution, technical limitations with impossibility to detect blood methanol levels, as well as a reduced index of clinical suspicion led to a delayed correct diagnosis, with inadequate therapy (no antidote, or hemodialysis). Another particularity of our case was represented by inexplicable correction of metabolic acidosis without antidote treatment. In conclusion, the presence of CT findings of bilateral ischemic or necrosis lesions in putamen and cerebral deep white matter, in a patient with severe high anion gap metabolic acidosis, are strong criteria for methanol poisoning diagnosis.
Cristina Bologa MD Internal Medical Department II Internal Medical Clinic “Sf. Spiridon” Clinical Emergency Hospital “Gr.T.Popa” University of Medicine Iasi, Romania Laura Ciuhodaru MD Intensive Care Unit “Sf. Spiridon” Clinical Emergency Hospital Iasi, Romania
Adorata Coman MD Ovidiu Petris MD II Internal Medical Clinic “Sf. Spiridon” Clinical Emergency Hospital “Gr.T.Popa” University of Medicine Iasi, Romania Laurentiu Sorodoc MD Catalina Lionte MD Internal Medical Department II Internal Medical Clinic “Sf. Spiridon” Clinical Emergency Hospital “Gr.T.Popa” University of Medicine Iasi, Romania E-mail address: [email protected] http://dx.doi.org/10.1016/j.ajem.2014.02.034 References [1] Jain N, Himanshu D, Verma SP, Parihar A- Case report. Methanol poisoning: characteristic MRI findings. Ann Saudi Med 2013, January-February. www. annsaudimed.net. [2] Askar A, Al-Suwaida A. Methanol intoxication with brain hemorrhage: catastrophic outcome of late presentation. Saudi J Kidney Dis Transpl 2007;18:117–22. [3] Gaul HP, Wallace CJ, Auer RN, Fong TC. MR Findings in methanol intoxication. AJNR Am J Neuroradiol 1995;16:1783–6. [4] Phang PT, Passerini L, Mielke B-. Brain hemorrhage associated with methanol poisoning. Crit Care Med 1988;16:137–40. [5] Giudicissi FM, Holanda CV, Nader NA, et al. Bilateral putaminal hemorrhage related to methanol poisoning: a complication of hemodialysis? Case report. Arch Neuropsiquiatr 1995;53:485–7. [6] Hernandez MA, Holanda MS, Tejerina EE, Gonzalez C, Lopez M. Methanol poisoning and heparin: a dangerous couple? AJEM 2004;22(7):620–1. [7] Andresen H, Schmoldt H, Matschke J, Flachskampf FA, Turk EE. Fatal methanol intoxication with different survival times- morphological findings and postmortem methanol distribution. Forensic Sci Int 2008;179:206–10. [8] Liesivuori J, Savolainen H. Methanol and formic acid toxicity: biochemical mechanisms. Pharmacol Toxicol 1991;69:157–63. [9] Gupta N, Sonambekar D, Tomar L. A rare presentation of methanol toxicity. Ann Indian Acad Neurol 2013;16:249–51.
Please cite this article as: Bologa C, et al, Unusual cause of spontaneous unilateral intracerebral hematoma—acute methanol poisoning: case report, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.02.034
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Case Report
Unusual cause of spontaneous unilateral intracerebral hematoma—acute methanol poisoning: case report Abstract Brain hemorrhage is a rare but lethal complication in methanol poisoning. We report a case of massive unilateral intraparenchymatous insular hematoma in a 34-year-old woman with unintentional methanol poisoning. She was admitted to a territorial hospital 72 hours post-ingestion of an unknown dose of methanol for high anion gap metabolic acidosis and confusion. Computed tomographic (CT) scan showed lesions in putamen and cerebral deep white matter. Sixteen days after methanol exposure, she suddenly developed coma, followed by cardiorespiratory arrest. A second CT scan revealed massive unilateral intraparenchymatous insular hematoma which led to death. Emergency physicians should be aware of this unusual complication of a methanol exposure. A 34-year-old woman was brought to a territorial hospital by ambulance in a critical condition, with acidotic breathing, confusion, blood pressure of 80/60 mmHg, tachycardia 130 beats/minute. According to the husband's statement, 72 hours before admission she complained of abdominal pain, nausea, and repeated vomiting. Her arterial blood analysis showed severe high anion gap metabolic acidosis: pH of 6.98, PCO2 22 mmHg, PO2 78 mmHg, Na 143 mmol/L, K 3.8 mmol/L, Cl 101 mmol/L, HCO3 5 mmol/L, anion gap 41.8, lactate 4 mmol/L. ABCs were started—orotracheal intubation, IV line with crystalloid administration, and vasopressors, followed by repeated sodium bicarbonate administration. Forty-eight hours from admission, she was still intubated, was hemodinamically stable, and maintained confusional state. Her chest radiograph, electrocardiogram, blood glucose level, and renal function tests were normal. Metabolic acidosis has been corrected. Her abdominal echography and Computed tomographic (CT) scan were normal. Cerebral CT scan was performed and revealed hypodense areas in lenticular nucleus bilateral, that were interpreted as cerebral ischemic lesions. Fundoscopic examination showed toxic optic neuropathy. According to information from the patient's husband that she is a drinker, in the presence of severe high anion gap metabolic acidosis associated with optic neuropathy and ischemic brain CT scan lesions, methanol poisoning was suspected. Her husband was sent back home to search for a clue, and he found a 500-mL recipient with only 200 mL methanol left. The patient was transferred to the intensive care unit of our hospital toxicology department 5 days after methanol ingestion. At presentation she was intubated, with 8 Glasgow Coma Scale, 100/60 mmHg blood pressure, 120 beat/min heart rate. Arterial blood analysis and renal function tests were normal. Coagulation parameters were normal. Endotracheal intubation was suspended 48 hours after arrival in our hospital. The renal function was maintained normal
without renal replacement therapies. Neurological status was improved with persistence of confusion. Repeated fundoscopic examination revealed bilateral optic neuropathy with optic atrophy and bilateral blindness. The blood methanol level could not be measured in our hospital, because of technical limitations. Ten days after methanol ingestion she suddenly developed severe bradycardia, 40 beat/min, associated with collapse 60/40 mmHg, that responded to atropine administration. After this episode she developed fever 39 to 40 degrees and maintained a confusional state. We repeated brain CT scan that revealed hypodense areas both in basal nuclei and right thalamus, right cerebral peduncle, midbrain and pons, as well as in the right cerebellum hemisphere. Sixteen days after methanol exposure, she suddenly presented an abrupt deterioration of the consciousness, with profound coma (Glasgow Coma Scale 3), followed by cardiorespiratory arrest that was successfully resuscitated. A new cerebral CT scan showed an intraparenchymatous hematoma in the right insula and right internal capsule, with important perilesional edema which realized mass effect, displacing towards right with approximately 8 mm transtentorial and subtentorial the median line structures, compressing the third ventricle and right lateral ventricle, with important cerebral edema, and hypodensity in basal ganglia, pons and midbrain. She was transferred in neurosurgery department, where decompressive craniotomy was performed, followed by death in the next 24 hours. Cerebral toxicity in methanol poisoning is characterized by bilateral ischemic or necrotic lesions in basal ganglia and subcortical areas, or putaminal hemorrhage [1-3]. Hemorrhagic brain lesions are found in severe methanol poisoning, having almost always a bad prognosis, leading to a patient's death. Orthner was the first that describe lesions of hemorrhagic necrosis in putamen and white matter as a consequence of acute methanol poisoning. Then, Phang and his team communicated 6 cases of bilateral extensive hemorrhagic necrosis in basal ganglia, interesting also the ventricles, as a complication of methanol poisoning possibly favored by heparin administration during hemodialysis [4-6]. We presented this case because, to the extent of our knowledge, there is only one case reported in literature by Hernandez and colleagues, with methanol exposure and transformation of bilateral brain infarction into extensive unilateral intraparenchymal hematoma [6]. Another particularity of our case is represented by the presence of unilateral putaminal hemorrhage associated with insular subcortex white matter necrosis that is known to have a poor clinical outcome. The definite selective neurotoxicity mechanism explaining the lesions is still unclear. It is supposed that all of these are the consequence of a “histotoxic” hypoxia induced by methanol and its metabolites, especially formic acid, determined both by insufficient venous drainage from lenticular nuclei, and by inappropriate arterial
0735-6757/$ – see front matter © 2014 Elsevier Inc. All rights reserved.
Please cite this article as: Bologa C, et al, Unusual cause of spontaneous unilateral intracerebral hematoma—acute methanol poisoning: case report, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.02.034
2
C. Bologa et al. / American Journal of Emergency Medicine xxx (2014) xxx–xxx
flux at this level [7,8]. Another mechanism involved is the so called “metabolic vulnerability” of the putamen to the hypoxia produced by formic acid excess [1,7]. This region is known to have much higher oxygen and glucose demands, as compared to the white matter nearby or other areas in basal ganglia [1]. Recently, Li and colleagues described another possible mechanism for methanol-induced cerebral toxicity, represented by increased intracitosolic calcium leading to cerebral vasospasm, followed by ischemic brain lesions [9]. In our case, intraparenchymal hemorrhage appeared 16 days after methanol ingestion, a quite large interval. Delayed presentation to the hospital was determined by late development of symptoms, as a consequence of ethanol coingestion. Lack of history data about a toxic ingestion and circumstances of appearance, presentation to the hospital after 3 days evolution, technical limitations with impossibility to detect blood methanol levels, as well as a reduced index of clinical suspicion led to a delayed correct diagnosis, with inadequate therapy (no antidote, or hemodialysis). Another particularity of our case was represented by inexplicable correction of metabolic acidosis without antidote treatment. In conclusion, the presence of CT findings of bilateral ischemic or necrosis lesions in putamen and cerebral deep white matter, in a patient with severe high anion gap metabolic acidosis, are strong criteria for methanol poisoning diagnosis.
Cristina Bologa MD Internal Medical Department II Internal Medical Clinic “Sf. Spiridon” Clinical Emergency Hospital “Gr.T.Popa” University of Medicine Iasi, Romania Laura Ciuhodaru MD Intensive Care Unit “Sf. Spiridon” Clinical Emergency Hospital Iasi, Romania
Adorata Coman MD Ovidiu Petris MD II Internal Medical Clinic “Sf. Spiridon” Clinical Emergency Hospital “Gr.T.Popa” University of Medicine Iasi, Romania Laurentiu Sorodoc MD Catalina Lionte MD Internal Medical Department II Internal Medical Clinic “Sf. Spiridon” Clinical Emergency Hospital “Gr.T.Popa” University of Medicine Iasi, Romania E-mail address: [email protected] http://dx.doi.org/10.1016/j.ajem.2014.02.034 References [1] Jain N, Himanshu D, Verma SP, Parihar A- Case report. Methanol poisoning: characteristic MRI findings. Ann Saudi Med 2013, January-February. www. annsaudimed.net. [2] Askar A, Al-Suwaida A. Methanol intoxication with brain hemorrhage: catastrophic outcome of late presentation. Saudi J Kidney Dis Transpl 2007;18:117–22. [3] Gaul HP, Wallace CJ, Auer RN, Fong TC. MR Findings in methanol intoxication. AJNR Am J Neuroradiol 1995;16:1783–6. [4] Phang PT, Passerini L, Mielke B-. Brain hemorrhage associated with methanol poisoning. Crit Care Med 1988;16:137–40. [5] Giudicissi FM, Holanda CV, Nader NA, et al. Bilateral putaminal hemorrhage related to methanol poisoning: a complication of hemodialysis? Case report. Arch Neuropsiquiatr 1995;53:485–7. [6] Hernandez MA, Holanda MS, Tejerina EE, Gonzalez C, Lopez M. Methanol poisoning and heparin: a dangerous couple? AJEM 2004;22(7):620–1. [7] Andresen H, Schmoldt H, Matschke J, Flachskampf FA, Turk EE. Fatal methanol intoxication with different survival times- morphological findings and postmortem methanol distribution. Forensic Sci Int 2008;179:206–10. [8] Liesivuori J, Savolainen H. Methanol and formic acid toxicity: biochemical mechanisms. Pharmacol Toxicol 1991;69:157–63. [9] Gupta N, Sonambekar D, Tomar L. A rare presentation of methanol toxicity. Ann Indian Acad Neurol 2013;16:249–51.
Please cite this article as: Bologa C, et al, Unusual cause of spontaneous unilateral intracerebral hematoma—acute methanol poisoning: case report, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.02.034
