American Journal of Therapeutics 22, e40–e42 (2015)
Acute Reversible Neurologic Deficits Due to Ethyl Chloride Sniffing: A Case Report and Review of Literature Mourad H. Senussi, MD* and Shyam Chalise, MD
Ethyl chloride (CH3CH2Cl) or chloroethane is a colorless volatile halogenated hydrocarbon gas found in many commercially available solvents, and it may be used as an inhalant of abuse. Neurologic toxicity has been reported, as well as deaths. We present a case of a 47-year-old HIV-positive man who presented with acute reversible neurologic deficits secondary to inhalational exposure to ethyl chloride. Laboratory studies and neuroimaging are nondiagnostic in ethyl chloride–induced neurotoxicity and thus requires a high index of clinical suspicion. The mainstay of treatment is supportive with withdrawal of the offending agent and observation for resolution of neurologic symptoms. Keywords: ethyl chloride neurotoxicity, inhalant abuse
INTRODUCTION
CASE PRESENTATION
Chlorinated hydrocarbons, such as ethyl chloride, are abused by sniffing or direct inhalation for their depressant effects on central nervous system (CNS) that mimic alcohol intoxication, as well as enhancing sexual pleasure. These volatile solvents are found in a wide array of different household cleaning products that are readily available and easy to obtain and thus provide a potential for widespread abuse. Although rare, deaths have been reported in both acute and chronic exposure. Acute inhalational exposure to ethyl chloride may produce neurologic symptoms, which include confusion, lightheadedness, hallucinations, impaired concentration and memory, lack of coordination, and feelings of drunkenness.
In June 2012, a 47-year-old HIV-positive man presented to the emergency room with complaints of unsteadiness of his gait and an increased drooling 1-day before presentation. He reported dizziness, unsteadiness, and considerable difficulty in speech, which was noted to be slurred by his coworkers. He denied any headaches, visual disturbances, numbness, tingling, or weakness of his extremities. He had initially denied any illicit drug use other than smoking cannabis 4 days before admission; however, he eventually revealed that he had inhaled ethyl chloride gas in the form of the commercially available volatile solvent “Maximum Impact” the night before. Medical history is extensive and includes HIV with the most recent CD4 count of 409 cells/microliter 2 months before admission, longstanding liver cirrhosis, esophageal banding secondary to variceal bleeding, right-sided Bell’s palsy with residual right facial weakness, chronic hepatitis C, depression, and Crohn’s disease. His medications included atripla (efavirenz-emtricitabine-tenofovir), duloxetine, spironolactone, and mesalamine. On examination, blood pressure was 113/73 mm Hg, pulse 79/min, oral temperature 97.8°F (36.6°C), respiratory rate 20/min, and SpO2 97% on ambient air. The patient was alert and oriented to time, place, and
Department of Internal Medicine, Saint Joseph Hospital, Chicago, IL. The authors have no conflicts of interest to declare. *Address for correspondence: Department of Internal Medicine, Saint Joseph Hospital, 2900 N Lake Shore Dr, Chicago, IL 60657. E-mail: [email protected]
1075–2765 Copyright Ó 2013 Wolters Kluwer Health, Inc. All rights reserved.
www.americantherapeutics.com
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Acute Reversible Neurologic Deficits Due to Ethyl Chloride Sniffing
person. Positive findings included right facial droop, mild dysarthria, mild aphasia, and difficulty with word finding. No dysphagia was noted. The patient had intact motor strength, full visual fields, reflexes, and no sensory deficits. Tongue movements were normal. Gross coordination skills were intact. No atrophy or fasciculation was noted. The patient exhibited mild unsteadiness of gait with a negative Romberg sign. A complete blood count revealed white blood count of 3.2 3 103/mm3, hemoglobin of 12.5 g/dL, mean corpuscular volume of 88.9 fl, and platelets of 68 3 103/mm3. A comprehensive metabolic panel was within the normal limits. A urine toxicology screen was positive for cannabinoids. Further laboratory studies included erythrocyte sedimentation rate (10 mm/h), blood alcohol level (,10 mg/dL), vitamin B12 level (615 pg/mL), thyroid stimulating hormone (2.4 uIU/mL), homocysteine (34.3 Umol/L; normal, 3.7–13.9), ammonia (28; normal, 16–60), nonreactive syphilis screen, and a negative antinuclear antibody test. A 12-lead electrocardiography showed normal sinus rhythm with a prolonged QT interval (QT/QTc 416/491 milliseconds). Unenhanced computed tomographic scan of the head revealed normal size and configuration of the basal cisterns, ventricles, and sulci. There was no evidence of acute intracranial hemorrhage. The bone windows demonstrated no acute fractures. Magnetic resonance imaging of the brain showed no acute intracranial abnormality. There was no evidence of acute cerebrovascular accident on diffusion-weighted imaging, and no abnormal enhancing intraaxial lesions were noted. Noncontrast magnetic resonance angiography of the brain was unremarkable as well, showing no vascular malformation or aneurysmal dilatation. There was no evidence of any significant stenosis, and the anterior and posterior communicating arteries were intact. Other imaging studies included bilateral carotid artery duplex ultrasound, which revealed mild internal carotid artery stenosis bilaterally with ,50% stenosis on both the right and left sides. Over the course of 1 week, the patient symptomatically improved with complete resolution of gait, unsteadiness, and slurred speech. He underwent physical therapy and was counseled on the detrimental effects of inhalant abuse.
DISCUSSION Ethyl chloride (CH3CH2Cl) or chloroethane is a colorless volatile halogenated hydrocarbon gas found in many commercially available solvents and may be used as an inhalant of abuse. Chlorinated hydrocarbons, such as ethyl chloride, are usually abused by www.americantherapeutics.com
e41
sniffing or direct inhalation. Neurologic toxicity has been reported, as well as deaths. Volatile solvents are found in a wide array of different household cleaning products that are readily available and easy to obtain and thus provide a potential for widespread abuse. Inhalant abuse poses a significant health risk and has been on the rise.1 Although reported risk factors include low socioeconomic class, male gender, and ethnicity, inhalant abuse has become more prevalent with the middle class youth given its widespread availability.2 Although rare, deaths have been reported in both acute and chronic exposure. There are 2 reported deaths attributed to inhalational exposure to ethyl chloride.3,4 Inhalants act as CNS depressants and are highly lipophilic, thus readily crossing the blood– brain barrier and often mimics alcohol intoxication. Humans subjected to acute inhalational exposure to ethyl chloride frequently exhibit neurologic symptoms, which include confusion, lightheadedness, hallucinations, impaired concentration and memory, lack of coordination, and feelings of drunkenness. Finch and Lobo5 reported a case of a 41-year-old HIV-positive African American man with acute neurologic deficit characterized by tremulousness, ataxia, and dysarthria secondary to ethyl chloride use associated with delayed neurologic recovery. Their patient was a habitual inhaler for almost 2 years of the commercially available solvent “Maximum Impact” (the same solvent used by our patient) who had a significantly increased exposure 2 weeks before presentation with the most recent exposure being on the day of admission. Similar to our case, the patient had presented with acute onset of gait instability hours after inhalational exposure, which resolved spontaneously over the course of 1 week. Our patient had exhibited predominantly cerebellumrelated symptoms, such as ataxia and slurred speech, similar to that reported by Hes et al,6 and Soult and Walker.7 Demarest et al8 reported a case of a 47-year-old HIV-positive man who presented with acute reversible neurologic deficits in the form of slurring of speech and difficulty in walking after inhaling ethyl chloride. However, unlike our patient, the neurologic examination was significant for wide-based gait, bilateral upgoing plantars, symmetrically brisk deep tendon reflexes, and bilateral ankle and patellar clonus.8 Initial management of ethyl chloride intoxication includes removal of any ongoing exposure. Intoxication may involve significant CNS depression manifested by altered mental status, ataxia, and horizontal nystagmus, which mimic ethanol intoxication. Patients may develop respiratory arrest and require supplemental oxygen and/or an advanced airway. However, the CNS depressant effects are usually rapid in onset and resolve quickly. Concomitant use of other drugs/toxins American Journal of Therapeutics (2015) 22(2)
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
e42
should always be considered. Cardiac dysrhythmias may occur with ethyl chloride toxicity, and therefore, patients should be monitored for cardiac arrhythmias during the initial stages of acute inhalation. Observation and supportive measures is the mainstay of treatment with most neurologic symptoms resolving spontaneously within 1 week. Inhalants should be considered in the differential diagnosis of patients presenting with acute mental status changes and neurologic symptoms. The use of inhalants should be specifically sought out. Urine toxicology screens are negative, and a high index of clinical suspicion is required. Treatment is supportive with withdrawal of the offending agent and observation for resolution of neurologic symptoms.
CONCLUSIONS Inhalant abuse with chlorinated hydrocarbons such as ethyl chloride, is common given the widespread availability of these products and its potential for abuse. Ethyl chloride neurotoxicity secondary to acute inhalational exposure may present with nonlocalizing nonspecific reversible neurologic signs. Clinicians should consider the possibility of inhalant abuse in patients who present with confusion, hallucinations, ataxia, dysarthria,
American Journal of Therapeutics (2015) 22(2)
Senussi and Chalise
weakness, and tremor that cannot be explained by other drugs or medical causes.
REFERENCES 1. Garland EL, Howard MO. Volatile substance misuse: clinical considerations, neuropsychopharmacology and potential role of pharmacotherapy in management. CNS Drugs. 2012;26:927–935. 2. Williams JF, Storck M; American Academy of Pediatrics Committee on Substance Abuse, American Academy of Pediatrics Committee on Native American Child Health. Inhalant abuse. Pediatrics. 2007;119:1009–1017. 3. Yacoub I, Robinson CA, Simmons GT, et al. Death attributed to ethyl chloride. J Anal Toxicol. 1993;17:384–385. 4. Broussard LA, Broussard AK, Pittman TS, et al. Death due to inhalation of ethyl chloride. J Forensic Sci. 2000;45: 223–225. 5. Finch CK, Lobo BL. Acute inhalant-induced neurotoxicity with delayed recovery. Ann Pharmacother. 2005;39:169–172. 6. Hes JP, Cohn DF, Streifler M. Ethyl chloride sniffing and cerebellar dysfunction (case report). Isr Ann Psychiatr Relat Discip. 1979;17:122–125. 7. Soult TA, Walker JS. Ethyl chloride intoxication. Am J Emerg Med. 1993;11:313–315. 8. Demarest C, Torgovnick J, Sethi NK, et al. Acute reversible neurotoxicity associated with inhalation of ethyl chloride: a case report. Clin Neurol Neurosurg. 2011;113:909–910.
www.americantherapeutics.com
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Acute Reversible Neurologic Deficits Due to Ethyl Chloride Sniffing: A Case Report and Review of Literature Mourad H. Senussi, MD* and Shyam Chalise, MD
Ethyl chloride (CH3CH2Cl) or chloroethane is a colorless volatile halogenated hydrocarbon gas found in many commercially available solvents, and it may be used as an inhalant of abuse. Neurologic toxicity has been reported, as well as deaths. We present a case of a 47-year-old HIV-positive man who presented with acute reversible neurologic deficits secondary to inhalational exposure to ethyl chloride. Laboratory studies and neuroimaging are nondiagnostic in ethyl chloride–induced neurotoxicity and thus requires a high index of clinical suspicion. The mainstay of treatment is supportive with withdrawal of the offending agent and observation for resolution of neurologic symptoms. Keywords: ethyl chloride neurotoxicity, inhalant abuse
INTRODUCTION
CASE PRESENTATION
Chlorinated hydrocarbons, such as ethyl chloride, are abused by sniffing or direct inhalation for their depressant effects on central nervous system (CNS) that mimic alcohol intoxication, as well as enhancing sexual pleasure. These volatile solvents are found in a wide array of different household cleaning products that are readily available and easy to obtain and thus provide a potential for widespread abuse. Although rare, deaths have been reported in both acute and chronic exposure. Acute inhalational exposure to ethyl chloride may produce neurologic symptoms, which include confusion, lightheadedness, hallucinations, impaired concentration and memory, lack of coordination, and feelings of drunkenness.
In June 2012, a 47-year-old HIV-positive man presented to the emergency room with complaints of unsteadiness of his gait and an increased drooling 1-day before presentation. He reported dizziness, unsteadiness, and considerable difficulty in speech, which was noted to be slurred by his coworkers. He denied any headaches, visual disturbances, numbness, tingling, or weakness of his extremities. He had initially denied any illicit drug use other than smoking cannabis 4 days before admission; however, he eventually revealed that he had inhaled ethyl chloride gas in the form of the commercially available volatile solvent “Maximum Impact” the night before. Medical history is extensive and includes HIV with the most recent CD4 count of 409 cells/microliter 2 months before admission, longstanding liver cirrhosis, esophageal banding secondary to variceal bleeding, right-sided Bell’s palsy with residual right facial weakness, chronic hepatitis C, depression, and Crohn’s disease. His medications included atripla (efavirenz-emtricitabine-tenofovir), duloxetine, spironolactone, and mesalamine. On examination, blood pressure was 113/73 mm Hg, pulse 79/min, oral temperature 97.8°F (36.6°C), respiratory rate 20/min, and SpO2 97% on ambient air. The patient was alert and oriented to time, place, and
Department of Internal Medicine, Saint Joseph Hospital, Chicago, IL. The authors have no conflicts of interest to declare. *Address for correspondence: Department of Internal Medicine, Saint Joseph Hospital, 2900 N Lake Shore Dr, Chicago, IL 60657. E-mail: [email protected]
1075–2765 Copyright Ó 2013 Wolters Kluwer Health, Inc. All rights reserved.
www.americantherapeutics.com
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Acute Reversible Neurologic Deficits Due to Ethyl Chloride Sniffing
person. Positive findings included right facial droop, mild dysarthria, mild aphasia, and difficulty with word finding. No dysphagia was noted. The patient had intact motor strength, full visual fields, reflexes, and no sensory deficits. Tongue movements were normal. Gross coordination skills were intact. No atrophy or fasciculation was noted. The patient exhibited mild unsteadiness of gait with a negative Romberg sign. A complete blood count revealed white blood count of 3.2 3 103/mm3, hemoglobin of 12.5 g/dL, mean corpuscular volume of 88.9 fl, and platelets of 68 3 103/mm3. A comprehensive metabolic panel was within the normal limits. A urine toxicology screen was positive for cannabinoids. Further laboratory studies included erythrocyte sedimentation rate (10 mm/h), blood alcohol level (,10 mg/dL), vitamin B12 level (615 pg/mL), thyroid stimulating hormone (2.4 uIU/mL), homocysteine (34.3 Umol/L; normal, 3.7–13.9), ammonia (28; normal, 16–60), nonreactive syphilis screen, and a negative antinuclear antibody test. A 12-lead electrocardiography showed normal sinus rhythm with a prolonged QT interval (QT/QTc 416/491 milliseconds). Unenhanced computed tomographic scan of the head revealed normal size and configuration of the basal cisterns, ventricles, and sulci. There was no evidence of acute intracranial hemorrhage. The bone windows demonstrated no acute fractures. Magnetic resonance imaging of the brain showed no acute intracranial abnormality. There was no evidence of acute cerebrovascular accident on diffusion-weighted imaging, and no abnormal enhancing intraaxial lesions were noted. Noncontrast magnetic resonance angiography of the brain was unremarkable as well, showing no vascular malformation or aneurysmal dilatation. There was no evidence of any significant stenosis, and the anterior and posterior communicating arteries were intact. Other imaging studies included bilateral carotid artery duplex ultrasound, which revealed mild internal carotid artery stenosis bilaterally with ,50% stenosis on both the right and left sides. Over the course of 1 week, the patient symptomatically improved with complete resolution of gait, unsteadiness, and slurred speech. He underwent physical therapy and was counseled on the detrimental effects of inhalant abuse.
DISCUSSION Ethyl chloride (CH3CH2Cl) or chloroethane is a colorless volatile halogenated hydrocarbon gas found in many commercially available solvents and may be used as an inhalant of abuse. Chlorinated hydrocarbons, such as ethyl chloride, are usually abused by www.americantherapeutics.com
e41
sniffing or direct inhalation. Neurologic toxicity has been reported, as well as deaths. Volatile solvents are found in a wide array of different household cleaning products that are readily available and easy to obtain and thus provide a potential for widespread abuse. Inhalant abuse poses a significant health risk and has been on the rise.1 Although reported risk factors include low socioeconomic class, male gender, and ethnicity, inhalant abuse has become more prevalent with the middle class youth given its widespread availability.2 Although rare, deaths have been reported in both acute and chronic exposure. There are 2 reported deaths attributed to inhalational exposure to ethyl chloride.3,4 Inhalants act as CNS depressants and are highly lipophilic, thus readily crossing the blood– brain barrier and often mimics alcohol intoxication. Humans subjected to acute inhalational exposure to ethyl chloride frequently exhibit neurologic symptoms, which include confusion, lightheadedness, hallucinations, impaired concentration and memory, lack of coordination, and feelings of drunkenness. Finch and Lobo5 reported a case of a 41-year-old HIV-positive African American man with acute neurologic deficit characterized by tremulousness, ataxia, and dysarthria secondary to ethyl chloride use associated with delayed neurologic recovery. Their patient was a habitual inhaler for almost 2 years of the commercially available solvent “Maximum Impact” (the same solvent used by our patient) who had a significantly increased exposure 2 weeks before presentation with the most recent exposure being on the day of admission. Similar to our case, the patient had presented with acute onset of gait instability hours after inhalational exposure, which resolved spontaneously over the course of 1 week. Our patient had exhibited predominantly cerebellumrelated symptoms, such as ataxia and slurred speech, similar to that reported by Hes et al,6 and Soult and Walker.7 Demarest et al8 reported a case of a 47-year-old HIV-positive man who presented with acute reversible neurologic deficits in the form of slurring of speech and difficulty in walking after inhaling ethyl chloride. However, unlike our patient, the neurologic examination was significant for wide-based gait, bilateral upgoing plantars, symmetrically brisk deep tendon reflexes, and bilateral ankle and patellar clonus.8 Initial management of ethyl chloride intoxication includes removal of any ongoing exposure. Intoxication may involve significant CNS depression manifested by altered mental status, ataxia, and horizontal nystagmus, which mimic ethanol intoxication. Patients may develop respiratory arrest and require supplemental oxygen and/or an advanced airway. However, the CNS depressant effects are usually rapid in onset and resolve quickly. Concomitant use of other drugs/toxins American Journal of Therapeutics (2015) 22(2)
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
e42
should always be considered. Cardiac dysrhythmias may occur with ethyl chloride toxicity, and therefore, patients should be monitored for cardiac arrhythmias during the initial stages of acute inhalation. Observation and supportive measures is the mainstay of treatment with most neurologic symptoms resolving spontaneously within 1 week. Inhalants should be considered in the differential diagnosis of patients presenting with acute mental status changes and neurologic symptoms. The use of inhalants should be specifically sought out. Urine toxicology screens are negative, and a high index of clinical suspicion is required. Treatment is supportive with withdrawal of the offending agent and observation for resolution of neurologic symptoms.
CONCLUSIONS Inhalant abuse with chlorinated hydrocarbons such as ethyl chloride, is common given the widespread availability of these products and its potential for abuse. Ethyl chloride neurotoxicity secondary to acute inhalational exposure may present with nonlocalizing nonspecific reversible neurologic signs. Clinicians should consider the possibility of inhalant abuse in patients who present with confusion, hallucinations, ataxia, dysarthria,
American Journal of Therapeutics (2015) 22(2)
Senussi and Chalise
weakness, and tremor that cannot be explained by other drugs or medical causes.
REFERENCES 1. Garland EL, Howard MO. Volatile substance misuse: clinical considerations, neuropsychopharmacology and potential role of pharmacotherapy in management. CNS Drugs. 2012;26:927–935. 2. Williams JF, Storck M; American Academy of Pediatrics Committee on Substance Abuse, American Academy of Pediatrics Committee on Native American Child Health. Inhalant abuse. Pediatrics. 2007;119:1009–1017. 3. Yacoub I, Robinson CA, Simmons GT, et al. Death attributed to ethyl chloride. J Anal Toxicol. 1993;17:384–385. 4. Broussard LA, Broussard AK, Pittman TS, et al. Death due to inhalation of ethyl chloride. J Forensic Sci. 2000;45: 223–225. 5. Finch CK, Lobo BL. Acute inhalant-induced neurotoxicity with delayed recovery. Ann Pharmacother. 2005;39:169–172. 6. Hes JP, Cohn DF, Streifler M. Ethyl chloride sniffing and cerebellar dysfunction (case report). Isr Ann Psychiatr Relat Discip. 1979;17:122–125. 7. Soult TA, Walker JS. Ethyl chloride intoxication. Am J Emerg Med. 1993;11:313–315. 8. Demarest C, Torgovnick J, Sethi NK, et al. Acute reversible neurotoxicity associated with inhalation of ethyl chloride: a case report. Clin Neurol Neurosurg. 2011;113:909–910.
www.americantherapeutics.com
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
