Ethylene glycol intoxication presenting as a mimic of acute stroke: report of three cases

Ethylene glycol intoxication presenting as a mimic of acute stroke: report of three cases | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Ethylene glycol intoxication presenting as a mimic of acute stroke: report of three cases Máté Héja, László Oláh This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-2524829/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Background: Stroke is a major cause of death and disability presenting with acute focal neurological symptoms of vascular origin. Several other disorders may cause symptoms similar to a stroke, referred as stroke mimics. Misdiagnosis of stroke mimics may lead to potentially harmful treatments, including thrombolysis. Intoxication is a rare, but possible cause of stroke mimic. We present three cases of ethylene glycol poisoning presenting as acute stroke mimic within the time window of thrombolytic therapy. Case presentations: The first patient (54-year-old, male) had nystagmus, dysarthria and truncal ataxia on admission. Cerebral CT and CT-angiography were negative. Vertebrobasilar stroke was suspected and intravenous thrombolysis was performed. A few hours later confusion, somnolence and hyperventilation developed. Arterial blood gas analysis showed metabolic acidosis. Toxicology screening revealed the presence of ethylene glycol in a toxic range. Due to the prompt treatment the patient was discharged 9 days later in a symptom-free state. The second patient (78-year-old, male) was admitted with central type of nystagmus, gaze palsy, dysarthria and ataxia. In the absence of exclusion criteria, thrombolysis was performed. A few hours later his condition deteriorated, he became comatose and tetraplegic with partially absent brainstem reflexes. Arterial blood gas analysis revealed severe metabolic acidosis. The ethylene glycol level was 159 mg/dL. Despite the appropriate treatment, he died. The third patient (54-year-old, male) with a history of chronic alcoholism was presented after an epileptic seizure with mixed aphasia and confusion. Stroke could not be excluded, therefore thrombolysis was performed. Arterial blood gases were normal, however toxicological screening revealed a serum etyhlene-glycol concentration of 16,54 mg/dL. Six days after admission he became symptom-free and was discharged home. Conclusions: Our cases show that ethylene glycol intoxication in its early phase may mimic acute stroke resulting in an unnecessary thrombolytic therapy. Symptoms not characteristic of a stroke, such as hyperventilation, agitation, and disturbance of consciousness, may appear later and warn of intoxication. The final diagnosis of ethylene-glycol intoxication can be established by a severe metabolic acidosis and toxicological screening. Close monitoring of symptoms might contribute to early recognition of ethylene-glycol intoxication and its effective treatment. acute stroke ethylene glycol stroke mimic intravenous thrombolysis intoxication Figures Figure 1 Introduction Cerebrovascular diseases are the second most common cause of death and the leading cause of disability worldwide [ 1 ]. Stroke is classically defined as a rapidly developing clinical signs of focal (or global) disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin [ 2 ]. There are several other non-vascular diseases that may mimic stroke symptoms, including both neurological and non-neurological causes, known as stroke-mimics [ 3 ]. The most common stroke mimics are seizures, peripheral vestibular lesion, migraine, brain tumours, metabolic disorders, e.g. hypoglycaemia, and functional disorders [ 4 ]. Stroke mimics are often indistinguishable from an actual stroke and misdiagnosis ranges from 5–31% of patients depending on the diagnostic methods. However, if a stroke mimic is misdiagnosed as a stroke, it could lead to unnecessary and potentially harmful treatments, including intravenous thrombolysis [ 3 ]. Intravenous recombinant tissue plasminogen activator (rt-PA) is an effective and safe treatment for acute ischemic stroke (AIS) administered within 4,5 hours after the onset of symptoms [ 5 , 6 ]. In the acute setting, after exclusion of cerebral hemorrhage with brain CT, the diagnosis of AIS is mainly clinical. Moreover, due to the short time window in AIS, there is no time for detailed investigations. Therefore, it is not suprising that a subset of patients presenting with focal neurological deficits are misdiagnosed as stroke and treated with rt-PA. The most feared complication of intravenous thrombolysis (IVT) is the intracranial hemorrhage which is rare, but not insignificant. Based on the literature, rate of stroke mimics treated with rt-PA varies from 1–20% [ 7 , 8 ], and the rate of symptomatic intracranial hemorrhage (sICH) has been around 0,5% − 1% in these patients [ 9 , 10 ]. Intoxication is a rare, but possible cause of stroke mimic, accounting for approximately 2% of cases [ 4 ]. Here we present three cases of ethylene glycol poisoning presenting as an acute stroke mimic within the time window of thrombolytic therapy. To the best of our knowledge, this is the first report of ethylene-glycol intoxication that mimicked stroke symptoms and led to intravenous thrombolysis. Case Reports Case 1 A 54-year-old smoker male patient with no major illnesses in his medical history presented to our department as a stroke-alert with sudden onset of slurred speech, nystagmus and gait disturbance started at 9:30 am (Fig. 1 ). On admission (1:20 p.m.), his neurological examination revealed severe dysarthria, horizontal and vertical gaze-directed nystagmus and severe truncal and limb ataxia (NIHSS: 4 points). He was fully alert, afebrile, moderately hypertensive (165/90 mmHg) and slightly tachycardic (103/min, sinus rhythm). Pulse oximetry showed a hemoglobin saturation of 98% on room air. Non-contrast cerebral computed tomography (NCCT) showed no signs of bleeding or acute ischemic lesion. CT-angiography (CTA) showed hypoplastic vertebral artery on the left side but no occlusion was seen on major intracranial arteries. His laboratory values showed no significant changes in routine laboratory parameters (Table 1 ). Based on the clinical symptoms, vertebrobasilar territory stroke was suspected and IVT was started (1:40 p.m., door-to-needle time: 20 minutes, onset-to-needle-time: 250 min). A total dose of 73 mg alteplase was administered. The patient’s neurological status did not change during thrombolysis. However, late in the afternoon (5 p.m.) somnolence, agitation and hyperventilation were noticed. Due to the disturbance of consciousness cranial CT was repeated to exclude intracranial hemorrhage, but it was negative again. Arterial blood gas (ABG) analysis disclosed severe metabolic acidosis (pH: 7.03, PaCO 2 21 mmHg, serum bicarbonate 5.9 mMol/L, base excess − 22.7 mMol/L, anion gap: 24.7 mMol/L, Table 2 ). The patient’s agitation increased which required sedation, endotracheal intubation and mechanical ventilation. Intravenous sodium bicarbonate was administered to correct the acidosis. Meanwhile, the patient’s wife arrived and said that the patient had seemed depressed in the past few weeks and had mentioned suicidal thoughts several times which increased the probability of an intoxication. Based on the metabolic acidosis we suspected methanol or ethylene glycol poisoning and an infusion of 10 g of 10% ethanol was started immediately. Within the next hours, toxicological screening revealed an ethylene glycol serum concentration of 95.85 mg/dL with toxic levels defined as > 20 mg/dL and “possibly fatal” levels defined at > 30 mg/dL. Later, the patient was transferred to the Intensive Care Unit of the Internal Medicine Department and urgent hemodialysis was initiated. Within 48 hours his renal function deteriorated from a glomerulal filtration rate [GFR] of 90 mL/min/1.73 m 2 to 45 mL/min/1.73 m 2 GFR (Table 1 ) and the examination of urine sediment was positive for calcium oxalate crystals. The patient became febrile and chest X-ray showed pneumonia, therefore intravenous antibiotics were started. His condition improved significantly in the following days. Control NCCT 24 hours after rt-PA treatment showed no abnormalities. The control toxicology test on the second day no longer confirmed the presence of ethylene glycol in the blood and the pH returned to normal, therefore hemodialysis could be discontinued. Five days after his admission mechanical ventilation was stopped and the patient could be extubated. After he regained his consciousness, he admitted to drinking antifreeze liquid with suicidal intent (approximately 0.5-1 dL) a few hours before his admission. On day 9, he was transferred to the psychiatric ward for further treatment. At discharge, he was symptom-free. Case 2 A 78-year-old male patient with a history of hypertension, diabetes mellitus and Parkison’s disease was admitted as a thrombolysis candidate with an ictal onset of vertigo, unsteadiness and speech disturbance. According to his wife, he was asymptomatic in the morning on the day of admission, then at 12:00 he was noted to have difficulties in standing and walking without assistance and his speech was slurred (Fig. 1 ). The patient denied alcohol consumption or taking sedatives. On arrival (3 p.m.), horizontal gaze-directed nystagmus, right sided horizontal gaze palsy, severe dysarthria and severe truncal and limb ataxia causing inability to walk were found (NIHSS: 5 points). At baseline, he was vigilant and fully oriented, his vital parameters were in normal range. NCCT and CTA were negative. Laboratory screening on admission (including renal function) did not reveal significant abnormalities (Table 1 ). Since there were no exclusion criteria, thrombolysis was performed (onset-to-needle time: 194 min). After thrombolysis, his neurological symptoms did not improve. Moreover, a few hours later (9 p.m.) the patient deteriorated rapidly and lost consciousness, requiring intubation and mechanical ventilation. At that time, he was comatose, tetraplegic, showed bilateral Babinski-signs, and his oculocephalic and pupillary light reflexes were absent resembling an acute basilar artery occlusion or brainstem hemorrhage. NCCT and CTA were repeated but no signs of bleeding or large vessel occlusion were found. ABG revealed extremely severe metabolic acidosis (pH 15 mMol/L), low serum bicarbonate (< 3 mMol/L) level and a wide anion gap (28 mMol/L). Despite several fluid boluses and sodium bicarbonate administration, the acidosis and lactate levels did not improve and the patient became hemodynamically unstable requiring continuous catecholamin infusion to maintanin blood pressure. Urgent toxicological screening proved ethylene glycol intoxication with a serum ethylene glycol level of 159 mg/dL. Repeated laboratory tests (9 hours after his admission) showed a sodium of 147 mMol/L, potassium of 5,9 mMol/L, creatinine of 1,69 mg/dL and GFR of 38 ml/min/1,73 m 2 (Table 1 ). The patient was transferred to the Intensive Care Unit of the Internal Medicine Department and ethanol infusion was started immediately accompanied by continuous renal replacement therapy (CRRT). Continuous infusion of bicarbonate was maintained to alkalinize the urine, and thiamin and pyiridoxin were also given intravenously to facilitate conversion of glycolate into less toxic metabolites. Ethylene glycol levels and blood pH were monitored regularly. When the pH returned to normal and ethylene glycol levels remained < 20 mg/dL, ethanol was stopped. Despite the aferomentioned therapy the patient became completely anuric and his renal function continued to deteriorate with elevations in creatinine over the next 10 days to a peak of 6.2 mg/dL. Urine analysis revealed calcium oxalate crystals. On the 5th day after admission, pneumonia developed with markedly elevated inflammatory markers, which required administration of broad spectrum antibiotics. Despite withdrawal of sedation, the patient remained comatose. Unfortunately, he died on the 10th day after admission. We were informed later that the patient’s mood had been depressed lately and although he didn’t mention suicidal thoughts, an empty bottle of antifreeze liquid was found in his garage. Case 3 A 54-year-old man was transported to our department with a suspicion of epileptic seizure. His medical history was significant for hypertension, chronic alcoholism, alcohol intoxication, delirium, and prior right hemispheric ischemic stroke. According to his mother, the patient lost his consciousness for a few minutes at 1:30 p.m. on the day of admission (Fig. 1 ). After that, he was confused, disoriented and his speech was unintelligible. Recent alcohol consumption was not reported. In addition to the moderate-severe left-sided spastic hemiparesis and Babinksi-sign due to the previous stroke, severe mixed aphasia and extreme agitation were found during the physical examination (NIHSS: 7 points). In order to treat agitation, clonazepam and tiapride were administered intravenously. No direct or indirect signs of convulsion were detected. NCCT showed chronic infarction in the right internal capsule, but neither hemorrhage nor hyperacute ischemic lesion was described. CTA showed no evidence of arterial occlusion or stenosis in the intracranial vessels. On admission, laboratory parameters were significant for mild hyponatraemia (122 mMol/L, Table 1 ). Since the patient was within the thrombolytic time window, he had severe symptoms and had no exclusion criteria for intravenous thrombolysis, we decided to administer rt-PA in the standard dose of 0.9 mg/kg (5:20 p.m., onset-to-needle time: 230 min). His neurological status did not change during the thrombolysis. Considering potential alternative diagnoses, alcohol intoxication could not be excluded, therefore blood was sent to toxicological examination. Athough toxicological screening was negative for ethanol, it revealed ethylene-glycol intoxication with an ethylene-glycol serum level of 16.54 mg/dL (6:35 p.m.) ABG was obtained but it showed physiological acid-base parameters (Table 2 ). The patient was admitted to the Intensive Care Unit of the Internal Medicine Department, where intravenous ethanol was adminstered. Renal function did not show any worsening, so hemodialysis was not indicated. The next day, there was no detectable amount of ethylene glycol in his blood. The patient’s aphasia and agitation gradually diminished. Hyponatremia was considered as a consequence of chronic alcoholism and was corrected slowly with saline infusions. On the 3rd day of hospitalization he was able to walk with minor assistance and was able to take care of himself. He denied consuming antifreeze intentionally. On the 6th day of admission he was discharged home with residual neurological symptoms consistent with his previous condition. Table 1 Laboratory values on admission and at 48 hours. Abnormal values are bolded (GFR: glomerulal filtration rate; LDH: lactate dehydrogenase; AST: aspartate aminotransferase; ALT: alanine aminotransferase; GGT: gamma-glutamyl transferase; CRP: C-reactive protein; WBC: white blood count; INR: international normalized ratio; EG: ethylene glycol) Laboratory values Case 1 Case 2 Case 3 On admission Sodium (mmol/L) 139 143 122 Potassium (mmol/L) 4.9 4.8 5.5 Glucose (mmol/L) 5.8 5.6 4.5 Creatinine (mg/dL) 0.72 0.95 0.53 GFR (mL/min) > 90 76 > 90 LDH (U/L) 224 217 182 AST (U/L) 32 17 21 ALT (U/L) 40 16 9 GGT (U/L) 116 14 10 CRP (mg/L) 1.12 2.3 9.2 WBC (G/L) 10.75 8.43 12.47 Hemoglobin (g/L) 170 150 148 Platelet (G/L) 306 197 271 INR 0.98 1.0 0.96 EG (mg/dL) 95.85 159 16.54 At 48 hours Sodium (mmol/L) 149 152 135 Potassium (mmol/L) 5.4 5.9 3.9 Glucose (mmol/L) 6.4 6.5 7.0 Creatinine (mg/dL) 1.69 2.56 0.57 GFR (mL/min) 45 23 > 90 LDH (U/L) 273 422 225 AST (U/L) 23 37 53 ALT (U/L) 27 20 16 GGT (U/L) 93 21 11 CRP (mg/L) 51.9 124 42.3 WBC (G/L) 14.54 19.87 7.49 Hemoglobin (g/L) 141 152 129 Platelet (G/L) 191 141 208 INR 1.05 1.15 1.15 EG (mg/dL) 0 0 0 Table 2 Arterial blood gas parameters of the 3 cases on admission (BE: base excess; AG: anion gap) ABG parameters on admission Case 1 Case 2 Case 3 pH 7.03 < 6.8 7.45 PaO 2 (mmHg) 74 83 87 PaCO 2 (mmHg) 21 24 29 HCO 3 − (mmol/L) 5.9 15 > 15 1.4 Ca 2+ (mmol/L) 1.27 0.84 0.24 Discussion And Conclusions Stroke is characterized by suddenly developed focal neurological symptoms of vascular origin. Diagnosing a stroke can be challenging because there are multiple diseases that may mimic its presentation. Stroke mimics are not uncommon in daily clinical practice and are reported to represent 8% up to 43% of patients admitted to the emergency department [ 11 ]. When acute stroke patients arrive directly at neurology department, as in our instituition, the neurologists have to face this differential diagnostic challenge. In this report, we describe 3 patients presenting with a rare cause of stroke mimic caused by ethylene glycol consumption. Ethylene glycol is a colorless, odorless, sweet-tasting toxic alcohol most commonly found in antifreeze liquid for car engines and hydraulic brake fluids. Poisoning can be accidental or intentional motivated by a suicide attempt. Ethylene glycol is rapidly absorbed through the gastrointestinal tract after ingestion and quickly converted to its toxic metabolites, such as glycolaldehyde and glycolic acid via alcohol dehydrogenase. Although ethylene glycol intoxication is uncommon in medical practice, it is crucial to recognise because early diagnosis and prompt treatment can prevent severe morbidity and mortality [ 12 ]. Clinical manifestation of acute toxicity includes central nervous system depression, cardiopulmonary symptoms and renal insufficiency [ 12 ]. Our cases demonstrated that ethylene glycol poisoning can mimic the symptoms of an acute stroke. Acute alcohol intoxication is a frequently described vertebrobasilar stroke mimic as the two diseases share common symptoms of dysarthria, nystagmus and gait disturbance [ 13 , 14 ]. Ethylene glycol is a more potent central nervous system depressant than ethanol and due to its rapid absorption, toxic effects usually appear within 0,5 − 2 hours of ingestion. The most common initial symptoms of ethylene-glycol poisoning are the same as those of alcohol intoxication and vertebrobasilar stroke, including slurred speech, ataxia and disturbance of consciousness [ 15 ]. In line with literature data, two of our three patients presented with central type of nystagmus, severe dysarthria and ataxia. As intoxication was not known at arrival, vertebrobasilar stroke was diagnosed. Our third patient was a real diagnostic challenge, because the most prominent symptom was a temporary loss of consciousness that raised the suspicion of an epileptic seizure, followed by severe aphasia and extreme agitation, the latter of which is also characteristic of the early phase of ethylene glycol intoxication [ 12 ]. Although not a typical stroke symptom, epileptic seizure can be associated with stroke. Moreover, epilepsy is also known as a stroke mimic, because postictal focal symptoms including hamiparesis and/or aphasia are commonly present in stroke [ 16 ]. Differentiation between stroke and epilepsy with postictal hemiparesis and/or aphasia might be rather difficult in the hyperacute stage of the diseases. Cerebral CT usually does not help, and CTA might also be negative in both diseases. Diffusion-weighted imaging, the most sensitive magnetic resonance imaging (MRI) method for cerebral ischemia [ 17 ], could be useful, but MRI is not everywhere and not always available, and motion artifacts may also limit its evaluation. Moreover, in an acute situation, when “time is brain” and rt-PA treatment requires specific time criteria, sometimes the treatment cannot be delayed by time consuming examinations. Therefore, the general rule is that if the clinical examination strongly suggests stroke, the worst should be assumed, and thrombolysis should be performed. To the best of our knowledge, this is the first report in the literature of ethylene glycol poisoning that not only mimicked acute stroke but also led to thrombolytic treatment. All of our patients were referred by paramedics as a stroke alert within the time window of thrombolysis, and no evidence of intoxication was mentioned on admission in any of the patients. If the history and symptoms suggest ischemic stroke within the time window, imaging excludes cerebral hemorrhage and does not indicate other intracranial disease, thrombolysis should be considered if the patient is otherwise eligible for rt-PA treatment. There were no exclusion criteria in any of our cases and since our presumptive diagnosis was the acute stroke, and the patients’ had disabling symptoms, thrombolysis was performed. In our 1st and 2nd patients, the symptoms on admission were typical for vertebrobasilar stroke without any other alternative diagnosis. In their case, the possibility of a stroke mimic arose only after the thrombolysis was completed. As we discussed earlier, the third patient’s case was more complicated. The preceding loss of consciousness that raised the suspicion of an epileptic seizure was considered as stroke mimic, and extreme agitation is neither typical in ischaemic stroke. However, as the thrombolysis is an effective therapy in ischemic stroke [ 18 ], and a stroke mimic is associated with no or minimal risk of intracranial hemorrhage [ 19 ], it is not recommended to exclude patients who are potential candidates for rt-PA treatment based on the sole concern that their neurological symptoms may be attributed to a stroke mimic [ 20 ]. Our cases underline this statement, because none of our patients suffered intracranial hemorrhage after thrombolysis, nor did they have any other disadvantages from administration of rt-PA. Our observations suggest that symptoms of the first phase of ethylene glycol intoxication may overlap with the symptoms of an acute stroke which may delay the diagnosis of this life-threatening condition. On the other hand, close monitoring during and after thrombolysis can facilitate the early recognition of the disease underlying the stroke mimic. As our cases have shown, the first symptoms of ethylene glycol poisoning, including nystagmus, dysarthria and truncal ataxia, are also common in ischemic stroke. However, later symptoms, such as hyperventilation, agitation and disturbance of consciousness are no longer characteristic for stroke and may draw attention to a stroke mimic. Besides the variable clinical symptoms, the hallmarks of ethylene glycol intoxication are 1) presence of metabolic acidosis; 2) elevated anion or osmolar gap; 3) positive findings for calcium oxalate crystals in the urine, and 4) toxicological detection of ethylene glycol in the serum or urine [ 21 ]. It is important to recognize those alarming signs that may warn of intoxication during the observation of patients. Despite the thrombolysis, none of our patients’ neurological symptoms improved, however, progressive disturbance of consciousness, agitation or hyperventilation developed during the course of the disease. ABG revealed severe metabolic acidosis with wide anion gap in Case 1 and Case 2. These findings raised the suspicion of intoxication with alcohol derivatives which was also confirmed by the toxicological screening. Later, both patients had evidence of nephrotoxicity, which is also a characteristic feature of ethylene glycol intoxication, demonstrated by elevated creatinine levels and decreased GFR values. However, in Case 3 ABG was normal and renal function was not impaired. Its explanation is probably that the serum ethylene glycol did not reach the toxic value and the prompt treatment prevented the formation of toxic metabolites. Quite contrary, in our 2nd patient, where the serum level was a multiple of toxic value, very severe metabolic changes and central nervous system depression developed. A suspected stroke diagnosis in stroke mimics, even if wrong, may carry not only a disadvantage, but also an advantage. Because stroke requires emergency care, patients with stroke symptoms, caused by either stroke or stroke mimics, usually reach the hospital in a very short time. Moreover, if reperfusion therapy is performed, the patient is carefully monitored not only during the rt-PA treatment, but also in the subsequent 24 hours. It means that patients with stroke or stroke mimics are investigated and observed in the initial stage of the disease, allowing recognition the first signs and symptoms, and thus early diagnosis and treatment. In our cases this management led to early diagnosis of ethylene glycol intoxication and early start of the appropriate treatment resulting in a good clinical outcome in 2 of our 3 patients. The importance of anamnesis should also be highlighted. A report of ingestion of toxic agents makes the diagnosis obvious, however the physician should ask specifically about drinking antifreeze or similar substances in cases of suspected toxicity. Often, the patient is unwilling or unable to give an accurate history. Ideally, a bottle of antifreeze or other solvent is found at the scene, but if not, the family as well as the prehospital team should be thoroughly questioned and instructed to search for potentially toxic substances. Previous suicidal ideations and history of depression are also key information. At the presention of our patients these information were lacking, and they became known only after the diagnosis was made. In conclusion, our observations show that ethylene glycol intoxication in its early phase may mimic acute stroke and thus even lead to thrombolytic treatment, which has not been reported earlier. If focal neurological deficits are accompanied by agitation, hyperventilation, or disturbance of consciousness, an alternative diagnosis, including intoxication, should be considered. The differential diagnosis in these cases can be facilitated by ABG and toxicological screening. Abbreviations AIS acute ischemic stroke ABG arterial blood gas CTA computed tomography angiography CRRT continuous renal replacement therapy GFR glomerular filtration rate IVT intravenous thrombolyis ICU Intensive Care Unit MRI magnetic resonance imaging NIHSS National Institutes of Health Stroke Scale NCCT non-contrast computed tomography rt-PA recombinant tissue plasminogen activator sICH symptomatic intracranial hemorrhage Declarations Ethics approval and consent to participate Not applicable Consent for publication Informed written consent was obtained from patients after discharge from the hospital (Case 1 and 3). They were able to fully understand and answer our questions and were oriented in time, place and their personal data. However, in the case of the patient who died in the hospital (Case 3), informed written consent was given by a family member (wife). Availability of data and materials The datasets supporting the conclusions of this case report are included within the article. Competing interests The authors declare that they have no conflict of interest. Funding None. Authors' contributions MH was involved in clinical work-up, manuscript preparation, editing and submission. LO revised the manuscript critically for important content. All authors have read and approved the final manuscript. Acknowledgements The authors wish to express their sincere thanks to the co-workers of the Intensive Care Unit of the Department of Neurology and the Intensive Care Unit of the Internal Medicine Department, University of Debrecen. References GBD 2016 Stroke Collaborators. Global, regional, and national burden of stroke, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet Neurol. 2019 May;18(5):439-458. doi: 10.1016/S1474-4422(19)30034-1. Epub 2019 Mar 11. PMID: 30871944; PMCID Aho K, Harmsen P, Hatano S, Marquardsen J, Smirnov VE, Strasser T. Cerebrovascular disease in the community: results of a WHO collaborative study. Bull World Health Organ. 1980;58(1):113-30. PMID: 6966542; PMCID: PMC2395897. Long B (2016) Stroke Mimics: Pearls and Pitfalls. www.emdocs.net/stroke-mimics-pearls-andpitfalls (Last accessed: 9 November 2018.) Fernandes PM, Whiteley WN, Hart SR, Al-Shahi Salman R. Strokes: mimics and chameleons. Pract Neurol. 2013 Feb;13(1):21-8. doi: 10.1136/practneurol-2012-000465. PMID: 23315456. Hacke W, Kaste M, Bluhmki E, Brozman M, Dávalos A, Guidetti D, Larrue V, Lees KR, Medeghri Z, Machnig T, Schneider D, von Kummer R, Wahlgren N, Toni D; ECASS Investigators. Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke. N Engl J Med. 2008 Sep 25;359(13):1317-29. doi: 10.1056/NEJMoa0804656. PMID: 18815396. Wahlgren N, Ahmed N, Dávalos A, Hacke W, Millán M, Muir K, Roine RO, Toni D, Lees KR; SITS investigators. Thrombolysis with alteplase 3-4.5 h after acute ischaemic stroke (SITS-ISTR): an observational study. Lancet. 2008 Oct 11;372(9646):1303-9. doi: 10.1016/S0140-6736(08)61339-2. Epub 2008 Sep 12. PMID: 18790527. Winkler DT, Fluri F, Fuhr P, Wetzel SG, Lyrer PA, Ruegg S, Engelter ST. Thrombolysis in stroke mimics: frequency, clinical characteristics, and outcome. Stroke. 2009 Apr;40(4):1522-5. doi: 10.1161/STROKEAHA.108.530352. Epub 2009 Jan 22. PMID: 19164790. Lee VH, Howell R, Yadav R, Heaton S, Wiles KL, Lakhani S. Thrombolysis of stroke mimics via telestroke. Stroke Vasc Neurol. 2022 Jun;7(3):267-270. doi: 10.1136/svn-2020-000776. Epub 2022 Feb 1. PMID: 35105730; PMCID: PMC9240458. Tsivgoulis G, Zand R, Katsanos AH, Goyal N, Uchino K, Chang J, Dardiotis E, Putaala J, Alexandrov AW, Malkoff MD, Alexandrov AV. Safety of intravenous thrombolysis in stroke mimics: prospective 5-year study and comprehensive meta-analysis. Stroke. 2015 May;46(5):1281-7. doi: 10.1161/STROKEAHA.115.009012. Epub 2015 Mar 19. PMID: 25791717. Zinkstok SM, Engelter ST, Gensicke H, Lyrer PA, Ringleb PA, Artto V, Putaala J, Haapaniemi E, Tatlisumak T, Chen Y, Leys D, Sarikaya H, Michel P, Odier C, Berrouschot J, Arnold M, Heldner MR, Zini A, Fioravanti V, Padjen V, Beslac-Bumbasirevic L, Pezzini A, Roos YB, Nederkoorn PJ. Safety of thrombolysis in stroke mimics: results from a multicenter cohort study. Stroke. 2013 Apr;44(4):1080-4. doi: 10.1161/STROKEAHA.111.000126. Epub 2013 Feb 26. PMID: 23444310. Merino JG, Luby M, Benson RT, Davis LA, Hsia AW, Latour LL, Lynch JK, Warach S. Predictors of acute stroke mimics in 8187 patients referred to a stroke service. J Stroke Cerebrovasc Dis. 2013 Nov;22(8):e397-403. doi: 10.1016/j.jstrokecerebrovasdis.2013.04.018. Epub 2013 May 13. PMID: 23680681; PMCID: PMC3812364. Hess R, Bartels MJ, Pottenger LH. Ethylene glycol: an estimate of tolerable levels of exposure based on a review of animal and human data. Arch Toxicol. 2004 Dec;78(12):671-80. doi: 10.1007/s00204-004-0594-8. Epub 2004 Sep 15. PMID: 15372138. Hassing LT, Verschoof MA, Koppen H. Alcohol Intoxication as a Stroke Mimic and the Incidence of Acute Alcohol Intoxication in Stroke. J Stroke Cerebrovasc Dis. 2019 Dec;28(12):104424. doi: 10.1016/j.jstrokecerebrovasdis.2019.104424. Epub 2019 Oct 15. PMID: 31624037. Arokszallasi T, Balogh E, Csiba L, Fekete I, Fekete K, Olah L. Acute alcohol intoxication may cause delay in stroke treatment - case reports. BMC Neurol. 2019 Jan 29;19(1):14. doi: 10.1186/s12883-019-1241-6. PMID: 30696413; PMCID: PMC6350361. Davis DP, Bramwell KJ, Hamilton RS, Williams SR. Ethylene glycol poisoning: case report of a record-high level and a review. J Emerg Med. 1997 Sep-Oct;15(5):653-67. doi: 10.1016/s0736-4679(97)00145-5. PMID: 9348055. Rolak LA, Rutecki P, Ashizawa T, Harati Y. Clinical features of Todd's post-epileptic paralysis. J Neurol Neurosurg Psychiatry. 1992 Jan;55(1):63-4. doi: 10.1136/jnnp.55.1.63. PMID: 1548500; PMCID: PMC488937. Chalela JA, Kidwell CS, Nentwich LM, Luby M, Butman JA, Demchuk AM, Hill MD, Patronas N, Latour L, Warach S. Magnetic resonance imaging and computed tomography in emergency assessment of patients with suspected acute stroke: a prospective comparison. Lancet. 2007 Jan 27;369(9558):293-8. doi: 10.1016/S0140-6736(07)60151-2. PMID: 17258669; PMCID: PMC1859855. National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med. 1995 Dec 14;333(24):1581-7. doi: 10.1056/NEJM199512143332401. PMID: 7477192. Artto V, Putaala J, Strbian D, Meretoja A, Piironen K, Liebkind R, Silvennoinen H, Atula S, Häppölä O; Helsinki Stroke Thrombolysis Registry Group. Stroke mimics and intravenous thrombolysis. Ann Emerg Med. 2012 Jan;59(1):27-32. doi: 10.1016/j.annemergmed.2011.09.011. Epub 2011 Oct 14. PMID: 22000770. Tsivgoulis G, Alexandrov AV, Chang J, Sharma VK, Hoover SL, Lao AY, Liu W, Stamboulis E, Alexandrov AW, Malkoff MD, Frey JL. Safety and outcomes of intravenous thrombolysis in stroke mimics: a 6-year, single-care center study and a pooled analysis of reported series. Stroke. 2011 Jun;42(6):1771-4. doi: 10.1161/STROKEAHA.110.609339. Epub 2011 Apr 14. PMID: 21493900. Iqbal A, Glagola JJ, Nappe TM. Ethylene Glycol Toxicity. 2022 Sep 26. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan–. PMID: 30725694. Additional Declarations No competing interests reported. Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-2524829","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":172975920,"identity":"b7211e24-c40b-43d8-b16e-a7e7e83a1c9d","order_by":0,"name":"Máté Héja","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAABBUlEQVRIiWNgGAWjYBACAwaGBAiLvYGBgQdIszEksDEwNhDWIsHAc4B4LQwQLRIJEC0MhLSYszc8/MCYY1fHL/k68cEbhsN5fOzJxx4w7jiMU4tlz4FkCcZtyRKSs3M3G85hOFzMxvMs3YDxDG4tBjcSEoBamCUMbuduk+ZhOJzYJpFjJsHYhkfL/QfJPxi31UvY3zy7/TdES/43/FpuMKQBbTksYSDBu40Zagsbfi1nEtIsErcdl5xxJnez5ByD9MQ2nmfmBolt6bi1HD+TfOPjtmp+/vazGz+8qbBOnN+e/OzBxzZrnFqAcZEAi38GRDQlYFMJB+wH8EqPglEwCkbBKGAAABXWVhueg/OyAAAAAElFTkSuQmCC","orcid":"","institution":"University of Debrecen","correspondingAuthor":true,"submittingAuthor":false,"prefix":"","firstName":"Máté","middleName":"","lastName":"Héja","suffix":""},{"id":172975921,"identity":"a59831a7-775a-4b4c-8477-1206eaf33244","order_by":1,"name":"László Oláh","email":"","orcid":"","institution":"University of Debrecen","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"László","middleName":"","lastName":"Oláh","suffix":""}],"badges":[],"createdAt":"2023-01-28 23:59:06","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-2524829/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-2524829/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":32532557,"identity":"6e140ccf-e937-46ec-86ad-4074e3df016a","added_by":"auto","created_at":"2023-02-06 14:41:33","extension":"jpg","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":254063,"visible":true,"origin":"","legend":"\u003cp\u003eTimeline of the 3 cases (NCCT: non-contrast cerebral computed tomography; CTA: computed tomography angiography; IVT: intravenous thrombolysis; ONT: onset to needle time; ABG: arterial blood gas; EG: ethylene glycol; ICU: intensive care unit)\u003c/p\u003e","description":"","filename":"Figure1.jpg","url":"https://assets-eu.researchsquare.com/files/rs-2524829/v1/5fce709c919afb6fc46a79d4.jpg"},{"id":37246043,"identity":"42b3528f-4e5d-4f8e-aa66-a6ab467975ab","added_by":"auto","created_at":"2023-05-19 14:59:36","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":480015,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-2524829/v1/6e343344-720e-4666-82ac-acf21a8021d3.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Ethylene glycol intoxication presenting as a mimic of acute stroke: report of three cases","fulltext":[{"header":"Introduction","content":"\u003cp\u003eCerebrovascular diseases are the second most common cause of death and the leading cause of disability worldwide [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]. Stroke is classically defined as a rapidly developing clinical signs of focal (or global) disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. There are several other non-vascular diseases that may mimic stroke symptoms, including both neurological and non-neurological causes, known as stroke-mimics [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. The most common stroke mimics are seizures, peripheral vestibular lesion, migraine, brain tumours, metabolic disorders, e.g. hypoglycaemia, and functional disorders [\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]. Stroke mimics are often indistinguishable from an actual stroke and misdiagnosis ranges from 5\u0026ndash;31% of patients depending on the diagnostic methods. However, if a stroke mimic is misdiagnosed as a stroke, it could lead to unnecessary and potentially harmful treatments, including intravenous thrombolysis [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. Intravenous recombinant tissue plasminogen activator (rt-PA) is an effective and safe treatment for acute ischemic stroke (AIS) administered within 4,5 hours after the onset of symptoms [\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e, \u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]. In the acute setting, after exclusion of cerebral hemorrhage with brain CT, the diagnosis of AIS is mainly clinical. Moreover, due to the short time window in AIS, there is no time for detailed investigations. Therefore, it is not suprising that a subset of patients presenting with focal neurological deficits are misdiagnosed as stroke and treated with rt-PA. The most feared complication of intravenous thrombolysis (IVT) is the intracranial hemorrhage which is rare, but not insignificant. Based on the literature, rate of stroke mimics treated with rt-PA varies from 1\u0026ndash;20% [\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e, \u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e], and the rate of symptomatic intracranial hemorrhage (sICH) has been around 0,5% \u0026minus;\u0026thinsp;1% in these patients [\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e, \u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eIntoxication is a rare, but possible cause of stroke mimic, accounting for approximately 2% of cases [\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]. Here we present three cases of ethylene glycol poisoning presenting as an acute stroke mimic within the time window of thrombolytic therapy. To the best of our knowledge, this is the first report of ethylene-glycol intoxication that mimicked stroke symptoms and led to intravenous thrombolysis.\u003c/p\u003e"},{"header":"Case Reports","content":"\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003ch2\u003eCase 1\u003c/h2\u003e \u003cp\u003eA 54-year-old smoker male patient with no major illnesses in his medical history presented to our department as a stroke-alert with sudden onset of slurred speech, nystagmus and gait disturbance started at 9:30 am (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). On admission (1:20 p.m.), his neurological examination revealed severe dysarthria, horizontal and vertical gaze-directed nystagmus and severe truncal and limb ataxia (NIHSS: 4 points). He was fully alert, afebrile, moderately hypertensive (165/90 mmHg) and slightly tachycardic (103/min, sinus rhythm). Pulse oximetry showed a hemoglobin saturation of 98% on room air. Non-contrast cerebral computed tomography (NCCT) showed no signs of bleeding or acute ischemic lesion. CT-angiography (CTA) showed hypoplastic vertebral artery on the left side but no occlusion was seen on major intracranial arteries. His laboratory values showed no significant changes in routine laboratory parameters (Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). Based on the clinical symptoms, vertebrobasilar territory stroke was suspected and IVT was started (1:40 p.m., door-to-needle time: 20 minutes, onset-to-needle-time: 250 min). A total dose of 73 mg alteplase was administered. The patient\u0026rsquo;s neurological status did not change during thrombolysis. However, late in the afternoon (5 p.m.) somnolence, agitation and hyperventilation were noticed. Due to the disturbance of consciousness cranial CT was repeated to exclude intracranial hemorrhage, but it was negative again. Arterial blood gas (ABG) analysis disclosed severe metabolic acidosis (pH: 7.03, PaCO\u003csub\u003e2\u003c/sub\u003e 21 mmHg, serum bicarbonate 5.9 mMol/L, base excess \u0026minus;\u0026thinsp;22.7 mMol/L, anion gap: 24.7 mMol/L, Table\u0026nbsp;\u003cspan refid=\"Tab2\" class=\"InternalRef\"\u003e2\u003c/span\u003e). The patient\u0026rsquo;s agitation increased which required sedation, endotracheal intubation and mechanical ventilation. Intravenous sodium bicarbonate was administered to correct the acidosis. Meanwhile, the patient\u0026rsquo;s wife arrived and said that the patient had seemed depressed in the past few weeks and had mentioned suicidal thoughts several times which increased the probability of an intoxication. Based on the metabolic acidosis we suspected methanol or ethylene glycol poisoning and an infusion of 10 g of 10% ethanol was started immediately. Within the next hours, toxicological screening revealed an ethylene glycol serum concentration of 95.85 mg/dL with toxic levels defined as \u0026gt;\u0026thinsp;20 mg/dL and \u0026ldquo;possibly fatal\u0026rdquo; levels defined at \u0026gt;\u0026thinsp;30 mg/dL. Later, the patient was transferred to the Intensive Care Unit of the Internal Medicine Department and urgent hemodialysis was initiated. Within 48 hours his renal function deteriorated from a glomerulal filtration rate [GFR] of 90 mL/min/1.73 m\u003csup\u003e2\u003c/sup\u003e to 45 mL/min/1.73 m\u003csup\u003e2\u003c/sup\u003e GFR (Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e) and the examination of urine sediment was positive for calcium oxalate crystals. The patient became febrile and chest X-ray showed pneumonia, therefore intravenous antibiotics were started. His condition improved significantly in the following days. Control NCCT 24 hours after rt-PA treatment showed no abnormalities. The control toxicology test on the second day no longer confirmed the presence of ethylene glycol in the blood and the pH returned to normal, therefore hemodialysis could be discontinued. Five days after his admission mechanical ventilation was stopped and the patient could be extubated. After he regained his consciousness, he admitted to drinking antifreeze liquid with suicidal intent (approximately 0.5-1 dL) a few hours before his admission. On day 9, he was transferred to the psychiatric ward for further treatment. At discharge, he was symptom-free.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec4\" class=\"Section2\"\u003e \u003ch2\u003eCase 2\u003c/h2\u003e \u003cp\u003eA 78-year-old male patient with a history of hypertension, diabetes mellitus and Parkison\u0026rsquo;s disease was admitted as a thrombolysis candidate with an ictal onset of vertigo, unsteadiness and speech disturbance. According to his wife, he was asymptomatic in the morning on the day of admission, then at 12:00 he was noted to have difficulties in standing and walking without assistance and his speech was slurred (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). The patient denied alcohol consumption or taking sedatives. On arrival (3 p.m.), horizontal gaze-directed nystagmus, right sided horizontal gaze palsy, severe dysarthria and severe truncal and limb ataxia causing inability to walk were found (NIHSS: 5 points). At baseline, he was vigilant and fully oriented, his vital parameters were in normal range. NCCT and CTA were negative. Laboratory screening on admission (including renal function) did not reveal significant abnormalities (Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). Since there were no exclusion criteria, thrombolysis was performed (onset-to-needle time: 194 min). After thrombolysis, his neurological symptoms did not improve. Moreover, a few hours later (9 p.m.) the patient deteriorated rapidly and lost consciousness, requiring intubation and mechanical ventilation. At that time, he was comatose, tetraplegic, showed bilateral Babinski-signs, and his oculocephalic and pupillary light reflexes were absent resembling an acute basilar artery occlusion or brainstem hemorrhage. NCCT and CTA were repeated but no signs of bleeding or large vessel occlusion were found. ABG revealed extremely severe metabolic acidosis (pH\u0026thinsp;\u0026lt;\u0026thinsp;6.8), unmeasurable high lactate level (\u0026gt;\u0026thinsp;15 mMol/L), low serum bicarbonate (\u0026lt;\u0026thinsp;3 mMol/L) level and a wide anion gap (28 mMol/L). Despite several fluid boluses and sodium bicarbonate administration, the acidosis and lactate levels did not improve and the patient became hemodynamically unstable requiring continuous catecholamin infusion to maintanin blood pressure. Urgent toxicological screening proved ethylene glycol intoxication with a serum ethylene glycol level of 159 mg/dL. Repeated laboratory tests (9 hours after his admission) showed a sodium of 147 mMol/L, potassium of 5,9 mMol/L, creatinine of 1,69 mg/dL and GFR of 38 ml/min/1,73 m\u003csup\u003e2\u003c/sup\u003e (Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). The patient was transferred to the Intensive Care Unit of the Internal Medicine Department and ethanol infusion was started immediately accompanied by continuous renal replacement therapy (CRRT). Continuous infusion of bicarbonate was maintained to alkalinize the urine, and thiamin and pyiridoxin were also given intravenously to facilitate conversion of glycolate into less toxic metabolites. Ethylene glycol levels and blood pH were monitored regularly. When the pH returned to normal and ethylene glycol levels remained\u0026thinsp;\u0026lt;\u0026thinsp;20 mg/dL, ethanol was stopped. Despite the aferomentioned therapy the patient became completely anuric and his renal function continued to deteriorate with elevations in creatinine over the next 10 days to a peak of 6.2 mg/dL. Urine analysis revealed calcium oxalate crystals. On the 5th day after admission, pneumonia developed with markedly elevated inflammatory markers, which required administration of broad spectrum antibiotics. Despite withdrawal of sedation, the patient remained comatose. Unfortunately, he died on the 10th day after admission. We were informed later that the patient\u0026rsquo;s mood had been depressed lately and although he didn\u0026rsquo;t mention suicidal thoughts, an empty bottle of antifreeze liquid was found in his garage.\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec5\" class=\"Section2\"\u003e \u003ch2\u003eCase 3\u003c/h2\u003e \u003cp\u003eA 54-year-old man was transported to our department with a suspicion of epileptic seizure. His medical history was significant for hypertension, chronic alcoholism, alcohol intoxication, delirium, and prior right hemispheric ischemic stroke. According to his mother, the patient lost his consciousness for a few minutes at 1:30 p.m. on the day of admission (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). After that, he was confused, disoriented and his speech was unintelligible. Recent alcohol consumption was not reported. In addition to the moderate-severe left-sided spastic hemiparesis and Babinksi-sign due to the previous stroke, severe mixed aphasia and extreme agitation were found during the physical examination (NIHSS: 7 points). In order to treat agitation, clonazepam and tiapride were administered intravenously. No direct or indirect signs of convulsion were detected. NCCT showed chronic infarction in the right internal capsule, but neither hemorrhage nor hyperacute ischemic lesion was described. CTA showed no evidence of arterial occlusion or stenosis in the intracranial vessels. On admission, laboratory parameters were significant for mild hyponatraemia (122 mMol/L, Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). Since the patient was within the thrombolytic time window, he had severe symptoms and had no exclusion criteria for intravenous thrombolysis, we decided to administer rt-PA in the standard dose of 0.9 mg/kg (5:20 p.m., onset-to-needle time: 230 min). His neurological status did not change during the thrombolysis. Considering potential alternative diagnoses, alcohol intoxication could not be excluded, therefore blood was sent to toxicological examination. Athough toxicological screening was negative for ethanol, it revealed ethylene-glycol intoxication with an ethylene-glycol serum level of 16.54 mg/dL (6:35 p.m.) ABG was obtained but it showed physiological acid-base parameters (Table\u0026nbsp;\u003cspan refid=\"Tab2\" class=\"InternalRef\"\u003e2\u003c/span\u003e). The patient was admitted to the Intensive Care Unit of the Internal Medicine Department, where intravenous ethanol was adminstered. Renal function did not show any worsening, so hemodialysis was not indicated. The next day, there was no detectable amount of ethylene glycol in his blood. The patient\u0026rsquo;s aphasia and agitation gradually diminished. Hyponatremia was considered as a consequence of chronic alcoholism and was corrected slowly with saline infusions. On the 3rd day of hospitalization he was able to walk with minor assistance and was able to take care of himself. He denied consuming antifreeze intentionally. On the 6th day of admission he was discharged home with residual neurological symptoms consistent with his previous condition.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab1\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eLaboratory values on admission and at 48 hours. Abnormal values are bolded (GFR: glomerulal filtration rate; LDH: lactate dehydrogenase; AST: aspartate aminotransferase; ALT: alanine aminotransferase; GGT: gamma-glutamyl transferase; CRP: C-reactive protein; WBC: white blood count; INR: international normalized ratio; EG: ethylene glycol)\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"4\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLaboratory values\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eCase 1\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eCase 2\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eCase 3\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eOn admission\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e\u0026nbsp;\u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eSodium (mmol/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e139\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e143\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e122\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePotassium (mmol/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e4.9\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e4.8\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e5.5\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eGlucose (mmol/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e5.8\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e5.6\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e4.5\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eCreatinine (mg/dL)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.72\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.95\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.53\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eGFR (mL/min)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e\u0026gt;\u0026thinsp;90\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e76\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u0026gt;\u0026thinsp;90\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLDH (U/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e\u003cb\u003e224\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e217\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e182\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAST (U/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e32\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e17\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e21\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eALT (U/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e40\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e16\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e9\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eGGT (U/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e\u003cb\u003e116\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e14\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e10\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eCRP (mg/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1.12\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e2.3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e9.2\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eWBC (G/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e10.75\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e8.43\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e12.47\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHemoglobin (g/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e170\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e150\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e148\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePlatelet (G/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e306\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e197\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e271\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eINR\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.98\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e1.0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.96\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eEG (mg/dL)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e\u003cb\u003e95.85\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e159\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e16.54\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eAt 48 hours\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eSodium (mmol/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e149\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e152\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e135\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePotassium (mmol/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e\u003cb\u003e5.4\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e5.9\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e3.9\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eGlucose (mmol/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e\u003cb\u003e6.4\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e6.5\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e7.0\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eCreatinine (mg/dL)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e\u003cb\u003e1.69\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e2.56\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.57\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eGFR (mL/min)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e\u003cb\u003e45\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e23\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u0026gt;\u0026thinsp;90\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLDH (U/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e\u003cb\u003e273\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e422\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e225\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAST (U/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e23\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e37\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e53\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eALT (U/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e27\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e20\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e16\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eGGT (U/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e\u003cb\u003e93\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e21\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e11\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eCRP (mg/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e\u003cb\u003e51.9\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e124\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e42.3\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eWBC (G/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e\u003cb\u003e14.54\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e19.87\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e7.49\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHemoglobin (g/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e141\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e152\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e129\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePlatelet (G/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e191\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e141\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e208\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eINR\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1.05\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e1.15\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e1.15\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eEG (mg/dL)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab2\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 2\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eArterial blood gas parameters of the 3 cases on admission (BE: base excess; AG: anion gap)\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"4\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eABG parameters on admission\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eCase 1\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eCase 2\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eCase 3\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003epH\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e7.03\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;6.8\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e7.45\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePaO\u003csub\u003e2\u003c/sub\u003e (mmHg)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e74\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e83\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e87\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePaCO\u003csub\u003e2\u003c/sub\u003e (mmHg)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e21\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e24\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e29\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHCO\u003csub\u003e3\u003c/sub\u003e\u003csup\u003e\u0026minus;\u003c/sup\u003e (mmol/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e5.9\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e20.2\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHCO\u003csub\u003e3\u003c/sub\u003e\u003csup\u003e\u0026minus;\u003c/sup\u003estd (mmol/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e7.3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e-\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e20.8\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eBE (mmol/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e-22.7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e-27.6\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e-2.5\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAG (mmol/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e24.7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e28\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e15.6\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLactic acid (mmol/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e\u0026gt;\u0026thinsp;15\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026gt;\u0026thinsp;15\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e1.4\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eCa\u003csup\u003e2+\u003c/sup\u003e (mmol/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1.27\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.84\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.24\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003c/div\u003e"},{"header":"Discussion And Conclusions","content":"\u003cp\u003eStroke is characterized by suddenly developed focal neurological symptoms of vascular origin. Diagnosing a stroke can be challenging because there are multiple diseases that may mimic its presentation. Stroke mimics are not uncommon in daily clinical practice and are reported to represent 8% up to 43% of patients admitted to the emergency department [\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e]. When acute stroke patients arrive directly at neurology department, as in our instituition, the neurologists have to face this differential diagnostic challenge. In this report, we describe 3 patients presenting with a rare cause of stroke mimic caused by ethylene glycol consumption.\u003c/p\u003e \u003cp\u003eEthylene glycol is a colorless, odorless, sweet-tasting toxic alcohol most commonly found in antifreeze liquid for car engines and hydraulic brake fluids. Poisoning can be accidental or intentional motivated by a suicide attempt. Ethylene glycol is rapidly absorbed through the gastrointestinal tract after ingestion and quickly converted to its toxic metabolites, such as glycolaldehyde and glycolic acid via alcohol dehydrogenase. Although ethylene glycol intoxication is uncommon in medical practice, it is crucial to recognise because early diagnosis and prompt treatment can prevent severe morbidity and mortality [\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e]. Clinical manifestation of acute toxicity includes central nervous system depression, cardiopulmonary symptoms and renal insufficiency [\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eOur cases demonstrated that ethylene glycol poisoning can mimic the symptoms of an acute stroke. Acute alcohol intoxication is a frequently described vertebrobasilar stroke mimic as the two diseases share common symptoms of dysarthria, nystagmus and gait disturbance [\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e, \u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e]. Ethylene glycol is a more potent central nervous system depressant than ethanol and due to its rapid absorption, toxic effects usually appear within 0,5\u0026thinsp;\u0026minus;\u0026thinsp;2 hours of ingestion. The most common initial symptoms of ethylene-glycol poisoning are the same as those of alcohol intoxication and vertebrobasilar stroke, including slurred speech, ataxia and disturbance of consciousness [\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e]. In line with literature data, two of our three patients presented with central type of nystagmus, severe dysarthria and ataxia. As intoxication was not known at arrival, vertebrobasilar stroke was diagnosed. Our third patient was a real diagnostic challenge, because the most prominent symptom was a temporary loss of consciousness that raised the suspicion of an epileptic seizure, followed by severe aphasia and extreme agitation, the latter of which is also characteristic of the early phase of ethylene glycol intoxication [\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e]. Although not a typical stroke symptom, epileptic seizure can be associated with stroke. Moreover, epilepsy is also known as a stroke mimic, because postictal focal symptoms including hamiparesis and/or aphasia are commonly present in stroke [\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e]. Differentiation between stroke and epilepsy with postictal hemiparesis and/or aphasia might be rather difficult in the hyperacute stage of the diseases. Cerebral CT usually does not help, and CTA might also be negative in both diseases. Diffusion-weighted imaging, the most sensitive magnetic resonance imaging (MRI) method for cerebral ischemia [\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e], could be useful, but MRI is not everywhere and not always available, and motion artifacts may also limit its evaluation. Moreover, in an acute situation, when \u0026ldquo;time is brain\u0026rdquo; and rt-PA treatment requires specific time criteria, sometimes the treatment cannot be delayed by time consuming examinations. Therefore, the general rule is that if the clinical examination strongly suggests stroke, the worst should be assumed, and thrombolysis should be performed.\u003c/p\u003e \u003cp\u003eTo the best of our knowledge, this is the first report in the literature of ethylene glycol poisoning that not only mimicked acute stroke but also led to thrombolytic treatment. All of our patients were referred by paramedics as a stroke alert within the time window of thrombolysis, and no evidence of intoxication was mentioned on admission in any of the patients. If the history and symptoms suggest ischemic stroke within the time window, imaging excludes cerebral hemorrhage and does not indicate other intracranial disease, thrombolysis should be considered if the patient is otherwise eligible for rt-PA treatment. There were no exclusion criteria in any of our cases and since our presumptive diagnosis was the acute stroke, and the patients\u0026rsquo; had disabling symptoms, thrombolysis was performed. In our 1st and 2nd patients, the symptoms on admission were typical for vertebrobasilar stroke without any other alternative diagnosis. In their case, the possibility of a stroke mimic arose only after the thrombolysis was completed. As we discussed earlier, the third patient\u0026rsquo;s case was more complicated. The preceding loss of consciousness that raised the suspicion of an epileptic seizure was considered as stroke mimic, and extreme agitation is neither typical in ischaemic stroke. However, as the thrombolysis is an effective therapy in ischemic stroke [\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e], and a stroke mimic is associated with no or minimal risk of intracranial hemorrhage [\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e], it is not recommended to exclude patients who are potential candidates for rt-PA treatment based on the sole concern that their neurological symptoms may be attributed to a stroke mimic [\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e]. Our cases underline this statement, because none of our patients suffered intracranial hemorrhage after thrombolysis, nor did they have any other disadvantages from administration of rt-PA.\u003c/p\u003e \u003cp\u003eOur observations suggest that symptoms of the first phase of ethylene glycol intoxication may overlap with the symptoms of an acute stroke which may delay the diagnosis of this life-threatening condition. On the other hand, close monitoring during and after thrombolysis can facilitate the early recognition of the disease underlying the stroke mimic. As our cases have shown, the first symptoms of ethylene glycol poisoning, including nystagmus, dysarthria and truncal ataxia, are also common in ischemic stroke. However, later symptoms, such as hyperventilation, agitation and disturbance of consciousness are no longer characteristic for stroke and may draw attention to a stroke mimic. Besides the variable clinical symptoms, the hallmarks of ethylene glycol intoxication are 1) presence of metabolic acidosis; 2) elevated anion or osmolar gap; 3) positive findings for calcium oxalate crystals in the urine, and 4) toxicological detection of ethylene glycol in the serum or urine [\u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e]. It is important to recognize those alarming signs that may warn of intoxication during the observation of patients. Despite the thrombolysis, none of our patients\u0026rsquo; neurological symptoms improved, however, progressive disturbance of consciousness, agitation or hyperventilation developed during the course of the disease. ABG revealed severe metabolic acidosis with wide anion gap in Case 1 and Case 2. These findings raised the suspicion of intoxication with alcohol derivatives which was also confirmed by the toxicological screening. Later, both patients had evidence of nephrotoxicity, which is also a characteristic feature of ethylene glycol intoxication, demonstrated by elevated creatinine levels and decreased GFR values. However, in Case 3 ABG was normal and renal function was not impaired. Its explanation is probably that the serum ethylene glycol did not reach the toxic value and the prompt treatment prevented the formation of toxic metabolites. Quite contrary, in our 2nd patient, where the serum level was a multiple of toxic value, very severe metabolic changes and central nervous system depression developed.\u003c/p\u003e \u003cp\u003eA suspected stroke diagnosis in stroke mimics, even if wrong, may carry not only a disadvantage, but also an advantage. Because stroke requires emergency care, patients with stroke symptoms, caused by either stroke or stroke mimics, usually reach the hospital in a very short time. Moreover, if reperfusion therapy is performed, the patient is carefully monitored not only during the rt-PA treatment, but also in the subsequent 24 hours. It means that patients with stroke or stroke mimics are investigated and observed in the initial stage of the disease, allowing recognition the first signs and symptoms, and thus early diagnosis and treatment. In our cases this management led to early diagnosis of ethylene glycol intoxication and early start of the appropriate treatment resulting in a good clinical outcome in 2 of our 3 patients.\u003c/p\u003e \u003cp\u003eThe importance of anamnesis should also be highlighted. A report of ingestion of toxic agents makes the diagnosis obvious, however the physician should ask specifically about drinking antifreeze or similar substances in cases of suspected toxicity. Often, the patient is unwilling or unable to give an accurate history. Ideally, a bottle of antifreeze or other solvent is found at the scene, but if not, the family as well as the prehospital team should be thoroughly questioned and instructed to search for potentially toxic substances. Previous suicidal ideations and history of depression are also key information. At the presention of our patients these information were lacking, and they became known only after the diagnosis was made.\u003c/p\u003e \u003cp\u003eIn conclusion, our observations show that ethylene glycol intoxication in its early phase may mimic acute stroke and thus even lead to thrombolytic treatment, which has not been reported earlier. If focal neurological deficits are accompanied by agitation, hyperventilation, or disturbance of consciousness, an alternative diagnosis, including intoxication, should be considered. The differential diagnosis in these cases can be facilitated by ABG and toxicological screening.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003e\u003cstrong\u003eAIS \u003c/strong\u003eacute ischemic stroke\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eABG\u003c/strong\u003e arterial blood gas\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCTA \u003c/strong\u003e computed tomography angiography\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCRRT \u003c/strong\u003e continuous renal replacement therapy\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eGFR\u003c/strong\u003e glomerular filtration rate\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eIVT \u003c/strong\u003e intravenous thrombolyis\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eICU\u003c/strong\u003e Intensive Care Unit\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eMRI\u003c/strong\u003e magnetic resonance imaging\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eNIHSS \u003c/strong\u003eNational Institutes of Health Stroke Scale\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eNCCT \u003c/strong\u003e non-contrast computed tomography\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003ert-PA\u003c/strong\u003erecombinant tissue plasminogen activator\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003esICH \u003c/strong\u003e symptomatic intracranial hemorrhage\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthics approval and consent to participate\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eInformed written consent was obtained from patients after discharge from the hospital (Case 1 and 3). They were able to fully understand and answer our questions and were oriented in time, place and their personal data. However, in the case of the patient who died in the hospital (Case 3), informed written consent was given by a family member (wife).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and materials\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe datasets supporting the conclusions of this case report are included within the article.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare that they have no conflict of interest.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNone.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors\u0026apos; contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eMH was involved in clinical work-up, manuscript preparation, editing and submission. LO revised the manuscript critically for important content. All authors have read and approved the final manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgements\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors wish to express their sincere thanks to the co-workers of the Intensive Care Unit of the Department of Neurology and the Intensive Care Unit of the Internal Medicine Department, University of Debrecen.\u003c/p\u003e"},{"header":"References","content":"1.\tGBD 2016 Stroke Collaborators. Global, regional, and national burden of stroke, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet Neurol. 2019 May;18(5):439-458. doi: 10.1016/S1474-4422(19)30034-1. Epub 2019 Mar 11. PMID: 30871944; PMCID\n2.\tAho K, Harmsen P, Hatano S, Marquardsen J, Smirnov VE, Strasser T. Cerebrovascular disease in the community: results of a WHO collaborative study. Bull World Health Organ. 1980;58(1):113-30. PMID: 6966542; PMCID: PMC2395897.\n3.\tLong B (2016) Stroke Mimics: Pearls and Pitfalls. www.emdocs.net/stroke-mimics-pearls-andpitfalls (Last accessed: 9 November 2018.)\n4.\tFernandes PM, Whiteley WN, Hart SR, Al-Shahi Salman R. Strokes: mimics and chameleons. Pract Neurol. 2013 Feb;13(1):21-8. doi: 10.1136/practneurol-2012-000465. PMID: 23315456.\n5.\tHacke W, Kaste M, Bluhmki E, Brozman M, Dávalos A, Guidetti D, Larrue V, Lees KR, Medeghri Z, Machnig T, Schneider D, von Kummer R, Wahlgren N, Toni D; ECASS Investigators. Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke. N Engl J Med. 2008 Sep 25;359(13):1317-29. doi: 10.1056/NEJMoa0804656. PMID: 18815396.\n6.\tWahlgren N, Ahmed N, Dávalos A, Hacke W, Millán M, Muir K, Roine RO, Toni D, Lees KR; SITS investigators. Thrombolysis with alteplase 3-4.5 h after acute ischaemic stroke (SITS-ISTR): an observational study. Lancet. 2008 Oct 11;372(9646):1303-9. doi: 10.1016/S0140-6736(08)61339-2. Epub 2008 Sep 12. PMID: 18790527.\n7.\tWinkler DT, Fluri F, Fuhr P, Wetzel SG, Lyrer PA, Ruegg S, Engelter ST. Thrombolysis in stroke mimics: frequency, clinical characteristics, and outcome. Stroke. 2009 Apr;40(4):1522-5. doi: 10.1161/STROKEAHA.108.530352. Epub 2009 Jan 22. PMID: 19164790.\n8.\tLee VH, Howell R, Yadav R, Heaton S, Wiles KL, Lakhani S. Thrombolysis of stroke mimics via telestroke. Stroke Vasc Neurol. 2022 Jun;7(3):267-270. doi: 10.1136/svn-2020-000776. Epub 2022 Feb 1. PMID: 35105730; PMCID: PMC9240458.\n9.\tTsivgoulis G, Zand R, Katsanos AH, Goyal N, Uchino K, Chang J, Dardiotis E, Putaala J, Alexandrov AW, Malkoff MD, Alexandrov AV. Safety of intravenous thrombolysis in stroke mimics: prospective 5-year study and comprehensive meta-analysis. Stroke. 2015 May;46(5):1281-7. doi: 10.1161/STROKEAHA.115.009012. Epub 2015 Mar 19. PMID: 25791717.\n10.\tZinkstok SM, Engelter ST, Gensicke H, Lyrer PA, Ringleb PA, Artto V, Putaala J, Haapaniemi E, Tatlisumak T, Chen Y, Leys D, Sarikaya H, Michel P, Odier C, Berrouschot J, Arnold M, Heldner MR, Zini A, Fioravanti V, Padjen V, Beslac-Bumbasirevic L, Pezzini A, Roos YB, Nederkoorn PJ. Safety of thrombolysis in stroke mimics: results from a multicenter cohort study. Stroke. 2013 Apr;44(4):1080-4. doi: 10.1161/STROKEAHA.111.000126. Epub 2013 Feb 26. PMID: 23444310.\n11.\tMerino JG, Luby M, Benson RT, Davis LA, Hsia AW, Latour LL, Lynch JK, Warach S. Predictors of acute stroke mimics in 8187 patients referred to a stroke service. J Stroke Cerebrovasc Dis. 2013 Nov;22(8):e397-403. doi: 10.1016/j.jstrokecerebrovasdis.2013.04.018. Epub 2013 May 13. PMID: 23680681; PMCID: PMC3812364.\n12.\tHess R, Bartels MJ, Pottenger LH. Ethylene glycol: an estimate of tolerable levels of exposure based on a review of animal and human data. Arch Toxicol. 2004 Dec;78(12):671-80. doi: 10.1007/s00204-004-0594-8. Epub 2004 Sep 15. PMID: 15372138.\n13.\tHassing LT, Verschoof MA, Koppen H. Alcohol Intoxication as a Stroke Mimic and the Incidence of Acute Alcohol Intoxication in Stroke. J Stroke Cerebrovasc Dis. 2019 Dec;28(12):104424. doi: 10.1016/j.jstrokecerebrovasdis.2019.104424. Epub 2019 Oct 15. PMID: 31624037.\n14.\tArokszallasi T, Balogh E, Csiba L, Fekete I, Fekete K, Olah L. Acute alcohol intoxication may cause delay in stroke treatment - case reports. BMC Neurol. 2019 Jan 29;19(1):14. doi: 10.1186/s12883-019-1241-6. PMID: 30696413; PMCID: PMC6350361.\n15.\tDavis DP, Bramwell KJ, Hamilton RS, Williams SR. Ethylene glycol poisoning: case report of a record-high level and a review. J Emerg Med. 1997 Sep-Oct;15(5):653-67. doi: 10.1016/s0736-4679(97)00145-5. PMID: 9348055.\n16.\tRolak LA, Rutecki P, Ashizawa T, Harati Y. Clinical features of Todd's post-epileptic paralysis. J Neurol Neurosurg Psychiatry. 1992 Jan;55(1):63-4. doi: 10.1136/jnnp.55.1.63. PMID: 1548500; PMCID: PMC488937.\n17.\tChalela JA, Kidwell CS, Nentwich LM, Luby M, Butman JA, Demchuk AM, Hill MD, Patronas N, Latour L, Warach S. Magnetic resonance imaging and computed tomography in emergency assessment of patients with suspected acute stroke: a prospective comparison. Lancet. 2007 Jan 27;369(9558):293-8. doi: 10.1016/S0140-6736(07)60151-2. PMID: 17258669; PMCID: PMC1859855.\n18.\tNational Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med. 1995 Dec 14;333(24):1581-7. doi: 10.1056/NEJM199512143332401. PMID: 7477192.\n19.\tArtto V, Putaala J, Strbian D, Meretoja A, Piironen K, Liebkind R, Silvennoinen H, Atula S, Häppölä O; Helsinki Stroke Thrombolysis Registry Group. Stroke mimics and intravenous thrombolysis. Ann Emerg Med. 2012 Jan;59(1):27-32. doi: 10.1016/j.annemergmed.2011.09.011. Epub 2011 Oct 14. PMID: 22000770.\n20.\tTsivgoulis G, Alexandrov AV, Chang J, Sharma VK, Hoover SL, Lao AY, Liu W, Stamboulis E, Alexandrov AW, Malkoff MD, Frey JL. Safety and outcomes of intravenous thrombolysis in stroke mimics: a 6-year, single-care center study and a pooled analysis of reported series. Stroke. 2011 Jun;42(6):1771-4. doi: 10.1161/STROKEAHA.110.609339. Epub 2011 Apr 14. PMID: 21493900.\n21.\tIqbal A, Glagola JJ, Nappe TM. Ethylene Glycol Toxicity. 2022 Sep 26. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan–. PMID: 30725694.\n"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"acute stroke, ethylene glycol, stroke mimic, intravenous thrombolysis, intoxication","lastPublishedDoi":"10.21203/rs.3.rs-2524829/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-2524829/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cstrong\u003eBackground: \u003c/strong\u003eStroke is a major cause of death and disability presenting with acute focal neurological symptoms of vascular origin. Several other disorders may cause symptoms similar to a stroke, referred as stroke mimics. Misdiagnosis of stroke mimics may lead to potentially harmful treatments, including thrombolysis. Intoxication is a rare, but possible cause of stroke mimic. We present three cases of ethylene glycol poisoning presenting as acute stroke mimic within the time window of thrombolytic therapy.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCase presentations:\u003c/strong\u003e The first patient (54-year-old, male) had nystagmus, dysarthria and truncal ataxia on admission. Cerebral CT and CT-angiography were negative. Vertebrobasilar stroke was suspected and intravenous thrombolysis was performed. A few hours later confusion, somnolence and hyperventilation developed. Arterial blood gas analysis showed metabolic acidosis. Toxicology screening revealed the presence of ethylene glycol in a toxic range. Due to the prompt treatment the patient was discharged 9 days later in a symptom-free state. The second patient (78-year-old, male) was admitted with central type of nystagmus, gaze palsy, dysarthria and ataxia. In the absence of exclusion criteria, thrombolysis was performed. A few hours later his condition deteriorated, he became comatose and tetraplegic with partially absent brainstem reflexes. Arterial blood gas analysis revealed severe metabolic acidosis. The ethylene glycol level was 159 mg/dL. Despite the appropriate treatment, he died. The third patient (54-year-old, male) with a history of chronic alcoholism was presented after an epileptic seizure with mixed aphasia and confusion. Stroke could not be excluded, therefore thrombolysis was performed. Arterial blood gases were normal, however toxicological screening revealed a serum etyhlene-glycol concentration of 16,54 mg/dL. Six days after admission he became symptom-free and was discharged home.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConclusions:\u003c/strong\u003e Our cases show that ethylene glycol intoxication in its early phase may mimic acute stroke resulting in an unnecessary thrombolytic therapy. Symptoms not characteristic of a stroke, such as hyperventilation, agitation, and disturbance of consciousness, may appear later and warn of intoxication. The final diagnosis of ethylene-glycol intoxication can be established by a severe metabolic acidosis and toxicological screening. Close monitoring of symptoms might contribute to early recognition of ethylene-glycol intoxication and its effective treatment.\u003c/p\u003e","manuscriptTitle":"Ethylene glycol intoxication presenting as a mimic of acute stroke: report of three cases","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2023-02-06 14:41:29","doi":"10.21203/rs.3.rs-2524829/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"bd504224-ddd6-4f75-9def-041287c67816","owner":[],"postedDate":"February 6th, 2023","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2023-05-19T14:59:23+00:00","versionOfRecord":[],"versionCreatedAt":"2023-02-06 14:41:29","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-2524829","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-2524829","identity":"rs-2524829","version":["v1"]},"buildId":"cBFmMYwuxLRRLfASyISRj","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}