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The management of GBM remains controversial. The lesion should be surgically removed whenever possible and some authors recommend early aggressive surgical removal of easily accessible tumors with a mass effect. Hassaneen et  al. advocated multiple craniotomies in the same sitting for multiple GBM without any added mortality or morbidity.[6] Review of literature suggests that most patients die approximately 6‑8 months after the onset of symptoms, although in some studies the outcome was worse ranging from 2.8 to 4.8 months. Sushil Kumar, Amit Handa, Rohan Sinha, Ravi Tiwari Department of Neurosurgery, St. Stephen’s Hospital, Tis Hazari, Delhi, India Address for correspondence: Dr. Amit Handa, Department of Neurosurgery, St. Stephen’s Hospital, Tis Hazari, Delhi ‑ 110 054, India. E‑mail: [email protected]

References Utsuki S, Oka H, Suzuki S, Shimizu S, Tanizaki Y, Kondo K, et al. Pathological and clinical features of cystic and noncystic glioblastomas. Brain Tumor Pathol 2006;23:29‑34. 2. Kleihues P, Ohgaki H. Primary and secondary glioblastomas: From concept to clinical diagnosis. Neuro Oncol 1999;1:44‑51. 3. Batzdorf  U, Malamud N. The problem of multicentric gliomas. J Neurosurg 1963;20:122‑36. 4. Cugati G, Jain PK, Pande A, Symss NP, Chakravarthy V, Ramamurthi R. Pediatric multifocal glioblastoma multiforme with fulminant course. J Neurosci Rural Pract 2012;3:174‑7. 5. Maldaun MV, Suki D, Lang FF, Prabhu S, Shi W, Fuller GN, et al. Cystic glioblastoma multiforme: Survival outcomes in 22 cases. J Neurosurg 2004;100:61‑7. 6. Hassaneen W, Levine NB, Suki D, Salaskar AL, de Moura Lima A, McCutcheon IE, et al. Multiple craniotomies in the management of multifocal and multicentric glioblastoma. Clinical article. J Neurosurg 2011;114:576‑84. 1.

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DOI: 10.4103/0976-3147.120196

Ethylene glycol toxic encephalopathy Sir, The neurological clinic is the most frequent and early to appear in the Ethylene Glycol  (EG) intoxication. It

is characterized by inebriation symptoms very early (from 30 minutes till 12 hours), from lethargy to coma. Seizures can occur and even status epilepticus. Other neurological signs are papiledema, ophtalmoplegia, nystagmus, ataxia, and tetany. In patients who died at this stage are described cerebral swelling, brain hemorrhage, aseptic meningitis, and encephalitis, and crystal formation in central neurological system (CNS).[1] The diagnosis is based on the suspicion of ingestion, the presence of visual disorders, high anion gap metabolic acidosis and an osmolar gap, and elevated levels of creatine kinase (CK). The confirmation is provided by the determination of plasma levels or in gastric juice of EG. We present a case of a 53‑year‑old man, found by his neighbors at home, with low level of consciousness. He was transferred to the Emergency Department who arrived in coma (GCS 3‑4) and hypotensive. Laboratory studies reveled a severe metabolic acidosis (pH of 6.96, pCO2 of 36 mm Hg, HCO3 of 8.1 mmol/L with a base deficit of ‑23’5), plasma osmolarity of 333 mOsm/L, anion gap of 46 mmol/L, lactate of 9.92 mmol/L, creatinine of 9.37  mg/dl, urea of 258  mg/dl, CK of 5940 U/L, thrombocytopenia of 73.000/µL, and leukocytosis of 13.600/µL. Urine analysis of drugs and blood alcohol was negative. A computed tomography (CT) scan was performed at admission, without pathological findings. For the clinical situation of unknown cause of coma, analytical data of severe high anion gap metabolic acidosis, anuric renal failure and rhabdomyolysis, methanol or EG poisoning was suspected; so, ethanol and dialysis treatment was started. We provide 10% ethanol bolus of 1 g/kg/iv for 30 'and then an infusion of 1.5 ml/kg/h for serum levels of 150 mg dl. The metabolic problem was resolved, but the renal failure persisted requiring dialysis, and also the coma status with a maximum GCS of 9 (4‑1‑4). The determination of toxics was held in a blood sample by gas chromatography technique attached to mass spectrometry (GC/MS), confirming the presence of EG. Estimated concentration EG was 285 mg/dl. Six days after admission, a new CT scan was performed, and it showed multiple areas of hypodensity at the basal ganglia (head of caudate nucleus) and in bordering territories [Figure 1]. After a month, the patient didn’t suffer neurological changes, remained comatose. The 80% of the EG absorbed is metabolized mainly in the liver by the enzyme, alcohol dehydrogenase, and the rest is excreted unchanged by kidneys, such as calcium oxalate. The EG metabolites are glycoaldehyde, glycolic acid, glyoxylic acid, oxalic acid, and calcium oxalate. The blocking of conversion of glycolic acid to

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References 1. 2. 3. 4. Figure 1: Cerebral computed tomography show multiple areas of hypodensity at the basal ganglia

glyoxylic will induce a metabolic acidosis by the high ratio NADH/NAD.[2] Ethanol is a competitive substrate for alcohol dehydrogenase, which has greater affinity for ethanol than for ethylene glycol. Therefore, ethanol is effective and inhibits the metabolism of ethylene glycol. Although it is difficult to dose and has sedative and behavioral effects, ethanol is inexpensive and easily obtained. An alternative is fomepizole (4‑methylpyrazole). It is also a competitive inhibitor of alcohol dehydrogenase and prevents the formation of toxic acid metabolites. It is easy to dose, easy to administer, and side‑effects are rare. However, it is expensive and not available in all hospitals. Hemodialysis is used to clear both EG and its toxic metabolites more quickly. It is a characteristic finding on the CT scan, or in the postmortem examination, the presence of necrosis in areas of the optic nerve and in some areas of the cerebral white matter, which typically affects the caudate and putamen nuclei, as it was observed in our patient. The putaminal lesion seems to be a selective toxic effect and can be associated with more extensive neuronal damage of cerebral cortex and other gray nuclei, being uncommon lesions of the white matter. The lesions are correlated with the clinical findings and are similar to those observed in trichloroethane poisoning, carbon monoxide, hypoxia‑anoxia, Wilson’s disease, Leigh disease, Kearns‑sayre syndrome, and Leber’s optic atrophy striatal degeneration.[3‑5] Luciano Santana‑Cabrera, Edwin Verdugo Espinosa, Erika Camelia Zborovszky, Cristina Rodríguez‑Escot, Manuel Sánchez Palacios Department of Intensive Care Unit, Universitary Hospital Insular in Gran Canaria, Las Palmas of Gran Canaria, Spain Address for correspondence: Dr. Luciano Santana‑Cabrera, Avenida Marítima del Sur s/n. Las Palmas de Gran Canaria, Canary Islands - 35016, Spain. E‑mail: [email protected] 478

5.

Kruse JA. Methanol and ethylene glycol intoxication. Crit Care Clin 2012;28:661‑711. Eder AF, McGrath CM, Dowdy YG, Tomaszewski JE, Rosenberg FM, Wilson RB, et al. Ethylene glycol poisoning: Toxicokinetic and analytical factors affecting laboratory diagnosis. Clin Chem 1998;44:168‑77. Blanco M, Casado R, Vázquez F, Pumar JM. CT and MR imaging findings in methanol intoxication. AJNR Am J Neuroradiol 2006;27:452‑4. Pelletier J, Habib MH, Khalil R, Salamon G, Bartoli D, Jean P. Putaminal necrosis after methanol intoxication. J Neurol Neurosurg Psychiatry 1992;55:234‑5. Chattopadhyay S, Chandra P. Images in clinical medicine. Putaminal necrosis. N Engl J Med 2007;356:e23. Access this article online Quick Response Code:

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DOI: 10.4103/0976-3147.120198

Commentary Nowadays, poisoning with an abundant variety of substances is not unknown to the clinical practitioner– regardless to the local setting. The patient’ status is imminent for further treatment; priority lies in stabilization, airway assessment and (maybe) drug sample drawing, as well as taking a myriad of (often) useless blood tests. Nevertheless, most alcohol poisonings present in the same manner: An almost or already comatose patient with maybe a history of substance abuse in a fast deteriorating condition. It is imminent to assess his or her neurological status (check for seizures, ataxia, tetany, etc.) and to exclude neurological diseases which may need urgent treatment, for example, diffuse cerebral swelling, meningitis, or brain hemorrhage; just to name a few. A cranial computed tomography (CT) is indispensable at that moment. After excluding these life‑threatening diseases, turn your attention to the blood tests you have taken: At least there should be arterial blood gases (ABG), glucose level, lactate level, creatinine, urea, creatine kinase, white blood cell count (WBC), and ethanol level. Necessary is also a urine analysis for drugs and hematuria. In the case of “simple” ethanol intoxication, treatment possibilities lie somewhere between a “wait and see” strategy and a more aggressive therapy, like hemodialysis.

Journal of Neurosciences in Rural Practice | October - December 2013 | Vol 4 | Issue 4

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