Rasim Babayev

National Nuclear Research Center

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MŞ

Murat Şakir Ekşi̇

Istanbul University

Deniz Konya

Bahçeşehir University

Emel Ece Özcan‐Ekşi

Acıbadem University

Bahadur Abbasov

VA Fanarjian National Center of Oncology

SÖ

Serdar Özgen

Acıbadem University

Arzu Ger ek

Marmara University

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А. Э. Казимов

Sechenov University

Cooperative Institutions

Marmara University

Acıbadem University

Bahçeşehir University

Brigham and Women's Hospital

Harvard University

University of California, San Francisco

October 6 University

Scientific and Technological Research Council of Turkey

Hakkari University

State Hospital

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Delayed Recovery from General Anesthesia from Intracranial Tumor

Anesthesia & Analgesia (2006)

Arzu Ger ek Deniz Konya Rasim Babayev Serdar Özgen

To The Editor: A 66-year-old 80 kg woman underwent lumbar laminectomy. Her medical history included hypertension, diabetes mellitus, and hypothyroidism. Her preoperative laboratory values were within normal ranges. Anesthesia was induced with propofol 2 mg/kg and remifentanil 1 μg/kg. After induction, the patient received vecuronium bromide 0.15 mg/kg and dexamethasone 0.2 mg/kg. After endotracheal intubation, she was placed in prone position. Anesthesia was maintained with 50% N2O and 1% sevoflurane in O2 and remifentanil 0.25 μg · kg−1 · min−1 infusion. Surgery lasted 270 min. At the end of the surgery, we reversed the muscle relaxant with 30 μg/kg prostigmine and 15 μg/kg atropine. Twenty minutes after turning off the anesthetics, her spontaneous respiration was irregular and she did not respond to verbal comments. Painful stimulus resulted in eye opening accompanied by right sided-flexor response. Her pupils were anisocoric. To exclude the possibility of an intracranial event (e.g., hemorrhage, emboli, or infarction), we performed emergent computerized tomography, which revealed a right frontal, intracranial contrast-enhanced lesion and midline shift (Fig. 1a). Intracranial tumor with peripheral edema was diagnosed with magnetic resonance imaging (Fig. 1b). Twenty-four hours later the patient underwent craniotomy and tumor excision, with complete neurological recovery.Figure 1.: (a) Cranial axial noncontrast computed tomography, showing a large hypointense area in the frontal lobe that may have been caused by hypotensive cerebral infarction, infiltrating neoplasm, inflammation, etc. (b) Cranial axial T1-weighted magnetic resonance image showing contrast-enhanced frontal tumor (arrow A) causing midline shift (arrow B).Several factors likely contributed to the exacerbation of mass effect and neurological sequelae after the laminectomy, including prone position, intraoperative fluid administration, surgical stress, and residual anesthesia. Delayed recovery from general anesthesia accompanied by neurological findings may be the first sign of intracranial tumor. Arzu Gerçek, MD Department of Anesthesiology Deniz Konya, MD Rasim Babayev, MD Serdar Ozgen, MD Department of Neurosurgery Marmara University Institute of Neurological Science Istanbul, Turkey [email protected]

Midline shift

Brain tumor

10.1213/01.ane.0000248176.95402.57

Cite

Citations (5)

A common pathology in an uncommon location: posterior migrated epidural disc herniation

The Spine Journal (2016)

Rasim Babayev Emel Ece Özcan-Ekşi̇А. Э. Казимов Murat Şakir Ekşi̇

Intervertebral Disc Displacement

Intervertebral Disc

Back Pain

10.1016/j.spinee.2016.01.216