Surgery_Schwartz

Surgery_Schwartz. pelvic radia-tion therapy in intermediate risk endometrial adenocarci-noma: a Gynecologic Oncology Group study. Gynecol Oncol. 2004;92:744-751. 110. Holloway RW, Abu-Rustum NR, Backes FJ, et al. Sentinel lymph node mapping and staging in endometrial cancer: a Society of Gynecologic Oncology literature review with consensus recommendations. Gynecologic Oncology. 2017;146:405-415. 111. Aarnio M, Mecklin JP, Aaltonen LA, Nystrom-Lahti M, Jarvinen HJ. Life-time risk of different cancers in hereditary non-polyposis colorectal cancer (HNPCC) syndrome. Int J Cancer. 1995;64:430-433. 112. Reichardt P. The treatment of uterine sarcomas. Ann Oncol. 2012;23(suppl 10):x151-x157. 113. Jacobs IJ, Menon U, Ryan A, et al. Ovarian cancer screening and mortality in the UK Collaborative Trial of Ovarian Cancer Screening (UKCTOCS): a randomised controlled trial. Lancet. 2016;387:945-956. 114. Buys SS, Partridge E, Black A, et al. Effect of screening on ovarian cancer mortality: the prostate, lung,


Surgery_Schwartz

Surgery_Schwartz. Cancer Screening (UKCTOCS): a randomised controlled trial. Lancet. 2016;387:945-956. 114. Buys SS, Partridge E, Black A, et al. Effect of screening on ovarian cancer mortality: the prostate, lung, colorectal and ovarian (PLCO) cancer screening randomized controlled trial. JAMA. 2011;305:2295-2303. 115. van Nagell Jr JR, Miller RW, DeSimone CP, et al. Long-term survival of women with epithelial ovarian cancer detected by ultrasonographic screening. Obstet Gynecol. 2011;118:1212-1221. 116. Kobayashi H, Yamada Y, Sado T, et al. A randomized study of screening for ovarian cancer: a multicenter study in Japan. Int J Gynecol Cancer. 2008;18:414-420. 117. Goff BA, Mandel LS, Drescher CW, et al. Development of an ovarian cancer symptom index: possibilities for earlier detec-tion. Cancer. 2007;109:221-227. 118. Kurman RJ, Shih Ie M. Molecular pathogenesis and extraovar-ian origin of epithelial ovarian cancer—shifting the paradigm. Hum Pathol. 2011;42:918-931.Brunicardi_Ch41_p1783-p1826.indd


Surgery_Schwartz

Surgery_Schwartz. RJ, Shih Ie M. Molecular pathogenesis and extraovar-ian origin of epithelial ovarian cancer—shifting the paradigm. Hum Pathol. 2011;42:918-931.Brunicardi_Ch41_p1783-p1826.indd 182418/02/19 4:35 PM 1825GYNECOLOGYCHAPTER 41 119. Jarboe EA, Folkins AK, Drapkin R, Ince TA, Agoston ES, Crum CP. Tubal and ovarian pathways to pelvic epithelial cancer: a pathological perspective. Histopathology. 2009; 55:619. 120. Steffensen KD, Waldstrom M, Grove A, Lund B, Pallisgard N, Jakobsen A. Improved classification of epithelial ovarian cancer: results of 3 Danish cohorts. Int J Gynecol Cancer. 2011;21:1592-1600. 121. Kurman RJ, Shih Ie M. The dualistic model of ovarian car-cinogenesis: revisited, revised, and expanded. Am J Pathol. 2016;186:733-747. 122. Collaborative Group on Epidemiological Studies of Ovarian C. Ovarian cancer and oral contraceptives: collabora-tive reanalysis of data from 45 epidemiological studies includ-ing 23 257 women with ovarian cancer and 87 303 controls. Lancet.


Surgery_Schwartz

Surgery_Schwartz. of Ovarian C. Ovarian cancer and oral contraceptives: collabora-tive reanalysis of data from 45 epidemiological studies includ-ing 23 257 women with ovarian cancer and 87 303 controls. Lancet. 2009;371:303-314. 123. Al Bakir M, Gabra H. The molecular genetics of hereditary and sporadic ovarian cancer: implications for the future. Br Med Bull. 2014;112:57-69. 124. Weissman SM, Weiss SM, Newlin AC. Genetic testing by cancer site: ovary. Cancer J. 2012;18:320-327. 125. Walsh T, Casadei S, Lee MK, et al. Mutations in 12 genes for inherited ovarian, fallopian tube, and peritoneal carcinoma identified by massively parallel sequencing. Proc Natl Acad Sci U S A. 2011;108:18032-18037. 126. Walker JL, Powell CB, Chen LM, et al. Society of Gyneco-logic Oncology recommendations for the prevention of ovar-ian cancer. Cancer. 2015;121:2108-2120. 127. Pal T, Permuth-Wey J, Betts JA, et al. BRCA1 and BRCA2 mutations account for a large proportion of ovarian carcinoma cases. Cancer.


Surgery_Schwartz

Surgery_Schwartz. the prevention of ovar-ian cancer. Cancer. 2015;121:2108-2120. 127. Pal T, Permuth-Wey J, Betts JA, et al. BRCA1 and BRCA2 mutations account for a large proportion of ovarian carcinoma cases. Cancer. 2005;104:2807-2816. 128. Norquist BM, Harrell MI, Brady MF, et al. Inherited muta-tions in women with ovarian carcinoma. JAMA Oncol. 2016;2:482-490. 129. Wentzensen N, Poole EM, Trabert B, et al. Ovarian can-cer risk factors by histologic subtype: an analysis from the Ovarian Cancer Cohort Consortium. J Clin Oncol. 2016;34: 2888-2898. 130. Antoniou A, Pharoah PDP, Narod S, et al. Average risks of breast and ovarian cancer associated with BRCA1 or BRCA2 mutations detected in case series unselected for family his-tory: a combined analysis of 22 studies. Am J Human Genet. 2003;72:1117-1130. 131. Alsop K, Fereday S, Meldrum C, et al. BRCA mutation frequency and patterns of treatment response in brca mutation– positive women with ovarian cancer: a report from the Australian Ovarian Cancer


Surgery_Schwartz

Surgery_Schwartz. K, Fereday S, Meldrum C, et al. BRCA mutation frequency and patterns of treatment response in brca mutation– positive women with ovarian cancer: a report from the Australian Ovarian Cancer Study Group. J Clin Oncol. 2012;30:2654-2663. 132. Arts-de Jong M, de Bock GH, van Asperen CJ, Mourits MJE, de Hullu JA, Kets CM. Germline BRCA1/2 mutation testing is indicated in every patient with epithelial ovarian cancer: a systematic review. Eur J Cancer. 2016;61:137-145. 133. Zhang S, Royer R, Li S, et al. Frequencies of BRCA1 and BRCA2 mutations among 1,342 unselected patients with inva-sive ovarian cancer. Gynecol Oncol. 2011;121:353-357. 134. Daly MB, Axilbund JE, Buys S, et al. Genetic/familial high-risk assessment: breast and ovarian. J Natl Compr Canc Netw. 2010;8:562-594. 135. Mavaddat N, Peock S, Frost D, et al. Cancer risks for BRCA1 and BRCA2 mutation carriers: results from pro-spective analysis of EMBRACE. J Natl Cancer Inst Monogr. 2013;105:812-822. 136. Piek JM, van Diest PJ,


Surgery_Schwartz

Surgery_Schwartz. N, Peock S, Frost D, et al. Cancer risks for BRCA1 and BRCA2 mutation carriers: results from pro-spective analysis of EMBRACE. J Natl Cancer Inst Monogr. 2013;105:812-822. 136. Piek JM, van Diest PJ, Zweemer RP, et al. Dysplastic changes in prophylactically removed Fallopian tubes of women predisposed to developing ovarian cancer. J Pathol. 2001;195:451-456. 137. Kuhn E, Kurman R, Shih I-M. Ovarian cancer is an imported disease: fact or fiction? Curr Obstet Gynecol Rep. 2012;1:1-9. 138. Kauff ND, Satagopan JM, Robson ME, et al. Risk-reducing salpingo-oophorectomy in women with a BRCA1 or BRCA2 mutation. N Engl J Med. 2002;346:1609-1615. 139. ACOG. Elective and risk-reducing salpingo-oopherectomy. ACOG Practice Bulletin. 2008;89:1-12. 140. Madsen C, Baandrup L, Dehlendorff C, Kjær SK. Tubal ligation and salpingectomy and the risk of epithelial ovarian cancer and borderline ovarian tumors: a nationwide case– control study. Acta Obstetricia et Gynecologica Scandinavica.


Surgery_Schwartz

Surgery_Schwartz. C, Kjær SK. Tubal ligation and salpingectomy and the risk of epithelial ovarian cancer and borderline ovarian tumors: a nationwide case– control study. Acta Obstetricia et Gynecologica Scandinavica. 2015;94:86-94. 141. Bijron JG, Seldenrijk CA, Zweemer RP, Lange JG, Verheijen RH, van Diest PJ. Fallopian tube intraluminal tumor spread from noninvasive precursor lesions: a novel meta-static route in early pelvic carcinogenesis. Am J Surg Pathol. 2013;37:1123-1130. 142. McAlpine JN, Hanley GE, Woo MM, et al. Opportunistic sal-pingectomy: uptake, risks, and complications of a regional initiative for ovarian cancer prevention. Am J Obstet Gynecol. 2014;210:e471. 143. Young RC, Walton LA, Ellenberg SS, et al. Adjuvant therapy in stage I and stage II epithelial ovarian cancer. N Engl J Med. 1990;322:1021-1027. 144. Bell J, Brady MF, Young RC, et al. Randomized phase III trial of three versus six cycles of adjuvant carboplatin and paclitaxel in early stage epithelial ovarian carcinoma: a


Surgery_Schwartz

Surgery_Schwartz. 1990;322:1021-1027. 144. Bell J, Brady MF, Young RC, et al. Randomized phase III trial of three versus six cycles of adjuvant carboplatin and paclitaxel in early stage epithelial ovarian carcinoma: a Gynecologic Oncology Group study. Gynecol Oncol. 2006;102:432-439. 145. Young RC, Decker DG, Wharton JT, et al. Staging laparotomy in early ovarian cancer. JAMA. 1983;250:3072-3076. 146. Chang SJ, Hodeib M, Chang J, Bristow RE. Survival impact of complete cytoreduction to no gross residual disease for advanced-stage ovarian cancer: a meta-analysis. Gynecol Oncol. 2013;130:493-498. 147. Vergote I, Trope CG, Amant F, et al. Neoadjuvant chemo-therapy or primary surgery in stage IIIC or IV ovarian cancer. N Engl J Med. 2010;363:943-953. 148. Kehoe S, Hook J, Nankivell M, et al. Primary chemotherapy versus primary surgery for newly diagnosed advanced ovar-ian cancer (CHORUS): an open-label, randomised, controlled, non-inferiority trial. Lancet. 2015;386:249-257. 149. Gómez-Hidalgo NR,


Surgery_Schwartz

Surgery_Schwartz. versus primary surgery for newly diagnosed advanced ovar-ian cancer (CHORUS): an open-label, randomised, controlled, non-inferiority trial. Lancet. 2015;386:249-257. 149. Gómez-Hidalgo NR, Martinez-Cannon BA, Nick AM, et al. Predictors of optimal cytoreduction in patients with newly diagnosed advanced-stage epithelial ovarian cancer: time to incorporate laparoscopic assessment into the standard of care. Gynecol Oncol. 2015;137:553-558. 150. McGuire WP, Hoskins WJ, Brady MF, et al. Cyclophospha-mide and cisplatin compared with paclitaxel and cisplatin in patients with stage III and stage IV ovarian cancer [see com-ments]. N Engl J Med. 1996;334:1-6. 151. Armstrong DK, Bundy BN, Wenzel L, et al. Intraperitoneal cisplatin and paclitaxel in ovarian cancer. N Engl J Med. 2006;354:34-43. 152. Walker JL, Armstrong DK, Huang HQ, et al. Intraperitoneal catheter outcomes in a phase III trial of intravenous versus intraperitoneal chemotherapy in optimal stage III ovarian and primary peritoneal


Surgery_Schwartz

Surgery_Schwartz. JL, Armstrong DK, Huang HQ, et al. Intraperitoneal catheter outcomes in a phase III trial of intravenous versus intraperitoneal chemotherapy in optimal stage III ovarian and primary peritoneal cancer: a Gynecologic Oncology Group Study. Gynecol Oncol. 2006;100:27-32. 153. Chi DS, Phaeton R, Miner TJ, et al. A prospective outcomes analysis of palliative procedures performed for malignant intestinal obstruction due to recurrent ovarian cancer. Oncolo-gist. 2009;14:835-839. 154. Markman M, Reichman B, Hakes T, Jones W. Responses to second-line cisplatin-based intraperitoneal therapy in ovarian cancer: influence of a prior response to intravenous cisplatin. J Clin Oncol. 1991;9:1801-1805. 155. Gershenson DM. Treatment of ovarian cancer in young women. Clin Obstet Gynecol. 2012;55:65-74. 156. Mangili G, Sigismondi C, Lorusso D, et al. The role of stag-ing and adjuvant chemotherapy in stage I malignant ovarian Brunicardi_Ch41_p1783-p1826.indd 182518/02/19 4:35 PM 1826SPECIFIC


Surgery_Schwartz

Surgery_Schwartz. G, Sigismondi C, Lorusso D, et al. The role of stag-ing and adjuvant chemotherapy in stage I malignant ovarian Brunicardi_Ch41_p1783-p1826.indd 182518/02/19 4:35 PM 1826SPECIFIC CONSIDERATIONSPART IIgerm cell tumors (MOGTs): the MITO-9 study. Ann Oncol. 2017;28:333-338. 157. Merard R, Ganesan R, Hirschowitz L. Growing teratoma syn-drome: a report of 2 cases and review of the literature. Int J Gynecol Pathol. 2015;34:465-472. 158. Lurain JR. Gestational trophoblastic disease II: classification and management of gestational trophoblastic neoplasia. Am J Obstet Gynecol. 2011;204:11-18. 159. Ngan HYS, Seckl MJ, Berkowitz RS, et al. Update on the diagnosis and management of gestational trophoblastic dis-ease. Int J Gynecol Obstet. 2015;131:S123-S126. 160. Seckl MJ, Sebire NJ, Berkowitz RS. Gestational trophoblastic disease. Lancet. 2010;376:717-729. 161. Sinha R, Sundaram M, Mahajan C, et al. Single-incision total laparoscopic hysterectomy. J Minim Access Surg. 2011;7:78-82. 162. Sinha


Surgery_Schwartz

Surgery_Schwartz. Gestational trophoblastic disease. Lancet. 2010;376:717-729. 161. Sinha R, Sundaram M, Mahajan C, et al. Single-incision total laparoscopic hysterectomy. J Minim Access Surg. 2011;7:78-82. 162. Sinha RY, Raje SR, Rao GA. Three-dimensional lapa-roscopy: principles and practice. J Minim Access Surg. 2017;13:165-169. 163. Gaia G, Holloway RW, Santoro L, Ahmad S, Di Silverio E, Spinillo A. Robotic-assisted hysterectomy for endome-trial cancer compared with traditional laparoscopic and laparotomy approaches: a systematic review. Obstet Gynecol. 2010;116:1422-1431. 164. Llarena NC, Shah AB, Milad MP. Bowel injury in gyneco-logic laparoscopy: a systematic review. Obstet Gynecol. 2015;125:1407-1417. 165. Sharp HT, Adelman MR. Prevention, recognition, and man-agement of urologic injuries during gynecologic surgery. Obstet Gynecol. 2016;127:1085-1096. 166. Teeluckdharry B, Gilmour D, Flowerdew G. Urinary tract injury at benign gynecologic surgery and the role of cystos-copy: a systematic review


Surgery_Schwartz

Surgery_Schwartz. surgery. Obstet Gynecol. 2016;127:1085-1096. 166. Teeluckdharry B, Gilmour D, Flowerdew G. Urinary tract injury at benign gynecologic surgery and the role of cystos-copy: a systematic review and meta-analysis. Obstet Gynecol. 2015;126:1161-1169. 167. Centers for Disease Control and Prevention. Sexually Trans-mitted Diseases Treatment Guidelines: Pelvic Inflammatory Disease. Available: https://www.cdc.gov/std/tg2015/pid.htm. Accessed August 11, 2018. 168. Dearking AC, Aletti GD, McGree ME, Weaver AL, Som-merfield MK, Cliby WA. How relevant are ACOG and SGO guidelines for referral of adnexal mass? Obstet Gynecol. 2007;110:841-848. 169. Mutch DG, Prat J. 2014 FIGO staging for ovarian, fallopian tube and peritoneal cancer. Gynecol Oncol. 2014;133:401-404.Brunicardi_Ch41_p1783-p1826.indd 182618/02/19 4:35 PM


Surgery_Schwartz

Surgery_Schwartz. NeurosurgeryAshwin G. Ramayya, Saurabh Sinha, and M. Sean Grady 42chapterOverview 1827Neuroanatomy 1827Neurologic Examination 1829Diagnostic Studies / 1829Neurologic and Neurosurgical Emergencies 1831Raised Intracranial Pressure / 1831Brain Stem Compression / 1833Stroke / 1833Seizure / 1833Trauma 1833Head Trauma / 1833Spine Trauma / 1842Peripheral Nerve Trauma / 1847Cerebrovascular Disease 1849Ischemic Diseases / 1849Thrombotic Disease / 1849Embolic Disease / 1849Hemorrhagic Diseases / 1850Tumors of the Central Nervous System 1854Intracranial Tumors / 1854Metastatic Tumors / 1854Glial Tumors / 1855Neural Tumors and Mixed Tumors / 1857Neural Crest Tumors / 1857Miscellaneous Tumors / 1857Embryologic Tumors / 1858Spinal Tumors / 1859Future Directions / 1861Spine: Basic Concepts 1861Stability / 1861Neural Compression / 1862Patterns of Disease / 1862Spine Fusion Surgery / 1865Spinal Instrumentation / 1865Arthrodesis / 1866Peripheral Nerve 1866Peripheral Nerve Tumors / 1866Entrapment


Surgery_Schwartz

Surgery_Schwartz. / 1861Neural Compression / 1862Patterns of Disease / 1862Spine Fusion Surgery / 1865Spinal Instrumentation / 1865Arthrodesis / 1866Peripheral Nerve 1866Peripheral Nerve Tumors / 1866Entrapment Neuropathies / 1867Autoimmune and Inflammatory Disorders / 1867Infection 1867Cranial / 1867Spine / 1868Functional Neurosurgery 1869Epilepsy Surgery / 1869Deep Brain Stimulation / 1869Trigeminal Neuralgia / 1871Stereotactic Radiosurgery 1871Arteriovenous Malformations / 1872Vestibular Schwannomas / 1872Intracranial Metastases / 1872Congenital and Developmental Anomalies 1872Dysraphism / 1872Spina Bifida Occulta / 1872Spina Bifida With Myelomeningocele / 1872Encephalocele / 1872Craniosynostosis / 1872Hydrocephalus / 1873Chiari I Malformation / 1873OVERVIEWNeurologic surgery provides the operative and nonoperative man-agement (i.e., prevention, diagnosis, evaluation, treatment, criti-cal care, and rehabilitation) of disorders of the central, peripheral, and autonomic nervous systems (ANSs).


Surgery_Schwartz

Surgery_Schwartz. and nonoperative man-agement (i.e., prevention, diagnosis, evaluation, treatment, criti-cal care, and rehabilitation) of disorders of the central, peripheral, and autonomic nervous systems (ANSs). Such disorders include those of the brain, meninges, skull and skull base, and their blood supply, including surgical and endovascular treat-ment of disorders of the intracranial and extracranial vasculature supplying the brain and spinal cord; disorders of the pituitary gland; disorders of the spinal cord, meninges, and vertebral col-umn, including those that may require treatment by fusion, instru-mentation, or endovascular techniques; and disorders of the cranial and spinal nerves throughout their distribution.An accurate history is the first step toward neurologic diagnosis. A history of trauma or of neurologic symptoms is of obvious interest, but general constitutional symptoms are also important. Neurologic disease may have systemic effects, while diseases of other systems may affect


Surgery_Schwartz

Surgery_Schwartz. or of neurologic symptoms is of obvious interest, but general constitutional symptoms are also important. Neurologic disease may have systemic effects, while diseases of other systems may affect neurologic function. The patient’s general medical ability to withstand the physi-ologic stress of anesthesia and surgery should be understood. A detailed history from the patient and/or family, along with a reliable physical examination, will clarify these issues.NEUROANATOMYAn understanding of neuroanatomy is the foundation of com-prehensive neurologic examination and diagnosis. Salient fea-tures will be considered, from cephalad to caudad. The cerebral hemispheres (or telencephalon) consist of the cerebral cortex, underlying white matter, the basal ganglia, hippocampus, and amygdala. The cerebral cortex is the most recently evolved part of the nervous system. Its functions are mapped to discrete ana-tomic areas. The frontal areas are involved in executive function, decision making, and


Surgery_Schwartz

Surgery_Schwartz. cortex is the most recently evolved part of the nervous system. Its functions are mapped to discrete ana-tomic areas. The frontal areas are involved in executive function, decision making, and restraint of emotions. The motor strip, or precentral gyrus, is the most posterior component of the frontal lobes, and is arranged along a homunculus with the head inferior and lateral to the lower extremities superiorly and medially. The motor speech area (Broca’s area) lies in the left posterior inferior frontal lobe in almost all right-handed people and in up to 90% of left-handed people. The parietal lobe lies between the central sulcus anteriorly and the occipital lobe posteriorly. The postcen-tral gyrus is the sensory strip, also arranged along a homunculus. The rest of the parietal lobe is involved with awareness of one’s body in space and relative to the immediate environment, body orientation, and spatial relationships. The occipital lobes are most posterior. The visual cortex is


Surgery_Schwartz

Surgery_Schwartz. is involved with awareness of one’s body in space and relative to the immediate environment, body orientation, and spatial relationships. The occipital lobes are most posterior. The visual cortex is arrayed along the apposing 1Brunicardi_Ch42_p1827-p1878.indd 182701/03/19 7:16 PM 1828medial surfaces of the occipital lobes. The left occipital lobe receives and integrates data from the left half of each retina. A left occipital lesion would therefore result in an inability to see objects right of center. The temporal lobes lie below the Sylvian fissures. The hippocampus, amygdala, and lower optic radia-tions (Meyer’s loops) are important components of the temporal lobe and are involved in memory, emotion, and vision, respec-tively. The receptive speech area (Wernicke’s area) typically is found in the area of the left posterior superior temporal lobe and inferior parietal lobe. The basal ganglia include the caudate, putamen, globus pallidus, subthalamic nucleus, substantia nigra, and


Surgery_Schwartz

Surgery_Schwartz. found in the area of the left posterior superior temporal lobe and inferior parietal lobe. The basal ganglia include the caudate, putamen, globus pallidus, subthalamic nucleus, substantia nigra, and nucleus accumbens. These structures are involved in the selection, activation and termination of movement, and facilitate learning of appropriate context-dependent motor behaviors.Lying deep to the cerebral hemispheres is the diencepha-lon, which includes the thalamus and hypothalamus. The thala-mus is a key processor and relay circuit for most motor and sensory information traveling to or from cortex. The hypothala-mus regulates homeostasis via the autonomic and neuroendo-crine systems.The brain stem consists of the midbrain (mesencephalon), pons (metencephalon), and medulla (myelencephalon). Longi-tudinal fibers run through the brain stem, carrying motor and sensory information between the cerebral hemispheres and spi-nal cord. The corticospinal tract is the major motor tract, while the


Surgery_Schwartz

Surgery_Schwartz. Longi-tudinal fibers run through the brain stem, carrying motor and sensory information between the cerebral hemispheres and spi-nal cord. The corticospinal tract is the major motor tract, while the medial lemniscus and spinothalamic tracts are the major sensory tracts. The nuclei of cranial nerves III through XII are also located within the brain stem. These nerves relay the motor, sensory, and special sense functions of the eye, face, mouth, and throat.The cerebellum arises from the dorsal aspect of the brain stem. It integrates somatosensory, vestibular, and motor infor-mation for coordination and timing of movement. Midline, or vermian, lesions lead to truncal ataxia. Lateral, or hemispheric, lesions lead to tremor and dyscoordination in the extremities.The ventricular system is the cerebrospinal fluid (CSF)–containing contiguous space inside the brain, continuous with the subarachnoid space outside the brain. The paired lateral ventricles consist of temporal, occipital, and


Surgery_Schwartz

Surgery_Schwartz. the cerebrospinal fluid (CSF)–containing contiguous space inside the brain, continuous with the subarachnoid space outside the brain. The paired lateral ventricles consist of temporal, occipital, and frontal horns, as well as the main body. CSF travels from each lateral ventricle through the foramina of Monroe to the third ventricle, located between the left and right thalami. CSF then drains through the cerebral aqueduct to the fourth ventricle within the brain stem. The foramen of Magendie (midline) and paired foram-ina of Luschka (lateral) drain to the subarachnoid space. The approximate CSF volume in an average adult is 150 mL, and the choroid plexus produces approximately 500 mL of CSF per day.The spinal cord starts at the bottom of the medulla and extends caudally through the spinal canal to the first lumbar ver-tebra, approximately. Motor tracts (efferent pathways) continue from the brain stem down via the lateral and anterior corticospi-nal tracts to anterior horn cells, and


Surgery_Schwartz

Surgery_Schwartz. canal to the first lumbar ver-tebra, approximately. Motor tracts (efferent pathways) continue from the brain stem down via the lateral and anterior corticospi-nal tracts to anterior horn cells, and then exit via ventral nerve roots. Sensory information (afferent pathways) enters via dorsal nerve roots, travels cranially via the dorsal columns (proprio-ception and fine touch) or spinothalamic tract (pain and tem-perature), and into the brain stem. Paired nerves exit the spinal cord at each level. There are 31 pairs: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal.The dorsal and ventral nerve roots at each level fuse to form mixed motor-sensory spinal nerves and spread through the body to provide innervation to muscles and sensory organs. The C5–T1 spinal nerves intersect in the brachial plexus and divide to form the main nerve branches to the arm, including the median, ulnar, and radial nerves. The L2–S4 spinal nerves intersect in the lumbosacral plexus, and divide to


Surgery_Schwartz

Surgery_Schwartz. the brachial plexus and divide to form the main nerve branches to the arm, including the median, ulnar, and radial nerves. The L2–S4 spinal nerves intersect in the lumbosacral plexus, and divide to form the main nerve branches to the leg, including the femoral and sciatic nerves.The principal motor tract of the spinal cord is the cortico-spinal tract. It is a two-neuron path, including an upper motor neuron and a lower motor neuron. The upper motor neuron cell body is located within the motor strip of the cerebral cortex. The axon travels through the internal capsule to the brain stem, decussates at the brain stem–spinal cord junction, and travels down the contralateral corticospinal tract to the lower motor Key Points1 Neurologic surgery specializes in primarily surgical manage-ment of central, peripheral, and autonomic nervous system disorders.2 Although clinical examination is paramount, neurosurgical diagnosis and treatment are aided largely by a variety of modalities, such as


Surgery_Schwartz

Surgery_Schwartz. central, peripheral, and autonomic nervous system disorders.2 Although clinical examination is paramount, neurosurgical diagnosis and treatment are aided largely by a variety of modalities, such as magnetic resonance imaging and intra-cranial pressure monitoring.3 The common treatment goals for traumatic brain and spinal injury are aimed at preventing secondary insults of hypoxia and hypotension.4 Aneurysmal subarachnoid hemorrhage remains one of the most morbid and intensive neurosurgical diseases. Endovas-cular therapy is a growing technology that allows for safer securing of ruptured aneurysms.5 Brain tumors can arise from primary or metastatic tissues. Treatment typically involves resection, followed by radia-tion and/or chemotherapy, depending on the type and grade of tumor.6 Spinal instrumentation is used for surgical stabilization of many types of spinal instability, including traumatic, infec-tious, oncologic, and degenerative.7 Infection of the nervous system is a serious and


Surgery_Schwartz

Surgery_Schwartz. is used for surgical stabilization of many types of spinal instability, including traumatic, infec-tious, oncologic, and degenerative.7 Infection of the nervous system is a serious and prevalent medical problem. Operative management is indicated for most conditions in which there is symptomatic compression of neural structures.8 Functional neurosurgery via device implantation is a rapidly evolving discipline that has already become the standard of care in treating medically refractory Parkinson’s disease and essential tremor. A wider variety of deep brain stimulation targets will treat additional neuropsychiatric diseases.9 Stereotactic radiosurgery is a powerful treatment option for intracranial disease, whether it is primary or adjunct. Gamma knife surgery can be used to treat tumors, vascular malfor-mations, and cranial neuralgias.Brunicardi_Ch42_p1827-p1878.indd 182801/03/19 7:16 PM 1829NEUROSURGERYCHAPTER 42neuron in the anterior horn at the appropriate level. The lower motor


Surgery_Schwartz

Surgery_Schwartz. malfor-mations, and cranial neuralgias.Brunicardi_Ch42_p1827-p1878.indd 182801/03/19 7:16 PM 1829NEUROSURGERYCHAPTER 42neuron in the anterior horn at the appropriate level. The lower motor neuron axon then travels via peripheral nerves to its tar-get muscle. Damage to upper motor neurons typically results in hyperreflexia and mild atrophy. Damage to lower motor neurons results in flaccidity and significant atrophy.The two major sensory tracts are three-neuron pathways. Fine touch and proprioceptive signals enter the spinal cord via the dorsal root ganglia and then ascend ipsilaterally via the dorsal columns. Then they synapse and decussate in the lower medulla, travel up the contralateral medial lemniscus to make a second synapse in the thalamus, and then finally ascend to the sensory cortex. Pain and temperature fibers first synapse in the dorsal horn of the spinal cord at their entry level, decussate, and then travel up the contralateral spinothalamic tracts to the thalamus. The


Surgery_Schwartz

Surgery_Schwartz. cortex. Pain and temperature fibers first synapse in the dorsal horn of the spinal cord at their entry level, decussate, and then travel up the contralateral spinothalamic tracts to the thalamus. The second synapse occurs in the thalamus, and the output axons ascend to the sensory cortex.The aforementioned motor and sensory tracts together constitute the somatic nervous system. In addition to this sys-tem, the ANS is the other constituent of the nervous system. The ANS carries messages for homeostasis and visceral regu-lation from the central nervous system (CNS) to target struc-tures such as arteries, veins, the heart, sweat glands, and the digestive tract.1 CNS control of the ANS arises particularly from the hypothalamus and the nucleus of the tractus solitarius. The ANS is divided into the sympathetic, parasympathetic, and enteric systems. The sympathetic system drives the “fight or flight” response, using epinephrine to increase heart rate, blood pressure, blood glucose, and


Surgery_Schwartz

Surgery_Schwartz. into the sympathetic, parasympathetic, and enteric systems. The sympathetic system drives the “fight or flight” response, using epinephrine to increase heart rate, blood pressure, blood glucose, and temperature, as well as to dilate the pupils. It arises from the thoracolumbar spinal segments. The parasympathetic system promotes the “rest and digest” state and uses acetylcholine to maintain basal metabolic func-tion under nonstressful conditions. Parasympathetic fibers arise from cranial nerves III, VII, IX, and X, and from the second to fourth sacral segments. The enteric nervous system controls the complex synchronization of the digestive tract, especially the pancreas, gallbladder, and small and large bowels. It can run autonomously but is regulated by the sympathetic and parasym-pathetic systems.NEUROLOGIC EXAMINATIONThe neurologic examination is divided into several components and generally is done from head to toe. First, one must assess men-tal status. A patient may be awake,


Surgery_Schwartz

Surgery_Schwartz. systems.NEUROLOGIC EXAMINATIONThe neurologic examination is divided into several components and generally is done from head to toe. First, one must assess men-tal status. A patient may be awake, lethargic (will follow com-mands and answer questions, but then returns to sleep), stuporous (difficult to arouse), or comatose (no purposeful response to voice or pain). Cranial nerves may be thoroughly tested in the awake patient, but pupil reactivity, eye movement, facial symmetry, and gag are the most relevant measures when mental status is impaired. Motor testing is based on maximal effort of major muscle groups in those able to follow commands, while assessing for amplitude and symmetry of movement to deep central pain may be all that is possible for stuporous patients. Table 42-1 details scoring for motor assessment tests. Characteristic motor reactions to pain in patients with depressed mental status include withdrawal from stimulus, localization to stimulus, flexor (decorticate)


Surgery_Schwartz

Surgery_Schwartz. scoring for motor assessment tests. Characteristic motor reactions to pain in patients with depressed mental status include withdrawal from stimulus, localization to stimulus, flexor (decorticate) posturing, extensor (decerebrate) posturing, or no reaction (in order of wors-ening pathology). Figure 42-1 diagrams the clinical patterns of posturing. This forms the basis of determining the Glasgow Coma Scale (GCS) motor score, as detailed in Table 42-2. Light touch, proprioception, temperature, and pain testing may be useful in awake patients but is often impossible without good cooperation. It is critical to document sensory patterns in spinal cord injury (SCI) patients. Muscle stretch reflexes should be examined. Often com-paring left to right or upper extremity to lower extremity reflexes for symmetry is the most useful for localizing a lesion. Check for ankle-jerk clonus or up-going toes (Babinski’s test). Presence of either is pathologic and signifies upper motor neuron


Surgery_Schwartz

Surgery_Schwartz. reflexes for symmetry is the most useful for localizing a lesion. Check for ankle-jerk clonus or up-going toes (Babinski’s test). Presence of either is pathologic and signifies upper motor neuron disease.Diagnostic StudiesPlain Films. Plain X-rays of the skull may demonstrate frac-tures, osteolytic or osteoblastic lesions, radiolucent foreign bodies, or pneumocephaly (air in the head). Plain films of the cervical, thoracic, and lumbar spine are used to assess for evi-dence of bony trauma or soft tissue swelling suggesting fracture. Spinal deformities and osteolytic or osteoblastic pathologic pro-cesses also will be apparent. However, the use of plain films has decreased given the rapid availability and significantly increased detail of computed tomography (CT) scans. They are typically used for assessing alignment in patients with known fractures, for intraoperative localization, and postoperative assessment of spinal instrumentation.Computed Tomography. The noncontrast CT scan of the


Surgery_Schwartz

Surgery_Schwartz. for assessing alignment in patients with known fractures, for intraoperative localization, and postoperative assessment of spinal instrumentation.Computed Tomography. The noncontrast CT scan of the head is an extremely useful diagnostic tool in the setting of new focal neurologic deficit, decreased mental status, or trauma. It is rapid and almost universally available in hospitals in the United States. Its sensitivity allows for the detection of acute hemorrhage. Fine-slice CT scanning of the spine is helpful for defining bony anatomy and pathology and is the method of choice for iden-tifying fractures of the spine. By providing an assessment of spinal alignment, CT scans can provide an indirect assessment of ligamentous injury, for example, “Rule of Spence” for assess-ing transverse ligament injury during Jefferson fractures (see “Spine Trauma” section later in this chapter). Conventional con-trast-enhanced CT scan will help show neoplastic or infectious processes. In the current


Surgery_Schwartz

Surgery_Schwartz. injury during Jefferson fractures (see “Spine Trauma” section later in this chapter). Conventional con-trast-enhanced CT scan will help show neoplastic or infectious processes. In the current era, contrast CT generally is used for those patients who cannot undergo magnetic resonance imaging (MRI) scanning due to pacemakers or metal in the orbits (see following section for discussion of CT angiography, venogra-phy, and perfusion).Magnetic Resonance Imaging. Magnetic resonance imaging (MRI) provides excellent imaging of soft tissue structures in the head and spine. It is a complex and evolving science. Several of the most clinically useful MRI sequences are worth describing. T1 sequences made before and after gadolin-ium administration are useful for detecting neoplastic and infec-tious processes. T2 sequences facilitate assessment of 2Table 42-1Motor scoring systemGRADEDESCRIPTION0No muscle contraction1Visible muscle contraction without movement across the joint2Movement in the


Surgery_Schwartz

Surgery_Schwartz. processes. T2 sequences facilitate assessment of 2Table 42-1Motor scoring systemGRADEDESCRIPTION0No muscle contraction1Visible muscle contraction without movement across the joint2Movement in the horizontal plane, unable to overcome gravity3Movement against gravity4Movement against some resistance5Normal strengthBrunicardi_Ch42_p1827-p1878.indd 182901/03/19 7:16 PM 1830SPECIFIC CONSIDERATIONSPART IITable 42-2The Glasgow Coma Scale scoreaMOTOR RESPONSE VERBAL RESPONSE EYE-OPENING RESPONSE Obeys commands6Oriented5Opens spontaneously4Localizes to pain5Confused4Opens to speech3Withdraws from pain4Inappropriate words3Opens to pain2Flexor posturing3Unintelligible sounds2No eye opening1Extensor posturing2No sounds1 No movement1 aAdd the three scores to obtain the Glasgow Coma Scale (GCS) score, which can range from 3 to 15. Add “T” after the GCS if intubated and no verbal score is possible. For these patients, the GCS can range from 3T to 10T.lesion-associated edema in the brain and


Surgery_Schwartz

Surgery_Schwartz. score, which can range from 3 to 15. Add “T” after the GCS if intubated and no verbal score is possible. For these patients, the GCS can range from 3T to 10T.lesion-associated edema in the brain and neural compression in the spine by the presence or absence of bright T2 CSF signals. Fluid-attenuated inversion recovery (FLAIR) imaging is a T2 sequence with suppression of the CSF signal, so as to emphasize lesions and edema, particularly adjacent to the ventricles. Diffu-sion-weighted images is the gold-standard for identifying isch-emic stroke within 12 hours of symptom onset.2 Gradient echo sequences (GRE) can be used to identify acute-subacute blood products and are used to assess for micro-hemorrhages in trau-matic diffuse axonal injury (DAI), amyloid angiopathy, and also in the diagnosis of cavernous malformations. In the spine, short-tau inversion recovery (STIR) or fat-suppressed T2 sequences are useful for assessing for the acuity of fractures (by measuring bone edema), and


Surgery_Schwartz

Surgery_Schwartz. of cavernous malformations. In the spine, short-tau inversion recovery (STIR) or fat-suppressed T2 sequences are useful for assessing for the acuity of fractures (by measuring bone edema), and identifying ligamentous injury.CT and MR Angiography. Recent advances in CT technol-ogy such as short acquisition times with multidetector technol-ogy has allowed for imaging of vascular anatomy. Fine-slice CT scans can be combined with a timed-bolus of intravenous contrast in the arterial phase (angiography, CTA) and venous phase (venography, CTV) to assess arterial and venous vascu-lature, respectively. Although traditional catheter-based angiog-raphy still serves as the gold-standard, CTA and CTV provide Figure 42-1. Patterns of motor responses associated with various lesions. A. Left hemispheric lesion with right hemiplegia and left local-ization. B. Deep cerebral/thalamic lesion with bilateral flexor posturing. C. Midbrain or pontine lesion with bilateral extensor posturing. D. Medullary


Surgery_Schwartz

Surgery_Schwartz. lesion with right hemiplegia and left local-ization. B. Deep cerebral/thalamic lesion with bilateral flexor posturing. C. Midbrain or pontine lesion with bilateral extensor posturing. D. Medullary lesion with general flaccidity. (Adapted with permission from Rengachary SS, Ellenbogen RG: Principles of Neurosurgery, 2nd ed. New York, NY: Elsevier/Mosby; 2005.)Brunicardi_Ch42_p1827-p1878.indd 183001/03/19 7:16 PM 1831NEUROSURGERYCHAPTER 42noninvasive alternative for the initial screening assessment and follow-up of patients with suspected or known vascular lesions, as well as the evaluation of vasospasm. Similarly, fine-slice time-of-flight axial images can be reformatted in three dimen-sions to build MRI angiograms and MRI venograms. MRI angiograms can detect stenosis of the cervical carotid arteries or intracranial aneurysms >3 mm in diameter. MRI venograms can assess the dural venous sinuses for patency or thrombosis. Two-dimensional time of flight imaging performs vascular


Surgery_Schwartz

Surgery_Schwartz. carotid arteries or intracranial aneurysms >3 mm in diameter. MRI venograms can assess the dural venous sinuses for patency or thrombosis. Two-dimensional time of flight imaging performs vascular reconstructions purely based on flow and does not require gado-linium contrast administration.CT and MR Perfusion. Perfusion scans have recently emerged as a method to a global assessment of the vascular integrity in the cerebral hemispheres, which is very important in the assess-ment of ischemic stroke (see “Stroke”). CT perfusion scans gen-erate quantitative color maps that indicate various physiologic parameters such as cerebral blood flow (CBF), cerebral blood volume (CBV), and mean transit time (MTT) through quan-titative analysis of rapidly acquired image sequences during intravenous contrast administration. Similar to perfusion CT, perfusion MRI can be used to generate quantitative color maps of relative cerebral CBV and MTT. These perfusion-based mea-sures can be used along with


Surgery_Schwartz

Surgery_Schwartz. administration. Similar to perfusion CT, perfusion MRI can be used to generate quantitative color maps of relative cerebral CBV and MTT. These perfusion-based mea-sures can be used along with diffusion-weighted imaging in the evaluation of ischemic stroke, particularly to identify an isch-emic “penumbra” or tissue that is ischemic but not yet infarcted, and may be salvageable with intervention.3,4Angiography. Transarterial catheter-based angiography remains the gold standard for evaluation of vascular pathology of the brain and spine. The current state of the art is biplanar imaging to reduce dye load and facilitate interventional proce-dures. Digital subtraction technologies minimize bony inter-ference in the resultant images. Bilateral carotid arteries and bilateral vertebral arteries may be injected and followed through arterial, capillary, and venous phases for a complete cerebral angiogram.Electroencephalography. Electroencephalography (EEG) involves measuring weak electrical


Surgery_Schwartz

Surgery_Schwartz. may be injected and followed through arterial, capillary, and venous phases for a complete cerebral angiogram.Electroencephalography. Electroencephalography (EEG) involves measuring weak electrical signals from the brain that are transmitted through the skull through electrodes that are applied to the scalp. The voltage fluctuations detected by EEG are thought to reflect summed membrane potentials from under-lying brain tissue. Clinically, EEG is useful for detecting sei-zures, interictal markers of epileptogenic tissue, and widespread abnormalities in brain function, such as diffuse encephalopathy. EEG is also used in concert with electrical stimulation to detect sensory evoked potentials that can be useful for intraoperative mapping during cranial and spine surgery.Electromyography and Nerve Conduction Studies. Electromyography and nerve conduction studies (EMG/NCS) are useful for assessing the function of peripheral nerves. EMG records muscle activity in response to a proximal


Surgery_Schwartz

Surgery_Schwartz. Nerve Conduction Studies. Electromyography and nerve conduction studies (EMG/NCS) are useful for assessing the function of peripheral nerves. EMG records muscle activity in response to a proximal stimulation of the motor nerve. NCS record the velocity and amplitude of the nerve action potential. EMG/NCS typically is performed approximately 3 to 4 weeks after an acute injury, as nerves distal to the injury continue to transmit electrical impulses normally until degeneration of the distal nerve progresses.Invasive Monitoring. The most reliable monitor, always, is an alert patient with a reliable neurologic examination. If a reliable neurologic examination is not possible due to the pres-ence of brain injury, sedatives, or paralytics, or if there is active and unstable intracranial pathology, invasive monitoring is required. There are several methods of monitoring intracranial physiology. The methods described in the following sections are bedside intensive care unit (ICU) procedures


Surgery_Schwartz

Surgery_Schwartz. invasive monitoring is required. There are several methods of monitoring intracranial physiology. The methods described in the following sections are bedside intensive care unit (ICU) procedures that allow for continuous monitoring. Both procedures involve making a small hole in the skull with a hand-held drill. They generally are placed in the right frontal region to minimize the neurologic impact of possible complications such as hemorrhage.External Ventricular Drain. An external ventricular drain is also known as a ventriculostomy. A perforated plastic catheter is inserted into the frontal horn of the lateral ventricle. An uninter-rupted fluid column through a rigid tube allows transduction of intracranial pressure (ICP). CSF also can be drained to reduce ICP or sampled for laboratory studies.Intraparenchymal Physiologic Monitoring. Intraparenchy-mal monitors can be inserted into the brain through a threaded post locked securely into a burr hole, commonly referred to as a bolt. A


Surgery_Schwartz

Surgery_Schwartz. studies.Intraparenchymal Physiologic Monitoring. Intraparenchy-mal monitors can be inserted into the brain through a threaded post locked securely into a burr hole, commonly referred to as a bolt. A bolt allows ICP monitoring with a fiber-optic pressure transducer, but it is smaller and less invasive than a ventriculos-tomy and may be associated with fewer complications, although the data do not clearly support this. Furthermore, a bolt can also be used to introduce probes to measure brain tissue oxygenation, brain temperature, and to perform microdialysis of parenchymal samples; however, the utility of these latter measures in clinical practice is still under investigation. Patients with severe brain injury due to trauma or aneurysmal hemorrhage may benefit from placement of these sensors in addition to a ventriculos-tomy to drain CSF for control of ICP. Such monitoring requires two twist-drill holes, which may be placed on adjacent or oppo-site sides of the head.NEUROLOGIC AND


Surgery_Schwartz

Surgery_Schwartz. in addition to a ventriculos-tomy to drain CSF for control of ICP. Such monitoring requires two twist-drill holes, which may be placed on adjacent or oppo-site sides of the head.NEUROLOGIC AND NEUROSURGICAL EMERGENCIESRaised Intracranial PressureICP normally varies between 4 and 14 mmHg. Sustained ICP levels above 20 mmHg can injure the brain. The Monro-Kellie doctrine states that the cranial vault is a rigid structure, and therefore, the total volume of the contents determines ICP. The three normal contents of the cranial vault are brain tis-sue, blood, and CSF. The brain’s contents can expand due to swelling from traumatic brain injury (TBI), stroke, or reactive edema. Blood volume can increase by extravasation to form a hematoma, or by reactive vasodilation in a hypoventilating, hypercarbic patient. CSF volume increases in the setting of hydrocephalus. Figure 42-2 demonstrates the classic CT find-ings of hydrocephalus. The addition of a lesion, such as a tumor or abscess, also will


Surgery_Schwartz

Surgery_Schwartz. patient. CSF volume increases in the setting of hydrocephalus. Figure 42-2 demonstrates the classic CT find-ings of hydrocephalus. The addition of a lesion, such as a tumor or abscess, also will increase ICP. The pressure-volume curve depicted in Fig. 42-3 demonstrates a compensated region with a small ΔP/ΔV, and an uncompensated region with large ΔP/ΔV. In the compensated region, increased volume is offset by decreased volume of CSF and blood.Increased ICP can injure the brain in several ways. Focal mass lesions cause shift and herniation. Temporal lesions push the uncus medially and compress the midbrain. This phenom-enon is known as uncal herniation. The posterior cerebral artery (PCA) passes between the uncus and midbrain and may be occluded, leading to an occipital infarct. Masses higher up in the hemisphere can push the cingulate gyrus under the falx cerebri. This process is known as subfalcine herniation. The anterior cerebral artery (ACA) branches run along the medial surface


Surgery_Schwartz

Surgery_Schwartz. up in the hemisphere can push the cingulate gyrus under the falx cerebri. This process is known as subfalcine herniation. The anterior cerebral artery (ACA) branches run along the medial surface of the cingulate gyrus and may be occluded in this case, leading to medial frontal and parietal infarcts. Diffuse increases in pressure Brunicardi_Ch42_p1827-p1878.indd 183101/03/19 7:16 PM 1832SPECIFIC CONSIDERATIONSPART IIin the cerebral hemispheres can lead to central, or transtento-rial, herniation. Increased pressure in the posterior fossa can lead to upward central herniation or downward tonsillar hernia-tion through the foramen magnum. Uncal, transtentorial, and tonsillar herniation can cause direct damage to the brain stem. Figure 42-4 diagrams patterns of herniation.Patients with increased ICP, or intracranial hypertension, often will present with headache, nausea, vomiting, and progres-sive mental status decline. Cushing’s triad is the classic presen-tation of hypertension,


Surgery_Schwartz

Surgery_Schwartz. increased ICP, or intracranial hypertension, often will present with headache, nausea, vomiting, and progres-sive mental status decline. Cushing’s triad is the classic presen-tation of hypertension, bradycardia, and irregular respirations. Focal neurologic deficits such as hemiparesis may be present if there is a focal mass lesion causing the problem. Patients with these symptoms should undergo an immediate head CT and rapid neurosurgical evaluation.Initial management of intracranial hypertension includes airway protection and adequate ventilation. A bolus of man-nitol up to 1 g/kg causes free water diuresis, increased serum osmolality, and extraction of water from the brain. The effect is delayed by about 20 minutes and has a transient benefit. Driv-ing serum osmolality above 300 mOsm/L is of indeterminate benefit and can have deleterious cardiovascular side effects, such as hypovolemia that leads to hypotension and decreased brain perfusion. A ventriculostomy and/or craniectomy may


Surgery_Schwartz

Surgery_Schwartz. is of indeterminate benefit and can have deleterious cardiovascular side effects, such as hypovolemia that leads to hypotension and decreased brain perfusion. A ventriculostomy and/or craniectomy may be needed for definitive decompression.It is critical to note that lethargic or obtunded patients often have decreased respiratory drive. This causes the partial pressure of arterial carbon dioxide (Paco2) to increase, resulting in cerebral vasodilation and worsening of intracranial hyperten-sion. This cycle causes a characteristic “crashing patient,” who rapidly loses airway protection, becomes apneic, and herniates. Emergent intubation and ventilation to reduce Paco2 to roughly 35 mmHg can reverse this process.Figure 42-2. Head computed tomography scan demonstrating hydrocephalus. The third ventricle (3rd) is widened and rounded, the anterior horns of the lateral ventricles are plump, and pressure-driven flow of cerebrospinal fluid into brain parenchyma adjacent to the ventricles is


Surgery_Schwartz

Surgery_Schwartz. ventricle (3rd) is widened and rounded, the anterior horns of the lateral ventricles are plump, and pressure-driven flow of cerebrospinal fluid into brain parenchyma adjacent to the ventricles is seen (arrowhead). This is known as transepen-dymal flow of cerebrospinal fluid.Intracranial volume (arbitrary units)Intracranial pressure (mmHg)0102030405060708090100110120130102030405060708090100˜V˜P˜V˜P˜V˜PLow complianceecnailpmoc oNecnailpmoc hgiHFigure 42-3. Pressure-volume curve demonstrating the effect of changing the volume of intracranial contents on intracranial pressure. Note the compensated zone, with little change of pressure with change of volume, and the uncompensated zone, with significant change of pres-sure with change of volume. (Adapted with permission from Ellenbogen RG, Abdulrauf SI, Sekhar LN: Principles of Neurosurgery, 3rd ed. Philadelphia, PA: Elsevier/Saunders; 2012.)Brunicardi_Ch42_p1827-p1878.indd 183201/03/19 7:16 PM 1833NEUROSURGERYCHAPTER 42Brain Stem


Surgery_Schwartz

Surgery_Schwartz. Abdulrauf SI, Sekhar LN: Principles of Neurosurgery, 3rd ed. Philadelphia, PA: Elsevier/Saunders; 2012.)Brunicardi_Ch42_p1827-p1878.indd 183201/03/19 7:16 PM 1833NEUROSURGERYCHAPTER 42Brain Stem CompressionThe posterior fossa (brain stem and cerebellum) requires special consideration because the volume of the posterior fossa within the cranial vault is small. Posterior fossa lesions such as tumors, hemorrhage, or stroke can cause mass effect that can rapidly kill the patient in two ways. Occlusion of the fourth ventricle can lead to acute obstructive hydrocephalus, raised ICP, herniation, and eventually death. This mass effect can also lead directly to brain stem compression (Fig. 42-5). Symptoms of brain stem compression include hypertension, agitation, and progressive obtundation, followed rapidly by brain death. A patient exhibit-ing any of these symptoms needs an emergent neurosurgical evaluation for possible ventriculostomy or suboccipital crani-ectomy (removal of the bone


Surgery_Schwartz

Surgery_Schwartz. followed rapidly by brain death. A patient exhibit-ing any of these symptoms needs an emergent neurosurgical evaluation for possible ventriculostomy or suboccipital crani-ectomy (removal of the bone covering the cerebellum). This situation is especially critical, as expeditious decompression can lead to significant functional recovery.StrokePatients presenting with acute focal neurologic deficits at a clearly defined time of onset (i.e., when the patient was last seen in a normal state of health) must be evaluated as rapidly as possible. An emergent head CT scan should be done. The study is often normal because CT changes from ischemic stroke may take up to 24 hours to appear (Fig. 42-6). A patient with a clinical diagnosis of acute stroke <4.5 hours old, without hemor-rhage on CT, may be a candidate for thrombolytic therapy with tissue plasminogen activator (tPA). When a proximal large-vessel obstruction is suspected, patients should be evaluated for endovascular mechanical


Surgery_Schwartz

Surgery_Schwartz. may be a candidate for thrombolytic therapy with tissue plasminogen activator (tPA). When a proximal large-vessel obstruction is suspected, patients should be evaluated for endovascular mechanical thrombectomy if therapy can be initiated within 6 to 8 hours of symptom onset. Intravenous tPA should be given regardless, but a noninvasive intracranial vas-cular study such as CT angiography should also be obtained in these cases. An emergent MRI is helpful but not always diag-nostically necessary.SeizureA seizure is defined as an uncontrolled synchronous organiza-tion of neuronal electrical activity. A new-onset seizure often signifies an irritative mass lesion in the brain, particularly in adults, in whom tumors commonly present with seizure. Patients with traumatic intracranial hemorrhage are at risk for seizure. In addition to airway and ventilatory problems, a seizing patient is also at risk for neural excitotoxicity if the activity is prolonged, such as in status epilepticus. Any


Surgery_Schwartz

Surgery_Schwartz. are at risk for seizure. In addition to airway and ventilatory problems, a seizing patient is also at risk for neural excitotoxicity if the activity is prolonged, such as in status epilepticus. Any patient with a new-onset sei-zure should have imaging of the brain after the seizure is con-trolled and the patient is resuscitated.TRAUMATrauma is the leading cause of death in children and young adults; however, the incidence of death and disability from trauma has been slowly decreasing. This decline is partly attrib-utable to increased awareness of safety devices such as seat belts and motorist helmets. Nonetheless, trauma remains a major cause of morbidity and mortality, and it can affect every major organ system in the body. The three main areas of neurosurgical focus are: traumatic brain injury (TBI), spinal cord injury (SCI), and peripheral nerve injury.Head TraumaGlasgow Coma Scale Score. The initial assessment of the trauma patient includes the primary survey, resuscitation,


Surgery_Schwartz

Surgery_Schwartz. brain injury (TBI), spinal cord injury (SCI), and peripheral nerve injury.Head TraumaGlasgow Coma Scale Score. The initial assessment of the trauma patient includes the primary survey, resuscitation, 1324Figure 42-4. Schematic drawing of brain herniation patterns. 1. Subfalcine herniation. The cingulate gyrus shifts across midline under the falx cerebri. 2. Uncal herniation. The uncus (medial tem-poral lobe gyrus) shifts medially and compresses the midbrain and cerebral peduncle. 3. Central transtentorial herniation. The dien-cephalon and midbrain shift caudally through the tentorial inci-sura. 4. Tonsillar herniation. The cerebellar tonsil shifts caudally through the foramen magnum. (Reproduced with permission from Wilkins RH, Rengachary SS: Neurosurgery, 2nd ed. New York, NY: McGraw Hill Education; 1996.)Figure 42-5. Maturing cerebellar stroke seen as a hypodense area in the right cerebellar hemisphere (arrowhead) on head computed tomography in a patient with rapidly progressing


Surgery_Schwartz

Surgery_Schwartz. Hill Education; 1996.)Figure 42-5. Maturing cerebellar stroke seen as a hypodense area in the right cerebellar hemisphere (arrowhead) on head computed tomography in a patient with rapidly progressing obtundation 2 days after the initial onset of symptoms. Swelling of the infarcted tissue causes posterior fossa mass effect. The fourth ventricle is obliterated and not visible, and the brain stem is being compressed.Brunicardi_Ch42_p1827-p1878.indd 183301/03/19 7:16 PM 1834SPECIFIC CONSIDERATIONSPART IIsecondary survey, and definitive care. Neurosurgical evalua-tion begins during the primary survey with the determination of the GCS score (usually referred to simply as the GCS) for the patient. The GCS is determined by adding the scores of the best responses of the patient in each of three categories. The motor score ranges from 1 to 6, verbal from 1 to 5, and eyes from 1 to 4. The GCS therefore ranges from 3 to 15, as detailed in Table 42-2. Tracheal intubation or severe facial or


Surgery_Schwartz

Surgery_Schwartz. categories. The motor score ranges from 1 to 6, verbal from 1 to 5, and eyes from 1 to 4. The GCS therefore ranges from 3 to 15, as detailed in Table 42-2. Tracheal intubation or severe facial or eye swelling can impede verbal and eye responses. In these circumstances, the patient is given the score of 1 with a modifier, such as verbal “1T” where T = tube.Scalp Injury. Blunt or penetrating trauma to the head can cause injury to the densely vascularized scalp, and significant blood loss can result. Direct pressure initially controls the bleeding, allowing close inspection of the injury. If a simple laceration is found, it should be copiously irrigated and closed primarily. If the laceration is short, a single-layer, percutaneous suture clo-sure will suffice. If the laceration is long or has multiple arms, the patient may need debridement and closure in the operating room, with its superior lighting and wider selection of instru-ments and suture materials. Careful reapproximation of the


Surgery_Schwartz

Surgery_Schwartz. multiple arms, the patient may need debridement and closure in the operating room, with its superior lighting and wider selection of instru-ments and suture materials. Careful reapproximation of the galea will provide a more secure closure and better hemostasis. ACBFigure 42-6. A. Head computed tomography scan of a patient with a 4-day-old stroke that occluded the right middle cerebral and posterior cerebral arteries. The infarcted tissue is the hypodense (dark) area indicated by the arrowheads. The patient presented with left-sided weakness and left visual field loss, but then became less responsive, prompting this head computed tomography. Note the right-to-left midline shift. B. Same patient status post decompressive right hemicraniectomy. Note the free expansion of swollen brain outside the normal confines of the skull. C. Patient with a right middle cerebral artery ischemic stroke with areas of hemorrhagic conversion, seen as hyperdense (bright) areas within the infarcted


Surgery_Schwartz

Surgery_Schwartz. outside the normal confines of the skull. C. Patient with a right middle cerebral artery ischemic stroke with areas of hemorrhagic conversion, seen as hyperdense (bright) areas within the infarcted tissue. This patient also required hemicraniectomy for severe mass effect. Note the lack of midline shift postoperatively.Brunicardi_Ch42_p1827-p1878.indd 183401/03/19 7:16 PM 1835NEUROSURGERYCHAPTER 42Blunt trauma also can cause crush injury with subsequent tissue necrosis. These wounds require debridement and consideration of advancement flaps to cover the defect.Skull Fractures. The usual classification system for bony fractures may be applied to the skull. The fracture may be characterized by skull X-rays or head CT.5 A closed fracture is covered by intact skin. An open, or compound, fracture is associated with disrupted overlying skin. The fracture lines may be single (linear); multiple and radiating from a point (stellate); or multiple, creating fragments of bone (comminuted).


Surgery_Schwartz

Surgery_Schwartz. fracture is associated with disrupted overlying skin. The fracture lines may be single (linear); multiple and radiating from a point (stellate); or multiple, creating fragments of bone (comminuted). Closed skull fractures do not normally require specific treatment. Open fractures require repair of the scalp and operative debridement. Indications for craniotomy include depression greater than the cranial thickness, intracranial hematoma, and frontal sinus involvement.6 Skull fractures generally indicate that a signifi-cant amount of force was transmitted to the head and should increase the suspicion for intracranial injury. Fractures that cross meningeal arteries can cause rupture of the underlying vessels and subsequent epidural hematoma (EDH) formation.Depressed skull fractures may result from a focal injury of significant force. The inner and outer cortices of the skull are disrupted, and a fragment of bone is pressed in toward the brain in relation to adjacent intact skull. The


Surgery_Schwartz

Surgery_Schwartz. from a focal injury of significant force. The inner and outer cortices of the skull are disrupted, and a fragment of bone is pressed in toward the brain in relation to adjacent intact skull. The fragment may overlap the edge of intact bone, or it may plunge completely below the level of adjacent normal skull. The inner cortex of the bone fragments often has multiple sharp edges that can lacerate dura, brain, and vessels. Craniotomy is required to ele-vate the fracture, repair dural disruption, and obtain hemostasis in these cases (Fig. 42-7). However, fractures overlying dural venous sinuses require restraint. Surgical exploration can lead to life-threatening hemorrhage from the lacerated sinus.Fractures of the skull base are common in head-injured patients, and they indicate significant impact. They are gener-ally apparent on routine head CT, but they should be evaluated with dedicated fine-slice coronal-section CT scan to document and delineate the extent of the fracture and


Surgery_Schwartz

Surgery_Schwartz. impact. They are gener-ally apparent on routine head CT, but they should be evaluated with dedicated fine-slice coronal-section CT scan to document and delineate the extent of the fracture and involved structures. If asymptomatic, they require no treatment. Skull base fractures requiring intervention include those with an associated cranial nerve deficit or CSF leak. A fracture of the temporal bone, for instance, can damage the facial or vestibulocochlear nerve, resulting in vertigo, ipsilateral deafness, or facial paralysis. A communication may be formed between the subarachnoid space and the middle ear, allowing CSF drainage into the pharynx via the Eustachian tube or from the ear (otorrhea). Extravasation of blood results in ecchymosis behind the ear, known as Battle’s sign. A fracture of the anterior skull base can result in anos-mia (loss of smell from damage to the olfactory nerve), CSF drainage from the nose (rhinorrhea), or periorbital ecchymosis, known as raccoon eyes.Copious


Surgery_Schwartz

Surgery_Schwartz. of the anterior skull base can result in anos-mia (loss of smell from damage to the olfactory nerve), CSF drainage from the nose (rhinorrhea), or periorbital ecchymosis, known as raccoon eyes.Copious clear drainage from the nose or ear makes the diagnosis of CSF leakage obvious. Often, however, the drain-age may be discolored with blood or small in volume if some drains into the throat. In indeterminate cases, it is important to consider radiographic findings on the CT scan near the fracture that suggest CSF leak, such as pneumocephalus, subarachnoid, or intraparenchymal blood at the fracture site. The “halo” test assesses for a double ring when a drop of the fluid is allowed to fall on an absorbent surface, but it has been shown to have poor clinical utility.7 The fluid can be sent for β-2 transferrin testing, a carbohydrate-free isoform of transferrin exclusively found in the CSF; however, these tests often take 1 to 2 weeks to result and also can be difficult to incorporate into


Surgery_Schwartz

Surgery_Schwartz. β-2 transferrin testing, a carbohydrate-free isoform of transferrin exclusively found in the CSF; however, these tests often take 1 to 2 weeks to result and also can be difficult to incorporate into clinical practice.BAFigure 42-7. A. Bone-window axial head computed tomography (CT) of a patient who presented aphasic after being struck with the bot-tom of a beer bottle. CT demonstrates a depressed skull fracture in the left posterior temporoparietal area. B. Brain-window axial head CT demonstrating intraparenchymal hematoma caused by laceration of cortical vessels by the edge of the fractured bone. Arrowhead indicates traumatic subarachnoid hemorrhage in the sylvanian fissure.Brunicardi_Ch42_p1827-p1878.indd 183501/03/19 7:16 PM 1836SPECIFIC CONSIDERATIONSPART IIMany CSF leaks will heal with elevation of the head of the bed for several days. An elevation of the head of the bed reduces the hydrostatic pressure of the CSF fluid column in the cranial vault, near the site of the


Surgery_Schwartz

Surgery_Schwartz. heal with elevation of the head of the bed for several days. An elevation of the head of the bed reduces the hydrostatic pressure of the CSF fluid column in the cranial vault, near the site of the defect. As such, when the CSF leak is in the lumbar thecal sac, the head of the bed should be flat so as to maximize hydrostatic pressure of the CSF fluid column at the cranial vault, away from the site of the defect. In addi-tion, lumbar drain can be used to reduce CSF pressure. When there is a contraindication, to lumbar drain placement (such as an intracranial mass lesion or hematoma), an extraventricular drain should be used for CSF diversion. Although persistent CSF leaks have been shown to increase the risk of meningitis,8 there is no evidence supporting the use of prophylactic antibi-otic use for preventing meningitis in patients with CSF leaks.9Traumatic cranial neuropathies generally can be managed conservatively, with documentation of the extent of impairment and signs of recovery.


Surgery_Schwartz

Surgery_Schwartz. use for preventing meningitis in patients with CSF leaks.9Traumatic cranial neuropathies generally can be managed conservatively, with documentation of the extent of impairment and signs of recovery. Patients with traumatic facial nerve pal-sies may benefit from a course of steroids, although their benefit is unproven. Patients with facial nerve palsy of abrupt onset, who do not respond to steroids within 48 to 72 hours, may be considered for surgical decompression of the petrous portion of the facial nerve. Patients also may present with delayed-onset facial nerve palsy. Again, steroids are used and surgery can be considered, with mixed results.Closed Head Injury. Closed head injury (CHI) is the most common type of TBI and a significant cause of morbidity and mortality in the United States. There are two important factors that affect the outcome of CHI in general. The initial impact causes the primary injury, defined as the immediate injury to neurons from transmission of the force


Surgery_Schwartz

Surgery_Schwartz. There are two important factors that affect the outcome of CHI in general. The initial impact causes the primary injury, defined as the immediate injury to neurons from transmission of the force of impact. The long, delicate axons of the neurons can shear as they undergo differ-ential acceleration or deceleration along their projecting path-ways. Prevention strategies, such as wearing helmets, remain the best means to decrease disability from primary injury. Sub-sequent neuronal damage due to the sequelae of trauma is referred to as secondary injury. Hypoxia, hypotension, hydro-cephalus, intracranial hypertension, thrombosis, and intracranial hemorrhage may all be mechanisms of secondary injury. One focus of basic research in TBI, critical care medicine, and neurosurgical intervention is to decrease the effects of sec-ondary injury.The Brain Trauma Foundation’s most recent summary of management recommendations for TBI patients was published in 2016 and is endorsed by the American


Surgery_Schwartz

Surgery_Schwartz. is to decrease the effects of sec-ondary injury.The Brain Trauma Foundation’s most recent summary of management recommendations for TBI patients was published in 2016 and is endorsed by the American Association of Neuro-logical Surgeons, Congress of Neurological Surgeons, and the World Health Organization.10 The guidelines standardize the care of these patients with the hope of improving outcomes. Level I recommendations are based on a body of high-quality evidence, such as large, well-received randomized controlled trials. Level II and III recommendations are based on moderate and low quality evidence, respectively. Some of the common patterns of CHI, including concussion, contusion, and diffuse axonal injury, are discussed in “Types of Closed Head Injury.”11Initial Assessment The initial evaluation of a trauma patient remains the same whether or not the primary surveyor suspects head injury. The first three elements of the ABCDs of resus-citation—airway, breathing, and


Surgery_Schwartz

Surgery_Schwartz. initial evaluation of a trauma patient remains the same whether or not the primary surveyor suspects head injury. The first three elements of the ABCDs of resus-citation—airway, breathing, and circulation—must be assessed and stabilized. Hypoxia and hypotension are known to worsen outcome in TBI (due to secondary injury), making cardiopul-monary stabilization critical. Patients who cannot follow com-mands require intubation for airway protection and ventilatory control. The fourth element, assessment of “D,” for disability, is undertaken next. Motor activity, speech, and eye opening can be assessed in a few seconds and a GCS score assigned.The following is an example of how a primary surveyor may efficiently assess disability and GCS: Approach the patient and enter his or her field of view. Observe whether the patient is visually attentive. Clearly command: “Tell me your name.” Then ask the patient to lift up two fingers on each side sequen-tially, and wiggle the toes. A visually or


Surgery_Schwartz

Surgery_Schwartz. Observe whether the patient is visually attentive. Clearly command: “Tell me your name.” Then ask the patient to lift up two fingers on each side sequen-tially, and wiggle the toes. A visually or verbally unresponsive patient should be assessed for response to peripheral stimuli such as nail-bed pressure, or deep central painful stimulation, such as a firm, twisting pinch of the sensitive supraclavicular skin. Watch for eye opening and movement of the extremities, whether purposeful or reflexive. Assess the verbal response. The motor, verbal, and eye-opening scores may be correctly assigned using this rapid examination. An initial assessment of the probability of significant head injury can be made, assuming that pharmacologic and toxic elements have not obscured the examination. The surveyor must also take note of any external signs of head injury, including bleeding from the scalp, nose, or ear, or deformation of the skull or face.Classification TBI can be classified as mild,


Surgery_Schwartz

Surgery_Schwartz. surveyor must also take note of any external signs of head injury, including bleeding from the scalp, nose, or ear, or deformation of the skull or face.Classification TBI can be classified as mild, moderate, or severe. For patients with a history of head trauma, classifica-tion is as follows: severe head injury if the GCS score is 3 to 8, moderate head injury if the GCS score is 9 to 12, and mild head injury if the GCS score is 13 to 15. Many patients present to emergency rooms and trauma bays with a history of TBI. A tri-age system must be used to maximize resource utilization while minimizing the chance of missing occult or progressing injuries.TBI patients who are asymptomatic, who have only headache, dizziness, or scalp lacerations, and who did not lose consciousness, have a low risk for intracranial injury and may be discharged home without a head CT scan.12,13 Head-injured patients who are discharged should be sent home with reliable family or friends who can observe the patient


Surgery_Schwartz

Surgery_Schwartz. intracranial injury and may be discharged home without a head CT scan.12,13 Head-injured patients who are discharged should be sent home with reliable family or friends who can observe the patient for the first postin-jury day. Printed discharge instructions, which describe moni-toring for confusion, persistent nausea, weakness, or speech difficulty, should be provided to the caretaker. The patient should return to the emergency department for evaluation of such symptoms.Patients with a history of altered consciousness, amne-sia, progressive headache, skull or facial fracture, vomiting, or seizure have a moderate risk for intracranial injury and should undergo a prompt head CT. If the CT is normal, and the neuro-logic examination has returned to baseline (excluding amnesia of the event), then the patient can be discharged to the care of a responsible adult, again with printed criteria for returning to the emergency room. Otherwise the patient must be admitted for a 24-hour observation


Surgery_Schwartz

Surgery_Schwartz. the patient can be discharged to the care of a responsible adult, again with printed criteria for returning to the emergency room. Otherwise the patient must be admitted for a 24-hour observation period.Patients with depressed consciousness, focal neurologic deficits, penetrating injury, depressed skull fracture, or changing neurologic examination have a high risk for intracranial injury. These patients should undergo immediate head CT and admis-sion for observation or intervention as needed.Types of Closed Head Injury Concussion A concussion is defined as temporary neuronal dysfunction following nonpenetrating head trauma. The head CT is normal, and deficits resolve over minutes to hours. Defini-tions vary; some require transient loss of consciousness, while others include patients with any alteration of mental status. Memory difficulties, especially amnesia of the event, are very 3Brunicardi_Ch42_p1827-p1878.indd 183601/03/19 7:16 PM 1837NEUROSURGERYCHAPTER 42common. Concussions


Surgery_Schwartz

Surgery_Schwartz. alteration of mental status. Memory difficulties, especially amnesia of the event, are very 3Brunicardi_Ch42_p1827-p1878.indd 183601/03/19 7:16 PM 1837NEUROSURGERYCHAPTER 42common. Concussions may be graded. One method is the Col-orado grading system.14 Head trauma patients with confusion only are grade 1, patients with amnesia are grade 2, and patients who lose consciousness are grade 3. Studies have shown that the brain remains in a hypermetabolic state for up to a week after injury. The brain is also much more susceptible to injury from even minor head trauma in the first 1 to 2 weeks after concus-sion. This is known as second-impact syndrome, and patients should be informed that, even after mild head injury, they might experience memory difficulties or persistent headaches. Return to play guidelines after sports-related concussions are contro-versial and are under active debate.15Contusion A contusion is a bruise of the brain, and occurs when the force from trauma is


Surgery_Schwartz

Surgery_Schwartz. Return to play guidelines after sports-related concussions are contro-versial and are under active debate.15Contusion A contusion is a bruise of the brain, and occurs when the force from trauma is sufficient to cause breakdown of small vessels and extravasation of blood into the brain. The contused areas appear bright on CT scan, as seen in Fig. 42-8. The frontal, occipital, and temporal poles are most often involved. The brain sustains injury as it collides with rough, bony surfaces. Contu-sions themselves rarely cause significant mass effect as they represent small amounts of blood in injured parenchyma rather than coherent blood clots. Edema may develop around a contu-sion, causing mass effect. Contusions may enlarge or progress to frank hematoma, particularly during the first 24 hours. Contu-sions also may occur in brain tissue opposite the site of impact. This is known as a contre-coup injury. These contusions result from deceleration of the brain against the skull.Diffuse Axonal


Surgery_Schwartz

Surgery_Schwartz. Contu-sions also may occur in brain tissue opposite the site of impact. This is known as a contre-coup injury. These contusions result from deceleration of the brain against the skull.Diffuse Axonal Injury Diffuse axonal injury (DAI) is caused by damage to axons throughout the brain, due to rotational acceleration and then deceleration. Axons may be completely disrupted and then retract, forming axon balls. Small hemor-rhages can be seen in more severe cases, especially on MRI. Hemorrhage is classically seen in the corpus callosum and the dorsolateral midbrain. DAI can be considered to be a severe form of a concussion, often with irreversible consequence. It can often explain a poor neurological examination (such as impaired arousal) in cases without clear radiographic signs of global bran injury, particularly when there is damage in struc-tures, such as the pontine reticular activating system or bilateral thalami, that are necessary for arousal. In these cases, alternative


Surgery_Schwartz

Surgery_Schwartz. global bran injury, particularly when there is damage in struc-tures, such as the pontine reticular activating system or bilateral thalami, that are necessary for arousal. In these cases, alternative explanations of poor arousal, such as a basilar thrombus, must also be investigated.Penetrating Injury These injuries are complex and must be evaluated individually. The two main subtypes are missile (e.g., due to bullets or fragmentation devices) and nonmissile (e.g., due to knives or ice picks). Some general principles apply. If available, skull X-rays and CT scans are useful in assessing the nature of the injury. Cerebral angiography must be considered if the object passes near a major artery or dural venous sinus. Operative exploration is necessary to remove any object extend-ing out of the cranium, as well as for debridement, irrigation, hemostasis, and definitive closure. Small objects contained within brain parenchyma are often left in place to avoid iat-rogenic secondary brain


Surgery_Schwartz

Surgery_Schwartz. the cranium, as well as for debridement, irrigation, hemostasis, and definitive closure. Small objects contained within brain parenchyma are often left in place to avoid iat-rogenic secondary brain injury. High-velocity missile injuries (from high-powered hunting rifles or military weapons) are especially deadly, because the associated shock wave causes cavitary tissue destruction of an area that is much larger than the projectile itself. Projectiles that penetrate both hemispheres or traverse the ventricles are almost universally fatal. Antibiot-ics are given to decrease the chances of meningitis or abscess formation; however, the evidence supporting the use of antibi-otics following missile injury is weak and largely comes from retrospective case studies and expert opinion. Recent guidelines published in regard to preventing combat-related infections recommend antimicrobial therapy for 5 days or until resolu-tion of the associated CSF leak, albeit with limited supporting


Surgery_Schwartz

Surgery_Schwartz. guidelines published in regard to preventing combat-related infections recommend antimicrobial therapy for 5 days or until resolu-tion of the associated CSF leak, albeit with limited supporting evidence.16Traumatic Intracranial Hematomas. The various traumatic intracranial hematomas contribute to death and disability sec-ondary to head injury. Hematomas can expand rapidly and cause brain shift and subsequent herniation. Emergent neurosurgical evaluation and intervention often are necessary.Epidural Hematoma EDH is the accumulation of blood between the skull and the dura. EDH usually results from arte-rial disruption, especially of the middle meningeal artery. The dura is adherent to bone, and some pressure is required to dis-sect between the two. On head CT, the blood clot is bright, biconvex in shape (lentiform), and has a well-defined border that usually respects cranial suture lines. An EDH is typically found over the convexities but may rarely occur in the posterior fossa as well.


Surgery_Schwartz

Surgery_Schwartz. in shape (lentiform), and has a well-defined border that usually respects cranial suture lines. An EDH is typically found over the convexities but may rarely occur in the posterior fossa as well. EDH has a classic, three-stage clinical presenta-tion that is probably seen in only 20% of cases. The patient is initially unconscious from the concussive aspect of the head trauma. The patient then awakens and has a “lucid interval,” while the hematoma subclinically expands. As the volume of the hematoma grows, the decompensated region of the pressure-volume curve is reached, ICP increases, and the patient rapidly becomes lethargic and herniates. Uncal herniation from an EDH classically causes ipsilateral third nerve palsy and contralateral hemiparesis.Open craniectomy for evacuation of the congealed clot and hemostasis generally is indicated for EDH. In some cases, EDH can be caused from bony venous bleeding that is self-limited Figure 42-8. Severe bilateral contusions in the basal aspect


Surgery_Schwartz

Surgery_Schwartz. clot and hemostasis generally is indicated for EDH. In some cases, EDH can be caused from bony venous bleeding that is self-limited Figure 42-8. Severe bilateral contusions in the basal aspect of the frontal lobes, caused by the brain moving over the rough, irregular skull base during sudden cranial acceleration.Brunicardi_Ch42_p1827-p1878.indd 183701/03/19 7:16 PM 1838SPECIFIC CONSIDERATIONSPART IIand may not require surgical intervention. Generally, patients who meet all of the following criteria may be managed conser-vatively: clot volume <30 cm3, maximum thickness <1.5 cm, and GCS score >8.10 Prognosis after successful evacuation is better for EDH than subdural hematoma (SDH). EDHs are associ-ated with lower-energy trauma with less resultant primary brain injury. Good outcomes may be seen in 85% to 90% of patients, with rapid CT scan and intervention.11 In some cases, EDH can also be caused by dural venous sinus tears that rapidly expand and are typically associated with a


Surgery_Schwartz

Surgery_Schwartz. may be seen in 85% to 90% of patients, with rapid CT scan and intervention.11 In some cases, EDH can also be caused by dural venous sinus tears that rapidly expand and are typically associated with a high degree of morbidity when treated surgically.Acute Subdural Hematoma An acute SDH is the result of an accumulation of blood between the arachnoid membrane and the dura. Acute SDH usually results from venous bleed-ing, typically from tearing of a bridging vein running from the cerebral cortex to the dural sinuses. The bridging veins are sub-ject to stretching and tearing during acceleration/deceleration of the head because the brain shifts in relation to the dura, which firmly adheres to the skull. Elderly and alcoholic patients are at higher risk for acute SDH formation after head trauma due to brain atrophy.On head CT scan, the clot is bright or mixed-density, cres-cent-shaped (lunate), may have a less distinct border, and does not cross the midline due to the presence of the falx.


Surgery_Schwartz

Surgery_Schwartz. due to brain atrophy.On head CT scan, the clot is bright or mixed-density, cres-cent-shaped (lunate), may have a less distinct border, and does not cross the midline due to the presence of the falx. Most SDHs occur over the cerebral hemispheres, but they may also occur between the hemispheres or layer over the tentorium.Open craniotomy for evacuation of acute SDH is indicated for any of the following: thickness >1 cm, midline shift >5 mm, or GCS drop by two or more points from the time of injury to hospitalization. Nonoperatively managed hematomas may sta-bilize and eventually reabsorb, or evolve into chronic SDHs.17 This management requires frequent neurologic examinations until the clot stabilizes based on serial head CT scans.The prognosis for functional recovery is significantly worse for acute SDH than EDH because it is associated with greater primary injury to brain parenchyma from high-energy impacts. Prompt recognition and intervention minimizes sec-ondary injury. The elderly


Surgery_Schwartz

Surgery_Schwartz. for acute SDH than EDH because it is associated with greater primary injury to brain parenchyma from high-energy impacts. Prompt recognition and intervention minimizes sec-ondary injury. The elderly patients with low admission GCS, or high postoperative ICP do poorly, with as few as 5% attaining functional recovery.18Chronic Subdural Hematoma Chronic SDH is a collection of blood breakdown products that is at least 2 to 3 weeks old. Acute hematomas are bright white (hyperdense) on CT scan for approximately 3 days, after which they fade to isodensity with brain, and then to hypodensity after 2 to 3 weeks. A true chronic SDH will be nearly as dark as CSF on CT. Traces of white are often seen due to small, recurrent hemorrhages into the col-lection. These small bleeds may expand the collection enough to make it symptomatic. This phenomenon is referred to as an acute-on-chronic SDH. Figure 42-9 demonstrates the CT appearance of an acute-on-chronic SDH. Vascularized mem-branes form within


Surgery_Schwartz

Surgery_Schwartz. enough to make it symptomatic. This phenomenon is referred to as an acute-on-chronic SDH. Figure 42-9 demonstrates the CT appearance of an acute-on-chronic SDH. Vascularized mem-branes form within the hematoma as it matures. These mem-branes may be the source of acute hemorrhage.Chronic SDHs often occur in patients without a clear his-tory of head trauma as they may arise from minor head injury. Alcoholics, the elderly, and patients on anticoagulation are at higher risk for developing chronic SDH. Patients may present with headache, seizure, confusion, contralateral hemiparesis, or coma.A chronic SDH >1 cm or any symptomatic SDH should be surgically drained. Unlike acute SDH, which consists of a thick, congealed clot, chronic SDH typically consists of a viscous fluid with the texture and dark brown color reminiscent of motor oil. A simple burr hole can effectively drain most chronic SDHs. However, the optimal treatment of chronic SDH remains con-troversial.19 Recent data suggest that


Surgery_Schwartz

Surgery_Schwartz. dark brown color reminiscent of motor oil. A simple burr hole can effectively drain most chronic SDHs. However, the optimal treatment of chronic SDH remains con-troversial.19 Recent data suggest that open craniotomy is effec-tive at reducing recurrence, but may be associated with more short-term complications.20 Most authorities agree that burr hole drainage should be attempted first to obviate the risks of formal craniotomy.21 A single burr hole placed over the dependent edge of the collection can be made, and the space is copiously irri-gated until the fluid is clear. A second, more anterior burr hole can then be placed if the collection does not drain satisfactorily due to containment by membranes. The procedure is converted to open craniotomy if the SDH is too congealed for irrigation drainage, the complex of membranes prevents effective drain-age, or persistent hemorrhage occurs that cannot be reached with bipolar cautery through the burr hole. The required surgi-cal prepping and


Surgery_Schwartz

Surgery_Schwartz. drainage, the complex of membranes prevents effective drain-age, or persistent hemorrhage occurs that cannot be reached with bipolar cautery through the burr hole. The required surgi-cal prepping and draping are always performed to allow simple conversion to craniotomy, and the scalp incision and burr holes are placed to allow easy incorporation into larger skin flaps.There are various strategies to prevent reaccumulation of blood. Subdural or subgaleal drains may be left in place for 1 to 2 days. Subdural drains have been shown to reduce the risk of recurrence, whereas corticosteroid use in this patient popula-tion has been associated with higher morbidity without benefit.20 Mild hydration and bedrest with the head of the bed flat may Figure 42-9. Head computed tomography scan of an elderly patient with progressing left hemiplegia and lethargy, demonstrat-ing an acute-on-chronic subdural hematoma. History revealed that the patient sustained a fall 4 weeks before presentation.


Surgery_Schwartz

Surgery_Schwartz. an elderly patient with progressing left hemiplegia and lethargy, demonstrat-ing an acute-on-chronic subdural hematoma. History revealed that the patient sustained a fall 4 weeks before presentation. Arrowheads outline the hematoma. The acute component is slightly denser and is seen as the hyperdense area in the dependent portion.Brunicardi_Ch42_p1827-p1878.indd 183801/03/19 7:16 PM 1839NEUROSURGERYCHAPTER 42encourage brain expansion. High levels of inspired oxygen may help draw nitrogen out of the cavity. Regardless of the strategy used, follow-up head CT scans are required postoperatively and approximately 1 month later to document resolution.Intraparenchymal Hemorrhage Isolated hematomas within the brain parenchyma are most often associated with hyper-tensive hemorrhage or arteriovenous malformations (AVMs). Bleeding may occur in a contused area of brain. Mass effect from developing hematomas may present as a delayed neuro-logic deficit. Delayed traumatic intracerebral


Surgery_Schwartz

Surgery_Schwartz. arteriovenous malformations (AVMs). Bleeding may occur in a contused area of brain. Mass effect from developing hematomas may present as a delayed neuro-logic deficit. Delayed traumatic intracerebral hemorrhage is most likely to occur within the first 24 hours. Patients with contusion on the initial head CT scan should be reimaged 24 hours after the trauma to document stable pathology. Indica-tions for craniotomy include: any clot volume >50 cm3 or a clot volume >20 cm3 with referable neurologic deterioration (GCS 6–8) and associated midline shift >5 mm or basal cistern compression.22Pneumocephalus Pneumocephalus, or air in the intracranial cavity, is commonly seen in neurosurgical patients following head trauma or following intracranial surgery.23 Pneumoceph-alus requires a defect in the skull that allows air to enter the intracranial cavity. This may occur following may represent an iatrogenic defect created following cranial surgery or follow-ing head trauma. Approximately 66% of


Surgery_Schwartz

Surgery_Schwartz. skull that allows air to enter the intracranial cavity. This may occur following may represent an iatrogenic defect created following cranial surgery or follow-ing head trauma. Approximately 66% of postcraniotomy CT scans demonstrate some extent of pneumocephalus.24 The iden-tification of pneumocephalus following head trauma can offer important clues about the extent of injury, such as the presence of skull based fractures or a CSF leak. In rare cases, pneumo-cephalus can also be seen in association with skull based tumors or infections.A tension pneumocephalus occurs when the intracranial air pocket is under tension which can result in life threatening herniation if left untreated. This is a neurosurgical emergency and requires an urgent neurosurgical consultation. Two radio-graphic features have been associated with a tension pneumo-cephalus25 (Fig. 42-10). First, the “Mount Fuji” sign, where the air pocket separates the frontal lobes and widens the inter-hemi-spheric fissure,


Surgery_Schwartz

Surgery_Schwartz. features have been associated with a tension pneumo-cephalus25 (Fig. 42-10). First, the “Mount Fuji” sign, where the air pocket separates the frontal lobes and widens the inter-hemi-spheric fissure, mimicking the silhouette of Mount Fuji. Second, the “air bubble” sign, where there are multi-focal pockets of air throughout the subarachnoid cisterns, putatively within the sub-arachnoid space. These radiographic findings are helpful clues; however, the diagnosis of tension pneumocephalus also requires a worsening neurological exam consistent with increased intra-cranial pressure and impending herniation. A burr hole may be used to relieve intracranial pressure per the discretion of the neurosurgical team.When not associated with tension dynamics, the clinical significance and management of pneumocephalus depends on the underlying mechanism. There are thought to be two major mechanisms by which pneumocephalus develops.24 First, the “ball valve” mechanism involves the passage of air into


Surgery_Schwartz

Surgery_Schwartz. pneumocephalus depends on the underlying mechanism. There are thought to be two major mechanisms by which pneumocephalus develops.24 First, the “ball valve” mechanism involves the passage of air into the intracranial cavity during periods of positive pressure, whereby the defect in the skull acts as a one-way valve. In these cases, management involves avoiding positive pressure ventilation, and laying the head of the bed flat to minimize air traveling upwards into the cranial cavity. Second, the “inverted bottle” mechanism involves air entering the intracranial space due to a negative pressure gradient created by the drainage of CSF. In most cases, drainage occurs through a traumatic or iatrogenic CSF leak, but it may also occur through ventricular or lumbar drainage. In these cases, management should be focused on minimizing CSF drainage through the defect. If the CSF leak is at the skull base, as is the case following basilar skull fractures, or those involving the mastoid air


Surgery_Schwartz

Surgery_Schwartz. management should be focused on minimizing CSF drainage through the defect. If the CSF leak is at the skull base, as is the case following basilar skull fractures, or those involving the mastoid air cells, then the head of bed must be elevated so as to reduce hydrostatic pressure in the ven-tricular CSF fluid column, and controlled CSF diversion can be performed using an extraventricular or lumbar drain (see “Skull Fractures” for further discussion). Definitive repair of the skull-based defect can also be considered, but this is often done on an elective basis. In general, nontension pneumocephalus will resolve on its own with time as it is resorbed into the blood stream. Supplemental 100% oxygen may be used to increase the rate of resorption by increasing the diffusion gradient of nitro-gen-predominant intracranial air pocket and the blood stream.26Management of Traumatic Brain Injury General Medical Management Several medical steps may be taken to minimize secondary injury and the


Surgery_Schwartz

Surgery_Schwartz. intracranial air pocket and the blood stream.26Management of Traumatic Brain Injury General Medical Management Several medical steps may be taken to minimize secondary injury and the systemic con-sequences of head injury. Patients with a documented CHI and evidence of intracranial hemorrhage or a depressed skull fracture should receive a 1 g Keppra loading dose, followed by 1 week of therapeutic maintenance Keppra, typically 500 mg twice a day. Antiseizure prophylaxis has been shown to decrease the incidence of early posttraumatic seizures.27 There is no evi-dence to support long-term use of prophylactic antiepileptic agents. Even though the clinical studies supporting early anti-seizure prophylaxis used phenytoin, Keppra is typically used in clinical practice due to a more favorable side effect profile. Blood glucose levels should be closely monitored by free blood sugar checks and controlled with sliding scale insulin. Fevers also should be evaluated and controlled with


Surgery_Schwartz

Surgery_Schwartz. side effect profile. Blood glucose levels should be closely monitored by free blood sugar checks and controlled with sliding scale insulin. Fevers also should be evaluated and controlled with antipyretics, as well as source-directed therapy when possible. Hyperglycemia and hyperthermia are toxic to injured neurons and contribute to secondary injury. Head-injured patients have an increased prevalence of peptic ulceration and GI bleeding. Peptic ulcers occurring in patients with head injury or high ICP are referred to as Cushing’s ulcers. Ulcer prophylaxis should be used. Com-pression stockings or athrombic pumps should be used when the patient cannot be mobilized rapidly for prophylaxis of deep venous thrombosis.Steroids and Traumatic Brain Injury Per a level 1 recom-mendation (high-quality evidence) from the Brain Trauma Foundation,10 steroids are not recommended for the management of TBI or reduction of elevated ICP. Also, high-dose methyl-prednisolone is contraindicated in severe


Surgery_Schwartz

Surgery_Schwartz. evidence) from the Brain Trauma Foundation,10 steroids are not recommended for the management of TBI or reduction of elevated ICP. Also, high-dose methyl-prednisolone is contraindicated in severe TBI. A large random-ized controlled trial (CRASH; n = 9673, 6-month follow-up,28 Figure 42-10. CT image on left illustrates “Mt. Fuji sign” (arrow-head) and intraparnchymal air (arrow). CT image on R illustrates brain herniation into the ethmoid sinus (arrowhead).Brunicardi_Ch42_p1827-p1878.indd 183901/03/19 7:16 PM 1840SPECIFIC CONSIDERATIONSPART IIdemonstrated an increased risk of 6-month mortality in severe TBI (GCS 3–8) that received methylprednisolone (47%), as compared to placebo (42%, P = 0.0024). This effect was also present when analyzing TBI of all severity levels (25.7% meth-ylprednisolone vs. 22.3% placebo, P = 0.0001).Blood Pressure Management Blood pressure management in TBI is a complex issue. On one hand, hypotension results in hypoperfusion that may worsen brain injury