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Surgery_Schwartz. 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 that occurs follow-ing TBI. On another hand, hypertension may result in expansion of intracranial hematomas that are often seen in TBI.There is clear evidence from retrospective studies, that frank hypotension (SBP <90 mmHg) is associated with increased mortality in TBI, particularly in the prehospital setting and during resuscitation.29 A large retrospective cohort study (n = 15,733) identified hypotension thresholds that were associ-ated with an increased risk of mortality in patients with TBI of varying age.30 Based on these data, the Brain Trauma Founda-tion guidelines10 provide a level III (low-quality) recommenda-tion that maintaining systolic blood pressures >100 mmHg (ages 50–69 years), or >110 mmHg (ages 15–49 years or >70 years) may be considered to reduce mortality and improve outcomes.


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Surgery_Schwartz. recommenda-tion that maintaining systolic blood pressures >100 mmHg (ages 50–69 years), or >110 mmHg (ages 15–49 years or >70 years) may be considered to reduce mortality and improve outcomes. More recently, a large retrospective study31 demonstrated a dose-dependent relation between the duration of prehospital hypotension and increased mortality in patients with TBI, such that a 10-point increase in systolic blood pressure across a broad range (40–119 mmHg) was associated with an 18.8% decrease in adjusted odds of inhospital mortality. These results suggest that having a single “hypotension threshold” may not be suf-ficient in management of TBI and may require more aggressive management than currently employed. Furthermore, an impor-tant and underappreciated consideration in blood pressure man-agement is the baseline blood pressure of the patient. Future studies should assess blood pressure management goals that are tailored to each individual patient’s baseline blood pressure.On the


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Surgery_Schwartz. man-agement is the baseline blood pressure of the patient. Future studies should assess blood pressure management goals that are tailored to each individual patient’s baseline blood pressure.On the other hand, hypertension in TBI may have impli-cations for intracranial hematoma expansion. It is common in clinical practice to recommend that systolic blood pressures are maintained <160 mmHg to mitigate the risk of hematoma expan-sion. Evidence supporting this practice is largely extrapolated from non-TBI patients. A small retrospective study (n = 69)32 demonstrated an increased risk of postcraniotomy intracranial hematoma in patients with intraoperative hypertension (62% vs. 34% controls, P <0.001), and postoperative hyperten-sion in the first 12 hours after surgery (62% vs. 25% controls, P <0.001). A recent large retrospective study in patients with anti-coagulant-associated intracranial hematoma demonstrated that lowering SBP to less than 160 mmHg within 4 hours of admis-sion was


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Surgery_Schwartz. P <0.001). A recent large retrospective study in patients with anti-coagulant-associated intracranial hematoma demonstrated that lowering SBP to less than 160 mmHg within 4 hours of admis-sion was associated with a reduced risk of hematoma expan-sion (n = 691, 33.1% <160 mmHg vs. 52.4 % in ≥160 mmHg; P <.001).33 However, there are no specific recommendations from the Brain Trauma Foundation on a hypertension threshold to avoid in patients with traumatic intracranial hematoma.Anticoagulation Reversal and Prophylaxis Patients with intracranial hematoma who are on anticoagulation for car-diovascular indications (atrial fibrillation, cardiac stents, or mechanical valves) or stroke prevention present a challenging population. Anticoagulation reversal is important to reduce the risk of hematoma expansion; however, anticoagulant reversal is also associated with thrombotic cardiovascular complications. A recent retrospective study in patients with nontraumatic, oral-anticoagulant–associated


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Surgery_Schwartz. expansion; however, anticoagulant reversal is also associated with thrombotic cardiovascular complications. A recent retrospective study in patients with nontraumatic, oral-anticoagulant–associated intracranial hematoma showed that lowering the INR to <1.3 within 4 hours of admission was an independent predictor of hematoma expansion (n = 853; 19.8% vs. 41.5% in INR of ≥1.3; P <.001). Furthermore, this study showed that the risk of ischemic complications was greater in patients that were not restarted on oral anticoagulation as com-pared to those that were subsequently restarted (n = 719; 5.2% vs. 15%, no restart, P <0.001); however, they did not observe a significant increase in the risk of hemorrhage with anticoagula-tion restart (n = 719; 8.1%, vs. 6.6%, P = 0.48). The median time to anticoagulation restart was 30 days after discharge (inter-quartile range 18–65), as such, these data do not speak to risks and benefits of restarting anticoagulation in the acute post-bleed interval.


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Surgery_Schwartz. restart was 30 days after discharge (inter-quartile range 18–65), as such, these data do not speak to risks and benefits of restarting anticoagulation in the acute post-bleed interval. It is important to note that the risks and benefits of restarting anticoagulation will vary based on the individual patient and the patient’s indications for anticoagulation (e.g., mechanical heart valve vs. atrial fibrillation). As such, close collaboration between the neurosurgery and cardiology teams are important in optimizing a management strategy for these patients.Anticoagulation prophylaxis for prevention of venous thrombosis also involves a risk-benefit analysis. Per a level III (low-quality) recommendation of Brain Trauma Foundation Guidelines,10 anticoagulation prophylaxis with low-molecular-weight heparin or low-dose unfractionated heparin may be used to reduce the risk of venous thrombosis, even though it is associ-ated with an increased risk of intracranial hematoma expansion. It may be


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Surgery_Schwartz. heparin or low-dose unfractionated heparin may be used to reduce the risk of venous thrombosis, even though it is associ-ated with an increased risk of intracranial hematoma expansion. It may be reasonable to initiate prophylactic anticoagulation 24 hours after an intracranial hematoma is deemed to be stable. A single-center retrospective study (n = 236) found that such a strategy was associated with a decreased risk of DVT (0% vs. 5.6% (n = 6), P <0.001), but did not observe significant differ-ences in the rates of pulmonary embolism (0.78% (n = 1) vs. 3.74% (n = 4), P = 0.18) or intracranial hematoma expansion (0.7% [1] vs. 2.8% [3], P = 0.3). However, because of the low rate of clinical events observed in this series, the study may have been underpowered to identify small differences in pulmonary embolism or hematoma expansion.Indications for Invasive Intracranial Monitoring In patients with severe TBI (GCS <8), the Brain Trauma Founda-tion guidelines endorse a level IIB


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Surgery_Schwartz. in pulmonary embolism or hematoma expansion.Indications for Invasive Intracranial Monitoring In patients with severe TBI (GCS <8), the Brain Trauma Founda-tion guidelines endorse a level IIB recommendation (low-quality of evidence) for ICP and cerebral perfusion pressure (CPP) to reduce short-term mortality (within 2 weeks of hospitalization). They also provide level IIB recommendations for treating ICP >22 mmHg and treating CPP level between 60 and 70 mmHg to optimize outcomes. These recommendations are supported by a recent retrospective cohort study (n = 459)34 that identified ICP and CPP thresholds that best discriminated between survi-vors and nonsurvivors in severe TBI, and also between survivors with “poor” and “favorable’ outcomes (Glasgow Outcome Scale 1–3 vs. 4–6). A large, multicenter randomized controlled trial performed in 6 hospitals in Equador and Bolivia did not sup-port the claim that intracranial monitoring in severe TBI results in improved clinical outcomes.


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Surgery_Schwartz. multicenter randomized controlled trial performed in 6 hospitals in Equador and Bolivia did not sup-port the claim that intracranial monitoring in severe TBI results in improved clinical outcomes. Chestnut et al in 2012 did not observe a significant difference in mortality or favorable out-comes (as assessed by the Glasgow Outcome Scale) when severe TBI patients were managed with an intracranial monitor (n = 56), or with imaging and clinical exam (n = 53, P = 0.43). Advanced multimodal monitoring such as brain tissue oxygen (PbrO2) mon-itoring, jugular bulb monitoring of arteriovenous oxygen content difference (AVDO2), cerebral autoregulation with TCD, and micro dialysis are under active investigation. Only jugular bulb monitoring of AVDO2 is associated with a level III (poor-quality evidence) recommendation to guide management in severe TBI. Brunicardi_Ch42_p1827-p1878.indd 184001/03/19 7:16 PM 1841NEUROSURGERYCHAPTER 42The Brain Tissue Oxygen Monitoring in TBI (BOOST) trials are


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Surgery_Schwartz. recommendation to guide management in severe TBI. Brunicardi_Ch42_p1827-p1878.indd 184001/03/19 7:16 PM 1841NEUROSURGERYCHAPTER 42The Brain Tissue Oxygen Monitoring in TBI (BOOST) trials are actively investigating the added benefit of brain tissue oxygen-ation beyond intracranial pressure monitoring in severe TBI.Decompressive Craniectomy for Severe TBI Decompressive craniectomy can be performed to relieve intracranial pressure associated with diffuse cerebral edema in cases of severe TBI without mass lesions (e.g., extra-axial hematoma). This is a controversial issue as there is a paucity of high-quality evi-dence providing clear support for or against this intervention. The DECRA trial (a multicenter, randomized, controlled trial, n = 155) compared bifrontal decompressive craniectomy to medical management for the treatment of patients with severe TBI and elevated intracranial pressure refractory to first-tier therapies (ICP >20 mmHg for at least 15 minutes within an hour). They


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Surgery_Schwartz. to medical management for the treatment of patients with severe TBI and elevated intracranial pressure refractory to first-tier therapies (ICP >20 mmHg for at least 15 minutes within an hour). They found no significant difference in mortality at six months, and found that functional outcomes (as measured by the Extended Glasgow Outcome Scale) were worse in patients who underwent surgery. They found a clear improvement in ICP and number of days in the ICU in patients that underwent surgery as compared to medical management. Of note, they used an intention-to-treat analysis, such that 18% of patients in the medical management group underwent a delayed cra-niotomy as a life-saving procedure. More recently, the RES-CUE-ICP trial36 (a multicenter, randomized, controlled trial, n = 408) compared decompressive craniotomy and ongoing medical care in patients with severe TBI (without mass lesions) with elevated ICP (>25 mmHg) refractory to firstand second-tier interventions (medical management


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Surgery_Schwartz. decompressive craniotomy and ongoing medical care in patients with severe TBI (without mass lesions) with elevated ICP (>25 mmHg) refractory to firstand second-tier interventions (medical management and ventriculostomy). Patients were randomized to either receive a barbiturate infu-sion (medical group) or undergo decompressive craniotomy (surgery group; unilateral hemicraniectomy vs. bifrontal crani-otomy depending on degree of bilateral swelling and surgeon discretion). Again, they used an intention-to-treat analysis such that 37% of patients of the medical group underwent decom-pressive hemicraniectomy. At 6 months, decompressive crani-ectomy in patients with traumatic brain injury and refractory intracranial hypertension resulted in lower mortality and higher rates of vegetative state, lower severe disability, and upper severe disability than medical care. The rates of moderate dis-ability and good recovery were similar in the two groups. The recent Brain Trauma Foundation


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Surgery_Schwartz. state, lower severe disability, and upper severe disability than medical care. The rates of moderate dis-ability and good recovery were similar in the two groups. The recent Brain Trauma Foundation Guidelines offer a level II (moderate-quality) recommendation against performing a bifrontal decompressive hemicraniectomy to improve func-tional outcomes at 6 months in patients with severe TBI with diffuse injury and no mass lesions, and with elevated ICP that is medically refractory. They note that this procedure has been demonstrated to reduce time in the ICU and ICP. However, they have not made an updated recommendation since the results of the RESCUE-ICP trial have been published.The results of the DECRA and RESCUE-ICP trials suggest caution and careful consideration prior to perform-ing decompressive craniotomy in treating severe TBI without mass lesions. There is now evidence that this procedure can be lifesaving and reduce mortality at 6 months; however, it is not clear that the


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Surgery_Schwartz. decompressive craniotomy in treating severe TBI without mass lesions. There is now evidence that this procedure can be lifesaving and reduce mortality at 6 months; however, it is not clear that the survivors have a favorable functional outcome (as grossly measured by the Extended Glasgow Outcome Scale). By improving ICP and reducing time in the ICU, it may hasten the recovery process by allowing patients to begin rehabilita-tion earlier. Also, several unanswered questions remain. For example, might outcomes be improved if decompressive cra-niectomy was performed earlier, prior to the patient develop-ing refractory ICP, and presumably secondary brain injury? As such, the decision of whether or not to perform decompressive craniotomy must be carefully considered within the context of each individual patient’s clinical scenario, the patient’s avail-able social support system, and the family’s disposition and goals of care.Vascular Injury. Trauma to the head or neck may cause damage to


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Surgery_Schwartz. individual patient’s clinical scenario, the patient’s avail-able social support system, and the family’s disposition and goals of care.Vascular Injury. Trauma to the head or neck may cause damage to the carotid or vertebrobasilar systems. Generally, dissection refers to violation of the vessel wall intima. Blood at arterial pressures can then open a plane between the intima and media, within the media, or between the media and adventitia. The newly created space within the vessel wall is referred to as the false lumen. Tissue or organs supplied by dissected ves-sels may subsequently be injured in several ways. Expansion of the hematoma within the vessel wall can lead to narrowing of the true vessel lumen and reduction or cessation of distal blood flow. Slow-flowing or stagnant blood within the false lumen exposed to thrombogenic vessel wall elements may thrombose. Pieces of thrombus may then detach and cause distal embolic arterial occlusion. Also, the remaining partial-thickness


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Surgery_Schwartz. the false lumen exposed to thrombogenic vessel wall elements may thrombose. Pieces of thrombus may then detach and cause distal embolic arterial occlusion. Also, the remaining partial-thickness vessel wall may rupture, damaging adjacent structures.Traumatic dissection may occur in the carotid artery (ante-rior circulation) or the vertebral or basilar arteries (posterior cir-culation). Dissections may be extradural or intradural. Intradural dissection can present with subarachnoid hemorrhage (SAH). Traditional angiography remains the basis of diagnosis and characterization of arterial dissection. Angiographic abnormali-ties include stenosis of the true lumen, or “string-sign,” visible intimal flaps, and the appearance of contrast in the false lumen. Four-vessel cerebral angiography should be performed when suspicion of dissection exists.Historically, patients with documented arterial dissec-tion have been anticoagulated with heparin and then warfarin to prevent thromboembolic stroke.


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Surgery_Schwartz. be performed when suspicion of dissection exists.Historically, patients with documented arterial dissec-tion have been anticoagulated with heparin and then warfarin to prevent thromboembolic stroke. Trauma patients often have concomitant absolute or relative contraindications to anticoagu-lation, complicating management. Antiplatelet therapy is often implemented in lieu of full anticoagulation, however, there is no randomized clinical trial comparing the two therapies.37 Consider surgical or interventional techniques for persisting embolic disease and for vertebral dissections presenting with SAH. Surgical options include vessel ligation and bypass graft-ing. Interventional radiology techniques include stenting and vessel occlusion. Occlusion techniques require sufficient col-lateral circulation to perfuse the vascular territory previously supplied by the occluded vessel.Carotid Dissection Carotid dissection may result from neck extension combined with lateral bending to the opposite


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Surgery_Schwartz. to perfuse the vascular territory previously supplied by the occluded vessel.Carotid Dissection Carotid dissection may result from neck extension combined with lateral bending to the opposite side, or trauma from an incorrectly placed shoulder belt tightening across the neck in a motor vehicle accident. Extension or bend-ing stretches the carotid over the bony transverse processes of the cervical vertebrae, while seat belt injuries cause direct trauma. Symptoms of cervical carotid dissection include con-tralateral neurologic deficit from brain ischemia, headache, and ipsilateral Horner’s syndrome from disruption of the sympa-thetic tracts ascending from the stellate ganglion on the surface of the carotid artery. The patient may complain of a bruit.Traumatic vessel wall injury to the portion of the carotid artery running through the cavernous sinus may result in a carotid-cavernous fistula (CCF). This creates a high-pressure, high-flow pathophysiologic blood flow pattern. CCFs


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Surgery_Schwartz. portion of the carotid artery running through the cavernous sinus may result in a carotid-cavernous fistula (CCF). This creates a high-pressure, high-flow pathophysiologic blood flow pattern. CCFs clas-sically present with pulsatile proptosis (the globe pulses out-ward with arterial pulsation), retro-orbital pain, and decreased visual acuity or loss of normal eye movement (due to damage Brunicardi_Ch42_p1827-p1878.indd 184101/03/19 7:16 PM 1842SPECIFIC CONSIDERATIONSPART IIto cranial nerves III, IV, and VI as they pass through the cav-ernous sinus). Symptomatic CCFs should be treated to preserve eye function. Fistulae may be closed by balloon occlusion using interventional neuroradiology techniques. Fistulae with wide necks are difficult to treat and may require total occlusion of the parent carotid artery.Vertebrobasilar Dissection Vertebrobasilar dissection may result from sudden rotation or flexion/extension of the neck, chiropractic manipulation, or a direct blow to the neck.


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Surgery_Schwartz. parent carotid artery.Vertebrobasilar Dissection Vertebrobasilar dissection may result from sudden rotation or flexion/extension of the neck, chiropractic manipulation, or a direct blow to the neck. Com-mon symptoms are neck pain, headache, and brain stem stroke or SAH. The risks and benefits of aspirin therapy are unclear when a vertebral dissection extends intracranially. The theoreti-cally increased friability of the vessel wall may increase the risk of SAH when coupled with an antiplatelet agent. Consultation of a stroke neurologist is recommended in this situation.Brain Death. Brain death occurs when there is an absence of signs of brain stem function or motor response to deep central pain in the absence of pharmacologic or systemic medical con-ditions that could impair brain function.Clinical Examination A neurologist, neurosurgeon, or inten-sivist generally performs the clinical brain death examination. Two examinations consistent with brain death 12 hours apart, or one


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Surgery_Schwartz. function.Clinical Examination A neurologist, neurosurgeon, or inten-sivist generally performs the clinical brain death examination. Two examinations consistent with brain death 12 hours apart, or one examination consistent with brain death followed by a consistent confirmatory study generally is sufficient to declare brain death (see following paragraphs). Hospital regulations and local laws regarding documentation should be followed closely.Establish the absence of complicating conditions before beginning the examination. The patient must be normotensive, euthermic, and oxygenating well. The patient may not be under the effects of any sedating or paralytic drugs.Documentation of no brain stem function requires the fol-lowing: nonreactive pupils; lack of corneal blink, oculocephalic (doll’s eyes), oculovestibular (cold calorics) reflexes; and loss of drive to breathe (apnea test). The apnea test demonstrates no spontaneous breathing even when Paco2 is allowed to rise above 60


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Surgery_Schwartz. (doll’s eyes), oculovestibular (cold calorics) reflexes; and loss of drive to breathe (apnea test). The apnea test demonstrates no spontaneous breathing even when Paco2 is allowed to rise above 60 mmHg.Deep central painful stimuli are provided by bilateral forceful twisting pinch of the supraclavicular skin and pressure to the medial canthal notch. Pathologic responses such as flexor or extensor posturing are not compatible with brain death. Spi-nal reflexes to peripheral pain, such as triple flexion of the lower extremities, are compatible with brain death.Confirmatory Studies Confirmatory studies are performed after a documented clinical examination consistent with brain death. A study consistent with brain death may obviate the need to wait 12 hours for a second examination. This is especially important when the patient is a potential organ donor, as brain-dead patients often have progressive hemodynamic instability. Lack of cerebral blood flow consistent with brain death may be


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Surgery_Schwartz. especially important when the patient is a potential organ donor, as brain-dead patients often have progressive hemodynamic instability. Lack of cerebral blood flow consistent with brain death may be documented by cerebral angiography or technetium radio-nuclide study. A “to-and-fro” pattern on transcranial Doppler ultrasonography indicates no net forward flow through the cere-bral vasculature, consistent with brain death. An electroenceph-alogram (EEG) documenting electrical silence has been used but generally is not favored because there is often significant artifact which impairs interpretation.Spine TraumaThe spine is a complex biomechanical structure. The spine pro-vides structural support for the body as the principal compo-nent of the axial skeleton, while protecting the spinal cord and nerve roots. Trauma may fracture bones or cause ligamentous disruption. Often, bone and ligament damage occur together. Damage to these elements reduces the strength of the spine and may cause


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Surgery_Schwartz. and nerve roots. Trauma may fracture bones or cause ligamentous disruption. Often, bone and ligament damage occur together. Damage to these elements reduces the strength of the spine and may cause instability, which compromises both supportive and protective functions. Spine trauma may occur with or without neurologic injury.Neurologic injury from spine trauma is classified as either incomplete or complete. If there is some residual motor or sensory neurologic function below the level of the lesion, as assessed by clinical examination, the injury is defined as incom-plete.38 A patient with complete neurologic dysfunction persist-ing 24 hours after injury has a very low probability of return of function in the involved area.Neurologic injury from spine trauma may occur immedi-ately or in delayed fashion. Immediate neurologic injury may be due to direct damage to the spinal cord or nerve roots from pen-etrating injuries, especially from stab wounds or gunshots. Blunt trauma may transfer


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Surgery_Schwartz. fashion. Immediate neurologic injury may be due to direct damage to the spinal cord or nerve roots from pen-etrating injuries, especially from stab wounds or gunshots. Blunt trauma may transfer sufficient force to the spine to cause acute disruption of bone and ligament, leading to subluxation, which is a shift of one vertebral element in relation to the adjacent level. Subluxation decreases the size of the spinal canal and neu-ral foramina and causes compression of the cord or roots. Such neural impingement can also result from retropulsion of bone fragments into the canal during a fracture. Transection, crush injury, and cord compression impairing perfusion are mecha-nisms leading to SCI. Delayed neurologic injury may occur dur-ing transportation, examination of an improperly immobilized patient, or during a hypotensive episode.The Mechanics of Spine Trauma. Trauma causes a wide variety of injury patterns in the spine due to its biomechanical complexity. A mechanistic approach


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Surgery_Schwartz. patient, or during a hypotensive episode.The Mechanics of Spine Trauma. Trauma causes a wide variety of injury patterns in the spine due to its biomechanical complexity. A mechanistic approach facilitates an understand-ing of the patterns of injury, as there are only a few types of forces that can be applied to the spine. Although these forces are discussed individually, they often occur in combination. Several of the most common injury patterns are then presented to illus-trate the clinical results of these forces applied at pathologically high levels.Flexion/Extension Bending the head and body forward into a fetal position flexes the spine. Flexion loads the spine anteriorly (the vertebral bodies) and distracts the spine posteriorly (the spi-nous process and interspinous ligaments). High flexion forces occur during front-end motor vehicle collisions, and backward falls when the head strikes first. Arching the neck and back extends the spine. Extension loads the spine posteriorly and


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Surgery_Schwartz. flexion forces occur during front-end motor vehicle collisions, and backward falls when the head strikes first. Arching the neck and back extends the spine. Extension loads the spine posteriorly and distracts the spine anteriorly. High extension forces occur dur-ing rear-end motor vehicle collisions (especially if there is no headrest), frontward falls when the head strikes first, or diving into shallow water.Compression/Distraction Force applied along the spinal axis (axial loading) compresses the spine. Compression loads the spine anteriorly and posteriorly. High compression forces occur when a falling object strikes the head or shoulders, or when landing on the feet, buttocks, or head after a fall from height. A pulling force in line with the spinal axis distracts the spine. Dis-traction unloads the spine anteriorly and posteriorly. Distraction forces occur during a hanging, when the chin or occiput strikes an object first during a fall, or when a passenger submarines under a loose


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Surgery_Schwartz. unloads the spine anteriorly and posteriorly. Distraction forces occur during a hanging, when the chin or occiput strikes an object first during a fall, or when a passenger submarines under a loose seat belt during a front-end motor vehicle collision.Rotation Force applied tangential to the spinal axis rotates the spine. Rotation depends on the range of motion of interverte-bral facet joints. High rotational forces occur during off-center Brunicardi_Ch42_p1827-p1878.indd 184201/03/19 7:16 PM 1843NEUROSURGERYCHAPTER 42impacts to the body or head or during glancing automobile accidents.Patterns of Injury. Certain patterns of injury resulting from combinations of the previously mentioned forces occur com-monly and should be recognized during plain film imaging of the spine. Always completely evaluate the spine. A patient with a spine injury at one level has a significant risk for additional injuries at other levels.Cervical The cervical spine is more mobile than the thoraco-lumbar


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Surgery_Schwartz. evaluate the spine. A patient with a spine injury at one level has a significant risk for additional injuries at other levels.Cervical The cervical spine is more mobile than the thoraco-lumbar spine. Stability comes primarily from the multiple liga-mentous connections of adjacent vertebral levels. Disruption of the cervical ligaments can lead to instability in the absence of fracture. The mass of the head transmits significant forces to the cervical spine during abrupt acceleration or deceleration, increasing risk for injury.Jefferson Fracture A Jefferson fracture is a bursting fracture of the ring of C1 (the atlas) due to compression forces. There are usually two or more fractures through the ring of C1. The open-mouth odontoid view may show lateral dislocation of the lateral masses of C1. The rule of Spence states that 7 mm or greater combined dislocation indicates disruption of the transverse liga-ment. The transverse ligament stabilizes C1 with respect to C2. Jefferson fractures


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Surgery_Schwartz. C1. The rule of Spence states that 7 mm or greater combined dislocation indicates disruption of the transverse liga-ment. The transverse ligament stabilizes C1 with respect to C2. Jefferson fractures dislocated <7 mm usually are treated with a rigid collar, while those dislocated 7 mm or greater usually are treated with a halo vest. Surgical intervention is not indicated.Odontoid Fractures The odontoid process, or dens, is the large ellipse of bone arising anteriorly from C2 (the axis) and projecting up through the ring of C1 (the atlas). Several strong ligaments connect the dens to C1 and to the base of the skull. Odontoid fractures usually result from flexion forces. Odontoid fractures are classified as type I, II, or III. A type I fracture involves the tip only. A type II fracture passes through the base of the odontoid process. A type III fracture passes through the body of C2. Types II and III are considered unstable and should be externally immobilized or fused surgically.


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Surgery_Schwartz. passes through the base of the odontoid process. A type III fracture passes through the body of C2. Types II and III are considered unstable and should be externally immobilized or fused surgically. Surgery often is undertaken for widely displaced fractures (poor chance of fus-ing) and for those that fail external immobilization. Type I frac-tures usually fuse with external immobilization only.Hangman’s Fracture Traditionally considered a hyperexten-sion/distraction injury from placement of the noose under the angle of the jaw, hangman’s fractures also may occur with hyperextension/compression, as with diving accidents, or hyper-flexion. The injury is defined by bilateral C2 pars interarticularis fractures. The pars interarticularis is the bone between superior and inferior facet joints. Thus, the posterior bony connection between C1 and C3 is lost. Hangman’s fractures heal well with external immobilization. Surgery is indicated if there is spinal cord compression or after failure of


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Surgery_Schwartz. Thus, the posterior bony connection between C1 and C3 is lost. Hangman’s fractures heal well with external immobilization. Surgery is indicated if there is spinal cord compression or after failure of external immobilization.Jumped Facets—Hyperflexion Injury The facet joints of the cervical spine slope forward. In a hyperflexion injury, the supe-rior facet can “jump” over the inferior facet of the level above if the joint capsule is torn. Hyperflexion/rotation can cause a unilateral jumped facet, whereas hyperflexion/distraction leads to bilateral jumped facets. Patients with unilateral injury usually are neurologically intact. Those with bilateral injury, however, typically suffer from spinal cord damage, since the anteropos-terior diameter of the spinal canal is compromised by bilateral injury, leading to spinal cord compression (Fig. 42-11).Thoracolumbar The thoracic spine is stabilized significantly by the rib cage. The lumbar spine has comparatively large vertebrae. Thus, the


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Surgery_Schwartz. injury, leading to spinal cord compression (Fig. 42-11).Thoracolumbar The thoracic spine is stabilized significantly by the rib cage. The lumbar spine has comparatively large vertebrae. Thus, the thoracolumbar spine has a higher thresh-old for injury than the cervical spine. A three-column model is useful for categorizing thoracolumbar injuries.39 The anterior longitudinal ligament and the anterior half of the vertebral body constitute the anterior column. The posterior half of the ver-tebral body and the posterior longitudinal ligament constitute the middle column. The pedicles, facet joints, laminae, spinous processes, and interspinous ligaments constitute the posterior column.Compression Fracture Compression fracture is a compression/flexion injury causing failure of the anterior column only. It is stable and not associated with neurologic deficit, although the patient may still have significant pain (Fig. 42-12).Burst Fracture Burst fracture is a pure axial compression injury


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Surgery_Schwartz. only. It is stable and not associated with neurologic deficit, although the patient may still have significant pain (Fig. 42-12).Burst Fracture Burst fracture is a pure axial compression injury causing failure of the anterior and middle columns. It is unstable, and perhaps half of patients have neurologic deficit due to compression of the cord or cauda equina from bone frag-ments retropulsed into the spinal canal.Chance Fracture Chance fracture is a flexion-distraction injury causing failure of the middle and posterior columns, sometimes with anterior wedging. Typical injury is from a lap seat-belt hyperflexion with associated abdominal injury. It often is unsta-ble and associated with neurologic deficit.Fracture-Dislocation Fracture-dislocation is failure of the anterior, middle, and posterior columns caused by flexion/dis-traction, shear, or compression forces. Neurologic deficit can result from retropulsion of middle column bone fragments into the spinal canal, or from subluxation


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Surgery_Schwartz. columns caused by flexion/dis-traction, shear, or compression forces. Neurologic deficit can result from retropulsion of middle column bone fragments into the spinal canal, or from subluxation causing decreased canal diameter (Fig. 42-13).Initial Assessment and Management. The possibility of a spine injury must be considered in all trauma patients. A patient with no symptoms referable to neurologic injury, a normal neu-rologic examination, no neck or back pain, and a known mecha-nism of injury unlikely to cause spine injury is at minimal risk for significant injury to the spine. Victims of moderate or severe trauma, especially those with injuries to other organ systems, usually fail to meet these criteria or cannot be assessed ade-quately. The latter often is due to impaired sensorium or signifi-cant pain. Because of the potentially catastrophic consequences of missing occult spine instability in a neurologically intact patient, a high level of clinical suspicion should govern patient


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Surgery_Schwartz. pain. Because of the potentially catastrophic consequences of missing occult spine instability in a neurologically intact patient, a high level of clinical suspicion should govern patient care until completion of clinical and radiographic evaluation.The trauma patient should be kept on a hard, flat board with straps and pads used for immobilization. A hard cervical collar is kept in place. These steps minimize forces transferred through the spine and therefore decrease the chance of causing dislocation, subluxation, or neural compression during transport to the trauma bay. The patient is then moved from the board to a flat stretcher. The primary survey and resuscitation are com-pleted. Physical examination and initial X-rays follow.For the examination, approach the patient as described in “Neurologic Examination” earlier in this chapter. Evaluation for spine or SCI is easier and more informative in awake patients. If the patient is awake, ask if he or she recalls details of the nature


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Surgery_Schwartz. “Neurologic Examination” earlier in this chapter. Evaluation for spine or SCI is easier and more informative in awake patients. If the patient is awake, ask if he or she recalls details of the nature of the trauma, and if there was loss of consciousness, numbness, or inability to move any or all limbs. Assess motor function by response to commands or pain, as appropriate. Assess pinprick, light touch, and joint position, if possible. Determining the ana-tomically lowest level of intact sensation can pinpoint the level of the lesion along the spine. Testing sensation in an ascending fashion will allow the patient to better discern the true stimulus Brunicardi_Ch42_p1827-p1878.indd 184301/03/19 7:16 PM 1844SPECIFIC CONSIDERATIONSPART IIas opposed to determine when it is extinguished. Document muscle stretch reflexes, lower sacral reflexes (i.e., anal wink and bulbocavernosus), and rectal tone.American Spinal Injury Association Classification The American Spinal Injury Association


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Surgery_Schwartz. Document muscle stretch reflexes, lower sacral reflexes (i.e., anal wink and bulbocavernosus), and rectal tone.American Spinal Injury Association Classification The American Spinal Injury Association provides a method of clas-sifying patients with spine injuries. The classification indicates completeness and level of the injury and the associated deficit. A form similar to that shown in Fig. 42-14 should be available in the trauma bay and completed for any spine injury patient. The association also has worked to develop recommendations and guidelines to standardize the care of SCI patients in an effort to improve the quality of care.Neurologic Syndromes. Penetrating, compressive, or isch-emic cord injury can lead to several characteristic presentations Figure 42-11. A. Lateral cervical spine X-ray of an elderly woman who struck her head during a backward fall. Arrowhead points to jumped facets at C5–C6. Note the anterior displace-ment of the C5 body with respect to the C6 body. B.


Surgery_Schwartz

Surgery_Schwartz. spine X-ray of an elderly woman who struck her head during a backward fall. Arrowhead points to jumped facets at C5–C6. Note the anterior displace-ment of the C5 body with respect to the C6 body. B. Sagittal T2-weighted magnetic resonance imaging of the same patient, revealing compromise of the spinal canal and compression of the cord. Note the bright signal within the cord at the level of compression, indicating spinal cord injury. C. Lateral cervical spine X-ray of same patient after application of cervical trac-tion and manual reduction. Note restoration of normal alignment. D. Lateral cervical spine X-ray after posterior cervical fusion to restabilize the C5–C6 segment of the spine.ABCDBrunicardi_Ch42_p1827-p1878.indd 184401/03/19 7:16 PM 1845NEUROSURGERYCHAPTER 42Figure 42-12. A. Lateral lumbar spine X-ray showing a compres-sion fracture of L2. Arrowhead points to anterior wedge deformity. Note the posterior wall of the vertebral body has retained normal height and alignment.


Surgery_Schwartz

Surgery_Schwartz. Lateral lumbar spine X-ray showing a compres-sion fracture of L2. Arrowhead points to anterior wedge deformity. Note the posterior wall of the vertebral body has retained normal height and alignment. B. Axial computed tomography scan through the same fracture. Arrowhead demonstrates a transverse discontinu-ity in the superior endplate of the L2 body.ABFigure 42-13. Sagittal reconstruction of an axial fine-slice com-puted tomography scan through the lumbar spine demonstrating a severe fracture-dislocation through the body of L2.based on the anatomy of injury. The neurologic deficits may be deduced from the anatomy of the long sensory and motor tracts and understanding of their decussations (Fig. 42-15). Four pat-terns are discussed. First, injury to the entire cord at a given level results in anatomic or functional cord transection with total loss of motor and sensory function below the level of the lesion. The typical mechanism is severe traumatic vertebral subluxation reducing spinal


Surgery_Schwartz

Surgery_Schwartz. in anatomic or functional cord transection with total loss of motor and sensory function below the level of the lesion. The typical mechanism is severe traumatic vertebral subluxation reducing spinal canal diameter and crushing the cord. Second, injury to half the cord at a given level results in Brown-Séquard syndrome, with loss of motor control and proprioception ipsilat-erally and loss of nociception and thermoception contralaterally. The typical mechanism is a stab or gunshot wound. Third, injury to the interior gray matter of the cord in the cervical spine results in a central cord syndrome, with upper extremity worse than lower extremity weakness and various degrees of numbness. The typical mechanism is transient compression of the cervical cord by the ligamentum flavum buckling during traumatic neck hyperextension. This syndrome occurs in patients with preex-isting cervical stenosis. Fourth, injury to the ventral half of the cord results in the anterior cord syndrome, with


Surgery_Schwartz

Surgery_Schwartz. during traumatic neck hyperextension. This syndrome occurs in patients with preex-isting cervical stenosis. Fourth, injury to the ventral half of the cord results in the anterior cord syndrome, with paralysis and loss of nociception and thermoception bilaterally. The typical mechanism is an acute disc herniation or ischemia from anterior spinal artery occlusion.Studies. Anteroposterior and lateral plain films provide a rapid survey of the bony spine. Plain films detect fractures and dislo-cations well. Adequate visualization of the lower cervical and upper thoracic spine often is impossible because of the shoul-der girdle. Complete plain film imaging of the cervical spine includes an open-mouth view to assess the odontoid process and the lateral masses of C1. Fine-slice CT scan with sagittal and coronal reconstructions provides good detail of bony anatomy and is good for characterizing fractures seen on plain films, as well as visualizing C7–T1 when not well seen on plain films. MRI


Surgery_Schwartz

Surgery_Schwartz. and coronal reconstructions provides good detail of bony anatomy and is good for characterizing fractures seen on plain films, as well as visualizing C7–T1 when not well seen on plain films. MRI provides the best soft tissue imaging. Canal compromise from subluxation, acute disc herniations, or ligamentous disrup-tion is clearly seen. MRI also may detect EDHs or damage to the spinal cord itself, including contusions or areas of ischemia.Brunicardi_Ch42_p1827-p1878.indd 184501/03/19 7:16 PM 1846SPECIFIC CONSIDERATIONSPART IIIndications for Screening for Vascular Injury With Cer-vical Spine Trauma It is important to consider the pres-ence of blunt cerebrovascular injury in patents with cervical spine trauma; however, the specific indications for obtaining a screening CT angiography study are controversial. Many trauma centers rely on the Denver Criteria.40 These criteria indicate that screening should be employed for a cervical ver-tebral body or transverse foramen fracture,


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Surgery_Schwartz. study are controversial. Many trauma centers rely on the Denver Criteria.40 These criteria indicate that screening should be employed for a cervical ver-tebral body or transverse foramen fracture, subluxation, or ligamentous injury at any level, or any fracture at the level of C1–C3, among other indications such as concerning mecha-nism, Lefort mid-face fractures, or basilar fractures through the carotid canal. A recent single-center retrospective study41 (n = 1717 cervical spine fractures) found a higher risk of ver-tebral artery injury only in the setting of fractures of C1 and C2 (combined), those that involve the transverse foramen, or had significant subluxation. They did not find that “high-risk” cervical spine fractures as defined by the Denver Criteria were associated with an increased risk of blunt cerebrovascular injury. Based on these data, we feel that it is appropriate to use a more defined set of screening criteria as outlined by Lock-wood et al to reduce cost and


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Surgery_Schwartz. increased risk of blunt cerebrovascular injury. Based on these data, we feel that it is appropriate to use a more defined set of screening criteria as outlined by Lock-wood et al to reduce cost and contrast-exposure in patients with cervical spine fractures.Figure 42-14. The American Spinal Injury Association system for categorizing spinal cord injury patients according to level and degree of neurologic deficit.Dorsal column(touch, vibration)Corticospinal tract(upper motor)Anterior horn(lower motor)Spinothalmic tract(pain, temperature)TransectionCentral cordBrown-SequardAnterior spinal a.Figure 42-15. Spinal cord injury patterns. a. = artery. (Adapted with permission from Hoff J, Boland M: Neurosurgery, in Schwartz SI: Principles of Surgery, 7th ed., New York, NY: McGraw-Hill Education; 1999.)Brunicardi_Ch42_p1827-p1878.indd 184601/03/19 7:16 PM 1847NEUROSURGERYCHAPTER 42Definitive Management Spinal-Dose Steroids Several studies have investigated the use of methylprednilosone in


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Surgery_Schwartz. 1999.)Brunicardi_Ch42_p1827-p1878.indd 184601/03/19 7:16 PM 1847NEUROSURGERYCHAPTER 42Definitive Management Spinal-Dose Steroids Several studies have investigated the use of methylprednilosone in acute spinal cord injury. The National Acute Spinal Cord Injury studies (NASCIS I, II, and III) provided some support for the view that administration of high-dose methylprednilosone in acute spinal cord injury results in improved neurologic outcomes. A post-hoc analy-sis performed as part of NASCIS II demonstrated improved neurologic outcomes if methylprednilosone was administered within 8 hours of injury. A post-hoc analysis in NASCIS III showed improved outcomes at 6 weeks and 6 months, but not 1 year when methylprednilosone was administered within 3 and 8 hours of injury.42,43,44 However, these findings are tempered by the fact that these benefits were modest and only demonstrated in post-hoc analyses, and by the high rate of medical compli-cations associated with corticosteroid


Surgery_Schwartz

Surgery_Schwartz. these findings are tempered by the fact that these benefits were modest and only demonstrated in post-hoc analyses, and by the high rate of medical compli-cations associated with corticosteroid administration. All three NASCIS trials showed that methylprednilosone was associated with a higher rate of complications such as pneumonia, severe sepsis, and poor wound healing. A recent Cochrane review did not observe a significant increase in complications or mortal-ity associated with methylprednilosone administration in acute spinal cord injury, but did observe a trend towards this effect.45 Despite the lack of clear evidence on this issue, the most recent acute spinal cord injury guidelines provide a controversial level I recommendation against the use of corticosteroids in acute spinal cord injury.46 Some authors have argued for the use of methylprednilosone within 8 hours of acute spinal cord injury in carefully selected patients (e.g., young males that are less prone to medical


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Surgery_Schwartz. cord injury.46 Some authors have argued for the use of methylprednilosone within 8 hours of acute spinal cord injury in carefully selected patients (e.g., young males that are less prone to medical complications associated with corticosteroids47). Thus, clear consensus on the use of spinal-dose steroids does not exist.48 A decision to use or not use spinal-dose steroids may be dictated by local or regional practice patterns, especially given the legal liability issues surrounding SCI. Patients with gunshot or nerve root (cauda equina) injuries, or those who are pregnant, <14 years old, or on chronic steroids were excluded from the NASCIS studies and should not receive spinal-dose steroids. In addition to steroids, hypothermia for SCI has also received attention. There is even less evidence supporting the use of this treatment, and thus, it is not currently recommended.49Orthotic Devices Rigid external orthotic devices can stabilize the spine by decreasing range of motion and


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Surgery_Schwartz. evidence supporting the use of this treatment, and thus, it is not currently recommended.49Orthotic Devices Rigid external orthotic devices can stabilize the spine by decreasing range of motion and minimizing stress transmitted through the spine. Commonly used rigid cervical orthoses include Philadelphia and Miami-J collars. Cervical collars are inadequate for C1, C2, or cervicothoracic instability. Cervicothoracic orthoses brace the upper thorax and the neck, improving stabilization over the cervicothoracic region. Minerva braces improve high cervical stabilization by brac-ing from the upper thorax to the chin and occiput. Halo vest assemblies provide the most external cervical stabilization. Four pins are driven into the skull to lock the halo ring in position. Four posts arising from a tight-fitting rigid plastic vest immobilize the halo ring. Lumbar stabilization may be provided by thoracolumbosacral orthoses. A variety of compa-nies manufacture lines of spinal orthotics. A


Surgery_Schwartz

Surgery_Schwartz. from a tight-fitting rigid plastic vest immobilize the halo ring. Lumbar stabilization may be provided by thoracolumbosacral orthoses. A variety of compa-nies manufacture lines of spinal orthotics. A physician familiar with the technique should fit a halo vest. Assistance from a trained orthotics technician improves fitting and adjustment of the other devices.Surgery Neurosurgical intervention has two goals: decompres-sion of the spinal cord and nerve roots, and stabilization of the spine. When spinal cord injury is caused by a hyperflexiondistraction injury that results in cord compression and an unstable spine, both surgical decompression and fusion are typically required. However, in cases of a hyperextension injury causing central cord syndrome due to chronic cervical stenosis, surgi-cal decompression may be needed without the need for inter-nal fixation. In cases where there significant anterolisthesis (subaxial cervical jumped or perched facets), reduction of the fracture may be


Surgery_Schwartz

Surgery_Schwartz. decompression may be needed without the need for inter-nal fixation. In cases where there significant anterolisthesis (subaxial cervical jumped or perched facets), reduction of the fracture may be important for both decompression and stabili-zation. However, in some cases, reduction of the fracture may not be sufficient for decompression, and further decompressive surgery may still be needed.50Several controversial topics require consideration here. First, the timing of surgery has been a controversial topic. In the past, it has been suggested that patients with incomplete injury, or a deteriorating exam warrant emergent decompres-sion, whereas patients with complete injuries can undergo sur-gery in a nonemergent manner. It is important to appreciate the risks of taking a medically unstable patient to surgery, such as a polytrauma patient with hemorrhagic shock or a complete spinal cord injury patient in neurogenic shock. However, there are clear benefits to early surgical


Surgery_Schwartz

Surgery_Schwartz. unstable patient to surgery, such as a polytrauma patient with hemorrhagic shock or a complete spinal cord injury patient in neurogenic shock. However, there are clear benefits to early surgical decompression: it can allow early mobilization, aggressive nursing care, and physical ther-apy. Furthermore, a recent prospective cohort study found that the odds of observing a two-point increase in ASIA grade at 6 months was higher in patients that underwent surgery within 24 hours, as compared to those that underwent surgery after 24 hours.51 These data suggest that a subpopulation of patients may significantly benefit from early surgery; however, the char-acteristics of these patients were not described, suggesting a het-erogeneous population in terms of preoperative ASIA grade and imaging.In general, spine trauma patients with complete neurologic deficit, without any signs of recovery, or those without any neu-rologic deficits who have bony or ligamentous injury requiring open fixation,


Surgery_Schwartz

Surgery_Schwartz. general, spine trauma patients with complete neurologic deficit, without any signs of recovery, or those without any neu-rologic deficits who have bony or ligamentous injury requiring open fixation, may be medically stabilized before undergoing surgery. Surgical stabilization may be indicated for some inju-ries that would eventually heal with conservative treatment. Solid surgical stabilization may also allow a patient to be man-aged with a rigid cervical collar who would otherwise require halo-vest immobilization.Continued Care. Regional SCI centers with nurses, respira-tory therapists, pulmonologists, physical therapists, physiat-rists, and neurosurgeons specifically trained in caring for these patients may improve outcomes. Frequently encountered ICU issues include hypotension due to neurogenic shock (due to loss of sympathetic tone) and aspiration pneumonia. The recent guidelines recommend maintaining MAPs >85 for 7 days after injury.46 Chronically, prevention and treatment of


Surgery_Schwartz

Surgery_Schwartz. neurogenic shock (due to loss of sympathetic tone) and aspiration pneumonia. The recent guidelines recommend maintaining MAPs >85 for 7 days after injury.46 Chronically, prevention and treatment of deep venous thrombosis, autonomic hyperreflexia, and decubitus ulcer for-mation are important. Many patients with cervical or high tho-racic cord injuries require prolonged ventilatory support until the chest wall becomes stiff enough to provide resistance for diaphragmatic breathing. Patients with high cervical cord inju-ries (C4 or above) will often require permanent ventilatory sup-port. Patients should be transferred to SCI rehabilitation centers after stabilization of medical and surgical issues.Peripheral Nerve TraumaThe peripheral nervous system extends throughout the body and is subject to injury from a wide variety of trauma. Periph-eral nerves transmit motor and sensory information from the CNS to the body. An individual nerve may have pure motor, pure sensory, or mixed motor and


Surgery_Schwartz

Surgery_Schwartz. to injury from a wide variety of trauma. Periph-eral nerves transmit motor and sensory information from the CNS to the body. An individual nerve may have pure motor, pure sensory, or mixed motor and sensory functions. The key Brunicardi_Ch42_p1827-p1878.indd 184701/03/19 7:16 PM 1848SPECIFIC CONSIDERATIONSPART IIinformation-carrying structure of the nerve is the axon. The axon transmits information from the neuronal cell body and may measure from <1 mm to >1 m in length. Axons that travel a significant distance are often covered with myelin, which is a lipid-rich, electrically insulating sheath formed by Schwann cells. Myelinated axons transmit signals much more rapidly than unmyelinated axons because the voltage shifts and currents that define action potentials effectively jump from gap to gap over the insulated lengths of the axon.Axons, whether myelinated or unmyelinated, travel through a collagenous connective tissue known as endoneurium. Groups of axons and their endoneurium


Surgery_Schwartz

Surgery_Schwartz. gap to gap over the insulated lengths of the axon.Axons, whether myelinated or unmyelinated, travel through a collagenous connective tissue known as endoneurium. Groups of axons and their endoneurium form bundles known as fascicles. Fascicles run through a tubular collagenous tissue known as perineurium. Groups of fascicles are suspended in mesoneurium. Fascicles and their mesoneurium run through another tubular collagenous tissue known as epineurium. The epineurium and its contents form the nerve.There are four major mechanisms of injury to peripheral nerves. Nerves may be lacerated, stretched, compressed, or contused. Knives, passing bullets, or jagged bone fractures may lacerate nerves. Adjacent expanding hematomas or dislocated fractures may stretch nerves. Expanding hematomas, external orthoses such as casts or braces, or blunt trauma over a super-ficial nerve may compress or crush nerves. Shock waves from high-velocity bullets may contuse nerves. These mechanisms of injury cause


Surgery_Schwartz

Surgery_Schwartz. orthoses such as casts or braces, or blunt trauma over a super-ficial nerve may compress or crush nerves. Shock waves from high-velocity bullets may contuse nerves. These mechanisms of injury cause damage to the various anatomic components of the nerve. The patterns of damage are categorized in “Types of Injury.”Certain nerve segments are particularly vulnerable to injury. The following four characteristics make a nerve seg-ment more vulnerable: proximity to a joint, superficial course, passage through a confined space, and being fixed in position.Types of Injury. The traditional classification system for peripheral nerve injury is the Seddon classification. Seddon described three injury patterns as defined in the “Neurapraxia,” “Axonotmesis,” and “Neurotmesis” sections. The Seddon clas-sification provides a simple, anatomically based approach to peripheral nerve injury.52Neurapraxia Neurapraxia is defined as the temporary failure of nerve function without physical axonal disruption.


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Surgery_Schwartz. provides a simple, anatomically based approach to peripheral nerve injury.52Neurapraxia Neurapraxia is defined as the temporary failure of nerve function without physical axonal disruption. Axon degeneration does not occur. Return of normal axonal function occurs over hours to months, often in the 2to 4-week range.Axonotmesis Axonotmesis is the disruption of axons and myelin. The surrounding connective tissues, including endo-neurium, are intact. The axons degenerate proximally and dis-tally from the area of injury. Distal degeneration is known as Wallerian degeneration. Axon regeneration within the con-nective tissue pathways can occur, leading to restoration of function. Axons regenerate at a rate of 1 mm per day. Significant functional recovery may occur for up to 18 months. Scarring at the site of injury from connective tissue reaction can form a neuroma and interfere with regeneration.Neurotmesis Neurotmesis is the disruption of axons and endoneurial tubes. Peripheral collagenous


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Surgery_Schwartz. the site of injury from connective tissue reaction can form a neuroma and interfere with regeneration.Neurotmesis Neurotmesis is the disruption of axons and endoneurial tubes. Peripheral collagenous components, such as the epineurium, may or may not be intact. Proximal and distal axonal degeneration occurs. The likelihood of effective axonal regeneration across the site of injury depends on the extent of neuroma formation and on the degree of persisting anatomic alignment of the connective tissue structures. For instance, an injury may damage axons, myelin, and endoneurium, but leave perineurium intact. In this case, the fascicle sheath is intact, and appropriate axonal regeneration is more likely to occur than if the sheath is interrupted.Management of Peripheral Nerve Injury. The sensory and motor deficits should be accurately documented. Deficits are usually immediate. Progressive deficit suggests a process such as an expanding hematoma and may warrant early sur-gical exploration.


Surgery_Schwartz

Surgery_Schwartz. and motor deficits should be accurately documented. Deficits are usually immediate. Progressive deficit suggests a process such as an expanding hematoma and may warrant early sur-gical exploration. Clean, sharp injuries may also benefit from early exploration and reanastomosis. Most other peripheral nerve injuries should be observed. EMG/NCS studies should be done 3-6 to weeks postinjury if deficits persist. Axon seg-ments distal to the site of injury will conduct action potentials normally until Wallerian degeneration occurs, rendering EMG/NCS before 3 weeks uninformative. Continued observation is indicated if function improves. Surgical exploration of the nerve may be undertaken if no functional improvement occurs over 3 months. If intraoperative electrical testing reveals conduction across the injury, continue observation. In the absence of con-duction, the injured segment should be resected and end-to-end primary anastomosis attempted. However, anastomoses under tension will not


Surgery_Schwartz

Surgery_Schwartz. the injury, continue observation. In the absence of con-duction, the injured segment should be resected and end-to-end primary anastomosis attempted. However, anastomoses under tension will not heal. A nerve graft may be needed to bridge the gap between the proximal and distal nerve ends. The sural nerve often is harvested, as it carries only sensory fibers and leaves a minor deficit when resected. The connective tissue structures of the nerve graft may provide a pathway for effective axonal regrowth across the injury.Patterns of Injury Brachial Plexus The brachial plexus may be injured in a variety of ways. Parturition or a motorcycle accident can lead to plexus injury due to dislocation of the glenohumeral joint. Attempting to arrest a fall with one’s hands can lead to a stretch injury of the plexus due to abrupt movement of the shoulder girdle. An api-cal lung (Pancoast) tumor can cause compression injury to the plexus. There are many patterns of neurologic deficits possible with


Surgery_Schwartz

Surgery_Schwartz. of the plexus due to abrupt movement of the shoulder girdle. An api-cal lung (Pancoast) tumor can cause compression injury to the plexus. There are many patterns of neurologic deficits possible with injury to the various components of the brachial plexus, and understanding them all would require extensive neuroana-tomic discussion. Two well-known eponymous syndromes are Erb’s palsy and Klumpke’s palsy. Injury high in the plexus to the C5 and C6 roots resulting from glenohumeral dislocation causes Erb’s palsy with the characteristic “bellhop’s tip” posi-tion. The arm hangs at the side, internally rotated. Hand move-ments are not affected. Injury low in the plexus, to the C8 and T1 roots, resulting from stretch or compression injury, causes Klumpke’s palsy with the characteristic “claw hand” deformity. There is weakness of the intrinsic hand muscles, similar to that seen with ulnar nerve injury.Radial Nerve The radial nerve courses through the axilla, then laterally and posteriorly in


Surgery_Schwartz

Surgery_Schwartz. deformity. There is weakness of the intrinsic hand muscles, similar to that seen with ulnar nerve injury.Radial Nerve The radial nerve courses through the axilla, then laterally and posteriorly in the spiral groove of the humerus. Improper crutch use can cause damage to the axillary portion. The section of the nerve traversing the spiral groove can be damaged by humerus fractures or pressure from improper posi-tioning during sleep. This classically occurs when the patient is intoxicated and is called “Saturday night palsy.” The key find-ing is wrist drop (i.e., weakness of hand and finger extensors). Axillary (proximal) injury causes triceps weakness in addition to wrist drop.Common Peroneal Neuropathy The common peroneal nerve forms the lateral half of the sciatic nerve (the medial half being the tibial nerve). It receives contributions from L4, L5, S1, and S2. It emerges as a separate nerve in the popliteal fossa and laterally wraps around the fibular neck, after which it splits to


Surgery_Schwartz

Surgery_Schwartz. being the tibial nerve). It receives contributions from L4, L5, S1, and S2. It emerges as a separate nerve in the popliteal fossa and laterally wraps around the fibular neck, after which it splits to Brunicardi_Ch42_p1827-p1878.indd 184801/03/19 7:16 PM 1849NEUROSURGERYCHAPTER 42form the deep and superficial peroneal nerves. The superficial, fixed location at the fibular neck makes the common peroneal nerve susceptible to compression. The classic cause of traumatic peroneal neuropathy is crush injury from a car bumper striking the lateral aspect of the leg at the knee. Symptoms of common peroneal neuropathy include foot drop (weakness of the tibialis anterior), eversion weakness, and numbness over the anterolat-eral surface of the lower leg and dorsum of the foot. In contrast, a foot drop due to L5 radiculopathy spares eversion because the S1 fibers are intact. Surgical exploration of a common peroneal crush lesion is typically a low yield endeavor. Rare cases may be due to


Surgery_Schwartz

Surgery_Schwartz. foot drop due to L5 radiculopathy spares eversion because the S1 fibers are intact. Surgical exploration of a common peroneal crush lesion is typically a low yield endeavor. Rare cases may be due to compressive fibers or adhesions that may be lysed, with the possibility of return of function.CEREBROVASCULAR DISEASECerebrovascular disease is the most frequent cause of new, rapid-onset, nontraumatic neurologic deficit. It is far more common than seizures or tumors. Vascular structures are subject to a vari-ety of chronic pathologic processes that compromise vessel wall integrity. Diabetes, high cholesterol, high blood pressure, and smoking – common comorbidities in the general population – are important risk factors for vascular disease. These conditions can lead to vascular damage by such mechanisms as atheroma deposition causing luminal stenosis, endothelial damage promot-ing thrombogenesis, and weakening of the vessel wall result-ing in aneurysm formation or dissection. These


Surgery_Schwartz

Surgery_Schwartz. such mechanisms as atheroma deposition causing luminal stenosis, endothelial damage promot-ing thrombogenesis, and weakening of the vessel wall result-ing in aneurysm formation or dissection. These processes may coexist. For instance, a vessel containing an atheromatous plaque will have a decreased luminal diameter. The plaque also may have compromised endothelium, providing the opportunity for thrombus formation, which can lead to acute total occlusion of the remaining lumen. Aneurysms and dissection often occur in atheromatous vessels. Specific patterns of disease relevant to the cerebrovascular system include atheromatous and thrombotic carotid occlusion, brain ischemia from proximal embolic disease, vessel wall rupture leading to hemorrhage, and rupture of abnor-mal, thin-walled structures, specifically aneurysms and AVMs.Ischemic DiseasesIschemic stroke accounts for approximately 85% of acute cerebrovascular events. Symptoms of acute ischemic stroke vary based on the functions of


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Surgery_Schwartz. specifically aneurysms and AVMs.Ischemic DiseasesIschemic stroke accounts for approximately 85% of acute cerebrovascular events. Symptoms of acute ischemic stroke vary based on the functions of the neural tissues supplied by the occluded vessel, and the presence or absence of collateral circulation. The circle of Willis provides extensive collateral circulation, as it connects the right and left carotid arteries to each other and each to the vertebrobasilar system. Patients with complete occlusion of the carotid artery proximal to the circle of Willis may be asymptomatic if the blood flow patterns can shift and provide sufficient circulation to the ipsilateral cerebral hemisphere from the contralateral carotid and the basilar artery. However, the anatomy of the circle of Willis is highly variable. Patients may have a congenitally hypoplastic or missing com-municating artery with resultant bilateral ACA supply by one carotid, or the PCA may be supplied by the carotid artery rather than


Surgery_Schwartz

Surgery_Schwartz. Patients may have a congenitally hypoplastic or missing com-municating artery with resultant bilateral ACA supply by one carotid, or the PCA may be supplied by the carotid artery rather than the basilar. Similarly, one vertebral artery is often domi-nant and the other is hypoplastic. These variations may make disease in a particular vessel more neurologically devastating than in a patient with full collateral circulation. Occlusion distal to the circle of Willis generally results in a stroke in the territory supplied by that particular artery.Neurologic deficit from occlusive disease may be tempo-rary or permanent. A patient with sudden-onset focal neurologic deficit that resolves within 24 hours has had a transient ischemic attack (TIA). A patient with permanent deficit has had a com-pleted stroke.Thrombotic DiseaseThe most common area of neurologically significant vessel thrombosis is the carotid artery in the neck. Disease occurs at the carotid bifurcation. Thrombosis of a carotid


Surgery_Schwartz

Surgery_Schwartz. stroke.Thrombotic DiseaseThe most common area of neurologically significant vessel thrombosis is the carotid artery in the neck. Disease occurs at the carotid bifurcation. Thrombosis of a carotid artery chronically narrowed by atheroma can lead to acute carotid occlusion. As discussed previously, this can be asymptomatic due to sufficient collateralization. The more common concern is thromboem-bolus. Intracranial arterial occlusion by local thrombus formation may occur, but it is rare compared to embolic occlusion.Management. Complete occlusion of the carotid artery with-out referable neurologic deficit requires no treatment. A patient with new neurologic deficit and an angiographically confirmed complete carotid occlusion contralateral to the symptoms should be considered for emergent carotid endarterectomy.53 Surgery should be performed within 2 hours of symptom onset and should not be performed on obtunded or comatose patients. These restrictions significantly reduce the number of


Surgery_Schwartz

Surgery_Schwartz. endarterectomy.53 Surgery should be performed within 2 hours of symptom onset and should not be performed on obtunded or comatose patients. These restrictions significantly reduce the number of opera-tive candidates. In nonemergent cases, the results of the large-scale North American Symptomatic Carotid Stenosis Trial (NASCET) demonstrated a stroke reduction benefit to surgical revascularization in patients with severe stenosis, defined as occlusion of 70% to 99% of the carotid.54 Practice guidelines recommend revascularization at this level of stenosis even if asymptomatic. Surgical options for these patients include both carotid endarterectomy and carotid stenting, which have been shown to produce equal outcomes over long-term follow-up.55Embolic DiseaseEmboli causing strokes may originate from a number of sources, including: the left atrium in atrial fibrillation, a hypokinetic left ventricular wall segment, valvular vegetations, an atheromatous aortic arch, stenotic/atheromatous


Surgery_Schwartz

Surgery_Schwartz. from a number of sources, including: the left atrium in atrial fibrillation, a hypokinetic left ventricular wall segment, valvular vegetations, an atheromatous aortic arch, stenotic/atheromatous carotid bifurcations, or from the systemic venous system in the presence of a right-to-left shunt, such as a patent foramen ovale. The majority of emboli enter the anterior (carotid) circulation rather than the posterior (vertebro-basilar) circulation. Characteristic clinical syndromes result from embolic occlusion of various vessels within these circulations.Common Types of Strokes Anterior Cerebral Artery Stroke The ACA supplies the medial frontal and parietal lobes as it courses into the inter-hemispheric fissure. Due to its vascular supply of the motor cortex, ACA stroke characteristically results in contralateral leg weakness.Middle Cerebral Artery Stroke The MCA supplies the lateral frontal and parietal lobes and the temporal lobe. MCA stroke results in contralateral face and arm


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Surgery_Schwartz. results in contralateral leg weakness.Middle Cerebral Artery Stroke The MCA supplies the lateral frontal and parietal lobes and the temporal lobe. MCA stroke results in contralateral face and arm weakness. Dominant-hemisphere MCA stroke causes language deficits due to its sup-ply of Broca’s area, Wernicke’s area, and the white matter tracts that connect the two. Proximal MCA occlusion with ischemia and swelling in the entire MCA territory can lead to significant intracranial mass effect and midline shift (see Fig. 42-6), termed malignant MCA stroke.Posterior Cerebral Artery Stroke The PCA supplies the occipital lobe. PCA stroke results in a contralateral homony-mous hemianopsia (see Fig. 42-6).Posterior Inferior Cerebellar Artery Stroke The PICA sup-plies the lateral medulla and the inferior half of the cerebellar Brunicardi_Ch42_p1827-p1878.indd 184901/03/19 7:16 PM 1850SPECIFIC CONSIDERATIONSPART IIhemispheres. PICA stroke results in nausea, vomiting, nystag-mus, dysphagia,


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Surgery_Schwartz. half of the cerebellar Brunicardi_Ch42_p1827-p1878.indd 184901/03/19 7:16 PM 1850SPECIFIC CONSIDERATIONSPART IIhemispheres. PICA stroke results in nausea, vomiting, nystag-mus, dysphagia, ipsilateral Horner’s syndrome, and ipsilateral limb ataxia. The constellation of symptoms resulting from PICA occlusion is referred to as the lateral medullary or Wallenberg’s syndrome.Management. Ischemic stroke management has two goals: reopen the occluded vessel and maintain blood flow to ischemic “penumbra” tissues bordering the vascular territory. Reopen-ing the vessel has historically been attempted with recombinant tPA.56 tPA administration within 3 hours of the onset of neu-rologic deficit improves outcome at 3 months. In the setting of suspected ischemic stroke, a head CT must be performed immediately to differentiate ischemic from hemorrhagic stroke. Intracranial hemorrhage, major surgery within the previous 2 weeks, GI or genitourinary hemorrhage in the previous 3 weeks, platelet


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Surgery_Schwartz. immediately to differentiate ischemic from hemorrhagic stroke. Intracranial hemorrhage, major surgery within the previous 2 weeks, GI or genitourinary hemorrhage in the previous 3 weeks, platelet count less than 100,000/µL, and systolic blood pressure >185 mmHg are among the contraindications to tPA therapy.In recent years, a paradigm shift in ischemic stroke man-agement has occurred with the advent of endovascular mechani-cal thrombectomy. Though tPA can be effective for strokes of smaller vessels, it produces recanalization in only 20% of large vessel ischemic strokes, and even less for internal carotid artery occlusion.57 In mechanical thrombectomy, the intracra-nial circulation is accessed endovascularly, and stent-retriever devices can be deployed to definitively remove clot and stent open involved vessels. Initial investigations into the technol-ogy began in 1999 with varied success. Technological advances proceeded, and in 2015, large-scale clinical trials investigating


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Surgery_Schwartz. stent open involved vessels. Initial investigations into the technol-ogy began in 1999 with varied success. Technological advances proceeded, and in 2015, large-scale clinical trials investigating mechanical thrombectomy for large vessel occlusion were pub-lished. The MR-CLEAN trial was one of these. In this trial, 500 patients were randomized to tPA and medical therapy vs. mechanical thrombectomy. The latter group had a significantly better 90-day outcome. A domino effect ensued in which four other similarly large-scale trials (e.g., REVASCAT)58 were ter-minated early.Benefits to mechanical thrombectomy include less strin-gent criteria than tPA administration, focused therapy, and time windows between 6 and 12 hours in trials. Currently, mechani-cal thrombectomy is being used for large vessel occlusion within 6 hours of symptom onset for those patients not eligible for tPA, which accounts for about 10% of ischemic stroke. Its indica-tions and associated technology continue to evolve.


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Surgery_Schwartz. occlusion within 6 hours of symptom onset for those patients not eligible for tPA, which accounts for about 10% of ischemic stroke. Its indica-tions and associated technology continue to evolve. It should be noted that current guidelines still support tPA as first-line therapy even for those eligible for mechanical thrombectomy.Patients not eligible for tPA or mechanical thrombectomy require hemodynamic optimization and neurologic monitoring. Admit such patients to the ICU stroke service for blood pres-sure management and frequent neurologic checks. Permissive hypertension allows for maximal cerebral perfusion. Systolic blood pressure >180 mmHg may require treatment, but the opti-mal mean arterial pressure goal is between 100 and 140 mmHg. Give normal saline solution without glucose (which could injure neurons in the penumbra due to osmotic fluid shift), and aim for normovolemia. A stroke patient who worsens clinically should undergo repeat head CT to evaluate for hemorrhage or


Surgery_Schwartz

Surgery_Schwartz. (which could injure neurons in the penumbra due to osmotic fluid shift), and aim for normovolemia. A stroke patient who worsens clinically should undergo repeat head CT to evaluate for hemorrhage or increas-ing mass effect from swelling, which typically peaks 3 to 5 days after the stroke. Significant swelling from an MCA or cerebellar stroke may cause herniation and brain stem injury. A decom-pressive hemicraniectomy or suboccipital craniectomy can be a life-saving intervention for these select stroke patients. In stud-ies of malignant MCA syndrome, decompressive hemicraniec-tomy showed favorable mortality and functional outcomes.59 This treatment option, however, should be considered with the understanding of potentially poor functional recovery regardless of therapy. One study showed that less than half of malignant MCA patients who underwent decompressive hemicraniectomy returned home following rehabilitation, which is even fewer for those undergoing medical therapy.60Hemorrhagic


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Surgery_Schwartz. less than half of malignant MCA patients who underwent decompressive hemicraniectomy returned home following rehabilitation, which is even fewer for those undergoing medical therapy.60Hemorrhagic DiseasesIntracranial hemorrhage from abnormal or diseased vascular structures accounts for approximately 15% of acute cerebrovas-cular events. Hypertension and amyloid angiopathy account for most intraparenchymal hemorrhages, although AVMs, aneu-rysms, venous thrombosis, tumors, hemorrhagic conversion of ischemic infarct, and fungal infections also may be the cause. The term intracranial hemorrhage is frequently used to signify intraparenchymal hemorrhage and will be used here. Intracra-nial hemorrhage causes local neuronal injury and dysfunction and also may cause global dysfunction due to mass effect if sufficiently large. The Intracerebral Hemorrhage (ICH Score) is commonly used to risk-stratify these patients, and it takes into account GCS, age, hemorrhage volume, presence of


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Surgery_Schwartz. due to mass effect if sufficiently large. The Intracerebral Hemorrhage (ICH Score) is commonly used to risk-stratify these patients, and it takes into account GCS, age, hemorrhage volume, presence of intraven-tricular hemorrhage, and location to predict mortality. AVM or aneurysm rupture (along with trauma, discussed previously in this chapter) result in subarachnoid hemorrhage (SAH) because the major cerebral and cortical blood vessels travel in the sub-arachnoid space, between the pia and the arachnoid membranes. SAH can cause immediate concussive-like neuronal dysfunc-tion by exposure of the brain to intra-arterial pressure pulsa-tions during the hemorrhage. Moreover, it can cause delayed ischemia from cerebral arterial vasospasm, which can present as acute worsening of the patient’s neurological status days to weeks after the injury. Patients presenting with intracranial hemorrhages that do not follow typical patterns should undergo cerebral angiography or MRI to evaluate for


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Surgery_Schwartz. neurological status days to weeks after the injury. Patients presenting with intracranial hemorrhages that do not follow typical patterns should undergo cerebral angiography or MRI to evaluate for possible underlying lesions, such as AVM or tumor.Hemorrhagic stroke most commonly occurs within the basal ganglia or cerebellum. The patient is usually hypertensive on admission and has a history of poorly controlled hyperten-sion. Such patients are more likely to present with lethargy or obtundation compared to those who suffer an ischemic stroke. Depressed mental status results from mass effect from the hema-toma in deep structures, which can produce midline shift or herniation. Ischemic stroke does not cause mass effect acutely. Therefore, patients are more likely to present with normal con-sciousness and a focal neurologic deficit. Hemorrhagic strokes tend to present with a relatively gradual decline in neurologic function as the hematoma expands, rather than the immediately maximal


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Surgery_Schwartz. and a focal neurologic deficit. Hemorrhagic strokes tend to present with a relatively gradual decline in neurologic function as the hematoma expands, rather than the immediately maximal symptoms caused by ischemic stroke. Table 42-3 pro-vides a listing of relative incidences of intracranial hemorrhage by anatomic distribution.Hypertension. Hypertension increases the relative risk of intracranial hemorrhage by approximately fourfold, likely due to chronic degenerative vasculopathy. Hypertensive hemor-rhages often present in the basal ganglia, thalamus, or pons, and result from breakage of small perforating arteries that branch off of much larger parent vessels (Fig. 42-16).Most hypertensive hemorrhages should be medically man-aged. The hematoma often contains intact, salvageable axons because the blood dissects through and along neural tracts, and surgical clot evacuation destroys these axons. Factors potentially favoring surgery include: superficial clot location, young age,


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Surgery_Schwartz. because the blood dissects through and along neural tracts, and surgical clot evacuation destroys these axons. Factors potentially favoring surgery include: superficial clot location, young age, nondominant hemisphere, rapid deterioration, and significant Brunicardi_Ch42_p1827-p1878.indd 185001/03/19 7:16 PM 1851NEUROSURGERYCHAPTER 42Table 42-3Anatomic distribution of intracranial hemorrhages and correlated symptoms% OF INTRACRANIAL HEMORRHAGESLOCATIONCLASSIC SYMPTOMS50Basal ganglia (putamen, globus pallidus), internal capsuleContralateral hemiparesis15ThalamusContralateral hemisensory loss10–20Cerebral white matter (lobar)Depends on location (weakness, numbness, partial loss of visual field)10–15PonsHemiparesis; may be devastating10CerebellumLethargy or coma due to brain stem compression and/or hydrocephalus1–6Brain stem (excluding pons)Often devastatingFigure 42-16. A. Head computed tomography scan of a patient with left-sided weakness and progressive lethargy reveals a right


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Surgery_Schwartz. and/or hydrocephalus1–6Brain stem (excluding pons)Often devastatingFigure 42-16. A. Head computed tomography scan of a patient with left-sided weakness and progressive lethargy reveals a right basal ganglia hemorrhage (arrowhead). The blood clot is bright white. Hypodensity around the clot represents cerebral edema. There is blood within the ventricular system. B. Another patient with intraventricular extension of a basal ganglia hemorrhage. The patient developed right-sided weak-ness and then lethargy. Head computed tomography indicated hydrocephalus. A ventriculostomy was placed for cerebrospinal fluid drainage (arrowhead indicates cross-sectional view of the catheter entering the anterior horn of the right lateral ventricle).mass effect. However, the most comprehensive randomized clinical trials to date did not show an overall improved outcome in surgically evacuated intracranial hemorrhage, except for the subgroup of patients with clot <1 cm from the cortical surface.61 More


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Surgery_Schwartz. clinical trials to date did not show an overall improved outcome in surgically evacuated intracranial hemorrhage, except for the subgroup of patients with clot <1 cm from the cortical surface.61 More recent studies have assessed the role of minimally-invasive catheter evacuation of clot; these investigations are ongoing.62 Medical management remains the gold standard, however, and includes moderate blood pressure control, normalizing platelet and clotting function, phenytoin or levetiracetam for seizure prophylaxis, and electrolyte management. Intubate patients who cannot clearly follow commands to prevent aspiration and hypercarbia. Follow and document the neurologic examination and communicate with the family regarding appropriateness for rehabilitation vs. withdrawal of care.Amyloid Angiopathy. The presence of pathologic amyloid deposition in the media of small cortical vessels compromises vessel integrity and tends to cause more superficial (lobar) hemorrhages than hypertensive


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Surgery_Schwartz. Angiopathy. The presence of pathologic amyloid deposition in the media of small cortical vessels compromises vessel integrity and tends to cause more superficial (lobar) hemorrhages than hypertensive intracranial hemorrhage. Amy-loid laden vessels may hemorrhage multiple times. The super-ficial location of amyloid hemorrhages may make surgical evacuation less morbid compared to typical deep hypertensive hemorrhages. Nonetheless, medical management and family counseling should be approached similarly to patients with hypertensive hemorrhages.Brunicardi_Ch42_p1827-p1878.indd 185101/03/19 7:16 PM 1852SPECIFIC CONSIDERATIONSPART IITable 42-5The Hunt-Hess clinical grading system for subarachnoid hemorrhageHUNT-HESS GRADECLINICAL PRESENTATION0Asymptomatic; unruptured aneurysm1Awake; asymptomatic or mild headache; mild nuchal rigidity2Awake; moderate to severe headache, cranial nerve palsy (e.g., cranial nerve III or IV), nuchal rigidity3Lethargic; mild focal neurologic deficit (e.g.,


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Surgery_Schwartz. or mild headache; mild nuchal rigidity2Awake; moderate to severe headache, cranial nerve palsy (e.g., cranial nerve III or IV), nuchal rigidity3Lethargic; mild focal neurologic deficit (e.g., pronator drift)4Stuporous; significant neurologic deficit (e.g., hemiplegia)5Comatose; posturingTable 42-4Prevalence of cerebral aneurysm by locationPREVALENCEANEURYSM LOCATION (VERNACULAR NAME)Anterior circulation 85% 30% Anterior communicating artery (A-Comm)25% Posterior communicating artery (P-Comm)20% Middle cerebral artery bifurcation10% OtherPosterior circulation 15% 10% Basilar artery, most frequently at the basilar tip5% Vertebral artery, usually at the posterior inferior cerebellar arteryCerebral Aneurysm. An aneurysm is a focal dilatation of the vessel wall and is most often a balloon-like outpouching, but may also be fusiform. Aneurysms usually occur at branch points of major vessels (e.g., internal carotid artery bifurca-tion), or at the origin of smaller vessels (e.g.,


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Surgery_Schwartz. balloon-like outpouching, but may also be fusiform. Aneurysms usually occur at branch points of major vessels (e.g., internal carotid artery bifurca-tion), or at the origin of smaller vessels (e.g., posterior com-municating artery or ophthalmic artery). Approximately 85% of aneurysms arise from the anterior circulation (carotid) and 15% from the posterior circulation (vertebrobasilar). Table 42-4 shows the percentage distribution of cerebral aneurysms by location. Aneurysms are thin walled and at risk for rupture. The major cerebral vessels, and therefore aneurysms, lie in the subarachnoid space. Rupture results in SAH. The aneurys-mal tear may be small and seal quickly, or it may not. SAH may consist of a thin layer of blood in the CSF spaces, or thick layers of blood around the brain and extending into brain parenchyma, resulting in a clot with mass effect. Because the meningeal linings of the brain are sensitive with free nerve endings, SAH usually results in a sudden, severe


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Surgery_Schwartz. and extending into brain parenchyma, resulting in a clot with mass effect. Because the meningeal linings of the brain are sensitive with free nerve endings, SAH usually results in a sudden, severe “thunderclap” headache. A patient will classically describe “the worst head-ache of my life.” Presenting neurologic symptoms may range from mild headache to coma to sudden death. The Hunt-Hess grading system categorizes patients clinically (Table 42-5). The World Federation of Neurological Surgery (WFNS) SAH Grading Scale is also used for this purpose. The Fisher Scale and a more recent modified form use head CT characteristics, described in the following section, to stratify patients based on risk of vasospasm-induced delayed cerebral ischemia. Both scales are used in conjunction as a quick way to communicate severity of aneurysmal SAH.Patients with symptoms suspicious for SAH should have a head CT immediately. Acute SAH appears as a bright signal in the fissures and CSF cisterns around the


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Surgery_Schwartz. to communicate severity of aneurysmal SAH.Patients with symptoms suspicious for SAH should have a head CT immediately. Acute SAH appears as a bright signal in the fissures and CSF cisterns around the base of the brain, as shown in Fig. 42-17. CT is rapid, noninvasive, and approxi-mately 95% sensitive. In patients with suspicious symptoms but negative head CT, a lumbar puncture (LP) should be per-formed. An LP with xanthochromia and high red blood cell counts (usually 100,000/mL), which do not decrease between tubes 1 and 4, is consistent with SAH. Negative CT and LP essentially rules out SAH. Patients diagnosed with SAH require four-vessel cerebral angiography within 24 hours to assess for aneurysm or other vascular malformation. Cathe-ter angiography remains the gold standard for assessing the patient’s cerebral vasculature, relevant anomalies, and pres-ence, location, and morphology of the cerebral aneurysms. Figure 42-18A demonstrates the typical anteroposterior digital subtraction


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Surgery_Schwartz. the patient’s cerebral vasculature, relevant anomalies, and pres-ence, location, and morphology of the cerebral aneurysms. Figure 42-18A demonstrates the typical anteroposterior digital subtraction angiographic view of a cerebral aneurysm. Figure 42-18B shows the anatomy of the circle of Willis in a simplified graphic representation to assist in visualizing the locations of various cerebral aneurysms.SAH patients should be admitted to the neurologic ICU. Hunt-Hess grade 4 and 5 patients require intubation and hemo-dynamic monitoring and stabilization. The current standard of care for ruptured aneurysms requires early aneurysmal occlu-sion. There are two options for occlusion. The patient may undergo craniotomy with microsurgical dissection and place-ment of a titanium clip across the aneurysm neck to exclude the aneurysm from the circulation and reconstitute the lumen of the parent vessel. The second option is to utilize an endovascular approach for treatment, which has traditionally


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Surgery_Schwartz. neck to exclude the aneurysm from the circulation and reconstitute the lumen of the parent vessel. The second option is to utilize an endovascular approach for treatment, which has traditionally taken the form of “coiling.” The patient is taken to the interventional neuro-radiology suite for placement of looped titanium coils inside the aneurysm dome. The coils support thrombosis and prevent Figure 42-17. Non contrast CT scan on the left shows diffuse subarachnoid blood in the cisterns with some concentration in the region of the anterior cerebral arteries. This is confirmed by the image on the right, a CT angiogram, where the arrow indicates an anterior communicating artery aneurysm.Brunicardi_Ch42_p1827-p1878.indd 185201/03/19 7:16 PM 1853NEUROSURGERYCHAPTER 42Figure 42-18. A. Anteroposterior view after injection of contrast dye in the right internal carotid artery demonstrates an aneurysm of the middle cerebral artery bifurcation. B. Figure depicting the anatomy of the circle


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Surgery_Schwartz. view after injection of contrast dye in the right internal carotid artery demonstrates an aneurysm of the middle cerebral artery bifurcation. B. Figure depicting the anatomy of the circle of Willis and the common sites for aneu-rysms. ICA = internal cerebral artery; MCA = middle cerebral artery. (Reproduced with permission from Osborn AG: Handbook of Neuroradiology: Brain and Skull. St. Louis, MO: Mosby-Year Book, Inc; 1991.)AIntracranial aneurysumsAnteriorcommunicating artery30% – 35%MCA bifurcation20%Basilar5%Posterior fossaMiscellaneous sites distalto circle of Willis1% – 3%ICA/posteriorcommunicating30% – 35%Bblood flow into the aneurysm. Newer endovascular options include flow diversion and stent-assisted coiling. Factors favor-ing craniotomy and clipping include young age, good medical condition, and broad aneurysm necks. Factors favoring coil-ing include age, medical comorbidities, and narrow aneurysm necks. Due to coil migration or compaction over time, surgical clipping is


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Surgery_Schwartz. condition, and broad aneurysm necks. Factors favoring coil-ing include age, medical comorbidities, and narrow aneurysm necks. Due to coil migration or compaction over time, surgical clipping is believed to result in a more definitive cure. The decision to clip or coil is complex and should be fully explored. Practice standards have changed in recent years with the advent of more nuanced endovascular techniques and treatment options, as described earlier. Current guidelines favor endovas-cular therapy as the preferred first-line approach. The Interna-tional Subarachnoid Aneurysm Trial researchers suggested that endovascular occlusion resulted in better mortality outcomes for certain types of cerebral aneurysms, although this trial was marred by poor selection and randomization techniques, and the validity of its conclusions have been questioned.63 Long-term outcomes may be better in younger patients with clipped aneurysms, as demonstrated in the Barrow Ruptured Aneurysm Trial (BRAT).64


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Surgery_Schwartz. the validity of its conclusions have been questioned.63 Long-term outcomes may be better in younger patients with clipped aneurysms, as demonstrated in the Barrow Ruptured Aneurysm Trial (BRAT).64 However, this trial has a number of similar criticisms as well. Debate also continues regarding optimal care for unruptured intracranial aneurysms, with a recent large-scale study showing no clear benefit to open surgical vs. endovascu-lar approaches.65SAH patients often require 1 to 3 weeks of ICU care after aneurysm occlusion for medical complications that accompany neurologic injury. In addition to routine ICU concerns, SAH patients are also at risk for cerebral vasospasm. In vasospasm, cerebral arteries constrict pathologically and can cause isch-emia or stroke from 4 to 21 days after SAH. Current vasospasm prophylaxis includes maintenance of optimal perfusion with hypertension and mild hypervolemia, as well as administration of nimodipine, a calcium channel blocker that may decrease the


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Surgery_Schwartz. vasospasm prophylaxis includes maintenance of optimal perfusion with hypertension and mild hypervolemia, as well as administration of nimodipine, a calcium channel blocker that may decrease the incidence and degree of spasm, though its mechanism is debated. Neurointerventional options for treating symptomatic vasospasm include intra-arterial papaverine or nicardipine, and balloon angioplasty for larger caliber vessels.Aneurysmal SAH has an approximate mortality rate of 50% in the first month. Approximately one-third of survivors return to pre-SAH function, and the remaining two-thirds have mild to severe disability. Most require rehabilitation after hospitalization.Arteriovenous Malformations. AVMs are abnormal, dilated arteries and veins without an intervening capillary bed. The nidus of the AVM contains a tangled mass of vessels but no neural tissue. AVMs may be asymptomatic or present with SAH, intra-parenchymal hemorrhage, or seizures. Small AVMs present with hemorrhage more often


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Surgery_Schwartz. the AVM contains a tangled mass of vessels but no neural tissue. AVMs may be asymptomatic or present with SAH, intra-parenchymal hemorrhage, or seizures. Small AVMs present with hemorrhage more often than large AVMs, which tend to present with seizures. Headache, bruit, or focal neurologic deficits are less common symptoms. AVMs hemorrhage at an average rate of 2% to 4% a year. Figure 42-19 demonstrates the angiographic appearance of an AVM in arterial and venous phases.For unruptured AVMs, recent evidence from over two hundred patients supports medical management alone rather than intervention due to risk of stroke.66 Because AVM rupture can present radiographically as SAH, it is important to consider several management differences as compared to aneurysmal SAH. Definitive therapy for the AVM usually is delayed 3 to 4 weeks to allow the brain to recover from acute injury. There is less risk of devastating early rebleeding from AVMs, and vasospasm is much less common. Three