Neurosurgery Sec. from Surgical Handbook PDF

| 02.07.20 - 17:35 14 Neurosurgery Edited by Michael Karsy, Hussam Abou-Al-Shaar, and Jian Guan 14.1 Traumatic Brain Injury Michael Karsy and Gregory W. J. Hawryluk 14.1.1 Assessment and Treat...

| 02.07.20 - 17:35 14 Neurosurgery Edited by Michael Karsy, Hussam Abou-Al-Shaar, and Jian Guan 14.1 Traumatic Brain Injury Michael Karsy and Gregory W. J. Hawryluk 14.1.1 Assessment and Treatment Traumatic brain injury (TBI): An alteration in brain function, or other evidence of brain pathology caused by an external force to the head. Initial injury is classified as primary traumatic brain injury (e.g., contusion, laceration, bone fragments, diffuse axonal injury). Delayed injury is termed secondary injury and occurs at the molecular level. Secondary insults occur at the level of the patient (e.g., hypoxia, hypotension) and can be treated by physicians. Assessment begins with Advanced Trauma Life Support (ATLS) primary and secondary surveys. Information evaluated by a neurosurgeon includes age and mechanism of injury; neurological status is examined including Glasgow Coma Scale (GCS; ▶ Table 14.1 and ▶ Table 14.2), pupils, brainstem reflexes (e.g., cough, gag, corneal), stigmata of cranial injury (e.g., raccoon’s eyes, Battle sign, CSF rhinorrhea or otorrhea, hemotympanum), associated traumatic injuries with prioritization of diagnostic studies and interventions. Facial injuries should be stabilized if able; ocular injuries can be assessed and treated by immediate lateral canthotomy; scalp lacerations can be immediately cleansed and stapled; intubation should be performed for airway protection prior to neurosurgical interventions. TBI severity can be divided by GCS: ○ GCS 15: Minimal/concussion. ○ GCS 13–15: Mild. ○ GCS 9–12: Moderate. ○ GCS ≤ 8: Severe, requires intubation. Table 14.1 Glasgow coma scale (GCS) Score Eyes Verbal Motor 6 Follows commands 5 Oriented Localizes to pain 4 Spontaneous Confused Withdraws from pain 3 To command Inappropriate words Flexor/decorticate posturing 2 To pain Incomprehensible sounds Extensor/decerebrate posturing 1 None None None Notes: GCS reported with total score and subcomponents (e.g., GCS 15 and E4V5M6); motor subcomponent is most predictive of 30-day outcome. Patients assigned 1 point for verbal subscore if intubated and a T is placed after the GCS score to communicate that the patient is intubated (e.g., GCS 8T). Table 14.2 Pediatric Glasgow coma scale Score Eyes Verbal Motor 6 Follows commands or spontaneous 5 Appropriate words/phrases; smiles/coos Localizes to pain 4 Spontaneous Inappropriate words; consolable crying Withdraws from pain 3 To command or shout Persistent and inappropriate crying Flexor/decorticate posturing 2 To pain Incomprehensible sounds, grunts, restlessness Extensor/decerebrate posturing 1 None None None 359 | 02.07.20 - 17:35 Neurosurgery Table 14.3 Canadian and New Orleans head CT rules Canadian head CT rule New Orleans head CT rule Applies to patients GCS 13–15, age > 16, no blood thinners, Applies to patients GCS 15 and normal and no postinjury seizures neurological exam CT obtained if any of the following is positive: CT obtained if any of the following is positive: GCS < 15 at 2 h postinjury Headache Suspected open or depressed skull fracture Vomiting Signs of basilar skull fracture Age > 60 Episodes ≥ 2 of vomiting Alcohol or drug intoxication Age ≥ 65 Persistent anterograde amnesia Retrograde amnesia to event ≥ 30 min Visible trauma above the clavicle Dangerous mechanism (e.g., pedestrian struck by motor vehicle, Seizure occupant ejected from motor vehicle, fall > 3 feet, fall > 5 stairs) GCS communicates severity of injury rapidly, has good interobserver reliability, and is predictive of discharge and long-term outcome especially motor score. CT evaluation of head includes soft-tissue and bone windows, Canadian CT rule or New Orleans trauma rule helps avoid unnecessary CT scans (▶ Table 14.3). ○ Low risk for intracranial injury: CT head not indicated, linear nondisplaced skull fractures not required, overnight observation considered. ○ Moderate or high risk for intracranial injury: CT imaging indicated, further clinical follow-up may be necessary. Concussion1: ○ Disturbance of brain function from direct or indirect force to the head. ○ Multiple grading systems were created but have been abandoned because of lack of validity. ○ American Academy of Neurology has guidelines emphasizing individual evaluation. ○ Sports concussion assessment tool 5 (SCAT5)1: Standardized method for evaluating concussion in athletes ≥ 13 years, child SCAT involved for children 5–12 years, involves a standardized form of multiple sections of questions, used to evaluate concussion severity and track change over time, recommends removal from play on the same day of injury with later medical clearance before returning to play. ○ Patients returned to full activity over six tiers of incremental increased activity with 24-hour increments as long as asymptomatic. ○ Postconcussive syndrome: Persistent headache, dizziness, exercise intolerance, memory dysfunction, emotional dysregulation, or intractable headaches that persist after a concussion; may require long-term rehabilitation. ○ Second impact syndrome: Rare condition with formation of malignant vasogenic edema resulting in coma and 50–100% mortality rate; occurs after second head injury while symptomatic from primary concussion. Radiological evaluation: ○ CT imaging indicated for head trauma; skull X-rays lack sensitivity. ○ Acute blood, bone, or bullets (e.g., fragments) show up as bright/hyperdense on CT scans; subacute blood is isointense; chronic blood is hypodense. ○ Scalp edema can help localize site of impact; contrecoup injury refers to a brain contusion remote from the site of impact as a result of brain movement within the skull. ○ Follow-up CT head utilized to rule out worsening of contusions; timing of repeat imaging varies on institution. ○ Marshall CT classification predicts outcome from injury severity: – I: No visible pathology on CT scan. – II: Cisterns present, midline shift 0–5 mm, no lesion > 25 cc. – III: Cisterns compressed, midline shift 0–5 mm, no lesion > 25 cc. – IV: Midline shift > 5 mm, lesion > 25 cc. – V: Any surgically evacuated lesion. – VI: Nonsurgically evacuated lesion, lesion > 25 cc. 360 | 02.07.20 - 17:35 Traumatic Brain Injury Table 14.4 Utah blunt cerebrovascular injury score2 Utah score (higher scores predict increased probability of injury) GCS ≤ 8 1 Focal neurological deficits 2 Carotid canal fracture 2 Petrous temporal bone fracture 3 Cerebral infarction on head CT 3 ○ CT angiography of head and neck vessels can be indicated to rule out blunt cerebrovascular injury seen in 1–2% of blunt trauma (▶ Table 14.4)2; particularly indicated in the context of fractures in proximity to major cerebral vessels (see Chapter 14.2.4 Medical management). ○ Delayed MRI can be helpful during hemorrhages, evaluation of diffuse axonal injury, and diagnosis of stroke. Radiological findings and treatment (▶ Fig. 14.1): ○ Epidural hematoma (EDH): Biconvex, may cross dural barriers, usually due to arterial bleeding from the middle meningeal artery, associated with temporal bone fractures (pterion) and lucid interval, surgically treated if ≥ 1 cm or progressively worsening. Better prognosis as often less direct brain injury. ○ Subdural hematoma: Crescent-shaped, does not cross dural barriers, most commonly found over the convexity but may also be found in tentorial or parafalcine areas, usually due to venous or bone bleeding. Correlates with higher impact trauma and marked brain injury; surgically treated if ≥1 cm thickness or ≥ 5 mm of midline shift. ○ Subarachnoid hemorrhage (SAH): A poor prognosticator; high-density blood typically over the convexity; when voluminous and near basal cisterns, strongly consider aneurysm rupture as an antecedent to the severe TBI. ○ Intracerebral hemorrhage (ICH): High-density blood within the parenchyma. ○ Hemorrhagic contusion: High-density blood adjacent to bony prominences (frontal and occipital poles, sphenoid wing, temporal lobe). ○ Intraventricular hemorrhage (IVH): Less likely in trauma. ○ Skull fractures: Linear, nondisplaced fractures can be conservatively managed; stellate, comminuted fractures, or injury to vascular structures may require surgical treatment; temporal bone fractures may require additional thin-cut views to evaluate facial nerve and otologic bones. ○ Depressed skull fractures generally require operative repair when depressed more than the width of the skull or when cosmetically sensitive. Open skull fractures require surgical debridement. ○ Pneumocephalus can often be managed conservatively; CSF otorrhea or rhinorrhea can be treated with ob- servation or CSF diversion and rarely requires surgical treatment; must watch these patients for meningitis! Medical treatments: ○ Intracranial pressure monitor placed for patients who meet criteria (see Chapter 2.2, Neurological Monitoring) and patients treated in intensive care settings with experience in head trauma. ○ Antiseizure medications: – Levetiracetam 20 mg/kg IV once followed by 10 mg/kg BID for 1 week; generally being used instead of Dilantin in contemporary practice. – Utilized to reduce risk of early posttraumatic seizure occurring within 1 week for moderate-to-severe TBI, no impact on late (>2 weeks after injury) posttraumatic seizures or epilepsy, level 2 evidence. – Other agents (e.g., phenytoin, valproate, carbamazepine) have been utilized. ○ Level I evidence that steroids are associated with harm after head injury.3 ○ Gastrointestinal prophylaxis with proton pump inhibitors or H2 blockers recommended to reduce risk of Cushing gastric ulcers in severe TBI. ○ Permissive hypertension with systolic blood pressure from 100 to 200 allowed to encourage cerebral perfusion. Surgical treatments4,5: ○ Decompressive hemicraniectomy: Remove or large cranial bone flap typically performed as a last resort to reduce ICP; can be unilateral or bifrontal; effective at reducing mortality but is associated with 361 | 02.07.20 - 17:35 Neurosurgery Fig. 14.1 Examples of findings seen in traumatic brain injury. Note basal cistern subarachnoid hemorrhage pattern due to an aneurysm and should not be mistaken for trauma. increased risk of vegetative outcome; requires second surgery to replace bone flap; overall 30% overall complication rate including hemorrhage, seizure, infection, bone flap absorption, and hydrocephalus.4,5 ○ Posterior fossa decompression can be used for evacuating hemorrhages causing brainstem compression and obstructive hydrocephalus. ○ Evacuation of ICH controversial for improving outcome, data better evaluated for spontaneous ICH.6 ○ Penetrating brain injury (e.g., bullets, knives) requires debridement of bone and shrapnel; hard-to-access fragments are left alone unless infected7. 14.1.2 Guidelines Guidelines for the Management of Severe Traumatic Brain Injury—4th Edition and Guidelines for the Management of Penetrating Brain Injury in 2001 by the Brain Trauma Foundation synthesize the literature and provide recommendations for care (with levels of evidence; ▶ Table 14.5)8. 362 | 02.07.20 - 17:35 Traumatic Brain Injury Table 14.5 Guidelines from the Brain Trauma Foundation8 Level of Recommendations evidence 2A Bifrontal decompressive hemicraniectomy does not improve 6-mo postinjury outcome in severe TBI with ICP levels > 20 mm Hg for more than 15 min within a 1-h period that are refractory to first-tier therapies; decompression reduces ICP and ICU days Frontotemporoparietal decompression measuring 12 × 15 cm or 15 cm diameter recommended 2B Early (within 2.5 h) and short-term (48 h postinjury) prophylactic hypothermia not recommended to improve outcomes None Hyperosmolar therapy may lower intracranial pressure but insufficient evidence to support specific recommendation 3 EVD system with continuous drainage can lower ICP more effectively than intermittent use CSF drainage to lower ICP with GCS < 6 during the first 12 h can be considered 2B Prolonged prophylactic hyperventilation (PaCO2 ≤ 25 mm Hg) not recommended 2B Barbiturates to induce burst suppression as prophylaxis against the development of elevated ICP not recommended Barbiturate administered to control elevated ICP refractory to maximal medical and surgical treatment recommended, hemodynamic stability essential before and after barbiturate therapy Propofol recommended for control of ICP but does not improve mortality or 6-mo outcome, high-dose propofol can produce morbidity 1 Steroids not recommended for improving outcome or reducing ICP 2A Basal caloric replacement by 5th day recommended to reduce mortality 2B Transgastric jejunal feeding recommended to reduce incidence of ventilator-associated pneumonia 2A Early tracheostomy reduces mechanical ventilation days but no evidence that it reduces mortality or rates of pneumonia Povidone-iodine does not reduce ventilator-associated pneumonia and may increase risk of acute respiratory distress syndrome 3 Antimicrobial-impregnate catheters may reduce catheter-related infections during EVD 3 Low-molecular-weight heparin or low-dose unfractionated heparin with mechanical prophylaxis may reduce risk of deep vein thrombosis; however, there is an increased risk for intracranial hemorrhage expansion 2A Prophylactic phenytoin or valproate not recommended for preventing late posttraumatic seizures Phenytoin decreases risk of early posttraumatic seizures (within 7 d of injury); early posttraumatic seizures have not been associated with worse outcomes Insufficient evidence to recommend levetiracetam over phenytoin for efficacy and safety 2B ICP monitoring reduces in-hospital and 2-wk postinjury mortality in severe TBI 2B Guideline-base recommendations for CPP monitoring decrease 2-wk mortality 3 Jugular bulb monitoring of arteriovenous oxygen content difference may reduce mortality and improve outcomes 3 and 6 mo postinjury Jugular venous saturation of < 50% may be a threshold to reduce mortality and improve outcomes 3 Systolic blood pressure ≥ 100 mm Hg for patients 50–69 y or ≥ 110 mm Hg for patients 15–49 y or over 70 y may decrease mortality and improve outcomes 2B Treatment of ICP ≥ 22 mm Hg recommended to reduce mortality 3 Combination of ICP and clinical CT findings used to make management decisions 2B CPP between 60 and 70 associated with favorable outcome but depends on patient’s autoregulatory status 3 Avoidance of CPP > 70 mm Hg recommended to reduce risk of adult respiratory failure Abbreviations: CPP, cerebral perfusion pressure; GCS, Glasgow coma scale; ICP, intracranial pressure; TBI, traumatic brain injury. 363 | 02.07.20 - 17:35 Neurosurgery Brain Trauma Foundation (BTF) guidelines cover medical and surgical treatments, neurological monitoring, and treatment thresholds.8 14.1.3 Brain Death Examination Guidelines from the American Academy of Neurology aimed to determine criteria that could be utilized to determine brain death (▶ Table 14.6)9; no case report of spontaneous functional recovery or recovery after maximal treatment has been seen for patients meeting such criteria. Difficult but not impossible to perform brain death testing immediately in the trauma bay due to requirements for normothermia, negative toxicology, and blood gas testing. 14.1.4 Outcome/Rehabilitation After initial treatment, rehabilitation is individualized to patient’s needs. Involves treatment with physical, occupational, speech/language, physical medicine, psychology/ psychiatry, and social support. Goals to return patients to society while managing injuries and deficits. Guidelines from the Ontario Neurotrauma Foundation10 and Brain Injury Association of America11 have discussed the role for rehabilitation after TBI. International Mission for Prognosis and Analysis of Clinical Trials in TBI (IMPACT)12 calculator useful as prognostic tool in adults with TBI and GCS ≤ 12; predicts 6-month mortality and 6-month unfavorable outcome; inputs include patient age, GCS motor score, pupillary exam, presence of hypoxia, presence of hypotension, Marshall brain injury CT classification, traumatic SAH on CT, epidural mass on CT, glucose and hemoglobin. 14.2 Spinal Injury Michael Karsy and Erica F. Bisson 14.2.1 Epidemiology Spinal cord injury (SCI): Injury to the spinal cord from trauma, infection, vascular anomalies, neoplasm (▶ Fig. 14.2), or a degenerative process.13 54 cases per million in the United States; 17,000 new hospitalizations/year + 4,000 patients who die on the scene. Average age at injury: 42 years; males account for 80% of new cases; younger patients are associated with trauma and older patients are associated with falls. Causes: 38% vehicular trauma, 30.5% falls, 13.5% violence, 9% sports, 5% medical/surgical, 4% other. 30% rate of rehospitalization one or more times after SCI. 14.2.2 Diagnosis Initial hemodynamic stabilization and CT imaging can be performed by the first-responding provider with early spine surgeon consultation for further imaging or clinical management (▶ Fig. 14.3). Stabilization of airway, breathing, and circulation (ABCs) takes precedence prior to further SCI workup. High-energy mechanisms, associated polytrauma, or cervical vertebral trauma should suspect SCI and associated vascular injuries. SCI classification aids in tracking neurological recovery and predicting outcome. The American Spinal Injury Association (ASIA) International Standards for Neurological Classification of Spinal Cord Injury, commonly referred to as the AIS, is used to communicate about injury location and severity (▶ Table 14.7). Numeric AIS scores are calculated by identifying the sensory level by pin prick and light touch for each side, the motor level for each side, and then a letter grade is assigned. Preserved sacral function is a key prognostic factor suggesting delayed improvement and thus key to an incomplete SCI. 364 | 02.07.20 - 17:35 Spinal Injury Table 14.6 Brain death testing9 Prerequisites Irreversible coma present and cause is known Neuroimaging explains coma CNS depressant drugs are absent, toxicology screen completed No evidence of residual paralytics Absence of severe acid–base, electrolyte, or endocrine abnormalities Normothermia or mild hypothermia (core temperature > 36 °C) Systolic blood pressure ≥ 100 mm Hg No spontaneous respirations Examination Pupils nonreactive (all must be checked) Corneal reflex absent Oculocephalic reflex absent, tested if C-spine stable Oculovestibular/cold caloric reflex absent No facial movement to stimulation at supraorbital or temporomandibular joint seen Gag reflex absent Couch reflex absent to tracheal suctioning Absent of motor response to noxious stimuli in all four extremities Apnea testing Patient is hemodynamically stable (all must be checked) Ventilator adjusted to provide normocarbia (PaCO2 34–45 mm Hg) Patient preoxygenated with 100% FiO2 for > 10 min to PaO2 > 200 mm Hg with a PEEP of 5 cm H2O Oxygen provided via suction catheter at the level of the carina at 6 L/min or via a T-piece with continuous positive airway pressure (CPAP) at 10 cm H2O Ventilator disconnected and spontaneous respirations are absent Arterial blood gas shows PCO2 ≥ 60 mm Hg or rise of 20 mm Hg from baseline, draws at 8–10 min or serial draws every 2 min can be performed Apnea test aborted if patient fails above or becomes hemodynamically unstable Ancillary testing (needs to be performed only in patients who cannot undergo apnea testing) Cerebral angiography Contrast should be injected in the aortic arch under high pressure and reach both anterior and posterior circulations No intracerebral filling should be detected at the level of entry of the carotid or vertebral artery to the skull External carotid circulation should be patent Filling of superior sagittal sinus may be delayed Electroencephalography Minimum of eight scalp electrodes used (EEG) Interelectrode impedance should be between 100 and 10,000 Ohm Integrity of recording system should be tested Distance between electrodes should be at least 10 cm Sensitivity should be increased to at least 2 μV for 30 min with inclusion of appropriate calibrations High-frequency filter should not be set below 30 Hz; low-frequency filter should not be set above 1 Hz EEG should demonstrate a lack of reactivity to intense somatosensory or audiovisual stimuli Transcranial Doppler TCD must have a reliable signal, may be less reliable in patients with a prior craniotomy ultrasonography (TCD) Abnormalities include reverberating flow, small systolic peaks in early systole Bilateral insonation of anterior and posterior circulation should be performed using the suboccipital transcranial window (temporal lobe, above the zygomatic arch and vertebrobasilar arteries) (Continued) 365 | 02.07.20 - 17:35 Neurosurgery Table 14.6 (Continued) Brain death testing9 Cerebral scintigraphy Isotope should be injected within 30 min of reconstitution (technetium Tc 99 m Anterior and lateral planar image counts (500,000) of the head should be performed hexametazime [HMPAO]) immediately, 30–60 min postinjection, and 2 h postinjection Optional to confirm injection with imaging of the liver No radionucleotide localization in the middle cerebral, anterior cerebral, or basilar artery territories should be seen No tracer in the superior sagittal sinus should be seen, minimal tracer from the scalp may be seen Fig. 14.2 Neoplastic diseases of the spine. A diagram of pathology types and specific locations of the spine is shown. Tumors can be characterized by their location, namely, extradural (typically metastatic cancer), intradural extramedullary (meningiomas and schwannomas), or intradural intramedullary (ependymomas and astrocytomas) tumors. Additional lesions of the spine include lymphoma, multiple myeloma, chordoma, and a variety of primary bone tumors. Injury types: 45% incomplete tetraplegia, 21.3% incomplete paraplegia, 20% complete paraplegia, 13.3% complete tetraplegia, 0.4% normal. Spine injury patterns (▶ Fig. 14.4) may be due to trauma or other injury mechanisms: ○ Tetraplegia: Injury of arms and legs. ○ Paraplegia: Injury of legs only. ○ Central cord syndrome: Characterized by injury to the traversing anterolateral spinothalamic tract, results in a cape-like distribution of numbness commonly at the level of the shoulder blades with weakness and/or numbness in the hands (distal > proximal) and possibly legs (proximal > distal). ○ Brown–Sequard syndrome: Hemisection of the spinal cord (i.e., bullet or knife injury); results in ipsilateral paralysis (corticospinal tract), ipsilateral loss of proprioception and vibration (dorsal columns), and contralateral loss of pain and temperature sensation (anterolateral spinothalamic). 366 | 02.07.20 - 17:36 Spinal Injury Fig. 14.3 Flow diagram of spinal cord injury management. ASIA, American Spinal Injury Association; ATLS, Ad- vanced Trauma Life Support; BMP, basic metabolic panel; CBC, complete blood count; CT, computerized tomography; INR, international normalized ratio; MAP, mean arterial blood pressure; PT, prothrombin time; PT/OT, physical therapy/occupational therapy; PTT, partial thromboplastin time; SCI, spinal cord injury. Table 14.7 American spinal injury association (ASIA) scale Type Injury Description A Complete No motor or sensory function in sacral segments S4–S5 B Incomplete Sensory but not motor function below injured level, sacral sparing at S4–S5 C Incomplete Motor function with < 3 strength in more than half of key muscle groups below injured level D Incomplete Motor function with ≥ 3 strength in more than half of key muscle groups below injured level E Normal Return of motor and sensory function after injury ○ Anterior spinal artery infarction: Deficits of the ventral horns and motor weakness. ○ Posterior spinal artery infarction: Injury of the dorsal horns resulting in deficits of proprioception and vibration. 14.2.3 Imaging CT scans have supplanted X-rays to image any presumed fracture of the spine due to improved sensitivity and wide availability. Allows improved classification of fracture pattern depending on location in spine. Rapid CT interpretation: Misalignment of anterior and posterior marginal lines, spinolaminar line, and interspinous line can allude to injury (▶ Fig. 14.5). Excessive prevertebral swelling (normal: < 7 mm at C2/3 or < 21 mm at C6/7) can allude to injury. 367 | 02.07.20 - 17:36 Neurosurgery Fig. 14.4 Spinal cord injury patterns. Fig. 14.5 Rapid CT assessment of spine instability. Assessment of the anterior marginal line (red), posterior marginal line (blue), spinolaminar line (green), and interspinous line (orange) can be a rapid method to evaluate spine malalignment and potential instability. Bone cortical surfaces evaluated for fragments and breaks. Soft-tissue swelling assessed (6 mm at C2 and 22 mm at C6 within normal limits). 368 | 02.07.20 - 17:36 Spinal Injury MRI used to evaluate ligamentous injury (anterior longitudinal ligament, posterior longitudinal ligament, ligamentum flavum), herniated disks, epidural hematoma, and spinal cord T2/STIR signal change. Cervical fractures with possible vertebral artery injury are evaluated with CT angiograms of the head/neck. Diagnostic cerebral angiograms are used for severe injuries or if requiring endovascular treatment. Isolated spinous and transverse process fractures do not necessitate expert consultation and are managed with pain control. 14.2.4 Medical Management Injury pathophysiology14: ○ Primary injury: Initial traumatic injury to the spinal cord via shear, laceration, contusion, and compression; not treatable. ○ Secondary injury: Subsequent neurological injury from molecular mechanisms (i.e., oxidative stress); optimized with medical treatment. ○ SCI → spine shock (areflexia/hyporeflexia and autonomic dysfunction) → neurogenic shock (disconnected sympathetic innervation, decreased heart rate, blood pressure, cardiac output, and systemic vascular resistance) → spasticity (hyperreflexia, increased muscle tone). Medical management14: ○ Immobilization of the level of injury until definitive decompression and/or stabilization. ○ Augmentation of mean arterial blood pressure (MAP) > 85 mm Hg for 3–7 days (with dopamine or norepinephrine). ○ Initiation of a SCI protocol (e.g., bowel regimen to prevent constipation and ileus). ○ Lower extremity compression stockings to reduce deep vein thrombosis (DVT) and pulmonary embolism (PE) risk. ○ Abdominal binder to improve MAP; cough assistance to reduce risk of pneumonia. ○ Nutritional support to prevent muscle atrophy and catabolism; peptic ulcer prophylaxis. ○ Rehabilitation consultation for subsequent care. ○ Early mobilization to improve recovery and reduce risk of DVT, PE, pneumonia, and pressure ulcers. ○ No specific medical drug exists for SCI currently.14 ○ Bracing (cervical thoracic orthosis, thoracolumbosacral orthosis, Jewett brace, Minerva) aims to reduce motion and improve pain control, limited efficacy, stability checked with upright X-rays in brace compared to initial supine imaging. ○ Dissection injuries to the vertebral artery are graded using the Biffl grade (▶ Table 14.8).15 Grade 1 and 2 dissections are treated with aspirin to prevent stroke formation as these heal well.16 Grade 3, 4, and 5 injuries are treated with a combination of anticoagulation, endovascular, or open treatments to either repair or sacrifice the vessel. Corticosteroid17,18,19: ○ Controversial and not recommended by the 2013 American Association of Neurological Surgeons/ Congress of Neurological Surgeons (AANS/CNS) Joint Taskforce guidelines statement.20 ○ National Acute Spinal Cord Injury Studies (NASCIS) were a series of three large randomized clinical trials evaluating methylprednisolone sodium succinate, NASCIS III demonstrated a 5-point improvement in motor score when treated between 3 and 8 hours; concern for higher rates of wound infection, pulmonary embolism, and pneumonia with steroid treatment. Table 14.8 Carotid or vertebral artery blunt injury (Biffl grade) Type Description Treatment I Luminal irregularity or dissection with < 25% narrowing Anticoagulation (e.g., aspirin) or carotid stenting II Dissection or intramural hematoma with > 25% luminal if progression of injury narrowing or intimal flap III Pseudoaneurysm Carotid stenting IV Occlusion Anticoagulation or endovascular vessel sacrifice V Transection with free extravasation Open repair, bypass, or sacrifice 369 | 02.07.20 - 17:36 Neurosurgery 14.2.5 Surgical Management Injury classification has evolved the surgical decision-making process, but much of the criteria for surgery continues to depend on expert opinion.20 ○ Denis model: Spine instability with disruption in two of three spine compartments. ○ AOSpine classification: Categorizes fractures by mechanism of injury, more commonly used by spine surgeons; compression (type A), extension (type B), translation/rotation (type C); fractures of type B and C patterns more commonly need surgical fixation while fractures of type A patterns can be often managed conservatively. ○ Thoracolumbar Injury Classification and Severity (TLICS) scale and the Subaxial Cervical Spine Injury Classification (SLIC) system (▶ Table 14.9) suggest surgery with score ≥ 5, easy to use. Fracture types: ○ Atlantooccipital dissociation: Separation of C1 from the occipital condyle (> 2.5 mm suggests dissociation on CT scan more accurately than cervical X-rays) due to disruption of the alar and capsular ligaments, highly unstable, and requires occipitocervical fusion. ○ Occipital condyle avulsions: Type 1 (impacted fracture, treated with collar), type 2 (basilar skull fracture extending into condyle, treated with collar), type III (avulsion injury, potentially unstable, and may require occipitocervical fusion). ○ C1/Jefferson fractures: Fractures of both the anterior and posterior tubercle of C1, treated with collar if minimally displaced with intact transverse ligament, C1–C2 fusion if significant fracture displacement or disrupted transverse ligament. ○ C2/Hangman fractures: Fracture with or without angulation of the C2 pars interarticularis, type 1 (< 3 mm displacement, treated with collar), type II (> 3 mm displacement and > 11-degree angulation, hard collar if reducible, C1–C2 or C2–C3 fusion if disrupted disk), type IIa (< 3 mm displacement and > 11-degree angulation, same treatment as type II), type III (associated facet dislocation, requires C1–C3 fusion). ○ Atlantoaxial rotatory subluxation: Hyperflexibility of cervical spine resulting in C1–C2 dislocation, often in children with trauma, can be reduced but often requires fixation. Table 14.9 TLICS or SLICS for prediction of surgical need TLICS SLICS Category Characteristic Score Characteristic Score Fracture morphology None 0 None 0 Compression 1 Compression 1 Burst 2 Burst 2 Translation/rotation 3 Distraction 3 Distraction 4 Rotation/translation 4 Integrity of posterior Intact 0 Intact 0 ligamentous Suspected injury 2 Indeterminate 1 complex Injured 3 Disrupted 2 Neurological status Intact 0 Intact 0 Nerve root injury 2 Nerve root injury 1 Complete injury 2 Complete injury 2 Incomplete injury 3 Incomplete injury 3 Cauda equina 3 Continuous cord compression with +1 neurodeficit Score: ≤ 3, nonoperative treatment; 4, nonoperative or operative at clinician discretion; ≥ 5, operative. Abbreviations: SLICS, Subaxial Cervical Spine Injury Classification system; TLICS, Thoracolumbar Injury Classification and Severity. 370 | 02.07.20 - 17:36 Spinal Injury ○ Dens fracture: Type I (fracture at superior tip, hard collar), type II (fracture at base of dens, controversial treatment in hard collar, halo fixation or C1–C2 fusion depending on patient age and risk for malunion), type III (fracture through base and body of C2, hard collar or halo). ○ Jumped or perched cervical facets: Injury from flexion and axial load, often associated with SCI, urgent traction performed at bedside or in operating room with need for fixation due to instability. ○ Spinous or transverse process fractures: Often nonoperative even when extends into facets or found at multiple contiguous levels. ○ Teardrop fracture: Hyperflexion injury with anteroinferior bone chip and sagittal split fracture, highly unstable and requires fixation, can be mistaken for avulsion fracture which is stable. ○ Compression fracture: Disruption of the superior or inferior vertebral endplate, usually treated nonoperatively with or without bracing. ○ Burst fracture: Disruption of the superior and/or inferior vertebral endplate with posterior displacement of a bone fragment into the spinal canal; can be treated nonoperatively in the setting of mild pain, no progressive deformity and no neurological symptoms; symptomatic lesions treated with spine fusion. ○ Chance fracture: Fracture across the bony elements extending from the posterior lamina through the vertebral bodies; can be managed nonoperatively if fragments are well apposed, otherwise requires surgical treatment. ○ Fraction/dislocation: Disruption, displacement, and malrotation of a spine fracture; almost always unstable and requires operative fixation. Various anterior and posterior surgical approaches possible with goal of bony fusion over 3–6 months; hardware can be removed for some fractures after healing (e.g., burst fractures, pediatric fractures). Timing of surgical decompression remains controversial, some evidence that surgery within 24 hours of injury shows improved outcomes after cervical cord injury.21 Sports-related fractures are more controversial and have limited data, thus require the use of expert opinion, evaluation of injury and anatomy, and regard to level of activity to determine return-to-play.22 14.2.6 Additional Topics Cauda equina syndrome (CES): ○ Neurological emergency but rare; significant morbidity or potential for recovery depending on treatment; earlier onset of symptoms and earlier treatment predicts improved recovery. ○ Occurs in 1–2% of herniated disks. ○ CES results from compression of the lumbosacral nerve roots below L1, and most often presents with asymmetric lower extremity weakness, perineal or saddle numbness (S3–S5 distribution), and bladder/bowel dysfunction, along with back pain and potential gait dysfunction. ○ Can mimic conus medullaris compression syndrome (compression of distal tip of the spinal cord; ▶ Table 14.10). ○ Up to 20% of patients can have continued urological or sexual dysfunction after treatment. ○ Treated with lumbar decompression. Malignant spinal cord compression (MSCC): ○ Causes (▶ Fig. 14.2): – Epidural disease directly results in cord compression. – Tumor causes pathological fractures resulting in spinal canal compromise. – Tumor hemorrhage or vascular insult results in acute neurological decline causing a spinal emergency. ○ Patients with a known history of aggressive primary cancer are counseled on monitoring for malignant spinal cord compression MSCC by evaluating changes in neurological symptoms. ○ Patients with known cancer and new-onset back pain should have MR imaging. ○ Surgical decompression followed by radiation shows improved outcomes than radiation alone for preservation of neurological function.23 ○ Surgery for MSCC follows the same general principles as for traumatic SCI, including rapid decompression of the spinal cord and nerves followed by stabilization if necessary. 371 | 02.07.20 - 17:36 Neurosurgery Table 14.10 Comparison of cauda equina and conus medullaris syndrome Clinical feature Cauda equina syndrome Conus medullaris syndrome Level L2 sacrum compression L1–L2 compression Presentation Sudden and unilateral Sudden and bilateral Reflexes Knee and ankle impacted Ankle impacted Radicular pain More severe Less severe Lower back pain Less More Impotence Absent Frequent Numbness Asymmetrical Symmetrical Motor strength Asymmetric, a reflexive paraplegia Symmetric, hyperreflexive, distal paresis of lower limbs Sensory Asymmetrical saddle anesthesia Symmetrical saddle anesthesia Sphincter Urinary retention, presents later Urinary and fecal incontinence, presents earlier Table 14.11 C-spine clearance NEXUS criteria for C-spine imaging Canadian C-spine rule Focal neurological deficit + 1 Age ≥ 65 y, extremity paresthesias or dangerous Midline spinal tenderness present + 1 mechanism (fall ≥ 3 feet/5 stairs, axial loading injury, high-speed motor vehicle collision, bicycle collision, motorized recreational vehicle) Altered level of consciousness present + 1 Absence of low-risk factors (sitting position in ED, ambulatory at any time, delayed neck pain, midline tenderness, simple rear end motor vehicle collision) Intoxication present + 1 Inability to rotate neck 45 degrees left and right Distracting injury present + 1 Yes to any factor suggests inability to clear patient without Score ≥ 1 suggests inability to clear patient without imaging imaging ○ Surgical approach to the cervical, thoracic, and lumbar spine varies based on tumor location, tumor type, and response to prior treatment (including radiation). For patients with back pain without neurologic symptoms, bracing, radiation, and kyphoplasty are potential treatment strategies. ○ Partial tumor resection with the goals of separating tumor from the spinal cord (i.e., separation surgery) can be useful for later stereotactic radiosurgery. Cervical spine clearance20: ○ NEXUS criteria (▶ Table 14.11) can be used to reducing imaging for spine clearance, 83–100% sensitivity for detecting cervical SCI. ○ Canadian C-spine Rule (▶ Table 14.11) shows improved sensitivity (99.4 vs. 90.7%) from NEXUS for detecting cervical SCI. ○ CT imaging better for evaluating fractures than X-rays. Normal CT has a high likelihood ratio of ruling out unstable cervical injury.24,25 ○ Clinical clearance attempted after normal CT imaging without pain. ○ Clearance in the setting of pain can be performed using flexion/extension films, MRI of the neck, or physician preference. 14.2.7 Rehabilitation SCI rehabilitation requires interdisciplinary inpatient and outpatient care over long time periods.26 Airway clearance: Ventilator dependence decreases survival and pneumonias are the leading cause of death after SCI; secretion clearance by cough assist, vest therapy, mucolytics (sodium bicarbonate, acetylcysteine); diaphragmatic stimulators can aid in high cervical SCI; early tracheostomy reduces ventilator time, sedation requirements, and ICU stay and improves suctioning. 372 | 02.07.20 - 17:36 Vascular Diseases Venous thromboembolism: Occurs in 50–100% of SCI patients, greatest incidence between 3 and 14 days; prevented with pneumatic compression stockings, heparin, screening ultrasounds, and inferior vena cava filters. Autonomic dysreflexia: Occurs with T6 or higher lesions, normal noxious stimuli generates uncontrolled hypertension due to an absent feedback mechanism; risk of stroke; treated by removing noxious stimuli (e.g., urinary catheterization, bowel movement, reducing pressure ulcers). Nutrition: Generally poor in acute postinjury period, continued muscle atrophy over time. Gastric motility: Reduced bowel motility due to hypotonic bowel and hypertonic sphincter; treated with bowel regimen. Neurogenic bladder: Bladder overdistension without feedback about fullness along with sphincter spasticity; treated with anticholinergics (e.g., oxybutynin, tolterodine, Botox) for bladder and alpha-adrenergics (e.g., terazosin, tamsulosin, Botox) for sphincter. Pressure ulcers: Occur in 20–30% of patients in rehab; most common in sacrum (39%), heels (13%), ischium (8%), occiput (6%); treated with early mobilization and wound care. Depression: Occurs in 30% of SCI patients compared to 10% in general population. Heart disease: Increased risk compared to general population. Orthostatic hypotension: Occurs with injuries above T6, treated with blood pressure augmenting agents. Heterotopic ossification: Bone deposits in soft tissue around hips and knees, difficult to treat. Hypo/hyperthermia. Chronic pain. Spasticity: Treated with baclofen, diazepam, Zanaflex, physical therapy, Botox. Sexual and reproductive health. 14.3 Vascular Diseases Jeyan Kumar, Yashar Kalani, and Min Park 14.3.1 Anatomy/Physiology The brain receives roughly 20% of the cardiac output with normal cerebral blood flow of 50 mL/100 mg/min. Paired carotid and vertebral arteries provide the majority of the vascular supply to the brain. Common carotid artery bifurcates at C4 into the internal carotid artery (ICA) and external carotid artery (ECA). ECA provides blood to the face and neck. ○ Can have multiple anastomoses with the ICA and vertebral arteries. ○ Seven branches (proximal to distal from bifurcation): Superior thyroid, ascending pharyngeal, lingual, facial, occipital, posterior auricular, superficial temporal, and internal maxillary arteries. Internal carotid artery: ○ Divided into seven segments, C1–C7. Becomes intradural at C5 (clinoidal) segment. ○ Terminates into two main branches: anterior cerebral artery and middle cerebral artery. Vertebral artery (VA): ○ Arises from the subclavian artery bilaterally and enters the foramen transversarium of the cervical vertebrae at C6, exits the foramen at C2 and crosses laterally on C1 prior to entering the dura at the foramen magnum. ○ Divided into four segments (V1–V4) and becomes intradural at V4. VAs combine to form the basilar artery. ○ Left VA dominant 50%, right VA 25%, and no dominance 25%. Circle of Willis: ○ Circulatory anastomoses of the anterior and posterior circulation via the anterior communicating and posterior communicating arteries with the internal carotid and posterior cerebral arteries. ○ Can maintain cerebral perfusion in situations of stenosis or occlusion. 373 | 02.07.20 - 17:36 Neurosurgery 14.3.2 Subarachnoid Hemorrhage Epidemiology: ○ Subarachnoid hemorrhage (SAH): Bleeding between the arachnoid membrane and pia mater (▶ Fig. 14.6). ○ Incidence of aneurysmal SAH in the United States: 9.7–14.5 per 100,000 persons.27 ○ Aneurysmal SAH incidence peaks at 55–60 years of age, 1.24 times more common in women, higher in African Americans and Hispanics compared to Caucasians.28 ○ Smoking, hypertension, and excessive alcohol consumption are important risk factors for the development of SAH.29 Etiology: ○ Major classification: Spontaneous versus traumatic. ○ Spontaneous causes: Aneurysmal (most common, 75–85%), cerebral arteriovenous malformation (AVM), CNS vasculitis, tumor, vessel dissection, coagulopathies (i.e., thrombocytopenia), dural sinus thrombosis, spinal AVM, illicit drug use (e.g., cocaine), sickle cell anemia, pituitary apoplexy, pretruncal aneurysmal SAH, no cause determined (14–22%).30 ○ SAH can be accompanied with intracerebral hemorrhage (ICH). Diagnosis (▶ Fig. 14.7): ○ Spontaneous SAH classically described as sudden, thunderclap headache. Described as the “worst headache of my life” and often accompanied with nausea, vomiting, AMS, HTN, nuchal rigidity (meningismus), and/or photophobia. Fig. 14.6 Representative images of various cerebrovascular diseases. (a) A patient presented with the “worst headache of their life” and modified Fisher Grade 4 subarachnoid hemorrhage (SAH) and (b) a CT angiography (CTA) demonstrating a ruptured left pericallosal aneurysm. (c) A diagnostic cerebral angiography following surgical clipping of the ruptured aneurysm. (d) A second patient with a spontaneous intracerebral hemorrhage presented with the “worst headache of their life” and acute onset of left-sided hemiparesis. The patient had an intracerebral hemorrhage (ICH) score of 1. (e) Arterial phase diagnostic cerebral angiography demonstrating a Spetzler–Martin grade 5 arteriovenous malformation (AVM) with ruptured Spetzler–Martin grade 5 AVM and (f) a late phase arterial angiography demonstrated the markedly enlarged deep venous drainage. 374 | 02.07.20 - 17:36 Vascular Diseases ○ Hunt-Hess Grade31: symptom-based classification of aneurysmal SAH. Grades 1–5 in order of increasing mortality (▶ Table 14.12). ○ World Federation of Neurological Societies (WFNS) grading of aneurysmal SAH32: Glasgow Coma Scale score with absence/presence of major neurologic deficit. Grades 0–5 in order of increasing mortality (▶ Table 14.13). ○ Fisher classification33 and modified Fisher classification34: imaging-based grading of aneurysmal SAH with severity predicting symptomatic vasospasm. Grades 1–4 in order of increasing risk of vasospasm (▶ Fig. 14.6a, ▶ Table 14.14). ○ Computed tomography (CT) and CT angiography (CTA) of the head to identify a possible vascular source for the SAH (▶ Fig. 14.6b). Fig. 14.7 Flow diagram of patient with intracranial hemorrhage. CTH, com- puted tomography of the head; AMS, altered mental status; CTA, computed tomography angiography; ICU, inten- sive care unit; Q1, every one hour; CSF, cerebrospinal fluid; ICH, intracerebral hemorrhage. Table 14.12 Hunt/Hess Score for aneurysmal SAH Symptoms Grade Slight headache or nuchal rigidity, asymptomatic, alert, and oriented 1 Moderate to severe headache, nuchal rigidity, no neurologic deficits other than cranial nerve palsies 2 Lethargy or confusion, mild focal neurological deficit 3 Stupor, moderate to severe neurologic deficit 4 Comatose, showing signs of severe neurologic deficit (decerebrate posturing) 5 Abbreviation: SAH, subarachnoid hemorrhage. 375 | 02.07.20 - 17:36 Neurosurgery Table 14.13 World Federation of Neurological Surgeons grading system for SAH Glasgow Coma Scale Motor deficit Grade 15 Absent 1 13–14 Absent 2 13–14 Present 3 7–12 Present or absent 4 3–6 Present or absent 5 Abbreviation: SAH, subarachnoid hemorrhage. Table 14.14 Modified Fisher Scale for subarachnoid hemorrhage Grade Description 0 No SAH and no IVH 1 Focal or diffuse, thin SAH, no IVH 2 Focal or diffuse, thin SAH, IVH present 3 Focal or diffuse, thick SAH, no IVH 4 Focal or diffuse, thick SAH, IVH present Abbreviations: IVH, intraventricular hemorrhage; SAH, subarachnoid hemorrhage. ○ Digital subtraction angiography (DSA) is the gold standard for imaging of CNS vasculopathies and is used to identify a vascular source for the SAH if the CT/CTA is negative. It may be used to better define the anatomy in preparation of surgical treatment or as a modality for intervention (see later). ○ Lumbar puncture can be used if clinical suspicion of SAH exists with a negative CT scan. Assesses for xanthochromia (yellow color of supernatant) and presence of red blood cells (compare tubes 1 and 4 for decreasing number of RBCs to differentiate traumatic tap vs. SAH). ○ MRI of the brain not routinely used for the initial assessment of SAH. Treatment (▶ Fig. 14.6): ○ Medical management: – Admission to an ICU. – Intubation, if required to protect the airway. – Blood pressure control to avoid significant hypertension (i.e., systolic blood pressure [SBP] < 140 or SBP < 160). – Correction of coagulopathies or thrombocytopenia. – Initiate deep vein thrombosis (DVT) prophylaxis with SCDs on admission and prophylactic subcutaneous low-molecular-weight heparin/heparin when appropriate. – Management of acute elevations in intracranial pressure (ICP) with hyperosmotic agents (i.e., mannitol, hypertonic saline). – Physical, occupational, and speech therapy for assessment and treatment. ○ Surgical management: – CSF diversion with external ventricular drain or lumbar drain (not common) in the presence of hydrocephalus and/or for elevated ICP management. – Endovascular intervention for embolization of the aneurysm and/or intra-arterial treatment of vasospasm. – Craniotomy for clipping of ruptured aneurysms. – Possible craniectomy for surgical treatment of brain swelling. Complications: ○ Cerebral vasospasm: – Symptomatic narrowing of arterial vessels following subarachnoid hemorrhage. Remains a significant cause of morbidity and mortality in this patient population. 376 | 02.07.20 - 17:36 Vascular Diseases – Radiographic vasospasm is found in 43% of all aneurysmal SAHs and symptomatic vasospasm in 32.5%. There is a 30% mortality with symptomatic vasospasm and 34% of symptomatic vasospasm results in permanent neurologic deficits.35 – Radiographic evidence as early as day 4, peak incidence between days 10 and 17; mean time to symptomatic vasospasm is 7.9 days.35 – Potentially reversible with increasing blood pressure or vasodilation by intra-arterial treatment with calcium channel blockers (e.g., verapamil) or balloon angioplasty. Oral nimodipine is used as a neuroprotective agent for vasospasm. ○ Hydrocephalus: – Reported incidence between 6 and 67% for acute and chronic hydrocephalus. – Acute/subacute (days 0–13): Treated with external ventricular drain and potential ventriculoperitoneal shunt placement. – Chronic: Can present in a delayed fashion following SAH. 21.2% of patients required shunting after external ventricular drain, 26% of shunted patients received shunts after discharge.36 14.3.3 Spontaneous Intracerebral Hemorrhage Epidemiology: ○ Second most common cause of stroke comprising 10–15% of all strokes.37 ○ Worldwide incidence of 10–20 per 100,000 population. High incidence of mortality with 38% of patients passing away within the first year.38 ○ Increased incidence with age, gender (male > female), and ethnicity (African Americans > Caucasians).37 Causes/risk factors: ○ Hypertension: Cerebrovascular damage to small arteries and arterioles from long-standing hypertension (chronic) versus acute crisis such as with certain drugs (e.g., cocaine). ○ Alcohol consumption: Moderate to heavy consumption of alcohol within 24 hours or 1 week presents an increased risk of ICH in a dose-dependent manner.39 ○ Anticoagulant therapy increases the risk of ICH by seven- to ten-fold.37,40 ○ Liver disease or coagulopathy (e.g., leukemia or thrombocytopenia). ○ Neoplasm: Can be the initial presentation of a cerebral neoplasm: – Primary tumors: Most commonly glioblastoma multiforme and oligodendroglioma. – Most common hemorrhagic metastatic tumors: Renal cell, melanoma, prostate, or lung.37 ○ Hemorrhagic conversion of an ischemic stroke. ○ Vascular malformations: Cavernoma, AVM, or aneurysm (generally in conjunction with SAH). ○ Cerebral amyloid angiopathy, deposition of beta-amyloid within vessel walls. Can present with repeated lobar hemorrhages in the elderly. ○ Dural or venous sinus thrombosis. Diagnosis: ○ Can present with gradual progressive onset of neurological deficit versus ischemic stroke where deficits are maximal at onset, but can also present acutely. ○ CT of the head is used for the initial diagnosis and allows for measurement of clot volume, presence of intraventricular hemorrhage, and/or the presence of hydrocephalus. ○ CTA of the head and neck to evaluate for underlying vascular sources. ○ MRI of the brain to evaluate for underlying lesions. May need to be repeated in a delayed setting following resorption of the hematoma for suspicious lesions (suspected neoplasm) obscured by the hemorrhage. ○ DSA, if suspicion for underlying vascular lesion, such as AVM or aneurysm, that was not identified by the CTA of the head. ○ ICH score (▶ Table 14.15), five-point scale that evaluates 30-day mortality.41 Treatment: ○ Medical management: – Admission to a monitored unit (intensive care unit). – Intubation, if required, to protect the airway. – Blood pressure control to avoid significant hypertension (i.e., SBP < 140 or SBP < 160). 377 | 02.07.20 - 17:36 Neurosurgery Table 14.15 Intracerebral hemorrhage (ICH) score Description Score Glasgow coma scale GCS 3–4: + 2 GCS 5–12: + 1 GCS 13–15: 0 Age ≥ 80 +1 ICH volume ≥ 30 mL +1 Intraventricular hemorrhage +1 Infratentorial location of hemorrhage +1 Note: 30 day mortality for scores: 1 (13%), 2 (26%), 3 (72%), 4 (97%), 5 (100%). – Correction of coagulopathies or thrombocytopenia. – Initiate DVT prophylaxis with SCDs on admission and prophylactic subcutaneous low- molecular-weight heparin/heparin when appropriate. – Management of acute elevations in intracranial pressure (ICP) with hyperosmotic agents (i.e., mannitol, hypertonic saline). – Prophylactic antiepileptic drug treatment is controversial; 8% of patients with ICH will develop seizures within 30 days.42 – Physical, occupational, and speech therapy for assessment and possible treatment. ○ Surgical management: – External ventricular drain placement for treatment of hydrocephalus and/or intraventricular hemorrhages. – Craniectomy for infratentorial hemorrhages: Brainstem compression may cause rapid neurologic decline requiring surgical intervention. – Craniectomy for supratentorial hemorrhage: Role of surgical intervention remains controversial; Surgical Trial in Traumatic Intracerebral Haemorrhage (STICH) and STICH II demonstrated no significant benefits with surgery; Minimally Invasive Surgery with Thrombolysis in Intracerebral Haemorrhage Evacuation (MISTIE) III trial demonstrated that surgery did not improve outcomes after a year for moderate to large hemorrhages.43,44,45 – Clot location, size, presence of midline shift, persistently elevated ICP, pathology (e.g., tumor, AVM), and neurologic exam (GCS) used to determine candidacy for surgical evacuation. – Trials for minimally invasive evacuation of ICH are ongoing. 14.3.4 Stroke: Epidemiology: ○ Third leading cause of death in the United States; results in 140,000 annual deaths; leading cause of long-term disability in the United States. ○ Affects 795,000 people annually with 600,000 being first strokes; roughly every 40 seconds; affects 15 million people worldwide. ○ 75% of strokes occur in patients > 65 years of age. ○ Highest risk of death in the southeastern United States termed the “stroke belt.” Etiology: ○ 80% ischemic, 20% hemorrhagic. ○ Mechanisms. – Thrombosis: Obstruction of artery due to arteriosclerosis, dissection, fibromuscular dysplasia with or without superimposed thrombosis. – Embolism: Debris translocating from one area to another causing obstruction; occurs from cardiac, arterial, or unknown sources. – Hypoperfusion: Low circulatory flow for necessary tissue metabolism resulting in tissue injury. 378 | 02.07.20 - 17:36 Vascular Diseases ○ Definitions: – Transient ischemic attack: Change in neurological symptoms lasting less than 24 hours. – Large vessel occlusion: Obstruction of the extracranial (common and internal carotid) and intracranial (circle of Willis, proximal branches) arteries. – Small vessel disease: Disease of distal vessels from the vertebral, basilar, or middle cerebral artery; results in lipohyalinosis and atheroma. – Lacunar infarct: Injury to vessels of the basal ganglia, internal capsule, thalamus, or pons. – Cryptogenic stroke: Cerebral ischemia due to unknown origin after workup. ○ High-risk cardiac features for stroke include atrial fibrillation, valvular disease, or arrhythmia. ○ Hypercoagulopathy risk factors include blood disorders (e.g., sickle cell anemia) or coagulation disorders (e.g., factor V Leiden). ○ Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification of ischemic stroke divides stroke into five categories: large artery atherosclerosis, cardioembolism, small vessel occlusion, stroke of other determined etiology, and stroke of undetermined etiology. Diagnosis: ○ See Chapter 16.2 Intubation, ACLS/PALS, Cardiac Arrest, and Stroke Reference. ○ History, physical, and neurological exam performed; time of stroke onset noted from patient, family, and/or emergency medical services; evaluation of current patient anticoagulation performed; standard labs evaluated (complete blood count, complete metabolic panel, coagulation factors, type and screen, troponin); EKG used to evaluate cardiac arrhythmia as potential cause and rule out concomitant myocardial infarction; other select tests performed in select patients (liver function test, toxicology, blood alcohol, pregnancy tests, arterial blood gas, chest X-ray). ○ Rapid assessment of stroke includes evaluation of deficits in face, drift/weakness, and abnormal speech. ○ National Institutes of Health Stroke scale (see ▶ Table 16.21): Obtained with almost all protocolized brain attacks or stroke evaluations; scored 0–42 with 42 being highest possible score; scores of 5–15 indicate moderate stroke and scores > 22–25 suggest a higher risk of hemorrhage with use of tissue plasminogen activator (TPA). ○ Noncontrast CT of the head prerequisite for any medical management to identify stroke burden and rule out hemorrhagic stroke. ○ Vascular imaging involving CT angiography and CT perfusion most commonly used to rapidly assess areas of core stroke (i.e., nonsalvageable tissue) and penumbra (i.e., potentially salvageable tissue with hypoperfusion). ○ Further workup of stroke etiology may include lipid panels, A1c levels, transthoracic or transesophageal echocardiography, MRI of the brain, diagnostic cerebral angiography, laboratory evaluation of coagulopathy or vasculitis, as well as telemetry and Holter monitoring. Medical management: ○ Stabilization of airway, circulation, and blood pressure performed; hypoglycemia corrected to goal of 140–180 mg/dL; use of isotonic fluids (i.e., normal saline) used to avoid cerebral vasogenic edema. ○ Blood pressure stabilized ≤ 185 mm Hg systolic and ≤ 110 mm Hg diastolic for at least 24 hours after thrombolytic treatment utilizing labetalol, nicardipine, and clevidipine as the first-line therapy and IV nitroprusside as the second-line therapy. ○ Patient management in a stroke critical care unit has been associated with improved patient outcomes and reduced complications. ○ Tissue plasminogen activator (TPA) indicates for stroke < 4.5 hours’ duration with newer studies suggesting that CT perfusion and the presence of penumbra can potentially further this time window; checklist utilized to evaluate eligible patients (see ▶ Table 16.2); door-to-needle time of < 60 minutes recommended. ○ Aspirin initiated within 48 hours of ischemic stroke. ○ Control of blood sugar and administration of statin performed. ○ Inpatient or outpatient rehabilitation commonly recommended after acute stabilization. Surgical management: ○ Clot retrieval occurs via use of an stent retriever device and suction catheter; postoperatively patients closely monitored for reperfusion hemorrhage; intravascular stenting or carotid stenting with angio- plasty (i.e., balloon dilation of stenotic blood vessels) can be utilized for maintaining vessel patency. 379 | 02.07.20 - 17:36 Neurosurgery ○ Several key studies (MR CLEAN,46 SWIFT-PRIME,47 EXTEND IA,48 ESCAPE,49 and REVASCAT50) suggested improved outcomes for mechanical thrombectomy in the presence of large vessel occlusion with penumbra on advanced vascular imaging. ○ Newer studies (DAWN51) have extended the window for thrombectomy up to 24 hours based on vascular imaging. Complications: ○ Prophylactic treatment of deep vein thrombosis and pulmonary embolism initiated as soon as safe; later evaluation of dysphagia and aspiration risk performed in all stroke patients. ○ Patients with large hemispheric or cerebellar strokes are closely monitored for the potential need of decompressive craniectomy in the setting of worsened edema, hemorrhage, and/or mass effect; early decompression shown to improve outcome but does result in a higher number of patients who would have otherwise died to remain severely disabled or vegetative. ○ Medical complications are most common after stroke: Falls (25%), urinary tract infection (24%), pneumonia (22%), pressure sores (21%), depression (16%), shoulder pain (9%), deep vein thrombosis (2%), pulmonary embolism (1%), cardiac arrhythmia or myocardial infarction (1%), aspiration, gastrointestinal bleeding, and nutritional deficiencies. 14.3.5 Other Topics Unruptured cerebral aneurysms: ○ Five-year rupture rate of 1,692 patients was studied in the International Study of Unruptured Intracranial Aneurysms (ISUIA).52 ○ Increasing size of aneurysm, > 7 mm in maximal dimension, and location in the posterior circulation conferred increased risk of rupture.52 ○ Endovascular intervention and surgical clipping remain the two methods for aneurysm treatment. The best technique depends on both aneurysm and patient characteristics. Arteriovenous malformations (AVM)53: ○ Anomalous connection of arteries to veins without intermediary brain parenchyma or a capillary network. Predisposes patients to intracerebral and/or intraventricular hemorrhages. ○ Annual risk of hemorrhage is approximately 3%. ○ Deep venous drainage, deep seated lesions, and previous hemorrhage represent increased risk factors of hemorrhage. ○ Best identified with vessel imaging, such as CTA or DSA. ○ Spetzler–Martin grading scale, a five-point scale, helps determine whether or not to offer treatment of an AVM. Treatment is often recommended in Grades 1 and 2 patients, while conservative management is recommended for Grades 4 and 5 patients (▶ Table 14.16). Table 14.16 Spetzler–Martin grading of arteriovenous malformations Characteristic Number of points Size of arteriovenous malformation Small (6 cm) 3 Location Noneloquent 0 Eloquenta 1 Pattern of venous drainage Superficial only 0 Deep component 1 aEloquent cortex: sensorimotor, language, visual cortex,hypothalamus, thalamus, internal capsule, brainstem, cerebellar peduncles, or cerebellar nuclei. 380 | 02.07.20 - 17:36 Neurosurgical Neoplasms ○ Stereotactic radiosurgery (e.g., Gamma knife) has been shown to have good results with smaller lesions with obliteration rates between 2 and 4 years. ○ Endovascular intervention for embolization of feeding vessels for complete or partial occlusion of the AVM. Generally used as an adjunct for surgical resection in difficult cases. ○ Craniotomy for resection of Spetzler–Martin Grade 1 and 2 lesions have low morbidity and mortality compared with Grade 3 or higher.54 Dural arteriovenous malformations (dAVF)55: ○ An acquired pathologic connection between meningeal vessels and dural venous sinuses or cortical veins. ○ Rare, accounts for 10–15% of all intracranial vascular malformations. ○ Usually presents in the fifth and sixth decades of life with annual rates of hemorrhage reported between 7.4 and 19% for dAVF with cortical venous drainage and 1.4–1.5% without. ○ Classified most commonly by the Borden or Cognard classifications.56 ○ Can be managed conservatively in low-risk cases. Endovascular embolization is considered the first-line treatment for dAVFs requiring treatment. Stereotactic radiosurgery and surgical ligation remain options in select cases. Cerebral cavernous malformations57: