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Title: Care of Central Nervous System Injuries Author: Chesnut RM Journal: Surgical Clinics of North America 87(2007) 119-156 Key Points • Primary brain injury occurs at the time of the initial trauma and cannot be treated so efforts should focus or monitoring and aggressively treating the cause of secondary brain injury. • Careful monitoring of neurologic status, intracranial pressure, and CT scan is critical to detect decline and guide urgent treatment decisions. • Surgery may be necessary in cases where there is mass effect, sudden neurologic decline, or refractory intracranial hypertension. Clinical Conclusions Careful patient monitoring is the key to the prevention, detection, and management of those critical factors that can lead to poor outcome after traumatic brain injury. Section Highlights Primary and secondary brain injury • Primary brain injury is the damage to the brain that occurs or is initiated at the time of trauma and can be a product of direct force, contrecoup injury, rotational forces, and penetrating trauma in which damage is related to the object’s mass and velocity. • Secondary brain injury occurs from processes that take place after the initial injury and either worsen that injury or negatively influence recovery. o Because primary brain injury is not amenable to therapeutic intervention, current care is directed at minimizing or preventing secondary brain injury. o The most common secondary insult is hypotension which is independently associated with increased morbidity and mortality and should be treated with full-volume resuscitation with isotonic solutions. (Bullock, Chesnut et al. 1996) o Pre-hospital or in-hospital hypoxia (PaO2 < 60 mm Hg or apnea/cyanosis in the field) and pyrexia (core temperature > or equal to 38.5 degrees C) are also strong predictors of poor outcome and must be prevented and treated aggressively.(Chesnut, Marshall et al. 1993; Jones, Andrews et al. 1994) Intracranial pressure and cerebral perfusion pressure • Understanding and treatment of intracranial pressure (ICP) revolves around the Monro-Kellie doctrine which holds that because the volume of the skull is fixed, the pressure is proportional to the volume of the compartments within the skull. • When the volume of one compartment changes slowly, compensatory decreases in the volume of other compartments may prevent a rise in ICP but when the change is rapid or compensatory mechanisms are malfunctioning, the ICP increases. • Intracranial hypertension can produce two deleterious consequences: herniation and ischemia. o Herniation occurs when a pressure gradient across a fixed anatomic barrier causes a shift of brain matter. o Ischemia develops when intracranial hypertension lowers the cerebral perfusion pressure (CPP) Figure 1-2 Targeted therapy • The old linear algorithms to treat TBI are currently being replaced with targeted therapy which supports a physiology-based, parallel processing approach. Clinical care • Patient assessment should evaluate critically for possible brain injury even in patients with a Glasgow Coma Score (GCS) of > 8 • Imaging includes the most important tool in neurotrauma which is the CT scan which have largely replaced conventional skull radiographs and should be done in any case of suspected TBI to expedite diagnosis and treatment. o Epidural hematoma (blood collection between the dura mater and the skull), subdural hematomas (below the dura mater), and acute intracerebral hematomas all have unique appearances on CT scan. Figures 3-5 o Subarachnoid hemorrhage, cerebral edema and shear injury can also all be visualized on CT scan. Figures 7-9 • Treatment of patients with traumatic brain injury begins with the basic principles of trauma resuscitation with any patient with a GCS < or equal to 8 requiring airway control, adequate oxygenation, and controlled or assisted ventilation. Figure 10 o Hypoventilation before implantation of an ICP monitor should be limited to a PaCo2 range of 30-35 mm Hg and only used when there are clinical signs of intracranial hypertension (papillary changes, motor posturing, or neurologic deterioration. Figure 11 o Hypotension in an independent predictor of morbidity and mortality in TBI and should be aggressively treated with volume resuscitation with isotonic solution and temporary pressors if needed. • Disability from TBI needs to be limited by obtaining a baseline neurologic status that is frequently rechecked to provide immediate treatment for deterioration. Figure 11 • Monitoring ICP is indicated with cases of severe TBI, moderate TBI thought to be at risk of intracranial hypertension, or those who cannot be evaluated with serial examination (e.g. sedated patients). o Pre-ICU care should begin with rapid and vigorous resuscitation of all TBI patients, early CT imaging, neurosurgical consultation, placement of an ICP monitor, and transport to the ICU. Figure 10-11 o Initial ICU care should continue the goals of resuscitation while central venous and arterial pressures are continuously monitored. Efforts to reduce ICP include head-of bed elevation to 30 degrees to facilitate venous drainage of the brain and the use of analgesics and sedation to limit patient pain and agitation. Transfusion should be used with caution as it has been associated with acute respiratory distress syndrome and multisystem failure but may be necessary to avoid hypoperfusion of the injured brain.(Pietropaoli, Rogers et al. 1992; Fearnside, Cook et al. 1993; Pigula, Wald et al. 1993; Chesnut, Gautille et al. 1998; Hebert, Wells et al. 1999; Dutton, Lefering et al. 2006; Napolitano 2006) Hypertonic saline infusion is frequently used as prophylaxis for intracranial hypertension, albeit without significant research support. Anticonvulsants are used prophylactically but are not part of standard treatment algorithms except in cases of penetrating brain trauma when they should be given for the first week because of the high incidence of seizures associated with this mechanism.(Aarabi B 2001) The Guidelines for the Management of Severe Traumatic Brain Injury and the Guidelines for the Acute Medical Management of Severe Traumatic Brain Injury in Infants, Children, and Adolescents have created algorithms for managing intracranial hypertension in TBI. Figures 12-14 (Bullock, Chesnut et al. 1996; Adelson, Bratton et al. 2003) • Special considerations may be necessary in individual cases. o Early decompressive craniectomy has been experiencing a growing role in TBI management and should be considered in patients with diffuse unilateral or bilateral swelling where ICP control is initially difficult or in patient s with chest trauma or respiratory distress where management of both conditions is difficult. o Burr holes have two roles in the treatment of TBI: exploration when imaging has not yet or cannot be done and temporizing where herniation from an epidural hematoma occurs. o Intracranial pressure monitoring is mandated in cases of severe TBI with intraparenchymal and intraventricular monitoring devices preferable to subdural, subarachnoid, or epidural monitors.(Aarabi B 2001; Adelson, Bratton et al. 2003) o Cerebral spinal fluid rhinorrhea and otorrhea that persists beyond the first several days should be an indication to consider surgical closure to reduce the risk of infection. o Observation of TBI patients should be done in an ICU rather than a general floor bed to allow for close observation and hourly neurosurgical checks. Surgical issues for certain types of TBI • Epidural hematoma of >30 mL volume, clot thickness of > 15mm, or midline shift > 5mm should be emergently surgically evacuated regardless of GCS score; hematomas not meeting these criteria in patients with a GCS < or equal to 8 should also be surgically managed. • Subdural hematoma with a thickness of > 10 mm or midline shift > 5 mm should be surgically evacuated regardless of GCS scores or in any patient with a GCS < 8 if their score deteriorates 2 or more points, they have papillary abnormalities, or the ICP is > 20 mm Hg. • Intraparenchymal lesion treatment is controversial but generally surgery should be considered for mass lesions > 50 mL in volume and for mass lesion of a lesser size that are associated with neurologic deterioration, refractory intracranial hypertension, mass effect, midline shift > 5 mm, or cisternal compression. • Posterior fossa lesions do not produce classic signs of progressive mass effect but instead patients simply deteriorate into coma and die even under observation so urgent surgery should be considered with significant mass effect seen on CT or patient signs of deterioration. • Depressed skull fractures should be elevated if they are displaced beyond the inner table of the skull or if they show signs of gross contamination, significant hematoma, dural penetration, gross deformity, or frontal sinus involvement. • Penetrating brain injury treatment involves management of intracranial hypertension, avoiding infection, addressing vascular injury, and seizure prophylaxis with surgical debridement only indicated if there is significant mass effect. Summary • Primary brain injury has no treatment but secondary injury can be prevented by careful patient monitoring and aggressive treatment strategies. • Initial resuscitation efforts are similar to that of any other trauma patient but the high level of disability associated with TBI necessitates ICU monitoring and frequent checks for neurologic decline. • Surgery may be necessary if signs and symptoms of mass effect develop or patient status worsens. References Aarabi B, A. T., Chestnut RMD, et al. (2001). "Part 1: Guidelines for the management of penetrating brain injury. Introduction and methodology." J Trauma 51(2 Suppl): S3-6. Adelson, P. D., S. L. Bratton, et al. (2003). "Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents. Chapter 1: Introduction." Pediatr Crit Care Med 4(3 Suppl): S2-4. Bullock, R., R. M. Chesnut, et al. (1996). "Guidelines for the management of severe head injury. Brain Trauma Foundation." Eur J Emerg Med 3(2): 109-27. Chesnut, R. M., T. Gautille, et al. (1998). "Neurogenic hypotension in patients with severe head injuries." J Trauma 44(6): 958-63; discussion 963-4. Chesnut, R. M., L. F. Marshall, et al. (1993). "The role of secondary brain injury in determining outcome from severe head injury." J Trauma 34(2): 216-22. Dutton, R. P., R. Lefering, et al. (2006). "Database predictors of transfusion and mortality." J Trauma 60(6 Suppl): S70-7. Fearnside, M. R., R. J. Cook, et al. (1993). "The Westmead Head Injury Project. Physical and social outcomes following severe head injury." Br J Neurosurg 7(6): 643-50. Hebert, P. C., G. Wells, et al. (1999). "A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care. Transfusion Requirements in Critical Care Investigators, Canadian Critical Care Trials Group." N Engl J Med 340(6): 409-17. Jones, P. A., P. J. Andrews, et al. (1994). "Measuring the burden of secondary insults in head-injured patients during intensive care." J Neurosurg Anesthesiol 6(1): 4-14. Napolitano, L. (2006). "Cumulative risks of early red blood cell transfusion." J Trauma 60(6 Suppl): S26-34. Pietropaoli, J. A., F. B. Rogers, et al. (1992). "The deleterious effects of intraoperative hypotension on outcome in patients with severe head injuries." J Trauma 33(3): 403-7. Pigula, F. A., S. L. Wald, et al. (1993). "The effect of hypotension and hypoxia on children with severe head injuries." J Pediatr Surg 28(3): 310-4; discussion 315-6.
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