Neurotrauma

Martina Stippler, MD Department of Neurosurgery, Beth Israel Deaconess Medical Center, Boston, Massachusetts

M. Dustin Boone, MD Anesthesia, Critical Care and Pain Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, Massachusetts



Epidemiology

Traumatic brain injury (TBI) is a leading cause of morbidity and mortality in developed nations and accounts for almost one-third of all trauma-related deaths. Currently, 50,000 Americans die of TBI-related complications annually, and about 5.3 million live with TBI-related disabilities. Among survivors of severe TBI, cognitive deficits are common, which poses a long-term societal burden, given its prevalence in the young. Only one-third of the patients can return to their prior occupation and engage in social activities. Elderly patients have the worst outcome; although accounting for only 10% of the TBI cases, they represent 50% of TBI-related deaths. Road traffic crashes account for 50% of the cases. Falls represent the most common cause in the elderly. Whereas patients with mild TBI rarely seek medical attention, severe TBI requires rapid diagnosis and treatment to limit secondary injury and optimize outcome. Overall, mortality in patients with severe TBI is still poor. However, parallel improvements in the trauma response system and the development of subspecialization in neurocritical care have led to reductions in mortality. ’

Classification

TBI is classified according to mechanism, severity, and morphology. Blunt injury is the most common mechanism, with motor vehicle collisions and falls accounting for the majority of cases. The frequency of penetrating injuries has increased with recent military conflicts, but are also seen in the civilian population (Fig. 1).1 Gunshot wounds are the most lethal type of brain injury, with a 90% REPRINTS: MARTINA STIPPLER, MD, 110 FRANCIS ROAD SUITE 3B, BOSTON, MA 02215. E-MAIL: BIDMC.HARVARD.EDU

MSTIPPLE@

INTERNATIONAL ANESTHESIOLOGY CLINICS Volume 53, Number 1, 23–38 r 2015, Lippincott Williams & Wilkins

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Figure 1. Penetrating head injury.

mortality rate. Although contamination is a concern in some penetrating injuries, gunshot wounds are considered sterile because of the exposure of the bullet fragment to the heat from the firearm. It is not advised to remove the fragments as doing so can cause more brain damage.2 Surgical management is mainly limited to local wound care, debridement of nonviable tissue, and water-tight scalp closure. Any further intervention is based on the neurological examination and whether the injury is survivable. Generally, routine surgical removal of the bone or missile fragments remote from the entry site or in the eloquent areas of the brain is not recommended.3 In addition to serial neurological examinations and head computed tomographic (CT) scans, intracranial pressure (ICP) monitoring is often used to guide treatment. Although ICP monitoring is routinely used in severe nonpenetrating TBI, little evidence supports its use in penetrating brain injury.4 Vascular injury can occur with any type of TBI but is more common with penetrating trauma (25% to 36% incidence) than with blunt injuries (< 1%). Traumatic aneurysms, or pseudoaneurysms, may present as delayed subarachnoid hemorrhage (SAH). Therefore, patients with penetrating injuries should undergo a screening cerebral angiogram.5 Blast injury is rarely observed in civilians, but is common in combat. There are 3 types of blast injuries, all of which create damage as a result www.anesthesiaclinics.com

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of the propagation of supersonic waves.6,7 The brain is understandably susceptible to blast injury.8 The threshold for brain injury from blast exposure is unclear.9 Injury Severity

Although there are different methods to stratify TBI by severity, the Glasgow Coma Scale (GCS) is the most widely used. A GCS score of 13 to 15 is considered mild TBI, between 9 and 12 moderate, and 20 mm Hg for 10 min)

1. 2. 3. 4.

Verify ICP: Check whether waveform is present and adequate Check for 30-degree head elevation (unless patient on spinal precautions) Make sure cervical collar is not too tight Optimize analgesia and sedation: Sedation: Titrate propofol drip to a RASS Level of 4 to 5 or a BIS score of 30 Do not exceed 80 mcg/kg/min for more than 24 h If propofol is ineffective, or requires maximum dosage of propofol for >24 h, start 20 mg/kg/min and titrate to a RASS level of 4 to 5 Dexmedetomidine IV drip.; maintenance gtt = 0.2-0.7 mcg/kg/h to achieve RASS 4 to 5 Analgesia: Titrate fentanyl drip to a RASS level 4 to 5 maximal 100 mcg/h 6. Hyperosmolar therapy: Check last available sodium (Na) level If last Na < 130 mEq/L, start 3%Na Cl drip at 15 mL/h, give mannitol bolus 0.5-1.5 mg/kg, do not increase serum Na > 10 mEq/L within a 24 h period If last Na 130-150 mEq/L, give 23% NaCl 30 mL IV bolus and start 3% NaCl drip at 30 mL/h or increase existing drip by 20 mL/h If last Na > 150 mEq/L give 250 mL 3% NaCl IV bolus, do not start (or increase existing) NaCl drip If 3% NaCl is not effective in reducing ICP, mannitol may be administered at 0.5-1.5 mg/kg IV bolus once Check Na and serum osmolarity Q4H 4 after every bolus Check Na and serum osmolarity Q4H while on drip If Na > 160 mEq/L or serum osmolarity >320 sOsm/L check Osmolar gap If osmolar gap < 10 administer mannitol 0.5-1 g/kg 7. Hyperventilation: Avoid hyperventilation in the first 24 h, goal PaCO2 35-40 mm Hg Hyperventilate to 30-35 mm Hg only with signs of herniation 8. Consider surgery

examinations. A variety of sedation regimens can be used, but we tend to start with a propofol infusion. For analgesia, fentanyl may be administered as a bolus or infusion. Care must be taken to avoid prolonged infusions of high-dose propofol on account of the risk of propofol infusion syndrome. In addition, bolus and infusion medications should be dose-adjusted when inducing hypothermia. Midazolam infusions can be used to replace or supplement propofol infusions for patients requiring high-dose propfol (> 80 mcg/kg/min). To monitor the depth of sedation, some institutions use the BIS monitor. Neuromuscular blockade is used as a last resort, as its use impairs the ability to monitor neurological examinations. Hyperventilation to induce hypocapnia (PaCO2 30 to 35 mm Hg) is not recommended in routine management. It can be effective as a temporizing measure to decrease ICP in patients who show signs of herniation, while other therapies are being considered. Otherwise, induced hypocapnia is thought to put the patient at risk for cerebral www.anesthesiaclinics.com

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ischemia. Hypocapnia induces vasoconstriction, which has the effect of lowering ICP by decreasing cerebral blood volume. The current guidelines recommend maintaining eucapnia (PaCO2 35 to 40 mm Hg). Hyperosmolar drugs such as mannitol or hypertonic saline are effective in reducing ICP. At present, there is no evidence to support the superiority of one particular agent. In general terms, both mannitol and hypertonic saline work to reduce ICP in similar ways. As the brain has a high water content, the formation of an osmotic gradient across the blood-brain barrier will drive water from the brain to the intravascular space. In addition, mannitol is thought to induce changes in the rheology of blood, which results in cerebral vasoconstriction. This concept has been recently challenged. Mannitol is dosed between 0.25 and 1 g/kg every 4 to 6 hours. As mannitol acts a diuretic, care should be taken when administering to a patient who is hypovolemic. Serum osmolarity should be measured and a ceiling of 320 mOsm/L is recommended as the upper limit for redosing. We calculate the osmolar gap to decide when to redose mannitol (gap < 10). Hypertonic saline comes in a variety of concentrations (2% to 23.4%). The goal is to raise the serum sodium initially to 145 to 150 mmoL/L, and a step-wise increase in sodium in subsequent days if hyperosmolar therapy continues to be required. Hypertonic saline may be a good choice for patients who present hypovolemic as it acts as a volume expander. Care should be used in administering hypertonic saline in hyponatremic patients over concern for central pontine myelinolysis. In addition, a central line is required for the administration of concentrations greater than 3%. For both agents, the brain adapts to a hyperosmolar state by generating idiogenic osmoles. For this reason, stopping hyperosmolar therapy needs to be carried out gradually. Persistently elevated ICP, despite maximal medical therapy, may be an indication for decompressive hemicraniectomy (Figs. 2 and 3). Depending on the underlying pathology, one side of the skull or the frontal bone bilaterally (Kjellberg procedure) is removed. In 2011, the results of the randomized Decompressive Craniectomy trial were published.31 Decompressive craniotomy did not improve functional outcome. The results of an ongoing trial of craniectomy for head injury called the Randomized Evaluation of Surgery with Craniectomy for uncontrollable Elevation of Intracranial Pressure (RESCUEicp) may provide further insight.32–34 Although a decompressive craniectomy may be a useful option for intractable ICP, it is not without risk. One study showed a 35% rate of complications that included subdural effusion, hydrocephalus, and infection. The incidence of posttraumatic hydrocephalus is higher in patients after decompressive craniectomy (Fig. 4). This may be due to disturbance of CSF dynamics after decompressive craniectomy. Bilateral decompressive craniectomy is sometimes performed but is associated with an unfavorable outcome www.anesthesiaclinics.com

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Figure 2. Computed tomographic scan showing a subdural hematoma.

in 46% of cases.35 Some patients suffer delayed neurological deterioration, described as “syndrome of the trephined.” It is thought that the brain function is impaired by the atmospheric pressure. Temperature management in severe TBI is critical. It is postulated that most of the benefit seen with cooling is not from hypothermia but in the prevention of hyperthermia. This concept is known as therapeutic temperature modulation. Currently, aggressive treatment to maintain normothermia is recommended. A retrospective study found that maintaining normothermia decreased the ICP burden.36 To achieve and maintain normothermia advanced cooling methods, such as surface cooling or intravascular cooling, may be used. Conventional cooling methods, such as ice packs and acetaminophen are ineffective in modulating temperature.37 Intravascular cooling is the most effective method for maintaining normothermia.38 Hypothermia should be reserved for patients with refractory intracranial hypertension. A recent meta-analysis of all prospective TBI clinical trials found that therapeutic moderate hypothermia (32 to 341C, 89.6 to 93.21F) resulted in less mortality [relative risk (RR) 0.51; 95% confidence interval (CI), 0.33-0.79] and increased likelihood of a good www.anesthesiaclinics.com

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Figure 3. Patient from Figure 2, several days postinjury with refractory intracranial hypertension and now s/p decompressive hemicraniectomy.

outcome (RR 1.91; 95% CI, 1.28-2.85) compared with normothermia during acute care, but the risk of pneumonia increased (RR 2.37; 95% CI, 1.37-4.10).39 Problems associated with hypothermia include increased bleeding risk, arrhythmias, and increased susceptibility to infection and sepsis. Two large trials of hypothermia did not provide evidence to support hypothermia in severe TBI.40,41 The Guidelines for the Management of Severe Traumatic Brain Injury recommend high-dose barbiturate to control elevated ICP only after maximum standard medical and surgical treatment have failed. High-dose barbiturate therapy has shown to be effective in lowering ICP but has never been proven to improve outcome. Barbiturate therapy has major side effects including myocardial depression, hypotension, and immunosuppression. Multimodality monitoring is used in most centers specializing in TBI. Besides ICP, cerebral blood flow, partial brain-tissue oxygen tension (PbtO2), microdialysis variables, cerebral oximetry, and bispectral index are measured. Multimodal monitoring is discussed in more detail in this volume (see Neuromonitoring in the ICU). Multimodal monitoring increases the understanding of brain pathophysiology and may help to www.anesthesiaclinics.com

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Figure 4. Head computed tomography showing posttraumatic hydrocephalus.

limit secondary brain injury by detecting changes to brain oxygenation and metabolic substrates. PbtO2 is probably the most commonly applied and studied parameter. Numerous studies have examined the relationship between outcome and PbtO2. They found that likelihood of death increased with duration of time that PbtO2 was 20 mm Hg might not.48 Management of Focal Injuries

Patients with focal TBI and extra-axial bleeding with mass effect are treated surgically. A fronto-temporal or temporal-parietal craniotomy, with or without subtemporal decompressive craniectomy, is performed. In some cases, a prophylactic hemicraniectomy is performed at the same time if the brain appears swollen intraoperatively. The preoperative CT www.anesthesiaclinics.com

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Figure 6. Head computed tomography showing a right epidural hematoma.

can help predict malignant brain swelling. More midline shift than one would expect from the extra-axial hematoma, effacement of basal cisterns and sulci, and loss of gray-white matter differentiation are warning signs. A patient with an EDH can progress from having a normal neurological examination to coma rapidly (Figs. 5 and 6). Most often, the patient becomes agitated and restless and may have an episode of emesis secondary to increased ICP. This is often followed by the development of focal neurological signs such as hemiparesis, seizures, pupillary dilation, decrease in consciousness, and, if the EDH is not evacuated within several hours, decortication. Any EDH > 30 cm3 should be evacuated regardless of the GCS score. An EDH < 30 cm3 in volume and

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