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Home , Brain damage, Craniotomy, Head injury, Injury, Intracerebral hemorrhage, Intracranial hemorrhage

ACS TQIP BEST PRACTICES IN THE MANAGEMENT OF TRAUMATIC

Released January 2015 Table of Contents Introduction...... 3

Using the Glasgow Scale...... 3

Triage and Transport...... 5

Goals of Treatment...... 5

Intracranial Pressure Monitoring...... 6

Management of Intracranial ...... 9

Advanced Neuromonitoring...... 12

Surgical Management...... 13

Nutritional Support...... 14

Tracheostomy...... 15

Timing of Secondary Procedures...... 15

Timing of Pharmacologic Venous Thromboembolism Prophylaxis...... 17

Management Considerations for Pediatric with TBI...... 18

Management Considerations for Elderly Patients with TBI...... 19

Prognostic Decision-Making and Withdrawal of Medical Support...... 20

Outcome Assessment and Quality Improvement in TBI...... 22

Bibliography...... 24

Expert Panel...... 28

Acknowledgements...... 29

Disclaimer...... 29

2 INTRODUCTION USING THE (TBI) is a process that carries major Key messages: and socioeconomic consequences. In zz The Glasgow Coma Scale the alone, an estimated (GCS) provides a reliable tool 2.5 million visits for assessing disturbances of and hospitalizations are associated with across care paths TBI annually; and more than 50,000 individuals die from TBI. Moreover, a zz Standardized approaches considerable proportion of TBI survivors to GCS assessment and incur temporary or permanent . reporting are essential The estimated annual burden of TBI on zz The GCS should specify the score the United States economy is more than for each of the three components $76 billion, with the costs for disability (, verbal, motor) when and lost productivity outweighing reporting on individual patients the costs for medical care. zz The sum of the component scores Data from well-designed, controlled (GCS 3-15) is relevant for comparisons studies on acute management of TBI are at the group level for purposes sparse. Evidence-based guidelines for TBI of classification and management have been compiled, but the paucity of high-quality studies limits The Glasgow Coma Scale (GCS) was the strength and scope of their counsel. introduced forty years ago by Teasdale The TQIP Best Practice Guidelines for and Jennett as a practical method for the Management of Traumatic Brain assessing the full spectrum of disorders Injury present recommendations of consciousness, from very mild to regarding care of the TBI patients based severe. It has been broadly adopted, and on the best available evidence or, if is internationally utilized as an integral evidence is lacking, based upon the part of clinical practice and research. consensus opinion of the expert panel. The GCS aims to rate performance in three different domains of response: the eye, verbal, and motor response (Table 1). For individual patients, it is recommended that in that all three components be reported, e.g., E4V4M5, versus a sum score, e.g., GCS 13. The derived sum score of the GCS (3-15) is more relevant for comparisons at the group level and provides a useful tool for classification and prognosis.

3 A score of ≥13 correlates with a mild of the GCS are that it covers a broad brain injury, 9 to 12 is a moderate spectrum of disorders of consciousness, injury, and ≤8 a severe brain injury. is widely applicable, and offers an important tool for monitoring changes in If a GCS component is untestable due the level of consciousness. Standardized to , sedation, or another approaches to both its assessment and confounder, the reason for this should its reporting are required in order to be be recorded. Although often done, able to compare evaluations over time a score of 1 should not be assigned or when communicating with other because differentiation between a professionals. Spontaneous “true 1” and an untestable component responses are first observed without is relevant. Graphical display of the stimulating the in any way. three GCS components over time may First, verbal stimuli are applied, such as facilitate earlier detection of changes. asking a patient to obey commands and Assessment requires either a at the same time observing whether, spontaneous response or response e.g., an eye opening occurs. If a patient following application of a stimulus. is not responsive, a stimulus is applied At more severely disturbed levels of to elicit a response. The location of consciousness, the motor score has the stimulus (central or peripheral) better discrimination, but in milder should be standardized and used the eye and verbal components consistently. To describe the motor are more relevant. Thus, each component response, only the reaction of the arms of the scale (Eye, Verbal, Motor) provides should be observed, not the legs. complementary information. Strengths Table 1. Glasgow Coma Scale

Eye opening (E) None 1 To pressure 2 To sound 3 Spontaneous 4 Untestable Reason: Verbal response (V) None 1 Sounds 2 Words 3 Confused 4 Oriented 5 Untestable Reason: Motor response (M) None 1 Extension 2 Abnormal flexion 3 Normal flexion 4 Localizing 5 Obey commands 6 Untestable Reason:

4 Providing the initial resuscitative care AND in lower-level centers (III, IV, or non-designated ) may TRANSPORT occasionally be rationalized in some rural Key Message settings with long transport times (≥ 1 hour). However, these hospitals should zz Patients with a Glasgow Coma have predefined air/ground transfer Scale (GCS) ≤ 13 should be rapidly protocols and agreements in place to transported directly from the scene provide for the immediate transfer of to the highest level trauma center TBI patients to the highest level center available in a defined trauma system available within a defined trauma system. to allow for expedient neurosurgical assessment and intervention zz Patients with a combination of TBI GOALS OF TREATMENT (GCS score ≤ 15) and moderate to severe extra-cranial anatomic injuries These clinical parameters should be and Abbreviated Injury Score (AIS) ≥3 maintained as part of goal-directed TBI should be rapidly transferred to the treatment. Some of these goals are more highest level of care within a defined relevant for patients in the intensive care trauma system to allow for expedient unit (ICU) setting (e.g., CPP, ICP, PbtO2) neurosurgical and multidisciplinary while others are applicable to all TBI assessment and intervention patients. Adequate oxygenation and normocapnia should be maintained. Proper field triage is critical for patients Patients with significant pulmonary with suspected TBI. Trauma patients issues (e.g. Acute Respiratory Distress with TBI require rapid , Syndrome) may require lung-specific definitive operative management, and parameters. Systolic critical care capabilities to prevent (SBP) and secondary brain injury. The US Center for should be monitored closely to avoid Disease Control’s (CDC) 2011 Field Triage . The goal for temperature Guidelines for Injured Patients direct management is normothermia. Core EMS providers to transport all patients body temperature should be kept with a Glasgow Coma Scale (GCS) < 13, <38°C. The goal for electrolytes is to or those with any level of TBI (GCS ≤ 15) maintain within normal range. Specific and extracranial injuries (AIS ≥ 3) to the to the sodium level is crucial highest level trauma center that has the in TBI patients. Hyponatremia must be expertise, personnel, and facilities to avoided as this may worsen cerebral rapidly provide definitive care, usually . TBI patients may also develop a level I or II trauma center. Despite insipidus (DI) or the syndrome these guidelines, significant undertriage of inappropriate antidiuretic hormone of TBI victims has been documented (SIADH). Therefore patients should throughout the US in systems with have frequent monitoring of the serum and without trauma centers. sodium and osmolality levels. Both

5 Table 2. Goals of Treatment

Pulse Oximetry ≥ 95% ICP 20 - 25 mmHg Serum sodium 135-145

PaO2 ≥ 100 mmHg PbtO2 ≥ 15 mmHg INR ≤ 1.4

* 3 3 PaCO2 35-45 mmHg CPP ≥ 60 mmHg ≥ 75 x 10 / mm SBP ≥ 100 mmHg Temperature 36.0-38°C Hemoglobin ≥ 7 g/dl

PH 7.35-7.45 Glucose 80-180 mg/dL

PaO2: partial pressure of ; PaCO2: partial pressure of carbon dioxide; SBP: systolic blood pressure; ICP: ; PbtO2: brain tissue oxygen tension; CPP: cerebral pressure; INR: international normalized ratio; *depending on status of cerebral

and are receive early evaluation for detrimental to the outcome of patients with assessment for direct and indirect with TBI. Serum glucose levels must be cascades using INR to monitored closely in all TBI patients. identify medical, iatrogenic, or early post- More frequent monitoring is required traumatic coagulopathy when present. following the initiation of nutritional Utilization of newer assays of coagulation support, particularly in patients with capability ( known or suspected diabetes mellitus. or Rotational thromboelastometry, and/or function assays) and coagulopathy are common may provide additional information in patients with TBI and should be regarding the need for targeted monitored closely. There is considerable to reverse coagulopathy. practice variability in hemoglobin transfusion thresholds for TBI patients. A recent randomized clinical trial compared 2 hemoglobin transfusion thresholds INTRACRANIAL (7 and 10 g/dl) after TBI. There were no differences in neurological outcome. PRESSURE MONITORING However, the 10 g/dl threshold was Key Messages: associated with a higher of adverse events, supporting the best zz ICP monitoring is important, but it practice recommendation of a 7 g/dl does not replace careful neurological transfusion threshold. TBI patients should and radiographic examination

6 zz ICP monitoring is indicated in Elevated ICP is predictive of poor comatose patients (GCS ≤ 8) and if outcome. Furthermore, cerebral there is evidence of structural brain perfusion pressure (CPP), a parameter on initial CT imaging derived from ICP (Mean Arterial Pressure – ICP), is an important marker of cerebral zz ICP monitoring is generally not blood flow; augmenting CPP can help indicated in comatose patients to restore cerebral perfusion and without evidence of structural oxygenation. In addition to enabling or elevated ICP CPP measurement, ICP monitoring can (compressed/absent basal cisterns) provide advanced warning of impending on initial CT imaging. Patients structural brain derangements such may be observed with repeat CT as contusion/ progression, imaging and forego ICP monitoring increased , and if there is no progression postoperative complications. The zz ICP monitoring should be considered identification of ICP elevation can prompt in patients with a GCS > 8 who further imaging, timely intervention, have structural brain damage with and definitive management.. high risk for progression (large/ ICP monitoring remains a critical multiple contusions, coagulopathy) component in the management of zz ICP monitoring should be considered severe TBI. However, recent studies in patients who require urgent have highlighted the need to better for extracranial injuries, define how ICP monitoring is used in the who need treatment of TBI. In the largest study of because of extracranial injuries, ICP monitoring to date, observational or who evidence progression data from hospitals participating in of on CT imaging the ACS TQIP demonstrate that ICP or clinical deterioration monitoring utilization was associated with lower in- mortality. Other zz The preferred method for ICP institutional practices not captured in the monitoring is an external ventricular database, also appeared to contribute to drain (EVD) because it is both improved outcome. The only randomized diagnostic (measures ICP) and controlled trial compared treatment therapeutic (allows for drainage using ICP monitoring to maintain ICP of (CSF) ≤ 20 mm Hg to treatment based upon

7 imaging and The gold standard for ICP measurement in TBI patients from South America. is via an external ventricular drain (EVD), Although there was no difference in attached to an external -gauge outcomes between the groups, this transducer. The monitor, centrally does not support the discontinuation placed within the cerebral ventricles, of ICP monitoring in the treatment can measure global ICP and offers the of TBI. Rather, it demonstrates the therapeutic advantage of draining importance of aggressive treatment CSF to reduce intracranial volume. using ICP monitoring or frequent Intraparenchymal ICP monitoring clinical and radiographic examination is also a reliable method but does to identify intracranial hypertension. not allow for CSF drainage. Subdural This study also challenges the currently and epidural monitors have been accepted rigid ICP alert threshold used, but these are the least accurate of 20 mm Hg for all patients. The methods of ICP measurement. current accepted alert threshold is an ICP of 20 mm Hg, with a reasonable range of 20-25 mm Hg as a trigger for treatment of intracranial hypertension. Ongoing research may reveal that this threshold is dependent upon individual patient factors. An approach based on injury type and augmented by advanced neuromonitoring may lead to individualized treatment pathways.

8 THREE-TIERED MANAGEMENT OF INTRACRANIAL PRESSURE

TIER 1

zz Head of bed elevated at 30 degrees (reverse Trendelenburg) to improve cerebral venous outflow

zz Sedation and analgesia using recommended short-acting agents (for example, propofol, fentanyl, midazolam) in intubated patients

zz Ventricular drainage performed intermittently. Continuous drainage is not recommended unless an additional ICP monitor is placed, as when the drain is open, it does not accurately reflect the true ICP

zz Repeat CT imaging and neurological examination should be considered to rule out the development of a surgical mass and guide treatment

If ICP remains ≥ 20 - 25 mmHg proceed to Tier 2

TIER 2

zz In patients with a parenchymal ICP monitor an EVD should be considered to allow for intermittent CSF drainage

zz Hyperosmolar therapy should be given intermittently as needed for ICP elevation and not on a routine schedule

 should be administered in intermittent boluses (0.25 - 1 gm/ kg body weight). Caution should be taken in the hypovolemic patient when osmotic is instituted with mannitol. The serum sodium and osmolality must be assessed frequently (every 6 hours) and additional doses should be held if serum osmolality exceeds 320 mOsm/L. Mannitol may also be held if there is evidence of

 Hypertonic may be administered in intermittent boluses of 3% sodium chloride solution (250 ml over ½ hour) or other concentrations (e.g., 30cc of 23.4%). Serum sodium and osmolality must be assessed frequently (every 6 hours) and additional doses should be held if serum sodium exceeds 160 mEq/L

zz Cerebral autoregulation should be assessed (see Advanced Neuromonitoring section). If the patient is not autoregulating, the CPP goal should be lowered to reduce ICP (to no less than 50 mm Hg). Additional neuromonitoring (e.g., PbtO2, SjvO2, CBF) may help determine optimal CPP

9 zz PaCO2 goal of 30 - 35 mmHg should be maintained, as long as brain is not encountered. Additional neuromonitoring (e.g., PbtO2, SjvO2, CBF) may help determine optimal PaCO2

zz Repeat CT imaging and neurological examination should be considered to rule out development of a surgical mass lesion and guide treatment

zz Neuromuscular achieved with a bolus “test dose” of a neuromuscular blocking agent should be considered if the above measures fail to adequately lower ICP and restore CPP. If there is a positive response, continuous infusion of a neuromuscular blocking agent should be employed (Tier 3)

If ICP remains ≥ 20 - 25 mmHg proceed to Tier 3

TIER 3

(includes potential salvage )

zz Decompressive hemi-craniectomy or bilateral craniectomy should only be performed if treatments in Tiers 1 and 2 are not sufficient or are limited by development of of medical treatment

zz Neuromuscular paralysis via continuous infusion of a neuromuscular blocking agent can be employed if there is a positive response to a bolus dose. The infusion should be titrated to maintain at least two twitches (out of a train of four) using a peripheral stimulator. Adequate sedation must be utilized

zz or propofol ( dosage) coma may be induced for those patients who have failed to respond to aggressive measures to control malignant intracranial hypertension, however it should only be instituted if a test dose of barbituate or propofol results in a decrease in ICP, thereby identifying the patient as a “responder.” Hypotension is a frequent side effect of high dose therapy with these agents. Meticulous volume resuscitation should be ensured and infusion of vasopressor/ may be required. Prolonged use or high dose of propofol can lead to propofol infusion syndrome. Continuous EEG may be used to ensure targeting of the infusion to burst suppression

zz (<36 °C) is not currently recommended as an initial TBI treatment. Hypothermia should be reserved for “rescue” or salvage therapy after reasonable attempts at ICP control via the previous Tier 3 treatments have failed

10 Because there is often no single MANAGEMENT OF pathophysiological pathway of ICP elevation, management is complex. INTRACRANIAL Elevated ICP can be related to a variety HYPERTENSION of mechanisms, including: edema (cellular, extracellular), cerebral venous Key Messages outflow obstruction, hyperemia (loss zz ICP is a global measure that cannot of autoregulation, vasodilation), mass identify the specific mechanism(s) effect (expanding hematoma), and of pressure elevation. Additional disturbances in CSF circulation. ICP is a neuromonitoring and assessment global measure that cannot distinguish of cerebral autoregulation may among these mechanisms. Additional help to individualize treatment neuromonitoring of brain tissue oxygen tension (PbtO2), jugular venous zz The recommended “3-tiered” oxygenation (SjvO2), cerebral blood approach to ICP management flow (CBF), cerebral autoregulation, utilizes various treatments to and other parameters may be helpful target different mechanisms. in identifying a more individualized Higher tiers reflect more intensive approach to treatment. We have management that is associated recommended a “tiered” approach with increased complications to ICP management that utilizes various treatments to target different zz Failure to control ICP/CPP within one mechanisms. The higher tiers reflect tier, should prompt rapid progression more intensive management that is also to the next tier’s treatment options associated with increased complications. zz Repeat CT imaging and neurological examination should be considered to rule out the development of surgical lesion and guide management

11 severity of brain hypoxia along with a ADVANCED 10% reduction in mortality and a trend toward reduced mortality and improved NEUROMONITORING neurologic outcome at 6 months. This Key Messages trial supports the value of advanced multimodality monitoring in TBI patients. zz Advanced neuromonitoring and assessment of cerebral Cerebral pressure autoregulation autoregulation may be helpful in is the brain’s intrinsic ability to identifying a more individualized maintain constant CBF over a range approach to treatment of systemic blood pressures. This mechanism protects against cerebral zz Impaired cerebral oxygenation due to hypotension and can occur in the face of against excessive flow that can lead to normal ICP and CPP elevated ICP. Cerebral autoregulation can be assessed at the bedside in the zz Cerebrovascular pressure reactivity ICU with cerebrovascular pressure index (PRx) and cerebral blood reactivity index (PRx) monitoring, CBF flow (CBF) monitoring can assess monitoring, and autoregulation status, which (TCD) ultrasonography monitoring. The may help determine patient- PRx is quantified as the slope of the specific CPP and ICP goals regression line relating MAP and ICP TBI is a complex disease with substantial and can be used to establish patient- heterogeneity. ICP monitoring alone specific CPP thresholds. For patients cannot detect all potential insults to with impaired cerebral autoregulation the brain; ensuring adequate cerebral (PRx slope > 0.13), a lower CPP (50 – 60 blood flow and oxygenation are mm Hg) should be considered as an important goals. Multiple studies have option for treatment. Patients with intact demonstrated an association between autoregulation (PRx slope < 0.13) may low brain tissue oxygen tension benefit from a higher CPP (50 – 60 mm (PbtO2 ≤ 15 mm Hg) and episodes of Hg). When CBF is monitored directly, jugular venous oxygen desaturation autoregulation status can be assessed (SJvO2 ≤ 50 %) with poor outcome in with a hemodynamic challenge. In TBI. Importantly, brain tissue hypoxia patients with intact autoregulation, can occur even when ICP and CPP CBF will change minimally in response are normal. A recently completed to an increase in MAP. Conversely, Phase II prospective randomized CBF will rise with increasing MAP in clinical trial investigating PbtO2-based patients with impaired autoregulation. management of severe TBI compared Once determined, autoregulation treatment guided by ICP alone to status can be used to set CPP goals as treatment guided by both ICP and PbtO2 described above. In a similar fashion, (BOOST, NCT00974259). The ICP+PbtO2 TCD ultrasonography and hemodynamic management group had statistically challenge can also be used to assess significant decreased duration and autoregulation in TBI patients.

12 adequate resection; there is no role for SURGICAL attempted burr-hole drainage of these solid clots. Evidence-based guidelines MANAGEMENT for surgery have been compiled, but Key messages: the paucity of high-quality randomized studies in this area limits the strength zz A large traumatic hematoma of recommendations. In general, CT should be evacuated before evidence of raised ICP, such as midline neurological deterioration shift of ≥5 mm and/or compression of develops, irrespective of the GCS the basal cisterns is an indication for surgical evacuation of a traumatic mass zz A formal is necessary lesion. Even if a patient has a relatively to perform adequate resection high GCS score, a large traumatic zz TBI patients presenting to the hematoma should be evacuated before ED in coma should be taken to neurological deterioration develops surgery immediately upon arrival from enlargement of the hematoma if a large hematoma is identified or swelling of the underlying brain. A as the cause of the coma lower threshold for surgical intervention may apply to posterior fossa . zz Decompressive craniectomy is effective in controlling intracranial Decompressive Craniectomy (DC), in pressure, but uncertainty exists as which a large bone flap is deliberately to its potential to improve outcome removed or not replaced, has witnessed a surge of popularity in recent years. Surgery for TBI patients is most Sometimes the flap is left off because commonly performed to evacuate massive cerebral swelling develops epidural (EDH), subdural after evacuation of a hematoma, and hematomas (SDH), cerebral contusions, at other times, the anticipates or intracerebral hematomas (ICH) that are significant cerebral edema and pre- large enough to cause significant mass emptively leaves the bone flap off. In effect on the brain. Surgical evacuation of other cases, patients who would not these hematomas should be performed normally undergo surgery may be taken as soon as possible. TBI patients to the operating room for DC if ICP presenting to the ED in a coma should begins to rise. A recent study casts doubt be taken to surgery immediately upon on the clinical benefit of a DC in patients arrival if a large hematoma is identified with diffuse brain injury and raised ICP as the cause of the coma. Admitted refractory to medical management. patients who undergo neurological The randomized controlled DECRA trial deterioration from delayed development demonstrated that although patients or enlargement of a hematoma require who received craniectomy achieved prompt surgical evacuation to prevent effective lowering of ICP, their neurologic further neurological worsening. A formal outcomes at six months were worse craniotomy is necessary to perform than those of patients randomized to

13 maximal medical therapy. However, zz Full nutritional supplementation critics of this trial have highlighted should be achieved within unbalanced treatment groups, variability 7 days of injury in medical treatments for the control Patients with TBI demonstrate group, high crossover rate to the hypermetabolic and hypercatabolic surgical arm, and short-term follow-up activity lasting from 1 week to (six months) as arguments against the several months following their injury. conclusions of the study. The application Nutritional support should be initiated of decompressive craniectomy for severe as early as possible, usually as soon TBI remains a topic of lively debate. as the patient is hemodynamically Depressed fractures are commonly stabile and there are no significant elevated if the is greater than gastrointestinal issues. Studies have the depth of the adjacent inner table, demonstrated that early nutritional especially if located in a cosmetically support is associated with fewer important area like the forehead. Open and lower mortality. “Early” depressed fractures are best treated is most commonly defined as within surgically to prevent , but 24-48 hours of injury, and is adopted for nonoperative management may be these guidelines. This recommendation attempted in selected cases, limited is made in conjunction with the Brain to those without dural laceration, Trauma Foundation recommendation gross contamination or evidence of of achieving full nutritional infection, or injury to the frontal sinus. support within 7 days of injury. In general, a depressed When considering nutrition support, over the sagittal sinus should not be enteral nutrition is recommended treated surgically because of the high over the use of parenteral nutrition. If risk of uncontrollable hemorrhage. parenteral nutrition use is unavoidable, frequent glucose monitoring must be performed to insure that the patient NUTRITIONAL SUPPORT remains euglycemic. A recent meta- analysis of post-pyloric vs. gastric Key Messages: feeding methods found that post- pyloric placement was associated with zz Nutrition should begin early, a significant reduction in the rate of as soon as the patient is . The same analysis also hemodynamically stable, and ideally demonstrated a trend toward reduced within 24-48 hours of injury mortality and ventilator dependence. zz Enteral nutrition is recommended over the use of parenteral nutrition

zz Post-pyloric feeding methods are preferred as they are associated with a lower rate of pneumonia

14 Benefits of performing tracheostomy TRACHEOSTOMY for patients undergoing prolonged mechanical ventilation include improved Key Messages: patient comfort due to reduced oropharyngeal irritation and improved zz If level of consciousness remains pulmonary toilet, which might also persistently depressed, TBI patients accelerate liberation from mechanical should undergo tracheostomy ventilation. A recent propensity-matched to facilitate liberation from cohort study evaluated tracheostomy mechanical ventilation; this can timing among patients with isolated decrease risk of pneumonia and severe TBI using data from hospitals ventilator-induced lung injury participating in the American College of zz Relative contraindications Trauma Quality Improvement to tracheostomy include Program. In this observational study, high intracranial pressure, early tracheostomy (≤ 8 days) relative hemodynamic instability, and to late tracheostomy (> 8 days) was severe respiratory failure associated with shorter mechanical ventilation duration and shorter ICU and zz All TBI patients deemed not likely hospital stays. This study also suggested to improve rapidly should be that early tracheostomy is associated considered for early tracheostomy, with lower risks of pneumonia, deep within 8 days of injury venous , and decubitus ulcer. Patients suffering severe TBI require mechanical ventilation in intensive care units as a component of their initial post- TIMING OF SECONDARY injury care. If the level of consciousness remains persistently depressed, these PROCEDURES patients should undergo tracheostomy Key Messages to ensure a patent airway and thereby facilitate liberation from mechanical zz In patients with intracranial ventilation and, possible decrease in hypertension, consideration the associated risk of pneumonia and should be given to delaying ventilator-induced lung injury. There are trips to the operating room for no absolute contraindications for this non-intracranial procedures procedure. Relative contraindications include high intracranial pressure, zz If patients with TBI require hemodynamic instability and severe orthopedic operations, these respiratory failure requiring high levels should ideally be delayed 24 to of FiO2 (>50%) and PEEP (>10cm H2O). 48 hours for initial stabilization of intracranial hypertension

15 zz Laparoscopic procedures with delayed definitive treatment. This should be avoided minimizes the “second hit” neurological phenomenon, triggered by the zz Close monitoring is required inflammatory response, hypotension, during general anesthesia to avoid hypoxia, hyper- or hypocarbia, and high ICP, hypotension, hypoxia, intracranial hypertension, all of which are and hypo- or hypercarbia common occurrences with orthopedic zz Intravenous anesthesia is preferable procedures. Timing of spine fracture- for severe TBI patients. dislocation surgery should depend on spine stability and the need for zz Regional anesthetic techniques emergent in should be avoided in patients patients with injury. with intracranial hypertension In patients with intractable intracranial There are no large prospective studies hypertension, consideration should be defining the optimal timing of secondary given to delaying trips to the operating extracranial surgery in patients with room unless life-saving procedures are severe TBI. In making such decisions, required. Open or open close communication among the should be performed treating specialties is paramount. when needed, with adherence to the To avoid secondary brain injury, same general principles of avoiding close monitoring during anesthesia secondary brain injury, as noted above. is required to avoid hypotension, Laparoscopy should generally be hypoxia, and hypo- or hypercarbia. avoided, especially early on, because While a single episode of hypotension it raises intra-abdominal pressure doubles mortality, the combination of and also induces hypercarbia. The hypotension with hypoxia is associated contribution of hypercarbia to long- with up to 75% mortality. If ICP is being term adverse neurologic outcomes monitored, CPP must be maintained is debatable, however. Routine ICU at ≥ 60mm Hg. Because of the adverse procedures, e.g., tracheostomy effects of inhalational anesthesia on and percutaneous endoscopic ICP, intravenous anesthesia may be gastrostomy may be performed once preferable. Of note, regional anesthetic the patient’s condition has stabilized. techniques are contraindicated in patients with intracranial hypertension.

Timing of orthopedic procedures (primarily long bone repair) does not appear to have an overall effect on outcomes in patients with severe TBI, with the following provisions. After initial stabilization, damage control orthopedics with early external fixation is favored,

16 following TBI. The challenge in deciding TIMING OF when to initiate pharmacologic prophylaxis lies in determining when PHARMACOLOGIC the risk of progression of intracranial VENOUS hemorrhage has become sufficiently low. THROMBOEMBOLISM Evidence suggests that delays in initiation of > 4 days after injury substantially PROPHYLAXIS increases the risk of VTE, so balancing these risks is critical. One approach is to Key Messages ensure that the brain injury has stabilized zz Patients with TBI are at high risk for on CT before initiation of prophylaxis. venous thromboembolism (VTE), In several studies, pharmacologic with rates as high as 20-30% prophylaxis is withheld pending a CT scan at intervals ranging from 24-72 zz VTE prophylaxis should be hours post injury. In the absence of considered within the first 72 any changes on CT scan, prophylaxis hours following TBI in most with a low molecular weight patients. Earlier initiation of (LMWH) appears to be safe. Among pharmacologic prophylaxis (<72 patients who undergo evacuation of hours) appears to be safe in an intracranial bleed, it is advisable to patients at low risk for progression wait for the head CT findings to stabilize of intracranial and have before initiation of prophylaxis. a stable repeat head CT scan To provide some objective assessment zz Placement of a prophylactic inferior of the risk of progression and to guide vena cava (IVC) filter should be the timing of initiation of prophylaxis, considered in patients at high Berne and others derived the Modified risk for progression of intracranial Berne-Norwood criteria (Table 3). Using hemorrhage who cannot receive this approach, it appears to be safe to pharmacologic prophylaxis, initiate prophylaxis if the findings on including those with lower head CT are stable (i.e., unchanged) after extremity long bone fractures or the first 24 hours. Prophylaxis should be pelvic fractures in addition to TBI withheld for at least 72 hours in patients Patients with TBI are at high risk for who meet any of the moderate risk venous thromboembolism (VTE) with criteria or who demonstrate progression rates as high as 20-30%, even with at 24 hours. If the head CT is stable appropriate mechanical prophylaxis. at 72 hours, then prophylaxis may be In spite of these risks, providers initiated with low risk of progression. have traditionally erred on the side The high-risk group is perhaps the of withholding pharmacologic VTE most challenging to manage. Because prophylaxis, accepting a higher risk of a many such patients are excluded from VTE event in order to prevent potential observational studies, there are very few progression of data upon which to base a strategy. A

17 Table 3. Modified Berne-Norwood Criteria

Low risk Moderate risk High risk No moderate or high Subdural or ICP monitor placement risk criteria > 8 mm Craniotomy Evidence of Contusion or intraventricular progression at 72 hrs hemorrhage > 2 cm Multiple contusions per lobe with abnormal CT angiogram Evidence of progression at 24 hrs

Initiate pharmacologic Initiate pharmacologic Consider placement of an prophylaxis if CT prophylaxis if CT stable at 72 hrs IVC filter* stable at 24 hrs *Consider alternate strategies as described in text

retrievable IVC filter can be considered in these patients, particularly those who MANAGEMENT are very high risk for VTE (e.g., patients with lower extremity long bone fractures CONSIDERATIONS or pelvic fractures) and removed FOR PEDIATRIC after the risk is reduced. Alternatively, PATIENTS WITH TBI surveillance duplex ultrasound of the lower extremity can be undertaken Key Messages: and if a DVT is identified, a IVC filter zz Transferring children with TBI to can be conconsidered. Finally, some a pediatric trauma center leads to centers initiate LMWH in patients with decreased morbidity and mortality. ICP monitors and following craniotomy If this is not possible, they should be after a stable head CT, although this transported to an adult trauma center practice has not been investigated. capable of treating pediatric patients

zz Pediatric TBI protocols should incorporate age appropriate physiologic parameters

18 All aspects of care of the pediatric patient with TBI should be optimized MANAGEMENT starting with pre-hospital management throughout transport and admission. CONSIDERATIONS Transferring children with TBI to FOR ELDERLY a pediatric trauma center leads to PATIENTS WITH TBI decreased morbidity and mortality. If this is not possible, they should Key Messages: be transported to an adult trauma zz Neurologic evaluation of the elderly center capable of treating pediatric patient with TBI can be complicated patients. For adult trauma centers by pre-existing , cognitive that receive pediatric patients, the decline, or /vision deficits; development pediatric TBI protocols careful determination of pre-injury are recommended. Hypoxia and neurological baseline via family hypotension should be prevented at all and is important times during pre-hospital and in-hospital care. Because children of different zz and anti-platelets ages have differing blood pressure and can exacerbate the ventilation parameters, it is important sequelae of TBI; reversal of these to maintain meticulous adherence medications, if feasible, is an to age appropriate parameters. important early management goal

Data from well-designed, controlled zz Older age is associated with higher studies on acute management of TBI mortality and worse functional in the pediatric population are limited. outcomes following TBI. However, The “Guidelines for the Acute Medical age, in isolation, should not be Management of Severe Traumatic considered a valid reason for Brain Injury in Infants, Children, treatment limiting decisions and Adolescents” are aimed to be a comprehensive document reviewing History obtained from the patient or the literature on all aspects of pediatric family can be very helpful, as comorbid management. These conditions can profoundly affect the Guidelines were updated in 2012, and impact of a TBI on an elderly patient. In provide detailed TBI management addition, medications that are frequently algorithms for children supported utilized in the elderly can exacerbate by the current knowledge base. TBI (anticoagulants/anti-platelets) or confound evaluation. With the increasing With the exception of age appropriate use of Novel Oral Anticoagulants (NOAC) parameters for blood pressure, the (for example, rivaroxaban/apixaban, tiered approach for management of dabigatran) the approaches to reversal intracranial hypertension and operative are evolving. Case series have reported management outlined in previous success with and Factor sections also apply to children. Eight Inhibitor Bypass Activity (FEIBA)

19 to reverse dabigatran (with or without be complicated by comorbid conditions hemodialysis) and Prothrombin Complex and medications that are more common Concentrate (PCC) for rivaroxaban/ in the elderly patient sustaining TBI. Well- apixaban. It is suggested that each studied recommendations for optimal center develop its own protocol for rapid CPP thresholds in the elderly are lacking. reversal of anticoagulants using local It is clear that as age advances, the expertise. For more information about risks of mortality and poor functional reversal of anticoagulants in the elderly, outcome from TBI increase. This is true please refer to the ACS TQIP Geriatric for all types of brain injury, but most Trauma Management Guidelines. striking with a GCS < 9. Despite this Neurologic evaluation of the elderly grim prognosis, 30% of elderly TBI patient with TBI can often be patients with severe TBI can survive to complicated by pre-existing dementia, leave the hospital. There is tremendous cognitive decline, or hearing/vision variability in the aggressiveness of deficits. Family and caregivers can medical care following traumatic brain be invaluable sources of information injury. This likely is due to local, regional, when trying to determine a neurologic and cultural differences in how care “baseline.” Determining the appropriate is provided. Many of those level of diagnostic evaluation is occur early after brain injury and likely important. One study found that in reflect early decisions to withdraw elderly patients with mild head injury, life-sustaining therapy. At this time, 14% of patients had evidence of due to the lack of sufficient prognostic traumatic lesion on head CT, with 20% tools, it is difficult to determine which of those lesions requiring neurosurgical patients may go on to have a meaningful intervention. Therefore, the American recovery. Arbitrary age thresholds for College of Emergency limitations of care should be avoided. recommends that a head CT be Rather, a detailed discussion with the obtained in any patient age ≥ 65 years family and decision-makers should who presents with mild head injury. center around the severity of injury, comorbid conditions, and respect for a There is a paucity of information related patient’s previously expressed wishes. to acute management of intracranial hypertension resulting from TBI in the elderly. Age-related changes in intracranial space are known to lower ICP significantly, with a concomitant rise in CPP. Further, cerebral autoregulation and pressure reactivity indices are known to decrease over time. These changes can

20 developed on populations of patients PROGNOSTITC which may provide general guidance as to predicted outcome. The most DECISION-MAKING extensively validated of these are the AND WITHDRAWAL OF IMPACT and CRASH TBI models. Caution MEDICAL SUPPORT is recommended against using these outcome models for prognosticating on Key Messages: individual patients; all of these models are developed on specific populations zz Severe TBI patients should of patients and produce point estimates receive full treatment for at with confidence intervals. Physicians least 72 hours post-injury using these models to discuss prognosis zz Age alone should not be too often discuss the point estimates but considered a valid reason for do not include confidence intervals or treatment-limiting decisions explain the inherent uncertainty in these models (or in prognostication in general). zz Caution is advised when using prognostic models Numerous studies across various in individual patients, in neurocritical care conditions, including particular when considering , global treatment-limiting decisions cerebral ischemia after , and TBI, have found that reflexive default zz It is strongly encouraged that each to early care limitations such as do-not- hospital develop a brain resuscitate (DNR) orders or withdrawal determination policy that derives of medical support is associated with from accepted national standards worsened outcome independent of other patient characteristics. Other Patients with severe TBI are, by definition, studies have found that the ability to severely injured and at high risk of accurately and precisely prognosticate death or long-term disability. Decisions long-term outcome very early in a regarding treatment approaches must patient’s course after severe TBI is limited be made rapidly and at the time of initial and frequently incorrect (especially injury. Some physicians have advocated within the first day after injury). All that care should be limited in those of these findings have raised the patients deemed to have a very poor concern of a “self-fulfilling prophecy” prognosis for meaningful recovery as of poor outcome in those patients assessed by initial parameters such as who do not receive aggressive care. GCS score, pupillary reactivity, patient age, and findings on . Mathematical models have been

21 Given these concerns, the advocated best practice is to provide all severe OUTCOME ASSESSMENT TBI patients with a trial of aggressive therapy and not limit any interventions AND QUALITY for at least 72 hours post-injury. While IMPROVEMENT IN TBI this time period is somewhat arbitrary, it represents a minimum period Key messages: during which the effectiveness of zz Outcome assessment is essential initial interventions and the likelihood to benchmarking the quality of patient survival can be assessed. of care in TBI patients Exceptions would be patients who are brain-dead or in whom a pre- zz A standardized and structured injury Advance Directive states that outcome assessment using such intervention is not desired. the GOS-E at 6 months is A longer period of treatment and recommended for TBI patients observation is typically needed for TBI is a major cause of long-term change prognosis of neurological recovery. in functional, physical, emotional Age, taken in isolation, should not cognitive, and social domains. be considered a valid reason for Assessment methods have different treatment-limiting decisions. strengths and weaknesses, and few State law governs the criteria for can be applied across the complete the determination of . TBI severity spectrum. For a global However, standardized criteria for assessment of function, the Glasgow the determination of brain death Outcome Scale (GOS) or its expanded have been developed and should be version, the Glasgow Outcome Scale- utilized. Specifically, patients must Extended (GOS-E) is broadly used to have no response to central pain, assess outcome of TBI. While the GOS/ absent reflexes, and the GOS-E may be appropriate for rating inability to breathe independently. outcome in the long term, it is not suited The clinical examination should be for assessing outcome upon discharge. used rather than a confirmatory test, This is particularly notable for patients such as at the more severe end of the TBI or cerebral blood flow assessment, spectrum who have been admitted to unless prerequisites for using the the . These patients clinical examination cannot be met. It are often in poor condition on discharge is strongly encouraged that hospitals from the intensive care unit but improve develop a defined brain death over the weeks and months thereafter. determination policy that derives from Observing these changes and evaluating the accepted national standards. long term outcomes may provide

22 reinforcing evidence for establishing severe TBI as these patients are at best practices to treat patients high risk for infections. Other routine aggressively in the first days post-injury. measures of quality care, such as patient satisfaction surveys, may also Improvement after TBI may occur over be inappropriate for TBI patients due months or even years. Conversely, to cognitive and behavioural issues. a minority of patients may show deterioration over time. A standardized and structured functional outcome assessment using the GOS-E) at six months post-injury is recommended for all TBI patients. The six-month point for standardized outcome assessments reflects a compromise between what is clinically feasible and eventual long-term clinical outcome. TBI predictive models developed on large clinical series (> 8000 patients), such as IMPACT and CRASH, provide individualized risk estimates and thus can enable establishment of baselines for clinical audits and benchmarking by permitting analysis of observed/ expected outcome. These models have been developed not only for mortality but also for functional outcome. The IMPACT model has been externally validated in multiple studies and is now being used to benchmark care in a growing number of trauma centers.

Process indicators should be identified and monitored regularly for TBI. ICP monitoring, DVT prophylaxis, nutrition, tracheostomy, time to withdrawal of support, and 6-month outcome assessment are recommended. Some system-wide process indicators, such ventilator associated pneumonia (VAP), may not be appropriate for

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26 Management Considerations Turgeon AF, Lauzier F, Simard JF, Scales DC, KE, Moore L, Zygun DA, Bernard F, Meade MO, Dung for Pediatric Patients With TBI TC, Ratnapalan M, Todd S, Harlock J, Fergusson DA. (2003). Guidelines for the acute medical management Mortality associated with withdrawal of life-sustaining of severe traumatic brain injury in infants, children, and therapy for patients with severe traumatic brain injury: adolescents. Crit Care Med 31, S407-491. A canadian multicentre cohort study. CMAJ : Canadian Medical Association journal = journal de l’Association medicale canadienne. 2011;183:1581-1588

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Mack L, Chan S, Silva J, Hogan T. The use of head Hemphill JC, 3rd, Newman J, Zhao S, Johnston SC. computed tomography in elderly patients sustaining Hospital usage of early do-not-resuscitate orders and minor head trauma. J Emerg Med 2003; 24:157-162. outcome after intracerebral hemorrhage. ; a journal of cerebral circulation. 2004;35:1130 -1134 Jagoda AS, Bazarian JJ, Bruns JJ Jr, et al; American College of Emergency Physicians; Centers for Disease Kaufmann MA, Buchmann B, Scheidegger D, Gratzl Control and Prevention. Clinical policy: Neuroimaging O, Radu EW. Severe head injury: Should expected and decision-making in adult mild traumatic outcome influence resuscitation and first-day decisions? brain injury in the acute setting. Ann Emerg Med Resuscitation. 1992;23:199-206 2008;52(6):714-748. Wijdicks EF, Varelas PN, Gronseth GS, Greer DM. Utomo W, Gabbe B, Simpson P, Cameron P. Predictors of Evidence-based guideline update: Determining in-hospital mortality and 6-month functional outcomes brain death in adults: Report of the quality standards in older adults after moderate o severe traumatic brain subcommittee of the american academy of neurology. injury. Injury 40(2009) 973-977. Neurology. 2010;74:1911-1918

Hukkelhoven C, Steyerberg E, Rampen A, et al. Patient Nakagawa TA, Ashwal S, Mathur M, Mysore MR, Bruce age and outcome following severe traumatic brain D, Conway EE, Jr., Duthie SE, Hamrick S, Harrison R, Kline injury: an analysis of 5600 patients. J Neurosurg. 2003; AM, Lebovitz DJ, Madden MA, Montgomery VL, Perlman 99:666-673. JM, Rollins N, Shemie SD, Vohra A, Williams-Phillips JA. Guidelines for the determination of brain death in Livingston D, Lavery R; Mosenthal A, et al. Recovery at infants and children: An update of the 1987 task force One Year Following Isolated Traumatic Brain Injury: A recommendations. Critical care medicine. 2011;39:2139- Western Trauma Association Prospective Multicenter 2155 Trial. J Trauma, 2005; 59 (6): 1298-1304.

Moorman ML, Nash JE, Stabi KL. Emergency surgery and trauma in patients treated with the new oral Outcome Assessment and anticoagulants: dabigatran, rivaroxaban, and apixaban. Quality Improvement in TBI J Trauma Acute Care Surg. 2014 Sep;77(3):486-594. Wilson JT, Pettigrew LE, Teasdale GM. Structured interviews for the Glasgow Outcome Scale and the Prognostic Decision-Making and extended Glasgow Outcome Scale: guidelines for their use. J Neurotrauma. 15:573-85. 1998 Withdrawl of Medical Support Turgeon AF, Lauzier F, Burns KE, Meade MO, Scales DC, Zarychanski R, Moore L, Zygun DA, McIntyre LA, Kanji S, Hebert PC, Murat V, Pagliarello G, Fergusson DA. Determination of neurologic prognosis and clinical decision making in adult patients with severe traumatic brain injury: A survey of canadian intensivists, neurosurgeons, and neurologists. Critical care medicine. 2013;41:1086-1093

27 Randeep Jawa, MD Associate Professor of Surgery, Stony Brook Expert Panel School of Medicine, Stony Brook NY

H. Gill Cryer, MD, FACS (Co-Chair) Todd Kilbaugh, MD Professor of Surgery, Chief of the Trauma/Emergency Associate Professor of Anesthesia, Critical Care, Surgery and Critical Care Program, UCLA, and , Perelman School of Medicine at the Los Angeles, CA University of Pennsylvania, Philadelphia, PA

Geoffrey T. Manley, MD, PhD, FACS (Co-Chair) Rosemary Kozar, MD, FACS Professor of Neurosurgery, UCSF, Chief of Professor of Surgery and Chief of Trauma, Memorial Neurosurgery, San Francisco General Hospital, San Hermann Hospital, Houston, TX Francisco, CA Andrew I.R. Maas, MD, PhD P. David Adelson, MD, PhD, FACS Professor & Chairman Department of Neurosurgery Chief of Pediatric Neurosurgery Antwerp University Hospital, Edegem, Belgium Phoenix Childrens Hospital, Phoenix, AZ Lisa H. Merck, MD, MPH, FACEP Aziz S. Alali, MD Assistant Professor, and Sunnybrook Research Institute Diagnostic Imaging Department of Surgery, Sunnybrook The Warren Alpert of Brown Hospital, Toronto, ON University, Providence, RI

J. Forrest Calland, MD, FACS Avery B. Nathens, MD, PhD FACS Assistant Professor of Surgery, University of Virginia Professor of Surgery, University of Toronto, Surgeon Health System, Charlotte, VA in Chief Department of Surgery, Sunnybrook Hospital, Toronto, ON Mark Cipolle, MD, PhD, FACS, FCCM Chief, , Christiana Care Claudia Robertson, MD Health System, Wilmington, DE Professor of Neurosurgery, Baylor College of Medicine Houston, TX Chris Cribari, MD FACS Medical Director of Acute Care Surgery, Medical Guy Rosenthal, MD Center of the Rockies, University of Colorado Department of Neurosurgery, Haddasah-Hebrew Health, Denver, CO University Medical Center Jerusalem, Israel Matthew L. Davis, MD, FACS Assistant Professor of Surgery, Texas A&M COM, Phiroz Tarapore, MD Trauma Program Director, Scott and White Assistant Professor of Neurosurgery, UCSF Healthcare System, Temple, TX San Francisco General Hospital, San Francisco, CA

Odette A. Harris, MD, MD, MPH Shelley Timmons, MD, PhD, Associate Professor of Neurosurgery Professor and Director of Neurotrauma Director, Brain Injury Geisinger Medical Center, Danville, PA Stanford School of Medicine, Stanford, CA Jamie Ullman, MD Mark R. Hemmila, MD, FACS Associate Professor and Director of Neurotrauma Associate Professor of Surgery, University of North Shore University Hospital, Manhasset, NY Michigan Health Systems, Ann Arbor, MI Alex Valadka, MD J. Claude Hemphill, MD Chief of Neurosurgery Professor of Neurology, UCSF, Chief of Neurology, Seton Hospital, Austin, Texas San Francisco General Hospital, San Francisco, CA David W. Wright, MD Michael Huang, MD Associate Professor, Department of Emergency Assistant Professor of Neurosurgery, UCSF Medicine Emory University, Atlanta, GA San Francisco General Hospital, San Francisco, CA

28 The Management of Intracranial Hypertension and Goals of Treatment sections were adapted from the National Institute of Neurological Disorders and Stroke of the National Institutes of Health funded (Award Numbers NS062778, 5U10NS059032, U01NS056975) ProTECT III clinical trial protocol that was successfully implemented in 38 hospitals through the Neurological Emergencies Treatment Trials network. The protocol was developed by the ProTECT III Clinical Standardization Team (G. Manley, B. Aarabi, O. Harris, C. Hemphill, P. LeRoux, L. Merck, R. Narayan, D. Okonkwo, J. Pascual, J. Salomone, W. Schwab, A. Valadka, D. Wright). The ProTECT III protocol was based on the Brain Trauma Foundation Guidelines for the Treatment and Surgical Management of TBI and refined with consensus-based methodology. We also acknowledge the participation of members of the AANS/CNS Joint Section of Neurotrauma and Critical Care (G.M., D.A., O.H., M.H., D.O., P.T., S.T., J.U., A.V.), the Neurocritical Care Society (J.C.H., C.R.), and the American College of Emergency Medicine (D.W). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health or other supporting entities.

The intent of the ACS TQIP Best Practices Guidelines is to provide health care professionals with evidence-based recommendations regarding care of the trauma patient. The Best Practices Guidelines do not include all potential options for prevention, diagnosis, and treatment and are not intended as a substitute for the provider’s clinical judgment and experience. The responsible provider must make all treatment decisions based upon his or her independent judgment and the patient’s individual clinical presentation. The ACS shall not be liable for any direct, indirect, special, incidental, or consequential related to the use of the information contained herein. The ACS may modify the TQIP Best Practices Guidelines at any time without notice.

Published January 2015

29 Notes

30 Notes

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