(BQ) Part 2 book “Neurotrauma and critical care of the brain” has contents: Pediatric brain injury, neurological critical care, fluids resuscitation and traumatic brain injury, mechanical ventilation and pulmonary critical care, paroxysmal sympathetic hyperactivity,… and other contents.
Guidelines for the Surgical Management of Traumatic Brain Injury 16 Guidelines for the Surgical Management of Traumatic Brain Injury Michael Karsy and Gregory W.J Hawryluk Abstract Compared with other fields of medicine, there are relatively few data guiding management of traumatic brain injury (TBI) Nonetheless, the TBI field has led in the development of evidence-based guidelines with the available literature The TBI guidelines have become some of the most respected and adopted recommendations in medicine Numerous guidelines for TBI have been developed, predominantly by the Brain Trauma Foundation In addition to Guidelines for the Management of Severe TBI, additional guidelines are available specifically pertaining to pediatrics, prehospital management, prognosis, combat, penetrating TBI, and surgical management This chapter aims to review aspects of published guidelines relevant to the surgical treatment of patients with TBI along with updates from recent key studies Because of the difficulty inherent in studying the emergent surgical management of TBI, many of these recommendations are consensus-based Management of epidural hematoma, subdural hematoma, intraparenchymal hematoma, posterior fossa lesions, skull fractures, and penetrating brain injury will be discussed here Guidelines related to decompressive hemicraniectomy will also be presented Keywords: traumatic brain injury, epidural hematoma, subdural hematoma, contusion, posterior fossa lesions, depressed skull fracture, penetrating brain injury, decompressive hemicraniectomy, guidelines, surgery 16.1 Introduction Traumatic brain injury (TBI) encompasses a broad, heterogeneous constellation of pathoanatomic lesions including contusions, epidural hematoma (EDH), subdural hematoma (SDH), and others (▶ Table 16.1).1 These lesions almost always coexist A broad spectrum of injury severities can be seen ranging from concussion to mild, moderate, and severe TBI; severe TBI is synonymous with coma Neurosurgeons play a key role in the management of TBI Neurosurgery can be lifesaving for many patients with severe TBI, and placement of brain monitors can help optimize recovery of the brain Neurosurgeons have led the development of TBI guidelines, and evidence demonstrates that use of these guidelines improves patient outcomes.2 This chapter aims to review key studies and, in particular, published guidelines relevant to the surgical management of TBI 16.2 Basics of Traumatic Brain Injury 16.2.1 Definition, Epidemiology, Classification, and Prognostication of Traumatic Brain Injury TBI is defined as “an alteration in brain function, or other evidence of brain pathology, caused by an external force.”3 This definition was recently ascribed as part of a consensus meeting to better define TBI for clinical and research purposes Alteration implies any loss or decrease in consciousness, any amnesia before or after the event, neurological deficits, or change in mental status The use of imaging was also discussed as an important aspect of the modern understanding of TBI These definitions help clarify the heterogeneous nature of TBI TBI is a nationwide and global epidemic, accounting annually for 235,000 hospitalized cases for nonfatal TBI, 1.1 million patients treated in emergency departments, and 50,000 deaths in the United States alone.4,5 Approximately 40 to 50% of longterm survivors demonstrate long-term disability.5,6,7 Moreover, the cumulative costs in initial care, long-term comorbidity, and loss in productivity account for $60 billion annually in the United States Common causes of head injury are motor vehicle accidents (MVAs), falls, and assaults, with MVAs common in younger individuals and falls seen in the elderly.4 In addition, TBI has increased in frequency in the elderly and the developing world as a cause of patient morbidity and mortality.1 Table 16.1 Hemorrhage patterns of traumatic brain injury Type Mechanism Epidural hematoma ● ● ● ● Subdural hematoma ● ● Intraparenchymal hematoma aBruising Temporal bone fracture and disruption of middle meningeal artery Rupture of bridging veins and extra-axial sinuses Laceration of cerebral sinuses (e.g., transverse or sagittal sinus) Skull fracture bone bleeding Rupture of bridging veins and intra-axial vessels Parenchymal bleeding (e.g., contusions, intracerebral hematomas) Focal: contusion,a laceration, herniation, infarction, intracranial hematoma,b delayed intracerebral hematoma Nonfocal: edema, disseminated swelling, diffuse axonal injury of the brain most common against bony prominence or dural folds with more than two-thirds of its volume comprising blood They can form from contusions bHematomas Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 199 Management Because of the challenges inherent to classifying TBI, it is most frequently classified by severity.1 Patients with mild TBI (postresuscitation Glasgow Coma Scale [GCS] score of 13–15) can often be managed conservatively with a period of observation The Canadian CT Head Rules is a decision score that can aid in identifying patients with mild TBI in whom computed tomography (CT) imaging is warranted.8 The criteria were developed from 3,121 patients showing that five high-risk factors (failure to reach GCS of 15 within hours, suspected open skull fracture, any sign of basal skull fracture, more than two episodes of vomiting, or age > 65 years) were 100% sensitive and two medium-risk factors (amnesia before impact > 30 minutes and dangerous mechanism of injury) were 98.4% sensitive for predicting need for neurological intervention In addition, only 32% of patients with high-risk factors and 54% of patients with medium-risk factors would require CT imaging, suggesting that the clinical examination could be a powerful method to identify patients with mild TBI that are likely to deteriorate Moderate TBI (GCS 9–12) and severe TBI (GCS < 9) require hospital admission, intensive monitoring, and a greater likelihood for neurosurgical interventions.9,10,11 Prognostication is of critical importance in the management of TBI patients; it greatly assists communication with families and helps with resource allocation and level-of-care decisions Focal neurological deficits commonly seen in head injury include pupillary changes, focal neurological deficits, signs of transtentorial herniation, and seizures, which can also be important predictors of outcome.12,13,14,15,16,17 Moreover, general predictors of good outcome include higher GCS on admission, as well as absence of transtentorial herniation, basal cistern effacement, additional intracranial lesions (e.g., skull fractures), or widespread cortical injury The International Mission for Prognosis and Analysis of Clinical Trials in TBI (IMPACT) study has been a major advance for the TBI field as it has served to definitively inform prognostic variables affecting TBI patients Another major achievement of this effort has been outcome prediction.18 IMPACT started in 2003 and involved merging 11 large data sets of clinical trials and observational studies from North America and Europe.19 Multiple studies have been published from the data set, and a prognostic calculator has been developed for use in counseling patients’ families, evaluating trauma departments and institutions, and serving as a quality metric to improve care of TBI patients (http://www.tbi-impact.org/) 16.2.2 Guidelines in Traumatic Brain Injury The publication of the evidence-based Guidelines for the Management of Severe Traumatic Brain Injury in 1995, 2000, 2007, and 2016 by the Brain Trauma Foundation (BTF) helped increase standardization and wider application of best practices in post–head injury management.17 The success of these guidelines led to the development of additional guidelines for the management of TBI patients Guidelines on pediatric TBI,20 combat-related trauma,21 mild head injury,22 and prehospital TBI emergency care23 discuss various medical management strategies and will not be reviewed here Recent publication of the 4th version of the BTF guidelines has further added to the understanding of TBI.24 200 16.2.3 Medical Management of Adult Traumatic Brain Injury The third edition of the Guidelines for the Management of Severe Traumatic Brain Injury was published in 2000 and helped to significantly standardize the treatment of patients with severe TBI.17 Multiple studies have shown improved mortality, functional outcome, length of hospital stay, and costs when the guidelines are followed.2,24 Three class I, 10 class II, and 16 class III recommendations were made based on available literature on a variety of management topics The treatment recommendations provided in the guidelines delineate many best practices in the management of TBI patients, and they provide parameters for the close monitoring required to identify declining patients who may require surgical intervention Level II evidence supports the placement of an intracranial monitor, either an external ventricular drain or an intracranial pressure (ICP) bolt, for patients with GCS to and an abnormal head CT suggesting mass effect secondary to trauma Level III evidence supports placing a monitor in patients with two of the following: > 40 years of age, unilateral or bilateral motor posturing, or systolic blood pressure < 90 mm Hg The use of a monitor in these situations can be critical in determining patients who fail medical management and warrant surgical decompression 16.2.4 Preoperative Management For TBI patients for whom neurosurgery is planned, several steps can be important in avoiding complications despite the emergent nature of the procedure.25 Protection of the airway and hemodynamic stabilization are critical as antecedent steps to surgery as part of the advanced trauma life support (ATLS) guidelines.26 Maintenance of adequate blood pressure, oxygenation, and ICP (< 22 mm Hg) is essential.25 Hyperosmolar therapy can be employed to treat ICP elevation, or in the face of focal neurological changes or a declining neurological examination when ICP elevation is presumed Screening for coagulopathy is very important when considering surgery Patients with TBI exhibit high rates of disseminated intravascular coagulation, and elderly patients commonly present with an iatrogenic coagulopathy To screen for a coagulopathy, it is critical to diligently seek any history of anticoagulation use and to assess laboratory studies (which may include complete blood count, prothrombin time, partial thromboplastin time, thromboelastography) Preparation for an emergency craniotomy involves communication between neurosurgical, anesthesia, and operating room staff and other team members as well as a system where requisite resources can be promptly mobilized Blood products should be available Two large-bore (> 16 gauge) intravenous catheters should be placed, laboratory studies reviewed, and radiographic images of the chest and neck reviewed to rule out additional injury An arterial line, a central line, a Foley catheter, and a secured endotracheal tube are all highly desirable If family members are not available to provide consent, then emergency consent must be employed Lower-extremity sequential compression devices should be placed prior to surgery to reduce the risk of deep vein thrombosis Antibiotics (commonly 30 mg/kg of cefazolin) and antiepileptic medications (commonly 20 mg/kg of levetiracetam or 25 mg/kg of fosphenytoin) should be administered Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license Guidelines for the Surgical Management of Traumatic Brain Injury 16.2.5 Anesthesia Considerations Various strategies for reduction of ICP and maintaining cerebral perfusion during an emergency craniotomy can be utilized during anesthesia.25 Patients in whom ICP elevation is suspected generally receive little to no premedication to avoid causing hypercapnia and hypoxemia Patient positioning is often reviewed to ensure adequate decompression of the jugular veins to prevent ICP elevations Blood pressure is closely monitored, with avoidance of hypotension (systolic < 90 mm Hg) paramount, especially in the setting of head elevation where decreased cerebral perfusion may occur Invasive arterial monitoring may be essential for accurate hemodynamic monitoring Adequate communication between the anesthesiologist and neurosurgeon is essential during surgery to avoid complications and aid in reducing ICP by medical treatments until adequate decompression can be completed Selection of medications is also crucial during anesthesia Use of both volume and inotropes/vasopressors, including dopamine and norepinephrine, may be necessary Preferred agents are etomidate (0.3 mg/kg), thiopental (3–5 mg/kg), propofol (1– mg/kg), and benzodiazepines (e.g., midazolam mg), which can aid in lowering ICP and cerebral metabolism (CMRO2) but also lower cerebral perfusion pressure Inhalational anesthetics (isoflurane, halothane, sevoflurane, enflurane) have the potential to cause vasodilation and increase ICP but can also lower CMRO2 Nitric oxide (N2O) may increase cerebral metabolism, cause vasodilation, and increase ICP, making it an unfavorable drug for use in neurotrauma Use of succinylcholine (0.6 mg/kg) for neuromuscular blockade is controversial because the muscle fasciculations it causes can increase ICP Nondepolarizing agents are preferred as they avoid this effect Fentanyl (3–5 μg/kg) or lidocaine (1.5 mg/kg) can be useful in blunting the hemodynamic response to laryngoscopy and intubation Postintubation sedation is also essential for avoiding coughing and gagging that can increase ICP Use of propofol, midazolam, or inhalational gases can be considered for this purpose 16.3 Surgical Management of Blunt Traumatic Brain Injury Subtypes 16.3.1 Surgical Management Introduction The development of surgical guidelines providing direction on when neurosurgery should be performed on TBI victims has been a particularly important effort Because of the difficulty in studying aspects of emergent surgical management, relatively little literature (and even less of high quality) informs surgical decisions made for TBI victims The BTF broke new ground in publishing Guidelines for the Surgical Management of TBI in 2006, which were necessarily based largely on expert consensus opinion This document provides guidance on the surgical management of EDH,17 SDH,16 intraparenchymal lesions,13 posterior fossa lesions,13 depressed cranial fractures,14 and penetrating brain injury (PBI),12 which will be discussed in this chapter The recommendations contained within are generated from level II or III evidence because randomization and placebo control of emergent interventions for TBI patients are often impractical or unethical 16.3.2 Acute Epidural Hematoma EDH is a relatively rare entity following TBI, representing only 2.7 to 4% of all cerebral injuries; the mean age of patients is 20 to 30 years.15,27,28,29,30,31,32,33,34,35,36,37,38 EDH commonly occurs as a result of injury to the middle meningeal artery, middle meningeal vein, diploic veins (especially in children), or venous sinuses, resulting in a hematoma near the pterion In fact, arterial bleeding accounts for 36% of adult EDH and 18% of pediatric cases.39 EDHs are often bound by sutures and lentiform in shape (▶ Fig 16.1) A classical “lucid interval” in which patients regain consciousness after losing it at the time of injury, followed by a subsequent decline as the acute EDH expands, has been described This classic clinical pattern occurs in only 47% of cases.27,34,38,40,41 In fact, because limited injury to the brain parenchyma typifies these injuries, these patients can achieve excellent outcomes after expedient surgical decompression The goal of achieving zero mortality with this condition may be feasible with widespread access to trauma centers, CT imaging, and improved early recognition With regard to timing of surgery for EDH, some studies have failed to support a time–outcome relationship34,42 while others support early treatment.29,41,43,44 There are substantial limitations inherent to the performance and interpretation of these studies, however The overall findings (▶ Table 16.2) from the BTF guidelines suggest prompt surgical evacuation for clots > 30 mL, regardless of GCS, or midline shift (MLS) > mm Patients with EDH < 30 mL, MLS < mm, and GCS > without focal deficit can be followed with serial imaging and intensive observation The guidelines additionally and understandably recommend that patients with acute EDH and GCS < accompanied by anisocoria should also undergo surgical evacuation as soon as possible Various factors supported by the literature are used to aid in decisions to proceed to surgical decompression in these patients Important prognostic factors in patients with EDH include age, pupillary abnormalities, associated intracranial lesions, time between neurological deterioration and surgery, and ICP.15 Blood clot volumes > 30 mL and MLS > mm have been supported by level II evidence for evacuation to improve patient outcome.15 One study of 200 patients showed that 24% of patients with hematoma volumes > 50 mL had an unfavorable outcome (i.e., Glasgow Outcome Scale [GOS] score > 3), whereas 6.2% of patients with hematomas < 50 mL had an unfavorable outcome.34 In addition, mixed-density hematomas (which suggest acute bleeding), MLS > 10 mm, and partial or total basal cistern obliteration correlated with worse mortality and GOS Another study of 158 consecutive patients showed that MLS of > mm and hematoma thickness > 15 mm predicted eventual surgical treatment A multivariate logistic regression study of 33 pediatric patients showed that MLS, hematoma thickness, volume, and temporal location of clot correlated with undergoing surgical evacuation It is noteworthy that these findings were not universally replicated by other studies, however.38,45 Patients with smaller EDH or better GCS on admission can be safely managed conservatively, at least initially.28,46,47,48,49 Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 201 Management Fig 16.1 Case of an acute epidural hematoma This is a 31-year-old man who presented after a bicycle accident He initially presented to the trauma bay with a GCS of 14 with some confusion but he acutely declined to GCS of CT imaging demonstrates an acute right EDH measuring > 30 mL in volume and with > mm in MLS The patient underwent emergent craniotomy, based on the size of the clot, MLS, GCS on arrival, and declining GCS, for evacuation of the EDH and replacement of the bone flap No ICP monitor was placed An ICP monitor was considered if the postoperative wake up exam had not returned to baseline Table 16.2 Guidelines for management of epidural hematomas Guideline Indications for surgery ● ● An EDH > 30 mL should be surgically evacuated regardless of the patient’s GCS score An EDH < 30 mL and with < 15-mm thickness and with < 5-mm MLS in patients with a GCS score > without focal deficit can be managed nonoperatively with serial CT scanning and close neurological observation in a neurosurgical center Timing It is strongly recommended that patients with an acute EDH in coma (GCS score < 9) with anisocoria undergo surgical evacuation as soon as possible Methods There are insufficient data to support one surgical treatment method; however, craniotomy provides a more complete evacuation of the hematoma Abbreviations: CT, computed tomography; EDH, epidural hematoma; GCS, Glasgow Coma Scale; MLS, midline shift 16.3.3 Acute Subdural Hematoma Acute SDH is an important and unique injury pattern commonly seen following severe head trauma Acute SDH is seen in 12 to 29% of patients admitted for severe TBI50,51,52,53,54 and 11% of patients with mild TB.16,55,56 Acute SDH often arises from injury to bridging subdural veins (▶ Fig 16.2, ▶ Fig 16.3) Like EDH, SDH commonly occurs after MVAs and falls, but the energy required to cause SDH is generally much larger, resulting in greater cerebral injury Approximately 37 to 80% of patients with acute SDH present with a GCS < and are less likely to demonstrate a lucid interval than patients with EDH.27, 38,55,56,57 In addition, 60 to 70% of patients with SDH show other 202 intracranial and extracranial injuries.55,56 Surgical treatment of SDH can be lifesaving, but the level of recovery varies widely and is difficult to predict Chronic SDH, related to prior mild TBI, preceding acute SDH, anticoagulant use, and alcohol abuse as risk factors, represents a distinct entity from acute SDH and will not be discussed further here.58 Compared with patients with acute EDHs, patients with acute SDHs have a comparatively poor prognosis Overall mortality is 15 to 60% but varies depending on other factors, including additional systemic injury and comorbidities.29,59,60,61,62,63,64,65,66 These results suggest an often poor outcome with SDH related to injury to other parts of the brain or organ systems A modern series of acute traumatic SDH of 1,427 patients between 2005 Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license Guidelines for the Surgical Management of Traumatic Brain Injury Fig 16.2 Case of an acute subdural hematoma This is a 45-year-old man who presented after a motor vehicle collision with ejection Noncontrast CT imaging demonstrates an acute right frontal SDH measuring 10 mm in maximal dimension with associated tSAH There is associated rightto-left MLS of 10 mm On examination, the patient had a GCS of and had declined from an initial GCS of 12 Because of the thickness of the clot, MLS, and GCS, this patient underwent an emergent, right-sided decompressive hemicraniectomy with ICP monitor placement and close neurocritical care follow-up Fig 16.3 Case of an acute-on-chronic subdural hematoma This is a 65-year-old woman with a history of warfarin use for treatment of atrial fibrillation who presented after a ground-level fall A noncontrast CT shows an acute SDH with chronic components The SDH measured 13 mm in maximal dimension with mm of MLS The patient’s initial GCS was 7, and the international normalized ratio was 2.3 on arrival Based on clot thickness, MLS, and GCS, she was eligible for craniectomy; however, she was not yet optimized from a coagulopathy perspective She underwent treatment with fresh-frozen plasma and vitamin K prior to decompressive craniectomy Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 203 Management Table 16.3 Guidelines for management of acute subdural hematomas Guideline Indications for surgery ● ● ● An acute SDH with a thickness > 10 mm or MLS > mm on CT should be surgically evacuated, regardless of the patient’s GCS score All patients with acute SDH in coma (GCS score < 9) should undergo ICP monitoring A comatose patient (GCS score < 9) with an SDH with a thickness < 10 mm and midline shift < mm should undergo surgical evacuation of the lesion if any of the following are true: ○ The GCS score decreased between the time of injury and hospital admission by ≥ points ○ The patient presents with asymmetric or fixed and dilated pupils ○ The intracranial pressure exceeds 20 mm Hg Timing In patients with acute SDH and indications for surgery, surgical evacuation should be done as soon as possible Methods If surgical evacuation of an acute SDH in a comatose patient (GCS < 9) is indicated, it should be done using a craniotomy with or without bone flap removal and duraplasty Abbreviations: CT, computed tomography; GCS, Glasgow Coma Scale; ICP, intracranial pressure; MLS, midline shift; SDH, subdural hematoma and 2008 demonstrated a mortality rate of 15% in patients who underwent surgical evacuation and 17% in patients managed conservatively.62 Furthermore, 94% of patients on discharge showed GCS > 13, where only 58% of patients showed the same on presentation This study also demonstrated improvement in mortality compared with the results of prior studies, which was 60 to 66% in the 1980s to 1990s and 22 to 26% in the 1990s to 2000s, likely owing to the improvement of modern neurocritical care and implementation of standardized guidelines for treatment (▶ Table 16.3) An ongoing randomized clinical trial (the HypOthermia for Patients requiring Evacuation of Subdural Hematoma [HOPES] trial) aims to evaluate the putative benefit of hypothermia to 33 °C (35 °C prior to dural opening) during the treatment of SDH in improving outcome (clinicaltrials.gov, #NCT02064959) It is hoped that studying prophylactic hypothermia in a more homogeneous subset of TBI patients than has previously been examined may lead to a positive result Earlier time to operative treatment of acute SDH has been supported in a number of studies as improving prognosis.29,44, 53,54,67,68,69 This association has not been uniformly seen in published studies, however One study showed a 30% mortality rate in patients operated after hours compared with a 90% mortality rate in those treated < hours from injury.53 This study also showed a significantly longer operative time in patients who died (390 vs 170 minutes) A large retrospective study of 522 patients who underwent surgical treatment of traumatic SDH showed that increased time to surgical treatment yielded a significant decrease in mortality, suggesting preoperative resuscitation was an important, but poorly characterized, phase in improving recovery.68 Care is required in the interpretation of these studies, however, as patients surviving to undergo later surgery likely had less severe injuries Moreover, some studies have failed to show an impact on timing of surgery and outcome,55,56,61,70,71,72 while others have shown a contrary result Generally, patients with indications for decompression of SDH should be expedited to the operating room, but stabilization of airway and hemodynamic issues should take precedence Recommendations from the BTF include surgical evacuation for patients with declining GCS as well as enlarging SDH thickness and cerebral herniation Several studies support these recommendations Some have demonstrated a significant 204 correlation of GCS, SDH volume, MLS, and basal cistern effacement and overall mortality.56,70 One study demonstrated that patients with a clot thickness of < 10 mm had a 10% mortality rate, whereas those with a clot thickness of > 30 mm had a 90% mortality rate.66 In addition, MLS > 20 mm also correlated with a significant increase in mortality Conversely, another study failed to show an impact of SDH volume, MLS, or basal cistern effacement, suggesting additional factors are important for prognosis.38 Cutoffs used for identifying surgical candidates have been evaluated by some groups, who have suggested evacuation of clots > 10 mm and MLS > mm and in patients with worsening ICP levels > 22 mm Hg.63,73,74 One recent study showed that a difference between MLS and clot thickness of ≥ mm correlated with a worse outcome.75 In fact, a good outcome was seen in 67% of patients in the nonoperative group compared with 23% of patients who required eventual surgery The BTF guidelines (▶ Table 16.3) recommend surgery for hematomas > 10 mm in thickness or MLS > mm.16 Patients with SDH and GCS < should undergo ICP monitoring.16 In addition, patients with SDH < 10 mm in thickness, MLS < mm, and GCS < should undergo evacuation if GCS declines between injury and hospitalization by ≥ points, if the patient presents with asymmetric or fixed and dilated pupils, or if the patient’s ICP is > 22 mm Hg.16 Patients with acute SDH should be evaluated as soon as possible, and surgical interventions should involve a craniotomy with or without bone flap removal and duraplasty 16.3.4 Traumatic Intraparenchymal Lesions Traumatic intraparenchymal lesions account for 13 to 35% of severe TBI, with most small lesions not requiring surgical evacuation.13,76,77,78,79,80,81 Primary mechanisms of traumatic parenchymal lesions can be divided into focal and nonfocal subtypes Focal subtypes include contusion, laceration, and intracerebral hematoma (ICH), whereas nonfocal lesions include edema, diffuse swelling, traumatic subarachnoid hemorrhage (tSAH), and diffuse axonal injury Lacerations involve significant trauma resulting in skull fracture and penetration of the brain by skull fragments Contusion often involves bruising of the brain due to capillary damage most prominent at the frontotemporal poles Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license Guidelines for the Surgical Management of Traumatic Brain Injury Fig 16.4 Case of an acute intraparenchymal hemorrhage This is a 54-year-old man who presented after a motor vehicle collision CT imaging demonstrates an acute right frontal intraparenchymal hemorrhage measuring > 50 mL with marked mass effect, effacement of the right frontal ventricle, and 10 mm of right-to-left MLS There is associated right frontal pneumocephalus from a comminuted fracture Based on the GCS, MLS, and lesion volume, the patient was indicated for a decompressive procedure and clot evacuation The patient had a GCS of on arrival, and he underwent decompressive craniectomy with evacuation of the hematoma and repair of the skull fracture due to coup-contrecoup injury ICH involves focal hemorrhage, where blood collection makes up more than two-thirds of the lesion, within the brain parenchyma (▶ Fig 16.4, ▶ Fig 16.5) tSAH involves hemorrhage within the subarachnoid space, outside of the brain parenchyma In addition, multiple intraparenchymal lesions commonly coexist or accompany SDH and EDH Importantly, ICHs can appear or enlarge in delayed fashion after initial presentation This phenomenon has been termed delayed traumatic ICH (DTICH), which is defined as a lesion of increased attenuation developing after admission with an initial normal CT scan of the head; it is often seen in areas of cerebral contusion.82,83 The incidence ranges from 3.3 to 7.4% of patients with moderate-to-severe TBI and 1.6% of evacuated ICH.82,84,85 In addition, DTICH is associated with increased incidence of secondary systemic insults, incidence after decompressive surgery, and coagulopathy, along with a mortality ranging from 16 to 72%.83,85,86,87,88 These results suggest a underlying pathological mechanism for DTICH distinct from those of other types of traumatic intraparenchymal injury and provide strong rationale for early invasive monitoring, which can identify the delayed appearance or expansion of these mass lesions Multiple studies have sought to improve prognostic accuracy by combining clinicoradiographic metrics A key study defining the Marshall classification of intracerebral injury showed that CT parameters could predict mortality independent from age and GCS.89 This study of 746 patients with severe TBI showed better favorable outcomes (23 vs 11%) with ICH volumes > 25 mL and led to the development of further studies regarding predictive metrics in ICH.89 Another large study of 218 patients showed that SAH, ICH volumes > 40 mL, and compressed cisterns correlated with a decline in GCS by points or pupillary dilation.90 Furthermore, delayed deterioration was associated with hypoxic events Patients with GCS < and ICH volumes of > 20 mL demonstrated better outcome with surgical evacuation compared with conservatively managed patients Subgroups of patients with MLS of ≥ mm, GCS ≥ 10, temporal contusions, MLS, or obliteration of the basal cisterns also benefited from craniotomy A retrospective study 202 patients with traumatic ICH showed that low GCS and hematoma > 16 mL independently predicted poor outcome.91 Similarly, patients with reduced ICP prior to evacuation demonstrated improved mortality and morbidity.92,93 These results supported the recommendations of BTF guidelines (▶ Table 16.4 and ▶ Table 16.5) including surgical decompression of patients with progressive neurological deterioration, medically refractory intracranial hypertension, or mass effect on CT In addition, patients with GCS > to and frontotemporal contusions > 20 mL, MLS > mm, or cisternal compression should be treated operatively As well, patients with lesions > 50 mL in volume should undergo decompression surgery Patients without neurological compromise, with controlled ICP, and with no significant mass effect can be managed nonoperatively with intensive monitoring and serial imaging Surgical evacuation should include a craniotomy for focal lesions; bifrontal decompressive craniectomy for diffuse posttraumatic cerebral edema and medically refractory intracranial hypertension; or subtemporal decompression, Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 205 Management Fig 16.5 Case of diffuse traumatic subarachnoid hemorrhage This is a 25-year-old man who presented after a skiing accident CT imaging shows diffuse tSAH with a right frontal SDH No significant mass effect or MLS is identified On examination, the patient had a GCS of Based on the GCS exam, lack of mass effect, or MLS, the patient underwent placement of an ICP monitoring device and close neurocritical care followup Table 16.4 Guidelines for management of intraparenchymal lesions Guideline Indications for surgery ● ● ● Timing and methods ● ● ● Patients with parenchymal mass lesions and signs of progressive neurological deterioration referable to the lesion, medically refractory intracranial hypertension, or signs of mass effect on CT scan should be treated operatively Patients with GCS score 6–8 with frontal or temporal contusions > 20 mL in volume with midline shift > mm and/ or cisternal compression on CT scan, and patients with any lesion > 50 mL in volume should be treated operatively Patients with parenchymal mass lesions who not show evidence for neurological compromise, have controlled ICP, and show no significant signs of mass effect on CT scan may be managed nonoperatively with intensive monitoring and serial imaging Craniotomy with evacuation of mass lesion is recommended for those patients with focal lesions and the surgical indications listed above Bifrontal decompressive craniectomy within 48 hours of injury is a treatment option for patients with diffuse, medically refractory posttraumatic cerebral edema and resultant intracranial hypertension Decompressive procedures, including subtemporal decompression, temporal lobectomy, and hemispheric decompressive craniectomy, are treatment options for patients with refractory intracranial hypertension and diffuse parenchymal injury with clinical and radiographic evidence for impending transtentorial herniation Abbreviations: CT, computed tomography; GCS, Glasgow Coma Scale; ICP, intracranial pressure temporal lobectomy, and decompressive craniectomy for evidence of impending transtentorial herniation 16.3.5 Posterior Fossa Lesions Compressive posterior fossa lesions secondary to trauma are rare entities but can require emergent attention because of their direct compression of the cerebellum and brainstem as well as the risk of causing hydrocephalus A location in the posterior fossa is found in 1.2 to 12.9% of EDH, 0.5 to 2.5% of SDH, and 1.7% of intraparenchymal hemorrhages.13,94,95,96,97,98,99,100 206 Nonoperative management has also been employed for patients with no CT evidence of mass effect and intact neurological examination.94,95,101 Studies generally support hematoma evacuation on an emergent basis, with improved outcome in patients with early presentation and greater GCS Caution should be noted in that patients can rapidly decline with posterior fossa lesions and brainstem compression In addition, supratentorial ICP monitoring may not always reflect localized intracranial hypertension in the posterior fossa One study of 81 patients showed favorable outcome (GOS or 5) in 95% of patients with GCS ≥ Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license Guidelines for the Surgical Management of Traumatic Brain Injury Table 16.5 Guidelines for management of intraparenchymal lesions in infants, children, and adolescents Guideline Indications for surgery ● ● ● Decompressive craniectomy should be considered in pediatric patients with severe TBI, diffuse cerebral swelling, and intracranial hypertension refractory to intensive medical management Decompressive craniectomy should be considered in the treatment of severe TBI and medically refractory intracranial hypertension in infants and young children with abusive head trauma Decompressive craniectomy may be particularly appropriate in children with severe TBI and refractory intracranial hypertension who have a potentially recoverable brain injury Decompressive craniectomy appears to be less effective in patients who have experienced extensive secondary brain insults Surgery may be favorable for patients who experience a secondary deterioration on the GCS and/or evolving cerebral herniation syndrome within the first 48 h after injury may represent a favorable group, whereas surgery may be unfavorable for patients with an unimproved GCS of Abbreviations: GCS, Glasgow Coma Scale; TBI, traumatic brain injury Table 16.6 Guidelines for management of posterior fossa mass lesions Guideline Indications for surgery ● ● Patients with mass effect on CT scan or with neurological dysfunction or deterioration referable to the lesion should undergo operative intervention Mass effect on CT scan is defined as distortion, dislocation, or obliteration of the fourth ventricle, compression or loss of visualization of the basal cisterns, or the presence of obstructive hydrocephalus Patients with lesions and no significant mass effect on CT scan and without signs of neurological dysfunction may be managed by close observation and serial imaging Timing In patients with indications for surgical intervention, evacuation should be performed as soon as possible because these patients can deteriorate rapidly, thus worsening their prognosis Methods Suboccipital craniectomy is the predominant method reported for evacuation of posterior fossa mass lesions and is therefore recommended Abbreviation: CT, computed tomography but poor outcome (GOS 1–3) in 81% of patients with GCS < 8.95 One study of 25 patients showed that those with EDH volumes < 10 mL, thickness < 15 mm, and MLS < mm had better survival.101 A study of 73 patients with posterior fossa lesions showed 14 patients could be managed conservatively and 59 required surgical evacuation.94 Furthermore, overall mortality was 5.4%, but it was confounded by secondary cerebral hemorrhages and poor preoperative neurological examination findings The BTF guidelines (▶ Table 16.6) recommend decompression for patients with mass effect or neurological dysfunction specific to the posterior fossa lesion, including compression of the fourth ventricle or basal cisterns, and obstructive hydrocephalus Patients without symptoms or mass effect on CT can be managed by observation and imaging, while surgical intervention should be performed rapidly for deteriorating patients Suboccipital craniectomy and evacuation of posterior fossa mass lesions are the preferred treatment strategy 16.3.6 Cranial Vault Fractures Depressed cranial fractures involve discontinuity of the skull arising from either blunt or sharp trauma to the head Fractures are described by shape (linear or stellate), location (including calvarial vs basilar), displacement (diastatic/nondisplaced vs displaced/depressed), number of bone pieces (hinge door vs comminuted), and exposure to environment (simple/closed vs compound/open) Traumatic skull fractures can also be associated with facial and orbital fractures The traumatic growing skull fracture is a separate entity related to a laceration of the dura resulting in spacing of the fracture edges due to cerebrospinal fluid (CSF) pulsations in a growing pediatric cranium.102 The AOCMF skull fracture classification system has been one of many approaches in quantifying craniofacial skull fracture patterns and location.103 General indications for surgical treatment of skull fractures include those that are depressed in frontal or other cosmetically sensitive areas, fractures over vascular sinuses with the presence of intracranial hemorrhage, open/comminuted fractures or fractures with > 1-cm depression, and when repair of CSF leak is necessary Linear, diastatic, and nondisplaced fractures can often be managed nonoperatively Additional vascular imaging may be indicated when fractures extend through areas with vulnerable vessels, such as when skull base fractures extend through the petrous carotid canal In addition to repair of skull fragments and wound debridement, removal of loose bone fragments is advocated; however, evidence for surgical treatment is at best class III evidence.104 The BTF guidelines (▶ Table 16.7) recommend operative repair of open fractures greater than the thickness of the skull to prevent infection unless there is no clinical or radiographic evidence of dural penetration, intracranial hematoma, depression > cm, frontal sinus involvement, gross cosmetic deformity, wound infection, pneumocephalus, or gross wound contamination Simple depressed fractures can be managed nonoperatively Surgery should be performed early with elevation, debridement, and Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 207 Management Table 16.7 Guidelines for management of depressed skull fractures Guideline Indications for surgery ● ● ● Patients with open (compound) skull fractures depressed greater than the thickness of the skull should undergo operative intervention to prevent infection Patients with open (compound) depressed skull fractures may be treated nonoperatively if there is no clinical or radiographic evidence of dural penetration, significant intracranial hematoma, depression > cm, frontal sinus involvement, gross cosmetic deformity, wound infection, pneumocephalus, or gross wound contamination Nonoperative management of closed (simple) depressed skull fractures is a treatment option Timing Early operation is recommended to reduce the incidence of infection Methods ● ● ● Elevation and debridement is recommended as the surgical method of choice Primary bone fragment replacement is a surgical option in the absence of wound infection at the time of surgery All management strategies for open (compound) depressed fractures should include antibiotics antibiotics as well as replacement of the primary bone fragment if wound infection is absent Management of open air sinus injury from skull fractures represents a unique aspect of surgical management because of the potential for CSF leak and intracranial infection Obliteration, cranialization, and exoneration of sinuses may be necessary for fractures through the air sinuses to reduce risk of CSF leak and cerebral infection Unfortunately, criteria distinguishing sinuses at risk of delayed complications remain elusive Mucoceles, the accumulation and retention of mucoid within paranasal sinuses, can occur with fractures that occlude the nasofrontal ducts and can present in a delayed fashion after TBI.105 Meningitis and encephalitis are risks of CSF leak after mucocele formation Mucopyoceles involve infection of the mucoid retention, and complicate clinical management Frontal sinus injuries occur in to 12% of patients with severe facial trauma, can involve the inner table, outer table, or both, and can be associated with cerebral infection (although they heal without intervention in 66% of patients).106 Compound fractures show a significant rate of infection from 1.9 to 10.6%, most commonly a Streptococcus species, neurological morbidity of 11%, and incidence of late epilepsy of 15%.107,108, 109,110,111 One series of 33 patients discussed the importance of surgical cranialization of the frontal sinus after injury and CSF leak along with obliteration of the nasofrontal outflow tract.112 Management guidelines on the repair of open-sinus fractures remain limited, with recent reviews recommending recognition of this potential complication, close posttrauma follow-up, interdisciplinary specialty management, and cranialization of posterior table comminuted fractures or those with CSF leak.105 Treatment of skull fractures in pediatric patients presents a unique situation because of the ongoing growth of the patients’ craniums These fractures are almost uniformly associated with a linear fracture and dural tear with entrapment of the arachnoid or brain within the fracture in children < years of age The incidence of growing fractures is 0.05 to 1.6% of patients with linear fractures of the cranium and usually attributed to the growth of the brain and skull preventing healing of the fracture.102 A series of 180 patients < years of age showed only patients required nonemergent surgical treatment of depressed skull fracture and overall outcome was uniformly positive, likely because of the limited traumatic mechanism.113 Repair of the growing fracture involves adequate repair of the dural tear, with earlier treatment favoring improved outcome.102 208 Cranial fracture alone or when associated with additional intracranial lesions can predict a poor outcome.63,114,115,116 One study of 1,178 adolescents with intracranial injury showed that cranial fracture was the only independent factor predicting poor outcome.114 Another study of 923 pediatric patients demonstrated that temporal bone fracture, age ≥ years, MVA mechanism, and concomitant organ injury were associated with worse prognosis.117 Furthermore, parietal fractures were more frequent in younger age groups, while frontotemporal fractures were more common in older ages (> years) A study of 850 patients with cranial fracture found that 71% showed an intracranial lesion compared with only 46% of 533 patients without a fracture.116 Replacement of bone fragments has been shown in multiple studies to not increase risk of infectious complications with surgery within 72 hours regardless of the level of contamination at the time of surgery.107,111,118 A metaanalysis of randomized clinical trials and 17 nonrandomized clinical trials showed that antibiotic prophylaxis after traumatic skull fracture did not reduce risks of infection or all-cause mortality after trauma and was generally not recommended.119,120 16.4 Surgical Techniques for Traumatic Brain Injury 16.4.1 Decompressive Craniectomy Decompressive hemicraniectomy is a surgical option in patients requiring evacuation of large intracranial hematomas and those with ICP elevation refractory to less aggressive treatment The Monro–Kellie doctrine dictates that cerebral tissue, CSF, and blood occupy a fixed intracranial volume Decompressive hemicraniectomy is designed to expand the intracranial volume in settings of hematoma or edema, in hopes of preventing brain herniation, decreased perfusion, and cerebral ischemia Generally, a minimum diameter of 12 cm has been widely accepted as necessary for decompression.121,122,123,124,125 Unilateral, bifrontal, or posterior fossa decompressive craniotomies can be performed when indicated Survival advantage after decompressive hemicraniectomy greatly depends on appropriate patient selection during neurosurgical emergencies In a meta-analysis of 12 studies, including randomized clinical trials, decompressive hemicraniectomy with open dural flaps offered significantly improved mortality and GOS score.121 Moreover, retrospective studies in this Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license Socioeconomics Table 32.13 Types of economic evaluation analysis Cost-effectiveness analysis ● ● ● ● Cost–utility analysis ● ● ● ● ● Cost–benefit analysis ● ● ● ● Net benefit analysis ● ● ● Most straightforward Takes into account differences in outcomes in clarifying choices (one-dimensional) Comparisons made between different injury prevention programs in terms of cost per unit of outcome Those with lowest cost per unit of outcome are most efficient More advanced Special form of cost-effectiveness analysis Costs per unit of utility (person’s well-being) are calculated Most common unit of health-related utility is disability-adjusted life years (DALYs) which incorporate quality of life and years of life into one measure DALYs measure physical, emotional, mental health, and social aspects relevant and important to an individual’s well-being Divides total benefits by intervention costs, yielding a return on investment of the intervention Supports direct comparison across diverse interventions with different objectives Advantage: clearly indicates whether an intervention is worthwhile implementing Disadvantage: requires putting a dollar value on a DALY which is difficult and which some find distasteful A companion to cost–benefit analysis Net benefit = benefits – costs Some interventions where benefits > costs may not be worthwhile as (1) investments that offer a larger return may be available and (2) uncertainty means that return will vary up or down from the average judgment, as no threshold or cutoff values exist Approaches that can be used to derive these cutoff values include comparing the cost per unit of outcome with other programs, “rules of thumb,” and inferences from past decisions.25 32.6.2 Cost–Utility Analysis Cost–utility analysis is more advanced than cost-effectiveness analysis Information from cost-effectiveness analyses is useful in clarifying choices between different programs on the basis of an outcome measure that is one-dimensional However, a limitation of cost-effectiveness analysis is when comparisons need to be made between interventions for different injury causes where the unit of outcome varies across the alternative options In addition, if outcomes are measured using a generic unit such as life years saved, then cost-effectiveness analysis does not account for differences in quality of life resulting from the intervention This makes it inappropriate for comparing programs that are primarily lifesaving with those for which the major objective is an improvement in quality of life Cost–utility analysis was developed as a special form of costeffectiveness analysis, in which the costs per unit of utility (units that relate to a person’s well-being) are calculated.2 The most commonly used units of health-related utility is DALYs prevented or QALYs saved These measures incorporate some components of quality of life as well as quantity (or length) of life into a single measure The number of life years (quantity of life) gained as a result of an intervention is combined with some judgment on the quality of those life years to calculate the number of QALYs gained or DALYs prevented Quality of life is a multidimensional concept measuring the physical, emotional, mental health, and social aspects that are relevant and important to a person’s well-being Conventionally, quality is measured on a QALY scale from to 1, where is equivalent to death and is equivalent to good health A DALY equals minus a QALY Results are presented in terms of cost per QALY gained from the alternative options, and the option with the lowest 402 cost per QALY gained is the most efficient Since outcomes are being measured in commensurate units of utility in cost–utility analysis, comparisons can be made across diverse interventions for different injury causes Again, no threshold or cutoff values exist below which the cost per QALY represents value for money and a similar assessment must be made as for costeffectiveness analysis, based on comparisons with other programs, “rules of thumb,” or inferences from past decisions As a general guide, around the world, interventions that cost more than $40,000 to $60,000 per QALY saved generally would not be implemented The U.S threshold exceeds $130,000 32.6.3 Benefit–Cost Analysis Benefit–cost analysis divides total benefits by intervention costs, yielding the return on investment in the intervention In this analysis, all benefits are either monetized or omitted from the calculation Benefit–cost analysis supports direct comparison across diverse interventions with different objectives Also, as with cost–utility analysis, multiple benefits can be captured in benefit–cost analysis if the interventions under consideration produce multidimensional outcomes An advantage of benefit– cost analysis over cost-effectiveness analysis and cost–utility analysis is that it clearly indicates whether an intervention is worthwhile to implement 32.6.4 Net Benefit Analysis Net benefit analysis generally is a companion to a benefit–cost analysis The net benefit equals the benefits minus the costs Any intervention where the benefits are greater than the costs is worthwhile (i.e., net benefits greater than zero or benefit– cost ratio greater than 1) When comparing two alternatives, depending on budget constraints, the intervention with the greatest net benefit or the one with the highest benefit–cost ratio may be the preferred option Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license Cost of Traumatic Brain Injuries in the U.S and the Return on Helmet Investments 32.7 Bicycle Helmets and Head Injury: A Benefit–Cost Analysis (▶ Table 32.14) This section presents an example of a benefit–cost analysis of an intervention to encourage the use of bicycle helmets by both children (under 15 years) and adults The example updates the estimate for child bicycle helmets in Miller and Levy24 and adds an adult estimate We follow the steps suggested in the preceding section Define the intervention The intervention is bicycle helmet purchase for every pedal cyclist in the United States, which equates to analyzing the average return on investment in a helmet We examine the benefits over the 5-year period that we assume a helmet would be used before needing replacement What is the perspective? We adopt a societal perspective to reflect the fact that the program is motivated in the public interest This perspective includes cost savings from avoiding lost work and pain and suffering We also present breakdowns from an insurer’s perspective How are future values adjusted? We used a 3% discount rate to discount future injury cost savings Medical costs were adjusted using the appropriate components of the Price Indexes for Personal Consumption Expenditures published by the U.S Bureau of Economic Analysis Work loss costs and quality-of-life losses were adjusted using the Employment Cost Index for Total Compensation for All Civilian Workers, published by the U.S Bureau of Labor Statistics What would these helmets cost? Average cost per bike helmet was $34.93 in 2015 (http://www.bicycleretailer.com/studiesreports/2016/05/12/nsga-bike-units-dollar-sales-2015# V0MSWdQrLvY) Further data on prices for bicycle helmets that meet U.S Consumer Product Safety Commission standards came from a search of the websites of the three largest retail companies that currently sell helmets in the United States Lowend models ranged from $12.42 to $21.99 plus sales tax (4–7% in many states) for adult helmets and from $10.59 to $15.95 for child helmets The analysis uses an $18 price (with sensitivity analysis at $15 and $40) for adults and $13 (with sensitivity analysis at $11 and $25) for children In the United States, an estimated 89.5 million people over age 15 and 35.3 million age 15 or less rode bicycles in 2012.26 The number of helmets purchased per year would be one-fifth of this rider count (assuming a 5-year life span for helmets) Annual helmet-related spending would be $92 million for children under 15 years old ([35.3 million/5] × $13) and $322 million for older cyclists ([89.5 million/5] × $18) How large is the bicycle-related head injury toll? HCUP and Vital Statistics data indicate that, in 2012, bicycle crashes caused 423 fatal head injuries, 42,419 nonfatal TBIs, and 49,444 other nonfatal head (face or scalp) injuries What bicycle-related head injuries cost? From the cost estimates developed above, estimated lifetime comprehensive costs (in 2012 dollars) for injury under age 15 totaled $0.2 billion for fatal head injuries, $1.8 billion for nonfatal TBIs, and $1.7 billion for other head injuries (▶ Table 32.16) Over age 15, the respective totals were $2.1 billion, $10.5 billion, and $2.9 billion (▶ Table 32.15) Lifetime medical spending due to bicycle-related head injuries was $150 million annually for children under 15 years old The other losses were much larger—$462 million in future work loss and almost $1.5 billion in lost quality of life For adults, the respective totals were $553 million, $2.0 billion, and $13.0 billion How effective are helmets? If universally used, helmets prevent 49 to 56% of bicycle related head injury deaths, 68 to 80% of nonfatal TBIs, and 65% of other head injuries.27,28,29,30 We used midpoint estimates for helmet effectiveness (i.e., we assumed that helmets prevent 53.5% of bicycle-related head injury deaths, 74% of nonfatal TBIs, and 65% of other head injuries) Given that only 69% of children and 38% of adults who own bicycles regularly use helmets, we assumed that only 69% of the effectiveness was achieved in children and 38% in adults How many cyclist deaths and injuries can helmet use prevent? Parents reported 64% of bicyclists under age 16 used helmets all or most of the time in 2012, higher than the self-reported 39% use among those age 16 and over.26 We used these estimates as if the age break were 15 If no cyclist under 15 used a helmet in 2012, 38 TBI deaths would have occurred in this population (▶ Table 32.16) This estimate was derived using the formula 28/(1 – 0.535 × 0.64) with 28 actual fatal injuries, 53.5% helmet effectiveness, and 64% helmeted Using a parallel calculation for nonfatal injuries, cyclists under age 15 would have survived 71,602 head injuries in 2012 if none wore helmets If every cyclist under age 15 wore a helmet in 2012, only 18 TBI deaths would have occurred in this population This estimate was derived by multiplying the number of injuries at 0% helmet use times minus the percentage effectiveness in reducing head injury deaths [38 × (1 – 0.537)] Similarly, only 22,408 head injuries would have occurred Thus, relative to no use, universal helmet use by cyclists under age 15 would have prevented an estimated 20 deaths, 21,807 nonfatal TBIs, and 27,387 other nonfatal head injuries in 2012 ▶ Table 32.17 presents parallel estimates for adults What cost savings and benefit–cost ratio would helmet use yield? Universal helmet use by cyclists under age 15 (as opposed to no use at all) would have resulted in almost $7.0 billion in injury cost savings It would have saved medical costs, work loss, and quality of life valued at $0.2 billion, $0.6 billion, and $6.2 billion, respectively More realistically, only 78.0% of helmet owners under age 15 routinely wear them, so universal helmet ownership would yield only 78% of the potential benefits The benefit–cost ratio of universal helmet ownership by bicyclists under age 15 is 56 ($7.0 billion × 78% × 4.717 present value years/[$13 × 35.3 million]) On average, a $13 child bicycle helmet saves $728, including $21 in present-value medical spending, $60 of work loss, and quality of life valued at $647 Universal helmet use by cyclists age 15 and over (as opposed to no use at all) would have resulted in an estimated $14.9 billion in injury cost savings, including $0.55 billion in medical spending, $1.9 billion in work loss, and $12.4 billion in quality of life preserved However, only 72.2% of these helmet owners routinely use them The benefit–cost ratio for adult bicycle helmets is 31.5 On average, an $18 adult bicycle helmet saves $566, including $21 in present-value medical spending, $72 of work loss, and quality of life valued at $473 What uncosted outcomes will result? Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 403 Socioeconomics Table 32.14 Bicycle helmets and head injury: an example of a cost–benefit analysis Intervention defined ● Bicycle helmet purchase for every cyclist in the United States (analyzing average return on investment in a helmet over a 5-y period) Perspective ● ● Societal perspective—everyone’s costs and benefits count Perspective includes cost savings from avoiding lost work and pain and suffering Future values adjusted ● 3% discount rate used to discount future injury cost savings Cost of helmets ● Analysis uses $18 adult and $13 child helmets In 2012, 35.3 million people under age 15 and 89.5 million people over age 15 rode bicycles With a 5-year average helmet life, no of helmets purchased would be 1/5 of this rider count Annual helmet spending: ○ $92 million for < 15 y ○ $322 million for ages ≥ 15 y ● ● ● Bicycle-related head injury toll In 2012: ● 423 fatal head injuries ● 42,419 nonfatal TBIs ● 49,444 nonfatal other head injuries Cost of bicycle head injuries Lifetime comprehensive costs: ● Under age 15: ○ $0.2 billion for fatal head injuries ○ $3.5 billion for nonfatal TBIs ○ $1.7 billion for nonfatal scalp injuries ● Ages 15 and over: ○ $2.1 billion for fatal head injuries ○ $10.5 billion for nonfatal TBIs ○ $2.9 billion for nonfatal scalp injuries Effectiveness of helmets ● ● ● Prevention of cyclist death and injury via helmet use ● ● ● Percentage of owners who wore their helmet all or most of the time when bicycling in 2012 ● ● Prevent 49–56% of fatal head injuries Prevent 68–80% of nonfatal TBIs Prevent 65% of other head injuries Estimated 180 TBI deaths under age 15 in 2012 if no helmets used Estimated 86 TBI deaths in children in 2012 if every child wore a helmet If universal helmet use by child cyclists had been instituted in 2012, the estimated effects would have been ○ Prevented 94 deaths ○ Prevented 46,400 nonfatal TBIs ○ Prevented 106,600 other nonfatal head injuries 78.2% under age 16 72.2% age 16 and over Cost savings and cost–benefit ratio of universal helmet use: Children Cost savings per $13 helmet ● ● ● ● Adult Benefit–cost ratio 56 Cost savings per $18 helmet ● ● ● ● Benefit–cost ratio Uncosted outcomes ● ● ● Changes in insurance payments Injury cost saving = $728 Medical cost saving = $21 Work loss saving = $60 DALY saving = $647 ● ● ● Injury cost saving = $567 Medical cost saving = $21 Work loss saving = $73 DALY saving = $473 31 Parents spend less time and expense caring for injured children Lawyers file fewer lawsuits seeking compensation for cyclists Ride bike less often because helmet is uncomfortable: ○ Increase in obesity ○ Decrease in bicycle-related injuries Save approximately $45 per child helmet Save approximately $50 per adult helmet Auto insurers process less claims Abbreviation: TBI, traumatic brain injury 404 Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license Cost of Traumatic Brain Injuries in the U.S and the Return on Helmet Investments Table 32.15 Cost of TBI and other head injuries, U.S cyclists age < 15, 2012 (M of dollars) Injury type Outcome Incidence Medical Work loss Quality of life Total TBI Fatal 25 0.6 39.6 157.4 197.6 TBI Nonfatal 15,512 102.7 246.3 3,160.2 3,509.2 Other head Nonfatal 24,606 47.0 175.7 1,471.6 1,694.3 40,143 150.2 461.6 4,789.3 5,401.0 Total If no cyclist used a helmet TBI Fatal 38 0.8 59.6 237.1 297.5 TBI Nonfatal 29,468 195.1 467.9 6,003.5 6,666.5 Other head Nonfatal 42,134 80.4 300.9 2,519.9 2,901.1 71,640 276.3 828.4 8,760.4 9,865.1 Total If every cyclist used a helmet TBI Fatal 18 0.4 28.3 112.6 141.3 TBI Nonfatal 7,662 50.7 121.7 1,560.9 1,733.3 Other head Nonfatal 14,747 28.1 105.3 882.0 1,015.4 Total 22,426 79.3 255.3 2,555.5 2,890.0 Savings 49,213 197 573 6,205 6,975 Abbreviation: TBI, traumatic brain injury Table 32.16 Cost of TBI and other head injuries, U.S cyclists age ≥ 15, 2012 (M of dollars) Injury type Outcome Incidence Medical Work loss Quality of life Total TBI Fatal 398 10.3 445.0 1,624.5 2,079.7 TBI Nonfatal 26,907 455.9 1,313.4 8,757.4 10,526.7 Other head Nonfatal 24,838 87.1 278.5 2,575.6 2,941.2 52,143 553.2 2,036.9 12,957.5 15,547.7 Total If no cyclist used a helmet TBI Fatal 500 13.0 559.5 2,042.7 2,615.2 TBI Nonfatal 37,822 640.8 1,846.3 12,310.1 14,797.2 Other head Nonfatal 33,273 116.6 373.1 3,450.3 3,940.0 71,595 770.4 2,778.9 17,803.1 21,352.4 Total If every cyclist used a helmet TBI Fatal 238 6.2 265.8 970.3 1,242.2 TBI Nonfatal 9,834 166.6 480.0 3,200.6 3,847.3 Other head Nonfatal 11,645 40.8 130.6 1,207.6 1,379.0 Total 21,717 213.6 876.4 5,378.5 6,468.5 Savings 49,878 557 1,903 12,425 14,884 Abbreviation: TBI, traumatic brain injury Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 405 Socioeconomics ● ● ● Parents will spend less time and expense caring for injured children Lawyers will file fewer lawsuits seeking compensation for bicyclist injuries Some people will find helmets uncomfortable or inconvenient, which may cause them to ride their bicycles less often, possibly increasing obesity or preventing other bicyclerelated injuries How will insurance payments change? Health insurers, public and private, will save almost all of the medical payments, saving an estimated $20 per helmet Auto insurers also will process fewer claims Twenty-five percent of injured bicyclists were in motor vehicle crashes.31 Auto insurers compensate 36% of the work losses in highway crashes and 18% of the medical costs.32 That implies auto insurers will save an estimated $25 per child helmet and $30 per adult helmet How sensitive are the results? The benefit–cost ratios here are for low-cost helmets Bulk purchase program prices would be lower At an $11 price, the benefit–cost ratio for a child helmet would be 66 Conversely, families buying fancier $25 child bicycle helmets can expect a return of $29 for each dollar spent If adults buy $40 helmets, the return would be $14 for each dollar spent and if they buy $15 helmets, the return would be $38 Our estimate of the benefit–cost ratio assumes an average 5year life span for helmets If adult helmets had an 8-year life span instead, the benefit–cost ratio would rise from 31 to 55 If the average helmet was used for instead of years, the benefit–cost ratios would be 35 for a child helmet and 19 for an adult helmet We used midpoint estimates for helmet effectiveness If high-point estimates were used instead, the benefit–cost ratio would be 63 for child helmets and 34 for adult helmets If low-point estimates were used, the benefit–cost ratio would be 50 for child helmets and 29 for adult helmets How the savings compare with savings from other helmets? Benefit–cost ratios are available for two types of more costly helmets ATV helmets cost an average of $120, with an estimated benefit–cost ratio of 5.33 Motorcycle helmets typically cost at least $125 They have a benefit–cost ratio of 52 if worn voluntarily.34 When a law mandates their use, costs of discomfort, inconvenience, and lost personal freedom reduce the benefit–cost for new users to 32.8 Limitations (▶ Table 32.17) No single data source for calculating TBI costs exists Consequently, we were forced to combine information from myriad data sources, each with limitations Some sources were old, others were based on nonnationally representative samples, and all were subject to reporting and measurement error These limitations not only increase the lack of precision around the estimates, but also may result in additional bias Several factors make our cost estimates conservative First, they omit injury treatment by mental health professionals and alternative medicine providers Second, TBI follow-up care is hard to fully track A good life care plan might identify many unmet needs omitted from the costs Third, sequelae of minor TBI often are missed in our data sets Moreover, physician ratings of prognosis deal with typical outcomes, not the occasional bad-outcome case The helmet benefit–cost analysis deals with averages Benefits for individual riders will vary widely with exposure (miles or hours bicycled), skill, risk-taking behavior, and where the bicycle is ridden (e.g., along busy roads, on paved bicycle paths, on unpaved trails) Still, the benefit–cost ratios are so high that even occasional riders who are not daredevils are likely to benefit from helmet use 32.9 Conclusion Economic analysis provides a compact way to measure the burden that TBI imposes on individuals and society It also supports comparison of the return on competing investments in preventive measures TBI is a large problem costing U.S society more than $750 billion a year, with additional costs for combat-related injuries The comprehensive cost of TBI represented 15% of the total cost of injury in the United States in 2012 Moreover, TBI caused 1% of total U.S medical spending Leading causes of TBI in terms of costs were motor vehicle crashes, falls, and, for men, firearms As the bicycle helmet benefit–cost analysis illustrates, prevention can be much cheaper than the consequences of not preventing Preventive measures such as helmets specifically target TBI Other effective TBI prevention targets broader objectives such as reducing falls or road crashes or better protecting vehicle occupants in crashes More research on TBI consequences is needed, especially on less-than-catastrophic TBIs The disability associated with such injuries could result in high costs to society 32.10 Disclaimer Preparation of this chapter was funded in part by Department of Defense cooperative agreement W81XWH-16–2-0005 and by the Health Resources and Services Administration under cooperative agreement U49MC28422, which funds the Children’s Safety Network The views expressed in this work are exclusively those of the authors and not necessarily reflect the official policy or position of the Department of Defense, the Health Resources and Services Administration, or the U.S Government Table 32.17 Study limitations Factors making cost Treatment by mental health and alternative estimates conservative medicine providers may be omitted Hard to track TBI follow-up care Sequelae of minor TBI often are missed Abbreviation: TBI, traumatic brain injury 406 References [1] Hendrie D, Miller TR Economic evaluation of injury prevention and control programs In: McClure R, Stevenson M, McEvoy S, eds The Scientific Basis of Injury Prevention and Control Sydney, Australia: IP Communications; 2004:372–390 Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license Cost of Traumatic Brain Injuries in the U.S and the Return on Helmet Investments [2] Gold MR, Siegel JE, Russell LB, Weinstein MC, eds Cost-Effectiveness in Health and Medicine New York, NY: Oxford University Press; 1996 [3] U.S Supreme Court Jones and Laughlin Steel Corp v Pfeifer Washington, DC: 103 Supreme Court Reporter; 1983 [4] U.S Office of Management and Budget Guidelines and Discount Rates for Benefit-Cost Analysis of Federal Programs Washington, DC: Office of Management and Budget; 1994: Circular A-94 [5] Viscusi WK Discounting health effects for medical decisions In: Sloan FA, ed Valuing Health Care: Costs, Benefits, and Effectiveness of Pharmaceuticals and Medical Technology New York: Cambridge University Press; 1995 [6] Murray CJL, Lopez AD Global Comparative Assessments in the Health Sector: Disease Burden, Expenditures and Intervention Packages Geneva: World Health Organization; 1994 [7] Rice DP, Hodgson TA, Kopstein AN The economic costs of illness: a replication and update Health Care Financ Rev 1985; 7(1):61–80 [8] Moore R, Mao Y, Zhang J, Clarke K Economic Burden of Illness in Canada, 1993 Ottawa, Ontario, Canada: Canadian Public Health Association; 1997 [9] Lawrence BA, Miller TR Medical and Work Loss Cost Estimation Methods for the WISQARS Cost of Injury Module Calverton, MD: Pacific Institute for Research and Evaluation; 2014 [10] Finkelstein EA, Corso PC, Miller TR, Fiebelkorn IA, Zaloshnja E, Lawrence BA Incidence and Economic Burden of Injuries in the United States, 2000 New York, NY: Oxford University Press; 2006 [11] Rice DP, MacKenzie EJ, Jones AS, et al Cost of Injury in the United States: A Report to Congress San Francisco, CA: Institute for Health & Aging, University of California, and Injury Prevention Center, The Johns Hopkins University; 1989 [12] Lawrence BA, Miller TR, Jensen AF, Fisher DA, Zamula WW Estimating the costs of non-fatal consumer product injuries in the United States Inj Control Saf Promot 2000; 7(2):97–113 [13] Miller TR, Romano EO, Spicer RS The cost of childhood unintentional injuries and the value of prevention Future Child 2000; 10(1):137–163 [14] Zaloshnja E, Miller T, Romano E, Spicer R Crash costs by body part injured, fracture involvement, and threat-to-life severity United States, 2000 Accid Anal Prev 2004; 36(3):415–427 [15] Grosse SD, Krueger KV, Mvundura M Economic productivity by age and sex: 2007 estimates for the United States Med Care 2009; 47(7) Suppl 1:S94– S103 [16] Miller TR, Pindus NM, Douglass JB, Rossman SB Databook on Nonfatal Injury: Incidence, Costs, and Consequences Washington, DC: The Urban Institute Press; 1995 [17] Murray CJ, Barber RM, Foreman KJ, et al GBD 2013 DALYs and HALE Collaborators Global, regional, and national disability-adjusted life years (DALYs) for 306 diseases and injuries and healthy life expectancy (HALE) for 188 countries, 1990–2013: quantifying the epidemiological transition Lancet 2015; 386(10009):2145–2191 [18] National Academies of Sciences, Engineering, and Medicine Advancing the Power of Economic Evidence to Inform Investments in Children, Youth, and Families Washington, DC: The National Academies Press; 2016 [19] Miller TR The plausible range for the value of life: red herrings among the mackerels J Forensic Econ 1990; 3(3):17–39 [20] Viscusi WK, Aldy JE The value of a statistical life: a critical review of market estimates throughout the world J Risk Uncertain 2003; 27(1):5–76 [21] Barell V, Aharonson-Daniel L, Fingerhut LA, et al An introduction to the Barell body region by nature of injury diagnosis matrix Inj Prev 2002; 8(2):91–96 [22] Orman JA, Geyer D, Jones J, et al Epidemiology of moderate-to-severe penetrating versus closed traumatic brain injury in the Iraq and Afghanistan wars J Trauma Acute Care Surg 2012; 73(6) Suppl 5:S496–S502 [23] Taylor BC, Hagel EM, Carlson KF, et al Prevalence and costs of co-occurring traumatic brain injury with and without psychiatric disturbance and pain among Afghanistan and Iraq War Veteran V.A users Med Care 2012; 50 (4):342–346 [24] Miller TR, Levy DT Cost outcome analysis in injury prevention and control: a primer on methods Inj Prev 1997; 3(4):288–293 [25] Weinstein M From cost-effectiveness ratios to resource allocation: where to draw the line? In: Sloan FA, ed Valuing Health Care: Costs, Benefits, and Effectiveness of Pharmaceuticals and Other Medical Technologies Cambridge: Cambridge University Press; 1996:77–97 [26] Schroeder P, Wilbur M 2012 National survey of bicyclist and pedestrian attitudes and behavior, volume 2: Findings report DOT HS 811 841 B Washington, DC: National Highway Traffic Safety Administration; 2013 [27] Bambach MR, Mitchell RJ, Grzebieta RH, Olivier J The effectiveness of helmets in bicycle collisions with motor vehicles: a case-control study Accid Anal Prev 2013; 53:78–88 [28] Thompson DC, Rivara FP, Thompson RS Effectiveness of bicycle safety helmets in preventing head injuries A case-control study JAMA 1996; 276 (24):1968–1973 [29] Thompson DC, Nunn ME, Thompson RS, Rivara FP Effectiveness of bicycle safety helmets in preventing serious facial injury JAMA 1996; 276 (24):1974–1975 [30] Sacks JJ, Holmgreen P, Smith SM, Sosin DM Bicycle-associated head injuries and deaths in the United States from 1984 through 1988 How many are preventable? JAMA 1991; 266(21):3016–3018 [31] Miller TR, Zaloshnja E, Lawrence BA, Crandall J, Ivarsson J, Finkelstein AE Pedestrian and pedalcyclist injury costs in the United States by age and injury severity 48th Proceedings, Association for the Advancement of Automotive Medicine Barrington, IL: AAAM; 2004:265–284 [32] Miller TR, Viner JG, Rossman SB, et al The Costs of Highway Crashes Washington, DC: The Urban Institute; 1991 [33] Miller TR, Finkelstein AE, Zaloshjna E, Hendrie D The cost of child and adolescent injuries and the savings from prevention In: Liller K, ed Injury Prevention for Children and Adolescents: Research, Practice, and Advocacy 2nd ed Washington, DC: American Public Health Association; 2012:21–81 [34] Miller TR, Hendrie D Economic evaluation of public health laws and their enforcement In: Wagenaar A, Burris S, ed Public Health Law Research: Theory and Methods, San Francisco: Jossey-Bass; 2013:347–378 Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 407 Index Note: Page numbers set bold or italic indicate headings for figures, respectively A ABC (Awakening and Breathing Controlled trial) 296 ABCDE bundle (spontaneous awakening trial) 295 abusive head trauma (AHT) 113 acceleration/deceleration forces 34 access to health care and TBI prognosis 373 acute brain injury 68 Acute Concussion Evaluation (ACE) 152 acute inpatient rehabilitation programs 353 – criteria for admission 354, 354 – interdisciplinary programs 354 – therapy services and care team 354, 355 acute lung injury 378 acute respiratory distress syndrome (ARDS) 287 advance directives 391, 392 advanced trauma life support (ATLS) – ER management of head injury 163 – fluid resuscitation guidelines 101 – protocols and certification 99 aerobic metabolism 41 Africa, TBI incidence 18 age factors – aging and neurodegenerative disease 379 – in MVT-related TBI 21 – in TBI incidence 14 – in TBI prognosis 372 – vascular damage and shear forces 38 Agency for Healthcare Research and Quality Methods Guide 127 aggression, posttraumatic 362 agitation, posttraumatic 361 alcohol drinking, see substance abuse ambulation, neurorehabilitation for 357 American Association of Neurological Surgeons (AANS) 132 amnesia, posttraumatic 375 aneurysm, traumatic 189 angiography, see computed tomography angiography (CTA) – intracranial – MRI/MA 81 antibiotic resistance 337, 338 antibiotics – C difficile diarrhea caused by 343 – catheter-related bloodstream infections 339 – cerebritis/cerebral abscess 329 – device-related infections 335 – epidural empyema 331 – postneurosurgical meningitis 334, 335 – posttraumatic meningitis 333 – stewardship in ICU 344, 344 – subdural empyema 330 – ventilator-associated pneumonia (VAP) 256, 256, 291, 292 antihypertensive drugs 315 408 – choice of 315, 316 – neuroprotective effects 316, 316 – vasopressors 316, 316 apolipoprotein E (APOE) allele 373 apoptosis – cell necrosis vs 43, 44 – cytochrome c as biomarker 45 – genetic regulation of 44 – NMDA-induced 45 – TUNEL method for following 44 ARDS (acute respiratory distress syndrome) 287 arginine 301 arterial pressure 314 artificial nutrition and hydration (ANH) 308 Asia and Oceana, TBI incidence 18 aspiration risk factors 306 assault-related traumatic brain injury – incidence 14 – inflicted injuries 233 – nonaccidental trauma evaluation in children 167, 167 – prevention 22 assist control ventilation (ACV) 283 athletic injuries, see sports/recreation (SR) related TBI atlanto-occipital dislocation (AOD) – classifications 229, 229 – instability of 228 – treatment 229 atlas (C1) fractures, see C1 (atlas) fractures ATLS, see advanced trauma life support (ATLS) Australia and New Zealand, TBI incidence 18 automobile driving, see motor vehicle traffic (MVT)–related TBI autonomic dysfunction 314, 315 autoregulatory reserve 76 Awakening and Breathing Controlled (ABC) trial 296 Awakening and Breathing Coordination, Delirium Monitoring and Management, and Early Mobility (ABCDE) bundle 295 awareness 106 axis (C2) fractures, see C2 (axis) fractures axons – cytoskeletal damage 38 – shear forces effects on 37, 37 B Balance Error Scoring System (BESS) 111 barbiturates – adverse events 279 – for severe TBI 180 – pharmacology 278, 279 – TBI considerations 279 barotrauma 290 basilar skull fracture 237, 239 bcl-2 gene superfamily 44 behavioral and emotional dysfunction 361 – acute management 361, 362 – agitation 361 – depression 363 – hypoarousal 363 – postacute management 363 – TBI prognosis and 373 benefit-cost analysis 402 BEST TRIPs (RCT) 130 beta-blockers 378–379 bifrontal decompression 209 biomarkers 49 – blood-based 50 – body fluid assays 50 – categories 49 – clinical applications –– decisions to withhold or withdraw care 54 –– dementia risk, posttraumatic 55 –– discharge counseling 52 –– disruption of neural circuits 56 –– early detection of secondary brain injury 53 –– epilepsy risk, posttraumatic 56 –– in chronic phase after TBI 55 –– in Emergency Department 52 –– in ICU 53 –– in rehabilitation unit 55 –– point-of-care tests 51 –– prehospital use 51 – context of use 50 – cytochrome c and apoptosis 45 – definitions 49 – diagnostic 49 – future perspectives 56 – introduction 49 – pathophysiology 49 – TBI prognosis 376 – validated, absence for neurotrauma 49 biomechanics 34, 34, 38 bladder management, posttraumatic 360 blast injury 30, 113 blood biomarkers 49–50 blood pressure, see hypotension and hypoxia – cerebral autoregulation and 313, 313, 314, 314 – CPP management and 178, 313 – mean arterial blood pressure 109 – vasoactive agents 315, 315 blood products 269, 269, 270 – See also transfusion of blood products blood tissue oximetry 270 blood-brain barrier (BBB) 38, 50, 54 blunt cardiovascular injury (BCVI) 176 body fluids 49, 50 body mass index (BMI) 301 BOLD (blood oxygen level dependent) MRI 95 Bozza-Marrubini Coma Scale 31 bradycardia 275 brain death – criteria for 393 – declaration of death 394 – ethical challenges 393 brain edema, see cerebral edema brain injury imaging, see specific techniques and injury types – advanced techniques 95 – clinical practice guidelines 134, 134 – introduction 81 – loss of consciousness and 109 – neuroimaging guidelines and classifications 81 – primary injuries 82 – secondary injuries 91 brain oxygenation, see cerebral oxygenation brain tissue oxygenation monitoring (PbtO2) 74 – data 250, 256 – physiology 250 – technical considerations 250 – transfusions and 179 Brain Trauma Foundation (BTF) – prehospital care guidelines 99, 172 – severe TBI guidelines 132, 200 brainstem injuries and TBI prognosis 378 breathing trials, spontaneous 294 Brussels Coma Scale 31 C C1 (atlas) fractures – classification 229 – treatment 230 – types of 228 C2 (axis) fractures – classifications 229, 230 – treatment 230 – types of 228 calcium channels, voltage-gated 42 calorimetry, indirect (IC) 303, 303 Canadian Assessment of Tomography for Childhood Head Injury (CATCH) 114 Canadian CT Head Rule 82, 82 capillary blood flow 40 carbon dioxide (CO2) 77 cardiac uncoupling 378 cardiovascular complications of TBI – antihypertensive agents 315, 315– 316 – arterial pressure 314 – autonomic dysfunction 314, 315 – cerebral autoregulation and blood pressure 313, 313 – hypotension 312, 312 – initial assessment 313, 314 – introduction 312 – pathophysiology 312, 312, 314 caregivers, TBI impact on 363 Caribbean, TBI incidence in 18 carotid-cavernous fistulas (CCFs) – management of 226 – pathophysiology 90, 91 – vascular injury and formation of 225 caspases 45 catechol-O-methyltransferase (COMT) 373 catecholamines and TBI prognosis 377 catheter-related bloodstream infections 338 – clinical features 339 – diagnosis 339 – epidemiology 338 – management 339, 340–342 – microbiology 339 – neurocritical care and 257 Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license Index – pathogenesis and risk factors 338 ced-3 genes 45 cell necrosis, apoptosis vs 43, 44 cellular fibronectin (cFn) 54 CENTER-TBI study (European Union) 31 Centers for Disease Control and Prevention (CDC) 19, 29 cerebral abscess, see cerebritis and cerebral abscess cerebral autoregulation – blood pressure and 313, 313, 314, 314 – cerebral blood flow and 76, 77 – CO2 cerebrovascular reactivity 77 – dynamic rate of autoregulation (RoR) 77 – phase shift, blood pressure waves 77 – static testing 77 – transient hyperemic response test 77 cerebral blood flow – cerebral autoregulation and 76, 313, 313 – hyperventilation effects on 286 – multimodality monitoring 74 – reduced, and tissue damage mechanisms 39 cerebral edema – blood-brain barrier and 54 – cytotoxic 39, 91 – imaging 91 – medical treatment – osmotic therapy 249 – pathophysiology in TBI 38 – vasogenic 38, 91 cerebral herniation syndromes 91, 92 – central or transtentorial herniation 91–92, 93, 255 – falcine or cingulate herniation 255 – neurocritical care and 255, 255 – subfalcine herniation 91, 92 – tonsillar herniation 92, 93, 255 – uncal or tentorial herniation 255 cerebral intraparenchymal pressure monitoring 69 cerebral ischemia, delayed (DCI) 78 cerebral oxygenation – monitoring 60, 74 – near-infrared spectroscopy 64 – reduced, secondary brain damage and 40, 41, 74 cerebral perfusion pressure (CPP) 73, 73 – autoregulatory curve 73, 73 – blood pressure and management of 178, 313 – calculation of 60 – clinical practice guidelines 135, 139 – ICP treatment and 179, 247 – mean arterial blood pressure and 109 – optimal 60, 73 – pathophysiology 285, 286 – positive end-expiratory pressure and 285 – resuscitation goals – TBI prognosis and 375 cerebral resection 209 cerebral salt wasting 254, 254 cerebral venous pressure monitoring 69 cerebral venous sinus injuries 226 cerebritis and cerebral abscess 328 – clinical features 329 – definitions 328 – diagnosis 329 – epidemiology 328 – management 329 – risk factors 328 cerebrospinal fluid (CSF) – bacterial meningitis findings 333 – biomarkers in 49 – leakage in penetrating brain injury 208, 212 – measurement techniques – shunt infections 335 cerebrovascular injuries, traumatic 189 cerebrovascular reactivity, CO2 77 cervical spine injury – clinical practice guidelines 134 – prehospital care 101, 101 child abuse – incidence 167, 238 – inflicted injuries 233 – nonaccidental trauma 167, 238, 239 children, see pediatric brain injury – clinical practice guidelines and TBI treatment outcomes 140 – fall-related TBI, risk factors and prevention 21 – loss of consciousness, see pediatric loss of consciousness – moderate TBI in 167 – skull fractures, see skull fractures, pediatric Children’s Head Injury Algorithm for the Prediction of Important Clinical Events (CHALICE) 114 China, TBI incidence in 18 chronic traumatic encephalopathy (CTE) 15, 155 – biomarkers 55 – pathology 155 – preventive measures 156 – stages of 89 classification of traumatic brain injury 29 – challenges 29 – classification methods, generally 29 – clinical examination and symptoms 31 – common data elements (CDEs) 30 – defining condition 29 – future of 31 – injury location 30 – introduction 29 – mechanism of injury 30 – prognosis and 31 – VA/DoD classification 354, 356 clinical decision rules (CDRs) 114 clinical ethics 387 clinical examination and severity of symptoms 31, 31 clinical practice guidelines (CPG) 124 – advantages and disadvantages 125 – balance with precision medicine 143 – bundles of care 141 – cervical trauma 134 – concussion 133 – conflicting guidelines 125 – definition and function of 124 – development of 126 –– development group formation 126 –– factors in 126 –– initial tasks 126 –– judging guideline quality 128, 128 –– literature review 127 –– recommendation development 127 – economic issues 125 – evidence-based medicine in 128 – guideline adherence and compliance 135 –– between-center variation 136 –– deviation from CPG and treatment outcome 141 –– factors affecting adherence 135 –– importance of full compliance 140 –– in severe TBI 135 –– quality of care and 142, 143 –– ways to improve 136 – intracranial hypertension 248 – introduction 124 – neurocritical care 142 – neurotrauma 131, 132, 136 – observational studies vs 131 – organized trauma care 142 – origin of 124 – overview, national and international 213 – real-world use of 143 – traumatic brain injury –– combat-related 212 –– imaging in 134 –– limitations of 131 –– mild TBI 133, 213 –– penetrating injuries 210, 211 –– prehospital TBI emergency care 214 –– severe TBI 132, 133, 177 –– severe TBI, pediatric 212 –– surgical management 199 ––– See also neurosurgery, specific topics and lesions – treatment outcomes, influence on 136, 137 –– ICP and CPP adherence 139 –– mature economies vs LMIC countries 140 –– mild TBI 140 –– pediatric TBI 140 –– pre- and post-CPG implementation studies 139 clinical trials, see randomized clinical trials (RTC) – biomarkers in patient selection for 53–55 – prehospital neuroprotectants 102 – TBI classification by prognosis and eligibility for 31 – TBI prognosis and insight from 380 Clostridium difficile diarrhea 342 – clinical features 343 – diagnosis 343 – epidemiology and risk factors 342 – management 343 – pathogenesis 343 coagulopathy 110 cognitive impairments 364, 365 colloids – for fluid resuscitation 268, 268 – for subarachnoid hemorrhage 268 – normal saline vs albumin, for fluid replacement 268 coma 107, 375 – See also Glasgow Coma Scale (GCS) combat support hospitals (CSH) 189 common data elements (CDEs) 30 communication, and handover of patients 117 comorbidities 16, 376 compensatory reserve (RAP index) – autoregulation vs 77 – definition 76 – pressure-volume curve and 71, 72 compliance (ventilation) 289, 289 compressive neuropathy 218 computed tomography (CT) – as primary imaging modality for head trauma 81 – biomarkers identifying patients for cranial scan 52 – clinical practice guidelines, TBI 134, 134 – contusions and intraparenchymal hemorrhage 86, 87–88 – epidural hematoma 83, 83, 84 – findings and TBI prognosis 377 – head injuries in children 114 – history of – loss of consciousness and 109 – moderate TBI 163 – penetrating injuries 89, 90 – severe traumatic brain injury 176 – subarachnoid hemorrhage (SAH) 86, 86 – subdural hematoma 84, 84–85 – TBI classification 30 – vascular injuries 90, 90 computed tomography angiography (CTA) – loss of consciousness and 109 – severe TBI 176 – uses for 81 concomitant injuries 218 concussion 110 – See also chronic traumatic encephalopathy (CTE), mild traumatic brain injury (mTBI), postconcussive syndrome – biomechanics 151 – clinical practice guidelines 133 – comorbid conditions 154 – definitions 110, 151 – epidemiology 151 – initial assessment 111, 152 –– neuroimaging role 152 –– secondary survey 152 –– sideline assessment tools 111, 152 – long-term management 153 – monitoring with serial assessment 153 – multimodal approach 153 – neuropsychological tests 112, 153, 153 – pathophysiology 151 – return to activity 154, 154 – second impact syndrome 154 – seizure activity 154 – subconcussion 155 – symptoms 112, 152, 153 – technologies for detecting in field 112 Congress of Neurological Surgeons (CNS) 132 consciousness 106, 357 – See also loss of consciousness (LOC) context of use 50, 54 contusions, intraparenchymal hemorrhage and 86 corticosteroids Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 409 Index – as neuroprotectants 102 – contraindications in severe TBI 181 cost-effectiveness analysis 401 cost-utility analysis 402 costs of traumatic brain injury 395 – bicycle helmets and head injury, benefit-cost analysis 403, 406 –– costs for adult cyclists 406 –– costs for cyclists under age 15 403, 405 –– helmets preventing deaths and injuries 403, 405 –– limitation of analysis 406 – comprehensive costs 398 –– by gender and age 399, 400 –– by gender and cause 398, 400 –– by level of treatment 398 –– by nature of treatment 398, 399 –– by severity of injury 398, 399 –– combat-related TBIs 399 –– military personnel 399 – cost categories 396, 396 – cost concepts 395, 395 – economic evaluation analyses 401, 402 –– benefit-cost analysis 402 –– cost-effectiveness 401 –– cost-utility analysis 402 –– net benefit analysis 402 – framework for economic evaluation with injury cost data 399, 401 – introduction 395 – medical cost estimates 396, 397 – methods for determining 396, 399 – quality-of-life costs 398, 398 – work loss costs 397, 397 CPG, see clinical practice guidelines (CPG) cranial impact forces vectors 34 cranial vault fractures, see skull fractures craniectomy, decompressive (DCC) 130, 208, 242 cranioplasty 212 critical care, neurological, see neurocritical care critical closing pressure 69, 70 critical illness neuromyopathy (CINM) 253 CTE, see chronic traumatic encephalopathy (CTE) Cushing triad cyclic adenosine monophosphate (cyclic AMP) 42 cysteine proteases 45 cystitis 340–341 cytochrome c 45, 45 cytokines 43 cytoskeleton 38 cytotoxic edema 39, 91 D data sources, TBI epidemiology decision-making, informed 52, 54 decompression, surgical – acute epidural hematoma 201 – bifrontal 209 – craniectomy 130, 208, 242 – frontotemporoparietal hemicraniectomy 209 – posterior fossa 210 decubitus ulcer infection 343 410 deep vein thrombosis (DVT), see venous thromboembolism (VTE) – inferior vena cava (IVC) filters, prophylactic 325 – prevention of 165 – prophylaxis and treatment 257, 359 – prophylaxis in penetrating injuries 189 – surveillance ultrasonography guidelines 326 delayed cerebral ischemia (DCI) 78 delayed traumatic intracranial hemorrhage (DTICH) 205 dementia, posttraumatic 55, 379 depression 363, 373 device-related infections 335 – clinical features 335 – diagnosis 335 – epidemiology 335 – management 335 – pathophysiology 335 – risk factors 335 dexmedetomidine – adverse reactions 275 – pharmacology 275, 275 – TBI considerations 275 diabetes insipidus 254 diarrhea, C difficile, see Clostridium difficile diarrhea diffuse axonal injury (DAI) – as most severe TBI 34 – as shearing injury 88 – coma and severity of 38 – imaging 88, 89 – pathophysiology 37, 37 – pediatric 235, 236 – staging of 88, 89 diffusion weighted imaging (DWI) 95, 96 disconnection theory, conventional 319 disorders of consciousness 357 distracted driving 21 do-not-resuscitate (DNR) orders 391, 392 dopamine 315 drug abuse, see substance abuse drug-related fever 344 DTICH (delayed traumatic intracranial hemorrhage) 205 dual venous sinus thrombosis 94, 94 dural sinuses, pressure monitoring 69 DVT, see deep vein thrombosis (DVT) dynamic rate of autoregulation (RoR) 77 dysautonomia 254 dysphagia 361 E education and TBI prognosis 372 electroencephalography (EEG), continuous 65, 77 electrolyte solutions, balanced 269 electrolytes and fluid balance 178, 254 electrophysiology 77 Emergency Department (ED) 52 Emergency Neurological Life Support (ENSL) 107, 108 emotional dysfunction, see behavioral and emotional dysfunction employment status and TBI prognosis 373 encephalomalacia 92, 95 end of life nutrition support 308, 309 enteral nutrition (EN) 257, 305 – aspiration risk factors 306 – complications 306 – drug-nutrient interactions 304, 308 – early initiation of 165, 165, 305 – guidelines 307 epidemiology – behavioral and environmental risk factors –– alcohol and drugs 15 –– comorbidities and prescription drugs 16 –– protective equipment reducing 16 – data sources – definitions 7, 23 –– clinical –– ICD-9-CM morbidity definition –– ICD-9-CM to ICD-10-CM transition challenges –– ICD-10-based TBI-related mortality definition –– ICD-10-CM-based TBI-related morbidity definition –– ICD-based 7, 7, –– TBI severity – future directions 23 – hospitalizations, TBI-related 11 –– by age group 12, 12 –– by external cause 12 –– by sex 11, 11 – incidence 170 –– measurement of –– work-related TBI 20 –– worldwide 18, 170, 199 – incidence, U.S 10, 107 –– by age group 10, 10, 11, 13 –– by external cause 10, 14 –– by severity of injury 14 –– by sex 10, 10 –– emergency department visits, TBIrelated 10, 10 –– in institutionalized persons 17 –– in military service members and veterans 16, 17 –– in rural areas 16 –– in special populations 16 – long-term consequences, measurement of – medical and socioeconomic consequences 19, 20 – mortality, TBI-related 12 –– by age group (U.S.) 12, 13 –– by external cause (U.S.) 12 –– by sex (U.S.) 12, 13 –– worldwide 18 – prevalence, estimated 17, 19 – prevention, data-based 19 –– alcohol and substance abuse 22 –– evidence-based interventions 23 –– fall-related TBI 20 –– methods for preventing 22 –– MVT-related TBI 21 –– public health role in 19 –– sports/recreation-related TBI 21 –– violence-related TBI 22 –– work-related TBI 20 – recurrent TBI 15 – risk factors 14, 19 – summary and conclusions 22 – surveillance 9, 23 epidural empyema 331 – clinical features 331 – diagnosis 331 – epidemiology 331 – introduction 331 – management 331 – risk factors 331 epidural hematoma – acute –– clinical pattern 201, 202 –– surgical decompression 201 –– surgical guidelines 201, 202 – imaging 83, 83 – pediatric 234, 235 – subdural hematoma vs 84 epilepsy, posttraumatic – identifying patients at risk for 56 – risk factors in children 243 – risk factors in moderate TBI 167, 167 esmolol 315 estrogens 38 ethics, medical 387 – clinical ethics, basics of 387 –– conflicting values of patient and physician 387, 387 –– futility of treatment 389 –– informed consent 389, 389 –– principles and guidelines 388, 388 –– values loss and preservation 388, 388 – end of life nutrition support 308, 309 – introduction 387 – neurotrauma issues –– advance directives and DNR orders 391, 392 –– brain death 393, 393 –– curing vs palliative care 390 –– justice of limited resources 390, 390 –– pediatric patients 393 –– pregnant patients 392 –– surrogate decision makers 391, 391 – withholding or withdrawing care 54, 389 Europe, TBI incidence in 18 evidence-based medicine 128, 131 excitatory inhibitory ratio (EIH) 319 external ventricular drainage (EVD) – drain infections 335 – history of 3, 60 – indications for placement 68 extra-axial manifestations, in brain imaging 82 extradermal hematoma, see epidural hematoma extubation, see weaning from mechanical ventilation F facial anatomy 222 facial fractures 222 – See also orbital injuries – classifications 223 – examination 223 – orbitofacial injuries 192, 194 – treatment 224, 224 – types of 222 –– See also specific fracture type falls-related TBI 14, 20 family adjustment to TBI 364, 366 fentanyl – adverse events 277 Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license Index – for severe TBI 180 – pharmacology 277 – TBI considerations 277 fever – as secondary complication of TBI 328 – drug-related 344 – management in moderate TBI 165 – noninfectious causes 336, 337, 343 – nosocomial infections 336, 337 FIO2 (fraction of inspired oxygen) 284 firearms-related TBI, see gunshot wounds – prevention of 22 – suicide- and homicide-related 14 fluid resuscitation 262 – blood products transfusion effects on 269 – fluid and intravascular volume management 178 – goals 262, 262 – introduction 262, 270 – prehospital care 101 – treatments 263 –– balanced electrolyte solutions 269 –– colloids 268, 268 –– hydroxyethyl starch 268, 269 –– hypertonic saline 263, 263 –– lactated Ringer's vs normal saline 101, 265, 266 –– mannitol 266, 267, 289 focal brain injury 35, 35 found-down patients 117 fraction of inspired oxygen concentration (FIO2) 284 free radicals 42 frontobasilar fractures 222, 223, 223 Full Outline of UnResponsiveness (FOUR) score scale 31 Functional Independence Measure (FIM) 172 functional MRI (fMRI) 95 futility of treatment 389 G gender – costs of TBI and 398–399, 400 – sex hormones and TBI vulnerability 38 – TBI incidence 15 – TBI prognosis and 372 genetics 44, 373 Glasgow Coma Scale (GCS) 4, 29 – components 100, 100, 170 – loss of consciousness and 108, 109 – mild head injury 81 – moderate TBI 162 – readiness to wean from ventilation and 293, 295 – severe TBI 170 – TBI classification 31, 31, 170, 171 – TBI prognosis and 374 Glasgow Outcome Scale (GOS) – as standardized outcome tool for TBI recovery 171, 171 – extended (GOS-E) 172, 172 glial fibrillary acidic protein (GFAP) 50–52, 54 glucose metabolism, brain injury and 300 glutamate, intracellular 42 glutamine 300 Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) scale 127 Grady Coma Scale 31 growing skull fracture (leptomeningeal cyst) 237, 238 guidelines, see clinical practice guidelines (CPG) gunshot wounds, see firearms-related TBI – pathophysiology 36 – TBI classification 30 H Haber-Weiss reaction 43 hangman's fracture 228, 230 head injury, see brain injury imaging, skull fractures – bicycle helmets preventing, benefitcost analysis 403, 404, 406 – infarction vs selective neuronal loss 40 – prevention in children 243 – primary vs secondary lesions 82 headache 329 health costs, see costs of traumatic brain injury heat shock proteins (Hsp) 43 helmets – bicycle helmets and head injury, benefit-cost analysis 403, 404, 406 – for TBI prevention – reducing TBI risk 16 hematoma 235, 235 – See also epidural hematoma, subdural hematoma (SDH) hemicraniectomy, decompressive frontotemporoparietal 209 hemorrhage patterns, TBI 199 heterogeneity of traumatic brain injury 29 heterotopic ossification 360 high intracranial pressure (HIPC), see intracranial pressure (ICP) regulation HIV infections 329 homicide and traumatic brain injury 14 hospital-acquired infections (HAI) 337 hospital-related complications, and TBI prognosis 378 – acute-care length of stay 379 – discharge site and status 379 – functional status and 379 – length of stay in rehabilitation 379 – length of time to rehabilitation admission 379 hydroxyethyl starch 268, 269 hyperglycemia – in brain injury 300 – management 165 – TBI prognosis and 377 hypernatremia, iatrogenic 254 hyperosmolar euvolemic therapies 240 hyperpyrexia 190 hypertension – antihypertensive drugs 315, 315– 316 – intracranial, see intracranial pressure (ICP) – loss of consciousness and 107 hyperthermia, posttraumatic 254 hypertonic saline (HTS) – fluid resuscitation with 263, 263 – for intracranial hemorrhage, animal models 264 – for intracranial hypertension 180, 249, 265, 286 – for pediatric intracranial hypertension 240 – lactated Ringer's vs 265–266 – mannitol vs 250, 265–266, 266 – mechanisms of action 264, 264 – prehospital TBI treatment 173 hyperventilation – cerebral perfusion pressure and 286 – prehospital care 102, 173 – severe TBI management and 177 hypoarousal 363 hypoglycemia 173 hyponatremia 377 hypopituitarism – management 165, 166 – risk factors 166 hypotension and hypoxia – clinical management 313 – management in ICU 178, 246 – prehospital care 100, 100, 172 – TBI prognosis and 376–377 hypothermia – acute subdural hematoma surgical outcome and 204 – as prehospital neuroprotectant 102 – induced, for penetrating TBI 190 – limited role in neurocritical care 250 – prophylactic, for severe TBI 181 – targeted temperature management 349 – TBI prognosis and 376 hypotonic solutions, intravenous 174, 249 hypovolemic shock 262 hypoxemic respiratory failure 292 hypoxia, see hypotension and hypoxia hypoxic-ischemic injury, global 94, 94 I I:E (Inspiration:expiration) ratio 284, 285 ICP, see intracranial pressure (ICP) ICU-acquired weakness 253 imaging, see brain injury imaging, specific techniques immunonutrition 300 impulsive loading 34 indirect calorimetry (IC) 303, 303 infection and TBI – C difficile diarrhea 342 – catheter-related bloodstream infections 338 – cerebritis and cerebral abscess 328 – decubitus ulcer infection 343 – device-related infections 335 – epidural empyema 331 – fever, noninfectious causes of 343 – introduction 328 – meningitis 333 – nosocomial infections and fever 336, 336 – osteomyelitis 332 – penetrating brain injuries 212 – pneumonia 337 – subdural empyema 329 – urinary tract infections 340 inferior vena cava (IVC) filters 325 inflammatory response 41, 43 informed consent – as ongoing process 389 – conditions for 389 – purpose of 389 informed decision-making 52, 54 infrared pupillometry 64 injury location – focal vs diffuse 30, 31 – TBI classification 30 injury severity and TBI prognosis 374 Innsbruck Coma Scale 31 inspiration:expiration (I:E) ratio 284, 285 inspiratory flow rate 284 institutionalized persons, TBI incidence in 17 intensive care medicine – See also neurocritical care intensive care units (ICUs) – aggressive surgical / medical care for head injuries – antibiotic stewardship in 344, 344 – early detection of secondary brain injury 53 – expansion of – ICU-acquired weakness 253 – informed decisions to withhold or withdraw care 54 – neurorehabilitation team and services 352 – selection of patients for clinical trials 54 – severe TBI management 176 – TBI biomarker applications 53 interleukin- beta (IL-1?) 43 intermittent positive pressure ventilation (IPPV) internal carotid artery (ICA) 226 International Initiative for Traumatic Brain Injury (InTBIR) 31 International Mission for Prognosis and Analysis of Clinical Trials in TBI (IMPACT) 31 intracerebral hematoma, pediatric 235, 235 intracerebral hemorrhage (ICH) 115, 204 intracranial angiography intracranial lesions, diagnosis of intracranial pressure (ICP) – BEST TRIPs randomized clinical trial 130 – clinical practice guidelines 135, 139 – components of 70 – elevated, prehospital care 101 – hyperosmolar euvolemic therapies 179, 240 – hypertension, intracranial –– CCP-directed therapies 247 –– ICP-directed therapies 247 –– management guidelines 248 –– neurological deficits – Lundberg's waves 70, 71 – management –– brain edema treatment –– external ventricular drain 60 –– improvements in –– in children 239, 239, 240 –– in severe TBI 179 –– loss of consciousness and 109 – monitor-related infections 335 – monitoring in moderate TBI 164 Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 411 Index – monitors, noninvasive 61 –– infrared pupillometry 64 –– optic nerve fundoscopy 63 –– optic nerve sheath diameter ultrasonography 63, 64 –– transcranial color-coded duplex sonography (TCCS) 61 –– transcranial Doppler ultrasonography 61 –– tympanic membrane displacement 63 – multimodality monitoring 69 – narcotics and sedatives for 180 – prehospital care 101 – TBI prognosis and 375 – waveforms 70, 71 intraparenchymal hemorrhage 86, 205 intraparenchymal lesions, traumatic – clinicoradiographic metrics and prognostication 205 – subtypes and mechanisms of 204, 205–206 – surgical management guidelines 204, 206 intravenous device-related infections, see catheter-related bloodstream infections intrinsic positive end-expiratory pressure (PEEPi) 289 intubation – indications for –– airway protection and loss of patency 281 –– central vs peripheral respiratory failure 282 –– centralized 281 –– gas exchange abnormalities 282 –– respiratory pump failure 282 – prehospital 100 ischemia and infarction, cerebral – delayed, continuous EEG monitoring for 78 – dual venous sinus thrombosis 94, 94 – hypoxic-ischemic injury, global 94, 94 – imaging 92 – secondary to TBI 39 – vasospasm 91, 93 ischemic stroke 115, 226 IVC (inferior vena cava) filters 325 J Jefferson fracture 228 Jouvet Coma Scale 31 jugular bulb oximetry 76 K ketamine – adverse events 277 – pharmacology 277, 278 – TBI considerations 278 L laboratory testing 107 lactated Ringer's solution – hypertonic saline vs 265–266 – normal saline vs 101, 265, 266 laser Doppler flowmetry (LDF) 76 412 Latin America and Caribbean, TBI incidence in 18 leptomeningeal cyst (growing skull fracture) 237, 238 levetiracetam 181 Lindegaard ratio 61 lipid metabolism 300 loss of consciousness (LOC) 106 – as event vs diagnosis 106 – blast injury 113 – characteristics 107 – communication and handover of patients 117 – concussion 110 –– See also mild traumatic brain injury –– definitions 110 –– detecting in field 112 –– initial assessment 111 –– symptoms following 112 – definitions of consciousness 106 – differential diagnosis 107 – disorders of consciousness 357 – duration of coma and TBI prognosis 375 – Emergency Neurological Life Support protocol 107, 108 – found-down patient 117 – initial assessment –– blood pressure, autoregulation, and cerebral perfusion pressure 109 –– coagulopathy 110 –– focal neurological findings 108 –– Glasgow Coma Scale 108, 109 –– imaging and 109 –– intracranial pressure monitoring and control 109 –– laboratory investigations 110 –– limitations of 110 –– miscellaneous tests 110 –– physical examination 108 –– resuscitation, stabilization, and laboratory testing 107 – introduction 106 – nontraumatic 107 – patients who talk and die 117 – pediatric 113 –– See also pediatric loss of consciousness – stroke and 115 – syncope and 115 –– See also syncope – syncope vs seizure 117 – traumatic brain injury and 107 – types of 106 low- and middle-income countries (LMIC) 140 lumbar drainage, postoperative 335 lumbar puncture – for cerebritis/cerebral abscess 329 – ICP measurements and – loss of consciousness and 109 Lundberg's waves 70, 71 lung-protective ventilation 287, 290 M Maddocks Questions 111 magnetic resonance imaging (MRI) – brain injury evaluation 81 – contusions and intraparenchymal hemorrhage 87, 88–89 – diffuse axonal injury (DAI) 89, 89 – epidural empyema 331 – epidural hematoma 83 – findings and TBI prognosis 378 – FLAIR MRI vs CT for subarachnoid hemorrhage 86 – for cerebritis and cerebral abscess 329 – subdural empyema 330 – subdural hematoma 85 magnetic resonance spectroscopy (MRS) 95 malnutrition 301, 301 mannitol – for brain edema 3, 249 – for fluid resuscitation 249, 267 – for ICP/CPP management 173, 179 – hypertonic saline vs 250, 265–266, 266 – pediatric use 240 Marshall CT classification 30, 82, 82, 170, 171 mastoiditis 332 matrix metalloproteinase-9 (MMP9) 54 mean arterial blood pressure (MAP) 109 mean index (Mx) 71 mechanical ventilation, see weaning from mechanical ventilation – basic modes 282, 283 –– assist control 283 –– pressure support 283 –– setting ventilation parameters 284 –– synchronized intermittent mandatory ventilation 283 – complications 289–290 – indications for intubation 281, 281 – introduction 281 – neurological effects and conditions –– acute respiratory distress syndrome 287 –– cerebral perfusion pressure 285, 286 –– neurogenic pulmonary edema 287 – noninvasive positive pressure ventilation 282 – patient monitoring 288 –– compliance 289, 289 –– intrinsic positive end-expiratory pressure (PEEPi) 289 –– peak airway pressure 71, 288, 288 –– plateau pressure 288 – prolonged, tracheostomy in 296 – setting up ventilator 282 mechanism of injury, TBI classification by 30 medical assessment, pediatric l 114 medical costs of TBI 396, 397 medical evacuation of patients, penetrating TBI 190 medications – antihypertensives 315, 315 – medication classes to avoid in TBI 353 – vasoactive agents 315, 315 meningitis 333 – device-related 335 – postneurosurgical 334 –– clinical features 334 –– diagnosis 334 –– epidemiology 334 –– management 335 –– risk factors 334 – posttraumatic 333 –– clinical features 333 –– diagnosis 333–334 –– epidemiology 333 –– management 333, 334 –– risk factors 333 mental disorders, see behavioral and emotional dysfunction metabolism, disruption following TBI 41 methicillin-resistant Staphylococcus aureus (MRSA) 338, 338 methicillin-susceptible Staphylococcus aureus (MSSA) 338 microdialysis, cerebral blood flow monitoring 75, 75 microvasculature, shear force effects on 35 midazolam – adverse reactions 274 – pharmacology 274 – propofol vs 274 – TBI considerations 275 mild traumatic brain injury (mTBI) 151 – See also concussion – biomarkers 53 – clinical practice guidelines 213 – comorbid conditions 154 – CPG influence on treatment outcomes 140 – definitions 8, 110, 111 – epidemiology 151 – imaging guidelines 81, 134, 134 – in children 233 – loss of consciousness and 107 – patient selection for clinical trials 53 – patients who talk and die 117 – post-acute management 354 – subconcussion 155 Military Acute Concussion Evaluation (MACE) 152 military medicine – brain trauma and – TBI incidence in service members and veterans 16, 17 missile injuries, pathophysiology 36 Model Trauma Care System Plan (MTCSP) 142 moderate traumatic brain injury 162 – clinical management 163 –– ATLS protocol 163 –– clinical and radiologic findings 163, 163 –– deep vein thrombosis, prevention of 165 –– fever management 165 –– ICP monitoring 164 –– in-hospital care 163, 164 –– initial evaluation 163 –– neurological status evaluation 163 –– nutritional support 164, 165 –– posthospital 165 –– prehospital management principles 163 –– principles of 164 – definition – epidemiology 162 – in pediatric population 167 –– long-term outcome 168, 168 –– nonaccidental trauma evaluation 167, 167 –– posttraumatic seizures 167, 168 – loss of consciousness and 107 – outcome and prognosis 166 Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license Index –– long-term sequelae 167, 167 –– poor recovery risk factors 166, 167 –– posttraumatic epilepsy risk 167, 167 – pathophysiology 162 – population at risk 162, 162 – postacute management 356 – presentation 162 monitoring, see monitoring, noninvasive, multimodality monitoring (MMM) morphine, for severe TBI 180 Moscow Coma Scale 31 motor vehicle traffic (MVT)–related TBI – age factors in 21 – increase following World War II – morbidity and mortality 14 – prevention 21 MRI/MA angiography 81 multidrug-resistant pathogens, risk factors in ventilator- and hospital-acquired pneumonia 337, 338 multimodality monitoring, severe head injury 270 multimodality monitoring (MMM) 68 – brain monitoring modalities 69, 69 – brain pressures 69 –– cerebral perfusion pressure 73, 73 –– intracranial pressure (ICP) 69 –– optimal cerebral perfusion pressure 73, 74 –– secondary indices of cerebral blood flow and ICP 70 – cerebral blood flow and autoregulation 74 – electrophysiology 77 – guidelines and indications for 68 – indications for extraventricular drain placement 68 – introduction 68 – purposes in neurocritical care 68 multitrauma and TBI prognosis 374 N narcotics and sedatives, for ICP management 180 naso-orbital-ethmoidal (NOE) fractures 222 – classification 223, 223 – treatment 224, 225 near-infrared spectroscopy (NIRS) 64 – cerebral blood flow monitoring 76 net benefit analysis 402 neuroanesthesia, history of neurocritical care 142, 246 – See also intensive care units (ICU) – catheter-related infections 257 – cerebral edema and osmotic therapy 249, 250, 250 – hypothermia in 250 – hypoxia and hypotension management 178, 246 – initial patient evaluation 246 – intracranial hypertension management 247 –– CCP–directed therapy 247 –– guidelines for 248 –– ICP–directed therapy 247 – introduction 246 – mechanical ventilation and 281, 285 – neurological complications in TBI 252 –– cerebral salt wasting (CSW) 254, 254 –– diabetes insipidus 254 –– dysautonomia 254 –– electrolyte abnormalities 254 –– herniation syndromes 255, 255 –– hypernatremia, iatrogenic 254 –– ICU-acquired weakness 253 –– pituitary dysfunction and electrolyte abnormalities 253 –– seizures 252 –– syndrome of inappropriate antidiuretic hormone (SAIDH) 253, 254 – neuromonitoring 176 Neurocritical Care Society neurodegenerative disease and aging 379 neuroendocrine dysfunction 361 neurofilaments (NF) – NF-L (TBI biomarker) 53 – pathophysiology 38, 52 neurogenic pulmonary edema (NPE) 287 neurogenic stress cardiomyopathy 313, 314 neurological damage, ischemic, secondary to TBI 39, 92 neurological examination, initial trauma management 174 neurological resuscitation, prehospital care 101 neurological step-down units 353, 353 neuromonitoring, noninvasive 60 – continuous EEG 65 – introduction 60 – limitations of invasive monitoring 60 – near-infrared spectroscopy (NIRS) 64 – noninvasive ICP monitors 61 – visual-evoked potentials 65 neuromyopathy, critical illness (CINM) 253 neuron-specific enolase (NSE) 52, 54 neuroprotectants, prehospital, clinical trials 102 neuroprotective agents, for severe TBI 180 neuropsychological tests, concussion and 153, 153 neurorehabilitation 352 – behavioral and emotional dysfunction 361 – cognitive impairments 364, 365 – family adjustment to TBI 364, 366 – functional implications of TBI 357 – introduction 352 – levels of treatment 352, 353 – medical complications of TBI 358 –– bladder management 360 –– DVT prophylaxis and treatment 359 –– heterotopic ossification 360 –– neuroendocrine dysfunction 361 –– nutrition and 361 –– pain management 358 –– seizures, prophylaxis and treatment 360 –– spasticity 359 –– swallowing 361 – mental health professionals in 364 – motor disturbances and recovery 357 – postacute management of TBI 354 – sensory deficits 358 – severity of TBI and 354, 356 – TBI biomarkers unavailable for 55 neurorehabilitation facilities and services – acute inpatient rehabilitation 353 – intensive care units 352 – neurological step-down units 353 – postacute residential brain injury rehabilitation program 354 – subacute rehabilitation units 354 neurostimulants 255 neurosurgery – as separate specialty – blunt TBI injuries, guidelines –– cranial vault fractures 207, 208 –– epidural hematoma, acute 201 –– posterior fossa lesions 206, 207 –– subdural hematoma, acute 202, 204 –– traumatic intraparenchymal lesions 204, 206 – epidural empyema 331 – evolution since World War I 185, 185 – for cerebritis/cerebral abscess 329 – guidelines for TBI management 199 –– anesthesia considerations 201 –– introduction 199, 199, 201 –– medical management 200 –– preoperative care 200 –– publication of 200 – Matson's tenets 185, 186 – penetrating brain injury management 210–211 – post-World War II expansion of – subdural empyema 330 – techniques 208 –– bifrontal decompression 209 –– cranioplasty 210 –– decompressive craniectomy 208 –– decompressive frontotemporoparietal hemicraniectomy 209 –– posterior fossa decompression 210 –– surgical complications, avoiding 210 – wartime penetrating injuries –– orbitofacial injuries 192 –– suboccipital or occipital injuries 194, 196 –– transtemporal injuries 192, 195– 197 –– vertex or parietal entrance 197 neurotrauma – absence of validated TBI biomarkers 49 – biomechanical characteristics 34, 34 – clinical practice guidelines 131, 132, 136 – cyclic AMP and 42 – ethical issues, see ethics, medical New Orleans Criteria 82, 82 NF-L (biomarker) 53 nicardipine 315 non-neurological issues 255 nonconvulsive seizures (NCS), continuous EEG for 65, 164 noninvasive neuromonitoring, see neuromonitoring, noninvasive noninvasive positive pressure ventilation 282 norepinephrine 377 normal saline 268 nosocomial infections, fever and 336 nutrition assessment 301 – energy intake insufficiency 301 – malnutrition 301, 301 – refeeding syndrome prevention 302, 302 nutrition in brain injury 300 – energy requirements –– factors affecting energy needs 304, 304 –– indirect calorimetry 303, 303 –– predictive equations 303, 304 – immunonutrition 300 –– arginine 301 –– glutamine 300 – moderate TBI 164, 165 – neurocritical care and 257 – neurorehabilitation and 361 – pathophysiology and metabolism –– glucose utilization 300 –– lipid utilization 300 – protein requirements 304 – severe TBI 182, 257 nutrition support 304 – algorithm for delivery route 305 – end of life care 308, 309 – enteral nutrition 305 – oral diet 304, 305 – parenteral nutrition 306 O observational studies, randomized clinical trials vs 128 occipital condyle fractures 227, 229 Oceana, TBI incidence in 18 ocular injuries – examination 219 – fractures and 218 – management of 222 odontoid fracture 228 older adults, fall-related TBI, risk factors and prevention 20 oncosuppressor protein p53 44 opioid withdrawal syndrome 277 opioids – fentanyl 277 – remifentanil 277 optic nerve fundoscopy 64 optic nerve sheath diameter ultrasonography 63, 64 oral diet 304, 305 orbit, anatomy of 218, 219–220 orbital apex syndrome 218 orbital injuries, see facial fractures, ocular injuries – classification 220, 220 – examination of 219 – fractures –– management of 221, 221 –– types of 218 – orbitofacial injuries 192, 194 organ donation, ethical issues 394 organized trauma care 142 osmotic therapies, for brain edema ossification, heterotopic 360 osteomyelitis 332 – clinical features 332 – diagnosis 332 – introduction 332 – management 332 – risk factors 332 Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 413 Index Oxford Centre for Evidence-Based Medicine, levels of evidence 127 P pain management 358 parenteral nutrition (PN) 257, 306 – disease indications for 306, 308 – guidelines 306 – peripheral vs total parenteral nutrition 306, 308 paroxysmal sympathetic hyperactivity (PSH) 318 – activities triggering 320 – as cardiovascular complication 312, 314–315 – common features 319 – diagnosis 319, 320 – diseases associated with 318 – history of 318 – introduction 318 – management 320 – natural history 319 – pathophysiology 319 – pharmacologic interventions 321, 321–322 – spinal cord injury and 318 – symptoms 318 partial pressure of oxygen monitoring, brain tissue (PbtO2) 74 pathophysiology of traumatic brain injury 34 – biomarker discoveries in TBI 49 – biomechanics of neurotrauma 34, 34 – brain swelling and resolution of edema 38, 39 – cytoskeletal damage 38 – focal injury 35 – gender-based differences 38 – intracellular and molecular mechanisms 41–42 –– apoptosis 43, 44, 44 –– calcium/glutamate interactions 42 –– cell membranes and ion channels 42 –– free radical generation 42 –– heat shock proteins 43 –– inflammatory response 41, 43 –– second messenger systems 42 – introduction 34 – penetrating injuries 36 – secondary brain damage mechanisms 39 – shear forces effects –– on axons 37, 37 –– on microvasculature 35 –– on synapses and synaptic function 36 – subdural hematoma, acute 35, 35 –– See also subdural hematoma – vascular damage from shear forces and age 38 patient selection, for randomized clinical trials 129 patient transport to hospital 99, 173 – ambulance vs helicopter 99 – EMS vs physician responders and patient outcome 99 peak airway pressure 71, 288, 288 pediatric brain injury 233 – classification 233, 234 – clinical practice guidelines –– severe TBI 212 414 –– treatment outcomes and 140 – decompressive craniectomy 242 – epidemiology 233, 233 – ethical challenges 393 – focal injuries 234, 234 – head injury prevention 243 – hyperosmolar therapy 240 – hypothermia for ICP control 242 – incidence 113, 233 – intracranial pathologies –– diffuse axonal injury 235, 236 –– diffuse brain swelling 235 –– extradural hematoma 234, 235 –– intracerebral hematoma 235, 235 –– subdural hematoma 234, 235 – intracranial pressure management 239, 239, 240 – introduction 233 – mild TBI 233 – moderate TBI 167 – nonaccidental trauma 238, 239 –– evaluation in moderate TBI 167 –– inflicted injuries 233 – posttraumatic seizures 243 –– risk factors 243 –– seizure prophylaxis, indications for 243 – primary vs secondary 233 – skull fractures 236, 236 Pediatric Emergency Care Applied Research Network (PECARN) 114 pediatric loss of consciousness 113 – abusive head trauma 113 – CT scans and clinical decision rules 114 – medical assessment 114 – nonneurological causes 115 – nontraumatic causes 114 – syncope 114, 116 PEEP (positive end-expiratory pressure) 284 penetrating brain injuries, see wartime penetrating injuries – complications, management of 212 – Cushing classification 186 – imaging 89, 90, 211 – introduction 210 – management –– guidelines 210, 210, 211 –– initial management 210 –– intracranial monitoring 211 –– surgical management 211 ––– See also neurosurgery – pathophysiology 36 – prognosis 381 – seizures following 212 – TBI prognosis 381 pentobarbital 180, 278, 279 perforating injuries 190, 191 perfusion imaging 95, 109 peroxiredoxin-6 (PRDX6) 50 pharmacodynamic biomarkers 49, 54, 56 phenylephrine 315 phenytoin 181, 243 physical examination 108 pituitary dysfunction 253 plateau pressure 288 pneumonia 337 – See also ventilator-associated pneumonia (VAP) – antibiotic resistance risk factors 337, 338 – clinical features and diagnosis 337 – definitions 337 – epidemiology and risk factors 337 – hospital-acquired (HAP) –– antibiotic therapy 338, 338 –– epidemiology and risk factors 337 – management of 337 – risk factors for multidrug-resistant pathogens 337, 338 Population, Intervention, Control, Outcome (PICO) process 127, 127 positive end-expiratory pressure (PEEP) – intracranial pressure and 285 – intrinsic (PEEPi) 289 – mechanical ventilation and 284 positive pressure ventilation, artificial postacute residential brain injury rehabilitation program 354 postconcussive syndrome (PCS) 153 – biomarkers and informed ED discharge counseling 52 – definition 52, 111 – mild traumatic brain injury as 111 – postacute management 356 – risk factors 154 – treatments 154 posterior fossa decompression 210 posterior fossa lesions 206, 207 posttraumatic dementia 55, 379 posttraumatic epilepsy (PTE), see epilepsy, posttraumatic posttraumatic stress disorder (PTSD) 15 Potts' puffy tumor 330 PRDX6 (peroxiredoxin-6) 50 predictive biomarkers 49 Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA) 127 pregnant patients 392 prehospital care 99 – cervical spine injury 101, 101 – fluid resuscitation 101 – guidelines 99, 172, 214 – hypotension and hypoxia 100, 100, 172 – initial assessment and vital signs 100 – introduction 99 – neurological assessment 100, 100 – neurological resuscitation 101 – patient transport to hospital 99 – prehospital intubation 100 – prehospital neuroprotectants, clinical trials, 102 – principles of 99 – severe TBI 172 – summary of recommendations 103 preoperative care, guidelines 200 prescription drugs, and TBI risk 16 pressure reactivity index (PRx) 71, 72 pressure support ventilation (PSV) 283, 294 primary injuries, see specific types of injuries – extra-axial manifestations 82 – imaging of 82 – intra-axial manifestations 86 – pathophysiology 82, 172 – TBI classification 30 primary survey (ABCDEs) 173, 173 – airway 173 – breathing and ventilation 174 – circulation and hemorrhage control 174 – disability and neurological evaluation 174 – exposure and environmental control 174 progesterone 38, 102 prognosis for traumatic brain injury, see under specific topics – aging and neurodegenerative disease 379 – biomarkers 49, 54, 376 – clinical decision making and 200, 371 – clinical trials 380 – demographics and premorbid characteristics 372 – elements of 372 – genetics and 373 – hospital-related complications and discharge status 378 – ICP and CPP in 375 – injury severity and 374, 380 – injury, illness, and medical comorbidities 376 – interrelationships and variables 371 – introduction 371 – key clinical points 381 – mechanism of injury and 374 – moderate TBI 166 – posttraumatic amnesia duration and 375 – pupillary reactivity and 375 – severe TBI 170 – TBI classification by 31 – threshold values in reporting 381 propofol – adverse reactions 273 – for severe TBI 180 – midazolam vs 274 – pharmacology 273 – TBI considerations 274 propofol infusion syndrome 180, 274 proteins, dietary 304 prothrombin time 377 pseudoaneurysms 196, 196 public health approach (CDC) – data analysis 19 – role in TBI prevention 19 – steps in 19 pulsatility index (PI), Gosling's 61, 62 pupillary examination, prehospital 100 pupillary reactivity and TBI prognosis 375 pupillometry, infrared 64 pyelonephritis 341 Q quality of care and CPG compliance 142, 143 quality of life, TBI impact on 363 Quality of Well-Being (QWB) scale 373 quality-of-life costs of TBI 398, 398 R race and ethnicity 372 Rancho Los Amigos Level of Cognitive Functioning Scale 352, 353 Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license Index randomized clinical trials (RTC) – BEST TRIPs trial 130 – decompressive craniectomy 130 – evidence-based medicine and 128, 131 – failure of 129 – in critical care 129 – patient selection 129 – surgical, challenges of 130 – traumatic brain injury 129 RAP index (compensatory reserve) 71, 72 refeeding syndrome 302, 302 rehabilitation, see neurorehabilitation remifentanil 277 resistivity index (RI), Pourcelot's 61–62 respiratory failure – central respiratory drive abnormalities 293 – determining cause of 292 – hyperinflation, dynamic 293 – hypoxemic 292 – prevention of – pump failure 282, 292 – respiratory muscle abnormalities 293 respiratory flow rate 284 respiratory rate (ventilation parameter) 284 responsiveness, level of 108 resuscitation 107, 188 retraction balls, axonal discontinuity and 37 RoR (dynamic rate of autoregulation) 77 Rotterdam CT score 30, 82, 83 rural population, TBI incidence in 16 S S100B (biomarker) 52, 54 safety devices 21 SAIDH (syndrome of inappropriate antidiuretic hormone) 253, 254 saliva, biomarkers in 49–50 second impact syndrome (SIS) 154, 356 second messenger systems 42 secondary brain injuries, see specific types of injuries – biomarkers in TBI 49, 53 – characteristics 49 – definition 82 – early detection of 53 – imaging 91 – mechanisms 39, 53, 172 –– capillary blood flow 40 –– infarction vs selective neuronal loss 40 –– ischemic neurological damage 39, 92 –– metabolic changes 41 –– reduced cerebral blood flow 39 –– reduced cerebral oxygenation 40, 41, 74 – TBI classification 30 sedation and analgesia 273 – barbiturates 278, 279 – choice of sedation 273 – dexmedetomidine 275, 275 – introduction 273 – ketamine 277, 278 – midazolam 274 – opioids 276, 276 – propofol 273, 274 seizures – ICU management of 252 – nonconvulsive, continuous EEG for monitoring 65, 252 – post-concussion 154 – posttraumatic 164, 252 –– in pediatric population 243 –– penetrating brain injury and 212 –– prophylaxis and treatment 181, 200, 360 – prehospital management 102 – syncope vs 117 sensory deficits 358 severe traumatic brain injury 170 – classification of injury and prognosis 170 – clinical practice guidelines 135, 177 – continuous EEG monitoring 78 – definition – epidemiology 170 – injury mechanisms and pathophysiology 172 – loss of consciousness and 107 – management 172 –– initial trauma 173 –– neurosurgical assessment and intervention 174, 175, 176 –– prehospital 172 –– primary survey (ABCDEs) 173, 173 –– radiographic assessment 176 –– secondary survey 174 – management in ICU 176 –– See also neurocritical care –– blood pressure and CPP management 270 –– fluid and intravascular volume management 178 –– hyperosmolar euvolemic therapies 179 –– hypothermia, prophylactic 181 –– intracranial pressure and CPP treatment 179 –– neuromonitoring 176 –– neuroprotective agents 180 –– nutrition and 182, 257 –– seizure prophylaxis 181 –– steroids contraindicated for 181 –– ventilation, oxygenation, and CO2 management 178 – postacute management 356 – transcranial Doppler ultrasonography 61 sex factors, see gender shear forces – effects on axons 37, 37 – effects on microvasculature 35 – effects on synapses synaptic function 36 – vascular damage and 38 shearing injury 88 Sideline Concussion Assessment Tool (NFL) 111 Sideline Concussion Assessment Tool (SCAT3) 152 Simoa (single molecule array) assay 50, 53 skull fractures – pediatric –– basilar fracture 237, 239 –– depressed 236, 237 –– growing fracture (leptomeningeal cyst) 237, 238 –– ping-pong (pond) fracture 236, 237 –– treatment in children 208 – surgical management guidelines 207, 208 Society of Critical Care Medicine socioeconomics – costs of traumatic brain injury 19, 20 – status and TBI prognosis 373 sodium levels and TBI prognosis 377 sodium nitroprusside 315 sodium/potassium ATPase pump 39, 42 spasticity, management of 359 spectroscopy, near-infrared (NIRS) 64 spinal cord injury (SCI) – clinical practice guidelines 135 – paroxysmal sympathetic hyperactivity and 318 spine fractures 227 – anatomy and 228 – areas at risk for injury 227 – classifications 229 – examination of 228 – stable vs unstable injuries 227 – treatment 229, 231 spontaneous awakening trial (SAT) 295 Sport Concussion Assessment Tool (SCAT2) 111 sports/recreation (SR) related TBI – concussion guidelines 133 – incidence 14 – prevention 21 stab wounds 36 Standardized Assessment of Concussion (SAC) 111 status epilepticus (SE) 77 stroke – intracerebral hemorrhage 115 – ischemic stroke 115 – loss of consciousness and 115 subacute rehabilitation units 354 subarachnoid hemorrhage (SAH) – acute respiratory distress syndrome and 287 – colloids for 268 – imaging 86, 86, 206 subaxial cervical spine injuries – classification 229, 230 – pathophysiology 228 – treatment 230 subconcussion 155 subdural empyema 329 – clinical features 330 – diagnosis 330 – epidemiology 330 – introduction 329 – management 330 – risk factors 330 subdural hematoma (SDH) – as most severe TBI 34 – contusion related 36 – epidural hematoma vs 84 – imaging 83, 84 – of arterial origin 36 – parenchymal small vessels, coalescence and rupture of 36 – pathophysiology 35, 35 – pediatric 234, 235 – rupture of bridging veins 36 – surgical management guidelines 202, 204 –– injury pattern 202, 203 –– prognosis 202 –– time to treatment and surgical outcome 204 subdural hygroma 85, 85 suboccipital or occipital injuries 194, 196 substance abuse – prevention following TBI 22 – TBI prognosis and 373 – TBI risk and 15 suicide and traumatic brain injury 14 superior orbital fissure syndrome 218 surgical management of TBI, see neurosurgery swallowing 361 sweat, biomarkers in 49–50 sympathetic storms, see paroxysmal sympathetic hyperactivity (PSH) synapses and synaptic function 36 synchronized intermittent mandatory ventilation (SIMV) 283, 294 syncope – as transient loss of consciousness 115 – differential diagnosis 116 – incidence 116 – medical workup 116 – pediatric 114, 116 – seizure vs 117 syndrome of inappropriate antidiuretic hormone (SAIDH) 253, 254 systematic reviews, in CPG development 127, 144 T T-tube ventilation 294 targeted temperature management (TTM) – clinical studies 349 – intraoperative 350, 350 – introduction 349 – postoperative outcome 350 – preclinical studies 349 tau protein (biomarker) 53, 55 TBI, see traumatic brain injury (TBI) terminal care, nutrition support in 308, 309 text messaging while driving (TMWD) 21 thermal diffusion 74 thiopentone 278, 279 threshold values 381 tidal volume 284 tight glycemic control 300 tracheostomy – patient need for 256, 256 – prolonged mechanical ventilation and 296 TRACK-TBI study (North America) 31 tranexamic acid (TXA) 102 transcranial color-coded duplex sonography (TCCS) 61, 74 transcranial Doppler (TCD) ultrasonography 61, 74 – advanced methods 63 – application in severe TBI 61, 62 – cerebral autoregulation studies 62 – principles of 61 Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 415 Index transesophageal echocardiogram (TEE) 313 transfusion of blood products – brain tissue oxygenation monitoring and 179 – effects on fluid resuscitation 269, 269 – indications for 257 – risks and benefits in TBI 269–270 transient hyperemic response test (THRT) 77 transtemporal injuries 192, 195–197 trauma centers – classification 99 – organized trauma care 142 – severe TBI requirements and 173 – suspected TBI and level of care 99 – Trauma Center Verification program 142 trauma management, initial 173, 173 traumatic brain injury (TBI), see individual topics – basics of 199 – brain trauma and critical care, history of – burden of, U.S and world-wide 10, 23 – classification 29 – clinical practice guidelines 124 – concomitant injuries 218 – costs of 395 – definition 29, 199 – epidemiology – ethical issues 387 – loss of consciousness in 107 – management, history of 1–2 – neurorehabilitation 352 – pathophysiology 34 – prehospital care 99 – prevention 19 – prognosis 366, 371 – recurrent 15 – severity of – standardized terminology and data collection – surgical management guidelines 199 – targeted temperature management 349 416 Traumatic Coma Data Bank (TCDB) trephination tumor necrosis factor- ? (TNF-?) 43 TUNEL ((terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling) 44 tympanic membrane displacement (TMD) 63 U ubiquitin C-terminal hydrolase (UCHL1) 51–52 urinary incontinence 360 urinary tract infections 340 – catheter-associated 340 – clinical features 340 – diagnosis 341 – epidemiology and risk factors 340 – management 341 – pathogenesis 340 urine, biomarkers in 49–50 V valproate 181 VAP, see ventilator-associated pneumonia (VAP) vascular cellular adhesion molecule (VCAM) 50 vascular injuries 224 – anatomy and 226 – classifications 226 – examination, neurological 226 – imaging 90 – mechanisms and pathophysiology 225 – shearing forces and age 38 – treatment 226, 227 vasoactive agents 315, 316 vasogenic edema 38, 91 vasopressors 316, 316 vasospasm 91, 93, 189 venous thromboembolism (VTE), see deep vein thrombosis (DVT) – introduction 323 – prophylaxis 257, 323 –– guideline recommendations 325 –– insufficient data in TBI population 323 –– pharmacologic, timing of 324 –– radiographic surveillance and IVC filters 325 –– risk factor-associated TBI progression 323 – risk factors in TBI 323 ventilator-associated pneumonia (VAP) 256, 290 – antibiotic therapy 256, 256, 291, 292, 338 – clinical features and diagnosis 337 – definition and incidence 290 – diagnosis 290, 337 – epidemiology and risk factors 337 – prevention 256, 291 – time of onset 290 – treatment 290, 291 ventilator-induced lung injury (VILI) 289 ventilatory support, history of – See also mechanical ventilation ventricular catheters, antibiotic-impregnated (AIVC) 336 ventriculitis, device-related 335 vertebral artery – anatomy 226 – blunt injury and ischemic stroke 226 – dissection, imaging 90, 90 vestibular dysfunction, neurorehabilitation for 357 violence-related traumatic brain injury, see assault-related traumatic brain injury visual-evoked potentials 65 vital signs, stabilization of 107 voltage-gated ion channels 42 W wakefulness 106 wartime penetrating injuries – combat-related TBI guidelines 212 – description of 190 –– penetrating 190, 191 –– perforating 190, 191 – historical background 185, 185 –– Cushing's treatment principles 185 –– Matson's tenets 185, 186 –– neurosurgical approach, evolution of 185, 185 – management 188 –– DVT prophylaxis 189 –– far-forward treatment 189 –– initial resuscitation 188 –– injury patterns and 192, 193 –– medical evacuation of patients 190 –– neurovascular injuries 189 –– orbitofacial injuries 192, 194 –– suboccipital or occipital injuries 194, 196 –– temperature control 190 –– transtemporal injuries 192, 195– 197 –– vertex or parietal entrance 197 – missiles and mechanisms of 186 –– criteria for removal of intracranial fragment 188, 188 –– metallic fragments 186, 186 –– nonmetallic fragments 187, 187– 188 weaning from mechanical ventilation 291 – ABCDE bundle (spontaneous awakening trial) 295 – Awakening and Breathing Controlled (ABC) trial 296 – determining cause of respiratory failure 292 – determining readiness to wean 293, 293 – predictors of outcome 293 – spontaneous breathing trials 294, 295 work loss costs of TBI 397, 397 work-related TBI 20 Z zygomaticomaxillary complex (ZMC) fractures 222 – classification 223, 223 – treatment 224, 225 Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1-62623-336-2), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license ... rate of 8% and infection rate of 6%.1 42 The PBI guidelines recommend local wound care and closure with Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1- 626 23-336 -2) ,... anterior to the tragus and above the zygoma and running to the midline behind the hairline After the incision is opened, the Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN... A modern series of acute traumatic SDH of 1, 427 patients between 20 05 Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed (ISBN 978-1- 626 23-336 -2) , copyright © 20 18 Thieme Medical