Maximizing Survival from Severe Traumatic Brain Injury: Applying Guidelines to Clinical Practice: Part I
Maximizing Survival from Severe Traumatic Brain Injury: Applying Guidelines to Clinical Practice: Part I
Head injury can mean many things, from a bump on the forehead to an open wound with extruding brain. This review focuses on patients with severe closed head injuries. Like many other areas of medicine, we have good evidence for what is the best care. The principles may seem simple, but applying them is not always easy. The challenge is to deliver optimal care consistently and continuously, from the scene, during transport, in the emergency department, through the operating room and ICU. This is the first of a two-part series on severe traumatic brain injury, focusing on the evidence for optimal care.
J. Stephan Stapczynski, MD, Editor
Introduction
Case Scenario. Paramedics are called to a private residence in response to a 54-year-old male. His wife reports that he fell 5 feet from a step ladder and struck the back of his head. The patient is a marathon runner who recently has been diagnosed with atrial fibrillation for which he is taking warfarin. Upon emergency medical service (EMS) arrival, he has sonorous respirations, symmetric pupils, and a Glasgow Coma Score (GCS) of 7: E1 M4 V2. His systolic blood pressure (SBP) is 85 mmHg, and his heart rate is 140 beats/minute and irregular. His oxygen saturation is 88%. Paramedics identify his low GCS and consider endotracheal intubation (ETI), but, given his clenched jaw and their short transport time, they elect to treat him with a non-rebreather facemask and high-flow oxygen. The patient is placed in a rigid cervical collar for immobilization and then transferred onto a backboard while maintaining cervical spine precautions. His oxygen saturations climb to the mid 90s. Five hundred milliliters of normal saline is administered, and his SBP rises to 105 mmHg with a drop in his heart rate to the 120s. He is transported to the nearest Level I trauma center with neurosurgical capabilities.
Upon arrival, the trauma team observes that the patient's pupils are symmetric and reactive. During preoxygenation, stat labs are sent, and an electrocardiogram demonstrates atrial fibrillation. The emergency physician successfully performs rapid sequence intubation (RSI) after premedication with lidocaine. The patient is taken emergently to radiology on the monitor with an advanced trauma life support (ATLS) trained nurse for non-contrast CT scans of the head and cervical spine. The neurosurgical consultant is simultaneously called. Upon return from CT, the patient is noted to have a dilated, non-reactive right pupil and begins to posture. The ventilator is set for a target PCO2 of 30-35 using continuous capnography monitoring for guidance. The CT scan reveals a large right-sided subdural hematoma with midline shift and evidence of herniation. The patient's INR returns at 3.0. The neurosurgeon is now at the bedside. The patient's SBP is 110 mmHg, and his heart rate is 100 beats/minute. The neurosurgeon requests mannitol, noting that his cardiovascular status appears to have stabilized. Four units of fresh frozen plasma (FFP) are ordered, and the patient is transported to the operating room for evacuation of his subdural hematoma.
Epidemiology and Societal Impact of Traumatic Brain Injury
Traumatic brain injury (TBI) is a leading cause of death and disability worldwide. In the United States, 1.4 million cases of TBI are reported annually, with 1.1 million cases treated in the emergency department and 235,000 cases hospitalized each year.1,2 The incidence of TBI peaks at ages 15-24 years, with smaller peaks at the extremes of age, younger than 5 and older than 70 years of age.3 TBIs frequently are the result of falls and motor vehicle collisions, which comprise 28% and 20%, respectively.1 Fall-associated TBI rates are highest for children ages 0-4 years and adults 75 years and older, while motor vehicle-related TBI rates are highest in adolescents aged 15-19.1 Child abuse is the leading cause of death from TBI in those younger than 2 years of age.4 TBI is prevalent on the battlefield, with more than 60% of military personnel returning to the Walter Reed Army Medical Center from Operation Enduring Freedom/Operation Iraqi Freedom having suffered a blast-induced TBI.5
Each year in the United States, approximately 50,000 people die from TBI, 2,685 of whom are younger than 15 years old.1 Nearly half of those who die from TBI do so in the first two hours.6 In children and adults, TBI is the most important determinant of outcome from trauma.6 The mortality rate from blunt trauma without TBI is 1%, and with TBI it skyrockets to 30%.7
Severe Traumatic Brain Injury. TBI is most often classified by using the GCS.8 The GCS is a sum score of three aspects of neurologic function: eye opening, verbal response, and motor response. The scores for each category should be reported separately and are subsequently added together, with the lowest possible total being three and the highest 15. It should be noted that the GCS has several limitations, such as the level of consciousness being impacted by paralysis, intoxication, and medical sedation.9,10 A GCS of 8 or less is considered severe TBI, GCS 9-13 moderate TBI, and GCS 14-15 mild TBI.11,12 Mild TBI comprises 80% of TBI cases, while moderate and severe TBI each contribute 10%.3
Primary and Secondary Brain Injury. TBI is described by both primary and secondary brain injury. Primary brain injury refers to the damage that occurs or is initiated at the time of the traumatic event, while secondary brain injury is a result of factors that occur after the initial trauma and either worsen injury or negatively influence outcome. Primary brain injury is a result of external forces to the head (direct impact, rapid acceleration and deceleration, penetrating object, or blast waves) that cause injury to neurologic and vascular tissue both locally and remote from the site of injury. Many of the deleterious mechanisms leading to secondary injury, such as disruption of cellular homeostasis, excitotoxicity of glutamate and aspartate, and superoxide generation, are not currently amenable to therapy.6 As such, clinical efforts are aimed at minimizing second insults to the brain, including hypotension, hypoxia, hypocapnea, pyrexia, coagulopathy, and anemia. Data from the Traumatic Coma Data Bank (TCDB) demonstrate that a single hypotensive measurement (SBP < 90 mmHg) occurred in one-third of severe TBI victims between injury and resuscitation and was independently associated with a doubling of mortality.13 Similar findings have been shown in the pediatric population.14 Hypoxia (O2 saturation < 90%) in both the prehospital and in-hospital settings is also associated with poor outcomes.13,15 While induced hypocapnea (PaCO2 < 35 mmHg) is used as a salvage technique during herniation, the potential benefits of prophylactic hypocapnea to decrease intracranial pressure (ICP) are more than offset by reductions in cerebral blood flow (CBF) and subsequent ischemia.16-20 Pyrexia (T > 100.4 °F) is common and is also strongly correlated with poor outcomes.15 (See Table 1.)
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Anatomy and Pathophysiology
The brain is semisolid and weighs approximately 3 lbs. Despite its diminutive size, it receives about 15% of total cardiac output and accounts for approximately 20% of total body oxygen consumption.12,21
A normally functioning brain maintains its blood flow through autoregulation. The cerebral perfusion pressure (CPP) serves as an estimate of CBF and is defined as the difference between the mean arterial pressure (MAP) and the ICP (CPP=MAP-ICP). The brain with a MAP between 60-150 is able to regulate cerebral blood flow by constricting and dilating the vasculature depending on the conditions.22 Hypertension, alkalemia, and hypocapnea result in cerebral vasoconstriction and decreased CBF, while hypotension, acidemia, and hypercapnea result in vasodilation and increased CBF. The volume of the skull is fixed and, as such, the Monro-Kellie Doctrine states that the ICP is directly related to the volume of the intracranial contents. The normal intracranial contents are brain parenchyma, blood, and cerebrospinal fluid (CSF).6 Cerebral edema after TBI can increase brain volume and is either vasogenic or cytotoxic. Vasogenic edema is the result of a compromised blood-brain barrier, and cytotoxic edema, the primary culprit in TBI, is a result of brain cell death.6,12,23 Blood volume can increase for several reasons, including venous outflow obstruction, metabolic derangements (e.g. pyrexia and seizures), or vasodilatation from loss of autoregulation.6 Finally, CSF volume can increase if drainage is obstructed, such as with an intraventricular lesion or obstruction of outflow through the posterior fossa.6
Intracranial hypertension from any of the aforementioned causes can result in both ischemia and herniation. Ischemia is caused by a decreased CPP and ultimately leads to cell death. Herniation occurs when there is a pressure gradient across a fixed anatomic barrier. This most commonly occurs at the tentorial membrane separating the cerebral hemispheres from the posterior fossa. When transtentorial herniation (often referred to as uncal herniation) occurs, pressure is exerted on the brainstem, the cranial nerves, and the local vasculature. This may result in anisocoria, posturing, autonomic disturbances, and/or death.6 (See Figure 1.)
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Brain Trauma Foundation Guidelines. During the past 30 years, it has been demonstrated that compliance with evidence-based in-hospital protocols that emphasize monitoring and the maintenance of cerebral perfusion has resulted in a drop in TBI mortality from 50% to less than 25%.24-30 In 2007, the Brain Trauma Foundation (BTF) published the third edition of the Guidelines for the Management of Severe Traumatic Brain Injury.31 The BTF is a national non-profit organization of neurosurgical experts that was founded to improve the outcomes of patients with TBI by creating evidence-based best practice guidelines, performing clinical research, and educating health professionals.32 Since the publication of the initial BTF guidelines, there have been several studies demonstrating that BTF guideline-based care decreases mortality, length of hospital stay, and costs while improving functional outcomes.24,25,29 A recent study showed that the use of BTF guidelines for treatment of severe TBI improved health outcomes and costs and suggested that widespread implementation of these guidelines would result in substantial savings in medical costs, annual rehabilitation costs, and lifetime societal costs.33 Despite widespread dissemination of the in-hospital guidelines, adoption has been limited.27 In 2007, the BTF published the first separate Guidelines for Prehospital Management of Traumatic Brain Injury (evidence through July 2006) in Prehospital Emergency Care.34 Little is known about the utilization of guideline-based care in the prehospital setting.
Prehospital Care
Brain Trauma Foundation. There is growing evidence that what happens in the initial "platinum 10 minutes" following TBI may profoundly impact the effectiveness of subsequent definitive care. EMS providers typically are the first healthcare providers to treat patients with TBI, making their assessment and treatment a critical link in the chain of survival.35 In accordance with the Guidelines for the Prehospital Management of Traumatic Brain Injury, the following section on the prehospital management of severe TBI will be divided into "assessment" and "treatment" topics.34
Assessment. Maintaining adequate oxygenation and blood pressure are critical steps in maximizing outcomes in patients with TBI.36 Given the well-documented negative impact of hypotension and hypoxemia following TBI, patients with suspected TBI should be monitored closely in the prehospital setting and have measures taken to prevent both conditions.13,14 Guidelines state that oxygen saturation levels and blood pressure (systolic and diastolic) should be monitored as often as possible, preferably continuously. For children, appropriate size pediatric oximeters and blood pressure cuffs are recommended. Hypoxemia is defined as arterial hemoglobin oxygen saturation < 90% in both children and adults. Adult hypotension has been defined as SBP below 90 mmHg, while for children it is age-dependent, ranging from < 60 mmHg for those between 0-28 days old to < 90 for those aged 10 years or older.34
The GCS should be evaluated repeatedly to monitor improvement or deterioration of the patient's condition (pediatric GCS for children < 2 years of age). (See Table 2.) It should be measured after the ABCs are assessed and treated and prior to administering sedatives or paralytic agents (or after metabolism of these drugs). Pupils should be assessed in both adults and children to aid in the subsequent determination of diagnosis, treatment, and prognosis. They should be measured after the patient has been resuscitated and stabilized. Asymmetry is defined as > 1 mm difference in diameter. A fixed pupil is defined as < 1 mm response to bright light.34
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Standard initial assessments of comatose patients also should be performed, such as a blood glucose measurement.
Treatment. The primary goals in the prehospital management of TBI are to prevent hypotension and hypoxia, to avoid hyper- and hypocapnia, and to triage to the appropriate center.34,37 In the prehospital setting, hypoxia is discovered in 44-55% of cases, and hypotension is found in 20-30%.37-39 The introduction of a prehospital system capable of normalizing blood pressure and oxygenation has been associated with improved outcomes in various locations.40,41
Hypoxemia (oxygen saturation < 90%) should be corrected immediately upon detection. A definitive airway should be established in patients who have a GCS of 8 or less and either the inability to maintain an adequate airway or hypoxemia not corrected with supplemental oxygen. The BTF guidelines state that ground-transported patients in an urban environment who are spontaneously breathing and are maintaining their oxygen saturations above 90% on supplemental oxygen should not be treated with paralytic medications to assist ETI.34 When RSI is indicated, protocols should include monitoring serial blood pressure, oxygenation, and end-tidal CO2 (ETCO2). Endotracheal tube placement should be confirmed via lung auscultation and ETCO2 determination. Normal breathing rates confirmed by ETCO2 of 35-40 mmHg should be maintained and hyperventilation (ETCO2 < 35 mmHg) should be absolutely avoided unless the patient shows signs of cerebral herniation.34
Hypotensive patients with TBI should be treated with isotonic fluids. The BTF guidelines support hypertonic fluid resuscitation as a treatment option for adult TBI patients with a GCS < 8.34 It should be noted, however, that a recent large Resuscitation Outcomes Consortium (ROC) trial of prehospital hypertonic saline (HTS) for severe TBI victims was halted by The National Heart, Lung and Blood Institute (NHLBI) because HTS did not improve outcomes when compared to standard treatment with normal saline.42
Patients should be assessed frequently for signs of acute herniation, such as dilated, unreactive, or asymmetric pupils; a motor examination with extensor posturing or no response; and acute neurological deterioration. While prophylactic hyperventilation should be avoided, hyperventilation therapy might be necessary for brief periods in patients who are normoventilated, well oxygenated, and normotensive and still have signs of herniation. Hyperventilation should be titrated to effect and be discontinued when clinical signs of herniation resolve. The goal of hyperventilation is an ETCO2 of 30-35 mmHg. The current literature does not support the use of mannitol or HTS to treat herniation in the prehospital setting.34
To ensure the best possible outcomes for TBI patients, the BTF recommends that all regions should have an organized trauma care system and protocols in place to direct EMS personnel regarding destination decisions for patients with severe TBI. Patients with TBI should be transported directly to a facility with immediate CT availability, neurosurgical capability, and the ability to monitor ICP and treat intracranial hypertension. The mode of transport should minimize prehospital time. Pediatric patients should be transported directly to a pediatric trauma center when available. If a pediatric trauma center is not available, preference should be given to an adult trauma center with added qualifications to treat children.34
Patel and colleagues demonstrated a doubling of the odds of death for patients with severe TBI treated in non-neurosurgical centers versus neurosurgical centers.43 Maas et al. suggest that all treatable patients with severe TBI be treated in large neurotrauma centers that offer surgical therapy and access to neurocritical care.44-47 Greater experience treating severe TBI leads to higher quality care and better outcomes.48-50
Prehospital RSI. Several recent studies have suggested that prehospital RSI is associated with worse outcomes.51-55 Subsequent analysis has shown that RSI per se was not directly responsible, but that hypoxia during induction and inadvertent hyperventilation after intubation were common and likely contributed to the poorer outcomes in the RSI groups.56-59 In fact, prehospital RSI can improve outcomes in severe TBI.60-64
Hyperventilation/hypocapnea results in vasoconstriction of the cerebral arterioles, thereby reducing CBF, cerebral blood volume (CBV), ICP, and cerebral oxygen delivery. In reality, the potentially favorable drop in ICP due to hypocapnea is more than offset by the negative consequences of decreased CBF with subsequent cerebral ischemia and secondary injury of the traumatized brain.16-20 Positive pressure ventilation may cause additional secondary insults by increasing intrathoracic pressure, which decreases venous return to the heart. This can result in systemic hypotension and increased ICP by causing congestion in the jugular venous system.16,65,66 Additionally, an increase in intrathoracic pressure is transmitted through the CSF and the spinal veins, causing an increase in ICP.67
As early as 1991, randomized controlled trial evidence of negative outcomes from prolonged hyperventila- tion in severe TBI patients led to the recommendation that routine hyperventilation be avoided.31,34,68 Despite the evidence and the BTF recommendation, hyperventilation is common during the prehospital resuscitation of TBI patients.56,62,69 In addition to hyperventilation, hypoventilation also has deleterious effect on the injured brain. A PaCO2 of > 45 mmHg (severe hypercapnea) on arrival at the ED is associated with hypotension, hypoxia, metabolic acidosis, and a significant increase in mortality.55 Prehospital airway management must concentrate not only on the quality of the intubation, but on the subsequent ventilation management.61 Responders must be trained to ventilate at a set rate and tidal volume. More controlled ventilation methods such as autoventilators should be considered to ensure maintenance of target ETCO2 without inadvertent hyper- or hypoventilation.16 The target ETCO2 for prehospital patients with TBI is 35-40 mmHg.34,70 Patients arriving at the hospital within the target range have better outcomes.31,55
The BTF guidelines recommend prehospital end-tidal capnography as a way to target ventilation in cases of severe TBI.34 It must be noted that while ETCO2 values match PaCO2 values closely in the operating room, there is question about how well they correlate in the emergency setting.71-73 Correlation appears to be best in patients with isolated TBI.16 Further research is necessary to establish firm ventilation recommendations based on this monitoring method.16
The BTF assembled a panel of experts to interpret the existing literature and to make recommendations regarding the use of RSI in the field for severe TBI. Table 3 outlines their recommendations in question-and-answer format.61
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Emergency Department Care
Initial Evaluation. The cornerstone of the initial emergency department management of severe TBI remains the ABCs and the maintenance of spinal immobilization. Estimates suggest that 35-60% of severe TBI victims have another traumatic injury.74,75 If the EMS report is suggestive of severe TBI, the trauma team should be activated when available. Upon arrival, the lead physician should perform the primary survey with continuous maintenance of cervical spine precautions. Neurologic status should be assessed early to establish a baseline. Attention should be focused on the GCS and pupillary exams (prior to RSI and administration of paralytics). Signs of herniation, such as pupillary asymmetry and loss of reaction to light, should be identified rapidly. In a patient not responsive to verbal cues, a noxious stimulus should be applied to all four limbs. Interventions such as ETI should be performed as indicated during the standard ATLS sequence. A report should be taken from EMS providers to ascertain any information that might help in management. Vital signs, ETCO2, and blood glucose should be obtained. A thorough secondary survey should be performed as soon as the initial survey is complete to assess for other injuries.76
History. The initial history must be detailed and accurate but also efficient. An effective method is the AMPLE categories. Allergies, Medications, Past medical history, Last meal and Events/Environment related to the injury.76 A history from EMS personnel, family, and bystanders should be obtained when available. Important additional questions include those related to the mechanism of injury, loss of consciousness, history of seizures, and alcohol or drug intoxication.
Physical Examination. A complete trauma examination should be performed for severe TBI patients, with special attention paid to coma scoring and the pupil exam. The GCS was developed by neurosurgeons Teasdale and Jennett at Glasgow University in 1974 to gauge and communicate coma progression and to predict outcome.8,77-80 While the GCS remains the most commonly used coma score and is advocated by the BTF, it should be noted that it is not without limitations. For example, if a patient undergoes field RSI, the chemical sedation and paralysis render the scale of little utility.81 In its original form, the initial score was obtained at 6 hours after injury, giving the injury time to declare itself.8 As such, early GCS scores can be inaccurate and can be altered significantly by alcohol and drug ingestion. Winkler et al. and Bazarian et al. both have shown that the prehospital GCS can differ significantly from the GCS upon arrival at the emergency department.82,83
There are other concerns with the GCS score. Gill et al. showed that the inter-rater reliability is low, and Teoh et al. have demonstrated that GCS scores with different permutations of eye, verbal, and motor can have different meanings.84,85 Finally, and perhaps most importantly, using the GCS alone to make treatment decisions can lead to unnecessary and perhaps deleterious intubations. In the San Diego Paramedic RSI trial, Davis et al. showed that when using GCS alone to determine the need for intubation, 27% of patients who were intubated did not have a significant head injury.51,86 This was particularly common in the intoxicated cohort. Additionally, many of their historical controls who would have met GCS < 8 intubation criteria were oxygenating and ventilating adequately on hospital arrival.51,86
There are a number of coma scoring systems that attempt to balance simplicity and ease of use with adequate detail to provide utility. The FOUR (Full Outline of UnResponsiveness) Score is a new coma score that shows promise.87 (See Table 2.) It has four components: eye response, motor response, brainstem reflexes, and respirations. Each component has a score between 0-4, and the components are not totaled. The FOUR Score coma scale has been validated in the neurointensive care unit and in the emergency department by both physicians and nurses and appears to be performed as reliably as the GCS while providing more detailed information.87,88
Differential Diagnosis. As in all cases of critical illness, it is imperative that a broad differential diagnosis is maintained. The possibility of medical illness as the precipitant of the trauma always should be considered, (e.g., syncope, cardiac arrest, seizure, hypoglycemia, stroke). It has been estimated that more than 60% of TBIs are related to the abuse of alcohol or another substance.89 Hypoglycemia can lead to traumatic injury as a result of altered mental status and, if left undetected, can lead to permanent neurologic damage and death.90
There are a number of different types of TBI, and their management can vary. Early neuroimaging is used to distinguish between epidural hematoma, diffuse axonal injury (DAI), intraparenchymal hemorrhage, subarachnoid hemorrhage, and subdural hematoma.
Laboratory Tests. Many severely head-injured patients have suffered another traumatic injury.74,75 The laboratory studies obtained in severe TBI are those that are routinely obtained for major trauma victims. Traditional laboratory tests include the complete blood count, metabolic panel, coagulation panel, arterial blood gas, serum lactate level, and the blood type. An evaluation of serum alcohol and a urine drug screen also can be beneficial to exclude alternative etiologies of altered mental status.
Imaging. The imaging modality of choice is the non-contrast CT scan of the head.91 CT scans are widely and rapidly available and are highly sensitive in the detection of acute hemorrhage, mass effect, midline shift, and bony injuries.92 The CT scan should be obtained as early as possible with the intent of detecting lesions that require immediate neurosurgical intervention. Monitoring should be maintained during transport and imaging.6 A healthcare provider capable of recognizing and responding to deterioration should stay with the patient and have the requisite equipment and medications. A head CT will delineate the presence and type of acute injury to the brain, thereby directing subsequent management. If the situation arises in which resuscitation priorities preclude transport to the radiology suite, neurosurgery should be consulted immediately.6 In addition to providing critical information early in the care of severe TBI, the non-contrast head CT has prognostic value.77,93-96
MRI is not standard in the early management of severe TBI because of the lack of universal availability, the time needed for imaging, and the difficulties with monitoring.92 MRI is superior to CT for evaluating non-hemorrhagic lesions such as DAI and the secondary effects of trauma such as ischemic injury.92,97 Plain radiographs of the skull have limited utility. They will reveal evidence of fracture but do not provide sufficient intracranial detail to direct further management. CT and MR-angiography play little role in the management of blunt TBI but can be used to evaluate vascular injury in penetrating trauma.92
Imaging of the cervical spine should be obtained in all patients with severe TBI. Plain films historically have been used for this purpose, but CT should be considered given the critical nature of the victim's injury, the efficiency (the patient will already be in the CT scanner), and the recent literature showing the superiority of CT over plain radiographs to detect bony injury.77,98-101 Neither CT nor plain radiographs of the cervical spine identify soft-tissue injuries adequately to clear the cervical spine in the acute phase of injury. In the absence of a fracture, cervical spine precautions should be maintained until the patient is cleared by established protocol. Imaging of the chest, abdomen, and extremities often will be required in patients with severe TBI and should be considered.
CT Findings. Acute blood appears as high-attenuation. Traumatic intracranial hemorrhages are categorized as epidural hematomas (EDH), intraparenchymal hemorrhages, subarachnoid hemorrhages (SAH), and subdural hematomas (SDH). (See Figure 2.) An EDH is a collection of blood between the dura mater and the skull. It is primarily a condition of the young and accounts for 0.5-1% of all TBI patients.102 EDHs are less frequent in the very young (< 2 years) and in the elderly because of the close attachment of the dura to the skull.12 EDH classically occurs from a direct blow to the head (e.g. assault, fall on object, or motor vehicle collision) resulting in skull fracture and rupture of the middle meningeal artery. As such, EDHs in the temporal or lateral frontopareital region should be considered arterial and immediately life-threatening.6 Epidural blood also can be from venous or fracture bleeding.6 EDHs are classically lenticular in shape, smooth, and may cross the midline.6 They are associated with a lucid interval, but this occurs less than 50% of the time.6,103 The underlying brain parenchyma tends to be minimally interrupted, and the lesions are amenable to rapid surgical repair.104 EDHs greater than 30 cm3 in volume should be evacuated surgically regardless of the patient's GCS score.105
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An intraparenchymal hemorrhage is an accumulation of blood within the brain parenchyma or the surrounding meningeal spaces. Acute cerebral contusions appear as focal areas of high attenuation with scattered foci of low attenuation (uninjured tissue).6 The most common locations are the temporal lobes and the base of the frontal lobes because of contact with adjacent bony surfaces. Edema tends to develop gradually, which results in increased mass effect and subsequent delayed deterioration and/or death.6 Lesions in the temporal lobes are constrained by the bone of the middle cranial fossa, which focuses expansion toward the brainstem, increasing the risk of rapid herniation.6,106
Traumatic SAH commonly appears over the convexities, within the sylvian fissure, or in the basal cisterns. The blood is contained between the pia mater and arachnoid. The accumulation of blood in the subarachnoid space leads to elevated ICP and decreased cerebral perfusion. The quantity of subarachnoid blood is of prognostic significance, but it is unclear if this is a result of the blood itself or because the quantity of blood is a marker of parenchymal injury.107,108
An SDH lies beneath the dura mater. SDHs are distributed over the cortex, causing their appearance as a crescent shape with an irregular border. SDHs often extend beyond suture lines. They can arise from parenchymal bleeding and can be arterial, venous, or from rupture of the bridging cortical veins. They typically arise from acceleration-deceleration injuries and frequently are associated with underlying paranchymal injuries, which remarkably impact their outcome.6,12 The midline shift can be larger than the hematoma itself, suggesting underlying brain injury.109 Brain injury can also result as the hematoma creates direct pressure on adjacent tissue. SDHs are much more common than EDHs and occur in 12-29% of patients with severe TBI.110 Because of the associated brain injury, the delay in clinical signs, and the advanced age of the afflicted population, the mortality is much higher than with EDH. Guidelines recommend that acute SDHs with either a thickness greater than 10 mm or a midline shift greater than 5 mm be evacuated surgically regardless of the patient's GCS score.110
DAI is a result of shearing or rotational forces that occur when the head is accelerated and decelerated rapidly.77 The subsequent stretching of axons at the gray-white junction of the cerebral cortex results in their widespread and often spontaneous and irreversible damage.111 The physical disruption of the cytoskeleton precipitates a sequence of events that finally results in cell death.112,113 Shear injury can be difficult to detect by CT scan but may appear as widely distributed punctate areas of high attenuation in the white and deep nuclear matter. Cerebral edema appears as local or global loss of gray-white differentiation.6
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This is the first of a two-part series on severe traumatic brain injury, focusing on the evidence for optimal care.Subscribe Now for Access
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