Severe Traumatic Brain Injury In Adults (Trauma CME)

Severe Traumatic Brain Injury In Adults (Trauma CME)

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Table of Contents
Table of Contents
  1. Abstract
  2. Case Presentation
  3. Introduction
  4. Critical Appraisal Of The Literature
  5. Etiology And Pathophysiology
    1. Subdural Hematoma
    2. Epidural Hematoma
    3. Traumatic Subarachnoid Hemorrhage
    4. Cerebral Contusion
    5. Diffuse Axonal Injury
    6. Penetrating Injury
    7. Elevated Intracranial Pressure
    8. The Glasgow Coma Scale Score
  6. Differential Diagnosis
  7. Prehospital Care
    1. Optimizing Perfusion: Crystalloids
    2. Airway Management: Bag And Go Or Stay And Tube?
    3. Ventilatory Management
    4. Transport: To Where And By Whom?
  8. Emergency Department Evaluation
    1. Initial Stabilization
    2. Airway
      1. Pretreatment
        • Lidocaine
        • Fentanyl
        • Vecuronium, Rocuronium, And Pancuronium
        • Esmolol
      2. Sedation And Induction
      3. Paralysis
    3. Breathing
    4. Circulation
    5. Intracranial Pressure Management
  9. Diagnostic Studies
    1. Laboratory Tests
    2. Imaging
  10. Management Of Neurologic Deterioration
    1. Examination Findings Consistent With Deterioration
    2. Confounders Of The Neurologic Examination
    3. Predictors Of And Factors Associated With Deterioration
      1. Response To Deterioration
  11. Controversies And Cutting Edge
    1. Prophylactic Antiepileptic Medications
    2. Corticosteroids
    3. Progesterone
    4. Ketamine
    5. Hypothermia
    6. Antifibrinolytics: Tranexamic Acid
    7. Hyperosmolar Therapy
    8. Reversal Of Anticoagulation
  12. Disposition
  13. Summary
  14. Risk Management Pitfalls For Severe Traumatic Brain Injury
  15. Case Conclusions
  16. Clinical Pathway For Management Of Severe Traumatic Brain Injury
  17. Tables and Figures
    1. Table 1. Processes That Influence Secondary Injury
    2. Table 2. Current Brain Trauma Foundation Guidelines For Severe Traumatic Brain Injury
    3. Table 3. Glasgow Coma Scale
    4. Table 4. Targeted History
    5. Table 5. Continuous Infusion Medications For Sedation And Analgesia
    6. Table 6. Reversal Of Anticoagulation
    7. Figure 1. Subdural Hematoma On Computed Tomography
    8. Figure 2. Epidural Hematoma On Computed Tomography
    9. Figure 3. Traumatic Subarachnoid Hemorrhage On Computed Tomography
    10. Figure 4. Cerebral Contusions On Computed Tomography
    11. Figure 5. Diffuse Axonal Injury On Computed Tomography
    12. Figure 6. Targeted Physiologic Resuscitation
    13. Figure 7. Herniation Syndromes
    14. Figure 8. Spiral (Whirl) Sign In Epidural Hematoma
  18. References


Traumatic brain injury is the most common cause of death and disabilityin young people, with an annual financial burden of over $50 billion per year in the United States. Traumatic brain injury is defined by both the initial primary injury and the subsequent secondary injuries. Fundamental to emergency department management is ensuring brain perfusion, oxygenation, and preventing even brief or transient episodes of hypotension, hypoxia, and hypocapnia. Cerebral perfusion pressure is a function of intracranial pressure and systemic blood pressure, and it must be monitored and maintained. Current research is devoted towards the prevention and treatment of secondary injury. The emergency clinician must be vigilant in maintaining homeostasis while coordinating the downstream care of the patient, including the intensive care unit and/or the operating room.

Keywords: severe traumatic brain injury, TBI, craniocerebral trauma, intracranial pressure, herniation syndromes, neurologic deterioration

Case Presentation

It is 2 AM on a relatively busy shift on a Saturday night in the ED. EMS arrives with a 27-year-old male involved in a high-speed motor vehicle collision. He was not wearing a seat belt, and he was found ejected from the vehicle. Upon EMS arrival on scene, the paramedics found him unresponsive, with a GCS score of 9 (E2, V3, M4). The patient had been alone in the car, and he did not have identifying information with him. His vital signs included: blood pressure of 110/80 mm Hg, heart rate of 126 beats per minute, shallow respiratory rate of 8 breaths per minute, and oxygen saturation of 96% on room air. The paramedics attempted an oral airway, but it was aborted, because the patient exhibited a gag reflex. Bilateral nasal trumpets were placed, and a nonrebreather facemask with 100% oxygen was administered. He had deformities to his right ankle and left forearm. He smelled of alcohol. The patient was transported on a backboard with a rigid cervical spine collar to maintain immobilization. As you evaluate him on arrival to the ED, his vitals are essentially unchanged; however, you note that his GCS score is now 7 (E2, V2, M3), as he flexes his right arm to painful stimulus. IV access is established, and as you prepare to endotracheally intubate him, you recognize that this patient’s survival and ultimate neurologic outcome may depend on your initial management.

Upon successful completion of rapid sequence intubation (without hypoxia or hypotension!) of your first patient, another ambulance presents with an 84-year-old female who fell at home. Her anxious daughter informs you that she tripped on the carpet, fell backwards, and hit her head, but she did not lose consciousness. On your assessment, the patient has a GCS score of 13 (E3, V4, M6) with blood pressure of 174/92 mm Hg, irregular heart rate of 124 beats per minute, respiratory rate of 14 breaths per minute, and oxygen saturation of 100% on the nonrebreather mask placed during transport. As the patient is transferred to the stretcher, she becomes unresponsive, with a GCS score of 5 (E1, V1, M3), with flexion of both arms. You note that her right pupil is now 6 mm and minimally responsive, and her left pupil is 3 mm. You request mannitol (1 g/kg IV) and prepare to emergently intubate her. As her daughter is escorted to the waiting room with the social worker, she hands the nurse a medication list, which includes warfarin. You recall the necessary steps to stabilize and prepare the patient for the operating room, and you wonder if there is more you can provide aside from fresh frozen plasma and mannitol.


Traumatic brain injury (TBI) is one of the leading causes of death and disability in the United States. It is a common disease that emergency clinicians care for on a regular basis. TBI is a spectrum of disease, ranging from mild to severe. The military conflicts in Afghanistan and Iraq have highlighted TBI as the signature injury due to blast injuries from explosive devices. In addition, mild TBIs among high-profile athletes in professional and collegiate sports have brought increased attention to this spectrum of the disease. In the United States, 1.36 million cases of TBI are treated in emergency departments (EDs), with 275,000 patients hospitalized and 52,000 deaths each year.1

The long-range morbidity of TBI is staggering when one considers the profound and permanent neurologic disabilities and the significant financial and societal impacts. The United States Department of Defense has estimated almost 44,000 TBIs sustained during the Afghanistan and Iraq conflicts between 2003 and 2007, with an estimated $100 million in direct and purchased care and an additional $10.1 million in prescription drug costs.2 In the United States, direct medical costs and indirect costs (such as lost productivity) of TBI totaled an estimated $60 billion in 2000.3

Falls cause the greatest number of TBI-related ED visits and hospitalizations. Motor vehicle accidents are the leading cause of TBI-related mortality, which is highest in adults aged 20 to 24 years.1 The incidence of TBI is greatest in children aged 0 to 4 years, adolescents/young adults aged 15 to 24 years, and adults aged 65 years and older.1 Falls cause the majority of TBI in young children and older adults, and child abuse is the leading cause of death from TBI in children < 2 years of age.1,4

Nearly half of patients who die from TBI do so in the first 2 hours after injury, highlighting the role of the emergency clinician in the initial diagnosis and management.5 The pathophysiology of severe TBI can be viewed as a 2-step process that includes: (1) the initial primary injury, occurring at impact, which is irreversible and immediately present; and (2) the secondary injury that occurs after the initial impact, which evolves as a process. Secondary injury is potentially preventable and represents end points for goal-directed resuscitation and research. (See Table 1.)

Critical Appraisal Of The Literature

A literature search was conducted using Ovid MEDLINE® and PubMed. Search terms included craniocerebral trauma as a MeSH heading and severe traumatic brain injury as the keyword. Results were limited to English language and human publications and were further refined. Over 2500 abstracts were reviewed for inclusion. Emphasis was placed on clinical and randomized trials conducted in the prehospital, ED, and acute settings and those that reported clinical outcomes. The Cochrane Database of Systematic Reviews, National Guideline Clearinghouse (, and American College of Emergency Physicians (ACEP) clinical policies were also reviewed and queried using traumatic brain injury as the keyword. The Cochrane database yielded 36 results, 18 of which were applicable to this review. There were 63 guidelines found in the National Guideline Clearinghouse, 30 of which are applicable to the prehospital and ED management of patients with severe TBI. There are currently no ACEP clinical policies that apply to severe TBI.

Among the 30 available guidelines, the Brain Trauma Foundation (BTF) produced 27. There are currently 6 sets of BTF guidelines, 3 of which have relevance to TBI. (See Table 2.)

High-quality evidence to guide the management of severe TBI is currently lacking.6,7 Current guidelines, recommendations, and consensus statements are based on Class II (moderate-quality randomized controlled trials or good cohort- or case-controlled trials) and Class III evidence (poor-quality randomized controlled trials, moderate-quality cohort- or case-controlled studies, or case series).

Despite the lack of a single trial demonstrating an effective single therapy or medication for the treatment of severe TBI, it has been shown that compliance with protocols or guidelines that emphasize appropriate monitoring and goal-directed management of cerebral perfusion pressure (CPP) has resulted in a decrease in mortality from 50% to < 25% in the prehospital10 and inpatient settings while lowering costs and improving cost-effectiveness.11,12

Risk Management Pitfalls For Severe Traumatic Brain Injury

  1. “The patient was in a car crash and had an obvious femur fracture. I didn’t think he needed a point-of-care glucose, given the obvious trauma.”

    All patients with altered mental status must have point-of-care blood glucose testing. Hypoglycemia and hyperglycemia can cause altered mental status, and they are easily reversible with treatment. In patients with a severe TBI, hyperglycemia or hypoglycemia may worsen neurologic outcomes if it is not urgently addressed.

  2. “The patient smelled of alcohol and was obviously intoxicated.”

    Over 60% of all severe TBIs are complicated by alcohol or drug intoxication, which may worsen morbidity. Blood alcohol levels and urine toxicology screens may help prove concomitant intoxication, but based on available history and physical examination, a patient should be aggressively resuscitated for severe TBI.

  3. “I assumed her TBI took precedence and didn’t realize she also had a cervical spine fracture.”

    All patients with a severe TBI should be assumed to have a concomitant spine injury until proven otherwise, and spinal immobilization should be maintained. A patient with a severe TBI will be clinically unreliable, and the forces to generate a severe TBI should be assumed to have been transmitted to the spine.

  4. “The CT was normal, so I didn’t think she had a TBI.”

    Diffuse axonal injury often has a benign CT appearance, and it contributes significantly to the morbidity and mortality of severe TBI. Patients with diffuse axonal injury are especially susceptible to secondary injuries from hypotension and hypoxia and should be resuscitated aggressively, based on available history and the physical examination.

  5. “The patient had a GCS score of 13 when she arrived but then had a 3-minute generalized tonic-clonic seizure. Afterwards, she didn’t return to her previous baseline, so I presumed she was just postictal.”

    If a patient does not return to the previous neurologic baseline after a seizure, be concerned about nonconvulsive status epilepticus or a worsening intracerebral process. Repeat a noncontrast head CT and work quickly to arrange electroencephalograph monitoring. The patient should be aggressively treated for potential status epilepticus, and other causes for neurologic deterioration should be investigated.

  6. “The patient had a stable GCS score of 10 an hour ago, but we just discovered he has a blown pupil.”

    TBI is a dynamic process, especially in the first 24 hours. These patients should be monitored closely, and the emergency clinician should anticipate deterioration and be prepared to intervene immediately.

  7. “The patient had a GCS score of 3, and the intern performed the intubation. It went well, but the postintubation blood gas showed a PaCO2 of 20 mm Hg.”

    Care must be taken to avoid routine or prophylactic hyperventilation. Monitor the respiratory rate, especially immediately postintubation when the patient is hand-bagged. The resultant vasoconstriction from lowering the PaCO2 can decrease cerebral blood volume and CPP, worsening secondary injuries.

  8. “The patient’s blood pressure kept dropping to 80 mm Hg, and despite 4 L of normal saline, I couldn’t keep him normotensive, so I started norepinephrine.”

    Over 60% of patients with a severe TBI have other occult traumatic injuries. A hemodynamically unstable patient should initially be assumed to be in hemorrhagic shock and the source of bleeding investigated. Even a single episode of hypotension can worsen neurologic morbidity and mortality.

  9. “The patient had a GCS score of 9, and the CT didn’t look that bad, so I admitted him to our local community medical ICU.”

    Patients with a severe TBI should be managed with early collaboration with trauma surgery and neurosurgery. Special consideration should be given to managing these patients in a neurologic ICU by neurointensivists or intensivists with experience managing neurologic disorders and secondary injury after severe TBI.

  10. “I gave my patient lidocaine as an ICP pretreatment medication prior to intubation, but while I was waiting 3 minutes for it to circulate, her SpO2 kept dropping below 90% and she seemed to aspirate.”

    Prevention of hypoxia and hypotension are key in avoiding secondary injuries. Given the data on pretreatment to blunt ICP elevations prior to intubation, care should be taken to efficiently intubate the patient without hypoxia or hypotension, even at the expense of a pretreatment agent.

Tables and Figures

Table 1. Processes That Influence Secondary Injury

Table 2. Current Brain Trauma Foundation Guidelines For Severe Traumatic Brain Injury

Table 3. Glasgow Coma Scale


Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, randomized,

and blinded trial should carry more weight than a case report.

To help the reader judge the strength of each reference, pertinent information about the study will be included in bold type following the reference, where available. In addition, the most informative references cited in this paper, as determined by the authors, are noted by an asterisk (*) next to the number of the reference.

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Christopher Zammit, William A. Knight

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March 2, 2013

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