A 66-year-old man with a past medical history of atrial fibrillation on Warfarin is found down at home with a scalp laceration. The patient is conscious and alert but refuses to go to the hospital. Two hours later, emergency medical services (EMS) is called for worsening headache and nausea.

On initial evaluation, his heart rate is 126/min, blood pressure 97/64 mmHg, respiratory rate 18/min, SpO2 93%, and temperature 99°F (37.2°C). His Glasgow Coma Scale (GCS) score is 11 (Eyes 2, Verbal 4, Motor 5). His pupils are equal, round and reactive to light. EMS personnel place the patient in a cervical collar and begin transport to a Level 1 trauma center. Paramedics establish an intravenous line and provide supplemental oxygen via a non-rebreather mask. En route, the patient’s GCS score declines to 7 (Eye 2, Verbal 2, Motor 3). The paramedic crew notes the right pupil is now dilated. They perform rapid sequence intubation (RSI) using etomidate and succinylcholine, and they initiate manual ventilation with 100% oxygen delivered at 12 breaths per minute.

Upon trauma center arrival, the attending trauma surgeon and emergency physician perform an initial evaluation and order a computed tomography (CT) scan of the head and cervical spine. The CT scan shows a large epidural hematoma (EDH), likely caused by rupture of the right middle meningeal artery from a temporal bone fracture. The trauma team administers vitamin K and prothrombin complex concentrate (PCC) to reverse the blood thinning effects of Warfarin. Neurosurgeons decide to bring the patient to the operating room to perform emergency surgical decompression by a right craniotomy. After surgery, the patient is admitted to the intensive care unit (ICU) for further management.

What is a Traumatic Brain Injury?

Traumatic brain injury (TBI) is a disruption of normal brain function as the result of an acute blunt or penetrating head injury. The incidence of TBI continues to climb in the U.S. despite advances in medical science and motor vehicle safety, totaling nearly 2.8 million cases per year.1 A major contributor to this change is the aging U.S. population and the increasing use of blood thinning medications.2 Total TBI costs in the U.S. in 2010 were estimated to be $76.5 billion.3

In patients with severe TBI, the initial head trauma has already caused some amount of irreversible brain cell death – as well as additional, potentially reversible – damage to other neurons. While dead brain cells cannot be revived, some injured cells may be salvaged. Medical intervention in severe TBI aims to prevent post-traumatic loss of damaged neurons, referred to as secondary brain injury. Any clinically significant long-term functional deficits due to the initial trauma are potentially compounded by deficits associated with secondary brain injury. It is worth noting that mild TBI may not result in a clinically significant amount of neural death.

Secondary brain injury most commonly results from hypoxemia and hypotension. Injured brain cells need oxygen to survive and recover. TBI patients are prone to airway compromise, which impacts the amount of oxygen delivered to the lungs and brain. Secondly, polytrauma patients with TBI often have hypotension due to additional hemorrhage outside the cranium, which further impairs the delivery of oxygen rich blood to the injured brain. It is important to note that hypovolemic hypotension should not occur in TBI patients unless they have an additional source of hemorrhage that is outside the cranium.

For years, consensus guidelines advocated three key principles in prehospital TBI care: 1) avoid hypotension, 2) avoid hypoxia, and 3) avoid hyperventilation. The recent Excellence in Prehospital Injury Care (EPIC) study provides some of the first scientific evidence to support these practices.4 This Arizona statewide effort involved implementing a TBI treatment algorithm emphasizing avoidance of hypotension, hypoxia and hyperventilation, augmented by specific monitoring strategies. This strategy resulted in three-fold improved survival in the most critically injured TBI patients.4 It is also important to note, however, that precise management strategies for each individual component of care were not exclusively assessed in this study and that the improvements in survival for TBI patients were primarily predicated on the statewide implementation of a prehospital guideline for TBI care emphasizing avoidance of hypotension, hypoxia and hyperventilation.

What Are Principles of Good Prehospital TBI Care?

In patients with TBI, the primary goals of EMS personnel are to manage immediately life-threatening injuries and to minimize secondary brain injury. In keeping with Advanced Trauma Life Support principles, airway, breathing and circulation are the immediate management priorities.5 Importantly, care should be taken to avoid hypotension, hypoxia, and hyperventilation, as suggested by the EPIC study.

Obtain a Thorough History

A thorough history and physical exam is essential and will help guide hospital management of TBI patients. Of particular importance, especially in geriatric patients, is to determine the history of anticoagulant medication use, which is widespread and can cause severe, life-threatening hemorrhage in trauma patients. Potential reasons for the use of anticoagulants include a history of atrial fibrillation, an artificial heart valve, deep vein thrombosis, pulmonary embolism or severe coronary artery disease.

The most common anticoagulants that EMS providers should know and ask about specifically are included in Table 1, below. Without a proper history from EMS, hospital providers may not know which blood thinner the patient takes which can complicate patient management and potentially increase risk of exsanguination.

Table 1: Generic and brand names of commonly prescribed anticoagulant drugs

Commonly Prescribed Anticoagulants

Generic Name Brand Name
Warfarin Coumadin
Dabigatran Pradaxa
Rivaroxaban Xarelto
Apixaban Eliquis

Manage Oxygenation and Ventilation

A single hypoxic event (SaO2 < 90%) is associated with doubling of the risk of mortality in TBI patients.4 High-flow supplemental oxygen should be provided as needed to maintain SaO2 above 90%.6 If the patient becomes hypoxic (SaO2 < 90%), starts hypoventilating, vomiting, or exhibiting snoring respirations, escalate to bag-valve-mask ventilation, endotracheal intubation or supraglottic airway insertion. Blood oxygen saturation should be monitored continuously. Ventilation should be provided at normal rates (12-16 breaths/min). Hyperventilation is generally not recommended as first line therapy for TBI treatment because it causes cerebral vasoconstriction that results in brain hypoperfusion and secondary brain injury. However, in the persistently hypoxic patient or with signs of impending brain herniation, brief episodes of hyperventilation may be necessary.

Endotracheal intubation may be helpful for controlling oxygen saturation and ventilation. However, many TBI patients are combative or have intact protective airway reflexes, and therefore rapid sequence intubation (RSI) may be necessary to accomplish intubation. In addition to removing protective airway reflexes, RSI may prevent abrupt changes in oxygen saturation, blood pressure and intracranial pressure. Pretreatment for RSI is controversial and may worsen hypotension; if necessary to reduce reflexive response to laryngoscopy, give fentanyl 3 mcg/kg IV over 30 to 60 seconds.7 Use of lidocaine and/or beta blockers (i.e. esmolol) is no longer recommended for pretreatment.

Etomidate (0.3 mg/kg IV push) is recommended for induction because of its minimal effect on blood pressure and intracranial pressure. Ketamine is usually discouraged for RSI because it theoretically raises intracranial pressure.8 However, the effect of ketamine induction upon TBI outcomes remains unknown. Propofol and benzodiazepines can cause hypotension and thus are less favored for RSI in TBI. Succinylcholine (1.5 mg/kg IV) and rocuronium (1-1.2 mg/kg IV) are commonly used for neuromuscular blockade because of their rapid onset.

Supraglottic airways (SGA), such as the King Laryngeal Tube, laryngeal mask airway and i-gel are increasing popular in the prehospital setting for advanced airway management. However, the benefit and harms of prehospital SGA in the setting of TBI are unknown. In the setting of intubation difficult, SGAs may provide an important alternative. However, their effect on intracranial pressure is unknown.

Avoid Hypotension

A single episode of hypotension (SBP < 90 mmHg) is also associated with doubling mortality in TBI patients.4 It is equally important to monitor blood pressure frequently (every three minutes) in the immediate post-injury period. Peripheral intravenous access or (if unable to achieve IV) intraosseous access should be acquired as soon as possible. Hypotension or downward trending SBP should be aggressively managed with intravenous fluids; isotonic fluids such as normal saline, lactated ringers, PlasmaLyte or Isolyte should be used. If there is evidence of concurrent hemorrhage, blood products (red blood cells, plasma, platelets or whole blood) may be indicate. Hypertensive TBI patients should not be fluid resuscitated. Additionally, prehospital fluid therapy with solutions that disrupt normal plasma osmolarity (i.e. 5% dextrose in water, hypertonic/hypotonic saline) is not recommended. The Resuscitation Outcomes Consortium Hypertonic Saline trial found no difference in outcomes when hypertonic saline was used to treat severe TBI.9

Other Prehospital Care

Severe bleeding and/or edema within the cranium can result in a dangerously elevated intracranial pressure which can cause the brain to herniate through the foramen magnum, the large opening at the base of the skull. Cerebral herniation can compress the brain stem (the part of the central nervous system controlling respirations and heartbeat), resulting in death. Signs of cerebral herniation include asymmetric, dilated and unreactive pupils; flexor or extensor posturing on motor exam; and a rapid decline in the GCS score. GCS is an important marker of neurological status and should be assessed frequently to track any deterioration over time, though not as important for prehospital management. Note that any sedatives or pain medications given prior to assessment of GCS may alter the result. Most importantly, if the GCS falls to eight or less, the patient may require endotracheal intubation in order to protect the airway and facilitate oxygenation and ventilation, regardless of current oxygen saturation. Progression of GCS decline will be of importance to determination of hospital management strategies, especially emergent neurosurgical options. Pupil size and symmetry should also be documented frequently, as changes may suggest cerebral herniation.

TBI patients should be transported directly to a facility with immediately available computed tomography (CT), prompt neurosurgical care, and an intensive care unit that specializes in the management of brain injured patients.

What Happens in the Emergency Department?

In the setting of a recognized TBI, the ED may activate the trauma team. The patient is typically evaluated on ED arrival by a trauma team consisting of a trauma surgeon, emergency medicine physician, resident physicians, nursing staff and imaging technicians. The trauma team will perform primary and head-to-toe secondary surveys to evaluate for immediately life-threatening or unrecognized injuries. Laboratory tests are obtained to identify important abnormalities such as alterations in acid/base status and coagulopathy. Evaluating for coagulopathy is especially important in older patients, since they are more likely to take blood thinning agents such as those listed in Table 1, above. The ED team may use special drugs such as plasma, vitamin K, and prothrombin complex concentrate (PCC [Kcentra]) to reverse the effect of anticoagulants. Recombinant factor Xa (Andexxa) was also recently approved by the FDA as a novel reversal agent for rivaroxaban (Xarelto) and apixaban (Eliquis).

What is the Role of Computed Tomography in TBI?

Figure 1: Patient undergoing CT scan of the head to evaluate for intracranial hemorrhage.

In order to definitively diagnose and characterize intracranial hemorrhage, cross-sectional images of the brain may be obtained by computed tomography (Figure 1). Computed tomography (CT) is an advanced imaging technique where multiple sequential cross-sectional images of the brain are obtained, allowing clinicians to visualize injuries in three dimensions. A typical head CT may encompass over 50 individual images.

Figure 2: Intracranial anatomy (simplified).
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Figure 3: Epidural hematoma (EDH). Note the convex, lens-shaped area of bleeding.
Figure 4: Subdural hematoma (SDH). Note the concave “moon-shaped” area of bleeding.
Figure 5: Subarachnoid hemorrhage (SAH). Note the blood spilling around the center of the brain.

The goal of head CT is to identify the presence or absence of bleeding in the brain. There are three common patterns of intracranial hemorrhage seen on head CT, although there are many other types that can occur. Figure 2 offers a simplified depiction of relevant intracranial anatomy. Epidural hematoma (EDH) is caused by bleeding between the inner surface of the skull and the dura mater, producing a convex, lens-shaped lesion on head CT (Figure 3). Subdural hematoma (SDH) is produced by bleeding between the dura mater and the arachnoid mater, causing a concave, crescent-shaped finding on CT imaging (Figure 4). Subarachnoid hemorrhage (SAH) is characterized by bleeding between the pia mater of the brain and the arachnoid mater, resulting in a layering hyperdensity on the surface of the brain when viewed on CT (Figure 5). SAH can either be spontaneous, commonly due to cerebral aneurysms, or traumatic.

What Happens after Admission to the Hospital?

Prehospital care for TBI patients focuses on management of ventilation, blood oxygen content and blood pressure to prevent secondary brain injury. Hospital care for TBI patients additionally focuses on management of intracranial pressure, which can also cause secondary brain injury or cerebral herniation. Intracranial hypertension can be managed surgically and/or medically, depending on the characteristics of the patient’s condition. It is also worth noting that intracranial pressure must be measured directly via placement of an intracranial pressure monitor, typically using either an external ventricular drain (EVD) or an intraparenchymal bolt.

The dangers of intracranial hypertension are more readily recognized through an understanding of the Monro-Kellie doctrine. This states that the cranium has a fixed volume and that when the volume of the contents within the skull increases (either through bleeding or cerebral edema), the pressure must also increase. Put simply, there are three things in the cranium: brain, blood and cerebrospinal fluid. If any of these things increase in volume, pressure must also increase, or corresponding volume must decrease by decreasing perfusion or amount of brain within the cranium (herniation). Elevated intracranial pressure, regardless of the source (i.e. cerebral edema, blood, mass lesion) can cause compression of the brain, secondary brain injury and cerebral herniation through the opening in the base of the skull. Thus, timely management of intracranial hypertension is paramount in the hospital setting.

Patients with certain types of brain bleeding may need emergency surgical decompression. Neurosurgeons typically evacuate EDHs larger than 30 cm3 or when the GCS is ≤8. They also typically evacuate SDHs with a thickness >10 mm or when the brain is shifted to the left or right (a “midline shift”) >5 mm or when the GCS is ≤8 with a decline of at least two points between initial prehospital assessment and hospital admission.11 The last criterion for SDH evacuation further emphasizes the importance of prehospital GCS assessment. Patients with significant SAH may need to have an external ventricular drain placed for intracranial pressure monitoring and treatment of intracranial hypertension.

What Happens in the OR?

Figure 6: Craniectomy of epidural hematoma. Note the partially clotted blood that will be removed.
Figure 7: Craniectomy of subdural hematoma. A subdural hematoma lies below the dura mater covering the brain. Photo shows dura mater flaps pulled back to reveal the underlying hematoma.

Patients with severe intracranial hypertension and low GCS from an EDH or SDH typically require immediate surgical decompression. The chosen surgical procedure depends on the type of injury. In the case of severe bleeding, craniotomy/craniectomy and evacuation is the typical approach (Figures 6, 7). Both craniotomy and craniectomy first involve skull trepanation, in which multiple burr holes are drilled into the skull. A cranial drill is then used to create a bone “flap,” a section of bone that will be removed from the skull. The size of the bone flap may range from small (6×8 cm) to large (12×15 cm), depending on the patient presentation.

Hemicraniectomy involves half, or even more, of the skull being removed to relieve intracranial hypertension. Larger bone flaps are associated with better outcomes than smaller ones.12 Removal of the bone flap allows for hematoma evacuation and definitive hemostasis. If the bone flap is immediately replaced, the procedure is termed a craniotomy. If the bone flap is not immediately replaced, the procedure is termed a craniectomy, and is meant to allow for longer term intracranial pressure reduction. Craniectomy is typically reserved for patients with more severe brain injury and intracranial hypertension, especially those for which there is concern for postoperative swelling. Bone flaps may be kept frozen under sterile conditions for future replacement once the patient recovers, a procedure referred to as cranioplasty.

Figure 8: External ventricular drain (EVD) placement after SAH; catheter is placed in ventricle (fluid-filled space) around the brain to drain cerebrospinal fluid and reduce intracranial pressure. EVD can also be used to monitor intracranial pressure.

For patients with SAH, surgeons may place an external ventricular drain, which can be used to measure intracranial pressure, remove excess fluid, and therapeutically reduce intracranial pressure (Figure 8).

What Happens in the ICU?

In the ICU, the patients will be continuously monitored by staff with the medical team maintaining patient hemodynamics (BP, cerebral blood flow), ventilation, temperature, and blood glucose levels. Additional management of TBI patients typically involves sedation, vasospasm prevention, pain control and seizure prevention.

In TBI patients with intracranial hypertension for which procedural intervention is not indicated, hyperosmolar therapy may be used to reduce intracranial pressure. This involves administering high-solute agents such as mannitol and/or hypertonic saline which increase the osmolarity of the blood, causing excess extravascular fluid in the cranium to flow into the vasculature and be removed via venous drainage, thereby reducing intracranial pressure. Hyperosmolar therapy also reduces intracranial pressure via increase of the ratio of plasma to hematocrit, thus reducing cerebral blood volume. Use of these agents can be complicated by incidence of rebound intracranial hypertension and should only be done in a situation where close monitoring can take place over an extended period of time.


EMS personnel play an important role in the care of TBI. Proper evaluation, management, and transport of care are crucial aspects of prehospital care. Prehospital care should focus on avoidance of hypoxia and hypotension and monitoring for signs of cerebral herniation. EMS must also carefully choose a receiving hospital with appropriate neurosurgical capabilities.


1. Taylor CA, Bell JM, Breiding MJ, et al. Traumatic brain injury-related emergency department visits, hospitalizations, and deaths – United States, 2007 and 2013. MMWR Surveill Summ. (2017) 66:1–16. 10.15585/mmwr.ss6609a1.

2. Centers for Disease Control and Prevention. Rates of TBI-related emergency department visits, hospitalizations, and deaths – United States, 2001-2010. Atlanta, GA: U.S. Department of Health & Human Services, 2016

3. (CDC) C for DC and P. CDC grand rounds: reducing severe traumatic brain injury in the United States. MMWR Morb Mortal Wkly Rep. 2013;62:549.

4. Spaite DW, Bobrow BJ, Keim SM, et al. Association of Statewide Implementation of the Prehospital Traumatic Brain Injury Treatment Guidelines With Patient Survival Following Traumatic Brain Injury: The Excellence in Prehospital Injury Care (EPIC) Study JAMA Surg. Published online May 08, 2019. doi:10.1001/jamasurg.2019.1152.

5. ATLS subcommittee; American College of Surgeons’ Committee on Trauma; International ATLS working group. Advanced trauma life support (ATLS®): the ninth edition. J. Trauma Acute Care Surg., 74 (2013), pp. 1363-1366.

6. Badjatia, N, Carney, N, Crocco, TJ, et al. (2008). Guidelines for prehospital management of traumatic brain injury 2nd edition. Prehospital Emergency Care, 12(SUPPL. 1).

7. Jagoda A. Emergency Airway Management in the Patient with Elevated ICP. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. (accessed on September 17, 2019).

8. Green SM, Roback MG, Kennedy RM .Clinical practice guideline for emergency department ketamine dissociative sedation: 2011 update., Ann Emerg Med. 2011;57:449–461.

9. Bulger EM, May S, Brasel KJ, et al. Out-of-Hospital Hypertonic Resuscitation Following Severe Traumatic Brain Injury: A Randomized Controlled Trial. JAMA. 2010;304(13):1455–1464. doi:10.1001/jama.2010.1405.

10. Theodore N, Hadley M, Aarabi B, et al. Prehospital Cervical Spinal Immobilization After Trauma, Neurosurgery, Volume 72, Issue suppl_3, March 2013, Pages 22–34,

11. Bullock M, Chesnut R, Ghajar J, et al. Guidelines for the Surgical Management of Traumatic Brain Injury Author Group, Neurosurgery, Volume 58, Issue 3, March 2006, Page S2–vi,

12. Jiang J-Y, Xu W, Li W-P, et al. Efficacy of standard trauma craniectomy for refractory intracranial hypertension with severe traumatic brain injury: a multicenter, prospective, randomized controlled study. J Neurotrauma 2005; 22: pp. 623-628.