This clinical review feature article is presented in conjunction with the Department of Emergency Medicine Education at the University of Texas Southwestern Medical Center, Dallas.
>> Discuss the incidence and significance of severe traumatic brain injury (TBI).
>> Describe national guidelines for the management of severe TBI.
>> Identify current evidenced-based management for airway and breathing control for
patients with severe TBI.
>> Identify current evidenced-based assessment and management for circulatory and neurological issues in the patient with severe TBI.
>> Discuss the best transport/destination practices for patients with TBI.
Alpha-adrenergic agonist: Any agent that stimulates the alpha receptors of the sympathetic nervous system (fight-or-flight response), causing vasoconstriction and an increase in blood pressure.
Cerebral herniation: A condition in which the brain is squeezed or pushed through the opening at the base of the skull (foramen magnum) due to high pressure from trauma or illness.
Cerebral perfusion pressure (CPP): The blood pressure available to perfuse the brain. This pressure has a narrow range—too little and the brain becomes ischemic. Pressure that is too high leads to vascular congestion and cerebral edema.
CT scan: A computerized topography scan, sometimes referred to as a CAT scan, which allows for a cross-sectional image of the tissue being examined.
Esmolol: A very short-acting beta blocker. Beta blockers will block effects of the sympathetic nervous system, thus reducing heart rate and blood pressure.
Fentanyl: A synthetic narcotic approximately 100 times stronger than morphine, used for pain control (analgesia) as well as its sedative (anesthesia) properties.
Hyperosmolar: Describes a fluid with a high osmolarity or containing a high concentration of solutes in a solution. A hyperosmolar drug, such as mannitol, will cause increased water excretion by the kidneys, resulting in decreased extracellular fluid and draws fluid from the extracellular space into the intravascular space.
Ketamine: A drug that will induce rapid anesthesia.
Lidocaine: A drug used primarily for its cardiac anti-arrhythmic properties; used during rapid sequence intubation (RSI) and believed to help blunt the potential increase in intracranial pressure.
Mannitol: An osmotic diuretic traditionally thought to transiently help reduce intracranial pressure.
Mean arterial pressure (MAP): A term used to describe mean arterial pressure during a cardiac cycle. If MAP is too low, then tissue will become ischemic.
Methylprednisolone: A glucocorticosteroid used for its anti-inflammatory effects.
Oxygen-dissociation curve: A plotted graph that represents how readily hemoglobin in the red blood cells will hold onto oxygen or release it into the surrounding tissues.
Pathophysiology: The study of normal body functions and changes that occur as a result of disease or trauma.
Perfusion pressure: The gradient between arterial and venous pressure.
pH: The power or potential of hydrogen or a measure of acidity or base. The normal laboratory pH range for the human body is 7.35–7.45.
Phenylephrine: A powerful vasoconstrictor (alpha-adrenergic agonist) administered IV piggyback.
Rapid sequence intubation (RSI): The process of sedating, chemically paralyzing and intubating a patient.
Sympathetic tone: Vascular tone as a result of stimulation of the sympathetic nervous system.
Traumatic brain injury (TBI): Brain injury as a result of blunt or penetrating trauma or force. Brain function can be temporarily or permanently impaired.
The images of Olympic athlete Nodar Kumaritasvili flying off his luge and contacting a fixed steel beam at the recent Winter Olympics in Vancouver, British Columbia, were shocking. But the resultant injuries and death of the young athlete were not surprising to EMS personnel who witnessed the incident, because training and experience with similar mechanisms of injury intuitively teach us that these types of patients are susceptible to traumatic brain injury (TBI).
Worldwide, TBI is the leading injury cause of death and permanent disability. In the U.S. alone, 1.4 million cases of TBI present to emergency services every year. Many more cases go unreported and untreated. These TBIs lead to 235,000 hospitalizations and, ultimately, 50,000 deaths. For instance, blunt trauma alone kills 1% of those affected, but when a TBI is also involved, the mortality rate increases to 30%. Some 50% of those who die from TBI do so within the first two hours of injury, making emergent prehospital intervention critical. Preventing secondary injury by proper prehospital management can save brain function and lives.
Traumatic brain injuries affect all patient populations regardless of race, gender or age. However, certain populations are at increased risk of receiving a TBI. This includes children younger than five, teens and adults between 15 and 24, and geriatrics aged 70 and older.
The most common causes of TBIs in the U.S., in order of prevalence, are falls, motor vehicle collisions and struck by/against events. Most of these events can be prevented with education and safety equipment.
Unfortunately, the outcome of severe TBI is poor despite maximal treatment. However, as EMS providers, we can maximize the likelihood of good outcomes with simple interventions and by following the ABCs. Existing national guidelines for the management of severe TBI are based on the best currently available evidence-based medicine. To develop these guidelines, the Brain Trauma Foundation has pursued a multidisciplinary approach.
In addition, a consensus panel, organized by the Brain Trauma Foundation, authored guidelines for the prehospital management of TBI with the goal of improving overall survival and neurological outcome in severe TBIs. The recommendations herein refer to the care of severe adult TBIs—defined by a Glasgow Coma Scale (GCS) score of < 9—and may not represent the best treatment for pediatric TBI, which is beyond the scope of this article.
As with all trauma, C-spine precautions must be immediately implemented and continued throughout resuscitation. Although true C-spine injury resulting in an unstable spine is unlikely, the effects of improper management can be problematic.
Intubation is considered an essential skill for most prehospital providers, and with the implementation of rapid sequence intubation (RSI), many providers feel confident in promptly securing difficult-to-manage airways during trauma calls. However, current guidelines suggest that only a subset of the TBI population may benefit from prehospital intubation. The indications for intubation generally include:
- Hypoxia that isn’t corrected by supplemental oxygen;
- GCS < 9 (severe TBI); or
- Inability to maintain an adequate airway.
Isolated, severe TBI patients (GCS < 9), as well as severe TBI patients with other trauma, overall, have an improved outcome with prehospital intubation. However, research has shown that spontaneously breathing TBI patients with a pulse oximetry reading (SpO) of > 90% on supplemental oxygen who are transported by ground within an urban environment (transport time < 10 minutes) and intubated by RSI in the field have experienced equivocal or even worse patient outcomes. Therefore, RSI is currently not recommended in the population meeting these criteria.
RSI has become a standard of care in many prehospital arenas throughout the U.S. In severe TBI, the pre-medication of patients with such agents as lidocaine, fentanyl or esmolol hasn’t demonstrably reduced morbidity or mortality. These agents were once thought to blunt the effects of RSI on transiently increasing intracranial pressure (ICP). At this time, there’s insufficient evidence to advocate for or against their field use in a pre-medication capacity. In addition, there are no set guidelines on the selection of sedatives and paralytics for RSI. In general, avoid agents known to increase intracranial pressure, such as ketamine, although this is currently being challenged as well.
Local protocols should be carefully followed when implementing RSI or intubation alone, including accurate endotracheal (ET) tube placement confirmation. Guidelines recommend the use of both auscultation and EtCO monitoring to confirm tube placement. One study evaluating the ability of emergency medicine physicians in the prehospital setting to differentiate esophageal intubation from endotracheal intubation found that 50% of esophageal intubations were recognized on auscultation alone, but 100% were recognized when capnography was used in conjunction with auscultation. In addition, pulse oximetry, direct visualization and condensation in the ET tube are important indicators of proper tube placement.
A single episode of hypoxia, defined as SpO < 90% at any time, has been shown in numerous studies to increase death and disability in severe TBI. Further, the hypoxic episode doesn’t need to be sustained; one discrete reading can affect outcome.
One study showed 27% of TBI patients had at least one hypoxic episode prior to emergency department (ED) admission. Another study reported that 55% of helicopter-transported patients had an SpO < 90% at the scene prior to intubation. Therefore, one of the goals in managing TBI patients should be to attempt to prevent these hypoxic episodes to maximize patient survival and neurological outcome.
Current recommendations state that 100% supplemental oxygen via non-rebreather mask, bag-valve-mask or advanced airway should be provided immediately to any TBI patient. Continuous pulse oximetry and end-tidal CO (capnometry) monitoring should occur with all severe TBI patients.
First responders and BLS crews on scene prior to ALS arrival should carefully monitor airway seal and chest rise until capnometry can be placed. It’s imperative to avoid hypoxia or hypoventilation and rapidly correct them if present.
Although hypoxia and hypoventilation have proven detrimental to patient outcomes, the role of hyperventilation has long been thought to be beneficial in reducing intracranial pressure through cerebral vasoconstriction. Recent literature shows hyperventilation is instead detrimental to severe TBI patient outcomes in most instances.
Hyperventilation causes cerebral vasoconstriction, thereby transiently decreasing intracranial pressure (ICP). But it also decreases much needed blood flow to the already swollen brain, causing fewer nutrients and less oxygen to get to the brain cells. In addition, hyperventilation causes more carbon dioxide to be blown off, which increases the serum pH. This increased pH (alkalinity) shifts the oxygen-dissociation curve left, making oxygen dissociation from the hemoglobin more difficult and further reducing the amount of oxygen available to the brain.
Even if the pathophysiology doesn’t make sense to the individual provider, the important message is that hyperventilation is bad, except in the event of cerebral herniation, which we’ll discuss later.
Also, capnometry is imperative in severe TBI patients to ensure eucapnea, which is defined as maintaining CO levels in a normal state (35–40 mmHg). Even placing the patient on a ventilator doesn’t ensure proper eucapnea; therefore, the use of EtCO is a must.
For adults, the goals of ventilation include keeping an SpO greater than 95% and maintaining eucapnea with an end-tidal carbon dioxide (EtCO) of 35–40mmHg. In general, to obtain these parameters, ventilation is recommended at a rate of 10 breaths per minute with a tidal volume of 6–7 cc/kg delivered over one second each. Adjust each based on SpO and EtCO.
The role of transient hyperventilation in cerebral herniation is to bridge to more effective therapy for decreasing ICP. Prehospital signs of cerebral herniation include extensor (decerebrate) posturing, flaccid response (a 1 in the motor category of the GCS), dilated and non-reactive pupils, asymmetric pupils or a decrease in the GCS of greater than 2 from the prior best score (in patients with an initial GCS < 9).
If any one of these signs is present, ensure normo-ventilation, proper oxygenation and normo-tension. If these goals are met and the patient has continued signs of herniation, start transient hyperventilation until clinical signs of cerebral herniation have resolved or more definitive care is provided. The goal EtCO for transient hyperventilation is 30–35 mmHg. The starting ventilation rate to achieve this goal is typically 20 breaths per minute with a tidal volume of 6–7 cc/kg delivered over one second.
Along with hypoxia, hypotension is another major contributor to increased morbidity and mortality in severe TBI. Hypotension, defined as a systolic blood pressure (SBP) less than 90 mmHg, doubles mortality in severe TBI. Much like hypoxia, it doesn’t require a protracted duration for secondary insult to occur. Even during interfacility transport of severe TBI patients, the prehospital provider must be aware of prevention and rapid correction of hypotension.
Mean arterial pressure (MAP), calculated as SBP plus two times the diastolic blood pressure, all divided by three, represents the perfusion pressure seen by the organs. In general, a MAP of greater than 65 is necessary to avoid ischemia. This important indicator of true end-organ perfusion should also be monitored in severe TBI patients, as it may not necessarily correlate with the SBP alone.
For instance, a patient may have an SBP of 100, but the MAP may be 50, signifying an emergent need for resuscitation to prevent organ damage.
Cerebral perfusion pressure (CPP), the indicator of blood flow to the brain, is MAP minus ICP. As ICP increases due to a traumatic brain injury, MAP becomes critical to maintain CPP and brain blood flow.
Fluid resuscitation should be promptly incorporated into the prehospital care of severe TBI patients as indicated. Crystalloid, isotonic, dextrose-free solutions (0.9% normal saline or lactated ringers) should be administered with a two-liter initial bolus.
Hypertonic saline (2% or 3%) is a current treatment option for fluid resuscitation in adult severe TBI. Multiple small studies have previously reported a survival benefit, although the recent National Heart, Lung and Blood Institute study of concentrated saline for patients with traumatic brain injury didn’t show any 28-day survival benefit. This study, the largest of its kind, was terminated in March 2009 after enrollment of 1,000 patients failed to show a statistically significant difference in outcome compared to normal saline volume resuscitation.
Initial fluid resuscitation studies presented concern about increased intracranial bleeding; however, this wasn’t shown in any of the subsequent studies. Further, the Heart, Lung, and Blood Institute study didn’t show earlier death at six-month follow-up in the hypertonic saline group as compared to normal saline. The full results of this follow-up aren’t currently published, however, it’s currently felt that hypertonic saline and normal saline are equivocal. Using standard normal saline is probably the best management step at this point.
After either of the above initial fluid resuscitation approaches, packed red blood cells should be administered subsequently for continued fluid resuscitation. If not immediately available in the prehospital setting, continued resuscitation with crystalloid solutions is appropriate en route to definitive care.
If the patient is hypotensive, seek out extracranial injuries, because an adult can’t bleed enough into the brain to cause hemorrhagic shock. Strong considerations of alternative locations of hemorrhage, such as femoral fractures, pelvic fracture and thoraco-abdominal internal hemorrhage, must be considered. In addition, always consider non-traumatic causes of hypotension during the evaluation.
Hyperosmolar therapy in the form of mannitol has no current evidence-based support for its use in the prehospital setting for brain-targeted therapy. In addition, hypertonic saline is not recommended in the prehospital arena as brain-targeted therapy. Note that this use of hypertonic saline is different from the role of hypertonic saline as an initial fluid resuscitation agent discussed earlier. The in-hospital role of these agents in reducing ICP is currently being evaluated.
Although not part of the current guidelines, neurogenic shock is a rare entity that presents with both bradycardia and hypotension with spinal trauma. One would expect instead to observe tachycardia with shock. These patients may require an alpha-adrenergic agonist, such as phenylephrine, to cause peripheral vasoconstriction due to loss of sympathetic tone with the spinal cord injury. Volume resuscitation must be concurrently administered. Be aware, however, that the elderly may present with bradycardia with shock due to beta-blockers and other cardiac medications preventing a tachycardic response to volume loss. These patients would not benefit from pharmacologic treatment of pseudo-neurogenic shock and most likely would be harmed from it.
GCS has been validated by numerous studies to correlate to outcomes in TBI patients. The role of GCS in the prehospital setting is to communicate patient condition to the receiving hospital as well as to screen for cerebral herniation in severe TBI patients, mandating a thorough understanding of this important prognostic indicator.
GCS should be evaluated after the ABCs are secured; although, if a second provider is available, and obtaining a GCS doesn’t affect the completion of the ABCs, the GCS may be performed in conjunction with the ABCs. The GCS should be performed either prior to sedation and paralysis or after the medications are metabolized.
Pupillary response is also noted to be an important prognostic indicator in trauma, especially severe TBI. First, consider any evidence of orbital trauma, since this could affect the pupillary response without being an indicator of actual intracranial injury. Asymmetry, or anisocoria, is defined as > 1 mm difference in pupil diameter.
This finding has a positive predictive value of only 30% in studies, meaning that a single measurement isn’t adequate in identifying or localizing an intracranial lesion. Rather, serial evaluation is required to watch for change, much like blood pressure readings. That stated, pupillary asymmetry is rarely seen in TBI patients unless the ICP is greater than 20 mmHg (the upper limit of normal). Less than 1% of the population has pupillary asymmetry of greater than one-half millimeter.
Pupils must also be evaluated for response to bright light. Fixed pupils are defined as less than one millimeter of constriction in response to bright light. Fixed and dilated pupils are a poor prognostic indicator and may indicate cerebral herniation, as discussed earlier.
Blood glucose, or dextrose, levels should be evaluated in all TBI patients. Dextrose, in the form of IV dextrose (D50W in adults), should be administered only if clinically indicated (blood glucose < 70 mg/dL). Administration of glucose to patients with normal or elevated blood glucose levels can be detrimental. In addition, consideration of other causes of altered mental state, such as narcotic overdose, must be considered.
Steroids, such as methylprednisolone, were once thought to be potentially beneficial to TBI patients. However, these steroids have been proven in studies to increase mortality in this population without any improvement in lowering ICP. Steroids should not be administered for treatment of severe TBIs.
(E)xposure & Transport
All severe TBI patients have disruption of their ability to cope with environmental factors. The patient should be fully exposed to evaluate for extracranial injuries, but the prehospital provider must also prevent heat loss.
In addition, the importance of a secondary survey with any additional appropriate interventions cannot be stressed enough. Keep in mind, however, that prompt and emergent transport of these patients is imperative to their survival and neurological outcomes.
All EMS regions need an organized trauma care system. This has been proven to save lives and function of all trauma patients. Severe TBI destination decision protocols should be in place well before any incidents. Severe TBI patients require transport directly to a facility with immediate CT scan availability, prompt neurosurgical care, the ability to monitor intracranial pressure, and the ability to treat intracranial hypertension.
The appropriate provider level for prehospital care of the severe TBI patient is not known through evidence-based research at this time. However, the mode of transport should be such to minimize total prehospital time to an appropriate facility.
The importance of rapid transport to an appropriate facility has been demonstrated by one study, which showed a significant increase in mortality of severe acute subdural hematomas based on time to surgical intervention. These transport decisions include consideration of traffic, road conditions, aeromedical availability and local resources.
One study showed a 9% reduction in mortality for TBI patients transported by helicopter versus ground. Of note, the helicopter was staffed with a physician and nurse, where ground transport was with paramedics. The effect of these different service levels on outcome is unclear.
Another study also noted better odds (odds ratio of 1.90, 95% CI: 1.6–2.25) of survival with helicopter transport after controlling for numerous potential confounders.
The severe traumatic brain injured patient has a poor prognosis starting immediately with the incident; however, as EMS providers with a thorough understanding of the acute critical care of these patients, we can maximize their survival and neurological outcomes.
Typically, one-half of severe TBI patients die within two hours of the injury. With maximal therapy, including close attention to airway, breathing with pulse oximetry and end-tidal capnography, circulation, disability and exposure, we can save lives. After all, it all comes down to our ABCs. JEMS
- 1. National Center for Injury Prevention and Control. Facts about traumatic brain injury. www.cdc.gov/ncipc/tbi/TBI.htm
- 2. Novack T. TBI inform: Introduction to brain injury fact and stats. http://main.uab.edu/tbi/show.asp?durki=27492&site=2988&return=57898
- 3. National Association of State EMS Officials, National Association of EMS Educators & National Association of EMTs. Guidelines for the prehospital management of traumatic brain injury, 2nd edition. Prehosp Emerg Care. 2008;12 Suppl 1:S1–S52.
- 4. NICHCY disability fact sheet: Traumatic brain injury. www.nichcy.org/pubs/factshe/fs18.pdf
- 5. Brain Trauma Foundation, American Association of Neurological Surgeons/College of Neurological Surgeons, Joint Section on Neurotrauma and Critical Care: Guidelines for the management of severe traumatic brain injury, 3rd edition. J Neurotrauma. 2007;24 Suppl 1:S1–S95.
- 6. Winchell RJ, Hoyt DB. Endotracheal intubation in the field improves survival in patients with severe head injury. Arch Surg. 1997;132:592–597.
- 7. Jagoda A. Increased intracranial pressure. In Walls R, Luten RC, Murphy MF, et al (Eds). Manual of emergency airway management, second edition. Lippincott Wiliams and Wilkins: Philadelphia, 2004.
- 8. Silvay G. Ketamine. Mt Siani J Med, 1983;50:300–304.
- 9. Knuth T, Letart PB, Ling G, et al. Guidelines for the field management of combat-related head trauma. Treatment: Pain management and the use of analgesics for sedation. Brain Trauma Foundation, 2005.
- 10. Schmittner MD, Vajkoczy SL, Horn P, et al. Effects of fentanyl and S(+)-ketamine on cerebral hemodynamics, gastrointestinal motility, and need of vasopressors in patients with intracranial pathologies: A pilot study. J Neurosurg Anesthesiol. 2007;19:257–62.
- 11. Bourgoin A, Albanese J, Wereszczynski N. Effects of sufentanil or ketamine administered in target-controlled infusion on the cerebral hemodynamics of severely brain-injured patients. Crit Care Med. 2005;33:1109–13.
- 12. Bourgoin A, Albanese J, Wereszczynski, et al. Safety of sedation with ketamine in severe head injury patients: Comparison with sufentanil. Crit Care Med. 2003;31:711–717.
- 13. Albanese J, Arnaud S, Rey M. Ketamine decreases intracranial pressure and electroencephalographic activity in traumatic brain injury patients during propofol sedation. Anesthesiology. 1997;87:1328–34.
- 14. Grmec S, Mally S. Prehospital determination of tracheal tube placement in severe head injury. Emerg Med. 2004;21:518–520.
- 15. Davis DP, Dunford JV, Poste JC, et al. The impact of hypoxia and hyperventilation on outcome after paramedic rapid sequence intubation of severely head-injured patients. J Trauma. 2004;57:1–10.
- 16. Davis DP, Dunford JV, Ochs M, et al. The use of quantitative end-tidal capnometry to avoid inadvertent severe hyperventilation in patients with head injury after paramedic rapid sequence intubation. J Trauma. 2004;56:808–814.
- 17. Helm M, Schuster R, Hauke J, et al. Tight control of prehospital ventilation by capnography in major trauma victims. Br J Anaesth. 2003;90:327–332.
- 18. 2005 American Heart Association. CPR/ECC Guidelines.
- 19. Dunn LT. Secondary insults during the interhospital transfer of head-injured patients: an audit of transfers in the Mersey Region. Injury. 1997;28:427–431.
- 20. Chestnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determining outcome from severe brain injury. J Trauma. 1993;34;216–222.
- 21. Rose J, Valtonen S, Jennett B. Avoidable factors contributing to death after head injury. Br. Med J. 1977; 2:615–618.
- 22. Marmarou A, Anderson RL, Ward JD, et al. Impact of ICP instability and hypotension on outcome in patients with severe head trauma. J Neurosurg. 1991;75:S159–166.
- 23. National Heart, Lung and Blood Institute. Concentrated saline for patients with traumatic brain injury. https://roc.uwctc.org/tiki/tiki-index.php
- 24. Taylor W, et al. Quantitative pupillometry, a new technology: Normative data and preliminary observations in patients with acute head injury. J Neurosurg. 2006;98:205–221.
- 25. Meyer B. Incidence of anisocoria and difference in size of palpebral fissures in five hundred normal subjects. Arch Neurol Psychiatry. 1947;57:464–470.
- 26. Gabriel EJ, et al. Guidelines for pre-hospital management of TBI. New York: Brain Trauma Foundation, 2000.
- 27. Seelig JM, Becker DP, Miller JD, et al. Traumatic acute subdural hematoma. Major mortality reduction in comatose patients treated within four hours. N Engl J Med. 1981;304:1511–1518.
- 28. Baxt ED, Moody P. The impact of advanced prehospital emergency care on the mortality of severely brain-injured patients. J Trauma. 1987;27:365–369.
This article originally appeared in April 2010 JEMS as “The ABCs of TBI: Evidence-based guidelines for adult traumatic brain injury care.”