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EMS Evaluation and Treatment of Head Injuries

Editor: Evan A. Kuhl Updated: 9/3/2024 8:22:58 PM

Introduction

Traumatic brain injury (TBI) is a major global health issue, affecting approximately 69 million people annually. While most injuries are mild, severe TBI leads to approximately 2.53 million emergency department visits, hospitalizations, and deaths in the United States each year, most commonly affecting the extremes of age: children 4 years or younger and adults 75 or older.[1] The incidence of TBI is significantly higher in low- and middle-income nations, as well as in regions with housing insecurity or criminal justice system involvement, highlighting disparities in safety, healthcare infrastructure, and emergency response systems.[2][3]

A TBI occurs from a mechanical force exerting pressure on the brain or skull. TBI severity can vary from mild, manifesting as concussions, to severe, resulting in intracranial bleeding, permanent disability, and death. Mild presentations include temporary loss of consciousness and headaches. However, persistent, life-altering symptoms patients may experience include vertigo, tinnitus, memory loss, and vision changes.

Management ranges from conservative approaches, including hydration and avoidance of light, to more aggressive treatments like decompressive craniotomy.[4] Although prehospital interventions for TBI are limited, extensive evidence suggests that emergency medicine services (EMS) clinicians can help prevent secondary insults, which occur after the initial injury due to factors such as reduced brain perfusion, increased intracranial pressure, hypoxia, metabolic imbalances, and unstable body temperature.[5]

The primary EMS goals when evaluating and treating head injuries include rapidly identifying affected individuals, ensuring timely transport to appropriate medical facilities, and aggressively preventing further brain injury by closely monitoring and treating conditions such as hypoxia, hypocapnia, hypotension, and extreme body temperature changes.[6][7] Therefore, EMS plays a vital role in the early assessment and treatment of patients with TBI, making it critical to closely assess for and manage potentially reversible causes to reduce morbidity and mortality.

Issues of Concern

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Issues of Concern

The primary concern in prehospital TBI management is the prevention of secondary brain injuries. Secondary injuries after the initial insult can arise from hypoxemia, hypoperfusion, and ischemia. Cerebral perfusion pressure (CPP) is determined by intracranial pressure (ICP) and mean arterial pressure (MAP), typically represented by the equation CPP = MAP - ICP.[8] Even short hypotension and hypoxemia episodes can cause harm and synergistically worsen outcomes.[9] Prehospital care of patients with TBI should thus target optimizing brain perfusion, preventing secondary insults, and rapidly and safely transporting patients to the most appropriate facility.

Key targets for monitoring and treating individuals with TBI include early and continuous blood pressure, oxygenation, end-tidal carbon dioxide (ETCO2) monitoring, and euthermia maintenance. Specific conditions that should be closely monitored and treated include hypoxemia (oxygen saturation or SpO2 < 90%), hypotension (systolic blood pressure [SBP] < 100 mm Hg), hypertension (SBP > 150 mm Hg), hyperventilation (ETCO2 < 35 mm Hg), and hypothermia (temperature < 36 °C) or hyperthermia (temperature > 38 °C). These conditions have all been shown to worsen outcomes in patients with TBI. Prehospital providers should aggressively evaluate for and address these manifestations. In pediatric patients, blood pressure targets vary by age, with minimum SBP goals set to 70 mm Hg for neonates, 80 mm Hg for children aged 1 to 5 years, and 100 mm Hg for children 6 years and older.

Frequent reassessments are critical for patients with TBI, and vital signs should be taken every 5 to 10 minutes. Continuous capnography and frequent assessment of the Glasgow Coma Scale (GCS) score should be performed at least every 30 minutes.[10] Accurate GCS scoring is essential, as it informs prognosis and management strategies. A pupillary examination is an important aspect of assessment and reassessment, as changes in pupillary size, reactivity, and asymmetry are associated with impending neurologic deterioration and poor outcomes. 

Effective airway management is also of great concern in patients with TBI, as oxygenation and ventilation derangements contribute to secondary brain injuries, warranting significant preventive efforts. Prehospital airway management involves quickly identifying patients at risk for airway compromise, minimizing peri-intubation complications, and ensuring appropriate ventilation to prevent hypocarbia.

Early oxygen administration is crucial to avoid hypoxemia. The administration of 100% oxygen via a nonrebreather mask should be considered for all patients with TBI, especially if endotracheal intubation is likely. Even a single episode of profound hypoxemia (SpO2 < 70%) or desaturation (SpO2 < 90%) is associated with increased mortality.[11] Unfortunately, the combination of hypotension and hypoxemia has a synergistic effect on mortality, with an odds ratio of death of 6.1 (95% CI 4.20-8.86).[12]

Multiple management strategies historically used to treat head injuries are currently not recommended due to their risks. One such practice is the routine use of hyperventilation for all patients with TBI. Hyperventilation causes cerebral vasoconstriction, thereby decreasing brain perfusion. This intervention transiently reduces CPP but may also cause cerebral ischemia. Thus, hyperventilation is no longer recommended unless clear signs of impending herniation are evident.[13]

Another outdated approach is the use of aggressive fluid resuscitation to maintain blood pressure. This practice can exacerbate cerebral edema and increase ICP. Patients who receive more than 2 liters of intravenous crystalloid have worse outcomes than those who receive less intravenous fluid (adjusted odds ratio 2.25, P = .005).[14] The indiscriminate use of corticosteroids in TBI was likewise once common but has since been shown to increase mortality and is no longer recommended.[15] The above practices are a few examples that have been replaced by more targeted, evidence-based approaches focusing on maintaining adequate oxygenation and perfusion while avoiding secondary insults.

Clinical Significance

Secondary brain injury prevention is crucial during the prehospital treatment of TBI. Secondary brain injury may be due to hypoxemia, hypoperfusion, and ischemia, which negatively affect outcomes. Monitoring for signs of raised ICP and MAP is vital to ensuring optimal CPP. Short periods of hypotension and hypoxemia significantly worsen patient outcomes, requiring intensive evaluation and management of blood pressure, oxygenation, ETCO2, and temperature derangements.

Blood pressure goals in pediatric patients vary with age. Continued reassessment of vital signs, including GCS and pupillary examination, is essential to detect neurological deterioration. Effective airway management is critical to prevent hypoxemia and ventilation problems. Prehospital providers should prioritize timely airway interventions, early oxygen administration, and minimization of peri-intubation complications. Even brief episodes of hypoxemia are associated with increased mortality, especially when combined with hypotension, highlighting the importance of close monitoring and prompt intervention in patients with TBI.

References


[1]

Capizzi A, Woo J, Verduzco-Gutierrez M. Traumatic Brain Injury: An Overview of Epidemiology, Pathophysiology, and Medical Management. The Medical clinics of North America. 2020 Mar:104(2):213-238. doi: 10.1016/j.mcna.2019.11.001. Epub     [PubMed PMID: 32035565]

Level 3 (low-level) evidence

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Colclough Z, Estrella MJ, Joyce JM, Hanafy S, Babineau J, Colantonio A, Chan V. Equity considerations in clinical practice guidelines for traumatic brain injury and the criminal justice system: A systematic review. PLoS medicine. 2024 Aug:21(8):e1004418. doi: 10.1371/journal.pmed.1004418. Epub 2024 Aug 12     [PubMed PMID: 39134041]

Level 1 (high-level) evidence

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Chan V, Estrella MJ, Hanafy S, Colclough Z, Joyce JM, Babineau J, Colantonio A. Equity considerations in clinical practice guidelines for traumatic brain injury and homelessness: a systematic review. EClinicalMedicine. 2023 Sep:63():102152. doi: 10.1016/j.eclinm.2023.102152. Epub 2023 Aug 24     [PubMed PMID: 37662521]

Level 1 (high-level) evidence

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Lewis SR, Evans DJ, Butler AR, Schofield-Robinson OJ, Alderson P. Hypothermia for traumatic brain injury. The Cochrane database of systematic reviews. 2017 Sep 21:9(9):CD001048. doi: 10.1002/14651858.CD001048.pub5. Epub 2017 Sep 21     [PubMed PMID: 28933514]

Level 1 (high-level) evidence

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Thompson HJ, Tkacs NC, Saatman KE, Raghupathi R, McIntosh TK. Hyperthermia following traumatic brain injury: a critical evaluation. Neurobiology of disease. 2003 Apr:12(3):163-73     [PubMed PMID: 12742737]


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Mount CA, Das JM. Cerebral Perfusion Pressure. StatPearls. 2024 Jan:():     [PubMed PMID: 30725956]


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Godoy DA, Murillo-Cabezas F, Suarez JI, Badenes R, Pelosi P, Robba C. "THE MANTLE" bundle for minimizing cerebral hypoxia in severe traumatic brain injury. Critical care (London, England). 2023 Jan 12:27(1):13. doi: 10.1186/s13054-022-04242-3. Epub 2023 Jan 12     [PubMed PMID: 36635711]


[10]

Lulla A, Lumba-Brown A, Totten AM, Maher PJ, Badjatia N, Bell R, Donayri CTJ, Fallat ME, Hawryluk GWJ, Goldberg SA, Hennes HMA, Ignell SP, Ghajar J, Krzyzaniak BP, Lerner EB, Nishijima D, Schleien C, Shackelford S, Swartz E, Wright DW, Zhang R, Jagoda A, Bobrow BJ. Prehospital Guidelines for the Management of Traumatic Brain Injury - 3rd Edition. Prehospital emergency care. 2023:27(5):507-538. doi: 10.1080/10903127.2023.2187905. Epub 2023 Apr 20     [PubMed PMID: 37079803]


[11]

Davis DP, Dunford JV, Poste JC, Ochs M, Holbrook T, Fortlage D, Size MJ, Kennedy F, Hoyt DB. The impact of hypoxia and hyperventilation on outcome after paramedic rapid sequence intubation of severely head-injured patients. The Journal of trauma. 2004 Jul:57(1):1-8; discussion 8-10     [PubMed PMID: 15284540]


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Spaite DW, Hu C, Bobrow BJ, Chikani V, Barnhart B, Gaither JB, Denninghoff KR, Adelson PD, Keim SM, Viscusi C, Mullins T, Rice AD, Sherrill D. Association of Out-of-Hospital Hypotension Depth and Duration With Traumatic Brain Injury Mortality. Annals of emergency medicine. 2017 Oct:70(4):522-530.e1. doi: 10.1016/j.annemergmed.2017.03.027. Epub 2017 May 27     [PubMed PMID: 28559036]


[13]

Gouvea Bogossian E, Peluso L, Creteur J, Taccone FS. Hyperventilation in Adult TBI Patients: How to Approach It? Frontiers in neurology. 2020:11():580859. doi: 10.3389/fneur.2020.580859. Epub 2021 Jan 28     [PubMed PMID: 33584492]


[14]

Ko A, Harada MY, Barmparas G, Smith EJT, Birch K, Barnard ZR, Yim DA, Ley EJ. Limit Crystalloid Resuscitation after Traumatic Brain Injury. The American surgeon. 2017 Dec 1:83(12):1447-1452     [PubMed PMID: 29336770]


[15]

Alderson P, Roberts I. Corticosteroids for acute traumatic brain injury. The Cochrane database of systematic reviews. 2005 Jan 25:2005(1):CD000196     [PubMed PMID: 15674869]

Level 1 (high-level) evidence