The Head and the Heart: Hemodynamic Derangement in Isolated TBI

Gavrilovski M, El-Zanfaly M, Lyon RM. Isolated traumatic brain injury results in significant pre-hospital derangement of cardiovascular physiology. Injury 2018;49(9):1675–9. 


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Major trauma remains a significant cause of serious morbidity and mortality, particularly in the younger patient population. One of the leading causes of death in trauma is hemorrhage, and the resulting sequelae of hypotension, acidosis, hypothermia, and coagulopathy.  In the prehospital arena, many patients do not have overt external hemorrhage, and we do not have access to cross-sectional imaging to prove the presence or absence of internal hemorrhage.  Therefore, we must commonly use surrogate markers to decide whether or not to initiate prehospital blood product transfusion.  Typically, these markers will include trends in heart rate, blood pressure, and shock index, as well as “soft markers” such as mental status, diaphoresis, and skin color.

Unfortunately, we know that alterations in hemodynamics do not only occur in hemorrhagic shock.  Both obstructive (such as from tension pneumothorax) and neurogenic shock (for example, from a spinal cord transection), can result in hemodynamic compromise that would not be corrected by blood product administration.  

There have been some studies that have shown isolated traumatic brain injury (TBI) can also cause hemodynamic derangements. This paper attempted to examine the incidence of cardiovascular instability in patients with TBI.

This paper from Gavrilovsk, El-Zanfaly, and Lyon is out of Kent Surry and Sussex Air Ambulance Trust (KSSAAT), a HEMS service in England covering a population of 4.5 million.  They have doctor/paramedic teams that respond in either helicopter or response car, and attend approximately 2000 patients per year – all prehospital trauma patients.

Patients were eligible if they were adult patients who underwent prehospital RSI, and had subsequent isolated TBI confirmed on pan-scan.  TBI was defined as any radiologic abnormality of suspected traumatic origin, and so included epidural hematomas, subdural hematomas, subarachnoid hemorrhages, and hemorrhagic contusions.  Cardiovascular instability was defined as essentially any recorded tachycardia or hypotension.


Out of a possible pool of 3485 patients, 256 patients met all inclusion and exclusion criteria.  The most frequent mechanism of injury for isolated TBI was a fall, with other common MOIs being motor vehicle accidents and assaults.  121 of those were confirmed to have isolated TBI, and 133 had polytrauma – with or without TBI.  2 patients were excluded due to isolated skull fracture without TBI or other traumatic injuries.   44% of the isolated TBI patients were found to have hemodynamic instability.  Interestingly, 12% of these were hypotensive even prior to the administration of sedative agents or the induction of anesthesia.  8.2% of the isolated TBI patients received prehospital blood products, despite not having any other injuries or significant sources of bleeding found on later imaging.   


This study is limited for several reasons.  It was a retrospective, observational study based on data available from an electronic database, and relied on both prehospital and inhospital data sets, and so some patients were excluded due to incomplete data.  In addition, it was a single-center trial, and so may not be generalizable to other health systems or patient populations. Finally, a pre-requisite for this study was receiving prehospital RSI, and so it is certainly possible that there were patients with significant TBIs that did not undergo RSI for a variety of reasons, and so were not captured in the patient population.


We frequently manage prehospital trauma patients with hemodynamic instability, and this study potentially creates some doubts as to the etiology of their hemodynamic compromise.  As discussed earlier, hemodynamic instability in the traumatically injured patient is generally thought to arise from hemorrhagic shock.  We are generally adept at recognizing when alternative etiologies (such as obstructive or neurogenic shock) are at play, and treating those appropriately.

As our understanding of trauma continues to evolve, we have continued to expand the effects attributable to traumatic brain injuries.  For instance, it is well-documented that patients with significant intracranial bleeds can have ST-elevations present on their ECG’s, and concomitant cardiovascular compromise.  The phenomenon of Impact Brain Apnea has been recently described by Wilson et al, and is a suspected cause of respiratory collapse and resulting cardiac arrest in acutely head-injured patients.  This paper adds another potential layer of prolonged hemodynamic instability to the TBI patient.  The pathophysiology is complex, but generally felt to arise from catecholamine surges as well as autonomic system imbalances and pro-inflammatory cytokine responses.

There are many scenarios where it would be difficult to identify which trauma patients with suspected TBI are having cardiovascular instability from their TBI and not from additional internal injuries. Fortunately, this paper is helpful in addressing this potential issue, by documenting it and raising awareness. There are also additional findings which we can use to determine which patients have additional internal injuries, including close examination of the thorax, abdomen, and pelvis for evidence of trauma.  Finally, our prehospital ultrasound gives us an advantage in our ability to perform FAST scans and potentially confirm the presence of intrathoracic or intraperitoneal free fluid (although this cannot be used as a definitive “rule-out” study). 

Interestingly, in patients with isolated TBI, their hemodynamic instability is likely best treated with crystalloid or vasopressors, rather than blood products.  This is part of what makes our job and field of study so difficult.  I think this paper has made me more aware of this issue, but I still think I will personally err on the side of early blood product administration in unstable patients who I suspect any additional injuries other than TBI.  I still think the potential harm of withholding blood products from a patient in hemorrhagic shock is greater than an unneeded transfusion in a patient with isolated TBI.  These patients would likely also receive tranexamic acid (TXA), which is currently being studied for use in isolated TBI (CRASH-3).

To paraphrase Dr. John Hickam – “Patients can have as many diseases as they damn well please.”


  1. Gavrilovski M, El-Zanfaly M, & Lyon RM. Isolated traumatic brain injury results in significant pre-hospital derangement of cardiovascular physiology. Injury 2018;49(9):1675–9

  2. Wilson, M, Hinds, J. Grier, G., Burns, B., Carley, S., & Davies, G. Impact brain apnoea – A forgotten cause of cardiovascular collapse in trauma. Resuscitation, Volume 105 , 52 - 58.


Andrew Cathers, MD - Dr. Cathers is an Emergency Medicine Physician as well as Flight Physician, and Assistant Medical Director of University of Wisconsin Med Flight with a focus on Education and Training in their Program. He is kind enough to share recaps of recently published HEMS literature which should be posted quarterly here on TamingtheSRU

Peer Review/Editing/Posting provided by Jeffery Hill, MD MEd