The Changing Landscape of Trauma Care, Part 2

Damage Control Resuscitation

In the United States, trauma is the leading cause of death in patients younger than age 45 years and ranks as the fifth leading cause of death among all age groups. Hemorrhage remains the leading cause of preventable death in the trauma population,¹ and one of the most important recent changes in our care of the injured patient is the manner in which we manage hemorrhage. As noted earlier, there has been a paradigm shift away from large-volume crystalloid resuscitation and toward what has been termed “damage control resuscitation” (DCR).^2,3

The principles of the DCR strategy are aimed at preemptively treating the lethal triad of hypothermia, acidosis, and coagulopathy in conjunction with control of surgical bleeding using damage control surgery. The main principles of DCR include “permissive hypotension,” prevention of heat loss and/or active warming, minimizing the use of crystalloid infusions, and initiating resuscitation with blood products in a ratio that more closely resembles whole blood.²

Permissive Hypotension

Permissive hypotension, also referred to as hypotensive resuscitation, is not considered a goal or an endpoint, but rather a “bridge” to definitive surgical control of hemorrhage. The body’s initial response to injury involves vasoconstriction and early clot formation, a process facilitated by hypotension. The rationale for permissive hypotension is that attempting to drive the BP up to normal ranges may interfere with vasoconstriction, as well as physically disrupting this early clot, leading to increased bleeding and further hypotension.

This concept has been corroborated by many animal and human studies.³ In 1994, the landmark study by Bickell et al⁴ randomized patients with penetrating torso trauma and a systolic BP (SBP) of 90 mm Hg or lower to either immediate or delayed fluid resuscitation. Their study demonstrated that patients whose fluid resuscitation was delayed until they reached the operating room had improved outcomes. The study supported the long-time prehospital practice of the “scoop-and-run” strategy, especially in penetrating torso trauma.

In 2003, Sondeen et al⁵ used a swine model of aortic injury to find an inflection point for clot disruption and re-bleeding during volume resuscitation. They found the inflection point to be a mean arterial pressure (MAP) of 64 mm Hg and an SBP of 94 mm Hg, regardless of the size of the aortotomy. Using an animal model of hemorrhagic shock, Li et al⁶ demonstrated in 2011 that resuscitation to a MAP of 50 mm Hg was associated with a decreased amount of blood loss as well as with improved survival compared to patients who were resuscitated to a MAP of 80 mm Hg. However, they also showed that after a time period of more than 90 to 120 minutes, the lower MAP group had increased end organ damage and worse outcomes, emphasizing the importance of prompt surgical control of bleeding—regardless of preoperative resuscitation strategy.

Other studies, though, have not shown a clear benefit to permissive hypotension. A 2002 study by Dutton et al⁷ showed that titration of initial fluid to a lower SBP (70 mm Hg) did not affect mortality when compared to a target resuscitation MAP of more than 100 mm Hg. Further, in 2014, a plenary paper presented to the American Association for the Surgery of Trauma demonstrated that controlled resuscitation (CR) strategy was safe and feasible,⁸ but did not demonstrate a mortality benefit in the overall cohort, though patients with blunt trauma who received CR had improved survival at 24 hours.

The group at Ben Taub General Hospital in Houston, Texas recently performed a randomized controlled trial evaluating intraoperative hypotensive resuscitation strategies. Patients in hemorrhagic shock were randomized to either an intraoperative MAP goal of 50 mm Hg or 65 mm Hg.^9,10 Preliminary results suggested that targeting a lower MAP resulted in fewer blood product transfusions, less fluid administration, less coagulopathy, and lower mortality in the early postoperative period. Additionally, they demonstrated a nonsignificant trend toward improved 30-day mortality in the lower MAP group.⁹ Moreover, in this study there was no increased morbidity associated with the hypotensive strategy,¹⁰ suggesting that the approach was safe. Unfortunately, the trial was stopped early due to slow enrollment.

Despite the overall promising results with permissive hypotension, it is important to remember that it is contraindicated in patients with known or suspected traumatic brain injury, as hypotension has been shown to be detrimental in this population.¹¹

Hemostatic Resuscitation and Coagulopathy

Avoiding Aggressive Crystalloid Resuscitation. While the ideal MAP to target during DCR remains unclear, the potential harm caused by aggressive crystalloid resuscitation has become more evident. Infusing excessive amounts of crystalloid has been shown to be associated with increased ventilator days, multisystem organ failure, abdominal compartment syndrome, and surgical-site infections¹²—all of which have also been associated with systemic consequences of increased inflammation, including increased release of tumor necrosis factor-alpha and other proinflammatory cytokines.¹³