Permissive Hypotension in Trauma Resuscitation

 

 
 
 

Jeff Beeson, DO, FACEP, EMT-P & Trenton Starnes, NREMT-P | From the April 2013 Issue | Wednesday, March 27, 2013


A scene familiar to any provider in emergency medicine: Take an otherwise healthy patient, add in a significant mechanism of injury, throw in abnormal vital signs for extra emphasis and you have a critical trauma patient. Most of us remember our first trauma patient and can recall the smallest details from that day. This is what we are trained for: life-saving interventions that must be performed quickly and with precision. We feel the pressure of knowing that our patient’s survival can be directly linked to our actions. But even the accepted standards of trauma care that are universally recognized and practiced have differing levels of support in scientific evidence.

Education: What you were taught is wrong
Our initial education in EMS focuses on easy mnemonics to assist providers in the ability to rapidly assess and treat conditions. Every trauma course taught to physicians, nurses or EMS providers has similar mnemonics that start with the letter “A” (airway). We are all trained in a similar manner, and most of us can work through the “ABCs” of trauma resuscitation with ease.

There’s little to no debate regarding the need for aggressive airway management, represented by the letters “A” and “B.” We then address the “C” (circulation) by stopping hemorrhage and supporting the patient’s circulatory status. Should the patient’s hemorrhage remain uncontrolled, providers are directed to begin fluid resuscitation while transporting to a trauma facility.

Fluid resuscitation strategies are universally taught to be the means to address traumatic shock. We instinctually respond by establishing large-bore IVs (preferably bilaterally) and then rapidly infuse crystalloids. In fact, the term “large-bore IV” is nearly synonymous with trauma itself, for both EMS and hospital providers alike.

The formula for fluid resuscitation in patients with uncontrolled hemorrhage is deceptively simple: Measure something. We typically use the systolic blood pressure (SBP), heart rate (HR) or some combination of both. If they’re abnormal, we use something, usually IV crystalloids, to bring the said measurement back to an expected number.

This approach to fluid resuscitation is standard and can be lifted out of almost any emergency medical textbook. Generous crystalloid boluses are hailed as standard treatment for traumatic shock patients.  But are we measuring the correct things? Are we initiating the correct interventions to fix the so-called “abnormal” measurements?

As common as the recommendations are for fluid resuscitation, one might be forgiven for assuming that the scientific basis for the interventions are similarly common and well-established. This is simply not the case. In fact, we find little empirical, science-based evidence for our current practice of liberal crystalloid administration in traumatic patients suffering uncontrolled hemorrhage.

The question should be: What is the best resuscitation strategy to keep the victim alive until hemostasis can be achieved?

Blood: Harder to replace than you think
Before we discuss what to give a patient with uncontrolled hemorrhage, we must first examine what the patient is losing—namely, whole blood. When our patient bleeds, they lose red blood cells, white blood cells, plasma, water, electrolytes, clotting factors, proteins, glucose ... the list goes on. Each component of blood plays an important role in hemostasis. If our patient is becoming deficient with these components, how does normal saline, the most common crystalloid administered to these patients, help? Do we expect large quantities of salt water to replace whole blood loss?

When a patient has sustained a significant hemorrhage, infusing normal saline or other crystalloids essentially dilutes what is left of the patient’s circulating blood, rendering their remaining components less potent. Since the body is dependent on these components within blood to keep the patient alive and perfusing, it’s reasonable to assume that further dilution of whole blood with salt water will hamper the effectiveness of the body’s compensatory mechanisms, which depend on the clotting mechanisms found in blood to stop any hemorrhage.

Also, by infusing enough normal saline to artificially raise the patient’s blood pressure back to “normal,” we’re also sending the wrong signals to the patient’s body. One example is the liver, which is stimulated to release additional clotting factors during hypotensive states. When we administer crystalloids to bring SBP back to “normal,” the liver won’t release what the body really needs.

What pressure is required to allow the blood to form a clot? In 1993, several authors published the results of a study where they introduced hypovolemia through surgically created arterial incisions.1 Crystalloid resuscitation was initiated in a stepwise fashion, using mean arterial pressures (MAP) to guide progressive amounts of fluid therapy. MAPs of 40, 60 and 80 mmHg were targeted. Researchers found that introducing too much IV fluid actually placed pressure behind fresh blood clots, causing the clot to dislodge and hemorrhage to resume. In other words, the net effect of artificially raising the pressure to “normal” was to make things worse. Clots broke loose, clotting factors were diluted and blood loss exceeded cases with minimal amounts of IV crystalloids. The paper concluded that attempts to restore blood pressure with crystalloids resulted in increased hemorrhage volume and higher mortality.

Blood Pressure: Limited usefulness in trauma triage
We’re taught to evaluate the need for aggressive resuscitation based on the patient’s baseline vital signs as compared to “normal” ranges. Certified trauma facilities use algorithmic tables in decision-making when it comes to triaging patients. The decision to activate a trauma patient is often based on the SBP. But is the SBP in and of itself a reasonable measurement of the patient’s need for fluid therapy?

Blood pressure is one of the initial measurements obtained by EMS providers when performing an assessment on the trauma patient. This measurement then becomes the “baseline” for which decline, improvement or treatment efficacy is judged while rendering patient care. Often, the systolic number alone is used as a palpated blood pressure commonly obtained in critical patients.

This approach has several problems. If we step back and look at what the SBP actually represents, we’ll see it tells us little regarding actual cardiovascular status. The blood pressure is simply a measurement of the amount of pressure exerted by circulating blood on the walls of the blood vessels. Once you factor in each patient’s unique history and physiology, the measurement becomes confounding and less than useful. Take a patient who is on beta-blockers, or one who is normally hypo- or hypertensive, and you now have a confusing clinical picture that contains very little actionable information. Many patients don’t present with abnormal vital signs initially, but often suffer greater harm as a result of their own compensatory mechanisms hiding the true picture.

This leads us to challenges in over- and under-triaging patients by trauma teams, emergency departments and EMS systems. The systolic alone, and even the systolic with the heart rate, can often give us not only false negatives, but also false positives. These false activations can lead to a greater strain on resources and complacency in trauma team readiness.

Further studies are warranted to examine if there are more effective measurements in guiding our resuscitations. One study, recently concluded with the Resuscitation Outcomes Consortium (ROC), looked at prehospital point-of-care lactate as a biomarker to indicate the seriousness of the patient’s condition. The hypothesis is that lactate is a better marker of a patient’s need for fluid resuscitation when compared to systolic blood pressures alone.

Our agency in the MedStar Mobile Healthcare system in Fort Worth, Texas, participated in the initial study, and the feedback we received from our crews indicated the lactate measurement took no more effort or skill than a blood pressure measurement in the field. Further studies may show us that the systolic blood pressures should be replaced by measuring mean arterial pressures or even lactose levels to guide triage and resuscitation.

Crystalloids: Where did this begin?
Does crystalloid therapy have any benefits in patients with uncontrolled hemorrhage? The history of fluid therapy can guide us. IV fluids, at least the type we would recognize as being closely related to modern-day versions, were first documented in the early 19th century as physicians were battling large epidemics of cholera. Cholera is known to kill by causing rapid dehydration and volume depletion. It was implicated in a vast number of non-traumatic deaths during that time period. In an issue of Lancet during that time, O’Saughnessy published a paper outlining the life-saving properties of IV fluids administered to patients stricken with the disease.4

In this revolutionary report, O’Shaughnessy outlines the healing effects of IV fluid therapy by demonstrating that patients receiving IV fluids early had a higher likelihood of surviving the effects of cholera and had greater odds of recovery. He describes the need for fluids by claiming the victim’s blood “lost a large portion of its water” and goes on to state IV fluids were able to aid in recovery, in part because it gave blood the ability to return to its “natural specific gravity” by “replacing its deficient saline.” 4 Shortly thereafter, Latta also published a paper outlining IV fluid’s incredible abilities in other situations, such as pregnant women with septic shock or other serious effects.5 Other researchers followed.

IV Fluid Therapy: Not just for cholera anymore
Physicians began making the reasonable assumption that if IV fluid therapy was lifesaving for medical patients, it may also have similar effects on trauma patients. Not long after the O’Saughnessy article drew attention to the merits of IV administration of water, the U.S. found itself embroiled in a civil war, giving physicians plenty of opportunity to put their miraculous IV fluids to work on the battlefield while treating injured soldiers.

These efforts continued into World War I, and in 1918, Cannon et al. published an influential paper in the Journal of the American Medical Association entitled “The Nature and Treatment of Wound Shock and Allied Conditions.”2 This comprehensive paper outlines the appropriate clinical approach to critical battlefield patients, even to the point of describing the proper way to fold blankets on patients to minimize hypothermia.

The modern iteration of fluid resuscitation in severely injured patients finds roots in a more recent battlefield. Most trauma guidelines can be traced to research arising from battlefield physicians in the Vietnam War. Although the papers that emerged from the observations during this time were limited, they were indeed influential. This is where we find the first actual indication to use large amounts of crystalloids to treat patients with life-threatening hemorrhage and shock.

From their experience in this environment, several clinicians and researchers published papers outlining their theories regarding rapid boluses of large quantities of IV fluids for critically injured patients.6–8 The amount of crystalloid resuscitation suggested was aggressive by contemporary standards, and recommendations on the correct ratio of fluid-replacement-to-blood-loss ranged from the conservative 3:1 to as high as 8:1 for “significant shock.” This was considered necessary to “replace intravascular loss and interstitial deficits.”

The papers also describe the detrimental effects of shock in terms of “oxygen debts” and “interstitial losses,” for which fluid therapy was the recommended treatment. IV fluids were not intended as volume expanders, but interstitial replacements to a dehydration caused by trauma, whether perceived or real. Crystalloids were seen as “maximizing or supernormalizing cardiac output,” among other perceived benefits.

This research was loosely controlled and limited in scope, and it lacked substantive documentation. Regardless, the theories appeared sound enough and subsequently influenced generations of physicians, nurses and EMS providers in their understanding of the importance of fluids in trauma resuscitation.

Little has changed since the 1970s. Current trauma protocols are almost identical to those used in the Vietnam War. Our trauma guidelines, at the EMS level and beyond, haven’t progressed beyond “two large-bore IVs and rapid fluid boluses.” Even at most Level 1 trauma facilities, standing order protocols exist for registered nurses to initiate two large-bore IVs and administer at least one liter, if not more, to any Level 1 trauma activation.

There almost exists an unstated—but very perceptible—level of pride with paramedics regarding who can “get in” more fluid to traumatic patients prior to emergency department (ED) arrival, using pressure-infusion devices to assist.

There is, however, some light at the end of the tunnel. New “damage control” surgery techniques are designed to adequately resuscitate patients prior to lengthy surgical procedures. In fact, most centers today are using early massive transfusion protocols of blood and blood products instead of high-volume crystalloids.

Research: Where do we go from here?
We need to challenge our current beliefs. Simply doing what we have always done isn’t the answer. Literature is moving other medical disciplines beyond massive fluid resuscitation protocols. Many recent studies by anesthesiologists, surgeons and others outside the realm of emergency medicine have demonstrated not only benefits in limiting IV fluid therapy with certain patient populations, but have also indicated a definite trend toward increased mortality associated with the very same IV fluid therapy protocols we know, practice and, yes, even cherish.

What’s an effective amount of IV fluid for these traumatic patients, and what constitutes a harmful amount? Several studies recently have tried (or are currently attempting) to address that. In 2011, a paper was published in the Journal of the American Medical Association about resuscitation strategy in patients with hemorrhagic shock requiring emergent surgery (active hemorrhage).3

These patients were managed to maintain a mean arterial pressure of only 50 mmHg, which is a number that makes most providers feel uncomfortable. But their conclusion was remarkable. The patients who were given IV fluid therapies targeted to a MAP of 50 mmHg received far less blood products and IV fluids overall than did standard resuscitation patients who received IV fluid therapy titrated to maintain a mean arterial pressure of 65 mmHg. Patients receiving the therapies targeted at an MAP of 50 mmHg hypotensive post-op resuscitation strategy were also found to have significant lower mortality at 30 days, significant reduction in postoperative bleeding and were less likely to die from coagulopathy.

EMS research is also catching up. The Resuscitation Outcomes Consortium is currently studying prehospital fluid strategies for severely injured patients. The “Field Trial of Hypotensive Resuscitation vs. Standard Resuscitation in Patients with Hemorrhagic Shock,” or HypoRESUS, study is currently evaluating patient outcomes using both “standard” fluid resuscitation strategies and “permissive hypotension” strategies. A severely injured patient sustaining blood loss is enrolled in the field by EMS. If the patient has a systolic of 90 mmHg or less, they are eligible for the study and have the potential to be enrolled in either the standard arm of the study or the permissive hypotensive arm. The study kits are blinded, and EMS provider won’t know which arm the patient is enrolled to until after enrollment.

If enrolled in the “standard” arm, the paramedic administers normal saline in 1-liter increments until the patient reaches 110 mmHg systolic, at which point the fluids will be set to keep open. If enrolled in the hypotensive arm, the paramedics are only allowed to administer normal saline IV in 250 mL increments until the systolic reaches 70 mmHg. Once the pressure hits 70 mmHg, fluids are set at to keep open until ED arrival.

MedStar Mobile Healthcare, along with other ROC agencies, began enrolling patients in this pilot study this past year. So far, we’ve learned a lot. We’ve learned that old habits can be hard to break. This is, in part, due to our own internal discomfort with perceived risk to our patient, regardless of the lack of scientific evidence making us uncomfortable. We fight against ourselves and our own prejudices.

This struggle is also evident at the hospital. The HypoRESUS study doesn’t end at the emergency department doors. The study is designed to continue two hours post-ED arrival. Whether the patient is in the ED, intensive care unit or surgical suite, they’re only allowed to receive the amount of crystalloids dictated by study protocol until hemorrhage is controlled through surgical ligation or other means.

Looking Back to Move Forward
One paper in particular advocates for delayed and conservative fluid resuscitation in trauma reference. Although it’s simple, it flies in the face of everything we were or have been taught. The author is W.B. Cannon—the very same Cannon mentioned earlier, who is responsible for writing in 1918 about battlefield injuries. He advocates for delayed fluid resuscitation.2

We may benefit by looking at history while considering our future. Permissive hypotension isn’t a new concept, but it is one that was lost in the infancy of EMS.

We’re faced with exciting times ahead. Evidence-based protocols are now common in EMS, and it’s about time. However, although we can celebrate this shift, let us not underestimate the underappreciated challenger to change: habit. And as we begin to help others understand the implications of their crystalloid resuscitation habits, we must not lose sight of another underappreciated quality in EMS: patience.

Jeff Beeson, DO, FACEP, EMT-P, is the medical director for the Emergency Physicians Advisory Board of Fort Worth, which provides medical oversight for MedStar Mobile Healthcare Ambulance and the 15 first responder organizations of the system. He’s an emergency physician, a licensed paramedic, registered nurse and an active member of Texas Task Force One. His passion for evidence-based prehospital medicine keeps him busy as a highly sought-after speaker at conferences worldwide.
Trenton Starnes, NREMT-P, is the chief of staff for the Emergency Physicians Advisory Board, and is also a paramedic with MedStar Mobile Healthcare Ambulance. After selling his award-winning advertising agency in 2009, he decided to pursue a new career in prehospital medicine and is currently working on his BS in emergency health sciences. You can follow him at http://about.me/trenton.

References
1. Stern SA, Dronen SC, Birrer P, et al. Effect of blood pressure on hemorrhage volume and survival in a near-fatal hemorrhage model incorporating a vascular injury. Ann Emerg Med. 1993;22(2):155–163.
2. Cannon WB, Fraser J, Cowell EM. The preventive treatment of wound shock. JAMA. 1918;70:618–621.
3. Morrison CA, Carrick MM, Norman MA, et al. Hypotensive resuscitation strategy reduces transfusion requirements and severe postoperative coagulopathy in trauma patients with hemorrhagic shock: preliminary results of a randomized controlled trial. J Trauma. 2011;70(3):652–663.
4. O’Shaughnessy W. Experiment on the blood in cholera. Lancet. 1831;i:490.
5. Latta T. Malignant cholera. Lancet. 1832;ii:274–277.
6. Shires GT. Management of hypovolemic shock. Bull NY Acad Med. 1979;55(2):139–149.
7. Cervera AL, Moss G. Progressive hypovolemia leading to shock after continuous hemorrhage and 3:1 crystalloid replacement. Am J Surg. 1975;129(6):670–674.
8. Shoemaker WC, Hopkins JA, Greenfield S, et al. Resuscitation algorithm for management of acute emergencies. JACEP. 1978;7(10):361–367.

Resources
>> Alam HB, Rhee P. New developments in fluid resuscitation. Surg Clin North Am. 2007;87(1):55–72.
>> Bickell WH, Wall MJ Jr, Pepe PE, et al. Immediate vs. delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med. 1994;331(17):1105–1109.
>> Sondeen JL, Coppes VG, Holcomb JB. Blood pressure at which rebleeding occurs after resuscitation in swine with aortic injury. J Trauma. 2003;54(5 Suppl):S110–S117.




Connect: Have a thought or feedback about this? Add your comment now
Related Topics: Patient Care, Trauma, trauma, saline, permissive hypotension, normal saline, mean arterial pressure, MAP, large-bore IV, IV fluid therapy, IV, hypotension, delayed fluid resuscitation, crystalloids, BP, blood pressure, blood loss, Jems Features

 
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