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Traumatic Hemorrhagic Shock: Advances In Fluid Management (Trauma CME) - $30.00
Published: November 2011 (Volume 13, Number 11)
CME: This issue includes 4 AMA PRA Category 1 CreditsTM, 4 ACEP Category 1 credits, 4 AAFP Prescribed credits, and 4 AOA Category 2A or 2B CME credits.
Author
David Cherkas, MD, FACEP
Assistant Residency Director, Department of Emergency Medicine, Mount Sinai School of Medicine, Elmhurst Hospital Center, New York, NY
Peer Reviewers
Marie-Carmelle Elie, MD, RDMS, FACEP
Assistant Professor of Emergency Medicine, Critical Care, Hospice and Palliative Medicine, University of Florida School of Medicine, Gainesville, FL
Eric J. Wasserman, MD, FACEP
Chairman and Medical Director, Department of Emergency Medicine, Newark Beth Israel Medical Center, Newark, NJ
(Shawn) Xun Zhong, MD
Director of Emergency Critical Care, Nassau University Medical Center, East Meadow, NY
Abstract
A number of concerns have been raised regarding the advisability of the classic principles of aggressive crystalloid resuscitation in traumatic hemorrhagic shock. This issue reviews the advances that have led to a shift in the emergency department (ED) protocols in resuscitation from shock state, including recent literature regarding the new paradigm for the treatment of traumatic hemorrhagic shock, which is most generally known as damage control resuscitation (DCR). Goals and endpoints for resuscitation and a review of initial fluid choice are discussed, along with the coagulopathy of trauma and its management, how to address hemorrhagic shock in traumatic brain injury (TBI), and new pharmacologic treatment for hemorrhagic shock. The primary conclusions include the administration of tranexamic acid (TXA) for all patients with uncontrolled hemorrhage (Class I), the implementation of a massive transfusion protocol (MTP) with fixed blood product ratios (Class II), avoidance of large-volume crystalloid resuscitation (Class III), and appropriate usage of permissive hypotension (Class III). The choice of fluid for initial resuscitation has not been shown to affect outcomes in trauma (Class I).
Excerpt From This Issue
In the middle of your Saturday overnight shift, you are called to see a patient who drove himself to the hospital with a stab wound to the left upper back. This 19-yearold male states that he was on the way to church when he was accosted by “2 dudes” who stabbed him “out of the blue.” He said he may have run into something with his car while trying to get away from them. You find the patient awake, but sluggish. He is speaking and his airway appears patent. Breath sounds are equal bilaterally. The patient’s initial vital signs are: heart rate of 140 beats per minute, blood pressure of 80/50 mm Hg, respiratory rate of 20 breaths per minute, temperature of 97°F (36.1°C), and SpO2 of 100% on room air. He reports only the single injury and when he is fully undressed, no other signs of trauma are found. Peripheral pulses are palpable, and on close inspection, the wound appears to be bleeding only minimally. The trauma surgeon is notified and is en route to assist. Initial FAST examination is negative. Two 18-gauge IVs are placed, lab work is drawn, and 2 L of lactated Ringer solution are administered. The blood pressure rapidly rises to 110/75 mm Hg, and the patient starts to complain of shortness of breath. Chest x-ray reveals a large hemothorax, and the patient’s blood pressure drops to 75/55 mm Hg. You begin to wonder if your initial resuscitation is really helping this patient.
About 50 minutes later, EMS arrives with a pedestrian struck by a car. EMS states that this 24-year-old male was the victim of a hit-and-run accident in which the driver apparently backed over him after first clipping him with the car and knocking him to the ground. When you walk into the patient’s room, you find him awake and angry, complaining of pain in his right upper quadrant. He is on a backboard, wearing a cervical collar, and has obvious bruising to the right chest and abdomen. His airway is patent and his breath sounds are equal bilaterally. The patient’s initial vital signs are: heart rate of 125 beats per minute, blood pressure of 120/80 mm Hg, respiratory rate of 20 breaths per minute, temperature of 98°F (36.6°C), and SpO2 of 94% on room air. Per EMS, the patient was hypotensive on their arrival, with initial blood pressure of 80/40 mm Hg, but it rapidly improved with 2 L of crystalloid given in the field. A second large-bore IV is placed and labs are drawn. The FAST examination reveals significant hemoperitoneum. He then becomes diaphoretic, and repeat blood pressure is now 75/40 mm Hg. The nurse asks if you want 2 more liters of crystalloid…
