Practical Nuances of Resuscitation – Part I: Not All Are Created Equal
- Sep 15th, 2014
- Justin Bright
By Justin Bright, MD
Senior Staff Physician
Henry Ford Hospital, Dept. of Emergency Medicine
Edited by Alex Koyfman, MD
One of my colleagues likes to tell our residents, “they don’t come to the ED to die, they come here to live.” It is our skill in identifying critically ill patients and successfully resuscitating them that defines us as emergency medicine physicians. Resuscitation in its simplest term means to revive from unconsciousness or apparent death. However, there are a multitude of different disease processes that cause critical illness, and the approach to resuscitation of each illness is quite different. It is important to have a confident grasp of different resuscitation options and endpoints so you can best help your patients. If you try to resuscitate all of your patients in exactly the same manner, you will actually end up harming many of them instead.
The goal here is to understand the resuscitation technique and endpoints in trauma, sepsis, and diabetic ketoacidosis. The tried and true methods will be summarized, and areas where controversies exist will be discussed as well. As a result, there is a wealth of information that we need to get through. In order to lay it out for you in smaller, digestible bites, I am going to roll this out in installments. First up….trauma!
Nuances in Resuscitation Part I: Trauma
Trauma is often the sexiest of the resuscitations, particularly to eager medical students and newly minted interns. Patients show up in the emergency department bloodied and critically ill after being perfectly healthy just minutes before. The mechanism of trauma often dictates the diagnostic and treatment pathway a patient ends up following. The resuscitation process in trauma happens in a well-choreographed dance among a team of providers with clearly defined roles. In a trauma, the clock is ticking. In the golden hour of trauma, patients who present to the emergency department and are adequately resuscitated within an hour of injury have significantly better clinical outcomes. The end game in trauma resuscitation is shock: generally in the loss of blood volume causing hemodynamic instability, diminished tissue perfusion, and ultimately end-organ damage. If you remember back to your ATLS courses, there are 4 classes of hemorrhagic shock:
- Class I: Loss of up to 15% of blood volume with minimal (if any) changes in hemodynamic status or vital signs.
- Class II: 15-30% loss in blood volume, causing tachycardia, tachypnea, diminished pulse pressure, and delayed capillary refill.
- Class III: 30-40% loss in blood volume, now with hypotension and change in mentation. In addition, urine output now decreases. These are the first signs that the body is in a shock state. In regards to resuscitation, the providers are already behind, and need to act rapidly and decisively to help their patient fight for life.
- Class IV: More than 40% of blood loss. These patients are actively trying to die right in front of you. These patients have significant drops in blood pressure (although the pulse pressure is often narrow), tachycardia, mental status changes, and peripheral signs of hypoperfusion like pale and graying skin and diminished capillary refill.
Despite these clear-cut classifications, it is important to remember that our patients do not read the textbooks. Variables like temperature, alcohol, drugs (both street and prescription), in addition to factors such as being pregnant or elderly all make vital sign and mentation changes difficult to recognize. As a result, being hypervigilant is the rule when evaluating a patient in potential need of resuscitation.
The treatment priorities in trauma resuscitation are our tried and true ABCs. Indications for intubation, chest tubes, and pericardiocentesis will not be covered here because they diverge from the major theme here, which is the resuscitation of shock states. The most important way to reverse shock in trauma is to stop the bleeding and replenish blood volume. It’s that simple. In order to stop blood loss, providers need to have a firm grasp on the potential anatomic locations for severe blood loss. The most common is external hemorrhage, i.e. a traumatic injury that causes exposure of a blood vessel with the external environment and the patient actively bleeds out of it. The most common locations of internal bleeding include the thoracic cavity, peritoneal cavity, retroperitoneal space, and soft tissue spaces adjacent to long bones.
While it is agreed that whatever volume is lost in a trauma patient needs to be replaced, the type of solution used to replace it, as well as how much should be administered is a topic of much debate. It is generally agreed that the initial fluid resuscitation should consist of a 2 liter rapid bolus of crystalloid – either 0.9% NS or LR (controversial; many now starting with a 1 liter bolus of crystalloid). At that volume of administration, there is little to no risk, and there is no study that demonstrates a clear-cut superiority or inferiority of one versus the other. As fluid resuscitation requirements increase, there are important considerations. With normal saline, a non-anion gap hyperchloremic metabolic acidosis can develop. Conversely, large volume resuscitation using lactated ringers (LR) can cause a metabolic alkalosis, as lactate metabolism generates bicarbonate. Another important consideration with LR is that a separate IV access site and tubing must be used when also transfusing blood at the same time. The greater concept to understand is that as greater volumes are administered, a patient can develop coagulopathy as red blood cells and clotting factors are diluted out, thereby preventing hemostasis and in some instances, actually worsening hemorrhage.
Other topics in fluid administration generating debate include the use of osmotic agents to generate volume, as well as the concept of permissive hypotension (see recent post here: http://www.emdocs.net/foamed-roadmap-permissive-hypotension/). Hypertonic saline has been studied, with the theory being the hyperosmotic solution will pull fluid back into the vasculature, as well as modulate the inflammatory response caused by the traumatic injury. As of yet, studies on hypertonic saline have not definitively shown an improved outcome for patients. Other osmotic agents such as dextran and albumin have also been studied, but they too have failed to show a definitive benefit in morbidity and mortality. The theory of delayed or permissive hypotension hypothesizes that excessive fluid hydration will dilute clotting factors and promote hypothermia, thereby promoting bleeding. So rather than aggressive volume replenishment, you purposely allow systolic blood pressures to go as low as possible while maintaining normal mental status. Not all traumatic injuries are created equal though, and while the concept may work in a penetrating chest trauma going to the OR, the same concept may not benefit a TBI patient in need of adequate cerebral perfusion to prevent secondary injury to brain tissue.
In general, hypotensive trauma patients are not lacking in systemic vascular resistance. Spinal cord injuries causing neurogenic shock are the one notable exception. Use of vasopressors in trauma patients is rarely indicated, and their use is associated with a significantly higher morbidity and mortality. Trauma patients need replacement of whatever volume they have lost. If they haven’t shown an improvement in mentation and vital signs after a 2L fluid bolus, it is time to begin blood product transfusion. Furthermore, transfusion is indicated if it becomes apparent that the patient has extensive hemorrhage that isn’t going to be rapidly controlled, or if it is anticipated that the patient is going to require 4 units of PRBCs in the first hour, or 10 units in the first 24 hours. It is not appropriate to just transfuse PRBCs, as their rapid transfusion will promote hypothermia and coagulopathy in the same way that massive and rapid transfusion of IV crystalloid will. Instead, it is becoming widely accepted to utilize a massive transfusion protocol which calls for PRBCs, FFP, and platelets to be transfused in a 1:1:1 ratio (exact ratio is controversial and currently being researched). This approach to rapid transfusion gives a patient the necessary circulatory volume and oxygen-carrying capacity, while at the same time insuring clotting factors and platelets are not diluted out.
Like what you read? Tune in next time for a discussion of Early Goal Directed Therapy in Sepsis!