ISU_Steve said:
Mike, can you provide a list of all the "studies" you've had published? I'd like to read over all of them. Thank you.
And I would appreciate it if you could PM me with the text of the article from the "Air Medical Journal". I can't seem to find a copy of that one.
A PubMed search shows this as the only EM related article by MacKinnon MA. There is some Neurosurg work out of Scotland and some Toxicology stuff out of NJ, but this author is from AZ.
Be gentle guys, I don't think this is the response Mike expected when he wandered in here. I think he imagined that this article and his experience as a flight nurse would outpace the average here.
- H
_________
Permissive hypotension: A change in thinking
Mike A. MacKinnon CEN, CFRN, BSN, RN,
Air Evac Services, Phoenix, Ariz, USA
Available online 26 February 2005.
A call sends you to a local freeway where a single vehicle has lost control and struck another vehicle from behind. The patient, a 26-year-old man, was restrained, and his air bag deployed; he has total recall of the accident. Local emergency medical services personnel inform you that he has bilateral femur fractures, very low blood pressure, and fast heart rate, but he is mentating normally. You are 20 minutes from the nearest appropriate facility.
Certainly this call—a trauma involving a hemorrhagic emergency that will rapidly deteriorate—is commonplace to air medical crews across the country. Multiple trauma courses, the most prominent of which is the Advanced Trauma Life Support by the American College of Surgeons (ACS), have taught us how to manage these emergencies. The typical treatment regimen has been 2 large-bore intravenous lines and the 3:1 rule.[1] Our treatment goals have centered on normalizing numbers, such as blood pressure and heart rate, regardless of physiologic evidence to the contrary.
However, our thinking is finally starting to change. To discuss these changes in treatment and thinking, we must first define the problem. Patients who are involved in significant blunt or penetrating trauma are at risk for hemorrhagic shock. The ACS defines shock as a circulatory system abnormality resulting in inadequate organ and tissue oxygen delivery.[1] Shock can present in many forms, but the most common form in blunt and penetrating injury that decreases circulating volume is hemorrhagic shock.
As a patient begins to hemorrhage, compensatory mechanisms initiate to lower hydrostatic pressure in the vasculature. The adrenal glands release catecholamine, which increases heart rate and systemic vascular resistance, thereby increasing cardiac output and tissue perfusion pressure. Through osmosis, interstitial fluid moves into the vascular space as the hydrostatic pressure of the vessels decreases, based on Starlings law.[2] Second, the liver and spleen secrete stored erythrocytes and plasma into the bloodstream. Renin also is secreted from the kidneys, stimulating aldosterone and antidiuretic hormone and causing water retention. [2]
Compensation is finite and can be overcome by persistent hemorrhage, defined as intravascular volume depleted by 15%.[2 and 3] Perfusion to the heart and brain is maintained at the expense of the renal, skin, muscle, and splanchnic blood flow. [2, 3, 4, 5 and 6] This shift leads to organ ischemia and potential failure, significantly increasing the risk for multiple organ dysfunction syndrome. [2 and 5]
Decreasing availability of oxygen and glucose leads to anaerobic metabolism and gluconeogenesis, causing metabolic wastes to build up. This problem is compounded by the bloodstream's inability to remove the waste because of decreased intravascular volume. The combination of acidic, electrolytic, and enzymatic imbalance impairs cellular function, which may lead to intracellular damage, cellular death, and potentially patient demise.[5]
Fluid resuscitation has been the cardinal treatment for hemorrhagic shock, and normalized blood pressure has been the goal of that treatment. It seems logical that, if we restore intravascular volume and normalize pressure, we increase cardiac output and perfusion pressure, keeping the patient alive until surgery. The assumption that positive outcomes will be achieved if physiological parameters are normalized partially stemmed from experimental work on animal models of hemorrhage in the 1950s and 1960s. This was usually a controlled hemorrhage model in which a known amount of blood volume was removed by a vascular catheter. The animals then were treated with various fluid resuscitation schemes, eventually culminating in the 3:1 rule.[4, 7 and 8] However, hemorrhagic shock typically is uncontrolled with mounting blood loss. As with any physiologically different process, the treatment is usually sequela-specific. [9]
If maintaining blood pressure is the goal, fluid resuscitation is the treatment. Keeping in mind the definition of shock, our immediate goals clearly are to arrest hemorrhage and maintain oxygen delivery. Although acellular fluid resuscitation may increase cardiac preload, it also may disrupt the formation of thrombus, increase bleeding time, and hemodilute the existing hemoglobin, platelet, and coagulation factors.[4, 6, 7 and 9] Although essential, blood product administration is often beyond the scope of prehospital providers and, therefore, this article.
Because oxygen delivery is paramount, our challenge is to set goals and define measurable responses to treatment. Traditionally, we have relied on normalized blood pressure, heart rate, and urine output to gauge response to treatment of hemorrhagic shock. However, recent research has revealed that 80% of severely traumatized patients who are maintaining normal vitals and urine output still suffer subnormal oxygen delivery, evidenced by increased lactate.[4] It appears both the treatment and assessment tools are missing the mark of measuring oxygen delivery.
An ideological shift has occurred in the past 10 years toward limiting prehospital fluid resuscitation. This idea is certainly not new and was originally proposed by Cannon in 1918 while studying shock in casualties of World War I.[10] This challenge to the long-held dogma that acellular fluid resuscitation improves outcomes remains controversial, but evidence is mounting in its defense.
As hemorrhagic shock begins, the hypotension that ensues actually helps the patient meet 2 goals: arrest of exsanguination and maintenance of existing oxygen delivery. This is accomplished by sparring forming thrombus and maintaining coagulation factor and hemoglobin levels. Once aggressive fluid resuscitation is instituted, increasing blood pressure dislodges thrombus and hemodilutes hemoglobin, platelets, and clotting factors, therefore decreasing overall oxygen delivery.[6, 7, 8, 9 and 11]
The concept of permissive hypotension currently is used in the treatment of abdominal aortic aneurysms as a standard of care.[12 and 13] It has been established that patients suffering from leaking abdominal aortic aneurysms who are maintained at normal pressures result in repeated bleeding. Current treatment aims to keep patients' systolic blood pressure between 70 and 85 until operative intervention can be performed. [12 and 13] Blunt and penetrating trauma resulting in hemorrhagic shock follows a parallel concept.
A recent review of studies indicates that aggressive prehospital fluid resuscitation in hemorrhage does not lead to positive patient outcomes.[4, 5, 6, 7, 8, 9, 11, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24 and 25]
A 1994 study by Bickell et al[4] on penetrating torso trauma showed a 70% survival rate for delayed fluid resuscitation as opposed to a 62% for the aggressive fluid resuscitation group. This study included 598 patients with a prehospital systolic pressure < 90. The data suggested that patients who were fluid restricted in hypotensive states may be associated with lower mortality, shorter hospital stays, and fewer postoperative complications.
Another study by Kowalenko et al[17] using pigs with intraperitoneal hemorrhage to simulate hemorrhagic shock came to similar conclusions. Saline infusion to maintain a mean arterial pressure (MAP) of 40 in one group, 80 in the second, and none in the third revealed a survival rate of 87.5%, 37.5%, and 12.5%, respectively. [17]
A similar study done by Stern et al[18] using pigs with groups given saline to maintain MAP of 40, 60, and 80 were observed for 60 minutes or until death. The group maintained at 80 MAP had the highest mortality rate with a mean survival time of 44 minutes. The authors concluded that attempts to normalize blood pressure resulted in higher mortality rates and increased hemorrhage volumes. [18]
Yet another study[8] conducted at Ben Taub Trauma Center in Texas of 598 patients with penetrating torso injuries and prehospital hypotension came to similar conclusions. Those who received 2.5 liters of fluid had a 62% survival rate, but those administered < 0.5 liters had a 70% survival rate.
(to be continued)...
