Hemostatic Agents

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HEMOSTATIC AGENTS

Hemostatic Agents & Prehospital Provider Fluid Resusitation



Hemostatic Agents & Prehospital Provider Fluid Resusitation

Introduction

Currently there is considerable debate in the trauma literature, about the administration of intravenous isotonic fluids in hypotensive trauma patients with suspected uncontrolled hemorrhage, prior to control of the bleeding. The traditional approach of the emergency physician and the trauma surgeon is to correct any traumatic, hypovolemic hypotension as rapidly as possible. This stems from indoctrination during medical training that hypotension is uniformly deleterious to the patient. As a result, rapid infusion devices have become standard equipment in emergency rooms in trauma centers. This emphasis on immediate post-injury fluid resuscitation was based on early experimental data showing that rapid restoration of blood volume and pressure led to improvement of vital organ function and long term survival, by avoiding the late sequelae of hypovolemic shock (Asensio et al, 2001). However a number of trauma surgeons have challenged this conventional dictum. They expressed concern that overzealous fluid resuscitation before control of bleeding, may be detrimental to the patient by increasing the rate and amount of blood loss. On the other hand, many opponents of this concept suggest that uncorrected severe hypotension may lead to early death by increasing the risk of post resuscitative organ failure and exacerbating secondary brain injury in patients with associated traumatic brain injuries. This monologue will explore this evolving concept in greater detail and offer some guidelines.

Analysis

The concept of limited fluid resuscitation or even non-resuscitation of trauma patients is not novel. In the mid sixteenth century, the famous French surgeon Ambrose described the conservative treatment of a soldier with an abdominal gunshot wound, who survived with no operation or fluid resuscitation. Canon, in the early part of the twentieth century alluded to the disadvantages of giving fluids to a bleeding hypotensive patient, as it may "pop the clot" and hasten exsanguination. This has even greater applicability to the combat field setting, and consequently military medical research focussed on determining the ideal resuscitation method and type of fluids to use in war time casualties (Alspaugh et al, 2000).

Since then considerable experimental evidence has accumulated to support that aggressive fluid resuscitation leads to increased bleeding by a variety of proposed mechanisms. Increased mean arterial and venous pressure leads to a greater pressure-head for blood loss, by dislodging a nascent hemostatic clot, hemodilution of platelets and clotting factors and alterations in the viscosity and rheologic properties of blood. In addition there is some evidence that at the cellular level, hemodilution reduces the oxygen-carrying capacity of whole blood and decreases oxygen delivery to the tissues (Lepppaniemi et al, 1996). This is confounded by the proposed mechanism of "resuscitation injury" secondary to the ischemia-reperfusion phenomenon. Almost forty years ago, Shaftan et al3 demonstrated in a dog model of unrelenting arterial bleeding, that aggressive fluid resuscitation actually increased the amount of blood loss. This finding was confirmed by subsequent animal model studies on uncontrolled intra-abdominal and intra-thoracic hemorrhage (Dutton, Mackenzie, Scalea, ...