A Review of "Prehospital Hypotension as a Valid Indicator of Trauma Team Activation" (2000).

Prehospital hypotension has been utilized for decades as a surrogate marker of injury severity. Several studies have discussed the correlation between injury and hypotension both in the field as well as in the emergency department. Increases have been noted in injury severity score and mortality. Resource utilization is higher in this patient population. This study revisits our original work from 2000 and reviews the current literature regarding hypotension and injury severity. We also examine the role of prehospital hypotension as an indicator of trauma team activation and resource allocation. This review serves as a part of a Literary Festschrift in honor of Dr J David Richardson's role as the Editor-in-Chief of The American Surgeon.

The ebb and flow of fluid (as in resuscitation).

Since the early 1960's "resuscitation" following major trauma involved use of replacement crystalloid fluid/estimated blood loss in volumes of 3/1, in the ambulance, emergency room, operating room and surgical intensive care unit. During the past 20 years, MAJOR paradigm shifts have occurred in this concept. As a result hypotensive resuscitation with a view towards restriction of crystalloid, and prevention of complications has occurred. Improved results in both civilian and military environments have been reported. As a result there is new focus on trauma surgical involvement in all aspects of trauma patient management, focus on early aggressive surgical approaches (which may or may not involve an operation), and movement from crystalloid to blood, plasma, and platelet replacement therapy.

Jim Peters' collapse in the 1954 Vancouver Empire Games marathon.

On 7 August 1954, the world 42 km marathon record holder, Jim Peters, collapsed repeatedly during the final 385 metres of the British Empire and Commonwealth Games marathon held in Vancouver, Canada. It has been assumed that Peters collapsed from heatstroke because he ran too fast and did not drink during the race, which was held in windless, cloudless conditions with a dry-bulb temperature of 28 degrees C. Hospital records made available to us indicate that Peters might not have suffered from exertional heatstroke, which classically produces a rectal temperature > 42 degrees C, cerebral effects and, usually, a fatal outcome without vigorous active cooling. Although Peters was unconscious on admission to hospital approximately 60 minutes after he was removed from the race, his rectal temperature was 39.4 degrees C and he recovered fully, even though he was managed conservatively and not actively cooled. We propose that Peters' collapse was more likely due to a combination of hyperthermia-induced fatigue which caused him to stop running; exercise-associated postural hypotension as a result of a low peripheral vascular resistance immediately he stopped running; and combined cerebral effects of hyperthermia, hypertonic hypernatraemia associated with dehydration, and perhaps undiagnosed hypoglycaemia. But none of these conditions should cause prolonged unconsciousness, raising the possibility that Peters might have suffered from a transient encephalopathy, the exact nature of which is not understood.