The Neglected Prehospital Phase of Head Injury: Apnea and Catecholamine Surge

doi:10.4065/75.1.37

Mayo Clinic Proceedings

Volume 75, Issue 1, January 2000, Pages 37-47

https://doi.org/10.4065/75.1.37 Get rights and content

The prehospital phase of head injury, also called the critical phase, consists of trauma-induced apnea and stress catecholamine release. This immediate period after head injury remains poorly summarized in the literature and essentially ignored with respect to treatment. A MEDLINE search of the literature on apneustic response and catecholamine surge after head injury and a review of literature from my acquired references revealed 116 references (from more than 600) that were pertinent. Apnea induced by head injury produces hypoxia, hypercarbia, and subsequent cardiac failure and hypotension, which, along with substantially bstantially elevated catecholamine values, promote secondary mechanisms of organ injury. Treatment for this immediate period after head injury requires a rapid response to the scene of trauma and development of treatment options that can be instituted at the scene of injury.

Section snippets

CRITICAL PHASE OF HEAD INJURY

The critical phase of head injury is arbitrarily defined in this article as the first 10 minutes after the onset of a severe head injury since patients live or die based on the pathophysiology that occurs during this period. The phases of severe head injury are outlined in Table 1.1, 2 Miller¹ and Overgaard and Tweed² noted that both ischemic and hypoxic brain injury are substantial before hospital admissian, and they emphasized the importance of this critical phase in patient outcomes.

Two

DISCUSSION

Maciver et al¹⁰⁶ stated 40 years ago that the staggering morbidity and mortality of severe head injury could be substantially reduced by simply providing ventilation to such patients at the accident scene. When this measure was undertaken, the 90% mortality rate in these patients was dramatically decreased to 40%. Arguably, the most substantial reduction in trauma morbidity and mortality in the United States occurred with the 1966 publication of Accidental Death and Disability: The Neglected

CONCLUSIONS

The critical phase of head injury determines life or death at the scene. Even among persons who survive and are treated in a hospital, the critical phase of head injury sets into motion physiological and biochemical cascades that influence medical care and determine outcome. We must begin efforts to improve outcome of head injury by addressing this period, which has been relatively neglected despite overwhelming evidence of its importance. If we respond to head injury as rapidly as possible and

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This describes a physiological response to brain injury, which can’t necessarily be detected in gross pathological changes at post mortem. Within the critical phase of head injury, arbitrarily defined as the first ten minutes following injury [30], concussive pressure transmitted to the brainstem can lead to apnoea and a subsequent stress-related massive sympathetic discharge. The combined effects of hypoxia, hypercarbia, acidosis and blood pressure surge, as well as direct catecholamine effects on tissue lead to synergistic injurious effects.
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One hundred and thirty-four deaths met our inclusion criteria; 79% were male, average age at death was 53.6 years. Sixty-two were found dead (FD), fifty-eight died at scene (DAS) and fourteen were dead on arrival at hospital (DOA). The predominant mechanism of injury was fall (39%). The median ISS was 29 with 58 deaths (43%) having probability of survival of >50%. Post-mortem evidence of head injury was present in 102 (76%) deaths. A bystander was on scene or present immediately after injury in 45% of cases and prior to the Emergency Medical Services (EMS) in 96%. In 93% of cases a bystander made the call for assistance, in those DAS or DOA, bystander intervention of any kind was 43%.
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ReviewThe Neglected Prehospital Phase of Head Injury: Apnea and Catecholamine Surge

Section snippets

CRITICAL PHASE OF HEAD INJURY

DISCUSSION

CONCLUSIONS

Br J Anaesth

Mayo clin Proc

Am J Surg

Am Heart J

Hum Palhol

Lancet

Eur J Pharmacol

j Lmerg Med

Lancet

Cerebral circulation after bead injury, part 4: functional anatomy and boundary-zone flow deprivation in the firsl week of traumatic coma

J Neurosurg

Belträge zur experimentellen chirurgie

Arch Klin Chir

Recherches expérimentales: sur la commotion cérébrale

Rev Chir

A contribution to the theory of cerebral concussion

Ann Surg

Cerebral concussion

Arch Surg Chicago

Experimental cerebral concussion

Brain

The physiologic basis of concussion

J Neurosurg

Fluid percussion model of mechanical brain injury in the cat

JNeurosurg

Head injury in man and experimental animals: clinical aspects

Ac ta Neurochir Suppl /Wien)

Experimentat missile wound to the brain

J Neurosurg

Effect of posttraumatic hypoventilalion on cerebral energy metabolism

J Neurosurg

Characterization of edema by diffusion-weighted imaging in experimental traumatic brain injury

J Neurosurg

Effect of indo-methacin pretreatmenl on acute mortality in experimental brain injury

J Neurosurg

Combined effect of respirator-induced ventilation and Superoxide dismulase in experimental brain injury

J Neurosurg

Alcohol and head injury: an issue revisited

J Neuro-trauma

Paradoxical effects of acute cthanolism in experimental brain injury [published correction appears in J Neurosurg, 1998:89:348]

J Neurosurg

Effects of ethanol on respiratory function in traumatic brain injury

J Neurosurg

The early critical phase of severe head injury: importance of apnea and dysfunctional respiration

J Trauma

A new model of diffuse brain injury in rats, part I: pathophysiology and biomechanics

J Neurosurg

Role of apnea in nonaccidentat head injury

Pediatr Neurosurg

The role of secondary brain injury in determining outcome from severe head injury

J Trauma

Early and late systemic hypotension as a frequent and fundamental source of cerebral ischemia following severe brain injury in the Traumatic Coma Data Bank

Ada Neurochir Suppl(Wien)

The outcome of severe closed head injury

J Neurosurg

Reversal of incipient brain death from head-i njury apnea at the scene of accidents [letter]

N Engt J Med

Concerning a definite regulatory mechanism of the vasomotor centre which controls blood pressure during cerebral compression

Bull Johns Hopkins Hosp

On the changes produced in the circulation and respiration by increase of the inlracranial pressure or tension

Philos Trans

The early and remote effects of total and partial paravertebral sympathectomy on blood pressure

AnnSurg

Effect of progressive sympaüiectomy on hypertension produced by increased intracranial pressure

Am J Physiol

The role of the adrencrgic nervous system in the prcssor response due lo acute elevation of inlracranial pressure (Cushing's response): a pharmacological analysis

Arch tnt Pharmacodyn Ther

Mechanical brain injury: the sympathoadrenal response

J Neurosurg

Circulating catecholamines in cals before and after lethal head injury

Proc Soc Exp Biol Med

The activity of the sympathetic nervous system following severe head injury

Intensive Care Med

Hacmodynamic changes in patients with severe head injury

Act Neurochir (Wien)

Review
The Neglected Prehospital Phase of Head Injury: Apnea and Catecholamine Surge