1. Hypoxemia and hypotension are two considerable factors associated with poor prognosis in severe traumatic brain injury (TBI) patients in the prehospital setting.
2. All reasonable efforts should be made to avoid hypoxemia and hypotension in the brain injured casualty. Reasonable efforts will be dictated by situation, available resources, and the tactical situation.
   1. Hypoxemia should be prevented in the brain injured casualty. Pulse oxymetry should be instituted as soon as possible along the chain of evacuation. Low oxygenation should be addressed as soon as it is practical to do so along the chain of evacuating.
   2. Hypotension should be avoided. Blood pressure should be measured as soon as possible along the chain of evacuation. Fluid resuscitation should be instituted for patients with systolic pressure < 90 as soon as resources and the tactical situation allow.

Hypoxemia, as evidenced by apnea, cyanosis, saturations < 90% or a PaO2 < 60 mm Hg, and hypotension, as evidenced by as a single episode of systolic blood pressure < 90 mm Hg, have been shown to be among the top five predictors of poor outcome in patients with TBI. It is therefore felt to be appropriate to identify and address these conditions as soon as available resources and the tactical situation allow.

Recognizing that assessment and treatment modalities may not be readily available in the forward military environment, the following is but a guide to the level of care that is recommended within certain tactical and operational limitations:

1. Combat Medic/Tactical Assessment: Determine patency of airway and note any obstruction. Ask the patient to speak. Look at the patient's chest and observe breathing motion. Feel for carotid and radial pulses. Mental status is very useful in assessing non-comatose patients since inadequate oxygenation and blood pressure may also alter mental status.
2. Evacuation Assessment: Measure oxygenation with SPO2 monitor. Measure BP and record. When possible, place a BP monitoring device.
3. Battalion Aid Station Assessment: If possible, measure oxygenation with SPO2 monitor. When equipment is not available, assess patient as recommended for first responder. Measure BP and record. When equipment is not available, feel for carotid and radial pulses.
4. Forward Surgical Assessment: Measure oxygenation with SPO2 monitor. Measure BP with BP monitoring device.

MEDLINE was searched from 1966 to 2005 using the following search terms: "head injury" or "traumatic brain injury" and "airway" or "hypoxemia" or "hypotension" or "oxygenation assessment" or "blood pressure assessment" or "field assessment of oxygenation and blood pressure." References from the book, Guidelines for Prehospital Management of Traumatic Brain Injury, chapter on "Assessment: Oxygenation and Blood Pressure" were also reviewed. Some studies of in-hospital patients with severe head injury and hypotension were used to corroborate out-of-hospital hypotension studies.

Assessment of Oxygenation

The concept of secondary injury is fundamental to understanding the management of TBI. Hypoxia has long been known to be a significant source of secondary brain injury. Significant Class III data have validated the concept that patients with an oxygen saturation < 90% have significantly worse outcome than patients whose oxygen saturations are > 90%.1,2 It should be emphasized that this recommendation is based on epidemiological data.

While it has never been demonstrated that improving blood oxygen saturation in the field improves outcome, a significant body of clinical research seems to support the assertion that this should be so. Knowing that blood oxygen saturation is > 90% is a long way from knowing anything about oxygen delivery to the brain. While the brain's general susceptibility to hypoxia is understood in general terms, the unique susceptibility of the injured brain to hypoxia is very poorly understood.

It is well known that the brain has very little cellular or tissue oxygen reserve and so is highly dependent on timely delivery of oxygen via the circulation. In general, the brain can only survive for 7 minutes without oxygen before the threat of irreversible cellular damage becomes very high. The cellular physiology of this process has been investigated, as have the biochemical consequences of low oxygen availability and ATP depletion in nerve cells. Nerve cells, glial cells, and cerebral vascular endothelium all appear to have unique susceptibilities to low oxygen tension, and so it is not surprising that patients with low oxygen saturation in the blood after injury may fair worse.3 It appears that the injured brain is even more susceptible to hypoxia than the healthy brain, but this assertion remains untested by all but epidemiological data.

Clinical studies in humans have demonstrated that patients with less oxygen delivered to their brain after injury appear to have worse outcomes.4,5

One method for assessing the adequacy of the brain's oxygen delivery is to measure how much oxygen the brain uses. This can be estimated by knowing the oxygen content of the blood entering the cranial vault, the systemic oxygen content, and then measuring the content of the blood leaving the cranial vault, which is done by placing a sensor or sampling catheter high in the jugular vein. By subtracting the oxygen content of the blood leaving the head from the content of the blood entering the head, a rough estimate of the brain oxygen utilization can be obtained. The resulting number is known as the AVO2 difference.

This number reflects the balance between the oxygen delivered to the brain and the metabolic activity, and therefore the oxygen demand, of the brain. A metabolically active brain will require more oxygen and more delivery of oxygen than a quiet brain. The brain will be injured when this demand is not met. The AVO2 difference really assesses if brain demand is being met.

The AVO2 difference is useful, but some estimates of the adequacy of oxygen delivery to the brain can be made by simply measuring the saturation of blood leaving the brain in the jugular bulb, the SjvO2. Most patients have saturations of 55-69% in blood leaving the brain. Studies have shown that patients with jugular saturations < 50% have worse outcomes.6,7

The real issue, however, is cerebral tissue oxygen tension. This can be measured via cerebral tissue oxygen monitoring. Normal cerebral tissue oxygen pressures, PbrO₂, are approximately 32 mm Hg. Studies have shown that patients whose PbrO₂ is allowed to dip to 15 or lower do significantly worse. Elegant work has stratified patients into groups with episodes of progressively lower brain tissue oxygen pressures, with increasingly poorer outcomes as the brain tissue oxygen pressure is allowed to go lower and the time the brain stays at these suppressed levels increases.4 Some brain tissue data has suggested that hypoxic brain injury is cumulative, that periods of recovery between episodes of hypoxia do not erase the negative effect of the hypoxia and that in fact, multiple brief episodes of hypoxia can be as damaging as a single prolonged hypoxic event.

Assessment of Blood Pressure

The assessment of blood pressure follows much the same logic as that for assessment of oxygen. The ultimate problem appears to be the delivery of adequate supplies of oxygen and other substrate to the brain after injury. For adequate supplies of oxygen to reach the brain, the blood must be well oxygenated, the saturations give some indication of this, and cerebral blood flow must be adequate. While systemic blood pressure is a poor way to assess cerebral blood flow, it is not unreasonable to assume that patients with low systemic blood pressure are at higher risk for low cerebral blood flow and so should be at higher risk for poor outcomes.

In fact, good epidemiologic data has demonstrated that patients with low systolic pressure have poorer outcomes from head injury than patients who are not permitted to have their systolic blood pressure dip below 90 mm Hg.1,2,8-15 Again, this argument is an epidemiological one as is the selection of 90 mm Hg as a cutoff for poor outcomes. This level was simply selected and it turned out that patients whose blood pressure was below 90 mm Hg did worse. If there is a better cutoff value or what that value might be is unknown.

Manley et al.16 have given us some insight into the dynamics of oxygen delivery in an animal model. He looked at brain tissue oxygen pressures during hemorrhagic shock. He showed how brain tissue oxygen pressure declined as oxygen delivery was compromised by hypovolemia due to bleeding. The hypothesis is that patients with low oxygen saturation in their blood and low systemic blood pressure are at higher risk for low oxygen delivery to the cerebral parenchyma after injury and so are at higher risk for subsequent hypoxic and ischemic injury. Good Class III epidemiology seems to confirm this suspicion.1-3,9-15,17

In his analysis of the prospectively collected National Trauma Coma Data Bank data, Chesnut et al.1 looked at the impact of hypoxemia, defined as apnea, cyanosis, saturations < 90% or a PaO2 < 60 mm Hg, and hypotension, defined as a single episode of systolic blood pressure < 90 mm Hg on outcome. Each was in the top five independent predictors of poor outcome.

A smaller Class III study from Australia also found the hypotension and hypoxemia were significant predictors of mortality.8 An interesting prehospital study from Italy looked at arterial saturation in the field in 50 patients and found a significant association between arterial saturation and outcome.2

A single episode of hypotension was associated with a doubling of mortality and an increased morbidity when compared with a matched group of patients without hypotension (Table A). Notably, the TCDB study defined hypotension and hypoxemia as a single reported incidence that meets the definition of each and does not require a protracted duration for secondary insult.

Patients with hypoxemia or hypotension have poorer outcomes from TBI than patients who avoid these conditions. It would therefore seem appropriate to correct these conditions as soon as resources and tactical situation allow.

A structured and prioritized approach to combat casualties is important because it enables a clear assessment process for the medic to follow. We acknowledge the Advanced Trauma Life Support Course™ of the Committee on Trauma of the American College of Surgeons.19 The course prioritizes airway before breathing and breathing before blood pressure and these strategies have been adopted worldwide. Other accepted methodological approaches to the comprehensive assessment and management of the TBI patient can be found in various sources.20 Standardized assessments are crucial to the appropriate assessment and then subsequent proper management of casualties in the forward area.

1. Prospective evaluation of assessment tools.
2. What is the optimum threshold for systolic blood pressure resuscitation?
3. Are there better field resuscitation end points?
4. What is the optimum oxygen saturation in the field?