Catastrophic Non-Survivable Brain Injury

BACKGROUND

Catastrophic brain injury, for the purpose of this guideline, is defined as any brain injury that is expected after imaging evaluation and /or clinical exam to result in the permanent loss of all brain function above the brain stem level.

NOTE: For patients with potentially survivable but severe Traumatic Brain Injury (TBI), refer to Joint Trauma System CPG, Neurosurgery and Severe Head Injury, 02 Mar 2017.

1. The intent of this guideline is to provide clinically useful recommendations which will allow providers at all roles of care who encounter these injuries to optimize the opportunity for these casualties to be evacuated safely and appropriately to the next level of care.

2. It is not the purpose of this guideline to address the complexities of brain death determination, or at what role of care and by what types of providers this determination should be made.

3. If appropriately resuscitated and hemodynamically normalized, these patients are more likely to be re-united with their families at Role 4 facilities. Additionally, evacuation from a combat theater of operations preserves the potential to honor the expressed intent of a patient to participate as an organ donor. Experience at Landstuhl Regional Medical Center between 2003 and 2013 demonstrated this opportunity to be on par with higher performing centers in CONUS. (Publication in draft, J. Oh, personal communication, 05 Aug 2016)

Catastrophic brain injury is associated with profound physiologic alterations that result in diffuse vascular regulatory disturbances and widespread cellular injury.1, 2 Severe alterations in metabolism,3-5 endocrine function,6-9 immunology10 and coagulopathy11-17 also commonly manifest. These disturbances frequently lead to multiorgan system failure, cardiovascular collapse and asystole in up to 60% of patients if not appropriately managed.3

It is known from animal studies that this cardiovascular deterioration is associated with impaired oxygen utilization, a shift from aerobic to anaerobic metabolism, a depletion of glycogen and myocardial high-energy stores, and the accumulation of lactate.3,5,9 This irregular metabolism has been associated with low levels of triiodothyronine (T3), thyroxin (T4), and to a lesser extent cortisol and insulin.6-9 Therapeutic replacement with T3 has been associated with complete reversal of anaerobic metabolism and subsequent stabilization of cardiac function when applied to human brain dead subjects.6,7 In addition, the use of T3 and similar thyroid replacement preparations have been associated with significant improvements in cardiovascular status, reductions in inotropic support, and decreases in donors lost from cardiac instability.5, 18-20 The etiology of this functional “hypothyroid state” is poorly understood, but may be a result of lower than normal thyroid stimulating hormone levels caused by the irreversible damage to the hypothalamus and pituitary from ischemia.21 Another explanation is a decrease in the peripheral conversion of T4 to its more potent analogue T3, similar to the euthyroid sick syndrome. It should be noted that evidence which validates the efficacy of hormonal replacement in this population of patients is not conclusive.22, 23 While this subject matter continues to be evaluated it should be recognized that early, effective, conventional critical care management is the therapeutic mainstay in these patients.24