We found that half of the patients suffering multi-trauma in the mountains had concomitant TBI. One third of them was hypotensive with SBP ≤ 110 mmHg on hospital arrival, despite they received more fluids pre-hospitally than multi-trauma patients without admission hypotension. Hypotensive multi-trauma patients with TBI were more severely injured, had a more severe coagulopathy, lower hemoglobin levels and lower base excess values; body temperature was lower at hospital arrival. Hypotensive patients with TBI had the highest mortality rate compared to non-hypotensive multi-trauma patients with TBI and multi-trauma patients without TBI. No single variable or set of variables could reliably predict admission hypotension in multi-trauma patients with TBI.
Outdoor activities in the mountains have gained popularity over recent years.(16) In parallel, the number of SAR missions in mountainous environments has increased (17) and the proportion of potentially life threatening injuries has notably risen.(8, 9, 18) Data on TBI in severely injured trauma patients in mountainous areas is scarce. We found an incidence of TBI of about 50% among mountain multi-trauma patients, which is comparable to the rate of TBI among severely injured patients in urban or suburban areas.(19) The major cause leading to TBI in mountain accidents was fall during hiking.
Hypotension is common in severely injured patients (8, 9) and is tolerated to a certain degree in order to avoid the adverse effects of early and high-dose fluid resuscitation.(20) This concept of “permissive hypotension” is contraindicated in patients with TBI (2) because the maintenance of an adequate perfusion is essential to ensure tissue oxygenation of the injured central nervous system and to avoid secondary brain injury.(3–5, 21–23) The current guidelines of the Brain Trauma Foundation recommend to maintain SBP at ≥ 100 mmHg for patients 50 to 69 years old and at ≥ 110 mmHg for patients 15 to 49 or over 70 years old.(2) We found that one third of multi-trauma patients rescued in mountainous environment with TBI had SBP ≤ 110 mmHg on hospital arrival, in agreement with published data on urban trauma patients.(4, 6) These patients (group 1) had a marked drop of their SBP during the pre-hospital phase from a mean SBP of about 100 mmHg on scene to about 80 mmHg on hospital arrival, even though these patients received more aggressive fluid resuscitation as compared to the other groups of trauma patients. This might be due to several reasons. First, patients with TBI and admission hypotension were more severely injured and had a higher mean ISS compared to the other groups. We suspect that these patients had more severe traumatic bleeding, as they had lower hemoglobin levels, lower base excess values and more severe coagulopathy on hospital arrival, and hemorrhage is the most frequent cause of hypotension in trauma patients.(24) Yet, the higher ISS was mainly due to a higher AIS of the head/neck body region, where severe traumatic bleeding is relatively uncommon. Second, the drop of SBP during the pre-hospital phase could indicate that the treatment performed on scene was either insufficient or that no other treatment was feasible. Stopping the bleeding whenever possible and the administration of fluids (and possibly vasopressors) are the main options to maintain or augment blood pressure. Patients in with TBI and admission hypotension received significantly more fluids, though the fluid administration in all three patient groups was conservative with volumes of far less than one liter. Vasopressors were seldomly administered. The administration of vasopressors to maintain a sufficient cerebral perfusion pressure could play an important role in the treatment of multi-trauma patients with TBI, in particular in mountain SAR operations with prolonged pre-hospital times. Vasopressors allow to maintain target blood pressure and at the same time to limit the amount of fluid and the negative consequences associated with an excessive volume therapy (such as dilution coagulopathy, interstitial edema or hypothermia).(25) There is ongoing controversy regarding the role of vasopressor therapy in trauma patients.(26, 27) Current guidelines recommend the administration of vasopressors in addition to fluids to maintain target SBP in the presence of life-threatening hypotension (28) and recent studies on the use of vasopressin in trauma patients with hemorrhagic shock are promising.(29, 30) A third factor that could explain the drop in SBP during the pre-hospital phase in patients with TBI and admission hypotension is the induction of anesthesia and intubation on scene. Yet, the difference in the rate of pre-hospital intubation between TBI patients with and without admission hypotension was not different. Also, when comparing TBI patients with admission hypotension who were intubated on scene with TBI patients with admission hypotension who were not intubated on scene, no difference in SBP on admission was found.
We found that more than one third of patients in group 1 and 2 were hypothermic (body temperature < 35 °C) on hospital arrival while the rate of admission hypothermia was low in patients without TBI (group 3). This difference could be caused by the higher rate of anesthesia in group 1 and 2 compared to group 3. General anesthetics greatly impair thermoregulation, reducing the thresholds for vasoconstriction and shivering,(31) increasing the risk of hypothermia. Hypothermia is an independent predictor of mortality in trauma (32, 33) and hypothermia prevention is paramount, although often disregarded during the initial resuscitation and particularly difficult in the harsh environment encountered in mountain rescue.
We sought factors that could predict admission hypotension in order to identify at risk patients on scene and eventually adopt a more aggressive treatment. We used a relatively novel method in the field of medicine, i.e. classification trees.(13) Although a pre-hospital GCS of ≤ 11 could expectedly discriminate between patients with and without TBI, no single variable or any set of variables easily obtainable in the pre-hospital setting were able to predict admission hypotension with a reasonable sensitivity and specificity. Apart from GCS, the ISS and the AIS abdomen and AIS extremities were the variables most frequently selected in the classification trees. Both, the abdomen and the extremities can be a source of major bleeding, which affirms that hemorrhage is probably the main cause of hypotension multi-trauma patients with TBI and aggressive treatment of bleeding is paramount.
Limitations
First, the number of cases collected in the IATR is limited when compared to the large data sets of urban trauma cases. Second, some data were missing, which is a limitation inherent to almost all registries. Both limitations curb the possibility to draw specific treatment protocols for mountain trauma causalities from our analysis. This highlights the need to continue to prospectively collect high quality data on trauma patients in mountainous and remote areas to perform further in-depth analyses using a larger sample size. Third, in the IATR, head and neck injuries are grouped in a single category (head/neck) and therefore the rate of isolated or concomitant spinal cord injuries, which could contribute to hypotension and hypothermia, is unknown.