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The environmental and logistical constraints of the prehospital setting make it a challenging place for the treatment of trauma patients. This is perhaps more pronounced in the management of battlefield casualties before extraction to definitive care. In seeking solutions, interest has been renewed in implementing damage control resuscitation principles in the prehospital setting, a concept termed remote damage control resuscitation. These developments, while improving conflict survival rates, are not exclusive to the military environment, with similar situations existing in the civilian setting. By understanding the pathophysiology of shock, particularly the need for oxygen debt repayment, improvements in the assessment and management of trauma patients can be made. Technology gaps have previously hampered our ability to accurately monitor the prehospital trauma patient in real time. However, this is changing, with devices such as tissue hemoglobin oxygen saturation monitors and point-of-care lactate analysis currently being refined. Other monitoring modalities including newer signal analysis and artificial intelligence techniques are also in development. Advances in hemostatic resuscitation are being made as our understanding and ability to effectively monitor patients improve. The reevaluation of whole-blood use in the prehospital environment is yielding favorable results and challenging the negative dogma currently associated with its use. Management of trauma-related airway and respiratory compromise is evolving, with scope to improve on currently accepted practices. The purpose of this review is to highlight the challenges of treating patients in the prehospital setting and suggest potential solutions. In doing so, we hope to maintain the enthusiasm from people in the field and highlight areas for prehospital specific research and development, so that improved rates of casualty survival will continue.

In conclusion, these data suggest that BNP and NT-proBNP increase with ascent to HA both after exercise and at rest. We also report the novel finding that BNP is significantly greater in those with severe AMS at 5150 m.

High altitude exposure normally leads to a marked natriuresis and diuresis. Acute mountain sickness is often associated with fluid retention, to which an elevated cortisol may contribute. Most investigators report a rise in resting cortisol with ascent, but little data exist regarding the cortisol response to a day trekking. We therefore measured salivary cortisol during ascent to > 5000 m in a cohort of between 42-45 subjects following a 6-h trek (samples taken between 15:30-16:30 h) and between 15-20 subjects at rest (morning samples taken between 08:00-09:00 h). Morning resting cortisol [nmol/l, mean±sd, (range)] was 5.5±2.9 (2.13-13.61) at 1300 m; 4.7±6.8 (1.4-27.02) at 3400 m, and significantly (p=0.002) rose between 4270 m [3.5±2.1 (1.4-8.34)] and 5150 m [14.5±30.3 (1.9-123.1)]. Post-exercise cortisol [nmol/l, mean±sd, (range)] dropped between 3400 m [7±6 (1.5-33.3)] and 4270 m [4.2±4.8 (1.4-29.5)] (p=0.001) followed by a significant rise in post-exercise cortisol between 4270 m [4.2±4.8 (1.4-29.5)] and 5 150 m [9.2±10.2 (1.4-61.3)] (p<0.001). There were no significant associations between severity of acute mountain sickness and cortisol levels. There was a significant though weak correlation between cortisol post-exercise at 5150 m and oxygen saturation at 5150 m (rho= - 0.451, p=0.004). In conclusion, this is the largest cohort to have their resting and post-exercise cortisol levels ascertained at high altitude. We confirm the previous findings of an elevated resting morning cortisol at > 5000 m, but present the novel finding that the cortisol response to a day trekking at HA appears suppressed at 4270 m.

Acute mountain sickness (AMS) is common at high altitude (HA) and associated with a relative failure of the natriuresis and diuresis that occurs at HA. The role of Brain Natriuretic Peptide (BNP) in this context has not been thoroughly investigated. We aimed to clarify if BNP rises in response to exercise at HA and if so whether this is related to AMS. 32 healthy subjects had assessments of BNP, aldosterone and AMS scores [as assessed by the AMS-C score of the Environmental Symptom Questionnaire (ESQ) and Lake Louise questionnaire] made following exertion at sea-level (SL), 3,400, 4,300 and 5,150 m. Data were analysed in the 23 subjects who did not consume drugs known to affect acclimatization. BNP (pg/ml, mean ± SEM) was significantly higher at 5,150 m versus the lower altitudes (p < 0.001 for all): 7.1 ± 1; 6.1 ± 0.3; 6.8 ± 0.9 and 17.7 ± 5.1 at sea-level; 3,400, 4,300 and 5,150 m. In those that showed a BNP response at 5,150 m (n = 19) versus those that did not demonstrate a BNP response (n = 4) there was a significant difference in Lake Louise (LL) AMS scores at 5,150 m on day 10 of the expedition (mean LL score 3.3 vs. 0.75, p = 0.034) and day 11 (mean LL score 3.3 vs. 0, p = 0.003). This is the first report to demonstrate a significant rise in BNP at HA. A BNP response at 5,150 m may be associated with a greater likelihood of suffering AMS.