TBI related death has become the new epidemic in polytrauma: a 10-year prospective cohort analysis in severely injured patients

In this study of severely injured patients admitted to the ICU, the overall mortality rate was 18%, with a preventable death rate of 0.9%. Over the 10-year study period, there was no significant change in the mortality rate, nor was there a significant difference in the causes of death. Overall, 12% of patients in the studied population died of TBI which made TBI the main cause of both early and late death in all studied years. It should be noted that in the whole polytrauma population the median AIS_head was 3 (1–4) which means a serious, but often not life-threatening injury. However, in patients who later died median AIS_head was 4 (3–5), and in patients who died of TBI median AIS_head was 4 (4–5). The high frequency of TBI related deaths is comparable to data from other studies worldwide [2, 6,7,8, 21, 22]. The overall death rate by exsanguination was 0.9% (5/578) in this severely injured patient population during the studied decade. This is much lower than reported in literature, even in comparable study populations [2, 6,7,8, 21]. Although MODS occurred in 16% of patients, MODS related mortality was 0.7% in the whole population. This was lower than several other studies [6, 8, 21,22,23]. The incidence of ARDS was already low in early years and seemed to be virtually non-existent anymore in later years with an overall death rate of 0.2% (one patient died of ARDS in 10 years). Likely, a combination of short transport times, short times to treatment, decrease in crystalloids, hemostatic resuscitation, damage control surgery combined with early appropriate care for fractures and lung protective ventilation has attributed to this reduction in ARDS [4, 24, 25].

Independent predictors for mortality in the whole studied population were age, AIS_head, BD_ED, and BD_ICU, PaO2_ICU and crystalloids ≤ 24 h. Since age could not be influenced, and there is not much to be done to ameliorate the effects of primary TBI, efforts should be made to optimize brain perfusion (with focus on optimizing gas exchange as early as possible and limited crystalloid administration), and minimize secondary brain injury; Abnormalities in both partial pressure of oxygen (PaO2) and partial pressure of carbon dioxide (PaCO2) are detrimental for the brain. Further, hypotension should be prevented in patients with associated TBI, and the interval between injury and definitive bleeding control is most critical to prevent worsening of the brain injury [26]. Large volumes of fluids should be avoided since they cause an imbalance in intracellular and extracellular osmolarity which on its turn ignites an inflammatory response. Inflammatory complications such as MODS and ARDS are known to be associated with large crystalloid-based resuscitation strategies [27,28,29]. In the last years, research on TBI has focused on targeting the pathophysiology and decreasing the inflammatory response to diminish tissue damage and cell necrosis to slow down the process of nerve degeneration [30, 31].

In this study there was no difference in age during the studied period. This is in contrast with reports suggesting that age is rising in trauma patients [7, 8, 10, 32]. This might be attributed to the inclusion criteria since patients with isolated TBI and geriatric patients with low energy injuries were excluded from this study. With an aging general population TBI will only increase and become the next epidemic in trauma. TBI constitutes a major health and socioeconomic problem throughout the world. It has not only become the largest cause of death, but survivors from severe TBI will frequently need long and intensive rehabilitation, have often a life-long disability with frequently need of assistance with activities of daily living.

ISS was different between the studied years with a rise in the later years, especially in deceased patients. This suggests that at a certain injury level death becomes almost inevitable (6/8 deaths in 2023 had an ISS > 50, 3 of them had an ISS of 75). This increase in ISS is likely even higher since AIS coding was changed from AIS98 to AIS08 in the Dutch Trauma Registry in 2015, resulting in a general decrease in ISS in later years [33].

It is worth mentioning that patients included in this study did not exhibit severely disrupted physiology upon arrival in ED despite severe injuries (ISS 29) and 65% of them requiring urgent surgery. This occurrence, where severely injured patients from smaller service areas with brief transport times do not display disrupted physiological parameters upon arrival has been documented before [24].

It remains unclear why Prothrombin time (PT) measured in ED was prolonged in the first years since all other physiological and demographic parameters in ED were similar over the years. We did not collect data on anticoagulant use, but there is no reason to suspect that anticoagulant use has decreased over the years. It is however possible that this decrease in PT was influenced by the type of anticoagulant used, since there has been an overall change from vitamin K antagonists to non-vitamin K antagonist oral anticoagulants (NOAC) use which has minimal effect on PT [34].

Hemoglobin in ICU increased likely due to early PRBC administration both prehospitally and in ED. First measured BD and bicarbonate in ICU decreased even though pH remained unchanged. We have no clear explanation for this phenomenon since other parameters that are an expression of physiologic derangement were unchanged.

Although generally still a fairly large amount of crystalloids ≤ 24 h was given, a decrease in the usage of crystalloids was observed in ED, OR and first 24 h during the studied period. Interestingly, crystalloid reduction was most obvious in patients who later died. This could be explained by an increased reluctance to overload polytrauma patients with associated TBI with fluids. Likely, the implementation of initial administration of isotonic fluids from 2 to 1 L as recommended in the 10th edition in the ATLS Advanced Trauma Life Support in 2018 has attributed to an overall decrease in crystalloid administration [35]. The decrease in early crystalloid administration has probably influenced blood product administration since there was an increase in administration of PRBC and FFP in ED. FFPs were also increasingly administered ≤ 8 and ≤ 24 h. The increase in FFPs was most apparent in patients who survived suggesting that FFP resuscitation in these patients was beneficial.

Over the years there was a decrease in ventilator days, this was most obvious in 2020 and 2021. Also, ICU_LOS was lowest in these 2 study years. There was however no difference in mortality rate nor in time to death in those years compared to other years. Likely, these lower ventilator days and ICU_LOS were influenced by the COVID era, when ICU beds were limited [36].

As far as we know, this is the first paper to systematically observe a series of consecutively severely injured patients over a span of ten years, offering comprehensive data on their physiological status, early interventions, and eventual outcomes for comparison. One limitation was that the study was conducted at a single center, where both research and clinical care were overseen by the same team of practitioners. Additionally, no information regarding pre-existing conditions was recorded, and in only half the patients Glasgow Coma Scale scores were collected. Furthermore, data wasn't collected for patients who arrived deceased at the ED or those who passed away before being admitted to the ICU. Despite these limitations, we believe that the cohort studied, predominantly comprising cases of blunt trauma in a densely populated area with short transportation times, can be seen as representative of similar urban settings with a similar prevalence of blunt trauma incidents.

In conclusion, in this 10-year analysis of severely injured patients admitted to ICU there was no difference in mortality rate despite an increase in ISS in the later years. TBI was the single largest cause of both early and late death in all years. Demographics and early physiology were remarkable similar. Hypoxia and base deficit in ICU, and crystalloid resuscitation were independent predictors for mortality that could be influenced to potentially decrease secondary brain damage. Less crystalloids and more blood products in the first 24 h were administered over the years. It will be challenging to further improve physiology to diminish TBI related deaths while maintaining the current level of care. With an increasing elderly population, TBI will become the next epidemic in trauma in the near future. Research should not only focus on (primary and secondary) prevention of brain damage, but also on decreasing the inflammatory response as was successfully done in other parts of the body in the past decades.

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