Mounting evidence has identified the following independent risk factors for the development of acute coagulopathy after a TBI, including a GCS ≤ 8, pre-hospital intravenous fluid infusion ≥ 2000 ml, subarachnoid hemorrhage, and a midline shift on CT images [1, 2]. In addition, patients with a penetrating TBI had a higher incidence of coagulopathy and a higher mortality rate than patients with a closed craniocerebral injury . Intravenous mannitol and hypertonic saline are routinely used to control intracranial hypertension in patients with a severe TBI; however, the impact of a single bolus infusion of hypertonic fluids could worsen hypocoagulability and hyperfibrinolysis in patients with hemorrhagic shock trauma . The present study demonstrated that some risk factors, such as GCS on admission, ISS on admission, and abnormal pupil size, could be used to assess the severity of brain injury after trauma and predict the occurrence of coagulopathy for patients with a TBI within 72 h post-operatively. Notably, bilateral mydriasis pre-operatively was a strong predictor. Nevertheless, whether complicated by a coagulopathy or not, patients with a severe TBI, pupil mydriasis, and no light reflex, despite undergoing decompressive craniectomy, could have high mortality and disability rates.
In the setting of trauma or emergency surgery, intra-operative bleeding can be minimized with optimal pre-operative preparation, but cannot be prevented completely. In this study, duration of surgery (OR = 2.199) and intra-operative blood loss (OR = 1.002) were independent risk factors for post-operative coagulopathy. It has been confirmed that shortening the duration of surgery, avoiding unnecessary blood loss, and reducing blood transfusion may help save medical resources, reduce medical costs, and decrease the mortality rate [13, 14].
The main goals of fluid therapy for patients with a TBI are to optimize cerebral perfusion and maintain adequate cerebral oxygenation. The anesthesiologist may prefer rapid intra-operative fluid infusion to maintain blood pressure and cerebral blood flow stability when blood pressure decreases markedly after the induction of general anesthesia or relief of intracranial hypertension. Although this study confirmed that a large volume of intra-operative crystalloid resuscitation is an independent risk factor for patients who developed a coagulopathy in the early post-operative period (OR = 1.004), there is still considerable controversy about fluid resuscitation for trauma patients. Shin et al.  reported that the volume of intra-operative fluid administration (900–1100 ml) is consistently associated with optimal 30-day mortality, respiratory complications, acute kidney injury, and post-operative length of stay in adults undergoing non-cardiac surgery. Hahn et al.  recommended the intra-operative administration of 3–5 ml/kg/h of crystalloids; however, additional fluid should be administered to patients who have more bleeding during surgery. Crystalloid resuscitation (> 2000 ml) for patients with a TBI is associated with increased mortality; thus, limited resuscitation before and after surgery may be indicated [17, 18].
A coagulopathy in patients with a TBI has been strongly associated with progressive hemorrhagic injury. Approximately one-half of TBI patients with a coagulopathy could subsequently exhibit hemorrhagic progression of the initial brain contusions within 48 h . There were statistical differences in contusion expansion within 24 h (p = 0.014) between patients who did and did not develop a coagulopathy 1 week after surgery based on our research. Furthermore, a coagulopathy within 72 h post-operatively and contusion expansion during the early post-operative period were independent risk factors for non-survival of patients with a TBI. The research results conclusively prove that coagulopathy alone and contusion expansion secondary to a coagulopathy may be associated with increased mortality.
At different onset times, a coagulopathy could lead to different mortality rates, and a coagulopathy with early onset after injury and long duration is a marker of increased morbidity and poor outcomes . Carrick et al.  implied that coagulopathy increased from 21–41% from the 1st day to the 3rd day in patients with a TBI. Finally, the mortality rate was 62%, and the length of stay was increased by 1 day (p = 0.14) in such patients. In agreement with Solla et al.  and Corbett , we reported that coagulopathy within 72 h post-operatively may portend a higher mortality rate, whether 1 week, 3 months, or 6 months. Therefore, it is essential to prevent coagulopathy and shorten the duration of the coagulopathy to improve clinical neurologic outcomes.
We have been cautious in interpreting these findings because of the limitations in our study. First, a retrospective clinical study has a significant selection bias that might influence the results. Second, these data, including osmotic/diuretic drugs, fluid resuscitation, severe hypoxia or asphyxia, and blood loss in the pre-hospital emergency care, were not uniformly available for us to incorporate into the subgroup analysis. Third, traditional blood coagulation tests, as the most commonly used method to detect coagulation abnormalities, did not provide the status of platelets, fibrinogen function, and fibrinolysis in coagulation cascades. Indeed, thromboelastography could play an essential role in accurately diagnosing platelet dysfunction, fibrinogen deficiency, and hyperfibrinolysis.