Inflammation and the coagulation system may influence the genesis of chronic subdural hematoma (CSDH). The appearance of CSDH on computed tomography (CT) varies with the stage of the hematoma. This study investigated the pathogenesis and the recurrence of CSDH by comparing cytokine levels with the CT features of CSDH in 26 patients with 34 CSDHs who underwent single burr-hole surgery at our hospital between October 2004 and November 2006. The hematoma components removed during the procedure were examined, and the hematoma serum levels of cytokines measured such as thrombomodulin (TM), interleukin-6 (IL-6), tumor necrosis factor-α (TNFα), and interleukin-10 (IL-10). Using CT, mixed density hematomas were distinguished from other homogeneous hematomas, and found that the TM level was significantly higher in mixed density hematomas than in homogeneous hematomas (p = 0.043). Mixed density hematomas were classified into three subtypes (laminar, separated, and trabecular hematomas). The TM level was significantly higher in laminar and separated hematomas than in other hematomas (p = 0.01). The levels of IL-6, TNFα, and IL-10 were extremely high, but showed no significant differences in relation to the CT features. Mixed density hematomas had high recurrence rate, as reported previously, and TM level was high in mixed density hematomas such as laminar and separated mixed density hematomas. The present findings suggest that the types of CSDH associated with high TM levels tend to have higher recurrence rate.

Predictive variables of delayed cerebral ischemia (DCI) and pulmonary edema following subarachnoid hemorrhage (SAH) remain unknown. We aimed to determine associations between transpulmonary thermodilution-derived variables and DCI and pulmonary edema occurrence after SAH. We reviewed 34 consecutive SAH patients monitored by the PiCCO system. Six patients developed DCI at 7 days after SAH on average; 28 did not (non-DCI). We compared the variable measures for 1 day before DCI occurred (DCI day -1) in the DCI group and 6 days after SAH (non-DCI day -1) in the non-DCI group for control. The mean value of the global end-diastolic volume index (GEDI) for DCI day -1 was lower than that for non-DCI day -1 (676 ± 65 vs. 872 ± 85 mL/m, P = 0.04). Central venous pressure (CVP) was not significantly different (7.8 ± 3.1 vs. 9.4 ± 1.9 cm H2O, P = 0.45). At day -1 for both DCI and non-DCI, 11 patients (32%) had pulmonary edema. Global end-diastolic volume index was significantly higher in patients with pulmonary edema than in those without this condition (947 ± 126 vs. 766 ± 81 mL/m, P = 0.02); CVP was not significantly different (8.7 ± 2.8 vs. 9.2 ± 2.1 cm H2O, P = 0.78). Although significant correlation was found between extravascular lung water (EVLW) measures and GEDI (r = 0.58, P = 0.001), EVLW and CVP were not correlated (r = 0.03, P = 0.88). Thus, GEDI might be associated with DCI occurrence and EVLW accumulation after SAH.

Background: The aim of this study was to evaluate the time course of recovery from cerebral vulnerability, using microdialysis (MD) technique and cerebral vascular autoregulation measurement, to clarify the appropriate timing of subsequent major surgical procedures, and to minimize the possibility of secondary brain injury in patients with severe traumatic brain injury (STBI). Methods: In 3,470 MD samples of 25 patients with STBI, cerebral extracellular biomarkers (glucose, lactate, pyruvate, glycerol, and glutamate) were measured. In addition, to estimate cerebral vascular autoregulaton, the pressure reactivity index (PRx) was calculated with intracranial pressure (ICP) and mean arterial pressure. The data with ICP, cerebral perfusion pressure (CPP), and PRx were collected hourly for 7 days after injury and they were compared with MD biomarkers daily. Results: During the study period, the average ICP and CPP remained stable and were within the threshold of STBI treatment guidelines. After injury, the extracellular glucose concentration decreased, and the levels of glycerol, glutamate, and lactate/pyruvate ratio (LPR), which indicate cerebral ischemia and neural cell damage, increased. On the fourth day after injury, the extracellular glucose concentration improved, and the value of LPR decreased. The average PRx decreased daily and became negative on the fifth day after injury. Conclusion: Our results indicated that cerebral vascular autoregulation would recover on the fourth day after STBI, and cerebral perfusion might be increased by recovery of autoregulation. Thus, subsequent nonemergent surgery should be performed at least 4 days after STBI to prevent secondary brain injury. In addition, we should keep in mind that the cerebral vulnerability might persist for 4 days after suffering STBI.

Objective: We conducted a systematic review to determine the prevalence and characteristics of earthquake-associated head injuries for better disaster preparedness and management.Methods: We searched for all publications related to head injuries and earthquakes from 1985 to 2018 in MEDLINE and other major databases. A search was conducted using “earthquakes,” “wounds and injuries,” and “cranio-cerebral trauma” as a medical subject headings.Results: Included in the analysis were 34 articles. With regard to the commonly occurring injuries, earthquake-related head injury ranks third among patients with earthquake-related injuries. The most common trauma is lower extremity (36.2%) followed by upper extremity (19.9%), head (16.6%), spine (13.1%), chest (11.3%), and abdomen (3.8%). The most common earthquake-related head injury was laceration or contusion (59.1%), while epidural hematoma was the most common among inpatients with intracranial hemorrhage (9.5%) followed by intracerebral hematoma (7.0%), and subdural hematoma (6.8%). Mortality rate was 5.6%.Conclusion: Head injuries were found to be a commonly occurring trauma along with extremity injuries. This knowledge is important for determining the demands for neurosurgery and for adequately managing patients, especially in resource-limited conditions.

Coagulopathy, a common complication of traumatic brain injury (TBI), is characterized by a hypercoagulable state developing immediately after injury, with hyperfibrinolysis and bleeding tendency peaking 3 h after injury, followed by fibrinolysis shutdown. Reflecting this timeframe, the coagulation factor fibrinogen is first consumed and then degraded after TBI, its concentration rapidly decreasing by 3 h post-TBI. The fibrinolytic marker D-dimer reaches its maximum concentration at the same time. Hyperfibrinolysis in the acute phase of TBI is associated with poor prognosis via hematoma expansion. In the acute phase, the coagulation and fibrinolysis parameters must be monitored to determine the treatment strategy. The combination of D-dimer plasma level at admission and the level of consciousness upon arrival at the hospital can be used to predict the patients who will "talk and deteriorate." Fibrinogen and D-dimer levels should determine case selection and the amount of fresh frozen plasma required for transfusion. Surgery around 3 h after injury, when fibrinolysis and bleeding diathesis peak, should be avoided if possible. In recent years, attempts have been made to estimate the time of injury from the time course of coagulation and fibrinolysis parameter levels, which has been particularly useful in some cases of pediatric abusive head trauma patients.