الفهرس | Only 14 pages are availabe for public view |
Abstract Traumatic brain injury can be defined as an alteration in brain function or other evidence of brain pathology caused by an external force. It is a leading cause of death and disability. Each year about 1.5 million persons die, and more than 10 million persons are hospitalized following TBI worldwide. There is no effective therapy for primary brain injury caused by the traumatic insult. Current treatment aimed to reduce the risk factors of secondary brain injury. One of the most important and devastating parts of the secondary pathologic cascade that may occur after the initial brain injury is the progression of intracranial hemorrhage (ICH), especially within the first 24 hours. Its frequency varies according to TBI severity. These observations raise the possibility that an intervention administered in the first hours after the injury may prevent the enlargement of intracranial bleeding and therefore might improve patients’ outcomes. The coagulation and fibrinolytic system are believed to be in a state of dynamic balance that maintains an intact vascular system. TXA as a potent antifibrinolytic agent reversibly blocks lysine binding sites on plasminogen and plasmin, and acts to prevent proteolytic degradation of fibrin clots formed in the normal physiologic process of hemostasis. Both plasminogen and plasmin are activators of fibrinolysis and active clot-lysing agents. TXA thus helps to stabilize fibrin clots, which in turn maintains coagulation and helps to control bleeding; with no apparent increase in vascular Summary 67 occlusive events, these findings raise the possibility that it might be effective in other situations in which bleeding can be life threatening or disabling. Our study assessed the effect of TXA on intracranial hemorrhage in patients with TBI. As well as worsening of glasgow coma scale, need for surgical intervention and blood transfusion. Our study was carried out upon 40 patients of traumatic brain injury with ICH in Critical Care Unit, Menoufia University hospitals during the period from January 2020 to January 2021. The inclusion criteria were adult patients (>16-year-old) with TBI within 8 hours of injury without indications for immediate surgical intervention and Glasgow Coma Scale (GCS) score of 4-12. The exclusion criteria were bilateral unreactive pupils at admission, unknown onset of injury, need for surgery, major extracranial bleeding, and cerebral edema with midline shift, hereditary or acquired coagulopahy. Initial brain CT scan was done immediately after admission and routine care. The baseline data including demographic data, mechanism of injury, and findings of initial brain CT scan (especially ICH volume) was entered. Patients were randomly classified using closed envelops into two groups (20 patients each): tranexamic group who received a loading dose of 1 g tranexamic acid infused over 10 minutes, followed by an iv infusion of 1 g over 8 hours and placebo group who received normal saline 0.9%. Our study revealed that there was significant increase ICH through the first 48 hours after TBI in placebo group. While, using of Summary 68 TXA resulted in significant reduction in the volume of ICH after 48 hours of admission, decreasing the incidence of complications. Moreover, there was no effect on coagulation profile In our study, tranexamic acid significantly improved the GCS after 48 hours than on admission, reduced the surgical intervention and the need of blood transfusion. The incidence of in-hospital complications recorded for 28 days (cerebral infarction, hydrocephalus, pulmonary embolism (PEs), and deep vein thrombosis (DVT) in placebo group were significantly more than that in TXA group. Early administration of tranexamic acid is associated with less hospital resources usage and better functional outcome. |