الفهرس 
Aim of the workOnly 14 pages are availabe for public view
 |  | from | 95 |  |  |
| | | from | 95 | | |
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.