A 38-year-old construction worker is brought to the emergency department after falling from a 3.1 m (10 ft) height. Bystanders reported that the patient hit his head on the concrete and had jerking movements for 30 seconds. In the emergency department, blood pressure is 152/90 mm Hg, pulse is 92/min, and respirations are 16/min. On physical examination, the patient opens his eyes to verbal commands, makes incomprehensible sounds, and localizes pain. Glasgow coma scale score is 10. There is boggy swelling of the temporoparietal scalp. No major injuries of the chest, abdomen, or extremities are apparent. CT scan of the head shows linear fractures of the temporal and parietal bones, and multiple frontal, parietal, and temporal lobe contusions. There is no shift of midline structures. No cervical spine fracture or dislocation is present. Tranexamic acid is administered. Which of the following is the most likely mechanism of the beneficial effect of this drug?

Question

A 38-year-old construction worker is brought to the emergency department after falling from a 3.1 m (10 ft) height.  Bystanders reported that the patient hit his head on the concrete and had jerking movements for 30 seconds.  In the emergency department, blood pressure is 152/90 mm Hg, pulse is 92/min, and respirations are 16/min.  On physical examination, the patient opens his eyes to verbal commands, makes incomprehensible sounds, and localizes pain.  Glasgow coma scale score is 10.  There is boggy swelling of the temporoparietal scalp.  No major injuries of the chest, abdomen, or extremities are apparent.  CT scan of the head shows linear fractures of the temporal and parietal bones, and multiple frontal, parietal, and temporal lobe contusions.  There is no shift of midline structures.  No cervical spine fracture or dislocation is present.  Tranexamic acid is administered.  Which of the following is the most likely mechanism of the beneficial effect of this drug?

Quizplus · Accepted Answer

Explanation: 11ec25c8_d82d_31d5_bc81_e5b3bc757f10_MD0003_00 Neurologic injury from traumatic brain injury (TBI) occurs in 2 phases: the primary injury caused by the mechanical impact and the secondary injury caused by subsequent local and/or systemic insults. All patients who sustain significant trauma, including patients with TBI, are at risk of secondary injury from acute traumatic coagulopathy. Acute traumatic coagulopathy is characterized by increased activation of the coagulation pathway (due to severe tissue injury), leading to uncontrolled coagulation and consumption of coagulation factors. This results in the following: Hypocoagulability from secondary coagulation factor deficiency (ie, consumptive coagulopathy) Hyperfibrinolysis, which may break down necessary clots In patients with TBI, hypocoagulability and hyperfibrinolysis can worsen existing intracranial hemorrhage (ICH) or cause delayed ICH. For this reason, antifibrinolytic therapy is recommended (Grade 1 B recommendation) for many patients with TBI. Tranexamic acid is an antifibrinolytic medication that should be administered to patients who have moderate TBI (Glasgow coma scale score of 9-12) and are within 3 hours of injury; in these patients, it has been shown to reduce mortality. Tranexamic acid may also be beneficial for some patients with mild TBI (eg, those with ICH) or severe TBI. Glasgow coma scale Another important aspect of TBI management is the maintenance of adequate cerebral perfusion pressure (CPP) to prevent the secondary insult of ischemia. Because CPP is the difference between mean arterial pressure (MAP) and intracranial pressure (ICP), this involves the following: Maintaining MAP: Fluids and vasopressors are used as needed to maintain adequate CPP. Reducing elevated ICP: Osmotic therapy (eg, hypertonic saline, mannitol) can decrease cerebral edema by creating an osmolar gradient that draws water out of edematous brain tissue (Choice B). Sedation (eg, propofol, midazolam) can decrease cerebral metabolic demand and, subsequently, total cerebral blood flow/volume (Choice C). (Choices A and E) Hyperthermia and seizures, which are common in TBI patients, both increase cerebral metabolic demand (and ICP) and require treatment. Antipyretics (eg, acetaminophen) and surface-cooling devices are the usual methods for achieving normothermia. Antiseizure medications (eg, levetiracetam) are commonly given to prevent post-traumatic seizures. Educational objective: Acute traumatic coagulopathy, a state of hypocoagulability and hyperfibrinolysis, can complicate traumatic brain injury (TBI). Antifibrinolytic therapy (ie, tranexamic acid) can improve outcomes for patients with moderate TBI if administered within the first 3 hours after injury. References: Effects of tranexamic acid on death, disability, vascular occlusive events and other morbidities in patients with acute traumatic brain injury (CRASH-3): a randomized, placebo-controlled trial. (http://www.ncbi.nlm.nih.gov/pubmed/31623894) The pathogenesis of traumatic coagulopathy. (http://www.ncbi.nlm.nih.gov/pubmed/25440402) Final results of MRC CRASH, a randomized placebo-controlled trial of intravenous corticosteroid in adults with head injury-outcomes at 6 months. (http://www.ncbi.nlm.nih.gov/pubmed/15936423)

A 38-Year-Old Construction Worker Is Brought to the Emergency Department