Stroke Secondary to Trauma

Introduction

Stroke is common following trauma. Indeed, direct cerebrovascular injury during a traumatic event can often lead to immediate ischemic and hemorrhagic complications. However, recent definitions for hemorrhagic stroke have, by policy, excluded etiologies that are secondary to trauma . This was done to emphasize differences in presentation and outcomes between traumatic and nontraumatic etiologies, with nontraumatic etiologies including arterial hypertension, vascular malformation, underlying mass lesion, or coagulopathy.

In many clinical situations, this distinction becomes diagnostically difficult for two reasons. First it is often impossible to determine whether a nontraumatic event preceded a traumatic one. For example, in situations involving an intracerebral hemorrhage after a fall, patients can be hypertensive as part of the Cushing reflex. In such situations, it can be clinically unclear whether the instigating event was the hypertensive bleed or the fall. Second, hemorrhagic complications can develop in a delayed fashion following a traumatic event. Thus, although they are not directly caused by the trauma, they are a secondary consequence of it and, in many situations, due to the same etiologies as nontraumatic hemorrhagic stroke, including vascular dysfunction and coagulopathy.

However, to accommodate the new definition of stroke, in this chapter we will focus only on hemorrhagic complications that are not directly related to the traumatic event. This is in contrast to prior editions of this chapter in that primary injuries following trauma, such as immediate posttraumatic intracerebral hemorrhage and subarachnoid hemorrhage (SAH), will not be discussed as they no longer fall within the definition of stroke. Similarly, extraaxial hematomas such as subdural and epidural hematomas will also not be discussed, even if they present in a delayed fashion, as they too no longer fall under the classification of stroke utilizing the new definitions. With these stipulations, there remain two broad categories for stroke following trauma, ischemic and hemorrhagic.

Ischemic Stroke

Ischemic stroke following traumatic injury to the head is common and evidence of ischemic damage has been found in approximately 90% of deaths secondary to traumatic brain injury . There are two methods in which this occurs. One is a primary injury that is directly from trauma to the brain parenchyma and local vasculature from the event itself. The other is delayed and is considered a secondary brain injury. Indeed, delayed ischemic development is considered one of the most common mechanisms of secondary brain injury after a traumatic event. Studies have shown that the time course of this ischemic development has two peaks . The first occurs within the first 24 h and the second develops at approximately 2–3 days following injury.

Decreased Cerebral Perfusion Pressure

The instigating factor for the acute ischemic development is usually an elevated intracranial pressure (ICP) from either posttraumatic hemorrhage or edema. As the ICP rises in the closed cranial cavity, there is diminished cerebral perfusion pressure to the parenchyma, leading to the decreased oxygen delivery and resulting ischemia. This can be a local effect, with decreased perfusion occurring only near the area of injury, or a more global effect, with a decrease in perfusion occurring throughout multiple areas of the brain.

A clarification needs to be made regarding the latter situation since global ischemic events are also no longer considered stroke according to recent definitions . However, this distinction was made to remove cases of global hypoperfusion typically from causes outside the central nervous system, such as cardiogenic shock, hypovolemia, or hypoxia from drowning. The situation in posttraumatic circumstances, however, more resembles that following a malignant middle cerebral artery infarct where cerebral edema is leading to increased ICP and further diminishing cerebral blood flow. In the posttraumatic situation, compounding the effect of cerebral hypoperfusion is the precarious state of the traumatized brain. It has been shown in multiple studies that the injured brain is inherently more vulnerable to secondary ischemic insults. This primarily stems from the loss of several neuroprotective mechanisms, including autoregulation, which would otherwise serve to preserve cerebral blood flow in the presence of a decreased cerebral perfusion pressure.

Given the relative frequency of hypoperfusion-mediated ischemic events, cerebral blood flow monitoring has become routine in traumatic brain injury situations. Although the gold standard method for detecting cerebral blood flow to the brain, positron emission tomography, is often impractical in critically injured patients, bedside devices designed for detecting both global and local ischemia have been developed and are recommended in the guidelines for the management of traumatic brain injury set forth by the Brain Trauma Foundation . These include an intraparenchymal brain oxygenation probe, which is great for monitoring local hypoperfusion and internal jugular monitors of venous oxygenation (SjvO2), which can assess for global cerebral hypoperfusion. Numerous studies have shown poor outcomes when values obtained from these monitors fall below certain thresholds. For SjvO2 monitors, this value is typically less than 50% oxygenation, although it is likely that an appreciable portion of the brain must become ischemic before this value is reached. Similarly, for intraparenchymal brain oxygenation monitors, the value utilized is usually less than a partial pressure of 20 mm Hg. Therapies guided by these instruments and aimed at promoting brain oxygenation by increasing oxygen delivery are suggested to improve outcomes, although no controlled clinical trial has yet been conducted .

When posttraumatic cerebral hypoperfusion is secondary to an elevated ICP, treatment options depend entirely on the etiology and are outlined in the traumatic brain injury guidelines . If a surgically addressable mass lesion is present, surgical evacuation is usually the most effective course of action. Alternatively, if there is global cerebral edema present, initial treatment options include elevating the head, intubation with hyperventilation, CSF drainage via a ventriculostomy, decreasing cerebral metabolism with sedation and paralytics, and osmotic diuresis with mannitol. If these strategies prove ineffective, decompressive hemicraniectomy is often the next step to promote cerebral perfusion pressure. Initiation of a pentobarbital coma can also be utilized to decrease cerebral metabolism.