Traumatic subarachnoid hemorrhage (tSAH)
Subarachnoid hemorrhage (SAH) entails bleeding in the arachnoid space, which lies between the surface of the brain and the arachnoid mater. Trauma is the most common cause of SAH and is associated with high morbidity. The incidence of traumatic SAH in patients with traumatic brain injury (TBI) ranges from 26%-53%1. Mortality can be as high as 50% in those with severe TBI1. Mechanisms of injury include rotational acceleration causing short-lasting oscillatory movements of the brain, vertebrobasilar artery stretch due to hyperextension, sudden rise of intra-arterial pressure from a blow to the cervical carotid artery, tearing of the bridging veins or pial vessels and diffusion of blood from the contusion into the subarachnoid space.Traumatic SAH is distinctly different than spontaneous SAH, which usually originates from a ruptured aneurysm. Traumatic subarachnoid hemorrhage (tSAH) involves cortical surfaces in contrast to spontaneous subarachnoid hemorrhage, which usually involves the basal cisterns. Traumatic subarachnoid hemorrhage usually does not put patient at risk for vasospasm and potential secondary ischemic stroke, in contrast to spontaneous subarachnoid hemorrhage. Therefore isolated traumatic subarachnoid hemorrhage usually has a good outcome.
Hemorrhagic contusion, also known as traumaticcerebral contusion, is typically caused by sudden deceleration, where the brain impacts on bony prominences as in a coup or contrecoup injury3. An area of high density is observed on CT scan3. Traumatic cerebral contusions usually expand over time3. They may appear with a delay, but most present by 72 hours following injury3. Late expansion up to 1 week after trauma is not very unusual. Patients with deteriorating neurologic status, medically refractory intracranial hypertension, mass effect on CT or large-volume traumatic cerebral contusion (>50 ml) should undergo surgical evacuation immediately3. Individuals with GCS 6-8 and frontal or temporal contusion volume >20 ml and mid-line shift ≥ 5 mm and/or compressed basal cisterns should also receive surgical evacuation3. Non-operative management includes maximal medical therapy with hypertonic saline to keep serum sodium up to 155 for osmotic drive of the extracellular fluid out of the brain for cerebral relaxation, prophylactic seizure therapy, close surveillance of neurological exam in the ICU and serial imaging, for neurologically intact patients with controlled intracranial pressure and no significant mass effect on CT3.
A closed fracture is a simple fracture of the skull3. Closed fractures may be managed operatively or non-operatively. Indications for surgery include hematoma formation, dural penetration, sinus involvement, presence of infection and bony depression >1 cm3.
An open fracture is a compound fracture of the skull3. These may also be managed surgically or non-surgically depending on the risk factors as listed above for closed fractures3. Open – contaminated A contaminated fracture suggests infectious involvement of the fracture that may affect the brain. A contaminated fracture should be taken to the operating room for debridement, and the patient should receive parenteral antibiotics.
Epidural hematoma (EDH) is most commonly caused by traumatic laceration of the middle meningeal artery in the foramen spinosum, a bony channel of the skull. Another cause is bleeding from a skull fracture onto the epidural space. Blood forms between the skull and the outer covering of the brain, called the dura mater. Blood expansion is limited horizontally by suture lines but may continue to bleed vertically. This tends to be a slow process resulting in a “lucid interval” for patients that may last up to 24 hours, in which they do not experience neurologic deficits. However, eventual brain compression causing mass effect and even herniation may result in sudden neurologic deterioration. Epidural hematomas are diagnosed using CT scan, indicating a lentiform pattern of bleeding. Patients with epidural hematoma>30 cm3 on imaging, with or without an altered neurologic exam, should undergo surgical evacuation immediately3. Those with an intact exam and hematoma volume 30 cm3 may be monitored with serial CT scans in the neurologic ICU3.
A subdural hematoma (SDH) is defined as a collection of blood between the outer layers that cover the brain, the dura mater and the arachnoid mater. The most common cause of subdural hematoma is trauma. Anticoagulation therapy and coagulopathy are less common causes. In younger individuals trauma is usually caused by motor vehicle collision, while in the elderly population, falls are the most common cause. As older individuals have greater age-related brain atrophy, they can accommodate larger hematoma collections without presenting symptomatically. This is a reason why the elderly most commonly present with chronic subdural hematoma (cSDH), while young persons become symptomatic acutely. The mechanism of injury is related to either hematoma formation around a focus of severe parenchymal injury, which presents acutely, or bridging vein laceration in the subdural space from acceleration-deceleration injury, which most commonly presents in the chronic setting.
The hyperacute phase of subdural hematoma formation takes place in approximately the first hour following hemorrhage. CT scan reveals a fluid collection relatively isodense to the adjacent cortex, although mixed density may be observed due to a mixture of clot, serum and ongoing unclotted blood4.
Acute SDH (aSDH) occurs in the first 1-3 days following hemorrhage. The classic finding on head CT is a crescent-shaped hyperdensity adjacent to the inner table, many times associated with brain edema. The four possible locations are over the convexity, interhemispheric, layered on the tentorium and in the posterior fossa. Convexity aSDH is generally less threatening than a temporo-parietal aSDH of the same size3. Operative indications include aSDH thickness greater than 1 cm or midline shift greater than 5 mm on CT scan. In the absence of these imaging findings, exam findings that prompt surgery include a drop in the GCS of 2 points or greater from time of injury to admission, asymmetric or fixed and dilated pupils, or intracranial pressure greater than 20 mm Hg3. Craniotomy is undergone for surgical drainage. Mortality is reported to be 50-90%, with the elderly and individuals on anticoagulation experiencing higher mortality rates3.
The time period of a sub-acute SDH ranges between 3 days and 2-3 weeks. Sub-acute SDHs appear isodense on head CT. Membrane formation occurs after 4 days of SDH formation3.
A chronic SDH (cSDH) is any SDH present for greater than 3 weeks. As discussed above, cSDH most commonly occurs in the elderly, with average age of 63 years3. Although falls are the most common cause, others include alcohol abuse, seizures and anticoagulation/coagulopathy3. Bilateral cSDH occurs in about 20-25% of cases3. cSDH is hypodense to brain parenchyma on head CT. Grossly, the blood appears to have a “motor oil” consistency that does not clot3. Presenting symptoms may be minor, including headache, confusion and language difficulties (such as word-finding problems). In more severe cases, symptoms may include hemiplegia, focal seizures or varying degrees of coma3. Symptomatic cSDH or those greater than 1 cm in maximum thickness should undergo surgical drainage. Burr hole drainage is the most common procedure, with either 2 burr holes or 1 large bur hole placed. Subdural drain may be placed. Craniotomy is less common.
Ventriculostomy may refer to placement of an external ventricular drain (EVD) for diagnosis and surveillance of intracranial pressure (ICP) and CSF-diversion as temporary treatment of hydrocephalus. EVDs are generally placed in the setting of trauma or aneurysmal rupture. Most patients are acutely ill and have hydrocephalus from CSF outflow obstruction or non-obstructive hydrocephalus due to resorption disturbance from intraventricular or subarachnoid hemorrhage. All patients with EVDs are monitored in the neuro-ICU. Placement can be done at the bedside. The approach is usually from the right frontal lobe (Kocher’s point) to the foramen of Monroe, although anywhere in the lateral ventricle such as Keen’s point, Frazier’s point and Dandy’s point are reasonable but less accessible in a bed-side setting6. CSF is drained via a catheter from the ventricle to an external drainage bag. Resistance to flow is adjustable. Intracranial pressure (ICP) is simultaneously monitored through a transducer on the EVD. After the patient is stabilized and pathology source removed, resistance is increased to maximum threshold, at which time CT scan is obtained. Should the ventricles remain stable in size, suggesting normal CSF outflow through the ventricular system, the EVD can then be removed. This is also done at the bedside. Endoscopic Third Ventriculostomy (ETV) is indicated for obstructed hydrocephalus. It is a procedure in which the floor of the third ventricle is endoscopically enlarged to allow for greater CSF flow through the third ventricle. It is usually used in setting of tectal tumors or aqueductal stenosis and seldom used in traumatic setting. The success rate is estimated to be approximately 56% and is most successful for infants with untreated aqueductal stenosis3. Overall success is dependent on patient age, pathology type, and shunt history3.
Various forms of intracranial pressure (ICP) monitoring exist for patients in critical condition, typically following traumatic injury. Indications include EDH, SDH, ICH, contusion, brain herniation and severe edema. ICP monitoring allows neurosurgeons to medically maintain ICP within normal range (typically < 20 mm Hg) or may prompt emergent surgical treatment, as necessary. The most reliable method is an intraventricular catheter, also known as an external ventricular drain (EVD), discussed separately. An advantage of the EVD is that it allows therapeutic drainage of CSF to decrease ICP directly, although it may be difficult to insert into compressed or displaced ventricles. When an EVD is not possible, the next best possible option is an intraparenchymal monitor, which is also a catheter inserted in to the right or left prefrontal cortex. Less accurate methods include a subarachnoid screw (also known as a bolt) or a subdural or epidural catheter.
Decompressive craniectomy is a procedure in which part of the skull is removed in the setting of intracranial hypertension and marked cerebral edema, generally following traumatic injury. The skull flap is left off for an indeterminate period of time, typically 2-3 months, to allow the brain to first expand without compression by the skull and then for swelling to resolve. A unilateral craniectomy or hemicraniectomy, is indicated for unilateral hemispheric swelling and midline shift after traumatic brain injury, ischemic stroke or SAH5. A major complication of this approach is brain herniation through the surgical site, from a craniectomy that is too small in proportion to the extent of the injury. Bilateral craniectomy can be considered for diffuse cerebral edema5. This may be performed as two separate craniectomy sites or a bifrontal craniectomy that extends from the floor of the anterior fossa to the coronal suture and the pterion bilaterally5.
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