Stroke & Vascular Disorders
Cerebellar infarction and cerebellar hemorrhage
Oct. 26, 2023
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Traumatic intracranial aneurysms result from either penetrating head trauma causing direct injury to the vascular wall or from severe closed head injury producing torsion or stretching of an intracranial vessel against the hard edge of dural membranes, bony protrusions, or fractured bones. As traumatic intracranial aneurysms have a high rate of growth and rupture, they need to be detected early and treated aggressively. Experience from the military conflict in the Iraq war has provided the most extensive descriptions of traumatic aneurysms. However, other series from civilian populations have also emerged.
• Traumatic intracranial aneurysms result from severe penetrating head trauma or closed head injuries, causing direct mural injury or indirect stretching injury to arterial walls.
• Although traumatic aneurysms constitute a small fraction of all aneurysms in adults, they carry a high risk of progressive growth and rupture and, therefore, are important to detect and treat in the setting of head trauma.
• Surgical risks of treatment of traumatic aneurysms are high, often requiring sacrifice of the parent vessel for effective exclusion of the aneurysm from the circulation.
• Developing endovascular therapies are increasingly used to treat traumatic aneurysms and can be effective with preservation of the parent artery.
An autopsy-proven case of a middle meningeal artery aneurysm after head injury was first recorded in 1829 (43). Later, in 1891, Bollinger postulated that 4 cases of "delayed apoplexy" after head injury were due to the rupture of a traumatic aneurysm (10). Guibert reported a case involving the infraclinoid internal carotid artery, but Birley and Trotter were the first to describe a case of an intracranial aneurysm after severe head injury (19; 07). Tonnis demonstrated the first case proven by angiography and Cairns provided a comprehensive description of these aneurysms (46; 11). Aneurysm formation after a depressed skull fracture was described by Krauland in 1949, and angiographically demonstrated after a closed head injury in 1962 (21).
It may be that detection of traumatic aneurysms has decreased from the 1970s to the present due to reliance on noncontrast computerized tomography, rather than traditional angiography, for screening evaluation of head-injured patients with traumatic aneurysms sometimes overlooked. Vigilance is required in patients with high-risk injuries; with awareness of the need for screening for vascular injury in appropriate patients, high rates of detection of traumatic aneurysms are reported (12).
Traumatic aneurysms have been traditionally divided into "true," "false," and "mixed," depending on whether the arterial wall is partially injured with ballooning of all layers ("true") or ruptured in intimal and medial layers with thin fibrous tissue, organized clot, or brain tissue forming the outer membrane containing the vascular space ("false"). “Pseudoaneurysm” is now a preferred term for false aneurysm. When a true aneurysm ruptures and forms a pseudoaneurysm outside the true one, the aneurysm is "mixed." Whatever the histologic classification, traumatic aneurysms have high risk of growth and rupture and call for urgent management.
Traumatic intracranial aneurysms are reported most frequently in the immediate setting of major head trauma, although multiple cases have been reported following relatively minor head injuries (30). Onset of clinical presentation of traumatic intracranial aneurysms can range from several hours to as long as 14 years after the injury, with a mean time of 2 to 3 weeks to presentation (13). Symptoms can develop from aneurysm expansion or from rupture, with acute or delayed hemorrhage in epidural, subdural, subarachnoid, or intraparenchymal compartments.
Clinical features of traumatic aneurysms include cranial nerve palsies, severe epistaxis, stupor, or coma, the latter most commonly as a result of delayed intracranial hemorrhage (14). Following trauma, the presence of these signs should raise suspicion of intracranial aneurysm. The clinical presentation can depend on the location of the aneurysm. Infraclinoid aneurysms can present with massive epistaxis, cranial nerve palsies, headaches, or diabetes insipidus. Mao and colleagues reviewed 2335 patients with cerebral aneurysms; 15 of these patients had traumatic intracranial aneurysms due to blunt trauma (34). Epistaxis and ophthalmic pathologies were the most common presenting symptoms, each accounting for 40% of symptoms. Most of the infraclinoid aneurysms presented with recurrent or massive epistaxis.
Supraclinoid traumatic intracranial aneurysms most commonly present with progressive cranial nerve palsies, including blindness and ptosis. Headache and coma due to subarachnoid or intraparenchymal hemorrhage can be seen in supraclinoid, vertebrobasilar, or parafalcine traumatic intracranial aneurysms. Distal cortical intracranial aneurysms can present with seizures or expanding skull fracture (34). When an intracavernous aneurysm ruptures into the cavernous sinus a carotid-cavernous fistula can result. Occasionally, in infants, a skull fracture may "grow" concomitant with the enlargement of an aneurysm because the skull sutures are not fused (16). Posterior circulation traumatic intracranial aneurysms are rare and can present with oculomotor nerve palsy. Traumatic aneurysms cannot be differentiated from saccular aneurysms by these presenting clinical features, although angiographic features may sometimes distinguish them.
The location of the aneurysm depends on the nature and path of the injury. Nonpenetrating or blunt trauma results in damage to the petrous, cavernous, or supraclinoid internal carotid artery, or to the peripheral cortical branches. Distal cortical branches underlying displaced skull fractures and distal anterior cerebral artery branches such as the pericallosal, which lies against the fixed falx cerebri, are at particular risk (14). Penetrating trauma destroys structures in the direct path of the injury. Transseptal and transcallosal trajectories put middle cerebral artery branches at risk for direct injury.
In a typical patient presenting with traumatic intracranial aneurysm, the level of consciousness is initially depressed due to the trauma itself followed by a lucent period after which secondary deterioration occurs because of intracranial hemorrhage (41). The hemorrhage may be subarachnoid, intracerebral, intraventricular, or subdural, depending on aneurysm location. Headache is prominent. Compressive cranial nerve palsies caused by the enlarging aneurysm may occur later, but an abducens palsy can be present within the first few days due to raised intracranial pressure. Epistaxis, which can be massive, develops when a petrous or intracavernous internal carotid artery aneurysm associated with a basal skull fracture ruptures. The aneurysm may be asymptomatic and discovered incidentally in 10% to 20% of cases during neuroimaging. In a patient with an extraventricular CSF drain, acute sanguinous ventriculostomy output may be the sign of underlying aneurysmal rupture (14).
During war, penetrating shell fragment injuries and gunshot wounds are frequent. Most victims die immediately from the direct effects of the injury, but should they survive, the next catastrophic event is often a ventricular or brain track hematoma. Experience from the Iraq war has produced the largest study of traumatic intracranial aneurysms yet reported (06). A total of 408 patients with closed or penetrating head injuries were evaluated, 187 of them with cerebral angiography. Forty seven of these patients experienced vascular injuries, with penetrating injuries from explosive blasts constituting the majority of the cases. Traumatic intracranial aneurysms were detected in 31 cases. Other vascular injuries observed were extracalvarial aneurysms, arterial dissections, and arteriovenous fistulae. Most (16) of the intracranial aneurysms were found in the anterior communicating artery and were due to penetrating fragments through the orbitofrontal region. The rest of the intracranial aneurysms were located in the middle cerebral, internal carotid, middle meningeal, and posterior inferior cerebellar arteries. The 6 vertebral artery lesions (4 extracalvarial aneurysms, 1 dissection, and 1 fistula) were all due to penetrating injury to the neck (06).
The prognosis of a patient with a traumatic aneurysm depends on the severity of the inciting injury, intactness of the aneurysm, treatment rendered, and the timing of treatment. Clinical factors that correlate with outcome include: (1) vital signs on admission; (2) Glasgow Coma Scale on admission; (3) bilaterality of hemispheric injury; (4) presence of intraventricular, subarachnoid, or intracerebral hemorrhage; (5) presence of missile or intracranial bony fragments; and (6) mass effect. Surprisingly, in one prospective study of penetrating craniocerebral injury, no correlation between the presence of intracerebral hemorrhage and outcome was evident, whereas a high correlation was evident after subarachnoid hemorrhage, carrying a mortality rate of 68% (31).
Current literature strongly supports active surgical or endovascular management of traumatic aneurysms compared to conservative therapy. Traumatic aneurysms tend to enlarge over days or weeks. Rupture occurs in half the cases with an estimated mortality of 31% to 70%, whereas the mortality of surgically treated persons prior to aneurysm rupture is less than 20%, depending largely on comorbid factors (25; 02). Spontaneous healing occurs in approximately 20% of cases, usually within a few months (03; 39; 28). Pseudoaneurysms tend to grow faster than true aneurysms and appear to rebleed more frequently (29).
Hydrocephalus, vasospasm, and cerebral edema are frequent complications.
A healthy, 6-year-old female was a restrained rear-seat passenger in an motor vehicle accident. The side impact imparted a significant rotational component to the injury. The patient was intubated in the field due to a Glasgow Coma Scale score of 4. Her initial head CT demonstrated large left frontal hemorrhage with interhemispheric extension.
Her hospital coursed involved CSF diversion by ventriculostomy and intense hyperosmolar therapy, with brief use of barbiturates to maintain intracranial pressure less than 20. Two weeks after the injury, routine head CT demonstrated new intraventricular density suggesting acute blood.
Consequently, angiography revealed a pericallosal artery aneurysm at the epicenter of the hematoma.
Typical traumatic aneurysm appearance of a broad base with irregular lumen convinced the surgeons to trap the aneurysm by craniotomy via a frontal interhemispheric approach. After opening the aneurysm and using suction to evacuate the intra-aneurysmal clot, a clip successfully isolated the aneurysm from the ACA circulation.
The patient recovered well and within 2 weeks was transferred to acute rehabilitation with right leg spastic paresis.
In civilian life, in non-violent settings, closed head injuries with blunt brain trauma account for the majority of traumatic intracranial aneurysms, from 60% to 92%, with penetrating and iatrogenic injuries accounting for smaller fractions (47; 02; 23). Blunt injury is most commonly due to motor vehicle accidents, followed by falls.
Penetrating injuries can be due to bullets, knives, or other objects. It is the irregularly shaped and slow velocity missiles that tend to cause traumatic intracranial aneurysm compared to high-velocity gunshot wounds. When a bullet is retained intracranially, it is where its velocity was lowest that a traumatic intracranial aneurysm forms (35). Stab wounds carry a higher risk of causing traumatic intracranial aneurysm than gunshot wounds (35). Traumatic intracranial aneurysms caused by accidental penetrating trauma with radio or TV antennae, umbrella tips, fishing poles, and other innocuous objects have also been described. Iatrogenic causes include craniotomy, skull base surgery, transsphenoidal procedures, arterial punctures, and endovascular procedures. One report describes 8 patients out of 299 who developed iatrogenic vascular injuries after external ventricular drain placement, with 2 of these patients developing traumatic aneurysms (27).
During modern warfare, the majority of traumatic intracranial aneurysms are due to blast injury with shell fragments or debris producing penetrating injury, whereas gunshot wounds, blunt head trauma, and knife injuries make up the remainder (01; 06). In the largest series to date, describing experience in the Iraq war, 33 of 47 vascular injuries were due to blast injury, 8 to gunshot wounds, 4 to blunt trauma from motor vehicle accidents, and 1 from a knife injury (06). Though a less common mechanism of injury in modern conflicts, on a per incident basis, stab wounds are more likely to result in aneurysms than are gunshot wounds (26). Aneurysms seen in a delayed setting after surgical treatment and debridement of a penetrating injury are defined as traumatic rather than iatrogenic, if they arise distant from the site of the cranial surgery.
The vast majority of missile-induced aneurysms are pseudoaneurysms, with disruption of the arterial wall due to direct trauma from low-velocity, sharp-edged shrapnel or bone fragments grazing the artery. Less often true aneurysms develop, with incomplete mural injury producing subsequent dilation of the intact vessel wall (14). Most of the time, the missile remains intracranially; in such instances, the aneurysm forms at the distal trajectory site (35).
Traumatic intracranial aneurysms secondary to blunt injury can also be classified into skull base and peripheral aneurysms. Skull base aneurysms are further divided into infraclinoid, supraclinoid, and vertebrobasilar categories because of different presentation and treatment options. Skull base traumatic aneurysms most commonly involve the petrous or cavernous carotid artery and are almost invariably associated with base of skull fracture. The peripheral traumatic intracranial aneurysms are divided into perifalx and distal cortical aneurysms. Perifalx aneurysms involve the anterior cerebral, posterior cerebral, or superior cerebellar arteries by compressing the arteries against the falx cerebri and tentorium cerebelli. Distal cortical traumatic aneurysms are due to depressed or linear skull fractures, or dural lacerations, injuring the surface cortical branches of the middle cerebral or anterior cerebral arteries (34). Traumatic intracranial aneurysms of the middle meningeal artery usually result from skull fracture crossing the artery in the temporal region (24).
In summary, traumatic intracranial aneurysms can be caused by direct mural injury by a penetrating object, by an acceleration-induced shearing force, or by indirect injury from brain shifting, producing forceful stretching or torsion of the vessel on adjacent structures like the falx cerebri, the tentorium cerebi, the sphenoid ridge, or sharp bony edges.
Traumatic intracranial aneurysms constitute less than 1% of adult aneurysms; however, they account for more than 20% of pediatric aneurysms (22; 34). Unlike in adults where female and male preponderance is the same, in pediatric population, it is more commonly males that are affected, and this is thought to be due to their higher risk of blunt head injury (30). Young adult men have the highest incidence, reflecting the population at highest risk for violent injuries. The incidence of traumatic intracranial aneurysms caused by penetrating trauma across studies is approximately 2% to 6% across studies (03). After a gunshot wound to the brain, the incidence of traumatic aneurysm in persons surviving 48 hours is 3% (31). Of 2187 persons with penetrating head injury in the Vietnam war, only 2 traumatic aneurysms were documented, but this number was probably an underestimate because not all brain-injured persons underwent angiography (17). When persons were evaluated systematically, as in the Iran-Iraq conflict, 3% of those with penetrating head wounds demonstrated an intracranial aneurysm (01). Among wartime patients with closed and penetrating head injuries deemed to warrant angiography, there was a 34% prevalence of vascular injuries, with traumatic intracranial aneurysms constituting the majority (06). Shrapnel and gunshot wounds show similar rates of aneurysm formation (01; 31). Stab wounds to the head, on the other hand, carry a much higher risk of all types of vascular injuries (30%), with aneurysm formation in 10% to 12% of cases (26; 15). Although closed head injury is the most common cause of traumatic aneurysms, the frequency with which they occur remains uncertain. The 10-year incidence of traumatic intracranial aneurysm after blunt traumatic brain injury was found to be 0.65% (49). In a single center experience, motor vehicle accidents were the most common cause of traumatic aneurysm after blunt head trauma (34). Males, younger age group, base of skull fracture, intracerebral hemorrhage, and high impact traumatic brain injury are risk factors for development of traumatic intracranial aneurysms (49).
The reported incidence of vascular injury in civilian penetrating brain injury (cvPBI) ranges between 38% and 50%. This risk is higher when a projectile penetrates the cranium in the fronto-basal region, when trajectory of the projectile traverses both hemispheres or is in close proximity to the circle of Willis, and when intraventricular or subarachnoid hemorrhage is present (08). Of all vascular injuries associated with civilian penetrating brain injury, traumatic intracranial aneurysms are the most common (39%), followed by arterial dissections (29%), arterial occlusion (21%), and arterio-venous fistulas (11%). Approximately 96% of the injuries are limited to the anterior circulation, namely the middle cerebral artery and internal carotid artery. Although CTA has limited overall sensitivity in detecting arterial injuries in civilian penetrating brain injury (72.7% sensitivity and 93.5% specificity), it is fairly reliable in identifying traumatic aneurysms in this patient population (100% sensitivity and specificity). Conventional angiography remains superior to CTA for detecting overall arterial injury; however, the clinical utility in the acute setting remains ambiguous (32).
A large series of civilian penetrating brain injury was reported from the level 1 trauma center at the University of Chicago. In this dataset, the frequency of vascular injury, including both the arterial and venous sinus systems, was found to be 57% higher than other civilian penetrating brain injury series (33). In part, this may be due to more inclusive definition of vascular injuries that is not restricted to only traumatic intracranial aneurysms. Analogous to the previously reported literature, arterial injury was observed in 26 out of 72 (36%) of the cohort. A total of 37 arterial injuries were described (some patients have more than one injury), the most prevalent of which was traumatic intracranial aneurysm (30%) and equal involvement of all major vessels in the anterior circulation (72% of all injured vessels), with an equal split amongst anterior cerebral artery, middle cerebral artery, and internal carotid artery.
Advance in design of helmet and body armor for soldiers of war has improved survival in soldiers; however, it has not eliminated the occurrence of traumatic aneurysms in military conflict (06). Nevertheless, by reducing rates of penetrating trauma and skull fracture, helmets may reduce the risks of traumatic aneurysm formation. Thus, helmets must be worn whenever major craniocerebral trauma is likely.
Traumatic aneurysms must be differentiated from saccular aneurysms. This is relatively simple when the trauma is recent and a fracture or missile track is evident, raising suspicion of a traumatic etiology. However, the diagnosis should also be considered when there is: (1) delayed neurologic deterioration after trauma; (2) unusual location of hemorrhage; (3) orbitofaciocranial injury; (4) recurrent epistaxis; (5) enlarging skull fracture; or (6) progressive cranial nerve palsies. The distinction between traumatic intracranial aneurysm and spontaneous aneurysms is of great importance for choosing the appropriate treatment. Although several angiographic features have been used to differentiate traumatic intracranial aneurysm from spontaneous aneurysms, it still remains a difficult task. The chance of traumatic intracranial aneurysm is much higher in the following situations: 1) a blurry or no aneurysm neck; 2) abrupt change in diameter and/or irregular wall in the parent artery; 3) aneurysm sac with delayed filling and emptying; and 4) irregular or strange aneurysm shape (37). Closed and penetrating head trauma can also cause cerebral contusion, arterial dissection, and arteriovenous fistulas, again necessitating angiography to distinguish the cause of traumatic hemorrhages. Vasospasm can sometimes hinder the diagnosis of traumatic intracranial aneurysms (06).
In head trauma patients, a head CT scan is performed to document the extent of the trauma as well as the presence of intracranial hemorrhage. Cerebral edema, missile tracts, bone and other fragments, and contiguous lesions may be seen. High-resolution contrast-enhanced CT scans combined with 4-vessel cerebral angiography provided adequate data for diagnosis of vascular injuries in most cases (04). MRI and MRA are also helpful in some instances; however, their role is often limited by the presence of retained metallic fragments. Although CT angiography is a sensitive noninvasive screening method for intracranial aneurysms, conventional cerebral angiography remains the reference standard for diagnosing cerebral aneurysm and is advocated as the initial screening modality by some authors (12; 14; 05). However, CT angiography has continued to advance in resolution and availability. One study, though limited by small sample size, reported that CT angiography had a 100% sensitivity and specificity in detecting traumatic intracranial aneurysms (09). With its ready availability and swift acquisition, CT angiography of the head and neck is the appropriate first-line investigation for neurovascular injury in most trauma patients, with conventional cerebral angiography employed for inconclusive CT angiography or in the setting of immediate operative intervention (48).
Penetrating head injuries produce a substantial risk of intracranial vascular injury, and they generally call for screening digital subtraction cerebral angiography, following initial stabilization of the patient. There should also be a high clinical suspicion for traumatic aneurysm and screening angiography, if following blunt craniofacial injury a patient has delayed neurologic deficits, intracranial bleed in unusual sites, recurrent epistaxis, or if the carotid canal is involved with a basilar cranial fracture (35). In military trauma patients, screening angiography has been recommended with a penetrating head injury of any kind, a known surgically treated traumatic intracranial aneurysm, a nonpenetrating blast injury to the head with a presenting Glasgow Coma Scale score of less than 8, evidence of vasospasm, or evidence of spontaneous decrease in cerebral blood flow (06). Radiographic risk factors for arterial injuries include the trajectory of the injury being proximal to the circle of Willis or being bihemispheric, the presence of subarachnoid hemorrhage or intraventricular hemorrhage, and a high severity score of the intraventricular hemorrhage or subarachnoid hemorrhage. Presence of these factors may help determine the need for a conventional angiogram (08).
The development of substantial and otherwise unexplained subarachnoid hemorrhage or delayed hematoma should also prompt consideration of vascular injury and angiography. The timing of angiography is still controversial. Late presenting aneurysms may be missed by early angiography, prompting some authorities to suggest delaying the procedure from initial presentation. Early angiography should be considered in the setting of severe head injuries, and a follow-up angiogram should be obtained if the initial study was negative (14). Bell and colleagues recommend a diagnostic angiography in war victims to be done as soon as possible; in their series, 2 aneurysms ruptured less than 10 days after the trauma (06). CT angiography has also been useful for preoperative surgical planning, allowing delineation of the aneurysmal shape and its anatomical relationship to surrounding vessels and bone (04; 45). When a carotid-cavernous fistula is documented, angiography with subtracted films must be carefully scrutinized because early filling of the fistula may mask an aneurysm.
A poorly defined aneurysmal neck, an irregular appearance, a location at the periphery of the vessel rather than at its bifurcation, and delayed filling and emptying of the aneurysm are angiographic features that may help differentiate traumatic from congenital or other acquired intracranial aneurysms (14).
Vasospasm may occur after either closed or penetrating head injury, but its frequency is uncertain and ranges widely in series of closed head injury (31). In wartime penetrating injuries causing traumatic aneurysms, the incidence of vasospasm can exceed 50% (06). When multiple aneurysms are present, the location of vasospasm is unreliable in determining which aneurysm has bled (20). Transcranial Doppler studies show increased velocities, suggesting vasospasm in about 40% of persons after closed head injury, which closely correlates with the amount of blood in the basal cisterns. Incidence of vasospasm peaks at 14 days and can be effectively treated with balloon angioplasty or intra-arterial nicardipine. Those with vasospasm have lower Glasgow coma scores compared to those without.
The aim of management is to prevent aneurysmal rupture and bleeding and to exclude the aneurysm from the circulation, irrespective of size, once the patient is stabilized. Although a few reports in the literature show that traumatic intracranial aneurysms can resolve with time (36; 42), many reports show a high rate of expansion and rupture, and a high morbidity and mortality with rupture (02). In addition, traumatic intracranial aneurysms have an unpredictable behavior, which makes observation risky (18). Thus, most sources strongly recommend treatment of traumatic intracranial aneurysms.
The surgical method of treatment depends on the location and morphology of the aneurysm as well as on the nature of the inciting injury. Mass lesions are evacuated and the wound debrided. Fragments are removed whenever readily accessible and dural lacerations repaired. The preferred treatment for the aneurysm itself is to clip it while maintaining the integrity of the parent vessel, but this is possible in only 10% to 15% of cases because of a lack of a discrete neck (01; 02). Because the wall of the majority of these aneurysms is made of clot, intraoperative rupture is common. The mortality rate with open surgery can be as high as 20% (23). Mortality is substantially lower when the aneurysm is unruptured. Intraoperative cerebral protection, such as barbiturate use combined with moderate hypothermia, is an essential consideration for patients in whom vessel reconstruction will require temporary occlusion of the parent vessel.
When the aneurysm is unclippable, trapping with excision, wrapping, or simple excision can be performed. For aneurysms that are difficult to access surgically, or in patients too unstable to withstand open brain surgery, endovascular approaches may be successful. Endovascular occlusion of traumatic aneurysms by coiling, stent-assisted coiling, flow diversion, or occlusion with liquid embolizing material has become increasingly described (38; 05; 40). The rate of preservation of the parent artery is higher with endovascular as compared to open brain surgery. In a study, 62% of 13 consecutive peripheral distal anterior cerebral artery (ACA) and middle cerebral artery (MCA) traumatic aneurysms were successfully embolized without compromising the parent vessel (12). Aneurysms treated endovascularly frequently require retreatment. The need for postoperative antiplatelet therapy can make endovascular treatment even more challenging, especially when a patient is presenting with trauma; however, risk of in-stent thrombosis often outweighs the risk of hemorrhage (18). Future designs may incorporate coated devices to lessen the dependence on antiplatelet agents after endovascular therapy (40).
Ligation of the proximal parent artery is the least preferred treatment and must be gradually accomplished over 48 hours to diminish the likelihood of aneurysm rupture. Aneurysms of the supraclinoid internal carotid artery should be clipped, failing which, they should be wrapped. Cavernous and petrous carotid aneurysms may be trapped surgically or endovascularly, wrapped, or excised. Peripheral branch lesions should be excised if clipping is not possible. The adequacy of collateral supply and tolerance to potential occlusion of the vessel should be assessed preoperatively whenever feasible. This may be done endovascularly in good grade patients with balloon occlusion while monitoring cerebral blood flow and neurologic status. Prophylactic intracranial revascularization prior to ligation of an aneurysm at the skull base is recommended.
Unlike the situation with spontaneous aneurysms, for traumatic intracranial aneurysms no recommendations exist regarding intervening at a certain aneurysm size. Although in the largest available series traumatic intracranial aneurysms that ruptured tended to be larger than unruptured aneurysms at diagnosis (8.275 mm vs. 3.15 mm), this was not statistically significant, and all of the aneurysms increased in size on follow-up angiography. Of 13 aneurysms that were not treated, primarily because of small size, most resolved or stabilized on follow-up angiograms, with 1 of 13 rupturing, resulting in death (06).
New technologies have made it increasingly possible to treat traumatic aneurysms and to achieve good outcomes by endovascular approaches, offering compelling alternatives to open surgical techniques (12; 40). Nevertheless, postoperative rupture may happen with interventional embolization because the fragile fibrous layer in traumatic intracranial aneurysm cannot provide enough support to ensure the stability of the coils inside the aneurysm. Therefore, special techniques have been developed. For instance, endovascular patch embolization has been used to treat traumatic intracranial aneurysm. By swaying the microcatheter, the partial coil is intentionally embolized in the space between the partially open stent and parent artery, and then the partial coil is patched and fixed after the stent is completely deployed (37).
Aneurysmal subarachnoid hemorrhage during pregnancy is a rare but serious obstetric complication. Literature on management is scant. In general, neurosurgical considerations take precedence over obstetric considerations. Ruptured aneurysms should be treated as they would in patients who are not pregnant, and unruptured aneurysms should be treated if they are symptomatic or enlarging (44).
Care should be taken to prevent raising intracranial pressure during surgery. Intracranial pressure should be monitored and appropriately lowered with osmotic therapies or with periodic hyperventilation. Barbiturates, etomidate, or isoflurane are preferred anesthetic agents because they decrease cerebral metabolic rate and provide some protection to the ischemic penumbra. Complete circulatory arrest with deep hypothermia is necessary in complex cases but has not been specifically evaluated in traumatic aneurysms.
All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.
Christos Lazaridis MD EDIC
Dr. Lazaridis of University of Chicago has no relevant financial relationships to disclose.See Profile
Steven R Levine MD
Dr. Levine of the SUNY Health Science Center at Brooklyn has no relevant financial relationships to disclose.See Profile
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