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Thursday, 28 November 2013

Cerebral aneurysm - The Complications

Cerebral aneurysm is defined as a cerebrovascular disorder causes of the blood vessel to bulge or balloon out of the wall of a blood vessel as a result of the weaken of blood vessels and veins and occurred mostly at the bifurcations and branches of the large arteries located at the Circle of Willis.
A. Complications
Complications during cerebral aneurysm embolization continue to occur even at high volume experienced centers. Such situations are unexpected, complex and can have devastating consequences(21). Others indicated that Systemic complications secondary to subarachnoid hemorrhage from an aneurysm are common (40%) and the mortality attributable to them (23%) is comparable to mortality from the primary lesion, rebleeding, or vasospasm(22).  Dr. Chen M. suggested that the two most serious neuroendovascular procedural complications-namely, aneurysm perforation and thromboemboli aims to propose a role based checklist(23). Other complications include 
1. Re-bleeding
there is a report of fifty-three of 236 consecutive patients (22.5%) who suffered a proved aneurysmal subarachnoid hemorrhage and who were admitted within 72 hours after subarachnoid hemorrhage to a primary emergency hospital had at least one rebleed within 6 months after the primary bleed. Two patients later had a rebleed within a mean of 3 years follow-up. Rebleeding was recorded if there was a sudden loss of consciousness and a verification by computed tomography, autopsy, lumbar puncture, or angiography. The peak incidence of rebleeding was within the first 24 hours and at the end of the first week after subarachnoid hemorrhage. The rebleed mortality rate was 74%, and only 19% of patients with a rebleed had a good outcome. The grade on admission, age, and sex do not affect the incidence nor the time of rebleeding(24).

2. Vasospasm.
In the continuation of a review of delayed vasospasm after aneurysmal subarachnoid haemorrhage, originally published in 1994 and partially updated at the ninth vasospasm conference in Turkey. The incidence of delayed ischaemic deficit (DID) or symptomatic vasospasm reported in 1994 was 32.5% in over 30,000 reported cases. In recent years, 1994-2009, it was 6,775/23,806, or 28.5%. Many of the recent reports did not specify whether a calcium antagonist was used routinely, and when this was stated (usually nimodipine or nicardipine), DID was noted in 22.0% of 10,739 reported patients. The outcome of delayed ischaemia in the earlier survey was a death rate of 31.6%, with favourable outcomes in 36.2%. In recent reports, though with fewer than 1,000 patients, the outcome is possibly better, with death in 25.6% and good outcome in 54.1%. It thus appears likely that delayed vasospasm is still common but less so, and that the overall outcome has improved(25).

3. Hydrocephalus
Dr. Harrigan MR and the team at University of Alabama at Birmingham indicated that Patients underwent treatment of the ruptured aneurysm an average of 47.4 hours after admission and received an average total dose of 40.6 g of EACA. The mean length of time of administration of EACA was 35.6 hours. There was a total of 5 rehemorrhages, for an overall rebleeding rate of 1.4% and a rate of rehemorrhage per 24-hour period of 0.71%. Overall, the rates of symptomatic vasospasm and permanent neurological deficits attributable to ischemic stroke were 11.5% and 7.2%, respectively, and the incidence of shunt-dependent hydrocephalus was 42.3%. Patients who were treated with coiling had higher rates of symptomatic vasospasm and ischemic complications than patients who had surgery(26).

4. Hyponatremia
Hyponatremia following subarachnoid hemorrhage (SAH) therefore appears to be the result of increased natriuresis, due to the inappropriate elevation of ANP rather than SIADH. In this situation, water restriction should not be recommended, since the circulatory volume is decreased(27).

5. Etc.

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