Cerebral aneurysm natural history, complications and prognosis: Difference between revisions
No edit summary |
|||
Line 29: | Line 29: | ||
[[Category:Needs overview]] | [[Category:Needs overview]] | ||
[[Category:Needs content]] | [[Category:Needs content]] | ||
[[Category:Emergency medicine]] | |||
[[Category:Disease]] |
Revision as of 14:39, 4 February 2013
Cerebral aneurysm Microchapters |
Diagnosis |
---|
Treatment |
Case Studies |
Cerebral aneurysm natural history, complications and prognosis On the Web |
American Roentgen Ray Society Images of Cerebral aneurysm natural history, complications and prognosis |
FDA on Cerebral aneurysm natural history, complications and prognosis |
CDC on Cerebral aneurysm natural history, complications and prognosis |
Cerebral aneurysm natural history, complications and prognosis in the news |
Blogs on Cerebral aneurysm natural history, complications and prognosis |
Risk calculators and risk factors for Cerebral aneurysm natural history, complications and prognosis |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Please help WikiDoc by adding more content here. It's easy! Click here to learn about editing.
Complications
Vasospasm
One complication of aneurysmal subarachnoid hemorrhage is the development of vasospasm. Approximately 1 to 2 weeks following the initial hemorrhage, patients may experience 'spasm' of the cerebral arteries, which can result in stroke. The etiology of vasospasm is thought to be secondary to an inflammatory process that occurs as the blood in the subarachnoid space is resorbed. It appears that macrophages and neutrophils that enter the subarachnoid space to phagocytose senescent erythrocytes and clear extracorpuscular hemoglobin, remain trapped in the subarachnoid space, die and degranulate 3-4 days after their arrival, and release massive quantities of endothelins and free radicals that in turn induce vasospasm. [1]. Vascular narrowing, however, is only one component of the transient inflammatory injury, which is extensive.
Vasospasm is monitored in a variety of ways. Non-invasive methods include transcranial Doppler, which is a method of measuring the velocity of blood in the cerebral arteries using ultrasound. As the vessels narrow due to vasospasm, the velocity of blood increases. The amount of blood reaching the brain can also be measured by CT or MRI or nuclear perfusion scanning.
The definitive, but invasive method of detecting vasospasm is cerebral angiography. It is generally agreed that in order to prevent or reduce the risk of permanent neurological deficits, or even death, vasospasm should be treated aggressively. This is usually performed by early delivery of drug and fluid therapy, or 'Triple H' (hypertensive-hypervolemic-hemodilution therapy) (which elevates blood pressure, increases blood volume, and thins the blood) to drive blood flow through and around blocked arteries. For patients who are refractive (resistant) to Triple H therapy, narrowed arteries in the brain can be treated with medication delivered into the arteries that are in spasm and with balloon angioplasty to widen the arteries and increase blood flow to the brain. Although the effectiveness of these treatments is well established, angioplasty and other treatments delivered by interventional radiologists have been in evolution over the past several years. It is generally recommended that aneurysms be evaluated at specialty centers which provide both neurosurgical and interventional radiology treatment and which also permit angioplasty, if needed, without transfer.
Some individuals with a ruptured cerebral aneurysm die from the initial bleeding. Other individuals with cerebral aneurysm recover with little or no neurological deficit.
Prognosis
- The prognosis for a patient with a ruptured cerebral aneurysm depends on the extent and location of the aneurysm, age , general health and neurological condition.
- The most significant factors in determining outcome are grade (see Hunt and Hess grade above) and age. Generally patients with Hunt and Hess grade I and II hemorrhage on admission to the emergency room and patients who are younger within the typical age range of vulnerability can anticipate a good outcome, without death or permanent disability. Older patients and those with poorer Hunt and Hess grades on admission have a poor prognosis. Generally, about two thirds of patients have a poor outcome, death, or permanent disability [2] [3]
References
- ↑ Gallo, GL (2006). "Leukocyte-endothelial cell interactions in chronic vasospasm after subarachnoid hemorrhage". Neurol. Res. 28 (7): 750–758. PMID 17164038. Unknown parameter
|coauthors=
ignored (help); Unknown parameter|month=
ignored (help) - ↑ Hop, Jeanette (1997). "Case-Fatality Rates and Functional Outcome after Subarachnoid Hemorrhage: A Systematic Review". Stroke. 28 (3): 660–664. PMID 11157554. Unknown parameter
|coauthors=
ignored (help); Unknown parameter|month=
ignored (help) - ↑ Ljunggren, B (1985). "Cognitive impairment and adjustment in patients without neurological deficit after aneurysmal SAH and early operation". Journal of Neurosurgery. 62: 673–679. PMID 3989590. Unknown parameter
|coauthors=
ignored (help)