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Intracranial pressure in patients with diffuse cerebral arterial spasm following ruptured intracranial aneurysms
Insights
Intracranial pressure (ICP) monitoring reveals a distinct pattern after subarachnoid hemorrhage (SAH). A delayed ICP decrease often coincides with cerebral arterial spasm, preceding a secondary rise due to ischemia.
Area of Science:
- Neurosurgery
- Neurology
- Critical Care Medicine
Background:
- Ruptured intracranial aneurysms frequently cause subarachnoid hemorrhage (SAH).
- Cerebral arterial spasm is a common complication following SAH.
- Intracranial pressure (ICP) dynamics are critical in managing SAH patients.
Purpose of the Study:
- To investigate the relationship between ICP fluctuations and cerebral arterial spasm after SAH.
- To characterize ICP patterns in the early phase following subarachnoid hemorrhage.
- To identify potential therapeutic interventions for managing secondary ICP increases.
Main Methods:
- Continuous ICP monitoring in 12 pre-operative patients with SAH and angiographic spasm.
- Recordings initiated within 13 days post-hemorrhage, lasting 1-7 days.
- Correlation of ICP trends with angiographic findings and neurological status.
Main Results:
- Initial ICP increase observed in 4 patients without spasm.
- A subsequent ICP depression occurred 7-12 days post-SAH in 11 patients, coinciding with arterial spasm.
- Secondary ICP rise due to ischemia/infarction led to neurological deterioration in survivors.
Conclusions:
- ICP monitoring reveals a biphasic pattern post-SAH, with a critical depression phase linked to vasospasm.
- This depressed ICP phase can precede ischemic complications and neurological deficits.
- Administration of isoproterenol and steroids during the depressed ICP phase may mitigate secondary ICP rises.
Abstract:
Intracranial pressure (ICP) was recorded continuously in 12 pre-operative patients with angiographic evidence of diffuse cerebral arterial spasm due to a ruptured intracranial aneurysm. Recordings were made for 1 to 7 days, starting within 13 days after the haemorrhage. 1. An increased ICP was observed in the first week after subarachnoid haemorrhage (SAH) in 4 of the patients without any signs of angiographic arterial spasm. 2. This initial increase was regularly followed by a depression of ICP in between 7--12 days after SAH. In 11 out of 12 patients such a depression was concomitant with the beginning of arterial spasm. During the period of depressed ICP pattern, 6 patients showed little or no neurological deterioration, whereas 5 patients showed impaired consciousness or neurological deficits. 3. A secondary rise of ICP thereafter always followed due to ischaemic brain swelling or infarction, and was usually associated with a serious neurological deterioration. 4. Continuous ventricular drainage was performed to control the secondary increased ICP in 7 patients who survived, 4 of them with good clinical improvement and 3 with severe neurological deficits. 5. In the stage of depressed ICP, the administration of isoproterenol and steroids is recommended in order to try to alleviate the secondary rise of ICP.