Nature’s wisdom during aneurysmal subarachnoid hemorrhage
Aneurysmal rupture of a large artery is an acute phenomenon that is potentially life-threatening. If the bleeding continues for more than a few moments, there can be a huge blood spill into the brain leading to instantaneous death. At the time of the rupture, the body responds in a variety of natural ways to control the bleeding, protect the brain and preserve life. An understanding of these natural events is necessary so that a philosophically appropriate treatment protocol can be instituted.
The issues that need to be assessed are:
1. Why does the patient become unconscious or drowsy at the time of the ictus? Why do hemispheric deficits like hemiplegia, hemiparesis or speech disturbances develop?
2. Is the post-ictal systemic hypertension pathological?
3. Does the post-ictal increase in the intracranial pressure merit emergency measures?
4. Does the angiographically demonstrated vasospasm need to be treated?
5. Is the operation on a patient having drowsiness, unconsciousness or hemispheric deficits different from that on a patient having similar aneurysm on angiography but without any neurological deficit?
The above issues can be settled through a rational analysis of the problems.
On the bursting of an aneurysm arising from a major intracranial artery, the potential volume and force of the bleeding into the subarachnoid space from the site of the rupture can be extremely high. However, in most instances, the blood spill is limited to the subarachnoid spaces adjoining the arterial rupture site. Large hemorrhages or clots are relatively rare. After an aneurysmal rupture, batteries of natural events come into play in all their wisdom to save the body. The course of these events and the part they play in the control of bleeding and saving of life need to be analyzed so that a rational therapy can be instituted aimed at assisting all the natural mechanisms.
Two major visible happenings that attempt to control the bleeding and minimize neurological damage are vasospasm and cerebral hypertension. The arterial spasm acts to control the bleeding from the site of the vascular rupture, and the raised intracranial pressure is probably an attempt to compress the bleeding site from exterior of the aneurysm. Both these intra-vascular and extra-vascular events can be visualized on radiological examination and observed during surgery.
The size of the aneurysmal rupture determines the extent of vasospasm necessary to control the hemorrhage. Larger the size of the rupture, more severe will be the extent of the vasospasm. The spasm is necessary to reduce the flow and the intensity of the bleeding thus providing an opportunity for clot formation at the site of the arterial rupture so as to stop bleeding. The greater the size of the ruptured vessel, the more intense would be the spasm, as also the neurological deficit. In effect, the extent of neurological deficits reflects the size of the tear in the aneurysm.
Following the aneurysm rupture, there is usually an immediate episode of transient unconsciousness followed by a period of drowsiness. During the period of unconsciousness, the spasm in the vessels may be so severe that there is a complete standstill of blood flow within the vessel. There is also a systemic response in the form of short-lived acute hypotension aimed at reducing intracranial blood flow. The momentary standstill of the blood flow is probably essential to control the bleeding and to allow clot formation for plugging the site of the vascular rupture.
Unconsciousness and drowsiness are due to the spasm of the small vessels. More prolonged the unconsciousness the more severe and prolonged is the spasm. Hemispheric deficits are due to large vessel spasm. Hemispheric deficits are relatively less common than the sensorial deficits. The swelling of the brain also assists in putting pressure over the aneurysm to control the bleeding. The brain swelling could be due to brain edema as a result of vasospasm and the resultant chemical changes in the brain. Brain edema can by itself be a cause of drowsiness. The higher the neurological grading of the patient, the more difficult the operation and more care will have to be taken during the dissection of the aneurysm. The more the brain edema the larger is the size of the arterial rent. It is often observed that surgery on an aneurysm in an acute stage can be significantly more difficult than surgery in the delayed stage.
The state of unconsciousness or severe drowsiness usually lasts for a few minutes. After an acute event and natural control of the bleeding from the ruptured aneurysm, the spasm of the vessels is gradually released. The patient regains consciousness and becomes more alert. The brain edema diminishes progressively. The actual bleeding from the ruptured aneurysm could be for less than a few seconds.
After the acute events and control of the bleeding, the spasm of the arteries and the cerebral edema gradually return towards normal. The systemic blood pressure now has to help intracranial blood vessels, which are in a state of spasm. If the blood does not reach the critical areas in good time there could be a permanent injury to these areas. The rise in the systemic blood pressure is a phenomenon assisting the body to force the blood into critical brain matter. The extent of the rise of blood pressure probably reflects the degree of intracranial vascular spasm. The rise in the systemic blood pressure is frequently resistant to various drugs and can persist for a long time.
The headache, which persists for a period of days, could be related to the blood spill in the subarachnoid spaces. The headache and the general body illness forces the patient to be in bed for a period of time. This enforced bed rest is probably necessary and allows for the treatment protocol to be appropriately executed.
It has to be understood that apart from these more obvious clinical events, there are a variety of other events that take place at a cellular and chemical level that result in the preservation of the integrity of the human body.
The probable post-ictal events discussed above suggest the following:
1. After an aneurysmal rupture, a spasm in the arteries is mandatory for bleeding to stop. Any attempt directed towards releasing the spasm may be counterproductive.
2. The intracranial hypertension in its own way assists in the control of the bleeding. Decongestants and lumbar drainage of CSF may not only be not indicated but may prove harmful.
3. Post-ictal systemic hypertension should not be aggressively treated.
4. Surgery on aneurysm in patients having moderate or severe neurological deficits is more difficult than surgery on neurologically intact patients.