Cerebral vasospasm following subarachnoid hemorrhage
Updates to Article Attributes
Cerebral vasospasm following subarachnoid haemorrhage is a major complication of subarachnoid haemorrhage (SAH). It is overtaking rebleed as the major cause of mortality and morbidity in the subgroup of patients with SAH who reach the hospital and receive medical care.
Epidemiology
It is seen in 40-70% of SAH patients on vascular imaging, and becomes clinically apparent in 20-30% of patients, typically from the 4th to 10th day post bleed 1.
Clinical presentation
Vasospasm can be clinically silent. However, symptomatic vasospasm is defined as new focal neurological symptoms or deterioration of the level of consciousness attributable to vasospasm-induced ischaemia after other aetiologies have been ruled out 2. As such, symptomatic vasospasm is often referred to as 'delayed cerebral ischaemia' in the medical literature 2.
About half of the symptomatic patients will show severe permanent neurological deficits or die 1.
Pathology
After decades of research the exact mechanism(s) responsible remain elusive although a number of candidate agents are demonstrated to play a role. These include:
- NO (nitrous oxide)
- endothelin 1
- oxyhaemoglobin
- others:
- thrombin
- serotonin
- thromboxane A2
- noradrenaline
- sphingosine-1-phosphate
Most likely the 'true' pathway involves multiple agents interacting with each other, both biochemically and via changes in gene expression, accounting for the delay of onset.
Oxyhaemoglobin, highest in concentration in arterial blood, appears to simultaneously up-regulate the expression of endothelin 1 (ET-1) and reduce the efficacy of NO.
This results in alteration of normal vascular tone, resulting in narrowing of the large vessels. Increasingly it is also becoming apparent that small calibre vessels which are in contact with blood in CSF blood are also narrowed also - down to 15 micrometres - far too small to be visualised on angiography, let alone CTA/MRA.
The result, if severe enough, is to reduce perfusion of brain parenchyma resulting in ischaemic symptoms, infarction, and its sequelae.
The degree of vasospasm is difficult to predict but correlates with the original Fisher scale and more accurately with the modified Fisher scale.
Radiographic features
Vasospasm associated with subarachnoid haemorrhage is usually characterised by diffuse narrowing without intervening regions of normal vessel calibre 10. It is often centred at the arterial bifurcation 10, giving the appearance of enlargement of the said bifurcation.
Treatment and prognosis
Aggressive, early and prophylactic treatment can markedly reduce the incidence of vasospasm but often requires early securing of the ruptured aneurysm. Three main modalities are employed:
Triple H therapy
Haemodilution, Hypertension, Hypervolaemia to maintain adequate cerebral perfusion pressure is achieved with hydration and inotropes, if necessary. This often requires admission to a neurological intensive care unit with a central venous catheter and intracranial pressure (ICP) monitoring.
Calcium channel blockers
Nimodipine is the best known and most widely used calcium channel blocker, which dilatedilates vessels, especially leptomeningeal collateralcollaterals.
Endovascular intervention
In severe cases, intra-arterial therapy can be beneficial. Intra-arterial delivery of a calcium channel blocker such as nimodipine or verapamil has replaced previously used drugs such as papaverine. They are administered by slow bolus injection into the relevant vascular territory via a standard diagnostic catheter, with careful monitoring of blood pressure. Treatment may need to be repeated daily for 3-5 days.
Balloon angioplasty is a more invasive neurointerventional technique requiring a guiding catheter and placement of an endovascular microballoon over a guidewire across the affected segment. Expanding the balloon disrupts the smooth muscle fibres within the vessel wall. There is a risk of vessel dissection or rupture. Once treated the spasm does not usually recur.
Other experimental treatments include:
- intrathecal sodium nitroprusside
- mechanical (surgical) evacuation of subarachnoid blood
- intrathecal fibrinolytic
Differential diagnoses
-</ul><p>Most likely the 'true' pathway involves multiple agents interacting with each other, both biochemically and via changes in gene expression, accounting for the delay of onset.</p><p>Oxyhaemoglobin, highest in concentration in arterial blood, appears to simultaneously up-regulate the expression of endothelin 1 (ET-1) and reduce the efficacy of NO.</p><p>This results in alteration of normal vascular tone, resulting in narrowing of the large vessels. Increasingly it is also becoming apparent that small calibre vessels which are in contact with CSF blood are narrowed also - down to 15 micrometres - far too small to be visualised on angiography, let alone CTA/MRA. </p><p>The result, if severe enough, is to reduce perfusion of brain parenchyma resulting in ischaemic symptoms, infarction, and its sequelae. </p><p>The degree of vasospasm is difficult to predict but correlates with the original <a href="/articles/fisher-scale">Fisher scale</a> and more accurately with the <a href="/articles/modified-fisher-scale">modified Fisher scale</a>.</p><h4>Radiographic features</h4><p>Vasospasm associated with subarachnoid haemorrhage is usually characterised by diffuse narrowing without intervening regions of normal vessel calibre <sup>10</sup>. It is often centred at the arterial bifurcation <sup>10</sup>, giving the appearance of enlargement of said bifurcation.</p><h4>Treatment and prognosis</h4><p>Aggressive, early and prophylactic treatment can markedly reduce the incidence of vasospasm but often requires early securing of the ruptured aneurysm. Three main modalities are employed:</p><h5>Triple H therapy</h5><p><strong>H</strong>aemodilution, <strong>H</strong>ypertension, <strong>H</strong>ypervolaemia to maintain adequate cerebral perfusion pressure is achieved with hydration and inotropes if necessary. This often requires admission to a neurological intensive care unit with a central venous catheter and intracranial pressure (ICP) monitoring.</p><h5>Calcium channel blockers</h5><p><a href="/articles/http-en-wikipedia-org-wiki-nimodipine">Nimodipine</a> is the best known and most widely used calcium channel blocker, which dilate vessels especially leptomeningeal collateral.</p><h5>Endovascular intervention</h5><p>In severe cases, intra-arterial therapy can be beneficial. Intra-arterial delivery of a calcium channel blocker such as nimodipine or verapamil has replaced previously used drugs such as papaverine. They are administered by slow bolus injection into the relevant vascular territory via a standard diagnostic catheter, with careful monitoring of blood pressure. Treatment may need to be repeated daily for 3-5 days.</p><p><a href="/articles/balloon-angioplasty-for-cerebral-vasospasm">Balloon angioplasty</a> is a more invasive neurointerventional technique requiring a guiding catheter and placement of an endovascular microballoon over a guidewire across the affected segment. Expanding the balloon disrupts the smooth muscle fibres within the vessel wall. There is a risk of vessel dissection or rupture. Once treated the spasm does not usually recur.</p><p>Other experimental treatments include:</p><ul>- +</ul><p>Most likely the 'true' pathway involves multiple agents interacting with each other, both biochemically and via changes in gene expression, accounting for the delay of onset.</p><p>Oxyhaemoglobin, highest in concentration in arterial blood, appears to simultaneously up-regulate the expression of endothelin 1 (ET-1) and reduce the efficacy of NO.</p><p>This results in alteration of normal vascular tone, resulting in narrowing of the large vessels. Increasingly it is also becoming apparent that small calibre vessels which are in contact with blood in CSF are also narrowed - down to 15 micrometres - far too small to be visualised on angiography, let alone CTA/MRA. </p><p>The result, if severe enough, is to reduce perfusion of brain parenchyma resulting in ischaemic symptoms, infarction, and its sequelae. </p><p>The degree of vasospasm is difficult to predict but correlates with the original <a href="/articles/fisher-scale">Fisher scale</a> and more accurately with the <a href="/articles/modified-fisher-scale">modified Fisher scale</a>.</p><h4>Radiographic features</h4><p>Vasospasm associated with subarachnoid haemorrhage is usually characterised by diffuse narrowing without intervening regions of normal vessel calibre <sup>10</sup>. It is often centred at the arterial bifurcation <sup>10</sup>, giving the appearance of enlargement of the said bifurcation.</p><h4>Treatment and prognosis</h4><p>Aggressive, early and prophylactic treatment can markedly reduce the incidence of vasospasm but often requires early securing of the ruptured aneurysm. Three main modalities are employed:</p><h5>Triple H therapy</h5><p><strong>H</strong>aemodilution, <strong>H</strong>ypertension, <strong>H</strong>ypervolaemia to maintain adequate cerebral perfusion pressure is achieved with hydration and inotropes, if necessary. This often requires admission to a neurological intensive care unit with a central venous catheter and intracranial pressure (ICP) monitoring.</p><h5>Calcium channel blockers</h5><p><a href="/articles/http-en-wikipedia-org-wiki-nimodipine">Nimodipine</a> is the best known and most widely used calcium channel blocker, which dilates vessels, especially leptomeningeal collaterals.</p><h5>Endovascular intervention</h5><p>In severe cases, intra-arterial therapy can be beneficial. Intra-arterial delivery of a calcium channel blocker such as nimodipine or verapamil has replaced previously used drugs such as papaverine. They are administered by slow bolus injection into the relevant vascular territory via a standard diagnostic catheter, with careful monitoring of blood pressure. Treatment may need to be repeated daily for 3-5 days.</p><p><a href="/articles/balloon-angioplasty-for-cerebral-vasospasm">Balloon angioplasty</a> is a more invasive neurointerventional technique requiring a guiding catheter and placement of an endovascular microballoon over a guidewire across the affected segment. Expanding the balloon disrupts the smooth muscle fibres within the vessel wall. There is a risk of vessel dissection or rupture. Once treated the spasm does not usually recur.</p><p>Other experimental treatments include:</p><ul>