Clinical review: Prevention and therapy of vasospasm in subarachnoid hemorrhage

Abstract

Vasospasm is one of the leading causes of morbidity and mortality following aneurysmal subarachnoid hemorrhage (SAH). Radiographic vasospasm usually develops between 5 and 15 days after the initial hemorrhage, and is associated with clinically apparent delayed ischemic neurological deficits (DID) in one-third of patients. The pathophysiology of this reversible vasculopathy is not fully understood but appears to involve structural changes and biochemical alterations at the levels of the vascular endothelium and smooth muscle cells. Blood in the subarachnoid space is believed to trigger these changes. In addition, cerebral perfusion may be concurrently impaired by hypovolemia and impaired cerebral autoregulatory function. The combined effects of these processes can lead to reduction in cerebral blood flow so severe as to cause ischemia leading to infarction. Diagnosis is made by some combination of clinical, cerebral angiographic, and transcranial doppler ultrasonographic factors. Nimodipine, a calcium channel antagonist, is so far the only available therapy with proven benefit for reducing the impact of DID. Aggressive therapy combining hemodynamic augmentation, transluminal balloon angioplasty, and intra-arterial infusion of vasodilator drugs is, to varying degrees, usually implemented. A panoply of drugs, with different mechanisms of action, has been studied in SAH related vasospasm. Currently, the most promising are magnesium sulfate, 3-hydroxy-3-methyl-glutaryl-CoA reductase inhibitors, nitric oxide donors and endothelin-1 antagonists. This paper reviews established and emerging therapies for vasospasm. IntroductionVasospasm is a common complication that follows aneurysmal subarachnoid hemorrhage (SAH). Ecker was first to point out the occurrence of arterial spasm following SAH [1]. Before him, Robertson had attributed ischemic brain lesions found on autopsy of patients with SAH to probable 'spasm of arteries ' [2]. Despite growing literature, skepticism regarding the association between angiographic vasospasm and clinical findings persisted [3], until CM Fisher and colleagues published a synopsis on the matter in 1977 [4]. This seminal publication comprehensively described the deficits accompanying vasospasm and, most importantly, made the association between vasospasm and neurological deficits, also known as delayed ischemic deficits (DID).The term vasospasm implies a reduction in the caliber of a vessel; however, in SAH it has multiple meanings. SAHinduced vasospasm is a complex entity due in part to a delayed and reversible vasculopathy, impaired autoregulatory function, and hypovolemia causing a regional reduction of cerebral perfusion to the point of causing ischemia [5,6].Radiographic evidence of vasospasm develops in 50% to 70% of patients with SAH, but only half of those experience symptoms of DID [7][8][9][10][11][12]. Proximal vessels, situated at the base of the brain, are preferentially affected; however, more distal arteries could also develop impaired vascular reactivity (autoregulation...

Vasopressin Increases Cerebral Perfusion Pressure but not Cerebral Blood Flow in Neurosurgical Patients with Catecholamine-Refractory Hypotension: A Preliminary Evaluation Using the Non-Invasive Quantix ND in Comparison to the Literature

“…They received volume and catecholamine therapy according to standard recommendations and in dependance on the occurance of cerebral vasospasm. The goal was to keep CPP > 70 mmHg [1]. The TBI patient was treated according to the Brain Trauma Foundation guidelines.…”

“…Despite many clincial trials so far no level I evidence for an ideal CPP exists, but the guidelines of the Brain Trauma Foundation recommend a CPP between 50-70 mmHg in trauma patients, depending on the patient's individual cerebral hemodynamic profile. For patients suffering from SAH there might be completely different needs for CPP levels since the major cause of death after SAH is delayed cerebal ischemia due to cerebral vasospasm [1]. For those patients a sufficient CCP is crucial.…”

Effects of iodinated contrast media in a novel model for cerebral vasospasm

“…This is important because patients with SAH have disturbances of cerebral blood regulation 25 , and many diagnostic and therapeutic procedures needed for their treatment may require the use of CM 12,13,14 . It has been shown that several types of CM may have potentially deleterious effects on the tone and reactivity of vessels from several vascular beds 15,16 .…”

“…Most diagnostic and therapeutic procedures needed for the treatment of SAH patients require the use of iodinated contrast media (CM) 12,13,14 . It has been shown that CM have adverse effects on vessels of the kidney and other vascular beds 15,16 .…”

Pharmacotherapy of neurological complications after cardiac surgery

“…[18] было отмечено увеличение общей летальности среди кардиохирургических больных, несмотря на хоро-шую перфузию ГМ. Однако блокаторы кальциевых кана-лов широко используются в лечении геморрагических ин-сультов на фоне спазма внутричерепных артерий [16].…”