Microneurosurgical Clip Ligation of Acutely Ruptured Cerebral Aneurysm Immediately Preceded by Intentional Subtotal Endovascular Coil Embolization Under a Single Anesthesia: Observations Using a Deliberate Combined Sequential Treatment Strategy in 13 Cases.

BACKGROUND: Endovascular coil embolization and craniotomy with clip ligation are the 2 most commonly used treatments for ruptured cerebral aneurysm. Although coiling maintains the advantages of brevity and complete avoidance of brain retraction and manipulation, clipping offers the benefits of decompression of the injured brain and lower rates of aneurysm recurrence. A combined, immediately sequential treatment strategy for acutely ruptured cerebral aneurysm that simultaneously maximizes the advantages of both techniques, while minimizing their respective disadvantages, may be a useful paradigm. OBJECTIVE: To demonstrate the complementarity of clipping and coiling in acutely ruptured cerebral aneurysm. METHODS: Patients with ruptured anterior circulation cerebral aneurysm standing to benefit from brain decompression were treated by a combination of coiling and microneurosurgery in rapid succession, under the same general anesthetic. Surgery consisted of clipping of the aneurysm via either craniotomy or craniectomy with expansion duraplasty in all cases, and ventriculostomy in selected cases. RESULTS: Coil embolization of the ruptured aneurysm was carried out rapidly and improved the efficiency of subsequent clipping by allowing early unequivocal identification of the aneurysm dome and decreased brain retraction, reducing risk of intraoperative rupture and obviating temporary occlusion. All aneurysms were shown eliminated by postoperative cerebral angiography. CONCLUSIONS: A deliberate combined treatment strategy that uses clipping immediately preceded by subtotal coiling under a single anesthetic may be ideal for selected ruptured cerebral aneurysms, takes advantage of the unique strengths of both techniques, makes both techniques easier, and maximizes opportunity for brain protection against delayed complications in the prolonged aftermath of aneurysmal subarachnoid hemorrhage.

Continuous monitoring of the microcirculation in neurocritical care: an update on brain tissue oxygenation.

PURPOSE OF REVIEW: This article summarizes recent clinical and experimental studies of parenchymal brain tissue oxygen monitoring and considers future directions for its use in neurocritical care. RECENT FINDINGS: Recent reports have focused on the relationship between brain tissue oxygen tension (PbrO2) and other physiologic parameters such as mean arterial pressure, cerebral perfusion pressure, cerebral blood flow, and fraction of inspired oxygen. PbrO2 appears to reflect both regional and systemic oxygen concentrations as well as microvascular perfusion through natural tissue gradients. Defining an absolute critically low PbrO2 threshold has been challenging, but levels below 14 mmHg may have a pathophysiologic basis. Newer studies have examined dynamic changes in PbrO2 during oxygen reactivity testing and during augmentation of cerebral perfusion pressure. PbrO2 monitoring has now been described in a wide range of neurocritical care conditions including head trauma, subarachnoid hemorrhage, nontraumatic intracerebral hemorrhage, brain death, and brain tumor resection. SUMMARY: The use of brain tissue oxygen monitoring is maturing as a tool to detect and treat secondary brain injury. PbrO2 measurements can provide continuous quantitative data about injury pathophysiology and severity that may help optimize neurointensive care management. Prospective trials of PbrO2 guided treatment protocols are now needed to demonstrate impact on clinical outcomes.

Optimizing blood pressure in neurological emergencies.

Excessive hypertension can challenge the brain's capacity to autoregulate cerebral blood flow, and can aggravate increased intracranial pressure (ICP) and cerebral edema. Hypotension may worsen ischemic damage in marginally perfused tissue, and in some cases can trigger cerebral vasodilation and ICP plateau waves. There is a lack of high-quality data regarding optimal BP management in these conditions. Existing guidelines for target BP levels are based largely on class III evidence. Class I data only exist for enteral candesartan and nimodipine use in acute ischemic stroke and aneurismal subarachnoid hemorrhage (SAH), respectively, and for parenteral magnesium use in eclampsia. Class II data exist for reducing BP to <180/105 mmHg in patients with ischemic stroke who are treated with intravenous tissue plasminogen activator, for elevating systolic BP to 180-220 mmHg in SAH patients with symptomatic vasospasm, and for maintaining cerebral perfusion pressure (CPP)>60 mmHg in traumatic brain injury. Short-acting continuous-infusion agents with a reliable dose-response relationship and favorable safety profile are desirable. To reduce BP, labetalol, esmolol, and nicardipine best meet these criteria. Sodium nitroprusside should be avoided in most neurological emergencies because of its tendency to raise ICP and cause toxicity with prolonged infusion. To elevate BP, the preferred agents are phenylephrine, dopamine, and norepinephrine.