Cerebral Aneurysm Clipping

Cerebral Aneurysm Clipping is one of the important modalities for the treatment of aneuryms apart from coiling so the anesthetic management of such cases is as follows.

Skull is a fixed vault and most intracerebral structures are relatively in compressible, hence even a small haemorrhage can result in a significant anatomic distortion producing significant rise in ICP and reduction in cerebral perfusion.

Patients with intracranial aneurysm often have a history of systemic hypertension and smoking. There are multiple perioperative considerations centering on neurological, cardiovascular, respiratory system and electrolyte disturbances.

In about a third of patients, rupture of aneurysm results in immediate death. Another 30% patients are exposed to the risk of rebleeding and serious pen-surgical complications.

Classically, subarachnoid hemorrhage (SAH) is graded from I-IV according to the severity, using the Hunt and Hess grade. This has prognostic significance because surgicalmorbidity and mortality increases with the grade. Subarachnoid haemorrhage (SAH) grade I or II patients and those having SAH grade III with uneventful intraoperative course and intact laryngeal reflexes are planned for extubation after ensuring satisfactory recovery from anesthesia.

Exceptions are made in patients with vertebral and basilar artery aneurysms who are judged individually in the postoperative period irrespective of their clinical preoperative SAH grade.

As no hard and fast rule exists to discriminate between anesthetic given and surgical complications, current practice is to avoid long acting anesthetic agents to facilitate early neurological evaluation. Sedative and analgesics have been reported to exacerbate or mask focal neurological findings in patients with previous strokes.

Long vascular Cerebral Aneurysm Clipping times, high retractor pressures and repeat surgical procedures can delay the emergence. Indicators of deterioration due to surgical causes are unequal pupils and new focal neurological deficits persisting for more than an hour after emergence from anesthesia.

These guidelines are based upon the assumption that anesthesia usually causes global depression and effect of residual anesthetics is usually dissipated within 30-60 minutes. Subsequently, neurological status is assessed every 15 minutes and deteriorating patients may require immediate CT scan or angiography. CT scan is often assessed according to Fisher grade.

Vasospasm (“intracranial arterial narrowing”) usually occurs three to fifteen days after the initial hemorrhage and is related to the amount of blood present in the subarachnoid space. Symptoms peak at about seven days and subside by the end of two weeks. 25% of the SAH patients may develop acute hydrocephalus due to interference with cerebrospinal fluid re-absorption necessitating emergency ventriculostomy.

The current management of SAH centers on nimodipine prophylaxis, blood pressure control, early surgery and volume expansion to prevent vasospasm. Contemporary management of intracranial aneurysm calls for “early” surgical intervention after SAH.

The definition of early varies up to and including first 72 hours after bleeding. Currently, some clinicians recommend ultra-early intervention, i.e., Cerebral Aneurysm Clipping within 18 hours of the initial SAH because, re-bleeding is most frequent within the first 24 hours after the initial haemorrhage and incidence declines with time. In our institute, patients admitted with cerebral aneurysm are operated within 6 hours of hospital admission.

From the anesthesiologist’s point of view, it is important to recognize that increasing clinical SAH grades are associated with possible impairment of cerebral autoregulation, decreased CO2 responsiveness, elevated ICP and increased surgical morbidity and mortality.

Because of these considerations patients with grade IV or V haemorrhages are electively ventilated postoperatively and allowed to wake up in an intensive care unit. Serial transcranial Doppler examinations and prophylactic “Triple H” therapy (hypovolaemic haemodilution with or without hypertension) are associated with improved outcome.

Other postoperative problems can be pulmonary oedema, pneumonia and cardiac dysrhythmias. In some patients, hypovolaemia may be paradoxically associated with hyponatraemia which is secondary to increased excretion of brain natriuretic peptide (cerebral salt wasting syndrome).

With fluid restriction, the risk of delayed cerebral ischemia and infarction further increases in these patients. Monitoring of central venous pressure (CVP) or pulmonary artery wedge pressure (PCWP) is required for optimization of fluid resuscitation in these hypovolaemic patients with raised ICR Correction of hyponatraemia is done with hypertonic or isotonic saline.

Patients with anterior circulation aneurysms may develop postoperative diabetes insipidus. Other late postoperative complications are hydrocephalus, delayed ischemic neurological deficits and infection.


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