Postoperative management

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Patient care following surgery to obliterate a ruptured cerebral aneurysm is complex and must be based on many considerations. Major immediate postoperative problems include brain swelling, bleeding into the operative site, fluid and electrolyte disturbances, hydrocephalus, and the onset of cerebral vasospasm. Complicating the picture is the fact that many postoperative complications present with similar symptoms but require entirely different treatments. Along with the neurological examination, frequent CT scanning, evaluation of vital signs, blood electrolyte determination, transcranial Doppler (TCD) evaluations, and cerebral blood flow determinations are particularly helpful in differentiating these various processes.

Patients who have undergone surgery to repair a ruptured aneurysm are predisposed to develop brain swelling and oedema. Irritation of the brain surface and vessels by subarachnoid clot, disturbance of cerebral vascular autoregulation, elevation of intracranial pressure, and infarction related to iatrogenic vessel occlusion or vasospasm all contribute to postoperative brain swelling. Patients are typically maintained on 16mg/day of dexamethasone during the first postoperative week. While no studies prove any benefit from corticosteroid therapy with SAH, we believe their inhibitory effects on phospholipase A2, inhibition of complement activation, depression of leucocyte migration, and inhibition of lymphocyte function may be beneficial in the prevention of vasospasm.189 For diabetics, glucose control with sliding scale or continuous infusion insulin may be necessary in the setting of SAH and corticosteroid use. Intravascular volume status is closely assessed with either central venous access monitors or pulmonary artery catheters, depending on the patient's condition. Judicious euvolaemic to very slight hypervolaemic fluid management can minimise cerebral swelling by avoiding systemic overload. Repletion of potassium and magnesium will decrease the incidence of arrhythmias, particularly in those patients being treated with induced hypertension for vasospasm. Monitoring of chest radiographs for signs of volume overload and nosocomial pneumonia is prudent during induced hypertensive therapy or for those patients who require prolonged mechanical ventilation. At the time of surgery the degree of brain swelling and the necessity for frontal or temporal lobectomy are assessed. In a similar fashion, lobectomy is considered postoperatively if clinical deterioration occurs concomitant with CT evidence of brain swelling.

Fluid and electrolyte disturbances are relatively common following SAH and surgery to repair a ruptured aneurysm. Takaku found an 88% incidence of electrolyte disturbances following aneurysm surgery.190 Hyponatraemia is the most common abnormality, occurring in 53%, whereas hypernatraemia had the highest mortality rate (42%). Hyponatraemia can be due to either inappropriate secretion of antidiuretic hormone or true natriuresis as a result of cerebral salt wasting.191,192 Both syndromes are characterised by a decrease in plasma sodium levels and osmolality, associated with increased urine sodium concentration greater than 25 mmol/L. Clinical differentiation of these syndromes is important because patients with primary salt wasting syndrome are hypovolaemic and require sodium and fluid replacement. Conversely, true inappropriate antidiuretic hormone secretion is treated with "free water" restriction.

As previously discussed, communicating hydrocephalus both before and after surgery can be seen in SAH patients. There have been some reports that early operation and subarachnoid clot removal may decrease the incidence of postoperative hydrocephalus.193 Others have proposed that preoperative antifibrinolytics contribute to the development of hydrocephalus.194 Regardless of the cause, hydrocephalus should be ruled out in any patient with a decline in mental status prior to and following aneurysm surgery.

Delayed ischaemic deficit secondary to cerebral vasospasm is the greatest cause of morbidity in patients surviving the initial SAH. Angiographic vasospasm occurs in 70% of patients, with 20% having clinically significant narrowing. Cerebral vasospasm has a peak incidence around the sixth to eighth day following SAH, although it can occur at any time up to about 14 days postbleed, beyond which it is extremely rare.195,196 When vasospasm develops, it may last several days to several weeks.195,197 The most reliable predictor of those patients predisposed to develop vasospasm is the amount and distribution of subarachnoid blood on the CT scan. Thick blood in the basal cisterns carries a higher risk of vasospasm than diffuse or focal loculations. Lobar haematomas and interhemispheric blood are associated with a low risk of vasospasm. Subarachnoid blood in the sylvian fissure appears to carry an intermediate vasospasm risk.198,199 Clinical vasospasm develops gradually over hours or days and is typically associated with gradual, progressive decline in neurological status. Headache, fever, and leucocytosis are often present and may herald the onset of vasospasm prior to neurological deterioration. Permanent neurological deficit or death occurs in approximately 12% of patients who develop severe clinical vasospasm.195,200

At present, the mainstay of treatment for clinically significant cerebral vasospasm is the induction of hypervolaemia and systemic hypertension, often referred to as hyperdynamic therapy. The neurological deficits seen with vasospasm are the result of arterial narrowing and increased cerebrovascular resistance. Because autoregulation is usually impaired after SAH, manoeuvres that increase cerebral perfusion pressure can increase cerebral blood flow in the ischaemic regions.201,202 Patients undergoing induced hypertension and intravascular volume expansion are best treated in an intensive care unit with arterial and central venous pressure monitoring. An indwelling arterial catheter assesses blood pressure, a Swan-Ganz catheter monitors pulmonary capillary wedge pressure, and transcutaneous pulse oximeters monitor oxygen saturation. Desaturations may indicate early pulmonary decompensation from hypervolaemic therapy. Fluid balance is assessed hourly.

As mentioned above, the initial therapy for symptomatic vasospasm consists of volume expansion with plasma protein fractionate to create a positive fluid balance. Pulmonary artery wedge pressure is usually maintained between 14 and 18 mmHg and central venous pressure is kept at approximately 10 mmHg. If clinical improvement is not seen soon after volume expansion, arterial blood pressure is elevated with dopamine, dobutamine, and/or noradrenaline (norepinephrine), and typically maintained with systolic pressures between 180 and 220 mmHg. Kassell has reported 58 patients treated for cerebral vasospasm with volume expansion and induced arterial hypertension in which he demonstrated reversal of neurological symptoms in 75%. He found neurological improvement to be permanent in 74%.144 As intravascular volume is expanded, patients may undergo a secondary diuresis which can make artificial elevation of the pulmonary capillary wedge pressure difficult. Use of low dose vasopressin can help minimise the diuresis and maintain an elevated intravascular fluid volume. Hypervolaemic and hypertensive therapy is continued until the neurological symptoms resolve, vasospasm clears as demonstrated by arteriography, or Doppler monitoring or complications from therapy require re-evaluation of the risk/benefit ratio of continuing this type of treatment. Complications include pulmonary oedema, congestive heart failure, brain oedema, hypertensive cerebral haemorrhage, systemic complications of prolonged vasopressor use, and myocardial infarction. Relative contraindications to hyperdynamic therapy include cerebral oedema, cerebral infarction, myocardial dysfunction, pulmonary oedema, adult respiratory distress syndrome, and increased intracranial pressure.203

When hyperdynamic therapy has proven unsuccessful or is contraindicated, we have found other manoeuvres helpful.

Selective intra-arterial infusion of papaverine hydrochloride (300 mg/100 ml normal saline over one hour) into the symptomatic vascular territory may reverse angiographic vasospasm in some patients. The results of this therapy can be clinically dramatic, but, in a similar fashion, may be extremely fleeting or completely unsuccessful.204-206 Further investigation needs to be performed in order to clarify both the role of intra-arterial infusions of vasodilator substances for treatment of cerebral vasospasm and the necessity for superselective infusion.207,208

Another potentially useful adjunct in the treatment of posthaemorrhagic cerebral vasospasm is transluminal balloon angioplasty of the large intracranial vessels (intracranial carotid artery, Ml segment of middle cerebral artery, vertebral and basilar arteries). A number of investigators have reported encouraging results with the use of this technique.209-214 We have witnessed marked improvement in cerebral perfusion following transluminal angioplasty but have also seen fatal complications due to vessel dissection or rupture. Linskey reported a fatal SAH that was produced by rupture of residual aneurysm neck by the angioplasty catheter.215 Despite the risks, however, we now routinely rely on angioplasty for those patients with vasospastic neurological deficit who do not respond quickly to medical therapy. Our own complication rate for this procedure over a four year period was 2 9% permanent neurological deficit and 6% death.

New pharmaceutical products may improve SAH patient outcome. Calcium channel blockers have been discussed earlier (nimodipine, 60 mg orally every four hours for 10-21 days). Their efficacy in reducing the detrimental effects of vasospasm has been shown in controlled studies,159-163 although the true mechanism of action remains elusive. A second drug currently under intense investigation is the free radical scavenger 21-aminosteroid U74006F (tirilazad, Upjohn Co., Kalamazoo, MI, USA). Four controlled studies have demonstrated a reduction in post-SAH morbidity in men administered this medication.216-219 Tirilazad has been shown to decrease the incidence of symptomatic vasospasm in patients with aneurysmal SAH, although the impact on overall patient mortality has been less impressive.220,221 The use of intraventricular sodium nitroprusside in patients with symptomatic vasospasm improved cerebral oxygenation and blood flow in preliminary studies, although further investigation into the efficacy of this therapy is needed.222

A frequently overlooked complication of SAH is Terson's haemorrhage (vitreous haemorrhage) and retinal haemorrhage, which are reported to occur in up to 40% of patients with ruptured cerebral aneurysms.223 Careful screening will permit detection and treatment with vitrectomy when necessary so that visual acuity is maximised in all patients in the long run.

A final consideration in the postoperative management of SAH patients is nutrition. SAH increases resting energy expenditures significantly, especially in patients with Hunt and Hess grades 3-5. Understanding of these metabolic derangements makes attention to nutritional supplementation of major importance.224

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