What the Anesthesiologist Should Know before the Operative Procedure

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1. What is the urgency of the surgery?

What is the risk of delay in order to obtain additional preoperative information?

In the case of acute aneurysmal subarachnoid hemorrhage (aSAH), surgical clipping or endovascular coiling should be performed as early as feasible. The risk of rebleeding is highest within the first 24 hours and potentially within the first 6 hours of hemorrhage. Ideally, an aneurysm is secured within 24 to 72 hours of the hemorrhage in order to minimize or eliminate the risk of re-hemorrhage. Re-hemorrhage is a complication of ruptured aneurysms, which carries very high morbidity and mortality. Early surgical management is done in an effort to prevent re-bleed and to allow for aggressive management of vasospasm or delayed cerebral ischemia (DCI).

Emergent: An aneurysm that ruptures while the patient is hospitalized may demonstrate an improved outcome if taken to the operating room emergently. In addition, clinical deterioration or cerebral herniation secondary to mass effect of a hematoma may warrant emergent intervention.

Urgent: Most ruptured aneurysms fall into the category of urgent. Outcomes are better if an aneurysm is secured within 24 to 72 hours of rupture. Unruptured aneurysms that present with cranial nerve compression or headache or are known radiographically to be rapidly expanding are also considered urgent type cases.

Elective: Most unruptured aneurysms are elective cases and should wait for a proper preoperative surgical and medical evaluation and optimization. Asymptomatic, incidental, unruptured aneurysms are managed by weighing the likelihood for future rupture against the morbidity of treatment. Considerations include the age of the patient, the location of the aneurysm, the size of the aneurysm, and high-risk anatomic features (such as daughter aneurysm). In general, young patients (<50 years), patients with large aneurysms (>5-6 mm), and patients with aneurysms in the posterior circulation (vertebral artery, basilar artery, and posterior cerebral artery) deserve consideration for treatment as opposed to observation and serial CTA or MRA imaging. The decision to treat via open surgery or endovascular means is highly institutional and practitioner dependent.

2. Preoperative evaluation

Evaluation of the patient with unruptured cerebral aneurysm should include a thorough history and physical, with care taken to focus on the neurologic system including cranial nerves, motor and sensory systems, and cognitive level of functioning. Cardiopulmonary vascular diseases such as coronary artery disease and chronic obstructive pulmonary disease are common comorbidities in this group of patients. Social diseases are also common–particularly tobacco and alcohol abuse. Illicit drugs, including methamphetamine, are also associated with intracranial aneurysms and subarachnoid hemorrhage. A family history of intracranial aneurysm syndrome places patients at a higher risk for having multiple aneurysms while risk for SAH is more common in autosomal dominant polycystic kidney disease and type IV Ehlers-Danlos syndrome.

Patients with ruptured aneurysm and SAH will often present with significant comorbidities as discussed below and the preoperative evaluation should take care to include a thorough review of each organ system but particularly cardiac function (ECG, echocardiography), chest x-ray, active infusions and medications, vascular access, recent laboratories (electrolytes, hemoglobin, coagulation tests, troponin), CT head, MRI brain, angiography, and transcranial Doppler. Gathering a social history to include questions regarding recent amphetamine, cocaine, or binge alcohol use is warranted.

Medically unstable conditions warranting further evaluation, including neurogenic stunned myocardium, can dangerously lower cardiac output and rarely result in end organ dysfunction. Like any other cardiomyopathy, invasive monitors such as TEE (transesophageal echo), pulmonary artery catheter, or PiCCO (pulse index continuous cardiac output) monitor, and noninvasive cardiac output monitors may be helpful to properly care for the patient while under anesthesia. However, use of these monitoring modalities has never been demonstrated to positively impact perioperative outcomes in aneurysm patients.

Delaying surgery may be indicated if cerebral vasospasm is present because it can create a high-risk environment for both the surgeon and the anesthesiologist. This is a unique consideration in the treatment of ruptured intracranial aneurysms. In some cases, patients may suffer a low-grade rupture presenting with a sentinel headache without other neurologic deficits, which may delay their presentation to a medical care provider. If a patient presents outside of the 72-hour window and if there is radiographic vasospasm, treatment (either by craniotomy and clipping or endovascular coiling) may be delayed due to the increased risk of cerebral ischemia, infarct, or even hemorrhage from manipulation of spastic vessels. In these cases, the risk of intervention to secure the aneurysm outweighs the risk of aneurysm re-rupture.

3. What are the implications of co-existing disease on perioperative care?

a. Cardiovascular system:

Acute/unstable conditions: In the patient with acute SAH, an impressive catecholamine release can lead to extremes of hypertension; ECG changes such as ST-segment elevation or depression, T-wave inversions, and QT prolongation; contraction band necrosis; B-type natriuretic peptide release; and systolic and diastolic dysfunction. Often early obtained ECGs may have a similar appearance to acute coronary ischemia, but the changes will be in all leads instead of one vascular territory.

Neurogenic stunned myocardium (NSM), also known as Takotsubo cardiomyopathy, is the most extreme form of this pathology. The cause is unclear at this time but the most commonly supported theories point to a surge of endogenous circulating catecholamines leading to myocardial dysfunction and contraction band necrosis. Cardiac catheterization is not warranted in this disease state as the pathology is not associated with coronary obstruction. Patients with NSM may develop transient lactic acidosis, pulmonary edema, and poor cardiac output state. Patients may require inotropic support in the form of milrinone or dobutamine. A pulmonary artery catheter or other cardiac output monitor can be useful to optimize patient care, in this setting. This pathology is largely reversible and the heart will return to its pre-injury ejection fraction within 3 to 5 days. In a small number of cases, the damage is permanent.

Baseline coronary artery disease or cardiac dysfunction—goals of management: The risk factors for aneurysm development and aneurysm rupture overlap with the most common risk factors for heart disease. Basic heart healthy management including avoiding tachycardia, maintaining a normal diastolic pressure, and avoiding extremes of afterload are appropriate goals of management.

b. Pulmonary:

Pulmonary complications may include neurogenic pulmonary edema, cardiogenic pulmonary edema, loss of oropharyngeal reflexes due to obtundation, aspiration pneumonitis, increased Alveolar-arterial oxygen gradient, volume overload secondary to treatment of vasospasm, acute lung injury secondary to high minute ventilation to avoid hypercapnia, and the need for prolonged mechanical ventilation due to poor neurologic state.

Neurogenic pulmonary edema can occur acutely within minutes of injury but may occur, less often, hours to days later. The classic radiographic finding is bilateral alveolar infiltrate. Clinically, patients may exhibit signs of dyspnea, hypoxia, cough, and less often mild hemoptysis due to alveolar hemorrhage. The etiology is less well understood but the hypothesis focus on two main areas; increased vascular permeability secondary to catecholamine surge and microvascular injury from acute increases in hydrostatic pressures. The treatment is largely supportive including supplemental oxygen and mechanical ventilation if necessary.

c. Renal-GI:

Electrolyte abnormalities are common. Hyponatremia is present in one quarter to nearly half of all patients with SAH due to syndrome of inappropriate excretion of antidiuretic hormone (SIADH), cerebral salt wasting (CSW), or both. Diuresis also tends to cause hypokalemia and hypomagnesemia. Hyperchloremic metabolic acidosis may present following infusion of normal saline (0.9% NS) or hypertonic saline solutions as therapy. These solutions often include 3% NaCl, 7.5% NaCl, and 23.4% NaCl. If significant acidosis results, one can consider switching to a 50% solution of hypertonic sodium acetate and sodium chloride. This creates a solution of 3% sodium, with half as chloride and the other half as acetate. The goal for the anesthesiologist should be to maintain the patient’s plasma sodium at the preoperative value. This may require checking intraoperative sodium levels at a frequency of approximately every 6 hours. Rapid correction of hyponatremia or augmentation to hypernatremia should be avoided as it may be associated with osmotic demyelination syndrome (also known as central pontine myelinolysis).

d. Neurologic:

In acute aSAH, the patient may be anywhere along the spectrum of alert and oriented to unarousable and ventilator-dependent. Seizures, hydrocephalus, intracranial hypertension, and cerebral herniation syndromes are all possible in this setting. In addition, intraventricular, subdural, epidural, and intraparenchymal hemorrhages may occur alongside SAH based on aneurysm location. An intraventricular or intraparenchymal fiberoptic or microdialysis catheter may be present for treatment of hydrocephalus or intracranial monitoring. Continuous electroencephalogram (EEG) is less commonly employed. It is important for the anesthesia team to familiarize themselves with these monitors, their respective management, and associated risks before assuming care of the patient. Acute hydrocephalus occurs in 20% to 30% of patients with aSAH. Treatment includes urgent placement of an intraventricular catheter. Cerebral salt wasting (CSW) can lead to extreme diuresis, loss of total body sodium, and intravascular volume depletion. Treatment includes serial monitoring of plasma electrolytes, sodium, and volume replacement.

Delayed cerebral ischemia and cerebral vasospasm are highly morbid complications of aSAH and occur in 30% to 70% of patients following SAH, depending on the grade of aSAH. The onset is typically 3 to 5 days after aneurysm rupture but may occur up to 3 weeks after injury. Treatment is multimodal. Nimodipine, a calcium channel blocker, decreases the incidence of ischemic injury, the mechanism of which is controversial, and is used almost universally. Other therapies including statins and magnesium have been shown not to improve neurologic outcome in randomized clinical trials. Endothelin receptor antagonists have been shown not to improve clinical outcomes, vasospasm-related cerebral infarction, or mortality, and increased the risk of lung complications, pulmonary edema, hypotension, and anemia. Historically, “triple-H” therapy has been a mainstay of treatment, although it has yet to be supported by randomized controlled trials. Triple-H therapy includes hypertension, hypervolemia, and hemodilution to increase cerebral perfusion pressure, enhance circulating blood volume and cerebral blood flow, and improve rheologic properties, respectively. Observational trials have correlated hypotension and hypovolemia with ischemic injury secondary to vasospasm. Avoidance of both hypotension and hypovolemia is prudent.

e. Endocrine:

While long-term survivors aSAH are noted to exhibit endocrinopathies, predominantly growth hormone and gonadal deficiencies, there is no significant evidence to suggest acute HPA (hypothalamic-pituitary-adrenal axis) dysfunction after aSAH. However, there may be a subpopulation of aSAH patients who exhibit vasopressor resistant hypotension and adrenal insufficiency who may need steroid augmentation to maintain or augment blood pressure. In addition, intraoperative hyperglycemia in patients undergoing open surgical intervention has been associated with worse long-term cognition and gross neurologic function.

f. Additional systems/conditions which may be of concern in a patient undergoing this procedure and are relevant for the anesthetic plan (e.g., musculoskeletal in orthopedic procedures, hematologic in a cancer patient)

Anemia is common due to initial blood loss but more often due to repeated phlebotomy as medical teams follow serial plasma electrolytes and markers of end organ function. A hematocrit of greater than 30 at the time of hemorrhage portends a better outcome. There are no data to support that transfusion of red cells to a hematocrit of 30 or greater will improve outcomes by minimizing ischemia. Coagulation studies are often abnormal secondary to consumptive coagulopathy as well as third spacing of coagulation factors following hypervolemic therapy for vasospasm. As microbleeds can be devastating within the fixed-volume cranial vault, it is important to optimize patient’s coagulation status as well as platelet function and number prior to surgical clipping. In the case of endovascular coil embolization, pre-procedural antiplatelet agents (aspirin and clopidogrel) and intra-procedural heparin may be employed to reduce in-stent thrombosis and a discussion with the endovascular surgeon prior to the case is best.

Infectious complications are not uncommon in the hospitalized patient. The most common infectious complications in aSAH are pneumonia, from aspiration due to obtundation and ventilator associated from prolonged mechanical ventilation, and catheter-associated urinary tract infection. Ventriculitis due to intraventricular catheters and bloodstream infections due to central venous access are much less common. In the operating suite, it is important to keep drainage bags from touching the floor and to use sterile technique if any in-dwelling device (e.g., IV, ventricular drain, etc.) is accessed for any reason.

4. What are the patient's medications and how should they be managed in the perioperative period?

Antihypertensive therapy should be continued up until the time of surgery. Although the relationship between aSAH and hypertension is uncertain, swings in blood pressure have been associated with aneurysm rupture and post-operative delirium. Particularly, beta-blockers should be continued as more information is coming out about the adrenergic system as a source of end organ dysfunction in aSAH.

In acute aSAH, antiplatelet agents should be discontinued immediately. Surgeons may insist on prophylactic platelet transfusions for patients who are on antiplatelet agents. For elective surgical clipping, antiplatelet agents should be discontinued 7 to 10 days prior to surgery, in conjunction with the prescribing provider. In elective endovascular coiling cases, the plans for peri-procedure management of antiplatelet agents should be discussed with the interventionalist, as she or he may elect to dose clopidogrel and/or aspirin before, during, or after surgery. OTCs and herbals that are known to inhibit platelet function should similarly be discontinued.

If the patient is on a statin preoperatively, continue this medication. The initiation of statins postoperatively as prophylaxis for DCI and vasospasm in aSAH has been shown to be not beneficial.

a. Are there medications commonly seen in patients undergoing this procedure and for which should there be greater concern?

Elective clipping or endovascular coiling patients commonly present on antihypertensive and antiplatelet agents. Antihypertensives should be continued and antiplatelet agents managed as noted above.

Hospitalized patients with aSAH will often be taking an antiepileptic, opioids, acetaminophen, a statin, hypertonic saline, nimodipine, and, in some institutions, antifibrinolytics such as tranexamic acid or aminocaproic acid. NMS may require support in the form of norepinephrine, vasopressin, milrinone, or dobutamine infusions. Conversely, hypertension is just as common and may require infusions of nicardipine or clevidipine to control hypertensive surge. A systolic pressure of less than 140 mm Hg is the recommendation for a patient with an unsecured aneurysm. This target may change in the setting of DCI or vasospasm with a blood pressure–dependent neurologic deficit on exam.

b. What should be recommended with regard to continuation of medications taken chronically?

Neuroleptics and mood stabilizers should be continued unless the patient is somnolent, unarousable, or obtunded. Anxiolytics, such as alprazolam or lorazepam, are controversial and may be continued at lower doses if prolonged hospitalization is suspected, with a low threshold to withdraw these medications due to oversedation and subsequent loss of a neurologic exam.

Chronic opioids should also be continued to avoid withdrawal and again may be withheld in the case of neurologic deterioration. Antidiabetic medications can and should be discontinued and replaced with short-acting insulin infusion.

c. Latex allergy – If the patient has a sensitivity to latex (e.g., rash from gloves, underwear, etc.) versus anaphylactic reaction, prepare the operating room with latex-free products.

Non-latex gloves and latex-free urinary catheters, central venous catheters, and cerebral ventricular catheters are all commonly available in modern hospitals.

d. Does the patient have any antibiotic allergies – Common antibiotic allergies and alternative antibiotics

Cefazolin or vancomycin is an adequate choice for clean neurosurgical cases. Clindamycin may be substituted in the case of a known beta-lactam allergy.

e. Does the patient have a history of allergy to anesthesia?

Malignant hyperthermia (MH)

Documented: Avoid all trigger agents such as succinylcholine and inhalational agents. Have a proposed general anesthetic plan and ensure that an MH cart is available [MH protocol].

Family history or risk factors for MH: TIVA is an appropriate anesthetic for surgical clipping or endovascular coiling. As with any TIVA, multiple working IV catheters, infusion pumps in places of open drip IV lines are recommended. As the surgical patient will most often be in cranial pins, it is important to ensure the patient does not move, with the use of either muscle relaxants or a deep anesthetic.

Local anesthetics/muscle relaxants

Following the initial stages of preparation, the surgical procedure should be minimally stimulating up until the point of aneurysm clip placement and again at closing of the dura, skull, and skin, and muscle paralysis is not necessary per se. The caveat is that the patient will be in cranial pins and care should be taken to avoid light anesthesia and the potential for patient movement. Patient movement while in pins can lead to very morbid injuries including damage to the operative site, eyes, face, and scalp, as well as significant blood loss. Never allow a patient to move while in pins. Additionally, while patient movement may seem minimal to the anesthesiologist, the neurosurgeon working under a microscope will “see” an exaggeration of this same movement and small changes can compromise the surgical field–especially during manipulation of the blood vessels or the aneurysm itself.

5. What laboratory tests should be obtained and has everything been reviewed?

Full electrolyte panel including magnesium, complete blood count, coagulation studies, troponin, urine drug screen, and blood alcohol levels (if patient with aSAH is unable to provide history) is useful for acute aSAH. For an elective case, either craniotomy for clipping or endovascular coiling, obtain electrolyte panel, complete blood count, and coagulation studies.

Hemoglobin levels: Anemia is common in the hospitalized patient. Transfusion of red cells carries with it significant risk. Hemoglobin levels higher than 8 are appropriate unless active coronary ischemia is present. As mentioned above, increased morbidity is associated with a hemoglobin of less than 10 at the time of presentation of cerebral injury. Transfusion of red cells to a hemoglobin of 10 does not eliminate the associated morbidity.

Electrolytes: Electrolyte abnormalities are common in aSAH–particularly hyponatremia, hypokalemia, and hypomagnesemia. Hyperchloremic metabolic acidosis is a common iatrogenic abnormality after administration of hypertonic saline. Hypertonic saline has been shown to augment cerebral perfusion and improve cerebral oxygenation in poor grade aSAH and is used liberally.

Coagulation panel: Normal coagulation is the goal preoperatively for any craniotomy patient. Usual goals are platelets > 100k and an INR < 1.4. Endovascular coiling patients may require antiplatelet agents as discussed above. Always speak with the interventionalist prior to the case to discuss goals of therapy.

Imaging: For acute aSAH, chest radiography, head CT or MRI, cerebral angiography, and transcranial Doppler or EEG. ECG is recommended for all patients and echocardiography if NMS is present or suspected.

Intraoperative Management: What are the options for anesthetic management and how to determine the best technique?

For intracranial surgery, a general anesthetic is the most common technique. Rarely, if the aneurysm is located near eloquent tissues, an awake craniotomy may be performed under local or MAC anesthesia. In addition, there may be intraoperative neuromonitoring employed including EEG, somatosensory evoked potentials (SSEP), and motor evoked potentials (MEP). A plan between the surgeon and the anesthesiologist should be decided with regard to maintaining anesthesia in the context of neuromonitoring.

Although it is common practice for surgeons to request burst-suppression of EEG using propofol, there are no data that suggest that approach would result in neuroprotection. Instead, measurement of regional brain oxygenation and pH (e.g., paratrend) data suggest that use of an inhaled anesthetic (rather than propofol) more effectively prevents regional ischemia during temporary clipping. Unfortunately, although high-dose inhaled anesthesia may be the most appropriate neuroprotective anesthetic during aneurysm surgery, this approach would greatly limit the ability to achieve meaningful neuromonitoring. For endovascular procedures, both MAC and general are appropriate techniques depending on the culture at your respective institution.

Regional anesthesia

A scalp block may be used in the case of an awake craniotomy. Postoperatively, a scalp block may assist in pain relief, although dural incision and brain parenchymal retraction are the main contributors to postoperative headache and these will not be covered by a regional technique.

General Anesthesia

This is the most commonly used technique, appropriate for all intracranial aneurysm clipping and most endovascular coiling cases.

Benefits are a completely still patient and the ability to tightly control blood pressure without the variability of patient discomfort. Drawbacks are loss of the neurologic exam and therefore feedback to the neurosurgeons should they be operating in important tissue areas such as the motor strip or speech center. Intubation should be completed with care to avoid significant increases in blood pressure and heart rate as prevention of aneurysm rupture or re-rupture in the setting of aSAH.

Monitored anesthesia care

MAC is appropriate for diagnostic endovascular angiography although not ideal for therapeutic angiography, particularly during the coiling period as the patient must remain prohibitively still. In the event of a complication, such as injury to an intracranial vessel, the anesthesiologist and surgeons may need to employ aggressive rescue resuscitation techniques. Fluoroscopy equipment surrounds the patient, making access to the airway and emergency venous access difficult or nearly impossible. Despite these drawbacks, some institutions perform all endovascular procedures under MAC. Both the anesthesiologist and surgeon should decide on a plan preoperatively on a case-by-case basis.

6. What is the author's preferred method of anesthesia technique and why?

General inhalation anesthesia or TIVA is preferred by this author. Careful and precise control of blood pressure and heart rate is easiest with a general anesthetic as the variability of patient comfort and cooperation is removed. Tight cardiovascular control may prevent aneurysm rupture during critical stages of surgical clipping and endovascular coiling. Additionally, PaCO2 and cerebral metabolic rate are easier to manipulate while the patient is under general anesthesia. An arterial catheter is important as cardiovascular medications in the form of infusions are likely to be used and tight blood pressure control cannot wait on noninvasive cuff cycling. A central venous catheter is not essential but is often helpful. A patient arriving on an elective basis may not require a central venous catheter unless the surgery is expected to be difficult or lengthy.

One consideration for placement of a central venous catheter includes the surgical approach. There may be instances during which the surgeon may want to expose the cervical segment of the carotid artery that may preclude an internal jugular central line and may necessitate a subclavian or femoral central line. Furthermore, if a femoral central line is considered, a left sided line may be preferred if there is consideration for intraoperative or postoperative angiography (as most interventionalists routinely use the right groin for access).

Tight blood pressure control is recommended. Though the relationship between hypertension and aSAH is unclear at best, swings in blood pressure may be associated with aneurysmal rupture. Infusions, as opposed to bolus injections of cardiovascular agents, are the better option to achieve tight control and avoid swings. Opioids or propofol will be helpful to blunt the hemodynamic response expected during the most stimulating portions of the surgery including placement of cranial pins, dural incision and retraction, and aneurysm manipulation. Swings in blood pressure can be troublesome for the surgeon during periods of aneurysm manipulation; tight pressure control is helpful during this time.

Appropriate mean arterial pressures should be maintained in an effort to optimally perfuse all organs. Induced hypotension is not recommended and may prove harmful to cerebral tissues at risk.

In aneurysm clipping, the surgical approach can be the most difficult and highly morbid portion of the case. Following aSAH, the brain may be edematous and surgical retraction and manipulation can be both difficult and traumatic. A mannitol bolus of 0.25 to 1 gram per kilogram body weight is appropriate to shrink brain parenchyma and aid the surgeon’s approach. However, some approaches, (e.g., trans-sylvian) are aided by cerebrospinal fluid within the subarachnoid space, and in these cases, mannitol is explicitly avoided. Take care to avoid significant preload depletion as this will ultimately decrease cerebral perfusion. Also try to avoid hypervolemia and volume over resuscitation as cerebral edema can make the surgical approach more difficult.

Moderate hyperventilation to a PaCO2 of 30 is appropriate for a period, to decrease cerebral volumes through vasoconstriction. Extremes of hypocapnia are associated with ischemic infarcts of not just the brain but also bowel and kidney and may lead to coronary spasm. Once the need for hyperventilation has resolved, usually after aneurysm clipping and dural closure, return the patient to a normocapneic state. Hypothermia has not demonstrated an improvement in outcome for patients undergoing aneurysm clipping in good grade aSAH. It may increase the risk of bacterial infection, but only slightly. Overall hypothermia is a fairly safe technique though there is no evidence to support its use.

The surgeon may employ temporary vascular occlusion in an effort to gain access to large or unapproachable aneurysms. This is a form of circulatory arrest to a specific vascular territory. Induced hypertension during these time periods has not been well studied though in specific cases this technique may not be unreasonable. Several studies demonstrate that an intact circle of Willis does not ensure adequate collateral flow during vessel occlusion testing. Various methods to decrease tissue oxygen demand and therefore improve supply/demand matching have been trialed.

Pharmacologic neuroprotection or burst suppression is also often used during aneurysm surgery. This requires intraoperative EEG and a neuromonitoring technologist. There is no good evidence to determine whether burst suppression is beneficial for temporary vascular occlusion. A recent randomized study demonstrated that in good-grade aSAH, neurologic outcome at discharge (measured by Glasgow Outcome Scale and mini-mental status examination) is not improved by propofol burst suppression during temporary vascular occlusion.

One study compared etomidate bolus to high percentage desflurane using brain tissue oxygenation and pH as surrogate markers of brain homeostasis. End tidal desflurane of 9% showed improved physiologic parameters as compared to etomidate during middle cerebral artery occlusion. No evaluation of cognitive function postoperatively or long-term outcomes were studied. Overall this technique is also reasonable and safe but change in outcome is unproven. Several institutions perform extracorporeal circulation and extreme hypothermia as a means of cerebral protection. However, clear evidence of neuroprotective efficacy is lacking.

Subarachnoid lumbar catheters are utilized by some neurovascular surgeons. Aneurysm approach may involve passage through or near one or more cisterns and CSF drainage can aid in visualization of the aneurysm and surrounding structures by allowing for brain relaxation. If this catheter is placed by the anesthesiologist or surgeon, it should be maintained with the care given any other monitor including careful recording of output, precautions to prevent infection such as avoiding contact with bed linens, body fluids and the floor, and securing the manometer safely to prevent accidental damage or detachment. Unintended overdrainage of cerebrospinal fluid from the lumbar catheter can place the patient at risk for cerebral herniation and death. This can potentially be corrected with injection of preservative free saline into the lumbar catheter.

Complications are not uncommon in aneurysm clipping or endovascular coiling. Intraoperative aneurysm rupture can occur in both open surgical and endovascular cases. If this occurs, avoid both hypertension and hypotension through infusions as opposed to bolus injections as swings in hypertension can make aneurysm access more difficult for the surgeon. Blood loss can be significant and rapid and maintenance of preload requires quick replacement of intravenous fluids. Adenosine induced cardiac arrest is used in some centers for vascular control of intra-operative aneurysm rupture or simply for improved surgical visualization of the aneurysm. In the case of intraoperative rupture during endovascular coiling, the patient may become acutely bradycardic and/or hypertensive due to raised intracranial pressure (Cushing reflex). This can be treated with an emergent ventriculostomy for CSF diversion and with hyperosmolar therapy, including hypertonic saline and mannitol.

Damage to surrounding tissues including ligation of branch arteries, localized edema, or tissue stunning from retraction and approach may not be obvious until a neurologic exam can be obtained postoperatively. Avoid heavy narcotic or benzodiazepine use in an effort obtain an adequate neurologic exam as soon as possible postoperatively. In some instances, the patient will not be safe to extubate and lightening anesthesia to obtain some degree of neurologic exam will be helpful.

Tachy- and bradydysrhythmias are common during dural incision, brain retraction, and aneurysm manipulation. The dura is extensively innervated by both cervical and cranial nerve projections. Preparation for a quick response and communication to surgical colleagues is the best defense.

Seizure is a rare occurrence and may present intraoperatively or postoperatively. Prophylactic antiepileptic dosing for this population, though commonly employed, is not supported in randomized trials to prevent seizures. Use of antiepileptics in the short term are probably not significantly deleterious, except in the case of phenytoin, whose use prophylactically in aSAH may be associated with worse cognitive outcomes. Newer antiepileptic medications, including levetiracetam (Keppra), may have a more favorable side effect profile with fewer cognitive effects and may see increased use.

a. If the patient is intubated, are there any special criteria for extubation?

A successful and safe extubation relies on a patient’s ability to breathe and maintain an appropriate minute ventilation in order to avoid hypercapnia, to control their oropharyngeal sensory and motor reflexes, to be alert, and to be cooperative to avoid aspiration. Postoperative imaging is common in most institutions. If the patient’s status is tenuous, extubation can be delayed for a short period if imaging is completed expeditiously.

b. Postoperative management

Pain control

Pain control is routinely a problem in the postoperative period. Headache associated with craniotomy and with aSAH be moderately well managed, although the side effects of somnolence, decreased respiratory rate, and clouding of the neurologic exam make pain control a complex balancing act. Non-narcotic options like acetaminophen are useful. Other NSAIDs may minimally inhibit platelet function and should probably be avoided. Endovascular coiling is a much less painful procedure. Discomfort associated with lying flat for several hours post procedure is a common complaint but easily managed with narcotics.

Bed acuity

Both surgical clipping and endovascular coiling patients should be admitted to the intensive care unit for careful postoperative monitoring. aSAH patients will usually arrive from the ICU and therefore return postoperatively.

Common Postoperative Complications

Intracerebral hemorrhage in the epidural, subdural, or intraparenchymal spaces could prove fatal: routine postoperative imaging is appropriate and emergent imaging is warranted if the patient acutely declines neurologically. Postoperative hemorrhage can originate from several sources including: incompletely secured aneurysm and subsequent rupture, dural veins or arteries, scalp vessels, and intraparenchymal hemorrhage along the surgical tract.

Neurologic deficit or failure to awaken from anesthesia is a feared complication of any neurologic surgery. Avoiding heavy narcotic or benzodiazepine use intraoperatively can improve sensorium postoperatively. Reversal of narcotics can cause hypertension, which is best avoided postoperatively. Reversal of benzodiazepines can change seizure thresholds and is best avoided in favor of the tincture of time for metabolism. A neurologic exam postoperatively or post extubation is helpful with special care taken to examine pupils, facial symmetry, extremity movement, brainstem reflexes, and spontaneous respiratory effort.

Neurologic deficit can be due to edema and neuron stunning associated with brain retraction, cranial nerve compression, operative site edema, or ligation of branch arteries. Emergent imaging is best for diagnosis of acute bleed, while ischemic stroke is unlikely to present as early on CT head and is better diagnosed in the early period by MRI. If an embolic stroke is suspected, endovascular options may exist, depending on each institution’s capabilities and the location of the embolus. Quick communication with the surgical team when a neurologic deficit is noted is important. In the interim period, continue to support blood pressure and avoid hypoxemia.

Cerebral vasospasm, hydrocephalus, and seizure can also contribute to delayed emergence or neurologic deterioration. Seizure may be obvious clinically but subclinical seizures (epileptiform brain activity with body motor response) are also possible. Hydrocephalus is diagnosed by head CT and treatment is placement of an intraventricular catheter. Vasospasm is more difficult to diagnose. Transcranial Doppler or angiography are two methods of diagnosis but unlikely to be employed in the PACU. This diagnosis should ideally be managed by the ICU team.

Acute and profound diuresis in the PACU could be a continued response to mannitol administered intraoperatively. Cerebral salt washing is also likely. In either case, checking serum and urine electrolytes for hyponatremia and replacing fluids to achieve euvolemia are the first steps in management. Repeated serum electrolytes may reveal plasma hyponatremia which will also need to be repleted.

Retroperitoneal or groin hematoma, following an endovascular procedure, requires immediate attention. Lower extremity pulse and groin exams should be completed hourly. Blood loss can be occult and a check of the hematocrit in a hemodynamically unstable patient should be a first thought. An abdominal CT may ultimately be necessary to diagnose a retroperitoneal hematoma.

What's the Evidence?

Preoperative Planning

Komotar, RJ, Mocco, J, Solomon, RA. “Guidelines for the surgical treatment of unruptured intracranial aneurysms: the first annual J Lawrence pool memorial research symposium – controversies in the management of cerebral aneurysms”. Neurosurgery. vol. 62. 2008. pp. 183-94. (Discusses surgical timing of aneurysm treatment, risks for rupture, and high-risk populations.)

Intraoperative Management

Bederson. “Guidelines for the management of aneurysmal subarachnoid hemorrhage: a statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association”. Stroke. vol. 40. 2009. pp. 994-1025. (Discusses Level 1 through Level 3 guidelines for management of subarachnoid hemorrhage including literature defense of each argument.)

Todd, M, Hindman, B. “Mild intraoperative hypothermia during surgery for intracranial aneurysm”. N Engl J Med. vol. 352. 2005. pp. 135-45. (The most complete hypothermia trials for aneurysm surgery – IHAST trial.)

Laskowitz, DT, Kolls, BJ. “Neuroprotection in subarachnoid hemorrhage”. Stroke. vol. 41. 2010. pp. S79-84. (Updates on theory behind neuroprotection: what works, what's proved, what's safe.)

Colby, GP, Coon, AL, Tamargo, RJ. “Surgical management of aneurysmal subarachnoid hemorrhage”. Neurosurg Clin N Am. vol. 21. 2010. pp. 247-61. (An insight into the surgeon's perspective of timing, approach, and treatment options for aneurysmal SAH.)

Rinkel, GJ, Klihn, CJ. “Prevention and treatment of medical and neurological complications in patients with aneurysmal subarachnoid hemorrhage”. Pract Neurol. vol. 9. 2009. pp. 195-209. (Technique to medically optimize patients in an effort to prevent secondary injury in SAH.)

Hoffman. “Comparison of the effect of etomidate and desflurane on brain tissue gases and pH during prolonged middle cerebral artery occlusion”. Anesthesiology. vol. 88. 1998. pp. 1188-94.

Kirkpatrick, PJ, Turner, CL, Smith, C, Hutchinson, PJ, Murray, GD. “Simvastatin in aneurysmal subarachnoid haemorrhage (STASH): a multicentre randomised phase 3 trial”. Lancet Neurol. vol. 13. 2014. pp. 666-75. (No benefit of simvastatin for long-term or short-term outcome in patients with aSAH.)

Connolly, ES, Rabinstein, AA, Carhuapoma, JR. “Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association”. Stroke. vol. 43. 2012. pp. 1711-37.

Guinn, NR, McDonagh, DL, Borel, CO. “Adenosine-induced transient asystole for intracranial aneurysm surgery: a retrospective review”. J Neurosurg Anesthesiol. vol. 23. 2011. pp. 35-40.

Al-Rawi, PG, Tseng, MY, Richards, HK. “Hypertonic saline in patients with poor-grade subarachnoid hemorrhage improves cerebral blood flow, brain tissue oxygen, and pH”. Stroke. vol. 41. 2010. pp. 122-8.

Mees, S, Dorhout, M. “Magnesium for Aneurysmal Subarachnoid Haemorrhage (MASH-2): A Randomised Placebo-Controlled Trial”. Lancet. vol. 380.9836. 2012. pp. 44-49.

Vergouwen, MDI, Algra, A, Rinkel, GJE. “Endothelin Receptor Antagonists for Aneurysmal Subarachnoid Hemorrhage: A Systematic Review and Meta-Analysis Update”. Stroke. vol. 43. 2012. pp. 2671-76.

Spetzler, RF, McDougal, CM, Zabramski, JM. “The Barrow Ruptured Aneurysm Trial: 6-year results”. J Neurosurg. vol. 123. 2015. pp. 609-617.

Lin, N, Cahill, KS, Frerichs, KU, Friedlander, RM, Claus, EB. “Treatment of ruptured and unruptured cerebral aneurysms in the USA: a paradigm shift”. J NeuroIntervent Surg. vol. 4. 2012. pp. 182-89.

Mahajan, C, Chouhan, RS, Rath, GP. “Effect of intraoperative brain protection with propofol on postoperative cognition in patients undergoing temporary clipping during intracranial aneurysm surgery”. Neurol India. vol. 62. 2014. pp. 262-68. (No effect on cognition with burst suppression during aneurysm surgery.)

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Cerebral Aneurysm Clipping