Avoidance of Complications in Neurosurgery

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CHAPTER 22 Avoidance of Complications in Neurosurgery

As with all neurosurgical procedures, avoidance of complications is as important as treatment of disease. In general, avoidance of surgical complications requires attention to making the correct diagnosis, choosing the appropriate surgery, and correctly selecting patients. This chapter is intended to review how to prevent complications of neurosurgical procedures in general, with additional emphasis placed on the specific complications that might be encountered in particular approaches to the spine and brain.

Avoidance of complications in neurosurgery begins with the correct selection of patients who are likely to benefit from the surgical intervention planned. When possible, patients with nonmedical issues that have a known association with poor outcomes, such as workers’ compensation claims or pending lawsuits, should be investigated further to determine the patient’s motivation for recovery.¹^–⁷ Taking the time to explain the probable risks and benefits of the procedure allows the patient to make an informed decision and protects the surgeon in the event of an adverse outcome from claims of inadequate consent. The remainder of this chapter focuses on prevention of complications once the patient has arrived in the operating room. Intraoperative complications may be related to anesthetic issues, positioning of the patient, or technical or anatomic aspects of the specific surgery selected.

Before induction of anesthesia, the surgeon and anesthesiologist must discuss the case in detail and review what is likely to happen and the possible risks. Ideally, an experienced neuroanesthesiologist should be available for neurosurgical procedures. Adequate venous access, placement of a single- or double-lumen tube as required by the surgical approach, and insertion of an intracardiac central venous pressure line to potentially remove air emboli must be planned in advance. The presence of blood products in proximity to the operating room and notification of the blood bank that more may be required depend on the scope of the surgical procedure. Antibiotics should be administered within 1 hour before incisions to ensure therapeutic blood levels.⁸

Complications Related to Patient Positioning

After the anesthesiologist has determined that the airway has been adequately secured and that all lines and monitoring equipment are in place, the patient is ready to be positioned. Several common positioning errors can lead to complications,⁹^–²¹ but most can be prevented with meticulous positioning protocols.

Supine Positioning

Exposure, bleeding, and complications such as air embolism depend on the angle of the head relative to the operative site and the patient’s heart. Overflexing the neck may lead to kinking of the endotracheal tube in the pharynx or obstruction of the jugular vein, which may increase venous pressure in the head and cause increased bleeding or decreased perfusion. The heels, gluteal area, shoulders, and head need to be sufficiently padded. Preferably, rolls are placed under both knees so that they are slightly flexed, and the feet should be suspended by padding under the calves. This position prevents heel pressure ulcers and compression on the Achilles tendon. If the arms are to be secured at the patient’s side, adequate padding of the elbow and wrist and any points of contact with monitoring devices need to be verified before the procedure starts.

Prone Positioning

Nerve palsies and compression injuries are the most frequent complications seen and the most easily preventable. Radial and ulnar neuropathies can occur as a result of positioning the patient in the prone position with the arms extended if padding is inadequate or an inappropriate position is used. Keeping the arms in a mildly flexed position prevents excessive traction in either direction. Padding may be in the form of sheets or blankets placed under the elbows and forearms, or egg-crate foam padding can be used. Brachial plexus injuries can occur with rostral or caudal traction on the shoulders ²² and is frequently seen in the prone position when the arms are extended in the cruciate position or too far above the head. Downward traction, such as when the shoulders need to be pulled down for x-ray localization in the low cervical or cervicothoracic junction, can also cause brachial plexus injury. If possible, any tension placed on the patient’s shoulders during radiography should be removed after the x-ray film has been obtained. Neurophysiologic monitoring of the ulnar nerve with somatosensory evoked potentials during spinal procedures has been shown to be effective in correcting and preventing position-related stretch injuries to the brachial plexus.²³^,²⁴ Another common peripheral neuropathy associated with the prone position is inadequate padding of the anterior superior iliac crest, which can lead to pain or numbness in the distribution of the lateral femoral cutaneous nerve.²⁵ A rare complication is obstruction of the external iliac artery or femoral artery from prolonged compression in the inguinal region.²⁶^,²⁷

Starting at the top, the face and head should be gently suspended without any compression on any one area (discussed later in the chapter in further detail). If the patient is being placed on chest rolls or chest bolsters, the ideal position is to have the shoulders slightly overhanging the chest rolls. Breasts should be tucked between the two rolls to prevent excessive pressure. Prone positioning on a spinal table (e.g., Jackson table, Orthopedic Systems, Inc., Union City, CA) requires placement of the hip pads (of a size appropriate for the patient) so that the top of the pad is at the anterior superior iliac crest. The thigh pads are placed just below the hip pads. The ankles should be allowed to dangle off the edge of the leg supports, if possible. Inadequate padding of the anterior superior iliac crest can cause pressure necrosis of the overlying skin. Male genitalia should be examined to verify that they are not being compressed between the thighs or gluteal folds and that a Foley catheter, if present, is not causing undue traction on the penis. The knees need to be padded, and a padded roll should be placed underneath the ankles so that the feet hang suspended.

The abdomen should be hanging suspended to prevent venous compression and improve venous return to the heart. This point is critical because excessive venous compression can lead to significant intraoperative bleeding secondary to epidural venous hypertension. If the abdomen cannot be adequately suspended, the three-quarter prone position can be used instead (discussed later), particularly in morbidly obese patients, who may not fit on any chest bolstering system, such as the Kamden frame, the four-post Relton frame, or chest rolls. This position allows the abdomen to remain free while the surgeon works from behind, but the position also makes intraoperative radiography very difficult.

Another difficulty with positioning for spine surgery is the difference between the ideal position for a decompressive procedure, with the spine and hips flexed, and that for spinal fusion, with the spine in a more lordotic position and the hips and spine in neutral positions. Many patients have been subjected to iatrogenic flat-back syndrome because of improper position during a fusion procedure.²⁸

Surgeons must be aware of the potential for unilateral or bilateral blindness after prolonged prone surgery. Causes have been hypothesized to be occlusion of the retinal artery or vein, direct trauma, orbital compartment syndrome, and ischemic optic neuropathy. Although rare, devastating complications have been described even when no direct trauma occurred, and therefore patients’ eyes should be checked frequently during the procedure. Minimizing blood loss and hypotensive episodes and maintaining a slightly elevated head of the bed may reduce the chance for this complication. If orbital compartment syndrome is suspected, emergency orbital decompression is the best chance for recovery.²⁹^–³³

Lateral Positioning

The lateral or three-quarters lateral decubitus position carries with it specific risks for peripheral nerve injuries. Stretch on the brachial plexus can be prevented by placement of an axillary roll slightly thicker than the diameter of the upper part of the arm. This roll should be placed approximately four fingerbreadths below the armpit to prevent compression of the long thoracic nerve. Failure to place an adequately sized roll may lead to excessive stretch of the brachial plexus, with the greatest effects on the C5 and C6 nerve roots. The upper extremities need to be supported in relatively neutral positions to prevent ulnar neuropathies. Horner’s syndrome can occur when the head is inadequately padded and allowed to hang laterally in such a manner that excessive tension is placed on the superior cervical ganglion.³⁴ Excessive traction on the lateral femoral cutaneous nerve can be caused by undue extension of the upper part of the leg at the hip while bending the dependent leg. Compression of the common peroneal nerve can occur as a result of inadequate padding laterally under the knee.

Various electrophysiologic modalities can be used to detect subtle signs of neurological compromise before they become fixed deficits. The use of intraoperative monitoring can reduce the likelihood of significant neurological deficits in the appropriate circumstances. Some positioning complications can be avoided with the concomitant use of intraoperative monitoring.^9,³⁵^–³⁹ At our institution, we use motor evoked potentials or somatosensory evoked potentials before and after positioning that may result in injury to the cervical cord. We have found excellent correlation between the lack of changes in evoked potentials and patient outcome. Monitoring is not necessary or indicated in all cases because it is time-consuming, can cause inappropriate movement of the patient, results in bleeding, and has the potential for needlestick injury to the operating room staff. However, in procedures with a potential for significant risk to the cord or neural structures, neurological monitoring is a helpful adjunct to the surgeon. Electrophysiologic neurological monitoring can consist of somatosensory evoked potentials, motor evoked potentials, intraoperative electromyographic responses, nerve action potential monitoring, direct spinal cord stimulation, and other methods.^36,^37,⁴⁰^–⁴⁴ The information gleaned from these modalities can be used to determine whether manipulation of the neural elements is compromising conduction. Numerous authors have published series in which the surgeon has changed some portion of the procedure as a reaction to changes in electrophysiologic monitoring.^9,^{35–39,43–48} Changes in ulnar nerve somatosensory evoked potentials can also indicate traction injury to the brachial plexus and is increasingly being used to monitor positioning, even with lumbar and thoracic procedures.²³^,²⁴

Although not appropriate to monitor for position-related changes, direct epidural electrode motor evoked potential monitoring provides real-time evaluation of the spinal motor tracts and allows quantification of the measured output. This technique may be used during intramedullary spinal cord tumor resection and has been suggested to be helpful in minimizing injury during intramedullary resection.⁴⁹

Cranial Fixation Complications

Positioning of the head for cranial fixation is a frequent source of complications. In sacral, lumbar, and midthoracic surgery performed in the prone position, the head does not need to remain immobile, nor does the cervical spine need to be kept straight. In these circumstances, the head is positioned on loose foam padding (with a cutout for the airway and no compression on the eyes), or the head is turned to the side on loose padding. The objective is to prevent compression on the eyes, face, and forehead. However, for many types of cranial, craniocervical, cervical, or cervicothoracic surgery, it is necessary to firmly immobilize the head and prevent unwanted motion of the neck. Several devices can be used to immobilize the head, the most effective of which is the Mayfield head clamp. This clamp involves three-point pin fixation into the skull so that the skull and neck are rigid relative to the table and, assuming that the body is adequately secured to the table, rigid relative to the body. Because it is more difficult to correct spine deformities after the head is secured in this manner, if part of the goal is to reconstitute cervical lordosis, this issue needs to be considered when positioning.

Pin site complications include lacerations,⁵⁰ skull fractures, associated intracranial hemorrhage (i.e., epidural, subdural, or subarachnoid hemorrhages), and infections that can lead to osteomyelitis.⁵¹^–⁵⁶ Lacerations can be prevented by making sure that the two-pin arm swivels freely so that the force is evenly distributed between the two pins without one pin being shielded from tension, which can potentially result in pivoting on the other pin. If the pins are placed into muscle, it is wise to recheck tension on the single pin to make sure that the muscle has not settled and reduced the pressure. The three pins should be placed slightly below the center of gravity of the head when it is in final position to prevent gravity or personnel from pulling the head down and out of the pins. Ideally, the pins should not be placed directly into the coronal suture or temporal squamosal bone because these bones are most prone to fracture.⁵⁷^–⁵⁹ Pins should be tightened to 60 to 80 lb in adults and 40 to 60 lb in children younger than 15 years. Pins are generally avoided in children younger than 2 years; however, some skull clamp systems do exist for these patients for procedures in which they are required.⁶⁰

Pivoting within the pins by one of these methods or by inadequately locking the clamp before positioning the patient can result in changes in neck position (which can cause cervical spinal cord injury), lacerations, or compression on the eyes and subsequent blindness. These complications can also occur with Gardner-Wells–type tong traction.

Other forms of head support include the horseshoe headrest and the four-cup headrest. Because the horseshoe headrest is not a rigid form of fixation, the head may shift during the procedure, and thus it is imperative that the anesthesiologist continuously observe for any signs of movement. The four-cup headrest is an excellent alternative to the horseshoe, although blindness, skin and scalp compression, and abnormal cervical motion are possible with either support. Alopecia has been reported as a result of scalp compression.⁶¹^–⁶⁷

Dependent Edema

One complication associated with the prone position is the development of orofacial edema when the head is dependent. This complication occurs more frequently with longer procedures and when the spine is more flexed for facilitation of the surgical approach. Such edema can be prevented by minimizing the amount of fluid given by the anesthesiologist and by placing the patient slightly more in a reverse-Trendelenburg position to elevate the head relative to the heart. Facial edema can result in lingual or laryngeal edema and resultant airway obstruction. If obstruction occurs, the patient should be kept intubated until the edema has improved or resolved. Premature attempts at extubation can result in hypoxia and may necessitate emergency tracheotomy.

Catastrophic Medical Complications

Venous Air Embolism

In positioning patients for neurosurgical procedures, the anesthesia team and the surgeons must be aware of the gradient between the patient’s head and the right atrium. Venous air embolism (VAE) is most often encountered with the patient in the seated position for posterior fossa surgery or cervical spine surgery.⁶⁸^–⁷³ It has also been described in patients who have undergone procedures in the prone, supine, and lateral positions.^68,⁷¹^–⁷⁷ Dehydration or blood loss leading to decreased central venous pressure may potentiate the risk for VAE. Patients with a patent foramen ovale or a known right-to-left shunt should be given special consideration before the seated position is used because the risk for paradoxical air embolism after VAE appears to be higher.

Most VAEs are thought to be caused by air entering noncollapsible veins, dural sinuses, or diploic veins. They also have arisen from central venous lines and pulmonary artery catheters. Air travels from the head down the venous system to the heart and eventually to the lungs, where pulmonary constriction and pulmonary hypertension ensue, or in patients with a right-left heart shunt, paradoxical air embolism may occur. Peripheral resistance decreases, and cardiac output initially increases to compensate and maintain blood pressure. Later, as the volume of air infused increases, cardiac output drops, as does blood pressure. Without intervention, cardiac arrest may occur.

Given the dangers of VAE, early detection of the embolus is paramount in reducing the severity of this complication. Monitors used to detect emboli include precordial Doppler ultrasonography, capnography or mass spectrometry, transesophageal echocardiography, transcutaneous oxygen, esophageal stethoscope, and right heart catheter.^68,^69,⁷¹^–⁷⁴ ^,77 The most sensitive are transesophageal echocardiography and Doppler, followed by expired nitrogen and end-tidal carbon dioxide. Electrocardiographic changes, hypotension, and heart murmurs are late signs. Because no single monitor is completely reliable, two or more should be used simultaneously. In awake patients, the presence of a cough may be the earliest sign of VAE, and it can be treated before the VAE becomes hemodynamically significant.⁷⁸ Detection of VAE has increased over the past several decades, but serious morbidity and mortality have decreased. Its incidence varies from 1.2% to 60%, with morbidity and mortality rates of less than 3% in most series.

Treatment of VAE includes aspiration of air through a right atrial catheter, discontinuation of nitrous oxide because it may enlarge the air bubble, and administration of pure oxygen. Surgeons should immediately seal the portals of entry with bone wax, electrocautery, and full-field irrigation. Arrhythmias, hypotension, and hypoxemia should be corrected quickly. Repositioning the patient in the left lateral decubitus position may facilitate removal of air from the right atrium. Stabilization of the patient’s hemodynamic status becomes the first priority, and the procedure may have to be prematurely terminated if hemodynamic stabilization cannot be achieved easily.

Deep Venous Thrombosis and Pulmonary Embolism

Deep venous thrombosis (DVT) and pulmonary embolism are major contributors to morbidity and mortality in postoperative neurosurgical patients. The incidence of DVT, as measured by the labeled fibrinogen technique, ranges from 29% to 43%.⁷⁹^–⁹¹ Most DVTs are asymptomatic and never come to medical attention. Pulmonary embolism, however, is thought to subsequently occur in 15% of such patients.^80,^84,^89,^92,⁹³ Significant thrombi are thought to arise from the popliteal and iliofemoral veins. Risk factors include prolonged surgery and immobilization, previous DVT, malignancy, direct lower extremity trauma, limb weakness, use of oral contraceptives, gram-negative sepsis, advanced age, hypercoagulability, pregnancy, and congestive heart failure.^79,^81,^{83–89,92–100}

A diagnosis of DVT made by clinical examination is generally unreliable. Ankle swelling, calf pain, calf tightness, and a positive Homans sign may all be absent, even in the presence of significant DVT. Doppler ultrasonography and impedance plethysmography are useful in detecting proximal venous thrombosis and are the mainstay of diagnosis, with sensitivities exceeding 90%. When Doppler results are equivocal, extremity venography can be used to diagnose distal and proximal DVTs.

Because of the often-fatal result of pulmonary embolism, prophylaxis against DVT is of major importance in neurosurgery. Many studies have confirmed the utility of sequential pneumatic leg compression devices in preventing DVT.^80,^81,^83,^84,^89,^90,^101,¹⁰² These devices are placed on the patient preoperatively and should be continued until the patient is ambulatory. Early mobilization of postoperative patients is important in preventing thrombus formation. The prophylactic use of low-dose (minidose) subcutaneous heparin (e.g., 5000 IU twice daily) has been well studied over the past 25 years and has been demonstrated to be efficacious in preventing DVT.^86,¹⁰²^–¹⁰⁷ However, some studies have shown an increase in the rate of postoperative intracranial bleeding with minidose administration of heparin.¹⁰²^,¹⁰³ Low-molecular-weight heparin (LMWH) has more recently been used for DVT prophylaxis in surgical patients. Several meta-analyses have been conducted, but it remains unclear whether unfractioned heparin or LMWH is superior for DVT prophylaxis in neurosurgical patients or whether increased efficacy correlates with increased hemorrhagic complications.¹⁰⁸^–¹¹¹

Despite the use of such prophylactic methods, thrombi inevitably develop in one or both lower extremities in some patients. Management options include full-dose heparinization or inferior vena cava interruption. In the immediate and early postoperative period, many neurosurgeons believe that neurosurgical patients with documented DVT should undergo transvenous Greenfield filter placement.^80,^81,^83,^84,^88,^89,^98,¹⁰² There appears to be a general consensus that full anticoagulation is acceptable 1 to 3 weeks after surgery; our institution uses the 1-week rule. Treatment with intravenous heparin (target partial thromboplastin time of 45 to 60 seconds) is followed by oral warfarin sulfate (target international normalized ratio of 2) when not contraindicated. Anticoagulation should be continued for 6 weeks to 3 months in uncomplicated cases. Gastrointestinal bleeding is the most common serious complication encountered.

Patients experiencing pulmonary embolism complain of pleuritic chest pain, hemoptysis, and dyspnea. Jugular venous distention, fever, rales, tachypnea, hypotension, and altered mental status may be found on physical examination. Arterial blood gas determination reveals a PO₂ of less than 80 mm Hg in 85% of patients, accompanied by a widened alveolar-arterial gradient. The level of fibrin degradation products is elevated in most cases. In patients with massive embolism, right axis deviation, right ventricular strain, or right bundle branch block may be identified on electrocardiography. Chest radiography demonstrates an effusion or infiltrate in 90% of cases. A nuclear medicine ventilation-perfusion scan is sensitive in detecting pulmonary embolism but is not specific. The entire clinical scenario, including patient examination, laboratory results, and radiographic evaluation, leads to the diagnosis.^80,^84,^89,^93,¹¹²^–¹¹⁶ Spiral computed tomography (CT) has become the preferred diagnostic study for pulmonary embolism.¹¹⁷ However, pulmonary angiography is the “gold standard” and may be necessary to confirm the diagnosis in as many as half of patients.

Hemorrhagic and Transfusion-Related Issues

Two significant and somewhat similar complications related to bleeding are diffuse intravascular coagulation and transfusion reactions. Both are a consequence of excessive bleeding and transfusions. The first results in a consumptive coagulopathy and further paradoxical bleeding. The other is a reaction to incompatible blood and can result in fever, rash, or shock. Both can be prevented by meticulous hemostasis. When bone is bleeding in an area where the need for fusion precludes the use of bone wax, thrombin-soaked Gelfoam can be rubbed on the bleeding bone surfaces and acts in much the same way as bone wax. When hemostasis alone is not enough to minimize transfusion requirements, as with some long spinal procedures, autologous blood salvage (e.g., Cell Saver) can be used to recycle the patient’s own blood. Other modalities to minimize allogeneic transfusions include autologous blood donation (with or without the use of preoperative erythropoietin), hemodilution, or induced hypotension. Patients about to undergo neurosurgery should, when medically suitable, avoid the use of aspirin products in the week before surgery and other nonsteroidal anti-inflammatory agents on the day before surgery.

Wound Complications

Because of the vascularity of the scalp, most cranial wounds heal well. Postoperative pseudomeningocele formation from persistent leakage of cerebrospinal fluid (CSF) is more common when the normal CSF reabsorption pathways are impaired, as with hydrocephalus, subarachnoid hemorrhage, and meningitis. CSF finds the path of exit of least resistance from the head.

Several potential problems related to the wound area and wound closure can be anticipated and prevented. The first category is postoperative blood collections, or hematomas. Ideally, postoperative hematomas can be prevented by meticulous hemostasis during the procedure, but such is not always the case. The use of postoperative drainage devices (e.g., Hemovac, Jackson-Pratt drain) in wounds for which hemostasis was difficult to achieve before closure can reduce the incidence of postoperative hematoma. Postoperative drainage may also be advantageous in patients in whom postoperative anticoagulation may be required because some of these patients have slightly delayed hematoma formation.¹¹⁸ An obese patient undergoing spine surgery may have significant serous exudation that can continue for up to 5 days or longer postoperatively. It is best to keep a drain in the submuscular space during this time to prevent a postoperative seroma that can become infected.

Several factors can predispose to loss of wound integrity. Prolonged steroid use, irradiation or chemotherapy, reoperations, and malnutrition can predispose patients to poor wound healing. Patients who are likely to lie on their incisions because of an inability to move or the location of an incision are also likely to experience wound breakdown because of pressure-related ischemia and failure to heal adequately. Known or unknown intraoperative violations of sterility may lead to subcutaneous infection and resultant loss of wound integrity. Failure to use perioperative antibiotics can also lead to local infection and failure of the incision line. Maintenance of a dry, sterile wound area results in better wound healing, and if a dressing becomes significantly stained or wet, it must be changed immediately. One way to prevent wound breakdown in a compromised host is the use of an incision that avoids the impaired area. Craniotomies may require a larger incision, such as a bicoronal or larger curvilinear incision that avoids a focused radiation area. In spine surgery, this means use of a paramedian incision. By removing the incision from the avascular midline plane and creating a vascularized myocutaneous flap, patients with cancer or severe malnutrition can have the same or better wound-healing rates as healthy patients. By making the incision off the midline, the pressure is also not directly on the wound and the instrumentation.

Other modalities being investigated include the use of cultured keratinocytes or fibroblasts injected back into the wound area, supplemental or hyperbaric oxygen therapy for several days after surgery, and injection of various growth factors into the wounds.

Risk Factors Related to Anatomy or Technique in Specific Surgeries

Cranial Surgery

Postoperative Seizures

The risk for postoperative seizures within the first week after supratentorial procedures has been well described in the literature.¹¹⁹^–¹³² The underlying cause of these seizures may be metabolic derangements, cerebral hypoxia, preoperative structural defects, stroke and vascular abnormalities, or congenital seizure disorder. Manipulation of brain tissue, postoperative edema, and hematoma formation are common causes of surgically induced seizures. The overall incidence of immediate and early seizures after craniotomy is 4% to 19%.

It is important to identify any risk factors that may contribute to the development of seizures postoperatively. Lesions of the supratentorial intracranial compartment are responsible for seizures after craniotomy in most situations; seizures after infratentorial procedures are attributed to the resultant retraction or movement of supratentorial structures.^119,^120,^{124–129,131,133–136} Brain abscesses, hematomas, intra-axial and extra-axial tumors, aneurysms, arteriovenous malformations, and shunts have been reported to be epileptogenic.^128,¹³⁶^–¹⁴⁹ Patients with a preoperative history of epilepsy are at a higher risk for seizures postoperatively. Patients with subtherapeutic levels of prophylactic agents are also at a higher risk for immediate and early postoperative seizures.^126,^129,^134,¹⁵⁰^–¹⁵³

All types of seizures can occur after neurosurgery. The diagnosis of a postoperative epileptic event is usually obvious. Multiple episodes are more common than single episodes, but status epilepticus is relatively uncommon. Seizures can occur in unconscious, comatose patients and may be manifested as nonconvulsive status epilepticus. An electroencephalogram may be useful in these situations.

The consequences of seizures are neurological and systemic and include neuronal damage, increased cerebral blood flow, and increased intracranial pressure (ICP). Metabolic acidosis, hyperazotemia, hyperkalemia, hypoglycemia, hyperthermia, and hypoxia may develop and exacerbate the situation, thereby leading to further seizure activity.

Preventing a seizure is preferable to treating one that has already begun. Adequate preoperative loading of parenteral or oral phenytoin has definitively been shown to decrease the incidence of postoperative seizures.¹⁵⁴^–¹⁵⁶ In patients unable to tolerate phenytoin, phenobarbital or carbamazepine may be substituted. It follows that therapeutic preoperative levels should be measured in patients undergoing supratentorial procedures whenever possible. Administration of the anticonvulsant should continue through the acute and early postoperative period. Electrolyte abnormalities should be corrected immediately in the postoperative period to further reduce the chance for a seizure.

Most seizures in neurosurgical patients are self-limited and last between 2 and 4 minutes. A chemistry profile should be obtained and any abnormalities corrected. Blood levels of antiseizure medications should also be verified and brought into the therapeutic range. Multiple seizures or any seizure lasting longer than 5 minutes should be aggressively treated rather than waiting 30 minutes to fulfill the criteria for status epilepticus. Treatment may entail the administration of lorazepam, diazepam, or midazolam, followed by fosphenytoin. Cardiorespiratory support measures may need to be initiated as well. For refractory cases, reintubation followed by phenobarbital coma or general anesthesia may be necessary. In most cases, it is probably best to image the patient postoperatively after the seizure episode has been treated. The possibility of intracranial hemorrhage, edema, infarction, or pneumocephalus must be entertained and the appropriate surgical or medical management initiated as soon as possible.

Reports have called into question the routine practice of phenytoin prophylaxis for patients without a history of seizures.^126,^152,¹⁵⁷ How this will affect practices remains to be seen because a full medicoeconomic and medicolegal analysis is not yet available.

Postoperative Edema and Increased Intracranial Pressure

Neurosurgical procedures involving direct manipulation of brain tissue may lead to postoperative swelling. The amount of edema is related to many factors. The duration and force of tissue retraction on central nervous system tissue are directly related to the amount of postoperative swelling in the supratentorial and infratentorial compartments. Bipolar coagulation can further contribute to this edema when cortical bleeding is caused by retraction. The edema may be worsened if venous drainage is impaired and results in local congestion. Sustained venous hypertension may cause infarction and petechial hemorrhage, often with disastrous consequences. Noncompliance of the cranium then leads to increased ICP. Cerebral perfusion is limited, and neurological dysfunction ensues. In severe cases, herniation follows.

For lengthy procedures or when significant brain retraction is necessary, the use of a rigid, self-retaining retractor system combined with rigid head fixation can help limit the damage caused by tissue manipulation. Preservation of the cerebral vasculature during surgery, with limited coagulation and careful tissue handling, can reduce the occurrence of severe edema postoperatively.

The neurological deficits caused by brain swelling may be permanent or transient, and the severity of the deficit depends on the patient. Edema usually begins within 5 hours after the procedure and reaches its maximum approximately 48 to 72 hours later.¹⁵⁸^–¹⁶⁶ Altered mental status, cranial nerve deficits, and motor or sensory dysfunction can all occur. The diagnosis may be confirmed with non–contrast-enhanced CT, and hemorrhage, hydrocephalus, and pneumocephalus may be ruled out. Cerebral hypodensity, sulcal effacement, midline shift, loss of the gray-white matter interface, and small lateral ventricles are the hallmarks of postoperative edema. If impaired venous drainage secondary to the incompetence of venous sinuses is suspected, conventional venous-phase angiography or magnetic resonance venography may be helpful in diagnosing the location and severity of the occlusion. Appropriate surgical and medical measures may then be instituted.

The goal of treatment of increased ICP is to maintain cerebral perfusion pressure (CPP) at greater than 55 to 60 mm Hg while reducing the amount of cerebral edema.¹⁶⁶^–¹⁷³ This entails measuring arterial blood pressure and ICP continuously. Induction of arterial hypertension with vasopressors may be necessary to achieve the desired CPP. Short-term hyperventilation to a PCO₂ of 30 mm Hg can reduce ICP effectively. High-dose dexamethasone should be given to patients with vasogenic edema to alleviate tumor-related swelling. Increasing the head of the bed to 30 to 45 degrees can assist in venous return, and maintaining a neutral midline head position and administering diuretics such as furosemide and mannitol can further reduce ICP. When using diuretics, it is important that serum chemistries and osmolalities be monitored to ensure that the patient does not become severely dehydrated. Hypertonic saline solutions are now increasingly being used with success for the treatment of vasogenic edema.¹⁷⁴^,¹⁷⁵ In refractory cases, sedation may be used to suppress cerebral metabolism and paralysis induced to reduce ICP by limiting agitation and muscle exertion. As a final resort, barbiturate coma with mild hypothermia or temporal lobectomy may be used to control ICP and maintain CPP.

Specific Cranial Disorders

Supratentorial Craniotomy

Numerous lesions may be approached via supratentorial craniotomy. In low-grade gliomas, long-term control and cure are possible. Because high-grade gliomas are not curable by surgery, surgery represents a palliative treatment aimed at reducing tumor bulk and maximizing quality of life. Patients with metastatic brain lesions can have a significant improvement in their survival by removal of brain metastases. It is therefore incumbent on neurosurgeons to minimize complications when patients are in the early stages of their disease and their clinical condition is best. The decision about whether surgery is warranted involves carefully weighing the possible surgical complications against the potential benefits. Studies have shown that craniotomies for intraparenchymal lesions typically result in mortality rates of 2.2% and morbidity rates of 15% (Table 22-1).¹⁷⁶^–¹⁷⁹

TABLE 22-1 Morbidity and Mortality Rates for Cranial Parenchymal Tumors

Tumors located in eloquent or deep brain areas are more difficult to surgically debulk and carry a higher risk for neurological morbidity. Surgery on gliomas typically results in more morbidity and mortality than does surgery on brain metastases.¹⁷⁸ Surgical outcome is closely tied to the patient’s age and preoperative neurological status as measured by the Karnofsky Performance Status score.¹⁷⁶^–¹⁷⁸ Patients are at risk for general complications of craniotomies, including complications related to positioning, anesthesia, infection, seizures, hemorrhage, and neurological compromise. Neurological compromise may result from resection or retraction of normal functional brain tissue or compromise of the vascular supply. Neurological morbidities usually consist of motor or sensory deficits or aphasias (Table 22-2). Occasionally, visual field deficits can occur.

TABLE 22-2 Neurological Complications in Intraparenchymal Tumor Surgery

COMPLICATION	RATE (%)
Motor or sensory deficit	7.5
Aphasia	0.5
Visual field deficit	0.5

From Sawaya R, Hammoud M, Schoppa D. Neurosurgical outcomes in a modern series of 400 craniotomies for treatment of parenchymal tumors. Neurosurgery. 1998;42:1044-1055.

Gliomas lack a well-defined boundary between abnormal and normal tissue. Pathologic analysis demonstrates tumor cells in grossly normal-appearing tissue. The result is a tradeoff between radical tumor resection and risk for resection of functional brain tissue and subsequent neurological deterioration. Avoidance of vascular compromise involves meticulous attention to detail and preservation of all significant vasculature seen to supply normal brain tissue. If significant vessels are taken during surgery, postoperative CT or magnetic resonance imaging (MRI) can reveal the evolution of an infarction in the vessel’s vascular distribution.

Computer-assisted stereotactic systems enhance the ability of the surgeon to delineate between normal brain and tumor. Stereotactic systems also facilitate targeting of tumors that cannot be visualized at the brain’s surface. Intraoperative functional mapping helps identify and avoid injury to eloquent cortex. Craniotomy performed while the patient is awake is particularly helpful in resecting lesions surrounding the speech centers. Using an awake craniotomy technique, Taylor and Bernstein reported an overall complication rate of 16.5% and a mortality rate of 1%.¹⁷⁹ New postoperative neurological deficits were seen in 13% of patients, but they were permanent in just 4.5%. Increasingly, functional imaging is being applied intraoperatively, with evidence suggesting that it allows more complete resection while minimizing the risk for deficits. Functional MRI and diffusion-weighted imaging can be integrated with most neuronavigation systems to allow identification and protection of motor tracts.¹⁸⁰^–¹⁸³

Hemorrhage into the postoperative tumor bed represents a serious complication that may require reoperation for evacuation of hematoma. Prevention begins with checking preoperative coagulation studies and ensuring that the patient has not been taking an aspirin-containing product. Intraoperatively, meticulous hemostasis must be achieved with a variety of hemostatic agents and bipolar electrocautery. The tumor cavity may be lined with hemostatic agents such as Surgicel. Tight blood pressure control during extubation and in the postoperative period is important. Rarely, distal intracerebral or intracerebellar hemorrhages can occur, although their cause is unexplained.¹⁸⁴

All patients undergoing surgery have a risk for thromboembolic events, but those with malignant gliomas are at significantly increased risk. Prophylaxis with low-dose heparin and external pneumatic leg muscle compression must be initiated promptly. The neurosurgical staff must maintain a high index of suspicion for phlebitis and pulmonary embolism so that treatment can be initiated early. Inferior vena cava filters may be placed to prevent the occurrence of pulmonary embolism. Full anticoagulation is preferable in patients seen more than 3 weeks after surgery.⁹⁰^,¹⁸⁵

Wound infection and wound dehiscence occur rarely with craniotomies and develop in less than 1% of patients.¹⁷⁸ The routine use of steroids in patients with intraparenchymal tumors apparently has little effect on overall wound healing.

Surgery for gliomas is rarely curative, and many patients with recurrences are subject to reoperation. However, studies have demonstrated that reoperation does not necessarily predispose patients to a greater complication rate.^176,^178,¹⁸⁶

Meningiomas differ from parenchymal tumors in that they are often associated with venous sinuses, and thus venous infarction or injury to the sinuses is an additional risk. These tumors can invade the wall of sinuses and eventually narrow and obliterate the sinus lumen. When meningiomas are located in proximity to a sinus, preoperative venous angiography, magnetic resonance angiography, or magnetic resonance venography is essential to avoid complications. Entering a patent sinus can result in difficult bleeding that may require surgical reconstruction or bypass of the sinus. Sacrifice of a major venous sinus should be avoided. Complications associated with sacrificing a major venous sinus include increased ICP as a result of of brain edema and venous hemorrhagic infarction. Obtundation and seizures can develop in such patients (Table 22-3).¹⁸⁷^–¹⁸⁹ Aggressive ICP management is essential in controlling this complication. Prudent surgical management may necessitate leaving a portion of the tumor adherent to the sinus and using adjuvant therapy or observation with surveillance MRI.¹⁹⁰ Postoperative seizures are seen with convexity and parasagittal meningiomas.¹⁸⁸ Sacrifice of a significant vein can result in venous infarction and an increased risk for seizures. The mortality rate for craniotomies performed for convexity and parasagittal meningiomas is 3.7% to 13%.^188,¹⁹¹^–¹⁹⁸

TABLE 22-3 Meningiomas and Seizure Frequency

Posterior Fossa Craniotomy

Infratentorial craniotomies carry many of the same risks as do supratentorial craniotomies. However, some risks are more pronounced when operating in the posterior fossa.

Leakage of CSF is seen frequently after a posterior fossa craniotomy and occurs in 3% to 15% of patients.¹⁹⁹^–²⁰¹ Leakage can occur from the wound or be manifested as rhinorrhea or otorrhea. Openings into the mastoid air cells and air cells in the vicinity of the meatus can lead to otorrhea. Fluid can drain into the nasopharynx through the eustachian tube. Packing the mastoid air cells with bone wax can prevent CSF leakage. Aggressive drilling of the porus acusticus and larger tumor size have been associated with an increasing risk for CSF leaks.²⁰² To minimize the risk for postoperative rhinorrhea, we apply bone wax aggressively to all mastoid air cells exposed during the craniectomy, as well as fibrin glue before closure. However, unroofing of air cells within the internal auditory canal can lead to persistent leakage, and we routinely apply a muscle plug, Gelfoam, and fibrin glue in this region to minimize the risk for leakage. In addition, routine prophylactic high-volume lumbar puncture may be performed daily for 3 days postoperatively to minimize the risk for leakage. When leakage occurs, management typically involves placement of a spinal drain. Operative repair may be necessary in patients who fail a trial of spinal drainage. Early recognition plus treatment of CSF leaks is imperative because CSF leakage places patients at risk for meningitis.²⁰¹ Meningitis occurs in about 1% of patients, and early treatment with appropriate antibiotics is essential. Aseptic meningitis also occurs infrequently after surgery. Patients may have some elements of ataxia postoperatively, but these symptoms are usually limited and resolve within a few days. Significant headaches occur in half of patients postoperatively, and 25% complain of headaches persisting for more than a year after surgery.²⁰³

Mortality from infratentorial surgery is generally higher than that seen with supratentorial procedures. Compromise of the anterior inferior cerebellar artery and the resultant lateral pontine infarction are implicated in a third of postoperative deaths.²⁰⁴ The second biggest contributor to postoperative mortality is aspiration pneumonia resulting from lower cranial nerve deficits. Patients may require placement of a feeding tube and a tracheostomy to prevent aspiration pneumonia. Cerebellar contusions or hematomas can occur as a result of overaggressive retraction. Distant supratentorial hemorrhages occasionally occur for unclear reasons.²⁰⁵ Surgeons must be prepared to place an occipital ventricular catheter intraoperatively on an emergency basis if acute hydrocephalus results.

Transsphenoidal Surgery

Transsphenoidal surgery is commonly used to reach tumors in the sellar region. This procedure can be performed with extremely low mortality and low morbidity. Deaths have occurred in 0% to 1.75% of patients (Table 22-4). Laws²⁰⁶ reported 7 deaths in 786 procedures (0.9%), and Wilson²⁰⁷ reported 2 deaths (0.2%) in a series of 1000 patients. At our institution, 2 deaths occurred in 1800 procedures. Morbidities associated with the transsphenoidal approach are distinct from general neurosurgical complications because the approach is quite different from most transcranial approaches.

TABLE 22-4 Common Complication Rates in Transsphenoidal Surgery

COMPLICATION	RATE (%)
Mortality	0-1.75
Nasal septum perforation	1-3
Sinusitis	1-4
Epistaxis	2-4
Visual disturbances	0.6-1.6
Transient diabetes insipidus	10-60
Permanent diabetes insipidus	0.5-5
Anterior pituitary insufficiency	1-10
Cerebrospinal fluid leakage	1-4
Meningitis	0-1.75

Avoidance of complications begins with appropriate patient selection. Patients with sphenoid sinus infections should not undergo transsphenoidal surgery because of the risk for meningitis. Tumor morphology may also dictate the operative approach. Tumors located eccentrically may not be accessible transsphenoidally and instead might require a transcranial approach. In tumors with dumbbell morphology, a constrictive diaphragma sellae may limit adequate tumor decompression. Tumor consistency also influences the surgical outcome. Most adenomas have a soft consistency and are easily and safely removed with curets and suction. Firm tumors, seen in 5% of patients, can be difficult to remove transsphenoidally. Adequate preoperative radiologic evaluation is essential because of the wide range of pathologies that are found in the sella. For example, misdiagnosis of an aneurysm as an adenoma can result in a potentially fatal complication. Any vascular anomalies in the sellar region may be a contraindication to the transsphenoidal approach.

Anesthetic complications in transsphenoidal surgery are rare. Acromegalic patients exhibit cardiomyopathy and macroglossia, which may complicate airway management. Patients with pituitary lesions are often deficient in one or more pituitary hormones. A comprehensive preoperative endocrine analysis is essential, and adequate stress doses of steroids should be administered. Postoperatively, the patient’s endocrine status should be carefully monitored. Other medical complications are relatively rare and are commensurate with complications in other elective procedures.

Several complications can arise as a consequence of the transsphenoidal approach. If a sublabial incision is used, anesthesia of the upper lip and anterior maxillary teeth can occur, although this condition is usually transient.²⁰⁸ Removal of the superior cartilaginous septum may result in a saddle nose deformity.²⁰⁹ Perforation of the nasal septum occurs in 1% to 3% of patients and is more likely with reoperations.²⁰⁶ Postoperative sinusitis can occur in 1% to 4% of patients and may be reduced by postoperative antibiotics.²¹⁰ Opening the speculum can result in diastasis of the maxilla or fracture of the medial orbital wall.²⁰⁶^,²¹¹ Damage to the optic nerve or the carotid arteries can occur if the speculum is advanced too far. Inadequate removal of mucosa in the sphenoid sinus can lead to the postoperative formation of a mucocele.²¹²

Vascular injuries represent serious morbidities and can lead to death. Intraoperative mucosal bleeding and delayed postoperative bleeding from the mucosal branch of the sphenopalatine artery can occur. If postoperative epistaxis persists, embolization of the internal maxillary artery may be necessary.²¹³ Damage to the carotid arteries can occur in the sphenoid sinus or in the sella. Maintaining a midline trajectory is vital to avoid the carotid artery, and preoperative radiologic studies are essential in localizing the carotids. There are significant variations in the carotid’s parasellar course, and the distance between the two arteries may be as little as 4 mm.²⁰⁸ Frameless stereotaxis can be used to maintain a midline approach and may be especially useful in reoperations.²¹⁴ Endoscopy is increasingly being used to minimize tissue trauma and to obtain more expansive views than those provided by microscopic visualization alone.²¹⁵^,²¹⁶ Excessive arterial bleeding signals intraoperative injury to the carotid artery, and the only treatment involves packing the operative field.²¹³ Other maneuvers are limited by the exposure, although if packing fails, ligation of the carotid may be required. Carotid artery injury can result in subarachnoid hemorrhage, vasospasm, false aneurysms, and carotid cavernous fistulas. A postoperative cerebral angiogram is essential to identify any of these complications.²¹⁷ About 25% of deaths occurring during transsphenoidal operations are attributable to vascular injuries.²¹^,²¹³ Visual disturbances are also possible because of the close association of the chiasm, optic nerve, and pituitary. Damage can occur as a result of direct trauma, traction injury, or vascular compromise. Visual disturbances are more likely after reoperations because of adhesion formation between the chiasm and sella. Adhesions predispose the chiasm, optic nerve, and hypothalamus to traction injuries. In general, visual disturbances occur in 0.6% to 1.6% of patients.²¹⁸ Postoperative visual loss can also signal the formation of a hematoma in the tumor bed. Such hematomas can be prevented by meticulous hemostasis. They can occur in 0.3% to 1.2% of cases.^206,^210,²¹² Injuries to the hypothalamus can also take place and potentially result in death.²¹³ These patients are comatose and exhibit hyperthermia. Hypothalamic injury is the most common cause of death in patients undergoing transsphenoidal operations.²¹³

Several complications can be anticipated in the postoperative period, and early recognition and appropriate treatment can circumvent catastrophic results. Patients should be closely monitored for diabetes insipidus (DI) with frequent serum sodium evaluations and careful accounting of patients’ fluid intake and urine output. An elevated serum sodium level or urine output may indicate DI. Temporary postoperative DI can occur in 10% to 60% of patients.²¹⁰^,²¹⁹ Permanent DI is much less common and occurs in just 0.5% to 5% of patients.²¹⁰ Delayed onset of the syndrome of inappropriate antidiuretic hormone secretion can also occur about a week postoperatively.²¹³

Postoperative anterior pituitary insufficiency is one of the most commonly seen postoperative complications. Its incidence varies from 1% to 10%.²⁰⁶^,²⁰⁷ Postoperative steroid therapy should be used in all postoperative patients until a thorough endocrine evaluation is complete. Adrenal insufficiency is a potentially serious complication if adequate steroid replacement therapy is not initiated.

CSF rhinorrhea is another commonly encountered complication of the transsphenoidal approach and occurs in 1% to 4% of patients.²⁰⁶^,²¹³ Intraoperatively, penetration of the arachnoid membrane can result in a gush of CSF into the operative field and the potential for postoperative CSF rhinorrhea. Packing the sella intraoperatively with an autologous fat graft and bone from the removed vomer can help prevent CSF leakage. Care must be taken to not overpack the sella, which may lead to compression of the chiasm.²¹² Patients in whom CSF rhinorrhea develops are first treated by spinal drainage for several days. Failure to close a CSF fistula with spinal drainage may indicate the need for reoperation and repacking of the sella. Early recognition and treatment of CSF rhinorrhea are important because a CSF leak can lead to meningitis. The incidence of meningitis in patients undergoing transsphenoidal surgery has been reported to be 0% to 1.75%.^210,^212,²²⁰ Patients with diabetes mellitus are at greater risk for the development of meningitis.

Cranial Base Surgery

Cranial base lesions represent a heterogeneous group of pathologies associated with the cranial base bony structures. Although once considered inaccessible, advances in microsurgery and neurodiagnostics have extended the neurosurgeon’s reach into the cranial base. The surgical approaches for cranial base surgery are challenging, and minimizing surgical morbidity is essential to achieve good outcomes. Complications are generally related to the lesion’s location and the surgical approach necessary for exposure.

The surgical approaches often call for brain retraction to adequately expose the lesion. Overly aggressive retraction can lead to tissue damage and infarction, with postoperative swelling resulting in increased ICP. Several maneuvers, including adequate bone removal, CSF drainage, and diuretics, can aid in achieving adequate exposure without excessive brain retraction. Resection of noneloquent brain tissue may be required to prevent contusions and possible postoperative herniation occurring from retraction injuries. Retraction can also compromise or injure venous outflow and result in venous stasis and hemorrhagic infarctions. This is especially important in regard to the vein of Labbé. Excessive retraction of the posterior temporal lobe can lead to tearing of the vein of Labbé and severe hemorrhagic temporal lobe edema.²²¹

Postoperative hematomas can also develop. Prevention involves meticulous hemostasis, tight blood pressure control in the postoperative period, and prompt correction of any coagulopathy. Early recognition involves having a high index of suspicion and performing early postoperative CT. Treatment usually involves operative evacuation of the hematoma.

CSF leakage is one of the most common postoperative complications in cranial base surgery. The surgery often creates a communication between the CSF space and the facial sinuses. The sphenoid sinus is most commonly involved because of its association with the clivus and cavernous sinus.²²¹ CSF leaks occur in about 8% of patients undergoing cranial base operations.²²¹ A persistent CSF fistula may develop. Leaks generally occur in the immediate postoperative period, or they rarely develop months after surgery.²²¹ CSF leaks are clinically manifested as clear spinal fluid draining from the nose, ear, or wound. The fluid can be collected on a pledget, and the presence of β₂-transferrin confirms the discharge as CSF. Confirmatory radiographic examinations can be performed. Radioisotopic cisternography with cotton pledgets in the nasal cavity can corroborate the presence of a CSF leak. CT cisternography with intrathecal metrizamide or magnetic resonance cisternography can be used to localize the leak.²²²

A watertight dural closure can prevent CSF leaks, but invasion of the dura by tumor or anatomic considerations often make closing the dura impossible. If watertight closure cannot be achieved, the cranial base should be reconstructed with muscle, fat, and fascia packing. Spinal fluid drainage can divert CSF and allow the dura or reconstruction to seal. Initial treatment of a postoperative CSF leak is a trial period of lumbar spinal drainage. CSF leaks that fail to resolve or CT demonstrating progressive increases in intracranial air requires surgical repair. A leak that recurs after spinal drainage is stopped necessitates re-exploration with repacking and reconstruction of the cranial base. Early recognition of hydrocephalus is important because increased ICP can predispose a patient to a CSF leak and correction of hydrocephalus may prevent a CSF leak.

Pneumocephalus is another postoperative complication frequently encountered in cranial base surgery. Air may be found in the extradural or intradural spaces. Intracranial air can produce alterations in a patient’s mental status that result in lethargy or agitation. Some degree of pneumocephalus is commonly found on postoperative CT, and the air is usually reabsorbed quickly. Patients operated on in the sitting position have a higher incidence of pneumocephalus.²²³ Increasing amounts of intracranial air signal the presence of a communication between the subarachnoid space and air sinuses and implies an undetected CSF leak. Having patients lie flat in bed and discontinuing external spinal drainage can facilitate the absorption of intracranial air. Passing a spinal needle through the bur-hole site into the air pocket can decompress the subdural air in the event of a tension pneumocephalus.²²¹

Skull base lesions often involve the cranial blood vessels. Tumors can encase or displace these vessels, and adequate tumor removal may require sacrifice of vessels. The neurosurgeon must know the consequences of sacrificing cranial base blood vessels to minimize morbidity. Sacrifice of vessels can result in ischemic neurological deficits and infarctions in a vascular territory or watershed distribution. Preoperatively, balloon occlusion testing and xenon-enhanced CT cerebral blood flow testing can determine whether patients can tolerate sacrificing a blood vessel. Patients in whom neurological deficits develop with the balloon occlusion test or who have cerebral blood flow of less than 35 mL/100 g per minute cannot tolerate vessel sacrifice and may require a bypass graft.²²⁴

Cranial nerve morbidity is commonly encountered with cranial base surgery, and the dysfunction may be temporary or permanent. Accurate preoperative cranial nerve examination is important because postoperative dysfunction is more likely in patients with preoperative deficits. Neurophysiologic monitoring is an important adjuvant for localizing cranial nerves and preventing injury. Cranial nerve VII may be monitored via continuous facial electromyographic responses. A nerve stimulator can help locate the facial nerve. Cranial nerve XI can be localized with a nerve stimulator and observation of shoulder twitching.¹⁹⁸

Cranial nerve injury can occur as a result of nerve retraction or direct injury during tumor dissection. Cranial nerves may also be injured by compromise of the nerves’ blood supply during surgical dissection distant from the nerves. Damage to the cranial nerves is especially significant during surgery in the cavernous sinus. Optic nerve damage occurs in 0% to 6% of patients.¹⁹⁷^,²²⁵ Permanent damage involving extraocular nerve function (i.e., cranial nerves III, IV, and VI) occurs in 20% to 30% of patients.¹⁹⁶^,¹⁹⁷ The incidence of V1 neuropathy is 8% to 20%.^196,^197,²²⁵

Certain cranial nerves are more susceptible to injury than others. Cranial nerves I, II, and VIII are very sensitive to injury. Minimal manipulation can result in profound deficits, and the loss of function is often irreversible. Cranial nerves III, IV, and VI are less sensitive to manipulation, and some recovery typically occurs postoperatively if the nerve’s continuity is maintained. Injury to these nerves results in diplopia. Loss of cranial nerve IV function can be corrected by tilting the head or the use of prism glasses. Oculoplastic procedures may be necessary to correct persistent diplopia caused by injury to cranial nerve III or VI. Cranial nerve V damage is generally well tolerated, with the exception of damage to the V1 segments, which mediate the corneal reflex. Damage to the V1 division results in corneal sensory dysfunction, and patients must have meticulous eye care to prevent corneal abrasions and loss of vision in the desensitized eye.²²¹

Damage to cranial nerve VII results in significant cosmetic morbidity as a consequence of facial paralysis and functional loss because of an inability to close the eye effectively. Damage can occur from direct injury to the nerve, injury to the geniculate ganglion, or nerve traction. Traction can occur during retraction of the greater superficial petrosal nerve or caudal retraction of the mandible after dislocating the temporomandibular joint (TMJ). Maintaining nerve continuity offers the best chance of functional recovery. Direct end-to-end anastomosis can be performed, or a cable graft using a sural nerve graft may be necessary. Other options include XII-VII or XI-VII anastomoses. Tarsorrhaphy or insertion of a gold weight implant in the upper eyelid may be necessary if eye closure is not adequate. In the immediate postoperative period, eye care with artificial tears and eye lubricants is essential to prevent keratitis.

Cranial nerves IX and X are usually injured together. Unilateral, slowly developing lesions are usually well tolerated because of the patient’s compensatory mechanisms. Acute lesions result in difficulty swallowing, inability to protect the airway, and unilateral vocal cord paralysis. Long-term dysfunction requires treatment with a tracheostomy and placement of a gastrostomy tube. Tracheostomies and feeding tubes may be removed if patients recover function sufficiently or compensatory mechanisms develop. Failure to initiate such measures can lead to malnutrition and aspiration pneumonia.

Unilateral injury to cranial nerve XII is generally well tolerated. When combined with other cranial nerve injuries, such as injury to cranial nerves VII, IX, or X, significant dysarthria can occur. Bilateral cranial nerve XII injury results in severe functional limitation and ultimately requires a tracheostomy and placement of a feeding tube.²²¹

Cranial base surgery can cause morbidity from TMJ manipulation. Dislocation of the TMJ can result in postoperative trismus. Resection of the mandibular condyle may be preferred because it avoids retraction of the mandible and associated postoperative trismus. Resection of the condyle leads to a contralateral jaw deviation but no functional loss.²²¹

Complications of Stereotactic Brain Surgery

Advances in medical technology have resulted in a host of neurosurgical procedures using three-dimensional stereotactic guidance systems. Many procedures involve the use of stereotactic guidance in performing conventional craniotomies or other operations. This section deals with complications related to stereotactic procedures performed through small bur holes or using focused radiation (i.e., Gamma Knife). Such procedures include brain biopsy, cyst aspiration, functional lesioning, and stereotactic radiosurgery.

A stereotactic frame is applied to the patient, and CT or MRI is performed. The most commonly used frames are the Leksell (Elektra Instruments, Atlanta, GA) and the Brown-Roberts-Wells (Radionics, Burlington, MA) systems.²²⁶ The fiducial markers on the frame are registered into the system and allow accurate three-dimensional navigation and localization in reference to the neuroimaging. Proper application of the stereotactic frame and precise registration are essential to achieve accurate results. Frameless systems that use cutaneous fiducial markers are available, as well as some that use surface landmarks alone, with no need to place cutaneous fiducial markers.

One of the most commonly performed stereotactic procedures is brain biopsy. Brain biopsies are safe and effective procedures. The procedure can usually be performed under monitored anesthesia care and can avoid the complications associated with general anesthesia. CT or MRI is used to stereotactically guide biopsy of a lesion through a small bur hole. Possible complications include hemorrhage, neurological deficits, seizures, and infections.²²⁶ The mortality rate in several large series has been less than 1%, and complication rates vary from 0% to 7% (Table 22-5).²²⁶^–²³³ Seizures and infections are rare during brain biopsy. The most serious complication usually involves postoperative hematoma formation. Properly performed brain biopsies are more than 90% effective in establishing a tissue diagnosis in patients with radiographic lesions.²²⁶

TABLE 22-5 Complications of Stereotactic Brain Biopsy

Preventing complications related to brain biopsy requires adequate preoperative planning. Only patients in whom the results of brain biopsy may change medical management should undergo biopsy. Because thrombocytopenia or coagulopathies predispose patients to intracranial hemorrhage, all candidates should have normal coagulation profiles and platelet counts. Preoperative radiographic imaging is essential to rule out vascular lesions that may result in serious hemorrhage when biopsied. The planned trajectory must avoid vessels and important structures. Intraoperative hypertension may predispose patients to hemorrhage.²²⁶

When bleeding is discovered during a brain biopsy, allowing the blood to drain out of the needle may prevent the formation of a hematoma.²²⁶ Craniotomy may be required to control persistent hemorrhage. Instillation of thrombin through the biopsy canula has been used to control hemorrhage.²³⁴ Routine postoperative CT can be performed to rule out hematoma formation, and asymptomatic hematomas are often discovered postoperatively. Neurological deficits develop in about 10% of patients with asymptomatic postoperative hematomas.²³⁵ Most postoperative hematomas are managed by observation and serial CT.

Brain biopsies are increasingly being performed on patients infected with human immunodeficiency virus (HIV), who may be subject to several central nervous system infections or neoplasms. Biopsies in patients with acquired immunodeficiency syndrome have higher complication rates. Skolasky and coworkers reviewed 435 HIV-positive patients undergoing biopsy and determined that the morbidity rate was 8.4% and the mortality rate was 2.9%.²³⁶ Complications were associated with preoperative poor functional status and thrombocytopenia. It is not clear whether the presence of HIV infection predisposes to higher complication rates.