8 Postoperative Care in Skull Base Surgery
Parul Goyal, Devyani Lal, and Peter H. Hwang
Introduction
Postoperative care after endoscopic skull base surgical procedures is important in ensuring optimal outcomes. Initially, postoperative care focuses on diagnosis and treatment of neurologic, rhinologic, and systemic problems that may arise in the immediate postoperative period. Long term, adequate postoperative care is necessary to ensure patent and functional sinus ostia.
General Care
Certain aspects of postoperative care start even before the patient leaves the operating room. At the completion of the procedure, it is important to communicate with the anesthesia team to ensure as smooth an emergence and extubation as possible. Avoidance of excessive coughing or “bucking” on the endotracheal tube helps to minimize bleeding and risk for disruption of grafts at the reconstruction site. If a lumbar drain is placed for the purpose of cerebrospinal fluid (CSF) diversion after skull base reconstruction, it is left unclamped at the time of extubation to minimize large changes in intracranial pressure.
In the recovery room, patients should be monitored closely with particular attention to neurologic status. For patients who have undergone more extensive skull base resections, postoperative observation in the intensive care unit may be indicated to facilitate close monitoring of neurologic status and fluid balance.
Packing
Various packing materials and protocols have been described for patients after endoscopic skull base surgery, both to support graft materials at the site of reconstruction as well as to promote hemostasis. In cases where a small skull base defect has been repaired, or where no CSF leak has occurred, a minimal amount of absorbable packing may be sufficient; absorbable gelatin sponges, fibrin glue, and polymerized hydrogel are among the many options for bioabsorbable packing material. However, in cases where a large defect has been repaired using composite grafting materials, it may be desirable to support the graft with additional nonabsorbable packing. For example, an inflatable balloon in the form of a Foley catheter or a posterior epistaxis pack may be placed against the graft to support the skull base repair for several days postoperatively. Nonabsorbable sponges or gauze may also be used. Packing removal should be done with extreme care so as not to disrupt the surgical repair, and endoscopic debridement of the repair site should be deferred for several weeks until definitive closure of the repair site has been ascertained. Because patients often find packing removal to be among the most uncomfortable parts of the postoperative process, our practice is to avoid large amounts of packing after endoscopic procedures whenever possible, balancing functional necessity for packing against patient comfort.
Antibiotics
There are no standardized recommendations for postoperative antibiotic use after endoscopic skull base surgical procedures. The procedures can best be classified as clean-contaminated procedures given the fact that instruments and graft materials must be passed through the nose to the operative site, allowing for contamination by nasal flora. Standardized regimens of antibiotics have been described in patients undergoing open skull base surgical procedures. Kraus and colleagues1 investigated the use of a standardized regimen of antibiotics in patients undergoing traditional (open) skull base surgical procedures. Their study included 211 patients, 90 of whom were treated with a standard regimen of ceftazidime, metronidazole, and vancomycin for a mean of 7.7 days. Patients who were treated with this standard regimen had significantly fewer infectious complications when compared with patients treated with various other antibiotic regimens.
With regard to endoscopic skull base procedures, the existing data suggest that endoscopic procedures may be associated with a lower likelihood of severe postoperative infections compared with open skull base procedures, perhaps due to qualitative differences between endoscopic and nonendoscopic techniques. Thus, endoscopic skull base surgery may have different perioperative antibiotic requirements. Brown and colleagues2 investigated the role of prophylactic postoperative antibiotics after endoscopic skull base surgery. Their study included 90 patients treated for pituitary tumors, encephaloceles, meningiomas, and craniopharyngiomas. Intravenous antibiotics were given at the time of induction and were continued for 24 to 48 hours postoperatively until the patients’ nasal packing was removed. The authors had no cases of intracranial infections or meningitis. However, 21% of the patients did need outpatient antibiotics within the first 3 months for nasal or sinus cavity infections.
In our practice, patients undergoing endoscopic skull base surgery receive a single preoperative dose of an intravenous antibiotic. Postoperatively, the use of antibiotics varies according to the extent of skull base resection and the amount of packing used. Smaller cases such as pituitary tumor resection are not treated with postoperative antibiotics, whereas larger skull base resections are treated prophylactically with a 2-week course of amoxicillin-clavulanate or quinolone. This may help to decrease the relatively high rate of postoperative sinus infections described by Brown et al.2 Patients who develop sinusitis are treated in a culture-directed fashion.
Cerebrospinal Fluid Leak
Reconstruction of the skull base is a critical part of endoscopic skull base surgery. The goal of reconstruction is to create a watertight seal so that complications associated with a persistent CSF leak can be avoided. Many different algorithms have been described for reconstruction after endoscopic skull base procedures.3–5 Although there is inadequate evidence to support one algorithm over another, vascularized flap reconstruction in general provides more favorable closure for large skull base defects. At the conclusion of endoscopic skull base surgery, careful inspection of the operative site facilitates visualization of most CSF leaks that may be present. Occasionally it can be difficult to identify a CSF leak at the time of surgery when the CSF may be obscured by blood, clots, and nasal secretions. Intrathecal fluorescein can be used to help identify and localize occult CSF leaks. However, its role as a routine intraoperative diagnostic tool is limited by the fact that it must be injected before the start of the procedure.
It is important to assess patients postoperatively for a CSF leak. In most instances, patients who have a postoperative CSF leak manifest the leak in the first 24 to 48 hours after surgery. However, it is important to search for a delayed leak when the patient is seen in outpatient follow-up. Some patients with a postoperative CSF leak may have obvious clear rhinorrhea, making the diagnosis straightforward. Other patients may have subtle signs, in which case imaging studies (computed tomography cisternogram) or surgical reexploration may be indicated. Nasal drainage that can be collected can be sent for β-2-transferrin assay to differentiate CSF from nasal secretions. In most institutions, this assay is not performed in the hospital’s own laboratory and must be sent to a different facility. It is often not practical to wait several days for the results of the testing; thus the diagnosis of a CSF leak is often made based on history and clinical suspicion, before the results of such tests are available.
After a CSF leak is diagnosed, treatment options include lumbar drainage for CSF diversion versus surgical reexploration. Cases in which a meticulous, layered reconstruction was performed at the time of surgery may initially be managed with lumbar drainage to allow for any small leak sites to seal. Patients who continue to have a persistent leak after a 48- to 72-hour trial of lumbar drainage should be taken back to the operating room for reexploration and revision of the reconstruction.
Bleeding
Although some degree of postoperative oozing is unavoidable after endoscopic skull base surgery, bleeding can typically be controlled at the conclusion of surgery with relatively limited amounts of nasal packing (or no packing). Thus our practice is to avoid large amounts of packing at the conclusion of endoscopic procedures. Patients are told before surgery to expect some minor oozing and expression of clots from the nose.
Heavy bleeding that occurs postoperatively is most commonly related to arterial injury. During the course of transsphenoidal surgery, the posterior septal branch of the sphenopalatine artery can be injured. Similarly, the anterior and posterior ethmoid arteries may be subject to injury during anterior cranial base surgery. Arterial nasal bleeding can be managed with nasal packing, surgical exploration and control, or, for posterior bleeding, angiography and embolization. We prefer the option of surgical exploration and control in most patients with suspected bleeding from branches of the sphenopalatine artery. If the bleeding site can be localized, the area can be controlled directly with bipolar cauterization. Alternatively, endoscopic techniques can be used to ligate the sphenopalatine artery as the vessel exits the sphenopalatine foramen. At our institutions, this method is preferred over embolization because of its effectiveness and low morbidity.
Injury to the carotid artery is rare, but can have serious immediate and long-term consequences. Patients typically present with profuse bleeding. Direct surgical repair is generally not feasible, and the best chance for control is by way of angiography and endovascular treatment.6,7 When patients present with profuse bleeding, it is important to control the bleeding and stabilize the patient by applying direct pressure at the bleeding site. A large Foley catheter or other form of nasal packing can help stabilize the bleeding enough to allow for angiography.
Postoperative Debridement
It is important to ensure patent sinus ostia after endoscopic skull base surgical procedures to avoid postoperative sinus obstruction and sinusitis. Our routine care includes postoperative endoscopy approximately 2 weeks after surgery. Debris and crusting can be removed from areas that are not adjacent to areas of skull base reconstruction. It is important to avoid aggressive debridement because manipulation can disrupt grafts at the site of skull base reconstruction. At subsequent follow-up visits, endoscopy is used to ensure patent sinus ostia and satisfactory healing at the surgical site. Saline nasal irrigations can be used after the first few weeks to help clear residual debris and crusting.
Endocrine Dysfunction
Patients undergoing parasellar skull base surgery are commonly vulnerable to transient or permanent derangements in the hypothalamic-pituitary-adrenal axis.8 Changes in the water-sodium balance result from abnormalities of antidiuretic hormone (ADH). Also, patients with functioning pituitary tumors may have unique hemodynamic and endocrine changes associated with conditions such as acromegaly, Cushing’s disease, or thyrotoxicosis.
Diabetes Insipidus
Diabetes insipidus (DI) is a common complication of transsphenoidal pituitary surgery, occurring in 0.5 to 25% of cases.9 DI typically manifests 1 to 2 days after pituitary surgery and is characterized by polyuria with dilute urine. Urine output can range from 4 to 18 L/day, with a urine specific gravity less than 1.005.10 After endoscopic pituitary surgery, most patients are awake and oriented, with increased thirst and polydipsia. Therefore, critical hypernatremia (over 150 mmol/mL), severe volume contraction, and hyperosmolality are rare.9 DI is transient in most patients and usually resolves by the third postoperative day.10 Hensen and colleagues11 found DI in 31% of patients in the early postoperative period, but in only 6% one week after surgery. Permanent DI requires the degeneration of 90% of the magnocellular neurons bilaterally and is very uncommon.10
| Cause | Features |
| Diabetes insipidus (DI) | Line specific gravity <1.005 Hypernatremia |
| Diuresis of perioperatively administered intravenous fluids | Urine specific gravity >1.005 Low to normal sodium levels Increased body weight |
| Glycosuria (diabetes mellitus) | Falsely elevated serum, urine osmolarity Increased serum and urine glucose Falsely decreased sodium levels |
A triphasic DI may occur in some patients with complete stalk resection.10 The first phase of transient DI over 1 to 3 days is followed by a period of antidiuresis 1 week later due to the release of ADH from degenerating neurons. In this second phase, patients may have hyponatremia and hypoosmolarity. Permanent DI follows these first two phases.
Screening for DI is performed by measuring intake and output, serial plasma osmolarity, serum chemistry, and urine specific gravity. Urine output >250 mL/hour over two consecutive hours supports the diagnosis of DI. Other causes of increased postoperative urine output must be considered (Table 8.1). Increased body weight with normal or low sodium and urine specific gravity >1.005 suggests postoperative fluid diuresis. This is a self-limited homeostatic response and should not be treated. Hypernatremia with urine specific gravity less than 1.005 is seen in DI. Elevated serum glucose with hyperglycemia is suggestive of glycosuria.
Treatment of DI is directed to restoring electrolyte homeostasis. Patients with intact thirst mechanisms, stable sodium levels, and stable osmolarity should be monitored closely with accurate measurements of intake-output and serum electrolytes. Water deficit should be accurately calculated, and fluid can be replaced orally or intravenously over a period of 24 to 48 hours. Treatment with desmopressin [deamino-8-D-arginine vasopressin (DDAVP)], a synthetic ADH analogue, is considered if there is significant discrepancy between fluid intake and output, serum sodium above 145 mEq/L, or when polyuria interferes with sleep.9 DDAVP administered intranasally, orally, subcutaneously and intravenously is quick and effective. An initial 1 μg of DDAVP subcutaneously and an oral dose of 0.1 mg are equally effective.10 Urine output and serum electrolyte monitoring is mandatory as hyponatremia can occur.
Syndrome of Inappropriate Antidiuretic Hormone and Other Causes of Postoperative Hyponatremia
Delayed hyponatremia is common following pituitary surgery, being present in 9 to 25% of patients.10 In such patients, ADH is secreted in spite of hyponatremia. Free water intake exceeds free water excretion, and increased urinary sodium excretion in the context of inappropriately concentrated urine is observed. The syndrome of inappropriate antidiuretic hormone (SIADH) is diagnosed by the presence of low serum sodium (usually <135 mEq/L), serum hypo-osmolarity, hyperosmolar urine with excess sodium excretion (>40 mEq/L), and euvolemia. Patients usually exhibit symptoms about 1 week after surgery. Symptoms include confusion, delirium, agitation, headache, appetite loss, nausea, vomiting, and lethargy. Seizures may occur if sodium levels drop below 115 mmol/L.
Cerebral salt wasting (CSW), adrenal insufficiency, hypothyroidism, and hyperglycemia are other factors that can contribute to postoperative hyponatremia. SIADH has a delayed onset, and this helps distinguishing SIADH from other causes of hyponatremia (Table 8.2). CSW is the renal loss of sodium after intracranial surgery, causing hyponatremia and hypovolemia. SIADH is characterized by euvolemia or mild hypervolemia, with decreased uric acid level with normal blood urea nitrogen (BUN) and creatinine. In contrast, CSW patients have volume contraction, elevated BUN and creatinine, and may have increased uric acid level. Patients with CSW lose weight, whereas patients with SIADH gain weight.
Adrenal insufficiency is important to rule out in early postoperative hyponatremia. Cortisol inhibits ADH secretion, and deficient or absent cortisol levels cause increased ADH secretion, leading to impairment in excreting free water.12 Treatment with cortisone replacement corrects hyponatremia. Hypothyroidism may cause hyponatremia by poorly understood mechanisms.10 Hyperglycemia may cause “pseudo”-hyponatremia by drawing intracellular water into the extracellular space due to increased intravascular osmotic load.
Therapy for hyponatremia is based on its severity, acuteness of onset, and associated symptoms. In SIADH, fluid restriction is the key. Fluid intake is restricted to less than 1000 mL/day, and serum electrolytes are measured at least daily.10 If sodium levels do not improve over the next several days, then fluid restriction to less than 600 mL is initiated. Although mild cases of SIADH may be managed on an outpatient basis, severely hyponatremic patients must be treated as inpatients. Refractory SIADH or patients with severe symptomatic hyponatremia (<120 mEq/L, with headache, nausea, vomiting, altered mentation, or seizures) may need treatment with intravenous hypertonic saline. Over-rapid correction must be avoided to prevent central pontine myelinolysis. The correction rate should not exceed 1 mmol/L/hour in the acute setting, and 0.5 mmol/L/ hour in the chronic setting.9,10 Hypertonic therapy should not be used for more than 12 to 24 hours; it should be discontinued once there is partial correction and resolution of symptoms. Serum electrolytes should be measured frequently (every 6 hours). Intravenous urea may also be used as an adjunct in severe hyponatremia.
| Cause | Features |
| Syndrome of inappropriate antidiuretic hormone(SIADH) | Delayed onset at 1 week Euvolemia |
| Cerebral salt wasting | Early postoperative onset Hypovolemia |
| Adrenal insufficiency | Early postoperative onset Low serum cortisol Hyponatremia responsive to cortisol therapy |
| “Pseudo”-hyponatremia | Early postoperative onset Falsely decreased sodium due increased glucose levels (diabetes mellitus, Cushing’s disease, acromegaly) |
Diabetes insipidus and SIADH are the most common causes of disruption in fluid homeostasis postoperatively, and the clinical features of these disorders are summarized in Table 8.3.
Other Endocrine Considerations and Perioperative Management
Perioperative stress dosing with glucocorticosteroids is controversial. The rationale for administering steroids is based on the assumption that surgery may disturb the hypothalamic-pituitary-adrenal axis (HPA). If patients have preoperative cortisol deficiency, perioperative steroids are indicated. A dose of 50 to 100 mg of intravenous hydrocortisone every 6 hours, then tapered to the oral preoperative dose, is usually used. Patients with Cushing’s disease require postoperative cortisol level assessment to determine results form surgery, and in these patients perioperative steroids may be avoided.
Acromegaly is associated with major cardiac-related morbidity and mortality. Hypertension and left ventricular failure may be seen in about half these patients.9 Diastolic dysfunction and cardiomyopathy, conduction abnormalities, and coronary artery disease may be present. Airway obstruction may occur secondary to hypertrophic facial bones and soft tissue or laryngeal stenosis, leading to difficulties in intubation. Obstructive sleep apnea (OSA) is also common in these patients. Postoperatively, close monitoring of patients’ airway and cardiac status is important. Patients with acromegaly have brisk diuresis following tumor resection, and early DDAVP should be avoided.13
| DI | SIADH | |
| Onset | 1–2 days after surgery | 1 week after surgery |
| Symptom/sign | Polyuria, polydipsia | Chemistry: hyponatremia Symptoms rare |
| Serum osmolarity | Hypertonic (>310 mOsm/L) | Hypotonic (<275 mOsm/L) |
| Serum sodium | Increased (>145 mEq/L) | Decreased (<135 mEq/L) |
| Urine volume | High (4–18 L) | Low |
| Urine osmolarity | Low (<200 mOsm/L) | High (>100 mOsm/L) |
| Treatment | Supportive | Fluid restriction |
| Hydration | Hypertonic saline | |
| Hypertonic saline | ||
Source: Modified from Nemergut EC, Dumont AS, Barry UT, Laws ER. Perioperative management of patients undergoing transsphenoidal pituitary surgery. Anesth Analg 2005;101(4):1170–1181.
Cushing’s disease patients commonly have systemic hypertension, electrocardiogram (ECG) abnormalities, and left ventricular hypertrophy.9 OSA is common. Impaired glucose tolerance (60%) and frank diabetes mellitus (in one third) are common. Tight glycemic control must be achieved in these patients to correct polyuria and unmask any underlying DI.
Thyrotoxicosis and hyperthyroidism due to thyroid-stimulating hormone (TSH)-producing adenoma are rare. However, these tumors are larger and more invasive at the time of diagnosis due to initial treatment for other causes of hyperthyroidism. Therefore, these tumors may be associated with higher blood loss. Hyperthyroidism should be controlled preoperatively.
Conclusion
Endoscopic skull base surgery is a rapidly advancing field, and regimens for postoperative care continue to evolve. There is little consensus on the specifics of postoperative care for these patients. The most commonly encountered postoperative problems include neurologic sequelae, endocrine disturbances, bleeding, and cerebrospinal fluid leaks. Postoperative care should be directed toward carefully monitoring and treating patients for these types of problems.
References
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