34 Postoperative and Neurocritical Care Management of Patients after Endonasal Endoscopic Transsphenoidal Pituitary Surgery

Jeffrey P. Greenfield and Theodore H. Schwartz

As the number of transsphenoidal surgeries being performed for an ever-widening array of skull base lesions increases, the recognition and management of the potential postoperative complications these procedures carry with them are of fundamental importance for the neurosurgeons performing the surgeries. Perhaps equally important is the relevance to an ever-widening array of clinicians involved in the postoperative management of these patients. Lesions approached endoscopically through the sphenoid sinus represent a diverse spectrum of disease. Although pituitary tumors remain the lesions most regularly approached endoscopically, experienced surgeons now use the endonasal endoscopic approach to resect meningiomas, chordomas, and craniopharyngiomas and to repair traumatic and spontaneous cerebrospinal fluid (CSF) leaks. In addition, intracranial disease being approached transsphenoidally need not arise from the sella turcica; lesions located anteriorly along the planum sphenoidale, the infundibulum proper, and as inferior as the clivus are now routinely biopsied and resected using these approaches.

This diversity of pathology and location presents serious challenges, as neural structures including the optic nerves and chiasm and pituitary stalk and gland, and their variable blood supplies, are often intimately related to the lesions being resected. Even when these structures remain intact at the conclusion of the procedure, gentle traction, suction, irrigation, or tamponade upon these structures can produce transient effects in the tissue that may affect the patient’s postoperative homeostasis. The care of these patients requires vigilance extending beyond assessment of perturbations of the hypothalamic-pituitary axis and visual pathways as postoperative complications that include CSF leak and secondary meningitis or pneumocephaly are significant concerns.

The incidence and complications associated with trans-sphenoidal surgeries have been studied.^1,2 In a survey-based report,² 958 respondent neurosurgeons reported performing transsphenoidal surgery. As one might expect, the incidence of complications was statistically significantly higher among surgeons with less experience performing transsphenoidal surgery. The overall operative mortality rate was 0.9%. The most frequent complications were anterior pituitary insufficiency (19.4%) and diabetes insipidus (DI) (17.8%). The incidence of CSF fistula was 3.9%. Other significant complications, such as carotid artery injuries, hypothalamic injuries, loss of vision, and meningitis, occurred with incidence rates between 1 and 2%.

In this chapter we review the immediate and extended postoperative management of patients undergoing endonasal, endoscopic, transsphenoidal neurosurgical procedures. We focus on the early recognition and appropriate management of fluid balance disorders, endocrine disturbances, CSF fistulas, and other emergent situations one might encounter in the recovery room or intensive care unit postoperatively.

Disorders of Fluid Balance

Understanding the normal metabolism of water and sodium is at the core of managing the patient who has had surgery that transiently or permanently disrupts the hypothalamic-pituitary axis. We explain the pathophysiology of the pathways governing this homeostasis and then examine how perturbations of various aspects of those pathways lead to specific deficits and how best to recognize, diagnose, and definitively treat those deficits.

Pathophysiology of Water and Sodium Metabolism

Total body water content approximates 60% of the body weight of a healthy adult male. Two thirds of total body water is intracellular fluid (ICF) and one third is extracellular fluid (ECF). Of the ECF, 75% is in the interstitial space and the remainder is contained within the vasculature. An average adult with normal kidney function requires 400 to 500 mL of water to excrete a normal 24-hour solute load in maximally concentrated urine. The major intracellular cation is potassium (K⁺) at 140 mEq/L. The extracellular concentrations are very tightly regulated at much lower concentrations, 3.5 to 5.0 mEq/L. The major extracellular cation is sodium (Na⁺), which has an average serum concentration of 140 mEq/L and an intracellular concentration of 12 mEq/L. Water movement between compartments is controlled by the osmolality of the compartments. The ECF and ICF are both roughly 290 mOsm/kg water. Water movement is secondary to changes in cation concentration, which are regulated by the energy-dependent Na⁺/K⁺–adenosine triphosphatase (ATPase) responsible for moving Na⁺ out of cells in exchange for K⁺.

Body fluid osmolality can be precisely determined by this formula: plasma osmolality (mOsm/kg) = 2(Na⁺_plasma) + (glucose/18) + (blood urea nitrogen [BUN]/2.8). Na⁺ is by far the major determinant of plasma osmolality, and doubling the plasma Na⁺ level to get a rough estimate often suffices in emergency situations where quickly raising the plasma osmolality to 300 mOsm/kg to combat intracranial swelling is the major concern. Tight glycemic control must be maintained postoperatively, as hyperglycemia can raise plasma osmolality. Without insulin, glucose remains extracellular, drawing water into the ECF and diluting the serum Na⁺ by as much as 1.5 to 2.4 mEq/L for every 100-mg/dL increment in the plasma glucose level above normal.3

Thirst mechanisms, antidiuretic hormone (ADH) secretion, and kidney function all regulate a patient’s water volume.⁴ Receptors in the anterolateral hypothalamus are stimulated by elevations in plasma osmolality and then release ADH from the posterior pituitary. Circulating ADH increases the absorption of water by making the distal nephron permeable to water. The pathways leading to thirst and ADH release are exquisitely sensitive, triggered by as little as a 2% increase in ECF osmolality.

Sodium also regulates total body volume by regulating ECF. When total Na⁺ in the ECF is low, the ECF volume is low by definition. This is sensed by pressure-dependent receptors in the cardiac atria, resulting in renal sodium retention. Conversely, the carotid sinus and renal juxtaglomerular apparatus respond to high volume secondary to high sodium by increasing natriuresis to adjust volume.

Hyperosmolality and Hypernatremia

After endoscopic endonasal transsphenoidal surgery, the evaluation of a single elevated serum sodium value should focus on the possible presence of DI. Postoperative hypernatremia is due to the loss of body water in excess of body solutes,⁵ because of either insufficient water intake or excessive water excretion. The clinical ECF volume status of a patient is crucial to assess. It can be measured by comparing preoperative and current weight, central venous pressure (CVP) if available through a central venous catheter, or strictly measured intakes and outputs. Postoperative laboratory values to assess include plasma electrolytes, glucose, BUN, creatinine, urine electrolytes and osmolality, and urine glucose. As mentioned previously, the marked elevation of plasma glucose, such as occurs in nonketotic hyperglycemic hyperosmolar coma, can result in an elevated plasma osmolality with a normal volume status.

When a postoperative patient is determined to be hyperosmolar by the above criteria, an assessment of the patient’s ability to concentrate urine provides useful direction for their care. Disorders of hyperosmolality can be subdivided into those in which renal water conservation mechanisms are intact but are unable to compensate for inadequately replaced losses of hypotonic fluid and those in which renal concentrating defects are a contributing factor to the deficiency of body water. If the urine is appropriately concentrated (>800 mOsm/kg water), the possibility of primary renal cause is eliminated. An inappropriately low urine osmolality (<800 mOsm/kg water) in a hyperosmolar patient indicates that the kidney is unable to concentrate the urine. In the absence of glucosuria or other causes of osmotic diuresis, inadequately concentrated urine in a hyperosmolar patient indicates DI. In the postoperative patient population, this algorithm is often unnecessary to scrutinize due to the knowledge of both normal preoperative fluid homeostasis and intraoperative pituitary stalk manipulation. Nevertheless, if these straightforward values are assessed in all postoperative endoscopic patients, their fluid management will be less complicated and their return to fluid homeostasis, either naturally or pharmacologically, will be expedited.

Diabetes Insipidus and Pathophysiology of Arginine Vasopressin

Hypotonic polyuria due to inadequate arginine vasopressin (AVP) secretion is the definition of DI. Broadly speaking, DI is a syndrome that can be classified as central (acquired or congenital lesion of the hypothalamic-pituitary axis) due to surgery, trauma, infarction, thrombosis, or granulomatous disease, or as nephrogenic (most commonly congenital due to defects in the AVP V² receptor or aquaporin-2 water channel). In the postoperative patient, disordered AVP secretion due to manipulation or transection of the pituitary stalk is the etiology unless proven otherwise. L-Arginine vasopressin (AVP, ADH) is synthesized in the bodies of magnocellular neurons in the paired supraoptic nuclei and paraventricular nuclei and is transported in granules down the pituitary stalk to be stored in the posterior pituitary axons terminals. Stores are sufficient for 5 to 10 days of maximum antidiuresis or 1 month of normal antidiuresis. AVP binds to V₂ receptors in the kidney and stimulates the production of cyclic adenosine monophosphate (cAMP), which leads to synthesis of aquaporin-2 water channels in cells of the collecting tubules. AVP secretion maintains plasma osmolality tightly at 280 to 290 mOsm/kg.6,7

The presence of DI preoperatively from a pituitary tumor is fairly unusual because AVP synthesis occurs in the hypothalamus. A lesion to the pituitary gland redirects the AVP into the bloodstream closer to its site of synthesis intracranially, rather than in the sella. If DI is present preoperatively, alternative diagnoses should be considered, including craniopharyngioma, meningioma, or disease directly involving the hypothalamus.

A central etiology for DI can be proven in the postoperative hypernatremic patient by evaluating the response to the administration of AVP or the AVP V² receptor agonist, desmopressin (deamino-8-D-arginine vasopressin [DDAVP]). An increase in urine osmolality with a concomitant decrease in plasma sodium values after DDAVP administration indicates insufficient endogenous AVP secretion and a central cause for the DI. No response to DDAVP suggests renal resistance to AVP and a nephrogenic cause for the DI. When treating postoperative DI, the premise is to first correct any preexisting water deficits and then to reduce any ongoing urinary water losses. Awake and ambulatory patients with an intact thirst mechanism will have little body water deficit but may still benefit from pharmacologic control of polyuria and polydipsia, especially at night. Hospitalized patients with various degrees of disruption of mental status or thirst mechanisms may have more dangerous hyperosmolality. To establish a patient’s water deficit, the following formula is used: water deficit = 0.6 × preoperative weight × (1–140/[Na⁺]). The osmolality should be corrected over 24 to 48 hours to avoid causing cerebral edema.⁷ The fluid can be replaced orally as water or through intravenously administered dextrose 5% in water (D₅W).

Multiple options exist for replacing insufficient AVP in the postoperative patient. Arginine vasopressin (pitressin) is a synthetic form of a naturally occurring human AVP. It has a relatively short half-life and can cause acute increases in blood pressure when administered intravenously. It may have limited usefulness in the immediate management of postoperative DI, but it is not optimal for longer DI management because it requires frequent dosing. A better option is DDAVP. It has a longer half-life and lacks the pressor effects of pitressin.^8,9 It is available as an intranasal form, an oral form, and a parenteral form that can be administered intravenously, intramuscularly, or subcutaneously. The dosage is usually started at 1 to 2 μg subcutaneously or intravenously, urine output should be reduced promptly, and the duration is usually 6 to 12 hours. This patient population also usually receives stress-dose glucocorticoids postoperatively,¹⁰ which sometimes cause acute hyperglycemia and resultant polyuria. This confounding variable should be quickly controlled with appropriate doses of insulin before further treatment is initiated for DI. Postoperative diuresis from excess fluid administration is also a consideration in a polyuric patient. Normal postoperative diuresis is monitored by following serial serum sodium levels. In a patient with stable serum sodium levels, polyuria is managed by gradually weaning the intravenous fluids and continuing to monitor serum sodium levels and urine outputs.

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