Hyponatremia in the Neurosurgical Patient: Diagnosis and Management

Hyponatremia in the Neurosurgical Patient: Diagnosis and Management

Neurosurg Focus 16 (4):Article 9, 2004, Click here to return to Table of Contents Hyponatremia in the neurosurgical patient: diagnosis and management CHAD D. COLE, M.SC., OREN N. GOTTFRIED, M.D., JAMES K. LIU, M.D., AND WILLIAM T. COULDWELL, M.D., PH.D. Department of Neurosurgery, University of Utah School of Medicine, Salt Lake City, Utah Hyponatremia is frequently encountered in patients who have undergone neurosurgery for intracranial processes. Making an accurate diagnosis between the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and cerebral salt wasting (CSW) in patients in whom hyponatremia develops is important because treatment differs great- ly between the conditions. The SIADH is a volume-expanded condition, whereas CSW is a volume-contracted state that involves renal loss of sodium. Treatment for patients with SIADH is fluid restriction and treatment for patients with CSW is generally salt and water replacement. In this review, the authors discuss the differential diagnosis of hyponatremia, distinguish SIADH from CSW, and highlight the diagnosis and management of hyponatremia, which is commonly encountered in patients who have undergone neurosurgery, specifically those with traumatic brain injury, aneurysmal subarachnoid hemorrhage, recent transsphenoidal surgery for pituitary tumors, and postoperative cranial vault reconstruction for craniosynostosis. KEY WORDS • hyponatremia • syndrome of inappropriate antidiuretic hormone secretion • cerebral salt wasting • intracranial disease Hyponatremia is a common electrolyte disorder en- characterized by a volume-contracted state.47 It is impor- countered in patients in the neurosurgical ICU.1,56 The tant to make an accurate diagnosis because treatment dif- causes of hyponatremia are diverse and the associated fers greatly between these conditions. Fluid restriction is risks of morbidity vary widely.5,17 The etiological range of the treatment of choice in SIADH, whereas salt and vol- this electrolyte disorder can be subcategorized into hy- ume replacement are the treatment for CSW. ponatremia associated with high, normal, or low osmolal- Although there are a variety of possible causes of hypo- ity (Fig. 1).1,3 Neurological dysfunction is the principal natremia, in this review we will focus on hyponatremia manifestation of hyponatremia, which may be exacerbat- that is commonly encountered in the neurosurgical ICU. ed by other disease processes or underlying conditions, es- Specifically, we will focus on SIADH, the putative asso- pecially in those patients in whom a pathological condi- ciated condition of CSW, and adrenal insufficiency in the tion is located intracranially. Awareness of other potential settings of TBI, aneurysmal SAH, transsphenoidal surgery causes of hyponatremia is required to provide appropriate for pituitary tumors, and cranial vault reconstruction. management and avoid deleterious outcomes, which may occur when the electrolyte deficiency is overcorrected or corrected too rapidly. Therefore, early diagnosis and ef- DIFFERENTIAL DIAGNOSIS fective treatment of hyponatremia is critical for hypona- Hyperosmotic Hyponatremia tremic patients with intracranial disease.30 In hyperosmotic (or translocational) hyponatremia dis- Both SIADH and CSW are potential causes of hypona- orders, solutes confined to the extracellular compartment tremia in patients who have undergone neurosurgery. It induce shifts in transcellular water.1 As an example, may be difficult to distinguish between these two condi- hyperglycemia or the retention of hypertonic mannitol tions in some cases because their clinical presentations may result in hyponatremia because water shifts from the sometimes overlap. The primary distinction lies in the intracellular to the extracellular space, causing dehydra- assessment of the patient’s volume. The SIADH is char- tion of cells. Symptoms common to hyperglycemia in- acterized by a volume-expanded state, whereas CSW is clude nausea, vomiting, dry axillae and oral mucosae, lower jugular venous pressure, and abdominal pain.68 A Abbreviations used in this paper: ADH = antidiuretic hormone; different set of changes is seen when mannitol is given to patients with underlying renal failure or when it is admin- ANP = atrial natriuretic peptide; BNP = brain natriuretic peptide; 10,54 CSW = cerebral salt wasting; DI = diabetes insipidus; ECV = effec- istered in very high doses. Not only does the rise in tive circulating volume; ICP = intracranial pressure; ICU = intensive plasma osmolality cause hyponatremia, but the fluid shift care unit; SAH = subarachnoid hemorrhage; SIADH = syndrome of may also lead to volume expansion and possibly pulmon- inappropriate secretion of ADH; TBI = traumatic brain injury. ary edema, metabolic acidosis, and hyperkalemia.10 Neurosurg. Focus / Volume 16 / April, 2004 1 Unauthenticated | Downloaded 10/01/21 12:33 PM UTC C. D. Cole, et al. Isosmotic Hyponatremia Hyposmotic Hyponatremia Isosmotic hyponatremia may be observed in patients Most hyponatremic disorders are associated with hyp- who undergo transurethral resection of the prostate or hys- osmolality. Also known as “dilutional hyponatremia,” terectomy (Fig. 1). During these procedures, patients may these disorders may be caused by excessive water intake, absorb large quantities of hyposmotic glycine or sorbitol but are more commonly caused by water retention.1 This irrigating solutions leading to a dilutional reduction in subcategory of hyponatremia may be further differentiat- the plasma sodium concentration. The extent of isosmotic ed according to volume status (Fig. 1). First, volume-ex- hyponatremia is related to both the quantity and rate of panded hyponatremia occurs when the intake of salt and fluid that is absorbed.34 The earliest symptom is nausea, water exceeds renal and extrarenal losses. The sodium and with more severe hyponatremia leading to confusion, dis- water retention may be primary, from an increased ECV, orientation, twitching, seizures, and hypotension.34 On the or secondary, in response to a decreased ECV.3 Diagnoses other hand, a less common condition of hyponatremia as- associated with an increased ECV due to primary water sociated with normal serum osmolality is seen in patients retention by the kidney include acute renal failure and with extreme hyperlipidemia and hyperproteinemia. Also advanced chronic renal failure. Those diagnoses associat- known as “pseudohyponatremia,” this finding is based on ed with a decreased ECV include congestive heart failure, a laboratory artifact of non–ion-selective techniques to cirrhosis, nephrotic syndrome, sepsis, anaphylaxis, and measure serum electrolyte conditions and has been essen- pregnancy.1,3 The latter conditions are characterized by tially eliminated with the increasing use of ion-selective high plasma concentrations of arginine vasopressin, de- electrodes for these measurements.1,3,46 spite the presence of hypotonicity. The retention of renal Fig. 1. Flow chart showing the diagnostic approach to hyponatremia. 2 Neurosurg. Focus / Volume 16 / April, 2004 Unauthenticated | Downloaded 10/01/21 12:33 PM UTC Hyponatremia in patients following neurosurgery sodium and water, which produces hypervolemic hypona- active ions present in the total body water, specifically the tremia and leads to an increased capillary hydrostatic pres- ratio of exchangeable sodium and potassium.3 sure, consequently favors a fluid shift from the intravas- The complications of hyposmotic hyponatremia oc- cular to the interstitial space (Fig. 1).3 cur most often in patients with excessive water retention.1 Other causes of volume-expanded hyponatremia are In these conditions, the hypotonic hyponatremia causes due to a reduced rate of salt resorption by the diluting seg- transcellular shifts in water from the extracellular into the ment of the kidney (hypothyroidism, secondary adrenal intracellular space. Because the cranium limits the expan- insufficiency, cancers), sustained nonosmotic release of sion of the brain by the imposed edema, an increase in ICP ADH (SIADH), or a combination of these two factors develops along with a risk of brain herniation. Fortunately, (Fig. 1).3 Less common causes include a decreased intake the degree of swelling is ameliorated as solutes leave the of solutes and primary polydipsia. In these latter causes of brain tissues within hours, allowing for some water loss hyponatremia, there is an increase in the intravascular vol- within the hypertensive environment.13,45 This adaptive ume with a minimal shift into the interstitial space. process limits the degree of central nervous system com- Conversely, volume-contracted hyponatremia is mainly plications if the severity of hyponatremia develops slow- caused by fluid loss from the intravascular space, which is ly. Nevertheless, this adaptation also gives rise to the risk induced by an intrinsic or a secondary renal loss of sodi- of osmotic demyelination (central pontine myelinolysis), um, an extrarenal loss of sodium, or hypokalemia (Fig. which can develop between 1 and several days after rap- 1).1,3 The consequential decrease in tissue perfusion stim- id correction of hyponatremia (Fig. 2).37,43,45,62,69 Thus, the ulates a release of ADH that is mediated by baroreceptors clinical manifestations of hyposmotic hyponatremia are within the carotid sinus, which sense a reduction in pres- more evident when the decrease in the serum sodium con- sure or stretch. The response of baroreceptors to the de- centration is large or when the decrease

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