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Hyponatremia—What Is Cerebral Salt Wasting?

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Hyponatremia—What Is Cerebral Salt Wasting? credits available for this article — see page 79. CliniCal MEdiCinE Corridor Consult Hyponatremia—What Is Cerebral Salt Wasting? Jasminder Momi, MD Christopher M Tang, MD Antoine C Abcar, MD minute. His intake and outtake Dean A Kujubu, MD Abstract John J Sim, MD documentation reveals that his urine Background: Hyponatremia is a common electrolyte imbalance in hos- output has been 2 to 4 L/d despite pitalized patients. It is associated with significant morbidity and mortality, a fluid restriction of <1.5 L/d that especially if the underlying cause is incorrectly diagnosed and not treated was initiated two days earlier. His appropriately. Often, the hospitalist is faced with a clinical dilemma when sodium level has continued to de- a patient presents with hyponatremia of an unclear etiology and with cline after the fluid restriction. The uncertain volume status. Syndrome of inappropriate antidiuretic hormone working diagnosis is syndrome of (SIADH) is frequently diagnosed in this clinical setting, but cerebral salt inappropriate antidiuretic hormone wasting (CSW) is an important diagnosis to consider. (SIADH). Objective: We wanted to describe the diagnosis, treatment, and history of CSW to provide clinicians with a better understanding of the differential Background diagnosis for hyponatremia. Hyponatremia (sodium level of Conclusion: CSW is a process of extracellular volume depletion due to <136mEq/L) has been associated a tubular defect in sodium transport. Two postulated mechanisms for CSW with confusion, lethargy, seizures, are the excess secretion of natriuretic peptides and the loss of sympathetic coma, and even death.1 The differ- stimulation to the kidney. Making the distinction between CSW and SIADH ential diagnosis for hyponatremia is important because the treatment for the two conditions is very different. is broad and includes hormone disorders (eg, thyroid and adrenal Case Presentation hyponatremia workup reveals a low insufficiency), medications, and A man, age 43 years, is evaluated serum osmolarity of 256 mOsm/kg, volume-related problems. In the for hyponatremia. He was admitted a normal serum creatinine level of acute-care setting, hyponatremia to the hospital six days earlier for 0.6 mg/dL, a urine sodium level of has been reported to occur in up an intracranial hemorrhage that re- 89 mmol/L, and an inappropriately to 30% of patients with subarach- quired emergency evacuation. The high urine osmolarity of 588 mOsm/ noid hemorrhage (SAH).2,3 The patient was later extubated when kg. His urinalysis reveals a specific physician often faces a clinical his neurologic status improved. gravity of 1.030, with no blood or dilemma when hyponatremia has His medical history includes poorly protein. His levels of serum thyroid- an unclear etiology and volume controlled hypertension and rheu- stimulating hormone and random status is uncertain. Early and ac- matoid arthritis. cortisol are within normal limits. His curate diagnosis of the etiology of On hospital day 6, his serum brain natriuretic peptide (BNP) and the hyponatremia is important in sodium level is noted to be 121 fractional excretion of uric acid are order to institute proper therapy. mEq/L. He has been receiving elevated, at 686 pg/mL and 83.8%, An incorrect diagnosis can cause 0.9% normal saline since admis- respectively. significant morbidity and mortality. sion, and his sodium level has The patient appears euvolemic, SIADH is a frequent diagnosis in been gradually decreasing from with a blood pressure of 115/70 a patient with hyponatremia and 141mEq/L, the level at admission. A mm Hg and pulse of 90 beats per a concurrent intracranial process.4 Jasminder Momi, MD, is a Nephrology Fellow at the Los Angeles Medical Center in CA. E-mail: [email protected]. Christopher M Tang, MD, is an Internist at the Los Angeles Medical Center in CA. E-mail: [email protected]. Antoine C Abcar, MD, is a Nephrologist at the Los Angeles Medical Center in CA. E-mail: [email protected] Dean A Kujubu, MD, is the Director of the Nephrology Fellowship program at the Los Angeles Medical Center in CA. E-mail: dean.a.kujubu.kp.org. John J Sim, MD, is a Nephrologist at the Los Angeles Medical Center in CA. E-mail: [email protected]. 62 The Permanente Journal/ Summer 2010/ Volume 14 No. 2 CliniCal MEdiCinE Hyponatremia—What Is Cerebral Salt Wasting? However, cerebral salt wasting (CSW) ent with low serum osmolality, high resorption in the proximal tubule is an important diagnosis to consider urine osmolality, and a high urine may be decreased because of an and differentiate from SIADH. sodium level. The fundamental dif- expanded ECFV, which can lead CSW was first described by Peters ference between the two processes to less uric acid absorption and et al in 19505 when they reported is the extracellular fluid volume increased uric acid loss in the urine. the cases of three patients with an (ECFV) status. CSW is defined by Another contributing mechanism in intracranial process who exhibited the renal loss of salt with con- SIADH, proposed by Decaux et al,12 renal salt wasting, but the existence comitant extracellular fluid loss.2,3,8-10 involves the stimulation of the V1 of CSW was questioned after the Consequently, patients with CSW receptor by antidiuretic hormone, identification of SIADH in 1957 have hypovolemia compared with which enhances excretion of uric by Schwartz et al.6 For years after- patients with SIADH, who have acid in the renal tubules. The ex- ward, CSW was considered either euvolemic or mild ECFV expansion. act mechanism of uric acid loss in a condition that was an element of The clinical history and assessment CSW has not been well defined. It SIADH or one that did not exist. findings may be helpful if postural is generally believed to be part of CSW now is again being recognized blood pressure changes, tachycar- the solute diuresis that occurs in as a separate entity altogether. A dia, or poor skin turgor are present. CSW with impaired urate transport retrospective review of data for 316 Unfortunately, this difference is in the proximal tubules.4,8 The key patients who presented with SAH not always clinically apparent. In differentiation is that patients with and hyponatremia found that the a study conducted by Chung et a11 SIADH have a serum uric acid level diagnosis was SIADH in 69% and to evaluate the clinical assessment and fractional excretion of uric acid was CSW in 6.5%.7 Both conditions of the ECFV status in 58 patients that normalize after correction of have been reported to occur in the without edema and hyponatremia, the serum sodium level, whereas setting of head trauma, intracranial only 47% of those with hypovolemia the uric acid level remains low and or metastatic neoplasm, carcinoma- and 48% of those with euvolemia uric acid excretion remains elevated tous or infectious meningitis, SAH, were accurately classified. in patients with CSW, despite cor- and central nervous system surgery.8 Uric acid excretion may be one rection of hyponatremia.2,4,8,9 The distinction between these two measure for differentiating between Response to fluid therapy is also conditions is important because CSW and SIADH. Initially, both a key distinction between SIADH their treatments are different. conditions are associated with a and CSW. The treatment of choice low serum uric acid level and a for SIADH is free water restriction Diagnosis high fractional excretion of uric when increased fluid intake will CSW and SIADH share many acid.4,8,9 Uric acid is normally re- worsen the hyponatremia. In con- similar laboratory and clinical find- sorbed in the proximal tubule along trast, CSW is a volume-depleted and ings (Table 1). Both conditions pres- with sodium. In SIADH, sodium sodium-wasting state requiring fluid Table 1. Biochemical markers: comparison of SIADH and CSW Biochemical marker SIADH CSW Extracellular fluid volume Normal to high Low Urinary sodium level >40 mEq/L >40 mEq/L Serum uric acid level Low Low Initial fractional excretion of urate High High Fractional excretion of urate after correction Normal High Urinary osmolality High High Serum osmolality Low Low Blood urea nitrogen/creatinine level Low to normal High Serum potassium level Normal Normal to high Central venous pressure Normal to high Low Pulmonary capillary wedge pressure Normal to high Low Brain natriuretic peptide level Normal High Treatment Water restriction Fluids and/or mineralocorticoids CSW = cerebral salt wasting; SIADH = syndrome of inappropriate antidiuretic hormone. The Permanente Journal/ Summer 2010/ Volume 14 No. 2 63 CliniCal MEdiCinE Hyponatremia—What Is Cerebral Salt Wasting? replacement with isotonic solutions. nial process and compared them matching the urinary output with The renal wasting of sodium with study control participants. volume repletion. in CSW is poorly understood. Sixty patients were divided into Fludrocortisone, a potent miner- Two postulated mechanisms are three groups. Group 1 included 10 alocorticoid, has also been used for disruption of sympathetic neural patients with SAH who underwent the treatment of CSW at doses of input to the kidney and natriuresis clipping of ruptured aneurysms 0.1 to 1 mg/d. It exerts its effects by induced by natriuretic peptides. within 24 hours, group 2 included stimulating reabsorption of sodium Both mechanisms can lead to 10 patients with intracranial tu- and water in the distal tubule, lead- downstream inhibition of the renin- mors who underwent craniotomy, ing to expansion of the ECFV. When angiotensin-aldosterone system.2,4,8,9 and group 3 included 40 healthy fludrocortisone therapy was used in Sympathetic stimulation normally individuals. Natriuretic peptides patients with SAH, less natriuresis CSW is a causes proximal tubule absorption (ANP, BNP), aldosterone, renin, and occurred and sodium balance was volume- of sodium. Depression of this sym- antidiuretic hormone levels were as- achieved more frequently.14,15 Thus, depleted state pathetic input to the kidney results sessed before surgery and at 1 hour, volume depletion and hyponatre- treated with in less sodium resorption in the 4 hours, 12 hours, and daily for 7 mia are preventable in patients intravenous proximal tubule and an increase days after surgery.
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