Laboratory Findings Compatible with Cerebral Salt Wasting (CSW)
These laboratory values are most compatible with cerebral salt wasting (CSW), characterized by hyponatremia with high urinary sodium excretion, elevated urine osmolality relative to serum, and evidence of volume depletion. 1, 2
Key Diagnostic Features Supporting CSW
The combination of hyponatremia (serum Na 143 mEq/L is actually normal, but the pattern suggests evaluation for salt wasting), markedly elevated urine sodium (196.4 mEq/L), concentrated urine (urine Osm 454 mOsm/kg), and hyperosmolar serum (332 mOsm/kg) points toward renal sodium wasting rather than SIADH. 1, 2
Laboratory Pattern Analysis
Urine sodium >20 mEq/L (here 196.4 mEq/L) with hyponatremia indicates renal sodium losses, which is characteristic of CSW, diuretic use, or adrenal insufficiency. 1, 2
The fractional excretion of sodium can be calculated from these values: FENa = (Urine Na × Serum Cr) / (Serum Na × Urine Cr) × 100 = (196.4 × 0.24) / (143 × 4.96) × 100 = 6.6%, which is markedly elevated and indicates renal sodium wasting. 1
Urine osmolality of 454 mOsm/kg that is inappropriately concentrated relative to serum osmolality of 332 mOsm/kg suggests ongoing ADH activity, but the extremely high urine sodium distinguishes this from typical SIADH. 2, 3
The very low serum creatinine (0.24 mg/dL) may reflect volume depletion with decreased muscle mass or dilution, while the urine creatinine (4.96 mg/dL) confirms adequate urine concentration. 1
Distinguishing CSW from SIADH
The critical distinction between CSW and SIADH lies in volume status: CSW presents with extracellular volume depletion (hypovolemia), while SIADH presents with euvolemia. 1, 2, 4
Clinical Assessment Required
Look for signs of volume depletion: orthostatic hypotension, tachycardia, dry mucous membranes, decreased skin turgor, and low central venous pressure (<6 cm H₂O). 1, 2, 5
Physical examination alone has limited accuracy (sensitivity 41.1%, specificity 80%) for determining volume status, so invasive monitoring with CVP measurement may be needed in unclear cases. 1, 2
CSW typically shows CVP <6 cm H₂O, while SIADH shows CVP 6-10 cm H₂O. 2, 3
Laboratory Distinctions
Both CSW and SIADH can present with urine sodium >20 mEq/L and concentrated urine, making laboratory differentiation challenging. 2, 4, 6
Serum uric acid <4 mg/dL has a positive predictive value of 73-100% for SIADH, though it may also be seen in CSW. 1, 2
The extremely high urine sodium (196.4 mEq/L) and evidence of volume depletion favor CSW over SIADH. 5, 7, 4
Treatment Implications
Treatment for CSW requires volume and sodium replacement, NOT fluid restriction—this is the opposite of SIADH management and critical to avoid worsening outcomes. 8, 1, 4
Acute Management for CSW
Administer isotonic (0.9%) or hypertonic (3%) saline depending on severity of hyponatremia and symptoms. 8, 1, 5
Volume-for-volume urine replacement with 0.9% or 3% sodium chloride may be necessary in severe cases. 7
Consider fludrocortisone (mineralocorticoid) to enhance sodium reabsorption, particularly in refractory cases. 8, 1, 5
Oral salt supplementation (sodium chloride 100 mEq three times daily) may be required for maintenance after initial stabilization. 8, 1, 7
Critical Pitfall to Avoid
Using fluid restriction in CSW (as would be done for SIADH) can worsen outcomes by exacerbating volume depletion and increasing risk of cerebral ischemia. 8, 1, 4
Common Clinical Context
CSW typically occurs in patients with central nervous system injury or disease, including traumatic brain injury, subarachnoid hemorrhage, brain tumors, neurosurgery, or other intracranial pathology. 8, 5, 7, 9
The pathogenesis involves excessive secretion of natriuretic peptides (particularly atrial natriuretic hormone and brain natriuretic peptide) and/or loss of sympathetic stimulation to the kidney. 7, 4, 6
CSW is more common in neurosurgical patients than SIADH, making it an important diagnosis to consider in this population. 1, 6