ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Cerebral salt wasting

Cerebral salt wasting
Literature review current through: Sep 2023.
This topic last updated: Jun 28, 2022.

INTRODUCTION — Hyponatremia is a common electrolyte disorder in the setting of central nervous system (CNS) disease. This is usually attributed to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) [1-4].

Cerebral salt wasting (CSW) is another potential cause of hyponatremia in those with CNS disease, particularly patients with subarachnoid hemorrhage. CSW is characterized by hyponatremia and extracellular fluid depletion due to inappropriate sodium wasting in the urine [5]. However, some authorities contend that CSW does not really exist and is only a misnomer for what is actually SIADH, with the putative salt wasting being due to unappreciated volume expansion [6,7].

Issues related to CSW, including the differentiation from SIADH, will be reviewed here. The causes and diagnosis of hyponatremia, causes and treatment of SIADH, and the general management of patients with subarachnoid hemorrhage are presented separately:

(See "Causes of hypotonic hyponatremia in adults".)

(See "Diagnostic evaluation of adults with hyponatremia".)

(See "Pathophysiology and etiology of the syndrome of inappropriate antidiuretic hormone secretion (SIADH)".)

(See "Treatment of hyponatremia: Syndrome of inappropriate antidiuretic hormone secretion (SIADH) and reset osmostat".)

(See "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis".)

PATHOPHYSIOLOGY — With respect to pathophysiology, two issues need to be addressed: the mechanism of salt wasting and the mechanism of hyponatremia.

The mechanism by which cerebral disease might lead to renal salt wasting is poorly understood. Two putative mechanisms are disruption of neural input to the kidney and central elaboration of a circulating natriuretic factor [8,9]:

The sympathetic nervous system promotes sodium, uric acid, and water reabsorption in the proximal tubule, as well as renin release. Thus, impaired sympathetic neural input could explain the reductions in proximal sodium and urate reabsorption as well as the impaired release of renin and aldosterone. The failure of serum aldosterone to rise in response to volume depletion would explain the absence of potassium wasting despite the increase in distal sodium delivery.

The second theory is that a circulating factor that impairs renal tubular sodium reabsorption is released in patients with brain injury [6,10-13]. The primary candidate is brain natriuretic peptide (BNP), which decreases sodium reabsorption and inhibits renin release [11,12,14]. BNP may also decrease autonomic outflow via effects at the level of the brainstem [14,15]. A discussion of the various actions of these hormones is available in a separate topic review. (See "Natriuretic peptide measurement in heart failure".)

One report suggested that BNP might be the more probable candidate [11]. In this prospective observational study, 10 patients with subarachnoid hemorrhage were compared with a control group of 10 patients who underwent craniotomy for resection of cerebral tumors and 40 controls. The patients with subarachnoid hemorrhage had increases in urine volume and sodium excretion that correlated with a marked significant increase in mean plasma BNP (15.1 versus 1.6 pmol/L in the other two groups) and with the increase in intracranial pressure. The concentration of ANP was normal, while that of aldosterone was reduced, an effect that may be mediated in part by BNP.

It was suggested that BNP was released from hormone-producing neurons in the brain in response to increased intracranial pressure. Some have speculated that renal salt wasting and the resultant volume depletion is a protective measure, limiting extreme rises in intracranial pressure. In addition, the vasodilatory properties of BNP might decrease the tendency for vasospasm in subarachnoid hemorrhage.

With respect to the mechanism of hyponatremia, renal salt wasting leads to volume depletion, which provides a baroreceptor stimulus for the release of ADH, thereby impairing the ability of the kidney to elaborate a dilute urine and leading to hyponatremia. (See "Causes of hypotonic hyponatremia in adults" and "General principles of disorders of water balance (hyponatremia and hypernatremia) and sodium balance (hypovolemia and edema)".)

Is cerebral salt wasting real? — Some authors have suggested that CSW may not exist [6,7]. They contend that most patients who are given a diagnosis of CSW may be excreting excess sodium physiologically, either because of reduced venous capacitance caused by catecholamine-induced vasoconstriction or because of volume expansion with intravenous fluids. As an example, patients with subarachnoid hemorrhage are at risk for cerebral vasospasm that is thought to be precipitated by reduced cerebral blood flow. As a result, they are typically given large volumes of isotonic saline. (See "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis".)

If volume expansion were induced by saline administration, a high rate of sodium excretion would not be an indicator of salt wasting. In a survey of patients admitted to a neurosurgical unit, a positive balance for sodium could be documented in over 90 percent of those believed to have CSW when calculations included all infusions from the time of first contact with medical or paramedical personnel [6,7].

However, many authorities feel that CSW is a distinct entity. In the setting of CNS disease, patients with CSW meet the traditional laboratory criteria for the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) but clearly have decreased extracellular volume due to excessive urinary sodium excretion [16-20]. By comparison, SIADH is associated with a slightly increased or normal extracellular volume.

EPIDEMIOLOGY AND CAUSES — The incidence of CSW is unclear, particularly given that its existence is disputed [6,7]. Among patients with CNS disease, CSW is a much less common cause of hyponatremia than the syndrome of inappropriate secretion of antidiuretic hormone (SIADH).

Although CSW has been most often described in patients with subarachnoid hemorrhage, it accounts for only a small proportion of cases of hyponatremia in these patients (7 percent in one series compared to 69 percent due to SIADH) [2]. Furthermore, the frequency of CSW as a cause of hyponatremia in this setting may be diminishing since the usual management of patients with subarachnoid hemorrhage consists of providing large volumes of isotonic saline. In another prospective cohort of 100 patients with acute nontraumatic aneurysmal subarachnoid hemorrhage, hyponatremia developed in 49 percent of subjects [21]. Hyponatremia was attributable to SIADH in 71 percent of patients and to glucocorticoid deficiency in 8 percent. Incorrect choice or insufficient use of fluids or hypovolemia accounted for the remainder of the cases. There were no cases that met the accepted criteria for CSW. This study is noteworthy in that all patients underwent serial assessment of volume status by an experienced clinician along with measurement of plasma cortisol, arginine vasopressin, and brain natriuretic peptide. (See 'Diagnosis' below and "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis", section on 'Hyponatremia'.)

CSW has also been reported in patients with carcinomatous or infectious meningitis, encephalitis, poliomyelitis, and central nervous system tumors, as well as following CNS surgery [5,22-26]. Rare cases have been described in children [27-29].

Some investigators who use the fractional excretion of urate following correction of hyponatremia as an indicator of salt wasting have identified this phenotype in patients both with and without neurologic disease, leading them to suggest the terminology should be changed from CSW to renal salt wasting [30]. In addition, these authors have identified a protein, haptoglobin-related protein without signal peptide, in salt-wasting patients that possesses characteristics of a proximally acting diuretic [31]. While these reports are of interest, better characterization of these patients is needed.

CLINICAL FEATURES — Patients with CSW may have moderate or severe hyponatremia and polyuria [32,33]. The typical onset of hyponatremia due to CSW is within the first 10 days following a neurosurgical procedure or event. However, case reports have described later onset (eg, one month after transsphenoidal surgery for treatment of a pituitary macroadenoma) [22].

CSW is associated with extracellular fluid depletion. As a result, hypotension, decreased skin turgor, and/or an elevated hematocrit may be observed.

Theoretically, the volume depletion seen with CSW may worsen cerebral perfusion directly, and the associated hypotension may precipitate vasospasm in those with subarachnoid hemorrhage [34,35]. Whether hyponatremia itself potentiates vasospasm is uncertain, but it may worsen cerebral edema and therefore contribute to mental status decline. (See "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis", section on 'Hyponatremia'.)

DIAGNOSIS — CSW should be considered in any patient with CNS disease and hyponatremia. A directed history and physical examination and appropriate laboratory tests are essential. The general approach to the diagnosis of hyponatremia is discussed separately. (See "Diagnostic evaluation of adults with hyponatremia".)

In the setting of CNS disease, CSW is diagnosed in the patient with clinical evidence of hypovolemia who has the following characteristics:

Hyponatremia (less than 135 mEq/L) with a low plasma osmolality

An inappropriately elevated urine osmolality (above 100 mosmol/kg and usually above 300 mosmol/kg)

A urine sodium concentration usually above 40 mEq/L

A low serum uric acid concentration due to urate wasting in the urine

Clinical evidence of hypovolemia is crucial since all of these laboratory findings are also seen in the syndrome of inappropriate secretion of antidiuretic hormone (SIADH).

Given the overlap and the frequent difficulty in determining whether a patient has mild hypovolemia, the diagnosis of CSW should require that volume repletion leads to a dilute urine, which would be due to the removal of the hypovolemic stimulus to ADH release. Excretion of a dilute urine would lead to correction of the hyponatremia.

Although difficult to perform accurately, evidence of net negative sodium balance prior to therapy is also consistent with the diagnosis of CSW [6,29]. Calculation of the sodium intake includes that obtained via intravenous and oral routes (including sodium supplements and food), while sodium excretion involves frequent measurement of urine sodium concentrations combined with knowledge of urine volumes.

Formation of a dilute urine with volume repletion has not been demonstrated, and, in many if not most reported cases, clear evidence of hypovolemia has not been present [6,7].

DIFFERENTIAL DIAGNOSIS — In the setting of CNS injury, CSW must be distinguished from other causes of hyponatremia, principally the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) [5]. Glucocorticoid deficiency as a cause of increased vasopressin should be excluded in patients with sellar or suprasellar disease [36,37]. General discussions concerning the causes and diagnosis of hyponatremia are presented separately:

(See "Causes of hypotonic hyponatremia in adults".)

(See "Diagnostic evaluation of adults with hyponatremia".)

CSW versus SIADH — Some authorities suggest that the distinction between CSW and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is critically important, with possible adverse consequences if the incorrect therapeutic strategy is administered [5,38]. Others suggest that the distinction is less important since all hyponatremic patients (where due to CSW or SIADH) who have active intracranial pathology (eg, recent intracranial surgery or subarachnoid hemorrhage) should be treated with 3 percent (hypertonic) saline to ensure a prompt increase in the serum sodium concentration and to avoid a decrease in extracellular fluid volume [39].

In addition to hyponatremia, CSW and SIADH share the following features:

The urine osmolality is inappropriately high in the presence of hyponatremia (which normally suppresses ADH release) due to increased release of ADH. This response is appropriate in CSW, due to the volume depletion, but inappropriate in SIADH.

The urine sodium is usually >40 mEq/L due to volume expansion in SIADH and putative salt wasting in CSW.

The serum uric acid concentration is typically reduced due to urinary losses, perhaps due to a putative hormone such as BNP in CSW and to volume expansion and a direct effect of ADH on the V1 receptor in SIADH [40].

It is only the presence of clear evidence of volume depletion (eg, hypotension, decreased skin turgor, elevated hematocrit, possibly increased BUN/serum creatinine ratio) despite a urine sodium concentration that is not low that suggests that CSW might be present rather than SIADH [6,8]. By comparison, extracellular fluid volume is normal or slightly increased with SIADH. (See "Etiology, clinical manifestations, and diagnosis of volume depletion in adults".)

Theoretically, evaluation of the response to isotonic saline would help distinguish between CSW and SIADH. (See "Diagnostic evaluation of adults with hyponatremia".)

Restoration of euvolemia in CSW should remove the stimulus to ADH release, resulting in a dilute urine and correction of the hyponatremia [41]. As mentioned above, this has not been documented in CSW. Lack of urinary dilution does not necessarily preclude CSW since it might be expected that patients with subarachnoid hemorrhage would also have SIADH.

By contrast, isotonic saline often worsens the hyponatremia in SIADH as the salt is excreted and some of the water is retained. (See "Treatment of hyponatremia: Syndrome of inappropriate antidiuretic hormone secretion (SIADH) and reset osmostat", section on 'Intravenous hypertonic saline'.)

However, we discourage treatment of hyponatremia with isotonic saline in patients with cerebral disease because of the dangers of a further fall in serum sodium concentration.

Calculation of the fractional excretion of uric acid (FEUA) before and after correction of hyponatremia has been proposed as an alternative way of distinguishing SIADH from cerebral salt wasting [41]. According to this theory, before correction of hyponatremia, FEUA is >11 percent in both SIADH and salt wasting. Conversely, after correction of hyponatremia, a FEUA that remains >11 percent is said to indicate salt wasting, caused by impaired proximal tubule sodium reabsorption, whereas a FEUA <11 percent identifies patients with SIADH. However, serial measurements of FEUA have not been validated with a consistent, rigorous, and convincing gold standard for identifying salt wasting [42-44] . For this reason, the diagnostic validity of these measurements is unproven.

Although unlikely, it is also possible that some patients have preexisting hyponatremia due to some other disorder that is associated with a urine sodium that is not low (eg, thiazide diuretics and hypoaldosteronism). (See "Causes of hypotonic hyponatremia in adults".)

Hyponatremia and hyperkalemia are the two major manifestations of adrenal insufficiency. The hyponatremia is mediated by increased release of ADH, which can be due to any cause of cortisol deficiency or hypoaldosteronism, while hyperkalemia only occurs with primary adrenal disease. The diagnosis of adrenal insufficiency is discussed separately. (See "Hyponatremia and hyperkalemia in adrenal insufficiency" and "Determining the etiology of adrenal insufficiency in adults".)

TREATMENT — Fluid restriction, the usual first-line therapy for the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), is not advised in hyponatremic patients with subarachnoid hemorrhage. In such patients, fluid restriction may increase the risk of cerebral infarction among patients who actually have CSW because ongoing salt losses may worsen the volume depletion and lower the blood pressure. (See "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis" and "Treatment of hyponatremia: Syndrome of inappropriate antidiuretic hormone secretion (SIADH) and reset osmostat".)

Instead, we treat with 3 percent (hypertonic) saline to raise the serum sodium (algorithm 1). All patients with active intracranial pathology (eg, recent intracranial surgery or subarachnoid hemorrhage) should have a prompt increase in the serum sodium concentration and should avoid a decrease in extracellular fluid volume. (See "Overview of the treatment of hyponatremia in adults".)

Some authorities suggest that isotonic saline be used as initial therapy in patients with CSW since, theoretically, it will suppress the release of ADH, thereby permitting excretion of the excess water and correction of the hyponatremia. However, if CSW is the sole cause of the hyponatremia, volume repletion would reduce the urine osmolality to below 100 mosmol/kg. However, dilution of the urine in response to isotonic saline is rare in patients with hyponatremia caused by subarachnoid hemorrhage or other intracranial disorders. (See "Overview of the treatment of hyponatremia in adults", section on 'Isotonic saline in true volume depletion'.)

Lack of urinary dilution does not necessarily preclude CSW since it might be expected that patients with subarachnoid hemorrhage would also have SIADH. Volume repletion would have little effect on urine osmolality in SIADH since ADH secretion in this disorder is not mediated by hypovolemia [8,9,45]. Hypertonic saline will increase the serum sodium concentration in patients with both CSW and SIADH.

For patients with documented CSW, salt tablets can be administered once the patients are able to take oral medications. Salt tablets may also be effective in patients with SIADH. Administration of a mineralocorticoid, such as fludrocortisone, can also be used [29,46-48].

Long-term therapy of CSW is not necessary since CSW tends to be transient [9]. Resolution usually occurs within three to four weeks.

THERAPY OF SIADH ASSOCIATED WITH SAH — The optimal therapy for hyponatremia due to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in patients with subarachnoid hemorrhage (SAH) is not clear since the standard initial therapy, fluid restriction, may increase the risk of cerebral infarction [49]. We generally prefer the administration of 3 percent (ie, hypertonic) saline in such patients. (See "Overview of the treatment of hyponatremia in adults".)

Although isotonic saline can also be given, particularly if the serum sodium is normal, careful monitoring is required since isotonic saline can lower the serum sodium in patients with SIADH. The administered sodium will be excreted (there is no defect in sodium handling in SIADH), but some of the water will be retained if the urine osmolality is substantially higher than 300 mosmol/kg (the osmolality of isotonic saline). Such patients should be treated with hypertonic saline. How this occurs is discussed elsewhere:

(See "Treatment of hyponatremia: Syndrome of inappropriate antidiuretic hormone secretion (SIADH) and reset osmostat", section on 'Intravenous hypertonic saline'.)

(See "Treatment of hyponatremia: Syndrome of inappropriate antidiuretic hormone secretion (SIADH) and reset osmostat", section on 'Subarachnoid hemorrhage'.)

In patients with subarachnoid hemorrhage, a separate issue is the possible administration of a mineralocorticoid, such as fludrocortisone, to prevent volume depletion and delayed cerebral ischemia [29,50,51]. The potential efficacy of this approach was examined in a trial of 91 patients with newly diagnosed subarachnoid hemorrhage who were randomly assigned to fludrocortisone (0.2 mg twice daily) or control therapy for a maximum of 12 days [50]. Plasma volume was measured by the isotope dilution technique during the first day as well as days 6 and 12, and sodium balance was ascertained using estimates of intake and measurement of urinary sodium excretion. Significantly fewer patients in the treatment group developed negative sodium balance (38 versus 63 percent in the control group at 6 days, 29 versus 70 percent at 12 days). There was a suggestion that fludrocortisone might reduce cerebral ischemia (22 versus 31 percent).

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Hyponatremia" and "Society guideline links: Fluid and electrolyte disorders in adults".)

SUMMARY AND RECOMMENDATIONS

Cerebral salt wasting (CSW) is characterized by hyponatremia and extracellular fluid depletion due to inappropriate sodium wasting in the urine in the setting of acute disease in central nervous system (CNS), usually subarachnoid hemorrhage. CSW is a much less common cause of hyponatremia in patients with cerebral injury than the syndrome of inappropriate ADH secretion (SIADH). (See 'Introduction' above and 'Epidemiology and causes' above.)

The pathophysiology of CSW is related to impaired sodium reabsorption, possibly due to the release of brain natriuretic peptide and/or diminished central sympathetic activity. Regardless of the mechanism, sodium wasting can lead sequentially to volume depletion, increased ADH release, hyponatremia due to the associated water retention, and possibly increased neurologic injury. (See 'Pathophysiology' above.)

Some authorities contend that CSW does not exist and that the laboratory findings are due to SIADH. However, we feel that CSW is a distinct entity. (See 'Is cerebral salt wasting real?' above.)

Specific laboratory findings include hyponatremia with a low plasma osmolality, an inappropriately elevated urine osmolality (above 100 mosmol/kg and usually above 300 mosmol/kg), a urine sodium concentration above 40 mEq/L, and a low serum uric acid concentration due to urate wasting in the urine. Since CSW is associated with extracellular fluid depletion, hypotension and decreased skin turgor may also be observed. (See 'Clinical features' above.)

CSW mimics all of the laboratory findings in the SIADH. The only clue to the presence of CSW rather than SIADH is clinical evidence of extracellular volume depletion, such as hypotension and decreased skin turgor, and/or increased hematocrit, in a patient with a urine sodium concentration above 40 mEq/L. Unlike SIADH, volume repletion in CSW leads to a dilute urine, due to removal of the hypovolemic stimulus to ADH release, and subsequent correction of the hyponatremia. This finding has not been convincingly demonstrated, which could reflect concurrent SIADH due to the CNS disease. (See 'Differential diagnosis' above.)

Regardless of whether hyponatremia is caused by CSW or SIADH, hyponatremic patients who have active intracranial pathology (eg, recent intracranial surgery or subarachnoid hemorrhage) should be treated with 3 percent (hypertonic) saline to ensure a prompt increase in the serum sodium concentration and to avoid a decrease in extracellular fluid volume. (See 'Treatment' above.)

  1. Hasan D, Wijdicks EF, Vermeulen M. Hyponatremia is associated with cerebral ischemia in patients with aneurysmal subarachnoid hemorrhage. Ann Neurol 1990; 27:106.
  2. Sherlock M, O'Sullivan E, Agha A, et al. The incidence and pathophysiology of hyponatraemia after subarachnoid haemorrhage. Clin Endocrinol (Oxf) 2006; 64:250.
  3. Wartenberg KE, Schmidt JM, Claassen J, et al. Impact of medical complications on outcome after subarachnoid hemorrhage. Crit Care Med 2006; 34:617.
  4. Qureshi AI, Suri MF, Sung GY, et al. Prognostic significance of hypernatremia and hyponatremia among patients with aneurysmal subarachnoid hemorrhage. Neurosurgery 2002; 50:749.
  5. Gutierrez OM, Lin HY. Refractory hyponatremia. Kidney Int 2007; 71:79.
  6. Singh S, Bohn D, Carlotti AP, et al. Cerebral salt wasting: truths, fallacies, theories, and challenges. Crit Care Med 2002; 30:2575.
  7. Carlotti AP, Bohn D, Rutka JT, et al. A method to estimate urinary electrolyte excretion in patients at risk for developing cerebral salt wasting. J Neurosurg 2001; 95:420.
  8. Palmer BF. Hyponatremia in patients with central nervous system disease: SIADH versus CSW. Trends Endocrinol Metab 2003; 14:182.
  9. Palmer BF. Hyponatraemia in a neurosurgical patient: syndrome of inappropriate antidiuretic hormone secretion versus cerebral salt wasting. Nephrol Dial Transplant 2000; 15:262.
  10. Al-Mufti H, Arieff AI. Hyponatremia due to cerebral salt-wasting syndrome. Combined cerebral and distal tubular lesion. Am J Med 1984; 77:740.
  11. Berendes E, Walter M, Cullen P, et al. Secretion of brain natriuretic peptide in patients with aneurysmal subarachnoid haemorrhage. Lancet 1997; 349:245.
  12. Berger TM, Kistler W, Berendes E, et al. Hyponatremia in a pediatric stroke patient: syndrome of inappropriate antidiuretic hormone secretion or cerebral salt wasting? Crit Care Med 2002; 30:792.
  13. Harrigan MR. Cerebral salt wasting syndrome: a review. Neurosurgery 1996; 38:152.
  14. Levin ER, Gardner DG, Samson WK. Natriuretic peptides. N Engl J Med 1998; 339:321.
  15. Steele MK, Gardner DG, Xie PL, Schultz HD. Interactions between ANP and ANG II in regulating blood pressure and sympathetic outflow. Am J Physiol 1991; 260:R1145.
  16. Nelson PB, Seif SM, Maroon JC, Robinson AG. Hyponatremia in intracranial disease: perhaps not the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). J Neurosurg 1981; 55:938.
  17. Wijdicks EF, Vermeulen M, ten Haaf JA, et al. Volume depletion and natriuresis in patients with a ruptured intracranial aneurysm. Ann Neurol 1985; 18:211.
  18. Levine JP, Stelnicki E, Weiner HL, et al. Hyponatremia in the postoperative craniofacial pediatric patient population: a connection to cerebral salt wasting syndrome and management of the disorder. Plast Reconstr Surg 2001; 108:1501.
  19. Sivakumar V, Rajshekhar V, Chandy MJ. Management of neurosurgical patients with hyponatremia and natriuresis. Neurosurgery 1994; 34:269.
  20. Lenhard T, Külkens S, Schwab S. Cerebral salt-wasting syndrome in a patient with neuroleptic malignant syndrome. Arch Neurol 2007; 64:122.
  21. Hannon MJ, Behan LA, O'Brien MM, et al. Hyponatremia following mild/moderate subarachnoid hemorrhage is due to SIAD and glucocorticoid deficiency and not cerebral salt wasting. J Clin Endocrinol Metab 2014; 99:291.
  22. Filippella M, Cappabianca P, Cavallo LM, et al. Very delayed hyponatremia after surgery and radiotherapy for a pituitary macroadenoma. J Endocrinol Invest 2002; 25:163.
  23. Sengupta K, Ali U, Andankar P. Cerebral salt wasting. Indian Pediatr 2002; 39:488.
  24. Ti LK, Kang SC, Cheong KF. Acute hyponatraemia secondary to cerebral salt wasting syndrome in a patient with tuberculous meningitis. Anaesth Intensive Care 1998; 26:420.
  25. Erduran E, Mocan H, Aslan Y. Another cause of hyponatraemia in patients with bacterial meningitis: cerebral salt wasting. Acta Paediatr 1997; 86:1150.
  26. Oster JR, Perez GO, Larios O, et al. Cerebral salt wasting in a man with carcinomatous meningitis. Arch Intern Med 1983; 143:2187.
  27. Ganong CA, Kappy MS. Cerebral salt wasting in children. The need for recognition and treatment. Am J Dis Child 1993; 147:167.
  28. Jiménez R, Casado-Flores J, Nieto M, García-Teresa MA. Cerebral salt wasting syndrome in children with acute central nervous system injury. Pediatr Neurol 2006; 35:261.
  29. Taplin CE, Cowell CT, Silink M, Ambler GR. Fludrocortisone therapy in cerebral salt wasting. Pediatrics 2006; 118:e1904.
  30. Maesaka JK, Imbriano LJ, Miyawaki N. High Prevalence of Renal Salt Wasting Without Cerebral Disease as Cause of Hyponatremia in General Medical Wards. Am J Med Sci 2018; 356:15.
  31. Maesaka JK, Imbriano LJ, Pinkhasov A, et al. Identification of a Novel Natriuretic Protein in Patients With Cerebral-Renal Salt Wasting-Implications for Enhanced Diagnosis. Am J Med Sci 2021; 361:261.
  32. Bettinelli A, Longoni L, Tammaro F, et al. Renal salt-wasting syndrome in children with intracranial disorders. Pediatr Nephrol 2012; 27:733.
  33. Spatenkova V, Bradac O, de Lacy P, Skrabalek P. Polyuria in relation to dysnatraemias in neurocritical care. Br J Neurosurg 2015; 29:650.
  34. Naval NS, Stevens RD, Mirski MA, Bhardwaj A. Controversies in the management of aneurysmal subarachnoid hemorrhage. Crit Care Med 2006; 34:511.
  35. Wijdicks EF, Vermeulen M, Murray GD, et al. The effects of treating hypertension following aneurysmal subarachnoid hemorrhage. Clin Neurol Neurosurg 1990; 92:111.
  36. Hannon MJ, Behan LA, O'Brien MM, et al. Chronic hypopituitarism is uncommon in survivors of aneurysmal subarachnoid haemorrhage. Clin Endocrinol (Oxf) 2015; 82:115.
  37. Verbalis JG. Hyponatremia with intracranial disease: not often cerebral salt wasting. J Clin Endocrinol Metab 2014; 99:59.
  38. Maesaka JK, Imbriano LJ, Ali NM, Ilamathi E. Is it cerebral or renal salt wasting? Kidney Int 2009; 76:934.
  39. Sterns RH, Silver SM. Cerebral salt wasting versus SIADH: what difference? J Am Soc Nephrol 2008; 19:194.
  40. Maesaka JK, Venkatesan J, Piccione JM, et al. Abnormal urate transport in patients with intracranial disease. Am J Kidney Dis 1992; 19:10.
  41. Maesaka JK, Imbriano LJ, Miyawaki N. Evolution and evolving resolution of controversy over existence and prevalence of cerebral/renal salt wasting. Curr Opin Nephrol Hypertens 2020; 29:213.
  42. Sterns RH, Rondon-Berrios H. Cerebral Salt Wasting Is a Real Cause of Hyponatremia: CON. Kidney360 2023; 4:e441.
  43. Palmer BF, Clegg DJ. Cerebral Salt Wasting Is a Real Cause of Hyponatremia: COMMENTARY. Kidney360 2023; 4:e445.
  44. Maesaka JK, Imbriano LJ. Cerebral Salt Wasting Is a Real Cause of Hyponatremia: PRO. Kidney360 2023; 4:e437.
  45. Diringer MN, Wu KC, Verbalis JG, Hanley DF. Hypervolemic therapy prevents volume contraction but not hyponatremia following subarachnoid hemorrhage. Ann Neurol 1992; 31:543.
  46. Misra UK, Kalita J, Kumar M. Safety and Efficacy of Fludrocortisone in the Treatment of Cerebral Salt Wasting in Patients With Tuberculous Meningitis: A Randomized Clinical Trial. JAMA Neurol 2018; 75:1383.
  47. Albanese A, Hindmarsh P, Stanhope R. Management of hyponatraemia in patients with acute cerebral insults. Arch Dis Child 2001; 85:246.
  48. Kinik ST, Kandemir N, Baykan A, et al. Fludrocortisone treatment in a child with severe cerebral salt wasting. Pediatr Neurosurg 2001; 35:216.
  49. Wijdicks EF, Vermeulen M, Hijdra A, van Gijn J. Hyponatremia and cerebral infarction in patients with ruptured intracranial aneurysms: is fluid restriction harmful? Ann Neurol 1985; 17:137.
  50. Hasan D, Lindsay KW, Wijdicks EF, et al. Effect of fludrocortisone acetate in patients with subarachnoid hemorrhage. Stroke 1989; 20:1156.
  51. Ishikawa SE, Saito T, Kaneko K, et al. Hyponatremia responsive to fludrocortisone acetate in elderly patients after head injury. Ann Intern Med 1987; 106:187.
Topic 2367 Version 24.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟