Cerebral salt wasting syndrome: Review (original) (raw)
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Review article Cerebral salt wasting syndrome: Review
2000
Hyponatremia is the most frequent electrolyte disorder in critically neurological patients. Cerebral salt wasting syndrome (CSW) is defined as a renal loss of sodium during intracranial disease leading to hyponatremia and a decrease in extracellular fluid volume. The pathogenesis of this disorder is still not completely understood. Sympathetic responses as well as some natriuretic factors play a role in this
Cerebral salt wasting following traumatic brain injury
Endocrinology, diabetes & metabolism case reports, 2017
Hyponatraemia is the most commonly encountered electrolyte disturbance in neurological high dependency and intensive care units. Cerebral salt wasting (CSW) is the most elusive and challenging of the causes of hyponatraemia, and it is vital to distinguish it from the more familiar syndrome of inappropriate antidiuretic hormone (SIADH). Managing CSW requires correction of the intravascular volume depletion and hyponatraemia, as well as mitigation of on-going substantial sodium losses. Herein we describe a challenging case of CSW requiring large doses of hypertonic saline and the subsequent substantial benefit with the addition of fludrocortisone. The diagnosis of CSW requires a high index of suspicion. Distinguishing it from SIADH is essential to enable prompt treatment in order to prevent severe hyponatraemia.The hallmarks of substantial CSW are hyponatraemia, reduced volume status and inappropriately high renal sodium loss.Substantial volumes of hypertonic saline may be required fo...
YPONATREMIA is a frequent finding in neurosurgical patients. Although hyponatremia is a hallmark of SIADH, it should not be viewed as a critical component for the diagnosis of CSW for the following reasons. Hyponatremia develops if there is a source of electrolyte-free water and vasopressin to prevent its excretion. Patients with CSW have multiple stimuli for the release of vasopressin, including central nervous system lesions, pain, stress, high intracranial pressure, and the drugs they have been given. 22 Therefore, if their renal concentration process is intact, they will have very high concentrations of Na + in their urine. 14,26 If this is combined with the infusion of isotonic saline, electrolyte-free water will be generated by desalination of the intravenous saline and will be retained in the body. 26 Accordingly, hyponatremia will develop, but only as a secondary event. In fact, hyponatremia can be prevented if the concentration of Na + in the intravenous solution is equal to that in the urine. 5 Therefore, with proper treatment, hyponatremia will not be present in a patient with CSW. It is particularly important to avoid making an incorrect diagnosis of CSW or SIADH in these patients because the treatments of these disorders differ. For example, although treatment of CSW includes a large infusion of saline, this therapy can lead to a more severe degree of hyponatremia in a patient due to desalination of the infused saline. Because the essential feature of CSW is Na + wasting, there should be a negative balance for Na + plus K + and/ or for Cl Ϫ when the diagnosis of CSW is established. Because urine electrolytes are not usually measured on the first few days the patient spends in the ICU, balance data would not be available when the patient is seen at consultation (usually 3-5 days after the appearance of the CNS lesion).
More on Renal Salt Wasting Without Cerebral Disease: Response to Saline Infusion
Clinical Journal of the American Society of Nephrology, 2009
The existence and prevalence of cerebral salt wasting (CSW) or the preferred term, renal salt wasting (RSW), and its differentiation from syndrome of inappropriate antidiuretic hormone (SIADH) have been controversial. This controversy stems from overlapping clinical and laboratory findings and an inability to assess the volume status of these patients. The authors report another case of RSW without clinical cerebral disease and contrast it to SIADH. Three patients with hyponatremia, hypouricemia, increased fractional excretion (FE) of urate, urine sodium >20 mmol/L, and concentrated urines were infused with isotonic saline after collection of baseline data. One patient with RSW had pneumonia without cerebral disease and showed increased plasma aldosterone and FEphosphate, and two patients with SIADH had increased blood volume, low plasma renin and aldosterone, and normal FEphosphate. The patient with RSW responded to isotonic saline by excretion of dilute urines, prompt correction of hyponatremia, and normal water loading test after volume repletion. Hypouricemia and increased FEurate persisted after correction of hyponatremia. Two patients with SIADH failed to dilute their urines and remained hyponatremic during 48 and 110 h of saline infusion. The authors demonstrate appropriate stimulation of ADH in RSW. Differences in plasma renin and aldosterone levels and FEphosphate can differentiate RSW from SIADH, as will persistent hypouricemia and increased FEurate after correction of hyponatremia in RSW. FEphosphate was the only contrasting variable at baseline. The authors suggest an approach to treat the hyponatremic patient meeting criteria for SIADH and RSW and changing CSW to the more appropriate term, RSW
Pediatric Neurosurgery, 2002
The association between hyponatremia and intracranial pathology has been well described. When accompanied by natriuresis, hyponatremia has most commonly been attributed to inappropriate secretion of antidiuretic hormone. However, there is growing evidence to suggest that many of these patients may actually have cerebrally mediated salt losses, a disorder referred to as the cerebral salt wasting syndrome (CSWS). While this syndrome has been reasonably well described in adults, data regarding CSWS in pediatric-aged patients remains sparse. Since fluid management of these disorders is different, it is important that the clinician be able to rapidly differentiate between them. We report three cases of CSWS in acutely brain-injured children and comment on the role that early quantitation of urine volume and urine sodium concentration had in rapidly establishing the correct diagnosis.
BMC Neurology
Background To explore the underlying mechanisms leading to the occurrence of hyponatremia and enhanced urinary sodium excretion in brain trauma patients using sodium balance and urinary biochemical analysis. Methods We conducted a retrospective analysis of a local database prospectively collected in 60 brain trauma patients without chronic renal dysfunction. Metabolic and hemodynamic parameters were averaged over three consecutive periods over the first seven days after admission. The main outcome investigated in this study was the occurrence of at least one episode of hyponatremia. Results Over the study period, there was a prompt decrease in sodium balance (163 ± 193 vs. -12 ± 154 mmol/day, p
Disturbances of Sodium in Critically Ill Adult Neurologic Patients
Journal of Neurosurgical Anesthesiology, 2006
Disorders of sodium and water balance are common in critically ill adult neurologic patients. Normal aspects of sodium and water regulation are reviewed. The etiology of possible causes of sodium disturbance is discussed in both the general inpatient and neurologic populations. Areas of importance are highlighted with regard to the differential diagnosis of sodium disturbance in neurologic patients and management strategies are discussed. Specific discussions of the etiology, diagnosis and management of cerebral salt wasting syndrome, the syndrome of inappropriate antidiuretic hormone secretion and central diabetes insipidus are presented, as well as the problems of over-treatment. The importance of diagnosis at an early stage of these diseases is stressed, with a recommendation for conservative management of milder cases.
Pediatric Nephrology, 2012
The syndrome of inappropriate antidiudresis (SIAD) and cerebral salt wasting (CSW) are similar conditions with the main difference being the absence or presence of volume depletion. The two conditions may be indistinguishable at presentation, as volume status is difficult to assess, which can lead to under-diagnosis of CSW in patients with central nervous system (CNS) disease. Carefully conducted studies in patients with CNS disease have indicated that CSW may be more common than SIAD. CSW may be differentiated from SIAD based on the persistence of hypouricemia and increased fractional excretion of urate following the correction of hyponatremia. Hyponatremia should be prevented if possible and treated promptly when discovered in patients with CNS disease as even mild hyponatremia could lead to neurological deterioration. Fluid restriction should not be used for the prevention or treatment of hyponatremia in hospitalized patients with CNS disease as it could lead to volume depletion especially if CSW is present. 0.9% sodium chloride may not be sufficiently hypertonic for the prevention of hyponatremia in hospitalized patients with CNS disease and a more hypertonic fluid may be required. The preferred therapy for the treatment of hyponatremia in patients with CNS disease is 3% sodium chloride.