9
views
0
recommends
+1 Recommend
2 collections
    0
    shares

          The flagship journal of the Society for Endocrinology. Learn more

      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Cerebral salt wasting following traumatic brain injury

      research-article

      Read this article at

      ScienceOpenPublisherPMC
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Summary

          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.

          Learning points:
          • 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 for a prolonged period of time to correct volume and sodium deficits.

          • Fludrocortisone has a role in the management of CSW. It likely reduces the doses of hypertonic saline required and can maintain serum sodium levels of hypertonic saline.

          Related collections

          Most cited references5

          • Record: found
          • Abstract: found
          • Article: not found

          Secretion of brain natriuretic peptide in patients with aneurysmal subarachnoid haemorrhage.

          Subarachnoid haemorrhage is commonly associated with natriuresis and hyponatraemia. One possible explanation for these features is a defect in the central regulation of renal sodium reabsorption with increased secretion of a natriuretic factor. We investigated whether excess sodium secretion in patients with subarachnoid haemorrhage is related to increased secretion of natriuretic peptides or to the presence of digoxin-like immunoreactive substances. We measured the plasma concentrations of digoxin-like immunoreactive substances (by a fluorescence polarisation immunoassay) and natriuretic peptides, aldosterone, renin, and antidiuretic hormone (by radioimmunoassay) in ten patients with aneurysmal subarachnoid haemorrhage, ten patients undergoing elective craniotomy for cerebral tumours, and 40 healthy controls of similar age and sex distribution. Samples were collected before surgery, 1 h, 4 h, and 12 h after surgery, then daily until 7 days postoperatively in the two groups of patients. All patients with subarachnoid haemorrhage, but none of the tumour patients, showed increased urine output and urinary excretion of sodium (p = 0.018 for comparison of means of curves to 7 days). The patients with subarachnoid haemorrhage had much higher plasma concentrations of brain natriuretic peptide (BNP) than controls, on admission (mean 15.1 [SE 3.8] vs 1.6 [1.0] pmol/L, p < 0.001) and throughout the study period, accompanied by lower than normal aldosterone concentrations and normal plasma concentrations of atrial and C-type natriuretic peptides (ANP, CNP). The patients with tumours had similar plasma concentrations of ANP, BNP, and CNP to the controls. We did not detect digoxin-like immunoreactive substances in either group of patients. Salt-wasting of central origin may induce hyponatraemia in patients with aneurysmal subarachnoid haemorrhage, possibly as a result of increased secretion of BNP with subsequent suppression of aldosterone synthesis.
            • Record: found
            • Abstract: found
            • Article: not found

            Cerebral salt wasting: pathophysiology, diagnosis, and treatment.

            Cerebral salt wasting (CSW) is a syndrome of hypovolemic hyponatremia caused by natriuresis and diuresis. The mechanisms underlying CSW have not been precisely delineated, although existing evidence strongly implicates abnormal elevations in circulating natriuretic peptides. The key in diagnosis of CSW lies in distinguishing it from the more common syndrome of inappropriate secretion of antidiuretic hormone. Volume status, but not serum and urine electrolytes and osmolality, is crucial for making this distinction. Volume and sodium repletion are the goals of treatment of patients with CSW, and this can be performed using some combination of isotonic saline, hypertonic saline, and mineralocorticoids. Copyright 2010 Elsevier Inc. All rights reserved.
              • Record: found
              • Abstract: not found
              • Article: not found

              A salt-wasting syndrome associated with cerebral disease.

                Author and article information

                Journal
                Endocrinol Diabetes Metab Case Rep
                Endocrinol Diabetes Metab Case Rep
                EDM
                Endocrinology, Diabetes & Metabolism Case Reports
                Bioscientifica Ltd (Bristol )
                2052-0573
                04 April 2017
                2017
                : 2017
                : 16-0142
                Affiliations
                [1 ]Department of Diabetes and Endocrinology , University Hospital of Wales, Heath Park, CardiffUK
                [2 ]Thyroid Research Group , Division of Infection and Immunity, School of Medicine, Cardiff University, Heath Park, CardiffUK
                [3 ]Department of Neurosurgery , University Hospital of Wales, Heath Park, CardiffUK
                [4 ]Department of Diabetes and Endocrinology , North Devon District Hospital, BarnstapleUK
                [5 ]Institute of Neuroscience and Mental Health Research Institute , School of Medicine, Cardiff University, CardiffUK
                Author notes
                Correspondence should be addressed to P Taylor; Email: taylorpn@ 123456cardiff.ac.uk
                Article
                EDM160142
                10.1530/EDM-16-0142
                5404462
                ddb530ba-2d48-4a40-8d28-79112c8b6b40
                © 2017 The authors

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License.

                History
                : 26 February 2017
                : 2 March 2017
                Categories
                Novel Treatment

                Comments

                Comment on this article

                Related Documents Log