Cerebral Salt Wasting Syndrome

Cerebral Salt Wasting Syndrome

• 1.
  CEREBRAL SALT WASTINGSYNDROME (CSWS) Ade Wijaya, MD October 2017
• 2.
  OUTLINE: • Physiology ofcells in hyponatremia • CSWS (introduction and etiology) • Patophysiology • Clinical manifestation and diagnosis • Treatment • Summary
• 3.
  CELLS DURING HYPONATREMIA FLUID,ELECTROLYTE, AND ACID-BASE PHYSIOLOGY: A PROBLEM-BASED APPROACH, 4th EDITION
• 4.
  BRAIN CELLS VOLUMEIN HYPONATREMIA FLUID, ELECTROLYTE, AND ACID-BASE PHYSIOLOGY: A PROBLEM-BASED APPROACH, 4th EDITION
• 5.
  CSWS • Renal lossof sodium during intracranial disorders leading to hyponatremia and a decrease in extracellular fluid volume • First described by Peters, et al (1950) • Cause: SAH, Brain Injury, CNS infections (TB meningitis, viral encephalitis), carcinomatpus meningitis, metastatic carcinoma, transsphenoidal surgery. PetersJP, Welt LG, Sims EA, Orloff J, Needham J. A salt-wasting syndrome associated with cerebral disease. Trans Assoc Am Physicians 1950;63:57-64. Cerdà-Esteve, M., Cuadrado-Godia, E., Chillaron, J. J., Pont-Sunyer, C., Cucurella, G., Fernández, M., ... & Roquer, J. (2008). Cerebral salt wasting syndrome. European journal of internal medicine, 19(4), 249-254.
• 6.
  PATOPHYSIOLOGY • Disruption ofhypothalamo-renal pathways • Imbalance of sympathetic output with decreased renal sympathetic activity • Direct injury to the anterior and posterior pituitary • Brain Natriuretic Peptide (BNP) • Local production of natriuretic peptides within the adrenal medulla  paracrine inhibitory effects on mineralocorticoid synthesis  aldosterone and renin levels fail to rise despite the presence of hypovolaemia • Downregulation of renal sodium transporters due to extracellular volume expansion and the adrenergic surge that occurs in the early phase of brain injury might cause pressure natriuresis Dholke, H., Campos, A., Reddy, C. N. K., & Panigrahi, M. K. (2016). Cerebral salt wasting syndrome. Journal of Neuroanaesthesiology and Critical Care, 3(3), 205.
• 7.
  THE ROLE OFBNP IN CSWS Kim, D. K., & Joo, K. W. (2009). Hyponatremia in patients with neurologic disorders. Electrolytes & Blood Pressure, 7(2), 51-57.
• 8.
  CLINICAL MANIFESTATION Dholke, H.,Campos, A., Reddy, C. N. K., & Panigrahi, M. K. (2016). Cerebral salt wasting syndrome. Journal of Neuroanaesthesiology and Critical Care, 3(3), 205.
• 9.
  TREATMENT • Salt andwater replacement (isotonic or hypertonic NaCl 3%)  slow correction, CPM! • Fludrocortisone - 0.05 to 0.1 mg twice daily - adverse effects: hypokalemia, hypertension, pulmonary oedema, hyperglycemia - only used if salt and water replacement fail to treat CSWS Dholke, H., Campos, A., Reddy, C. N. K., & Panigrahi, M. K. (2016). Cerebral salt wasting syndrome. Journal of Neuroanaesthesiology and Critical Care, 3(3), 205. Cerdà-Esteve, M., Cuadrado-Godia, E., Chillaron, J. J., Pont-Sunyer, C., Cucurella, G., Fernández, M., ... & Roquer, J. (2008). Cerebral salt wasting syndrome. European journal of internal medicine, 19(4), 249-254.
• 10.
  SUMMARY • CSWS causehyponatremia in patients with brain insults • CSWS vs SIADH • Treatment: salt and water replacement, avoid too rapid correction  CPM
• 11.
  THANK YOU