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WHERE’S WALDO?

WHERE’S WALDO?. Case studies in hyponatremia. Who really knows?. WE CAN’T FIND WALDO.

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WHERE’S WALDO?

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  1. WHERE’S WALDO? Case studies in hyponatremia

  2. Who really knows?

  3. WE CAN’T FIND WALDO • Waldo B. was a fifty-something schizophrenic, a denizen of the general medical wards when I was an intern. He was frequently admitted with recurring hyponatremia. In the wee hours the call came from Nurse Zirkel- “We can’t find Waldo !”

  4. FOLLOW THE WATER The search for causes of hyponatremia can be elusive but it’s rooted in the understanding of basic osmoregulation

  5. ADH / VASOPRESSIN • Synthesized in the hypothalamus in response to increased plasma osmolality, decreased arterial pressure, and reductions in cardiac volume • The effects of vasopressin are mediated by three vasopressin receptor subtypes • V1-Vasoconstriction • V2-Water reabsorption • V3-CNS effects

  6. VASOPRESSIN AND OSMOREGULATION • Increased plasma osmolality triggers ADH release from the posterior pituitary and triggers thirst • Significantly decreased tissue perfusion mediated by baroreceptors in the carotid sinus can overcome the inhibitory effect of hyponatremia on ADH secretion and lead to increased free water retention in the kidneys

  7. ADH / VASOPRESSIN

  8. WATER INTAKE AND ADH • In normal circumstances a water load will be rapidly excreted as the dilutional fall in plasma osmolality suppresses ADH release allowing excretion of a dilute urine • The maximum rate of water excretion on a regular diet is over 10 liters a day allowing an enormous range of protection against development of hyponatremia

  9. WALDO’S DILEMMA • Psychogenic polydipsia • Normally the threshold for thirst is roughly equal to or slightly higher than the trigger for ADH release • In primary polydipsia the triggers are reversed. The threshold for thirst is lower than the threshold for ADH release and a maximally dilute urine is produced. Compulsive water drinking can then rapidly lead to severe hyponatremia if enough free water is consumed

  10. OTHER ISSUES IN THIS POPULATION • Common drugs may stimulate thirst • Stress of illness may stimulate ADH (vasopressin as stress hormone) • Increase in renal response to vasopressin • Drug-induced SIADH –carbamazepine, increased renal sensitivity to ADH • Question of SSRI’s causing SIADH • Nephrogenic DI with lithium

  11. DIAGNOSTIC APPROACH IN HYPONATREMIC PSYCHIATRIC PATIENT • Measure urine osmolality • In primary polydipsia the urine should be maximally dilute-less than 100 mosmol/kg • A higher urine osmolality suggests a contributory role for increased ADH release or responsiveness • Consider drugs-carbamazepine, lithium, SSRIs, ecstasy

  12. SIADH • Characterized by inappropriately concentrated urine • Hypotonic hyponatremia • Urine osmolality > 100 mmol/kg • Absence of extracellular volume depletion • Normal thyroid and adrenal function • Normal cardiac, hepatic, and renal function

  13. SIADH • Should be SIWR (Syndrome of Inappropriate Water Retention) • CNS disturbances • Tumor • Drugs • Major Surgery • Pulmonary disease • Hormonal Therapy • HIV • Hereditary SIADH • Idiopathic

  14. “MARATHON MALADIES” • 44 yo surgeon from Baton Rouge presented to Meriter ER following completion of the recent Iron Man competition with headache and confusion. Serum Na was 115 meq/l • April 2005 Article in NEJM by Levine and Thompson traced some of the history of medical attention to the extreme sports

  15. “MARATHON MALADIES CONTINUED” In the NEJM study the most important factors predicting development of hyponatremia were weight gain and race time. A consensus panel was convened and several recommendations were made for the prevention of exercise-induced hyponatremia.

  16. EXERCISE RELATED HYPONATREMIA • Likely related to excessive consumption of hypotonic solutions during and immediately following races • Nontraumatic deaths in the past thought related to heat stroke and exertional rhabdomyolysis. This led to recommendations for aggressive fluid consumption

  17. RECOMMENDATIONS • Avoid fixed global recommendations for water intake • Athletes should rely on thirst as a guide to fluid replacement • Monitor weight before and after training and races--avoid weight gain • Medical personnel should avoid hypotonic solutions in persons with exercise related collapse--especially when serum Na unknown • Hypertonic supplements in the form of salt containing gels may play a role

  18. TREATMENT • Symptoms of hyponatremia are due to osmotic swelling of the brain as plasma tonicity decreases. Symptoms depend on acuity and severity of hyponatremia • Early signs nonspecific— nausea, vomiting, headaches • Decreased mental status and seizures • Coma, respiratory arrest, and death

  19. CPM / EPM • The 800 pound gorilla in the management of hyponatremia. Also known as osmotic demyelination syndrome. • Based on autopsy findings, many, if not most, cases go unreported • Clear correlation with overly rapid correction of hyponatremia • Other comorbid conditions include alcoholism, liver transplantation, hypoxemia

  20. CPM

  21. CPM

  22. TREATMENT OF ASYMPTOMATIC PATIENTS • If hypovolemic, restoring volume with NS will inhibit ADH and facilitate correction of hyponatremia • If hypervolemic (CHF, liver disease/cirrhosis, renal disease) treat underlying condition.

  23. TREATMENT OF EUVOLEMIC PATIENTS WHO ARE SYMPTOMATIC • Acute onset <48 hrs. Fluid restrict and stop offending drugs/hypotonic fluids • Infuse hypertonic saline 3% as a 100 ml bolus. Goal is to remove patients with severe symptoms from immediate danger • Secondary goal is to use isotonic solution and to limit rate of correction to 10-20 meq/l over 48 hrs

  24. CHRONIC ONSET • Stop offending drugs/hypotonic fluids • If symptomatic, treat with hypertonic saline but aim for a slower correction .5-1 mmol/hr to a max of 12 mmol over 24 hrs

  25. TREATMENT • Management is based on treatment of the clinical symptoms of hyponatremia and not serum sodium levels • Goals of therapy are to remove patients from immediate danger, correct patient to a mild hyponatremic, asymptomatic state, and maintain slow correction to less than normonatremic levels to allow brain time to adjust to new tonicity

  26. REFERENCE • American Journal of Medicine (2006) Vol 119 Symposium on Hyponatremia

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