+ All Categories
Home > Documents > WHERE’S WALDO?

WHERE’S WALDO?

Date post: 07-Jan-2016
Category:
Upload: svea
View: 68 times
Download: 0 times
Share this document with a friend
Description:
WHERE’S WALDO?. Case studies in hyponatremia. Who really knows?. WE CAN’T FIND WALDO. - PowerPoint PPT Presentation
26
WHERE’S WALDO? WHERE’S WALDO? Case studies in Case studies in hyponatremia hyponatremia
Transcript
Page 1: WHERE’S WALDO?

WHERE’S WALDO?WHERE’S WALDO?

Case studies in hyponatremiaCase studies in hyponatremia

Page 2: WHERE’S WALDO?

Who really knows?Who really knows?

Page 3: WHERE’S WALDO?

WE CAN’T FIND WALDOWE CAN’T FIND WALDO

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

Page 4: WHERE’S WALDO?

FOLLOW THE WATERFOLLOW THE WATER

The search for causes of hyponatremia can The search for causes of hyponatremia can be elusive but it’s rooted in the be elusive but it’s rooted in the understanding of basic osmoregulationunderstanding of basic osmoregulation

Page 5: WHERE’S WALDO?

ADH / VASOPRESSINADH / VASOPRESSIN

Synthesized in the hypothalamus in Synthesized in the hypothalamus in response to increased plasma osmolality, response to increased plasma osmolality, decreased arterial pressure, and decreased arterial pressure, and reductions in cardiac volumereductions in cardiac volumeThe effects of vasopressin are mediated The effects of vasopressin are mediated by three vasopressin receptor subtypesby three vasopressin receptor subtypesV1-VasoconstrictionV1-VasoconstrictionV2-Water reabsorptionV2-Water reabsorptionV3-CNS effectsV3-CNS effects

Page 6: WHERE’S WALDO?

VASOPRESSIN AND VASOPRESSIN AND OSMOREGULATIONOSMOREGULATION

Increased plasma osmolality triggers ADH Increased plasma osmolality triggers ADH release from the posterior pituitary and triggers release from the posterior pituitary and triggers thirstthirst

Significantly decreased tissue perfusion Significantly decreased tissue perfusion mediated by baroreceptors in the carotid sinus mediated by baroreceptors in the carotid sinus can overcome the inhibitory effect of can overcome the inhibitory effect of hyponatremia on ADH secretion and lead to hyponatremia on ADH secretion and lead to increased free water retention in the kidneysincreased free water retention in the kidneys

Page 7: WHERE’S WALDO?

ADH / VASOPRESSINADH / VASOPRESSIN

Page 8: WHERE’S WALDO?

WATER INTAKE AND ADHWATER INTAKE AND ADH

In normal circumstances a water load will In normal circumstances a water load will be rapidly excreted as the dilutional fall in be rapidly excreted as the dilutional fall in plasma osmolality suppresses ADH plasma osmolality suppresses ADH release allowing excretion of a dilute urinerelease allowing excretion of a dilute urine

The maximum rate of water excretion on The maximum rate of water excretion on a regular diet is over 10 liters a day a regular diet is over 10 liters a day allowing an enormous range of protection allowing an enormous range of protection against development of hyponatremiaagainst development of hyponatremia

Page 9: WHERE’S WALDO?

WALDO’S DILEMMAWALDO’S DILEMMA

Psychogenic polydipsiaPsychogenic polydipsia

Normally the threshold for thirst is roughly equal Normally the threshold for thirst is roughly equal to or slightly higher than the trigger for ADH to or slightly higher than the trigger for ADH releaserelease

In primary polydipsia the triggers are reversed. In primary polydipsia the triggers are reversed. The threshold for thirst is lower than the The threshold for thirst is lower than the threshold for ADH release and a maximally threshold for ADH release and a maximally dilute urine is produced. Compulsive water dilute urine is produced. Compulsive water drinking can then rapidly lead to severe drinking can then rapidly lead to severe hyponatremia if enough free water is consumedhyponatremia if enough free water is consumed

Page 10: WHERE’S WALDO?

OTHER ISSUES IN THIS OTHER ISSUES IN THIS POPULATIONPOPULATION

Common drugs may stimulate thirstCommon drugs may stimulate thirst

Stress of illness may stimulate ADH Stress of illness may stimulate ADH (vasopressin as stress hormone)(vasopressin as stress hormone)

Increase in renal response to vasopressinIncrease in renal response to vasopressin

Drug-induced SIADH –carbamazepine, Drug-induced SIADH –carbamazepine, increased renal sensitivity to ADHincreased renal sensitivity to ADH

Question of SSRI’s causing SIADHQuestion of SSRI’s causing SIADH

Nephrogenic DI with lithiumNephrogenic DI with lithium

Page 11: WHERE’S WALDO?

DIAGNOSTIC APPROACH IN DIAGNOSTIC APPROACH IN HYPONATREMIC PSYCHIATRIC HYPONATREMIC PSYCHIATRIC

PATIENTPATIENTMeasure urine osmolalityMeasure urine osmolality

In primary polydipsia the urine should be In primary polydipsia the urine should be maximally dilute-less than 100 mosmol/kgmaximally dilute-less than 100 mosmol/kg

A higher urine osmolality suggests a A higher urine osmolality suggests a contributory role for increased ADH contributory role for increased ADH release or responsivenessrelease or responsiveness

Consider drugs-carbamazepine, lithium, Consider drugs-carbamazepine, lithium, SSRIs, ecstasySSRIs, ecstasy

Page 12: WHERE’S WALDO?

SIADHSIADH

Characterized by inappropriately Characterized by inappropriately concentrated urineconcentrated urine

Hypotonic hyponatremiaHypotonic hyponatremia

Urine osmolality > 100 mmol/kgUrine osmolality > 100 mmol/kg

Absence of extracellular volume depletionAbsence of extracellular volume depletion

Normal thyroid and adrenal functionNormal thyroid and adrenal function

Normal cardiac, hepatic, and renal Normal cardiac, hepatic, and renal functionfunction

Page 13: WHERE’S WALDO?

SIADHSIADH

Should be SIWR (Syndrome of Inappropriate Water Should be SIWR (Syndrome of Inappropriate Water Retention)Retention)CNS disturbancesCNS disturbancesTumorTumorDrugsDrugsMajor SurgeryMajor SurgeryPulmonary diseasePulmonary diseaseHormonal TherapyHormonal TherapyHIVHIVHereditary SIADHHereditary SIADHIdiopathicIdiopathic

Page 14: WHERE’S WALDO?

““MARATHON MALADIES”MARATHON MALADIES”

44 yo surgeon from Baton Rouge 44 yo surgeon from Baton Rouge presented to Meriter ER following presented to Meriter ER following completion of the recent Iron Man completion of the recent Iron Man competition with headache and confusion. competition with headache and confusion. Serum Na was 115 meq/l Serum Na was 115 meq/l

April 2005 Article in NEJM by Levine and April 2005 Article in NEJM by Levine and Thompson traced some of the history of Thompson traced some of the history of medical attention to the extreme sportsmedical attention to the extreme sports

Page 15: WHERE’S WALDO?

““MARATHON MALADIES MARATHON MALADIES CONTINUED”CONTINUED”

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

Page 16: WHERE’S WALDO?

EXERCISE RELATED EXERCISE RELATED HYPONATREMIAHYPONATREMIA

Likely related to excessive consumption of Likely related to excessive consumption of hypotonic solutions during and immediately hypotonic solutions during and immediately following racesfollowing races

Nontraumatic deaths in the past thought related Nontraumatic deaths in the past thought related to heat stroke and exertional rhabdomyolysis. to heat stroke and exertional rhabdomyolysis. This led to recommendations for aggressive This led to recommendations for aggressive fluid consumptionfluid consumption

Page 17: WHERE’S WALDO?

RECOMMENDATIONSRECOMMENDATIONS

Avoid fixed global recommendations for water Avoid fixed global recommendations for water intakeintakeAthletes should rely on thirst as a guide to fluid Athletes should rely on thirst as a guide to fluid replacementreplacementMonitor weight before and after training and Monitor weight before and after training and races--avoid weight gainraces--avoid weight gainMedical personnel should avoid hypotonic Medical personnel should avoid hypotonic solutions in persons with exercise related solutions in persons with exercise related collapse--especially when serum Na unknowncollapse--especially when serum Na unknownHypertonic supplements in the form of salt Hypertonic supplements in the form of salt containing gels may play a rolecontaining gels may play a role

Page 18: WHERE’S WALDO?

TREATMENTTREATMENT

Symptoms of hyponatremia are due to Symptoms of hyponatremia are due to osmotic swelling of the brain as plasma osmotic swelling of the brain as plasma tonicity decreases. Symptoms depend on tonicity decreases. Symptoms depend on acuity and severity of hyponatremiaacuity and severity of hyponatremia

Early signs nonspecific—Early signs nonspecific—

nausea, vomiting, headachesnausea, vomiting, headaches

Decreased mental status and seizuresDecreased mental status and seizures

Coma, respiratory arrest, and deathComa, respiratory arrest, and death

Page 19: WHERE’S WALDO?

CPM / EPMCPM / EPM

The 800 pound gorilla in the management of The 800 pound gorilla in the management of hyponatremia. Also known as osmotic hyponatremia. Also known as osmotic demyelination syndrome.demyelination syndrome.

Based on autopsy findings, many, if not most, Based on autopsy findings, many, if not most, cases go unreportedcases go unreported

Clear correlation with overly rapid correction of Clear correlation with overly rapid correction of hyponatremiahyponatremia

Other comorbid conditions include alcoholism, Other comorbid conditions include alcoholism, liver transplantation, hypoxemialiver transplantation, hypoxemia

Page 20: WHERE’S WALDO?

CPMCPM

Page 21: WHERE’S WALDO?

CPMCPM

Page 22: WHERE’S WALDO?

TREATMENT OF TREATMENT OF ASYMPTOMATIC PATIENTSASYMPTOMATIC PATIENTS

If hypovolemic, restoring volume with NS If hypovolemic, restoring volume with NS will inhibit ADH and facilitate correction of will inhibit ADH and facilitate correction of hyponatremiahyponatremia

If hypervolemic (CHF, liver disease/cirrhosis, If hypervolemic (CHF, liver disease/cirrhosis, renal disease) treat underlying condition.renal disease) treat underlying condition.

Page 23: WHERE’S WALDO?

TREATMENT OF EUVOLEMIC TREATMENT OF EUVOLEMIC PATIENTS WHO ARE PATIENTS WHO ARE

SYMPTOMATICSYMPTOMATIC

Acute onset <48 hrs. Fluid restrict and Acute onset <48 hrs. Fluid restrict and stop offending drugs/hypotonic fluidsstop offending drugs/hypotonic fluids

Infuse hypertonic saline 3% as a 100 ml Infuse hypertonic saline 3% as a 100 ml bolus. Goal is to remove patients with bolus. Goal is to remove patients with severe symptoms from immediate dangersevere symptoms from immediate danger

Secondary goal is to use isotonic solution Secondary goal is to use isotonic solution and to limit rate of correction to 10-20 and to limit rate of correction to 10-20 meq/l over 48 hrsmeq/l over 48 hrs

Page 24: WHERE’S WALDO?

CHRONIC ONSETCHRONIC ONSET

Stop offending drugs/hypotonic fluidsStop offending drugs/hypotonic fluids

If symptomatic, treat with hypertonic If symptomatic, treat with hypertonic saline but aim for a slower correction saline but aim for a slower correction

.5-1 mmol/hr to a max of 12 mmol over .5-1 mmol/hr to a max of 12 mmol over

24 hrs24 hrs

Page 25: WHERE’S WALDO?

TREATMENTTREATMENT

Management is based on treatment of the Management is based on treatment of the clinical symptoms of hyponatremia and clinical symptoms of hyponatremia and not serum sodium levelsnot serum sodium levels

Goals of therapy are to remove patients Goals of therapy are to remove patients from immediate danger, correct patient to from immediate danger, correct patient to a mild hyponatremic, asymptomatic state, a mild hyponatremic, asymptomatic state, and maintain slow correction to less than and maintain slow correction to less than normonatremic levels to allow brain time normonatremic levels to allow brain time to adjust to new tonicityto adjust to new tonicity

Page 26: WHERE’S WALDO?

REFERENCEREFERENCE

American Journal of Medicine (2006) Vol American Journal of Medicine (2006) Vol 119 Symposium on Hyponatremia 119 Symposium on Hyponatremia


Recommended