Dr. Simon Prince, FACP, FASN Assistant Professor of Medicine NYU School of Medicine North Shore Nephrology Hyponatremia
Dr. Simon Prince, FACP, FASNAssistant Professor of Medicine NYU School of MedicineNorth Shore Nephrology
Hyponatremia
Sodium
The problems with sodium has little to do with direct effects of the ion. Disregulation of sodium causes changes in cell volume. WATER PROBLEM
OSMOSIS
Why we care about osmolality
Alterations in cell size disrupt tissue function.
Sodium is an indicator of osmolality
The clinically important
variable is
tonicity.
Tonicity vs. Osmolality
• OsmolalityoTotal concentration
of all particles• Tonicity
oOnly impermeable particles contribute to tonicity.
Only impermeable particles cause changes in cell volume.
Why are we interested in TONICITY?
o When elevated, water leaves the cells causing
cell shrinkage and dysfunction.o When decreased water moves into the cells
causing cellular swelling and dysfunction. • We are interested in sodium because it
usually tells us the plasma tonicity.
Pseudohyponatremia: high osmolality
• Elevated glucose raise plasma tonicity which draws water from the intracellular compartment diluting plasma sodium.
Hillier TA, Abbott RD, Barrett EJ. Am J Med 1999; 106: 399-403.
Pseudohyponatremia: high osmolality
• Correcting the sodium for hyperglycemia.
o Add 1.6 to the sodium for every 100 mg/dL the glucose is over 100.
o Example: Na = 126 mEq/L. Glucose = 600 mg/dL: 600 - 100 = 500. So the glucose is five 100’s over 100 5 x 1.6 = 8 126 + 8 =134 True sodium equals 134 mEq/L To remember 1.6 think “Sweet 16”
• If a person drinks more water than the kidney is capable of clearing the excess water will dilute the plasma.
Causes of hyponatremia: Increased fluid intake
• To exceed the maximal renal clearance of water an adult needs to drink about 18 liters a day.
True hyponatremia
• Hyponatremia does not occur when sodium excretion exceeds sodium intake.
Negative salt balance causes hypovolemia
Causes of Hyponatremia:Defect in Free H2O clearance
Etiology of Hyponatremia: 3 steps to generating dilute urine
1.Delivery of water to the diluting segments of the nephron.
2.Functional diluting segments.
3.Collecting tubule impermeable to water (lack of ADH)
1400
285
100 50
Failure to Generate dilute urine
Lack of water delivery to the diluting segments.
• Renal Failure• Volume deficiency• Cirrhosis• Heart failure• Nephrotic syndrome
Failure to Generate dilute urine
• Ineffective solute reabsorption diluting segments:o Thick ascending limb
of the loop of Henle (TALH)o Distal convoluted
tubule. Diuretics Non-oliguric ATN
Failure to Generate dilute urine
Permeable collecting ducts (ADH)
o Volume related ADHo SIADH
Drug induced Paraneoplastic CNS Pulmonary disease
o Adrenal insufficiencyo Hypothyroidism
ADds Hydration to the body.
ADHOsmolality
ADH is normally used to regulate osmolality
We start with an increase in the plasma osmolalityThis is detected by the brainThe brain releases ADHADH acts on the kidneyThe kidney reacts by retaining water and producing a small amount of concentrated urine.
The retained watergoes here
not here
Clinical Approach
What Studies Are Needed?
Tests to send...
oUA, Urine: Na and OsmolalityoBMPoSerum osmolality, TSH, uric acid, BNP, cortisol
oCXRoHead CT
What is the Volume Status?
1.Hypovolemic2.Euvolemic
3.Hypervolemic
Hypovolemic Hyponatremia
Volume expansion with SALINE
Hypervolemic Hyponatremia
•Fluid restrict•Diurese
EUVOLEMIC HYPONATREMIA
•Excess intake in Free Water
•Defect in Free Water Clearance
•ADH problem
ADH Should NOT Be Present When...1.Euvolemic / Hypervolemic states2.Serum Osmolality is low - normal range
If ADH is elevated... that would be INAPPROPRIATE
Diagnostic Criteria for SIADH
1.Hypoosmolar hyponatremia2.Euvolemic3.Urine Na >254.Urine Osmolality elevated
o >350 mOsmo >200 higher than Serum Osmolality
Causes of SIADH
• Neurological:o Meningitiso Tumorso Traumao SAH
• Pulmonary disease:o Asthmao Mechanical ventilationo Pneumoniao TB
• Stresso Paino Vomitingo Post-surgical
• Medicationo Antipsychoticso SSRIo First generation sulfonylureaso Pitocin/Oxytocino Narcoticso Cyclophosphamideo Ecstasy
• AIDS
TREATMENT
Conservative vs. Aggressive
Who should get treated and why?
Symptomatic Hyponatremia
oMental status changesoNauseaoVomittingoHead acheoMovement abnormalitiesoSeizuresoHypoxia / respiratory failure
Symptomatic vs. Asymptomatic
Symptomatic HYPERTONIC SALINE
Asymptomatic Conservative approach is best
Acute symptomatic hyponatremia
• In patients with neurologic symptoms due to hyponatremia: 3%.
• Increase sodium until symptoms abate or 6 mmol/L, which ever comes first.
• Increase Na < 24 mEq/L in the first 24 hours.
• Goal is not more than 0.5 mEq/L/hour
The problem with compensation
The starting point is after compensation has reduced the amount of intracellular solute and the ICP
Now, an over-eager intern sees the low sodium and starts an infusion of 3% NaCl to raise the sodium to normal.
Sodium
108Sodium
134
The sodium draws water from the inside of the cells causing the brain to shrivel.
Central Pontine Myelinolysis
• Brain Shrinkage o Quadriplegiao Respiratory paralysiso Mental status changeso Usually fatal within three to five
weeks• Risk factors:
o Hyponatremia for > 24 hourso Over-correction of
hyponatremia (> 24 mEq/L/day)o Rapid correction (greater than
1–2 meq/hr)o Alcoholismo Malnutritiono Liver disease
Damned if you do. Damned if you don’t
• Without treatment patients have cerebral edema.
• With mistreatment patients are at risk of CPM.
TAKE HOME POINTS
• Hyponatremia is a WATER problem, not sodium problem
• In general best strategy in ER if not symptomatic... DO NOTHING (Primum non nocere) ... including holding NS unless dehydrated
• Repeat blood tests to confirm and watch for psuedohyponatremia, send off urine studies
• Careful hypertonic saline (3%) if symptomatico rule of thumb start hourly rate @0.5 LBM (kg)
CASE REPORTS