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Hyponatremia and Hypernatremia
Sodium and water
Terms in this set (74)
Na < 120
Na 120 to 130
131 to 135
> 295. Translocation of water leads to low sodium. I.e. Hyperglycemia and mannitol
275 to 295. Pseudo ~ Hyperlipidemia
< 275. Evaluate volume status
Examples of Hypervolemic hyponatremia
Examples of Euvolemic Hyponatremia
- CNS disorders
- Drug induced
- Pulmonary disease
Examples of Hypovolemic Hyponatremia
Cerebral salt wasting
Bicarbonaturia, glucosuria, ketonuria
Third space loss
Causes of AVP Stimulation
Hyperosmolality ~ Osmoreceptors in hypothalamus
Hypovolemia can trigger this at more than 7 to 10% loss
Decreased circulatory blood volume ~ baroreceptors in left atrium and aortic arch
1. AVP synthesis
2. AVP storage
3. AVP Secretion
4. AVP binding to V2 receptors in renal collecting duct
5. cAMP activation
6. The translocation of vesicles to place aquaporin 2 on apical surface of renal collecting duct
7. Water reabsorption
8. Decrease osmol, increase EABV
AVP on V1a
Vascular smooth muscle cells, PLTs, lymphocytes and monocytes, liver. when activated vasoconstriction, PLT aggregation, cytokine release, glycogenolysis.
AVP on V1b
Anterior pituitary to release ACTH and beta endorphin
Dysregulation of normal AVP response
HF, cirrhosis, CAP, AIDS, neurologic injury, extreme exercise
Excessive levels of ADH.
ADH is not suppressed appropriately. Despite hypoosmolality in the serum
Leading to Impaired water excretion, increased TBW and hyponatremia.
High urine osmolality in setting of inappropriately low serum osmolality
1. UNa > 40 with normal sodium intake
2. Clinical euvolemia
3. Normal hepatic, renal, cardiac
4. Normal thyroid, adrenal
5. No diuretics
Leads to cerebral swelling.
Extracellular space has less Na/more water which creates an osmotic gradient for water to enter cells (high water to low water). This causes symptoms when swelling is > 8%.
Rapid correction okay.
Loss of electrolytes and osmolytes decreases brain solute content.
Rapid correction ~ dehydration and ODS risk
Risks of Hyponatremia
Gait instability, falls
Mortality in Hyponatremia
Increases significantly with HF and Cirrhosis
Goal Sodium Change in Hyponatremia
Raise Na by < 8 to 12 mEq in 24h
Raise Na by < 18 to 24 mEq in 48h
Symptomatic 1 mEq/L/hr until neuro symptoms resolve or Na > 120 mEq/L
Natural Adaptations of Brain in Hyponatremia
Sodium, potassium, and chloride loss (rapid) + organic osmolyte loss (slow)
Treatment of Acute HypoNa
3% of 100 mL or 1 ml/kg bolus followed by 100 ml/hr or 1-2 ml/kg/hr.
30 ml of 23.4% ~ changes serum sodium by 5 mEq
Reverses symptoms which usually takes 4-6
Hypertonic saline dosing
3% = 512 mEq/L = 0.5 mEq/ml
TBW = 0.5 L/kg body weight
1 mL 3% NaCl per kg = Change of 1 mEq/L
Greater increase if urine is dilute and smaller increase if urine sodium is high
Risk factors for ODS
Na < 105 mEq/L
Reversibly impaired water excretion
AVP synthesis high
Then urine osm fall to < 100
Then urine output increase to > 500 ml/hr
Na increases by > 2.5 mEq/L/hr
This equivalent water diuresis to using 3% (i.e. change in sodium is 1 mEq/L for 3 ml/kg water loss.)
Maximally dilute urine can increase serum sodium by > 2mEq/L/hr.
States of Reversibly impaired water excretion
Drug induced SIADH
Stress induced SIADH ~ nausea
Fluid restriction for Hyponatremia
~ 800 ml/d
Predictors of failure
- High Urine osm > 500
- Urine Na and K > serum Na
- 24h urine output < 1500
- Increase serum Na < 2 in 24h
Vaptans for Hyponatremia
Increases sodium by 6 to 8 mEq/L over a few days
No use with CYP3A4 and PGP inhibitors
Better for patients with Uosm > 600
Urea use in Hyponatremia
Induces osmotic extraction of free water without associated electrolyte depletion
Diminishes natriuresis with increased medullary urea content in SIADH
Similar efficacy to vaptans
Deficit of water in relation to sodium
Mutations in the AVPR2 gene ~ 90%
Mutations in the AQP2 gene ~ 10%
Renal disease ~ medullary cystic disease
Hypercalcemia or hypokalemia
Drugs ~ lithium, demeclocycline, foscarnet, methoxyflurane, amphotericin B, vasopressin V2-receptor antagonists
Cause of Hypernatremia
Lack of water
Hypernatremia Rate of Correction
Acute - 1 mEq/L/hr
Chronic - 10 mEq/L/d
Why does edema not occur in non physiologic ADH secretion?
Volume receptors active.
Appropriate increase in UNa and water excretion possibly due to ANP (ADH escape). Steady state urine sodium reflects intake sodium
Urine flow components
1. Volume of urine needed to excrete solutes at concentration of solutes in plasma (i.e. isotonic or osmolar clearance)
2. Remaining urine volume is solute free water (electrolyte free water clearance, cH2O)
V = Cosm + cH2O
Cosm = Uosm x Vurine / Posm
cH2O = V [1- Uosm/Posm]
Effective osmoses ~ Na and K
So CH2Oe = V [1-(Una+Uk)/Pna]
Electrolyte free water clearance
If cH2O is negative = water is being absorbed and sodium will fall.
If cH2O is positive = free water is lost and sodium will rise.
Obligatory Urine Volume Calculation
Solute load (600 mOsm/d average) / concentrating ability (1000 to 1200 mOsm/L) = 0.5 L per day
If patient's urine osm is 150 mOsm/L then = 4L
Change in serum sodium = (infusate sodium - serum sodium) / (Total body water + 1)
If K is in solution, add it to the infusate sodium.
Does not take urine losses of solute or water.
Often actual rate of correction is more than correct.
Hypernatremia + dilute urine
Some degree of DI.
Water deprivation Test
Tea and Toast / Beer Drinkers potomania
Increase water intake and decrease solute intake
Water excretion requires Na, K, urea
Carbs get converted to CO2 and H2O
Low solute limits water excretion
Plasma Na and Plasma Osm low
Urine Osm High
Urine Na high (high meaning not low)
Uric acid low
Releases serotonin, dopamine, NE (ADH)
Causes rhabdo, hyperthermia, AKI, arrhythmias, and hyponatremia
More common in women than men with high mortality rate (higher copeptin levels, estrogen stems ADH secretion and up regulates ADH)
Estrogen and Hyponatremia relationship
Women have more neurologic sequalae
Estrogen reduces brain cell Na-K-ATPase ~ more brain edema
AVP more vasoconstrictive in females
Treatment for polyuria in DI
Increase urine osm (DDAVP in central DI)
Decrease solute intake (Na and protein restriction)
Urine electrolyte free water clearance
Urine output - [Urine output x (urine sodium + urine potassium)/Plasma sodium]
Treatment for SIADH
Decrease urine osm (ADH antagonists, loop diuretics, demeclocycline)
Increase solute intake (protein intake, oral urea, NaCl)
300 mosm/d increase
9 g of NaCl
18 g of urea
Serum Osm Calculation
2Na + glucose/18 + BUN/2.8 (mg/dl)
Pseudo hyponatremia examples
Hyperlipidemia, hyperproteinemia (waldenstrom or MM)
Method by which to evaluate pseudohyponatremia
Direct potentiometry = blood gas machine
Should be normal sodium level by this method and low by indirect (most labs)
Hyperglycemia, no osmolal gap
Hyponatremia + Osmolal gap
Plasma osm normal
Indirect potentiometry is low
Direct potentiometry is normal
Water deficit calculation
TBW x (1-[140/Na])
Can underestimate TBW and free water losses
Nephrogenic DI response to water deprivation
Urine osm never increases
Complete Central DI response to water deprivation
No response but when you give DDAVP, the urine will concentrate but not to normal as the medullary concentrating gradient is washed out
Partial Central DI response to water deprivation
Partial response and better response after DDAVP but not normal
Primary Polydipsia response to water deprivation
Good response but not normal due to washout of medullary concentrating gradient
Amphotericin B - Electrolyte disorders
Nephrogenic DI ~ decrease response to vasopressin
Type 1 distal RTA
Hypokalemia induced DI
K < 3.0 (usually within 2 weeks of low K)
Modest reduction in urinary concentrating ability
Decreased collecting tubule responsiveness to vasopressin by down regulation of AQP2 and decreased NaKCC transporter with decreased medullary concentrating gradient.
CRRT Rx for to avoid overcorrection in hypoNa
Total Na in Circuit per hour / total therapy fluid amount per hour
[(Replacement fluid Na x rate) + (dialysate Na x rate)] / total fluid amount
Does uremia increase the risk of ODS?
No because as sodium goes up, urea goes down
Fractional Excretion Calculation
Does urine sodium have to be high in SIADH?
No, as urine sodium reflect steady state in SIADH so if sodium intake is low then urine sodium will also be low.
Clinical utility of uric acid in SIADH?
Low serum uric acid may be helpful as Fractional excretion of uric acid increases in SIADH
Urine osm x urine volume =
150 x 1.5L = 225 mosm/d
where 600 mosm/d is normal
What test can be used to differentiate between partial central DI and primary polydipsia?
Copeptin and urine osm after hypertonic saline.
Must ensure urine volume is > 3L.
Copeptin levels will increase.
In irrigation procedures that use iso-osmolar agents what would the values be for osm and sodium after the procedure?
Low serum sodium
Measured serum osm is normal
Osmolal gap present (due to irrigant)
Electrolyte free water clearance response to normal saline when UNa + UK > PNa ?
Desalination and plasma sodium falls
Electrolyte free water clearance response to fluid restriction when UNa + UK > PNa ?
Too slow because there is no EFW clearance from the urine
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