4. Sodium and Water III Flashcards
the majority of cases of hypernatremia are due to what?
water loss/water deficiency
in patients with access to water, hypernatremia is common or rare?
rare, because thirst is a very powerful driving force
with hypernatremia, why does a faster onset cause more severe CNS symptoms?
because the brain hasn’t had time yet to alter its idiogenic osmoses (takes a few days to adjust)
CNS sx of hypernatremia?
lethargy, irritability, weakness, seiz, coma
Renal losses of free water? (3 types)
central DI
nephrogenic DI
osmotic diuresis
diabetes insipidus: what are symptoms?
polyuria, polydipsia
central DI: where is defect?
in the hypothal or posterior pituitary (where ADH is produced/secreted)
central DI: treatment?
desmopressin
nephrogenic DI: what meds can cause this?
lithium, demeclocycline
GI fluid loss: diarrhea is iso/hypo/hypertonic?
diarrhea typically hypotonic (lose more volume than solute)
GI fluid loss: vomit is iso/hypo/hypertonic?
hypotonic. (lose more volume than solute)
if hypernatremia is due to inadequate intake, what might be the reason?
hypothalamic injury, no access to water
in hypernatremia, what urine osmolarity is appropriate?
high: greater than 500 mosm/L
acute hypernatremia (<24h): correct rapidly or slowly?
can be corrected rapidly
chronic hypernatremia: correct rapidly or slowly? why?
slowly. brain idiogenic osmoses require time to adjust; rapid correction can lead to cerebral edema
formula for estimated water deficit?
0.6 * weight * [(Na/140)-1]
recommended rate of correction of hypernatremia?
0.5 mEq/L/h at maximum
Hypernatremia: overall, due to water loss from what?
kidney loss, GI tract, skin (sweat, insensible loss)
Hypernatremia: what should I always calculate?
the water deficit!
what is pseudohyponatremia?
large amounts of lipid or protein will occupy volume, but will be electrolyte free. yields falsely low serum Na results.
what are some causes of low-ADH hyponatremia?
renal failure
primary polydipsia
beer potomania (tea/toast syndrome)
what does low-ADH hyponatremia mean?
there is hyponatremia (too much water) for a reason that is not high ADH. NOT due to inappropriate reab of free water.
how can renal failure contribute to low-ADH hyponatremia?
if kidney cannot clear water (GFR is low) normal water intake can exceed maximum amount pt can excrete.
how can primary polydipsia contribute to low-ADH hyponatremia?
commonly associated with psychiatric disturbances. have to drink more than ~15L/day
what is an average osmolar excretion per day?
~600 mosm/day
how is it possible to get beer potomania/tea and toast sx?
carbohydrates don’t contribute to osmolar excretion level: they are just metabolized to CO2 and water. need enough osmoles to be able to create urine
Low ADH hyponatremia - what is the mechanism of overwhelming water excretory capacity
low GFR - renal failure
too few osmoles - beer potomania or tea/toast syndrome
too much water - primary polydipsia
high-ADH hyponatremia with volume depletion: what is happening?
elevated ADH is appropriate or inappropriate: volume is being maintained at the expense of osmolarity
high-ADH hyponatremia - what causes it? (3)
decreased ECV
Reset osmostat
SIADH
What are some causes of a decreased ECV? (7)
True volume depletion Diuretic therapy (esp. thiazides) CHF Cirrhosis Nephrotic syndrome Hypothyroidism Hypoadrenalism
Is water an efficient blood volume expander?
No, it is an inefficient blood volume expander but it is better than nothing.
Which one does the body maintain in urgent cases - volume or osmolarity?
Volume - organ perfusion is improved at the expense of osmolarity
How do thiazides induce hyponatremia? (2)
1) Thiazides impair urine dilution by blocking NaCl absorption (which increases osmolarity in DCT lumen)
(DCT is impermeable to H2O and urine is normally diluted in the DCT as NaCl is reabsorbed)
2) Volume depletion stimulates ADH production
Both mechanisms promote hyponatremia
How does CHF, cirrhosis, and nephrotic syndrome decrease ECV?
diverts fluid out of the arterial system
CHF and cirrhosis - fluid pools in the venous system
Nephrotic syndrome - fluid leaks from the capillaries into the interstitial space
What happens when the ECV is decreased? What happens when ECV is decreased but total body fluid is normal or increased?
ADH + aldosterone stimulated (despite normal or increased total body fluid)
How does hypoadrenalism cause decreased ECV? What is the response to this?
What are some of the laboratory findings of this?
no cortisol -> impaired cardiac function.
no aldosterone -> volume depletion
net: ECV decreased
response: ADH stimulated
labs: high urine Osms, but urine Na may not be low without aldosterone
How does hypothyroidism cause decreased ECV? What is the response to this?
What are some of the laboratory findings of this?
thyroxine deficiency impairs cardiac function; ECV falls and ADH is stimulated
Patients are often not clinically volume depleted.
How does reset osmostat cause decreased ECV? What is the response to this?
It actually doesn’t cause decreased ECV. Some patients just have a lower ADH setpoint than normal and no treatment is needed or effective.
What characterizes SIADH? (3)
What are the typical lab findings for this in terms of:
- urine Na
- creatinine
- uric acid
- urine osms
How is it diagnosed?
euvolemic
hyposmolar
hyponatremia
Urine Na = >40
Cr = normal or low
Uric acid = low
Urine osms = inappropriately high (often fixed at ~300mOsm/kg)
Diagnosis of exclusion (r/o hypothyroidism, hypoadrenalism, etc)
What are some causes of SIADH?
CNS, lungs, Drugs, pain, nausea, post-op state, HIV/AIDs
What are 3 considerations that you must take in when diagnosing hyponatremia?
Serum osmolality
Urine osmolality
Volume status
What is the serum osmolality of most hyponatremic patients?
low
What do you suspect if the serum osmolality a hyponatremic patient is low? high?
low = normal for hyponatremic patient
high = presence of another osmole (glucose, glycine, mannitol, sorbitol, renal failure, or pseudohyponatremia)
what is pseudohyponatremia?
presence of lipids or proteins skew the measurement of Na.
What does urine osmolality generally indicate?
ADH activity
How do you distinguish between physiologic ADH vs SIADH?
volume status assessment
What does a LOW urine osmolality indicate in a hyponatremic patient?
high fluid intake, not enough osmoles or reset - H2O is appropriately secreted.
- primary polydipsia
- low osmolar intake (beer potomania, tea/toast syndrome
- reset osmostat
What does a HIGH urine osmolality (>300) indicate?
elevated ADH activity - can be appropriate or inappropriate
What are some causes of HYPERvolemic HYPOnatremia? (4)
How do they do this?
ADH is inappropriate
Renal Failure - low GFR limits water excretion
Nephrotic syndrome, CHF, cirrhosis - results in decreased ECV, which stimulates ADH production.
Urine Na+ generally < 20 unless diuretics are being used
What is a major cause of HYPOvolemic HYPOnatremia?
How do they do this?
What is the labs like?
ADH is appropriate
- diuretic use
labs: low urine Na (suggests volume depletion)
What are some causes of EUvolemic hyponatremia (3)
SIADH
Hypothyroidism
Hypoadrenalism
When do symptoms of hyponatremia occur?
usually below 120
What happens if you rapidly correct hyponatremia?
How can you diagnose it?
osmotic demyelination - stroke-like syndrome of neurologic deficits (dysarthria, dysphagia, paresis, lethargy, coma)
Occurs when Na is corrected >10-12mEq in the first 24hrs or >18mEq in the first 48hrs
Dx: CT/MRI, but changes are not evident for 2-4 wks
How do you treat hyponatremia?
slowly - cellular adaptations (loss of intracellular osmoles) begins within 24hrs
How fast should you correct a hyponatremic patient who is asymptomatic? mildly symptomatic? severely symptomatic?
Asymptomatic = very slowly
Mildly symptomatic = 0.5 mEq/L/h
Severely symptomatic = 1-2 mEq/L/h
Total correction should not exceed 8-12 mEq/L/d
What are the methods used to correct a hyponatremic patient? (3)
Water restriction
V2 receptor antagonists (Vaptans)
Na+ supplementation
What is the preferred method for hypervolemic patients?
water restriction
What cases of hypervolemia is V2 receptor antagonist useful? (3)
useful in cases where hypervolemia is caused by elevated ADH: SIADH, CHF, cirrhosis
How does Na supplementation work in treating hypervolemia? What happens if you give NS? What happens if you give hypertonic saline?
NS will suppress ADH in hypovolemia (remember all NS stays in extracellular space)
Hypertonic saline overwhelms the concentrating ability of the kidney, forcing free water excretion (as in the case of SIADH)
How does NS help to treat hyponatremic patients? What cases is it useful? What situations is it harmful?
provides osmoles in beer potomania/Tea&Toast syndrome to enable diuresis
restores intravascular volume and shuts down ADH production in hypovolemia
Hypervolemic states
SIADH - urine mosms are usually fixed above 300 mOsm/kg, giving NS will actually cause them to retain water!
How do you treat SIADH patients? (hint - there are different treatments for symptomatic and asymptomatic)
Asymptomatic: fluid restrict
Symptomatic: 3% saline
Why is giving NS in SIADH patients B-A-D?
NS has an osmolality of 308 mosm/kg
SIADH = urine osmolality is fixed at 616 mOsm/kg, 308 mOsm will be excreted in 500cc urine.
This will result in the net retention of 500cc free water and serum Na+ will fall
Distinguishing SIADH from hypovolemia is critical because of this difference
What are some indications for rapid correction of hyponatremia?
Severe neurologic symptoms
(seizures, coma, lethargy, mental status changes, severe headache)
Known acute hyponatremia
(postoperative, exercise-induced)
How fast should you correct a hyponatremic patient?
What should you do once the target correction is achieved?
Raise Na+ by 1-2 mEq/L/h initially and monitor hourly.
Halt correction at 8-10mEq or when symptoms resolve.
Expected Na+ correction calculation?
What does this calculation indicate?
What is the delta Na for a 70kg patient (42L TBW) with [Na+] 100 is given 3% saline (contains 513 mEq NaCl/L or 1026 mosm/L)?
delta Na = (fluid Na - [Na] ) / (TBW+1)
indicates how much Na will rise with a given saline infusion, and is the desired correction in 24hrs
Thus for a 70kg patient (42L TBW) with [Na+] 100 is given 3% saline (contains 513 mEq NaCl/L or 1026 mosm/L), the delta Na is 9.6
1L of 3% saline would be expected to raise [Na+] by 9.6 in this patient
How do you treat chronic SIADH? (4)
Education and fluid restriction
high salt to promote solute diuresis
Demeclocycline - induces nephrogenic DI and provides resistance to ADH
V2 antagonist
