01-03 Sodium and Water IIb: Sodium Disorders

Question 1

Hypo- and hypernatremia are d/o of _____ regulation, NOT _____ regulation.

Answer 1

Hypo- and hypernatremia are d/o of WATER regulation, NOT Na+ regulation.

Question 2

What is hypernatremia and what causes it?

Answer 2

Hypernatremia is too little water for the amount of salt present
—usu. 2°to dehydration
—can be from halophagia or iatrogenic admin of hypertonic saline

Question 3

Sx of Hypernatremia

Answer 3

Sx severity depends on rapidity of ∆

—CNS Sx: lethargy, weakness, szs, coma

Question 4

How long does it take the brain to synth idiogenic osmoles to counteract the hyperosmolarity caused by hypernatremia?

Answer 4

24-48 hrs

Question 5

Causes of hypernatremia?

Answer 5

WATER LOSSES:
—renal (DI, osmotic diuresis), GI or insensible
SALT OVERLOAD:
—salt poisoning
—NaHCO3 therapy
—hypertonic NaCl
INADEQUATE INTAKE
—hypothal lesion (hypodypsia)
—no access to water

Question 6

Iatrogenic cause of DI?

Answer 6

mannitol

Question 7

Diabetes Inspidus
—Types & Mech
—UA Findings
—TX

Answer 7

TYPES & MECH
—Central: hypothalamus makes too little ADH or post. pit. can’t release it
—Nephrogenic: renal resistance to ADH
——reversible = hypoK+ and hyperCa2+, vaptans
——irreversible = lithium demeclocycline*
*actually drug of choice for SIADH

UA FINDINGS
—polyuria (3-20L/day!)
—low osmolarity no matter what the serum Osm

TX
—DDAVP (exogenous vasopressin)

Question 8

Causes of osmotic diuresis

Answer 8

1.DM
—hyperglycemia
2. IATROGENIC
—mannitol
—hypertonic saline
3. Large osmolar load
—high protein diet
—parenteral nutrition

Question 9

GI Losses water losses

Answer 9

—diarrhea and vomit are both isotonic

—vomiting impairs water intake obvi

Question 10

What are insensible and sensible losses?

Answer 10

INSENSIBLE
—Stools; urine; evap* from skin & resp tract
*Fever/burns/skin disruptions ↑ evap losses

SENSIBLE
—sweat is hypotonic
—evaporative losses from skin have

Question 11

Dx Hypernatremia

Answer 11

UA can distinguish between renal and extrarenal losses
—usually the source of sodium excess or water loss is apparent
—watch out for crazy transferred Münchausen in kids whose parents give them salt water =(

Question 12

Expected urine osmolarity in setting of hypernatremia?

Answer 12

expect HIGH urine osmolarity (>500mOsm/L)

—low osmolarity is inappropriate and may mean DI

Question 13

Time course of hypernatremia & its tx

Answer 13

Acute = < 24hrs
Chronic = > 24hrs
—If hypernatremia has acute onset you can correct rapidly
—when in doubt, correct slowly b/o r/o CR

TX
—Correct no more than 10-12mEq/L/d

Question 14

Equation for estimated water deficit

Answer 14

0.6 X wt. X [(Na+/140) - 1]

—always calc this; usu larger than you think!

Question 15

Estimate the water deficit in a 70kg pt w/ [Na+] of 160

Answer 15

deficit = 0.6 X 70 X [(160/140) - 1]
= 0.6 X 70 X 0.14
= 5.88L
—Write for that but also order q4hr labs

Question 16

What IVF to Rx in pts w/ hypernatremia?

Answer 16

Depends on volume status:
—If hypovolemic give NS
—If euvolemic give 1/2 NS

Question 17

General Def of hyponatremia

Answer 17

Low serum Na typically characterized by hyposmolarity & water excess*
*can have iso- or hyperosmolar hyponatremia

Question 18

Sx of Hyponatremia

Answer 18

sx depend of rate of onset and are related to CE
—nausea
—malaise
—h/a
—lethargy
—decr consciousness 
—szs
—coma

Question 19

Majority of hyponatremia is _______osmolar.

Answer 19

Majority of hyponatremia is hyposmolar.

Question 20

Iso- or hyperosmolar hyponatremia

Answer 20

1. Hyperglycemia causes iso- or hyperosmolar hyponatremia
2. Other causes are rare:
   —iatrogenic (glycine, sorbitol, mannitol)
   —pseudohyponatremia: hyperlipidemia, hyperproteinemia (e.g. MM) causes lab to “see” low Na+
   ——osmoreceptors only see aqueous face

Question 21

Hyposmolar hyponatremia

Answer 21

Water retention that is either:
—ADH independent where the volume of filtrate overwhelms the kidney's ability to excrete excess water
——renal failure (low GFR)
——1° polydypsia (too much water)
——beer potomania (too few osmoles)
—ADH dependent (SIADH)

Question 22

Equation for water excess

Answer 22

0.6 X wt X ([Na+]-140]/140

Question 23

Beer potomania

Answer 23

—beer has no osmoles (no electrolytes and no protein to make urea)
—impaired ability to excrete urine (most dilute urine still has 50 mOsm/L of solutes and you are only taking in ~100mOsm/d; lose normal urea gradient)
—urinating a lot (increased intake + EtOH suppresses ADH)

Question 24

Tea & Toast

Answer 24

Cause of Low ADH Hyponatremia
—Low serum
—eating carbs supreses catabolism that would normally create protein from muscle stores in starvation

Question 25

High ADH Hyponatremia Causes

Answer 25

Can be appropriate or inappropriate
—‪↓‬ ECV: true vol depl
——diuretics (esp thiazides)
——CHF/cirrhosis/nephrotic (ADH/Aldo stim)
——hypothy, hypoadrenalism: both ‪↓‬ thyroxine and ‪↓‬ cortisol cause ‪↓‬ C.O. → ↓‬ ECV → ADH stim
—Reset osmostat: super rare; Na+ ~130, no Tx needed
—SIADH: euvolemic, hyposmolar, hyponatremia (high Urine Na+ and osmolarity)

Question 26

Thiazide Hyponatremia

Answer 26

—causes vol depletion and impairs Na+ reuptake which both cause hyponatremia
—usually the DCT dilutes urine b/c it is impermeable to water but reuptakes Na+
—since the filtrate leaving the DCT is non-dilute, the minimum urine osmolarity is ↑ and water excretion is impaired

Question 27

Causes of SIADH

Answer 27

—CNS tumor/infx
—pulm tumor/infx
—pain
—n
—post-op state
—narcotics!!
—HIV/AIDS
—neuropsych drugs: SSRIs, neuroleptics, anticonvulsants
—chemo

Question 28

Approach to diagnosis of hyponatremia

Answer 28

LOOK AT SLIDE 67 DRAW IT
—Ignore below?

ADH excess or not?
—If so inappropriate or not?
Look at serum & urine osmolality; volume status

SERUM OSMOLARITY
—usually low
—If high, look for other osmoles (gluc, lipids, prot, glycine, mannitol, sorbitol, renal failure

URINE OSMOLARITY
—Once estab’d ‪↓‬ serum osm, check urine osm to determine ADH activity
—Low Urine Osm → appropriate water excretion and a dx of beer, T&T, reset osmostat
—High Urine Osm → means ADH activity which still could be approp or inappro
——Inapp: Nephrotic, CHF, cirrhosis
——Approp: hypovolemic (e.g. w/ diuretic use)

Question 29

Causes of euvolemic hyponatremia

Answer 29

—SIADH (usually the cause)
—hypothyroidism
—hypoadrenalism

Question 30

What happens when you correct hyponatremia too quickly?

Answer 30

osmotic demyelination (formerly “Central Pontine Myelinosis” but now known to affect other brain regions)
—stroke-like syndrome of neurologic deficits
—dysarthria, dysphagia, paresis, lethargy, coma
—usually 2-6 day s/p correction
—most important risk factor is the rate of correction in the first 24-48hrs (assoc’d w/ correction >10-12mEq in first 24 or >18 in first 48hrs
—DX w/ CT or MRI but only after 2-4 weeks
—?relower Na+?

Question 31

Methods to Correct Hyponatremia

Answer 31

• water restriction (if hypervolemic)
• V2 receptor antagonist (only if elev ADH)
• Na+ supplementation**tricky b/c this is NOT a salt problem it’s a too much water problem and you have to worry about the brain

Question 32

Pros/Cons of NS to Tx Hyponatremia

Answer 32

PROS
provides osmoles in beer potomania, T&T → enables water diuresis
—restores intravascular volume in hypovolemia

CONS
—exacerbates hypervolemic states
—worsens SIADH

Question 33

Why is NS bad in SIADH?

Answer 33

In SIADH you are making hyper concentrated urine, urine that may be as much as twice NS concentration, so you end up secreted all the salt in a bag of saline in only have the volume. Therefore, you’ve essentially just given your pt 500mL of free water exacerbating their hypervolemia.

Question 34

Tx for SIADH

Answer 34

—fluid restrict if asymptomatic

—if symptomatic, give 3% NS

Question 35

Indications for rapid correction of hyponatremia

Answer 35

—severe neuro sx (szs, coma, lethargy, MS∆s, severe h/a)
—if you know for sure the ∆was acute (e.g. post-op or exercise-induced)
—Call nephrology or endocrine

Question 36

Chronic tx of SIADH

Answer 36

—educate and fluid restrict
—high salt can provoke solute diuresis
—demeclocycline can induce nephrogenic DI which makes kidney resistant to ADH
—V2 antagonists in the future ($$ now)