01-03 Sodium and Water IIb: Sodium Disorders Flashcards
Hypo- and hypernatremia are d/o of _____ regulation, NOT _____ regulation.
Hypo- and hypernatremia are d/o of WATER regulation, NOT Na+ regulation.
What is hypernatremia and what causes it?
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
Sx of Hypernatremia
Sx severity depends on rapidity of ∆
—CNS Sx: lethargy, weakness, szs, coma
How long does it take the brain to synth idiogenic osmoles to counteract the hyperosmolarity caused by hypernatremia?
24-48 hrs
Causes of hypernatremia?
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
Iatrogenic cause of DI?
mannitol
Diabetes Inspidus
—Types & Mech
—UA Findings
—TX
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)
Causes of osmotic diuresis
1.DM —hyperglycemia 2. IATROGENIC —mannitol —hypertonic saline 3. Large osmolar load —high protein diet —parenteral nutrition
GI Losses water losses
—diarrhea and vomit are both isotonic
—vomiting impairs water intake obvi
What are insensible and sensible losses?
INSENSIBLE
—Stools; urine; evap* from skin & resp tract
*Fever/burns/skin disruptions ↑ evap losses
SENSIBLE
—sweat is hypotonic
—evaporative losses from skin have
Dx Hypernatremia
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 =(
Expected urine osmolarity in setting of hypernatremia?
expect HIGH urine osmolarity (>500mOsm/L)
—low osmolarity is inappropriate and may mean DI
Time course of hypernatremia & its tx
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
Equation for estimated water deficit
0.6 X wt. X [(Na+/140) - 1]
—always calc this; usu larger than you think!
Estimate the water deficit in a 70kg pt w/ [Na+] of 160
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
What IVF to Rx in pts w/ hypernatremia?
Depends on volume status:
—If hypovolemic give NS
—If euvolemic give 1/2 NS
General Def of hyponatremia
Low serum Na typically characterized by hyposmolarity & water excess*
*can have iso- or hyperosmolar hyponatremia
Sx of Hyponatremia
sx depend of rate of onset and are related to CE —nausea —malaise —h/a —lethargy —decr consciousness —szs —coma
Majority of hyponatremia is _______osmolar.
Majority of hyponatremia is hyposmolar.
Iso- or hyperosmolar hyponatremia
- Hyperglycemia causes iso- or hyperosmolar hyponatremia
- 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
Hyposmolar hyponatremia
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)
Equation for water excess
0.6 X wt X ([Na+]-140]/140
Beer potomania
—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)
Tea & Toast
Cause of Low ADH Hyponatremia
—Low serum
—eating carbs supreses catabolism that would normally create protein from muscle stores in starvation
High ADH Hyponatremia Causes
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)
Thiazide Hyponatremia
—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
Causes of SIADH
—CNS tumor/infx —pulm tumor/infx —pain —n —post-op state —narcotics!! —HIV/AIDS —neuropsych drugs: SSRIs, neuroleptics, anticonvulsants —chemo
Approach to diagnosis of hyponatremia
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)
Causes of euvolemic hyponatremia
—SIADH (usually the cause)
—hypothyroidism
—hypoadrenalism
What happens when you correct hyponatremia too quickly?
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+?
Methods to Correct Hyponatremia
- 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
Pros/Cons of NS to Tx Hyponatremia
PROS
provides osmoles in beer potomania, T&T → enables water diuresis
—restores intravascular volume in hypovolemia
CONS
—exacerbates hypervolemic states
—worsens SIADH
Why is NS bad in SIADH?
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.
Tx for SIADH
—fluid restrict if asymptomatic
—if symptomatic, give 3% NS
Indications for rapid correction of hyponatremia
—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
Chronic tx of SIADH
—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)
