Electrolyte Disorders - Hyponatremia Flashcards
Def. hypoN and RFs
-Serum Na <135.
CHF Cirrhosis nephrotic syndrome PNA legionella post-op ICU older pt meds
2 main systems that regulate sodium?
- ADH system (amount of ADH is indirectly related to amount of urine produced!)
- thirst mechanism.
What is normal Na
280-290 mOsm/L
What two stimuli trigger ADH to be released? the goal here would be to make urine that is NOT dilute
- Osmotic stimuli: osmoreceptors detect high osmolarity in serum –> concentrate urine to get rid of extra solutes
- Non-osmotic stimuli: baroreceptors detect low BP or blood volume –> concentrate urine to conserve fluid
What are other non-osmotic stimuli that trigger ADH release
Baroreceptors Nausea Hypoxia Pain Opiates & Antidepressants Pregnancy
Pathogen. of HypoN: what happens when you have decreased serum osmolarity i.e. too much free water retention?
- Thirst suppression and suppression of ADH release
- ADH suppression= more urine= dilute urine
Pathogen. of HypoN: what happens when you have increased serum osmolarity i.e. too little free water?
- Thirst stimulation and stimulation of ADH release
- ADH release=little urine=concentrated urine
Defective urine diluting ability (so all you’re doing is concentrating your urine!) + excess water intake = ?
Hyponatremia
Defective urine concentrating ability + inadequate water intake = ?
Hypernatremia
What results in hyponatremia?
Increases in TBW, not really from actual Na changes. Increased TBW due to excessive intake or decreased renal excretion …
(renal one is usually due to inability to suppress ADH…if you can’t suppress ADH you produce less urine thus increasing TBW and diluting out your Na)
Timing of acute v. chronic hyponatremia
Acute: <48h
Chronic: >48 h or unknown amount of time
Sx of hyponatremia
Usually present at <125mEq/L
HA, fatigue, dizziness, nausea, gait instability/falls, confusion, psychosis, seizures, coma due to cerebral edema
Whats the 2 step systematic approach to dx hypoN
- Measure serum osmolarity to determine if hypoN is hypotonic (true), isotonic or hypertonic (secondary)
- If it is hypotonic, assess fluid volume status because each volume status correlates w/ diff. etiologies.
2a. Measure random urine Na level and urine osmolarity to weed out etiology. If considering SIADH, take serum uric acid. If low, could be SIADH.
What’s special about the labs in hyponatremia?
Must be drawn simultaneously ideally before any tx is given b/c that could alt. lab values
Hypovolemia PE
HypoTN Orthostatics Tachy Poor cap refill Increased skin turgor Dry mucosa/fissuring Flat JV Decreased urine output >50% collapse of IVC during inspo on ECHO
Hypervolemia PE
HTN, Edema, JVD, Dilated IVC on ECHO
Etiology:
- Hypovolemic
- Urine osm>300
- Urine Na>20
RENAL FLUID LOSS
- diuretic excess
- adrenal insufficiency
- osmotic diuresis
- post obstructive diuresis post hydronephrosis
- RTA
- cerebral salt wasting
- salt losing nephropathy
Etiology:
- Hypovolemic
- Urine osm>300
- Urine Na<20
EXTRARENAL FLUID LOSS
- V/D
- 3rd spacing (burns, pancreatitis)
- Blood loss
- Sweating
- Lung losses
Etiology:
- Euvolemic
- Urine osm<100
Psych issue causing primary polydipsia
Etiology:
- Euvolemic
- Urine osm>300
- Urine Na>20
-SIADH (tumor i.e. paraneoplastic syndrome pf #1 SCLC, CNS/pulm, SSRI, Nausea, Pain, hypoxia)
- Hypothyroid
- Adrenal insufficiency
- Thiazides (one of the most common causes!!!)
Etiology:
- Hypervolemic
- Urine osm>300
- Urine Na<20
Nephrotic syndrome
CHF
Cirrhosis
all these lead to a defective circ. volume –> RAAS activation
Etiology:
- Hypervolemic
- Urine osm>300
- Urine Na>20
Acute or chronic kidney failure (will have low GFR)
How is SIADH dx?
Exclude cortisol def., hypothryoid, other causes
Most common causes of SIADH
SCLC!
Post-op!
Pulmonary disorders
Nervous system disorders
What drugs are associated w/ SIADH
Antidepressants Anticonvulsants Antipsychotics Cyclophosphamide for cancer Opiates MDMA
Correction of acute hyponatremia
Can have rapid correction w/ little risk of ODS
Correction of chronic hyponatremia
-Raise by 8-10 mEq/L/day w/ no more than 18mEq/L in first 48 hours
If a pt is seizing (a complication of hypoN), what should you do?
Give HYPERTONIC SALINE (3%) to quickly raise Na by 3-4 mEq/L and stop sizure. Then slowly raise to normal.
How to fix an overcorrection of Na?
- D5W i.e. free water
- DDAVP i.e. desmopressin
- D5W and DDAVP
- Discontinue therapies that are raising Na
Tx for hypovolemic hypoN (both renal and extrarenal)
- Isotonic saline if w/o sx
- Hypertonic saline if w/ sx
Tx of euvolemic hypoN due to primary polydipsia
- Water restriction
- Hypertonic saline if w/ sx
Tx of euvolemic hypoN due to SIADH
- Water restriction
- Furosemide
- Salt or urea tabs
- Vaptans to inhibit ADH in kidney
- Demeclocycline
-Other tx: thyroid replacement, prednisone, discontinue thiazine
Tx of hypervolemic hypoN (both etiologies)
Water restriction and Furosemide
Sx of ODS
- Dysarthria and dysphagia
- Paralysis
- Behavior issues
- Pseudobulbar palsy
- Seizures
- Lethargy
- Confusion
- Coma (*locked-in syndrome…terrifying)
- Death
Dx of ODS
MRI Head. Initial normal MRI does not R/O ODS b/c it can take 4 weeks for MRI abnormalities to be seen.
Steps of developing ODS
- Normal brain w/ normal osmolality
- Sudden onset of hypotonic state
- Water moves ECM to ICM b/c there are more solutes IN the cells
- Rapid adaptation: we try to fix the edema by having Na, K, and Cl leave our cells so water will follow
- Slow adaptation: organic osmolytes leave
- BRANCH POINT:
- proper therapy: slow increase of osmolytes and Na, K, Cl, etc.
- overcorrection: cells shrink, axonal shear damage, BBB disruption all lead to demyelination
