Moffitt Morning Report Pearls: Hyponatremia!

Thank you to Kendra W. for presenting an awesome case of an elderly woman who presented with AMS, found to be hyponatremia with a Na 113. Her hyponatremia was attributed to volume overload in the s/o heart failure, and she improved with diuresis.

TLC (Tim and Laura, your Chiefs)

 

Definition

  • Definition: Na < 135
  • Why? Either too much water, or too little sodium

Why is it important? Consequences of severe, untreated hyponatremia include:

  • AMS
  • Seizures
  • Coma
  • Herniation and death (usually in hyper acute causes)

Diagnostic workup:

Step 1: Is sodium the problem (AKA: Is the blood hypotonic)? Check serum osms!

How much stuff (aka solute) is in the blood? Sodium is the major solute, so if sodium really is low then the serum osms should also be low unless there is another process going on. Test = serum osms! Can order this from the lab or calculate it.

  1. High serum osms (>295): Hypertonic hyponatremia: Presence of osmotic substrates– glucose, mannitol, maltose/sucrose (IVIG). Remember to correct for hyperglycemia: glucose >100, every additional 100, Na = +1.6
  2. Normal serum osms (280-295): Pseudohyponatremia (high proteins/lipids), mixed picture
  3. Low serum osms (<280): Go to step 2

Pearl: Measured sodium includes non-osmoticly active things like glycol. Calculated does not have glycine and such in it). If the measured serum osms are normal but calculated are low, it may be because of high ethanol concentrations

Step Is the kidney responding appropriately (AKA: is ADH off?) Check urine osms!

ADH causes increased reabsorption of water at the collecting ducts. In hyponatremia, you want to get rid of the excess water, so ADH should be off. Test = Urine osms!

  1. If urine osms <100: That means the problem is not in the kidney, it’s in how much water or salt you’re taking in.
    • Water = Primary polydipsia (12-20L a day) – psychosis, ecstasy, marathon running
    • Solute = Beer potomania/tea and toast – diet deficient in solute. This doesn’t allow the kidneys to produce as much urine as someone with normal solute intake.
  2. If urine osms >300: Proceed to Step 3

Pearl: If intermediate urine osm, or even if low, think about CKD. In severe renal disease, can’t concentrate appropriately, and may end up with hyponatremia.

Step 3: Is ADH on for a hemodynamic reason? (AKA: Low effective arterial blood volume) Check volume status and UNa!

Test: Volume exam, urine sodium (remember that we use FENA for AKI to tell if it’s pre renal. The same concept goes here. If you have low circulating blood volume, you should have low urine sodium).

  1. Hypovomeia: Hypovolemiaà RAASà ADH increases renal H2O absorb w/o more Na. Urine Na <20, pt orthostatic, JVP low, etc. Note UNa may be higher if diuretics on board or post-ATN diuresis
  2. Hypervolemic: Heart failure, cirrhosis, nephrotic syndrome. Typically urine Na <20

Step 4: Is ADH on for a non-hemodynamic reason? These are the euvolemic etiologies we think about.

  1. Euvolemic:
  • SIADH (malignancy, lung dx, intracranial, psych meds, chemo, DDAVP, pain, NSAIDs, HIV) (typically UNa >40)
  • Glucocorticoid deficiency / adrenal insufficiency (Check cortisol!)
  • Hypothyroid (Check TSH!)
  • Psychogenic polydipsia, tea+toast, beer podomania (Remember step 2, urine osms <100 for these bc ADH off vs. rest urine osms >300 as discussed above)

Treatment:

  • General principles:
    • Don’t correct too fast- Risk central pontine myelinolysis (see below)
    • If Na <118, involve renal and typically admit to the ICU, check Na q1-2hr
    • Pearl: Something that I didn’t know and learned this morning! Giving potassium will increase your sodium bc it’s osmotically active, so factor this in to your decision making regarding correction in hyponatremic patients!
  • Treatment by etiologies:
    • Hypovoemic: Give fluids and recheck
    • Euvolemic: Address underlying cause. Then also1st line = Free water restriction, 2nd line= Loop diuretic + salt tabs, 3rd line = Consider demeclocycline or vasopressin antagonists if refractory
    • Hypervolemic: Free water restriction, diurese, if HF vasopressin antagonists can be helpful (tolvaptan and conivaptan)
    • Can consider DDAVP to turn off kidneys and then give hypertonic saline to take control of the process, but only do this at the instruction of the renal team.

Complication of correction that is too rapid: Central Pontine Myelinolysis (CPM)

  • Do not correct sodium by more than 10meq/24hr
  • Higher risk population: Very low sodium <110 (in most cases), malnourished patients, alcoholics, pre-menopausal women, chronic hyponatremia (always assume chronic unless documented as acute in the hospital)

 

This review of hypernatremia has some helpful images:

Hyponatremia review

Evernote: https://www.evernote.com/shard/s638/sh/18d5bdee-6e84-4cc0-be60-a9cbb0543232/a8c36b391581e08a2f5348c330c58355

 

Advertisements

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out /  Change )

Google+ photo

You are commenting using your Google+ account. Log Out /  Change )

Twitter picture

You are commenting using your Twitter account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

Connecting to %s