Inpatient / Nephrology


Last Updated: 2/12/2023

# *** Hyponatremia [symptomatic; acute vs. chronic >48 hours; mild 130-134, moderate 120-129, severe <120]

-- ABCs: 
if severe (<120) or symptomatic, page renal and consider ICU due to need for close monitoring and frequent lab draws
-- Chart Check: baseline Na, medication use
-- Admission Criteria: *** no strict criteria
-- HPI Intake: diet, alcohol, meds, co-morbidities including CHF, cirrhosis, ESRD, cancer
-- Can't Miss: *** EtOH use, seizure risk, rapid overcorrection
-- Admission Orders: *** serum Osm, Urine Osm, Urine Na, strict I/O's, BNP if evidence of CHF; fluids vs diuretics
-- Initial Treatment to Consider: if severe with symptoms - immediate hypertonic (3%) saline 100mL bolus over 10 mins to get Na up 4-6 points

-- History: *** meds, diet, EtoH use, hx of CHF, cirrhosis, CKD, cancer, endocrine disorder
-- Clinical: *** seizure, N/V, weakness
-- Exam: *** AMS, weakness, volume exam
-- Data: *** Na, Serum Osm, Urine Osm, Urine Na (SOsm <300 if hypotonic, UOsm >100 if ADH present, UNa <30 if RAAS active)
-- Etiology/DDx: *** hypovolemia, decreased effective circulating volume (3rd spacing), SIADH (infection, malignancy, meds, primary brain injury or lesion), ESRD, primary polydipsia, low solute

Working Through The Differential:
Is this hypotonic hyponatremia? (SOsm <300) - if not, "pseudohyponatremia" from hyperglycemia, protein
Is ADH present? (UOsm > 100) - if not, primary psychogenic polydipsia, tea and toast, beer potomania
Is RAAS On? (UNa <30) - if yes, hypovolemia or 3rd spacing 2/2 CHF or cirrhosis; if no, salt wasting via SIADH, diuretic use, ESRD, or endocrine etiology

The patient's HPI is notable for ***. Exam showed ***. Labwork and data were notable for ***. Taken together, the patient's presentation is most concerning for ***, with a differential including ***.

-- Serum Osm, Urine Osm, Urine Na
-- if unclear etiology, can also send TSH, lipid screen, SPEP/UPEP, serum cortisol and ACTH, UDS, BNP
-- BMP q ***

-- Correction Goal: *** at a rate of 4-6 per 24 hours
-- Volume: *** (IVF vs diuresis) Severe with Sxs - 3% NaCl 100mL bolus over 10 min (to Na raise 1-3) given up to 3x to get Na up 4-6; Severe without Sxs - 3% Na Cl drip until Na >125; Otherwise, volume repletion by exam
-- if ADH Absent - restrict fluids, slow introduction of solute; high risk of overcorrection
-- if ADH on, RAAS Active - replete if hypovolemic, diuresis if CHF, nephrotic syndrome
-- if ADH on, RAAS Off - likely SIADH, restrict 0.8L/day, salt tabs 1g TID; consider Lasix, vaptans

If You Remember Nothing Else

Hyponatremia is a common (often incidental) finding in the inpatient setting. It is often clinically insignificant and will correct on its own with treatment of the patient's underlying disease process (usually giving fluid or diuretics), but in severe circumstances will lead to symptoms and require renal involvement and hypertonic (3%) fluid administration to rapidly raise the sodium to get it out of the severe symptomatic range.

Hyponatremia represents an excess of water compared to sodium and thus determining the etiology comes down to whether your body is holding on to water appropriately or not. The most common causes are by far hypovolemia, decreased effecive circulating volume (3rd spacing) from CHF or cirrhosis, and ESRD. In general, if SOsm is <300 it is true hyponatremia, if UOsm is >100 then ADH is present, and if UNa is <30 RAAS is active.

Osmotic Demyelination Syndrome (ODS) is the feared complication of overcorrection >8 in 24 hours or >18 in 48 hours since it can lead to locked-in syndrome. However, there is low risk overall if starting Na is >120. Be on alert and get renal involved if Na <105, the patient has chronic malnutrition, or uses EtOH as these all increase the risk of ODS. If you overcorrect, give D5W.

Clinical Pearls

  • Differentiate between acute vs. chronic >48 hours; mild 130-134, moderate 120-129, severe <120; symptomatic vs asymptomatic
  • Hyponatremia is seen in up to 30% of hospitalized patients
  • Hyponatremia is a relative excess of water compared to sodium in extracellular space - more commonly caused by excess water rather than depleted sodium
  • Hypothalamus responds to tonicity, not volume - if hypertonic, makes you thirsty or releases ADH which reabsorbs free water in the collecting ducts
  • Tonicity implies there is a membrane - anything that is an “effective” osmole can’t go through the membrane on its own - think Na+, K+, Glucose, etc; BUN, ethanol, lactate are all “ineffective” - they move between membranes and thus don’t impact tonicity
  • Sodium drives almost all of tonicity since it is the most important osmotically active particle in the extracellular space; remember the equation for serum osmolality is 2*Na + BUN/2.8 + glucose/18; note that BUN contributes to serum Osm, but is not and effective osmole
  • Tonicity impacts fluid shifts, and thus cell size. Fluid going into or out the cells (swelling vs shrinking) is what leads to clinical manifestations of hyponatremia, mostly when it affects the cells in the CNS
  • A short-term goal for severe hypoNa is to get Na >125, and in most cases raising sodium 4-6 will help alleviate many of the life-threatening symptoms when you give hypertonic saline
  • NEVER bolus free water - if you do by accident, give hypertonic fluid to even out
  • Osmotic Demyelination Syndrome (ODS) is the feared complication of overcorrection >8 in 24 hours or >18 in 48 hours - can lead to locked-in syndrome; low risk overall if starting Na is >120; risks include Na <105, chronic malnutrition, EtOH use; if overcorrected give D5W
  • K and Na are freely exchanged - if you replete potassium, you are essentially giving Na - make sure you are careful not to overcorrect in severe chronic cases
  • Is this hypotonic hyponatremia? (SOsm <300) - Isotonic “pseudohyponatremia” is caused by hyperproteinemia from myeloma, lipidemia; Hypertonic "hyponatremia" can be caused by hyperglycemia (not actual hyponatremia, its a lab issue - need to correct), mannitol, sorbitol, and IVIG
  • Is ADH present? (UOsm >100; ranges from 50-1200) - if ADH Absent - kidney not able to dilute any further - too much H2O or not enough solute - primary psychogenic polydipsia (too much water), marathon (mix of too much water in the setting of low solute), tea+toast (low solute), beer potomania (low solute)
  • A shortcut to calculate UOsm - the last two digits on Serum Gravity on UA x30 can approximate UOsm
  • Tea+Toast is a weird and unintuitive case where hyponatremia is not driven by ADH - you have a mininum amount of solute you need to eliminate free water into your urine since the minimal UOsm your kidneys can dilute to is 50 - if you don't take in enough solute in your diet, your kidneys can't physiologically put more urine out
  • ESRD limits ability of kidneys to maximally dilute and concentrate urine and thus can affect our inerpretation of UOsm
  • Is ADH appropriate? (in response to high Osm or sensed decreased effective circulating volume) In other words, is RAAS on or off? (UNa <30 suggests RAAS is on); note these measures are less reliable if on diuretics - utilize FeUrea; if RAAS on (UNa <30) - hypovolemia or 3rd spacing (decreased effective volume); if RAAS off (UNa >30) - salt wasting via SIADH, diuretic, ESRD, adrenal
  • Common causes of SIADH include pneumonia, malignancy (ectopic ADH from small cell lung cancer), meds including SSRIs and AEDS, and primary brain injury or lesion
  • Note thay diuretics increase UNa, and in such cases FeUrea <55% can be used to suggest RAAS is on
  • These buckets are of course fluid and patients don't always fit nicely into one or the other

Trials and Literature

  • Review of disorders of plasma sodium (NEJM, 2015)
  • A study comparing the utility and limitations of different frameworks for approaching hyponatremia - in sum, relying on volume status in the framework will lead to challenges since this is often difficult to interpret (Am J Med, 2010)

Other Resources