HYPONATREMIA

DR SATISH K DHAM
SENIOR CONSULTANT(INTERNAL
MEDICINE(IMMUNOLOGY)
UMKAL HOSPITAL GURGAON
 HYPONATREMIA
• Defined as serum sodium below 135meq/l
• Mild 130mq/moderate up to 120mq/l and severe<
120mq/l
• Most common disorder of electrolyte, occurring in more
than 22% of hospitalized ICU patients
• Generally considered a disorder of water as against a
disorder of salt,ie results from increased water retention
 HYPONATREMIA
• Recognition important as acute severe
hyponatremia can cause significant morbidity and
mortality.
• Rapid correction of chronic hyponatremia can
result in severe neurological complications and
even death.
 HYPONATREMIA
• To maintain a normal sodium, ingestion of
water must be matched with an equal
amount of water excretion.
• Any process that limits the elimination of
water, or expands the volume around a fixed
sodium content may lead to decrease in
sodium concentration.
 HYPONATREMIA
STEPS REQUIRED FOR THE KIDNEY TO EXCREATE A WATER LOAD
1 Glomerular filtration and delivery of water and electrolytes to the diluting
sites of nephron.
2Active reabsorption of Na and Cl without water in the thick ascending limb of
the loop of Henle.
3 Maintenance of dilute urine due to impermeability of the collecting duct to
water in the absence of ADH.
ABNORMALITES IN ANY OF THE STEPS CAN RESULT IN IMPAIRED FREE WATER
EXCRETION AND HYPONATREMIA
 HYPONATREMIA
• Na is mainly extracellular, K is intracellular
• Osmolality is defined as the number of osmoles of solute per kilogram of
solvent Osm/kg.
• Serum osmol = 2(Na)+ BUN/2.8 + Gluc/18
• Sodium is the primary determinant
• Serum osmol tightly regulated (275 – 290)
• Mechanisms for regulation(renal water handling)
• If osmol↑ → 1. thirst mechanism, 2. ADH↑
• ↓Effective circulating volume also → ADH↑
 HYPONATREMIA
• Causes of expansion of space around the Na content.
• Pseudohyponatremia Increase plasma protein or lipids.
• Hyperosmolar hyponatremia as seen in hyperglycemia drawing water in ECF
diluting Na(1.6 to2.4meq/l for every 100mg/dl rise in plasma glucose.
• Post TURP Syndrome.Glycine,mannitol,sorbitol can be absorbed in the ECF
during bladder irrigation.
• Psychogenic Polydipsia, beer potomania,tea and toast diet. Water ingested
exceeds the capacity of water excretion by kidneys
 PATHOPHYSIOLOGY

• Simply, hyponatremia is due to inability to match water excretion with

water ingestion
• 1. Defect in water excretion
• SIADH (inappropriate ADH release)
• Hypovolemic state(appropriate ADH release)
• Hypervolemic, CHF, Cirrhosis, Nephrotic syndrome
 DEFINING HYPONATREMIA

• Abnormal ratio of Na to water

• Na < 135

• Most often due to retention of free water

• 2ndary to impaired excretion of free water

• Occ. due to Na loss exceeding water loss

• i.e. thiazide-induced hypoNa (elderly women)
 CLINICAL MANIFESTATIONS

• INTRACELLULAR WATER SHIFT LEADING TO CEREBRAL EDEMA

SYMPTOMS DEPENDENT ON SEVERITIY AND RAPIDITY OF FALL OF Na
• <2 days, SYMPTOMS INCLUDE nausea, malaise, headache, confusion,
stupor, seizures and coma.
• IN chronic >3 days adaptive mechanisms protect and minimize increase in
ICF
 WORKUP

• First test to obtain: serum osmolality

• Helps exclude two easier to remember causes of hyponatremia
• 1. Hyperosmolar hypoNa (osmo > 290)
• Hyperglycemia, mannitol
• 2. Iso-osmolar hypoNa (nl serum osmo)
• Severe hyperlipidemia or hyperproteinemia
• “pseudohyponatremia” not a true hypoNa
 WORKUP
• Hypo-osmolar hypoNa (most common)
• Three types (based on volume status)
• Hypervolemic (congested states)
• CHF, cirrhosis, nephrotic syndrome, ARF / CRI
• Hypovolemic (appropriate ADH secretion)
• renal loss (diuretics, nephropathy, hypoAldosteron)
• GI loss (vomiting, diarrhea, NGT)
• Skin loss (sweating, burns, cystic fibrosis)
• Peritonitis or sepsis
 WORKUP
• Euvolemic (normal volume state)
• SIADH
• Pain and nausea can cause non-osmotic ADH release
• Post-op state, especially TURP
• Hypercortisolism or hypothyroidism
• Psychogenic polydipsia (water intoxication)
• Reset osmostat(pregnancy, psych disorders)
• In this case, body thinks “normal” is lower -> no Tx
 WORKUP

• Next lab value: Urine osmolality

• Is free water excretion, or ability to dilute the urine, intact in the face of
hypoNa?
• Remember: problem is too much water
• Normal physiologic response = excrete water
• If Uosm < 100, means appropriate excretion of dilute urine
• Psychogenic polydipsia or reset osmostat
• If Uosm > 200, reflected impaired water excretion (usu due to inability to
stop ADH)
 WORKUP

• Final lab value: Urine sodium

• UNa < 30 implies hypovolemic or reduced effective circ
volume (CHF, nephrotic, cirrhosis)
• Kidneys reabsorb solutes to retain water and volume
• UNa > 30 seen in the euvolemic types
 TREATMENT URGENT

• If symptomatic & urgent, give hypertonic saline

• Do not correct more than 8mEq / day

• Risk of central pontine myelinolysis(CPM)

 TREATMENT OF ASYMPTOMATICS
• Correct the underlying cause in the DDx
• Hypovolemic → give volume
• Hypervolemic → Na & water restriction
• Loop diuretics if CHF or nephrotic syndrome
• Tolvaptans
• Euvolemic → water restriction (because excretion can’t match it)
• Specifics: if it’s hypothyroid → give thyroxine
• Also use loops or, rarely, demeclocycline - causes opposite problem
(diabetes insipidus)
• TOLVAPTAN
 SUMMARY

• If asked to work-up hypoNa, first: H&P

• History of fluid loss (vomit/diarrhea) or diuretics.
• On exam: mucous membranes, skin turgor, peripheral edema/ascites (CHF or cirrhosis)
• Labs: ask for serum osmolality FIRST
• Rule out the hyper & iso-osmolar forms
• #2: assess volume status if hypo-osmolar
• Determine if it’s Hyper- / Eu- / Hypovolemic form
• Ask for urine osmolality & urine sodium
• Identify the cause of hypoNa, then treat
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