This document provides guidelines for the diagnosis and management of hyponatremia. It defines hyponatremia as a serum sodium concentration of less than 135 mEq/L. It notes that hyponatremia is commonly seen in hospitalized patients and can cause neurological symptoms if left untreated. The guidelines recommend a systematic approach to hyponatremia involving assessing volume status, urine and serum osmolality to determine the cause (hypovolemic, euvolemic, or hypervolemic), and correcting any underlying conditions and sodium levels slowly to avoid complications. Newer vasopressin receptor antagonists called vaptans can be useful for treating euvolemic or hypervolemic hy

1. HYPONATREMIA - GUIDELINES
Dr. Ratan Jha (consultant
nephrologist)
Dr. Mohd Viquasuddin (dnb resident)

2. introduction
• Diagnosis and management of hyponatremia is
challenging
• inappropriate treatment can be harmful.
• is often missed, misdiagnosed or poorly managed
• can cause substantial morbidity, mortality
• No single treatment protocol so often mismanaged.
• Rapid correction is frequently associated with
increased morbidity and mortality.
• Recently available vasopressin-receptor antagonists
(Vaptans) are specific and more effective method to
treat hyponatremia.

3. Prevalence & epidemiology
• Most common electrolyte disorder
• Affects 15 -30 % of hospitalized patients
• Affects 7 % of ambulatory patients
• Causes 1 million hospitalizations/ year
• Higher incidence in cirrhosis and heart failure
• Higher incidence in geriatric populations
• Hospital acquired hyponatremia common

5. Risk factors
• Primarily due to elevated Vasopressin (ADH)
• ADH released due to elevated plasma
osmolality and hypovolemia / hypotension
• ADH cause excess water reabsorption
• Etiology based on classification
• 1. hypovolemic
• 2. euvolemic
• 3. hypervolemic

6. Hypovolemic hyponatremia
• Decreased Total body water and Na , greater decrease in Na
• Gastro-intestinal losses : diarrhea, vomiting
• 3rd space losses : burns, pancreatitis, peritonitis,
rhabdomyolysis
• Renal losses : diuretics, mineralocorticoid deficiency.
• osmotic diuresis : glucose, mannitol, urea
• Salt losing nephropathies : interstitial nephritis, medullay
cystic kidney disease, partial urinary tract obstruction,
polycystic kidney disease.

7. Euvolemic hyponatremia
• Increased Total body water with normal total
body Na
• Drugs : carbamazepine, clofibrate, opioids,
cyclophosphamide, NSAID’s, oxytocin.
• Disorders : addison’s disease,
hypothyroidism,SIADH
• Increased intake of fluids : primary polydipsia
• Non-osmotic release of ADH : nausea, pain,
emotional stress

8. Hypervolemic hyponatremia
• Increased Total body Na with a greater
increase in Total body water
• Extra-renal disorders : cirrhosis, heart failure
• Renal disorders : acute kidney injury, chronic
kidney disease, nephrotic syndrome

12. Why neurological symptoms ?
• Symptoms are primarily neurological
• Reduction in ECF not responsible
• increase in volume of ICF responsible
• particularly in the volume of brain cells
• Hyponatremia leads to hypoosmolality of ECF, so water
moves into cells (ICF).
• Swelling of brain cells in enclosed space with fixed volume
of rigid skull leads to increased intracranial pressure
resulting in reduction of cerebral blood flow causing
hypoxic brain damage.
• if left untreated, can lead to herniation of the brain stem
into the foramen magnum

13. Chronic hyponatremia
• hyponatremia lasting more than 48 hours or with
an unknown duration
• neurological symptoms are less
• in gradually developing hyponatremia, brain cells
compensate by cellular exit of solutes that
promote water loss and lessen brain swelling
• not necessarily “asymptomatic”
• can cause osteoporosis due to increased bone
resorption

14. Approach to Hyponatremia
• requires a systemic and sequential approach
• Step 1. History and examination.
• Step 2. Assessment of serum osmolality to confirm
diagnosis of true hypotonic hyponatremia and rule out
misleading results (hypertonic hyponatremia and
pseudo-hyponatremia).
• Step 3. Approach to true hypotonic hyponatremia by
assessment of volume status and urine sodium
concentration.
• Step 4. Laboratory tests to assess underlying causes of
hyponatremia.

15. Step 1
• detailed history and examination needed
• Vomiting, diarrhea with hypotonic fluid ingestion, recent surgery,
improper IV fluid administration
• Associated diseases (i.e. psychiatric illness, CHF, cirrhosis, renal
failure)
• Recent head injury, intracranial surgery, subarachnoid hemorrhage,
stroke, brain tumor, meningitis or brain abscess can cause SIADH.
• Cough, shortness of breath, or pleuritic chest pain should prompt
consideration of respiratory causes of SIADH
• Use of medications
• Skin turgor, mucous membrane appearance and postural
hypotension
• Detection of ascites, peripheral edema, pulmonary rales and S 3
• Measuring blood pressure, JVP, CVP and PCWP

16. Step 2
• Measure plasma osmolality with osmometer
• osmometer provides actual (correct) osmolality
• Normal plasma osmolality is 280 - 295 mOsm/kg
• low plasma osmolality (POsm < 280 mOsm/kg)
confirms diagnosis
• normal plasma osmolality (POsm 280–295 mOsm/kg)
suggests isotonic pseudo hyponatremia : check for
hyperproteinemia, hyperlipidemia
• high plasma osmolality (POsm > 295 mOsm/kg)
suggests hypertonic hyponatremia : check for
hyperglycemia, mannitol therapy and contrast dyes.

17. Step 3
• classified into hypovolemic, hypervolemic and
euvolemic
• treatment protocols are absolutely different in
all three categories
• Volume status should be measured
• Urinary sodium should be measured

19. Diagnostic criteria for SIADH
• Essential diagnostic criteria for SIADH
• • Decreased measured serum osmolality (<275 mOsm/kg
H2O)
• • Clinical euvolaemia. Exclude hypovolemia and
hypervolemia
• • Urinary osmolality >100 mOsm/kg H2O during hypo-
osmolality
• • Urinary [Na+] >40 mmol/L with normal dietary sodium
intake
• • Normal thyroid and adrenal function. Exclude renal
failure and use of diuretic agents within the week prior to
evaluation
• • No hypokalemia, no acid base disorders

20. Diagnostic criteria for SIADH
• Supporting diagnostic criteria for SIADH
• • Serum uric acid <4 mg/dL
• • Blood urea nitrogen <10 mg/dL
• • Fractional sodium excretion >1%; fractional
urea excretion >55%c
• • Failure to improve or worsening of
hyponatremia after 0.9% saline infusion
• • Improvement of hyponatremia with fluid
restriction

21. Step 4
• Check urine Osmolality with osmometer.
• distinguishes between hyponatremia with normal
water excretion and hyponatremia due to
impaired water excretion
• Urine osmolality below 100 mOsm/kg indicates
that antidiuretic hormone (ADH) secretion is
completely and appropriately suppressed
• urine osmolality exceeding 100 mOsm/kg
indicates impaired water excretion which reflects
impaired renal diluting mechanism (SIADH)

22. Step 4
• urine osmolality and urine Na helps in differential
diagnosis of the etiology of hyponatremia
• Urine Na (>40) and urine osmolarity(>150) will be
high in SIADH, adrenal insufficiency & cerebral
salt wasting syndrome
• Low Urine Na (<30) and high urine osmolarity
(>150) indicate hypovolemia
• Low values of serum uric acid and blood urea
favour euvolemic hyponatremia
• high values of serum uric acid and blood urea
favour hypovolemic hyponatremia.

23. Step 4
• Specific etiologic tests
• Blood sugar: To rule out hyperglycemia
• Serum creatinine: To rule out renal failure
• Serum protein: High in multiple myeloma and low in cirrhosis of liver
• Serum triglycerides: To rule out pseudohyponatremia
• Serum potassium: High in Addison's disease and low in person with
diuretics therapy, diarrhea and vomiting.
• Thyroid function tests: To rule out hypothyroidism
• Adrenal functions: ACTH & ACTH stimulation tests to rule out Addison's
disease.
• Acid-base balance: Metabolic alkalosis occurs in diuretic use or vomiting.
Metabolic acidosis occurs in diarrhea or laxative abuse and primary
adrenal insufficiency.
• Head CT scan and Chest X-ray to rule out cerebral salt wasting syndromes

24. management
• manage underlying cause of hyponatremia
• Acute symptomatic hyponatremia may be
corrected relatively rapidly
• serum sodium should not be raised more than
8-10 mEq in first 24 hours
• Chronic asymptomatic hyponatremia should
be corrected slowly
• Rate of serum sodium correction may be 6-8
mEq in 24 hours.

25. Serum sodium <120 mEq/L
– 1. Water restriction to raise s. Sodium level
– 2. 3% saline (hypertonic saline) or
– 3. Diuretic + oral salt
– Correction with hypertonic saline is more predictable
(accurate)
– careful with management of hyponatremia and may
require hospitalization and regular monitroing.
– Once serum sodium reaches 120 mEq/L then vaptan
may be initiated if underlying cause cannot be
corrected

26. Serum sodium 120-135 mEq/L
– Asymptomatic – water restriction initially, if not
controlled – use vaptans
– Symptomatic – water restriction initially along
with vaptan
– (as water restriction will not work for long term,
compliance issue with water restriction)

27. Acute symptomatic
--Fluid restriction
– 3% sodium chloride (hypertonic saline)
• If rate of correction is rapid use 5% dextrose
• Acute asymptomatic (Less likely)
• Fluid restriction

28. Chronic asymptomatic
– Fluid restriction
– Improve protein intake in elderly
-- Data suggests chronic asymptomatic hyponatremia
develop cognitive dysfunction, bone demineralization and
likely to develop symptomatic hyponatremia
chronic hyponatremia patients should be treated
•
– Severe hyponatremia should be treated
• Fluid restriction
• 3% saline (hypertonic saline)
• If hyponatremia is persistent, vaptans may be started/added once
serum sodium reaches >120 mEq/L with other interventions
•

29. Use of vaptans in hyponatremia
– Euvolemic and hypervolemic hyponatremia
– Chronic symptomatic hyponatremia where underlying cause can not
be corrected and long term treatment is required
– Can be started once serum sodium >120 mEq/L
– For initiating vaptan patient should be admitted for 3-4 days, i.e.
Vaptan therapy should be initiated in hospital
– Monitoring of serum sodium after discharge, initially at 3-4 days, then
every 15 days for a month and then monthly monitoring till therapy is
continued
– Liver function should be monitored intially, at 15 days for 2-3 months
and then every 3 monthly
– Ensure proper intake (good quantity) of water (fluid) while patients
are on vaptan
– Vaptan (tolvaptan) is contraindicated if patient can not drink
water/can not feel thirst
– Vaptans produce good quanttiy of water loss

30. ….
• thank you
• The end