HYPONATREMIA - GUIDELINES

Dr. Ratan Jha (consultant nephrologist)

Dr. Mohd Viquasuddin (dnb resident)

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.

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

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

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.

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

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

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

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

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.

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

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.

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

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

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

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)

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.

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

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.

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

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)

Acute symptomatic

--Fluid restriction– 3% sodium chloride (hypertonic saline)

• If rate of correction is rapid use 5% dextrose• Acute asymptomatic (Less likely)• Fluid restriction

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

•

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

….

• thank you• The end