SODIUM
By Dr.Keerthana
EDPG-1
TOTAL BODY WATER
Calculation of TBW
• Children and adult men: Body weight (kg)*0.6
• Adult women: Body weight (kg)*0.5
• Elderly men: Body weight (kg)*0.5
• Elderly women: Body weight (kg)*0.45
WATER REGULATION
1)Response to water deficit:
• Water intake is regulated by thirst and its stimuli are
*Dehydration
*Fall in BP
*Increased solute concentration
• Water excretion is regulated by ADH
2)Response to water excess:
• Decrease ADH:
Water reabsorption by collecting duct decrease and urine output
increases
• Increase in ANP:
Volume expansion lead to increased secretion of ANP due to atrial
stretching which promotes diuresis and natriuresis
SODIUM
• Major ECF cation
• Normal Na: 135-145mEq/l
• 85-90% sodium is extracellular
PLASMA INTERSTITIUM ICF 0.9% 3% RL
NS NS
142 mEq/l 144 mEq/l 10 154 513 130mEq
mEq/l mEq/l mEq/l /l
• Sodium is responsible for >90% of total osmolality of ECF
• Maintain ECF volume and blood pressure
• ECF volume is reflection of total body sodium content
• Daily requirement of sodium is <2.3 grams of sodium or about 5
grams of sodium chloride
• Salt is about 40% sodium
• 1 gram of salt contains about 400mg of sodium
SODIUM REGULATION
1)Response to sodium deficit:
• Deficiency of sodium in body will lead to hypovolemia and activates
Angiotensin-2 and aldosterone
• By acting on the kidneys, Angiotensin-2 helps to increase sodium
absorption at proximal tubules
• Aldosterone acts on the kidneys at the collecting duct and help in
absorption of sodium and water
2)Response to sodium excess:
• Excess sodium lead to increased ECF volume leading to decreased
angiotensin-2 , aldosterone and increased ANP
• Decreased angiotensin-2 and aldosterone leads to decreased renal
reabsorption of sodium
• Increased ANP will lead to natriuresis and diuresis
• When two solutions are separated by a membrane that is permeable
only to water, water moves into the compartment with more
concentrated solution to equalise the ion concentration in each
• The force driving this movement is the osmotic pressure
• Sodium contributes the most to the osmotic pressure
• Others: anions like HCO3- , Cl- and glucose
Formula to calculate effective osmolality
Effective osmolality = 2[Na] + glucose/18
Normal range: 275-290 mOsm/L
ECF CONCENTRATION DISTURBANCES:
• Sodium is the most important osmotically active ion in ECF
• So change in serum sodium concentration produces change in
osmolality
• Major abnormalities in fluid concentration are
*Hyponatremia
*Hypernatremia
HYPONATREMIA
• Hyponatremia is defined as the serum sodium less than 135 mEq/l
• In the setting of normal water intake, high circulating levels of ADH
with subsequent water retention are a prerequisite for development of
hyponatremia
• Urine osmolality is always >100 mOsm/l with the exception of
psychogenic polydipsia
• Concentration of sodium does not give information regarding volume
status
• First step in evaluation should include clinical evaluation of ECF
volume status and comparing measured and calculated plasma
osmolalities
• Plasma osmolality is calculated by
2[Na] + (glucose/18) + (BUN/2.8)
HYPONATREMIA :
Hyperosmolar Hyponatremia
Iso-osmolar Hyponatremia
Hypo-osmolar Hyponatremia
HYPEROSMOLAR HYPONATREMIA
• Plasma osmolality >295 mOsm/l
• Occurs when large quantities of osmotically activate solutes
accumulate in ECF space
• There is movement of water from ICF to ECF, thereby diluting the
ECF sodium
• Commonly happens with severe hyperglycemia
• Each 100mg/dl increase in plasma glucose above normal level of
100mg/dl , decreases serum sodium by 1.6 mEq/l
• Other causes of hypertonic hyponatremia are administration of
osmotic agents such as mannitol, glucose and maltose causing an
osmolar gap and hyponatremia
• Osmolar gap is the difference between measured osmolality and
calculated osmolality
• Normal: around 10 mOsm/l
• If it is >15 mOsm/l, it means that a non detectable agent with osmotic
activity is present causing an osmolar gap
• A consequent osmotic diuresis will cause sodium deficit with volume
depletion
ISO-OSMOLAR HYPONATREMIA
• Plasma osmolality: 275-295 mOsm/l
• Pseudohyponatremia is a factitiously low value of sodium that occurs
in severe hyperproteinemia or hyperlipidemia yielding a measurement
error
• High concentrations of lipids or proteins can displace serum water,
which causes laboratory misinterpretation of normal sodium
• Patients are asymptomatic
• Treatment is not needed
HYPO-OSMOLAR HYPONATREMIA
1) Hyponatremia with hypovolemia:
• Extrarenal loss (urinary sodium <15 mEq/l)
*Vomiting
*Diarrhoea
*Peritonitis
• Renal loss (urinary sodium >20 mEq/l)
*Excessive diuretics
*Salt losing nephropathy
*Cerebral salt wasting syndrome
2) Hyponatremia with hypervolemia:
• Urinary sodium <20 mEq/l:
*CHF
*Cirrhosis
*Nephrotic syndrome
• Urinary sodium >20 mEq/l:
*Renal failure
3) Hyponatremia with euvolemia:
Urinary sodium >20 mEq/l
*Psychogenic polydypsia
*SIADH
*Glucocorticoid deficiency
*Drug induced
*Hypokalemia
*Hypothyroidism
Clinical features of Hyponatremia
MILD MODERATE SEVERE
Anorexia Personality changes Drowsiness
Headache Muscle cramps Diminished reflexes
Nausea Muscular weakness Convulsions
Vomiting Confusion Coma
Lethargy Ataxia Death
Physiological basis of clinical features
Hyponatremia leads to hypo-osmolality of ECF
In brain, water moves into ICF and cells swell
Causes increase in ICP causing decrease in cerebral blood flow
Hypoxic brain damage
• In severe cerebral edema, increased brain cell volume results in
significant increase in ICP leading to herniation
• Herniation is characterised by
*Unequal or fixed dilated pupils
*Hypoventilation
*Cardiovascular instability
*Urinary or faecal incontinence
*Respiratory arrest
Diagnosis
• History
• Physical examination
• Diagnostic tests
Serum Sodium
Serum osmolality
Urinary sodium
Urine osmolality
• Acute (<24 hrs) or Chronic (>48 hrs) Hyponatremia
• If urine osmolality is not readily available from the laboratory, it can
be estimated using urinary specific gravity
• Consider the numerals in hundredths and thousandths decimal places
of specific gravity as whole numbers and multiple them by 35 to
obtain urine osmolality
• Example: specific gravity-1.005
Urine osmolality = 05*35= 175 mOsm/l
• Plasma osmolality:
If normal - Pseudohyponatremia
• Urine osmolality:
If <100 mOsm/l or specific gravity <1.003 – primary polydypsia
If >100 mOsm/l – other causes of hyponatremia in which water excretion is
impaired
• Urine sodium:
If <1O mEq/l : Effective volume depletion (diarrhoea, vomiting) and in
edematous patients
If >20 mEq/l : Other causes of hyponatremia
Treatment
Based on
• Severity of symptoms
• Rate of onset
• Volume status
• Serum sodium
Symptomatic or acute (<2 days):
• Treat the underlying cause
• Water restriction
• Hypertonic 3%NaCl at rate of 1-2 mEq/l/hr until symptoms settle
• Calculate rate and composition of fluid using the formula
Change in serum sodium by one litre of infused fluid
= (Infused Na/l - serum Na) / (TBW(l) +1)
• Once the symptoms improve, correct serum sodium concentration at
rate not greater than 0.5 mEq/l/hr or 12 mEq/l/day
• Consider adding Tolvaptan PO starting at 15 mg Q24h, Conivaptan IV
starting at 20 mg in 100ml of 5%dextrose over 30 mins or
Demeclocycline PO 300-600 mg bd if resistant to initial measures
Asymptomatic and chronic (>2 days)
• No immediate correction needed if mild hyponatremia
• Treat underlying cause
• Water restriction
• Correct at the rate not greater than 0.5 mEq/l/hr or 12 mEq/l/day
To estimate the effect of 1 litre of any infusate on serum sodium:
Change in Na= Infusate Na/l - serum Na / TBW(l) +1
Example: one litre of 3%NaCl for patient with serum Na of 110
=513-110 / 0.6*60 + 1
=403 / 36 + 1 = 10.9 mEq/l
Initial goal:To increase Na by 4 mEq/l in initial 4 hours
To increase Na by 10.9 mEq/l, 1000ml of 3%NaCl is required
To increase Na by 4 mEq/l, amount of 3%NaCl required is 366ml
( 4/10.9 *1000 = 366 ml )
Required rate of infusion of 3%NaCl is 366/4 = 92 ml/hr
Complication of treatment
OSMOTIC DEMYELINATION SYNDROME
• Caused by rapid correction of hyponatremia (>12 mEq/l/24hr) as
water moves from cells to ECF yielding intracellular dehydration
• Risk factors: sodium <120 mEq/l, chronic heart failure, alcoholism,
cirrhosis, hypokalemia, malnutrition
• Symptoms: dysarthria, dysphagia, lethargy, paraparesis or
quadriparesis, seizures and coma
• Treatment: 5%DW at 3ml/kg/hr, loop diuretics and desmopressin
HYPERNATREMIA
• Hypernatremia is defined as serum sodium >145 mEq/l and
hyperosmolarity (serum osmolality >295 mOsm/l
• Hypernatremia results from a deficit in TBW or net gain of sodium
(less comm)
• If sodium and osmolality increase, normal subjects become thirsty and
drink free water and sodium levels return towards normal
• Any clinical situation that impairs patient’s sense of thirst, limits the
availability of water, limits kidney’s ability to concentrate urine or
results in increased salt intake predispose to hypernatremia
• High risk: elderly patients, decompensated diabetics, infants,
hospitalised patients
• Hypernatremia may result from of loss of free water in diarrhoea or
urine
• Symptoms will be more severe and evident when the onset is rapid
• After 48 hrs there is an adaptation of brain cells with an increase in
electrolytes and thus increased intracellular water partly correcting the
initial cell shrinking
• If severe hypernatremia develops from minutes to hours such as from
a massive salt overdose, suddenly shrinking brain may prompt
intracranial hemorrhage
• Hypernatremia classification based on volume status
*Hypovolemic hypernatremia
*Hypervolemic hypernatremia
*Normovolemic hypernatremia
Etiology of Hypernatremia:
• Excess water loss:
Insensible loss:
*Dermal: Heat exposure, severe burns, severe exercise
*Respiratory: patient on mechanical ventilator
Renal loss:
*Diabetes insipidus (central or nephrogenic)
*Excessive diuretics, uncontrolled DM
GI losses: Osmotic diarrhoea
• Water deficit due to impaired thirst
*Primary hypodypsia
*Confused or comatose conditions
• Sodium retention
*Excessive IV hypertonic NaCl or NaHCO3
Clinical features:
• Clinical features of hypernatremia are primarily neurological and they
depend upon rapidity of onset, its duration and its magnitude
• Dry sticky mucous membrane is characteristic and body temperature is
generally elevated
• Major neurological symptoms include nausea, muscular weakness,
altered mental status, neuromuscular irritability, focal neurological
deficit and occasional coma or seizures
Diagnostic Testing:
• In addition to routine serum values, serum osmolarity and urine
sodium concentration and osmolality should be obtained
• The degree of hypernatremia almost always equals the TBW deficit in
adults
• TBW deficit = TBW * (serum Na - 140) / 140
Management:
• To quickly correct underlying shock, hypoperfusion, or significant
hypovolemia with normal saline
• To treat the underlying cause of hypernatremia such as fever, vomiting
or diabetes insipidus
• To lower the serum sodium level usually by replacement of the total
water deficit
• In addition to water deficit, ongoing and insensible loss needs to be
replaced
• Correct the total fluid deficit over 48-72 hrs
• In acute hypernatremia, water deficit can be replaced relatively rapidly
without increasing the risk of cerebral edema
• In acute hypernatremia, the targeted rate of correction of
hypernatremia is1-2 mEq/l/hr
• In Chronic and asymptomatic patients, the rate of correction is no
greater than 0.5 mEq/l/hr
• Treatment of hypernatremia is water
• Route of administration of water is by mouth or via nasogastric tube
• Acute hypernatremia is treated vigorously with D5% infusion
• Large and rapid infusion of D5% will lead to hyperglycaemia and
osmotic diuresis which may aggravate hypernatremia
• If required, hyperglycaemia can be combated with insulin therapy
• If there is severe loss of ECF volume with hypotension and azotemia,
isotonic saline is given initially until the ECF volume is restored
• Subsequently water deficit can be replaced with water by mouth or IV
D5% or 0.45% NaCl
• Sodium concentration of 0.9% NaCl (154 mEq/l) is greater than
normal serum sodium but is generally lower than serum sodium
concentration in hypernatremia
• So initial therapy with 0.9% NaCl can rapidly correct hypotension and
avoiding rapid fall of serum sodium
• Hypernatremia with increased ECF volume: In these patients
hypernatremia is secondary to solute administration
• These patients are usually volume overloaded
• Loop diuretic is administered along with water to facilitate sodium
excretion
• In patient with massive overload or renal failure, dialysis may be
necessary
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