DISORDERS OF SODIUM CONCENTRATION:HYPONATREMIA

HYPERNATREMIA

Prepared by

DR.MUHAMMAD FAIZAN

Contents Fluid compartment & Osmolality Sodium control Definition of hyponatremia Epidemiology Types clinical manifestation Diagnosis Treatment Definition of hypernatremia Clinical manifestation Diagnosis Treatment

Total body water 60% of lean body weight in men and 50% in women. 2/3 comprises ICF & 1/3 ECF. 25% of ECF is intravascular & 75% in

interstitial spaces.Sodium is the main solute in Ecf where is potassium is main in Icf.

Disturbances in TBW manifest primarily as changes in osmolality of fluid compartments.

Osmolality Solute concentration is measured by osmolality i.e osmoles/kg

water. 285-295 mosm/kg Tonicity – osmolytes impermeable to cell membrane, they are

effective osmolyte. e.g: Na, gluccose. Ineffective osmolytes – permeate cell membrane. e.g:

urea,ethanol.

Plasma osmolality= 2Na + glucose/18 +BUN/2.8

Effective plasma osm= 2Na It is obvious that Na is intimately related to osmolality. Because of their relation to osmolality ,hyponatremia &

hypernatremia are primarily disorders of water balance & water distribution across fluid compartment.

Since 85-90% total body Na is in ECF,alterations manifest clinically as ECF volume depletion(hypotension,tachycardia) or ECF volume overload(peripheral/pulmonary edema).

Sodium control

Serum sodium conc is regulated by:

1. Stimulation of thirst

2. Secretion of ADH

3. Renin-Angiotensin-Aldosterone

4. Renal handling of Na.

Stimulation of thirst

○ Osmolality increasesMain driving forceOnly requires an increase of 2% - 3%

○ Blood volume or pressure is reducedRequires a decrease of 10% - 15%

○ Thirst center is located in the anteriolateral center of the hypothalamus Respond to NaCL and angiotensin II

Secretion of ADH

• Synthesized by the neuroendocrine cells in the supraoptic and paraventricular nuclei of the hypothalamus

• Triggers:– Osmolality of body fluids

» A change of about 1%– Volume and pressure of the vascular system

Actions of ADH 1. Increases the water permeability of

the collecting tubule2. Mildly increases vascular resistance

Renin-Angiotensin-Aldosterone• Renin

– Stimuli are perfusion pressure, sympathetic activity, and NaCl delivery to the macula densa

– Increase in NaCl delivery to the macula decreases the GFR by decrease in the renin secretion

• Aldosterone– Reduces NaCl excretion by stimulating it’s resorption

» Ascending loop of Henle» Distal tubule» Collecting duct

HYPONATREMIA

DEFINITION: Defined as sodium concentration < 135 mEq/L Generally considered a disorder of water as opposed to disorder of

salt 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)

EPIDEMIOLOGY

○ Hyponatremia is the most common electrolyte disorder○ incidence of approximately 1%○ prevalence of approximately 2.5%

Mortality/Morbidity○ Acute hyponatremia (developing over 48 h or less) are

subject to more severe degrees of cerebral edemasodium level is less than 105 mEq/L, the mortality is over

50%○ Chronic hyponatremia (developing over more than 48 h)

experience milder degrees of cerebral edema Brainstem herniation has not been observed in patients

with chronic hyponatremia

TYPES

HYPOOSMOLAR Hypovolumic Renal or Non-Renal

Thiazide diuretics,cerebral salt wasting.

Vomiting,diarrhea.

EuvolumicSIADH, hypothyroidism, psychogenic polydipsia.

HypervolumicCHF,Hepatic cirrhosis,severe nephrotic syn.

HYPEROSMOLAR EUOSMOLAR PSEUDONATREMIA

Clinical manifestation most patients with a serum sodium concentration exceeding 125

mEq/L are asymptomatic Patients with acutely developing hyponatremia are typically

symptomatic at a level of approximately 120 mEq/L Most abnormal findings on physical examination are

characteristically neurologic in origin and are related to osmotic intracellular water shift leading to cerebral edema.

Depends on the severity of fall of plasma Na conc and rate of development.

Acute (<48 hrz),chronic (>76 hrz) Mild ( =125mEq/L): anorexia, nausea, lethargy Mod (115-125mEq/L): disoriented, agitated, neuro deficit Sev (<115mEq/L): seizures, coma, death

Algorithm for Diagnosis

Step 1 Sna > 145 => Hypernatremia Sna< 135 => Hyponatremia Step 2 Calculate Serum Osmolarity Hyponatremia = Is it Hypoosmolar, Isoosmolar or

Hyperosmolar Step 3 Does calculated serum osmolarity agree with

measured serum osmolarity to within 10 meq/l. Step 4 Determine ECV status euvolemic, hypovolemic, or

hypervolemic (ECV status) Step 5 Obtain Urine Sodium and Urine Osmolarity. Is Urine sodium <or> 20 meq/l ? Is Urine osmolarity <or> 400 meq/l ?

Mandatory Lab Test

Serum OsmolalityUrine OsmolalityUrine Sodium Concentration

Additional tests:TSH, cortisol (Hypothryoidism or Adrenal

insufficiency)Albumin, BMP, triglycerides and SPEP

(psuedohyponatremia, cirrhosis, MM)

Interpretation of Test

Serum Osmolality Can differentiate between true hyponatremia,

pseudohyponatremia and hypertonic hyponatremia Urine Osmolality

Can differentiate between primary polydipsia and impaired free water excretion

Urine Sodium concentration Can differentiate between hypovolemia hyponatremia and

SIADH

DIFFERENTIAL DIAGNOSIS

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

Ddx(contd)

2nd test to obtain: urine osmolalityPlasma osmolality < 275 mosmol/kg+ urine osmolality

>100 mosm/l○ Increased volume,

CHF, cirrhosis, nephrotic syndrome○ Euvolemic

SIADH, hypothyroidism, psychogenic polydipsia, beer potomania, postoperative states

○ Decreased volumeGI loss, skin, 3rd spacing, diuretics

Ddx(contd)

3rd test:Urine sodium for dehydrated patients UNa < 20 ,i.e Na and water are lost other then via kidneys

Diarrhea,vomiting,burns,trauma,heat exposure. UNa > 20 ,i.e Na is lost via kidneys

Renal failure,diuretic excess,addison’s disease.

Uric Acid Level○ < 4 mg/dl consider SIADH

FeNa○ Help to determine pre-renal from renal causes

Treatment

Four issues must be addressed○ Asymptomatic vs. symptomatic○ acute (within 48 hours)○ chronic (>48 hours)○ Volume status

Treatment (contd) 1st step is to calculate the total body water:

○ total body water (TBW) = 0.6 × body weight

2nd step is to decide what our desired correction rate should be:

Symptomatic:

1. 1.5 to 2 mEq/L per hour for first 3-4 hours until symptoms resolve

2. Increase by no more than 10 mEq/L in first 24 hrs

3. Increase by no more than 18 mEq/L in first 48 hrs

The risks of correcting hyponatremia too rapidly are volume overload and development of central pomtine myelinolysis(CPM),due to shrinkage of neuron away from their myelin sheaths.The risk of precipitaing cpm is increased with correction of Na >12 meq/l in 24 hrz.

The absolute magnitude of correction in 24 hrz is more important then the rate.

Treatment(contd)o Na deficit = TBW x (desired [Na] - actual [Na]) (mmol)Change in sodium from 1 litre of fluid:o Change in Na={(Na I)+(k i) –(Na s)} /TBW

When do you need to Rx quickly? Acute (<24h) severe (< 120 mEq/L) Hyponatremia

○ Prevent brain swelling or Rx brain swelling Symptomatic Hyponatremia (Seizures, coma, etc.)

○ Alleviate symptoms

“Quickly”: 3% NS, 1-2 mEq/L/h until:○ Symptoms stop○ 3-4h elapsed and/or Serum Na has reached 120 mEq/L

Then SLOW down correction to 0.5 mEq/L/h with 0.9% NS or simply fluid restriction. Aim for overall 24h correction to be < 10-12 mEq/L/d to prevent myelinolysis

Treatment(contd) When to Rx slowly (correct < 0.5 mEq/L/h, 10-

12 mEq/L/d)

Symptomatic/Acute: rapid Rx has resolved symptoms and brought serum Na up to 120 mEq/L

Asymptomatic, mild, chronic hyponatremia Want to prevent myelinolysis(Symptoms include:

dysarthria, dysphagia, paraparesis, quadriparesis, lethargy, coma or even seizures)Increased risk: Women, alcoholics, malnourished

Treatment (contd)

Treatment in asymptomatics:

Correct the underlying cause in the DDx Hypovolemic → give volume Hypervolemic → Na & water restriction

Loop diuretics if CHF or nephrotic syndrome 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

Treatment (contd) IV Fluids

One liter of Lactated Ringer's Solution contains:○ 130 mEq of sodium ion = 130 mmol/L○ 109 mEq of chloride ion = 109 mmol/L ○ 28 mEq of lactate = 28 mmol/L○ 4 mEq of potassium ion = 4 mmol/L ○ 3 mEq of calcium ion = 1.5 mmol/L

One liter of Normal Saline contains:○ 154 mEq/L of Na+ and Cl− (total osm=308)

One liter of 3% saline contains:○ 514 mEq/L of Na+ and Cl− (total osm=1028)

Example 60 kg woman with sodium level of 116 How much sodium will bring him up to 124 in the next 24 hours? Sodium needed = 0.5 x 60 x (124-116) = 240 Hypertonic saline contains 500 mEq/L of sodium Normal saline contains 154 mEq/L of sodium The patient needs 240 mEq in next 24 hours That averages to 10 mEq per hour or 20 mL of hypertonic saline per hour However, this will only raise the serum sodium by 0.33 per hour therefore, increasing

the rate 60 mL to 90 mL will produce the desired rate of serum sodium increase of 1.0 to 1.5 mEq per hour until symptoms resolve

Take Home Points

If asked to work-up hypoNa, first: H&PHistory of fluid loss (vomit/diarrh) 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

Treatment is based on symptomsSevere symptoms = Hypertonic SalineMild or no symptoms = Fluid restriction

HYPERNATREMIADEFINITION

Hypernatremia is defined as sa plasma Na >145 mEq/L and represents a state of hyperosmolality.

TYPES May be caused by a primary water deficit or Na gain.

Primary water deficit:

1. Impaired thirst response

2. Non renal water losses( diarrhea,sweating,burns)

3. Renal water loss( osmotic diuresis or diabetes inspidus).

Na gain:

4. Mineralocortecoid excess

5. NaHco3 excess

CLINICAL MANIFESTATION

Initial symptoms include lethargy, weakness and irritability Can progress to twitching, seizures, obtundation or coma Resulting decrease in brain volume can lead to rupture of

cerebral veins leading to hemorrhage Severe symptoms usually occur with rapid increase to

sodium concentration of 158 mEq or more Sodium concentration greater than 180 mEq are associated

with high mortality

ALGORITHM FOR DIAGNOSIS

First asses Ecf volume Second to asses urine volume. Third to measure the urine osmolality If urine osmolality >800,then 4th test to do Urine Na level if urine osmolality 300-800 ,then 4th to measeure Urine osmole excretion per day If urine osmolality <300,then 4th to do Response to dDAVP

DIFFERENTIAL DIAGNOSIS

First check Ecf volume. Hypervolemic

Helps exclude 2 common causes:

1. Hypertonic Na load

2. Cushing syndrome

Ddx (contd)

If hypovolemic or euvolemic then check urine volume and measure urine osmolality:

If urine volume <800 and urine osmolality >800 mosm/l

1. Insensible losses

2. Gi losses

3. Loop diuretic

4. Primary hupodipsia If urine volume >1000 ml and urine osmolality 300-800 Urine osmole excretion per day > 900 mosm/day

1. Osmotic diuresis( glucosuria,mannitol,high solute loads,) If urine volume >1000ml and urine osmolality <300 and

response to dDAVP :

1. Complete CDI(if +)

2. Partial CDI(if-)

TREATMENT

Therapeutic goals are:

1. Reduce serum sodium concentration to 145 mmol/L

2. Determine rate of correction

3. Correct the water deficit

4. Correct the underlying disorder

TREATMENT (CONTD)

Hypernatremia that developed over a period of hours (accidental loading) Rapid correction improves prognosis without cerebral

edema Accumulated electrolytes in brain rapidly extruded Reducing Na+ by 1 mmol/L/hr appropriate

Hypernatremia of prolonged or unknown duration a slow pace of correction prudent full dissipation of brain solutes occurs over several days maximum rate 0.5 mmol/L/hr to prevent cerebral edema A targeted fall in Na+ of 10 mmol/L/24 hr

TREATMENT (CONTD)

Administration of Fluids: Preferred route: oral or feeding tube IV fluids if oral not feasible Except in cases of frank circulatory compromise,

isotonic saline is unsuitable Only hypotonic fluids are appropriate-pure water,

5% dextrose, 0.2 % saline, 0.45% saline-the more hypotonic the infusate, the lower the infusion rate required

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