Physiology of Hyponatremia Hyponatremia results from either the excessive intake or inability to...

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Physiology of Hyponatremia Hyponatremia results from either the excessive intake or inability to excrete free water. Water intakedilutional fall in plasma osmolality suppression of ADH. Plasma osmolality is elevated OR effective circulating volume is lowADH secretion Normals can excrete over 10 L of free water a day.

Transcript of Physiology of Hyponatremia Hyponatremia results from either the excessive intake or inability to...

Page 1: Physiology of Hyponatremia Hyponatremia results from either the excessive intake or inability to excrete free water. Water intake  dilutional fall in.

Physiology of Hyponatremia

• Hyponatremia results from either the excessive intake or inability to excrete free water.

• Water intakedilutional fall in plasma osmolality suppression of ADH.

• Plasma osmolality is elevated OR effective circulating volume is lowADH secretion

• Normals can excrete over 10 L of free water a day.

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Differential Diagnosis

• Conditions in which ADH levels are elevated:

1. Volume depletion (vomiting, diarrhea, hemorrhage, profuse sweating)

2. CHF, cirrhosis (effective volume depletion)

3. Diuretic use 4. Adrenal insufficiency5. SIADH

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Differential Diagnosis• Conditions in which ADH levels are

suppressed:1. Advanced renal failure2. Primary polydipsia3. Low dietary solute intake 4. Beer potomania

• Pseudohyponatremia—rare1. High Sosms: hyperglycemia, mannitol2. Normal Sosms: hyperlipidemia,

hyperproteinemia

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Workup

• History and PE are focused on volume status• Later on, pattern recognition helps

– The elderly lady on a tea and toast diet who is also taking a diuretic

– The cirrhotic with worsening ascites, edema

• Early on, be complete with the evaluation: send UA (specific gravity is the poor man’s Sosm); serum osmolality, urine osmolality, urine electrolytes

• Urine electrolytes give another assessment of volume status (Na+ should be <10 in volume depletion, unless on diuretic), K+ handling

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Workup

• A normal or elevated Uosm (above 100) in the setting of low Posms makes the diagnosis of SIADH.

--usually Na+ is >40--usually Creatinine is normal--normal acid-base, K+ handling

• Low Uosm (less than 100) seen in primary polydipsia, poor solute intake

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Workup

• Distinguishing hypovolemia/diuretic induced from SIADH (or presence of both):

--Urine Na+ usually low --PE reveals signs dehydration--Creatinine may be elevated--hold diuretic and hydrate; if the

Urine Na+ rises to above 40 and the Uosms remain above 100 the patient also has SIADH.

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Treatment

• Goal: to prevent cerebral edema and encephalopathy (lethargy, obtundation, seizures, coma, arrest) while preventing central pontine myelinolysis (correcting sodium too rapidly.)

• More rapid therapy (1.5 to 2 mEq per hour) can be used in the first few hours if there is serious cerebral dysfunction. Otherwise, maximum rate of elevation: 10-12 mEq during the first 24 hours and 18 mEq/L in the first two days.

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Ways to Raise Serum Sodium

• Water restriction—chronic primary therapy for hyponatremia in edematous states (CHF, cirrhosis) and in SIADH

• SIADH in the acute setting must be treated with IVF that exceeds the Uosm (NS or hypertonic saline)

• In volume depletion—use normal saline

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Calculation of the Sodium Deficit

• TBW times the net sodium gain• 0.5 times the weight in kilos for women,

0.6 for men• Example of 50 kg female, sodium of 122• So, if we wish her sodium to be raised by

12 mEq in the first 24 hours:--0.5 x 50 kg x 12 = 300 mEq

• Hypertonic saline contains roughly 1 mEq of sodium per 2 cc, so 600 cc should be given over 24 hours (25 cc/hour)

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Ddx of SIADH

• CNS: head trauma, neurosurgery, psychiatric illness, stroke, infection

• Tumor: ectopic ADH due to small cell Ca of the lung (most common), also seen in bronchogenic Ca, pancreatic Ca, neuroblastoma (rarer)

• Drugs: Carbamazepine, chlorpropamide, highdose IV cyclophosphamide, SSRIs

• Major surgery• Pulmonary disease (particularly pneumonia)