SIADH
also see Water and Salt Metabolism, Diabetes Insipidus

Discussion:

Hypo-osmolality and Hyponatremia

• excess H2O relative to solute in the ECF
  • either by depletion of body solute more than body water, or by dilution of body solute from increases in body water more than body solute
• Pseudohyponatemia: produced by marked elevation ofof plasma lipids, proteins, or glucose
• Correction for hyperglycemia: correct serum [Na+] by 1.6 mmol/L for each 100mg/dL increase in plasma glucose above 100mg/dl

Hypoosmolarity with Decreased ECF Volume

• signs of clinical hypovolemia
• Causes:
  • diuretic use
  • Salt-wasting nephropathies (I.e. PCKD, obstructiveuropathy,Bartter’ssyndrome)
  • Addison’sdisease
• low urine [Na+] suggests a non-renal cause of solute depletion

Hypo-osmolarity with Normal ECF Volume

• indicated by a high urine [Na+] (>30 mmol/L)
• Most common cause: SIADH

SIADH

• Inappropriately elevated plasma AVP (arginine vasopressin) levels with respect to concurrent body osmolality
• ADH excess > water retention > incr ECF > incr urinary Na excretion > low serum Na (hypo-osmolality <270 mOsm/L)
• Hallmark:
  • Hyponatremia
  • Low serum osmolality
  • High serum AVP
    • High urineosmolality (inappropriate for low serumosm)-indicated by urine that is less than maximally dilute: Uosm > 100mOsm/kg H2O
    • Low urine volume
    • Elevated urine [Na+] > 40 mEq/L
• Diagnosis of exclusion

Etiology

CNS disorders, Pulmonary diseases, Drug effects

• Tumors-lung, pancreas; Tumors produce ADH
• Pneumonia, TB
• CNS disease-stroke, head injury, encephalitis, subarachnoid hemorrhages
• Post op-pain, anesthesia
• Drug-vincristine, fluoxetine
• Cardiothoracic: diminished return of blood to left side of heart)

Symptoms

• Sx’slargely NEUROLOGIC-due to brain edema
• Depend on time-course over which hypo-osmolality develops
• Usually not seen until serum [Na+] falls below 125mmmol/L: HA, confusion, nausea, irritability, combativeness
• When serum sodium <110 meq/L: Seizures, stupor, coma

Treatment

• Too rapid correction of severe hyponatremia can produce pontine and extrapontine myelinolysis
• Treating underlying problem
• IF less severe or chronic hyponatremia (most cases of mild to moderate SIADH): Fluid restriction to about 50% to 60% of maintenance.
•  IF severe, acute symptomatic pts: Sodium replacement
• Demeclocycline: Block AVP’s action on the collecting duct

Treatment Parameters

• Controlled correction!!
• Maximal rate of correction of serum [Na+] in range of 1-2 mmol/L/hour, not to exceed 12 mmol/l in first 24 hours and 18 mmol/L in the first 48 hours
• Careful monitoring of serum [Na+] levels at frequent intervals

Summary DI vs SIADH

DI:

• Lack of AVP or End organ resistance to AVP

• Labs:

  • Polyuria: >5ml/kg/hr

  • Hypernatremic dehydration

  • Urine SG: < 1.010

  • Urine/plasma: osmolality <0.7

• Tx: 

  • Central: DDAVP

  • Nephrogenic: Thiazide diuretic, salt restriction

SIADH

• Inappropriate SIADH release with respect to low serum osmolality

• Labs

  • Low urine volume

  • Hyponatremia

  • High urinary sodium concentration >40mEq/L

  • High urine osmolality > 100 mOsm/L

  • Low serum osmolality < 270 mOsm/L (normal 280-300)

• Treatment

  • Treat underlying problem

  • Fluid restriction 50-60% of maint

  • Sodium replacement if severe or symptomatic

CHLA Board Review 2005