Pathophysiology
In SIADH, the inappropriately elevated level of ADH enhances the reabsorption of water, thus concentrating the urine. It is the excess free water absorption that causes hyponatremia.
*Note that although water excretion is impaired, salt handling is NORMAL.
Signs and Symptoms
headache, nausea / vomiting, muscle cramps, restlessness, lethargy, confusion, decreased reflexes, seizure, coma, death
*these signs and symptoms are secondary to hyponatremia and are not specific for SIADH
Diagnosis
- clinically euvolemic (e.g. assess postural BP and pulse, JVP, mucus membranes and skin turgor)
- serum hypoosmolarity (serum osm <280 href="http://www.uwo.ca/cns/resident/pocketbook/medicine/kidney/hyponatremia.html">hyponatremia (serum sodium <135>20 mmol/L
- urine osmolarity > serum osmolarity
*The diagnosis of SIADH cannot be made if the patient is on diuretics or if renal, thyroid or adrenal function is abnormal
NOTE: It is possible for a patient to be hypovolemic and have SIADH. In this setting, urine sodium may be <20 align="left">
Causes
- CNS disturbance: stroke, subarachnoid hemorrhage, infection (meningitis / encephalitis), trauma, psychosis
- Tumor (ectopic production of ADH): small cell lung cancer most commonly, more rarely other types of lung cancers, pancreatic cancer, colon adenocarcinoma, olfactory neuroblastoma, lymphoma, leukemia
- Drugs: carbamazepine, cyclophosphamide, vincristine, ecstasy (MDMA), neuroleptics, TCAs, SSRIs, MAOIs, NSAIDs
we come in many different colors and flavors (:
Wednesday, April 21, 2010
Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)
- Major surgery: abdominal, thoracic, transphenoidal surgery (after pituitary surgery, SIADH may occur on its own or as a transient event as part of a “triphasic response” i.e. early post-op period of diabetes insipidus followed by SIADH followed by diabetes insipidus)
- Pulmonary disease: pneumonia (bacterial, TB, Aspergillosis), bronchiectasis, occasionally with asthma, atelectasis, pneumothorax, acute respiratory failure
- AIDS
- Other: nausea (potent stimulus for ADH secretion), pain, severe stress (these 3 factors may explain some of the etiologies of SIADH above e.g. surgery)
- Idiopathic
-Hospital-acquired hyponatremia: often seen secondary to overzealous administration of hypotonic IV fluids
- Pulmonary disease: pneumonia (bacterial, TB, Aspergillosis), bronchiectasis, occasionally with asthma, atelectasis, pneumothorax, acute respiratory failure
- AIDS
- Other: nausea (potent stimulus for ADH secretion), pain, severe stress (these 3 factors may explain some of the etiologies of SIADH above e.g. surgery)
- Idiopathic
-Hospital-acquired hyponatremia: often seen secondary to overzealous administration of hypotonic IV fluids
***In the setting of CNS disturbances, especially subarachnoid hemorrhage, SIADH must be differentiated from cerebral salt wasting.
Investigation
Laboratory Studies
1.Serum: Electrolytes, blood urea nitrogen (BUN), creatinine, glucose levels, and osmolality
Laboratory Studies
1.Serum: Electrolytes, blood urea nitrogen (BUN), creatinine, glucose levels, and osmolality
--Hyponatremia (sodium <135>Hypokalemia and metabolic alkalosis suggest diuretic therapy or vomiting.
--BUN and serum uric acid levels tend to fall because of plasma dilution and increased excretion of nitrogenous products.
--Low serum osmolality (<280>
--BUN and serum uric acid levels tend to fall because of plasma dilution and increased excretion of nitrogenous products.
--Low serum osmolality (<280>
--Hyperkalemia and metabolic acidosis coexisting with hyponatremia suggest adrenal insufficiency.
--Elevated glucose levels decrease the measured serum sodium levels by 1.6 mEq/L for every 100 mg/dL increase in glucose. This results from the osmotic effect of glucose drawing water into the intravascular space. The serum sodium level rises as hyperglycemia is corrected.
--Elevated glucose levels decrease the measured serum sodium levels by 1.6 mEq/L for every 100 mg/dL increase in glucose. This results from the osmotic effect of glucose drawing water into the intravascular space. The serum sodium level rises as hyperglycemia is corrected.
2.Urine: Electrolytes and osmolality (specific gravity is nonspecific but sensitive)
--Elevated urinary sodium level (>20 mmol/L). It would be preferable to check urine electrolytes at the same time as the serum electrolytes to determine the fractional excretion of sodium or FeNa.
--Urine osmolality generally >100 mOsm/L
3.Plasma cortisol level may be obtained to exclude adrenal insufficiency.
4.Pseudohyponatremia occurs with severe hyperlipidemia and with hyperproteinemia (levels >10 g/dL, as seen in multiple myeloma).
Imaging Studies
1.Chest radiographs may reveal an underlying cause (eg, pulmonary disease, lung carcinoma).
2.CT scan of the head may be appropriate in selected cases.
--CT scan may show evidence of cerebral edema (eg, narrowing of the ventricles) or may identify a CNS disorder responsible for SIADH (eg, brain tumor).
--CT helps rule out other potential causes of acute changes in neurologic status.
Treatment
*CORRECT SLOWLY because of risk of central pontine myelinolysis (brain cell dysfunction caused by the destruction of the layer myelin sheath in the pons.)
The maximum correction rate should be a rise of serum sodium no greater than 0.5 mmol/L/h or 8 mmol/L/day. In patients with severe symptoms, can increase the initial rate to 1 mmol/L./h for 2-3 hours and then decrease to above rate (especially if the drop in sodium was acute rather than chronic)
1. Water restriction (0.8-1.5L/day) is usually sufficient on its own
2. High salt, high protein diet
3. Consider a loop diuretic e.g. lasix 20 mg IV (impairs renal responsiveness to ADH, excrete more water than sodium) 4. Salt infusion is only required if hyponatremia persists despite the above methods. Nephrology or Internal medicine should be consulted if administration of hypertonic saline is required.
NOTE: In order to correct hyponatremia
the osmolality of the fluid given must exceed the osmolality of the
urine .
urine .
e.g. A patient with SIADH has a urine osmolality = 600 mmol/L and is
given 1L of 0.9% normal saline. There are 150 mEq of Na and Cl in normal saline
and, therefore the Osm of normal saline = 300 mEq/L. Given that salt handling is
NORMAL in SIADH, all the NaCl will be excreted but in only 500 ml (i.e. the
urine osm = 600 and therefore 300 mEq of NaCl will be excreted in 500 ml = 600
mEq/L). Giving normal saline, therefore, will actually make the hyponatremia
WORSE by increasing fluid volume another 500ml! The serum concentration of
sodium may transiently rise but then it will fall.
If the same patient is given 1L of 3% saline, which contains 513 mEq of Na and Cl (Osm=1026), all the NaCl will be excreted but in a LARGER volume. i.e. 1024 mEq / 600 mEq/L = 1700 ml. A net loss of 700 ml of water will occur.
5. MONITOR serum electrolytes frequently to ensure that the serum sodium level is being corrected and that the rate of rise is less than 8 mmol/L/day.
6. Treat underlying condition if possible
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