Sunday, May 18, 2008

Hyponatremia in TBI

1. What is SIADH? What are common causes of SIADH?
2. What are the symptoms of SIADH?
3. What is the treatment for mild, severe, and chronic SIADH?
4. What is the most common cause of hyponatremia in TBI?
5. What is the volume status of patients with SIADH? Cerebral salt wasting (CSW)?
6. What is the pathophysiology behind CSW? What are the symptoms?
7. How is CSW treated?

Answers:
1. Excessive ADH secretion from the neurohypophysis. Causes include head trauma, brain thrombotic or hemorrhagic events, CNS infections, lung disease, malignancy, and medications.
2. Mild SIADH may have no symptoms or anorexia, nausea/vomiting. Severe SIADH results in increased body weight, restlessness, irritability, confusion, coma, or convulsions. Peripheral edema is rare.
3. Fluid restriction (1L/day), monitor weight and Na levels. Hypertonic saline should only be used with severe symptoms and Na should not be increased by more than 10mEq/L in 24 hours. Chronic SIADH can be treated with demeclocycline, which inhibits ADH in the kidney.
4. Cerebral salt wasting.
5. SIADH is isovolemic. CSW is hypovolemic.
6. CSW occurs because of direct neural effect on renal tubular function, which causes Na to be lost in the urine. This results in hypovolemia, which triggers ADH secretion (which is appropriate in this case). Symptoms resemble that of dehydration.
7. Treat with fluid replacement and Na correction.

1 comment:

Curtis and Audrey said...

4.What is the most common cause of hyponatremia in TBI?

Most sources state: SIADH(possible ~33% of TBI) > Cerebral salt wasting.