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Antipsychotics have been reported to cause hyponatremia in a review of medical articles from 1946 to 2016. [25] Available evidence suggests that all classes of psychotropics, i.e., antidepressants, antipsychotics, mood stabilizers, and sedative/hypnotics can lead to hyponatremia. Age is a significant factor for drug induced hyponatremia. [26]
Importantly CSWS can be associated with subarachnoid hemorrhage (SAH) which may require fluid supplementation rather than restriction to prevent brain damage. [16] Most cases of hyponatremia in children are caused by appropriate secretion of antidiuretic hormone rather than SIADH or another cause. [17]
The cornerstone of therapy for SIADH is reduction of water intake. If hyponatremia persists, then demeclocycline (an antibiotic with the side effect of inhibiting ADH) can be used. SIADH can also be treated with specific antagonists of the ADH receptors, such as conivaptan or tolvaptan. [citation needed] Another cause is psychogenic polydipsia. [3]
Class Ib drugs tend to be more specific for voltage gated Na channels than Ia. Lidocaine in particular is highly frequency dependent, in that it has more activity with increasing heart rates. This is because lidocaine selectively blocks Na channels in their open and inactive states and has little binding capability in the resting state.
The low GFR causes a lowered rate of osmole excretion, and an increase in the amount of water reabsorbed; thus, hyponatremia occurs when the amount of water intake exceeds the renal water excretion capacity. [2] Medications, such as thiazides and antidepressants, may exacerbate symptoms of hyponatremia. [2]
[14] [3] Dilutional hyponatremia can happen in diabetics as high glucose levels pull water into the blood stream causing the sodium concentration to be lower. [14] [3] Diagnosis of the cause of hyponatremia relies on three factors: volume status, plasma osmolality, urine sodium levels and urine osmolality. [14] [3]
Common ADRs include: hyponatremia, hypokalemia, hypomagnesemia, dehydration, hyperuricemia, gout, dizziness, postural hypotension, syncope. [17] The loss of magnesium as a result of loop diuretics has also been suggested as a possible cause of pseudogout (chondrocalcinosis). [18]
V 2 R antagonists have become a mainstay of treatment for euvolemic (i.e., SIADH, postoperative hyponatremia) and hypervolemic hyponatremia (i.e., CHF and cirrhosis). [9] V 2 RAs predictably cause aquaresis leading to increased [Na +] in majority of patients with hyponatremia due to SIADH, CHF, and cirrhosis. The optimum use of VRAs has not yet ...