Search results
Results from the WOW.Com Content Network
In severe or acute hypoosmolar hyponatremia, swelling of brain cells causes various neurological abnormalities, which in severe or acute cases can result in convulsions, coma, and death. The symptoms of chronic syndrome of inappropriate antidiuresis are more vague, and may include cognitive impairment, gait abnormalities, or osteoporosis. [2]
Although hyponatremia is a fairly common condition, many patients have only mildly decreased blood sodium. Dr. Jeff Hersh explains the cause of hyponatremia, and how it should be treated Skip to ...
The treatment of hyponatremia depends on the underlying cause. [12] How quickly treatment is required depends on a person's symptoms. [12] Fluids are typically the cornerstone of initial management. [12] In those with severe disease an increase in sodium of about 5 mmol/L over one to four hours is recommended. [12]
Hyponatremia, or low sodium, is the most commonly seen type of electrolyte imbalance. [12] [13] Treatment of electrolyte imbalance depends on the specific electrolyte involved and whether the levels are too high or too low. [3] The level of aggressiveness of treatment and choice of treatment may change depending on the severity of the ...
Therapy can include the use of zinc supplements to reduce the duration of diarrhea in infants and children under the age of 5. [1] Use of oral rehydration therapy has been estimated to decrease the risk of death from diarrhea by up to 93%. [2] Side effects may include vomiting, high blood sodium, or high blood potassium. [1]
In general, hyponatremia is usually asymptomatic until severe. [10] Typical laboratory findings for tea and toast syndrome include a low serum osmolality (hypotonicity) with normal urine osmolality since antidiuretic hormone levels are normal. A common laboratory finding for the tea and toast phenomenon is manifestation as hyponatremia.
the physiologic response to a decrease in kidney perfusion is an increase in sodium reabsorption to control hyponatremia, often caused by volume depletion or decrease in effective circulating volume (e.g. low output heart failure). above 2% [citation needed] or 3% [2] acute tubular necrosis or other kidney damage (postrenal disease)
Linkage analysis on patients with the severe form of PHA excluded the possibility of linkage of the disease with the mineralocorticoid receptor gene region. [25] Later, the severe form of PHA was discovered to be due to mutations in the genes SCNN1A , SCNN1B , and SCNN1G that code for the epithelial sodium channel subunits, α, β, and γ ...