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LAS VEGAS – Hyponatremia is not a salt problem, it’s a water problem.
That was the lead message in a well-attended rapid-fire session on hyponatremia at the annual meeting of the Society of Hospital Medicine.
“It’s almost always associated with pathologic elevations of ADH [antidiuretic hormone], and it’s that retention of water that dilutes the serum and drops the sodium, which causes the cerebral edema,” said Thomas Yacovella, MD, assistant professor of medicine at the University of Minnesota, Minneapolis.
“Remember that hyponatremia is a bad actor, especially when associated with a chronic disease,” Dr. Yacovella said. Serum sodium levels are a reliable surrogate for chronic heart failure related to hyponatremia. End-stage disease is when sodium levels are at 125 or less.
A basic work-up for hyponatremia starts with assessing fluid intake, history of medications and of any causes of ADH release, volume status assessment, and laboratory evaluations of blood and urine. The three keys to knowing how quickly hyponatremia can be reversed are severity of symptoms, how long it took for the condition to develop, and the risk of herniation vs. the risk of osmotic demyelination, he said.
In cases of osmotic demyelination, Dr. Yacovella advised monitoring urine osmolality and cases where ADH release could be quickly reversed. “When you don’t know for sure, go slow,” he said.
Exercise-associated hyponatremia is often caused by the perfect storm of sodium loss, high emotion, vomiting, pain, excessive water intake, and high ADH levels. This form of hyponatremia can occur postoperatively, but is more typically associated with the copious water ingestion that can occur during psychosis, extreme exercise, ecstasy ingestion, and “stupid” contests that involve extreme behavior, Dr. Yacovella said. His pearls for acute management of these kinds of hyponatremia were to administer a 100-mL bolus of hypertonic saline, and that a large output of dilute urine indicates corrective aquaresis.
Dr. Yacovella emphasized that in addition to remembering that hyponatremia is a water and not a salt problem, physicians should always look to “the path of physiology of the disease, and how long it took to develop the hyponatremia, and that will inform how quickly you can treat the patient.”
He had nothing to disclose.
wmcknight@frontlinemedcom.com
On Twitter @whitneymcknight
LAS VEGAS – Hyponatremia is not a salt problem, it’s a water problem.
That was the lead message in a well-attended rapid-fire session on hyponatremia at the annual meeting of the Society of Hospital Medicine.
“It’s almost always associated with pathologic elevations of ADH [antidiuretic hormone], and it’s that retention of water that dilutes the serum and drops the sodium, which causes the cerebral edema,” said Thomas Yacovella, MD, assistant professor of medicine at the University of Minnesota, Minneapolis.
“Remember that hyponatremia is a bad actor, especially when associated with a chronic disease,” Dr. Yacovella said. Serum sodium levels are a reliable surrogate for chronic heart failure related to hyponatremia. End-stage disease is when sodium levels are at 125 or less.
A basic work-up for hyponatremia starts with assessing fluid intake, history of medications and of any causes of ADH release, volume status assessment, and laboratory evaluations of blood and urine. The three keys to knowing how quickly hyponatremia can be reversed are severity of symptoms, how long it took for the condition to develop, and the risk of herniation vs. the risk of osmotic demyelination, he said.
In cases of osmotic demyelination, Dr. Yacovella advised monitoring urine osmolality and cases where ADH release could be quickly reversed. “When you don’t know for sure, go slow,” he said.
Exercise-associated hyponatremia is often caused by the perfect storm of sodium loss, high emotion, vomiting, pain, excessive water intake, and high ADH levels. This form of hyponatremia can occur postoperatively, but is more typically associated with the copious water ingestion that can occur during psychosis, extreme exercise, ecstasy ingestion, and “stupid” contests that involve extreme behavior, Dr. Yacovella said. His pearls for acute management of these kinds of hyponatremia were to administer a 100-mL bolus of hypertonic saline, and that a large output of dilute urine indicates corrective aquaresis.
Dr. Yacovella emphasized that in addition to remembering that hyponatremia is a water and not a salt problem, physicians should always look to “the path of physiology of the disease, and how long it took to develop the hyponatremia, and that will inform how quickly you can treat the patient.”
He had nothing to disclose.
wmcknight@frontlinemedcom.com
On Twitter @whitneymcknight
LAS VEGAS – Hyponatremia is not a salt problem, it’s a water problem.
That was the lead message in a well-attended rapid-fire session on hyponatremia at the annual meeting of the Society of Hospital Medicine.
“It’s almost always associated with pathologic elevations of ADH [antidiuretic hormone], and it’s that retention of water that dilutes the serum and drops the sodium, which causes the cerebral edema,” said Thomas Yacovella, MD, assistant professor of medicine at the University of Minnesota, Minneapolis.
“Remember that hyponatremia is a bad actor, especially when associated with a chronic disease,” Dr. Yacovella said. Serum sodium levels are a reliable surrogate for chronic heart failure related to hyponatremia. End-stage disease is when sodium levels are at 125 or less.
A basic work-up for hyponatremia starts with assessing fluid intake, history of medications and of any causes of ADH release, volume status assessment, and laboratory evaluations of blood and urine. The three keys to knowing how quickly hyponatremia can be reversed are severity of symptoms, how long it took for the condition to develop, and the risk of herniation vs. the risk of osmotic demyelination, he said.
In cases of osmotic demyelination, Dr. Yacovella advised monitoring urine osmolality and cases where ADH release could be quickly reversed. “When you don’t know for sure, go slow,” he said.
Exercise-associated hyponatremia is often caused by the perfect storm of sodium loss, high emotion, vomiting, pain, excessive water intake, and high ADH levels. This form of hyponatremia can occur postoperatively, but is more typically associated with the copious water ingestion that can occur during psychosis, extreme exercise, ecstasy ingestion, and “stupid” contests that involve extreme behavior, Dr. Yacovella said. His pearls for acute management of these kinds of hyponatremia were to administer a 100-mL bolus of hypertonic saline, and that a large output of dilute urine indicates corrective aquaresis.
Dr. Yacovella emphasized that in addition to remembering that hyponatremia is a water and not a salt problem, physicians should always look to “the path of physiology of the disease, and how long it took to develop the hyponatremia, and that will inform how quickly you can treat the patient.”
He had nothing to disclose.
wmcknight@frontlinemedcom.com
On Twitter @whitneymcknight