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6 Idiosyncratic ACE inhibitor reactions ACE inhibitors can cause central polydipsia and increased ADH secretion, both of which result in severe, symptomatic hyponatremia ACE does not block the conversion of angiotensin I to angiotensin II in the brain Thus, angiotensin II converted in the brain stimulates thirst and ADH secretion 7 Endurance exercise hyponatremia Hyponatremia after endurance exercise (eg, triathlon events) may be caused by a combination of excessive hypotonic fluid intake and continued ADH secretion Reperfusion of the exercise-induced ischemic splanchnic bed causes delayed absorption of excessive quantities of hypotonic fluid ingested during exercise Sustained elevation of ADH prevents water excretion in this setting The retention of hypotonic fluid may be further exacerbated by nonsteroidal anti-inflammatory drugs (NSAIDs) frequently used by athletes New guidelines encourage runners to drink between 400 mL/h and 800 mL/h as opposed to the previous as much as possible advice However, the clinical relevance of this new recommendation remains to be determined 8 Mineralocorticoid-responsive hyponatremia in the elderly In a subgroup of elderly patients, hyponatremia does not resolve in response to water restriction even though they are euvolemic with high ADH levels These patients may respond to fludrocortisone treatment 9 Adrenal deficiency This is an important but often overlooked cause of euvolemic hyponatremia The adrenal insufficiency may be either primary or secondary, due to adrenocorticotropin (ACTH) deficiency Routine laboratory data may not easily distinguish hyponatremia due to ACTH deficiency from that of SIADH However, low plasma bicarbonate (or total CO2) levels suggest ACTH deficiency 10 Methylenedioxymethylamphetamine ( Ecstasy ) abuse Abuse of 3,4-methylenedioxymethylamphetamine (MDMA), also known as Ecstasy, can lead to severe neurologic symptoms, including seizures, brain edema, and herniation from severe hyponatremia MDMA and its metabolites have been shown to induce enhanced ADH release from the hypothalamus 11 Selective serotonin reuptake inhibitors (SSRIs) SIADH induced by selective serotonin (or epinephrine) reuptake inhibitors, such as fluoxetine, paroxetine, and citalopram, is fairly common in geriatric patients Enhanced secretion or action of ADH may result from increased serotonergic tone 12 Amiodarone SIADH during amiodarone-loading has been reported Hyponatremia usually improves with dose reduction 13 Hyponatremia in HIV-infected patients Hyponatremia is seen in up to 50% of patients hospitalized for HIV infection and in 20% of ambulatory AIDS patients, often associated with pneumonia and central nervous system processes If hyponatremia is present at the time of hospital admission, it is just as likely to be due to hypovolemic gastrointestinal loss as to euvolemic SIADH However,
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if hyponatremia develops after hospital admission, most patients have euvolemic SIADH Infrequently, hypovolemic hyponatremia is due to adrenal insufficiency from infections or ketoconazole toxicity, isolated mineralocorticoid deficiency with hyporeninemic hypoaldosteronism, or an HIV-specific impairment in renal sodium conservation
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Hyponatremia with increased ECF volume is seen when hyponatremia is accompanied by edema-associated disorders such as congestive heart failure, cirrhosis, nephrotic syndrome, and advanced renal disease (Figure 21 1) In congestive heart failure, total body sodium is increased, yet effective circulating volume is sensed as inadequate by baroreceptors Increased ADH and aldosterone results, with retention of water and sodium The urine sodium concentration is generally less than 10 mEq/L unless the patient has been taking diuretics
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Whether hyponatremia becomes symptomatic depends on the magnitude and speed (within 1 to 2 days) of the decline of the plasma sodium Mild hyponatremia (plasma sodium levels of 130 135 mEq/L) is usually asymptomatic; nausea and malaise can occur when the plasma sodium is below 125 130 mEq/L Headache, lethargy, and disorientation are seen with plasma sodium levels of 115 120 mEq/L The most serious symptoms of severe and rapidly developing hyponatremia are seizure, coma, permanent brain damage, respiratory arrest, brainstem herniation, and death Premenopausal women in whom hyponatremic encephalopathy develops are about 25 times more likely than menopausal women to die or suffer permanent brain damage, suggesting a hormonal role in the pathophysiology of this disorder Natriuresis compensates for the slight increase in volume from ADH secretion The expansion of ECF volume is not large enough to cause clinical hypervolemia, hypertension, or edema
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