Syndrome of inappropriate antidiuretic hormone

50 Syndrome of inappropriate antidiuretic hormone

Overview/pathophysiology

Syndrome of inappropriate antidiuretic hormone (SIADH) or syndrome of inappropriate antidiuresis (SIAD) is a condition of abnormal release of antidiuretic hormone (ADH, vasopressin [VP]) in response to changes in plasma osmolality that result in hyponatremia. Hyponatremia is defined as an excess of water in relation to the amount of sodium in the extracellular fluid. SIADH is the most frequent cause of hyponatremia, which is the most common electrolyte imbalance in hospitalized patients. Mild hyponatremia (serum sodium less than135 mEq/L) occurs in 15%-22% of hospitalized patients and 7% of ambulatory patients, while moderate hyponatremia (serum sodium less than 130 mEq/L) occurs in 1%-7% of hospitalized patients. Hyponatremia is often caused by extracellular fluid volume depletion associated with many diuretics that cause a significant loss of sodium along with water. Hyponatremia is important to manage because of its potential morbidity and should be recognized as an indicator of underlying disease.

ADH (VP) is produced in the hypothalamus, stored in the posterior pituitary, and regulates free water volume in the kidney. Hyponatremia resulting from chronic SIADH is not always caused by reduced water excretion or volume overload. Plasma ADH level may not be high and measurement is often not helpful in establishing the diagnosis. Findings may reflect dilute (hypo-osmolar) plasma and hyponatremia with a normal circulating blood volume. Morbidity and mortality of hyponatremia associated with SIADH stem from cerebral edema and abnormal nerve function. Values of serum sodium less than 100 mEq/L are life threatening.

ADH is a key component in the regulation of fluid and electrolyte balance through direct effects on renal water regulation. Water is reabsorbed in the distal nephron, where the kidney both concentrates and dilutes urine in response to the ADH level. VP stimulates the nephron to produce aquaporin (AQP), a specific water channel protein, on the surface of the interstitial cells lining the collecting duct. The presence of AQP in the wall of the distal nephron allows resorption of water from the duct lumen according to the osmotic gradient and excretion of concentrated urine.

Health care setting

Assessment

Signs and symptoms:

Decreased urine output with concentrated urine. Signs of water intoxication may appear, including altered level of consciousness (LOC), fatigue, headache, diarrhea, anorexia, nausea, vomiting, and seizures. Note: Because of loss of Na⁺, edema will not accompany the fluid volume excess.

Physical assessment:

Weight gain without edema, elevated blood pressure (BP), altered mental status. Laboratory values must be correlated with physical findings. The goal of assessment is to differentiate between SIADH and a compensatory response of ADH release in patients with chronic, mild volume depletion/dehydration.

History of:

Cancers of the lung, pancreas, duodenum, and prostate, which can secrete a biologically active form of ADH. Other common causes include pulmonary disease (e.g., tuberculosis, pneumonia, chronic obstructive pulmonary disease, empyema), acquired immunodeficiency syndrome, head trauma, brain tumor, intracerebral hemorrhage, meningitis, and encephalitis. Positive-pressure ventilation, physiologic stress, chronic metabolic illness, and a wide variety of medications (chlorpropamide, acetaminophen, oxytocin, narcotics, general anesthetic, carbamazepine, thiazide diuretics, tricyclic antidepressants, neuroleptics, angiotensin-converting enzyme inhibitors, cancer chemotherapy agents) all have been linked to SIADH.

Diagnostic tests

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Jul 18, 2016 | Posted by admin in NURSING | Comments Off

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