SIADH vs. DI: what is the difference?

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) and diabetes insipidus (DI) are two disorders which can be obscure and are sometimes confused. These complex conditions involving antidiuretic hormone (ADH) activity require immediate attention and treatment.
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The antidiuretic hormone, arginine vasopressin (AVP), is released by the pituitary gland in response to changes in plasma volume, blood pressure and osmolality. ADH, a key regulator of renal water absorption, plays opposing roles in SIADH and DI. Simply put, SIADH is precisely what it states, abnormal secretion of ADH. Too much ADH prevents urine production and results in excess water retention, hyponatremia and hypoosmolality (Lippincott Advisor, 2021a). SIADH could also be attributable to central nervous system (CNS) disorders, cancer, mesothelioma, cardiopulmonary diseases comparable to asthma, atelectasis, myocardial infarction, vascular diseases, multiple sclerosis, Guillain-Barre syndrome, porphyria, myxedema, and psychosis. Complications are significant and include water intoxication, cerebral edema, non-cardiogenic pulmonary edema, heart failure, seizures, coma and death (Lippincott Advisor, 2021a).
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In the case of diabetes insipidus, the effect is the alternative. There are two varieties of DI: central (also often called pituitary, neurogenic, or neurohypophyseal) and nephrogenic. In central DI, either the hypothalamus doesn’t produce enough ADH or the pituitary gland doesn’t secrete enough ADH. Without vasopressin, the filtered water is excreted within the urine as a substitute of being reabsorbed. In nephrogenic DI, ADH production and secretion are normal, however the kidneys are proof against the antidiuretic effects of the hormone. The lead to each subtypes is polyuria, greater than 3 L/24 hours in adults and greater than 2 L/24 hours in children. In severe cases of DI, the every day amount of urine excreted may reach 10–20 l/day. The causes of those diseases could also be damage to the hypothalamus or pituitary gland, developmental defects of the central nervous system, certain medications, kidney diseases and genetic defects. The major complications of DI include hypovolemia, hyperosmolality, circulatory collapse, CNS changes, lack of consciousness, bladder distention, and hydronephrosis (Lippincott Advisor, 2021b).
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Since SIADH causes water retention, remember the “SI” meaning “soaked from the inside”. With DI, excess fluid leaves the body, so take into consideration “mid-flow.” Here is a table showing the essential differences between SIADH and DI.
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Monitoring

Monitoring might be similar for each SIADH and DI, with a couple of differences. For each conditions, vital signs, intake and output, in addition to every day weight ought to be rigorously monitored. Assess urine and serum electrolyte levels, especially sodium, and monitor for changes in neurological status and level of consciousness. It is significant to evaluate heart rate and rhythm, heart and lung sounds, and assess the patient’s response to treatment. In the case of DI, blood urea nitrogen levels, urine specific gravity and osmolality, and 24-hour urine volume also needs to be checked in response to institutional policies. Additionally, monitoring for signs and symptoms of hypovolemic shock is incredibly vital in patients with DI.
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I hope you discover this temporary outline helpful. More detailed information will be present in the NursingCenter Pocket Card, Understanding the Syndrome of Inappropriate Antidiuretic Hormone (SIADH) and Diabetes Insipidus (DI).
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Lippincott’s advisor. (2021a, April 2). Diseases and conditions: Syndrome of inappropriate secretion of antidiuretic hormone. https://advisor.lww.com/lna/document.do?bid=4&did=1009704&searchTerm=SIADH&hits=siadh

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Lippincott’s advisor. (2021b, October 1). Diseases and conditions: diabetes insipidus. https://advisor.lww.com/lna/document.do?bid=4&did=1064604&searchTerm=diabetes%20insipidus&hits=diabetes,insipidus

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