Syndrome of Inappropriate Antidiuretic Hormone
Syndrome of Inappropriate Antidiuretic Hormone
The endocrine system is made up of multiple organs located throughout the body and are responsible for hormone secretion directly into the blood stream (Huber & VanMeter, 20180. One hormone of the endocrine system released directly into the blood stream is Antidiuretic Hormone (Vasopressin). Antidiuretic hormone (ADH) is produced in the hypothalamus and then transported to the posterior pituitary where it remains until stimulated for release. The stimulation for normal release is directly connected to plasma osmolality. The role of ADH when released is to increase reabsorption of water in the distal convoluted tubule and collecting ducts of the kidneys (Huber & VanMeter, 2018). The purpose of this post is to review the effects of the excessive release of ADH called Syndrome of Inappropriate Antidiuretic Hormone (SIADH). This review will include symptoms, diagnostics, treatment plans, and links to routine screening tools related to SIADH.
Syndrome of inappropriate ADH is due to excess ADH being released from the posterior pituitary. In some cases, this may be caused by an acute situation such as stress and will be temporary or may be caused by an ectopic source such as a tumor, leading to a more chronic state (CHOP, 2020). The excessive release of ADH leads to fluid retention. The excess fluid retention often leads to hyponatremia and presents with related symptoms that can mild to severe. Mild symptoms include headache, lethargy, poor concentration, depressed mood, impaired memory, falls, muscle cramps, and nausea. Moderate to advanced symptoms include disorientation, hallucinations, limb weakness, and dysarthria. Most severe symptoms include seizures, hemiplegia, respiratory insufficiency, coma, and death (Gross, 2012)
The cornerstone diagnosis for SIADH is hyponatremia, a sodium level lower than 136 mmol/l. In order to identify serum sodium levels bloodwork must be drawn. A CMP would be appropriate in this case so the clinician can assess sodium levels as well as potassium. A CMP will also allow the clinician to assess creatinine, uric acid, and BUN levels due to decreased urinary output. A UA should also be obtained to identify osmolality. These lab value assessments will aid the clinician in determining the patient’s volume status. The assessment of lab values in addition to hyponatremia that is paired with peripheral edema, jugular vein distention without cardiac valve involvement, and dyspnea on physical assessment aid in the diagnosis of SIADH (Pliquette & Obermuller, 2017).
Standard Treatment Plan
Treatment of SIADH is dependent on multiple factors such as the degree of hyponatremia, presence of symptoms, urine osmolality, and causative factor. When treating patients, attention must be paid to the rate of correction and starts with fluid restriction, sodium administration, and possibly medication administration. Fluid restriction is suggested to be set at a goal intake of less than 800 ml/day. Sodium intake via IV solution or salt tablets in addition to dosing a loop diuretic or a vasopressin receptor antagonist will produce increased sodium levels and decrease fluid retention. Treatment and rate of correction are dependent on patient presentation and clinical findings (Sterns, 2019).
Links to Routine Screening and Treatment
Understanding the signs and symptoms of SIADH, especially for patients at a higher risk for acquiring SIADH, will help patients practice safe monitoring. Making sure patients are aware of changes in their balance, level of alertness, and urinary output are some ways in which a patient can self-screen or monitor for symptoms related to hyponatremia. In addition, patients at risk for hyponatremia or hypervolemia can weigh themselves daily for water retention. Any changes in the patients baseline will need to be reported to the patients clinician for a further workup.
In the early 1950’s routine measurement testing became available to measure serum sodium concentration levels. Since that time, it has been determined that hyponatremia is the most common electrolyte disorder encountered. Despite the common occurrence of hyponatremia, clinicians did not have a specific treatment therapy. In the last 15 years there have been two vasopressin receptor antagonists, collectively called vaptans, that have been approved for clinical use in North America. Use of vaptans correct hyponatremia efficiently and quickly reducing patients time in hospitals and need for ongoing fluid restrictions (Gross, 2012).
Grave’s disease is an autoimmune disease which is a form of hyperthyroidism characterized by increased T3 and T4 secretion. The immune system attacks the thyroid causing excessive production of thyroid hormones. The orbital connective tissue, eyelids, and extraocular muscles are also affected by this autoimmune attack (Plazinska et al., 2020). This condition occurs more frequently in women older than 30 years old. Patients with Grave’s disease experience signs of hypermetabolism, stimulation of the sympathetic nervous system, and toxic goiter (Hubert & VanMeter, 2018). The purpose of this post is to discuss Grave’s disease, common presenting symptoms, diagnostic tests, treatment plan and links to routine screening and treatment guidelines.
Some of the most obvious signs of Grave’s disease are enlarged thyroid, protruding eyes and decreased eye movements which is the result of increased orbital tissue mass and increased sympathetic stimulation. Other symptoms include tachycardia, heat intolerance, frequent bowel movements or diarrhea, goiter, nervousness or irritability, trembling hands, tiredness or muscle weakness, trouble sleeping, and weight loss diabetes. Complications like optic nerve damage, corneal ulceration, and thyrotoxic crisis can occur if Grave’s disease is left untreated. Other complications include osteoporosis and irregular heartbeats which can lead to blood clots, heart failure and stroke (National Institute of Diabetes and Digestive and Kidney Diseases [NIDDK], 2017).
Blood tests analyzing TSH, T3, T4 and uptake of radioactive iodine are important in diagnosing Grave’s disease. CT scans, MRI, thyroid scans or ultrasounds might be indicated as diagnostic tools. In Grave’s disease, a thyroid scan will show iodine distributed throughout the thyroid gland (NIDDK, 2017).
Treatment of Grave’s disease include radioactive iodine, use of antithyroid drugs or surgical removal of the thyroid gland. It is very important for advanced practice registered nurses to continue to monitor these patients as they are at risk for developing hypothyroidism or hypoparathyroidism (Hubert & VanMeter, 2018).
Links to Routine Screening and Treatment Guidelines
American Thyroid Association recommends beginning TSH screening in all adults at age 35, with the test repeated every 5 years (Garbar et al. 2012). According to Spencer et al. (2015), thyroid screening is recommended for pregnant women because thyroid dysfunction pre-pregnancy and during pregnancy is associated with increased risk of negative short term and long-term outcomes for mothers and infants. Links to screening and treatment guidelines are as follows:
Nuggets of Information
An interesting discovery while researching this topic is a study that found that cigarette smoking reduces the efficacy of radioactive iodine in the treatment of Grave’s disease. Nicotine was found to constantly affect thyroid function, therefore counteracting the effect of radioactive iodine (Plazinska et al., 2020).