Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)


Article Author:
Muhammad Yasir


Article Editor:
Oren Mechanic


Editors In Chief:
David Wood
Andrew Wilt
Mary Cataletto


Managing Editors:
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Frank Smeeks
Kristina Soman-Faulkner
Benjamin Eovaldi
Radia Jamil
Sobhan Daneshfar
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Hajira Basit
Phillip Hynes


Updated:
4/2/2019 12:27:42 AM

Introduction

Syndrome of inappropriate antidiuretic hormone ADH release (SIADH) is a condition defined by the unsuppressed release of antidiuretic hormone (ADH) from the pituitary gland or nonpituitary sources or it's continued action on vasopressin receptors. The condition was first detected in two lung cancer patients by William Schwartz and Frederic Bartter in 1967. They developed the classic Schwartz and Bartter criteria for the diagnosis of SIADH which has not changed. SIADH is characterized by impaired water excretion leading to hyponatremia with hypervolemia or euvolemia.[1][2][3]

Etiology

Most commonly, SIADH occurs secondary to another disease process elsewhere in the body. Hereditary SIADH, also known as nephrogenic SIADH, has been ascribed to the gain of function mutation in vasopressin 2 (V2) receptors in the kidneys. 

Conditions Frequently Leading to SIADH

Central nervous system disturbances:  Any central nervous system (CNS) abnormality can enhance ADH-release from the pituitary gland, leading to SIADH. These disorders include stroke, hemorrhage, infection, trauma, mental illness, and psychosis.

Malignancies: Small cell lung cancer (SCLC) is the most common tumor leading to ectopic ADH production. Less commonly, extrapulmonary small cell carcinomas, head and neck cancers, and olfactory neuroblastomas also cause ectopic ADH release.

Drugs: A number of drugs that are associated with SIADH act by enhancing the release or affect of ADH. The most common drugs include carbamazepine, oxcarbazepine, chlorpropamide, cyclophosphamide, and selective serotonin reuptake inhibitors (SSRI). Carbamazepine and oxcarbazepine act in part by increasing the sensitivity to ADH. Chlorpropamide increases the number of V2 receptors in collecting tubules. As high-dose intravenous cyclophosphamide is given with a fluid load to prevent hemorrhagic cystitis, SIADH in such patients is a particular problem, leading to potentially fatal hyponatremia. SSRIs cause SIADH by an unknown mechanism, but people above 65 years of age are more at risk. "Ecstasy" (methylenedioxymethamphetamine), a drug of abuse, is particularly associated with the direct release of ADH. (It also stimulates thirst, which farther worsens hyponatremia.) Less commonly, NSAIDs, opiates, interferons, methotrexate, vincristine, vinblastine, ciprofloxacin, haloperidol, and high dose imatinib have been linked with SIADH. 

Surgery: Surgical procedures are often associated with hypersecretion of ADH, a response that is probably mediated by pain afferents.[4]

Pulmonary disease: Pulmonary diseases, particularly pneumonia (viral, bacterial, tuberculous), can lead to SIADH by unknown mechanism. A similar response has infrequently been seen in patients with asthma, atelectasis, acute respiratory failure, and pneumothorax.

Hormone deficiency:  Both hypopituitarism and hypothyroidism may be with hyponatremia and an SIADH picture that can be corrected by hormone replacement. 

Hormone administration:  SIADH can by induced by exogenous hormone administration, as with vasopressin (to control gastrointestinal bleeding), desmopressin (dDAVP, to treat von Willebrand disease, hemophilia, or platelet dysfunction), and oxytocin (to induce labor). All three act by increasing the activity of the vasopressin-2 (V2; antidiuretic) receptors.

HIV infection: A common laboratory manifestation seen in HIV infection, either with the acquired immune deficiency syndrome (AIDS) or early symptomatic HIV infection, is hyponatremia. It can be due to SIADH, or it can be due to volume depletion, secondary to adrenal insufficiency or gastrointestinal losses. Pneumonia, due to Pneumocystis carinii or other organisms and CNS infections by opportunistic pathogens is also responsible for SIADH. [5]

Hereditary SIADH:  A gain of function mutation in the gene for the renal V2 receptors (located on X chromosome) is responsible for hereditary SIADH. Such mutation locks the renal V2 receptors in a continuous active state, leading to excessive water absorption and hyponatremia, which in turn is resistant to vasopressin receptor antagonists. 

Epidemiology

The incidence of SIADH increases with age but, recently, a higher incidence of SIADH has been reported in children. Children and older adults are found to be more hyponatremic, particularly when they were hospitalized for respiratory and CNS infections like pneumonia or meningitis. SIADH is also more prevalent is hospitalized, post-operative patients due to the administration of hypotonic fluids, drugs, and the body's response to stress. 

Pathophysiology

ADH, also known as arginine vasopressin, is formed in the hypothalamus and stored in the posterior pituitary via a pituitary stalk. The main function of ADH is osmoregulation. However, a severe reduction in effective blood volume, shifts the function of ADH to volume regulation, even at the expense of effective plasma osmolality or tonicity. "Plasma osmolality" should be differentiated from "effective plasma osmolality" or "plasma tonicity," as the latter is determined by effective osmoles in extracellular fluid  (ECF) such as sodium (which is not freely permeable across cell membranes), the main component of the ECF. Glucose and urea also increase the plasma osmolality, but these are ineffective osmoles as they are freely permeable across the cell membranes and do not take part in maintaining plasma tonicity.  

Osmoregulation

The most important and primary function of ADH is to maintain the plasma tonicity, primarily by an alteration in water balance. Osmoreceptors detect the change in effective plasma osmolality in the hypothalamus. A decrease in tonicity prevents ADH release and prevents water retention. An increase in tonicity causes ADH release, which acts on V2 receptors on the luminal surface of cortical and medullary collecting tubular cells. Under the influence of ADH, unique aquaporin-2 water channels are formed by the fusion of pre-formed cytoplasmic vesicles in the tubular cells and water is absorbed down the concentration gradient. Once the water is absorbed, these channels are removed by endocytosis and returned to the cytoplasm. The osmoreceptors are extremely sensitive, responding to alterations in the plasma tonicity of as little as 1%. [6] The osmotic threshold for ADH release in humans is about 280 to 290 mOsmol/kg. Below this level, their is little circulating ADH, and the urine should be maximally diluted with an osmolality below 100 mOsmol/kg. Above the osmotic threshold, their is a relatively linear rise in ADH secretion. This system is so efficient that the plasma osmolality does not typically vary by more then 1% to 2%, despite wide water intake fluctuations. [7]

In patients with SIADH, levels of ADH are high even in the presence of decreased plasma osmolality and/or hyponatremia. Excess water absorption keeps the blood volume high or normal. 

Volume Regulation

An acute drop in blood pressure as sensed by " volume receptors" rather then "osmoreceptors" causes ADH release (along with other hormones like rennin and epinephrine) which generates free water absorption from the kidneys. This can potentially lead to hyponatremia and a decrease in effective ECF osmolality. So, the main focus in rapid and/or substantial decrease in blood volume is "volume regulation," even at the cost of osmolality. This affect is more prominent in patients with liver disease or cardiac disease, and hyponatremia in such patients is the direct predictor of a worse prognosis.[8]

History and Physical

Clinical manifestations of SIADH can be due to hyponatremia and decreased ECF osmolality which causes the water to move into the cells causing cerebral edema. Signs and symptoms depend upon the rate and severity of hyponatremia and the degree of cerebral edema. The earliest clinical manifestations of acute hyponatremia include nausea and malaise, which may be seen when the serum sodium concentration falls below 125 to 130 mEq/L (normal 135 to 145mEq/L). Vomiting is an ominous sign for patients with acute hyponatremia. With a more severe and acute fall in sodium concentration, headache, lethargy, obtundation, and eventually, seizures can occur. Coma and respiratory arrest can occur if the serum sodium level falls below 115 to 120 mEq/L. Acute hyponatremic encephalopathy may be reversible, but permanent neurologic damage or death can occur, particularly in premenopausal women.

Chronic hyponatremia allows cerebral adaptation, and the patients remain asymptomatic despite a serum sodium concentration below 120mmol/L. Nonspecific symptoms like nausea, vomiting, gait disturbances, memory and cognitive problems, fatigue, dizziness, confusion, and muscle cramps can occur with chronic hyponatremia. Sign and symptoms or mild and chronic hyponatremia are often subtle and missed during history and physical examination. Nausea and vomiting effect approximately one-third of patients with chronic hyponatremia who have a serum sodium concentration less then 120 mmol/L. The Idiopathic SIADH is more common in patients over 65 years of age, and mild to moderate hyponatremia in such patients may contribute to fractures in addition to a higher risk of falls and gait problems. 

History must include inquiry about head injury, chronic pain, smoking, weight loss, pulmonary symptoms, drug intake or substance abuse (particularly heroin and ecstasy), in addition to all the above-mentioned symptoms. The source of excess fluid should be evaluated, and chronicity of the condition should be considered. 

Physical examination should include assessment of volume status, as these patients are typically euvolemic. Skin turgor and blood pressure are within normal range. Moist mucus membranes with no evidence of JVP or edema typically indicate euvolemia. Detailed neurological and chest examination should be done.

Evaluation

Their is no single best test to diagnose SIADH. Patients usually present with hyponatremia with normal volume status. Schwartz and Bartter made a clinical criterion in 1967 which is still valid up to the date.[9][10][11]

The Schwartz and Bartter Clinical Criterion

  • Serum sodium less then 135mEq/L
  • Serum osmolality less then 275 mOsm/kg
  • Urine sodium greater then 40 mEq/L (due to ADH-mediated free water absorption from renal collecting tubules)
  • Urine osmolality greater then 100 mOsm/kg
  • The absence of clinical evidence of volume depletion - normal skin turgor, blood pressure within the reference range
  • The absence of other causes of hyponatremia - adrenal insufficiency, hypothyroidism, cardiac failure, pituitary insufficiency, renal disease with salt wastage, hepatic disease, drugs that impair renal water excretion.
  • Correction of hyponatremia by fluid restriction

Renal function tests and random blood sugar test should be done to check hyperglycemia and uremia as these are the potential causes of pseudohyponatremia. 

Tests for SIADH

  • Serum osmolality and serum sodium
  • Urine sodium concentration and osmolality
  • Renal function tests: BUN and creatinine
  • BSR (Blood sugar random)
  • Thyroid profile
  • Serum cortisol
  • Serum K+, bicarbonate, chloride
  • Fasting lipid profile
  • Liver function tests

Hypothyroidism and adrenal insufficiency must be ruled out before labeling the patient with SIADH. Farther tests should be done to find out underlying cause according to the history. Patients with long-standing smoking history, weight loss, or pulmonary symptoms must have a chest X-ray and CT scan to look for SCLC. 

Treatment / Management

The patients with SIADH have a combination of ADH-induced water retention and secondary solute loss. The overall solute loss is more prominent then water retention in patients with chronic SIADH. The treatment of SIADH involves correction and maintenance of corrected sodium levels and correction of underlying abnormalities such as hypothyroidism or pulmonary or CNS infection. The goal of sodium correction is more then 130 mEq/L.

The choice of treatment depends essentially upon the severity of symptoms at presentation. A mild but rapid fall in sodium levels can cause severe symptoms like delirium, confusion, and seizures while chronic but significant hyponatremia (less then 125 mEq/L) may produce mild or no symptoms. So, in patients with mild to moderate symptoms, the mainstay of the treatment is the restriction of oral water intake with the goal of less then 800 mL/day. If hyponatremia is persistent, sodium chloride in the form of oral salt tablets or intravenous saline can be given. Loop diuretics such as furosemide (20 mg twice daily) also can be added to salt tablets as it helps to decrease the urine concentration and thereby increasing water excretion particularly among the patients who's urine osmolality is much higher then serum osmolality (greater then 500 mOsm/kg).[12]

 To correct sodium levels, it should be known that urine osmolality in such patients is usually twice the amount of serum osmolality, i.e., greater then 500 mOsm/kg. So, the fluid needed to correct the sodium levels must have an osmolality that is more then urine osmolality. Isotonic saline may not correct hyponatremia in such patients or it may even worsen hyponatremia and symptoms. Therefore, a solution with an electrolyte concentration greater then the urine electrolyte concentration must be used. Three percent hypertonic saline (osmolality 513 mOsm/kg) is used for this purpose in patients with severe symptomatic or resistant hyponatremia. Also, the rate of correction is an important factor. It should not exceed more then 8 mEq/L per 24 hours or 0.5 to 1 mEq/L per hour. More rapid correction can result in osmotic demyelination of the CNS leading to severe lethal complications such as osmotic demyelination syndrome ("Locked-in" syndrome) causing quadriplegia.[13]

Patients presenting with severe symptoms such as seizures, confusion, or delirium need urgent initial correction with hypertonic saline infusion for first few hours rather then just water restriction. A 100 mL bolus of 3% hypertonic saline is given in the first 3 to 4 hours, and sodium levels are measured within 2 to 3 hours so that farther doses can be adjusted to avoid correcting too rapidly. A rise of 3 to 4 mEq/L within the first few hours in such distressing conditions can be justified. If the patient's mental status does not improve, more boluses of 100 mL hypertonic saline can be given in the same way as above until symptoms get better. 

Vasopressin receptor antagonists such as conivaptan (IV) or tolvaptan (oral) are also available and approved for severe persistent SIADH. These drugs prevent ADH-mediated free water retention by antagonizing V2 receptors and correct hyponatremia. Tolvaptan is hepatotoxic and should not be given to the patients with liver disease. Intravenous conivaptan is very effective in correcting hyponatremia and baseline mental status in hospitalized patients. Other therapies, like lithium or demeclocycline, are also effective in SIADH, but both drugs are nephrotoxic and have other potential side effects; therefore, they should only be used when other therapies fail.[14]

Enhancing Healthcare Team Outcomes

The management of patients with SIADH is multidisciplinary because of the diverse causes and the challenge to treat the patient successfully without causing further complications. The aim is to control the primary condition causing SIADH as well as monitoring the fluid status and electrolytes. The nursing staff and clinicians involved must work as an interdisciplinary team to minimize complications and provide the best care. Several newer agents are available that can lower or block actions of ADH, but expertise is necessary when using these medications. The prognosis for patients with SIADH depends on the cause. For benign causes, the prognosis is excellent but those cases caused by malignancies tend to have a poor outcome. [15][16](Level V)


Interested in Participating?

We are looking for contributors to author, edit, and peer review our vast library of review articles and multiple choice questions. In as little as 2-3 hours you can make a significant contribution to your specialty. In return for a small amount of your time, you will receive free access to all content and you will be published as an author or editor in eBooks, apps, online CME/CE activities, and an online Learning Management System for students, teachers, and program directors that allows access to review materials in over 500 specialties.

Improve Content - Become an Author or Editor

This is an academic project designed to provide inexpensive peer-reviewed Apps, eBooks, and very soon an online CME/CE system to help students identify weaknesses and improve knowledge. We would like you to consider being an author or editor. Please click here to learn more. Thank you for you for your interest, the StatPearls Publishing Editorial Team.

Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) - Questions

Take a quiz of the questions on this article.

Take Quiz
Which drug is used as an ADH antagonist to treat SIADH?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
Which of the following is least likely to cause SIADH?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
Which of the following drugs is often used to treat central SIADH?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
Which antibiotic or antibiotic class is used to treat ADH secreting tumors?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
Which of the following is the best treatment for patients with symptomatic syndrome of inappropriate antidiuretic hormone (SIADH)?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A male is seen in the endocrine clinic with complaints of fatigue and general malaise. He says that for the past several months he has had to quit his job because of his fatigue. Besides the headaches and nausea, he has little appetite. Blood work reveals that he has a sodium of 112, potassium of 4.1, white blood cell count of 5.5, hemoglobin of 9.0, and a hematocrit of 29. You suspect that he may have the syndrome of inappropriate antidiuretic hormone (SIADH) secretion and you decide to treat him with which of the following?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
Which of the following is a feature of the syndrome of inappropriate secretion of anti-diuretic hormone (SIADH)?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
Which is the cardinal laboratory feature of the syndrome of inappropriate antidiuretic hormone secretion (SIADH)?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 62-year-old male who is a heavy smoker presents to you with complaints of general malaise, occasional cough, and weight loss. He says that he has lost 10 lbs over the last 2 months. He denies any travel, recent infections, or use of any medications. He does have borderline diabetes which he has controlled with diet. Examination reveals that he has some mild peripheral edema in the extremities, and he has clubbing bilaterally. Blood works reveals a mild anemia and sodium of 122. What is the next test to order?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 66-year-old male with a long history of alcoholism and smoking presents confused and is found to have a BP of 112/70, normal orthostatics, a normal physical exam, and the following lab values: Na 112 mEq/L, K 3.6 mEq/L, Cl 84 mEq/L, HCO3 20 mEq/L, BUN 6 mg/dL, Creatinine 0.6 mg/dL, Glucose 99 mg/dL, Urine specific gravity 1.016. What is the most likely diagnosis?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 67-year-old male with a long history of alcoholism and smoking presents with confusion. He has a BP of 110/76, normal orthostatics, and normal physical exam. Blood work reveals Na 116 mEq/L, K 3.5 mEq/L, Cl 87 mEq/L, HCO3 22 mEq/L, BUN 7 mg/dL, Creatinine 0.7 mg/dL, Glucose 90 mg/dL, and Urine specific gravity of 1.014. What is the most likely diagnosis?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
Which is least likely to be found in a patient with the syndrome of inappropriate antidiuretic hormone secretion (SIADH)?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
Lung cancer and syndrome of inappropriate secretion of antidiuretic hormone (SIADH) are associated with which of the following electrolyte abnormalities?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
Which of the following conditions is least likely to cause SIADH?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
Which of the following statements about syndrome of inappropriate antidiuretic hormone, SIADH is correct?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
Which of the following statements concerning the treatment for SIADH is incorrect?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
An 11-year-old is admitted to intensive care after a head injury. After 6 hours of intravenous fluids, the urine output is 1 ml/kg/hour and the serum sodium is 124 milliequivalent/L. The patient's central venous pressure is 7 cm H2O. Select the best management.



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
After a motor vehicle accident with traumatic brain injury a patient has syndrome of inappropriate antidiuretic hormone (SIADH). Which of the following is least important to follow treatment of this condition?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 38-year-old woman presents for her annual physical. She reports feeling well. Physical exam is unremarkable; however, laboratory findings show hyponatremia with a markedly elevated urine osmolality. Which of the following is the most likely etiology of these findings?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A female with a 45 pack year history presents with weight gain and a lung mass on chest radiograph. She has hyponatremia and hyperosmolar urine. What is the most probable diagnosis?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A patient presents to the clinic with numerous complaints. He claims that over the past few months he has no appetite, intermittent nausea, weakness, headache, muscle cramps, and confusion. He denies any trauma, does not smoke, and has no medical issues except for being a smoker. The physical exam is unremarkable. Blood work reveals sodium of 120; serum osmolality is 230 and a high urine osmolality. The urine sodium is more than 40 mEq/L. The blood urea nitrogen is low but the potassium levels are normal. CT scan reveals the presence of cerebral edema. What should the initial treatment be in this patient?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A patient has lung cancer and develops syndrome of inappropriate antidiuretic hormone secretion (SIADH). Which of the following suggests the treatment prescribed is working? Select all that apply.



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A patient with a past medical history of long-term smoking and a recent diagnosis of small cell lung carcinoma has a sodium level of 123 mEq/L and serum osmolality of 240 milliosmoles/kg. On further testing, the urine osmolality is found to be 500 milliosmoles/kg. Based on the most likely diagnosis, this patient's lab findings are due to which of the following?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up

Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) - References

References

Lockett J,Berkman KE,Dimeski G,Russell AW,Inder WJ, Urea treatment in fluid restriction-refractory hyponatraemia. Clinical endocrinology. 2019 Jan 7;     [PubMed]
Monden MAH,van der Vorst LP,Martens HJM,van der Wolk A, [The syndrome of inappropriate diuretic hormone secretion (SIADH) ending lethal during the use of paliperidon and lamotrigine]. Tijdschrift voor psychiatrie. 2018;     [PubMed]
Baba Y,Harada H,Shimada S,Sasaki Y,Murai S,Abe M,Fujiwara S,Arai N,Kawaguchi Y,Kabasawa N,Tsukamoto H,Uto Y,Ariizumi H,Yanagisawa K,Hattori N,Saito B,Nakamaki T, [Syndrome of inappropriate secretion of antidiuretic hormone in multiple myeloma patients treated with bortezomib, lenalidomide, and dexamethasone combination therapy]. [Rinsho ketsueki] The Japanese journal of clinical hematology. 2018;     [PubMed]
Silveira MAD,Seguro AC,da Silva JB,Arantes de Oliveira MF,Seabra VF,Reichert BV,Rodrigues CE,Andrade L, Chronic Hyponatremia Due to the Syndrome of Inappropriate Antidiuresis (SIAD) in an Adult Woman with Corpus Callosum Agenesis (CCA). The American journal of case reports. 2018 Nov 12;     [PubMed]
Rondon-Berrios H,Tandukar S,Mor MK,Ray EC,Bender FH,Kleyman TR,Weisbord SD, Urea for the Treatment of Hyponatremia. Clinical journal of the American Society of Nephrology : CJASN. 2018 Nov 7;     [PubMed]
Berardi R,Antonuzzo A,Blasi L,Buosi R,Lorusso V,Migliorino MR,Montesarchio V,Zilembo N,Sabbatini R,Peri A, Practical issues for the management of hyponatremia in oncology. Endocrine. 2018 Jul;     [PubMed]
Seltzer J,Wedemeyer MA,Bonney PA,Carmichael JD,Weiss M,Zada G, Outcomes following transsphenoidal surgical management of incidental pituitary adenomas: a series of 52 patients over a 17-year period. Journal of neurosurgery. 2018 May 1;     [PubMed]
Humayun MA,Cranston IC, In-patient Tolvaptan use in SIADH: care audit, therapy observation and outcome analysis. BMC endocrine disorders. 2017 Nov 6;     [PubMed]
Steele A,Gowrishankar M,Abrahamson S,Mazer CD,Feldman RD,Halperin ML, Postoperative hyponatremia despite near-isotonic saline infusion: a phenomenon of desalination. Annals of internal medicine. 1997 Jan 1;     [PubMed]
Robertson GL, Regulation of arginine vasopressin in the syndrome of inappropriate antidiuresis. The American journal of medicine. 2006 Jul;     [PubMed]
Robertson GL,Shelton RL,Athar S, The osmoregulation of vasopressin. Kidney international. 1976 Jul;     [PubMed]
Vitting KE,Gardenswartz MH,Zabetakis PM,Tapper ML,Gleim GW,Agrawal M,Michelis MF, Frequency of hyponatremia and nonosmolar vasopressin release in the acquired immunodeficiency syndrome. JAMA. 1990 Feb 16;     [PubMed]
Cooke CR,Turin MD,Walker WG, The syndrome of inappropriate antidiuretic hormone secretion (SIADH): pathophysiologic mechanisms in solute and volume regulation. Medicine. 1979 May;     [PubMed]
Adrogué HJ,Madias NE, Hyponatremia. The New England journal of medicine. 2000 May 25;     [PubMed]
Rose BD, New approach to disturbances in the plasma sodium concentration. The American journal of medicine. 1986 Dec;     [PubMed]
Greenberg A,Verbalis JG, Vasopressin receptor antagonists. Kidney international. 2006 Jun;     [PubMed]

Disclaimer

The intent of StatPearls is to provide practice questions and explanations to assist you in identifying and resolving knowledge deficits. These questions and explanations are not intended to be a source of the knowledge base of all of medicine, nor is it intended to be a board or certification review of Pediatric. The authors or editors do not warrant the information is complete or accurate. The reader is encouraged to verify each answer and explanation in several references. All drug indications and dosages should be verified before administration.

StatPearls offers the most comprehensive database of free multiple-choice questions with explanations and short review chapters ever developed. This system helps physicians, medical students, dentists, nurses, pharmacists, and allied health professionals identify education deficits and learn new concepts. StatPearls is not a board or certification review system for Pediatric, it is a learning system that you can use to help improve your knowledge base of medicine for life-long learning. StatPearls will help you identify your weaknesses so that when you are ready to study for a board or certification exam in Pediatric, you will already be prepared.

Our content is updated continuously through a multi-step peer review process that will help you be prepared and review for a thorough knowledge of Pediatric. When it is time for the Pediatric board and certification exam, you will already be ready. Besides online study quizzes, we also publish our peer-reviewed content in eBooks and mobile Apps. We also offer inexpensive CME/CE, so our content can be used to attain education credits while you study Pediatric.