Syndrome of inappropriate antidiuretic hormone overview: Difference between revisions
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===Electrocardiogram=== | ===Electrocardiogram=== | ||
[[EKG]] may be helpful in the [[diagnosis]] of [[SIADH]] | [[EKG|Electrocardiogram (EKG)]] may be helpful in the [[diagnosis]] of [[SIADH]]. Findings on an [[EKG]] suggestive of [[SIADH]] are like classic [[Brugada]] like pattern, include downward coving of [[ST-segment]] and [[T-wave inversion]] in the anterior [[precordial]] leads. The [[EKG]] changes will be normalized after the [[sodium]] levels were corrected. | ||
===Xray=== | ===Xray=== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Vindhya BellamKonda, M.B.B.S [2]
Overview
The syndrome of inappropriate antidiuretic hormone (SIADH) is a condition commonly found in individuals hospitalized for central nervous system (CNS) injury. SIADH is a syndrome characterized by excessive release of antidiuretic hormone (ADH or vasopressin) from the posterior pituitary gland or any other source, resulting in hyponatremia, and sometimes fluid overload. Syndrome of inappropriate antidiuretic hormone production (SIADH) leads to excessive water retention and thus a decrease in sodium concentration. SIADH may be occur as a result of central nervous system diseases, cancers, pulmonary diseases and some drugs. Signs and symptoms of SIADH vary widely. Some patients with SIADH may become severely ill while others may have no symptoms at all. Common symptoms include nausea, vomiting, loss of appetite, fatigue, weakness and altered consciousness. Blood tests of hyponatremia (sodium <135 mEq/L) and low serum osmolality (<280 mOsm/kg) may prompt the diagnosis of SIADH. Treatment of SIADH depends on the cause. Restriction of water intake and supplementation of sodium may lead to improvement. Prognosis of SIADH varies depending on the cause.
Historical Perspective
In 1951, Leaf and Mambi first described SIADH. Later it was described by Dr Frederic Bartter in two patients with lung cancer from Boston (MA) and Bethesda (MD), in 1957.
Classification
SIADH may be classified into several sub-types based on the pattern of arginine vasopressin (AVP) secretion in response to a range of plasma osmolalities into type A, type B, type C, and type D.
Pathophysiology
Clinical picture of SIADH may result from genetic disorders that result in antidiuresis. A mutation affecting the gene for the renal V2 receptor is implicated in the pathogenesis. Congenital nephrogenic diabetes insipidus typically has a resistance of the renal collecting duct to the action of the arginine vasopressin hormone responsible for the inability of the kidney to concentrate urine. In the X-linked form, inactivating mutations of the V2 receptor gene leading to functional loss of the mutated receptors are seen.
Causes
Syndrome of inappropriate antidiuretic hormone is caused by excess of renal water reabsorption through inappropriate antidiuretic hormone secretion. There are various causes attributed to SIADH ranging from malignancies, medications, central nervous system causes, and infectious. Some of the most common causes of SIADH include malignancies, like small cell lung cancer and medications, such as selective serotonin reuptake inhibitors and carbamazepine.
Differential diagnosis
Syndrome of inappropriate antidiuretic hormone consists of hyponatremia, inappropriately elevated urine osmolality, excessive urine sodium, and decreased serum osmolality in a euvolemic patient without edema. These findings should occur in the absence of diuretic treatment with normal cardiac, renal, adrenal, hepatic, and thyroid function. Hyponatremia occurs in about 30% of hospitalized patients and SIADH is the most frequent cause of hyponatremia. Differentiating SIADH from other causes of hyponatremia becomes essential to evaluate the treatment plan.
Epidemiology and Demographics
Syndrome of inappropriate antidiuretic hormone (SIADH) can occur at any age. Its incidence depends on various possible etiologies. Prevalence of SIADH was estimated to be 2,500-30,000 cases per 100,000 individuals. The incidence and prevalence of SIADH in particular is less thoroughly studied in the literature.
Risk Factors
The most common risk factors of Syndrome of inappropriate antidiuretic hormone (SIADH) are malignancy, pulmonary disorders, CNS disorders and medications.
Screening
There is insufficient evidence to recommend routine screening for SIADH.
Natural History, Complications, and Prognosis
The symptoms of SIADH can occur at any age. If left untreated can lead to complications, such as confusion, seizures, stupor, and coma. Some of the complications of SIADH treatment are include cerebral edema and central pontine myelinolysis, which are seen with rapid sodium correction. The prognosis of Syndrome of inappropriate antidiuretic hormone (SIADH) depends primarily on its cause. The prognosis of Syndrome of inappropriate antidiuretic hormone (SIADH) depends primarily on its cause. If the cause is medications, SIADH usually improves after discontinuing the medication. SIADH secondary to an infection, improves with the treatment of the infection. SIADH secondary to cancers, has poor outcome. Patients with SIADH have different signs, symptoms and prognosis depending on the etiology of SIADH. Serum sodium concentration at short-term follow-up is predictive of long-term survival. Rapid correction of serum sodium concentration can lead to various complications.
Diagnosis
History and Symptoms
Symptoms of SIADH depend on the level of sodium in the blood and the rate at which the level of sodium falls. Symptoms may be non-specific, such as generalized fatigue and weakness; but if become severe, then symptoms, such as irritability, nausea, vomiting, muscle weakness and cramps, loss of appetite, confusion, personality changes, hallucinations, seizures, stupor, and coma may be seen.
Physical Examination
Physical examination of patients with syndrome of inappropriate antidiuretic hormone (SIADH) is usually remarkable for ill and sometimes confused appearance, orthostatic hypotension, Cheyne-Stokes respiration, dysarthria, altered mental status, confusion, disorientation, delirium, generalized muscle weakness, generalized seizures, coma, myoclonus, tremor, asterixis, hyporeflexia, and ataxia.
Laboratory Findings
Laboratory findings which are helpful in diagnosing Syndrome of inappropriate antidiuretic hormone (SIADH) include serum electrolytes (especially sodium), blood urea nitrogen (BUN), creatinine, glucose levels, and osmolality. Laboratory findings in patients with SIADH may show hyponatremia (sodium <135 mEq/L) and low serum osmolality (< 280 mOsm/kg). Patients with SIADH have elevated urinary sodium level (> 20 mMol/L) and urine osmolality (generally > 100 mOsm/L). Patients with SIADH also have low BUN, normal creatinine, hypouricemia, and hypoalbuminemia.
Electrocardiogram
Electrocardiogram (EKG) may be helpful in the diagnosis of SIADH. Findings on an EKG suggestive of SIADH are like classic Brugada like pattern, include downward coving of ST-segment and T-wave inversion in the anterior precordial leads. The EKG changes will be normalized after the sodium levels were corrected.
Xray
Imaging Studies, such as x-ray, CT and MRI may be help find the causes of syndrome of inappropriate antidiuretic hormone.
CT scan
Imaging Studies, such as x-ray, CT and MRI may be help find the causes of syndrome of inappropriate antidiuretic hormone.
MRI
MRI is one of the important diagnostic tool to find the CNS causes of SIADH
Ultrasound
There are no ultrasound findings associated withSIADH.
Other Imaging Findings
There are no other specific imaging findings forSIADH
Other Diagnostic Studies
There are no additional diagnostic findings for SIADH.
Treatment
Medical Therapy
Treatment of syndrome of inappropriate antidiuretic hormone depends on the etiology. For immediate improvement, all patients with SIADH require strict restriction of their dailywater intake and correction of serum sodium levels. The serum sodium can can be corrected depending on the initial sodium levels of the patient. Mild cases can be managed easily with exclusive fluid restriction. Moderate cases of SIADH are treated with loop diuretics and normal saline, whereas, 3% hypertonic saline may be used in severe cases. In emergency settings, Vasopressin-2 receptor antagonists, ( such as conivaptan ortolvaptan) are used. The definitive treatment of SIADH involves treatment of the underlying condition. Urea, demeclocycline and lithium are also used in the treatment of SIADH.
Surgery
The definitive treatment of SIADH involves treatment of the underlying condition. SIADH resulting from a carcinoma may require surgery, radiation therapy, or chemotherapy.
Primary prevention
Effective measures for the primary prevention of SIADH include regular monitoring of drugs by the health care provider and screening for cancers.
Secondary prevention
There are no secondary preventive measures available for SIADH.