Syndrome of inappropriate antidiuretic hormone differential diagnosis

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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

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) was initially described by Leaf and Mamby. SIADH consists ofhyponatremia, 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 hyponatremia due to SIADH from other causes of hyponatremia becomes essential to evaluate the treatment plan. Syndrome of inappropriate antidiuretic hormone must be differentiated from cerebral salt wasting , adrenal insufficiency, hypopituitarism, hypothyroidism,psychogenic polydipsia

Differentiating Syndrome of inappropriate antidiuretic hormone from other Diseases

SIADH must be differentiated from cerebral salt wasting, adrenal insufficiency, hypopituitarism, hypothyroidism, psychogenic polydipsia

Disease	Causes	Symptoms	Diagnosis and treatment
SIADH	SIADH is a syndrome characterized by excessive release of antidiuretic hormone (ADH or vasopressin) from the posterior pituitary gland or another source. The result is hyponatremia, and sometimes fluid overload.	Symptoms are variable. Ranging from nausea/vomiting,cramps,depressed mood,irritability,confusion andhallucinations. In severe cases seizures ,stupor or coma may result.	Hyponatremia <135 mmol/l Decreased effective serum osmolality<275mosm Urine sodium concentration>40mmol/litre Plasma uric acid <200;FeUrate>12% Absence of edematous disease likecardiac failure, liver cirrhosis,nephrotic syndrome. normal adrenal and thyroid function
Cerebral salt wasting	Cerebral salt wasting is defined as the renal loss of sodium during intracranial disease leading to hyponatremia and a decrease in extracellular fluid volume.	polyuria,polydipsia,lightheadedness, muscle cramps,orthostatic hypotension,headaches	The patient ishypovolemic and hyponatremic. Treatment is with adequate hydration and sodium replacement.
Adrenal insufficiency	Adrenal insufficiency ranges from mild nonspecific symptoms to life-threatening shock condition. An important distinction in these patients is the presence ofmineralocorticoid deficiency. Those with secondary or tertiary adrenal insufficiency will typically have preserved mineralocorticoid function due to the separate feedback systems. Adrenal insufficency can be primary, secondary or tertiary. Common causes of primary adrenal insufficiency: Autoimmune Iatrogenic Drugs Others- adrenal hemorrhage, cancer,infection. congenital. Secondary adrenal insufficiency refers to decreased adrenocorticotropic hormone (ACTH) stimulation of the adrenal cortex and therefore does not affect aldosterone levels. Traumatic brain injury (TBI) and panhypopituitarism are common causes. Tertiary adrenal insufficiency refers to decreased hypothalamic stimulation of the pituitary to secrete ACTH. Exogenous steroid administration is the most common cause of tertiary adrenal insufficiency.	fatigue muscle weakness loss of appetite weight loss abdominal pain diarrhea Vomiting Chronic disease is characterized by weight loss,sparse axillary hair,hyperpigmentation of the skin,orthostatic hypotension. Acute addisonian crisis is characterized by fever and hypotension. A low sodium with a high potassium level and mild acidosis are also present.	The diagnosis of Addison disease is made through rapid ACTH administration and measurement of cortisol.Lab findings include white blood cell count with moderate neutropenia,lymphocytosis,and eosinophilia;elevated serum potassium and urea nitrogen;low sodium;low blood glucose;and morning low plasma cortisol. The definitive diagnosis is the cosyntropin or ACTH stimulation test. A cortisol level is obtained before and after administering ACTH. A normal person should show a brisk rise in cortisol level after ACTH administration. Management: The management of Addison disease involves glucocorticoid,mineralocorticoid,and sodium chloride replacement. Adrenal crisis: In adrenal crisis,get a cortsol level,then rapidly administer fluids and hydrocortisone. Adrenal crisis may occur in: previously undiagnosed patient with adrenal insufficiency who has undergone surgery,has a serious infection,or any major stressful conditions. Bilateral adrenal infarction or hemorrhage, Patient who is abruptly withdrawn from chronic glucocorticoid therapy
Hypopituitarism:	Hypopituitarism is defined as the partial or complete loss of anterior pituitary function that can result from acquired or congenital causes. Etiology is as follows: Pituitary tumors Sellar tumors Head trauma Infection empty sella infiltration Idiopathic congenital	Signs and symptoms of hypopituitarism vary, depending on the deficient hormone and severity of the disorder,some of the symptoms may be as follows: Fatigue Weight loss Decreased libido Decreased appetite Facial puffiness Anemia Infertility Cold insensitivity. amenorrha,inability to lactate in breast feeding women Decreased facial or body hair in men Short stature in children	The diagnosis is based on detailed investigation of symptoms of target endocrine gland function relative to the corresponding pituitary hormone deficiency. The clinical manifestations of hypopituitarism result from the degree of the specific hormone deficiency. A thorough and longitudinal history and physical examination, including visual field testing, are important. Hypopituitarism may involve from one to all endocrine axes regulated by the pituitary (in order of frequency: growth hormone deficiency>secondary hypogonadism>secondary hypothyroidism>secondary adrenal failure).The treatment of permanent hypopituitarism consists of replacement of the peripheral hormones (hydrocortisone, DHEA, thyroxine, testosterone or oestradiol, growth hormone. surgery, and/or radiotherapy to restore normal endocrine function and quality of life. Patients with hypopituitarism require lifelong monitoring of serum hormone levels and symptoms of hormone deficiency or excess. Long-term care and monitoring of patients with hypopituitarism requires a experienced endocrinologist.
Hypothyroidism	Hypofunctioning of the thyroid gland due to multifactorial etiology ranging from congenital to autoimmune causes described below: Congenital Autoimmune Drugs Post surgery post radiation Infiltrative e.g., amyloid	Fatigue Constipation Dry skin Weight gain Cold intolerance Puffy face Hoarseness Muscle weakness Elevated blood cholesterol level Bradycardia Myopathy Depression Impaired memory	Diagnosis of hypothyroidism is based on blood tests,T3(triiodothyronine),T4(Thyroxine) and TSH (thyroid stimulating hormone). Signs and symptoms are neither sensitive nor specific for the diagnosis. TSH is the most sensitive tool for screening,diagnosis and treatment follow up, when pituitary is normal. The drug of choice for treatment is Levothyroxine.
Psychogenic polydipsia	Also called as primary polydipsia is characterized by polyuria and polydipsia. Causes could be: Defect in the hypothalamus Adverse effect of a medication Traumatic brain injury Psychiatric disorders such as schizophrenia	polyuria,polydipsia,confusion,lethargy,psychosis,seizures and sometimes, even death.	Evaluation of psychiatric patients with polydipsia warrants a comprehensive evaluation for other medical causes of polydipsia, polyuria, hyponatremia, and the syndrome of inappropriate secretion of antidiuretic hormone. The management strategy in psychiatric patients should include fluid restriction and behavioral and pharmacologic modalities. The water deprivation test is the gold standard test to differentiate central or nephrogenic diabetes insipidus (DI) from primary polydipsia (PP) in patients with polyuria and polydipsia. n healthy subjects, water deprivation causes the plasma osmolality to rise above 280–290 mOsmol/kg, which leads to the release of AVP into the circulation. In the collecting ducts of the kidney, AVP binds to the vasopressin type 2 receptor and this is followed by expression of aquaporin 2 channels. This results in increased water retention with a rise in urine osmolality to a maximum of 1000–1200 mOsmol/kg and restoration of plasma osmolality toward the reference range.

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