Polydipsia
Soraya Nasraty
Polydipsia is a symptom that can be attributed to medical or psychogenic causes and has a prevalence of 3% to 39% among chronic psychiatric inpatients (1). It is
a common symptom in patients with diabetes mellitus (DM) (Chapter 14.1) and prominent in patients with diabetes insipidus (DI). Polydipsia is usually seen with polyuria.
Approach
Initially try to classify and identify the cause of polydipsia.
A. Poorly resorbed solutes. DM should be suspected in any patient with polydipsia and polyuria of recent onset that is caused by the osmotic diuresis from glucose (Chapter 14.1). Mannitol, sorbitol, or urea can also cause polyuria.
B. Primary polydipsia. Increased fluid intake of up to 20 L/day may be seen in patients with psychogenic polydipsia. This can be caused by hyperactivity of hypothalamic thirst centers or by the anticholinergic effects of neuroleptic medications which cause dry mouth. Other patients may have delusions leading to increased fluid intake (1).
C. Diabetes insipidus can result from either a central (neurogenic DI) or renal cause (nephrogenic DI).
1. Central (complete or partial) DI is caused by a defect in the secretion of antidiuretic hormone (ADH) by the pituitary gland. Neurogenic DI can be idiopathic or be caused by an intracranial event such as a brain tumor, head trauma, neurosurgery, toxic brain injury, or metastatic cancer. Rare forms include granulomatous disease (tuberculosis, sarcoidosis) and an inherited autosomally dominant form. Vasopressin-induced DI occurs in the last trimester of pregnancy and is often associated with preeclampsia.
2. Nephrogenic DI is caused by the nephrons not responding to ADH, which could be congenital or acquired. It can be secondary to medications (lithium, methoxyflurane, demeclocycline) or result from systemic hypokalemia and hypercalcemia.
D. Iatrogenic polydipsia can occur because a patient misinterprets the physician’s instructions to drink plenty of water (2).
History
Thirst, which is the chief complaint of patients with DM, DI, and psychogenic polydipsia, is associated with polyuria. Nocturia occurs more frequently with DM and DI than with psychogenic polydipsia. Polydipsia usually starts abruptly in central DI and patients often have a preference for ice cold water (3). In eliciting the history, take note of neurologic symptoms (problems with visual fields, headaches, numbness), a prior history of cancer (particularly metastatic brain cancer), a history of trauma, neurosurgery, and infections (e.g., encephalitis). The patient’s psychiatric history may also be relevant.
Physical examination
A thorough general physical examination, including vital signs, is helpful in making the diagnosis, but the emphasis is on the neurologic examination (i.e., visual fields, cranial nerve deficits, oculomotor palsies, and reflexes). Signs of recent weight loss or presence of peripheral neuropathy is helpful in making the diagnosis of DM (Chapters 2.13 and 4.6).
Testing
A. Clinical laboratory tests. A urinalysis needs to be performed to look for glucosuria of DM or the low specific gravity associated with DI. A chemistry panel is helpful in checking for elevated serum glucose levels of DM or an elevated creatinine seen with renal disease or nephrogenic DI. A calcium level could be useful if hypercalcemia is suspected (Chapter 17.4). Serum and urine osmolality are useful in differentiating between DI, which presents with increased serum osmolality and in an appropriately low urine osmolality (specific gravity < 1.005), and excessive water intake, which presents with low or normal serum osmolality and an appropriately low urine osmolality. Normal serum values are between 285 and 295 mOsm/L.
B. Diagnostic imaging. Magnetic resonance imaging (MRI) of the head may be indicated to exclude pituitary or hypothalamic tumors. In neurogenic DI, MRI is quite specific because the normal bright spot of a functioning pituitary gland will be absent (3).
C. Water deprivation test. This indirect test may be useful in making the diagnosis of DI and to differentiate between neurogenic and nephrogenic DI by determining the effects of water deprivation (mild dehydration) on ADH secretion by measuring serum, urine osmolality, urine-specific gravity, and serum sodium in a controlled environment (3). This test needs to be carefully supervised by someone able to treat severe hypertonic dehydration if necessary. Patients with mild polydipsia are placed on fluid restriction starting at midnight prior to testing, but fluids are restricted in those with severe polydipsia during the day only. Baseline body weight, plasma osmolarity, serum sodium, and urine osmolarity are determined. Urine osmolarity and weight are assessed on an hourly basis. Adequate dehydration is noted by a decrease in body weight by 5% and serum osmolarity by more than 275 mOsm/L. A normal response would show normal plasma osmolarity and sodium concentration with decreased urine output and increasing urine osmolarity to more than 800 mOsm/L (i.e., two to four times greater than the plasma). In contrast to healthy patients, patients with DI cannot concentrate their urine in response to dehydration. Patients with central DI respond to desmopressin (a synthetic analog of vasopressin) administered intranasally, whereas patients with nephrogenic DI do not (4). Sometimes patients do not fall into definite categories (e.g., partial central DI). The direct form of testing where ADH levels are measured after infusing hypertonic saline is rarely performed.
Diagnostic assessment
Often important clues about the cause of polydipsia can be obtained with a directed clinical history with particular attention paid to the onset of symptoms, the presence of nocturia, and the medication history. The value of the physical examination is limited unless signs are evident of defects caused by a pituitary tumor (e.g., progressive headaches, visual field defects) or endocrinologic symptoms (e.g., amenorrhea, galactorrhea, acromegaly, Cushing’s disease). Often the diagnosis is made with routine laboratory tests. Sometimes a water deprivation test needs to be performed to make the diagnosis, but this test should be done in a hospital setting with the patient monitored closely for dehydration.
References
1. Greendyke RM, Bernhardt AJ, Tasbas HE. Polydipsia in chronic psychiatric patients. Neuropsychopharmacology 1998;18:272–281.
2. Olpade-Olaopa EO, Morley RN, Ahiaku ER, Bramble FJ. Iatrogenic polydipsia: a rare cause of water intoxication in urology. Br J Urol 1997;7:488.
3. Adam P. Evaluation and management of diabetes insipidus. Am Fam Physician 1997;55:2146–2153.
4. Blevins LS Jr, Wand GS. Diabetes insipidus. Crit Care Med 1992;20:69–79.>
Book Source Details
- Book Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter
- Author(s): Robert B. Taylor (editor)
- Year of Publication: 2000
- Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2000 Lippincott Williams & Wilkins.
Other Book Chapters Related to Diabetes insipidus
Read excerpts from these other book chapters related to Diabetes insipidus:
Medical Books Excerpts
- POLYDIPSIA
- "Algorithmic Diagnosis of Symptoms and Signs" (2003)
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- "Professional Guide to Signs & Symptoms (Fifth Edition)" (2006)
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- "The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter" (2000)
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- "Signs & Symptoms: A 2-in-1 Reference for Nurses" (2007)
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Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2008 Williams & Wilkins.
More About Causes of Diabetes insipidus
» Next page: Diabetes insipidus (Handbook of Diseases)
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