POLYDIPSIA

KERRY CAPERELL, MD, MS AND RONALD I. PAUL, MD

Polydipsia, or excessive thirst, is an uncommon complaint in children. Although fluid consumption varies greatly among individuals, pathologic conditions exist when excessive drinking of fluids interferes with daily life or is accompanied by bizarre behavior, such as drinking from a toilet bowl. Polydipsia is routinely accompanied by urinary frequency (see Chapter 74 Urinary Frequency). Other accompanying symptoms depend on the underlying cause.

PATHOPHYSIOLOGY

The sensation of thirst and subsequent fluid intake is influenced by complex mechanisms that involve the hypothalamus, extracranial thirst receptors, and kidneys. As water is lost from the body, thirst centers in the hypothalamus are stimulated by an increase in serum osmolality. In response to signals from the hypothalamus, the pituitary gland releases an antidiuretic hormone, vasopressin, which causes reabsorption of water in the collecting ducts of the kidney. In addition to physiologic controls of thirst, cortical involvement and social conditioning also play a role and may be responsible for the wide variability in fluid consumption.

DIFFERENTIAL DIAGNOSIS

Diabetes mellitus (DM) is the single most common cause of polydipsia (Table 59.1). Additional prominent symptoms of DM include weight loss and polyuria. Other common causes of polydipsia include sickle cell anemia and diabetes insipidus (DI) (Table 59.2). In sickle cell anemia, chronic sickling of cells in the medulla of the kidney results in a limited ability to concentrate urine and mild polydipsia. In DI, a wide variety of lesions in the hypothalamus and neurohypophysis result in a deficiency of antidiuretic hormone. Inherited forms of nephrogenic DI may be autosomal dominant, autosomal recessive, or X-linked recessive. In instances in which the cause of DI cannot be readily determined, patients are diagnosed as idiopathic. These patients need frequent reevaluations because many are later diagnosed with intracranial tumors.

Less common metabolic and endocrine causes of polydipsia include electrolyte imbalances, catecholamine excess, and cystinosis. Primary renal causes of hyposthenuria include interstitial nephritis, renal tubular acidosis, medullary cystic disease (nephronophthisis), and obstructive uropathy. In nephrogenic DI, the renal tubule is unresponsive to antidiuretic hormone. Patients with nephrogenic DI usually have onset of symptoms in infancy and present with recurrent episodes of dehydration, fever, failure to thrive, and psychomotor retardation. Pharmacologic causes of polyuria and polydipsia include methylxanthines, amphotericin B, and diuretics. In addition, chronic lithium therapy may result in nephrogenic DI.

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