Pediatric emergency medicine trisk 307

FIGURE 63.1 A diagnostic approach to palpitations. a Especially caffeine, diet
supplements, herbal preparations, sympathomimetic medications, cocaine, or
amphetamines. EKG, electrocardiogram; SVT, supraventricular tachycardia; VT,
ventricular tachycardia; WPW, Wolff–Parkinson–White; CHF, congestive heart failure;
Hgb, hemoglobin; POTS, postural orthostatic tachycardia syndrome.

Suggested Readings and Key References
Ginsburg GS, Riddle MA, Davies M. Somatic symptoms in children and
adolescents with anxiety disorders. J Am Acad Child Adolesc Psychiatry
2006;45:1179–1187.
Kizilbash SJ, Ahrens SP, Bruce BK, et al. Adolescent fatigue, POTS, and
recovery: a guide for clinicians. Curr Probl Pediatr Adolesc Health Care
2014;44:108–133.
Marzuillo P, Benettoni A, Germani C, et al. Acquired long QT syndrome: a
focus for the general pediatrician. Pediatr Emerg Care 2014;30(4):257–
261.
Patel S, Sedaghat-Yazdi F, Perez M. Management of pediatric chest pain,
palpitations, syncope, and murmur presenting to the emergency
department. Clin Ped Emer Med 2018;19(4):328–339.
Rivera RF, Chambers P, Ceresnak SR. Evaluation of children with
palpitations. Clin Pediatr Emerg Med 2011;12(4):278–288.
Sedaghat-Yazdi F, Koenig PR. The teenager with palpitations. Pediatr Clin
North Am 2014;61(1):63–79.


CHAPTER 64 ■ POLYDIPSIA
KERRY CAPERELL, RONALD I. PAUL

INTRODUCTION
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 78 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
64.1 ). Additional prominent symptoms of DM include weight loss and polyuria.
Other common causes of polydipsia include sickle cell anemia and diabetes
insipidus (DI) ( Table 64.2 ). 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. Instances in which the cause of DI cannot be readily determined,
patients are diagnosed as idiopathic. These patients need frequent reevaluations
because many are ultimately 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, psychomotor
retardation, and marked thirst. Such infants will have a history of frequent and
heavy wet diapers and often show a preference for cold water over anything else,
including food. Pharmacologic causes of polyuria and polydipsia include
methylxanthines, amphotericin B, and diuretics. In addition, chronic lithium
therapy may result in nephrogenic DI.
Primary polydipsia is diagnosed when the ingestion of water is in excess of that
needed to maintain water balance. It can be caused by an inappropriate
psychological thirst drive (psychogenic polydipsia or compulsive water drinking)
or by hypothalamic damage that alters thirst but not antidiuretic hormone release
(neurogenic polydipsia).
Most children with polydipsia have serious but nonacute problems. Potential
life-threatening conditions may develop in certain circumstances ( Table 64.3 ).
Patients with DI or nephrogenic DI may develop severe dehydration if water is
withheld for prolonged periods. Conversely, urgent management of
hypernatremia is usually unnecessary if patients are able to drink and may be
harmful if it is of chronic duration. Diabetic ketoacidosis may be an initial
presentation of patients with DM, and can result in extreme electrolyte and acid–
base imbalances. Patients with primary polydipsia who overload their kidneys’
ability to excrete free water may present with hyponatremic seizures. Many of the
brain lesions that cause DI can become life-threatening. Patients with severe brain
injury often develop DI toward the end of life.

EVALUATION AND DECISION
When evaluating a child with polydipsia, the physician should seek information
from the parent regarding the quantity and type of fluid ingested each day, and
whether the child has used any unusual methods to satiate thirst. A history of
nocturnal polydipsia and polyuria is helpful because most children with
psychogenic polydipsia do not wake in the middle of the night for fluids. A
medical history should include questions on growth and development, as well as
past episodes of severe dehydration. Inquiries should be made about known
causes of polydipsia such as sickle cell disease, DM, chronic kidney disorders,
head trauma, and medications ( Fig. 64.1 ). The physical examination should
include a careful evaluation for known systemic and intracranial causes of DI,
and particularly a full neurologic examination.