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 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 ... 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