Psychogenic Polydidsia Review: Etiology, Differential, and Treatment
Department of Neuropsychiatry and Behavioral Sciences, University of South Carolina School of Medicine, Columbia, SC 29203, USA. Current Psychiatry Reports
(Impact Factor: 3.24).
07/2007; 9(3):236-41. DOI: 10.1007/s11920-007-0025-7
Psychogenic polydipsia (PPD), a clinical disorder characterized by polyuria and polydipsia, is a common occurrence in inpatients with psychiatric disorders. The underlying pathophysiology of this syndrome is unclear, and multiple factors have been implicated, including a hypothalamic defect and adverse medication effects. Hyponatremia in PPD can progress to water intoxication and is characterized by symptoms of confusion, lethargy, and psychosis, and seizures or 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.
Available from: Alberto Javier Espay
- "In normovolemic hyponatremia, the shortlist of diagnostic possibilities includes SIADH, hypothyroidism , adrenal insufficiency, or psychogenic polydipsia. Low urine sodium and low urine osmolality imply psychogenic polydipsia (Dundas et al., 2007). If urine sodium and osmolality are high, then a TSH and cosyntropin stimulation test will evaluate whether thyroid and adrenal function are depressed. "
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ABSTRACT: Electrolyte and acid-base disturbances are common occurrences in daily clinical practice. Although these abnormalities can be readily ascertained from routine laboratory findings, only specific clinical correlates may attest as to their significance. Among a wide phenotypic spectrum, acute electrolyte and acid-base disturbances may affect the peripheral nervous system as arreflexic weakness (hypermagnesemia, hyperkalemia, and hypophosphatemia), the central nervous system as epileptic encephalopathies (hypomagnesemia, dysnatremias, and hypocalcemia), or both as a mixture of encephalopathy and weakness or paresthesias (hypocalcemia, alkalosis). Disabling complications may develop not only when these derangements are overlooked and left untreated (e.g., visual loss from intracranial hypertension in respiratory or metabolic acidosis; quadriplegia with respiratory insufficiency in hypermagnesemia) but also when they are inappropriately managed (e.g., central pontine myelinolisis when rapidly correcting hyponatremia; cardiac arrhythmias when aggressively correcting hypo- or hyperkalemia). Therefore prompt identification of the specific neurometabolic syndromes is critical to correct the causative electrolyte or acid-base disturbances and prevent permanent central or peripheral nervous system injury. This chapter reviews the pathophysiology, clinical investigations, clinical phenotypes, and current management strategies in disorders resulting from alterations in the plasma concentration of sodium, potassium, calcium, magnesium, and phosphorus as well as from acidemia and alkalemia.
Handbook of Clinical Neurology 01/2014; 119:365-82. DOI:10.1016/B978-0-7020-4086-3.00023-0
- "Psychogenic polydipsia (PPD), a clinical disorder characterized by polyuria and polydipsia, is defined by hyponatremia found in 10-20% of those presenting with compulsive drinking. Symptoms are not typically seen until the patient reaches their limit of maximal urine dilution (100 mosmol/kg with minimum urine osmolality). "
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ABSTRACT: Psychogenic polydipsia, in its most severe form, can lead to acute water intoxication by way of extreme hyponatremia. This results in cerebral edema, mental status deterioration and can lead to life threatening intracranial hypertension if not identified and treated urgently. However, this treatment rarely involves surgical intervention. Herein, we describe a 47-year-old man who presented to our emergency department who was found down with a decline in mental status and generalized tonic clonic seizures. He was comatose with glasgow coma score of 5. His exam was notable for sluggishly reactive pupils, absence of corneal reflexes, decorticate posturing, and globally increased tone and hyper-reflexia with upgoing toes bilaterally. Lab work revealed sodium of 107 mmol/L. CT scan of the head showed global cerebral edema with sulcal effacement. A ventriculostomy was placed with an opening pressure of 35-cm H(2)O, and cerebrospinal fluid was drained to maintain normal intracranial pressure. Fluid restriction and hypertonic saline were used to carefully correct the hyponatremia. The patient improved and at day five was neurologically intact. His history later revealed schizophrenia and a predilection for drinking greater than 8 L of diet cola daily.
Journal of Emergencies Trauma and Shock 04/2012; 5(2):193-5. DOI:10.4103/0974-2700.96496
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ABSTRACT: Summary form only given. The SABRE accelerator was originally designed to operate as low impedance voltage adder with 40-ohm maximum output impedance in negative polarity operation and approximately 20 ohms in positive polarity. Because of the low impedance and higher that expected energy losses in the pulse forming network, the operating input cavity voltage is of the order of 800 kV which limits the total output voltage to ~8 MV for negative polarity and 5 to 6 MV for positive polarity. The modifications presented here aim to increase the output voltage in both polarities. A new high impedance central electrode was designed capable of operating both in negative and positive polarities, and the number of pulse forming lines feeding the ten inductively isolated cavities was reduced to half
IEEE International Conference on Plasma Science 01/1996; DOI:10.1109/PLASMA.1996.550837
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