Psychogenic polydipsia is a condition in which the patient exhibits a compulsive consumption of fluids. This is commonly observed in patients with psychiatric disorders such as schizophrenia.
Typically, the medical staff notices water seeking behavior and excessive drinking in patients with polydipsia, a condition commonly occurring in individuals with psychiatric illness. Also, schizophrenic patients tend to have polydipsia .
With regards to asymptomatic hyponatremia, it is typically observed in the hospital setting. Hyponatremia is defined as a plasma sodium level below 135 mEql/L, in which there is excess water compared to sodium. This electrolyte imbalance occurs in 10% to 20% of individuals with polydipsia and is more prevalent in patients with cardiac, renal, and hepatic pathology.
In acute episodes of hyponatremia, the clinical picture may feature nausea, headache, muscle cramping, dysarthria, lethargy, confusion, delirium, and seizures. Further outcomes such as coma and death may also occur.
The serum calcium concentration corresponds to certain symptoms. For example, gastrointestinal (GI) symptoms occur when sodium concentration ranges between 125 and 130 mEq/L, while neurologic manifestations are observed in sodium levels below 125mEq/L.
Physical exam findings for symptomatic hyponatremia are positive for decreased tendon reflexes and mental status changes.
Workup consists of a detailed history, including a psychiatric evaluation, a physical exam and laboratory tests.
Water restriction and administration of exogenous ADH
The water restriction study used conjunctively with the administration of exogenous ADH is used to confirm the diagnosis. This is performed to evaluate urine osmolality. In polydipsia prior to water restriction, urine is diluted, with an osmolality less than 100 mOsm/kg H2O. However, after the study is performed, osmolality increases to >750 mOsm/kg H2O. This finding confirms PPD  and excludes diabetes insipidus. Note that this study will yield characteristic findings to differentiate between DI and SIADH.
If serum ADH is measured before and after the study, the initial low levels in PPD increase following the test.
Other laboratory studies
Plasma sodium levels and osmolality, as well as urine sodium concentration and osmolality are obtained. The latter values are obtained by 24-hour urine collection, as polyuria and polydipsia are reflected in this investigation. Plasma urine is below 100 mOsm/kg H2O, while urine osmolality is less than 280 mOsm/kg H2O.
Further beneficial tests are the complete metabolic panel, urinalysis and urea. These will yield information about the full clinical picture. Additionally, these results will rule out diabetes mellitus and other possible diseases.
A chest radiograph is obtained to test for lung malignancy, as this may account for SIADH.
The therapeutic goals of PPD are related to treating the underlying cause. Furthermore, the medical team should pay special attention to the onset, severity and presentation of hyponatremia. It is also mandatory to address any coexisting neurologic diseases.
In patients with profound or symptomatic hyponatremia, this electrolyte should be corrected. There is a delicate balance between correcting the sodium levels and the complications secondary to this abnormality. To aid in the treatment, nephrology consultation is very beneficial.
This correction consists of infusing the patient with hypertonic saline (3%). Frequent surveillance of the electrolytes is warranted to reduce the probability of developing certain sequelae associated with rapid correction such as central pontine myelinolysis and osmotic demyelination.
Regarding monitoring, electrolytes should be assessed very 2 to 3 hours in the early stages of acue hyponatremia. Sodium replacement should be pursued until symptoms are alleviated and the level is above 118 to 120 mEq/L. Once this concentration range is reached, this is followed by conservative treatment until a concentration of 25 mEq/L .
In patients with longstanding symptoms and a mild sodium imbalance, treatment consists of fluid restriction. Additionally, loop diuretics can be used to promote excretion of water. Weight can be monitored periodically to assess fluid ingestion.
Behavioral therapy with positive feedback may be beneficial in these patients. Professional therapists can employ cognitive techniques that address the reasons for compulsive drinking. Also, patients can be enrolled in a program that targets impulse control and offers alternate coping skills. These patients should be closely assessed wth periodic follow-up appointments.
The atypical antipsychotics used to treat schizophrenia, bipolar disorder and other psychiatric illnesses help improve the symptoms of PPD. Clozapine has demonstrated success . The off-label use of this drug was observed to normalize plasma osmolality. Another medication, risperidone, improves polydipsia.
Lithium is an ADH antagonist that was prescribed in the treatment of polydipsia at one point. However, it is associated with adverse effects on the kidneys and thyroid .
Outcomes of PPD
PPD can be quite detrimental as it is linked to increased morbidity and mortality. In schizophrenics, polydipsia can be life-threatening, as one study observed that these patients with PPD have a 74% higher probability of dying sooner than schizophrenics without PPD .
Congestive heart failure is one of the longstanding complications of PPD. Additionally, polydipsia can lead to intestinal and bladder dilation and advanced diseases such as hydronephrosis and kidney failure.
Outcomes of hyponatremia
The etiology of PPD has not been fully established. This condition commonly affects patients with mental illnesses such as schizophrenia, developmental disorders, affective disorders, personality disorders, and anorexia nervosa.
With regards to the aforementioned disorders, PPD is observed in patients exhibiting positive symptomatology in schizophrenia; patients also employ it as a method to cope with stress and the side effects of anticholinergic drugs.
Additionally, one study assessing PPD in developmental conditions demonstrated a prevalence of 3.5% in its subjects . Autism and Kleine-Levin syndrome are examples of these disorders.
Another consideration is tobacco smoking, as nicotine stimulates the release of antidiuretic hormone (ADH). Hence, smoking is implicated in a large proportion of those with PPD. In fact, one study linked compulsive water consumption and subsequent symptomatic hyponatremia with heavy smokers .
PPD is observed in 6% to 20% of the psychiatric population , especially in those with schizophrenia, developmental disorders, and women with anxiety disorders . It is also present in conditions such as anorexia nervosa, affective disorders, and personality disorders. Specifically, it is observed in 10% to 20% of patients with schizophrenia although symptomatic hyponatremia manifests in only 2% to 5%. .
With regards to patient demographics, there may be a gender preference towards women. Furthermore, it is observed in all races.
As a common condition in hospitalized individuals, hyponatremia is prevalent in 1% to 2% .
Normally, ADH prompts the reabsorption of water from the distal tubules and collecting duct. Additionally, this hormone exerts its action on arteriolar vasoconstriction leading to an increase in blood pressure.
ADH is not secreted in cases where the plasma osmolality is below under 280 mOsm/kg H2O. Moreover, the thresholds at which inhibition of ADH and thirst occur are set closely to each other. Hence, thirst is suppressed either before or during the same time that ADH is suppressed.
With regards to hyponatremia, there are protective renal mechanisms to prevent this from occurring. This electrolyte imbalance becomes symptomatic when the kidney's excretion capacity is overwhelmed .
Polydipsia in PPD
The pathogenesis of PPD is dependent on numerous factors. The hypothalamic thirst control center does not function properly. In fact, the threshold for ADH and thirst suppression are altered and there is now a difference between them. Therefore, polydipsia develops even though there is inhibition of ADH release.
Interestingly, investigations regarding polydipsia in schizophrenics patients corroborated ADH and oxytocin involvement. During psychotic episodes, the osmostat for ADH release is modified, and this produces malfunction in water excretion.
In patients with PPD and coexisting diabetes insipidus (DI), the heavy water consumption can produce ADH dysregulation by impairing the feedback regulation .
PPD may result in hyponatremia in 10% to 20% of patients. Symptoms develop after excessive fluid intake, which is likely 3 to 4 liters in volume. Hyponatremia also occurs in those who drink large amounts of fluid after urine reaches its maximum dilution and suppression of ADH has occurred. . The kidneys cannot dilute the urine and, hence, hyponatremia forms.
In patients with SIADH or inappropriate secretion of ADH, this hormone cannot be suppressed. Excess fluid ingestion in these individuals will result in significant hyponatremia.
Psychogenic polydipsia (PPD) refers to the strong desire to seek and drink large volumes of fluid regardless whether a stimulus is present. This type of polydipsia occurs in psychiatric illnesses such as schizophrenia, bipolar disorder, depression, anorexia nervosa, and others. While the cause has not been determined, a chemical imbalance may play a role. The complex pathogenesis is multifactorial and involves principal changes in the key regulatory pathways involved in water homeostasis.
The chronic and excessive intake of water and fluids can dilute the serum sodium concentration resulting in hyponatremia. If this decline occurs rapidly, symptoms such as nausea, headache, lethargy, confusion, seizures, coma, or even death can manifest. However, gradual development of hyponatremia allows the body to adapt and tolerate the new status.
Diagnosis is achieved by certain studies, such as water restriction and other helpful laboratory tests. Also, management involves the limitation of fluid intake in which resources such as cognitive behavioral therapy could be beneficial. Additionally, atypical antipsychotics may be helpful. Another crucial therapeutic aspect addresses any profound hyponatremia with careful correction.
Psychogenic polydipsia is a condition in which an individual exhibits a strong urge to drink large amounts of fluids. This type of polydipsia is found in patients with psychiatric illnesses such as schizophrenia, anorexia nervosa, developmental disorders, and middle-aged women with anxiety. Psychogenic polydipsia is thought to occur due to chemical imbalances,
The following conditions are associated with the development of psychogenic polydipsia:
Prolonged drinking of large fluid quantities can develop a condition called hyponatremia, in which the water in the body is in excess, compared to the concentration of sodium. The following symptoms occur:
The main method to confirm the diagnosis of psychogenic polydipsia is through a test called the water restriction test.
Also, blood and urine tests are used to assess the osmolality and levels of sodium.
In patients with severe hyponatremia, intravenous fluids with sodium are administered carefully and cautiously to avoid neurological damage.
Antipsychotic medications such as clozapine can be used to treat polydipsia.
Behavioral therapy can be beneficial as a professional can help the patient quit excessive drinking. Additionally, a therapist helps the patient develop other coping skills and mechanisms to replace the polydipsia.