Complications

Complication
Timeframe
Likelihood
long term
low

Chronic complication of polydipsia. Results from bladder dilation. May lead to renal failure.

long term
low

Can predispose a person to hyponatremia (with low plasma osmolality and hypervolemia). In addition, congestive heart failure has been noted as a long-term complication of excessive fluid consumption.

One case report found that hyponatremia led to stress cardiomyopathy in a patient with PPD and severe obsessive compulsive disorder. It is hypothesized that excessive catecholamine release, a downstream effect of hyponatremia, may play a role in the onset of stress cardiomyopathy.[86]

Chronic congestive heart failure

long term
low

Osteopenia, osteoporosis, and increased risk of fractures have been seen in people with chronic schizophrenia and polydipsia. In one small study, bone density was normal in the control (schizophrenia without polydipsia) group, but was abnormally low in schizophrenia patients with polydipsia, who had a markedly increased incidence of fractures.[87]

Osteoporosis

variable
high

In an epidemiologic study of the prevalence of PPD in 241 psychiatric inpatients, somatic consequences of excessive fluid intake included enuresis and urinary incontinence.[5]

variable
high

In 10% to 20% of patients, PPD is characterized by low plasma sodium (hyponatremia). Typically, hyponatremia is mild and asymptomatic in the absence of another contributing comorbidity.[4] Symptomatic hyponatremia is more likely after an acute 3- to 4-liter fluid ingestion, or if patients continue to drink excessively (>10 liters daily) after reaching their limit of urine dilution (100 mOsm/kg H₂O in osmolality) and antidiuretic hormone suppression.[4][22] It may be more likely in heavy smokers.[20] Acute symptomatic hyponatremia can develop over a period of <48 hours, and presents clinically with symptoms related to central nervous system dysfunction as a result of cerebral edema. The rapidity and severity of serum sodium decline dictates the severity of neurologic symptoms. Underlying neurologic diseases or metabolic abnormalities (e.g., hypoxia, hypercapnia, or acidosis) influence the neurologic manifestations.

Correction strategies include the use of hypertonic saline (3%) infusions. Vigilant and frequent monitoring of serum sodium and electrolytes during this process is essential.[67]

For some patients who develop chronic hyponatremia and present with severe symptoms, hypertonic saline and a loop diuretic can be given together.[43]

variable
low

Rhabdomyolysis secondary to dilutional hyponatremia has been reported.[45][46]

variable
low

An acute drop in serum sodium to <125 mEq/L can manifest clinically with neurologic symptoms, including headache, nausea, cramping, hyporeflexia, dysarthric speech, restlessness, lethargy, confusion, seizures, and delirium. Coma and even sudden death can ensue as sodium status worsens.[43][44]

variable
low

Rapid correction of hyponatremia increases the risk of central pontine myelinolysis and osmotic demyelination.[88]

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