Complications
Chronic complication of polydipsia. Results from bladder dilation. May lead to renal failure.
Can predispose a person to hyponatraemia (with low plasma osmolality and hypervolaemia). In addition, congestive heart failure has been noted as a long-term complication of excessive fluid consumption.
One case report found that hyponatraemia led to stress cardiomyopathy in a patient with PPD and severe obsessive compulsive disorder. It is hypothesised that excessive catecholamine release, a downstream effect of hyponatraemia, may play a role in the onset of stress cardiomyopathy.[83]
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.[84]
In an epidemiological study of the prevalence of psychogenic polydipsia (PPD) in 241 psychiatric inpatients, somatic consequences of excessive fluid intake included enuresis and urinary incontinence.[5]
In 10% to 20% of patients, PPD is characterised by low plasma sodium (hyponatraemia). Typically, hyponatraemia is mild and asymptomatic in the absence of another contributing comorbidity.[4] Symptomatic hyponatraemia is more likely after an acute 3- to 4-litre fluid ingestion, or if patients continue to drink excessively (>10 litres 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 hyponatraemia can develop over a period of <48 hours and presents clinically with symptoms related to central nervous system dysfunction as a result of cerebral oedema. The rapidity and severity of serum sodium decline dictate the severity of neurological symptoms. Underlying neurological diseases or metabolic abnormalities (e.g., hypoxia, hypercapnia, or acidosis) influence the neurological 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.[65]
For some patients who develop chronic hyponatraemia and present with severe symptoms, hypertonic saline and a loop diuretic can be given together.[41]
An acute drop in serum sodium to <125 mmol/L (<125 mEq/L) can manifest clinically with neurological 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.[41][42]
Rapid correction of hyponatraemia increases the risk of central pontine myelinolysis and osmotic demyelination.[85]
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