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Potomania is a disorder characterized by the excessive intake of fluids without an underlying physical disorder. It can manifest as polydipsia when it refers to drinking excessive water, psychogenic polydipsia (when it is associated with mental disorders), and beer potomania when this excessive consumption is of beer [,]. An adult under normal physiological conditions drinks an average of 2 L of water daily, and symptoms are generally rare when fluid consumption is less than 10 L per day []. However, when an excess of water intake exceeds the kidneys’ elimination capacity, hypotonic hyponatremia can occur, with a reduction in plasma osmolality [,]. Potomania is defined as a clinical condition characterized by excessive fluid intake, particularly of liquids with low solute content, in the context of insufficient dietary protein and electrolyte consumption. This imbalance reduces renal solute availability, limiting the kidneys’ capacity to excrete free water and predisposing individuals to dilutional hyponatremia. The condition often arises from a combination of contributing factors, including maladaptive social behaviors (e.g., detox practices, competitive drinking), nutritional deficiencies, and underlying psychiatric disorders such as schizophrenia, obsessive-compulsive disorder (OCD), and bipolar disorder, which are frequently associated with psychogenic polydipsia [,].

Beer potomania is a specific subtype of potomania characterized by the chronic ingestion of large volumes of beer alongside a diet low in protein and electrolytes. Unlike general potomania, which may involve excessive intake of any hypo-osmolar liquid, beer potomania involves a unique combination of a solute-poor beverage and restricted solute intake from food. Since beer contains minimal electrolytes and negligible protein, it provides insufficient solute to facilitate water excretion, impairing free water clearance and leading to hyponatremia. Although both conditions share the mechanism of dilutional hyponatremia secondary to fluid overload, their etiologies, clinical contexts, and treatment approaches differ substantially [].

The clinical importance of potomania lies in its potential to cause life-threatening hyponatremia, which can present with neurological symptoms such as seizures, altered mental status, and even osmotic demyelination syndrome if not carefully managed. Despite its severity, potomania is often underdiagnosed or misattributed to other causes of hyponatremia due to its rarity and overlapping clinical presentations. Diagnosis is further complicated by the lack of standardized criteria and reliance on patient history, which may be incomplete or unreliable, especially in those with psychiatric conditions or substance use disorders. Timely recognition and tailored interventions are critical to prevent complications and guide appropriate treatment [,].

In this review, cases were classified as potomania or beer potomania based on the following diagnostic criteria: (1) documented excessive intake of fluids—typically water or beer—with volumes generally exceeding 4–10 L per day; (2) presence of hypotonic hyponatremia (serum sodium < 135 mmO/L); (3) low urine osmolality (<100 mOsm/kg in most cases); (4) absence of alternative causes of hyponatremia such as renal failure, syndrome of inappropriate antidiuretic hormone secretion (SIADH), or adrenal insufficiency; and (5) dietary patterns indicating low solute or protein intake. For beer potomania, additional criteria included a reported history of chronic beer consumption with limited nutritional intake [,].

While individual case reports have highlighted unique presentations of potomania and beer potomania, there is a lack of synthesized evidence offering a comprehensive overview of their clinical characteristics, risk factors, and outcomes. No prior systematic review has compiled these cases to identify common patterns or to inform clinical decision-making. Given the growing recognition of fluid-induced hyponatremia and the need for awareness among clinicians, particularly in emergency and psychiatric settings, this systematic review aims to bridge the existing gap by analyzing and summarizing available evidence from case reports [,]. This synthesis will provide insights into diagnostic strategies, therapeutic interventions, and potential complications, supporting the development of clinical guidelines and future research directions.

A total of 44 individual cases were included in this systematic review. The mean age of patients was 45 years. Key demographic features are summarized in . Approximately 70% of the cases involved male patients. The cases were geographically diverse, with reports from Europe, North America, Asia, and South America. The detailed process of search results and selection is shown in . Hyponatremia was the primary clinical manifestation, with serum sodium levels ranging from 102 to 129 mmO/L. Most cases presented with severe hyponatremia (<120 mmO/L), and the most common symptoms were nausea, confusion, headache, altered mental status, seizures, and, in some cases, coma. Symptoms such as seizures and altered mental status were common, as previously described by Musch et al. [] and Sailer et al. []. Fluid intake and psychiatric comorbidities are described in . Urine osmolality was reported in 36 cases and was consistently low (around <100 mOsm/kg, referring to the average of the values found) in most patients, consistent with impaired renal capacity to excrete excess water due to low solute intake. Laboratory findings are detailed in . Psychiatric comorbidities were present in over half of the patients, including schizophrenia, bipolar disorder, and depression. Many of these patients also had a history of psychogenic polydipsia or compulsive water intake.

Beer potomania was described in 26 of the 44 cases, predominantly affecting middle-aged males with a history of chronic alcohol consumption and poor nutritional intake. In contrast, potomania was often associated with excessive intake of other fluids (e.g., water, soda, sports drinks). It was linked to restrictive diets, eating disorders, or excessive hydration due to exercise. Management strategies included the following: Fluid restriction ( n = 40); Intravenous saline or hypertonic saline ( n = 28); Electrolyte correction (e.g., potassium, magnesium, thiamine); Psychiatric evaluation and intervention, where applicable. Osmotic demyelination syndrome (ODS) was reported in five cases, all of which involved overcorrection of sodium (>10 mmO/L in 24 h). These cases emphasize the importance of cautious correction and close monitoring. Biochemical reference values used for interpretation appear in . Outcomes were generally favorable with appropriate treatment but delayed diagnosis or overly aggressive sodium correction led to complications in a subset of patients. Mortality was reported in two cases.

The methodological quality of the included case reports was assessed using the Joanna Briggs Institute (JBI) checklist. Most cases scored well in domains such as clarity of clinical history and diagnostic reasoning. However, several reports lacked long-term follow-up or detailed outcome descriptions. These limitations were considered when interpreting the findings and drawing conclusions. Although case reports and series are considered lower levels of evidence due to their uncontrolled nature, they play an important role in advancing medical knowledge, especially in rare disorders such as potomania. They help inform clinical decision-making when higher-level evidence is lacking. In this review, all included case reports were critically appraised using the Joanna Briggs Institute (JBI) checklist. Most studies demonstrated acceptable methodological quality, particularly in reporting clinical history and diagnostic reasoning. However, some lacked detail on treatment outcomes or long-term follow-up, and these limitations were considered in the interpretation of findings [,]. All included case reports listed in , and are cited either in the main text or referenced within the tables themselves to ensure transparency and traceability of data sources.

The results of this review provide a broad overview of the clinical characteristics, manifestations, and outcomes associated with potomania and beer potomania. Across the 44 cases analyzed, distinct patterns of excessive fluid consumption, consistent clinical symptoms, and the development of hypotonic hyponatremia were observed in both conditions. Excessive fluid intake increases total body water, dilutes plasma osmolality, and suppresses vasopressin secretion, reducing urine concentration and promoting diuresis []. However, when fluid intake is not accompanied by sufficient solute intake, urinary osmolality drops to around 100 mOsm/kg, limiting renal water excretion and leading to dilutional hyponatremia [,]. This mechanism is particularly evident in beer potomania, a condition resulting from high-volume beer consumption combined with low dietary solute and protein intake. A low urine osmolality reflects intact renal dilution capacity, but hyponatremia occurs when solute excretion is insufficient to eliminate excess water [,]. This dissociation between urine dilution capacity and solute-dependent water clearance has also been explored by Wilke et al. [], who demonstrated vasopressin-independent regulation of aquaporin-2 under conditions of food deprivation.

Beer potomania was first described in the 1970s [,] and remains a reference for current understanding []. Excessive fluid intake increases total body water, dilutes plasma osmolality, and suppresses vasopressin secretion. Additionally, very low-sodium diets prompt the kidneys to retain more sodium and water, decreasing delivery of filtrate to diluting nephron segments and further limiting water excretion—even in the absence of vasopressin [,]. Examples include extreme weight loss diets [], beer potomania [], and intake of carbohydrate-rich but sodium-poor beverages such as malted soy drinks [], which can exacerbate hyponatremia compared to complete starvation []. Dietary solute intake, particularly protein and sodium, is essential for the renal excretion of free water. In patients with severely restricted diets, the low solute load impairs the kidneys’ ability to eliminate excess water, even when the capacity to dilute urine is preserved [].

Patterns of fluid consumption and etiological context differ significantly between potomania and beer potomania. Potomania involved varied liquids, including water [], cider [], tea [,], Coca-Cola Zero ® [], isotonic drinks [], and soy-based drinks [], while beer potomania was specifically linked to high beer consumption [,]. These differences reflect broader social and dietary influences, including the predominance of beer potomania in males (19 out of 23 cases), potentially due to cultural norms around alcohol consumption []. Symptomatically, patients with both forms of potomania presented similar clinical features: fatigue, nausea, vomiting, confusion, seizures, and altered consciousness [,,]. Symptoms such as seizures and altered mental status were common, as previously described by Musch et al. [] and Sailer et al. []. Potomania, schizophrenia, bipolar disorder, OCD, and substance use disorders were frequently reported [,,,], as was psychogenic polydipsia, which affects approximately 6% to 20% of patients with schizophrenia and is also prevalent in individuals with intellectual disabilities or autism spectrum disorders [].

Diagnosis of beer potomania is based on a history of excessive beer intake, poor diet, and the exclusion of other causes of hyponatremia. It typically presents with low urine sodium and osmolality [,,]. Potomania due to other fluids is diagnosed by identifying excessive intake and ruling out other etiologies of hyponatremia. Laboratory criteria for diagnosis include serum sodium < 135 mEq/L, serum osmolality < 280 mOsm/kg, and urine osmolality < 100 mOsm/kg []. Treatment involves fluid restriction, correction of electrolyte imbalances, and cautious use of intravenous fluids to avoid rapid sodium correction []. Some case reports, such as that by Yu and Fisher [], emphasize the risks of initial fluid resuscitation in beer potomania, which may exacerbate hyponatremia if not properly monitored. In beer potomania, alcohol cessation and nutritional support are also essential []. Sodium correction should not exceed 10–12 mmO/L in 24 h or 18–25 mmO/L in 48 h [,]. In cases of overcorrection, 5% dextrose or desmopressin may be administered [,]. Some case reports, such as that by Yu and Fisher [], emphasize the risks of initial fluid resuscitation in patients with beer potomania, which may exacerbate hyponatremia if not properly monitored.

Osmotic demyelination syndrome (ODS) is a severe complication of rapid sodium correction and is characterized by symptoms such as paralysis, dysarthria, and dysphagia. Risk factors include alcoholism, malnutrition, liver disease, and correction rates > 25 mmO/L over 24–48 h [,,]. Three cases in this review reported ODS [,,], highlighting the need for careful management. When ODS occurs, lowering sodium using hypotonic solutions and dextrose infusions is recommended []. Psychiatric management also poses challenges, as several medications (e.g., lithium, carbamazepine, oxcarbazepine, valproate) may contribute to or exacerbate hyponatremia []. Conversely, some antipsychotics, such as risperidone and olanzapine, may reduce compulsive fluid intake behaviors []. Despite offering a comprehensive clinical synthesis, this study has limitations. Case reports may be subject to publication bias, with more severe or unusual presentations more likely to be reported. Additionally, the limited sample size and absence of control groups reduce the generalizability of findings. Diagnostic methods and interventions varied considerably across cases, making standardization difficult. Furthermore, sociocultural factors such as dietary habits and patterns of alcohol use may limit applicability to broader populations.

Potomania and beer potomania are uncommon but potentially life-threatening causes of hyponatremia, often overlooked in clinical practice. This systematic review highlights the importance of recognizing distinct fluid consumption patterns, psychiatric comorbidities, and nutritional deficiencies associated with both conditions. While potomania encompasses a broader range of liquid intakes, beer potomania is specifically linked to excessive beer consumption and low dietary solute intake. Timely diagnosis relies on thorough patient history and laboratory evaluation, including assessment of serum sodium and serum and urine osmolality. Effective treatment includes fluid restriction, correction of electrolyte imbalances, nutritional support, and careful monitoring to prevent osmotic demyelination syndrome. Special attention should be given to psychiatric assessment and management, especially in patients with psychogenic polydipsia or other mental health conditions. Although this review is based on case reports, which limits generalizability, it provides clinically relevant insights that can inform diagnosis and management in settings where higher-level evidence is lacking. Further research with standardized methodologies is necessary to better understand the epidemiology, outcomes, and optimal treatment approaches for these rare conditions.