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Beer potomania and hyponatremia

By: Patricia A. Zrelak, PhD, RN, FAHA, NEA-bc, SCRN, CNRN

Excellent nursing care is required to prevent potentially deadly overtreatment.


  • Beer potomania is an unusual syndrome of severe hyponatremia associated with excessive beer ingestion in the presence of alcohol use disorder and malnutrition.
  • Excellent nursing care is critical because too-rapid sodium correction can result in osmotic demyelination syndrome, a serious and frequently irreversible neurologic disorder.
  • Nursing care includes obtaining an accurate history to help to determine causation, anticipating judicious sodium correction, and closely monitoring the patient for changes in sensorium, neurologic status, and fluid and electrolyte balance.

Both alcohol use disorder and hyponatremia are common in hospitalized patients. Hyponatremia is the most frequent electrolyte abnormality in hospitalized patients; according to DeVita and colleagues, it occurs in up to 40% of all hospitalized patients and up to 30% of patients in specialized units (with rates higher in the young and elderly). It’s associated with many clinical conditions and may occur in the presence of hypovolemia, euvolemia, or hypervolemia. (See Hyponatremia causes.)

Beer potomania is an unusual syndrome of severe hyponatremia associated with excessive beer use. Several cases have been reported since the condition was first recognized in 1971, but few have addressed the nursing care of patients with this rare but potentially lethal syndrome. The following case presentation and evaluation provide valuable insight into treating and managing patients with beer potomania who are under for hyponatremia. 

Hyponatremia causes

The following conditions may be associated with significantly reduced serum sodium levels in adults.

·      Adverse drug reaction

·      Beer potomania

·      Cerebral salt wasting

·      Chronic renal failure

·      Cirrhosis with ascites

·      Congestive heart failure

·      Dermal losses (sweating, burns)

·      Endurance exercise

·      Excessive administration of parenteral hypotonic fluids

·      Extrarenal loss

·      Fresh water immersion

·      GI loss (vomiting, diarrhea)

·      Glucocorticoid deficiency (hypopituitarism)

·      Heat exhaustion–related fluid loss

·      Hypothyroidism

·      Hypervolemia

·      Mineralocorticoid deficiency (Addison’s disease)

·      Nephrotic syndrome

·      Pancreatitis, peritonitis, intestinal obstruction

·      Polydipsia—psychogenic

·      Polydipsia—environmental

·      Postsurgical complications

·      Pseudohyponatremia

·      Redistributive hyponatremia (fluid shift from intra- to extracellular compartments)

·      Renal loss

·      Response to diuretics (such as ACE-inhibitors)

·      Salt wasting nephropathy

·      Syndrome of inappropriate vasopressin secretion

·      Water intoxication

Case presentation

Tom Zerb*, a 48-year-old man is admitted with a chief complaint of acute change in mental status that began about 3 days ago. Mr. Zerb is unkempt and appears malnourished. On examination, he’s somnolent but able to answer questions when prodded, and he’s oriented to person, place, and time. Other than slight dysarthria, mild short-term memory problems, and upper extremity tremor, his neurologic examination doesn’t identify any other specific problems. 

A computed tomography scan is negative for hemorrhage or other mass lesions. Mr. Zerb’s medical history is positive for current alcohol use disorder, smoking, hypertension, and occasional illicit drug use (primary methamphetamine). According to his girlfriend, he drinks at least two six-packs of 12-ounce beers daily.

The patient’s vital signs are temperature 99° F (37.2° C), blood pressure 126/82 mmHg, heart rate 80 beats per minute, respiratory rate 20 breaths per minute, and oxygen saturation 94% on room air. Initial lab results are sodium 98 mEq/L (normal is 136-145 mEq/L), chloride 70 mEq/L (98-107 mEq/L), magnesium 1.5 mg/dL (1.6-2.6 mg/dL), blood urea nitrogen (BUN) 4 mg/dL (8.4-25.7 mg/dL), albumin 2.6 g/dL (3.5-5.0 g/dL), and serum alcohol 277 mg/dL (high). Other labs of interest include potassium 3.9 mmol/L (normal is 3.5-5.1 mEq/L), creatinine 0.38 mg/dL (0.70-1.30 mg/dL),uric acid 3.2 mg/dL (3.5-7.2 mg/dL), serum osmolality 280 mOsm/kg (270-300 mOsm/kg), urine osmolality 379 mOsm (500-800 mOsm), and spot urine sodium 6 mEq/L (greater than 20 mEq/L). 


Mr. Zerb is admitted to the medical ICU after receiving a 3% saline bolus in the emergency department (ED). The provider places him on nothing by mouth for the first 24 hours and until he passes a nurse swallow evaluation. His serum sodium is checked every 2 hours, urine osmolarity every 4 hours, and urine output every hour. After the saline bolus, Mr. Zerb has brisk urine output of more than 200 mL per hour. As the patient’s serum sodium levels begin to rise, his I.V. fluid is switched to dextrose 5% in water (D5W), and the I.V. rate is increased to match his urine output.

During Mr. Zerb’s first day in the hospital, his serum sodium levels increase by 13 mEq/L; by day 2 the levels are 129 mEq/L, and on day 3 they’re 136 mEq/L. Thus, he appears to be back at his baseline. On day 5, he complains of a moderate-to-severe headache and photosensitivity, and he appears anxious. Although Mr. Zerb is alert and oriented to person, place, and time, he’s forgetful, has a short attention span, and can’t perform tasks such as serial additions. A magnetic resonance imaging (MRI) scan is performed to rule out osmotic demyelination syndrome (ODS), a grave concern given his faster-than-recommended sodium correction. (See  ODS explained.)

The MRI is negative for brain structure changes. After ruling out other potential sources for the acute change in condition (such as infection), Mr. Zerb is diagnosed with alcohol withdrawal. With supportive care and benzodiazepine administration, his symptoms resolve over the next 2 days. He’s discharged home on day 8. A repeat brain scan performed as an outpatient at 6 weeks is negative for ODS.

ODS explained

Osmotic demyelination syndrome (ODS) is defined by symmetrical destruction of myelin sheaths primarily involving the brainstem’s central basis pontis without evidence of vascular involvement.


The exact mechanism of ODS isn’t known, but it appears to be at least partially due to cellular swelling that occurs when fluid shifts from the hypotonic extracellular space to the relative hypertonic intracellular space.

ODS is more likely to occur when the sodium correction treatment exceeds 10 to 12 mEq/L /day in the first 24 hours or more than 18 mEq/L /day in the first 48 hours.  However, case reports of ODS include correction rates less than 10 mEq/L per 24 hours because the risk is higher in the presence of hypokalemia. Although ODS can occur in many conditions with rapid sodium level correction, patients with beer potomania are at greater risk because of the degree and chronicity of hyponatremia, alcohol use, and underlying pathophysiology of the low solute load that increases the risk of too-rapid correction of sodium levels. Infusion of hypertonic saline is thought to increase ODS risk, but it’s also been seen in patients treated with infusion of normal saline or with fluid restriction alone. Other causes of hyponatremia that place a patient at risk for ODS include hypovolemia, polydipsia, desmopressin discontinuation, and glucocorticoid suppression.

Signs and symptoms

Clinical features of ODS are variable and may be biphasic. Symptoms can be related to damage to the corticospinal or corticobulbar tracts within the basis pontis or secondary to extrapontine involvement. Extrapontine myelinolysis involves the basal ganglia and thalamus and is seen in up to 10% of patients with ODS. A change in consciousness level ranging from mild confusion to coma that presents up to 3 or more days after the acute change in sodium levels frequently is the first symptom. Other symptoms include:

  • ataxia
  • seizures
  • encephalopathy
  • varying degrees of upper motor neuron signs
  • pseudobulbar palsy
  • spastic quadriparesis
  • dysarthria
  • dysphagia
  • oculomotor dysfunction.

Patients with severe ODS may develop locked-in syndrome—complete paralysis of all voluntary muscles except for the ones that control vertical eye movements of the eyes.

Diagnosis and prognosis

Diagnosis is based on the patient’s clinical history, laboratory values, and brain scans. ODS prognosis ranges from complete neurologic recovery and resolution of magnetic resonance imaging findings to deficit progression and death. No specific treatment is available for ODS, so prevention is critical.

Case evaluation

Typically, patients with beer potomania have a long history of beer drinking in conjunction with poor dietary intake, resulting in malnutrition. Similar to Mr. Zerb, they’ve recently binged on beer and are chronically hyponatremic. Early symptoms (including malaise, dizziness, muscle weakness, and headache) frequently are nonspecific and associated with hyponatremia, hypokalemia, or acute water intoxication. As the condition worsens, signs and symptoms of cerebral edema and increased intracranial pressure—such as neurologic impairment, seizures, coma, and death—may occur. The risk of cerebral edema is greatest when acute hyponatremia develops within 48 hours. Complicating the presentation are symptoms of potential alcohol intoxication (such as vomiting and GI absorptive problems) and withdrawal. It’s not uncommon for patients to appear malnourished. 


Well-nourished patients with normal renal function can excrete large amounts of free water, such as from excessive water ingestion (up to 20 L/day) without becoming hyponatremic. The reason is that under normal conditions, decreased serum osmolality or increased blood volume suppresses antidiuretic hormone (ADH) release, causing less water to be reabsorbed by the kidneys and diuresis of dilate urine. (See About serum osmolarity.)

The kidney’s ability to excrete free water depends on osmole excretion and the osmolarity of the blood. The blood’s osmolarity is generated primarily from protein breakdown (10 grams of protein produces approximately 50 mOsm of urea) as well as sodium and potassium intake. Typical osmolar excretion ranges between 600 to 900 mOsm per day; the maximum urinary dilution ability of healthy kidneys is as low as 50 mOsm/L.

About serum osmolarity

Serum osmolarity is a measure of the blood’s osmotic pressure. It’s defined as the amount of osmoles (the number of moles of solute [dissolved particles]) that contribute to the osmotic pressure of a solution (measured in milliosmoles [mOsm] per liter).

Important solutes that impact blood osmolarity include sodium, glucose, blood urea nitrogen from protein breakdown, and other electrolytes such as potassium. Solutions can be

  • isotonic with the same osmolarity as blood (normal levels are between 280 and 295 mOsm/L)
  • hypotonic with few solutes (<280 mOsm/L)
  • hypertonic with a high concentration of solutes (>295 mOsm/L).

Patients who are malnourished or have poor solute or protein intake (such as patients receiving most of their caloric intake from beer) are vulnerable to impaired water excretion by the kidneys. A beer diet contains little or no sodium, potassium, or protein, resulting in low solute intake and low serum osmolarity, which impairs free water clearance by the kidneys, leading to dilutional and, more frequently, euvolemic hyponatremia. Calories from beer are used before other forms of energy, preventing endogenous protein breakdown. The result is no urea or ketone generation, which further decreases the blood’s solute load, and therefore its osmolarity.

Lack of adequate serum osmolarity impairs the normal functioning electrolyte gradient that pulls water into urine, impairing the kidneys’ ability to excrete free water. If free water intake exceeds the amount of water excreted by the kidneys, dilutional hyponatremia can occur. For example, if Mr. Zerb excretes only 200-250 mOsm/per day given his poor solute intake and based on a maximum urinary dilution capability of 50 mOsm/L, then any fluid intake greater than 4 to 5 L (equivalent to 11.6 to 14 12-ounce cans of beer) may result in net water retention and dilutional hyponatremia. Because Mr. Zerb has no intrinsic urinary dilution defect, when adequate solute intake is restored, his kidneys will quickly excrete the free water, leading to a rapid and potentially lethal correction in serum sodium levels.


Beer potomania diagnosis is based on laboratory values and patient history, while ruling out other etiologies. Other potential causes of hyponatremia in patients with a history of alcohol use disorder include liver cirrhosis, syndrome of inappropriate antidiuretic hormone, cerebral salt wasting syndrome due to alcohol-induced cerebral atrophy, heart failure, hypovolemia, and pseudohyponatremia secondary to alcohol-induced severe hypertriglyceridaemia.


Beer potomania treatment can be challenging. Clinicians must be careful not to reverse sodium levels too rapidly. Based on a series of case reports and expert opinion, the following treatment regimen is suggested.

  • If the patient is asymptomatic or has minimal symptoms, fluid restriction and close monitoring is recommended, regardless of the degree of hyponatremia.
  • If the patient has neurologic symptoms, a 500 mL bolus of normal saline should be given.

The goal is to correct serum sodium levels by 1 to 2 mEq/L/h in the first 2 to 3 hours with a 24-hour goal of ≤ 10 mEq/L and a 48-hour goal of < 18 mEq/L. If the serum sodium levels rise too rapidly, a D5W infusion should be started to match urine output and adjusted every 2 hours based on serum sodium levels. (See Slow and steady.)

Slow and steady

Slow and carefully monitored serum sodium level increases in a patient with beer potomania helps ensure recovery and reduces the risk of potential neurologic deterioration. The table depicts an example of safe sodium level increase, which hadn’t occurred in the case study.

  Day 1 Day 2 Day 3 Day 4 Day 5 Day 6
Serum sodium level (mEq/L) 98 111 121 129 136 139
Change from day prior (mEq/L) n/a 13 10 8 7 3
Change from admission n/a 13 23 31 38 41

In several reported cases of neurologic deterioration due to rapid overcorrection of serum sodium, desmopressin (along with D5W) was successfully used to lower sodium levels. In these cases, neurologic deterioration was reversed. Desmopressin can be repeated every 12 hours until serum sodium goals are met.

ADH levels frequently are suppressed in patients with beer potomania, resulting in limited kidney free-water uptake. This can cause brisk diuresis when solute is introduced and a rapid rise in serum sodium levels over a relatively short period. Overtreating with solute (such as hypertonic saline) should be avoided. Sanghvi and colleagues recommend keeping patients NPO for 24 hours because of the risk of too rapid correction of serum osmolarity, particularly serum sodium, through the introduction of solutes in the diet (such as protein, sodium, and glucose). Caution also is needed when using the “banana bag” (normal saline solution with thiamine, magnesium, and multivitamin), a common treatment for patients with alcohol use disorder. 


Beer potomania prognosis depends on the level of sodium and electrolyte abnormalities, the patient’s co-morbidities, and the ability of the healthcare team to safely correct the electrolyte disturbances.

Severe hyponatremia (serum sodium concentration < 120 mEq/L) exposes the patient to brain damage from cerebral edema and increased intracranial pressure. Other consequences include seizures, pulmonary aspiration, falls, and death. Although correcting sodium levels is important, overcorrection or correcting them too quickly can lead to complications, including ODS. 

Nursing care

Your nursing care of patients with beer potomania starts with obtaining an accurate history that can help determine the cause of hyponatremia. Next, anticipate judicious sodium correction to prevent overcorrection, especially in the first several days. Closely monitor the patient for changes in sensory and neurologic status as well as electrolyte balance (including intake, output, and laboratory values). In addition to hyponatremia treatment, a patient with beer potomania may require monitoring and treatment for hypokalemia and the long-term effects of alcohol use disorder. Monitor the patient’s ECG for changes associated with hypokalemia; the co-occurrence of reversible first-, second-, and third-degree heart blocks has been described in a few published case reports. Changes in the patient’s condition may be the result of worsening fluid and electrolyte status, complications from acute alcohol intoxication or alcohol withdrawal, ODS, or other issue.

Patient education

Inpatient education should include dietary and fluid restriction precautions in the acute phase; discharge instructions should include avoiding excessive alcohol intake and referral to a substance use disorder rehabilitation program or counselor. Many patients with beer potomania are malnourished, so provide recommendations for nutritional counseling and a dietary consult.

Watch for dangers of overtreatment

Beer potomania is an unusual and little-known cause of hyponatremia that results from low solute intake. Treatment can be difficult. Avoiding overtreatment of hyponatremia is important to prevent ODS, which may not be recognized immediately and has been known to occur even when serum sodium replacement levels are in the acceptable range, especially in the presence of hypokalemia. Although beer potomania may be an unusual reason for admission to the ICU, hyponatremia is common for acutely ill patients. Critical care and ED nurses should be aware of the dangers of rapidly correcting long-standing hyponatremia, and clinical suspicion for ODS should be high in any patient presenting with new-onset neurologic symptoms with recent rapid sodium correction.

Beer potomania overview

Keep the following points in mind when monitoring patients with beer potomania who are being treated for hyponatremia.

  • Beer potomania is an unusual and little-known cause of hyponatremia that results from low solute intake.
  • Early symptoms of beer potomania frequently are nonspecific, and treatment may be challenging.
  • Careful correction of serum sodium and reintroduction of solutes are required to prevent overcorrection of sodium levels. Sodium levels typically rise more quickly when the cause of hyponatremia is beer potomania.
  • The treatment goal is to correct serum sodium levels by 1 to 2 mEq/L in the first 2 to 3 hours with a 24-hour goal of 10 mEq/L or less and a 48-hour goal of under 18 mEq/L.
  • Overcorrecting sodium levels can cause osmotic demyelination syndrome, a rare delayed and frequently deadly complication.
  • Patients with beer potomania being treated for hyponatremia should be closely monitored for sensory and neurologic status changes and fluid and electrolyte imbalances. Patients also may experience cardiac rhythm changes related to hypokalemia.

*Name is fictitious.

Patricia A. Zrelak is a clinical practice consultant in the department of clinical education, practice, and informatics at Kaiser Foundation Hospital in Sacramento, California.


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