Kristina Unterseher, MSN, FNP, CNN-NP

Q) A clinic patient of mine was recently admitted to the hospital with hyponatremia (serum sodium, 115 mEq/L). She was treated with 2 L of normal saline and discharged home 48 hours later, at her baseline mental status with a serum sodium level of 132 mEq/L. Two days later, she was readmitted for mental status changes, and MRI showed brain swelling. The neurologist stated this was a result of the initial treatment for her hyponatremia. How is this possible?

The cause-and-effect relationship between rapid correction of chronic hyponatremia and subsequent development of neurologic problems was discovered in the late 1970s. Central pontine and extrapontine myelinolysis (known as osmotic demyelination syndrome or ODS) is a neurologic condition that can occur from rapid sodium correction. It is diagnosed by MRI, which shows hyperintense lesions on T2-weighted images. Clinical signs include upper motor neuron signs, pseudobulbar palsy, spastic quadriparesis, and mental status changes ranging from mild confusion to coma.²

Treatment for hyponatremia should be guided by symptom management.^2,3 If a patient is asymptomatic, a simple and effective strategy is to keep NPO for 24 hours, except for medications. Simple food and fluid restriction will likely increase the serum sodium level because of obligate solute losses and urinary electrolyte free water loss.^2,4 While the first instinct is to feed these patients, as they often appear malnourished, this can cause a solute load leading to a too-rapid sodium correction. After 24 hours, if intake restriction is not effective, use 0.5% normal saline but with limited dosing orders, as usual saline dosing can cause too rapid a correction.²

For symptomatic patients (confusion, seizures, coma), the goal is to initially elevate sodium by 1 to 2 mEq/L per hour for the first two to three hours. Do not exceed 10 mEq/L in 24 hours or 18 mEq/L in 48 hours. Exceeding these limits puts patients at high risk for ODS. In fact, even when staying within these parameters, there is some risk for overcorrection. It is always better to go slowly.^2,3

In the patient with hyponatremia due to low solute intake (eg, beer potomania), diuresis can start spontaneously after a period of food and fluid restriction. It can also be initiated with just a small amount of solute. For example, administering an IV antibiotic with a base solution of 100 mL of normal saline or a “banana bag” (an IV solution containing 0.5 to 1 L of normal saline with multivitamins/minerals that cause the fluid to be yellow) can produce several liters of diuresis.² Once you open the floodgate, you can unintentionally cause too-rapid correction that could lead to ODS.  

In chronic hyponatremic patients, low antidiuretic hormone (ADH) levels are often found; thus when a solute is introduced, there is little ADH in the system to protect against excessive water loss and electrolyte imbalance. At the same time, excessive water loss can translate to higher sodium levels and increase the risk for cerebral edema. If rapid diuresis occurs, an infusion of D5W (5% dextrose in water) to match the rate of urine output may prevent a rapid serum sodium level rise. Frequent monitoring of serum sodium levels is often necessary. In instances where ODS is already present, there are case studies of improved neurologic outcomes with reduction of serum sodium levels.^2,3

While the treatment of hyponatremia at first glance seems straightforward—replace that which is lost—it can actually transform a seemingly simple problem into a complicated clinical course requiring intensive care, due to the need for frequent monitoring and intervention.

Kristina Unterseher, MSN, FNP, CNN-NP
Peacehealth St. John 
Medical Center
Longview, WA

REFERENCES
1. Hilden T, Swensen TL.  Electrolyte disturbances in beer drinkers: a specific “hypo-osmolaity syndrome.” Lancet. 1975;2(7928):245-246.

2. Sanghvi SR, Kellerman PS, Nanovic L. Beer potomania: an unusual cause of hyponatremia at high risk of complications from rapid correction. Am J Kidney Dis. 2007;50(4):673-680.

3. Bhattarai N, Poonam K, Panda M. Beer potomania: a case report. BMJ Case Rep. 2010; 2010: bcr10.2009.2414.

4. Campbell M. Hyponatremia and central pontine myelinolysis as a result of beer potomania: a case report. Prim Care Companion J Clin Psychiatry. 2010;12(4):PCC.09100936.

5. Thaler SM, Teitelbaum I, Beri T. “Beer potomania” in non-beer drinkers: effect of low dietary solute intake. Am J Kidney Dis. 1998;31(6):1028-1031.

Q) A clinic patient of mine was recently admitted to the hospital with hyponatremia (serum sodium, 115 mEq/L). She was treated with 2 L of normal saline and discharged home 48 hours later, at her baseline mental status with a serum sodium level of 132 mEq/L. Two days later, she was readmitted for mental status changes, and MRI showed brain swelling. The neurologist stated this was a result of the initial treatment for her hyponatremia. How is this possible?

The cause-and-effect relationship between rapid correction of chronic hyponatremia and subsequent development of neurologic problems was discovered in the late 1970s. Central pontine and extrapontine myelinolysis (known as osmotic demyelination syndrome or ODS) is a neurologic condition that can occur from rapid sodium correction. It is diagnosed by MRI, which shows hyperintense lesions on T2-weighted images. Clinical signs include upper motor neuron signs, pseudobulbar palsy, spastic quadriparesis, and mental status changes ranging from mild confusion to coma.²

Treatment for hyponatremia should be guided by symptom management.^2,3 If a patient is asymptomatic, a simple and effective strategy is to keep NPO for 24 hours, except for medications. Simple food and fluid restriction will likely increase the serum sodium level because of obligate solute losses and urinary electrolyte free water loss.^2,4 While the first instinct is to feed these patients, as they often appear malnourished, this can cause a solute load leading to a too-rapid sodium correction. After 24 hours, if intake restriction is not effective, use 0.5% normal saline but with limited dosing orders, as usual saline dosing can cause too rapid a correction.²

For symptomatic patients (confusion, seizures, coma), the goal is to initially elevate sodium by 1 to 2 mEq/L per hour for the first two to three hours. Do not exceed 10 mEq/L in 24 hours or 18 mEq/L in 48 hours. Exceeding these limits puts patients at high risk for ODS. In fact, even when staying within these parameters, there is some risk for overcorrection. It is always better to go slowly.^2,3

In the patient with hyponatremia due to low solute intake (eg, beer potomania), diuresis can start spontaneously after a period of food and fluid restriction. It can also be initiated with just a small amount of solute. For example, administering an IV antibiotic with a base solution of 100 mL of normal saline or a “banana bag” (an IV solution containing 0.5 to 1 L of normal saline with multivitamins/minerals that cause the fluid to be yellow) can produce several liters of diuresis.² Once you open the floodgate, you can unintentionally cause too-rapid correction that could lead to ODS.  

In chronic hyponatremic patients, low antidiuretic hormone (ADH) levels are often found; thus when a solute is introduced, there is little ADH in the system to protect against excessive water loss and electrolyte imbalance. At the same time, excessive water loss can translate to higher sodium levels and increase the risk for cerebral edema. If rapid diuresis occurs, an infusion of D5W (5% dextrose in water) to match the rate of urine output may prevent a rapid serum sodium level rise. Frequent monitoring of serum sodium levels is often necessary. In instances where ODS is already present, there are case studies of improved neurologic outcomes with reduction of serum sodium levels.^2,3

While the treatment of hyponatremia at first glance seems straightforward—replace that which is lost—it can actually transform a seemingly simple problem into a complicated clinical course requiring intensive care, due to the need for frequent monitoring and intervention.

Kristina Unterseher, MSN, FNP, CNN-NP
Peacehealth St. John 
Medical Center
Longview, WA

REFERENCES
1. Hilden T, Swensen TL.  Electrolyte disturbances in beer drinkers: a specific “hypo-osmolaity syndrome.” Lancet. 1975;2(7928):245-246.

2. Sanghvi SR, Kellerman PS, Nanovic L. Beer potomania: an unusual cause of hyponatremia at high risk of complications from rapid correction. Am J Kidney Dis. 2007;50(4):673-680.

3. Bhattarai N, Poonam K, Panda M. Beer potomania: a case report. BMJ Case Rep. 2010; 2010: bcr10.2009.2414.

4. Campbell M. Hyponatremia and central pontine myelinolysis as a result of beer potomania: a case report. Prim Care Companion J Clin Psychiatry. 2010;12(4):PCC.09100936.

5. Thaler SM, Teitelbaum I, Beri T. “Beer potomania” in non-beer drinkers: effect of low dietary solute intake. Am J Kidney Dis. 1998;31(6):1028-1031.

Q) A clinic patient of mine was recently admitted to the hospital with hyponatremia (serum sodium, 115 mEq/L). She was treated with 2 L of normal saline and discharged home 48 hours later, at her baseline mental status with a serum sodium level of 132 mEq/L. Two days later, she was readmitted for mental status changes, and MRI showed brain swelling. The neurologist stated this was a result of the initial treatment for her hyponatremia. How is this possible?

The cause-and-effect relationship between rapid correction of chronic hyponatremia and subsequent development of neurologic problems was discovered in the late 1970s. Central pontine and extrapontine myelinolysis (known as osmotic demyelination syndrome or ODS) is a neurologic condition that can occur from rapid sodium correction. It is diagnosed by MRI, which shows hyperintense lesions on T2-weighted images. Clinical signs include upper motor neuron signs, pseudobulbar palsy, spastic quadriparesis, and mental status changes ranging from mild confusion to coma.²

Treatment for hyponatremia should be guided by symptom management.^2,3 If a patient is asymptomatic, a simple and effective strategy is to keep NPO for 24 hours, except for medications. Simple food and fluid restriction will likely increase the serum sodium level because of obligate solute losses and urinary electrolyte free water loss.^2,4 While the first instinct is to feed these patients, as they often appear malnourished, this can cause a solute load leading to a too-rapid sodium correction. After 24 hours, if intake restriction is not effective, use 0.5% normal saline but with limited dosing orders, as usual saline dosing can cause too rapid a correction.²

For symptomatic patients (confusion, seizures, coma), the goal is to initially elevate sodium by 1 to 2 mEq/L per hour for the first two to three hours. Do not exceed 10 mEq/L in 24 hours or 18 mEq/L in 48 hours. Exceeding these limits puts patients at high risk for ODS. In fact, even when staying within these parameters, there is some risk for overcorrection. It is always better to go slowly.^2,3

In the patient with hyponatremia due to low solute intake (eg, beer potomania), diuresis can start spontaneously after a period of food and fluid restriction. It can also be initiated with just a small amount of solute. For example, administering an IV antibiotic with a base solution of 100 mL of normal saline or a “banana bag” (an IV solution containing 0.5 to 1 L of normal saline with multivitamins/minerals that cause the fluid to be yellow) can produce several liters of diuresis.² Once you open the floodgate, you can unintentionally cause too-rapid correction that could lead to ODS.  

In chronic hyponatremic patients, low antidiuretic hormone (ADH) levels are often found; thus when a solute is introduced, there is little ADH in the system to protect against excessive water loss and electrolyte imbalance. At the same time, excessive water loss can translate to higher sodium levels and increase the risk for cerebral edema. If rapid diuresis occurs, an infusion of D5W (5% dextrose in water) to match the rate of urine output may prevent a rapid serum sodium level rise. Frequent monitoring of serum sodium levels is often necessary. In instances where ODS is already present, there are case studies of improved neurologic outcomes with reduction of serum sodium levels.^2,3

While the treatment of hyponatremia at first glance seems straightforward—replace that which is lost—it can actually transform a seemingly simple problem into a complicated clinical course requiring intensive care, due to the need for frequent monitoring and intervention.

Kristina Unterseher, MSN, FNP, CNN-NP
Peacehealth St. John 
Medical Center
Longview, WA

REFERENCES
1. Hilden T, Swensen TL.  Electrolyte disturbances in beer drinkers: a specific “hypo-osmolaity syndrome.” Lancet. 1975;2(7928):245-246.

2. Sanghvi SR, Kellerman PS, Nanovic L. Beer potomania: an unusual cause of hyponatremia at high risk of complications from rapid correction. Am J Kidney Dis. 2007;50(4):673-680.

3. Bhattarai N, Poonam K, Panda M. Beer potomania: a case report. BMJ Case Rep. 2010; 2010: bcr10.2009.2414.

4. Campbell M. Hyponatremia and central pontine myelinolysis as a result of beer potomania: a case report. Prim Care Companion J Clin Psychiatry. 2010;12(4):PCC.09100936.

5. Thaler SM, Teitelbaum I, Beri T. “Beer potomania” in non-beer drinkers: effect of low dietary solute intake. Am J Kidney Dis. 1998;31(6):1028-1031.

Q) Recently, we had a patient admitted for hyponatremia with
a serum sodium level of 117 mEq/L. One of the hospitalists mentioned “beer potomania” in the differential. Not wanting to look dumb, I just agreed. What is beer potomania, and how is it related to low serum sodium?

Potomania is the excessive consumption of alcoholic beverages; beer potomania is used to refer to a dilutional hyponatremia caused by excessive consumption of beer.¹ First recognized in 1971, this cause of hyponatremia is not the most common but should be in the differential if the patient is a heavy alcohol imbiber who presents with encephalopathy and low serum sodium.

When considering this diagnosis, keep in mind that hyponatremia is common among chronic alcoholics and can be due to conditions such as cirrhosis, congestive heart failure, syndrome of inappropriate antidiuretic hormone (SIADH) secretion, and hypovolemia. Less common but still belonging in the differential are pseudohyponatremia secondary to alcohol-induced severe hypertriglyceridemia and cerebral salt wasting syndrome.^2,3

Beer potomania usually manifests as altered mental status, weakness, and gait disturbance with an average serum sodium concentration of 108 mEq/L.³ Other abnormal lab results consistent with this diagnosis include hypokalemia (mean potassium, 3 mEq/L) and low blood urea nitrogen and urine sodium levels.^2,3 Another fairly consistent finding is a recent personal history of binge drinking (more than about 5 L, or 14 cans of beer, in 24 hours) and/or history of illness (vomiting, diarrhea) that predisposed the patient to a rapid drop in serum sodium levels.²

Based on the information presented thus far, you may ask, “Why haven’t I seen this diagnosed more often? There are a lot of beer bingers out there!” Good question. Let’s review the pathophysiology of beer potomania. When patients have poor protein and solute (food, electrolytes) intake, they can experience water intoxication with smaller-than-usual volumes of fluid. The kidneys need a certain amount of solute to facilitate free water clearance (the ability to clear excess fluid from the body). A lack of adequate solute results in a buildup of free water in the vascular system, leading to a dilutional hyponatremia.³

Free water clearance is dependent on both solute excretion and the ability to dilute urine. Someone consuming an average diet will excrete 600 to 900 mOsm/d of solute. This osmolar load in-cludes urea generated from protein (10 g of protein produces about 50 mOsm of urea), along with dietary sodium and potassium. The maximum capacity for urinary dilution is 50 mOsm/L. In a nutritionally sound person, a lot of fluid—about 20 L—would be required to overwhelm the body’s capacity for urinary dilution.²

However, when you don’t eat, the body starts to break down tissue to create energy to survive. This catabolism creates 100 to 150 mOsm/d of urea, allowing you to continue to appropriately excrete a moderate amount of fluid in spite of poor solute intake ... as long as you are not drinking excessive amounts of water.⁵

Alcoholics get a moderate amount of their calories via beer consumption and do not experience this endogenous protein breakdown or its resultant low urea/solute level. With low solute intake, dramatically lower fluid intake (about 14 cans of beer) will overwhelm the kidneys’ ability to clear excess free water in the body.² Fortunately, most heavy beer drinkers continue to eat at least modestly, which is sufficient to avoid this rare type of hyponatremia. Chronic alcoholics who go on a drinking binge beyond their normal baseline alcohol consumption, or who develop a flulike illness that causes electrolyte depletion (via diarrhea or vomiting), are at higher risk for beer potomania.

Kristina Unterseher, MSN, FNP, CNN-NP
Peacehealth St. John 
Medical Center
Longview, WA

REFERENCES
1. Hilden T, Swensen TL.  Electrolyte disturbances in beer drinkers: a specific “hypo-osmolaity syndrome.” Lancet. 1975;2(7928):245-246.

2. Sanghvi SR, Kellerman PS, Nanovic L. Beer potomania: an unusual cause of hyponatremia at high risk of complications from rapid correction. Am J Kidney Dis. 2007;50(4):673-680.

3. Bhattarai N, Poonam K, Panda M. Beer potomania: a case report. BMJ Case Rep. 2010; 2010: bcr10.2009.2414.

4. Campbell M. Hyponatremia and central pontine myelinolysis as a result of beer potomania: a case report. Prim Care Companion J Clin Psychiatry. 2010;12(4):PCC.09100936.

5. Thaler SM, Teitelbaum I, Beri T. “Beer potomania” in non-beer drinkers: effect of low dietary solute intake. Am J Kidney Dis. 1998;31(6):1028-1031.

Q) Recently, we had a patient admitted for hyponatremia with
a serum sodium level of 117 mEq/L. One of the hospitalists mentioned “beer potomania” in the differential. Not wanting to look dumb, I just agreed. What is beer potomania, and how is it related to low serum sodium?

Potomania is the excessive consumption of alcoholic beverages; beer potomania is used to refer to a dilutional hyponatremia caused by excessive consumption of beer.¹ First recognized in 1971, this cause of hyponatremia is not the most common but should be in the differential if the patient is a heavy alcohol imbiber who presents with encephalopathy and low serum sodium.

When considering this diagnosis, keep in mind that hyponatremia is common among chronic alcoholics and can be due to conditions such as cirrhosis, congestive heart failure, syndrome of inappropriate antidiuretic hormone (SIADH) secretion, and hypovolemia. Less common but still belonging in the differential are pseudohyponatremia secondary to alcohol-induced severe hypertriglyceridemia and cerebral salt wasting syndrome.^2,3

Beer potomania usually manifests as altered mental status, weakness, and gait disturbance with an average serum sodium concentration of 108 mEq/L.³ Other abnormal lab results consistent with this diagnosis include hypokalemia (mean potassium, 3 mEq/L) and low blood urea nitrogen and urine sodium levels.^2,3 Another fairly consistent finding is a recent personal history of binge drinking (more than about 5 L, or 14 cans of beer, in 24 hours) and/or history of illness (vomiting, diarrhea) that predisposed the patient to a rapid drop in serum sodium levels.²

Based on the information presented thus far, you may ask, “Why haven’t I seen this diagnosed more often? There are a lot of beer bingers out there!” Good question. Let’s review the pathophysiology of beer potomania. When patients have poor protein and solute (food, electrolytes) intake, they can experience water intoxication with smaller-than-usual volumes of fluid. The kidneys need a certain amount of solute to facilitate free water clearance (the ability to clear excess fluid from the body). A lack of adequate solute results in a buildup of free water in the vascular system, leading to a dilutional hyponatremia.³

Free water clearance is dependent on both solute excretion and the ability to dilute urine. Someone consuming an average diet will excrete 600 to 900 mOsm/d of solute. This osmolar load in-cludes urea generated from protein (10 g of protein produces about 50 mOsm of urea), along with dietary sodium and potassium. The maximum capacity for urinary dilution is 50 mOsm/L. In a nutritionally sound person, a lot of fluid—about 20 L—would be required to overwhelm the body’s capacity for urinary dilution.²

However, when you don’t eat, the body starts to break down tissue to create energy to survive. This catabolism creates 100 to 150 mOsm/d of urea, allowing you to continue to appropriately excrete a moderate amount of fluid in spite of poor solute intake ... as long as you are not drinking excessive amounts of water.⁵

Alcoholics get a moderate amount of their calories via beer consumption and do not experience this endogenous protein breakdown or its resultant low urea/solute level. With low solute intake, dramatically lower fluid intake (about 14 cans of beer) will overwhelm the kidneys’ ability to clear excess free water in the body.² Fortunately, most heavy beer drinkers continue to eat at least modestly, which is sufficient to avoid this rare type of hyponatremia. Chronic alcoholics who go on a drinking binge beyond their normal baseline alcohol consumption, or who develop a flulike illness that causes electrolyte depletion (via diarrhea or vomiting), are at higher risk for beer potomania.

Kristina Unterseher, MSN, FNP, CNN-NP
Peacehealth St. John 
Medical Center
Longview, WA

REFERENCES
1. Hilden T, Swensen TL.  Electrolyte disturbances in beer drinkers: a specific “hypo-osmolaity syndrome.” Lancet. 1975;2(7928):245-246.

2. Sanghvi SR, Kellerman PS, Nanovic L. Beer potomania: an unusual cause of hyponatremia at high risk of complications from rapid correction. Am J Kidney Dis. 2007;50(4):673-680.

3. Bhattarai N, Poonam K, Panda M. Beer potomania: a case report. BMJ Case Rep. 2010; 2010: bcr10.2009.2414.

4. Campbell M. Hyponatremia and central pontine myelinolysis as a result of beer potomania: a case report. Prim Care Companion J Clin Psychiatry. 2010;12(4):PCC.09100936.

5. Thaler SM, Teitelbaum I, Beri T. “Beer potomania” in non-beer drinkers: effect of low dietary solute intake. Am J Kidney Dis. 1998;31(6):1028-1031.

Q) Recently, we had a patient admitted for hyponatremia with
a serum sodium level of 117 mEq/L. One of the hospitalists mentioned “beer potomania” in the differential. Not wanting to look dumb, I just agreed. What is beer potomania, and how is it related to low serum sodium?

Potomania is the excessive consumption of alcoholic beverages; beer potomania is used to refer to a dilutional hyponatremia caused by excessive consumption of beer.¹ First recognized in 1971, this cause of hyponatremia is not the most common but should be in the differential if the patient is a heavy alcohol imbiber who presents with encephalopathy and low serum sodium.

When considering this diagnosis, keep in mind that hyponatremia is common among chronic alcoholics and can be due to conditions such as cirrhosis, congestive heart failure, syndrome of inappropriate antidiuretic hormone (SIADH) secretion, and hypovolemia. Less common but still belonging in the differential are pseudohyponatremia secondary to alcohol-induced severe hypertriglyceridemia and cerebral salt wasting syndrome.^2,3

Beer potomania usually manifests as altered mental status, weakness, and gait disturbance with an average serum sodium concentration of 108 mEq/L.³ Other abnormal lab results consistent with this diagnosis include hypokalemia (mean potassium, 3 mEq/L) and low blood urea nitrogen and urine sodium levels.^2,3 Another fairly consistent finding is a recent personal history of binge drinking (more than about 5 L, or 14 cans of beer, in 24 hours) and/or history of illness (vomiting, diarrhea) that predisposed the patient to a rapid drop in serum sodium levels.²

Based on the information presented thus far, you may ask, “Why haven’t I seen this diagnosed more often? There are a lot of beer bingers out there!” Good question. Let’s review the pathophysiology of beer potomania. When patients have poor protein and solute (food, electrolytes) intake, they can experience water intoxication with smaller-than-usual volumes of fluid. The kidneys need a certain amount of solute to facilitate free water clearance (the ability to clear excess fluid from the body). A lack of adequate solute results in a buildup of free water in the vascular system, leading to a dilutional hyponatremia.³

Free water clearance is dependent on both solute excretion and the ability to dilute urine. Someone consuming an average diet will excrete 600 to 900 mOsm/d of solute. This osmolar load in-cludes urea generated from protein (10 g of protein produces about 50 mOsm of urea), along with dietary sodium and potassium. The maximum capacity for urinary dilution is 50 mOsm/L. In a nutritionally sound person, a lot of fluid—about 20 L—would be required to overwhelm the body’s capacity for urinary dilution.²

However, when you don’t eat, the body starts to break down tissue to create energy to survive. This catabolism creates 100 to 150 mOsm/d of urea, allowing you to continue to appropriately excrete a moderate amount of fluid in spite of poor solute intake ... as long as you are not drinking excessive amounts of water.⁵

Alcoholics get a moderate amount of their calories via beer consumption and do not experience this endogenous protein breakdown or its resultant low urea/solute level. With low solute intake, dramatically lower fluid intake (about 14 cans of beer) will overwhelm the kidneys’ ability to clear excess free water in the body.² Fortunately, most heavy beer drinkers continue to eat at least modestly, which is sufficient to avoid this rare type of hyponatremia. Chronic alcoholics who go on a drinking binge beyond their normal baseline alcohol consumption, or who develop a flulike illness that causes electrolyte depletion (via diarrhea or vomiting), are at higher risk for beer potomania.

Kristina Unterseher, MSN, FNP, CNN-NP
Peacehealth St. John 
Medical Center
Longview, WA

REFERENCES
1. Hilden T, Swensen TL.  Electrolyte disturbances in beer drinkers: a specific “hypo-osmolaity syndrome.” Lancet. 1975;2(7928):245-246.

2. Sanghvi SR, Kellerman PS, Nanovic L. Beer potomania: an unusual cause of hyponatremia at high risk of complications from rapid correction. Am J Kidney Dis. 2007;50(4):673-680.

3. Bhattarai N, Poonam K, Panda M. Beer potomania: a case report. BMJ Case Rep. 2010; 2010: bcr10.2009.2414.

4. Campbell M. Hyponatremia and central pontine myelinolysis as a result of beer potomania: a case report. Prim Care Companion J Clin Psychiatry. 2010;12(4):PCC.09100936.

5. Thaler SM, Teitelbaum I, Beri T. “Beer potomania” in non-beer drinkers: effect of low dietary solute intake. Am J Kidney Dis. 1998;31(6):1028-1031.