ACID-BASE AND ELECTROLYTE TEACHING CASE
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ACID-BASE AND ELECTROLYTE TEACHING CASE
Beer Potomania: An Unusual Cause of Hyponatremia at High Risk of
Complications From Rapid Correction
Shalin R. Sanghvi, MD,1,2 Paul S. Kellerman, MD,1,2 and Lisa Nanovic, DO1,2
INDEX WORDS: Beer; potomania; hyponatremia; management; algorithm; treatment; complications.
CASE REPORT hours after ED presentation. On the general medical floor,
she had urinary output of 500 mL/h, and serum sodium level
An unusual syndrome of hyponatremia was described in
beer drinkers dating back to the early 1970s. The syndrome increased by 6 mEq/L (mmol/L) over 4 hours (Fig 1).
“beer potomania” is used to describe a patient who presents Dextrose 5% in water (D5W) was started at a rate to match
with hyponatremia in conjunction with low daily solute urine output to prevent a further increase in serum sodium
intake and excessive beer drinking. This pathophysiological level. Because of excessive nursing needs for serial labora-
state results in patients at serious risk of rapid correction of tory draws, hourly recordings of urinary output, and titration
hyponatremia and its neurological sequelae. This article of IV fluids, the patient was transferred to the intensive care
reviews the literature for both beer potomania and osmotic unit 12 hours after ED presentation. The first urine osmolal-
demyelination syndrome (ODS). Two patients with beer ity measured 4 hours after ED presentation was 218 mOsm/L;
potomania with differing outcomes are presented, with cru- however, rechecks at 12 and 18 hours after presentation
cial differences in management. The article describes patho- showed values of 50 and 48 mOsm/L, respectively. The
physiological characteristics and the unique management patient was treated with IV clindamycin for empiric antibi-
challenges of beer potomania. Last, recommendations and otic coverage. Review of the patient’s records during the
an algorithm for the treatment of patients with hyponatremia first 24 hours showed a total of 8,500 mL of IV fluids (NS
caused by beer potomania are presented as a potential guide solution accounted for 1,200 mL) and 7,600 mL of urine
to prevent the catastrophic outcome of ODS. output. In the subsequent 24 hours, the patient received
4,300 mL of D5W and had 4,300 mL of urine output. Serum
Patient 1 sodium level increased 15 mEq/L (mmol/L) during the first
Clinical History 24 hours and 24 mEq/L (mmol/L) during the first 48 hours
(Fig 1). On day 7, her level of alertness started to decrease,
A 39-year-old woman was admitted to the hospital after and on day 9, magnetic resonance imaging of the brain
being brought by a family member because of a 24-hour showed findings consistent with pontine and extrapontine
history of increasing confusion. Her medical history was myelinolysis.
remarkable for long-standing alcohol use and an alcohol
withdrawal seizure approximately 2 years before this presen-
tation. Her daily intake was approximately 18 cans of beer. Patient 2
Recent history included antibiotic use for a tooth infection
and diarrhea after starting the antibiotics. The family mem- Clinical History
ber was unaware if there was recent binge drinking. The A 63-year-old man with a history of alcoholism presented
patient’s initial mental status showed a somnolent woman to the ED with weakness and dizziness after a 2-week
with mildly slurred speech and oriented to person, place, and history of binge drinking. The patient had been drinking
time, but with difficulty with short-term memory. Serum approximately 15 to 20 cans of beer daily and had very little
sodium level on presentation was 100 mEq/L (mmol/L;
food intake. On examination, the patient was oriented to
Table 1).
person, place, and time, with mild difficulty following com-
mands. Serum sodium level at the time of presentation was
Additional Investigations
104 mEq/L (mmol/L; Table 1).
The patient had no laboratory or clinical evidence of
cirrhosis or congestive heart failure. Computed tomographic
scan of the head on admission had normal findings.
Diagnosis From the 1University of Wisconsin, Madison; and 2Veter-
ans Affair Hospital, Middleton, WI.
Symptomatic severe hyponatremia was diagnosed, possi-
Received March 26, 2007. Accepted in revised form July
bly caused by beer potomania.
12, 2007.
Address correspondence to Shalin R. Sanghvi, MD, 3034
Clinical Follow-Up Fish Hatchery Rd, Fitchburg, WI 53713. E-mail:
In the emergency department (ED), the patient was admin- shalin.sanghvi@gmail.com
istered 1 g of intravenous (IV) cefazolin and 1 L of normal © 2007 by the National Kidney Foundation, Inc.
saline (NS) solution containing magnesium and thiamine. 0272-6386/07/5004-0019$32.00/0
The patient was transferred to a general medicine bed 5 doi:10.1053/j.ajkd.2007.07.015
American Journal of Kidney Diseases, Vol 50, No 4 (October), 2007: pp 673-680 673674
Table 1. Summary of Beer Potomania Cases
Presentation Laboratory Results
Patients Neurological Symptoms Na K BUN U osm U Na Serum Na
Author (year) no. on Presentation (mEq/L) (mEq/L) (mg/dL) (mosm/L) (mos m/L) Treatment Change Outcome
Demanet (71) 1 Unconscious, seizure 107 2.6 12 N/A N/A N/A N/A N/A
2 Weakness 105 1.3 15 N/A N/A N/A N/A Death - brain autopsy with atrophy
of mammillary bodies
3 Weakness 104 2.6 30 N/A N/A N/A N/A Death - no brain autopsy
4 Unconscious 103 2.5 13 N/A N/A 300 MEQ Na IV d 10 mmol/48 h N/A
1 and 2
5 Weakness, “grand mal” 101 1.4 19 N/A N/A N/A N/A Death - normal brain autopsy
6 Unconscious, “grand mal” 99 1.8 18 N/A N/A N/A N/A Death - brain autopsy with CPM
7 Unconscious, “grand mal” 98 4.4 30 N/A N/A N/A N/A N/A
Gwinup (72) 8 Weakness 122 5.1 N/A N/A N/A Fluid restriction 20 mmol/72 h No neurological sequelae
reported
Hilden (75) 9 Debility, dizziness, 123 2.7 N/A N/A N/A 0.9% NS 2–3 L 12 mmol/48 h No neurological sequelae
confusion reported
10 Debility, dizziness, 109 2.5 N/A 79 N/A No IVFs 15 mmol/48 h No neurological sequelae
confusion reported
11 Debility, dizziness, 108 2.7 N/A 69 N/A 0.9% NS 2–3 L 19 mmol/48 h No neurological sequelae
confusion reported
12 Debility, dizziness, 127 2.5 N/A N/A N/A No IVFs 2 mmol/48 h No neurological sequelae
confusion reported
13 Debility, dizziness, 117 3.1 N/A N/A N/A No IVFs 9 mmol/48 h No neurological sequelae
confusion reported
Swenson (76) 14 Weakness 106 3.8 N/A 199 5.6 Fluid restriction 8 mmol/48 h No apparent neurological
sequelae
Evans (85) 15 Confused, restless 118 4.1 2.3 N/A N/A 1.8% NS ⫻ 6 h then 10 9 mmol/48 h Long-term impaired memory,
DW or 0.9% NS confabulation
Joyce (86) 16 Agitation, confusion, 110 3 N/A N/A N/A 3% NS ⫻ 30 mL, 0.9% 14 mmol/24 h Discharged d 2, lost to follow-up
seizures NS @ 300 ml/h
Fenves (95) 17 Tremor 121 3.6 4 50 1 0.9% NS @ 100 mL/h 13 mmol/13 h Not reported
18 Unconscious, seizures 97 3.6 2 338 12 0.9% NS @ 150 mL/h 30 mmol/48 h No apparent neurological
and 3% NS @ 20 mL/ sequelae
h ⫻ 160 Ml
Kelly (98) 19 Unconscious 109 3.6 16 340 ⬍10 NS 3 L/24 h 20 mmol/48 h ODS
Lens (01) 20 Confusion/weakness 97 2.1 14 N/A N/A 0.45 NS ⫹ KCl 21 mmol/48 h ODS
supplements
Sanghvi (06) 21 Weakness 100 2.7 4 218 53 NS, later fluid restriction 15 mmol/24 h, ODS
with D5 24 mmol/
48 h
22 Weakness 104 4.3 7 547 10 Fluid restriction 7 mmol/24 h, 14 No apparent neurological
mmol/48 h sequelae
Sanghvi et al
Note: To convert BUN in mg/dL to mmol/L, multiply by 0.357; sodium and potassium in mEq/L and mmol/L are equivalent.
Abbreviations: Na, sodium; K, potassium; BUN, blood urea nitrogen; U osm, urine osmolality; U Na, urine sodium; N/A, not available; IV, intravenous; CPM, central pontine
myelinolysis; NS, normal saline solution; IVF, intravenous fluid; KCl, potassium chloride; ODS, osmotic demyelination syndrome.Risks and Management of Beer Potomania 675
Figure 1. Time graph for patients
1 and 2. Note: Sodium (Na) in mEq/L
and mmol/L is equivalent. Abbrevia-
tions: ER, emergency room; ICU, in-
tensive care unit; UO, urine output;
NS, normal saline; D5W, dextrose 5%
in water.
Additional Investigations quent urine osmolality was 71 mOsm/L (6 hours after ED
presentation). The 24-hour increase in serum sodium level
The patient was not being administered antibiotics and
had no laboratory or clinical evidence of cirrhosis or conges- was 7 mEq/L (mmol/L), and the 48-hour increase was 14
tive heart failure. mEq/L (mmol/L). The patient was discharged on hospital
day 6 without clinical evidence of neurological sequelae.
Diagnosis
Severe hyponatremia was diagnosed, possibly caused by DISCUSSION
beer potomania.
Background
Clinical Follow-Up
Cases of a hypo-osmolality syndrome in beer
Based on the tentative diagnosis of beer potomania and
drinkers were first described by Gwinup et al1 in
mild neurological symptoms, the patient’s fluid intake was
restricted to 1 L. The patient’s only IV fluids were a dose of 1972, and series of patients with similar presenta-
moxifloxacin (in 0.9% NS solution) in the ED. After transfer tions were described by Hilden and Svendsen2 in
to the intensive care unit 2 hours after ED presentation for 1975 and Swenson and Rater3 in 1976. In earlier
further monitoring, the patient had an impressive diuresis of
cases, the cause of hyponatremia was compli-
3,000 mL during the subsequent 2 hours. Serum sodium
level increased 7 mEq/L (mmol/L) during the first 9 hours cated by confounding factors, including diuretic
(Fig 1). D5W was started at a rate to match urine output. use and lack of evaluation for such diseases as
Diuresis decreased to approximately 150 mL/h. Total urine congestive heart failure or cirrhosis. However,
output during the first 24 hours was 6,500 mL, and total IV
with repeated documented cases of patients pre-
fluids were 4,500 mL (NS solution accounted for 250 mL).
Review of the patient’s laboratory test results showed urine senting with hyponatremia in conjunction with
osmolality at presentation of 547 mOsm/L; however, subse- excessive beer drinking and low daily solute676 Sanghvi et al intake, it is evident that there is a syndrome of and mental disorders ranging from mild confu- hyponatremia virtually unique in beer drinkers. sion to coma. Two retrospective reviews by Sterns Electrolyte abnormalities are not uncommon in et al15 and Ellis16 reported neurological sequelae patients admitted with a history of alcohol use. In in some patients when the change in serum the study by Liamis et al,4 17% of chronic alco- sodium during a 24-hour period was greater than holic patients had hyponatremia. Review of inter- 12 mEq/L (mmol/L) and 10 mEq/L (mmol/L), nal data from the University of Wisconsin and respectively. Case reports describe ODS in pa- Veterans Affairs Hospital in Middleton, WI, showed tients with a rate of correction less than 10 hyponatremia in greater than 5% of patients admit- mEq/L (mmol/L) per 24 hours.9 ted with alcoholism as a coding diagnosis. In addi- Our literature review found 22 cases (includ- tion to beer potomania, there are a number of other ing ours) of beer potomania. In these cases, 8 potential causes of hyponatremia in alcoholics, patients had complications (36%): 4 of the 8 had including cirrhosis, syndrome of inappropriate anti- ODS (18%), whereas the other 4 died (18%). diuretic hormone (ADH), congestive heart failure, Management varied from hypertonic saline solu- hypovolemia, and pseudohyponatremia secondary tion for brief periods to free-water restriction and to dyslipidemia.4 Laboratory values for 22 pub- even free-water supplementation in certain cases. lished cases, including the 2 mentioned here, were Brisk diuresis was common in many patients reviewed to identify features specific to beer poto- after admission (Table 1). Understanding the mania.1-3,5-11 Of the laboratory data available, con- pathophysiological state is pivotal to recognizing sistent findings among patients included severe the possibility of rapid correction and the pos- hyponatremia (mean serum sodium, 108 mEq/L sible complications. Furthermore, because ODS [mmol/L]), hypokalemia (mean serum potassium, may not present until 2 to 3 days after the change 3 mEq/L [mmol/L]), mild neurological symptoms in serum sodium levels, it is important to delin- on presentation (typically confusion), low blood urea eate management goals at the initial evaluation. nitrogen level, brisk diuresis in response to solute intake, and low urine sodium level. Although not Pathophysiology consistently reported in patients with beer potoma- Hyponatremia in beer drinkers occurs because nia, low urine osmolality on admission laboratory of water intake that exceeds excretory capacity test results was not a consistent finding (Table 1). (described next), modified by the possibility of Many similarities were noted in the presenta- inappropriate ADH secretion on admission. Our tion of patients with beer potomania. In addition review of the 22 cases shows that hyposthenuria to the history of excess beer drinking, often a on admission was not a consistent finding (al- recent history of binge drinking or illness was though urine sodium levels were low). Recogniz- present. This may potentially precipitate a rapid ing this finding prevents the erroneous dismissal decrease in serum sodium levels, which causes of beer potomania. In the majority of cases, after the patient to acutely present with such clinical admission, brisk water diuresis ensued, leading symptoms of hyponatremia as confusion, altered to the likelihood that when infections and vol- mental status, and gait disturbances. ume status were treated, the patient’s ADH secre- The relationship between neurological lesions tion decreased to a level commensurate with the and rapid correction of chronic hyponatremia degree of hypo-osmolality. was noted in the late 1970s, and a direct relation- Free-water clearance is dependant on solute ship was established in the early 1980s.12,13 excretion and urinary diluting capability.17 Based Specific neurological findings included central on a normal diet, typical osmole excretion is and extrapontine myelinolysis, now known as approximately 600 to 900 mOsm/d. This osmolar ODS. ODS is diagnosed by means of magnetic load is caused by urea generation from protein resonance image, with findings of hyperintense (10 g of protein produces ⬃50 mOsm of urea), in lesions on T2-weighted images. Most signal addition to dietary sodium and potassium intake. changes are located in the central part of the If the maximum urinary dilution capability is 50 pons, medulla oblongata, and mesencephalon.14 mOsm/L, a large amount of water (⬎20 L) must Clinical features include upper motor neuron be ingested under normal situations to over- signs, pseudobulbar palsy, spastic quadriparesis, whelm the capacity for urinary dilution, as seen
Risks and Management of Beer Potomania 677
in psychogenic polydipsia. If solute excretion sodium and potassium out of the cell, and a
decreases, the ability to excrete free water be- chronic response characterized by loss of intracel-
comes limited. For example, if the patient ex- lular organic osmoles because of the persistent
cretes only 100 mOsm/d, greater than 2 L of fluid osmotic imbalance.18 Because organic osmoles
intake with a urinary dilution capability of 50 take 5 to 7 days to return to normal levels, the
mOsm/L will result in net water retention and long-term adaptation is the major concern when
subsequently hyponatremia. correcting hyponatremia. Oligodendrocytes are
Patients with beer potomania have a history of particularly sensitive to the osmotic stress that
significant beer drinking, often long term, in occurs with correction at a rate that the intracellu-
conjunction with a poor diet. The net result is lar osmolality remains hypotonic relative to the
very low osmole intake because beer has very extracellular environment. Although the exact
little sodium and no protein, but has some calo- mechanism is not known, this stress leads to both
ries that prevent endogenous protein breakdown pontine and extrapontine myelinolysis, known as
(urea generation). Because the obligatory solute ODS.19 Symptoms can be related to damage of
loss in a day is approximately 250 mOsm in the corticospinal or corticobulbar tracts within
these patients,7 with a urinary dilution capability the basis pontis or secondary to extrapontine
of 50 mOsm/L, water intake greater than 5 L (or involvement and manifest as ataxia, movement
14 cans of beer) results in hyponatremia. disorders, or irregular behavior. Often the symp-
The net effect is an excess of solvent (electro- toms of ODS present as a biphasic course, with
lyte-free water) without the solute for diuresis. improvement in the initial symptoms of hypona-
ADH levels are expected to be suppressed in tremia and a secondary neurological decline.8
patients with beer potomania.4 The low ADH However, they also can be in a monophasic
levels limit free-water reuptake in the collecting course, making the diagnosis of ODS very diffi-
tubules of the kidney and explain why these cult.19
patients have brisk diuresis when solute is pre- Because of the underlying pathophysiological
sented. Sodium chloride in IV fluids is a com- state and risk of ODS, challenging questions at
mon source of the solute load while hospitalized. the time of initial evaluation include whether IV
Less obvious forms include “banana bag” (NS fluid is needed and, if so, what type and how
solution with thiamine, magnesium, and multivi- much IV fluid is needed, and last, what the
tamin), antibiotics, and food. Urine osmolality treatment goals are.
on recheck after the solute is introduced is low in
these patients because of the low ADH levels. Management
Based on a solute concentration of 308 mEq/L Although most patients with hyponatremia
(mmol/L) in 0.9% sodium chloride solution and present with increased ADH levels, beer potoma-
the kidney’s diluting ability of 50 mOsm/L, nia is unusual because the cause of hyponatremia
significant diuresis can occur with 1 L of NS is multifactorial, including low osmole intake.
solution in the setting of a low-ADH state. This Furthermore, as these patients convert to a low
water diuresis can produce large increases in ADH state, the rate of correction may be dra-
serum sodium levels in a short period. Attempt- matic. As stated, our review of the literature
ing to replace this with electrolyte-free water to found that 18% of patients presenting with beer
prevent a rapid increase in sodium levels can be potomania developed ODS. Patients who present
difficult. with beer potomania are at greater risk of devel-
In patients with hyponatremia, cellular swell- oping ODS because of the degree and chronicity
ing occurs because the fluid shifts from the of hyponatremia, alcohol use, and likelihood of
hypotonic extracellular space to the relative hy- correcting rapidly because of the underlying
pertonic intracellular space. Because of the con- pathophysiological state. Because these patients
fined space of the brain, this swelling can lead to often present with symptomatic severe hyponatre-
deleterious results, including cerebral herniation. mia, management can be challenging.
Cerebral adaptation occurs in response to de- Three large retrospective reviews of patients
creased intracellular tonicity. There is an acute who presented with symptomatic severe hypona-
response consisting of electrolyte shifts of mainly tremia (sodium ⬍ 120 mEq/L [mmol/L]) con-678 Sanghvi et al
cluded no benefit to aggressive correction of mEq/L (mmol/L) in the first 24 hours and less
chronic hyponatremia.15,16,20 Furthermore, all 3 than 18 mEq/L (mmol/L) in the first 48 hours
reviews showed a high complication rate of (Fig 2). If the patient has neurological symp-
treatment (⬎5%) in patients presenting with toms, correction of sodium level by 1 to 2 mEq/h
chronic hyponatremia.15,16,20 The complication (mmol/h) in the first 2 to 3 hours is reasonable.
rate for patients with chronic severe hyponatre- However, despite this initial more rapid correc-
mia correlated with both serum sodium level tion, both the 24- (10 mEq [mmol]) and 48-hour
change greater than 0.55 mEq/L/h until serum (18 mEq [mmol]) goals should not be exceeded.
sodium level was 120 mEq/L or greater (mmol/ If the patient is asymptomatic, fluid restriction
L)20 and serum sodium level change greater than and monitoring the patient despite the degree of
10 mEq (mmol) in 24 hours15,16 and 18 mEq hyponatremia is the recommended approach. If
(mmol) in the first 48 hours.15 Animal studies the serum sodium level increase occurs at a rate
showed a benefit in relowering serum sodium that will exceed the desired goal, D5W infusion
levels such that the net 24-hour change was less should be started to match urine output. The
than 20 mEq/L (mmol/L),21 as well as benefit D5W rate can be adjusted every 2 hours thereaf-
from relowering serum sodium level if there ter based on serum sodium level change. If
were neurological signs or symptoms consistent serum sodium levels increase to greater than
with ODS.22 Two documented clinical cases either the 24- or 48-hour goals, D5W rate should
showed neurological benefit in relowering serum be increased to decrease the serum sodium level
sodium levels after patients showed symptoms of to the recommended goal.
ODS.23,24 Desmopressin may be considered if diuresis
Based on the underlying pathophysiological occurs at an excessive rate that the infused D5W
state and the literature reviewed, a table of recom- is unable to match; based upon the current rate of
mendations (Table 2) and a treatment algorithm serum sodium level change, the goal will be
(Fig 2) are provided. It is well known that the exceeded despite D5W; the goal has been al-
most important risk factor for ODS is the rate of ready been exceeded; or last, symptoms of ODS
serum sodium level increase. Of the 22 cases of develop. Desmopressin was used successfully in
beer potomania reviewed, in 3 of the 4 cases 2 documented clinical cases.23,24 In both cases,
resulting in ODS, serum sodium level increase in patients presented with severe symptomatic hy-
48 hours was 20 to 24 mEq/L (mmol/L). Addition- ponatremia. In both cases, patients had improve-
ally, as stated, there were reports in animals and ment in neurological symptoms, but later showed
humans of benefit to relowering serum sodium deterioration. In the first patient, symptoms in-
levels.21-23 We believe that treatment goals for cluded confusion and hyperreflexia, and in the
patients presenting with beer potomania should second patient, quadriparesis and hyperreflexia
be a serum sodium level increase less than 10 were present. In the first patient, serum sodium
level change was 21 mEq/L (mmol/L) in 24
Table 2. Management Recommendations hours, and in the second patient, serum sodium
level changes at 24 and 48 hours were 12 mEq/L
Recommendations (mmol/L) and 23 mEq/L (mmol/L), respectively.
● NPO except medications for 24 h Because of concerns of the role of rapid correc-
● No IVFs unless symptomatic
tion of serum sodium levels in the neurological
● Prescribe IVFs in finite amounts if needed
● Intensive care status deterioration, desmopressin and D5W were used
● Serum sodium every 2 h to relower serum sodium levels. In both patients,
● Concrete goals mental status later improved. Although desmo-
S Na increase ⬍ 10 mEq/L in first 24 h pressin poses its own risks, in the appropriate
S Na increase ⬍ 18 mEq/L in first 48 h
clinical setting with close monitoring, its use
● Relower serum sodium levels if necessary
● Give all IV medications in D5W may benefit the patient.
● If caloric intake is needed, use D5W Our recommendations for the management of
Note: Sodium in mEq/L and mmol/L is equivalent. patients with beer potomania are listed in Table
Abbreviations: NPO, nothing by mouth; IVF, intravenous 2. Although the inclination is to feed these pa-
fluids; IV, intravenous; D5W, dextrose 5% in water. tients because of their malnourished state, ourRisks and Management of Beer Potomania 679
Figure 2. Treatment algorithm. Note: Sodium in mEq/L and mmol/L is equivalent. Abbreviations: NS, normal saline;
D5W, dextrose 5% in water; DDAVP, desmopressin; S Na, serum sodium.
recommendation is to wait 24 hours because of physicians. Beer potomania is a diagnosis of
the risk of osmole introduction and rapid correc- important consideration on initial evaluation
tion. If caloric intake is needed, we recommend of a patient presenting with hyponatremia.
D5W. With fluid and feeding restriction, the This syndrome of hyponatremia is unusual
patient’s serum sodium level likely will increase because patients have low levels of solute
because of obligate solute losses and urinary intake, and, if ADH secretion is not suppressed
electrolyte-free water loss. In addition, extrare- on admission, they likely will quickly convert
nal free-water loss will contribute to the increase to a state of low ADH secretion. The renal
in serum sodium levels. If the patient’s sodium response to exogenous solute loads can be both
level does not increase, 0.45% NS solution can dramatic and damaging. ODS is a known com-
be prescribed, but a finite amount is recom- plication of overzealous treatment of patients
mended to prevent exceeding serum sodium with hyponatremia, but can occur even when
goals. the serum sodium level increase is in the
historically acceptable range of less then 12
Conclusion mEq (mmol) per 24 hours, especially in pa-
Hyponatremia is a common biochemical ab- tients identified as high risk. Because ODS
normality presenting a therapeutic challenge to may not be recognized until 2 to 3 days after680 Sanghvi et al
the insult, treatment goals need to be identified 11. Tien R, Arieff AI, Kucharczyk W, Wasik A, Kucharc-
at the initial evaluation. A table and algorithm zyk J: Hyponatremic encephalopathy: Is central pontine
are presented to detail the management and myelinolysis a component? Am J Med 92:513-22, 1992
12. Decaux G, Soupart A: Treatment of symptomatic
goals of treatment. If the syndrome of beer hyponatremia. Am J Med Sci 326:25-30, 2003
potomania is recognized and treatment goals 13. Arieff AI, Guisado R: Effects on the central nervous
are met, ideally, ODS can be avoided. system of hypernatremic and hyponatremic states. Kidney
Int 10:104-116, 1976
ACKNOWLEDGEMENTS 14. Dervisoglu E, Yegenaga I, Anik Y, Sengul E, Turgut
Support: None. T: Diffusion magnetic resonance imaging may provide prog-
Financial Disclosure: None. nostic information in osmotic demyelination syndrome: Re-
port of a case. Acta Radiol 47:208-212, 2006
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