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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
An unusual syndrome of hyponatremia was described in
beer drinkers dating back to the early 1970s. The syndrome
“beer potomania” is used to describe a patient who presents
with hyponatremia in conjunction with low daily solute
intake and excessive beer drinking. This pathophysiological
state results in patients at serious risk of rapid correction of
hyponatremia and its neurological sequelae. This article
reviews the literature for both beer potomania and osmotic
demyelination syndrome (ODS). Two patients with beer
potomania with differing outcomes are presented, with crucial differences in management. The article describes pathophysiological characteristics and the unique management
challenges of beer potomania. Last, recommendations and
an algorithm for the treatment of patients with hyponatremia
caused by beer potomania are presented as a potential guide
to prevent the catastrophic outcome of ODS.
Patient 1
Clinical History
A 39-year-old woman was admitted to the hospital after
being brought by a family member because of a 24-hour
history of increasing confusion. Her medical history was
remarkable for long-standing alcohol use and an alcohol
withdrawal seizure approximately 2 years before this presentation. Her daily intake was approximately 18 cans of beer.
Recent history included antibiotic use for a tooth infection
and diarrhea after starting the antibiotics. The family member was unaware if there was recent binge drinking. The
patient’s initial mental status showed a somnolent woman
with mildly slurred speech and oriented to person, place, and
time, but with difficulty with short-term memory. Serum
sodium level on presentation was 100 mEq/L (mmol/L;
Table 1).
Additional Investigations
hours after ED presentation. On the general medical floor,
she had urinary output of 500 mL/h, and serum sodium level
increased by 6 mEq/L (mmol/L) over 4 hours (Fig 1).
Dextrose 5% in water (D5W) was started at a rate to match
urine output to prevent a further increase in serum sodium
level. Because of excessive nursing needs for serial laboratory draws, hourly recordings of urinary output, and titration
of IV fluids, the patient was transferred to the intensive care
unit 12 hours after ED presentation. The first urine osmolality measured 4 hours after ED presentation was 218 mOsm/L;
however, rechecks at 12 and 18 hours after presentation
showed values of 50 and 48 mOsm/L, respectively. The
patient was treated with IV clindamycin for empiric antibiotic coverage. Review of the patient’s records during the
first 24 hours showed a total of 8,500 mL of IV fluids (NS
solution accounted for 1,200 mL) and 7,600 mL of urine
output. In the subsequent 24 hours, the patient received
4,300 mL of D5W and had 4,300 mL of urine output. Serum
sodium level increased 15 mEq/L (mmol/L) during the first
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,
and on day 9, magnetic resonance imaging of the brain
showed findings consistent with pontine and extrapontine
myelinolysis.
Patient 2
Clinical History
A 63-year-old man with a history of alcoholism presented
to the ED with weakness and dizziness after a 2-week
history of binge drinking. The patient had been drinking
approximately 15 to 20 cans of beer daily and had very little
food intake. On examination, the patient was oriented to
person, place, and time, with mild difficulty following commands. Serum sodium level at the time of presentation was
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
Symptomatic severe hyponatremia was diagnosed, possibly caused by beer potomania.
Clinical Follow-Up
In the emergency department (ED), the patient was administered 1 g of intravenous (IV) cefazolin and 1 L of normal
saline (NS) solution containing magnesium and thiamine.
The patient was transferred to a general medicine bed 5
From the 1University of Wisconsin, Madison; and 2Veterans Affair Hospital, Middleton, WI.
Received March 26, 2007. Accepted in revised form July
12, 2007.
Address correspondence to Shalin R. Sanghvi, MD, 3034
Fish Hatchery Rd, Fitchburg, WI 53713. E-mail:
[email protected]
© 2007 by the National Kidney Foundation, Inc.
0272-6386/07/5004-0019$32.00/0
doi:10.1053/j.ajkd.2007.07.015
American Journal of Kidney Diseases, Vol 50, No 4 (October), 2007: pp 673-680
673
674
Table 1. Summary of Beer Potomania Cases
Presentation Laboratory Results
Author (year)
Demanet (71)
Patients
no.
Neurological Symptoms
on Presentation
Na
(mEq/L)
K
(mEq/L)
BUN
(mg/dL)
U osm
(mosm/L)
U Na
(mos m/L)
Treatment
Serum Na
Change
1
2
Unconscious, seizure
Weakness
107
105
2.6
1.3
12
15
N/A
N/A
N/A
N/A
N/A
N/A
N/A
N/A
3
4
Weakness
Unconscious
104
103
2.6
2.5
30
13
N/A
N/A
N/A
N/A
N/A
10 mmol/48 h
Gwinup (72)
5
6
7
8
Weakness, “grand mal”
Unconscious, “grand mal”
Unconscious, “grand mal”
Weakness
101
99
98
122
1.4
1.8
4.4
5.1
19
18
30
N/A
N/A
N/A
N/A
N/A
N/A
N/A
N/A
N/A
N/A
300 MEQ Na IV d
1 and 2
N/A
N/A
N/A
Fluid restriction
N/A
N/A
N/A
20 mmol/72 h
Hilden (75)
9
123
2.7
N/A
N/A
N/A
0.9% NS 2–3 L
12 mmol/48 h
109
2.5
N/A
79
N/A
No IVFs
15 mmol/48 h
108
2.7
N/A
69
N/A
0.9% NS 2–3 L
19 mmol/48 h
127
2.5
N/A
N/A
N/A
No IVFs
2 mmol/48 h
117
3.1
N/A
N/A
N/A
No IVFs
9 mmol/48 h
N/A
199
5.6
Fluid restriction
8 mmol/48 h
N/A
N/A
9 mmol/48 h
N/A
N/A
N/A
1.8% NS ⫻ 6 h then 10
DW or 0.9% NS
3% NS ⫻ 30 mL, 0.9%
NS @ 300 ml/h
0.9% NS @ 100 mL/h
0.9% NS @ 150 mL/h
and 3% NS @ 20 mL/
h ⫻ 160 Ml
NS 3 L/24 h
0.45 NS ⫹ KCl
supplements
NS, later fluid restriction
with D5
Swenson (76)
14
Debility, dizziness,
confusion
Debility, dizziness,
confusion
Debility, dizziness,
confusion
Debility, dizziness,
confusion
Debility, dizziness,
confusion
Weakness
106
3.8
Evans (85)
15
Confused, restless
118
4.1
Joyce (86)
16
110
3
Fenves (95)
17
18
Agitation, confusion,
seizures
Tremor
Unconscious, seizures
121
97
3.6
3.6
4
2
50
338
1
12
Kelly (98)
Lens (01)
19
20
Unconscious
Confusion/weakness
109
97
3.6
2.1
16
14
340
N/A
⬍10
N/A
Sanghvi (06)
21
Weakness
100
2.7
4
218
53
22
Weakness
104
4.3
7
547
10
10
11
12
13
2.3
Fluid restriction
14 mmol/24 h
Outcome
N/A
Death - brain autopsy with atrophy
of mammillary bodies
Death - no brain autopsy
N/A
Death - normal brain autopsy
Death - brain autopsy with CPM
N/A
No neurological sequelae
reported
No neurological sequelae
reported
No neurological sequelae
reported
No neurological sequelae
reported
No neurological sequelae
reported
No neurological sequelae
reported
No apparent neurological
sequelae
Long-term impaired memory,
confabulation
Discharged d 2, lost to follow-up
13 mmol/13 h
30 mmol/48 h
Not reported
No apparent neurological
sequelae
20 mmol/48 h
21 mmol/48 h
ODS
ODS
15 mmol/24 h,
24 mmol/
48 h
7 mmol/24 h, 14
mmol/48 h
ODS
No apparent neurological
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. Abbreviations: ER, emergency room; ICU, intensive care unit; UO, urine output;
NS, normal saline; D5W, dextrose 5%
in water.
Additional Investigations
The patient was not being administered antibiotics and
had no laboratory or clinical evidence of cirrhosis or congestive heart failure.
quent urine osmolality was 71 mOsm/L (6 hours after ED
presentation). The 24-hour increase in serum sodium level
was 7 mEq/L (mmol/L), and the 48-hour increase was 14
mEq/L (mmol/L). The patient was discharged on hospital
day 6 without clinical evidence of neurological sequelae.
Diagnosis
DISCUSSION
Severe hyponatremia was diagnosed, possibly caused by
beer potomania.
Background
Clinical Follow-Up
Based on the tentative diagnosis of beer potomania and
mild neurological symptoms, the patient’s fluid intake was
restricted to 1 L. The patient’s only IV fluids were a dose of
moxifloxacin (in 0.9% NS solution) in the ED. After transfer
to the intensive care unit 2 hours after ED presentation for
further monitoring, the patient had an impressive diuresis of
3,000 mL during the subsequent 2 hours. Serum sodium
level increased 7 mEq/L (mmol/L) during the first 9 hours
(Fig 1). D5W was started at a rate to match urine output.
Diuresis decreased to approximately 150 mL/h. Total urine
output during the first 24 hours was 6,500 mL, and total IV
fluids were 4,500 mL (NS solution accounted for 250 mL).
Review of the patient’s laboratory test results showed urine
osmolality at presentation of 547 mOsm/L; however, subse-
Cases of a hypo-osmolality syndrome in beer
drinkers were first described by Gwinup et al1 in
1972, and series of patients with similar presentations were described by Hilden and Svendsen2 in
1975 and Swenson and Rater3 in 1976. In earlier
cases, the cause of hyponatremia was complicated by confounding factors, including diuretic
use and lack of evaluation for such diseases as
congestive heart failure or cirrhosis. However,
with repeated documented cases of patients presenting with hyponatremia in conjunction with
excessive beer drinking and low daily solute
676
intake, it is evident that there is a syndrome of
hyponatremia virtually unique in beer drinkers.
Electrolyte abnormalities are not uncommon in
patients admitted with a history of alcohol use. In
the study by Liamis et al,4 17% of chronic alcoholic patients had hyponatremia. Review of internal data from the University of Wisconsin and
Veterans Affairs Hospital in Middleton, WI, showed
hyponatremia in greater than 5% of patients admitted with alcoholism as a coding diagnosis. In addition to beer potomania, there are a number of other
potential causes of hyponatremia in alcoholics,
including cirrhosis, syndrome of inappropriate antidiuretic hormone (ADH), congestive heart failure,
hypovolemia, and pseudohyponatremia secondary
to dyslipidemia.4 Laboratory values for 22 published cases, including the 2 mentioned here, were
reviewed to identify features specific to beer potomania.1-3,5-11 Of the laboratory data available, consistent findings among patients included severe
hyponatremia (mean serum sodium, 108 mEq/L
[mmol/L]), hypokalemia (mean serum potassium,
3 mEq/L [mmol/L]), mild neurological symptoms
on presentation (typically confusion), low blood urea
nitrogen level, brisk diuresis in response to solute
intake, and low urine sodium level. Although not
consistently reported in patients with beer potomania, low urine osmolality on admission laboratory
test results was not a consistent finding (Table 1).
Many similarities were noted in the presentation of patients with beer potomania. In addition
to the history of excess beer drinking, often a
recent history of binge drinking or illness was
present. This may potentially precipitate a rapid
decrease in serum sodium levels, which causes
the patient to acutely present with such clinical
symptoms of hyponatremia as confusion, altered
mental status, and gait disturbances.
The relationship between neurological lesions
and rapid correction of chronic hyponatremia
was noted in the late 1970s, and a direct relationship was established in the early 1980s.12,13
Specific neurological findings included central
and extrapontine myelinolysis, now known as
ODS. ODS is diagnosed by means of magnetic
resonance image, with findings of hyperintense
lesions on T2-weighted images. Most signal
changes are located in the central part of the
pons, medulla oblongata, and mesencephalon.14
Clinical features include upper motor neuron
signs, pseudobulbar palsy, spastic quadriparesis,
Sanghvi et al
and mental disorders ranging from mild confusion to coma. Two retrospective reviews by Sterns
et al15 and Ellis16 reported neurological sequelae
in some patients when the change in serum
sodium during a 24-hour period was greater than
12 mEq/L (mmol/L) and 10 mEq/L (mmol/L),
respectively. Case reports describe ODS in patients with a rate of correction less than 10
mEq/L (mmol/L) per 24 hours.9
Our literature review found 22 cases (including ours) of beer potomania. In these cases, 8
patients had complications (36%): 4 of the 8 had
ODS (18%), whereas the other 4 died (18%).
Management varied from hypertonic saline solution for brief periods to free-water restriction and
even free-water supplementation in certain cases.
Brisk diuresis was common in many patients
after admission (Table 1). Understanding the
pathophysiological state is pivotal to recognizing
the possibility of rapid correction and the possible complications. Furthermore, because ODS
may not present until 2 to 3 days after the change
in serum sodium levels, it is important to delineate management goals at the initial evaluation.
Pathophysiology
Hyponatremia in beer drinkers occurs because
of water intake that exceeds excretory capacity
(described next), modified by the possibility of
inappropriate ADH secretion on admission. Our
review of the 22 cases shows that hyposthenuria
on admission was not a consistent finding (although urine sodium levels were low). Recognizing this finding prevents the erroneous dismissal
of beer potomania. In the majority of cases, after
admission, brisk water diuresis ensued, leading
to the likelihood that when infections and volume status were treated, the patient’s ADH secretion decreased to a level commensurate with the
degree of hypo-osmolality.
Free-water clearance is dependant on solute
excretion and urinary diluting capability.17 Based
on a normal diet, typical osmole excretion is
approximately 600 to 900 mOsm/d. This osmolar
load is caused by urea generation from protein
(10 g of protein produces ⬃50 mOsm of urea), in
addition to dietary sodium and potassium intake.
If the maximum urinary dilution capability is 50
mOsm/L, a large amount of water (⬎20 L) must
be ingested under normal situations to overwhelm the capacity for urinary dilution, as seen
Risks and Management of Beer Potomania
in psychogenic polydipsia. If solute excretion
decreases, the ability to excrete free water becomes limited. For example, if the patient excretes only 100 mOsm/d, greater than 2 L of fluid
intake with a urinary dilution capability of 50
mOsm/L will result in net water retention and
subsequently hyponatremia.
Patients with beer potomania have a history of
significant beer drinking, often long term, in
conjunction with a poor diet. The net result is
very low osmole intake because beer has very
little sodium and no protein, but has some calories that prevent endogenous protein breakdown
(urea generation). Because the obligatory solute
loss in a day is approximately 250 mOsm in
these patients,7 with a urinary dilution capability
of 50 mOsm/L, water intake greater than 5 L (or
14 cans of beer) results in hyponatremia.
The net effect is an excess of solvent (electrolyte-free water) without the solute for diuresis.
ADH levels are expected to be suppressed in
patients with beer potomania.4 The low ADH
levels limit free-water reuptake in the collecting
tubules of the kidney and explain why these
patients have brisk diuresis when solute is presented. Sodium chloride in IV fluids is a common source of the solute load while hospitalized.
Less obvious forms include “banana bag” (NS
solution with thiamine, magnesium, and multivitamin), antibiotics, and food. Urine osmolality
on recheck after the solute is introduced is low in
these patients because of the low ADH levels.
Based on a solute concentration of 308 mEq/L
(mmol/L) in 0.9% sodium chloride solution and
the kidney’s diluting ability of 50 mOsm/L,
significant diuresis can occur with 1 L of NS
solution in the setting of a low-ADH state. This
water diuresis can produce large increases in
serum sodium levels in a short period. Attempting to replace this with electrolyte-free water to
prevent a rapid increase in sodium levels can be
difficult.
In patients with hyponatremia, cellular swelling occurs because the fluid shifts from the
hypotonic extracellular space to the relative hypertonic intracellular space. Because of the confined space of the brain, this swelling can lead to
deleterious results, including cerebral herniation.
Cerebral adaptation occurs in response to decreased intracellular tonicity. There is an acute
response consisting of electrolyte shifts of mainly
677
sodium and potassium out of the cell, and a
chronic response characterized by loss of intracellular organic osmoles because of the persistent
osmotic imbalance.18 Because organic osmoles
take 5 to 7 days to return to normal levels, the
long-term adaptation is the major concern when
correcting hyponatremia. Oligodendrocytes are
particularly sensitive to the osmotic stress that
occurs with correction at a rate that the intracellular osmolality remains hypotonic relative to the
extracellular environment. Although the exact
mechanism is not known, this stress leads to both
pontine and extrapontine myelinolysis, known as
ODS.19 Symptoms can be related to damage of
the corticospinal or corticobulbar tracts within
the basis pontis or secondary to extrapontine
involvement and manifest as ataxia, movement
disorders, or irregular behavior. Often the symptoms of ODS present as a biphasic course, with
improvement in the initial symptoms of hyponatremia and a secondary neurological decline.8
However, they also can be in a monophasic
course, making the diagnosis of ODS very difficult.19
Because of the underlying pathophysiological
state and risk of ODS, challenging questions at
the time of initial evaluation include whether IV
fluid is needed and, if so, what type and how
much IV fluid is needed, and last, what the
treatment goals are.
Management
Although most patients with hyponatremia
present with increased ADH levels, beer potomania is unusual because the cause of hyponatremia
is multifactorial, including low osmole intake.
Furthermore, as these patients convert to a low
ADH state, the rate of correction may be dramatic. As stated, our review of the literature
found that 18% of patients presenting with beer
potomania developed ODS. Patients who present
with beer potomania are at greater risk of developing ODS because of the degree and chronicity
of hyponatremia, alcohol use, and likelihood of
correcting rapidly because of the underlying
pathophysiological state. Because these patients
often present with symptomatic severe hyponatremia, management can be challenging.
Three large retrospective reviews of patients
who presented with symptomatic severe hyponatremia (sodium ⬍ 120 mEq/L [mmol/L]) con-
678
Sanghvi et al
cluded no benefit to aggressive correction of
chronic hyponatremia.15,16,20 Furthermore, all 3
reviews showed a high complication rate of
treatment (⬎5%) in patients presenting with
chronic hyponatremia.15,16,20 The complication
rate for patients with chronic severe hyponatremia correlated with both serum sodium level
change greater than 0.55 mEq/L/h until serum
sodium level was 120 mEq/L or greater (mmol/
L)20 and serum sodium level change greater than
10 mEq (mmol) in 24 hours15,16 and 18 mEq
(mmol) in the first 48 hours.15 Animal studies
showed a benefit in relowering serum sodium
levels such that the net 24-hour change was less
than 20 mEq/L (mmol/L),21 as well as benefit
from relowering serum sodium level if there
were neurological signs or symptoms consistent
with ODS.22 Two documented clinical cases
showed neurological benefit in relowering serum
sodium levels after patients showed symptoms of
ODS.23,24
Based on the underlying pathophysiological
state and the literature reviewed, a table of recommendations (Table 2) and a treatment algorithm
(Fig 2) are provided. It is well known that the
most important risk factor for ODS is the rate of
serum sodium level increase. Of the 22 cases of
beer potomania reviewed, in 3 of the 4 cases
resulting in ODS, serum sodium level increase in
48 hours was 20 to 24 mEq/L (mmol/L). Additionally, as stated, there were reports in animals and
humans of benefit to relowering serum sodium
levels.21-23 We believe that treatment goals for
patients presenting with beer potomania should
be a serum sodium level increase less than 10
Table 2. Management Recommendations
Recommendations
● NPO except medications for 24 h
● No IVFs unless symptomatic
● Prescribe IVFs in finite amounts if needed
● Intensive care status
● Serum sodium every 2 h
● Concrete goals
S Na increase ⬍ 10 mEq/L in first 24 h
S Na increase ⬍ 18 mEq/L in first 48 h
● Relower serum sodium levels if necessary
● Give all IV medications in D5W
● If caloric intake is needed, use D5W
Note: Sodium in mEq/L and mmol/L is equivalent.
Abbreviations: NPO, nothing by mouth; IVF, intravenous
fluids; IV, intravenous; D5W, dextrose 5% in water.
mEq/L (mmol/L) in the first 24 hours and less
than 18 mEq/L (mmol/L) in the first 48 hours
(Fig 2). If the patient has neurological symptoms, correction of sodium level by 1 to 2 mEq/h
(mmol/h) in the first 2 to 3 hours is reasonable.
However, despite this initial more rapid correction, both the 24- (10 mEq [mmol]) and 48-hour
(18 mEq [mmol]) goals should not be exceeded.
If the patient is asymptomatic, fluid restriction
and monitoring the patient despite the degree of
hyponatremia is the recommended approach. If
the serum sodium level increase occurs at a rate
that will exceed the desired goal, D5W infusion
should be started to match urine output. The
D5W rate can be adjusted every 2 hours thereafter based on serum sodium level change. If
serum sodium levels increase to greater than
either the 24- or 48-hour goals, D5W rate should
be increased to decrease the serum sodium level
to the recommended goal.
Desmopressin may be considered if diuresis
occurs at an excessive rate that the infused D5W
is unable to match; based upon the current rate of
serum sodium level change, the goal will be
exceeded despite D5W; the goal has been already been exceeded; or last, symptoms of ODS
develop. Desmopressin was used successfully in
2 documented clinical cases.23,24 In both cases,
patients presented with severe symptomatic hyponatremia. In both cases, patients had improvement in neurological symptoms, but later showed
deterioration. In the first patient, symptoms included confusion and hyperreflexia, and in the
second patient, quadriparesis and hyperreflexia
were present. In the first patient, serum sodium
level change was 21 mEq/L (mmol/L) in 24
hours, and in the second patient, serum sodium
level changes at 24 and 48 hours were 12 mEq/L
(mmol/L) and 23 mEq/L (mmol/L), respectively.
Because of concerns of the role of rapid correction of serum sodium levels in the neurological
deterioration, desmopressin and D5W were used
to relower serum sodium levels. In both patients,
mental status later improved. Although desmopressin poses its own risks, in the appropriate
clinical setting with close monitoring, its use
may benefit the patient.
Our recommendations for the management of
patients with beer potomania are listed in Table
2. Although the inclination is to feed these patients because of their malnourished state, our
Risks 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
the risk of osmole introduction and rapid correction. If caloric intake is needed, we recommend
D5W. With fluid and feeding restriction, the
patient’s serum sodium level likely will increase
because of obligate solute losses and urinary
electrolyte-free water loss. In addition, extrarenal free-water loss will contribute to the increase
in serum sodium levels. If the patient’s sodium
level does not increase, 0.45% NS solution can
be prescribed, but a finite amount is recommended to prevent exceeding serum sodium
goals.
Conclusion
Hyponatremia is a common biochemical abnormality presenting a therapeutic challenge to
physicians. Beer potomania is a diagnosis of
important consideration on initial evaluation
of a patient presenting with hyponatremia.
This syndrome of hyponatremia is unusual
because patients have low levels of solute
intake, and, if ADH secretion is not suppressed
on admission, they likely will quickly convert
to a state of low ADH secretion. The renal
response to exogenous solute loads can be both
dramatic and damaging. ODS is a known complication of overzealous treatment of patients
with hyponatremia, but can occur even when
the serum sodium level increase is in the
historically acceptable range of less then 12
mEq (mmol) per 24 hours, especially in patients identified as high risk. Because ODS
may not be recognized until 2 to 3 days after
680
Sanghvi et al
the insult, treatment goals need to be identified
at the initial evaluation. A table and algorithm
are presented to detail the management and
goals of treatment. If the syndrome of beer
potomania is recognized and treatment goals
are met, ideally, ODS can be avoided.
ACKNOWLEDGEMENTS
Support: None.
Financial Disclosure: None.
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