NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #211
Carol Rees Parrish, MS, RDN, Series Editor
48 PRACTICAL GASTROENTEROLOGY • JUNE 2021
NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #211
Beyond the Banana Bag: Treating Nutritional
Deficiencies of Alcohol Withdrawal Syndrome
Brian D. Peterson, MD, Internal Medicine Resident,
University of Virginia Health System, Charlottesville, VA
Matthew J. Stotts, MD MPH, Assistant Professor of
Medicine, Division of Gastroenterology & Hepatology,
University of Virginia Health System, Charlottesville, VA
Excessive alcohol consumption can lead to a variety of health complications. With abrupt
cessation or reduction in alcohol intake, individuals may experience alcohol withdrawal
syndrome (AWS), with symptoms ranging from mild tremors to life-threatening seizures. To
prevent well-described symptomatic nutritional deciencies and severe electrolyte abnormalities,
hospitalized patients are often placed on institutional protocols to manage both their withdrawal
symptoms and concomitant nutrient deciencies. These protocols often differ among health
systems in their approach to nutrient replacement, primarily due to a lack of high-quality
evidence for dosing. This review focuses on nutritional challenges seen in these individuals
with AWS, with specic focus on immediate repletion strategies to prevent the neurologic and
hematologic sequelae of common micronutrient deciencies. This review also offers practical
strategies to transition to outpatient repletion to minimize chronic nutritional deciencies.
Matthew J. StottsBrian D. Peterson
INTRODUCTION
A
lcohol use disorder (AUD) is a common
diagnosis encountered by health care
providers both in the hospital and outpatient
settings. The lifetime prevalence of AUD, as
dened by the Diagnostic and Statistical Manual
of Mental Disorders, 5th Edition (DSM-5), has
increased over the last 20 years, with estimates
up to 30% of non-institutionalized United States
adults, leading to higher incidences of alcohol-
related health problems such as liver dysfunction
and alcohol withdrawal syndrome (AWS).
1,2
While
patients with AUD are often admitted to hospitals
for reasons other than AWS, those at high risk for
AWS are often screened with the Prediction of
Alcohol Withdrawal Severity Scale (PAWSS) and
monitored with the Clinical Institute Withdrawal
for Alcohol (CIWA). The latter scoring system
correlates symptoms to the required dose of
benzodiazepines or barbiturates needed to prevent
life threatening symptoms of AWS.
Individuals with AUD are known to be at
high risk for nutritional deciencies and severe
electrolyte derangements. Hospital protocols
often include supplementing micronutrients such
as thiamine, folic acid, and a variety of minerals.
To date, there are few high-quality studies
investigating the optimal dosing of decient
nutrients for patients treated for AWS. This lack
NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #211
Beyond the Banana Bag: Treating Nutritional Deciencies of Alcohol Withdrawal Syndrome
PRACTICAL GASTROENTEROLOGY • JUNE 2021 49
NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #211
of standardized, evidenced-based dosing strategies
increases the potential that patients may receive
insufcient repletion, leading to progression of
nutritional deciencies and their sequelae.
Alternatively, they may receive a longer
duration of supplementation than required, leading
to a high pill burden without signicant benet.
Micronutrients
Individuals with AUD may be decient in
micronutrients for a variety of reasons. In addition
to heavy alcohol use often being associated with
a poor diet, alcohol ingestion can directly cause
malabsorption as well as electrolyte disturbances
through alterations in renal tubular function.
3
Providers must be aware of strategies for monitoring
and replacing these micronutrients.
Thiamine
Thiamine (Vitamin B1) is a common micronutrient
deciency seen in those with AUD. It is a ubiquitous
water-soluble vitamin found in whole grains, meats,
and sh and is absorbed in the small intestine by
both active transport and passive diffusion. Only
a small percentage is stored outside of the plasma,
primarily in the liver. Due to its short half-life
and limited stores (~ 21 days), frequent ingestion
of thiamine containing foods or supplements is
required.
4
Thiamine deciency is uncommon in healthy
individuals, as most developed countries fortify
their grains and cereals with thiamine to ensure
the population meets the adult recommended
daily allowance (RDA) of approximately 1.1-
1.2mg per day.
5
People with AUD can become
thiamine decient through a combination of
decreased intake of thiamine rich foods and
decreased hepatic storage. Animal models have
shown direct inhibition of duodenal transport by
ingested alcohol. However, the clinical relevance
is unclear with several clinical studies failing to
show decreased duodenal thiamine uptake with
active alcohol use.
6
There are two available ways
to assess thiamine status:
1. Directly measuring thiamine diphosphate
serum levels
2.
Measuring the function of the thiamine
dependent erythrocyte transketolase
enzyme.
7
The clinical utility of either test is unclear due to
a lack of experimental data showing an association
between low measured thiamine and severity of
clinical symptoms. Additionally, the turn-around
time is too long (7-10 days) to be useful in urgent
clinical decision making.
Early symptoms of thiamine deciency include
short-term memory loss, weakness, and peripheral
neuropathy. While thiamine deciency induced
congestive heart failure (wet beriberi) rarely
occurs in developed countries, Wernicke-Korsakoff
syndrome (WKS) is a common manifestation of
thiamine deciency in the United States.
8
WKS
initially presents with Wernicke’s Encephalopathy
(WE), a reversible clinical syndrome characterized
by a triad of altered mental status, gait ataxia,
and nystagmus. If untreated, WE can progress
to the chronic, irreversible neuronal changes
of Korsakoff’s Syndrome (KS), characterized
by retrograde and anterograde memory loss.
Different studies cite the prevalence of WKS as
high as 60% in patients with AUD.
9
Alarmingly,
about 80% of patients with WKS are diagnosed
at autopsy, indicating that the syndrome often
goes untreated.
11
It is difcult to predict which
patients are most at risk for developing symptoms
of thiamine deciency due to differences in genetic
susceptibilities, alcohol consumption, and diet.
Folic Acid
Folic acid (Vitamin B9) is an essential nutrient
obtained from leafy vegetables, broccoli, chickpeas
and fortied grains. Folic acid is an important
cofactor in DNA synthesis and amino acid
production. The liver accounts for 50% of the
total body folic acid storage with the remaining
50% stored in the blood and bone marrow
.
Patients
with AUD become decient through decreased
dietary intake, diminished intestinal absorption,
increased renal losses, and disrupted hepatobiliary
conversion to active metabolites. Fortunately, folic
acid deciency is uncommon in the United States
since widespread grain fortication in 1998.
3
The most common sign of folic acid deciency is
macrocytic anemia without the neurologic sequelae
of B12 deciency. Replacing folate may improve
macrocytic anemia, but could worsen neurologic
symptoms such as dementia, depression, peripheral
neuropathy, or subacute combined spinal cord
50 PRACTICAL GASTROENTEROLOGY • JUNE 2021
NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #211
Beyond the Banana Bag: Treating Nutritional Deciencies of Alcohol Withdrawal Syndrome
NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #211
degeneration if a B12 deciency is also present.
The mechanism for neurologic worsening after
folic acid replacement is poorly understood so it
is important to treat concomitant B12 deciencies
prior to giving folic acid.
10,12
Common symptoms
of folic acid deciency include weakness, fatigue,
shortness of breath and skin and hair changes.
13
There is also evidence that folate deciency and the
subsequent hyperhomocysteinemia can increase
the risk for alcohol withdrawal seizures.
14
Magnesium
Magnesium is a dietary nutrient found in leafy
vegetables, meats, and nuts. Hypomagnesemia
occurs in about 30% of patients with AUD due
to inadequate dietary intake, poor absorption, and
alcohol-induced urinary losses.
15
Importantly,
magnesium plays a role in the homeostasis of other
important electrolytes; hypomagnesemia can lead
to both hypocalcemia by inhibiting parathyroid
hormone and to hypokalemia through increased
urinary losses
15,16
Magnesium also plays a role in
thiamine homeostasis by functioning as a cofactor
for the enzyme transketolase. Patients with suspected
WE who fail to improve after thiamine repletion
may have a more robust response after magnesium
correction.
17,18
The degree of hypomagnesemia in
patients presenting with AWS correlates with more
severe symptoms of withdrawal and an increase in
1 year mortality.
5
Symptoms of hypomagnesemia
include neuromuscular manifestations (muscular
weakness, tremors, positive Trousseau’s sign) and
cardiac complications leading to arrhythmias and
possible sudden death.
15
Phosphorus
Phosphorus is an important micronutrient
commonly found in meats, nuts and dairy products.
Individuals with chronic alcohol use often have
decits in their total body stores of phosphorous
due to inadequate dietary intake of foods rich in
phosphate and frank malnutrition in some. These
patients also have urinary losses from alcohol-
induced renal tubular dysfunction.
15
A total body
decit of phosphorus often becomes apparent after
correction of underlying alcoholic ketoacidosis
and glucose administration, leading to phosphate
shifting into cells for glucose phosphorylation and
ATP production.
(continued from page 17)
Other Micronutrients
A variety of other micronutrient deciencies
have been associated with AUD, including other
water-soluble vitamins such as niacin, pyridoxine,
cobalamin (B12), riboavin in addition to fat-
soluble vitamins and trace elements like zinc,
selenium, and iron.
Initial Acute Management
When individuals with chronic heavy alcohol
use present to the hospital, providers should be
aware of the potential nutritional deciencies that
are likely present and aim to adequately replete
these nutrients to prevent both short and long-term
clinical consequences. Malnourished patients can
experience refeeding syndrome when starting
nutrition repletion, leading to life threatening uid
shifts and depletion in phosphorus, magnesium, and
potassium. Severely malnourished patients should
be closely monitored for clinical and laboratory
signs of refeeding syndrome and treated timely
and effectively.
19
Approach to Thiamine Repletion
Thiamine is a universal component of vitamin
repletion protocols in AWS. The goal of thiamine
repletion is to replenish circulating concentrations
as quickly as possible to ensure central nervous
system availability and both prevent and treat
Wernicke’s long before it develops into Korsakoff
syndrome.
The heterogeneity in alcohol consumption,
genetic predisposition, and dietary intake makes
it difcult to develop general thiamine replacement
guidelines in patients presenting with AWS.
20
A
Cochrane review from 2013 revealed a lack of
high-quality evidence to guide clinicians in
choosing the proper dose, route, and frequency of
thiamine for at risk patients.
21
Currently, dosing
strategies for thiamine rely on expert opinion and
often differ among institutions and professional
societies (Table 1). The historical dose of 100mg IV
thiamine daily was arbitrarily chosen in the 1950s
because it represented a high dose at that time.
This dose has persisted through use of the “banana
bag” for AWS, which often contained 100mg
IV thiamine per bag, among other vitamins and
minerals.
22
This thiamine dose is likely insufcient
(continued on page 52)
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NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #211
Beyond the Banana Bag: Treating Nutritional Deciencies of Alcohol Withdrawal Syndrome
NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #211
2.
Administering thiamine as soon as possible
given evidence for developing WE after
prolonged glucose administration without
thiamine replacement.
26
3.
Oral bioavailability in patients with AWS is
poor and initial therapy should favor IV/IM
repletion. Often the intravenous therapy is
continued for 2-3 days before transitioning
to an oral regimen.
4.
The short half-life of thiamine necessitates
multiple doses per day in high-risk patients.
5.
Long term oral supplementation should
be considered in individuals who remain
at nutritional risk with high probability of
continued alcohol misuse. Higher doses
than the typical RDA are likely needed to
compensate for poor absorption during
active alcohol consumption (typically
100mg oral thiamine/day).
in magnitude and dosing frequency for high-risk
individuals. The plasma half-life of thiamine is
approximately 1.5 hours, which leads some authors
to suggest a required dosing interval of every 8-12
hours in patients at risk for WE.
22,23
Notably, oral
preparations should be avoided in patients with
AWS due to poor intestinal absorption.
24
Data
from the UK National Health Service (NHS) has
shown that a 5-day course of IV/IM thiamine
supplementation was associated with large savings
compared to shorter courses, primarily through
preventing progression to Korsakoff syndrome and
associated costs caring for debilitated patients in
long term care facilities.
25
While high-quality data on dosing regimens and
duration are limited, potential guiding principles
for clinicians to consider include (Table 2).
1. Prophylactically replacing thiamine in all
patients presenting with alcohol withdrawal
syndrome can prevent permanent symptoms
of WKS and reduce associated healthcare
costs.
(continued from page 50)
(continued on page 54)
Table 1. Replacement Guidelines and Recommendations for Chronic Alcohol Use
and Alcohol Withdrawal Syndrome
American Society of Addiction Medicine
(recommendations IV.9 and V.7) (2020)
35
Ambulatory patients with AWS -100mg oral thiamine for 3-5
days
Admitted patients with AWS -100mg IV/IM for 3-5 days.
Oral thiamine can also be offered.
Australian Commonwealth Department of
Health Guidelines (2009)
36
Chronic alcohol use with poor dietary intake-300mg IV for
3-5 days
Followed by 300mg PO for several weeks
British Association for Psychopharmacology
(2012)
37
High risk for WE (malnourished, heavy alcohol use) -
250mg IV daily for 3-5 days
Suspected WE - >500mg IV daily for 3-5 days
European Journal of Neurology (2010)
38
Suspected WKS-200mg IV TID until no further improve-
ment in symptoms
National Institute for Health & Clinical
Excellence (NICE) Clinical Guideline
(2019)
39
IV thiamine followed by oral thiamine should be offered to
high-risk alcohol drinkers
Dosed at the upper end of the “British national formulary”
range
Royal College of Physicians (2002)
40
WE prophylaxis - 250mg IV daily
Presumptive WE - 250mg TID for 3 days. Stop if no re-
sponse. If improvement, 250mg IV daily for 5 more days
54 PRACTICAL GASTROENTEROLOGY • JUNE 2021
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Beyond the Banana Bag: Treating Nutritional Deciencies of Alcohol Withdrawal Syndrome
Approach to Folic Acid Repletion
The upper limit for folic acid supplementation in a
healthy adult is approximately 1 mg per day.
12
The
bioavailability of oral supplementation approaches
100% when consumed without food or alcohol.
In cases of severe, symptomatic megaloblastic
anemia when enteral access is lost or difcult to
obtain, IV or IM preparations can be used. There
are no high-quality studies or guidelines for how
long to treat with supplemental folic acid. It is
reasonable in patients with mild megaloblastic
anemia to supplement 1mg by mouth daily for
several months until their anemia has resolved.
Higher risk patients may benet from indenite
1mg oral folic acid supplementation. Concomitant
multivitamin with minerals supplementation should
be evaluated for folic acid content to avoid dosing
over the recommended daily upper limit. Typical
multivitamins contain about 400mcg folic acid.
Unlike thiamine, which does not seem to
have adverse physiologic effects from high
dosages, folic acid supplementation above the
recommended daily allowance (RDA) of 1 mg
by mouth daily is controversial and has been
linked to increased cancer risk and neurocognitive
changes in some populations.
27
To date, there are
no randomized controlled trials evaluating the
optimal folic acid dosing strategy for patients
at risk for alcohol withdrawal seizures. In 2015,
the National Toxicology Program with the US
Department of Health and Human Services
developed a comprehensive needs assessment for
(continued from page 52)
further research into optimal folic acid dosing.
28
This needs assessment should spur research into
optimal folic acid dosing to help guide future
patient management.
Approach to Magnesium Repletion
Serum magnesium levels are a poor representation
of total body magnesium status because 99% of
the body’s magnesium is stored intracellularly.
29
However, serum magnesium is the most common
test used to guide replacement. Clinicians should
be aware that a normal serum magnesium level may
mask a total body magnesium decit. See Table 3
for dosing strategies. Patients with reduced renal
function should receive approximately 25-50% of
the recommended dosages.
30
Oral dosing can be
split into two daily doses to avoid causing diarrhea.
Serum magnesium levels should be checked at
least daily in patients with AUD or more frequently
in patients with symptomatic hypomagnesemia.
Of note, patients receiving multiple intravenous
doses of magnesium should be monitored for EKG
changes. Magnesium replacement and monitoring
after hospital discharge should be considered in
some patients due to total body storage depletion
and continued urinary losses from alcohol induced
renal tubular dysfunction.
15
Approach to Phosphorus Repletion
Patients at risk for refeeding syndrome should be
treated in the hospital setting due to the need for
frequent laboratory monitoring.
31
While ongoing
alcohol use will place individuals at risk for ongoing
Table 2. Prophylactic Thiamine Replacement in AWS
39,41
Moderate Risk for WKS
• Normal dietary intake
• Stable housing and employment
• Existing familial support
High Risk for WKS
• Poor/unknown dietary intake
• Housing insecurity and unemployment
• Poor social support
Dosing Strategy
• High dose IV/IM thiamine daily for
3-5 days followed by oral repletion.
• Counsel alcohol cessation and consider
multivitamin with minerals containing
thiamine at discharge
Dosing Strategy
• High dose IV/IM thiamine >2 times a day for 3-5 days.
• Can continue high dose IV/IM thiamine daily until no
further neurologic improvement.
• Encourage multidisciplinary approach to minimize
risk factors of malnutrition.
• Can consider thiamine 100mg PO daily at discharge
NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #211
PRACTICAL GASTROENTEROLOGY • JUNE 2021 55
Beyond the Banana Bag: Treating Nutritional Deciencies of Alcohol Withdrawal Syndrome
phosphorus loss, abnormalities in the excretion of
urinary phosphate typically resolves after a few
weeks of ongoing abstinence. Table 3 gives an
approach to managing hypophosphatemia in the
inpatient and ambulatory settings. Importantly,
phosphorus repletion should be enteral except in
Table 3. Common Nutritional Deficiencies and Their Management in Alcohol Use Disorder
and Alcohol Withdrawal Syndrome
Nutrient Symptoms of
Deficiency
Initial Replacement
Strategy
Outpatient
Maintenance
Comments
Thiamine
(Vitamin B1)
• Wernicke’s
encephalopathy
• Korsakoff Syndrome
• Dry and wet
beri-beri
• Peripheral
neuropathy
• Asymptomatic and low
risk: 100mg oral daily
• Symptomatic or
moderate to high-risk:
high doses multiple
times daily (Table 3)
• Based on
nutritional risk
(Table 2)
• RDA: Male 1.2mg/
day, Female 1.1mg/
day (available in
multivitamin)
Folic Acid
(Vitamin B9)
• Macrocytic anemia
• Muscle weakness
• 1mg daily
(can consider IV or IM
dosing if no enteral
access)
• 400mcg/day(as
part of a MVM*)
• Consider 1 mg
daily if ongoing
deficiency
• RDA: 400 mcg/day
• NOTE: Consider
concomitant B12
deficiency
Magnesium
• Cardiovascular
dysfunction
• Neuromuscular
irritability
• Hypocalcemia,
Hypoparathyroidism
• Symptomatic (serum
level < 1mg/dL):
aggressive IV repletion
(Mg sulfate 8-12g in
1st 24 hours, 4-6g
daily for following 3-7
days)
• Asymptomatic (serum
level >1.2mg/dL): oral
Mg salts (MgOx, Mag
Citrate) or IV repletion
(Mg sulfate)
• Individualize oral
replacement based
on nutritional risk
factors and serum
levels
• RDA:
Male 400-420mg/day,
Female 310-320mg/
day
• NOTE: IV formulations
should be infused
over several hours to
avoid exceeding renal
threshold and further
urinary loss
• Oral formulations
cause diarrhea, which
can be reduced by
dividing doses across
the day
Phosphorous
• Cardiac dysfunction
• Rhabdomyolysis
• Serum level 1.0-
2.0mg/dL: oral
replacement
(level >1.5mg/dL give
1mmol/kg/day in 3-4
divided doses, level
<1.5 give 1.3mmol/
kg/day in 3-4 divided
doses)
• Serum level <1mg/dL:
IV replacement up to
1.5mmol/kg/day and
then transition to oral
as above
• Insufficient
Evidence for
Ambulatory
Replacement
• RDA: Male/Female
700mg/day
• IV Phosphorus
can chelate
serum calcium
causing dangerous
hypocalcemia
*MVM = Multivitamin/mineral
56 PRACTICAL GASTROENTEROLOGY • JUNE 2021
NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #211
Beyond the Banana Bag: Treating Nutritional Deciencies of Alcohol Withdrawal Syndrome
NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #211
cases of extreme depletion (<1.0mg/dL) due to the
risk of calcium chelation with rapid IV phosphorus
administration.
31
Other Micronutrient Deficiencies
In addition to the previously discussed
micronutrients, there are multiple other important
nutrient deciencies in patients presenting with AWS
that should be considered. These micronutrients
can be replaced using a daily multivitamin with
minerals (MVM), often continued indenitely
while actively consuming alcohol. Providers should
realize that over the counter multivitamins may not
include the essential minerals needed. Patients are
encouraged to ask their pharmacist or health care
provider for specic MVM recommendations.
Transition to Outpatient Management
After recovering from AWS with an initial period
of aggressive micronutrient supplementation, the
need for additional nutrient replacement depends on
an individual’s nutritional and social needs. Factors
such as employment status, social support, food
insecurity, and housing status have been shown to
correlate with increased alcohol use and worsened
nutritional status.
32
As an example, a meta-analysis
from 2018 investigated the efcacy of nutritional
interventions in homeless patients with AUD
and found that several interventions (particularly
providing meal services) could improve nutrition
related behavior, although the data was insufcient
in determining long term outcomes in nutrition
status and disease progression.
33
It is reasonable to discharge all individuals with
recommendations for nutritional supplementation
until they can be assessed by their outpatient
provider. A complete multivitamin with minerals
(MVM) is an efcient and affordable way to
deliver essential micronutrients. Notably the dose
of thiamine in these may be inadequate in those
with ongoing heavy alcohol use.
CONCLUSION
Strategies to replete micronutrient deciencies
in patients presenting with AWS vary among
institutions and individual providers due to a lack
of prospective or randomized studies. Thiamine
deciency is one of the most concerning and
potentially underdiagnosed nutrient deciencies
seen in this population. Thiamine replacement
should be given intravenously 2-3 times a day in
those who have symptoms of deciency or are
at high risk. Specic attention must be given to
magnesium and phosphorous repletion based
on serum levels in those at risk for refeeding
syndrome. Folic acid repletion at 1 mg daily
likely provides adequate treatment for decient
states. A daily MVM is a reasonable strategy to
provide the remaining vitamins and minerals that
are commonly decient in this population. There
are no studies examining long term benets of
outpatient nutrient replacement in patients with
AUD and, hence, providers should individualize
supplementation strategies based on the level of
ongoing alcohol use, dietary intake, nancial status
and signs and symptoms of deciency.
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EMPTY ING FA
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I D A O I N
NEEDS
NIP BLA
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S T R R C
MET ACHRONOUS R
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VALVE L YMPHOMAS
A
E I AR AP I
LEAK
EXCRETA S
1234
567
8
9
10 11
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17 18
19
20 21 22 23
24 25 26
27 28 29
30 31 32 33 34
35 36
37 38
Answers to this month’s crossword puzzle:
(continued from page 56)