Alcoholic Metabolic Emergencies

a,b a,b,
Michael G. Allison, MD , Michael T. McCurdy, MD *

KEYWORDS
 Ethanol intoxication  Beer potomania  Alcoholic ketoacidosis
 Alcohol encephalopathy  Wernicke encephalopathy  Korsakoff syndrome

KEY POINTS
 Hypoglycemia in the alcohol intoxicated adult is no more common than the rest of the
population; children often have hypoglycemia with alcohol overdose.
 Beer potomania can be treated with simple fluid restriction; isotonic resuscitation should
be approached with caution.
 Alcoholic ketoacidosis may not present with ketonemia.
 Alcoholic encephalopathy syndromes, such as Wernicke encephalopathy and Korsakoff
syndrome, should be treated with 500 mg intravenous thiamine every 8 hours.

INTRODUCTION

As all emergency providers are aware, habitual users of alcohol frequently find them-
selves seeking treatment in the Emergency Department (ED). Patients who abuse
alcohol, a term that is synonymous with ethanol for the purpose of this article, can pre-
sent with a myriad of complaints and may exhibit a range of clinical illnesses. Acute
alcohol intoxication and withdrawal make up the largest subsets of illnesses stemming
from alcohol abuse, and physicians may get lulled into a familiar management pattern
for patients with acute alcohol intoxication. However, because of the high risk of sig-
nificant morbidity if not recognized and treated appropriately, emergency physicians
must pay careful attention to the metabolic derangements that plague alcohol
abusers. This article discusses how to diagnose efficiently and provide appropriate
medical therapy for some key underrecognized alcohol emergencies.

Funding Sources: Nil.

Conflict of Interest: Nil.
a
Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of
Maryland School of Medicine, 110 South Paca Street, 2nd Floor, Baltimore, MD, USA;
b
Department of Emergency Medicine, University of Maryland School of Medicine, 110 South
Paca Street, 6th Floor, Baltimore, MD 21201, USA
* Corresponding author. Department of Medicine, University of Maryland School of Medicine,
110 South Paca Street, 2nd Floor, Baltimore, MD 21201.
E-mail address: [email protected]

Emerg Med Clin N Am 32 (2014) 293–301

http://dx.doi.org/10.1016/j.emc.2013.12.002 emed.theclinics.com
0733-8627/14/$ – see front matter Ó 2014 Elsevier Inc. All rights reserved.
294 Allison & McCurdy

ALCOHOL INTOXICATION

Acute alcohol intoxication, herein referred to as “intoxication,” is defined as the path-

ologic state produced by the ingestion of alcohol. Blood alcohol levels (BAL) are
sometimes used to supplement clinical decision-making in the ED, and a working un-
derstanding of the pharmacokinetics of ethanol is helpful in these circumstances. The
degree and duration of symptoms of intoxication are governed by the body’s absorp-
tion, metabolism, and elimination of alcohol over time. Ethanol is absorbed through the
gastrointestinal tract and achieves its concentration in the circulation within minutes to
a few hours. A standard drink is classified as 14 g of alcohol. Usually this equals about
1.5 ounces of liquor, 5 ounces of wine, or 12 ounces of beer. One serving will increase
the BAL by approximately 25 mg/dL. The character of symptoms associated with
intoxication varies with every drinker, so reliably predicting blood alcohol level on clin-
ical features alone is difficult.
Ethanol is metabolized via hepatic oxidation by zero-order kinetics, which means
that a set amount is metabolized per unit time. Prolonged ethanol exposure induces
hepatic enzymatic activity, resulting in increased alcohol degradation in chronic
drinkers.1 Drinkers who do not chronically abuse ethanol eliminate it at a rate of
15 mg/dL/h, whereas chronic abusers eliminate it around 25 mg/dL/h.1 Observational
data from ED patients have found clearance rates of 18 to 20 mg/dL/h with only minor
variability among habitual drinkers.2,3 Although these typically quoted studies provide
reasonable estimates of ethanol metabolism, their wide confidence intervals suggest
substantial clinical variability among patients. Therefore, acute alcohol intoxication
can be diagnosed clinically or by BAL.
To reduce the amount of unnecessary time intoxicated patients spend in the ED for
supportive measures, studies have attempted to identify the utility of various therapies
to enhance ethanol elimination. Unfortunately, these studies, which have included
naloxone, flumazenil, and intravenous fluids, have failed to demonstrate improvement
in ethanol clearance with anything other than time.4–6 Despite a lack of increasing
ethanol elimination, intoxicated patients should receive good supportive care until
they are lucid and competent and can be safely discharged.

INTOXICATION AND THE ENDOCRINE SYSTEM

Alcohol can cause clinical abnormalities of endocrine function. Its effects on gonadal
function, bone and mineral metabolism derangements, and glucocorticoid secretion
rarely result in acute illness requiring ED management.7 However, acute intoxication
may result in alterations in glucose metabolism requiring emergency treatment.
Habitual drinkers who consume alcohol in the absence of other nutrition have a
theoretical risk of developing hypoglycemia. Fasting states deplete existing
glycogen stores, forcing the body to rely on gluconeogenesis to maintain normogly-
cemia. The metabolism of alcohol by alcohol dehydrogenase creates a molecular
milieu that may prevent the normal conversion of amino acids and pyruvate into
glucose, allowing the development of hypoglycemia.7 However, clinical studies of
acutely intoxicated patients do not support this theory. Two different cohort studies,
using prospective convenience sampling and retrospective laboratory analysis of
intoxicated ED patients, found a low incidence of hypoglycemia (4% and 1%,
respectively).8,9 Although intoxicated adults do not seem to have a higher risk of
developing hypoglycemia, children who present following acute alcohol ingestion
are at risk for hypoglycemia.10 Finger-stick glucose evaluation should be used in
any intoxicated patient, similar to the evaluation in other ED patients with altered
mental status.
 Alcoholic Metabolic Emergencies 295

ELECTROLYTE DERANGEMENTS
Hyponatremia: A Consequence of Beer Potomania
First described in a 1971 case series, beer potomania is alcohol-induced hyponatre-
mia found in alcohol users with concomitant poor nutritional supplementation. A large
percentage of the patients in that initial case series consumed greater than or equal to
4 L of beer per day in the days preceding hospitalization.11 The lone consumption of
large quantities of beer causes total body deficiencies in sodium and protein. Because
of the kidney’s inability to match water excretion with the high volume of hypotonic
beer consumption, free water retention occurs, exhibited by a dilutional hyponatremia.

Presentation
Similar to other alcohol-related emergencies, patients with beer potomania often
exhibit neurologic abnormalities such as altered mental status, focal neurologic defi-
cits, or seizures. Unfortunately, the diagnosis of beer potomania is elusive due to these
similarities in presentation, and patients are often misdiagnosed. For example, alter-
ations in consciousness may also be found with acute intoxication, withdrawal, and
delirium tremens. Focal neurologic signs may be seen with alcohol-related head injury.
Agitation and disorientation can present as alcohol withdrawal, delirium tremens, or
acute psychosis. Seizures may be found with alcohol withdrawal. Only serum electro-
lyte measurements will reliably differentiate these clinical entities from the hyponatre-
mia associated with beer potomania.

Diagnosis
Hyponatremia in a recent beer drinker, in the absence of a comorbid condition altering
sodium levels, is the sine qua non of beer potomania. Because alcoholics are at risk for
various causes of hyponatremia, these causes must be ruled out (Box 1).12 In beer
potomania, hyponatremia may be particularly dramatic, with some reports citing so-
dium levels as low as 98 mg/dL.11 Potassium levels are usually also low, whereas
blood urea nitrogen and creatinine levels are typically normal because most patients
are euvolemic. Not surprisingly, urine studies reveal low urine osmolality and low urine
sodium concentration.13 Identifying hyponatremia in beer drinkers with these other
metabolic abnormalities will lead the clinician on the path to proper therapy.

Management
The safe restoration of intravascular solutes is the cornerstone of managing these pa-
tients. Patients with beer potomania are not hypovolemic, and excessively rapid
correction of hyponatremia may put a patient at risk for osmotic demyelination syn-
drome (ODS). Early reports on beer potomania found similar symptom improvement
with both 2 to 3 L of isotonic fluid and simple water restriction.14 The rapid restoration

Box 1
Causes of hyponatremia in habitual alcohol drinkers

 Hypovolemia
 Beer potomania
 Pseudohyponatremia—Hypertriglyceridemia or hyperproteinemia
 Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
 Cardiomyopathy
 Cirrhosis
 Cerebral salt-wasting syndrome
296 Allison & McCurdy

of normal sodium concentration with crystalloid, however, may have contributed to the
high incidence of ODS in these reports. A form of ODS, central pontine myelinolysis,
had been recognized in prior case series of beer potomania before the development of
the current understanding of the dangers of rapid sodium correction.11,15,16 Because
ODS/central pontine myelinolysis can occur when the sodium concentration is cor-
rected to greater than 10 mEq/L in the first 24 hours, a more cautious rate of correction
may be prudent, such as raising sodium levels by less than or equal to 10 mEq in the
first day and less than 18 mEq in the first 48 hours.13 These authors recommend this
careful correction of sodium after finding that 18% of patients with beer potomania
developed ODS in a review of the early literature.13 Life-threatening sequelae of
beer potomania (eg, seizures) may warrant the careful administration of small aliquots
of hypertonic saline along with close monitoring of serum sodium.15 However, no
benefit exists to treat asymptomatic hyponatremia aggressively because simple water
restriction is often sufficient to normalize sodium levels in these patients.

Hypomagnesemia
Hypomagnesemia among alcohol abusers is quite common. Up to 30% of chronic
alcoholics and 7% of acutely intoxicated patients will be hypomagnesemic.17,18 Hypo-
magnesemia in alcohol abusers can result from a variety of causes, which may include
dietary deficiency, gastrointestinal malabsorption, increased urinary excretion,
ketosis, and vitamin D deficiency.
Hypomagnesemia clinically manifests as muscle weakness, hyperreflexia, and
increased QT intervals, which can predispose patients to dysrhythmias. Acquired
long-QT syndrome from electrolyte abnormalities such as hypomagnesemia may pre-
dispose patients to the polymorphic ventricular tachycardia known as Torsades de
pointes. Magnesium therapy has been shown to be the first-line agent in treating Tor-
sades de pointes in hemodynamically stable patients, even in patients with normal
magnesium levels.19

Alcoholic Ketoacidosis
The presence of ketoacidosis in nondiabetics was first reported in 1940, and the au-
thors astutely noted that many of the patients recently used alcohol.20 However, it was
not until 1971 that Jenkins and colleagues21 coined the term “alcoholic ketoacidosis”
to describe patients with a similar constellation of symptoms after recent alcoholic
binges whose ketosis improved with intravenous hydration. These initial reports
helped to lay the foundation for the current understanding of the pathophysiology,
diagnosis, and management of alcoholic ketoacidosis.

Pathophysiology
Heavy alcohol use and malnutrition cause ketosis. During an alcohol binge, decreased
protein and carbohydrate intake results in the body having to use its glycogen stores.
In addition, hepatic alcohol dehydrogenase oxidizes ethanol into acetaldehyde, which
favors the reduction of nicotinamide adenine dinucleotide (NAD1) to nicotinamide
adenine dinucleotide (reduced form) (NADH).22 High NADH concentrations impair
gluconeogenesis, causing free fatty acid formation. Catecholamine surges and insulin
inhibition promote glucagon secretion, which further promotes the conversion of fatty
acids into ketones.23 Acetaldehyde, acetone, and b-hydroxybutyrate (BOHB) are all
elevated, but BOHB predominates. High concentrations of ketones cause an anion
gap metabolic acidosis. The acidosis is worsened by the concomitant lactic acidosis
often present in such patients.22 In summary, both inadequate stores of energy and
high ethanol consumption can cause ketogenesis and acidemia.
 Alcoholic Metabolic Emergencies 297

Presentation
Patients with alcoholic ketoacidosis generally present with the triad of abdominal pain,
nausea, and vomiting.20,21,24 The general sequence of events is as follows: a recent
alcoholic binge causing abdominal pain, which causes cessation of drinking and sub-
sequently leading to the alcoholic acidosis, which causes nausea and vomiting. Clin-
ical signs may include tachypnea, tachycardia, and hypotension from volume
depletion. Similar to diabetic ketoacidosis, the abdominal examination can elicit
tenderness without guarding or rebound. The nonspecific symptoms and signs asso-
ciated with alcoholic ketoacidosis often warrant ruling out concomitant anatomic
causes as well (Box 2).
Diagnosis
The diagnosis of alcoholic ketoacidosis requires appropriate clinical signs and symp-
toms in the presence of classic metabolic derangements on laboratory investigation.
Patients typically have an elevated anion gap acidosis, ketonuria, and occasionally
ketoacidemia. BOHB, the predominant ketone in the disease, is present in much
higher concentrations than in diabetic ketoacidosis.25 BOHB is not routinely tested
in most commercial serum or urine ketone assays, resulting in its underidentification.
Because alcohol consumption has typically ceased days before presentation, BAL is
often negative.22 Serum pH may also be normal due to the presence of a mixed meta-
bolic derangement, namely a ketoacidosis and a contraction alkalosis.22
Management
Early and proper recognition of alcoholic ketoacidosis is important because the treat-
ment is highly efficacious. Before this clinical entity was better understood, practi-
tioners used insulin and bicarbonate in select patients; however, these therapies are
no longer recommended because of their lack of benefit.20,21 A seminal paper on
the treatment of alcoholic ketoacidosis compared saline infusions to 5% dextrose
containing solutions for volume loading.26 All patients in the study did well and
resolved their ketoacidosis, but patients receiving dextrose-containing solutions
cleared their ketoacidosis in half the time. Current therapy for alcoholic ketoacidosis
should use isotonic volume expansion with dextrose-containing fluids, such as 5%
dextrose in normal saline.

Alcoholic Encephalopathy
As a consequence of carbohydrate-heavy alcohol consumption at the expense of
vitamin-rich food consumption, chronic alcohol abusers are at particular risk for en-
cephalopathy resulting from thiamine (Vitamin B1) deficiency. In 1880s, Wernicke27
described a syndrome characterized by confusion, ataxia, and ophthalmoplegia,

Box 2
Differential diagnosis of abdominal pain in patients consuming alcohol

 Pancreatitis
 Alcoholic hepatitis
 Gastritis/esophagitis
 Intra-abdominal sepsis
 Pneumonia
 Spontaneous bacterial peritonitis
298 Allison & McCurdy

and Korsakoff28 separately identified a syndrome of mental disturbance in patients

with either acute illness or alcohol abuse. The mental disturbance in Korsakoff’s pa-
tients took many forms, but often included confabulation. The syndromes became
linked in the mid-1900s when characteristic cerebral lesions were found in both disor-
ders. Wernicke encephalopathy (WE), a reversible form of the encephalopathy and the
Korsakoff syndrome (KS), a persistent state of encephalopathy characterized by
confabulation, are still present today and are underdiagnosed in the emergency
setting.

Cause and pathophysiology

Thiamine depletion occurs in 2 to 3 weeks in the absence of vitamin-rich foods or sup-
plementation. Because of an increased appreciation of thiamine deficiency as the
cause for both WE and KS, many countries now supplement their food with the
vitamin, which has decreased the number of cases by 40% in some instances.29
Resulting from policies enacted to supplement grains, alcohol abusers are now the
most notable risk group for alcoholic encephalopathy due to poor intake, decreased
absorption, and impaired storage of thiamine.30
For unknown reasons, thiamine deficiency selectively damages certain parts of the
brain that anatomically correlate with the clinical symptoms associated with WE and
KS. Classically, the mammillary bodies are the most affected, but other areas are
also prone to develop lesions, including the dorsomedial thalamus, ocular motor
nuclei, vestibular nuclei, locus ceruleus, and peri-aqueductal gray matter.30

Diagnosis
The diagnosis of WE and KS remains difficult. Some case series have found WE is first
diagnosed during autopsy 80% of the time.31 Often patients with the mental status
manifestations of WE and KS can be misdiagnosed as primarily psychiatric, resulting
in improper therapy and delayed diagnosis.32 A high level of suspicion must be main-
tained when evaluating alcohol abusers with altered mental status.
Because the classic triad of mental status changes, ophthalmoplegia, and ataxia is
not universally present, an operational definition has been established. The diagnostic
criteria for WE include the presence of any 2 of the following 4 conditions in a known
alcohol abuser: (1) nutritional deficiency, (2) ocular findings, (3) ataxia, and (4) mental
status changes.33 These 4 criteria for WE increase the diagnostic sensitivity of WE at
the expense of decreased specificity, resulting in potential overdiagnosis.
Thiamine levels have no role in the diagnosis of WE or KS in the ED. The tests take
days to perform and are rarely available when making diagnostic and treatment deci-
sions. Likewise, imaging studies should not be routinely used for making the diagnosis
of WE. A noncontrast brain magnetic resonance image will be able to determine if
pathologic lesions exist in the mammillary bodies or other areas characteristic for
the disease; however, this risks underdiagnosis because magnetic resonance image
has a low sensitivity of 53%. Computed tomographic scan performs even worse
with a sensitivity of 13%.34 Basing treatment decisions on imaging alone would
miss a large number of WE cases. WE remains a clinical diagnosis and, given the
benign nature of its treatment with thiamine replacement, emergency physicians
should not worry about the potential for overdiagnosis because the consequences
of underdiagnosis can be severe.

Treatment
Standard therapy for WE and KS is thiamine supplementation, although optimal
dosing remains elusive despite decades of experience treating these conditions.
Because of the risk of decreased intestinal absorption in alcoholics, most experts
 Alcoholic Metabolic Emergencies 299

recommend parenterally administering thiamine; however, a Cochrane Review found

inadequate evidence to recommend a particular dose or duration of thiamine supple-
mentation.35 In the only prospective study on the subject, patients responded most
favorably to a dose of 200 mg intramuscular injection, which happened to be the high-
est dose given in the study.36 Despite the lack of evidence, some national guidelines
suggest dosing thiamine at 500 mg 3 times a day.37 Higher doses of thiamine pose no
known risk, so emergency providers may wish to treat with the larger recommended
doses.
A commonly held belief by physicians is that glucose administration before thiamine
repletion in patients with suspected thiamine deficiency and hypoglycemia may pre-
cipitate WE or KS. On a cellular level, thiamine acts as a cofactor for glycolysis and
the ultimate production of ATP. Concerns about timing of glucose and thiamine ther-
apy stem from the fact that giving a glucose load to a thiamine-deplete person poten-
tially risks the utilization of all remaining thiamine stores, thus precipitating WE. The
origins of these concerns are a variety of case reports and case series, in which pa-
tients were given dextrose-containing solutions over many days without any thiamine
repletion.38–40 There is no clear human evidence that glucose loading before thiamine
supplementation results in acute deterioration of mental status, although animal
studies have shown documented cerebral changes after an acute glucose load in
thiamine-deficient rats.41,42 The authors of a literature review on the subject note there
is not good evidence evaluating this clinical question in humans in an acute setting.
Given the dangers of acute hypoglycemia, the authors suggest providing emergent
glucose supplementation followed by prompt thiamine supplementation.43

SUMMARY

The spectrum of metabolic derangements due to the habitual and recreational use of
alcohol is vast. Emergency physicians must be vigilant when treating the intoxicated
and altered patient. Many of the disease states previously discussed are curable if
managed in a timely fashion. Furthermore, many of the conditions discussed within
this article are preventable with abstinence from alcohol; as physicians, we should al-
ways attempt to engage our patients in discussions regarding health maintenance and
the need to seek help with addictions.

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