ARTICLE

Does Ethanol Explain the Acidosis Commonly Seen inEthanol-Intoxicated Patients?

Shahriar Zehtabchi, M.D., Richard Sinert, D.O., Bonny J. Baron, M.D.,Lorenzo Paladino, M.D., and Kabir Yadav, M.D.

Department of Emergency Medicine, Downstate Medical Center/Kings County Hospital Center,

State University of New York, Brooklyn, New York, USA

Objective. Emergency physicians frequently treat ethanol-intoxicated trauma patients. In patients with apparently minorinjuries, the presence of metabolic acidosis is often attributed toserum ethanol. We tested whether there is justification for thebias that ethanol reliably explains the acidosis commonly seen inalcohol-intoxicated patients. Methods. Prospective, observa-tional. Inclusion criteria: Ethanol-intoxicated patients admittedto the emergency department (ED) following significant traumamechanisms, in whom diagnostic evaluation revealed only minorinjury. Exclusion criteria: Major trauma (blood transfusions,drop in Hct >10 points over 24 h, or Injury Severity Score [ISS]>5) or positive urine toxicology screen. Definitions: EthanolIntoxication: (Blood Alcohol Level (BAL) �80 mg/dl), Acidosis:BD ��3.0 mMol/L; Lactic Acidosis (LAC >2.2 mMol/L). Datawere reported as mean±SD. Data were compared by t-tests orFishers exact test as appropriate (a=0.05, 2 tails) and correlationsby Pearson correlation coefficient. Results. 192 patients werestudied (84% male) with a mean age of 31.7±15.6 years. Acidosiswas observed in 19.3% (CI 95%, 14.5% to 25.0%) of all studypatients. We observed significant (p < 0.001) difference inprevalence of acidosis in ethanol intoxicated (42%) compared tononintoxicated (1%) patients. Comparing the two study groups,patients with ethanol intoxication had lower BD (�2.24±2.74 vs.�0.05±2.35, p<0.001) and higher LAC (2.69±1.48 vs. 2.00±1.78,p=0.02). However, ethanol levels did not correlate significantlywith BD (p= 0.50) or LAC (p=0.14). Conclusion. Ethanolintoxication is associated with acidosis, which does not correlatewith BD or LAC. The complexity of pathogenesis of acidosis inethanol intoxication justifies further diagnostic evaluation ofthese patients in order to rule out other causes of acidosis.

Keywords Ethanol; Lactic acidosis; Injuries; Toxins; Cocaine

INTRODUCTION

Approximately 100,000 alcohol-related deaths are reported

each year (1,2). Ethanol consumption is a major risk factor for

various types of injuries including motor vehicle crashes,

pedestrians struck, cycle injuries, falls, burns, drowning,

suicides, and assaults (2–4). Nearly 50% of trauma patients

have used alcohol prior to their injury (5) and more than half

of fatal motor vehicle crashes are alcohol related (6).

Ethanol-intoxicated patients present to the emergency

department (ED) with a spectrum of conditions ranging from

simple intoxication to complex medical or traumatic illnesses.

ED physicians are faced with the challenge of identifying

potentially life-threatening illnesses in uncooperative, intox-

icated patients with unreliable histories and physical exams.

Adjunctive laboratory tests may provide the only early clue as

to the patient’s degree of illness. These tests may, however,

further confuse an already complicated clinical picture.

Metabolic derangements may reflect illness or injury, or they

may be secondary to alcohol or illicit drugs.

Acid-base disturbances are commonly found in ethanol

intoxicated patients. Lamminpaa et al. documented abnor-

malities in acid-base equilibrium in 49% of 192 adult

alcoholic ED patients (7). Since mild to moderate acidosis

is so commonly seen in the ethanol-intoxicated patient, the

ED physician’s bias is often to ascribe a low base deficit

level to the direct effects of ethanol. This bias is not

completely unfounded since many published case series of

ethanol intoxicated patients have described a coexistent

metabolic acidosis (8,9). Prospective studies using both

healthy human volunteers (10,11) and animals (12,13) have

linked ethanol intake to the development of a metabol-

ic acidosis.

A difficult diagnostic question is whether the presence of

ethanol can completely account for the acidosis seen in

ethanol intoxicated patients. Previous studies which looked at

acidosis in acute and chronically ethanol-intoxicated patients

did not exclude coexisting medical or surgical problems and

Address correspondence to Shahriar Zehtabchi, M.D., Depart-ment of Emergency Medicine, Downstate Medical Center, StateUniversity of New York, Box: 1228, 450 Clarkson Ave., Brooklyn,NY 11203, USA; E-mail: zehtab@yahoo.com

161

Clinical Toxicology, 43:161–166, 2005

Copyright D Taylor & Francis Inc.

ISSN: 0731-3810 print / 1097-9875 online

DOI: 10.1081/CLT-200053083

Order reprints of this article at www.copyright.rightslink.com

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did not control for multiple intoxicants in addition to ethanol

(7–9). Healthy volunteers and animals have been used in

models of acute intoxication. Acute ethanol intoxication

combined with chronic ethanol intake, a pattern often seen

in ED patients, has not been extensively studied. In addition,

prospective studies utilizing human volunteers were limited by

ethical concerns which restricted the amount of ethanol

consumed, thus preventing analysis of a dose-response curve

of alcohol causing acidosis.

We designed a prospective study using ethanol-intoxicated

trauma patients who were diagnosed with only minor or no

injuries. After excluding patients with other co-intoxicants,

or additional known causes of acidosis, we attempted to

correlate ethanol level with degree of acidosis, in the

remaining patients. We hypothesized that a dose-response

curve could be produced to predict the expected acidosis for

any given level of ethanol. If ethanol levels could reliably

predict acidosis, then the ED physician could easily

determine if the acidosis in their intoxicated patient could

be attributed to ethanol alone or whether further diagnostic

workup was indicated.

METHODS

Study Design

Patients with significant mechanisms of blunt or pene-

trating trauma, who required laboratory analysis as part of

their diagnostic evaluation, were enrolled in the study. The

determination of significant trauma and the need for labo-

ratory evaluation was at the discretion of the emergency med-

icine attending physician in charge of the trauma resuscitation.

A convenience sample of trauma patients was enrolled by

emergency medicine residents and attendings.

The primary outcome variable was to investigate the

correlation of serum ethanol level with degree of metabolic

acidosis in ethanol-intoxicated trauma patients with only

minor injuries. The study was approved by the joint insti-

tutional review boards (IRB) of State University of New

York, Downstate Medical Center, and Kings County Hos-

pital Center. A policy of waived consent, which adhered

to the principle of implied consent, was approved by

the IRB.

Study Population and Setting

This study was conducted at Kings County Hospital Center

(KCHC) in Brooklyn, New York. KCHC is an urban, level one

trauma center. Data were collected from July 2002 to August

2003. Patients with blunt or penetrating trauma suspected of

having significant injury underwent diagnostic evaluation.

Patients found to have major injuries were excluded from the

data set. Significantly injured patients were excluded in order

to avoid any confounding effect of blood loss and tissue

ischemia on the metabolic acidosis caused by ethanol

intoxication. Patients with major injuries were defined as

those with any of the following: received blood transfusion,

drop in hematocrit (Hct) of greater than 10 points in the first

24 h, or injury severity score (ISS) >5. ISS �5 has previously

been used in the literature to define minor trauma (14). It is

associated with a mortality rate of less than 1% (15). Drop in

Hct and blood transfusions have also been used as indicators

of major trauma in previous studies (16).

Patients with positive urine toxicology (see Measurements)

were also excluded from the data set in order to rule out

additional exogenous causes of metabolic acidosis other

than ethanol.

Measurements

Age, gender, vital signs (systolic blood pressure, pulse

rate), mechanism of injury, and physical findings were

collected for all patients. Shortly after patients’ arrival to the

ED, blood samples were obtained for measurement of arterial

base deficit (BD), lactate (Radiometer ABL 725, Copenhagen,

Denmark), and serum ethanol level (AxSYM System, Abbott

Laboratories, IL). Urine toxicology screen (Utox) and serial

hematocrits were ordered for all the patients. In our institu-

tion urine toxicology screen is performed by using kinetic

interaction of microparticles in solution (KIMS) technique

(Roche Modular ISE1800 and D 2400) and detects the

following components: Opiates, Cannabinoids, Cocaine (Ben-

zoylecguanine), Benzodiazepines, Methadone, Barbiturates,

Methylqualone, Amphetamine, Phencyclidine, and Propoxy-

phene. The results of all diagnostic studies were recorded.

TABLE 1

Comparison of baseline predictor variables in ethanol-

intoxicated and nonintoxicated patients

Variable ETOH� ETOH+ p

n 147 45 –

BAL (mg/dl)+ 4±16 205±81

Age 31±17 34±13 0.31*

Gender (% male) 78 98 <0.001**

D Hematocrit (%) 2.19±2.76 2.97±2.75 0.09*

SBP$ (mmHg) 138±23 135±15 0.41*

Shock index

(HR/SBP)

0.65±0.18 0.72±0.13 0.01*

Lactate (mMol/L) 2±1.78 2.69±1.48 0.02*

Base deficit

(mMol/L)

�0.05±2.35 �2.24±2.74 <0.001*

+Blood alcohol level.

*Student’s t-test.

**Fisher’s exact test.$Systolic blood pressure.

S. ZEHTABCHI ET AL.162

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Units of transfused PRBCs and change in Hct over the initial

24 h were documented. ISS scores were calculated. Shock

Index was calculated by dividing the patients’ heart rate by

systolic blood pressure.

Ethanol Intoxication (ETOH+) was defined as blood

alcohol level �80 mg/dl, the legal definition for alcohol

intoxication in many states. Acidosis was determined by

analysis of BD. BD is defined by the amount of bicar-

bonate required to titrate a sample of blood to a pH of 7.40

with a PCO2 of 40 mmHg at 37�C (17). We chose a level

of BD ��3.0 mmol/L as the cutoff to define acidosis

based on previous studies of trauma patients (18). BD

��3.0 mmol/L is associated with an increase in serious

injury. A lactate level (LAC) >2.2 mmol/L was used to

define lactic acidosis, the cutoff value for normal lactate in

our laboratory.

Data Analysis

Data were reported as means±standard deviation. Student’s

t-tests or Fishers exact test were used for comparing the means

as appropriate. All tests were two-tailed, with a set at 0.05.

Pearson correlation coefficient was used for analysis of

covariants. Calculations were done using SPSS for Windows,

Rel. 11.0 1997. Chicago: SPSS Inc.

A sample size analysis was calculated assuming a

correlation between ETOH and BD of 0.40. This effect was

selected as the smallest effect that would be important to

detect, in the sense that any smaller effect would not be of

clinical significance. The criterion for significance (alpha) was

set at 0.050. The test was two-tailed, which means that an

effect in either direction would be interpreted. With the

proposed sample size of 44 ethanol-intoxicated patients, the

study would have power of 80.1% to yield a statistically

significant result. Sample size was calculated using Sample-

Power Re. 2.0. 2003, Chicago: SPSS Inc.

RESULTS

A total of 192 patients were enrolled. Study subjects

consisted of 156 males (81%) and 36 females (19%) with

mean age of 32±16 (range of 13 to 89 years old). Comparison

of baseline predictor variables in patients in two categories of

ethanol-intoxicated and nonintoxicated is presented in Table 1.

A total of 147 patients (77%) were classified as non-

intoxicated. Forty-five patients (23%) were ethanol-intoxicat-

ed with a mean BAL of 205±81 mg/dl. No significant

difference was observed between the intoxicated and non-

intoxicated groups when comparing age, systolic blood

pressure, and change in hematocrit over 24 h. A greater per-

centage of ethanol-intoxicated patients were male (p<0.001).

Although the mean shock index (heart rate divided by systolic

TABLE 2

Prevalence of ketonuria, low serum bicarbonate, increased anion gap, and elevated arterial lactate in

intoxicated vs. nonintoxicated patients

Ethanol+

P*

Ethanol�

P*BD<�3

mMol/L (n=19)

BD>�3

mMol/L (n=26)

BD<�3

mMol/L (n=14)

BD>�3

mMol/L (n=133)

Ketonuria 2 (10%) 1 (0.4%) 0.56 1 (0.7%) 15 (11%) 1.00

HCO3

<20 mMol/L

9 (47%) 3 (12%) 0.01 7 (50%) 8 (6%) <0.001

Anion gap >15 16 (89%) 11 (42%) 0.002 8 (54%) 37 (28%) 0.10

Lactate

>2.2 mMol/L

11 (58%) 8 (31%) 0.12 8 (54%) 17 (13%) 0.00

Ethanol+: Blood alcohol level �80 mg/dl.

*Fisher’s exact test.

FIG. 1. Scatterplot of serum ethanol level and arterial base deficit in

intoxicated patients.

163ACIDOSIS SEEN IN ETHANOL-INTOXICATED PATIENTS

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BP) was higher in the intoxicated group, there was no

difference (6.7% vs. 7.4%, p=1.00) in the percentage of

patients with an index greater than 0.9 in either group.

Comparing the two study groups, patients with ethanol

intoxication had lower BD (mean difference: 2.19 mMol/L,

95% CI, 1.37 to 3.01 mMol/L) and higher LAC (mean

difference: 0.69 mMol/L, 95% CI, 0.11 to 1.27 mMol/L).

We observed significant statistical difference (p<0.001) in

the prevalence of acidosis (BD ��3 mmol/L) when com-

paring intoxicated (42%) to nonintoxicated (1%) patients. Of

the 45 patients with ethanol intoxication, 19 (42%) were

acidotic. Among the intoxicated acidotic patients, anion gap

was elevated (AG �15) in 16 patients (84%) and arterial

lactate was elevated in 11 patients (58%). Prevalence of

ketonuria, low serum bicarbonate, high anion gap, and

elevated arterial lactate in intoxicated vs. nonintoxicated

patients are summarized in Table 2.

We tested the correlation (Pearson Correlation Analysis)

between the serum ethanol level, BD, and arterial lactate level

in the study subjects. We detected no significant (p=0.50)

correlation between BD and serum ethanol level in ethanol-

intoxicated patients (see Fig. 1). The correlation between

serum ethanol level and arterial lactate in ethanol-intoxicated

patients was also not statistically significant (p=0.14) (Fig. 2).

DISCUSSION

In our study, 42% of ethanol intoxicated patients (19/42)

had pure metabolic acidosis (BD ��3 mMol/L). This

association between ethanol consumption and metabolic

acidosis has been previously reported in several other studies.

Lamminpaa et al. (7), MacDonald et al. (14), and De Marchi

et al. (19) observed metabolic acidosis in 7.9%, 11.7%, and

33%, respectively, of ethanol-intoxicated patients treated in

their emergency departments. The difference in the prevalence

of metabolic acidosis can be explained by the various

definitions of acidosis used in each study. Lamminpaa (7)

used decreased pH (<7.35) and MacDonald (14) used lactate

level in excess of 2.4 mMol/L as the cutoff for defining

metabolic acidosis. De Marchi (19) compared means of serum

bicarbonate levels and arterial pH in intoxicated vs. non-

intoxicated patients. In our study, BD was used to identify

patients with metabolic acidosis. In contrast to pH, BD is not

affected by changes in PCO2. Changes in BD reflect multiple

causes of acidosis in addition to lactic acidosis.

In our study, although we observed a statistical difference

in BD between the ethanol-intoxicated and nonintoxicated

groups, this difference does not appear to be clinically

significant, as both means fall in the normal range. We also

did not detect a significant (p=0.50) correlation between

serum ethanol levels and arterial BD. Therefore, a dose-

response curve could not be generated between BD and BAL.

Dunham et al. (16) detected a significant but weak correlation

between BD and blood alcohol level (BAL). Unlike our study

population which only consisted of minor trauma patients,

Dunham’s analysis included both minor and major trauma.

Studying a group of hospitalized, acutely alcohol-intoxicated

patients, MacDonald et al. (14) found no significant

correlation (p=0.26) between serum lactate concentration

and BAL. Lamminpaa et al. studied the correlation between

BAL and metabolic acidosis in both ethanol-intoxicated adults

(7) and teenagers (20). Statistically significant correlation was

detected between the serum pH and BAL in adults (r=�0.45,

r2=0.20, p=0.0013) (7) but not in teenagers (r=�0.31,

p=0.16) (24). However, these studies included a significant

number of patients with respiratory acidosis secondary to

CNS depression from alcohol intoxication. In contrast to all

the studies mentioned previously, we specifically excluded

patients with major injuries or intoxications other than

ethanol in order to avoid additional potential causes of

metabolic acidosis.

The lack of correlation between ethanol and BD can be

explained by the complexity of the acid-base disturbances

induced by ethanol intoxication. Ethanol contributes to

metabolic acidosis by producing a high anion gap as well as

a non-anion gap acidosis (loss of bicarbonate in the urine)

(21–24). In our study 20% of acidotic ethanol-intoxicated

patients had a non-anion gap, and 80% had a high anion gap

metabolic acidosis. The high anion gap acidosis caused by

ethanol is due to increased production of lactic acid, aceto-

acetate, and beta hydroxybutyric acid (24–28). In addition, the

severity of acidosis in ethanol intoxication can be affected

by other acid-base disorders commonly observed in these

patients. Ethanol consumption can cause vomiting, resulting in

a metabolic alkalosis (29). Ethanol is capable of increasing the

respiratory rate (respiratory alkalosis) at low doses and

decreasing the respiratory rate (respiratory acidosis) at higher

FIG. 2. Scatterplot of serum ethanol level and arterial lactate in intoxicated

patients.

S. ZEHTABCHI ET AL.164

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doses (26,30). A study using rats given fixed doses of ethanol

intraperitoneally revealed that the degree of acidosis, reflected

by decreased arterial pH, was very variable (31). Study

investigators (Gilliam et al.) concluded that differences in

sensitivity to ethanol might be related to endogenous

variations in respiratory and cardiovascular regulatory mech-

anisms. Multiple mechanisms for production of acidosis,

combined with additional confounding factors such as chronic

consumption vs. acute intoxication make the occurrence and

severity of acidosis variable and unpredictable. In addition, the

rate of absorption and metabolism of ethanol varies in an

uncontrolled setting such as an emergency department and

provides another explanation for the poor correlation between

ethanol level and degree of acidosis. In a previous study (32),

we showed that ethanol intoxication did not affect the base

deficit and lactate even in patients with major trauma.

The contribution of lactate to the metabolic acidosis from

ethanol is controversial. Studies of normal volunteers have

shown a predictable rise in plasma lactate after ethanol

ingestion (24,33). However, other studies have reported that

clinically significant lactic acidosis is uncommon in ethanol

intoxicated patients (14,23). Lactate levels in excess of 2.4

mmol/L were associated with a significant increase in

mortality in critically ill patients (35,36). Investigators have

suggested that presence of severe lactic acidosis in ethanol

intoxicated patients warrants diagnostic work-up to investigate

other possible causes of increased lactate production such as

hypoxemia or hypoperfusion (34,35), thiamine deficiency

(36), seizure (37), renal dysfunction (38), sepsis (38–40), and

toxins (39).

We selected our study population to overcome many of the

methodological problems found in earlier studies, correlating

ethanol levels with acidosis. We chose to study trauma

patients because this population tends to be young and healthy.

This enabled us to control for additional metabolic derange-

ments that may occur in patients with acute medical illnesses.

We excluded patients with major trauma to eliminate the

metabolic effects of injury. Finally, in order to study the

metabolic effects of ethanol alone, we excluded any patients

with co-intoxications. This allowed us to study a representa-

tive group of ethanol-intoxicated patients who did not have

any obvious medical or trauma-related metabolic acidosis.

LIMITATIONS

Our study analyzed a convenience sample of trauma

patients, and our data represents only a portion of our

institution’s total trauma admissions. A further limitation

involves our definition of intoxication secondary to illicit

drugs. A urine toxicology screen qualitatively measures the

presence of a drug or its metabolites. A positive Utox may not

necessarily indicate an acute intoxication. The Utox for

cocaine, for example, can be positive for up to three days

postingestion and may not be an indicator of intoxication at the

point of testing. Exclusion of patients with positive Utox could

be a source of selection bias, since some of these patients may

not have acute intoxication. Similarly, we also did not obtain

information about the drinking history of our patients, and the

intoxicated group may have been a mixture of naive and

chronic drinkers. We only measured a single ethanol level and

thus we could not relate this to total volume and time of ethanol

ingestion. Finally, our definition of ethanol intoxication as a

blood alcohol level of 80 mg/dl uses a legal definition. This

may not represent a significant physiological cutoff.

CONCLUSION

We reject our research hypothesis that a dose-response

curve could be produced to predict the expected acidosis for

any given level of ethanol. Patients may exhibit a metabolic

acidosis as a result of ethanol intoxication. The degree of

acidosis, however, cannot be reliably predicted by the serum

ethanol level. Severe metabolic or lactic acidosis in intoxi-

cated patients cannot be safely attributed to ethanol consump-

tion alone. Diagnostic work-up is warranted in such patients to

search for causes of acidosis, other than ethanol intoxication.

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