Alcoholic Liver Disease Directed Readings In the Classroom

Transcription

Alcoholic Liver
Disease
July/August 2013 issue of Radiologic Technology
Directed Readings
In the Classroom
Instructions:
This presentation provides a framework for educators
and students to use Directed Reading content
published in Radiologic Technology. This information
should be modified to:
1.
Meet the educational level of the audience.
2.
Highlight the points in an instructor’s discussion or presentation.
The images are provided to enhance the learning
experience and should not be reproduced for other
purposes.
Introduction
In the United States, approximately 100 000 deaths are attributed to
alcohol abuse each year. In 2009, the World Health Organization listed
alcohol use as one of the leading causes of the global burden of
disease and injury. Alcoholic liver disease, a direct result of chronic
alcohol abuse, insidiously destroys the normal functions of the liver.
The end result of the disease, cirrhosis, culminates in a dysfunctional
and diffusely scarred liver.
This article discusses the clinical manifestations, imaging
considerations, and treatment of alcoholic liver disease and cirrhosis.
Normal liver function, liver hemodynamics, the disease of alcoholism,
and the deleterious effects of alcohol also are reviewed.
Embryonic Development
The liver initially develops from the foregut, an element of the early
primitive gut, within the first few weeks of embryonic development.
In the embryo, the liver is responsible for hemopoiesis, which is the
formation and development of blood cells. The primary liver cells, the
hepatocytes, form a series of branching and anastomosing plates that
constitute the normal hepatic architecture.
The tiny umbilical vein of the umbilical cord provides perfusion to the
developing liver. The umbilical vein enters the fetus superior to the
bladder and travels cephalically toward the liver. At the liver, the
umbilical vein bifurcates into right and left branches. The left branch
enters the liver and attaches directly to the left portal vein. The right
branch is essentially a shunt between the umbilical vein and the
inferior vena cava. This shunt, referred to as the ductus venosus,
allows some blood to bypass the liver and flow directly into the fetal
inferior vena cava (IVC). Once in the IVC, the blood can travel up to
the fetal heart and be dispersed throughout the fetus.
Shortly after birth, the ductus venosus collapses and becomes the
ligamentum venosum. Concurrently, the right branch of the umbilical
vein collapses. The remaining structure of the umbilical vein then is
referred to as the round ligament or the ligamentum teres. The
umbilical vein can recanalize, or reopen, and shunt blood away from a
liver that has been damaged. This condition, known as portal
hypertension, will be reviewed further in this article when common
complications of alcoholic liver disease (ALD) and cirrhosis are
discussed.
Anatomy and Physiology
of the Liver
The liver is the largest parenchymal organ of the body. Located within
the right upper quadrant and extending across the midline of the
body, the normal liver occupies 2 distinct abdominal regions — the
right hypochondrium and epigastrium. Anatomically, the liver consists
of 3 primary lobes, which can be differentiated by surrounding
landmarks and location. The largest, the right lobe, occupies much of
the right upper quadrant. The left lobe of the liver is located within
the midline of the abdomen. This lobe can traverse the midline and
may come in contact with the spleen. The third, and much smaller
lobe, is the caudate lobe. The caudate lobe is located posterior to the
left lobe, and is therefore located within the midline of the abdomen
as well.
of the Liver
The liver performs many vital functions that sustain life, including:
• Digestion.
• Excretion.
• Nutrient storage and conversion.
• Detoxification of destructive chemicals.
• The creation of new molecules.
of the Liver
The liver consists of several types of specialized cells that sustain
homeostasis, the body’s ability to preserve internal stability.
Externally, the liver has a protective covering referred to as the
Glisson capsule. Within the capsule, nearly 100 000 groups of cells
referred to as lobules create the mass of the liver. The primary cells
contained within these liver lobules are referred to as hepatocytes.
Hepatocytes are responsible for adjusting secretion and absorption
levels of nutrients within the liver and comprise 70% to 80% of the
liver mass. Hepatocytes are unique in that they have long life spans
and cannot only respond to disease, but in many cases restore
previously damaged hepatic tissue.
of the Liver
The nonparenchymal cells of the liver include Kupffer cells,
endothelial cells, hepatic stellate cells, and pit cells. The Kupffer cells
perform significant phagocytic functions, such as demolition of
pathogens, removing cell debris, and destruction of dysfunctional or
damaged red blood cells. The crucial role that Kupffer cells play in the
hepatic reaction to alcohol and its metabolites will be discussed
further in this article.
Hemodynamics of the Liver
Appreciating the normal blood flow within the liver is important
because hepatic perfusion is compromised with many forms of liver
disease. The hemodynamics of the liver are distinctive chiefly because
unlike many organs, the liver has a dual blood supply. The liver
receives most of its blood flow, approximately 70%, from the main
portal vein, which enters at the hilum of liver, an area also referred to
as the porta hepatis.
The main portal vein bifurcates within the liver into right and left
portal vein branches. The portal veins have minimal pulsatility when
examined with ultrasonography and pulsed-wave Doppler.
Hemodynamics of the Liver
A supplementary blood supply to the liver, the hepatic artery,
originates from the anterior aspect of the abdominal aorta via a
branch called the celiac artery (also called the celiac trunk or celiac
axis). The hepatic artery is one of 3 branches of the celiac artery. The
hepatic artery bifurcates once inside the liver into right and left
branches.
Filtered blood exits the liver by means of the hepatic veins. There are
typically 3 hepatic veins: middle, right, and left. These veins often are
used to differentiate the 2 main lobes of the liver and further
separate these lobes into segments. The hepatic veins empty the
filtered blood from the liver into the IVC.
Assessing Normal Liver Function
Serum liver function tests are a common clinical assessment used by
physicians to assess general well-being. A liver function blood test
includes a laboratory assessment of several levels, including an
evaluation of:
• Alanine aminotransferase.
• Aspartate aminotransferase.
• Alkaline phosphatase.
• Bilirubin.
• Albumin.
• Total protein.
Assessing Normal Liver Function
Of some importance to imaging professionals is the physical
manifestation of elevated bilirubin. Bilirubin, a major component of
bile, is the byproduct of hemoglobin breakdown. An elevation in
bilirubin can result in jaundice, which is the yellowing of the skin and
sclera of the eyes. Consequently, imaging professionals should be
capable of recognizing jaundice in patients that present with elevated
liver function test.
Hepatic Imaging Features
Ultrasonography provides a noninvasive, nonionizing, effective means
of evaluating the liver. The normal echotexture of the liver is said to
be smooth and homogeneous, consisting of medium-to-low echoes,
only occasionally disrupted by the hepatic vasculature and normal
hepatic fissures and ligaments. Representative images demonstrate
the hepatic and portal veins, the interface between the liver and right
kidney, and the hepatic lobes. An assessment of the biliary tract,
including the gallbladder, often is performed as well.
Hepatic Imaging Features
Computed tomography (CT) frequently is used to assess hepatic
maladies. Unenhanced CT readily demonstrates the homogeneous
parenchyma of the normal liver. The appearance of the attenuation
value of the unenhanced liver is often greater than the spleen;
although with contrast, this varies according to the time of image
acquisition. However, immediately after contrast administration, the
attenuation value of the liver often becomes less than that of the
spleen.
Alcoholism and the Effects of
Alcohol
In 2009, the World Health Organization listed alcohol use as one of the
leading causes of the global burden of disease and injury, surpassed only
slightly by childhood malnourishment and unsafe sex. This placed
alcohol use ahead of unsafe water and sanitation, hypertension, high
cholesterol, and tobacco use, and clearly affirms that alcohol is the most
widely abused substance in the world.
In the United States, approximately 100 000 deaths per year are
attributed to alcohol abuse. Alcohol use is an underlying cause of more
than 30 conditions and a definite contributing factor to many more,
including psychotic disorder, alcoholic cardiomyopathy, amnesic
syndrome, and alcoholic liver disease. Alcohol consumption is the
leading cause of liver disease in the United States, with approximately
40% of deaths from cirrhosis attributed to alcohol-induced liver disease.
Alcohol
The Mayo Clinic defined alcoholism as a chronic disease in which the
body becomes reliant upon alcohol (ethanol). Furthermore, it has
been referred to as a syndrome that consists of 2 phases: problem
drinking and alcohol addiction.
Problem drinking: characterized by consumption that is used to deal
with stressors and anxiety.
Alcohol addiction: described by the American Psychiatric Association
as a disease in which individuals become preoccupied with drinking,
have impaired control over drinking, suffer from compulsive drinking,
drink despite physical or psychological problems caused by drinking,
and have a tolerance for alcohol, and/or suffer from withdrawal
symptoms.
Alcohol
In the United States, 67% of the population aged 18 years or older
drink alcohol, while nearly 18 million Americans suffer from
alcoholism or alcohol-related health issues. A 2008 study performed
by the National Survey on Drug Use and Health claimed the rate of
youth alcohol consumption among those aged 12 to 17 years was
14.6%. In addition, 70% of 8th graders, 84% of 10th graders, and 88%
of 12th graders have at least tried an alcoholic beverage. It is
important to note that 22 is the average age when alcohol
dependency begins.
Alcohol
A standard alcoholic beverage has been described as any drink that
contains 14 g of pure alcohol. Therefore, the list includes a single 12 fl oz
can of beer, 5 fl oz of table wine, or a 1.5 fl oz shot of 80-proof spirits.
Irrespective of what form of alcohol is consumed, the greatest risk factor
appears to be the quantity of alcohol consumed. The definition for lowrisk drinking for men and women differs, because women suffer from
hepatic damage and cirrhosis with considerably smaller amounts of
alcohol consumption. Thus, a man should not drink more than 4 drinks
per day and no more than 14 drinks per week. A woman should not
drink more than 3 drinks per day and no more than 7 drinks per week.
However, we still have limited knowledge of the pathological factors that
cause liver damage, and there appears to be no “safe” limit for alcohol
consumption.
Alcohol Metabolism and the Liver
The liver is the principal organ for alcohol metabolism. The body
naturally recognizes ethanol alcohol as a foreign, toxic agent that can
disrupt normal homeostasis.
When we consume ethanol, it is rapidly absorbed by the upper
gastrointestinal tract. Ethanol is diffused throughout the body, but
exposure is greatest to the liver, via the main portal vein. Ethanol is
metabolized by the body in the gastric mucosa and the liver. These
organs manage an enzyme referred to as alcohol dehydrogenase,
which is used by the body to oxidize ethanol and convert it into
acetaldehyde and other metabolites. Acetaldehyde ultimately is
converted by the body into acetic acid, and then acetate.
Acetaldehyde affects protein synthesis.
Alcohol’s metabolites, especially acetaldehyde, damage vital liver cells
because of the excessive generation of free radicals (molecules with
unpaired electrons). One destructive byproduct is the reactive oxygen
species of free radicals. An excessive amount of this type of toxic free
radical causes oxidative stress, which results in the body’s inability to
prevent and repair hepatic damage and the destruction of
deoxyribonucleic acid.
Alcohol metabolism differs dramatically between sexes. Women are
much more likely to suffer from liver damage than men as a result of
alcohol consumption. However, this phenomenon is not clearly
understood.
Nonetheless, an estimated 5.3 million women in the United States
drink in a manner that is harmful to their health. In addition to sex,
the incidence of liver damage depends on the individual’s ethnicity,
genetic predisposition, and nutritional state.
In addition to the immediate damage of acetaldehyde and the free
radicals, the phagocytic cells of the liver, the Kupffer cells, also mount
an immune response. This response is the result of an increase in
toxins in the blood that leak from the intestinal wall and enter the
bloodstream because of alcohol consumption. The activation of
Kupffer cells is responsible for early ethanol-induced liver injury. In
fact, through an intricate chain of events, it is the activation of Kupffer
cells that ultimately leads to the death of hepatocytes. This damage
results in the manifestation of alcoholic liver disease, and eventually
to the development of fibrosis, or scar tissue, within the liver.
Alcoholic Liver Disease and
Alcoholic Cirrhosis
ALD is caused by alcoholism and can be divided into 3 types: hepatic
steatosis, alcoholic hepatitis (inflammation), and cirrhosis. It is
important to note that the components of ALD can be seen
independent of alcohol consumption and it appears that they are not
part of a continuum.
The mechanism behind the development of ALD is not completely
understood, because it is estimated that only 10% to 20% of
alcoholics develop cirrhosis. However, it is suspected that if other risk
factors are present, such as obesity and hepatitis C, there may be
increased likelihood of progression to cirrhosis.
Alcoholic Cirrhosis
Hepatic steatosis, commonly referred to as fatty liver, is a frequent
diagnosis that is not exclusive to patients suffering from ALD. Fatty
liver is the accumulation of triglycerides in the hepatocytes. Fatty liver
has been demonstrated in 90% to 100% of all heavy drinkers. Shortterm exposure to 80 g of alcohol (about 8 beers) over several days can
produce hepatic changes consistent with fatty liver disease.
Fatty liver disease can be reversed if alcohol consumption is stopped
or significantly reduced. However, there are often no clinical
symptoms, so fatty liver may be undiagnosed. Although fatty liver
may lead to an elevation in laboratory findings, it is often diagnosed
with imaging when the patient presents with unrelated symptoms.
Alcoholic Cirrhosis
Hepatitis is inflammation of the liver. In the Western world, fatty liver
with the development of hepatitis, referred to as steatohepatitis, has
been acknowledged as a precursor for the development of cirrhosis.
Alcoholic hepatitis results directly from alcohol abuse and is observed
in as many as 35% of heavy drinkers. Like other forms of hepatitis,
alcoholic hepatitis can be subclinical. Laboratory findings are more
predictive if the disease has progressed.
Approximately 40% of patients with alcoholic hepatitis who continue
to drink will develop alcoholic cirrhosis within 1 to 2 years.
Alcoholic Cirrhosis
Hepatocellular death with resulting fibrosis and regeneration is
collectively referred to as cirrhosis. Cirrhosis slowly destroys normal
hepatic architecture by interspersing fibrous bands of connective
tissue between the hepatic lobules, which results in the regeneration
of liver cells in nodules that are unrelated to normal vasculature.
A specific causative form of cirrhosis, alcoholic cirrhosis, is defined as
a condition in which there is continuing fibrosis resulting in the
subdivision of the liver into nodules of proliferating hepatocytes
surrounded by scar tissue as the direct result of chronic alcohol
abuse. Alcoholic cirrhosis is a debilitating disease that remains among
the top 10 causes of death worldwide, and the 12th leading cause of
death in the United States.
Alcoholic Cirrhosis
Alcoholic cirrhosis is an irreversible condition that has an estimated
frequency of 10% to 15% among people who consume 50 g of alcohol
daily over a 10-year period. It is characterized by both steatosis and
hepatitis, and fibrosis. If left unchecked and untreated, inflammation
of the liver certainly produces hepatic fibrosis.
Alcoholic Cirrhosis
The principal pathogenetic process in the development of cirrhosis is the
progressive fibrotic changes that occur within the liver parenchyma
combined with the disruption of the normal hepatic vasculature. The
fibrous tissue found in the liver with cirrhosis is formed from the
abnormal accumulation of a naturally occurring substance, collagen.
Excessive collagen is produced by the liver’s hepatic stellate cells as a
result of complex cellular changes from acetaldehyde exposure. This
accumulation of fibrotic tissue impedes normal liver function and
distorts normal hepatic architecture, thus leading to the manifestation of
cirrhosis. The liver becomes smaller, harder, and difficult to perfuse with
blood. The other characteristic of cirrhosis in addition to fibrosis is the
manifestation of regenerating nodules. The histologic classifications of
cirrhosis include micronodular (chronic), macronodular (acute), and
mixed forms of cirrhosis.
Alcoholic Cirrhosis
The early stages of cirrhosis are referred to as compensated cirrhosis.
In these stages, the liver, though permanently scarred, can perform
many of its vital functions. The final stages of cirrhosis are referred to
as decompensated cirrhosis. With decompensated cirrhosis, the liver
is irreparably scarred and hepatic function is compromised.
While patients with compensated cirrhosis can have the same survival
as the general population, those with decompensated cirrhosis have a
median survival of less than 2 years. It is important to note that
patients with alcoholic hepatitis can present with clinical features
similar to decompensated cirrhosis.
Alcoholic Cirrhosis
There are 4 stages of cirrhosis according to criteria agreed upon by
the Baveno IV conference:
• Stage 1: uncomplicated cirrhosis.
• Stage 2: cirrhosis with evidence of esophageal varices but without
bleeding and ascites.
• Stage 3: cirrhosis with ascites, with or without esophageal varices.
• Stage 4: cirrhosis with gastrointestinal bleeding, with or without
ascites.
Stages 1 and 2 correspond with compensated cirrhosis, while stages 3
and 4 correspond with decompensated cirrhosis. Hepatic failure
occurs when 80% to 90% of hepatic function is lost.
Sequelae and Complications of
Alcoholic Cirrhosis
The most common result of alcohol cirrhosis is a hemodynamic shift
referred to as portal hypertension. Portal hypertension is the
elevation of the blood pressure within the portal venous system. It
develops as a result of the resistance to normal blood flow to the liver
via the main portal vein. In turn, this resistance leads to elevated
pressure within the portal veins and an enlargement of the main
portal vein. The development of portal hypertension is the earliest
and most important complication of cirrhosis because most of the
physical problems associated with cirrhosis are attributable to it.
Alcoholic Cirrhosis
As the resistance within the portal vein increases, small tributaries
between the portal and systemic circulation develop. These are
referred to as portosystemic venous collaterals or portosystemic
shunts. One location for portosystemic shunts is the paraumbilical
vein, which collapses shortly after birth and becomes the ligamentum
teres. In patients with portal hypertension, the paraumbilical vein
may recanalize, or reopen, and blood is once again shunted away
from the liver. This is referred to as portosystemic shunting.
Alcoholic Cirrhosis
Although these tiny tributaries are vital for the patient suffering from
portal hypertension, they are highly prone to rupture.
Gastroesophageal varices are found in 65% of patients with advanced
cirrhosis. These fragile vessels rupture and lead to acute hemorrhage
and death in about half of patients. In some cases, hepatofugal flow
occurs within the portal veins. Hepatofugal flow is a reversal of flow;
therefore, instead of forward flow toward the liver, the portal veins
flow away from the liver.
Alcoholic Cirrhosis
Portal hypertension is a frequent cause of ascites in patients with
cirrhosis. Ascites is defined as the pathological accumulation of fluid
within the peritoneal cavity. Ascites develops as a result of the
buildup of fibrous tissue within the liver, increasing hydrostatic
pressure and the leakage of serous fluid from the cells. Occasionally
this fluid becomes infected, resulting in a condition known as
spontaneous bacterial peritonitis. This infection may be the result of
bacteria translocating from the intestines to the ascites via the
lymphatic channels or bloodstream. Concurrently, enlargement of the
spleen, referred to as splenomegaly, is a common finding in patients
with portal hypertension and cirrhosis.
Alcoholic Cirrhosis
Patients often suffer from hepatic encephalopathy as well, which is a
brain abnormality caused by the liver’s inability to remove toxins,
specifically ammonia, from the blood. These patients can suffer from
a wide range of central nervous system abnormalities that include
day-night reversal, mild intellectual impairment, and even coma.
Hepatorenal syndrome is another complication of advancing cirrhosis.
It is described as dysfunction of the kidneys characterized by reduced
renal circulation, retention of sodium and water, and excess urea in
the blood.
Alcoholic Cirrhosis
Cancer is a leading cause of death for patients with cirrhosis. There
appears to be a definite connection between long-standing cirrhosis
and the most common form of liver cancer, hepatocellular carcinoma
(HCC). Patients who drink more than 80 g of alcohol per day for more
than 10 years have a 5-fold increase in the risk for HCC.
Clinical findings of HCC include abdominal distention, abdominal
discomfort, anorexia, and an elevated serum alpha-fetoprotein.
Clinical Features and Diagnosis of
Cirrhosis
The clinical signs of cirrhosis can range from subtle onset to acute
manifestations that may cause irreversible physical debilitation. The
vague, nonspecific early signs and symptoms of cirrhosis include
weakness, malaise, disrupted sleep, muscle cramps, and weight loss.
As the disease progresses, the individual suffers from jaundice,
ascites, and peripheral edema. These clinical features result from
hepatic cell dysfunction, and most often are the result of portal
hypertension and portosystemic shunting.
Cirrhosis
Laboratory findings for cirrhosis are also nonspecific. However, there
are common indicators that point to hepatic damage. Gamma
glutamyl transferase (y-GT), also referred to as gamma-glutamyl
transpeptidase, is a liver enzyme that is especially sensitive for ALD.
The Child-Pugh-Turcotte scoring system for staging cirrhosis, which
includes both laboratory and clinical findings, has a sensitivity and
specificity of 78% and 83%, respectively. This scoring method
evaluates the bilirubin, albumin, and prothrombin laboratory findings.
It also includes an evaluation for ascites and encephalopathy.
Cirrhosis
Alcoholic cirrhosis can be suspected clinically in the presence of risk
factors such as obesity and chronic alcohol consumption. Diagnosis
can be based on the presence of ascites, varices, and spider
angiomas. However, liver biopsy remains the most definitive tool for
confirming hepatic scarring and vascular compromise.
The Role of Imaging in Diagnosing
Cirrhosis
Ultrasonography and CT play a vital function in the early detection of
alcoholic cirrhosis, associated abnormalities, and further assessment
of cirrhosis. The sonographic appearance of cirrhosis has been well
documented. Features include:
•Nodular hepatic architecture.
•Atrophic right lobe.
•Enlarged caudate lobe and left lobe.
•Difficult-to-penetrate liver.
•Increased echogenicity (in the presence of fatty infiltration).
•Coarse, heterogeneous echotexture.
•Ascites.
Cirrhosis
Patients with elevated liver functions should be closely examined
with ultrasonography for signs of cirrhosis. Some institutions use
ultrasonography for the initial identification of hepatic architectural
changes.
Hepatomegaly can be an early manifestation of the disease, as with
other instances of hepatitis. Further investigation of the abdomen
with ultrasonography may yield evidence of splenomegaly and
ascites. It is important to note that sonographers must further
examine the liver for signs of portal hypertension and HCC whenever
signs of cirrhosis are identified.
Cirrhosis
Evidence of portosystemic shunting can be visualized with
ultrasonography as well.
The transjugular intrahepatic portosystemic shunt (TIPS) is an
exceedingly effective treatment for patients suffering from
unmanageable variceal bleeding and ascites. Ultrasonography is used
following placement to document the stent’s patency.
Cirrhosis
CT is also useful for evaluating liver disease. CT imaging features of
cirrhosis include:
•Nodular hepatic architecture.
•Atrophic right lobe.
•Enlarged caudate lobe and left lobe.
•Evidence of confluent hepatic fibrosis.
•Heterogeneous texture.
•Ascites.
•Splenomegaly.
•Portosystemic collateral vessels.
Cirrhosis
Interventional radiologists may perform an assessment of the hepatic
venous pressure gradient (HVPG). HVPG is the gold standard for
assessing the severity of portal hypertension. This is an invasive
procedure performed under fluoroscopic guidance in which a
balloon-tipped catheter is advanced into the right hepatic vein via the
internal jugular vein. At this point, the hepatic venous pressure is
measured using an electromechanical transducer and polygraph.
Although HVPG remains the best way to assess the degree of portal
hypertension, ultrasonography has potential to provide a noninvasive
and highly efficient alternative.
Treatment and Prognosis
Abstinence from alcohol consumption is the most obvious treatment
for ALD, although it is difficult for many patients. For patients with
alcoholic cirrhosis who stop drinking, 90% live for another 5 years,
while those who continue to drink have a 70% chance of living less
than 5 years.
In those who abstain from alcohol consumption, less severe fatty liver
disease can be reversed in a few weeks, while resolution of alcoholic
hepatitis can take more than 6 months.
A TIPS, as mentioned earlier, is an effective means of treatment for
unmanageable ascites. For severe liver damage and severe alcoholic
hepatitis, corticosteroid treatment may be used to reduce the
inflammatory response.
Liver transplant is a controversial treatment for patients with alcoholinduced liver disease. Some people hold negative views concerning
alcoholics receiving liver transplants because they believe that
alcoholics bear full responsibility for their illness. Nevertheless, liver
transplants for ALD patients are often more successful than in
patients requiring a liver transplant because of other diseases. Most
ALD patients who undergo a liver transplant are younger than 60
years of age and are suffering severe liver impairment. Patients are
advised to be abstinent for at least 6 months prior to surgery. Many
complications of liver transplantation exist, including recurrence of
hepatocellular carcinoma and graft rejection. However, 5-year
survival rates have been reported to be as high as 80%.
There is current research on new approaches to treat or reverse
hepatic fibrosis. Of interest is the inverse relationship between coffee
intake and the risk of cirrhosis. Coffee intake has a favorable effect on
alcohol-related cirrhosis risk. One study evaluated more than 700
individuals and determined that espresso coffee represented a
definite modulator of alcoholic cirrhosis risk, although the connection
is not clearly understood.
The prognosis for patients with alcoholic cirrhosis depends on several
factors. Cirrhosis mortality rates are often 2 times higher in men than
women, although at any given level of alcohol consumption, women
have a higher likelihood of developing cirrhosis than men.
Treatment for Alcoholism
It is important to keep in mind that alcoholism has a wide range of
negative effects, not only on the individual, but on his or her family,
friends, and even strangers.
The Center for Substance Abuse Prevention offers information on all
aspects of alcohol abuse and other types of drugs. If you suspect that
alcoholism is having a negative effect on you or a loved one, it is vital
to remember that prevention, recognition, and early prevention, and
treatment are key. A simple screening tool for alcoholism, the CAGE
questionnaire, is often used by primary care physicians. It also can be
used by individuals who suspect that they or a family member may be
suffering from alcoholism.
Conclusion
Alcoholism is an insidious disease. Although the liver has a
remarkable ability to repair itself in some situations, it is clear that
alcohol has deleterious effects on normal liver function. Ultimately,
this can lead to a life-altering medical crisis.
The initial manifestations of ALD can be diagnosed clinically, and
imaging can aid in diagnosis. When the clinical signs of cirrhosis and
portal hypertension become life altering, imaging can further be used
to identify key features that may lead to better treatment and
improved outcomes. We must all recognize that alcoholism is a
chronic disease that can affect anyone, and that identifying clinical
and imaging precursors can lead to treatment opportunities and
extend the lives of our patients and loved ones.
Discussion Questions
Explain what constitutes alcohol abuse and the toxic
influence that alcohol has on the liver.
Identify the imaging modalities used for diagnosing
cirrhosis and list the imaging features of each.
Discuss the treatment options and prognosis for
alcoholism as well as some of the barriers that patients
and their families face.
Additional Resources
Visit www.asrt.org/students to find information
and resources that will be valuable in your
radiologic technology education.

Alcoholic Liver Disease Directed Readings In the Classroom

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