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Esophageal Varices
| Viewpoint: Current Edition
Management of Complications of Cirrhosis: Esophageal Varices
Esophageal varices, ascites and edema, and encephalopathy are three
complications of cirrhosis that can be managed medically. Physicians
should screen for these in cirrhotic patients and institute appropriate
therapy. This Viewpoint deals with management of esophageal varices. The
next Viewpoint will focus on fluid overload (ascites and edema) and
encephalopathy (the confusional state of liver disease)
Varices are large twisted blood vessels that develop in patients with
cirrhosis. They are most commonly found in the esophagus (swallowing
tube) but can also occur in the stomach. As excessive scar tissue is
deposited in the liver, the resistance to blood flow increases with an
accompanying increase in the pressure within the vein that feeds the
liver (portal vein). As a result, small or previously insignificant
blood vessels in the lining of the esophagus or the stomach become
engorged and can ultimately burst and bleed.
Bleeding from varices is often massive. Patients often throw up
blood, or pass blood from the rectum. The resultant low blood pressure
can lead to decreased perfusion of vital organs resulting in
complications such as loss of consciousness, heart attack and sometimes
death. Because of a high mortality rate from an episode of variceal
bleeding, it is recommended that physicians screen for the presence of
esophageal varices in cirrhotic patients. An upper endoscopy (a
procedure where a gastroeneterologist inserts a flexible tube with a
camera into the stomach) is performed to visualize the number and size
of the varices. If varices are present, patients are started on
medication to decrease the pressure within the veins. Mutiple studies
have shown that a decrease in the pressure of the veins reduces the risk
of bleeding and saves lives. If these veins are absent, the procedure
can be repeated in two years and medications started once the veins are
noted.
This information was last reviewed 1/4/02.
Page Content Credits
Viewpoint is an editorial column that expresses the opinion of the
specific Medical Director, who is solely responsible for its content.
Viewpoint does not represent the views or opinions of Veritas Medicine
and does not reflect the opinions of other physicians and researchers
If you have cirrhosis, or
suspect that you have cirrhosis, of the liver due to HCV , hereditary
hemochromatosis (or any other cause), you may have esophageal varices...75%
of patients with cirrhosis of the liver, have these "varicose veins"of
the esophagus. Knowing the warning signs of acute bleeding could save
your life...
Confirmation of esophageal varices is made during an endoscopy (a tube
with a light on the end of it put down your throat ( esophagus) and into
your stomach) while the patient is sedated...the doctor can view the
varices, their color, size, and predict their potential risk for a
"first bleed" or acute bleeding episode based on the pressure in the
veins, and other signs.
Warning signs include:
Nausea and vomiting blood (bright red blood or blood looking like
"coffee grounds"
Pallor or pale appearance
Shock
Sudden drop in blood pressure
Black stool (usually means an upper GI bleed of some kind)
If you have these symptoms, GO TO AN EMERGENCY ROOM IMMEDIATELY!
Patients with known or suspected varices should:
Wear a medic alert bracelet which states on it "esophageal varices"
Know their blood type
Not strain at stool
Try to avoid violent coughing, vomiting, or sneezing
Avoid aspirin or NSAIDS
Avoid coarse or sharp foods
Take beta blockers if indicated prescribed by their doctors to keep
their pulse slower than usual to reduce pressure in the varices
What can the patient with esophageal varices do to prevent a "first
bleed"?
The patient needs to follow the suggestions above
Discuss medical options with his/her doctor such as:
medications to slow down the heart rate by 20 to 30%
Ligation (Banding) of varices
Chemical treatment of the varices to stop or prevent bleeding
Make sure that family members, friends, and physicians know that you
have this condition
Web sites with further information, studies on esophageal varices, their
treatment, etc. are plentiful
on the Internet
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Encephalopathy (Hepatic or
Portal-systemic)
Updated April 2000
WHAT IS HEPATIC or PORTAL-SYSTEMIC ENCEPHALOPATHY?
There are numerous types of Encephalopathy from a number of different
causes, but we will be focusing on Hepatic or Portal-systemic
Encephalopathy. Encephalopathy is a degenerative disease of the brain,
and
refers to changes in the brain that can occur in some Hepatitis patients
with severe or advanced cirrhosis (it can occur in both acute and
chronic
Hepatitis cases).
IT HELPS TO UNDERSTAND 4 FEATURES OF ENCEPHALOPATHY (as stated by Dr.
Gregory T. Everson, Director of Hepatology, University of Colorado
Health
Sciences Center):
1 ~ Encephalopathy is usually brought on by some other problem, such as
gastrointestinal bleeding, infection or electrolyte imbalance);
2 ~ It's a completely reversible condition;
3 ~ Effective medical treatment exists and early therapy may prevent the
patient from lapsing into more advanced stages; and
4~ A successful liver transplant can completely reverse the condition.
Encephalopathy is caused by toxic waste compounds such as ammonia,
certain
fatty acids or other by-products of protein digestion which are not
cleared
by the liver from the bloodstream. This can happen once liver cells have
been damaged; liver function deteriorates, and these toxins cannot be
cleared from the blood as they would be with a healthy liver.
Encephalopathy can range from very slight (decline in memory or reduced
mental abilities and confusion) to moderate (loss of memory,
disorientation,
change in sleep habits, untidiness, muscle tremors or blackout spells)
to
severe (leading to a form of chronic dementia or even coma). It is very
important that this condition be properly diagnosed by your physician.
It's
a common mistake for Hepatitis patients to mistakenly self-diagnose
Encephalopathy when what the patient is experiencing are much less
severe
but similar symptoms occurring as a result or by-product of Chronic
Hepatitis (such as the typical "brain fog" so many experience in varying
degrees).
WHO GETS HEPATIC ENCEPHALOPATHY?
A patient with Chronic Hepatitis and advanced Cirrhosis, may; over time
develop Encephalopathy. It can range from barely discernible to very
severe, so no two cases are the same. The precise cause is unknown, but
it's clear that it correlates with worsening liver function in some
patients. Renal failure and constipation are suspect in causing the
condition to worsen. External stresses such as infections,
irregularities
of salts or electrolytes in the blood, some medications, excessive
protein
intake and the protein load caused by gastrointestinal bleeding may also
worsen encephalopathy.
Large amounts of protein in the diet can lead to the buildup of
protein
breakdown products in the blood which are normally eliminated through
the
liver. When we break down protein, one of the substances we make from it
is
called ammonia. This ammonia can circulate in the blood, and as it
passes
through the liver, the ammonia is converted to another breakdown
product,
urea. While urea is usually gotten rid of in the urine, ammonia builds
up
in the blood if the damaged liver is not able to properly convert it.
Our
bodies require protein to properly function, so restriction and diet
should
be a decision made between you, your doctor, and (when available) a
nutritionist.
Gastrointestinal bleeding is when an individual bleeds into the
stomach, and
the blood is broken down as it passes through the intestines. Partially
digested proteins in the blood are reabsorbed into the circulation,
placing
an increased load on the liver.
TREATMENT
The treatment of Hepatic Encephalopathy involves, first, the removal of
all
drugs that require detoxification in the liver and, second, the
reduction of
the intake of protein (as it tends to irritate the symptoms).
Restricting
the amount of protein in the diet will generally lower the levels of
amino
acids and ammonia in the bloodstream and brain. At the same time, it is
imperative that a Hepatitis patient with cirrhosis take in enough
protein to
avoid excessive muscle wasting and energy depletion, so it is imperative
to
seek early medical attention and follow up with your health care
specialist.
Some physicians advise their patients with this condition to carefully
monitor and limit the amount of protein they consume each day, and
recommend
the majority of this protein come from vegetables, milk and easily
digested
non-meat proteins.
Your doctor should be aware of your symptoms, and how much they have
changed
in a specific period of time. He may follow your progress with
Trailmaking
tests (a series of connect-the-numbered dots), clinical tests and lab
work,
as well as your observations.
Doctors will often prescribe lactulose; a non-absorbable sugar to
loosen
stools which may improve mental function. Some antibiotics, such as
Neomycin or Metronidazole are also used (in part, to lower amino acid
production) with some success. Certain amino acids can be used in
treatment, since they are considered less likely to cause mental
impairment.
A dietary supplement rich in these amino acids is used at many liver
transplant centers. It is very important that you are taking the correct
amino acids for your body ... so you should be a partner with your
doctor
and/or nutritionist when such decisions are made about your health care
and
maintenance. |
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| Friday June 29 5:01 PM ET
Cirrhosis-Blood Pressure Link Studied
By RANDOLPH E. SCHMID, Associated Press Writer
WASHINGTON (AP) - Researchers have discovered what they believe is
the cause of blood pressure problems in patients suffering cirrhosis,
potentially a first step in slowing the disease.
In people suffering advanced cirrhosis, blood vessels become dilated,
lowering blood pressure and increasing blood flow to the liver and gut.
Due to liver scarring, this increased blood flow meets with resistance,
resulting in elevated pressure where the vessels meet the liver.
That can cause fluid to accumulate in the abdomen and dilated blood
vessels to rupture - both life-threatening complications.
In tests on animals, the research team, led by Dr. George Kunos of
the National Institute of Alcoholism and Alcohol Abuse, found that
substances normally present in the body, called endocannabinoids, act on
the blood vessel walls to cause dilation.
The researchers found elevated levels of the endocannabinoid
anandamide associated with low blood pressure in two separate animal
studies of cirrhosis. Using a chemical that blocks the action of
anandamide, they raised blood pressure and reduced the so-called portal
pressure where the blood enters the liver.
In addition to finding higher levels of anandamide in the cirrhosis
cases, they also discovered that the blood vessels of the victims had
increased receptors to react to that chemical.
The finding may suggest an approach for therapy to assist patients
while they await a liver transplant, the researchers suggest in their
paper. The findings are reported in the July issue of the journal Nature
Medicine.
Kunos was out of the country and could not be reached
to discuss the work.
Dr. Bruce Bacon of the St. Louis University School of
Medicine, who was not involved in the study, said the finding is ``a
significant observation and an important one.''
But he cautioned, ``whether that will lead to
therapeutic intervention (in people) is yet to be determined.''
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Management of Bleeding in the Cirrhotic Patient
Important advances have been made in the management of variceal (enlarged
veins or arteries) bleeding. Despite these advances, bleeding in the patient
with cirrhosis (liver scarring) remains one of the most demanding clinical
challenges that a gastroenterologist or gastrointestinal surgeon may face.
This
article from the Journal of Gastroenterology and Hepatology addresses
the management of bleeding in the patient with cirrhosis.
The
aim of management is to identify the source of bleeding, control active
bleeding, and prevent re-bleeding. This requires a multidisciplinary team,
and the optimal management algorithm depends on the clinical circumstance of
the patient and the local availability of endoscopic, radiological, and
surgical expertise.
Injection sclerotherapy is effective in stopping acute variceal bleeding,
but has the drawback of a high incidence of complications.
Endoscopic variceal ligation is just as effective, and is associated with
fewer complications.
To
prevent re-bleeding, beta-blockers are recommended for all patients with
large varices (including those which have never bled).
Injection sclerotherapy or band ligation, conducted at weekly intervals
after the initial control of bleeding, is equally effective at obliterating
varices and decreasing the risk of further hemorrhage. Band ligation results
in fewer complications.
Other
newer treatment options for variceal bleeding, such as somatostatin analogs,
transjugular intrahepatic portosystemic shunt and liver transplantation,
offer more optimal approaches to control bleeding and prevent re-bleeding,
but may be prohibitively expensive.
Even
for the most affluent communities, affordability, cost-effectiveness, and
resource rationing are important considerations in management of patients
with cirrhosis complicated by gastrointestinal bleeding.
05/19/03
Source
S Chung. Journal of
Gastroenterology and Hepatology 17(4): 355-360. April 2002.
Available from Blackwell Science. 54 University Street, Carlton South 3053,
Victoria, Australia. +61393470300. Fax +61393475001. E-mail: Rob.Turner@blacksci-asia.com.au.
Website: www.blackwell-science.com.
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Salty Issues
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Author:
Contributing Editor Heidi Gennaro, RD
Author Date: 10/10/2001
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Reducing Salt for Edema, Advanced Cirrhosis
or Ascites
You have just returned from your doctor visit with a frown and a
prescription note in your hand that reads, "make an appointment with the
dietitian regarding a low sodium diet", or maybe a "2 gram sodium, fluid
restricted diet" or even worse a "no-salt diet."
Oh My! You have visions of dull-tasting food and constant deprivation.
Maybe you're a "pour salt on everything" type, or maybe you like "just a
little" salt on certain foods. In either case, you're worried that this
will be a tough road to take.
Why Do I Have to
Watch My Sodium Intake?
If you have edema,
advanced cirrhosis or ascites you need to know the answer
to this question...
Limiting sodium intake to
around 2000 milligrams (2 Grams)per day is important to any person who
has a disease that affects their heart. Why? Sodium retains water in
your body. Think about a sponge...and how much water it can hold. Sodium
acts the same way in your body. It holds on to the water you have in
your system.
If you have pulmonary
hypertension, part of the challenge in managing your disease is to
minimize the "fluid load" on your heart. Taking your "doctor prescribed"
medications, which often include a diuretic, and limiting the amount of
sodium in your diet, will help to decrease the amount of fluid in the
body. Therefore, the stress on your heart will be lessened.
Limiting salt at the table
or in cooking is your first step to controlling the amount of fluid you
retain in your body. And looking carefully for the amount of sodium in
pre-packaged and commercial foods is your second step. If you haven't
already, begin learning the art of 'label reading'. You would be
surprised at how much sodium may be in some of your favorite commercial
foods!
Be cautious about using
products containing "salt, soda, sodium, monosodium glutamate, bisodium
phosphate, baking powder, baking soda, or any other ingredients that
contain the word sodium".The bottom line is how much TOTAL SODIUM per
serving the product contains. Ask yourself: will this work in a 2000
milligram sodium food plan?
Also be careful of certain
medicines that may contain substantial amounts of sodium such as certain
cough medicines, stomach antacids, and laxatives, for example. It is
also a good idea to contact your city water municipality to find out the
sodium content in your drinking water, or having your well water tested
for sodium by a qualified laboratory.
Low Sodium Dining:
Some Practical Tips
Tips to consume less salt
and sodium:
Shop around and choose
grocery stores that offer more choices of lower-sodium foods. Or ask
your local grocer or supermarket to offer more low-sodium foods.
When selecting canned
foods, select those prepared with reduced or no sodium.
Remember that fresh fish,
poultry, and meat are lower in sodium than most canned and processed
ones.
Remember that many frozen
dinners, packaged mixes, canned soups, and salad dressings contain a
considerable amount of sodium.
Remember that condiments
such as soy and many other sauces, pickles, and olives are high in
sodium. Ketchup and mustard, when eaten in large amounts, can also
contribute significant amounts of sodium to the diet. Choose lower
sodium varieties.
Choose fresh fruits and
vegetables as a lower sodium alternative to salted snack foods.
Throw away your
saltshaker! If you salt foods in cooking or at the table, add small
amounts. Salt added to food in cooking or at the table accounts for 1/3
of all the sodium we eat. Yes, you can do it!
Ignore your "salt
tooth"...Of course you can learn to prefer low-sodium food... just by
eating it. Within 2 months, your tastes should adjust, and you won't
miss the salt. Try it!!
Experiment with salt-free
seasonings. Try lemon juice, pepper, onion, parsley, oregano on some of
those foods that you usually salt. Learn to use spices and herbs, rather
than salt, to enhance the flavor of food.
Consult with your doctor
before trying a salt substitute. Many brands contain potassium instead
of sodium and may interact with some of your medications.
Make food from scratch!!
This way you can control the amount of salt that goes into it.
Choose fresh fruits and
veggies. When planning meals, consider that fresh and most plain frozen
vegetables are low in sodium. Be radical: go for five servings a day!
Invest in a low-sodium
cookbook. There are a whole new variety of foods and recipes waiting to
be tested! Don't want to BUY a cookbook---then check one out at your
local library.
Request less salt in your
meals when eating out or traveling.If you dine out often, ask the staff
person if the nutritional information is available on the dish or
take-out fare that you are considering. If not, choose wisely and then
ask that they not ADD any additional salt.
Read the Nutrition Facts
Label to determine the amount of sodium in the foods you purchase. The
sodium content of processed foods -- such as cereals, breads, soups, and
salad dressings -- often varies widely. Get smart with common label
terms:
- 'Sodium free' - less
than 5mg of sodium per serving
- 'Very low sodium' -
35mg or less per serving
- 'Low sodium' - 140mg or
less per serving
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Small esophageal varices in
cirrhotic patients
SourceURL:http://www.gastrohep.com/news/news.asp?id=1868
Endoscopy surveillance should be planned taking into account cause and
degree of liver dysfunction, find researchers in the latest issue of the
Journal of Hepatology.
In this study, researchers from Italy prospectively evaluated 206
cirrhotics during a mean follow up of 37 months. Of these patients, 113
were without varices and 93 with small EV.
Patients with previous gastrointestinal bleeding or receiving any
treatment
for portal hypertension were excluded.
Endoscopy was performed every 12 months.
The research team found that the incidence of EV was 5% at 1 year and
28%
at 3 years.
In addition, the rate of EV progression was 12% at 1 year and 31% at 3
years.
The team identified post-alcoholic origin of cirrhosis, Child-Pugh's
class
B or C, and the finding of red wale marks at first examination, as
predictors for the variceal progression.
The 2-years risk of bleeding from EV was higher in patients with small
varices upon enrolment than in those without varices, 12% versus 2%,
respectively.
Predictor for bleeding was the presence of red wale marks at first
endoscopy.
In addition, predictor for bleeding was the presence of red wale marks
at
first endoscopy.
Dr Manuela Merli's team concluded, "In patients with no or small EV,
endoscopy surveillance should be planned taking into account cause and
degree of liver dysfunction".
In a related editorial in the same publication, Dr Roberto de Franchis
discusses the evaluation and follow-up of patients with cirrhosis and
esophageal varices.
Dr de Franchis considers the results of several studies concerning the
timing of follow-up endoscopies.
Concluding that, "It appears reasonable to maintain the recommended
interval of 1 to 2 years, adopting a shorter interval for patients with
alcoholic cirrhosis".
J Hepatology 2003; 38(3): 266-72
24 February 2003
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Cirrhosis and Bleeding: The Need for Very Early Management
Retrospective studies
suggest that the prognosis of patients with
cirrhosis and variceal hemorrhage has improved in more recent decades.
In a prospective cohort
study in which the choice of prophylactic therapy was left to each
practitioner, French researchers followed cirrhotic patients with
medium/large varices to determine factors predictive of bleeding and death.
Three hundred fourteen
patients with grades 2 or 3 esophageal varices (Child A and B/C: 218 and 96)
were enrolled at multiple medical centers.
One hundred seventy-three
patients had no previous history of variceal bleeding. Only 245 patients
(100% of patients with prior variceal hemorrhage, 61% of patients without
prior hemorrhage) were receiving some form of prophylactic therapy. The
median follow-up was 18 months.
There were 76 bleeding
events and 14 related deaths (18%); nine of these deaths occurred within 24
h of bleeding onset (two at home, two during hospital transfer, and five in
hospital, a mean of 2.5 h after onset; six involved Child C patients).
Twenty-five deaths were
not due to bleeding but were closely related to cirrhosis. In a Cox model,
the presence of tense ascites) and a prior history of hemorrhage were
independent predictors of variceal hemorrhage.
In patients without a
prior history of bleeding, bleeding risk was higher with more prolonged
prothrombin time and lower when patients were receiving propranolol.
The authors conclude,
“Despite the advent of effective drugs and endoscopic therapy for variceal
bleeding, about a quarter of deaths occur very early after bleeding onset,
confirming the need for rapid specific management.”
10/22/03
Reference
D Nidegger and
others. Cirrhosis and bleeding: the need for very early management.
Journal of Hepatology
39(4): 509-514. October 2003.
American Journal of Medicine February 15,
2003
Do Ammonia Levels Correlate with Hepatic Encephalopathy?
Hepatic encephalopathy in patients with chronic liver
dysfunction is believed to be caused by a failure of the liver to clear
toxic products from the stomach. The exact toxins that cause hepatic
encephalopathy have not been established, but ammonia may be involved.
Many physicians determine ammonia levels to diagnose
hepatic encephalopathy and as a guide to treatment. However, studies have
shown that the correlation between serum ammonia levels and severity of
hepatic encephalopathy is inconsistent.
A recent study suggested that the partial pressure of
ammonia may correlate more closely with the severity of hepatic
encephalopathy than the total plasma ammonia level.
Ong and associates evaluated the correlation between
plasma ammonia levels and the severity of hepatic encephalopathy. They also
determined the best of the four types of ammonia measurements for this
correlation by comparing arterial total ammonia, venous total ammonia,
arterial partial pressure of ammonia, and venous partial pressure of
ammonia.
Consecutive patients who were admitted to a tertiary
care center with the diagnosis of cirrhosis between September 1998 and
December 1999 were enrolled in the study. The diagnosis of cirrhosis was
established by biopsy or by signs of portal hypertension such as
gastroesophageal varices, previous variceal bleeding, or ascites.
Researchers collected clinical and laboratory data at the time of admission.
The mental status of the patients was assessed using the West Haven Criteria
for grading of mental status. A diagnosis of hepatic encephalopathy was
established when the patients' mental status was altered and other causes of
mental status changes had been excluded. After diagnosis, fasting arterial
and venous blood samples were obtained, and total ammonia and partial
pressure of ammonia were determined.
The 121 patients who were enrolled in the study had the
following West Haven Criteria grades: 30 patients (25 percent) had grade
zero encephalopathy; 27 patients (22 percent) had grade 1; 23 patients (19
percent) had grade 2; 28 patients (23 percent) had grade 3; and 13 patients
(11 percent) had grade 4. All four measurements of ammonia increased with
the severity of hepatic encephalopathy. The arterial total ammonia level had
the highest correlation, but it was not statistically significant. Other
variables that had a correlation to the severity of hepatic encephalopathy
included International Normalized Ratio (INR) values, serum creatinine
levels, bilirubin levels, and lactulose use. A multivariable ordered
logistic regression analysis revealed that only serum ammonia levels and INR
values were independently associated with the severity of hepatic
encephalopathy.
The authors conclude that venous total ammonia levels
do correlate with severity of hepatic encephalopathy and should be adequate
in evaluating patients with this condition. Total arterial ammonia levels
and partial pressure of ammonia levels had similar correlation but did not
prove to be better markers than venous total ammonia levels.
KARL E. MILLER, M.D.
Ong JP, et al. Correlation between ammonia levels and the
severity of hepatic encephalopathy. Am J Med February 15, 2003;114:188-93.
http://www.aafp.org/afp/20031001/tips/8.html
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