Non diabetic 67 years old patient Mohammad Abdul mannan admitted to Kasr
al Ainy hospital two weeks ago and complaining of abdominal distension with mild
pain, both lower limbs swelling extended to and above knee; left and right knee
respectively, and blurring of vision with yellowish discoloration of sclera of
both eyes one month ago. On patient physical examination show: 1. Ascites with
shifting dullness, 2. no hepatosplenomegaly felt due to obese patient with
marked Ascites, 3. jaundice, and 4. no other sign on psychical examination e.g.
dilated veins over abdomen especially around umbilicus and around frank of
abdomen. in the first day of admission, administer two pack of blood
transfusion, one in the first day and another on second or few days later. Pictures
show the sign below.
To diagnose or understand this case, you need to read the
article below:
Edema is an abnormal accumulation of fluid in the
interstesium, located beneath the skin and cavities of the body including
abdomen due to either 1. Increased
hydrostatic pressure;
2. Reduced oncotic pressure within blood vessels;
3. increased tissue oncotic pressure;
4. Increased blood vessel wall permeability e.g.
inflammation;
5. Obstruction of fluid clearance in the lymphatic system;
6. Changes in the water retaining properties of the tissues themselves.
Raised hydrostatic pressure often reflects retention of water and sodium by the
kidney; and 7. All of these due to either portal hypertension or hepatic cells
failure due to most common in Egypt HCV. You should remember, if there is
dilated vein around umbilicus and Melena or hematemasis suggest portal
hypertension results edema.
There are three differential diagnoses for this case, a.
hepatocelular failure, b. nepheotic syndrome, hypoalbuminemea and d. right sided
heart failure. About liver cell failure: Etiology is hepatitis C virus most
probably in this case due to HCV is more common in Egypt. Hepatitis C is an
infectious disease affecting primarily the liver, caused by the hepatitis C
virus. The infection is often asymptomatic, but chronic infection can lead to
scarring of the liver and ultimately to cirrhosis, which is generally apparent
after many years. In some cases, those with cirrhosis will go on to develop
liver failure, liver cancer, or life-threatening esophageal and gastric varices.
HCV is spread primarily by blood-to-blood contact associated
with intravenous drug use, poorly sterilized medical equipment, and
transfusions. An estimated 150–200 million
people worldwide are infected with hepatitis C. The existence of hepatitis C
(originally identifiable only as a type of non-A non-B hepatitis) was suggested
in the 1970s and proven in 1989.Hepatitis C infects only humans and
chimpanzees. It is one of five known hepatitis viruses: A, B, C, D, and E.
The virus persists in the liver in about 85% of those
infected. This chronic infection can be treated with medication: the standard
therapy is a combination of peginterferon and ribavirin, with either boceprevir
or telaprevir added in some cases. Overall, 50–80% of people treated are cured. Those who develop
cirrhosis or liver cancer may require a liver transplant. Hepatitis C is the
leading reason for liver transplantation, though the virus usually recurs after
transplantation. No vaccine against hepatitis C is available.
Mode of transmission:
In the beginning of HCV transmission in Egypt was due to
careless use of intravenous syringe and not wearing hand gloves during blood
sample taking.
The primary route of transmission in the developed world is
intravenous drug use (IDU), while in the developing world the main methods are
blood transfusions and unsafe medical procedures. The cause of transmission
remains unknown in 20% of cases; however, many of these are believed to be
accounted for by IDU.
Intravenous drug use:
IDU is a major risk factor for hepatitis C in many parts of
the world. Of 77 countries reviewed, 25 (including the United States) were
found to have prevalence’s of hepatitis C in the intravenous drug user
population of between 60% and 80%. Twelve countries had rates greater than 80%.
It is believed that ten million intravenous drug users are infected with
hepatitis C; China (1.6 million), the United States (1.5 million),
and Russia (1.3 million) have the highest absolute totals. Occurrence of
hepatitis C among prison inmates in the United States is 10 to 20 times that of
the occurrence observed in the general population; this has been attributed to
high-risk behavior in prisons such as IDU and tattooing with no sterile
equipment.
Healthcare exposure
Blood transfusion, transfusion of blood products, or organ
transplants without HCV screening carry significant risks of infection. The
United States instituted universal screening in 1992 and Canada instituted
universal screening in 1990. This decreased the risk from one in 200 units to
between one in 10,000 to one in 10,000,000 per unit of blood. This low risk
remains as there is a period of about 11–70 days
between the potential blood donor's acquiring hepatitis C and the blood's
testing positive depending on the method. Some countries do not screen for
hepatitis C due to the cost.
Those who have experienced a needle stick injury from
someone who was HCV positive have about a 1.8% chance of subsequently
contracting the disease themselves.[9] The risk is greater if the needle in
question is hollow and the puncture wound is deep.[19] There is a risk from
mucosal exposures to blood; but this risk is low, and there is no risk if blood
exposure occurs on intact skin.
Hospital equipment has also been documented as a method of
transmission of hepatitis C, including reuse of needles and syringes;
multiple-use medication vials; infusion bags; and improperly sterilized
surgical equipment, among others.[19] Limitations in the implementation and
enforcement of stringent standard precautions in public and private medical and
dental facilities are known to be the primary cause of the spread of HCV in
Egypt, the country with highest rate of infection in the world.
Sexual intercourse
Whether hepatitis C can be transmitted through sexual
activity is controversial. While there is an association between high-risk
sexual activity and hepatitis C, and multiple sexual partners are a risk factor
for hepatitis C, there is no conclusive evidence that hepatitis C can be
transmitted by sexual activity, since people who report transmission with sex
as their only risk factor may actually have used drugs but denied it. The
majority of evidence supports there being no risk for monogamous heterosexual
couples. Sexual practices that involve higher levels of trauma to the
anogenital mucosa, such as anal penetrative sex, or that occur when there is a
concurrent sexually transmitted infection, including HIV or genital ulceration,
do present a risk. The United States Department of Veterans Affairs recommends
condom use to prevent hepatitis C transmission in those with multiple partners,
but not those in monogamous relationships.
Body modification
Tattooing is associated with two to threefold increased risk
of hepatitis C. This can be due to either improperly sterilized equipment or
contamination of the dyes being used.Tattoos or piercings performed either
before the mid-1980s, "underground," or nonprofessionally are of
particular concern, since sterile techniques in such settings may be lacking.
The risk also appears to be greater for larger tattoos.[56] It is estimated
that nearly half of prison inmates share unsterilized tattooing equipment.[56]
It is rare for tattoos in a licensed facility to be directly associated with
HCV infection.
Shared personal items
Personal-care items such as razors, toothbrushes, and
manicuring or pedicuring equipment can be contaminated with blood. Sharing such
items can potentially lead to exposure to HCV. Appropriate caution should be
taken regarding any medical condition that results in bleeding, such as cuts
and sores. HCV is not spread through casual contact, such as hugging, kissing,
or sharing eating or cooking utensils. Neither is it transmitted through food
or water.
Vertical transmission
Vertical transmission of hepatitis C from an infected mother
to her child occurs in less than 10% of pregnancies. There are no measures that
alter this risk. It is not clear when transmission occurs during pregnancy, but
it may occur both during gestation and at delivery. A long labor is associated
with a greater risk of transmission. There is no evidence that breast-feeding
spreads HCV; however, to be cautious, an infected mother is advised to avoid
breastfeeding if her nipples are cracked and bleeding, or if her viral loads are high.
Sign and symptoms:
Acute infection
Hepatitis C infection causes acute symptoms in 15% of cases.
Symptoms are generally mild and vague, including a decreased appetite, fatigue,
nausea, muscle or joint pains, and weight loss and rarely does acute liver
failure result loss Most cases of acute infection are not associated with
jaundice. The infection resolves spontaneously in 10–50% of cases, which occurs more frequently in
individuals who are young and female.
Chronic infection
About 80% of those exposed to the virus develop a chronic
infection. This is defined as the presence of detectable viral replication for
at least six months. Most experience minimal or no symptoms during the initial
few decades of the infection. Chronic hepatitis C can be associated with
fatigue and mild cognitive problems. Chronic infection after several years may
cause cirrhosis or liver cancer. The liver enzymes are normal in 7–53%. Late relapses after
apparent cure have been reported, but these can be difficult to distinguish
from reinfection.
Fatty changes to the liver occur in about half of those
infected and are usually present before cirrhosis develops. Usually (80% of the
time) this change affects less than a third of the liver. Worldwide hepatitis C
is the cause of 27% of cirrhosis cases and 25% of hepatocellular carcinoma. About
10–30% of those infected develop
cirrhosis over 30 years. Cirrhosis is more common in those also infected
with hepatitis B, schistosoma, or HIV, in alcoholics and in those of male
gender. In those with hepatitis C, excess alcohol increases the risk of
developing cirrhosis 100-fold. Those who develop cirrhosis have a 20-fold
greater risk of hepatocellular carcinoma. This transformation occurs at a rate
of 1–3% per year. Being infected
with hepatitis B in addition to hepatitis C increases this risk further.
Liver cirrhosis may lead to portal hypertension, ascites
(accumulation of fluid in the abdomen), easy bruising or bleeding, varices
(enlarged veins, especially in the stomach and esophagus), jaundice, and a
syndrome of cognitive impairment known as hepatic encephalopathy. Ascites
occurs at some stage in more than half of those who have a chronic infection.
Acute infection
Hepatitis C infection causes acute symptoms in 15% of cases.
Symptoms are generally mild and vague, including a decreased appetite, fatigue,
nausea, muscle or joint pains, and weight loss and rarely does acute liver
failure result. Most cases of acute infection are not associated with jaundice.The
infection resolves spontaneously in 10–50%
of cases, which occurs more frequently in individuals who are young and female.
Chronic infection
About 80% of those exposed to the virus develop a chronic
infection. This is defined as the presence of detectable viral replication for
at least six months. Most experience minimal or no symptoms during the initial
few decades of the infection. Chronic hepatitis C can be associated with
fatigue and mild cognitive problems. Chronic infection after several years may
cause cirrhosis or liver cancer.The liver enzymes are normal in 7–53%. Late relapses after
apparent cure have been reported, but these can be difficult to distinguish
from reinfection.
Fatty changes to the liver occur in about half of those
infected and are usually present before cirrhosis develops. Usually (80% of the
time) this change affects less than a third of the liver. Worldwide hepatitis C
is the cause of 27% of cirrhosis cases and 25% of hepatocellular carcinoma. About
10–30% of those infected develop
cirrhosis over 30 years. Cirrhosis is more common in those also infected
with hepatitis B, schistosoma, or HIV, in alcoholics and in those of male
gender. In those with hepatitis C, excess alcohol increases the risk of
developing cirrhosis 100-fold. Those who develop cirrhosis have a 20-fold
greater risk of hepatocellular carcinoma. This transformation occurs at a rate
of 1–3% per year. Being infected
with hepatitis B in addition to hepatitis C increases this risk further.
Liver cirrhosis may lead to portal hypertension, Ascites
(accumulation of fluid in the abdomen), easy bruising or bleeding, varices
(enlarged veins, especially in the stomach and esophagus), jaundice, and a
syndrome of cognitive impairment known as hepatic encephalopathy. Ascites
occurs at some stage in more than half of those who have a chronic infection.
Acute infection
Hepatitis C infection causes acute symptoms in 15% of cases.
Symptoms are generally mild and vague, including a decreased appetite, fatigue,
nausea, muscle or joint pains, and weight loss[9] and rarely does acute liver
failure result. Most cases of acute infection are not associated with jaundice.
The infection resolves spontaneously in 10–50%
of cases, which occurs more frequently in individuals who are young and female.
Chronic infection
About 80% of those exposed to the virus develop a chronic
infection. This is defined as the presence of detectable viral replication for
at least six months. Most experience minimal or no symptoms during the initial
few decades of the infection. Chronic hepatitis C can be associated with
fatigue and mild cognitive problems. Chronic infection after several years may
cause cirrhosis or liver cancer. The liver enzymes are normal in 7–53%. Late relapses after
apparent cure have been reported, but these can be difficult to distinguish
from reinfection.
Fatty changes to the liver occur in about half of those
infected and are usually present before cirrhosis develops. Usually (80% of the
time) this change affects less than a third of the liver. Worldwide hepatitis C
is the cause of 27% of cirrhosis cases and 25% of hepatocellular carcinoma. About
10–30% of those infected develop
cirrhosis over 30 years. Cirrhosis is more common in those also infected
with hepatitis B, schistosoma, or HIV, in alcoholics and in those of male
gender.[9] In those with hepatitis C, excess alcohol increases the risk of
developing cirrhosis 100-fold. Those who develop cirrhosis have a 20-fold
greater risk of hepatocellular carcinoma. This transformation occurs at a rate
of 1–3% per year. Being infected
with hepatitis B in addition to hepatitis C increases this risk further.
Liver cirrhosis may lead to portal hypertension, ascites
(accumulation of fluid in the abdomen), easy bruising or bleeding, varices
(enlarged veins, especially in the stomach and esophagus), jaundice, and a
syndrome of cognitive impairment known as hepatic encephalopathy. Ascites
occurs at some stage in more than half of those who have a chronic infection.
Acute infection
Hepatitis C infection causes acute symptoms in 15% of cases.
Symptoms are generally mild and vague, including a decreased appetite, fatigue,
nausea, muscle or joint pains, and weight loss[9] and rarely does acute liver
failure result. Most cases of acute infection are not associated with jaundice.
The infection resolves spontaneously in 10–50%
of cases, which occurs more frequently in individuals who are young and female.
Chronic infection
About 80% of those exposed to the virus develop a chronic
infection. This is defined as the presence of detectable viral replication for
at least six months. Most experience minimal or no symptoms during the initial
few decades of the infection. Chronic hepatitis C can be associated with
fatigue and mild cognitive problems. Chronic infection after several years may
cause cirrhosis or liver cancer. The liver enzymes are normal in 7–53%. Late relapses after
apparent cure have been reported, but these can be difficult to distinguish
from reinfection.
Fatty changes to the liver occur in about half of those
infected and are usually present before cirrhosis develops. Usually (80% of the
time) this change affects less than a third of the liver. Worldwide hepatitis C
is the cause of 27% of cirrhosis cases and 25% of hepatocellular carcinoma. About
10–30% of those infected develop
cirrhosis over 30 years. Cirrhosis is more common in those also infected
with hepatitis B, schistosoma, or HIV, in alcoholics and in those of male
gender. In those with hepatitis C, excess alcohol increases the risk of
developing cirrhosis 100-fold. Those who develop cirrhosis have a 20-fold
greater risk of hepatocellular carcinoma. This transformation occurs at a rate
of 1–3% per year. Being infected
with hepatitis B in addition to hepatitis C increases this risk further.
Liver cirrhosis may lead to portal hypertension, Ascites
(accumulation of fluid in the abdomen), easy bruising or bleeding, varices
(enlarged veins, especially in the stomach and esophagus), jaundice, and a
syndrome of cognitive impairment known as hepatic encephalopathy. Ascites
occurs at some stage in more than half of those who have a chronic infection.
Acute infection
Hepatitis C infection causes acute symptoms in 15% of cases.
Symptoms are generally mild and vague, including a decreased appetite, fatigue,
nausea, muscle or joint pains, and weight loss and rarely does acute liver failure
result.[10] Most cases of acute infection are not associated with jaundice. The
infection resolves spontaneously in 10–50%
of cases, which occurs more frequently in individuals who are young and female.
Chronic infection
About 80% of those exposed to the virus develop a chronic
infection. This is defined as the presence of detectable viral replication for
at least six months. Most experience minimal or no symptoms during the initial
few decades of the infection. Chronic hepatitis C can be associated with
fatigue and mild cognitive problems. Chronic infection after several years may
cause cirrhosis or liver cancer. The liver enzymes are normal in 7–53%. Late relapses after
apparent cure have been reported, but these can be difficult to distinguish
from reinfection.
Fatty changes to the liver occur in about half of those
infected and are usually present before cirrhosis develops. Usually (80% of the
time) this change affects less than a third of the liver. Worldwide hepatitis C
is the cause of 27% of cirrhosis cases and 25% of hepatocellular carcinoma. About
10–30% of those infected develop
cirrhosis over 30 years. Cirrhosis is more common in those also infected
with hepatitis B, schistosoma, or HIV, in alcoholics and in those of male
gender. In those with hepatitis C, excess alcohol increases the risk of
developing cirrhosis 100-fold. Those who develop cirrhosis have a 20-fold
greater risk of hepatocellular carcinoma. This transformation occurs at a rate
of 1–3% per year. Being infected
with hepatitis B in addition to hepatitis C increases this risk further.
Liver cirrhosis may lead to portal hypertension, Ascites
(accumulation of fluid in the abdomen), easy bruising or bleeding, varices
(enlarged veins, especially in the stomach and esophagus), jaundice, and a
syndrome of cognitive impairment known as hepatic encephalopathy. Ascites
occurs at some stage in more than half of those who have a chronic infection.
Diagnosis:
There are a number of diagnostic tests for hepatitis C,
including HCV antibody enzyme immunoassay or ELISA, recombinant immunoblot
assay, and quantitative HCV RNA polymerase chain reaction (PCR). HCV RNA can be
detected by PCR typically one to two weeks after infection, while antibodies can
take substantially longer to form and thus be detected.
Chronic hepatitis C is defined as infection with the
hepatitis C virus persisting for more than six months based on the presence of
its RNA. Chronic infections are typically asymptomatic during the first few
decades, and thus are most commonly discovered following the investigation of
elevated liver enzyme levels or during a routine screening of high-risk
individuals. Testing is not able to distinguish between acute and chronic
Diagnosis in the infant is difficult as maternal antibodies may persist for up
to 18
Serology
Hepatitis C testing typically begins with blood testing to
detect the presence of antibodies to the HCV, using an enzyme immunoassay. If
this test is positive, a confirmatory test is then performed to verify the
immunoassay and to determine the viral load. An INFECTION a recombinant
immunoblot assay is used to verify the immunoassay and the viral load is
determined by a HCV RNA polymerase chain reaction. If there are no RNA and the
immunoblot is positive, it means that the person tested had a previous
infection but cleared it either with treatment or spontaneously; if the
immunoblot is negative, it means that the immunoassay was wrong. It takes about
6–8 weeks following infection
before the immunoassay will test positive. A number of tests are available as
point of care testing which means that results are available within
30 minutes.
Liver enzymes are variable during the initial part of the
infection and on average begin to rise at seven weeks after infection. The
elevation of liver enzymes does not closely follow disease severity.
Biopsy
Liver biopsies are used to determine the degree of liver
damage present; however, there are risks from the procedure. The typical
changes seen are lymphocytes within the parenchyma, lymphoid follicles in
portal triad, and changes to the bile ducts. There are a number of blood tests
available that try to determine the degree of hepatic fibrosis and alleviate
the need for biopsy.
Screening
It is believed that only 5–50%
of those infected in the United States and Canada are aware of their status. Testing
is recommended in those at high risk, which includes injection drug users,
those who have received blood transfusions before 1992, those who have been in
jail, those on long term hemodialysis, and those with tattoos.[56] Screening is
also recommended in those with elevated liver enzymes, as this is frequently
the only sign of chronic hepatitis. Routine screening is not currently
recommended in the United States. In 2012, the U.S. Centers for Disease Control
and Prevention (CDC) added a recommendation for a single screening test for
those born between 1945 and 1965.
Treatment:
HCV induces chronic infection in 50–80% of infected persons. Approximately 40–80% of these clear with
treatment. In rare cases, infection can clear without treatment. Those with
chronic hepatitis C are advised to avoid alcohol and medications toxic to the
liver, and to be vaccinated for hepatitis A and hepatitis B. Ultrasound
surveillance for hepatocellular carcinoma is recommended in those with
accompanying cirrhosis.
Medications
In general, treatment is recommended for those with proven
HCV infection and signs of liver inflammation. As of 2010, treatments consist
of a combination of pegylated interferon alpha and the antiviral drug ribavirin
for a period of 24 or 48 weeks, depending on HCV genotype. This produces cure
rates of between 70 and 80% for genotype 2 and 3, respectively, and 45 to 70%
for other genotypes. When combined with ribavirin, pegylated
interferon-alpha-2a may be superior to pegylated interferon-alpha-2b, though
the evidence is not strong.
Combining either boceprevir or telaprevir with ribavirin and
peginterferon alfa improves antiviral response for hepatitis C genotype 1. Adverse
effects with treatment are common, with half of people getting flu like
symptoms and a third experiencing emotional problems. Treatment during the
first six months is more effective than once hepatitis C has become chronic. If
someone develops a new infection and it has not cleared after eight to twelve
weeks, 24 weeks of pegylated interferon is recommended. In people with
thalassemia, ribavirin appears to be useful but increases the need for
transfusions.
Sofosbuvir with ribavirin and interferon appears to be
around 90% effective in those with genotype 1, 4, 5, or 6 disease. Sofosbuvir
with just ribavirin appears to be 70 to 95% effective in type 2 and 3 disease
but has a higher rate of adverse effects. Treatments that contain ledipasvir
and sofosbuvir for genotype 1 has success rates of around 93 to 99% but is very
expensive. In genotype 6 infection, pegylated interferon and ribavirin is
effective in 60 to 90% of cases. There is some tentative data for simeprevir
use in type 6 disease as well.
Surgery
Cirrhosis due to hepatitis C is a common reason for liver
transplantation though the virus usually (80–90%
of cases) recurs afterwards. Infection of the graft leads to 10–30% of people developing
cirrhosis within five years. Treatment with pegylated interferon and ribavirin
post transplant decreases the risk of recurrence to 70%.
Alternative medicine
Several alternative therapies are claimed by their
proponents to be helpful for hepatitis C including milk thistle, ginseng, and
colloidal silver. However, no alternative therapy has been shown to improve
outcomes in hepatitis C, and no evidence exists that alternative therapies have
any effect on the virus at all
Prevention:
As of 2011, no vaccine protects against contracting
hepatitis C. However, there are a number under development and some have shown
encouraging results. A combination of harm reduction strategies, such as the
provision of new needles and syringes and treatment of substance use, decreases
the risk of hepatitis C in intravenous drug users by about 75%. The screening
of blood donors is important at a national level, as is adhering to universal
precautions within healthcare facilities. In countries where there is an
insufficient supply of sterile syringes, medications should be given orally
rather than via injection (when possible) (from Wikipedia about HCV).
About nephrotic syndrome, hypoalbuminemia, and right sided
heart failure are excluded by history, sign, symptoms, and confirm the HCV by
its specific test.
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