4. EPIDEMIOLOGY
īĸ Â It is thought to account for 5 to 10
percent of patients with portal
hypertension in developed countries
īĸ And up to one third of patients in
developing countries
6. īĸ The portal vein drains blood from the
small and large intestines, stomach,
spleen, pancreas, and gallbladder.
īĸ The superior mesenteric vein and the
splenic vein unite behind the neck of the
pancreas to form the portal vein.
īĸ The portal trunk divides into 2 lobar
veins:-
īŧ right branch
īŧ left branch
7. īĸ . The right branch drains the cystic vein,
and the left branch receives the umbilical
and paraumbilical veins that enlarge to
form umbilical varices in portal
hypertension.
īĸ The left gastric vein (formerly, gastric
coronary vein), which runs along the
lesser curvature of the stomach, receives
distal esophageal veins, which also
enlarge in portal hypertension
14. īĸ TwoIMPORTANTÂ factorsâvascular resistance
and blood flowâexist in the development of
portal hypertension.
īĸ Ohm law is V = IR, where V is voltage, I is
current, and R is resistance.
īĸ This can be applied to vascular flow; ie, P = FR,
where P is the pressure gradient through the
portal venous system, F is the volume of blood
flowing through the system, and R is the
resistance to flow.
īĸ Changes in either F or R affect the pressure,
although in most types of portal hypertension,
both of these are altered.
15. īĸ Normal portal pressure is generally considered to
be between 5 and 10 mm Hg.
īĸ Once the portal pressure rises to 12 mm Hg or
greater, complications can arise, such as varices
 and ascites.
īĸ Indeed, esophageal varices are responsible for
the main complication of portal hypertension,
massive upper gastrointestinal (GI) hemorrhage.
16.
17.
18. SIGNS AND SYMPTOMS
īĸ Gastrointestinal hemorrhage may be the initial
presenting symptom
īĸ Ascites
īĸ hepatic encephalopathy
īĸ jaundice
īĸ coagulopathy, or spider angiomata.
īĸ Patients who are hemodynamically stable may
have warm skin
īĸ hyperdynamic pulses
īĸ low systolic blood pressures
19.
20. DIAGNOSTIC TEST
īĸ Complete history of patient
īĸ Physical examination
īĸ Various lab tests
īĸ Hepatic Venous Pressure Gradient measurement
has been accepted as the gold standard for
assessing the severity of portal hypertension
(<5mmHg)
īĸ X-ray tests
īĸ Endoscopic testÂ
īĸ doppler ultrasonography
21. MANAGEMENT
īĸ treatment depends on the severity of the
symptoms
īĸ GOAL-
īĸ To treat symptomatic causes
īĸ To prevent complication
22. Endoscopic
therapy.Â
īĸ This is usually the
first line of
treatment for
variceal bleeding
and consists of
either banding or
sclerotherapy
23. BANDING=
īĸ Banding is a procedure
in which a
gastroenterologist uses
rubber bands to block
off the blood vessel to
stop bleeding.
24.
25. SCLEROTHERAPY
īĸ Sclerotherapy is occasionally used when banding
cannot be used and is a procedure in which a
blood-clotting solution is injected into the
bleeding varices to stop bleeding.
26.
27. īĸ Medications.
īĸ  Nonselective beta-blockers (nadolol orÂ
propranolol) may be prescribed alone or in
combination with endoscopic therapy to reduce
the pressure in varices and further reduce the
risk of bleeding
īĸ The drug lactulose can help treat confusion and
other mental changes associated with
encephalopathy
29. Transjugular
intrahepatic
portosystemic shunt
(TIPS):Â
īĸ This procedure involves
placing a stent (a tubular
device) in the middle of the
liver.
īĸ The stent connects the
hepatic vein with the portal
vein, which reroutes blood
flow in the liver and helps
relieve pressure in abnormal
veins.
30. Distal splenorenal
shunt (DSRS):Â
īĸ This procedure connects
the vein from your
spleen to the vein from
the left kidney in order
to reduce pressure in
the varices and control
bleeding.
31.
32. īĸ Liver transplant . This is done in cases of end-
stage liver disease.
īĸ Devascularization. A surgical procedure
that removes the bleeding varices; this procedure
is done when a TIPS or a surgical shunt is not
possible or is unsuccessful in controlling the
bleeding.
īĸ Paracentesis. This is a procedure in which the
accumulation of fluid in the abdomen (ascites) is
directly removed. The results are usually
temporary and the procedure will need to be
repeated as needed.
35. DEFINITION
īĸ Cirrhosis is the scarring
of the liver - hard scar
tissue replaces soft
healthy tissue.
īĸ As cirrhosis becomes
worse, the liver will have
less healthy tissue. If
cirrhosis is not treated,
the liver will fail and will
not be able to work well
or at all.
36. PATHOPHYSIOLOGY
īĸ Regenerative process is disorganized, resulting in
abnormal blood vessel and bile duct from fibrosis
īĸ Normal lobular structure distorted by fibrotic
connective tissue
īĸ Lobules are irregular in size and shape with
impaired vascular flow
īĸ Insidious, prolonged course
40. SYMPTOMS
īĸ Loss of appetite
īĸ Tiredness
īĸ Nausea
īĸ Weight loss
īĸ Abdominal pain
īĸ Spider-like blood vessels
īĸ Severe itching
41.
42. īĸ Bilirubin> 2mg/dl to 40 mg/dl
īĸ AST, ALT, alkaline phosphatase
ī Aid in early diagnosis, prognosis, and response
to treatment
ī â ALkPo > 3 times normal indicate billiray
disease
43. Albumin
īĸ (non-specific protein) & Factor V and VII
(specific proteins) can provide information on
the functional capacity of the liver
īĸ Low albumin < 3 that does not respond to
therapy is bad prognosis
44. īĸPT
ī Prolongation due to impaired synthesis of
vitamin K dependant clotting factors
ī No response to VIT K is poor prognosis
īĸBUN
ī < 5 due to inadequate protein intake and
depressed hepatic capacity for urea synthesis
īĸBiopsy
ī Confirm the presence of cirrhosis
45.
46.
47. MANAGEMENT
Drug Therapy
īĸ There is no specific drug therapy for cirrhosis
īĸ Drugs are used to treat symptoms and
complications of advanced liver disease
48. NUTRITIONAL THERAPY
īĸ Diet for patient without complications:
ī High in calories
ī â CHO
ī Moderate to low fat
ī Amount of protein varies with degree of liver damage
īĸ Patient with hepatic encephalopathy
ī Very low to no-protein diet
īĸ Low sodium diet for patient with ascites and
edema
50. NURSING DIAGNOSES
īĸ Imbalanced nutrition: less than body
requirements related to inadequate diet
īĸ Ineffective breathing pattern related to intra-
abdominal fluid collection
īĸ Excess fluid volume related to increased sodium
and water intake
īĸ Risk for injury related to altered clotting factors
51. Overall goals:
ī Relief of discomfort
ī Minimal to no complications
ī Return to as normal a lifestyle as possible
52. 1. IMBALANCED NUTRITION: LESS THAN
BODY REQUIREMENTS
īĸ Measure dietary intake by calorie count.
īĸ Encourage patient to eat all meals including
supplementary feedings.
īĸ Restrict intake of caffeine, gas-producing or spicy
and excessively hot or cold foods.
īĸ Recommend cessation of smoking. Provide
teaching on the possible negative effects of
smoking.
īĸ Maintain NPO status when indicated.
īĸ Provide tube feedings, TPN, lipids if indicated.
53. 2. INEFFECTIVE BREATHING
PATTERN
īĸ Monitor respiratory rate, depth, and effort
īĸ Keep head of bed elevated. Position on sides.
īĸ Encourage frequent repositioning and deep-
breathing exercises and coughing exercises.
īĸ Monitor serial ABGs, pulse oximetry, vital
capacity measurements, chest x-rays.
īĸ Provide supplemental O2Â as indicated.
īĸ Demonstrate and assist with respiratory
adjuncts: incentive spirometer.
54. 3. EXCESS FLUID VOLUME RELATED TO
INCREASED SODIUM AND WATER
INTAKE
īĸ Measure I&O, weigh daily, and note gain of more
than 0.5 kg/day.
īĸ Measure abdominal girth.
īĸ Restrict sodium and fluids as indicated.
īĸ Auscultate lungs, noting diminished breath
sounds and developing adventitious sounds.
īĸ Monitor for cardiac dysrhythmias. Auscultate
heart sounds, noting development of S3/S4Â gallop
rhythm.
55. 4. RISK FOR INJURY
īĸ Observe for presence of petechiae,
ecchymosis, bleeding from one or more sites.
īĸ Monitor pulse, BP , Closely assess for signs and
symptoms of GIÂ bleeding
īĸ Encourage use of soft toothbrush, electric razor,
avoiding straining for stool, vigorous nose
blowing
īĸ Use small needles for injections. Apply pressure
to small bleeding and venipuncture sites for
longer than usual.
īĸ Advice to avoid aspirin-containing products.
56. HEALTH EDUCATION AND
DISCHARGE TEACHING
īĸ Do not use alcohol or street drugs.
īĸ Do not take any over-the-counter or prescription
drugs or herbal medicines without first
consulting your doctor or nurse. (Some
medications may make liver disease worse.)
īĸ Follow the dietary guidelines given by
your health care provider, including eating a low-
sodium (salt) diet. You will probably be required
to consume no more than 2 grams of sodium per
day. Reduced protein intake may be required if
confusion is a symptom.
58. LIVER FAILURE
īĸ Liver failure occurs when large parts of
the liver become damaged beyond repair and
the liver is no longer able to function.
īĸ Liver failure is a life-threatening condition that
demands urgent medical care. Most often, liver
failure occurs gradually and over many years.
However, a more rare condition known as acute
liver failure occurs rapidly (in as little as 48
hours) and can be difficult to detect initially.
59. WHAT CAUSES LIVER FAILURE?
The most common causes of chronic liver failure
(where the liver fails over months to years)
include:
īĸ Hepatitis B
īĸ Hepatitis C
īĸ Long-term alcohol consumption
īĸ Cirrhosis
īĸ Hemochromatosis (an inherited disorder that
causes the body to absorb and store too much
iron)
īĸ Malnutrition
60. īĸ The causes of acute liver failure, when the liver
fails rapidly, however, are often different. These
include:
īĸ Acetaminophen (Tylenol) overdose
īĸ Viruses including hepatitis A, B, and C
(especially in children)
īĸ Reactions to certain prescription and
herbal medications
īĸ Ingestion of poisonous wild mushrooms
61. SIGNS AND SYMPTOMS
Early symptoms include:
īĸ Nausea
īĸ Loss of appetite
īĸ Fatigue
īĸ Diarrhea
62. LATER SYMPTOMS
īĸ Jaundice
īĸ Bleeding easily
īĸ Swollen abdomen
īĸ Mental disorientation or confusion (known as
hepatic encephalopathy)
īĸ Sleepiness
īĸ Coma
63. īĸ How Is Liver Failure Treated?
īĸ If detected early enough, acute liver failure caused by
an overdose of acetaminophen can sometimes be
treated and its effects reversed.
īĸ Likewise, if a virus causes liver failure, supportive
care can be given at a hospital to treat the symptoms
until the virus runs its course. In these cases, the liver
will sometimes recover on its own.
īĸ For liver failure that is the result of long-term
deterioration, the initial treatment goal may be to save
whatever part of the liver is still functioning. If this is
not possible, then a liver transplant is required.
Fortunately, liver transplant is a common procedure
that is often successful.
64. LIVER TRANSPLANT
īĸ A liver transplant is the process of replacing a
sick liver with a donated, healthy liver.
Liver transplants require that the blood type and
body size of the donor match the person
receiving the transplant.
īĸ Donated livers come from living and non-living
donors. Liver transplant surgery usually takes
between four and twelve hours. Most patients
stay in the hospital for up to three weeks after
surgery.Â
65. THE PROCESS TO BE ELIGIBLE FOR A
LIVER TRANSPLANT IS:
īĸ Personâs doctor refers him or her to be seen at a
transplant center;
īĸ At the transplant center, the transplant team
evaluates the personâs overall physical and
mental health, plan to pay for transplant related
medical expenses, and emotional support family
and friends will provide;
īĸ Based on the findings, the team decides if the
person is eligible for a liver transplant;
īĸ If the person is eligible, the center will add him
or her to the transplant waiting list.
66. īĸ The waiting list is prioritized so the sickest
people are at the top of the list. The time a
person spends on the waiting list depends on:
īĸ Blood type
īĸ Body size
īĸ Stage of liver disease
īĸ Overall health
īĸ Availability of a matching liver
īĸ Most patients return to a regular lifestyle six
months to a year after a successful liver
transplant. In some patients, the liver disease
they had before the transplant comes back and
they may need treatment or another transplant.
Editor's Notes
Caput medusae- also known as palm tree sign. It is the appearance of distended and engorged superficial epigastric veins.
Used for varicose vein and spider veins. It involves an injection of a solution (salt sol.) directly into the vein. The solution irritates the lining of the blood vessel, causing it to collapse and stick together and the blood to clot. Over the time the vesle turn into scar tissue that fade from the view.
Chronic AlcoholismChronic alcoholism is the leading cause of cirrhosis in the United States. Drinking too much alcohol can cause the liver to swell, which over time can lead to cirrhosis. The amount of alcohol that causes cirrhosis is different for each person.
Chronic Viral HepatitisChronic hepatitis C is the second leading cause of cirrhosis in the United States. Hepatitis C causes the liver to swell, which over time can lead to cirrhosis. About one in four people with chronic hepatitis C develop cirrhosis. Chronic hepatitis B and hepatitis D also can cause cirrhosis.
Nonalcoholic steatohepatitis (NASH)Fat build up in the liver that is not caused by alcohol use, is nonalcoholic steatohepatitis (NASH). NASH can cause the liver to swell and can lead to cirrhosis. People with NASH often have other health issues including diabetes, obesity, high cholesterol, coronary artery disease and poor eating habits.
Bile Duct DiseaseBile duct disease limits or stops bile from flowing to the small intestine. The bile backs up in the liver causing the liver to swell and can lead to cirrhosis. Two common bile duct diseases are primary schlerosing cholangitis and primary biliary cirrhosis.
Genetic diseasesSome genetic diseases can lead to cirrhosis. These diseases include Wilson disease, hemochromatosis, glycogen storage diseases, Alpha-1 antitrypsin deficiency, and autoimmune hepatitis.