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PORTAL
HYPERTENSION, LIVER
CIRRHOSIS & LIVER
TRANSPLANT
PRESENTER-
Ms. Anshu
M.Sc Nursing 1st
yr
KGMU Institute of nursing
DEFINITION
ī‚ĸPortal hypertension is an increase in
the blood pressure within a system
of veins called the portal venous
system
EPIDEMIOLOGY
ī‚ĸ  It is thought to account for 5 to 10
percent of patients with portal
hypertension in developed countries
ī‚ĸ And up to one third of patients in
developing countries
ANATOMY OF PORTAL VEIN
ī‚ĸ The portal vein drains blood from the
small and large intestines, stomach,
spleen, pancreas, and gallbladder.
ī‚ĸ The superior mesenteric vein and the
splenic vein unite behind the neck of the
pancreas to form the portal vein.
ī‚ĸ The portal trunk divides into 2 lobar
veins:-
īƒŧ right branch
īƒŧ left branch
ī‚ĸ . 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.
ī‚ĸ 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
CAUSES PORTAL
HYPERTENSION
ī‚ĸInfrahepatic Causes
ī‚ĸHepatic Causes
ī‚ĸSuprahepatic Causes
PATHOPHYSIOLOGY
ī‚ĸ TwoIMPORTANT factors—vascular resistance
and blood flow—exist in the development of
portal hypertension.
ī‚ĸ Ohm law is V = IR, where V is voltage, I is
current, and R is resistance.
ī‚ĸ 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.
ī‚ĸ Changes in either F or R affect the pressure,
although in most types of portal hypertension,
both of these are altered.
ī‚ĸ Normal portal pressure is generally considered to
be between 5 and 10 mm Hg.
ī‚ĸ Once the portal pressure rises to 12 mm Hg or
greater, complications can arise, such as varices
 and ascites.
ī‚ĸ Indeed, esophageal varices are responsible for
the main complication of portal hypertension,
massive upper gastrointestinal (GI) hemorrhage.
SIGNS AND SYMPTOMS
ī‚ĸ Gastrointestinal hemorrhage may be the initial
presenting symptom
ī‚ĸ Ascites
ī‚ĸ hepatic encephalopathy
ī‚ĸ jaundice
ī‚ĸ coagulopathy, or spider angiomata.
ī‚ĸ Patients who are hemodynamically stable may
have warm skin
ī‚ĸ hyperdynamic pulses
ī‚ĸ low systolic blood pressures
DIAGNOSTIC TEST
ī‚ĸ Complete history of patient
ī‚ĸ Physical examination
ī‚ĸ Various lab tests
ī‚ĸ Hepatic Venous Pressure Gradient measurement
has been accepted as the gold standard for
assessing the severity of portal hypertension
(<5mmHg)
ī‚ĸ X-ray tests
ī‚ĸ Endoscopic test 
ī‚ĸ doppler ultrasonography
MANAGEMENT
ī‚ĸ treatment depends on the severity of the
symptoms
ī‚ĸ GOAL-
ī‚ĸ To treat symptomatic causes
ī‚ĸ To prevent complication
Endoscopic
therapy. 
ī‚ĸ This is usually the
first line of
treatment for
variceal bleeding
and consists of
either banding or
sclerotherapy
BANDING=
ī‚ĸ Banding is a procedure
in which a
gastroenterologist uses
rubber bands to block
off the blood vessel to
stop bleeding.
SCLEROTHERAPY
ī‚ĸ 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.
ī‚ĸ Medications.
ī‚ĸ  Nonselective beta-blockers (nadolol or 
propranolol) may be prescribed alone or in
combination with endoscopic therapy to reduce
the pressure in varices and further reduce the
risk of bleeding
ī‚ĸ The drug lactulose can help treat confusion and
other mental changes associated with
encephalopathy
SURGICAL MANAGEMENT
ī‚ĸ GOAL-
ī‚ĸ To manage condition of patient.
ī‚ĸ To prevent complication
Transjugular
intrahepatic
portosystemic shunt
(TIPS): 
ī‚ĸ This procedure involves
placing a stent (a tubular
device) in the middle of the
liver.
ī‚ĸ The stent connects the
hepatic vein with the portal
vein, which reroutes blood
flow in the liver and helps
relieve pressure in abnormal
veins.
Distal splenorenal
shunt (DSRS): 
ī‚ĸ 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.
ī‚ĸ Liver transplant . This is done in cases of end-
stage liver disease.
ī‚ĸ 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.
ī‚ĸ 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.
LIVER CIRRHOSIS
CIRRHOSIS
INTRODUCTION-
ī‚ĸ Cirrhosis refers to the replacement of normal
liver tissue with non-living scar tissue. It is
always related to other liver diseases.
DEFINITION
ī‚ĸ Cirrhosis is the scarring
of the liver - hard scar
tissue replaces soft
healthy tissue.
ī‚ĸ 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.
PATHOPHYSIOLOGY
ī‚ĸ Regenerative process is disorganized, resulting in
abnormal blood vessel and bile duct from fibrosis
ī‚ĸ Normal lobular structure distorted by fibrotic
connective tissue
ī‚ĸ Lobules are irregular in size and shape with
impaired vascular flow
ī‚ĸ Insidious, prolonged course
CAUSES OF CIRRHOSIS
ī‚ĸ chronic Alcoholism
ī‚ĸ Chronic Viral Hepatitis
ī‚ĸ Nonalcoholic steatohepatitis (NASH)
ī‚ĸ Bile Duct Disease
ī‚ĸ Genetic diseases
SYMPTOMS
ī‚ĸ Loss of appetite
ī‚ĸ Tiredness
ī‚ĸ Nausea
ī‚ĸ Weight loss
ī‚ĸ Abdominal pain
ī‚ĸ Spider-like blood vessels
ī‚ĸ Severe itching
ī‚ĸ Bilirubin> 2mg/dl to 40 mg/dl
ī‚ĸ AST, ALT, alkaline phosphatase
ī‚— Aid in early diagnosis, prognosis, and response
to treatment
ī‚— ↑ ALkPo > 3 times normal indicate billiray
disease
Albumin
ī‚ĸ (non-specific protein) & Factor V and VII
(specific proteins) can provide information on
the functional capacity of the liver
ī‚ĸ Low albumin < 3 that does not respond to
therapy is bad prognosis
ī‚ĸPT
ī‚— Prolongation due to impaired synthesis of
vitamin K dependant clotting factors
ī‚— No response to VIT K is poor prognosis
ī‚ĸBUN
ī‚— < 5 due to inadequate protein intake and
depressed hepatic capacity for urea synthesis
ī‚ĸBiopsy
ī‚— Confirm the presence of cirrhosis
MANAGEMENT
Drug Therapy
ī‚ĸ There is no specific drug therapy for cirrhosis
ī‚ĸ Drugs are used to treat symptoms and
complications of advanced liver disease
NUTRITIONAL THERAPY
ī‚ĸ Diet for patient without complications:
ī‚— High in calories
ī‚— ↑ CHO
ī‚— Moderate to low fat
ī‚— Amount of protein varies with degree of liver damage
ī‚ĸ Patient with hepatic encephalopathy
ī‚— Very low to no-protein diet
ī‚ĸ Low sodium diet for patient with ascites and
edema
NURSING MANAGEMENT
Nursing Assessment
ī‚ĸ Past health history
ī‚ĸ Medications
ī‚ĸ Chronic alcoholism
ī‚ĸ Weight loss
NURSING DIAGNOSES
ī‚ĸ Imbalanced nutrition: less than body
requirements related to inadequate diet
ī‚ĸ Ineffective breathing pattern related to intra-
abdominal fluid collection
ī‚ĸ Excess fluid volume related to increased sodium
and water intake
ī‚ĸ Risk for injury related to altered clotting factors
Overall goals:
ī‚— Relief of discomfort
ī‚— Minimal to no complications
ī‚— Return to as normal a lifestyle as possible
1. IMBALANCED NUTRITION: LESS THAN
BODY REQUIREMENTS
ī‚ĸ Measure dietary intake by calorie count.
ī‚ĸ Encourage patient to eat all meals including
supplementary feedings.
ī‚ĸ Restrict intake of caffeine, gas-producing or spicy
and excessively hot or cold foods.
ī‚ĸ Recommend cessation of smoking. Provide
teaching on the possible negative effects of
smoking.
ī‚ĸ Maintain NPO status when indicated.
ī‚ĸ Provide tube feedings, TPN, lipids if indicated.
2. INEFFECTIVE BREATHING
PATTERN
ī‚ĸ Monitor respiratory rate, depth, and effort
ī‚ĸ Keep head of bed elevated. Position on sides.
ī‚ĸ Encourage frequent repositioning and deep-
breathing exercises and coughing exercises.
ī‚ĸ Monitor serial ABGs, pulse oximetry, vital
capacity measurements, chest x-rays.
ī‚ĸ Provide supplemental O2 as indicated.
ī‚ĸ Demonstrate and assist with respiratory
adjuncts: incentive spirometer.
3. EXCESS FLUID VOLUME RELATED TO
INCREASED SODIUM AND WATER
INTAKE
ī‚ĸ Measure I&O, weigh daily, and note gain of more
than 0.5 kg/day.
ī‚ĸ Measure abdominal girth.
ī‚ĸ Restrict sodium and fluids as indicated.
ī‚ĸ Auscultate lungs, noting diminished breath
sounds and developing adventitious sounds.
ī‚ĸ Monitor for cardiac dysrhythmias. Auscultate
heart sounds, noting development of S3/S4 gallop
rhythm.
4. RISK FOR INJURY
ī‚ĸ Observe for presence of petechiae,
ecchymosis, bleeding from one or more sites.
ī‚ĸ Monitor pulse, BP , Closely assess for signs and
symptoms of GI bleeding
ī‚ĸ Encourage use of soft toothbrush, electric razor,
avoiding straining for stool, vigorous nose
blowing
ī‚ĸ Use small needles for injections. Apply pressure
to small bleeding and venipuncture sites for
longer than usual.
ī‚ĸ Advice to avoid aspirin-containing products.
HEALTH EDUCATION AND
DISCHARGE TEACHING
ī‚ĸ Do not use alcohol or street drugs.
ī‚ĸ 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.)
ī‚ĸ 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.
LIVER FAILURE
LIVER FAILURE
ī‚ĸ Liver failure occurs when large parts of
the liver become damaged beyond repair and
the liver is no longer able to function.
ī‚ĸ 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.
WHAT CAUSES LIVER FAILURE?
The most common causes of chronic liver failure
(where the liver fails over months to years)
include:
ī‚ĸ Hepatitis B
ī‚ĸ Hepatitis C
ī‚ĸ Long-term alcohol consumption
ī‚ĸ Cirrhosis
ī‚ĸ Hemochromatosis (an inherited disorder that
causes the body to absorb and store too much
iron)
ī‚ĸ Malnutrition
ī‚ĸ The causes of acute liver failure, when the liver
fails rapidly, however, are often different. These
include:
ī‚ĸ Acetaminophen (Tylenol) overdose
ī‚ĸ Viruses including hepatitis A, B, and C
(especially in children)
ī‚ĸ Reactions to certain prescription and
herbal medications
ī‚ĸ Ingestion of poisonous wild mushrooms
SIGNS AND SYMPTOMS
Early symptoms include:
ī‚ĸ Nausea
ī‚ĸ Loss of appetite
ī‚ĸ Fatigue
ī‚ĸ Diarrhea
LATER SYMPTOMS
ī‚ĸ Jaundice
ī‚ĸ Bleeding easily
ī‚ĸ Swollen abdomen
ī‚ĸ Mental disorientation or confusion (known as
hepatic encephalopathy)
ī‚ĸ Sleepiness
ī‚ĸ Coma
ī‚ĸ How Is Liver Failure Treated?
ī‚ĸ If detected early enough, acute liver failure caused by
an overdose of acetaminophen can sometimes be
treated and its effects reversed.
ī‚ĸ 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.
ī‚ĸ 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.
LIVER TRANSPLANT
ī‚ĸ 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.
ī‚ĸ 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. 
THE PROCESS TO BE ELIGIBLE FOR A
LIVER TRANSPLANT IS:
ī‚ĸ Person’s doctor refers him or her to be seen at a
transplant center;
ī‚ĸ At the transplant center, the transplant team
evaluates the person’s overall physical and
mental health, plan to pay for transplant related
medical expenses, and emotional support family
and friends will provide;
ī‚ĸ Based on the findings, the team decides if the
person is eligible for a liver transplant;
ī‚ĸ If the person is eligible, the center will add him
or her to the transplant waiting list.
ī‚ĸ 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:
ī‚ĸ Blood type
ī‚ĸ Body size
ī‚ĸ Stage of liver disease
ī‚ĸ Overall health
ī‚ĸ Availability of a matching liver
ī‚ĸ 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.
Portal hypertension, liver cirrhosis and liver transplant

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Portal hypertension, liver cirrhosis and liver transplant

  • 1. PORTAL HYPERTENSION, LIVER CIRRHOSIS & LIVER TRANSPLANT PRESENTER- Ms. Anshu M.Sc Nursing 1st yr KGMU Institute of nursing
  • 2.
  • 3. DEFINITION ī‚ĸPortal hypertension is an increase in the blood pressure within a system of veins called the portal venous system
  • 4. EPIDEMIOLOGY ī‚ĸ  It is thought to account for 5 to 10 percent of patients with portal hypertension in developed countries ī‚ĸ And up to one third of patients in developing countries
  • 6. ī‚ĸ The portal vein drains blood from the small and large intestines, stomach, spleen, pancreas, and gallbladder. ī‚ĸ The superior mesenteric vein and the splenic vein unite behind the neck of the pancreas to form the portal vein. ī‚ĸ The portal trunk divides into 2 lobar veins:- īƒŧ right branch īƒŧ left branch
  • 7. ī‚ĸ . 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. ī‚ĸ 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
  • 9.
  • 10.
  • 11.
  • 12.
  • 14. ī‚ĸ TwoIMPORTANT factors—vascular resistance and blood flow—exist in the development of portal hypertension. ī‚ĸ Ohm law is V = IR, where V is voltage, I is current, and R is resistance. ī‚ĸ 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. ī‚ĸ Changes in either F or R affect the pressure, although in most types of portal hypertension, both of these are altered.
  • 15. ī‚ĸ Normal portal pressure is generally considered to be between 5 and 10 mm Hg. ī‚ĸ Once the portal pressure rises to 12 mm Hg or greater, complications can arise, such as varices  and ascites. ī‚ĸ Indeed, esophageal varices are responsible for the main complication of portal hypertension, massive upper gastrointestinal (GI) hemorrhage.
  • 16.
  • 17.
  • 18. SIGNS AND SYMPTOMS ī‚ĸ Gastrointestinal hemorrhage may be the initial presenting symptom ī‚ĸ Ascites ī‚ĸ hepatic encephalopathy ī‚ĸ jaundice ī‚ĸ coagulopathy, or spider angiomata. ī‚ĸ Patients who are hemodynamically stable may have warm skin ī‚ĸ hyperdynamic pulses ī‚ĸ low systolic blood pressures
  • 19.
  • 20. DIAGNOSTIC TEST ī‚ĸ Complete history of patient ī‚ĸ Physical examination ī‚ĸ Various lab tests ī‚ĸ Hepatic Venous Pressure Gradient measurement has been accepted as the gold standard for assessing the severity of portal hypertension (<5mmHg) ī‚ĸ X-ray tests ī‚ĸ Endoscopic test  ī‚ĸ doppler ultrasonography
  • 21. MANAGEMENT ī‚ĸ treatment depends on the severity of the symptoms ī‚ĸ GOAL- ī‚ĸ To treat symptomatic causes ī‚ĸ To prevent complication
  • 22. Endoscopic therapy.  ī‚ĸ This is usually the first line of treatment for variceal bleeding and consists of either banding or sclerotherapy
  • 23. BANDING= ī‚ĸ Banding is a procedure in which a gastroenterologist uses rubber bands to block off the blood vessel to stop bleeding.
  • 24.
  • 25. SCLEROTHERAPY ī‚ĸ 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. ī‚ĸ Medications. ī‚ĸ  Nonselective beta-blockers (nadolol or  propranolol) may be prescribed alone or in combination with endoscopic therapy to reduce the pressure in varices and further reduce the risk of bleeding ī‚ĸ The drug lactulose can help treat confusion and other mental changes associated with encephalopathy
  • 28. SURGICAL MANAGEMENT ī‚ĸ GOAL- ī‚ĸ To manage condition of patient. ī‚ĸ To prevent complication
  • 29. Transjugular intrahepatic portosystemic shunt (TIPS):  ī‚ĸ This procedure involves placing a stent (a tubular device) in the middle of the liver. ī‚ĸ 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):  ī‚ĸ 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. ī‚ĸ Liver transplant . This is done in cases of end- stage liver disease. ī‚ĸ 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. ī‚ĸ 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.
  • 34. CIRRHOSIS INTRODUCTION- ī‚ĸ Cirrhosis refers to the replacement of normal liver tissue with non-living scar tissue. It is always related to other liver diseases.
  • 35. DEFINITION ī‚ĸ Cirrhosis is the scarring of the liver - hard scar tissue replaces soft healthy tissue. ī‚ĸ 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 ī‚ĸ Regenerative process is disorganized, resulting in abnormal blood vessel and bile duct from fibrosis ī‚ĸ Normal lobular structure distorted by fibrotic connective tissue ī‚ĸ Lobules are irregular in size and shape with impaired vascular flow ī‚ĸ Insidious, prolonged course
  • 37.
  • 38.
  • 39. CAUSES OF CIRRHOSIS ī‚ĸ chronic Alcoholism ī‚ĸ Chronic Viral Hepatitis ī‚ĸ Nonalcoholic steatohepatitis (NASH) ī‚ĸ Bile Duct Disease ī‚ĸ Genetic diseases
  • 40. SYMPTOMS ī‚ĸ Loss of appetite ī‚ĸ Tiredness ī‚ĸ Nausea ī‚ĸ Weight loss ī‚ĸ Abdominal pain ī‚ĸ Spider-like blood vessels ī‚ĸ Severe itching
  • 41.
  • 42. ī‚ĸ Bilirubin> 2mg/dl to 40 mg/dl ī‚ĸ AST, ALT, alkaline phosphatase ī‚— Aid in early diagnosis, prognosis, and response to treatment ī‚— ↑ ALkPo > 3 times normal indicate billiray disease
  • 43. Albumin ī‚ĸ (non-specific protein) & Factor V and VII (specific proteins) can provide information on the functional capacity of the liver ī‚ĸ Low albumin < 3 that does not respond to therapy is bad prognosis
  • 44. ī‚ĸPT ī‚— Prolongation due to impaired synthesis of vitamin K dependant clotting factors ī‚— No response to VIT K is poor prognosis ī‚ĸBUN ī‚— < 5 due to inadequate protein intake and depressed hepatic capacity for urea synthesis ī‚ĸBiopsy ī‚— Confirm the presence of cirrhosis
  • 45.
  • 46.
  • 47. MANAGEMENT Drug Therapy ī‚ĸ There is no specific drug therapy for cirrhosis ī‚ĸ Drugs are used to treat symptoms and complications of advanced liver disease
  • 48. NUTRITIONAL THERAPY ī‚ĸ Diet for patient without complications: ī‚— High in calories ī‚— ↑ CHO ī‚— Moderate to low fat ī‚— Amount of protein varies with degree of liver damage ī‚ĸ Patient with hepatic encephalopathy ī‚— Very low to no-protein diet ī‚ĸ Low sodium diet for patient with ascites and edema
  • 49. NURSING MANAGEMENT Nursing Assessment ī‚ĸ Past health history ī‚ĸ Medications ī‚ĸ Chronic alcoholism ī‚ĸ Weight loss
  • 50. NURSING DIAGNOSES ī‚ĸ Imbalanced nutrition: less than body requirements related to inadequate diet ī‚ĸ Ineffective breathing pattern related to intra- abdominal fluid collection ī‚ĸ Excess fluid volume related to increased sodium and water intake ī‚ĸ 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 ī‚ĸ Measure dietary intake by calorie count. ī‚ĸ Encourage patient to eat all meals including supplementary feedings. ī‚ĸ Restrict intake of caffeine, gas-producing or spicy and excessively hot or cold foods. ī‚ĸ Recommend cessation of smoking. Provide teaching on the possible negative effects of smoking. ī‚ĸ Maintain NPO status when indicated. ī‚ĸ Provide tube feedings, TPN, lipids if indicated.
  • 53. 2. INEFFECTIVE BREATHING PATTERN ī‚ĸ Monitor respiratory rate, depth, and effort ī‚ĸ Keep head of bed elevated. Position on sides. ī‚ĸ Encourage frequent repositioning and deep- breathing exercises and coughing exercises. ī‚ĸ Monitor serial ABGs, pulse oximetry, vital capacity measurements, chest x-rays. ī‚ĸ Provide supplemental O2 as indicated. ī‚ĸ Demonstrate and assist with respiratory adjuncts: incentive spirometer.
  • 54. 3. EXCESS FLUID VOLUME RELATED TO INCREASED SODIUM AND WATER INTAKE ī‚ĸ Measure I&O, weigh daily, and note gain of more than 0.5 kg/day. ī‚ĸ Measure abdominal girth. ī‚ĸ Restrict sodium and fluids as indicated. ī‚ĸ Auscultate lungs, noting diminished breath sounds and developing adventitious sounds. ī‚ĸ Monitor for cardiac dysrhythmias. Auscultate heart sounds, noting development of S3/S4 gallop rhythm.
  • 55. 4. RISK FOR INJURY ī‚ĸ Observe for presence of petechiae, ecchymosis, bleeding from one or more sites. ī‚ĸ Monitor pulse, BP , Closely assess for signs and symptoms of GI bleeding ī‚ĸ Encourage use of soft toothbrush, electric razor, avoiding straining for stool, vigorous nose blowing ī‚ĸ Use small needles for injections. Apply pressure to small bleeding and venipuncture sites for longer than usual. ī‚ĸ Advice to avoid aspirin-containing products.
  • 56. HEALTH EDUCATION AND DISCHARGE TEACHING ī‚ĸ Do not use alcohol or street drugs. ī‚ĸ 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.) ī‚ĸ 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 ī‚ĸ Liver failure occurs when large parts of the liver become damaged beyond repair and the liver is no longer able to function. ī‚ĸ 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: ī‚ĸ Hepatitis B ī‚ĸ Hepatitis C ī‚ĸ Long-term alcohol consumption ī‚ĸ Cirrhosis ī‚ĸ Hemochromatosis (an inherited disorder that causes the body to absorb and store too much iron) ī‚ĸ Malnutrition
  • 60. ī‚ĸ The causes of acute liver failure, when the liver fails rapidly, however, are often different. These include: ī‚ĸ Acetaminophen (Tylenol) overdose ī‚ĸ Viruses including hepatitis A, B, and C (especially in children) ī‚ĸ Reactions to certain prescription and herbal medications ī‚ĸ Ingestion of poisonous wild mushrooms
  • 61. SIGNS AND SYMPTOMS Early symptoms include: ī‚ĸ Nausea ī‚ĸ Loss of appetite ī‚ĸ Fatigue ī‚ĸ Diarrhea
  • 62. LATER SYMPTOMS ī‚ĸ Jaundice ī‚ĸ Bleeding easily ī‚ĸ Swollen abdomen ī‚ĸ Mental disorientation or confusion (known as hepatic encephalopathy) ī‚ĸ Sleepiness ī‚ĸ Coma
  • 63. ī‚ĸ How Is Liver Failure Treated? ī‚ĸ If detected early enough, acute liver failure caused by an overdose of acetaminophen can sometimes be treated and its effects reversed. ī‚ĸ 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. ī‚ĸ 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 ī‚ĸ 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. ī‚ĸ 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. 
  • 65. THE PROCESS TO BE ELIGIBLE FOR A LIVER TRANSPLANT IS: ī‚ĸ Person’s doctor refers him or her to be seen at a transplant center; ī‚ĸ At the transplant center, the transplant team evaluates the person’s overall physical and mental health, plan to pay for transplant related medical expenses, and emotional support family and friends will provide; ī‚ĸ Based on the findings, the team decides if the person is eligible for a liver transplant; ī‚ĸ If the person is eligible, the center will add him or her to the transplant waiting list.
  • 66. ī‚ĸ 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: ī‚ĸ Blood type ī‚ĸ Body size ī‚ĸ Stage of liver disease ī‚ĸ Overall health ī‚ĸ Availability of a matching liver ī‚ĸ 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

  1. Caput medusae- also known as palm tree sign. It is the appearance of distended and engorged superficial epigastric veins.
  2. 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.
  3. 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.