3. DEFINITION
Cirrhosis is a chronic disease characterized by
replacement of normal liver tissue with diffuse
fibrosis that disrupts the structure and function of the
liver.
63. PATHOPHYSIOLOGY
Cirrhosis with portal hypertension
↓
Splanchnic arterial vasodilation
↓
Decrease in circulating arterial blood volume
↓
Activation of renin-angiotensin and sympathetic nervous
systems and antidiuretic hormone
↓
Kidney retains sodium and water
↓
Hypervolemia
↓
Persistent activation of systems for retention of sodium and
water
↓
Ascites and edema formation
64. CLINICAL MANIFESTATIONS
Increased abdominal girth and rapid weight gain
Short of breath , enlarged abdomen, striae and distended
veins.
Fluid and electrolyte imbalances .
ASSESSMENT AND DIAGNOSTIC EVALUATION
1.History collection
2.Physical examination
Presence of fluid can be confirmed either by percussing
for shifting dullness or by detecting a fluid wave .
A fluid wave is likely to be found only when a large
amount of fluid is present
Daily measurement and recording of abdominal girth and
bodyweight
65. MEDICAL MANAGEMENT…
1. Dietary modification
The goal of treatment for the patient with ascites is a
negative sodium balance to reduce fluid retention.
Table salt, salty foods, salted butter and margarine, and
all ordinary canned and frozen foods should be avoided.
Daily sodium allowance may be reduced further to 500
mg.
2. Diuretics
Spironolactone an aldosterone blocking aldosterone
blocking agent, is most often the first-line therapy in
patients with ascites from cirrhosis.
Daily weight loss should not exceed 1 to 2 kg in patients
with ascites and peripheral edema or 0.5 to 0.75 kg in
patients without edema
66. MEDICAL MANAGEMENT…
3. Bed rest
Upright posture is associated with activation of the
renin-angiotensin-aldosterone system and
sympathetic nervous system.
Bed rest may be a useful therapy.
4. Paracentesis
Removal of fluid from the peritoneal cavity through
a small surgical incision or puncture made through
the abdominal wall under sterile conditions
67. OTHER METHODS OF TREATMENT
Insertion of a peritoneovenous shunt to redirect
ascitic fluid from the peritoneal cavity into the
systemic circulation is a treatment modality for
ascites.
The shunt is reserved for those who are resistant to
diuretic therapy, are not candidates for liver
transplantation, have abdominal adhesions.
68. HEPATIC ENCEPHALOPATHY
Hepatic encephalopathy, a life-threatening
complication of liver disease, occurs with profound
liver failure and may result from the accumulation of
ammonia and other toxic metabolites in the blood
69. CAUSES
Hepatitis
Bleeding esophageal varices or chronic GI bleeding
High-protein diet
Bacterial infections,
Uremia
Alkalosis
Hypokalemia
Excessive diuresis
Dehydration,
Surgery ,
Fever
Medications sedative agents, tranquilizers, analgesic
agents, and diuretic medications that cause potassium
loss.
70. PATHOPHYSIOLOGY
Ammonia accumulates because damaged liver cells
fail to detoxify and convert to urea the ammonia that
is constantly entering the bloodstream.
Ammonia enters the bloodstream as a result of its
absorption from the GI tract and its liberation from
kidney and muscle cells.
The increased ammonia concentration in the blood
causes brain dysfunction and damage, resulting in
hepatic encephalopathy.
71. STAGES OF HEPATIC ENCEPHALOPATHY
Stage 1
Normal level of consciousness with periods of lethargy
and euphoria; reversal of day–night sleep patterns
Stage 2
Increased drowsiness; disorientation ;inappropriate
behavior; mood swings ;agitation
Stage 3
Stuporous; difficult to rouse; sleeps most of time;
marked confusion; incoherent speech
Stage 4
Comatose; may not respond to painful stimuli
72. CLINICAL MANIFESTATIONS
The earliest symptoms of hepatic encephalopathy include
minor mental changes and motor disturbances.
The patient appears slightly confused, has alterations in
mood, becomes unkempt, and has altered sleep patterns.
Asterixis (flapping tremor of the hands) may occur.
Simple tasks, such as handwriting, become difficult.
Inability to reproduce a simple figure is referred to as
constructional apraxia.
Early stages of ,the deep tendon reflexes are hyperactive;
with worsening of hepatic encephalopathy, these reflexes
disappear and the extremities may become flaccid.
73. ASSESSMENT AND DIAGNOSTIC FINDINGS
History collection
Physical examination
The electroencephalogram (EEG) shows generalized
slowing, an increase in the amplitude of brain waves,
and characteristic tri phasic waves.
Fetor hepaticus , a sweet, slightly fecal odor to the
breath presumed to be of intestinal origin
Patient lapses into frank coma and may have
seizures.
74. MEDICAL MANAGEMENT
Lactulose is administered to reduce serum ammonia
levels.
(1) ammonia is kept in the ionized state, resulting in a
fall in colon pH, reversing the normal passage of
ammonia from the colon to the blood
(2) evacuation of the bowel takes place, which
decreases the ammonia absorbed from the colon
(3) the fecal flora are changed to organisms that do not
produce ammonia from urea
Benzodiazepine antagonists (flumazenil )
administered to improve encephalopathy whether or
not the patient has previously taken benzodiazepines.
75. NUTRITIONAL THERAPY IN HEPATIC
ENCEPHALOPATHY
• Keep daily protein intake between 1.0 and 1.5
g/kg.
• Provide small, frequent meals and an evening
snack of complex carbohydrates to avoid protein
loading.
76. ESOPHAGEAL VARICES
Bleeding or hemorrhage from esophageal varices
occurs in approximately one third of patients with
cirrhosis and varices.
It is one of the major causes of death in patients with
cirrhosis.
77. PATHOPHYSIOLOGY
Portal hypertension
↓
Development of pressure gradient of 12 mm Hg or
greater between portal vein and inferior vena cava
↓
Venous collaterals develop from high portal system
pressure to systemic veins in esophageal plexus,
hemorrhoidal plexus and retroperitoneal veins
↓
Abnormal varicoid vessels form in any of above
locations
↓
Vessels may rupture causing life-threatening
hemorrhage.
78. CLINICAL MANIFESTATIONS
The patient with bleeding esophageal varices may
present with hematemesis, melena, or general
deterioration in mental or physical status and often
has a history of alcohol abuse.
Signs and symptoms of shock (cool clammy skin,
hypotension, tachycardia)may be present
79. ASSESSMENT AND DIAGNOSTIC FINDINGS
1. Endoscopy
To identify the cause and the site of bleeding
After the examination, fluids are not given until
the gag reflex returns.
2.Portal venous pressure
Indirect measurement of the hepatic vein
pressure requires insertion of a fluid-filled
balloon catheter into the Antecubital or femoral
vein.
The catheter is advanced under fluoroscopy to a
hepatic vein. A “wedged” pressure is obtained
by occluding the blood flow in the blood vessel;
pressure in the un occluded vessel is also
measured.
80. LABORATORY TESTS
Liver function tests, such as serum aminotransferase,
bilirubin, alkaline phosphatase, and serum proteins.
Splenoportography, which involves serial or
segmental x-rays, is used to detect extensive
collateral circulation in esophageal vessels, which
would indicate varices.
Other tests are hepatoportography and celiac
angiography.
81. MEDICAL MANAGEMENT
PHARMACOLOGIC THERAPY
Nitrates such as isosorbide lower portal pressure
by veno dilation and decreased cardiac output
Vasopressin produces constriction of the
splanchnic arterial bed and a resulting decrease in
portal pressure.
It may be administered intravenously or by intra-
arterial infusion
Somatostatin and octreotide decreases bleeding
from esophageal varices without the
vasoconstrictive effects of vasopressin.
Nadolol , beta-blocking agents decrease portal
pressure
82. BALLOON TAMPONADE
Pressure is exerted against the bleeding varices by a
double-balloon tamponade (Sengstaken-Blakemore
tube).
The tube has four openings, each with a specific
purpose :gastric aspiration, esophageal aspiration,
inflation of the gastric balloon, and inflation of the
esophageal balloon.
The balloon in the stomach is inflated with 100 to
200 mL of air.
An x-ray confirms proper positioning of the gastric
balloon
Tube is pulled gently to exert a force against the
gastric cardia.
Traction may be applied with weights
84. ENDOSCOPIC SCLEROTHERAPY
A sclerosing agent is injected through a fiber optic
endoscope into the bleeding esophageal varices to
promote thrombosis and sclerosis.
Endoscopic variceal sclerotherapy has been used in
the primary prophylaxis of variceal bleeding.
After treatment, the patient must be observed for
bleeding, perforation of the esophagus, aspiration
pneumonia, and esophageal stricture.
85. ESOPHAGEAL BANDING
THERAPY(VARICEAL BAND LIGATION)
A modified endoscope loaded with an elastic rubber
band is passed through an over tube directly onto the
varix to be banded.
After suctioning the bleeding varix into the tip of the
endoscope, the rubber band is slipped over the tissue,
causing necrosis, ulceration, and eventual sloughing
of the varix.
Complications include superficial ulceration and
dysphagia, transient chest discomfort, and rarely
esophageal .
86. TRANSJUGULAR INTRAHEPATIC
PORTOSYSTEMIC SHUNTING
Method of treating esophageal varices in which a
cannula is threaded into the portal vein by the trans
jugular route.
An expandable stent is inserted and serves as an
intrahepatic shunt between the portal circulation and
the hepatic vein reducing portal hypertension
Complications may include bleeding, sepsis, heart
failure, organ perforation, shunt thrombosis, and
progressive liver failure
87. SURGICAL BYPASS PROCEDURES
Surgical decompression of the portal circulation can
prevent variceal bleeding if the shunt remains patent
Distal splenorenal shunt made between the splenic
vein and the left renal vein after splenectomy.
Mesocaval shunt is created by anastomosing the
superior mesenteric vein to the proximal end of the
vena cava or to the side of the vena cava using
grafting material.
Portocaval shunts divert all portal flow to the vena
cava via end-to-side or side-to-side approaches, so
they are considered nonselective shunts.
89. DEVASCULARIZATION AND TRANSECTION
Devascularization and staple gun transection
procedures to separate the bleeding site from the
high-pressure portal system have been used in the
emergency management of variceal bleeding.
The lower end of the esophagus is reached through a
small gastrostomy incision; a staple gun permits
anastomosis of the transected ends of the esophagus.
Re bleeding is a risk, and the outcomes of these
procedures vary among patient populations.
90. ASSESSMENT AND DIAGNOSTIC FINDINGS OF LIVER CIRRHOSIS
Serum albumin level tends to decrease and the serum globulin level
rises.
Enzyme tests indicate liver cell damage: serum alkaline phosphatase,
AST,ALT, and GGT levels increase, and the serum cholinesterase level
may decrease.
Bilirubin tests are performed to measure bile excretion or bile
retention.
Pro thrombin time is prolonged.
Ultrasound scanning is used to measure the difference in density of
parenchymal cells and scar tissue.
CT, MRI, and radioisotope liver scans give information about liver
size and hepatic blood flow and obstruction. Diagnosis is confirmed by
liver biopsy.
Arterial blood gas analysis may reveal a ventilation–perfusion i
hypoxia.
91. MEDICAL MANAGEMENT OF LIVER
CIRRHOSIS
Antacids are prescribed to decrease gastric
distress and minimize the possibility of GI
bleeding.
Vitamins and nutritional supplements promote
healing of damaged liver cells and improve the
general nutritional status.
Potassium-sparing diuretics.
An adequate diet and avoidance of alcohol are
essential
Colchicine, an anti- inflammatory agent used to
treat the symptoms of gout, may increase the
length of survival in patients with mild to
moderate cirrhosis.
