SIROSIS HEPATIS

Tria Firza Kumala., Skep., Ners.,M.Biomed

Review Anatomy Physiology Of Liver
Details of a portion of a liver lobule
• Aliran darah :
• Hati menerima darah dari
2 sumber :
• Darah yang
mengandung banyak
oksigen mengalir dari
arteri hepatik. ,
percabangan dari
aorta abdominal .
• Darah vena dari
pengeluaran saluran
gastrointestinal (terdiri
dari nutrien pada
intestine)  masuk ke
hati melalui vena portal
hepatik.
• Darah meninggalkan hati
melalui vena sentral pada
setiap lobusnya kemudian
mengalir ke vena hepatik.
• Sirosis adalah penyakit kronis dengan
karakteristik perubahan jaringan hati
yang normal dengan diffuse fibrosis
yang merusak struktur dan fungsi
hati.
• 3 jenis sirosis hepatis :
• Sirosis Alkoholic  jaringan skar
disekitar area portal.
• Sirosis Postnekrotik  Jaringan skar
terjadi akibat dari riwayat infeksi virus
hepatitis
• Sirosis Biliary  skar terjadi di hati dan
sekitar duktus biliary (biasanya
dihasilkan dari obstruksi kronis biliary
dan infeksi ).
1. Alcoholic cirrhosis  in which the
scar tissue characteristically surrounds
the portal areas  Common type of
cirrhosis.
2. Postnecrotic cirrhosis 
in which there are broad
bands of scar tissue as a
late result of a previous
bout of acute viral
hepatitis.
3. Biliary cirrhosis  in
which scarring occurs in
the liver around the bile
ducts.
This type usually is the
result of chronic biliary
obstruction and
infection (cholangitis)
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PATOPHYSIOLOGI

• GBR 38-15
Manifestations of Liver Cirrhosis

Fig. 42-5
 Clinical Manifestations
Early Manifestations

• Onset usually insidious

• GI disturbances:
– Anorexia
– Dyspepsia
– Flatulence
 Clinical Manifestations
Early Manifestations

• Abdominal pain
• Fever
• Lassitude
• Weight loss
• Enlarged liver or spleen
Clinical Manifestations
Late Manifestations

• Two causative mechanisms

– Hepatocellular failure
– Portal hypertension
 Clinical Manifestations
Jaundice

• Occurs because of insufficient

conjugation of bilirubin by the
liver cells, and local obstruction
of biliary ducts by scarring and
regenerating tissue
 Clinical Manifestations
Jaundice

• Intermittent jaundice is
characteristic of biliary cirrhosis
• Late stages of cirrhosis the patient
will usually be jaundiced
 Clinical Manifestations
Skin

• Spider angiomas (telangiectasia,

spider nevi)
• Palmar erythema
 Clinical Manifestations
Endocrine Disturbances

• Steroid hormones of the adrenal

cortex (aldosterone), testes, and
ovaries are metabolized and
inactivated by the normal liver
 Clinical Manifestations
Endocrine Disturbances

• Alteration in hair distribution

– Decreased amount of pubic hair
– Axillary and pectoral alopecia
 Clinical Manifestations
Hematologic Disorders

• Bleeding tendencies as a result of

decreased production of hepatic
clotting factors (II, VII, IX, and X)
 Clinical Manifestations
Hematologic Disorders

• Anemia, leukopenia, and

thrombocytopenia are believed
to be result of hypersplenism
Clinical Manifestations
Peripheral Neuropathy

• Dietary deficiencies of thiamine,

folic acid, and vitamin B12
 Complications

1. Portal hypertension and

esophageal varices
2. Peripheral edema and ascites
3. Hepatic encephalopathy
4. Fetor hepaticus
 Complications
Portal Hypertension

• Characterized by:
– Increased venous pressure in
portal circulation
– Splenomegaly
– Esophageal varices
– Systemic hypertension
 Complications
Portal Hypertension

• Primary mechanism is the increased

resistance to blood flow through the
liver
 Complications
Portal Hypertension
Splenomegaly

• Back pressure caused by portal

hypertension  chronic passive
congestion as a result of increased
pressure in the splenic vein
 Complications
Portal Hypertension
Esophageal Varices

• Increased blood flow through

the portal system results in
dilation and enlargement of
the plexus veins of the
esophagus and produces
varices
 Complications
Portal Hypertension
Esophageal Varices

• Varices have fragile vessel

walls which bleed easily
 Complications
Portal Hypertension
Internal Hemorrhoids

• Occurs because of the

dilation of the mesenteric
veins and rectal veins
 Complications
Portal Hypertension
Caput Medusae

• Collateral circulation involves the

superficial veins of the abdominal
wall leading to the development
of dilated veins around the
umbilicus
 Complications
Peripheral Edema and Ascites

• Ascites:
- Intraperitoneal
accumulation of watery
fluid containing small
amounts of protein
 Complications
Peripheral Edema and Ascites

• Factors involved in the

pathogenesis of ascites:
- Hypoalbuminemia
-  Levels of aldosterone
-  Portal hypertension
 Complications
Hepatic Encephalopathy

• Liver damage causes blood to

enter systemic circulation without
liver detoxification
• Result from the accumulation of
ammonia and other toxic
metabolites in the blood
• Frequently a terminal complication
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Fig. 42-6
 Pemeriksaan Diagnostik

• Serum kadar albumin menurun

• Serum kadar globulin meningkat
• Test Enzim indikasi kerusakan sel hati :
serum alkaline phosphatase, AST, ALT,
and GGT levels meningkat dan serum
cholinesterase level menurun
• Test Bilirubin meningkat
• Prothrombin time (PT) memanjang.
• Ultrasound scanning dilakukan untuk
mengukur skar jaringan
• CT, MRI, dan radioisotope
• Scaning hati : ukuran hati dan sirkulasi
darah di hati dan obstruksi
• Biopsi hati
• Analisa gas darah
Assessment and Diagnostic Findings

• The serum albumin level  decrease and the

serum globulin level  rises.
• Enzyme tests indicate liver cell damage =
– serum alkaline phosphatase, AST, ALT, and
GGT levels increase
– the serum cholinesterase level may decrease.
• Bilirubin tests are performed to measure bile
excretion or bile retention = elevated levels
Assessment and Diagnostic Findings

• Prothrombin time is prolonged.

• Ultrasound scanning is used to measure the
difference in density of parenchymal cells and
scar tissue. CT, MRI, and radioisotope
• Diagnosis is confirmed by liver biopsy.
• Arterial blood gas analysis may reveal a
ventilation– perfusion imbalance and hypoxia.
MEDICAL MANAGEMENT
1. Antacids  to decrease gastric distress and minimize the
possibility of GI bleeding.
2. Vitamins and nutritional supplements  promote healing of
damaged liver cells and improve the general nutritional
status.
3. Potassium-sparing diuretics (spironolactone [Aldactone],
triamterene [Dyrenium])  decrease ascites.
 NURSING PROCESS:
THE PATIENT WITH HEPATIC CIRRHOSIS
Nursing Assessment

• Past health history

• Medications
• Chronic alcoholism
• Weight loss
Nursing Diagnoses

1. Imbalanced nutrition: less

than body requirements
2. Impaired skin integrity
3. Ineffective breathing pattern
4. Risk for injury
Planning

• Overall goals:
– Relief of discomfort
– Minimal to no complications
– Return to as normal a lifestyle as
possible
Nursing Implementation

• Health Promotion
– Treat alcoholism
– Identify hepatitis early and treat
– Identify biliary disease early and
treat
Nursing Implementation

• Acute Intervention
– Rest
– Edema and ascites
– Paracentesis
– Skin care
– Dyspnea
– Nutrition
Nursing Implementation

• Acute Intervention
– Bleeding problems
– Balloon tamponade
– Altered body image
– Hepatic encephalopathy
Nursing Implementation

• Ambulatory and Home Care

– Symptoms of complications
– When to seek medical attention
– Remission maintenance
– Abstinence from alcohol
Evaluation

• Maintenance of normal body weight

• Maintenance of skin integrity
• Effective breathing pattern
• No injury
• No signs of infection