Hepatic Disorders

1. HEPATIC
DISORDERS
Presented by:
Mr. Rahul Ranjan
Nursing Tutor, NNC

2. Contents
 Jaundice
 Hepatic cirrhosis
 Portal hypertension
 Ascites
 Hepatic Encephalopathy and coma

3. JAUNDICE
 When the bilirubin concentration in the blood is abnormally
elevated, all the body tissues, including the sclera and the
skin, become yellow-tinged or greenish-yellow, a condition
called jaundice.
 Jaundice becomes clinically evident when the serum
bilirubin level exceeds 2.5 mg/dL.

4. Types of Jaundice
 There are several : hemolytic, hepatocellular, obstructive,
or jaundice due to hereditary hyperbilirubinemia.
 Hepatocellular and obstructive jaundice are the two types
commonly associated with liver disease.

5. 1. Hemolytic Jaundice
 Hemolytic jaundice is the result of an increased destruction
of the red blood cells.
 Fecal and urine urobilinogen levels are increased.

6. 2. Hepatocellular Jaundice
 Hepatocellular jaundice is caused by the inability of damaged liver
cells to clear normal amounts of bilirubin from the blood.
 The cellular damage may be from infection, such as in viral hepatitis
(eg, hepatitis A, B, C, D, or E) or other viruses that affect the liver
(eg, yellow fever virus, Epstein-Barr virus), from medication or
chemical toxicity (eg, carbon tetrachloride, chloroform, phosphorus,
arsenicals, certain medications), or from alcohol.
 AST and ALT levels may be increased, indicating cellular necrosis.

7. 3. Obstructive Jaundice
 Obstructive jaundice of the extrahepatic type may be caused by
occlusion of the bile duct by a gallstone, an inflammatory
process, a tumor, or pressure from an enlarged organ.
 The obstruction may also involve the small bile ducts within the
liver (ie, intrahepatic obstruction), caused, for example, by
pressure on these channels from inflammatory swelling of the
liver.

8. 4. Hereditary Hyperbilirubinemia
 Increased serum bilirubin levels (hyperbilirubinemia) resulting
from several inherited disorders can also produce jaundice.
 Gilbert’s syndrome is a familial disorder characterized by an
increased level of unconjugated bilirubin that causes jaundice.
 Dubin–Johnson syndrome (chronic idiopathic jaundice, with
pigment in the liver) and Rotor’s syndrome (chronic familial
conjugated hyperbilirubinemia without pigment in the liver).

9. Cirrhosis of Liver/Hepatic cirrhosis
 Cirrhosis is a late stage of scarring (fibrosis) of the liver
caused by many forms of liver diseases and conditions,
such as hepatitis and chronic alcoholism.
 Cirrhosis is a chronic disease characterized by replacement
of normal liver tissue with diffuse fibrosis that disrupts the
structure and function of the liver.

11.  A chronic liver disease characterized by fibrotic changes
and the formation of dense connective tissue within the
liver, subsequent degenerative changes, and loss of
functioning cells.

15. POST-NECROTIC CIRRHOSIS
 It is a complication of viral, toxic or idiopathic (autoimmune
hepatitis).
 Broad bands of scar tissue forms within the liver.
BILIARY CIRRHOSIS
 Biliary cirrhosis is associated with chronic biliary obstruction and
infection.
 There is diffuse fibrosis of the liver with jaundice as a main
feature.

16. CARDIAC CIRRHOSIS
 It results from long standing, severe right-sided heart
failure, constrictive pericarditis, and tricuspid insufficiency
 Elevated venous pressure transmitted via the inferior vena
cava and hepatic veins to the sinusoids of the liver, which
become dilated and engorged with blood.
 The liver becomes enlarged and swollen

17. CLINICAL MANIFESTATIONS
Early manifestations
 Anorexia
 Nausea and vomiting
 Change in bowel habits (Diarrhoea and constipation)
 Abdominal pain
 Fever
 Slight weight loss
 Liver and spleen enlargement

18. LATER MANIFESTATIONS
 It may be severe and result from liver
failure and its complications.
 Jaundice
 Skin lesions
 Spider angioma and Palmer erythema

19. Others
 Thrombocytopenia, leukopenia, anaemia, and coagulation
disorders.
 Coagulation problems manifested by epistaxis, easy bruising,
gingival bleeding, and heavy menstrual bleeding.
 Endocrine problems
 Men: Gynecomastia, loss of axillary, pubic hair, testicular
atrophy, impotence with loss of libido.
 Younger women: amenorrhoea, Older women: vaginal bleeding

20. D/E
 Bilirubin, Albumin
 Prothrombin time
 Leukopenia and neutropenia
 Coagulation defects
 Aspartate Aminotransferases (AST)
 Alanine transaminase (ALT)
 Alkaline phosphatase

21.  Fibroscan
 USG
 CT Scan
 MRI
 Liver Biopsy

22. COMPLICATIONS
 Portal hypertension
 Esophageal & gastric varices
 Hepatic Encephalopathy
 Hepatorenal Syndrome
 Peripheral edema
 Ascites

23. Treatment
 Treatment for alcohol dependency
 Infections: The patient will be given antibiotics for any infections that arise.
 Medications: To control liver cell damage caused by hepatitis B or C (Tenofovir,
Sofosbuvir) .
 A Sengstaken-Blakemore tube with a balloon
 Banding: A small band is placed around the base of the varices to control
bleeding.
 Transjugular intrahepatic portosystemic stent shunt (TIPSS)
 Liver Transplantation

24. Medications
 Diuretic: Increases urine production to get rid of excess salt and
water.
 Ammonia reducer: Reduces the amount of ammonia in the
body.
 Beta blocker: Slows heart rate and decreases blood pressure.
When taken in eye-drop form, it reduces eye pressure.
 Antibiotics: Stops the growth of or kills bacteria.
 Antiviral drug: Reduces viruses' ability to replicate.

28. NURSING MANAGEMENT
 Ineffective breathing pattern related to ascites and
restriction of thoracic excursion secondary to ascites,
abdominal distention, and fluid in the thoracic cavity.
 Chronic pain and discomfort related to enlarged tender liver
and ascites
 High risk for injury related to altered clotting mechanisms
and altered level of consciousness.

29.  Fluid volume excess related to ascites and edema
formation.
 Disturbed thought processes related to deterioration of liver
function and increased serum ammonia level.
 Imbalanced nutrition: less than body requirements, related
to abdominal distention, discomfort and anorexia.
 Activity intolerance related to fatigue, lethargy, and
malaise.

30. Portal hypertension
 Obstructed blood flow through the damaged liver results in
increased blood pressure (portal hypertension) throughout
the portal venous system.
 Portal hypertension may be caused by intrinsic liver
disease, obstruction, or structural changes that result in
increased portal venous flow or increased hepatic
resistance.

31.  Hepatic venous pressure gradient (HVPG)
 An HVPG of ≥5 mmHg defines portal hypertension, and if
the measurement exceeds 10 mmHg it is called clinically
significant portal hypertension.
 Above 12 mm Hg, variceal hemorrhaging may occur.

32. ASCITES
 Ascites is the accumulation of an excessive (larger than
normal) amount of fluid in the abdominal cavity.
 Ascites is the abnormal buildup of fluid in the abdomen.
Technically, it is more than 25 mL of fluid in the peritoneal
cavity.
 Symptoms may include increased abdominal size, increased
weight, abdominal discomfort, and shortness of breath

34. Causes
 Cirrhosis – 81% (alcoholic in 65%, viral in 10%, cryptogenic in 6%)
 Heart failure – 3%
 Constrictive pericarditis
 Kwashiorkor (childhood protein-energy malnutrition)
 Infection: Tuberculosis – 2% or spontaneous bacterial peritonitis
 Pancreatitis – 1%
 Nephrotic syndrome

35. Pathophysiology
 The mechanisms responsible for the development of ascites
are not completely understood.
 Portal hypertension and the resulting increase in capillary
pressure and obstruction of venous blood flow through the
damaged liver are contributing factors.
 The failure of the liver to metabolize aldosterone increases
sodium and water retention by the kidney.

36. Pathophysiology

38. Grades of Ascites
 Grade 1: mild, only visible on ultrasound and CT
 Grade 2: detectable with flank bulging and shifting dullness
 Grade 3: directly visible, confirmed with the fluid wave/thrill
test

39. Clinical Manifestations
 Increased abdominal girth and rapid weight gain are
common presenting symptoms of ascites.
 The patient may be short of breath and uncomfortable
from the enlarged abdomen, and striae and distended veins
may be visible over the abdominal wall.
 Fluid and electrolyte imbalances are common.

40. Medical Management
 The goal of treatment for the patient with ascites is a
negative sodium balance to reduce fluid retention.
 DIURETICS: Use of diuretics along with sodium restriction
is successful in 90% of patients with ascites.
 BED REST: In patients with ascites, an upright posture is
associated with activation of the renin-angiotensin-
aldosterone system and sympathetic nervous system.

41. PARACENTESIS
 Paracentesis is the removal of fluid (ascites) from the
peritoneal cavity through a small surgical incision or
puncture made through the abdominal wall under sterile
conditions.

44. Hepatic Encephalopathy and coma
 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.
 Hepatic Encephalopathy (HE) is a state of CNS dysfunction, resulting
from failure of liver to detoxify toxic agents because of hepatic
insufficiency and porto-systemic shunt.
 It occurs most often in patients with cirrhosis but also occur in acute
hepatic failure.
 Hepatic coma represents the most advanced stage of hepatic
encephalopathy.

45. HE

46. CLINICAL MANIFESTATION
 Disturbances in sleep
 Impaired memory
 Mental confusion
 Drowsiness / Somnolence
 Coma
 May be aggressive out burst
 Euphoric

48. Diagnosis
 Routine Investigations - CBC, LFTS, Electolytes, Urea,
Creatinine, Prothrombin time, Albumin , A/G ratio, Blood
ammonia level
 EEG: shows generalized slowing, an increase in the
amplitude of brain waves, and characteristic triphasic waves
 CSF culture
 CT Scan and MRI

49. MEDICAL MANAGEMENT
 Specific treatment aims at :
 Decreasing ammonia production in colon
 Elimination or treatment of precipitating factors