Chapter 43 Assessment & Management of Patients w/ Hepatic Disorders Flashcards
Liver
Largest gland in the body
- Located in patient’s RUQ
Functions of the Liver
Glucose Metabolism
Ammonia Conversion
Protein Metabolism
Fat Metabolism
Vitamin and Iron Storage
Bile Formation
- Bilirubin is excreted in bile
The Liver’s Role in Glucose Metabolism
Plays a major role in the metabolism of glucose & the regulation of blood glucose concentration
The Liver’s Role in Ammonia Conversion
The use of amino acids from protein for glycogenesis results in the formation of ammonia as a by-product
The liver converts this ammonia into urea which is excreted in the urine
The Liver’s Role in Protein Metabolism
Synthesis of almost all the plasma proteins such as albumin, and blood clotting factors
The Liver’s Role in Fat Metabolism
Can break down fatty acids to produce energy and ketone bodies (can provide a source of energy for muscles).
Primarily happens when glucose is not available for metabolism
The Liver’s Role in Vitamin & Iron Storage
Vitamins A, B and D plus several of the B-complex vitamins along with iron and copper are stored in the liver
The Liver’s Role in Bile Formation
Bile is continuously formed by the liver and stored in the gallbladder
Empties into the intestine when needed for digestion of fats
Age-Related Considerations
Atypical clinical presentation of biliary disease
Decreases in:
- Drug metabolism and clearance capabilities
- Intestinal & portal vein blood flow
- Rate of replacement and repair of liver cells after injury
- Size & weight of the liver, particularly
Increased prevalence of gallstones due to the increase in cholesterol secretion in bile
More rapid progression of Hep C infection & lower response rate to therapy
More severe complications of biliary tract disease
**Changes is drug metabolism and clearance → may need to reduce dosage to prevent toxicity
Risk Factors for Hepatic Disorders
Previous exposure to hepatotoxic agents/infectious agents
Any alcohol/IV drug use
Meds that cause hepatic dysfunction
Health History
Exposure to:
Substances toxic to the liver (hepatotoxins)
Industrial chemical for example
Infectious diseases
Alcohol Use Risk for Cirrhosis
- Men: 60-80 g/day
- Women: 40-60 g/day
Drug use
- Including IV drugs (exposure to infectious diseases)
- Use of Tylenol
- Acetaminophen
- Ketoconazole
- Valporic acid
Lifestyle behaviors
Sexual practices
Foreign travel
Physical Assessment
Early Symptoms are vague & non-specific
- Fatigue
- Vague abdominal symptoms: loss of appetite, n/v, indigestion, gas, RUQ pain
Advanced Liver Disease/ Cirrhosis Symptoms
- Pallor
- Jaundice
- Peripheral edema & ascites
- Skin changes: palmor erythema, spider nevi
- Confusion or disorientation
- Extremities: Muscle atrophy, edema, skin excoriation r/t to itching
Physical Assessment Findings Associated w/ Hepatic Disorders: Integumentary Assessment
Pallor (chronic illness)
Assess skin, mucosa, & sclera for jaundice
Assess extremities for muscle atrophy, edema, and skin excoriation from scratching
Assess skin for petechiae, ecchymosis, spider angiomas, and palmar erythema
Male patient considerations: asses for unilateral or bilateral gynecomastia and testicular atrophy
Physical Assessment Findings Associated w/ Hepatic Disorders: Neurological Assessment
Recall
Memory
Abstract thinking
General tremor, asterixis, weakness, and slurred speech
Assess for Associated Nervous System Disorders
- Depression
- Mood changes: anger & irritability
Physical Assessment Findings Associated w/ Hepatic Disorders: Percussion & Palpation
-Assess for the presence of abdominal fluid
-Assess the liver size and detect tenderness
-When palpable, the liver is in the right upper quadrant with a firm, sharp ridge
Tenderness indicates acute enlargement
Size of liver determined by percussion
Nurse notes and records size, consistency, tenderness, and whether its outline is regular or irregular
Patient Assessment Related to Genetic Hepatic Disorders
Assess for physical signs or history of the following:
- Abdominal bloating & constipation
- Changes to skin color or yellow hue to sclera
- Enlarged liver, abdomen, or spleen
- Episodes of n/v
- Hemorrhoids, esophageal varices, or gallstones
- Intolerance to fatty foods or alcohol
- Pale stools
- Presence & frequency of dyspepsia or reflux
- Unexplained weight loss
- Assess for associated blood-sugar problems
- Inquire about & assess for abnormal bleeding/ bruising
- Obtain & review lab values
-> LFTs, ammonia, bilirubin, & fat soluble vitamins
Cirrhosis
Chronic liver disorder characterized by fibrotic changes, the formation of dense connective tissue w/in the liver, subsequent degenerative changes, & loss of functional liver tissues
Asterixis
Involuntary flapping of the hands
Diagnostic Evaluation: Common Lab
Tests to Assess Liver Function
Liver enzymes: (Serum AST, ALT, GGT) are elevated
Total protein and albumin
will be decreased
Increased ammonia level
Elevated LDH
Increased serum bilirubin
Increased PT
Serum alkaline phosphatase
Increased lipids
Refer to Table 43-1 (pg.1370)
AST (SGOT) Range
10-40 U/mL
ALT (SPGT) Range
8-40 U/mL
Normal Albumin Range
3.5-5.2 g/dL
Normal PT & INR Range
PT: 11-13 secs
INR: <1.1
Alkaline Phosphate Range
52-142 U/L
Total Bilirubin Normal Range
0.3-1.0 U/L
At what total bilirubin level does jaundice manifest?
> 2.0 mg/dL
Liver Function Tests (LFTs)
Serum aminotransferases
* Levels increase primarily in liver disorders
* Used to monitor the course of hepatitis, cirrhosis, the effects of treatments that may be toxic to the liver
Alanine aminotransferase (ALT)
* Not specific to liver diseases
* Levels of AST may be increased in cirrhosis, hepatitis, and
liver cancer
Aspartate aminotransferase (AST)
* Levels are associated with cholestasis; alcoholic liver disease
Gamma-glutamyl transferase (GGT)
Diagnostic Evaluation
Diagnostic testing may include the following:
CT & ultrasound
Liver biopsy: confirms dx
Analysis of ascitic fluid
Radio Isotope Liver Scan
May be performed to assess liver size, blood flow, & obstruction
Liver Elastography
Uses ultrasound-based vibration & scanning to identify liver fibrosis & determine its extent
Magnetic Resonance Elastography
Uses mechanical shear waves to identify stiff tissue
Nursing Role in Liver Biopsy
Prior to sending a patient for biopsy:
Assess Vital Signs
**Make sure coagulation studies completed
Abnormalities are treated
Compatible donor blood is available
Post-procedure:
Assume the right side-lying position with a pillow placed under the right
costal margin.
VS per orders
Assess for S&S of bleeding
Which hepatic dysfunction is more common? Acute or Chronic?
Chronic
Hepatic Dysfunction
Acute or chronic - cirrhosis of the liver
Liver failure associated with alcohol use
Infection
Fatty liver disease
Nonalcoholic fatty liver disease (NAFLD)
Nonalcoholic steatohepatitis (NASH)
Fatty Liver Disease
Accumulation of lipids in the liver
Manifestations of Hepatic Dysfunction
Jaundice
Portal hypertension
Ascites and varices
Hepatic encephalopathy or coma
Nutritional deficiencies
Jaundice
Caused by the inability of damaged liver cells to clear normal amounts of bilirubin from the blood
Yellow- or greenish- yellow sclera and skin
Bilirubin level exceeds 2 mg/dL
Hemolytic,
hepatocellular,
obstructive
Hereditary hyperbilirubinemia
- Hepatocellular and
obstructive jaundice are
most associated with
liver disease
Stool changes w/jaundice
Clay-colored stool
Steatorrhea
“Fatty Stool”
Bulky, pale foul-smelling stool
Hemolytic Jaundice
Result of an increased destruction of RBCs
- Effect: Plasma is rapidly flooded w/bilirubin -> liver cannot excrete the bilirubin as quickly as it is formed
Encountered in patients w/ hemolytic blood transfusion reactions & other hemolytic disorders
Clinical Manifestations of Hemolytic Jaundice
Bilirubin is predominately unconjugated or free
Urine & fecal urobilinogen levels are increased (urine is free of bilirubin)
Unless hyperbilirubinemia is extreme, pts do not experience complications
If prolonged:
- Predisposes to formation of pigments stones in gall bladder
- Severe jaundice (bilirubin exceeds 20-25 g/dL)
- Poses a CNS risk
Hepatocellular Jaundice
Mild or severely ill
Lack of appetite, N/V, weight loss
Malaise, fatigue, weakness
Headache, chills, fever, infection
Obstructive Jaundice
Maybe caused by occlusion of the bile duct from a gallstone, inflammatory process, tumor, or pressure from enlarged organ
Dark orange-brown urine, clay-colored
stools
Dyspepsia and intolerance of fats,
impaired digestion
Pruritus
What skin changes occur w/jaundice?
Yellow pigmentation of the skin & pruritus
Portal HTN
Obstructed blood flow through the liver results in increased pressure throughout the portal venous system
Cirrhosis is the most common cause
Results in: Ascites & Esophageal varices
Physical Assessment Findings Associated w/ Portal HTN
Splenomegaly w/hypersplenism
Portal HTN results in…
…ascites and esophageal varices
Ascites
Accumulation of fluid in the abdominal cavity
Pathophysiological Processes of Ascites
1) Portal HTN resulting in increased capillary pressure and obstruction of venous blood flow
2) Vasodilatation of splanchnic circulation (blood flow to the major abdominal organs)
3) Changes in the ability to metabolize aldosterone, increasing fluid retention
4) Decreased synthesis of albumin, decreasing serum osmotic pressure
5) Movement of albumin into the peritoneal cavity
Clinical Manifestations of Ascites
Increased abdominal girth
Rapid weight gain
SOB due to enlarged abdomen
Distended veins may be visible over abdomen
Umbilical hernia may occur
Fluid and electrolyte imbalances are common
Edema of lower extremities
Assessment of Ascites
Record abdominal girth and weight daily
Patient may have striae, distended veins, and umbilical hernia
Assess for fluid in abdominal cavity by percussion for shifting dullness or by fluid wave
Monitor for potential fluid and electrolyte imbalances
Treatment of Ascites
Low Na+ diet
Diuretics
Bed rest
Paracentesis
Admin of albumin infusions: Ensure that BP doesn’t bottom out
Transjugular Intrahepatic Portosystemic Shunt (TIPS)
Advantages of Transjugular Intrahepatic Portosystemic Shunt(TIPS)
Reduces portal HTN
Decreases Na+ retention
Prevents reoccurrence of fluid accumulation
Medical Management of Ascites
Paracentesis
IV infusion of albumin
Provides only temporary removal of fluid
Paracentesis
Removal of large volume (5-6L) ascites from peritoneal cavity
Nursing Interventions for Paracentesis
Review labs
Monitor vitals
Post-procedure: assess puncture site for bleeding
Monitor for S&S of infection
Nursing Management of Ascites
Strict I&O
Measure abdominal girth
daily
Daily weights
Close monitoring of respiratory status
Monitoring of labs:
Serum ammonia
Creatinine
Electrolyte values
Hepatic Encephalopathy & Coma
Life-threatening complication of liver disease seen in profound liver failure.
Accumulation of ammonia and other toxic metabolites in the blood
Survival is 40% after first bout w/ hepatic encephalopathy
Two major alterations underlie its development in acute and chronic liver disease
- Hepatic insufficiency: the inability of the liver to detoxify toxic by-products of metabolism - Portosystemic shunting: collateral vessels develop allowing elements of the portal blood (laden with potentially toxic substances usually extracted by the liver) to enter the systemic circulation
Early signs: mental changes and motor disturbances
Hepatic Insufficiency
The inability of the liver to detoxify toxic by-products of metabolism
Portosystemic Shunting
Collateral vessels develop allowing elements of the portal blood (laden with potentially toxic substances usually extracted by the liver) to enter the systemic circulation
Hepatic Encephalopathy Clinical Manifestations
Early Signs:
Mental status changes
Confusion
Motor disturbances
Asterixis- involuntary flapping of the hands
Handwriting becomes difficult (Apraxia)
Sleeps during day
Insomnia at night
Late Signs:
Becomes difficult to awaken
Completely disorientated
Coma
Seizures
Assessment & Stages of Hepatic Encephalopathy
Assessment
EEG
Changes in LOC
Potential seizures
Fetor hepaticus
Monitor fluid, electrolyte, and ammonia levels
Stage 1 of Hepatic Encephalopathy
Normal LOC
Stage 2 of Hepatic Encephalopathy
Increased drowsiness
Stage 3 of Hepatic Encephalopathy
Stuporous
Difficult to arouse
Stage 4 of Hepatic Encephalopathy
Comatose
- May not respond to painful stimuli
Medical Management of Hepatic Encephalopathy
Eliminate precipitating cause
Lactulose to reduce serum ammonia levels
Oral
NG tube
Enema
IV glucose to minimize protein catabolism
Avoid protein restriction
Reduction of ammonia from GI tract by gastric suction, enemas, oral antibiotics
Discontinue sedatives, analgesics, and tranquilizers
Monitor or treat complications and infections
Nursing Management of Hepatic Encephalopathy
Maintain safe environment, prevent injury: Pad all 4 siderails
Monitor for respiratory compromise due to depressed neurological status
Positions changes every 2 hours
Prevent skin breakdown, atelectasis
Neuro checks every 2-4 hours
Strict I & O
Daily weights
Monitor results of Ammonia testing, electrolytes
Daily handwriting
Esophageal Varices
Occurs in 30% of patient with compensated cirrhosis and 60% of
patients with decompensated cirrhosis
First bleeding episode has a mortality rate of 10% to 30% depending on
severity
Manifestations include hematemesis, melena, general deterioration, and
shock
Patients with cirrhosis should undergo screening endoscopy every 2 to 3 years
Clinical Manifestations of Esophageal Varices
Hematemesis
Melena
Mental deterioration
Shock
-Tachycardia
-Hypotension
-Cool clammy skin
Melena
Black, tarry stool
Treatment of Bleeding Varices
Treat for shock; administer oxygen
IV fluids, electrolytes, volume expanders, blood and blood products
Vasopressin, somatostatin, octreotide to decrease bleeding
Nitroglycerin in combination with vasopressin to reduce coronary vasoconstriction
Propranolol and nadolol to decrease portal pressure; used in combination with other treatment
Balloon tamponade
Procedural Treatment of Bleeding Varices
Endoscopic sclerotherapy
Endoscopic variceal ligation (esophageal banding therapy)
Transjugular intrahepatic portosystemic shunt
Additional therapies
Surgical management
Surgical bypass procedures
Devascularization and transection
Endoscopic
Sclerotherapy
Nursing Management of Esophageal Varices
Maintain a safe environment
Prevent injury
Bleeding
Infection
Administer prescribed treatments and monitor for potential complications
Encourage deep breathing and position changes
Education and support of patient and family
Viral Hepatitis
A systemic viral infection that causes
necrosis and inflammation of liver cells with characteristic symptoms and cellular and biochemical
changes
Hep A
Spread via poor-hand hygeine; fecal oral route
Incubation: Between 2-6 weeks
Illness may last 4-8 weeks
Mortality rate <40 yrs: 0.5%
Clinical Manifestations of Hep A
Mild flu-like symptoms
Low-grade fever
Anorexia
Later jaundice and dark urine, indigestion and epigastric distress, enlargement of liver and spleen
Management of Hep A
Promote Prevention
-Good handwashing, safe H2O, & proper sewage disposal
-Vaccine
-Immunoglobulin injections (if not previously vaccinated) for sexual contacts and household members to provide passive immunity
Encourage bed rest during the acute stage
Provide nutritional support: frequent small feedings & IV fluids w/glucose
Hep B
Transmitted through blood, saliva, semen, and vaginal secretions; sexually transmitted; transmitted to the infant at the time of birth
A major worldwide cause of cirrhosis and liver cancer Long incubation period: 1 to 6 months
Clinical Manifestations of Hep B
Insidious and variable; similar to Hepatitis A
Loss of appetite
Dyspepsia
Abdominal pain
Generalized aching
Malaise, and weakness
Jaundice may or may not be evident
Management of Hep B
Administer medications for chronic hepatitis type B including alpha-interferon and antiviral agents: entecavir (ETV) and tenofovir (TDF)
Promote bed rest and nutritional support-gradual resumption of physical activity
Promote vaccine: for persons at high risk, routine vaccination of infants
Passive immunization for those exposed
Standard precautions and infection control measures
Screening of blood and blood products
Hep C
Transmitted by blood and sexual contact, including needle sticks and sharing of needles
The most common bloodborne infection
A cause of one-third of cases of liver cancer and the most common reason for liver transplant
Incubation period is variable: ranging from 15 to 160 days
Symptoms are usually mild
Chronic carrier state frequently occurs
Management of Hep C
Administer antiviral medications
Educate patient on avoiding alcohol and medications that affect the liver
Promote prevention: public health programs to decrease needle sharing among drug users
Screening of blood supply
Use safety needle
Hepatitis D
Only persons with Hepatitis B are at risk
Blood and sexual contact transmission
Use of IV or injection drugs, patients undergoing hemodialysis, and recipients of multiple blood transfusions
Likely to develop fulminant liver failure or chronic active hepatitis and cirrhosis
Incubation period between 30 and 150 days
Interferon alfa is the only licensed drug available in
the treatment for HDV infection
Hepatitis E
Transmitted by fecal–oral route, contaminated water
Incubation period: 15 to
65 days
Resembles Hepatitis A; self-limiting, abrupt onset, not chronic
Prevention: good hygiene,
handwashing
Pathophysiology of Hepatic Cirrhosis
Episodes of necrosis of hepatic celss
Destroyed liver cells replaced by scar tiss
Amount of scar tissue exceeds that of func liver tiss
Alcoholic Hepatic Cirrhosis
Scar tissue characteristically surrounds the portal areas
Postnecrotic Hepatic Cirrhosis
Broad bands of scar tissue from previous acute hepatitis
Biliary Hepatic Cirrhosis
Scarring occurs in the liver around the bile ducts
Clinical Manifestations of Hepatic Cirrhosis
Liver enlargement
Portal obstruction
Ascites
Infection and peritonitis
Varices, GI varices
Edema
Vitamin deficiency
Anemia
Mental deterioration
What skin changes occur w/jaundice?
Yellow pigmentation of the skin & pruritus
