Nursing management of adults with disorders of the liver
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NURSING MANAGEMENT OF ADULTS WITH DISORDERS OF THE LIVER. 2009. TOPICS TO BE REVIEWED. HEPATITIS CIRRHOSIS STEATOHEPATITIS (FATTY LIVER) HEPATIC ABSCESS LIVER TRAUMA CANCER OF LIVER LIVER TRANSPLANT. NORMAL FUNCTION OF LIVER. MAIN FUNCTIONS OF THE LIVER: storage, protection, metabolism

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NURSING MANAGEMENT OF ADULTS WITH DISORDERS OF THE LIVER

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Nursing management of adults with disorders of the liver

NURSING MANAGEMENT OF ADULTS WITH DISORDERS OF THE LIVER

2009


Topics to be reviewed

TOPICS TO BE REVIEWED

HEPATITIS

CIRRHOSIS

STEATOHEPATITIS (FATTY LIVER)

HEPATIC ABSCESS

LIVER TRAUMA

CANCER OF LIVER

LIVER TRANSPLANT


Normal function of liver

NORMAL FUNCTION OF LIVER

MAIN FUNCTIONS OF THE LIVER: storage, protection, metabolism

Maintains normal serum glucose levels

Ammonia conversion

Protein metabolism

Fat metabolism

Vitamin and Iron storage

Drug metabolism and detoxification


Liver function glucose metabolism

LIVER FUNCTION: GLUCOSE METABOLISM

What happens to glucose in the liver?

Where is it stored?

When is it released?

What is gluconeogenesis?

When does it take place?


Liver function ammonia conversion

LIVER FUNCTION: AMMONIA CONVERSION

When gluconeogenesis takes place what is the byproduct of the process?

What happens to the byproduct?

What do the bacteria in the intestines produce as a byproduct?

How is this byproduct removed?


Liver function protein metabolism

LIVER FUNCTION:PROTEIN METABOLISM

What is the liver’s job in terms of synthesizing plasma proteins?

What does the liver need to complete it’s job?


Liver function fat metabolism

LIVER FUNCTION: FAT METABOLISM

What is the liver’s job in terms of fat metabolism?

When does the liver do this?

What are the results of this metabolism used for?


Liver function vitamin iron storage

LIVER FUNCTION: VITAMIN & IRON STORAGE

Stores which fat soluble vitamins?

What other vitamins are stored in the liver?

What are these vitamins responsible for?

Which minerals are stored in the liver?


Liver function drug metabolism and detoxification

LIVER FUNCTION: DRUG METABOLISM and DETOXIFICATION

THE FOLLOWING CLASSIFICATION OF DRUGS ARE METABOLIZED BY THE LIVER?

What else is metabolized by the liver?

What does the liver do in terms of detoxification?


Normal function bile secretion

NORMAL FUNCTION: bile secretion

What is the liver’s job with Bile?

When is bile secreted?

Where is Bile collected and stored?

How is this related to Billirubin?

When do Billirubin levels increase?


Liver function protection

LIVER FUNCTION: PROTECTION

  • What does the liver’s protection function involve?

  • What do the cells do?


Liver function continued

LIVER FUNCTION CONTINUED

Inactivates Hormones

Estrogen

Testoterone

Progesterone

Aldosterone

cortisol

Sinusoids store blood (about 200-400 cc)


Disorder of the liver

DISORDER OF THE LIVER

HEPATITIS


Hepatitis

Hepatitis

Widespread viral inflammation of liver cells

Hepatitis A (HAV)

Hepatitis B (HBV)

Hepatitis C (HCV)

Hepatitis D (HDV)

Hepatitis E (HEV)

Hepatitis F and G are uncommon (HFV, HGV)

DRUG INDUCED HEPATITIS

Occurs as a secondary infection


Hepatitis a hav

Hepatitis A (HAV)

Similar to that of a typical viral syndrome; often goes unrecognized

Spread via the fecal-oral route by oral ingestion of fecal contaminants

Contaminated water, shellfish from contaminated water, food contaminated by handlers infected with hepatitis A

Also spread by oral-anal sexual activity

(Continued)


Hepatitis a hav continued

Hepatitis A (HAV)(Continued)

Incubation period for hepatitis A is 15 to 50 days.

Disease is usually not life threatening.

Disease may be more severe in individuals older than 40 years of age.

Many people who have hepatitis A don’t know it; symptoms are similar to a gastrointestinal illness.


Hepatitis b hbv

Hepatitis B (HBV)

Spread is via unprotected sexual intercourse with an infected partner, sharing needles, accidental needle sticks, blood transfusions, hemodialysis, maternal-fetal route.

Symptoms occur in 25 to 180 days after exposure; symptoms include anorexia, nausea and vomiting, fever, fatigue, right upper quadrant pain, dark urine, light stool, joint pain, and jaundice.

(Continued)


Hepatitis b hbv continued

Hepatitis B (HBV)(Continued)

Hepatitis carriers can infect others, even if they are without symptoms.


Hepatitis c hcv

Hepatitis C (HCV)

Spread is by sharing needles, blood, blood products, or organ transplants (prior to 1992), needle stick injury, tattoos, intranasal cocaine use.

Incubation period is 21 to 140 days.

Most individuals are asymptomatic; damage occurs over decades.

Hepatitis C is the leading indication for liver transplantation in the U.S.

NOT TRANSMITTED BY CAUSUAL OR INTIMATE HOUSEHOLD CONTACT


Hepatitis d hdv

Hepatitis D (HDV)

Transmitted primarily by parenteral routes

Incubation period 14 to 56 days

HDV coinfects with HBV and needs it presence to replicate


Hepatitis e hev

Hepatitis E (HEV)

Present in endemic areas where waterborne epidemics occur and in travelers to those areas (India, Asia, Africa, Middle East, Mexico, Central America & South America)

Also seen in travellers coming from these areas

Transmitted via fecal-oral route

Resembles hepatitis A

Incubation period 15 to 64 days


Clinical manifestations of all hepatitis

Clinical Manifestations of all Hepatitis

Abdominal pain

Changes in skin or eye color

Arthralgia (joint pain)

Myalgia (muscle pain)

Diarrhea/constipation

Wgt loss

Hepatomegaly

Fever

Lethargy/Malaise

Nausea/vomiting

Intolerance to fats/dyspepsia

Pruritus

CHANGES IN COLOR OF URINE AND STOOL


Assessment

ASSESSMENT

HEALTH HISTORY

Suspected exposure

Medical history

SIGNS/SYMPTOMS

Pre-icteric stage

Icteric stage

Post-icteric stage


Signs symptoms

SIGNS/SYMPTOMS

PRE-ICTERIC STAGE

Lasts about 1 week


Signs and symptoms

SIGNS AND SYMPTOMS

ICTERIC STAGE

Lasts 2-6 weeks

Jaundice appears

Yellow skin, sclera, mucous membranes

Dark amber urine

Clay colored stools


Signs and symptoms1

SIGNS AND SYMPTOMS

POST-ICTERIC STAGE

Lasts 2-6 weeks

Jaundice subsides

Liver decreases in size

Good appetite


Laboratory tests for hepatitis

LABORATORY TESTS FOR HEPATITIS

There will be an increase of liver enzymes and serologic markers INDICATING A PRESENCE OF HEPATITIS A, B, C


Laboratory tests for hepatitis a hav

LABORATORY TESTS FOR HEPATITIS A (HAV)

Presence of hepatitis A in client: when hepatitis A (HAV) antibodies (anti-HAV) are found in the blood

Presence of immunoglobulin M(IgM) antibodies means that ongoing inflammation of liver present (persisits for 4-6 wks)

Previous infection indicated by presence of immunoglbulin G (IgG) antibodies which provides permanent immunity to disease


Laboratory tests for hepatitis b hbv

LABORATORY TESTS FOR HEPATITIS B (HBV)

Serologic markers which indicate client has Hepatitis B (HBV) are:

HBsAg (Hepatitis B surface Antigen)

Anti-HBc IgM (IgM antibodies to hepatitis B core antigen)

If these levels are elevated after 6 months: chronic or carrier state

Presence of antibodies to HBsAb (hepatitis B surface antibody): indicates recovery and immunity to hepatitis B

Someone immunized will have a positive HBsAb


Laboratory tests for hepatitis c hcv

LABORATORY TESTS FOR HEPATITIS C (HCV)

ELISA (enzyme linked immunosorbent assay ) SCREENS INITIALLY & for HCV antibodies (anti-HCV): can detect antibodies in 4 wks

RIBA: (recumbent immunoblot assay): used to confirm that client has been exposed and has developed antibody

HCV PCR (HCV polymerase chain reaction test): confirms presence of circulating active virus


Laboratory test for hepatitis d hdv

LABORATORY TEST FOR HEPATITIS D (HDV)

Presence of virus confirmed by identification of intrahepatic delta antigen

Also by rise in hepatitis D virus antibodies (anti-HDV) titer

Found within a few days of infection


Lboratory tests for hepatitis e hev

LBORATORY TESTS FOR HEPATITIS E (HEV)

VIRUS CANNOT BE DETECTED

Presence of hepatitis E antibodies (anti-HEV) is found in people infected with virus


Laboratory tests continued

LABORATORY TESTS CONTINUED

A person having a previous infection is indicated by immunoglobulin G (IgG) antibodies. They persist in blood and provide permanent immunity to HAV


Laboratory tests indicating hepatitis

LABORATORY TESTS INDICATING HEPATITIS

TESTS WHICH ARE LOWERED:

Leukocytes (leukopenia)

Serum albumin

Serum glucose (hypoglycemia)

PT (prolonged)

TESTS WHICH ARE

ELEVATED:

serum bilirubin

Bilirubin in urine

ALT

AST

Alkaline phosphatase elevated or may be normal


Nonsurgical management

Nonsurgical Management

Physical rest

Psychological rest

Drug therapy includes:

Antiemetics

Antiviral medications

Immunomodulators

Corticosteroids

DECREASE # MEDS TO ALLOW LIVER TO REST


Drugs

DRUGS

ANTIVIRALS:

Lamivudine (Epivir-HBV)

Adefovir dipivoxil (Hepsera)

USED: to destroy Hepatitis B virus in chronic disease

SIDE EFFECTS: alters renal function; granulocytopenia


Drugs1

DRUGS

IMMUNOMODULATING DRUGS:

Interferon(peginterferon alfa-2a) (Pegasys)

Oral ribavirin (Virazole)


Nursing care

NURSING CARE

Diet therapy

Hydration

No alcohol

Low fat, moderate protein, high CHO diet, high calorie

Small frequent meals

Vit B, C, K


Patient education

PATIENT EDUCATION

Prevention to health care professionals

Knowledge of transmission routes

Proper personal hygiene and good sanitation

Gamma Globulin

Avoid sex until antibody results (negative)

Hepatitis A Vaccine

Hepatitis B vaccine

No vaccine for Hepatitis E

Hepatitis C mainly spread through blood transfusions: (screen blood products)


Cirrhosis defined

CIRRHOSIS DEFINED

Chronic

Degenerative

Causes liver enlargement

Causes loss of normal liver function


Pathophysiology

PATHOPHYSIOLOGY

Fibrotic bands of connective tissue change the structure of the liver

Inflammation causes degeneration and destruction of liver cells

Tissue becomes nodular

Nodules block bile ducts and normal blood flow throughout the liver

Blood flow changes occur from compression by the fibrous tissue


Types of cirrhosis

TYPES OF CIRRHOSIS

Laennec’s cirrhosis: chronic ETOH, nutritional deficiencies

Biliary

Postnecrotic cirrhosis: hepatic necrosis

Cardiac: congestion and tissue damage due to heart failure


Etiology

ETIOLOGY

Known causes of liver disease include:

Alcohol

Viral hepatitis

Autoimmune hepatitis

Steatohepatitis

Drugs and toxins

Biliary disease

(Continued)


Etiology continued

ETIOLOGY CONTINUED

Metabolic/genetic causes

Cardiovascular disease


Early signs and symptoms cirrhosis

EARLY SIGNS AND SYMPTOMS CIRRHOSIS

Same for all types regardless of the cause

Start out vague, like flu

General weakness, Fatigue

Anorexia, Indigestion

Abnormal bowel function (constipation, or diarrhea)

Abdominal pain/liver tenderness


Late s s

LATE S & S

Jaundice, pruritus, dry skin, warm bright red palms of hands (palmar erythema), rashes

Edema, ascites, significant wgt change, peripheral dependent edema extremities and sacrum

Bleeding tendencies/Anemia/petecchiae, echymosis

Infections

Menstrual irreg/gynecomastia/impotence

Renal failure/dark amber urine

Clay colored stools


Assessment1

ASSESSMENT

INSPECTION:

Jaundice

Caput medusae: dilated abd veins,

striae,

spider angiomas

Contour of abdomen: Distension: massive ascites

Everted umbilicus (umbilicus protrusion)

HEPATOMEGALY, SPLENOMEGALY


Other physical assessments

Other Physical Assessments

Assess nasogastric drainage, vomitus, and stool for presence of blood

Fetor hepaticus (breath odor)

Amenorrhea

Gynecomastia, testicular atrophy, impotence

Neurologic changes: changes in LOC, leading to coma, Asterixis


How to elicit asterixis

HOW TO ELICIT ASTERIXIS

Have client extend the arm,

dorsiflex the wrist

Extend the fingers

OBSERVE rapid non-rhythmic extensions and flexions


Laboratory assessment

Laboratory Assessment

AST: Aminotransferase serum levels and LDH: lactate dehydrogenase may be elevated from hepatic cell destruction.

Alkaline phosphatase levels may increase from obstructive jaundice.

Total serum bilirubin from hepatic disease and urobilinogen levels may rise from hepatocellular obstruction or liver disease.

decrease.

(Continued)


Laboratory assessment continued

Laboratory Assessment(Continued)

Fecal urobilinogen is decreased due to obstructive liver disease

Total serum protein and albumin levels decreased

Prothrombin time prolonged; platelet count low

Decreased hemoglobin and hematocrit values due to anemia and white blood cell count


Laboratory assessment continued1

LABORATORY ASSESSMENT CONTINUED

Elevated ammonia levels: liver cannot excrete ammonia

BUN and Serum creatinine level possibly elevated due to decreased renal function


Complications portal hypertension

COMPLICATIONS: PORTAL HYPERTENSION

Increase pressure in portal vein

Comes from obstruction of blood flow from pressure by CT bands (see patho)

New channels looked for

Blood flows back to spleen (splenomegaly)

Veins become dilated (esophagus, stomach, intestines, abdomen, rectum)


Portal hypertension continued

PORTAL HYPERTENSION (CONTINUED)

Results in:

Ascites

Esophageal varices

Prominent abdominal veins (caput medusae)

hemorroids


Complication ascites

COMPLICATION: ASCITES

DEFINED AS:

Accumulation of free fluid within the peritoneal cavity

With increased hydrostatic pressure from portal hypertension fluid leaks into peritoneal cavity

Albumin in fluid hypoalbuminemia


Ascites continued

ASCITES CONTINUED

Hypovolemia renal vasoconstriction

Renin-angiotensin system triggered

Sodium and water retention

Leads to increased hydrostatic pressure

Perpetuates the cycle of ASCITES


Complications

COMPLICATIONS

ASCITES:

Bed rest, HOB up 30 degrees or higher; or sitting in chair

Abdominal girth measurements

bid wgts standing

Strict fluid restriction; strict I & O, vitamin supplements

Salt free diet/diuretics/electrolyte replacement


Excess fluid volume continued

Excess Fluid Volume(Continued)

Paracentesis is insertion of trocar catheter into abdomen to remove & drain fluid from the peritoneal cavity.

Observe for possibility of impending shock, electrolyte imbalances: albumin IV.


Excess fluid surgical management continued

EXCESS FLUID SURGICAL MANAGEMENT CONTINUED

LAVEEN SHUNT (peritoneovenous shunt): surgical procedure, tube placed in peritoneal cavity, drain fluid into superior vena cava

PORTACAVAL SHUNT: (See p 1378

fig 62.4) surgical shunting diverts portal venous blood flow from the liver

TIPS (transjugular intrahepatic portalsystemic shunt): non surgical procedure creating a connection within the liver between the portal and systemic circulation to reduce portal pressure


Complication bleeding esophageal varices

COMPLICATION: BLEEDING ESOPHAGEAL VARICES

DEFINED: fragile thin walled esophageal veins become distended from pressure

Portal hypertension blood backs up from liver to esophageal and gastric vessels


Complications1

COMPLICATIONS

ESOPHAGEAL VARICES

MEDICAL EMERGENCY

LIFE THREATENING

S&S: hematemesis, melena, shock

Can occur spontaneously

Can be caused by any activity that

Abdominal pressure


Treatment of bleeding esophageal varices

TREATMENT OF BLEEDING ESOPHAGEAL VARICES

IV fluids/electrolytes/volume expander/ transfuse

ESOPHAGOGASTRIC BALLOON TAMPONADE: via Sengstaken-Blakemore tube

Compressing bleeding vessels with this tube


Sengstaken blakemore tube

SENGSTAKEN-BLAKEMORE TUBE

Used to control bleeding

Esophageal balloon

Gastric balloon

3 lumens

1 for gastric lavage

1 for inflating the esophageal balloon

1 for inflating the gastric balloon


Sengstaken blakemore tube nrsg care

SENGSTAKEN-BLAKEMORE TUBE: NRSG CARE

MD inserts tube with HOB 30-45 degrees

MOST SERIOUS COMPLICATION: ASPIRATION AND AIRWAY OCCLUSION

SURGICAL SCISSORS AT BEDSIDE

Monitor for respiratory distress

Suction saliva from upper esophagus, nasopharynx

Check nostrils frequently, cleanse and lubricate to prevent ulceration

Removed after bldg controlled


Rupture of esophageal varicies

RUPTURE OF ESOPHAGEAL VARICIES

Vasopressin: constriction arterial bed

Somatostatin: decreases bldg without vasoconstrictive effects of Vasopressin

Propranolol: beta blocker to decrease portal pressure


Complication coagulation defects

COMPLICATION: COAGULATION DEFECTS

synthesis of bile in liver

Prevents absorption of fat soluble vitamins (vit K)

Without vit K clotting factors are not produced

susceptible to bleeding

Abnormal PT (prolonged or )


Complication splenomegaly

COMPLICATION: SPLENOMEGALY

Backup of blood into spleen

Spleen destroys platelets

thrombocytopenia (first sign of liver dysfunction)


Complication jaundice

COMPLICATION: JAUNDICE

Liver cells cannot excrete bilirubin

circulating bilirubin levels

LABORATORY TESTS: changes with hepatocellular jaundice

Serum bilirubin (indirect and direct)

Urine bilirubin

Urobilinogen stool: normal to

Urobilinogen urine: normal to


Complications portal systemic encephalopathy pse

COMPLICATIONS: PORTAL SYSTEMIC ENCEPHALOPATHY (PSE)

Also called HEPATIC ENCEPHALOPATHY AND HEPATIC COMA

SEE: neurologic symptoms

Impaired LOC

Impaired thinking

Impaired neuromuscular disturbances

ACUTE AND REVERSIBLE with early intervention

CAUSED BY: elevated ammonia levels


Nursing diagnosis

NURSING DIAGNOSIS

Activity intolerance

Fluid volume deficit

Fluid volume excess

Ineffective breathing patterns

Risk for hemorrhage

Risk for infection

Altered nutrition

Pain

Sexual dysfunction


Nursing diagnosis continued

NURSING DIAGNOSIS CONTINUED

Altered thought processes

Risk for violence


Nursing care1

NURSING CARE

Bed rest with controlled activity, prevent clots

Prevent infection (pneumonia)

Assess for bleeding

Treat dry itching skin: no soap, soft linens, lotions, antihistamines

Assess F & E status, bid wgts, abd girth once shift, I&O, fluid restriction, amt of dietary protein

Assess neuro status q 2 hr

Psychological support/abstinence of alcohol


Fatty liver steatohepatitis

Fatty Liver (Steatohepatitis)

Fatty liver is caused by the accumulation of fats in and around the hepatic cells.

Causes include:

Diabetes mellitus

Obesity

Elevated lipid profile

Many clients are asymptomatic.


Hepatic abscess

Hepatic Abscess

Liver invaded by bacteria or protozoa causing abscess

Pyrogenic liver abscess; amebic hepatic abscess

Treatment usually involves:

Drainage with ultrasound guidance

Antibiotic therapy


Liver trauma

Liver Trauma

The liver is the most common organ injured in clients with penetrating trauma of the abdomen, such as gunshot wounds and stab wounds.

Clinical manifestations include abdominal tenderness, distention, guarding, rigidity.

Treatment involves surgery, multiple blood products.


Cancer of the liver

Cancer of the Liver

One of the most common tumors in the world

LIVER BX: done in same day surgery, local anesthetic, done through skin. CRITICAL THAT COAGULATION TESTING BE DONE. MAJOR SE: hemorrhage

Most common c/o: abd discomfort

Tx includes: Chemotherapy/Surgery


Liver transplantation

Liver Transplantation

Used in the treatment of end-stage liver disease, primary malignant neoplasm of the liver

Donor livers obtained primarily from trauma victims who have not had liver damage

Donor liver transported to the surgery center in a cooled saline solution that preserves the organ for up to 8 hours


Complications2

Complications

Acute, chronic graft rejection

Infection

Hemorrhage

Hepatic artery thrombosis

Fluid and electrolyte imbalances

Pulmonary atelectasis

Acute renal failure

Psychological maladjustment


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