As a nurse, you will often come across a patient with some kind of liver problem.  While a lot of the times it will be due to alcohol abuse or hepatitis resulting from unsafe sex or needle use it is important not to assume such is the case, despite the age or appearance of the patient.  As I learned from this lecture, there are quite a number of factors that lead to liver problems and liver disease.  The causes of liver problems aren’t always Tylenol, alcohol, unsafe sex, or sharing dirty needles.  What are the other causes?  Well, read on and find out.  By the end of this post you should be an expert on the ways of the liver, oh Nursing Ninjas.

Nursing Lecture Study: Liver Disorders Cirrhosis

Chronic and progressive disease that causes extensive destruction (scarring) of liver cells

Destroyed cells are replaced by scar tissue

Characterized by diffuse fibrotic band of connective tissue that distort the liver’s normal architecture

incidence and prevalence is not well known and deaths from cirrhosis is about 43, 000 per year.

Pathophysiology of Cirrhosis

inflammation from toxins or disease results in the destruction and degeneration of hepatocytes

with cirrhosis, the tissue becomes nodular.  The nodules can block bile ducts and normal blood flow throughout the liver

initially the liver is enlarged… further progression leads to liver shrinkage

Compensated and Decompensated Cirrhosis

Compensated Cirrhosis:

In compensated cirrhosis the liver has significant scarring but is still able to perform essential functions without significant signs and symptoms.

Decompensated Cirrhosis:

In decompensated cirrhosis there is significant impairment with obvious manifestations of liver failure.  There is also a loss of hepatic function.

Complications of Cirrhosis:

Portal Hypertension (Portal HTN):

Portal hypertension is the persistent and abnormal increase in the pressure within the portal vein portal hypotension is a major complication of cirrhosis.

Ascites:

Ascites is the distention of the abdomen from the accumulation of fluid in the peritoneal cavity caused by an increase in hydrostatic pressure from portal hypertension.  A paracentesis can be performed to remove this fluid.  However, removing abdominal fluid too quickly can cause a dangerous drop in blood pressure and shock.

Bleeding Esophageal Varices:

Blood that is backed up from the liver and enters the esophageal and gastric vessels cause little vessels to become distended.  Since these blood vessels are already fragile they are easily ruptured.

Coagulation Defects:

Since the liver plays a role in the synthesis of clotting proteins, impairment of the liver will affect coagulation.

Impaired Absorption of Fat Soluble Vitamins:

The decreased synthesis of bile in the liver leads to a decrease of absorption of fat soluble vitamins due to the lack of a sufficient amount of bile.

Jaundice:

yellowish coloration of the skin in patients with cirrhosis.  Jaundice is caused by one of two ways:

Intrahepatic obstruction jaundice

is a result of fibrosis, edema, or scarring of the hepatic bile channels and bile ducts.  This obstruction interferes with normal bilirubin in bile excretion.

Hepatocellular jaundice

this is a result of the liver’s inability to effectively excrete bilirubin and causes excessive circulating bilirubin levels.

Hepatocellular disease:

damage to the liver cell

Intrahepatic obstruction:

Result of fibrosis, edema, or scarring of the hepatic bile channels and bile ducts.

Hemolytic jaundice:

Portal-Systemic Encephalopathy (PSE):

Manifestations include neurological symptoms like altered level of consciousness, impaired thinking processes, and neuromuscular disturbances.  It is a clinical disorder seen in patients with cirrhosis and hepatic failure.  It is also known as hepatic encephalopathy and hepatic coma.  The hepatic coma is the latest stage.

Portal-Systemic Encephalopathy may be due to the shunting of portal Venice blood into central circulation, bypassing the liver:  toxic substances are broken down cause in elevated ammonia levels.  (This condition is not seen in all patients with high serum ammonia levels and vice versa.)

Precipitation factors of PSE

-          high-protein diet

-          infections

-          hyperkalemia and hypokalemia

-          constipation

-          GI bleed (causing high-protein load and intestines)

-          Drugs

Stages of PSE

stage I: Prodromal

subtle manifestations that may not be recognized immediately

personality changes

behavioral changes such as agitation and belligerence

emotional lability such as euphoria or depression

impaired thinking

inability to concentrate

fatigue drowsiness

slurred or slowed speech

disturbances in sleep pattern

stage II: Impending

continuing mental changes and mental confusion

disorientation to time place or person

Asterixis: hand flapping

stage III: Stuporus

progressive deterioration

marked mental confusion

Stuporus, drowsy but arousable

abnormal electroencephalogram tracing

muscle twitching

hyperflexia

Asterixis

stage IV: comatose

unresponsiveness bleeding to death in most patients progress and to the stage

unarousable, obtunded

response to painful stimulus

no Asterixis

positive Babinsky’s sign

muscle rigidity

fetor hepaticus – characteristic liver breath which is a musty, sweet order

seizures

Spontaneous Bacterial Peritonitis:

A potential infection in patients with ascites caused by bacteria in fluid accumulated in the peritoneum cavity.  Patients often have mild symptoms such as loss of appetite and a low-grade fever.  More severe symptoms include fever, abdominal pain, and a change in their mental status.

Cirrhosis Etiology

alcohol

viral hepatitis

autoimmune hepatitis

Steatohepatitis

drugs and toxins

biliary disease

primary biliary cirrhosis (PBC)

primary sclerosing cholangitis (PSC)

metabolic and genetic causes:

Hemachromatosis

Wilson’s disease

Alpha/antitrypsin deficiency

Cystic Fibrosis

cardiovascular disease

Nursing assessment for cirrhosis

history taking

age/gender/race

employment history such as exposure to harmful toxins

family history: alcoholism or liver disease

alcohol use and habits

liver disease history

previous medical conditions

jaundice/hepatitis

heart failure

respiratory disorders

physical assessment

abdomen

ascites: massive or minimal, measure girth around the umbilical

hepatomegaly

other

Melena

Fetor hepaticus

Gynecomastia

Asterixis (Flapping Tremor)

lab assessment

total serum Bili

indirect Bili elevated

urobilinogen elevated

fecal urobilinogen decreased

elevated due to enzymes released into blood during hepatic inflammation

aspartate aminotransferase (AST)

Alanine amniotransferase (ALT)

AST/ALT mayt not be elevated in severe disease as hepatocytes may be unable to create inflammatory response.

Lactate dehydrogenase (LDH)

radiographic assessment

x-rays

CT

Ultrasound

MRI

more diagnostics of cirrhosis

percutaneous biopsy

EGD

Clinical manifestations of cirrhosis

early manifestations include:

fatigue

significant change in weight

G.I. symptoms

abdominal pain and liver tenderness

pruritis

late manifestations include:

jaundice/icterus

dry skin

rashes

petechiae

Palmer erythema

spider angiomas

peripheral dependent edema

Nursing diagnoses related to liver problems

1. excessive fluid Valium related to edema (portal hypertension)

2. potential for hemorrhage

PC: Hemorrhage

interventions based on identifying the source of bleeding and stopping it

nonsurgical management

coagulation drug therapies goal is to prevent bleeding

beta blocker (Inderal LA)

if bleeding occurs…

gastric intubation

balloon tamponade

blood products

transjugular intrahepatic portal systemic shunt (TIPS)

endoscopic procedures:

Endoscopic injection Sclerotherapy

Endoscopic band ligation

Surgical management of hemorrhaging related to cirrhosis

surgical bypass shunting procedures

Portal-systemic shunts

Decrease portal hypertension by diverting a portion of the portal vein blood flow from the liver

Electrocautery, cryoablation and laser procedures

Monitor postoperatively for hemorrhaging – coagulation studies (PT/PTT, Plt, INR)

3. Potential for portal systemic encephalopathy

Nursing and Medical interventions of PSE

Diet

high carb/moderate fat/high protein

Drugs

Lactulose

Neomycin sulfate

Metronidazole

Pt. Education

Diet/drug/alcohol abstinence

Neural- monitoring

Medical management of cirrhosis

Diet therapy

Low-sodium restriction: 500 mg to 2 g

Fluid restrictions, which are not always necessary

Vitamin supplements added to IV therapy

Drug therapy

Diuretics such as Lasix and Aldactone

monitor potassium

Abdominal paracentesis

Performed at bedside; rapid removal of ascitic fluid leads to decreased abdominal pressure, contributing to vasodilation and shock

Comfort measures

Respiratory difficulty; head of bed up 30° or up in chair

Fluid and electrolyte management

Monitor electrolytes such as BUN, serum protein and Hct

Surgical management of cirrhosis

Peritoneovenous shunt

Portacaval shunt

Transjugular Intrahepatic portal-systemic shunt

Nursing management of jaundice

Assessment

Yellow sclera, yellow skin, Clay colored stool, tea colored urine, Pruritis, fatigue, anorexia

Impaired skin integrity

Change linens

Loose and soft clothing

Body image disturbance

Linens, clothing may be yellow; usually temporary

Hepatitis

Inflammation of the liver

3 phases of the virus

Phase 1

Lasts 1 to 21 days; ineffective in the is at its height; GI symptoms domine

Phase 2

Lasts 2 to 4 weeks; symptoms due to spread of bilirubin through pruritus; dark urine, Clay colored stools in jaundice

Phase 3

Lasts 2 to 4 months, jaundice results slowly

Client remains fatigue; hepatomegaly persists

Viral Hepatitis

Hepatitis A, B, C, D, E. (HAV, HBV, HCV, HDV, HEV)

Hepatitis A

A ribonucleic acid virus of the and enterovirus family

Mild course, similar to typical viral syndrome

Incubation is 15 to 50 days

Sources of infection include contaminated water and food contaminated by food handlers

Hepatitis B

Double shelled — DNA with core antigen, surface antigen, and another core antigen

circulates in the blood

Symptoms occur within 25 to 180 days of incubation; 40% have no symptoms

anorexia, fever, fatigue, right upper quadrant pain, dark urine with light stool, joint pain, jaundice

Sources of infection include unprotected sex, sharing meals, accidental needle sticks, hemodialysis, and maternal feeder route.

Blood tests confirmed infection and most adults recover however, & do not develop immunity and are hepatitis carriers

Hepatitis C

single-stranded RNA virus

transmitted from blood to blood and is most commonly spread by illicit IV drug needle sharing, blood to blood products or organ transplants reseed prior to 1992, needlestick injury, unsanitary tattoo equipment, sharing intranasal cocaine.

Damage is accumulated over decades by causing chronic inflammation in the liver — causes hepatocytes to scar and can lead to cirrhosis and is the leading indication for liver transplantation in the US.

Hepatitis D

Delta Hepatitis is a defective RNA virus that needs helper function of HBV.

Coincides with HBV and needs its presence for viral replication or can occur as a superinfection in a patient with chronic HBV

Superinfection will usually result in chronic HD

Incubation is 14 to 56 days and is transmitted through the parenteral routes

Hepatitis E

Non-envelope the single-stranded RNA virus originally identified by its association with waterborne epidemics of hepatitis in the Indian subcontinent

Clinical courses similar to hepatitis A

Incubation period 15 to 64 days

Its prevalence in the US is found only in travelers returning from endemic areas such as Asia, Africa, and Mexico.

Clinical findings of hepatitis

Jaundice                              vomiting

Lethargy                              pain

Irritability                           diarrhea/constipation

Myalgia                                hepatic encephalopathy

Anorexia                             anemia

Nausea                                 bleeding tendencies

Pharmacologic treatment of hepatitis

There is no direct pharmacological treatment for viral hepatitis; care is supportive only

No ABX

Antiemetics

Vitamin K

Antihistamines

Immunoglobulin for family and friends prophylaxis

Avoid estrogens, aspirin, acetaminophen, infinitives

Complications of hepatitis

Fulminant hepatitis

failure of liver cells to regenerate — progression of necrotic process and is often fatal

Chronic hepatitis

Dietary treatment of hepatitis

high-protein, high calorie food with low to moderate fat content as tolerated

4 to 6 small meals a day

no alcohol

Nursing management of hepatitis

Assessment

exposure to risk factors, jaundice, hepatic encephalopathy, liver function tests

Fatigue

bed rest, advance activity with frequent rest periods

Altered nutrition

Nutritious breakfast as anorexia worsens during the day; it calories with Candy, juice

Hepatitis: early client considerations

higher risk of liver damage and developing complications

Fatty liver

accumulation of fat which causes liver enlargement increases firmness and decreases liver function

elevated AST/ALT

causes include

diabetes mellitus,

obesity,

elevated lipid panel

chronic alcoholism

protein malnutrition

hepatotoxins

prolonged TPN

hepatic abscess

pathophysiology

liver abscesses

pyogenic liver abscess

amebic liver abscess

Liver trauma

most common organ to be injured in patients with penetrating trauma of abdomen

lacerations, GSW, crush injuries, tears

liver damage should be suspected whenever there is any upper abdominal or lower chest trauma

Kehr’s sign

interventions

Dr. performs exploratory laparoscopy

blood may be given if suspected bleeding

Liver cancer

primary hepatic cancer or hepatocellular carcinoma is one of the most common cancers worldwide

rates are increasing

chronic HBV in hCG cause cirrhosis which is a risk factor for liver cancer

liver cancer has a vague presentation

a CT may be performed to evaluate mets

surgical management may be indicated in some cases however 75% of liver cancer victims are not candidates

chemotherapy

VS surgically implanted infusion pump

chemo with contrast

liver transplantation to treat cancer

physiological and psychological assessment is needed

patients who are not candidates for liver transplant include

severe cardiovascular instability with advanced cardiac disease

severe respiratory disease

active EtOH/substance abuse

metastatic malignant disease

inability follow instructions regarding meds and self-care

complications of liver transplants

rejection

tachycardia, fever, right upper quadrant pain, decreased bile pigment in volume, increasing jaundice, labs

success greatly improved since 1980 with the use of immunosuppressive drug cyclosporine

the rejection occurs the patient is in need of an emergency re-transplantation

post-op

assess for signs of rejection

administer treatment for rejection as directed

IV methylprednisone (Solumedrol)