NDEE N3 Lecture ORIGINAL

Systemic, viral infection characterized by necrosis and inflammation of liver cells

Hepatitis A, B, C, D, and E

Hepatitis A

Hepatitis E

1. Viral replication phase --> asymptomatic; lab markers of hepatitis appear

2. Pre-icteric/prodromal phase --> s/s include anorexia, nausea/vomiting, fatigue, and pruritus

3. Icteric phase --> s/s include jaundice, dark urine; some pts experience abdominal pain secondary to enlarged liver

4. Convalescent phase --> s/s resolve; lab values return to normal

Caused by an RNA virus of the enterovirus family

Primarily transmitted through the fecal-oral route (e.g. poor hygiene, hand to mouth, contaminated foods and liquids, sexual activity)

Not transmitted by blood infusions

Most patients recover from Hepatitis A, and it RARELY progresses to acute liver necrosis or hepatic failure

Cirrhosis or death is uncommon in Hepatitis A cases

No carrier state exists

No chronic hepatitis associated with HAV

The virus is present only briefly in the serum

By the time jaundice occurs, the patient is likely to be noninfectious

Symptoms resemble those of a mild, flu-like upper respiratory tract infection, with low-grade fever

Anorexia --> Early symptom (often severe)

Jaundice and dark urine --> Late symptom

Indigestion --> vague epigastric distress, nausea, heartburn, flatulence

Strong dislike to taste of cigarettes, presence of cigarette smoke, and other strong odors

Liver and spleen are often moderately enlarged for a few days after onset

Other than jaundice, there are few other physical signs

HAV antigen may be found in the stool 7-10 days before illness and for 2-3 weeks after symptoms appear

HAV antibodies are detectable in the serum, usually not until symptoms appear

Analysis of subclasses of immunoglobulins can help determine whether the antibody represents acute or past infection

Scrupulous hand hygeine

Safe water supplies

Proper control of sewage disposal

The HAV vaccine is effective (95-100% after 2-3 doses) and safe

the two-dose vaccine is recommended for adults 18 years of age or older

Vaccination is recommended for:
- People traveling to locations with unsatisfactory sanitation and hygeine
- High-risk groups (e.g. gay sex, IV/injection drug users, daycare staff, healthcare personnel, those working with the virus in research or animal care settings)

HAV can be prevented by IM administration of immune globulin during the incubation period

Must be given within 2 weeks of exposure

Immune globulin may suppress overt symptoms of the disease

Immune globulin is recommended for household members and sexual contacts of people with HAV

Susceptible individuals in the same household are usually infected by the time diagnosis is made --> immune globulin is recommended

Institutional contacts of patients with HAV should also receive post-exposure prophylaxis with immune globulin

Bed rest during the acute stage

A nutritious diet

Frequent, small feedings

IV fluids with glucose should be supplemented PRN

Gentle persistence and creativity may be required to stimulate appetite.

Optimal food and fluid levels are necessary to counteract weight loss and speed recovery.

Management usually occurs in the home unless symptoms are severe

EDUCATION is key

Diet

Rest when fatigued

Avoid alcohol

Infection control measures, especially hand hygiene after bowel movements and before eating

Follow-up bloodwork → LFTs (AST, ALT), HAV antigen

Environmental sanitation (safe food and water supply, effective sewage disposal)

Infection control measures, especially hand hygiene after bowel movements and before eating, help prevent the spread of the virus.

Follow-up bloodwork should include liver function tests (LFTs) such as AST and ALT, as well as testing for HAV antigen.

Primarily transmitted through blood

Found in: blood, saliva, semen, vaginal secretions

Transmitted through mucous membranes or breaks in skin

Transferred from carrier mother to infant at birth or during close contact afterward

Not transmitted via umbilical vein

Long incubation period (1-6 months)

Replicates in the liver

Remains in the serum for long periods, facilitating virus transmission

Screening of blood donors has greatly reduced the occurence of HBV transmission through blood transfusions

>90% of people who contract HBV develop antibodies and recover spontaneously within 6 months

Hepatitis B has a much longer incubation period than Hepatitis A, ranging from 1-6 months

Anorexia (loss of appetite)

Abdominal pain

Generalized aching

Malaise and weakness

Fever and respiratory symptoms are rare

Fever and respiratory symptoms are rare

Some patients have arthralgias (joint pain) and rashes

GI symptoms such as dyspepsia (indigestion) and abdominal pain

Occurs because the liver infection can spread to the spleen and the entire GI system

Light-colored stools and dark urine are common --> issues with enzyme secretion and food breakdown

Liver may be tender and enlarged 12-14 cm vertically

Spleen may also be enlarged and palpable in a few patients

Posterior lymph nodes may be enlarged

HBsAg appears in 80-90% of patients 1-10 weeks after exposure to HBV and about 2-8 weeks before onset of symptoms or increased transferase levels

HBeAg (Hepatitis B e-antigen) --> indicates active viral replication in the liver

HBV DNA appears in the serum around the same time as HBeAg

Detected through polymerase chain reaction (PCR) testing

No, HBcAg is not always detected in the serum in HBV infection.

The goal is to reduce the disease burden by fostering immunization and educating the public on preventing Hepatitis B transmission.

Screening of blood donors for presence of HBAg

Individuals with a positive Hep B test cannot donate blood, even to themselves

The use of disposable syringes, needles, lancets, and needleless IV systems helps prevent transmission.

Work areas disinfected DAILY

Gloves are worn when handling blood, body fluids, or HBAg-positive specimens

Eating is PROHIBITED in areas exposed to blood or secretions

Educating patients about the nature of the disease, its infectiousness, and prognosis is key to preventing transmission and protecting others.

High risk groups such as:
- healthcare personnel
- patients undergoing hemodialysis
- people with HCV
- people with chronic liver disease

HEPLISAV-B is recommended for people >18 years of age

Administered in 2 doses given 1 month apart --> shorter schedule = increased completion rate

Prior to 2019, a yeast-recombinant hepatitis B vaccine was used

Provided protection >90% in healthy individuals

In those with normal immune systems, booster doses are not required

Booster doses are recommended for people who are immunocompromised

Healthcare workers with frequent blood contact are screened for anti-HBs to determine if immunity is present from previous exposure, and those without immunity are vaccinated.

Unvaccinated people evaluated for STIs

Those with a history of STIs

Multiple sex partners

People who have sex with injection drug users

Gay sex

Provides passive immunity to HBV

Indicated for people exposed to HBV who have never had hepatitis B AND have never received the Hepatitis B vaccine

Recommended for people exposed to HBV through sexual contact or percutaneous/transmucosal routes

Given at separate sites with separate syringes

Minimize infectivity

Reduce liver inflammation

Decrease symptoms

Bed rest until symptoms subside

Activities restricted until hepatic enlargement, serum bilirubin, and liver enzyme levels decrease

Gradually, activity increase is allowed

No, protein intake is not restricted

Maintaining adequate nutrition is essential for recovery

Antacids and antiemetics are used to control dyspeptic symptoms and malaise

Medications should be avoided if vomiting occurs

Persistent vomiting may require hospitalization and fluid therapy

Due to mode of transmission, patient is evaluated for other bloodborne diseases (like HIV)

Can be prolonged

Complete symptomatic recovery sometimes requires 3-4 months or LONGER

After jaundice has resolved

Separation from family and friends

Inability to work or engage in sexual contact during acute and infective stages

Planning with family involvement can reduce fears and anxieties about disease spread and minimize social isolation for the patient

Be prepared for care in the home

Ensure provision for adequate rest and nutrition

Risk for contracting HBV --> arrange for them to receive HBV vaccine or HBIG as prescribed

Be aware of early signs of HBV

Ways to reduce risk --> avoid all modes of transmission (blood and body fluids)

Avoid drinking alcohol

Assess patient's progress

Answer family members' questions about disease transmission

Reinforce education on care and prevention

Patient's physical and psychological status

Patient and family understand importance of rest and nutrition

Abstinence

Use of condoms

Keeping follow-up appointments

Participating in health promotion activities

Undergoing recommended health screenings

Reinforce the importance of adequate rest and nutrition

Strategies to prevent disease transmission

Sharing contaminated needles

Blood transfusions

Sexual contact

Unintentional needlesticks or injuries in healthcare settings

IV or injection drug users

Multiple sexual partners

Patients receiving frequent transfusions or large blood volumes

Healthcare workers

Similar to that of HBV --> symptoms usually mild or absent

Chronic carrier state often develops --> increased risk of chronic liver disease, cirrhosis, liver cancer

Small amounts of alcohol taken regularly appear to cause progression of the disease

Alcohol and medications that may affect the liver should be avoided

No benefit

Since 2011, highly effective HCV protease inhibitor therapies have been introduced
↓
Can acheive a sustained virologic response (SVR), indicating a cure of the infection

SVR --> absence of detectable virus 12 weeks after completing treatment

Indicates cure of HCV infection

Screening of blood supplies

Public health programs aimed at reducing shared needle use in IV drug use

Hepatitis D infection only occurs in people with Hepatitis B, as HDV requires the Hepatitis B surface antigen (HBsAg) for replication.

Confirmed by the presence of anti-delta antibodies along with HBsAg in testing

IV or injection drug users

Patients undergoing hemodialysis

Recipients of multiple blood transfusions

Individuals who engage in sexual contact with people who have Hepatitis B

varies between 30-150 days

Symptoms are similar

Patients with HDV are more likely to develop acute hepatic failure, chronic active hepatitis, and cirrhosis

Interferon alfa is the only licensed treatment for HDV

High-dose, long-duration therapy (at least 1 year) is recommended

Recurrence rate is high --> efficacy depends on the dose and treatment duration

Fecal-oral route (remember "Eat Ass")

Primarily through contaminated water in areas with poor sanitation

Incubation period ranges from 15-65 days

Presentation resembles Hepatitis A

Has a self-limited course, abrupt onset

Jaundice is almost always present

Major prevention method is good hygeine (e.g. handwashing), avoiding contact with virus

Effectiveness of immune globulin in protecting against HEV is uncertain

A – No
B – Yes
C – Yes
D – Yes
E - No

They are thought to be two different isolates of the SAME virus

Another form of hepatitis, believed to cause non A-E hepatitis in humans

Transmitted percutaneously

Risk factors similar to Hepatitis C (e.g. IV drug use, blood transfusions)

While persistent infection with HGV/GBV-C can occur, it does not seem to affect the clinical course or lead to progressive liver disease

Clinical significance remains uncertain

Liver damage caused by toxic chemicals --> leads to acute liver cell necrosis or toxic hepatitis

Occurs when the toxins are inhaled, injected parenterally, or ingested

Some chemicals commonly implicated in this disease include carbon tetrachloride and phosphorus.

These substances are true hepatotoxins

Toxic chemicals cause acute liver cell necrosis by damaging liver cells when they are inhaled, injected, or ingested, leading to toxic hepatitis

a condition where medications cause liver inflammation

Similar to acute viral hepatitis, but the liver parenchymal destruction is often more extensive

Isoniazid (for tuberculosis)

halothane

acetaminophen

methyldopa

certain antibiotics

antimetabolites

anesthetic agents

These medications cause Drug-Induced Hepatitis because they are metabolized by the liver, leading to liver inflammation or damage.

At the onset of disease, toxic hepatitis resembles viral hepatitis.

Symptoms include anorexia, nausea, vomiting, and jaundice

Hepatomegaly (enlarged liver) is also observed on physical assessment

Symptoms can be more intense in severely toxic patients

Recovery is rapid if hepatotoxic agent is identified early and removed, or if exposure has been limited

No effective antidotes for Toxic Hepatitis

In severe cases, symptoms intensify: Patient develops high fever, extreme weakness (prostration), and persistent vomiting, which may contain blood

Symptoms become progressively worse as the condition intensifies

Clotting abnormalities in toxic hepatitis are caused by the liver’s inability to produce clotting factors, which may lead to hemorrhages under the skin.

Severe GI symptoms may lead to vascular collapse

Delirium, coma, and seizures develop (unfiltered blood gets backed up into the brain)

Without liver transplant, patient may die of acute hepatic failure within days

Treatment focuses on maintaining fluid and electrolyte balance, blood replacement, and supportive care

Few options exist short of liver transplantation

Recovery is rare, but those who survive may develop chronic liver disease or postnecrotic cirrhosis

Drug-induced liver disease --> over 50% of all cases

Acetaminophen is the leading cause

Manifestations of sensitivity to a medication may occur on the first day of its use or not until several months later

Usually, the onset is abrupt

Chills, fever

Rash, pruritus

Arthralgia

Anorexia, nausea

Jaundice

Dark urine

Enlarged and tender liver

After the offending medication is withdrawn, symptoms may gradually subside

In severe hypersensitivity cases, high-dose corticosteroids may be used, although efficacy is uncertain

Liver transplantation is also an option, but with mixed outcomes

Clotting abnormalities can be severe --> lead to hemorrhages under the skin

Due to liver's ability to produce clotting factors being impaired

Severe GI symptoms may lead to vascular collapse --> lead to delirium, coma, and seizures

Without a liver transplant, patients may die of acute hepatic failure within a few days

Treatment focuses on maintaining fluid and electrolyte balance, blood replacement, and supportive care

Apart from liver transplantation, few treatment options exist for severe cases of drug-induced hepatitis

Some patients recover from acute drug-induced hepatitis only to develop chronic liver disease

If liver heals, scarring may occur, leading to postnecrotic cirrhosis

Universal precautions
- Gown
- Gloves
- Hand hygeine

ALF is a clinical syndrome of sudden and severely impaired liver function in a previously healthy perosn

Acute = less than 6 months

Neurologic dysfunction

Elevated PT and INR is ≥1.5

Viral hepatitis

Toxic medications (e.g., acetaminophen)

Chemicals (e.g., carbon tetrachloride)

Metabolic disturbances (e.g., Wilson disease)

Structural changes (e.g., Budd–Chiari syndrome)

Coagulation defects

Kidney disease and electrolyte imbalances

Cardiovascular abnormalities

Infection and hypoglycemia

Encephalopathy and cerebral edema

Plasmapheresis (replace plasma) --> correct coagulopathy and reduce serum ammonia levels

Lactulose --> laxative used to reduce ammonia levels (beware of loose stools 4+)

Ammonia levels

Liver function tests (LFTs)

PT/INR (prothrombin time and international normalized ratio)

Cerebral edema --> requires intracranial pressure monitoring

Careful fluid balance and hemodynamic assessments

Maintaining a quiet environment to avoid increasing intracranial pressure

Diuresis with mannitol, an osmotic diuretic, to reduce cerebral edema

A chronic disease characterized by the replacement of normal liver tissue with diffuse fibrosis, which disrupts the structure and function of the liver

1. Alcoholic cirrhosis --> scar tissue surrounds the portal areas, often caused by chronic alcoholism

2. Post-necrotic cirrhosis --> Broad bands of scar tissue form, typically following acute viral hepatitis

3. Biliary cirrhosis --> scarring occurs around bile ducts, usually due to chronic biliary obstruction and cholangitis

Portal and periportal spaces of the liver are chiefly involved in cirrhosis

These areas include the bile canaliculi, which form the liver bile ducts

In cirrhosis, the bile ducts become occluded with inspissated bile (thickened) and pus --> leads to inflammation and overgrowth of scar tissue

The liver attempts to form new bile channels --> leads to overgrowth of disconnected, newly formed bile ducts surrounded by scar tissue

Nutritional deficiency, particularly reduced protein intake, contributes to liver destruction in cirrhosis

Excessive alcohol intake is the major causitive factor in fatty liver and its consequences, which can lead to cirrhosis

Yes; cirrhosis can occur in people who do not consume alcohol and even in those with a normal diet BUT consume high amounts of alcohol

Exposure to certain chemicals (e.g. carbon tetrachloride, chlorinated naphthalene, arsenic, phosphorus)

Infectious schistomiasis

MEN are affected by cirrhosis twice as often as women

Alcoholic cirrhosisi is marked by episodes of necrosis involving liver cells.

Over time, scar tissue replaces destroyed liver cells, eventually exceeding the amount of functioning liver tissue

The cirrhotic liver develops a hobnail appearance due to islands of residual normal tissue and regenerating liver tissue projecting from the constricted areas.

Classified as either compensated (less severe, often vague symptoms) or decompensated (resulting from liver failure to synthesize proteins, clotting factors, and portal hypertension)

Caused by failure of liver to synthesize proteins, clotting factors, and other substances, along with manifestations of portal hypertension

Elevated pressure in the portal vein due to cirrhosis (scarring of the liver)

Early in the course of cirrhosis, the liver tends to be large and the cells are loaded with fat

Liver is firm and has a sharp edge that is noticeable on palpation

May occur due to recent, rapid enlargement of the liver which produces tension on the Glisson capsule (fibrous covering of the liver)

Later in the disease, the liver decreases in size as scar tissue contracts the liver tissue

The liver edge, if palpable, is nodular

Portal obstruction and ascites

Chronic liver failure and obstruction of the portal circulation

The cirrhotic liver prevents free blood passage, causing blood to back up into the spleen and GI tract.

They become stagnant with blood (chronic passive congestion) --> leads to indigestion and altered bowel function

Fluid rich in protein may accumulate --> ascites

Through percussion for shifting dullness or the presence of a fluid wave.

Bacterial peritonitis

Bacteremia due to translocation of intestinal flora.

Ascites leads to absent bowel sounds because fluid presses against the intestines in the peritoneum space.

Paracentesis --> clinical signs may be absent, making a paracentesis necessary for diagnosis

Fibrotic changes in the liver obstruct blood flow --> leads to collateral vessel formation and shunting of blood into vessels with lower pressures.

Caput medusae

ngl kinda looks like medusa

In the esophagus, stomach, and lower rectum.

May rupture and cause internal bleeding, leading to significant blood loss

Hemoglobin and Hematocrit (H&H) levels.

Observation for occult (hidden) and frank (visible) bleeding from the GI tract.

They are both distended blood vessels

Difference is in location --> hemorrhoids are in the rectal area

Prevent Bleeding

Prevent constipation --> high fiber diet, stool softeners (e.g. lactulose)

Rest helps reduce physical stress, which can prevent pressure on the varices and reduce the risk of bleeding.

Voice rest --> avoid strain on the esophageal area

late

Predisposes patient to the formation of edema and ascites

Lower and upper extremities

Presacral area

Facial edema is not typical

Overproduction of aldosterone --> also causes potassium excretion

Deficiencies in vitamins A, C, and K

Especially hemorrhagic phenomena associated with vitamin K deficiency.

Chronic gastritis

Impaired GI function

Inadequate dietary intake

Impaired liver function

Results in severe fatigue, poor nutritional status, and a diminished ability to perform daily activities

Deterioration of mental and cognitive function --> can lead to hepatic encephalopathy and hepatic coma

Serial neurologic assessments, including:
- evaluating general behavior
- cognitive abilities
- orientation to time and place
- speech patterns

Mental deterioration is often caused by increased ammonia levels --> treatment is lactulose (helps reduce ammonia)

a birth defect characterized by the obstruction of tubes that transport bile from the liver to the gallbladder

Bile cannot pass from liver to gallbladder --> liver damage, cirrhosis

Can be fatal if left untreated

Jaundice

Light-colored stool

Abdominal distention

Malaise

Decreased
- Serum albumin
- Serum cholinesterase

Increased
- Serum globulin
- LFTs (AST, ALT, GGT, alkaline phosphatase)
- Bilirubin
- PT/INR

Ultrasound

MRI

CT scan

Ultrasound scanning measures the difference in density between parenchymal cells and scar tissue.

Imaging studies that provide information on liver size, hepatic blood flow and obstruction, and presence of liver fibrosis

Diagnosis is confirmed by liver biopsy

Consent from the patient is required

Coagulation labs (PT/INR, PTT, vitamin K) must be reviewed

Prepare FFP (fresh frozen plasma) and protamine sulfate (heparin antidote) for possible use

Monitor for bleeding

Check for H/H (hemoglobin and hematocrit)

Regularly assess vital signs

Monitor for pain

Antacids

H2 histamine receptor antagonists (famotidine, cimetidine, ranitidine)

Promote healing of damaged liver cells

Improve patient's general nutritional status

Potassium-sparing diuretics (spironolactone, triamterene) --> minimize fluid and electrolyte imbalances

Avoid alcohol consumption

Maintaining an adequate diet

Cannot be reversed, but progression may be halted or slowed with appropriate measures

Colchicine

Angiotensin system inhibitors (ACE inhibitors and ARBs; -pril and -sartan)

Statins

Diuretics (e.g. spironolactone)

Immunosuppresants

Glitazones (e.g. pioglitazone, rosiglitazone)

Vitamin E

Chemokine receptor (CCR2/CCR5) inhibitors

Cause cell death of hepatic stellate cells, which potentiate fibrosis

Farnesoid X receptor agonists, such as obeticholic acid, help prevent chronic inflammation and liver fibrosis.

Milk Thistle (Silybum marianum)

Silymarin has anti-inflammatory and antioxidant properties that may benefit liver disease, particularly in hepatitis and alcohol-induced liver damage.

Promote rest

Improve nutritional status

Providing skin care

Reduce the risk of injury

Monitoring and managing potential complications

Ascites causes the skin to become tight and stretched, increasing the risk of skin breakdown and discomfort.

Promoting rest allows the liver to reestablish its functional ability, helping the patient recover from liver damage and manage symptoms.

It reduces the demands on the liver and increases blood supply, aiding in liver function and recovery

Daily weight and I&O (intake and output) --> used to monitor for fluid retention (edema, ascities)

Accurate weights are critical --> use same gown/clothes, zero out the bed

Positioning is crucial for maximal respiratory efficiency, especially when ascites is present, as it can interfere with thoracic excursion and breathing.

Oxygen therapy --> ensures adequate oxygenation of damaged liver cells and prevent further cell destruction

To prevent hazards of immobility, measures are initiated to avoid:
- atelectasis (use deep breathing exercises, incentive spirometry)
- pneumonia (hand washing, vaccination)
- venous thromboembolism (DVT prevention)
- pressure injuries

After nutritional status improvement and patient's strength increases, encourage a gradual increase in activity

Activity and mild exercise should be planned alongside rest to balance physical recovery and prevent exhaustion

Nutritious, high-protein diet supplemented with B complex vitamins and vitamins A, C, and K if tolerated

The nurse should encourage the patient to eat, especially if they do not have ascites or signs of hepatic coma.

small, frequent meals --> better tolerated than three large meals due to abdominal pressure

Probiotics are under ongoing research for managing hepatic encephalopathy, as imbalance of intestinal flora is common in these patients.

Water-soluble forms of fat-soluble vitamins A, D, and E, along with folic acid and iron to prevent anemia

Sodium restriction to help prevent formation of ascities

They may receive nutrients via enteral or parenteral route

It is important due to subcutaneous edema, immobility, jaundice, and increased susceptibility to skin breakdown and infection

Frequent changes in position

Irritating soaps

Adhesive tape

Lotion

Nurse should take measures to minimize scratching by the patient --> can worsen skin irritation

Ensure side rails are in place

Use pads in case patient becomes restless/agitated

Orient patient to time and place

Explain all procedures

Ask for assistance

Electric shaver

Soft-bristled toothbrush

Apply pressure to venipuncture sites

A major role of the nurse is monitoring the patient for complications related to cirrhosis.

Decreased production of prothrombin

Liver's decreased ability to synthesize necessary substances for blood coagulation

Monitor for bleeding, hemorrhage, coagulation disorders and other potential complications related to liver dysfunction

Hepatic encephalopathy is a complication of cirrhosis characterized by deteriorating mental status, which may present as delirium.

Signs of hepatic encephalopathy include deteriorating mental status, changes in cognition, and potential progression to coma.

Monitoring is essential to identify early deterioration in mental status, allowing for timely interventions.

Patients with advanced chronic liver disease may experience cardiovascular abnormalities and pulmonary compromise as complications of fluid volume excess.

Pulmonary compromise is a potential complication of ESLD due to plasma volume excess.

Administer diuretics --> monitor BP

Implement fluid restrictions

Enhance patient positioning

Ascites

Lower extremity edema

Dyspnea

Monitor I&O

Daily weight changes

Changes in abdominal girth

Edema formation

Monitor for nocturia and oliguria --> can indicate increasing severity of liver dysfunction

1. Exclude alcohol from the diet

2. Consider referral to AA (alcoholics anonymous), psychiatric care, or counseling

3. Avoid raw shellfish

4. Implement sodium restrictions --> may be necessary for a long time, if not permanently

Adherence to the therapeutic plan, including:
- Rest
- Lifestyle changes
- Adequate dietary intake
- Elimination of alcohol

Symptoms of impending encephalopathy

Possible bleeding tendencies

Susceptibility to infection

Recovery is often slow with frequent setbacks

Many patients find it difficult to refrain from alcohol for comfort or escape

Assisting patients in managing the transition from hospital to home care

The use of alcohol may have been an important part of patient's normal home and social life

Malignant (cancerous) tumors

Benign (non-cancerous) tumors

The widespread use of oral contraceptives in western countries, especially among women in their reproductive years.

The incidence has decreased with the development of modern contraceptives that contain less estrogen.

Being overweight or obese

Hemorrhage

Potential conversion to a malignant state

Few cancers originate in the liver

Primary liver tumors are relatively rare

Chronic liver disease

Hepatitis B and C infections

Cirrhosis

Resection (surgical removal) of primary liver cancer may be possible if found early; however, early detection is not common.

Cirrhosis

Chronic infection with HBV and HCV

Exposure to certain chemical toxins (e.g. vinyl chloride, arsenic)

Identified as a risk factor for liver cancer, especially when combined with alcohol consumption

it is a metabolite of the fungus Aspergillus flavus and may be a risk factor for liver cancer

Aflatoxin can contaminate ground nuts and grains, especially when stored unrefrigerated in tropical or subtropical climates.

Aflatoxin and other similar toxic molds may act as co-carcinogens with hepatitis B, increasing the risk of liver cancer.

Liver metastasis from other primary sites occurs 2.5x more frequently than tumors originating from primary liver cancers

Common primary sites include the digestive system, breast, and lung.

via the portal system, lymphatic channels, or through direct extension from an abdominal tumor

Continuous dull ache in the right upper quadrant, epigastrum, or back

Other symptoms include weight loss, anorexia, loss of strength, and anemia

The liver may be enlarged and irregular on palpation

Jaundice is present only if the larger bile ducts are occluded by the pressure of malignant nodules in the hilum of the liver.

Ascites develops if malignant nodules obstruct the portal veins or if tumor tissue is seeded in the peritoneal cavity.

Based on:
- clinical signs and symptoms
- history and physical examination
- results of laboratory and x-ray studies

Increased serum levels of: bilirubin, Alkaline phosphatase, AST, GGT, Lactic dehydrogenase

Other possible findings: Leukocytosis, Erythrocytosis, Hypercalcemia, Hypoglycemia, Hypocholesterolemia

Lung

Regional lymph nodes

Adrenals

Bone

Kidneys

Heart

Pancreas

Stomach

X-ray, CT scans

Ultrasound studies

MRI

Liver scans

Arteriography

Laparoscopy

PET (positron emission tomography) scans

CT scans

Ultrasound

Biopsy under imaging guidance (CT scan or ultrasound)

Laparoscopic biopsy

Assess biopsy site

Monitor labs q.1H for 3-6 hours per protocol

Local or systemic dissemination of tumor

Tumor seeding (0.5% to 2%)

Hemorrhage

False-negative results

Due to risk of dissemination (spreading) of malignant tumor, assessment of imaging characteristics is preferred

Confirmed diagnosis made by frozen section at time of the surgery

Surgical resection of the liver tumor

Radiation therapy

Chemotherapy

Prolong survival and improve quality of life by reducing pain and discomfort

Their major effect is palliative

Internal radiotherapy can lead to a reduction in tumor size, but its effect on survival is yet to be determined.

Systemic chemotherapy may be used to treat metastatic liver lesions.

Embolization produces anoxic necrosis with high concentrations of trapped chemotherapeutic agents.

An implantable pump has been used to deliver a high concentration of chemotherapy through the hepatic artery by constant infusion.

To bypass biliary ducts obstructed by tumors (liver, pancreatic, or bile duct) in patients with inoperable tumors or those at poor surgical risk.

A catheter is inserted through the abdominal wall and past the obstruction into the duodenum under fluoroscopy.

Reestablishes biliary drainage, relieves pressure and pain from bile buildup, decreases pruritus and jaundice, improving comfort, quality of life, and survival.

Observe bile for: amount, color, presence of blood and debris

Monitor for: fever, chills, vital signs

Complications: bile drainage around catheter, signs of biliary obstruction (increased pain, pressure, pruritus, jaundice)

Directs heat to tumors through various methods to cause necrosis of tumor cells while sparing normal tissue

A needle electrode is inserted into the liver tumor under imaging guidance, and radiofrequency energy passes through the non-insulated needle tip, causing heat and tumor cell death from coagulation necrosis.

Treatment modality under investigation --> lymphocytes with antitumor reactivity are administered to patients

Tumor regression has been observed in patients with metastatic cancer who have not responded to standard treatments

It interrupts arterial blood flow to small tumors by injecting small particulate embolic or chemotherapeutic agents into the artery supplying the tumor, resulting in ischemia and necrosis of the tumor.

It promotes dehydration of tumor cells and tumor necrosis through the injection of alcohol, which targets the tumor cells directly.

Surgical resection is treatment of choice when hepatocellular carcinoma (HCC) is confined to one lobe of the liver and function of the remaining liver is considered adequate for postoperative recovery

In the case of metastasis, hepatic resection can be performed if the primary site can be completely excised and the metastasis is limited.

Assess nutritional status

Evaluate fluid balance

Review general physical condition to ensure optimal preparation for surgery

Liver scan
Liver biopsy
Cholangiography
Selective hepatic angiography
Percutaneous needle biopsy
Peritoneoscopy
Laparoscopy
Ultrasound
CT scan
PET scan
MRI
Blood tests (particularly for serum alkaline phosphatase, AST, GGT, and isoenzymes)

surgical procedure involving removal of a lobe of the liver

Most common procedure for removal of a liver tumor

A thoracoabdominal incision is used for a right-liver lobectomy or an extended right lobectomy, which includes the medial left lobe.

An extensive abdominal incision is made for a left lobectomy.

Involves destroying tumor cells using chemicals (such as ethanol) or physical means (e.g. radiofrequency, microwave) in patients who are not candidates for resection or transplantation

Local ablation (e.g. radiofrequency ablation, microwave coagulation) under ultrasound or CT guidance

Can be done laparoscopically or percutaneously

Radiofrequency ablation is a standard mode of treatment that can effectively destroy a tumor up to 5 cm in size in one session.

Local pain or bleeding

Serious complications are rare