Jeffery L. Hicks, D.D.S.

Dept. of Comprehensive Care Dentistry

Largest internal organ

Weight ~3 lbs

Upper Right Quadrant of abdominal cavity

Beneath the diaphragm,

protected by rib cage

Four lobes

Hepatocytes / lobules

Lobule / central venule

Hepatic artery & portal vein peripheral to each lobule

Sinusoids carry blood between central venules and hepatic artery / portal vein branches

Via hepatic artery / portal vein

Portal vein drains intestines, stomach, spleen and esophagus

Portal vein provides 60% of the liver’s blood supply

Formation and excretion of bile

Regulation of carbohydrate homeostasis

Lipid synthesis and secretion of plasma lipoproteins

Control of cholesterol homeostasis

Formation of urea, serum albumin, clotting factors, enzymes

Detoxification of drugs and foreign substances

Inflammation of the liver

Hepatitis - viral, bacterial, toxic, drug-induced or idiopathic/cryptogenic

Hepatitis - acute or chronic

Hepatitis may lead to cirrhosis

Upon systemic entry, virus infects hepatocytes

Viral antigens are displayed on hepatocyte surfaces

Cytotoxic T-cells attack antigens on hepatocytes resulting in inflammation and necrosis

Incubation phase: variable depending on virus

Symptomatic preicteric phase: malaise, fatigue, nausea, appetite loss Symptomatic icteric phase: jaundice, light-colored stools, pruritis

Convalescence: clearance of jaundice and systemic symptoms

Hepatitis A virus (HAV) is a childhood disease

~ 50% of individuals in the US have been infected by adulthood

Associated with oral-fecal contamination (food, water)

Found in feces 2 or more weeks before onset of symptoms

Infectious until 2 weeks after symptoms begin

Presence of anti-HAV antibody in serum indicates prior sensitization to HAV and can offer protection from future infection

99% of people infected with HAV clear infection without treatment

Hepatitis B is caused by DNA viron with envelop

HBV components:envelope contains HBsAg (surface antigen)

HBcAG and HBeA (core antigens)

HBV found in mult. body fluids

Transmission via body fluid contact with a mucous membrane, non-intact skin, percutaneous exposure

HBV can survive on surfaces for over one week

Highest concentration of HBV particles are found in blood

No TX indicated for acute B

TX of chronic symptoms associated with HBV

Interferon reduces liver damage

in 30% symptomatic chronic

Adefovir (nucleotide analogs) results in viral load reduction

Liver transplant if dz progress

Hepatitis C is caused by enveloped RNA virus

Envelope protein rapid mutate

6 different genotypes with 50 subcategories with variations - quasispecies

“Mild” type of acute HCV has high rate of progression to chronic dz and eventual cirrhosis

Chronic Hepatitis C progresses ~10-30 yrs

Acute Hepatitis

Chronic Hepatitis

Fulminant Hepatitis

Cirrhosis

Cancer

Death

Subclinical Dz Symptomatic Dz

ELISA to detect HCV antibodies

RIBA as a confirmatory test

Hep C PCR with viral genotyping

LFT’s are performed to assay baseline liver enzyme which if elevated may indicate hepatocyte damage

Genotypes 2 and 3 are more likely to respond to treatment

10 goal is to eradicate HCV infection and reduce incidence of hepatocellular carcinoma

Interferon and ribavarin therapy

Pegylated interferonLiver transplant

HEV is an RNA virus with oral-fecal transmission

Also known as enteric non-A, non-B hepatitis

Occurs primarily in developing countries with poor sanitation

Epidemics have occurred in Mexico, India, Asia and Africa

Serologic test not available, diagnosis is one of exclusion

Incubation period is 15-64 days

Symptoms include nausea, vomiting, abnormal LFT’s

Treatment is supportive

Liver transplant if necessary

Also referred to as cryptogenic or autoimmune hepatitis

LFT’s are elevated without evidence of viral antigens

70-80% of patients are female

Treated with corticosteroids and immunosuppressive agents

Methylprednisone-1st line therapy as well as Imuran (Azathioprine)

Cirrhosis - chronic, progressive

Hepatocytes try to regenerate growth is uncontrolled and fibrous, leading to impeded vascular flow

Most common type

1st change - accumulation of fat in the liver cells

Fatty liver is reversible if ETOH use is stopped

If not, widespread scar formation occurs throughout the liver

Chronic biliary obstruction or infection

Diffuse fibrosis of the liver with jaundice

Abrupt onset of GI disturbances such as flatulence, nausea and vomiting, diarrhea or constipation due to altered liver metabolism of carbs, fats and proteins

Dull heavy pain in the right upper quadrant

Liver and spleen enlargement with a palpable liver

Later manifestations due to liver failure and portal hypertension

Jaundice Peripheral Edema Ascites Esophageal Varices Skin Lesions Hematologic Disturbances

Accumulation of fluid in the abdominal cavity

Protein moves from liver sinusoids into the lymph space

lymph leaks through capsule into the abdominal cavity

Paracentesis

Diuretics used to remove excess fluid (lasix, HCTZ)

Accumulation of fluid may lead to spontaneous bacterial peritonitis (SBP)

Cipro prophylactically to prevent (SBP)

Graded I – IV; occurs in 2/3 to ¾ of cirrhotic patients

Fibrosis causes portal vein HTN; blood flow is impeded collateral circ. develops

Veins of the esophagus thin, not elastic, fragile, bleed

Varices rupture in response GERD, ingestion of coarse, poorly chewed food, vomiting, straining at stool, coughing, sneezing or lifting heavy objectsResult- melena or hematemesis

Bleeding varicies the most life-threatening medical emergency

Collateral circulation of abdominal veins due to portal hypertension

Propranolol, nonselective beta blocker

Reduce hepatic blood flow by reducing cardiac output

Avoid epi use = unopposed alpha action = hypertensive crisis

Surgical shunting, namely TIPS (Transjugular Intrahepatic Portosystemic Shunt)

TIPS: needle inserted into right internal jugular vein, advanced into a hepatic vein and then into a large branch of the portal vein, this tract is widened with balloon and a wire mesh

stent is placed in the tract to maintain patency.

Spider angiomas small dilated blood vessels with a bright red center point and spider like branches

Occur on the nose, cheeks, upper trunk, neck and shoulders

Intraoral petechiae and ecchymosis are also common

NH3 produced in gut by bacterial breakdown of amino acids, amines, purines and urea.

NH3 shunted into systemic circulation and causes confusion, mental status changes, deep coma and death

Managed via Lactulose, laxative that is converted to acetic acid in the gut to decrease ph to discourage bacterial growth

Lactulose traps ammonia in the gut and the laxative effect expels ammonia in the feces.

Asterixis (liver flap) pt/ is unable to hold out arms with hands dorsiflexed

Rapid flexion and extension movements of hands occur

Liver panel

Serum bilirubinALPGGTASTALTSerum albuminPTT INR (PT) WBC

Platelet count

Consider antibiotic prophylaxis due to decrease of Kupffer cells No official recommendation exists

Obtain recent WBC, platelet count and PTT, INR, usually 1 month old labs may be suitable but if patient has severe liver disease then more recent labs needed due to unpredictability of values

When evaluating PTT, INR and platelet counts prior to Tx, decision to render treatment is made on a case-by-case basis

Platelet transfusion and FFP necessary if platelets are 50K or less and if INR is 2 or above and or if PTT is 2x normal value

Collaplug, Avitene, Topical Thrombin and primary closure necessary

for low platelet counts and elevated coagulation tests

Pt. may breakthough bleed due to clot breakdown/ fibrinolysis

Amicar mouthrinse to slow clot breakdown

May need cryoprecipatate

Oral stents as carrier for agents and apply pressure

10 Closure, always!

Analgesia - avoid all NSAIDS renal toxicity, hepatorenal syndrome

Acetaminophen acceptable at doses < 4 gms daily

Pt’s physician should be consulted for alternative medications

Increase in transplant success and survival rates: anti-rejection medications organ preservation solutions.

One-year patient survival rates 85% to 90% Five-year patient survival rates 65%

Average OR time: 8-12 hours

Average hospital stay: 2 weeks

Average blood transfusion: 5 units

Following transplantation patients are placed on immunosuppressive drugs

In the OR with varying doses.

Adjusting doses avoids risk of post-operative infection, tumor development and liver rejection.

Immunosuppressives

Corticosteroid, usually prednisone fluid build-up and puffiness of the face

Cyclosporine (Neoral) high blood pressure, kidney damage, growth of body hair Tacrolimus (Prograf) (Tacrolimus) lowest side effects

Frequent blood tests are required to monitor the patient's progress and reduce side effects.

As time passes, the amount of immunosuppression needed usually decreases

Be aware if patients are taking meds as indicated

Antibiotic prophylaxis is required for life in all organ transplant patients prior to invasive dental procedures