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Michael Brillantes, MD, FPCS, FPSGSLIVER By Michael Brillantes, MD, FPCS, FPSGS
Anatomy -1/50 of total body weight Surgically divided into the right and left lobe by a line through the IVC and gallbladder (Cantlie’s line)
-left lobe divided into medial and lateralsegments by falciform ligament -blood supply hepatic a. - 25% portal v – 75%
II. Liver function Circulatory function- material absorbed from the GI tract are brought to the liver through the dual blood supply to be used in the metabolic pool
B. Biliary passages- channel of exit formaterials secreted by the liver through the dual blood supply to be used in the metabolic pool
C. Reticuloendohelial system- containsphagocytic Kupffer cells and endothelial cells D. Metabolic Activity- anabolic and catabolic activities
III. Function Tests a. Albumin – half- life is 21 days; decrease means a chronic liver disease (more than 3 wks)
B. Carbohydrates and Lipids- hepaticdisease causes decrease in glycogenesis with resultant hyperglycemia
C. Enzymes Alkaline phospatase- increase indicates an obstructive pathology
2. SGOT and SGPT- increase indicates livercellular damage; SGPT more applicable for hepatic disease 3. Dye excretion
4. Coagulation factors a. Vit. K dependent clotting factors II, VII, IX, and X b. Inability to synthesize prothrombin
IV. Special Studies A. Needle Biopsy- provides pathologic diagnosis B. Ultrasound, CT scan, MRI C. Angiography
V. Pathology Trauma- 2nd most commonly injured organ 1. Clinical manifestation- shock, abdominal pain, spasm, and rigidity
2. Diagnostic- CT scan is the most useful- may also use ultrasound, paracentesis or peritoneal lavage
3. Treatment Correct shock- IVF and blood Surgery Control bleeders- perihepatic packaging, ligation of bleeders, Pringle maneuver Debridement External drainage
4. Complications Recurrent bleeding- inadequate homostasis or loss of coagulation factors secondary to massive transfusions Intraabdominal sepsis
C. Hematobilia- free communication between blood vessel and biliary tree- triad of abdominal pain, GI bleeding, and previous trauma - jaundice may be present
B. Hepatic Absdess 1. Pyogenic- most commonly due to cholangitis secondary to CBD obstruction; septicemia second most common etiology
- Fever with “picket fence” pattern, hepatomegally and tenderness-organism- usually e. coli -usually found in the right lobe, solitary or multiple
Presents with hepatic tenderness and feverDiagnostic i. CBC- leukocytosis, with count up to 18-20,000
ii. Radiograph- immobility or elevation of right hemidiaphragmiii. Ultrasound or CT scan
b. Treatment I .Antibiotics- IV for 2 wks, followed by 1 month oral form II. Drainage- percutaneous under ultrasound or CT guidance, or open
2. Amebic- reaches the liver via the portal vein from an ulceration in the bowel wall-organism- e. histolytica -occurs in the right lobe, usually solitary, with characteristic “anchovy paste”
Fever and liver pain, assoc. woth tender hepatomegally33% with antecedent diarrhea
Diagnostic i. CBC- leukocytosis ii. Indirect heme agglutinstion test iii. Ultrasound iv. Aspiration of trophozoites
b. Complications i. Secondary bacterial infection ii. rupture
c. Treatment i. Amebicidal drugs- Metronidazole 500 mg TID ii. Surgery – indicated for persistence of abscess, secondary infection
C. Cysts 1. Non- parasitic – usually solitary, found in the right lobe, watery content, with low internal pressure
-polycystic liver assoc. with polycystic kiny in 51.6% of cases-usually presents as a RUQ mass
Classification Blood or degenerative Dermoid Lymphatic Endothelial Retention – polycystic liver Proliferative cysts- cystadenomas
b. Diagnostic – ultrasound, CT scan, arteriography, scintillography, peritoneoscopyc. Asymptomatic- no treatment Symptomatic- drainage with unroofing or sclerotherapy
2. Hydatid cysts- caused by Echinococcus granulosus- with high internal pressure, causing rupture and anaphylactic reaction
Asymptomatic unless there are pressure symptoms on adjacent organsDiagnostic- radiograph, ultrasound and CT scan -Casoni’s skin test
b. Treatment i. small calcified cyst- no treatment ii. Sterilizationof cyst prior to surgery with hypertonic saline or alcohol followed by surgical removal
D. Benign Tumors 1. Classification a. Hamartomas- tissues normally found in the organ but arranged in a disorderly manner
b. Adenoma- associated with contraceptiveuse; may transform into hepatocellular carcinoma; high rate of bleeding
c. Focal nodular hyperplasia- reaction toinjury or a response to a preexisting vascular malformation d. Hemangioma- most common nodule in the liver
2. Diagnostic- ultrasound, CT scan, angiography3. Treatment- excision if symptomatic
E. Malignant lesions 1. Primary carcinoma- from Aspergillus flavus, kwashiorkor
Classification hepatoblastoma- usually affects children less than 2 years old.
ii. Fibrolamellar carcinoma- adolescent and young adults; large solitary lesioniii. Hepatocellular carcinoma- most common primary malignancy, usually follows postnecrotic cirrhosis (hepatitis B)
Manifested by mass, weight loss, abdominal pain, or intraperitoneal hemorrhage
b. Diagnostic i. Liver function test- alkaline phosphatase ii. Alpha Feto Protein
iii. Angiography iv. Ultrasound, intraoperative ultrasound, CT scan, MRI
c. Treatment- curative resection, chemotherapy with direct arterial infusion
2. Other Primary NeoplasmsSacroma- angiosacroma most common Mesenchymoma Infantile hemangioendothelioma
3. Metastatic neoplasms - most common malignant tumor of the liver - reach the liver by portal vein, hepatic artery, lymphatics, direct extension
Symptoms are usually referable to the liver (i. eSymptoms are usually referable to the liver (i.e. pain, ascites, weight loss, anorexia and jaundice
Diagnostic i. alkaline phosphatase ii. Serum marker referable to the primary carcinoma iii. SGOT iv. CT scan, MRI
b. Treatment Control primary tumor Check for other systemic metastases Patient should be able to tolerate a major resection Resection of metastasis should be feasible
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