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Surgical Anatomy of The Liver
  1. The liver is divided into a large right and a small left lobe by the falciform ligament.
  2. The morphology does not correspond to the surgical anatomy of the liver and functionally the liver is divided into a right and left hemi-liver by the principal plane (Rex-Cantlie line).  This is a plane passing through the gallbladder bed towards the vena cava. The middle hepatic vein lies in this plane.
  3. The right hemi-liver is divided into anterior and posterior sections by the right hepatic vein
  4. The left hemi-liver is divided into lateral and medial sections by the left hepatic vein.
  5. Further portal inflow division results in each section in turn being subdivided into two segments.
  6. The divisions of the portal vein are mirrored by divisions of the bile duct and hepatic artery forming a ‘portal triad’, a division of which supplies each segment.
  7. The right portal pedicle is short (less than 1 cm in most) and the vein divides to supply the right anterior section, subdivided into segments V (inferior) and VIII (superior) by portal vein divisions and the right posterior section subdivided into segments VI (inferior) and VII (superior) by portal vein divisions.
  8. The left portal pedicle is long. It gives of a caudate branch and thereafter the vein divides to supply a left lateral section and a left medial section.
  9. The left medial section is divided into two segments, III and IV, by a further portal vein division.
  10. The caudate lobe is a distinct anatomical segment and is labeled segment I. It receives branches of the portal trinity from the right and left liver and drains independently into the vena cava.
  11. As each segment of liver has its own supply from the portal trinity, independent of the other segments, these can therefore be resected independently of other segments.
  12. The numbering of the segment is in clockwise manner.
Hydatid disease
  1. Caused by helminth Ecchinococcus granulosa
  2. Adult worm is found in the dog (definitive host)
  3. Sheep (Intermediate host)
  4. Man is an accidental intermediate host
  5. Liver is the commonest organ involved
  6. Cysts are unilocular may be multiple
  7. Site: liver, lung, brain, heart, or the bones
  8. Pathologically hydatid liver cyst has three distinct layers:
    1. Ectocyst - fibrous advential layer due to host response
    2. Middle layer - laminated membrane of proteinaceous material
    3. Endocyst - inner germinal layer from which the scolices may be detached
  9. Clinical features
    1. Clinical presentation is often non-specific and may be asymptomatic
    2. 60% have right hypochondrial pain and 15% become jaundiced
    3. Other features include skin rashes, pruritus and allergic reactions
    4. Cysts can rupture resulting in broncho-biliary fistula
  10. Investigation
    1. Eosinophilia
    2. Plain abdominal x-ray may show calcification in cyst wall
    3. Ultrasound is the initial investigation of choice.
    4. CE CT is best radiological investigation.
    5. Aspiration should not be performed if hydatid disease is suspected
    6. Immunoblot (Western blot) and ELISA are 80-100% sensitive for liver cysts but only 50-56% for lungs and other organs.
    7. When a cyst ruptures there is an abrupt stimulation of antibodies.
    8. Senescent, calcified, or dead cysts are seronegative.
    9. If the CT shows a cyst regardless of confirmation by serology the diagnosis should be made.
  11. Management
    1. Pharmacological treatment is not curative
    2. Used as an adjunct to surgery to kill spilled scolices
    3. The drugs of choice are albendazole, mebendazole and praziquantel
    4. Albendazole is the drug of choice in treatment as it is best absorbed.
    5. Praziquantel is used as adjunct therapy as it only kills the inside of the hydatid cyst and not the germinal layer. It is currently being used as adjunct therapy with albendazole for pre and post-operative protection against cyst spillage.
    6. Surgical excision of the cyst is the treatment of choice for symptomatic cysts.
    7. Hepatic resection may be required for recurrent cysts
    8. Recurrence rate is approximately 5% at 5 years
  12. Complications
    1. Rupture of cyst or other means of cyst spillage produces infection, occasional obstruction or allergic reaction 90 (very rarely- anaphylactic shock) in affected organ.
    2. Rupture releases smaller cysts that may circulate to other organs.
Amebic Hepatic Abscesses
  1. Right lobe most commonly involved.
  2. Amebic liver abscess is the most frequent extraintestinal manifestation of Entamoeba histolytica infection.
  3. Most common route of spread ascending infection through bilary tract.
  4. Pathophysiology:
    1. E histolytica exists in 2 forms. The cyst stage is the infective form, and the trophozoite stage causes invasive disease.
    2. Cysts are resistant to gastric acid, but the wall is broken down by trypsin as it passes through the small intestine.
    3. Trophozoites are released and colonize the cecum. To initiate symptomatic infection, E histolytica trophozoites present in the lumen must penetrate the mucosal layer and adhere to the underlying mucosa.
    4. Liver involvement occurs following invasion of E histolytica into mesenteric venules. Amebae then enter the portal circulation and travel to the liver. The abscess contains acellular proteinaceous debris and is surrounded by a rim of amebic trophozoites invading the tissue.
  5. Constitutional symptoms
    1. Nausea and vomiting and Weight loss.
    2. Diarrhea: Diarrhea is present in < 33% and Bloody diarrhea is present in 7% of cases.
  6. Pulmonary symptoms
    1. Pulmonary symptoms are (18-26%), cough and chest pain.
    2. Odorless brown sputum like anchovy paste suggests development of bronchopleural fistula.
  7. Sign:
    1. Fever is the most common sign and is found in as many as 99% of cases.
    2. Hepatomegaly is present in some cases. Abdominal tenderness
    3. Pulmonary abnormalities
      1. Dullness and rales at the right lung base and nonproductive cough.
      2. Breath sounds over the right lung base may be diminished.
      3. Pleural rub may be audible.
    4. Jaundice (<10% of cases) mostly occurs in complicated cases with multiple abscesses or a large abscess compressing the biliary tract.
  8. Signs of complications
    1. Signs of peritoneal irritation, such as rebound tenderness, guarding, and absence of bowel sounds, are  present when the abscess ruptures in the peritoneal cavity.
    2. Pericardial friction rub is audible when the abscess extends into the pericardium.
    3. Signs of pleural effusion when the abscess ruptures in the pleural cavity.
  9. Investigation
    • Leukocytosis
    • Serologic testing
      Serologic testing is a more useful diagnostic tool than stool microscopy. It can be used for
    1. Diagnosis of symptomatic patients,
    2. Assessment of the risk of invasive disease in people who are asymptomatic and are passing cysts in onendemic areas (nonpathogenic strains do not cause seroconversion), and
    3. Testing patients with inflammatory bowel disease before starting corticosteroid therapy to prevent complications from unsuspected amebiasis.
    4. Indirect hemagglutination (IHA) testing is the most sensitive assay, with positive results occurring in 90-100% of patients with amebic liver abscess.
    5. Enzyme immunoassay (EIA) has now largely replaced IHA testing. EIA is relatively simpler, easy to perform, rapid, stable, and inexpensive.
  10. Imaging Studies:
    1. Ultrasonography initial diagnostic test.
    2. CECT is a best radiological investigation.
    3. Technetium-99m liver scanning is useful for differentiating an amebic liver abscess from a pyogenic abscess.
    4. Gallium scanning is helpful in differentiating pyogenic abscess (similar to technetium-99m nuclear hepatic scanning) but requires delayed images, which makes the test less helpful.
    5. Plain chest or abdominal films may show elevation and limitation of motion of the right diaphragm, basilar atelectasis, and right pleural effusion or gas within the abscess cavity.
  11. Treatment
    1. Medical Care:
      1. Metronidazole remains the drug of choice for amebic liver abscess.
      2. Chloroquine phosphate may be substituted or added in the event of failure of resolution of clinical symptoms with metronidazole or another nitroimidazole within 5 days or intolerance to metronidazole or a nitroimidazole.
      3. Emetine or dehydroemetine has a direct lethal action on the trophozoites of E histolytica. These agents are very toxic and, therefore, should be used only as a second-line therapy. Their toxicity includes cardiac arrhythmias, precordial pain, muscle weakness, vomiting, and diarrhea. Dehydroemetine is less toxic than emetine.
    2. Aspiration:
      1. Aspiration of the abscess content is indicated only if rupture of the abscess is thought to be imminent or if differentiation between amebic abscess and pyogenic abscess is critical.
      2. Aspiration may be done if no response to antibiotic has occurred after 3-5 days.
      3. Amebas rarely are recovered from the aspirate (15%), and often they are present only in the peripheral parts of the abscess, invading adjacent tissue.
    3. Surgical Care:
      1. High risk of abscess rupture, as defined by cavity size greater than 5 cm;
      2. Left lobe liver abscess, which is associated with higher frequency of peritoneal leak or rupture into the pericardium; and a failure to observe a clinical medical response to therapy within 3 - 5 days.
      3. Imaging-guided needle aspiration or catheter drainage is the procedure of choice. Q
Portal Hypertension
  1. Normal portal pressure = 5 - 10 mmHg          
  2. Portal hypertension is defined as a pressure > 12 mmHg
Prehepatic Intrahepatic Posthepatic
*Portal vein
*Splenic vein
Primary biliary cirrhosis
Chronic active hepatitis
Cirrhosis - post hepatitic, alcohol, cryptogenic, metabolic
(e.g. Wilson's, haemochromotosis)
Non-cirrhotic - cytotoxic drugs, Vitamin A intoxication
Budd-Chiari syndrome
Veno-occlusive disease
Caval abnormality
Most common cause of portal hypertension is cirrhosis.Q
  1. Pathophysiology
    1. Increased portal pressure reduces portal venous flow
    2. Encourages development of porto-systemic anastomoses
    3. Develop at site of connections between portal and systemic circulation
      1. Gastro-oesophageal junction
      2. Lower rectum
      3. Peri-umbilical veins
      4. Retroperitoneal veins of Retzius
      5. Peri-hepatic veins of Sappey

Grading of esophageal varices

  1. Dilated veins <5mm still at the level of surrounding tissue.
  2. Dilated straight veins >5mm protruding in to lumen but not obstructing
  3. Large tense, veins obstructing the lumen
  4. Near complete obstruction of lumen with impending rupture
  1. Clinical feature:
    1. Hepatocellular failure                
    2. Variceal bleeding        
    3. Ascites
    4. 90% of patient with cirrhosis develop esophageal varices and Bleeding will occur in 30% of these patient.
Severity of Cirrhosis
Variable Score
Score 5-6 = Class A
Score 7-9 = Class B
Score > 10 = Class C
  1 point 2 points 3 points
Encephalopathy Absent Mild / moderate Severe or coma
Bilirubin (μ mol/l) <34 34-51 >51
Albumin (g/l) >3.5 2.8-3.5 <2.8
Prothrombin time (secs above normal) 1-4 4-6 >6
Child-Turcotte-Pugh (CTP) Score
Variable 1 Point 2 Points 3 Points
Bilirubin level <2 mg/dL 2–3 mg/dL >3 mg/dL
Albumin level >3.5 g/dL 2.8–3.5 g/dL <2.8 g/dL
International normalized ratio <1.7 1.7–2.2 >2.2
Encephalopathy None Controlled Uncontrolled
Ascites None Controlled Uncontrolled
Child-Turcotte-Pugh class
Class A = 5–6 points
Class B = 7–9 points
Class C = 10–15 points
  1. Treatment: Medical Care: Gastroesophageal variceal hemorrhage is the most dramatic and lethal complication of portal hypertension.
Emergent treatment   
  • Bleeding from esophageal varices
  1. Initial resuscitation with replacement of blood volume loss
  2. Diagnosis of source of bleeding
  3. Specific treatment of bleeding lesion
  • Pharmacological therapy
  1. Terlipressin is vesopressior drug of choice.
  2. Somatostatin: is an endogenous hormone that decreases portal blood flow by splanchnic vasoconstriction.
  3. Octreotide is a synthetic analogue of somatostatin.
  4. Vasopressin is the most potent splanchnic vasoconstrictor. It reduces blood flow to all splanchnic organs, decreasing portal venous inflow and decreasing portal pressure.
  5. Adding nitrates to vasopressin therapy significantly improves efficacy.
  • Endoscopic therapy
  1. Upper GI endoscopy and banding is treatment of choice for acute varriceal bleed.
  2. Efficacy in achieving hemostasis is higher than 80%.
  • Endoscopic banding is now better than sclerotherapy.
  1. Several different sclerosants are available: 
    1. Sodium morrhuate, 
    2. Sodium tetradecyl sulfate, 
    3. Ethanolamine oleate.
  2. Complications are related to the toxicity of the sclerosant and include transient fever, stricture, dysphagia, perforation (rarely), chest pain, mediastinitis, ulceration, and pleural effusion.
  3. Sclerotherapy is very effective emergency treatment for acute variceal bleeding
    (not optimal for patients bleeding from gastric fundal varices). 
  • Other interventions
    Balloon-tube tamponade should be used only in massive bleeding as a temporizing measure until definitive treatment can be instituted. 
  1. Prognosis
    Predictors of mortality with variceal bleeding
    1. Active bleeding during endoscopy
    2. Encephalopathy
    3. Ascites
    4. Serum Bilirubin increased
    5. Aspartate Aminotransferase increased
    6. Prothrombin Time increased
  2. Prophylaxis:
    1. Beta-blockers – only for prophylactic use.
    2. Beta-blockers include propranolol and nadolol. Beta-blockers are noncardioselective and reduce portal and collateral blood flow. Reduction in cardiac output (blockade of beta1-adrenoreceptors) occurs. Splanchnic vasoconstriction (blockade of vasodilatory adrenoreceptors of the splanchnic circulation) also occurs.
  3. Surgical Care: Surgical care includes decompressive shunts, devascularization procedures, and liver transplantation. 
Decompressive shunts: These include
  1. Total portal systemic shunts      
  2. Partial portal systemic shunts      
  3. Selective shunts.
Role of shunts is to:
  1. Emergency control of variceal bleeding when no access to TIPS
  2. Reduce portal hypertension in patients awaiting transplantation
  3. Relieve intractable ascites
  4. Reduce bleeding from rectal, colonic or stomal varices
  1. Total portal systemic shunts
    1. These include any shunt larger than 10 mm in diameter between the portal vein (or one of its main tributaries) and the IVC (or one of its tributaries).
    2. There is no portal vein flow to liver
    3. 90% potency rate
    4. Examples are
  • End to side portocaval
  • Side to side portocaval
  • Mesocaval shunt
  • Central splenorenal shunt
  1. Excellent control of bleeding and ascites is achieved in more than 90% of patients. Encephalopathy (rate of 40-50%) and progressive liver failure are possible.
  2. Indications are massive variceal bleeding with ascites or acute Budd-Chiari syndrome without evidence of liver failure.
  1. Partial portal systemic shunts​
    1. These reduce the size of the anastomosis of a side-to-side shunt to 8 mm in diameter. Portal pressure is reduced to 12 mm Hg, and portal flow is maintained in 80% of patients.
    2. The operative approach is similar to side-to-side portacaval shunts, except the interposition graft (Small bore portocaval H-graft ) must be placed between the portal vein and the IVC.
    3. Some portal vein flow is maintained
    4. Have narrow diameter and partially decompress portal circulation
    5. 10% of patients will develop encephalopathy
  2. Selective shunts
    1. Example include
      • Distal splenorenal shunt (Warren shunt) – It is a surgical shunt of choice.
      • Distal spleno caval shunt
    2. These provide selective decompression of gastroesophageal varices to control bleeding while at the same time maintaining portal hypertension to maintain portal flow to the liver.
    3. One example is the distal splenorenal shunt, which is the most commonly used decompressive operation for refractory variceal bleeding..
    4. This shunt provides the best long-term maintenance of some portal flow and liver function with a lower incidence of encephalopathy (10-15%) compared to total shunts. The operation produces ascites because the retroperitoneal lymphatics are diverted.
    5. Lowest inciducule of encephalopathy
  • Devascularization procedures: These include splenectomy, gastroesophageal devascularization, and esophageal transection (at times).
  1. Incidence of liver failure and encephalopathy is low following devascularization procedures, presumably because of better maintenance of portal flow.
  2. Devascularization could be used in patients who have portal or splenic vein thrombosis in addition to cirrhosis.
  3. Splenectomy
  4. Gastroesophageal devascularization (Sugiura procedure)
  5. This should devascularize the whole greater curve of the stomach from the pylorus to the esophagus and the upper two thirds of the lesser curve of the stomach; the esophagus should be devascularized for a minimum of 7 cm.
  • Prevention of rebleeding
  1. For prevention of rebleeding, when pharmacological and/or endoscopic therapy has failed, consider surgery.
  2. TIPS is a useful procedure for continued bleeding despite medical and endoscopic treatment in patients with Child class C disease and selected patients with Child class B disease.
  3. It is effective only in portal hypertension of hepatic origin.
Hepatocellular carcinoma
The male-female ratio is about 4:1
HCC is the most common primary malignancy of the liver.
  1. Risk factor are:
    1. HBV
    2. HCV infection (Conversion to HCC is highest – 90%)
    3. Cirrhosis of liver is most common itiology for HCC.
    4. Alcoholic liver disease
    5. Hemochromatosis
    6. Tyrosinemia
    7. Primary biliary cirrhosis
    8. Aflatoxin B
    9. Any agent or factor that cause of chronic liver damage.
  2. Symptom
    1. Abdominal pain                                              
    2. Abdominal swelling                                        
    3. Weight loss
    4. Weakness                                                      
    5. Feeling of fullness and anorexia                  
    6. Vomiting
    7. Jaundice
  3. Physical examination
    1. Hepatomegaly                                
    2. Splenomegaly                                                
    3. Ascites
    4. Jaundice (Unusual)Q                       
    5. Fever                                                                                
    6. Hepatic bruit
    7. Mild cirrhosis
Jaundice is late sign occurs when significant deteriorations of liver function or bile duct obstruction occurs.

Jaundice is rare, unless significant detioration of liver function or mechanical obstructtion of the bile ducts occurs (Harrison’s 16 ed.; p; 534).

Jaundice as a presenting symptom of HCC occurs in upto one-half (50%) of all patients. Q The most common cause is hepatic insufficiency, on rare occasions results from biliary obstruction. (CANCER, principles & practice of oncology, 6 ed.; p: 1164).
  1. Spread by
    1. Centrifugal growth
    2. Parasinusoidal extension
    3. Verôus spread
    4. Distant metastasis
  1. Paraneoplastic syndrome
  1. Erythrocytosis                                              
  2. Hypercalcemia            
  3. Hypoglycemia,
  4. Carcinoid syndrome                                   
  5. Dysfibrinogenemia,    
  6. Cryoglobulinemia, 
  7. Hypercholesterolemia.
  1. Diagnostic approach
    1. CAT scans
    2. Ultrasound scans.
    3. Blood alpha-fetoprotein is a useful marker for the diagnosis of hepatocellular carcinoma.
    4. MRI most sensitive investigation can better detect lesion less than 1cm.
    5. The definitive diagnosis of hepatocellular carcinoma is made by biopsy.
    6. Role of FDG-PET is primarily useful in assessing the degree of differentiation & in staging moderately & poorly differentiated tumors, rather than in primary lesion detection.
Comparison of HCC with Fibrolamellar carcinoma.
Characterstic HCC Fibrolamellar HCC
Male-Female ratio 4:1-8:1 1:1
Median age 55 25
Tumor Invasive Well circumscribed
Respectability <25% 50-75%
Cirrhosis 90% 5%
AFP+ 80% 5%
Hep. B+ 65% 5%

AFB+, α-Fetoprotein positive
HCC = Hepatocellular carcinoma
Hep. B+ = Hepatitis B-positive.
  1. Staging
    1. TNM staging criteria for HCC
      1. T1 - Solitary tumor without vascular invasion
      2. T2 - Solitary tumor with vascular invasion or multiple tumors none more than 5 cm
      3. T3 - Multiple tumors more than 5 cm or tumor involving a major branch of the portal or hepatic vein(s)
      4. T4 - Tumor(s) with direct invasion of adjacent organs other than the gallbladder or with perforation of visceral peritoneum          
      5. N0 - Indicates no nodal involvement
      6. N1 - Indicates regional nodal involvement
      7. M0 - Indicates no distant metastasis
      8. M1 - Indicates metastasis presence beyond the liver
    2. Stage grouping
      1. Stage I = T1 + N0 + M0
      2. Stage II = T2 + N0 + M0
      3. Stage IIIA = T3 + N0 + M0
      4. Stage IIIB = T4 + N0 + M0
      5. Stage IIIC = TX + N1 + M0
        Stage IVB = TX + NX + M1
  2. Treatment methods
    1. In those with small tumors (<2 cm in diameter), limited stage I or II disease, and good hepatic function, surgical resection is the treatment of choice. It can achieve 5-year survival rates as high as 60% to 70%, rarely, cure the disease.
    2. Liver transplantation for hepatocellular carcinoma is indicated only in patients who have unresectable tumors less than 5 cm in diameter, focal tumor recurrence after resection, or hepatic failure.
    3. Specialized procedures, including
      1. Transcatheter arterial embolization
      2. Chemoembolization
      3. Lipoidal-targeted chemotherapy
      4. Transcatheter oily chemoembolization, can improve survival rates in patients with unresectable cancer.
      5. Percutaneous ethanol injection achieves a 3-year survival rate that is similar to that of resection, plus it is relatively inexpensive and widely available.
Hepato Blastoma
  1. It is an immature variant of HCC.
  2. MC primary malignant tamor of liver in children below 2 year of age.
  3. Typically there is very high level of serum AFP.
  4. Usually solitary.
  5. 5-yr. survival rate is better than HCC.

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