Hepatobiliary surgery - Liver surgery · 2016. 3. 11. · Hepatobiliary surgery - Liver surgery...

Hepatobiliary surgery- Liver surgeryEIRIN VESTENG

Outline

I. Surgical anatomy of the liver

II. Physiology of the liver

III. Diagnostic options in liver diseases

IV. Benigns lesions

V. Liver cysts

VI. Liver absesses

VII. Primary malignant neoplasms

VIII. Secondary malignant neoplasms

IX. Liver transplantation

1. Surgical

anatomy of the

liver

THE LIVER IS ONE OF THE LARGEST VISCERAL ORGANS IN OUR BODY, COVERING 2% OF TOTAL BODY WEIGHT.

IT DEVELOPS AS AN EMBRYOLOGIC OUTPOUCHING FROM THE DUODENUM.

1. Surgical anatomy of the liver

- Sectors & segments

The liver has a complex segmental anatomy, often simplified by characterized as

having 4 lobes – right, left, caudate (R) and quadrate (R), or just right & left lobes.



The anatomical right & left lobes are separated by an imaginary line called major lobar fissure (Cantlie line or principal plane) running from the medial aspect of the gallbladder fossa to the IVC, running parallel with the fissure of the round ligament. This division marks the course of the middle hepatic vein.

The right hepatic vein further subdivides the right liver into

anterior (segments V and VIII) and posterior (segments VI

and VII) sectors,

while the umbilical fissure subdivides the left liver into the

medial (segment IV) and left lateral sector (segments II and

III).



The liver is divided into 4 sectors & 8 segments based on the branching of theportal triads and hepatic veins.

The three main hepatic veins (left, right & middle) divide the liver into foursectors (portal sectors):

Right posterior sector (segments VI & VII)

Right anterior sector (segments V & VIII)

Left medial sector (segment IV)

Left lateral sector (segments II & III)

The caudate lobe (segment I) is an exception because its venous drainage is directly into the vena cava and is therefore independent of the major hepaticveins.



The portal sectors are supplied by independent portal pedicles arising from

the right or left main pedicles.

The divisions separating the sectors are called portal scissurae, within each

of which runs a hepatic vein.

Further branching of the pedicles subdivides the sectors into segments.

Segments I-IV comprise the left liver

Segments V-VIII comprise the right liver

Each segment is supplied by an independent portal pedicle, which forms

the basis of sublobar segmental resections.


- Portal circulation

The portal vein is formed by the

confluence of the splenic and superior

mesenteric veins at the level of the 2nd

lumbar vertebra behind the head of

the pancreas. It runs for approximately

6–9 cm to the hilum of the liver, where

it divides into the main right and left

branches.


- Venous blood supply

Both the portal and hepatic venous systems are valveless.

The main portal vein terminates in the porta hepatisby dividing into right and left branches.

The right branch divide into anterior and posterior sectoral divisions.

The left branch gives branches to segments II, III, and IV; a large branch to the caudate lobe

The hepatic veins (left, right & middle) represent the final common pathway for the central veins of the lobules of the liver IVC


- Arterial blood supply

The common hepatic artery arises from the celiac trunk, ascends in the hepatoduodenal ligament, and gives rise to the right gastric, gastroduodenal, and proper hepatic arteries;

The proper hepatic artery then divides into the right and left hepatic arterial branches in the liver hilum.

The hepatic artery supplies approximately 25%of the 1500 mL of blood that enters the liver each minute; the remaining 75% is supplied by the portal vein.

Within the liver, the hepatic arterial branchestravel with segmental bile ducts and portal veinbranches.


- Biliary drainage

The biliary tree arises within the liver from bile canaliculi, formed from specialized segments of the hepatocyte membrane. Bile canaliculi join to form progressively larger channels, resulting in segmental bile ducts that drain each segment.

The right anterior and right posterior sectoral ducts unite to form the main right hepatic duct, while the union of ducts draining segments II, III, and IV forms the left hepatic duct.

Drainage of segment I (caudate lobe) is principally into the left hepatic duct


- Lymphatics

Lymphatics draining superficial lobules of the

liver follow a subcapsular course to the

diaphragm, to the suspensory ligaments of the

liver, or to the posterior mediastinum, while

others enter the porta hepatis.

Lymphatics arising from lobules deep within the

liver travel either with the hepatic veins along

the vena cava or with the portal veins into the

porta hepatis.

Most of the lymphatic drainage of the liver is to

the hepatoduodenal ligament.


- Nerves

The liver and biliary tree are innervated by

sympathetic fibers arising from T7 to T10 and by

parasympathetic fibers from the right and left vagus

nerves.

The postganglionic sympathetic nerves arise from the

celiac ganglia.

Fibers derived from the celiac ganglia and vagus

nerves form a plexus of nerves that run along the

anterior and posterior aspects of the hepatic artery.

2. Physiology of

the liver

2. Physiology of the liver

Total hepatic blood flow (about 1500 mL/min; 30 mL/min per kg body weight) constitutes 25% of the cardiac output, though the liver accounts for only 2.5% of body weight.

About 30% of the hepatic volume is blood (12% of total blood volume).

2/3 of the flow enters through the portal vein and 1/3through the hepatic artery.

Pressure in the portal vein is normally low (10–15 cm H2O [7–11 mm Hg]).

The liver derives half of its oxygen from hepatic arterial blood and half from portal venous blood.


Blood flow within the liver is uniform.

Hepatic blood flow to the liver is regulated by a number of factors.

Muscular sphincters at the inlet and outlet of sinusoids

The cells lining the hepatic sinusoids

Portal venous and hepatic arterial blood becomes pooled after entering the periphery of the hepatic sinusoid.

Hepatic arterial flow increases or decreases reciprocally with changes in portal flow (arterial compensatory response); however, portal venous flow does not increase with reductions in arterial flow.


Occlusion of the right or left portal venous branches result in ipsilateral hepatic atrophy

and contralateral hypertrophy.

Intentional occlusion of a major portal vein branch (usually the right) is a procedure being

used with greater frequency prior to major hepatic resection, primarily when the

regenerative capacity of the future liver remnant is questionable (size concerns or

underlying parenchymal disease).

By causing atrophy of the liver to be resected and hypertrophy of the future liver remnant,

the risk of postop hepatic failure may be reduced!

3. Diagnostic

options in liver

diseases

3. Diagnostic options in liver diseases

Blood tests:

Liver function tests – ASAT, ALAT, ALP, GGT, bilirubin, albumin and prothrombin

time

other bloodtests for specific liver problems or genetic conditions.

Imaging tests:

CT, MRI, USG

Tissue analysis:

Biopsy

4. Benign lesions

HEPATIC HEMANGIOMA

HEPATOCELLULAR ADENOMA

FOCAL NODULAR HYPERPLASIA (FNH)

INFANTILE HEPATIC

HEMANGIOENDOTHELIOMA (IHH)

4. Benign lesions

- Hemangioma

Hemangioma is the most common benign hepatic tumor. No malignant potential known.

Women > men (4-6:1)

Sx: Hemangiomas are usually Asx and discovered incidentally. They may cause RUQ pain or fullness. May present ruptures (sx: severe abd pain, hemodynamic instability)

Dx: Suspicion after USG, Doppler. CT or MRI should be performed after suspicion. Do not biopsy.

TX:

ASx hemangiomas should be documented but left alone.

Irrespective of their size, the only reasons to resect hemangiomas are for Sx or diagnostic uncertainty.

Symptomatic hemangiomas should be excised by lobectomy or enucleation. Even large lesions can be safely removed.

Ruptured hemangiomas should be treated with hemodynamic stabilization followed by surgical resection or arterial embolization.

4. Benign lesions

- Hemangioma

4. Benign lesions

- Hepatic adenoma

Strongly ass w/the use of OCPs, anabolic steroids, pregnancy and certain fertility drugs.

Women > men (9:1). There is malignant potential (HCC)

Sx: usually Asx and discovered incidentally. RUQ pain or fullness, palpable abd mass. May present ruptured.

Dx: Suspicion is on USG. Besides biopsy, the most accurate dx test is MRI w / gadolinium enhancement. Workup may include α-FP.

Tx:

Asx hepatic adenomas should be documented but left alone and monitored. Pt should d/c any OCP.s, anabolic steroids and avoid pregnancy. Surgical resections should be undertaken if the adenomas is symptomatic, large or if the woman anticipates pregnancy. Monitor with sonography and annual α-FP

BUT, the general recommendation is that adenomas should be resected because of the risks of malignant change and spontaneous hemorrhage.

Small peripheral lesions may be removed with wedge excisions, but larger tumors require more extensive resections.

4. Benign lesions

- Hepatic adenoma

4. Benign lesions

- Focal nodular hyperplasia

FNH is the 2nd most common benign solid tumor of the liver with no malignant potential.

Female > Male, average 40 y.o, 85% are solitary tumors

Unlike hepatic adenoma - the use of OCP’s does not appear to predispose to the

development of FNH, but may stimulate growth.

Sx: usually Asx. Suspicion is on USG.

Dx: can be made radiologically via CT, with its characteristic “central scar” (80%).

Tc-99m sulfur colloid scan may helpful to differentiate it from hepatic adenoma & HCC).

Rupture is likely non-existant

Tx: D/c OCPs (?), routine monitoring w / USG

4. Benign lesions


4. Benign lesions


Tc-99m sulfur colloid scan

FNH «hot spot»

Tc-99m sulfur colloid scan

Not an FNH «cold spot»

5. Liver cysts

5. Liver cysts

A number of different cystic lesions may affect the liver.

Simple hepatic cysts, the most common, are unilocular fluid-filled lesions, generally no sx.

Many patients have multiple simple cysts, which should not be confused with polycystic liver disease, a progressive condition characterized by cystic replacement of virtually the entire liver.

The occasional large cyst may present as an upper abdominal mass or discomfort.

Solitary cysts lined with cuboidal epithelium are classified as cystadenomas and should be

resected, since they are premalignant.

Dx: MRI, USG, CT

Complex, multilocular (septated) cysts (if not echinococcal) are often neoplastic and should be resected.

5. Liver cysts

5. Liver cysts

There are few indications for aspirating hepatic cysts—simple cysts reaccumulate fluid

quickly, neoplastic cysts must be excised, and parasitic cysts might rupture and the

parasite thus be allowed to spread.

It is possible to eliminate small cysts by aspiration of the contents followed by an injection

into the lumen of 20–100 mL of absolute alcohol; however, small cysts almost never cause

symptoms and generally require no treatment.

Large symptomatic cysts are difficult to eradicate with alcohol injections, and serious

superinfection of the cyst cavity may occur. The simplest method of treatment consists of

laparoscopic cyst fenestration (wide excision of the cyst wall). A tongue of omentum is fixed so it lies in the residual cyst cavity as an ancillary measure to prevent the edges from

coapting. The operation is curative in nearly all patients.

5. Liver cysts

6. Liver

abscesses

6. Liver abscesses

Hepatic abscesses may be bacterial, parasitic, or fungal in origin. (US: bacterial > parasitic > fungal)

Cases are about evenly divided between those with a single abscess and those with multiple abscesses. About 90% of right lobe abscesses are solitary, while only 10% of left lobe abscesses are solitary.

In most cases, the dev. of a hepatic abscess follows a suppurative process elsewhere in the body.

About 40% of patients have an underlying malignancy. Other cases develop after generalized sepsis from bacterial endocarditis, renal infection, or pneumonitis. In 25% of cases, no antecedent infection can be documented ("cryptogenic" abscesses).

In most cases, the organism is of enteric origin.

Escherichia coli, Klebsiella pneumoniae, bacteroides, enterococci (eg, Streptococcus faecalis), anaerobic streptococci (eg, Peptostreptococcus), and microaerophilic streptococci are most common.

6. Liver abscesses

6. Liver abscesses

Sx: Asx, fever, jaundice, RUQ pain, chills, malaise, fatigue

Dx: USG, CT, MRI

Tx:

Antibiotics should be started promptly (aminoglycoside, clindamycin or metronidazole & ampicillin). Modified after culture results.

About 80% adequately treated by drainage catheters inserted percutaneously under ultrasound or CT guidance. Whether the patient has a single abscess or multiple abscesses, this is usually the most appropriate initial therapy. The catheters can be removed in 1–2 weeks after output becomes nonpurulent and scant.

Surgical intervention is more often necessary in cases of multiple, loculated collections or when the abscess cavity contains a large amount of necrotic debris. In such cases, open debridement should be considered early.

7. Primary

malignant

neoplasms

HEPATOCELLULAR CARCINOMA (HCC)

INTRAHEPATIC CHOLANGIOCARCINOMA

HEPATOBLASTOMA (CHILDREN)

HEPATIC ANGIOSARCOMA

7. Primary malignant neoplasms

Liver malignancy may arise from hepatocytes (hepatocellular carcinoma [HCC], the most common) or biliary epithelial cells (intrahepatic cholangiocarcinoma). A mixture of both have also been described.

Neonates may also develop a variant of HCC called hepatoblastoma.

Angiosarcoma of the liver, a rare fatal tumor, has been seen in workers intensively exposed to vinyl chloride for prolonged periods in polymerization plants.

Most pts w / malignancy of the liver will have RUQ pain, as well as high liver enzymes and anemia.

RUQ pain is often first followed by RUQ USG (to r/o biliary tract obstruction), but in suspicion of malignancy, CT w/contrast should always be performed.

In differentiating the type of malignancy, the pt’s history is of the utmost importance.

Achieving a cure for malignancies involving the liver & biliary tract will require resection of some sort.


- Hepatocellular carcinoma

HCC is the most common primary hepatic malignancy (85-90%)

Male > female (2:1) average 50 y.o

Risk factors include:

Cirrhosis, chronic HBV/HCV infection, hemochromatosis, schistosomiasis, environmental and occupational toxins (aflatoxin (Aspergillus spp), PVC, organochloride pestacides), thorotrast

Sx: dull, achy RUQ pain; malaise, jaundice, hepatomegaly, tender abd mass, fever, weight loss, acute hemorrhage/shock

Dx: May be suspected on USG, the best initial dx test on suspicion of HCC is CT w/contrast. Liver enzymes & a-FP (tumor marker) will be elevated. The most accurate test is biopsy.

Tx: Ideally resection; if non-resectable, transplantation is only hope of cure. There is no effective chemotherapy for HCC.

5-year survival rate for pts with HCC -


- Hepatocellular carcinoma


- Intrahepatic cholangiocarcinoma

Cholangiocarcinoma makes up a small fraction of primary liver cancers.

Unlike HCC, intrahepatic cholangiocarcinoma is less frequently associated with cirrhosis.

Risk factors: primary sclerosing cholangitis, liver fluke infection (Clonorchis sinensis) or sporadic. Emerging evidence also suggests chronic HCV, obesity, diabetes mellitus, chronic liver disease and smoking.

Intrahepatic cholangiocarcinoma generally presents as a large mass within the liver and is therefore clinically distinct from cholangiocarcinoma arising from the extrahepatic biliary tree.

Intrahepatic or extrahepatic spread of disease is not uncommon by the time the tumor is detected. These tumors infrequently cause symptoms at early stages and therefore often grow to a large size before they become apparent, frequently because of pain.


- Treatment

Liver Transplantation

HCC is the only solid neoplasm for which transplantation plays a significant role.

Is the optimal curative treatment for HCC

Milan criteria 5-year survival 70%

Partial Hepatectomy

Is the next best option

The minimal criteria of resectability that must be met are (1) disease confined to the liver and (2) disease amenable to a complete resection.

Anatomical segmentectomies are preferred to nonanatomical resections.


- Treatment

Ethanol injection (percutaneous ablative technique)

In pts with small, unresectable tumors.

USG or CT guidance 95% ethanol (5-20mL)

Can approach complete necrosis in 90-100% of tumors < 2 cm Ø

Radiofrequency Ablation (RFA) (percutaneous ablative technique – of choice)

In pts with small, unresectable tumors.

USG or CT needle + radiofrequency generator that generates thermal energy to bring about tumor destruction.

RFA can be used percutaneously, laparoscopically, or at laparotomy.

The goal of RFA is the same at that of ethanol injection: to achieve complete tumor necrosis.


- Treatment

Arterial Embolization (ablative technique)

This approach takes advantage of the fact that primary liver cancers

derive disproportionately greater blood supply from the hepatic arterial

circulation compared to the surrounding liver.

The strategy is to combine selective hepatic arterial injection of cancer

chemotherapeutic agents with arterial embolization, the latter to produce

tumor necrosis and slow the washout of the drugs.

Liver-directed therapy (under investigation)

Systemic therapy (under investigation)


- Treatment

8. Secondary

malignant

neoplasms

METASTATIC NEOPLASMS OFTHE LIVER

8. Secondary malignant neoplasms

By far the most common malignancy of the liver

In many instances pts are Asx until mets to the liver, after which liver failure ensues. Pt may also have the typical malignant hx of unintended weight loss, malaise and fatigue.

Nearly all solid tumors can potentially give rise to liver metastases.

Colon cancer is most likely to spread to the liver

Breast and lung are also common, pancreas, esophagus, stomach

The cirrhotic liver, which often gives rise to primary hepatic tumors, seems to be less susceptible than normal liver to implantation of metastases.

Dx: on CT or MRI: colonoscopy CXR often help to find the underlying cancer if it is in question. You may also consider CEA (colon cancer) titers.

TX: is targeted on the underlying primary malignancy. Unilobar malignancy may often be treated with partial hepatectomy. Malignancy in both lobes is not amenable for resection.

8. Secondary malignant neoplasms

9. Liver

transplantation

9. Liver transplantation

First successful human liver transplant, 1967 – Dr. Thomas Starzl

Most common indication: adults – cirrhosis due to chronic hepatitis C infection, children –

biliary atresia.

Current contraindication are few & are primarily related to evidence of cardiopulmonary

disease that probibits safe liver transplantation & active substance abuse.


- Donor selection

It is important that the liver is a rough size match for the donor.

Blood type compatibility is preferred but not an absolute requirement.

Matching of tissue antigens does not appear to be relevant

Donor organ Blood is flushed from the organ (prevent vascular occlusion) Decrease

metabolic requirement (cold – 4 °C) + preservation solution (eg. Viaspan) transplanted

within 10-24hours


- Operative technique

The operation is performed in three phases:

1. the dissection phase, during which the attachments of the diseased liver are dissected

and the vascular structures are prepared for resection

2. the anhepatic phase, which extends from the time the host liver is removed until the time

the donor liver is revascularized

3. the reperfusion phase, during which blood is circulating through the new organ and the

biliary tree is reconstructed.

Several techniques are available for handling the retrohepatic vena cava

The mainstay of immunosuppression for liver transplant recipients is a calcineurin inhibitor.


- Living Donor Liver Transplantation &

Split Liver Transplantation

The shortage of organs for small children in the late 1980s prompted the development of techniques to reduce the size of an adult liver graft by performing an anatomic resection of one or more lobes and transplanting the reduced graft.

The success of living donor liver transplantation from adult donors into children, together with the shortage of suitable adult donors, led to the development by Marcos and Tanaka of techniques to utilize the right lobe from a living donor to transplant into another adult. Nevertheless, living donor liver transplants have become a standard option when timely deceased donor liver transplantation is not possible.

By applying the living donor technique to deceased donors, two transplants can be obtained from a single adult liver from a deceased donor. This has been termed a split liver transplant. Typically, the lateral segment of the left lobe is used for a child or very small adult, while the remainder of the liver consisting of the right lobe plus the medial segment of the left lobe is used for an adult..


- Complications

Complications following liver transplantation are common, but most can be treated

effectively.

Coagulopathy ( bleeding),

primary nonfunctioning of the liver (5-10%) – most devastating complication

Vascular complication (5-10%)

Bile duct complication (20%)

Rejection (20-50%) – increase immonsuppressive therapy or corticosteroid pulse therapy

Fungal infections esp. Candida Albicans (“thrush”)

Sources:

Current diagnosis & treatment, 14th edt (G. doherty)

Step up to surgery, 2nd edt

Youtube – Paul Bohlin

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Hepatobiliary surgery - Liver surgery · 2016. 3. 11. · Hepatobiliary surgery - Liver surgery...

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