Liver, Mesentery & Omentum parenchyma at the hilar plate

By Dr. Edwin N. Lim LIVER: Blood supply

◦ Dual blood supply - hepatic artery (25%) and portal vein
LIVER: ANATOMY (75%) 20-25% of individuals have aberrant portal venous anatomy
◦ Largest solid organ in the body ◦ Hepatic Artery - 25%  portal vein trifurcation or an aberrant branch from the
◦ Weighs 1.5 kg in an adult → Arises from the celiac trunk/artery left portal vein supplying the right anterior lobe
◦ Surrounded by peritoneal membrane -Glisson’s capsule → gives off: common hepatic artery,left gastric, &
splenic artery  Superior pancreaticoduodenal vein
◦ Adjacent to diaphragm -Cephalad
◦ Common hepatic artery – arises from celiac trunk → comes off low in an anterior lateral position and is
◦ Adjacent to stomach, duodenum, colon -Caudad
divides into gastroduodenal artery and proper hepatic divided during pancreaticoduodenectomy
◦ Adjacent to right kidney & adrenal -posteriorly  Short branch (posterior lateral) to the caudate process on
artery the right side
LIVER: segments ◦ Hepatic artery proper – divides into the right and left → It is important to ligate during hilar dissection for
hepatic artery anatomic right hemihepatectomy to avoid avulsion.
◦ COUINAUD SYSTEM
→ Liver is divided into longitudinal planes drawn ◦ Cystic artery - arise from the right hepatic artery in the
triangle of calot LIVER: Drainage
through each hepatic vein to the vena cava & a
This “classic” or standard arterial anatomy is present in only  Hepatic Veins and Inferior Vena Cava
transverse plane at the level of the main portal
approximately 76% of cases, with the remaining 24% having → Most of the segments would drain to the hepatic
bifurcation veins
variable anatomy
◦ Cantlie’s line (portal fissure) → Three hepatic veins (right, middle, and left) that
 most common variant (10-15%) - replaced or accessory
→ Runs from the IVC to the gallbladder fossa’s tip Right Hepatic Artery from Superior Mesenteric Artery
pass obliquely through the liver to drain the blood to
→ divides the liver into the Right and Left lobes the suprahepatic IVC and eventually the right atrium
◦ Portal Vein - 75% Right hepatic vein Drains segments 5-8
Lobe of the Liver Segments → Formed by the confluence of superior mesenteric Middle hepatic vein Drains segment 4, 5, and 8
Right (60-70%) 5, 6, 7, 8 vein and splenic vein Left hepatic vein Drains segment 2 and 3
Left (30-40%) 2, 3, 4 → Normal Portal Vein Pressure - low at 3-5mmHg Small short hepatic vein Drains segment 1 (caudate
Caudate 1  Portal hypertension - 20-30mmHg into IVC lobe)
 Results in decompression of systemic circulation
by portocaval anastomosis via left gastric vein Large inferior accessory right hepatic vein in 15-20%
◦ Caudate lobe which produces esophageal and gastric  runs in the hepatocaval ligament that can be a source of
→ lies to the left and anterior of the IVC varices with propensity for major hemorrhage torrential bleeding if control is lost in right hepatectomy
→ contains three subsegments: Spiegel lobe, 1. Esophageal varices -coronary & L gastric
paracaval portion, caudate process V.
2. Caput medusa -round ligament LIVER: Innervation
◦ Falciform ligament - divides the left lateral segment 3. External hemorrhoids -IMV & hemorrhoidal  Parasympathetic
(segment 2 and 3) from the left medial segment plexus → Left vagus gives off anterior hepatic branch (LA)
(segment 4) → drains the splanchnic blood from the stomach, → Right vagus gives off posterior hepatic branch (RP)
pancreas, spleen, small intestine, and majority of  Sympathetic
Segment 1 Caudate lobe → greater thoracic splanchnic nerve
the colon to the liver before returning to the
Segments 2 and 3 left lateral segment systemic circulation → celiac ganglia
Segment 4 (quadrate lobe) → Inferior mesenteric vein - usually drains into the
◦ 4A - cephalad and just
→ splenic vein upstream from the confluence Right phrenic nerve
below the diaphragm  common source of referred pain to the right shoulder and
left medial segment  divides to give off segment 2 and 3
◦ 4B - caudad and branches to the left lateral segment scapula as well as the right side or back
adjacent to the  responsible for segment 4 branches  stimulated when Glisson’s is stretched or by diaphragmatic
gallbladder fossa Left Portal Vein
that supply the left medial segment irritation
Segments 5 and 8 right anterior lobe  provides the dominant inflow
Segments 6 and 7 right posterior lobe branch to the caudate lobe
Right Portal Its division is usually higher in the hilum
Vein and may be close to (or inside) the liver
 → ensures enough supply of glucose to CNS ◦ AST - its levels could also be elevated in liver, cardiac and
2. Lipid Metabolism skeletal muscle, lungs, kidney, brain, pancreas and red
→ bile formation, cholesterol & Fatty Acids production blood cells injury making them less specific
3. Protein Metabolism Common causes of elevated aminotransferase levels include
→ amino acid deamination  viral hepatitis
LIVER: Bile Ducts and Hepatic Ducts → production of ammonia & proteins  alcohol abuse
 In general, the hepatic ducts follow the arterial branching 4. Bilirubin Metabolism  medications
pattern inside the liver → Breakdown product of heme catabolism  genetic disorders (Wilson’s disease, hemochromatosis, α1-
Right anterior usually enters the liver above the hilar ◦ Bilirubin is bound to albumin in the circulation and sent to antitrypsin deficiency) & autoimmune diseases
hepatic duct plate the liver EVALUATION OF LIVER: Biliary obstruction (Cholestasis)
dives behind the right portal vein and  Unconjugated - insoluble bound to albumin ◦ Condition where bile does not go from liver to duodenum
Right posterior  Conjugated - to glucuronic acid to form bilirubin
can be found on the surface of the ◦ Disturbances in bile flow may be due to:
hepatic duct diglucuronide in a reaction catalyzed by the glucuronyl
caudate process before entering the liver  Intrahepatic causes - hepatocellular dysfunction
a longer extrahepatic course before transferase, making it water soluble  excreted into bile
canaliculi with small amounts dissolved in blood and  Extrahepatic causes - biliary tree obstruction
giving off segmental branches behind the
Left hepatic duct
left portal vein at the base of the excreted in urine ◦ Cholestasis often results in the release of certain enzymes
 The majority of conjugated bilirubin is excreted in the and can be detected by measuring the serum levels of
umbilical fissure
intestine as waste, however, it is permeable to bilirubin, ALP, and GGT
unconjugated bilirubin and urobilinogens ◦ Bilirubin – test done to check for cholestasis
Most common variation of these ducts occurs in 30-40% Unconjugated/
 The human liver can produce about 1L of bile daily Bilirubin Conjugated/ Direct
 nonstandard hepatic duct confluence with accessory or Indirect
LIVER: Synthetic function type Bilirubin
aberrant ducts Bilirubin
◦ Coagulation function insoluble & transported allowed excretion in
LIVER: Lymphatics → Single most sensitive test of liver function (INR,factor Description to the liver bound to bile
VII & factor V levels) albumin
 Lymph is produced within the liver
→ e.g Prothrombin time and % activity
 Drains via the perisinusoidal space of Disse and periportal  with addition of
◦ Albumin, acute phase proteins & cytokines
clefts of Mall→ larger lymphatics→ drain to hilar cystic another chemical is
→ e.g TPAG
duct lymph node (Calot’s triangle node), common bile necessary to
◦ Carbohydrate & lipid metabolism, bile synthesis and Different-
duct, hepatic artery, and retropancreatic and celiac lymph differentiate this do not have
bilirubin metabolism iation
nodes fraction from the addition of
through
Importance EVALUATION OF LIVER: Liver Function Tests fractionation whole other agents
 If you have Klatskin tumor or Hilar Cholangiocarcinoma, ◦ Term frequently used to refer to measurement of the  >90% of serum
there is high incidence of lymph node metastasis. levels of a group of serum markers for evaluation of liver bilirubin is
dysfunction unconjugated
 You should remove all the lymph nodes from liver hilum,
◦ Most commonly checked are: Indirect
common bile duct until the region below the pancreas hyperbilirubinemia
→ Aspartate Aminotransferase (AST) Direct
→ Alanine Aminotransferase (ALT)  increased bilirubin
hyperbilirubinemia
LIVER: PHYSIOLOGY production
→ Alkaline Phosphatase (ALP)  inherited or
◦ Functions - storage, metabolism, production, and (hemolytic disorders
→ Gamma- glutamyl transpeptidase (GGTP) Disturbance
and resorption of
acquired
secretion → Bilirubin in disorders of
hematomas)
◦ One crucial role is the processing of absorbed nutrients ◦ Liver function test are actually a misnomer because they
flow leads to
 defects (inherited
intrahepatic
through the metabolism of glucose, lipids, and proteins. excretion or
measure cell damage and not liver function or
◦ Responsible for the synthesis of most circulating plasma extrahepatic
◦ Serum albumin and prothrombin time - more accurate acquired) in hepatic
obstruction
proteins: albumin, factors of the coagulation and measurement of liver’s synthetic function uptake or
fibrinolytic systems, and compounds of the complement conjugation.
cascade EVALUATION OF LIVER: Parenchymal injury  Intrahepatic  Extrahepatic
◦ Detoxification ◦ AST and ALT - participate in gluconeogenesis by catalyzing cholestasis cholestasis
Suggests
◦ Immunologic responses through many immune cells in the transfer of amino groups from aspartic acid or alanine  Hepatocellular  Biliary tree
reticuloendothelial system to ketoglutaric acid to produce oxaloacetic acid and dysfunction obstruction
1. Carbohydrate Metabolism pyruvicacid, respectively (forming the SGOT, SGPT)
◦ ALP (alkaline phosphatase)
→ glycogenolysis, gluconeogenesis ◦ ALT - more specific → Found primarily in liver (bile duct epithelium) & bones
→ In conditions of biliary obstruction - levels rise as a result ▪ Cost to 10 days
of increased synthesis and release into the serum MRI ▪ T1/T2
▪ Availability
→ 7 days - half life
 it may take several days for levels to normalize ▪ Lack of exact Drainage ▪ Laparoscopic/open ▪ Aspiration rarely
even after resolution of the biliary obstruction. localization ▪ Anatomic resection needed except:
◦ GGTP (gamma-glutamyl transpeptidase) PET SCAN ▪ Metastatic tumor ▪ Ionizing radiation large abscess,
→ found in hepatocytes & released from bile duct epithelium ▪ Cost unresponse to
→ Elevation is an early marker for Hepatobiliary disease ▪ Availability medical therapy or
→ Like AP, it is also non-specific because it can be induced in superinfected left
certain medications, alcohol abuse, pancreatic disease,
lobe
myocardial infarction, renal failure and obstructive
RADIOLOGIC EVALUATION OF LIVER: Ultrasound
◦ Identify biliary duct stones and intrahepatic biliary
dilatation INFECTION OF LIVER
◦ Echo-texture: Liver contains the largest portion of the reticuloendothelial
system in the human body, therefore able to handle the ALGORITHM FOR INCIDENTAL FINDING OF LIVER MASS
→ Cirrhosis, fatty infiltration, solid & cystic tumors
◦ Screening of high-risk populations for HCC continuous low-level exposure to enteric bacteria that it
◦ radiologic charactersitic: receives through the portal venous system Mass identified incidentally by US or CT
 Cystic lesion - simple hepatic cyst has no internal
echoes and a thin smooth wall; with bright posterior PYOGENIC AMOEBIC History and PE
acoustic enhancement ▪ Acute ▪ Entamoeba
1. Doppler ultrasound appendicitis Abdominal pain/ weight loss
→ Patency of major hepatic vessels & tumor vascularity ▪ Impaired biliary
ETIOLOGY Liver disease/cirrhosis/
2. Intraoperative ultrasound (IOUS)
drainage Alcohol use
→ Gold standard for detecting liver lesions (20-30% Hepatittis/BT/tattoos
▪ Hematogenous
more metastaticlesions identified vs preoperative) OCP/hormone use/cancer hx
not seen prior to surgery ▪ Endocarditis
Jaundice/scleral icterus
→ Detect number, extent & association of tumors with ▪ Single/multiple Palpable mass/hepatomegaly
intrahepatic blood vessels ▪ Single ▪ Superior,anterio Stigmata of portal HPN
→ Mapping lines of resection ▪ Multiple- near diaphragm
→ Image-guided procedures (biopsy, radiofrequency honeycomb ▪ Necrotic central
ablation)
LOCATION Laboratory tests
▪ Right lobe of the portion
RADIOLOGIC EVALUATION OF LIVER: CT scan
◦ Useful in pre-op planning, assessment of hepatic vessels liver ▪ Anchovy paste or CBC, platelet count
and measurement of liver volume chocolate sauce Lytes/BUN/crea/glu/albumin
◦ Evaluation of the remainder of the abdomen, presence of ▪ RUQ pain, fever ▪ RUQpain, fever Liver function tests/ ammonia
peritoneal disease, portal lymphadenopathy and other Coagulation studies
▪ Jaundice - 1/3 ▪ Jaundice, unusual
remote lesions Hepatitis screen
▪ Leukocytosis ▪ Hepatomegaly Tumor markers
SYMPTOMS ▪ Increase ESR and ▪ Leukocytosis (CEA, AFP, CA 19-9)
RADIOLOGIC EVALUATION OF LIVER: MRI
◦ Provides additional tumor characteristic alkaline PO4 ▪ Mildly increase
◦ Less accurate in detecting colorectal liver metastatic but ▪ Elevated alkaline PO4 Additional imaging studies
more sensitive in detecting early HCC transaminases
◦ Distinguishes HCC from macro-regenerative nodules MANAGEMENT:
US
◦ MR cholangiography Culture ▪ 50% cases ▪ Flourescent CT or MRI scan
→ Evaluation of intrahepatic biliary tree Antibody (Enzyme Nuclear med
Advantages Disadvantages Angiogram
imminoassay EIA)
▪ Initial imaging ▪ Incomplete
ULTRASOUND
▪ Liver & biliary ▪ Obesity/bowel ▪ Empiric/culture- ▪ Metronidazole Liver biopsy(if needed)
Antibiotic
CT SCAN ▪ Contrast medium ▪ Ionizing radiation based 750mg TID for 7
 Occult primary evaluation
EGD
Colonoscopy
Mammogram
Gyn/PAP smear

Diagnosis
 LIVER LESIONS MANAGEMENT OF BENIGN LESIONS ▪ Resection of extra-hepatic tumor

BENIGN MALIGNANT ▪ Liver biopsy with caution, increase risk of Role Of Chemotherapy In Colorectal Liver Metastasis
Cyst Hepatocellular CA Hemangioma bleeding ◦ Conversion chemotheraphy
Hemangioma CholangioCA ▪ Main indication for resection: PAIN → To achieve resectability rather than a complete
Focal Nodular Hyperplasia Gallbladder CA Adenoma ▪ Resection response
Adenoma Metastatic Colorectal CA
Focal
▪ Main indication for surgery: ABDOMINAL ◦ If potentially resectable
Metastatic neuroendocrine PAIN → At least 4 courses of chemotherapy should be given
Biliary Hamartoma Nodular
(carcinoid) ▪ Oral contraception or estrogen should be first line
Hyperplasia
Metastatic cancers of other stopped
Abscess
cause ◦ Optimum timing for assessment of response to
MOST COMMON MALIGNANT: HEPATOCELLULAR CA chemotherapy (resectability)
▪ Viral hepatitis → Every 2 months
SYMPTOMS OF BENIGN LIVER LESIONS
▪ Alcohol hepatitis
▪ Most frequently encountered Risk factors
▪ Hemachromatosis Strategy for CRLM
▪ Congenital cyst
▪ Nonalcoholic steatohepatitis
Cyst ▪ Biliary cystadenoma Resectable Non-resectable
▪ Hypervascular in arterial phase
▪ Polycystic liver disease CT scan
▪ Hypodense in delayed phase
▪ Caroli’s disease MRI ▪ Variable T1 and hyperintense T2 +/- preoperative Chemotherapy 2-3
▪ Small liver lesion (2-4mm) surface Portal vein Chemotherapy months
Biliary duct ▪ Highly suggestive HCC
▪ Firm, yellow, smooth in appearance thrombosis
hamartoma
▪ Excisional biopsy
▪ Most common Resection
2ND MOST COMMON MALIGNANT: CHOLANGIOCARCINOMA
Hemangioma
▪ Gain, larger than 5-6cm (one or two stages)
▪ Spontaneous rupture is rare HILAR (Klatskin) PERIPHERAL
+/- PVE
▪ Malignant transformation Obstructive jaundice, painless Tumor mass
▪ Young woman(20-40) Locoregional
▪ Pain Treatment Poor survival Postoperative chemotherapy
▪ Solitary, sometimes multiple ▪ Surgical resection (absence ▪ Vascular invasion
Adenoma
▪ Prior or current use of contraceptives of PSC) ▪ Posotive margins TREATMENT OPTIONS
▪ Spontaneous rupture (10-25%) ▪ Chemoradiation ▪ Multiple tumors
Gold standard for HCC with cirrhosis
▪ Malignant transformation to HCC Improved outcome Prognostic factors Hepatic resection
▪ Childbearing ▪ Histologic (-) margin affecting survival (if Margin: 1cm)
Focal Nodular ▪ Oral contraceptive use ▪ Concomitant hepatic ▪ Absence of mucobilia HCC with cirrhosis
Hyperplasia ▪ Do not rupture resection ▪ Nonpapiliary tumor Recurrent rates (>50%)
▪ No significant risk of malignancy ▪ Well-differentiated ▪ Advance stage Liver Improved survival rates
▪ Nonhepatectomy transplantation Early stage(1,2); 1 tumor,5cm; 3
▪ Lack of pre-op chemo tumor,largest 3cm; absence of gross
CT SCAN result 3-5 year survival: 41.7% - 26.8% 3-year survival: 55% vascular invasion or extrahepa spread
Hemangiom ▪ Largely asymmetrical nodular peripheral HCC of 3 - 7.5cm
a 3rd MOST COMMON MALIGNANT: METASTATIC COLORECTAL Radiofrequency Recurrence rate after TFA vs resection
enhancement, isodense ablation (RFA) TFA=14.5%; resection=7.4%
▪ Sharply defined border, confused with CA
10-year survival Combination with TACE
metastatic tumors Ethanol ablation,
Adenoma ▪ Venous phase - isodense/hypodense ▪ Resection on fewer than 4 segments ▪ 4 or more: 29%
cryosurgery,
▪ Arterial phase - subtle hypervascular ▪ Solitary: 33% microwave ablation
enhancement Resectability is no longer defined on Chemoembolization
▪ Biphasic, well circumscribe with typical what actually is removed but on what Yttrium 90
central scar remain after resection Inoperable primary or metastatic liver
Focal micropheres (SIR-
▪ Venous phase - isodense or invisible ▪ Atleast 30-40% tumor
Nodular Spheres)
campared with background liver ▪ Use of neoadjuvant chemotherapy Stereotactic
Hyperplasia
▪ Arterial phase - Intense homogenous ▪ Portal ven embolization radiosurgery
enhancement ▪ Simultaneous ablation
Systemic
chemotherapy
 Table 31-9 Brisbane 2000 Liver Terminology

OLDER HEPATIC RESECTION

BRISBANE 2000 TERMINOLOGY
TERMINOLOGY

R hepatic lobectomy R hepatectomy/hemihepatectomy

L hepatic lobectomy L hepatectomy/hemihepatectomy
R trisegmentectomy R trisectionectomy or extended R
L trisegmentectomy hepatectomy/hemihepatectomy
L lateral segmentectomy L trisectionectomy or extended L
R posterior lobectomy hepatectomy/hemihepatectomy
L lateral sectionectomy or
Caudate lobectomy
bisegmentectomy 2,3
Right posterior sectionectomy
Caudate lobectomy or
segmentectomy 1

ALTERNATIVE “SECTOR”
TERMINOLOGY

R anterior sectorectomy
R posterior sectorectomy or R
lateral sectorectomy
L medial sectorectomy or L
paramedian sectorectomy
(bisegmentectomy 3,4)
L lateral sectorectomy
(segmentectomy 2)
LAPAROSCOPIC LIVER RESECTION OPEN VS LAPAROSCOPIC
▪ Trocar placement ◦ LLR is associated with less blood loss and shorter ACUTE LIVER FAILURE
▪ location hospital stay than open resection for CLM ETIOLOGY
◦ According to short term results, LLR is → Viral infection (hepatitis A, B, E)
equivalent to OLR in terms of oncologic → Drug-induced (acetaminophen)
outcomes
◦ Long term survival is comparable to CLINICAL PRESENTATION
conventional open approach → Jaundice & Encephalopathy
→ Hepatic Coma
MULTIPLE BILOBAR SYNCHRONOUS METASTASIS → Increased creatinine
→ Arterial pH <7.3
1. Chemotherapy if colonic tumor is not
→ Culture proven infection
symptomatic (obstructed etc)
2. After 6 cycles:
DIAGNOSIS & TREATMENT
The peripheral area of anterolateral segments A) Colonic resection → Liver biopsy
(segments 2, 5, 6, and lower part of 4) is considered to B) Clearance of the left lobe of liver → Rapid progression
be a favorable location of tumors for laparoscopic liver C) Right portal vein ligation → Acetaminophen overdose
resection, whereas the posterosuperior segments 3. After 2 months & 2 cycle of chemotherapy  Activated charcoal
(segments 1, 7, 8, and upper part of 4) of the liver are
A) Right hepatectomy  N-acetylcysteine
unfavorable locations.
→ ICU care
→ Prognosis is poor unless treated
THE INTERNATIONAL POSITION ON
LAPAROSCOPIC LIVER SURGERY: THE LOUISEVILLE RE-resection of recurrent CRLM
▪ 321 patient with primary resection & 14 in re- CIRRHOSIS
STATEMENT 2008 ▪ History and PE
resection (HK university)
→ Laparoscopic approach for LEFT LATERAL ▪ Lab findings:
SECTIONECTOMY is standard practice ▪ Univariate analysis  Mild normochromic anemia
→ Re-resection is not a risk factor in overall  Low WBC, platelet
→ Major resection should be reserved for  Bone marrow: Macronormoblastic
experienced surgeon survival
 Prolong PT, not responding to vitamin K
INDICATION CONTRAINDICATION ▪ Multivariate analysis  Bilirubin, transaminases, Alkal PO4 - elevated
▪ Small, superficial or ▪ Large tumor, deep → Postoperative complication, microscopic ▪ Liver biopsy with ultrasound or CT guided
peripheral seated or posteriorly margin (+) & multiple tumors were risk
▪ Cirrhosis - the final sequela of chronic hepatic insult and
▪ Segment 2,3,4b,5,6 located in right lobe factors
consequence of sustained wound healing in response
▪ Tumor closed to ▪ Re-resection of recurrent CRLM can achieve to chronic liver injury
portal bifurcation or favorable survival outcome ▪ Characterized by the presence of fibrous septa
suprahepatic junction throughout the liver subdividing the parenchyma into
hepatocellular nodules
▪ Approx 40% of patients are asymptomatic, but
progressive deterioration leading to the need for liver
transplantation or death is typical after the MANIFESTATIONS
development of end-stage liver disease (ESLD)  fatigue, anorexia, weight loss, jaundice, abdominal
 most common nonneoplastic cause of death pain, peripheral edema, ascites, GI bleeding, and
among patients with hepatobiliary and digestive hepatic encephalopathy
diseases  In Males - gynecomastia, loss of chest and axillary
hair, and testicular atrophy
CLASSIFICATION OF CIRRHOSIS
Micronodular characterized by thick regular  Jaundice - usually does not appear until the bilirubin rises
cirrhosis septa, small uniform above 2 to 3 mg/dL
regenerative nodules, and System Signs and symptoms
involvement of virtually every Neurologic  encephalopathy - ammonia goes to
hepatic lobule the brain since liver is bypassed
Macronodular  frequently has septa and  asterixis
cirrhosis regenerative nodules of varying Head and Neck  parotid gland swelling because of edema
sizes Skin  jaundice, angiomata, palmar
Mixed present when regeneration is erythema (alteration in sex hormone)
occur- ring in a micronodular liver Chest  Pleural effusion
and over time converts to a Abdomen  Ascites
macronodular pattern  caput medusa
 Cruveilheier-Baumgarten bruit - venous
hum that can be auscultated in the MODE FOR END-STAGE LIVER DISEASE SCORING SYSTEM
ETIOLOGY
epigastrium resulting from collaterals
 Alcoholic Liver Disease between the portal system and the  Model for End-Stage Liver Disease (MELD) is
 History of chronic alcohol abuse remnant of the umbilical vein a linear regression model based on
 Liver biopsy - would show hepatocyte necrosis,  Splenomegaly objective laboratory values
Mallory bodies, neutrophil infiltration, and Urogenital  testicular atrophy  INR
perivenular inflammation Extremities  clubbed fingers – consequence of  Bilirubin level
 Non-alcoholic steatohepatitis (NASH) hypoalbuminemia  Creatinine level
 history of diabetes mellitus or metabolic syndrome Dupuytren’scontractures  Used to predict mortality after transjugular
 the lack of a history of significant alcohol White nail beds intrahepatic portosystemic shunt (TIPS) and as
consumption, and exclusion of other causes of Musculoskeletal Muscle cramps - correlate with the sole method of liver transplant allocation
hepatic steatosis ascites,
 Biopsy - demonstration of steatohepatitis low mean arterial pressure, and
 Cryptogenic cirrhosis - cirrhosis without an apparent plasma
cause renin activity
 Chronic hepatitis C infection
 most common cause of chronic liver disease and ASSESSMENT OF SURGICAL RISK
the most frequent indication for liver
transplantation in US CHILD-TURCOTTE-PUGH SCORE
 Hemochromatosis (iron overload)  originally developed to evaluate the risk of
 most common metabolic disorder causing cirrhosis portocaval shunt procedures
 Autoimmune causes  shown to be useful in p redicting surgical risks of
 primary biliary cirrhosis other intra- a bdominal operations on cirrhotic
 primary sclerosing cholangitis patients
 autoimmune hepatitis
 Uncommon metabolic disorders Class A 10%
 Wilson’s Disease
Class B 30%
 A1-antitypsin deficiency
Class C 75-80%
PORTAL HYPERTENSION Clinically significant portal hypertension ▪ Hepatic encephalopathy
 Hepatic venous pulmonary gradient (HVPG) is >10 mmHg PORTOCAVAL ▪ Higher incidence of shunt thrombosis and
 Gastroesophageal varices SHUNT rebleeding
 Splenomegaly WARREN
▪ Lower rate of hepatic encephalopathy
SHUNT (distal
 Caput-medusae and decompensation
splenorenal)
TRANSJUGULAR
 Ascites INTRAHEPATIC ▪ >90% of cases refractory to medical
 Anorectal varices PORTOSYSTEMIC treatment
SHUNT (TIPS)
 Portal venous system contributes approximately 75%
of the blood and 72% of the oxygen supplied to the
liver
 In the average adult, 1000 to 1500 mL/min of portal
venous blood is supplied to the liver
SUGUIRA PROCEDURE
MANAGEMENT: ESOPHAGEAL VARICES
 this amount can be significantly increased in ▪ Abstinence from alcohol
Extrahepatic portal vein thrombosis & refractory
the cirrhotic patient bleeding
Prevention ▪ Avoidanceof aspirin/NSAIDs
 The portal venous system is without valves and drains
blood from the spleen, pancreas, gallbladder, and of variceal ▪ Administration of propanolol Extensive devascularization of the stomach and
bleeding ▪ Prophylactic Endoscopic Variceal Ligation
abdominal portion of the alimentary tract into the distal esophagus
liver (EVL) Transection of esophagus
 Normal portal venous pressure is 5-10 mmHg, and at
this pressure ▪ Blood resuscitation Splenectomy
Acute
variceal
▪ Fresh frozen plasma and platelet Truncal vagotomy
IMAGING OF THE PORTAL VENOUS SYSTEM AND ▪ Prophylactic antibiotics
MEASUREMENT OF PORTAL VENOUS PRESSURE
bleeding
▪ Vasopressin (0.2-0.8 units/min) Pyloroplasty
(5 days
▪ Somatostatin (initial bolus 50 units/IV)
 Abdominal ultrasonography - simplest initial hemostasis
▪ Surgical shunts/TIPS (refractory variceal
investigation is rate) HEPATIC TRANSPLANTATION
bleeding)
 large portal vein suggests portal
hypertension but is not diagnostic
▪ Balloon tamponade (<24 hours) Patients only chance of definitive therapy and
 Doppler ultrasound - is capable of outlining the long term survival
anatomy of the portal vein, excluding the presence of MANAGEMENT: GASTRIC VARICES Patients with variceal bleeding refractory to all
thrombosis, and identifying the direction of portal ▪ MELD score <15
venous blood flow form of management
SHUNTS ▪ Not candidate for transplant
 useful in evaluating blood flow through surgical
▪ Limited access to TIPS
Reverses most of the hemodynamic and
shunts and TIPS humoral changes associated with cirrhosis
Aim ▪ Reduceportal venous pressure
 Hepatic venography - most accurate method of ▪ Maintain total portal & hepatic blood
determining portal hypertension Not affected by previous EVL, TIPS, splenorenal,
flow
▪ Avoid a high incidence of complication medocaval shunt
 I. OMENTUM Omental Cysts
• Vague abdominal pain, nausea & vomiting
Anatomy • Lead point for omental torsion and infarction
o The cyst will eventually enlarge and the omentum will twist on itself causing infarction
• May transform to malignancy

• Diagnosis: CT scan and US – well circumscribed cystic appearing lesion arising from the
greater omentum

• Treatment: Open or Lap resection

o Laparoscopic unroofing or percutaneous drainage have a high chance of relapse so you do
Open or Lap resection
 Percutaneous drainage means referring to an interventional radiologist and by image
guidance, will aspirate the cyst. If the capsule remains intact, it will relapse.

Omental Neoplasm
• Metastatic – most common cause of omental neoplasm
Parts of lesser omentum • most common origin is ovarian CA
• Gastrohepatic ligament o Ovarian CA (most common) o Endometrial cancer
• Hepatoduodenal ligament – contains the portal triad o GI tract tumors o Kidney cancer
o Melanoma
Parts of greater omentum
• Gastrosplenic ligament – contains the short gastric vessels • Primary (rare)
• Gastrocolic ligament o Lipoma o Desmoid tumor
• Gastrophrenic ligament o Myxoma o Extra GI stromal tumor

Physiology II. MESENTERY

• “Policeman of the abdomen” – forms fibrin adhesions at sites of inflammation to wall off Anatomy
peritoneal infections
o Application: In practice, after surgery, surgeons use the omentum as a patch on the
surgical site. So, if ever there is a problem, the omentum will contain the infection.
o Ex. cholecystectomy, before closing the abdomen, get omentum and place it on the site
where the gallbladder was removed.
• Visceral fat – involved in metabolic functions
o Increased visceral fat – independent risk factor for insulin resistance and high
triglyceride levels

Omental Infarction
• Primary infarction – always remember when it’s primary, the problem is the organ itself.

Functions
o Torsion of the omentum from sudden/forceful movements
o Thrombosis or vasculitis of omental vessels
o Omental venous outflow obstruction • Diagnosis via imaging
• Secondary infarction – caused by other pathology o Ultrasound – hyperechoic non-compressible intraabdominal mass attached to the abdominal
o Hernia wall
o Tumors  Non-compressible means it is not the bowel
o Adhesions  Nice to know: another UTZ finding like this is the appendix (non-compressible)
• More common in male and obese patients o CT scan – streaking whirling pattern of fatty tissue in the anterior abdomen
 • Contiguous structure suspending & fixing bowel to the abdominal wall
• Treatment • Provides housing for arterial, venous, nervous, lymphatic structures
o Conservative – leads to abscess or adhesion formation
o Laparoscopic exploration and resection of infarcted tissue (partial omentectomy) – • White line of Toldt – lateral border of the ascending and descending large bowel; provides
treatment of choice avascular fascial plan between the colon, its mesentery and underlying retroperitoneal space
o This is usually accessed by the surgeon to mobilize the part of the bowel (like in the picture
below, the ascending colon) for example in colectomy procedures.
Anatomical Abnormalities
• Intestinal malrotation – congenital disorders secondary to defects in the proper rotation and
fixation of the bowel
o Leads to intestinal volvulus
• Intestinal herniation – common in paraduodenal or mesocolic areas
• Cecal volvulus - attachment of the cecum may degrade overtime leading to an area of laxity
• Sigmoid volvulus – sigmoid mesentery increases in size over time; more common than cecal
because it is not fixed unlike the cecum

Sclerosing Mesenteritis
• Idiopathic fibrosis of the mesentery affecting hollow viscera and mesenteric vessels
• Causes (Theories):
o Antecedent abdominal surgery
o Autoimmune disease
o Paraneoplastic syndrome
o Previous infection (typhoid, TB, influenza, rheumatic fever)
o Vascular insult
• Mesenteric lipodystrophy type if localized
• Mesenteric panniculitis type if diffused

• Clinical Manifestations: (vague presentation)

o Abdominal pain o Anorexia and weight loss
o Nausea and vomiting o Altered bowel habits
• Physical Exam:
o abdominal mass with aortic pulsations (mobile in all
directions)
• Diagnosis: Abdominal CT with IV contrast
o Soft tissue mass with a ↑ density than normal
mesenteric tissue
o “Tumor pseudocapsule” – hypodense zone
around the associated fibrotic mass
o “Fat ring sign” – area of preserved fat near
mesenteric vessels
coursing through areas of fibrosis Mesenteric Cysts
Diagnosis: Lap or open biopsy
• Disruption of the lymphatics in the mesentery due to
• Treatment: o Trauma, Mechanical obstruction, or Congenital ly
o Bowel and mesenteric resection - bowel ischemia • Most are unilocular
o Intestinal bypass – intestinal obstruction • Symptoms are due to local compression of abdomina
o Steroids, Hormonal therapy, Colchicine • Incidental finding in 45%
o Thalidomide, Cyclophosphamide
• Physical Exam: abdominal mass
 o Tillaux’s sign – abdominal mass lesion that is only mobile laterally
– freely mobile in all directions)
• Diagnosis: CT scan and US
• Treatment:
o Marsupialization and simple aspiration – ↑ rates of recurrence
o Enucleation – for benign lesions
 means removing without a margin of normal tissue
o Resection with clear margins – for malignant lesions
o All of these can be done either by Lap or open surgery

Mesenteric Tumors → Treatment: wide resection

Benign Malignant
Desmoid Tumors Lymphoma – most common
Lipoma GIST• Leiomyosarcoma
Cystic lymphangioma Carcinoids• Lymphangiosarcoma
Liposarcoma• Malignant fibrous
Lipoblastomahistioma