Liver, Mesentery & Omentum LIVER: Blood supply

By Dr. Edwin N. Lim ◦ Dual blood supply - hepatic artery (25%) and portal 20-25% of individuals have aberrant portal venous anatomy
 portal vein trifurcation or an aberrant branch from the
vein (75%) left portal vein supplying the right anterior lobe
LIVER: ANATOMY ◦ Hepatic Artery - 25%
◦ Largest solid organ in the body → Arises from the celiac trunk/artery  Superior pancreaticoduodenal vein
◦ Weighs 1.5 kg in an adult → gives off: common hepatic artery,left gastric, & → comes off low in an anterior lateral position and is
◦ Surrounded by peritoneal membrane -Glisson’s capsule splenic artery divided during pancreaticoduodenectomy
 Short branch (posterior lateral) to the caudate process on
◦ Adjacent to diaphragm -Cephalad ◦ Common hepatic artery – arises from celiac trunk the right side
◦ Adjacent to stomach, duodenum, colon -Caudad divides into gastroduodenal artery and proper hepatic → It is important to ligate during hilar dissection for
◦ Adjacent to right kidney & adrenal -posteriorly artery anatomic right hemihepatectomy to avoid avulsion.
◦ Hepatic artery proper – divides into the right and left
LIVER: segments hepatic artery LIVER: Drainage
◦ COUINAUD SYSTEM ◦ Cystic artery - arise from the right hepatic artery in the  Hepatic Veins and Inferior Vena Cava
→ Liver is divided into longitudinal planes drawn triangle of calot → Most of the segments would drain to the hepatic veins
→ Three hepatic veins (right, middle, and left) that
through each hepatic vein to the vena cava & a This “classic” or standard arterial anatomy is present in only
pass obliquely through the liver to drain the blood to
transverse plane at the level of the main portal approximately 76% of cases, with the remaining 24% having
variable anatomy the suprahepatic IVC and eventually the right atrium
bifurcation  most common variant (10-15%) - replaced or accessory Right hepatic vein Drains segments 5-8
◦ Cantlie’s line (portal fissure) Right Hepatic Artery from Superior Mesenteric Artery Middle hepatic vein Drains segment 4, 5, and 8
→ Runs from the IVC to the gallbladder fossa’s tip Left hepatic vein Drains segment 2 and 3
◦ Portal Vein - 75%
Small short hepatic vein Drains segment 1 (caudate
→ divides the liver into the Right and Left lobes → Formed by the confluence of superior mesenteric into IVC lobe)
Lobe of the Liver Segments vein and splenic vein
Right (60-70%) 5, 6, 7, 8 → Normal Portal Vein Pressure - low at 3-5mmHg Large inferior accessory right hepatic vein in 15-20%
 Portal hypertension - 20-30mmHg  runs in the hepatocaval ligament that can be a source of
Left (30-40%) 2, 3, 4 torrential bleeding if control is lost in right hepatectomy
 Results in decompression of systemic circulation
Caudate 1 by portocaval anastomosis via left gastric vein
which produces esophageal and gastric varices
◦ Caudate lobe with propensity for major hemorrhage LIVER: Innervation
→ lies to the left and anterior of the IVC 1. Esophageal varices -coronary & L gastric V.  Parasympathetic
→ contains three subsegments: Spiegel lobe, 2. Caput medusa -round ligament → Left vagus gives off anterior hepatic branch (LA)
paracaval portion, caudate process 3. External hemorrhoids -IMV & hemorrhoidal → Right vagus gives off posterior hepatic branch (RP)
plexus  Sympathetic
→ drains the splanchnic blood from the stomach, → greater thoracic splanchnic nerve
◦ Falciform ligament - divides the left lateral segment pancreas, spleen, small intestine, and majority of the → celiac ganglia
(segment 2 and 3) from the left medial segment colon to the liver before returning to the systemic
(segment 4) circulation Right phrenic nerve
Segment 1 Caudate lobe → Inferior mesenteric vein - usually drains into the  common source of referred pain to the right shoulder and
Segments 2 and 3 left lateral segment
→ splenic vein upstream from the confluence scapula as well as the right side or back
 divides to give off segment 2 and 3  stimulated when Glisson’s is stretched or by diaphragmatic
Segment 4 (quadrate lobe)
branches to the left lateral segment irritation
◦ 4A - cephalad and just  responsible for segment 4 branches
below the diaphragm left medial segment Left Portal Vein
that supply the left medial segment
◦ 4B - caudad and adjacent  provides the dominant inflow branch
to the gallbladder fossa to the caudate lobe
Segments 5 and 8 right anterior lobe Its division is usually higher in the hilum
Segments 6 and 7 right posterior lobe Right Portal Vein and may be close to (or inside) the liver
parenchyma at the hilar plate
LIVER: Bile Ducts and Hepatic Ducts ◦ Bilirubin is bound to albumin in the circulation and sent to EVALUATION OF LIVER: Biliary obstruction (Cholestasis)
 In general, the hepatic ducts follow the arterial branching the liver ◦ Condition where bile does not go from liver to duodenum
pattern inside the liver  Unconjugated - insoluble bound to albumin ◦ Disturbances in bile flow may be due to:
Right anterior usually enters the liver above the hilar  Conjugated - to glucuronic acid to form bilirubin  Intrahepatic causes - hepatocellular dysfunction
hepatic duct plate diglucuronide in a reaction catalyzed by the glucuronyl  Extrahepatic causes - biliary tree obstruction
dives behind the right portal vein and can transferase, making it water soluble  excreted into bile
Right posterior
be found on the surface of the caudate canaliculi with small amounts dissolved in blood and
◦ Cholestasis often results in the release of certain enzymes
hepatic duct and can be detected by measuring the serum levels of
process before entering the liver excreted in urine
bilirubin, ALP, and GGT
a longer extrahepatic course before  The majority of conjugated bilirubin is excreted in the
giving off segmental branches behind the intestine as waste, however, it is permeable to
◦ Bilirubin – test done to check for cholestasis
Left hepatic duct Unconjugated/
left portal vein at the base of the unconjugated bilirubin and urobilinogens Bilirubin Conjugated/ Direct
umbilical fissure  The human liver can produce about 1L of bile daily Indirect
type Bilirubin
Bilirubin
LIVER: Synthetic function insoluble & transported allowed excretion in
Most common variation of these ducts occurs in 30-40% to the liver bound to bile
◦ Coagulation function Description
 nonstandard hepatic duct confluence with accessory or → Single most sensitive test of liver function (INR,factor albumin
aberrant ducts
VII & factor V levels)  with addition of
→ e.g Prothrombin time and % activity another chemical is
LIVER: Lymphatics ◦ Albumin, acute phase proteins & cytokines necessary to
 Lymph is produced within the liver → e.g TPAG Different-
differentiate this do not have
 Drains via the perisinusoidal space of Disse and periportal ◦ Carbohydrate & lipid metabolism, bile synthesis and iation
fraction from the addition of
bilirubin metabolism through
clefts of Mall→ larger lymphatics→ drain to hilar cystic whole other agents
fractionation
duct lymph node (Calot’s triangle node), common bile duct,  >90% of serum
EVALUATION OF LIVER: Liver Function Tests
hepatic artery, and retropancreatic and celiac lymph nodes bilirubin is
Importance ◦ Term frequently used to refer to measurement of the levels
unconjugated
 If you have Klatskin tumor or Hilar Cholangiocarcinoma, of a group of serum markers for evaluation of liver
Indirect
there is high incidence of lymph node metastasis. dysfunction
hyperbilirubinemia Direct
 You should remove all the lymph nodes from liver hilum, ◦ Most commonly checked are:  increased bilirubin hyperbilirubinemia
common bile duct until the region below the pancreas → Aspartate Aminotransferase (AST) production  inherited or
→ Alanine Aminotransferase (ALT) Disturbance (hemolytic disorders acquired
LIVER: PHYSIOLOGY → Alkaline Phosphatase (ALP) in and resorption of disorders of
→ Gamma- glutamyl transpeptidase (GGTP) flow leads to hematomas) intrahepatic
◦ Functions - storage, metabolism, production, and  defects (inherited or excretion or
secretion → Bilirubin
◦ Liver function test are actually a misnomer because they acquired) in hepatic extrahepatic
◦ One crucial role is the processing of absorbed nutrients uptake or obstruction
through the metabolism of glucose, lipids, and proteins. measure cell damage and not liver function
conjugation.
◦ Responsible for the synthesis of most circulating plasma ◦ Serum albumin and prothrombin time - more accurate
measurement of liver’s synthetic function  Intrahepatic  Extrahepatic
proteins: albumin, factors of the coagulation and cholestasis cholestasis
fibrinolytic systems, and compounds of the complement Suggests
EVALUATION OF LIVER: Parenchymal injury  Hepatocellular  Biliary tree
cascade ◦ AST and ALT - participate in gluconeogenesis by catalyzing dysfunction obstruction
◦ Detoxification the transfer of amino groups from aspartic acid or alanine ◦ ALP (alkaline phosphatase)
◦ Immunologic responses through many immune cells in to ketoglutaric acid to produce oxaloacetic acid and → Found primarily in liver (bile duct epithelium) & bones
reticuloendothelial system pyruvicacid, respectively (forming the SGOT, SGPT) → In conditions of biliary obstruction - levels rise as a result
1. Carbohydrate Metabolism ◦ ALT - more specific of increased synthesis and release into the serum
→ glycogenolysis, gluconeogenesis ◦ AST - its levels could also be elevated in liver, cardiac and → 7 days - half life
→ ensures enough supply of glucose to CNS skeletal muscle, lungs, kidney, brain, pancreas and red  it may take several days for levels to normalize
2. Lipid Metabolism blood cells injury making them less specific even after resolution of the biliary obstruction.
→ bile formation, cholesterol & Fatty Acids production Common causes of elevated aminotransferase levels include ◦ GGTP (gamma-glutamyl transpeptidase)
3. Protein Metabolism  viral hepatitis → found in hepatocytes & released from bile duct epithelium
→ amino acid deamination  alcohol abuse → Elevation is an early marker for Hepatobiliary disease
→ production of ammonia & proteins  medications → Like AP, it is also non-specific because it can be induced in
4. Bilirubin Metabolism  genetic disorders (Wilson’s disease, hemochromatosis, α1- certain medications, alcohol abuse, pancreatic disease,
→ Breakdown product of heme catabolism antitrypsin deficiency) & autoimmune diseases myocardial infarction, renal failure and obstructive
RADIOLOGIC EVALUATION OF LIVER: Ultrasound INFECTION OF LIVER
◦ Identify biliary duct stones and intrahepatic biliary Liver contains the largest portion of the reticuloendothelial ALGORITHM FOR INCIDENTAL FINDING OF LIVER MASS
dilatation system in the human body, therefore able to handle the
◦ Echo-texture: continuous low-level exposure to enteric bacteria that it
→ Cirrhosis, fatty infiltration, solid & cystic tumors receives through the portal venous system Mass identified incidentally by US or CT
◦ Screening of high-risk populations for HCC
◦ radiologic charactersitic: PYOGENIC AMOEBIC History and PE
 Cystic lesion - simple hepatic cyst has no internal
echoes and a thin smooth wall; with bright posterior ▪ Acute ▪ Entamoeba
appendicitis Abdominal pain/ weight loss
acoustic enhancement Liver disease/cirrhosis/
1. Doppler ultrasound ▪ Impaired biliary Alcohol use
ETIOLOGY
→ Patency of major hepatic vessels & tumor vascularity drainage Hepatittis/BT/tattoos
2. Intraoperative ultrasound (IOUS) ▪ Hematogenous OCP/hormone use/cancer hx
→ Gold standard for detecting liver lesions (20-30% more Jaundice/scleral icterus
▪ Endocarditis Palpable mass/hepatomegaly
metastaticlesions identified vs preoperative) not seen
prior to surgery ▪ Single/multiple Stigmata of portal HPN
→ Detect number, extent & association of tumors with ▪ Single ▪ Superior,anterio
intrahepatic blood vessels ▪ Multiple- near diaphragm Laboratory tests
→ Mapping lines of resection LOCATION honeycomb ▪ Necrotic central
→ Image-guided procedures (biopsy, radiofrequency CBC, platelet count
ablation) ▪ Right lobe of the portion Lytes/BUN/crea/glu/albumin
RADIOLOGIC EVALUATION OF LIVER: CT scan liver ▪ Anchovy paste or Liver function tests/ ammonia
◦ Useful in pre-op planning, assessment of hepatic vessels chocolate sauce Coagulation studies
and measurement of liver volume Hepatitis screen
▪ RUQ pain, fever ▪ RUQpain, fever Tumor markers
◦ Evaluation of the remainder of the abdomen, presence of
▪ Jaundice - 1/3 ▪ Jaundice, unusual (CEA, AFP, CA 19-9)
peritoneal disease, portal lymphadenopathy and other
remote lesions ▪ Leukocytosis ▪ Hepatomegaly
SYMPTOMS ▪ Increase ESR and ▪ Leukocytosis Additional imaging studies
RADIOLOGIC EVALUATION OF LIVER: MRI alkaline PO4 ▪ Mildly increase
◦ Provides additional tumor characteristic ▪ Elevated alkaline PO4 US
◦ Less accurate in detecting colorectal liver metastatic but CT or MRI scan
transaminases Nuclear med
more sensitive in detecting early HCC
MANAGEMENT:
◦ Distinguishes HCC from macro-regenerative nodules Angiogram
◦ MR cholangiography Culture ▪ 50% cases ▪ Flourescent
→ Evaluation of intrahepatic biliary tree Antibody (Enzyme Liver biopsy(if needed)
Advantages Disadvantages imminoassay EIA)
▪ Initial imaging ▪ Incomplete Occult primary evaluation
ULTRASOUND EGD
▪ Liver & biliary ▪ Obesity/bowel ▪ Empiric/culture- ▪ Metronidazole Colonoscopy
Antibiotic
CT SCAN ▪ Contrast medium ▪ Ionizing radiation based 750mg TID for 7 Mammogram
▪ Cost to 10 days Gyn/PAP smear
MRI ▪ T1/T2
▪ Availability
▪ Lack of exact Drainage ▪ Laparoscopic/open ▪ Aspiration rarely Diagnosis
localization ▪ Anatomic resection needed except:
PET SCAN ▪ Metastatic tumor ▪ Ionizing radiation large abscess,
▪ Cost unresponse to
▪ Availability medical therapy or
superinfected left
lobe
 LIVER LESIONS MANAGEMENT OF BENIGN LESIONS Role Of Chemotherapy In Colorectal Liver Metastasis
BENIGN MALIGNANT ▪ Liver biopsy with caution, increase risk of ◦ Conversion chemotheraphy
bleeding → To achieve resectability rather than a complete
Cyst Hepatocellular CA Hemangioma
response
Hemangioma CholangioCA ▪ Main indication for resection: PAIN
Focal Nodular Hyperplasia Gallbladder CA Adenoma ▪ Resection ◦ If potentially resectable
Adenoma Metastatic Colorectal CA Focal ▪ Main indication for surgery: ABDOMINAL PAIN → At least 4 courses of chemotherapy should be given first
Metastatic neuroendocrine Nodular ▪ Oral contraception or estrogen should be line
Biliary Hamartoma
(carcinoid) Hyperplasia stopped ◦ Optimum timing for assessment of response to
Metastatic cancers of other chemotherapy (resectability)
Abscess
cause MOST COMMON MALIGNANT: HEPATOCELLULAR CA → Every 2 months
▪ Viral hepatitis
SYMPTOMS OF BENIGN LIVER LESIONS ▪ Alcohol hepatitis Strategy for CRLM
Risk factors
▪ Most frequently encountered ▪ Hemachromatosis Resectable Non-resectable
▪ Congenital cyst ▪ Nonalcoholic steatohepatitis
Cyst ▪ Biliary cystadenoma ▪ Hypervascular in arterial phase
CT scan
▪ Hypodense in delayed phase
+/- preoperative Chemotherapy 2-3
▪ Polycystic liver disease Chemotherapy months
MRI ▪ Variable T1 and hyperintense T2
▪ Caroli’s disease Portal vein
▪ Small liver lesion (2-4mm) surface ▪ Highly suggestive HCC Resection
Biliary duct thrombosis
▪ Firm, yellow, smooth in appearance (one or two stages)
hamartoma
▪ Excisional biopsy
▪ Most common
2ND MOST COMMON MALIGNANT: CHOLANGIOCARCINOMA +/- PVE
▪ Gain, larger than 5-6cm HILAR (Klatskin) PERIPHERAL
Hemangioma Postoperative chemotherapy
▪ Spontaneous rupture is rare Obstructive jaundice, painless Tumor mass
▪ Malignant transformation Locoregional
▪ Young woman(20-40) Treatment Poor survival TREATMENT OPTIONS
▪ Pain ▪ Surgical resection (absence ▪ Vascular invasion Gold standard for HCC with cirrhosis
▪ Solitary, sometimes multiple of PSC) ▪ Posotive margins Hepatic resection
Adenoma
▪ Prior or current use of contraceptives
(if Margin: 1cm)
▪ Chemoradiation ▪ Multiple tumors
▪ Spontaneous rupture (10-25%) HCC with cirrhosis
Improved outcome Prognostic factors
▪ Malignant transformation to HCC Recurrent rates (>50%)
▪ Histologic (-) margin affecting survival
▪ Childbearing Liver Improved survival rates
▪ Concomitant hepatic ▪ Absence of mucobilia
Focal Nodular ▪ Oral contraceptive use transplantation Early stage(1,2); 1 tumor,5cm; 3
resection ▪ Nonpapiliary tumor
Hyperplasia ▪ Do not rupture tumor,largest 3cm; absence of gross
▪ Well-differentiated ▪ Advance stage
▪ No significant risk of malignancy vascular invasion or extrahepa spread
▪ Nonhepatectomy
▪ Lack of pre-op chemo HCC of 3 - 7.5cm
Radiofrequency Recurrence rate after TFA vs resection
3-5 year survival: 41.7% - 26.8% 3-year survival: 55%
CT SCAN result ablation (RFA) TFA=14.5%; resection=7.4%
Combination with TACE
Hemangiom ▪ Largely asymmetrical nodular peripheral 3rd MOST COMMON MALIGNANT: METASTATIC COLORECTAL CA
Ethanol ablation,
a enhancement, isodense 10-year survival cryosurgery,
▪ Sharply defined border, confused with ▪ Resection on fewer than 4 segments ▪ 4 or more: 29% microwave ablation
metastatic tumors ▪ Solitary: 33% Chemoembolization
Adenoma ▪ Venous phase - isodense/hypodense Yttrium 90
Resectability is no longer defined on Inoperable primary or metastatic liver
▪ Arterial phase - subtle hypervascular micropheres
what actually is removed but on what tumor
enhancement (SIR-Spheres)
remain after resection
▪ Biphasic, well circumscribe with typical Stereotactic
▪ Atleast 30-40%
central scar radiosurgery
Focal ▪ Use of neoadjuvant chemotherapy
▪ Venous phase - isodense or invisible Systemic
Nodular ▪ Portal ven embolization
campared with background liver chemotherapy
Hyperplasia ▪ Simultaneous ablation
▪ Arterial phase - Intense homogenous
enhancement ▪ Resection of extra-hepatic tumor
 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 ACUTE LIVER FAILURE
▪ Trocar placement ◦ LLR is associated with less blood loss and shorter ETIOLOGY
▪ location hospital stay than open resection for CLM → Viral infection (hepatitis A, B, E)
◦ According to short term results, LLR is → Drug-induced (acetaminophen)
equivalent to OLR in terms of oncologic
outcomes CLINICAL PRESENTATION
◦ Long term survival is comparable to → Jaundice & Encephalopathy
conventional open approach → Hepatic Coma
→ Increased creatinine
MULTIPLE BILOBAR SYNCHRONOUS METASTASIS → Arterial pH <7.3
1. Chemotherapy if colonic tumor is not → Culture proven infection
symptomatic (obstructed etc)
2. After 6 cycles: DIAGNOSIS & TREATMENT
A) Colonic resection → Liver biopsy
The peripheral area of anterolateral segments B) Clearance of the left lobe of liver → Rapid progression
(segments 2, 5, 6, and lower part of 4) is considered to C) Right portal vein ligation → Acetaminophen overdose
be a favorable location of tumors for laparoscopic liver  Activated charcoal
3. After 2 months & 2 cycle of chemotherapy
resection, whereas the posterosuperior segments  N-acetylcysteine
(segments 1, 7, 8, and upper part of 4) of the liver are A) Right hepatectomy
→ ICU care
unfavorable locations.
→ Prognosis is poor unless treated
THE INTERNATIONAL POSITION ON RE-resection of recurrent CRLM
▪ 321 patient with primary resection & 14 in CIRRHOSIS
LAPAROSCOPIC LIVER SURGERY: THE LOUISEVILLE
re-resection (HK university) ▪ History and PE
STATEMENT 2008 ▪ Lab findings:
→ Laparoscopic approach for LEFT LATERAL ▪ Univariate analysis  Mild normochromic anemia
SECTIONECTOMY is standard practice → Re-resection is not a risk factor in overall  Low WBC, platelet
→ Major resection should be reserved for survival  Bone marrow: Macronormoblastic
▪ Multivariate analysis  Prolong PT, not responding to vitamin K
experienced surgeon  Bilirubin, transaminases, Alkal PO4 - elevated
→ Postoperative complication, microscopic ▪ Liver biopsy with ultrasound or CT guided
▪ Small, superficial or ▪ Large tumor, deep margin (+) & multiple tumors were risk
peripheral seated or posteriorly factors ▪ Cirrhosis - the final sequela of chronic hepatic insult and
▪ Re-resection of recurrent CRLM can achieve consequence of sustained wound healing in response
▪ Segment 2,3,4b,5,6 located in right lobe to chronic liver injury
▪ Tumor closed to favorable survival outcome ▪ Characterized by the presence of fibrous septa
portal bifurcation or throughout the liver subdividing the parenchyma into
suprahepatic junction 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
hepatic lobule Neurologic  encephalopathy - ammonia goes to
Macronodular frequently has septa and the brain since liver is bypassed

 asterixis
cirrhosis regenerative nodules of varying
sizes Head and Neck  parotid gland swelling because of edema
Mixed present when regeneration is Skin  jaundice, angiomata, palmar
occur- ring in a micronodular liver erythema (alteration in sex hormone)
and over time converts to a Chest  Pleural effusion
macronodular pattern Abdomen  Ascites
MODE FOR END-STAGE LIVER DISEASE SCORING SYSTEM
 caput medusa
 Cruveilheier-Baumgarten bruit - venous  Model for End-Stage Liver Disease (MELD) is
ETIOLOGY hum that can be auscultated in the a linear regression model based on
epigastrium resulting from collaterals objective laboratory values
 Alcoholic Liver Disease
between the portal system and the  INR
 History of chronic alcohol abuse
remnant of the umbilical vein  Bilirubin level
 Liver biopsy - would show hepatocyte necrosis,
 Splenomegaly  Creatinine level
Mallory bodies, neutrophil infiltration, and
Urogenital  testicular atrophy  Used to predict mortality after transjugular
perivenular inflammation
Extremities  clubbed fingers – consequence of intrahepatic portosystemic shunt (TIPS) and as
 Non-alcoholic steatohepatitis (NASH)
hypoalbuminemia the sole method of liver transplant allocation
 history of diabetes mellitus or metabolic syndrome
Dupuytren’scontractures
 the lack of a history of significant alcohol
White nail beds
consumption, and exclusion of other causes of
Musculoskeletal Muscle cramps - correlate with ascites,
hepatic steatosis
low mean arterial pressure, and plasma
 Biopsy - demonstration of steatohepatitis renin activity
 Cryptogenic cirrhosis - cirrhosis without an apparent
cause
 Chronic hepatitis C infection ASSESSMENT OF SURGICAL RISK
 most common cause of chronic liver disease and
CHILD-TURCOTTE-PUGH SCORE
the most frequent indication for liver
transplantation in US  originally developed to evaluate the risk of
 Hemochromatosis (iron overload) portocaval shunt procedures
 most common metabolic disorder causing cirrhosis  shown to be useful in predicting surgical risks of
 Autoimmune causes other intra- abdominal operations on cirrhotic
 primary biliary cirrhosis patients
 primary sclerosing cholangitis
 autoimmune hepatitis Class A 10%
 Uncommon metabolic disorders Class B 30%
 Wilson’s Disease Class C 75-80%
 A1-antitypsin deficiency
PORTAL HYPERTENSION MANAGEMENT: ESOPHAGEAL VARICES HEPATIC TRANSPLANTATION
 Gastroesophageal varices ▪ Abstinence from alcohol Patients only chance of definitive therapy and
Prevention ▪ Avoidanceof aspirin/NSAIDs long term survival
 Splenomegaly of variceal ▪ Administration of propanolol
 Caput-medusae bleeding ▪ Prophylactic Endoscopic Variceal Ligation
Patients with variceal bleeding refractory to all
 Ascites (EVL) form of management
 Anorectal varices Reverses most of the hemodynamic and
▪ Blood resuscitation
 Portal venous system contributes approximately 75% Acute
▪ Fresh frozen plasma and platelet
humoral changes associated with cirrhosis
variceal
of the blood and 72% of the oxygen supplied to the
bleeding
▪ Prophylactic antibiotics Not affected by previous EVL, TIPS, splenorenal,
liver ▪ Vasopressin (0.2-0.8 units/min)
 In the average adult, 1000 to 1500 mL/min of portal (5 days
▪ Somatostatin (initial bolus 50 units/IV)
medocaval shunt
venous blood is supplied to the liver hemostasis
▪ Surgical shunts/TIPS (refractory variceal
rate)
 this amount can be significantly increased in bleeding)
the cirrhotic patient ▪ Balloon tamponade (<24 hours)
 The portal venous system is without valves and drains
blood from the spleen, pancreas, gallbladder, and
abdominal portion of the alimentary tract into the MANAGEMENT: GASTRIC VARICES
liver ▪ MELD score <15
 Normal portal venous pressure is 5-10 mmHg, and at SHUNTS ▪ Not candidate for transplant
this pressure ▪ Limited access to TIPS
▪ Reduceportal venous pressure
IMAGING OF THE PORTAL VENOUS SYSTEM AND ▪ Maintain total portal & hepatic blood flow
MEASUREMENT OF PORTAL VENOUS PRESSURE Aim
▪ Avoid a high incidence of complication
 Abdominal ultrasonography - simplest initial ▪ Hepatic encephalopathy
investigation is PORTOCAVAL ▪ Higher incidence of shunt thrombosis and
 large portal vein suggests portal hypertension SHUNT rebleeding
but is not diagnostic WARREN
▪ Lower rate of hepatic encephalopathy and
 Doppler ultrasound - is capable of outlining the SHUNT (distal
decompensation
splenorenal)
anatomy of the portal vein, excluding the presence of
TRANSJUGULAR
thrombosis, and identifying the direction of portal INTRAHEPATIC ▪ >90% of cases refractory to medical
venous blood flow PORTOSYSTEMIC treatment
 useful in evaluating blood flow through surgical SHUNT (TIPS)
shunts and TIPS
 Hepatic venography - most accurate method of
determining portal hypertension
Clinically significant portal hypertension SUGUIRA PROCEDURE
 Hepatic venous pulmonary gradient (HVPG) is >10 mmHg Extrahepatic portal vein thrombosis & refractory
bleeding
Extensive devascularization of the stomach and
distal esophagus
Transection of esophagus
Splenectomy
Truncal vagotomy
Pyloroplasty
 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 Anatomy
sites of inflammation to wall off 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 • Contiguous structure suspending & fixing bowel to the abdominal wall
o Omental venous outflow obstruction • Provides housing for arterial, venous, nervous, lymphatic structures
• Secondary infarction – caused by other pathology
o Hernia • White line of Toldt – lateral border of the ascending and descending
o Tumors large bowel; provides avascular fascial plan between the colon, its
o Adhesions mesentery and underlying retroperitoneal space
• More common in male and obese patients o This is usually accessed by the surgeon to mobilize the part of
the bowel (like in the picture below, the ascending colon) for
• Diagnosis via imaging example in colectomy procedures.
o Ultrasound – hyperechoic non-compressible intraabdominal
mass attached to the abdominal wall
 Non-compressible means it is not the bowel
 Nice to know: another UTZ finding like this is the appendix
(non-compressible)
o CT scan – streaking whirling pattern of fatty tissue in the
anterior abdomen

• Treatment
o Conservative – leads to abscess or adhesion formation
o Laparoscopic exploration and resection of infarcted tissue
(partial omentectomy) – treatment of choice
 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 Mesenteric Cysts
mass • Disruption of the lymphatics in the mesentery due to:
o “Fat ring sign” – area of o Trauma, Mechanical obstruction, or Congenital lymphatic malformations
preserved fat near mesenteric • Most are unilocular
vessels • Symptoms are due to local compression of abdominal structures
coursing through areas of fibrosis • Incidental finding in 45%
Diagnosis: Lap or open biopsy
• Physical Exam: abdominal mass
• Treatment: o Tillaux’s sign – abdominal mass lesion that is only mobile laterally (vs. omental
o Bowel and mesenteric resection cysts – freely mobile in all directions)
- bowel ischemia
o Intestinal bypass – intestinal • Diagnosis: CT scan and US
obstruction • Treatment:
o Steroids, Hormonal therapy, o Marsupialization and simple aspiration – ↑ rates of recurrence
Colchicine o Enucleation – for benign lesions
o Thalidomide, Cyclophosphamide
 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
• Lipoblastoma histioma