liver anatomy and physiology medicine

7/17/2019 Liver anatomy and physiology medicine

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ODESSA BACUD

TIANGCO, MD

ANATOMY

HEPATIC VEIN

● Small

hepaticveins

HEPATIC ARTERY

● Replacedhepatic

artery

● Accessoryhepatic

artery

PORTAL VEIN

PORTAL VEIN●

75%● Posterior to the

bile duct & hepatic

artery

● valveless

● 3-5 mm Hg

BILIARY SYSTEM

LYMPHATICS & INNERVATION

● Spaces of Disse & clefts of Mall → sub-Glissonian

&periportal → cisterna chyli

● Vagus nerve & celiac plexus

C3 & C4

LIVER LOBE

● Coagulation

factors

● Plasma proteins-

eg. albumin

● Glucose

● Lipoproteins

● Triglyceride

PHYSIOLOGY:SYNTHETIC FUNCTIONS

● Cholesterol →

● Bile salt

BILIRUBIN METABOLISM

uncojugated

conjugated

● Bile

● 85% water

● 10% bile salts

● 3% mucus & pigments

● 1% fats

● 0.7% inorganic salts

● BILE ACIDS

● Primary : cholic &

chenodeoxycholic

● Secondary : deoxycholic& lithocholic

BILE & ENTEROHEPATIC

CIRCULATION

500-1000ML/24H

LIVER FUNCTION TESTS

● PARENCHYMAL- AST, ALT

BILIARY - Alkaline phosphatase

● SYNTHETIC - INR, factors V & VII, bilirubin,

albumin

RADIOLOGIC EVALUATION OF THE

ULTRASOUND

Economical● Screen for HCC

● Biliary tract stones

● Intrahepatic biliary

ductal dilation

ULTRASOUND

● Microbubblecontrast

● Doppler UTZ

● laparoscopic

● IOUS- gold standard

to detect number,extent & blood vessel

association of tumors

COMPUTED TOMOGRAPHY SCANS

● Highly sensitive

Dual- & triple-phase IV contrast

● 3-D

● PRE-OPERATIVE

EVALUATION-

inflow & outflow

of hepatic bloodvessel

● -Liver volume

● Primary vs.

metastatic

MAGNETIC RESONANCE IMAGING

● Less sensitive at spatial discrimination

● More sensitive for detecting early HCC &

distinguishing HCC for macroregenerativenodules

● Contrast- cystic vs. Hemangioma

● MRC

● PET Scan

F-flurodeoxyglycose

Angiography ● Hepatic arterial chemoembolization

● Percutaneous biopsy

● Diagnostic laparoscopy

LIVER FAILURE

● Hepatic insufficiency---> encephalopathy

● ACUTE

● Rapid massive loss of hepatocyte functional mass

without pre-existing liver disease

● CHRONIC

● Viral hepatitis, metabolic diseases, alochol abuse,

toxins

● Ongoing & progressive hepatocyte necrosis →

fibrosis & regeneration→ cirrhosis

ACUTE LIVER FAILURE

● Development of encephalopathy within 26

weeks of onset of any hepatic symptom

● Fulminant Hepatic Failure

● Subfulminant Hepatic Failure

ACUTE LIVER FAILURE

● Etiology

● Acetaminophen overdose

● Viral hepatitis

● Other drug toxicities

● 20% will survive--> N liver function

HEPATIC ENCEPHALOPATHY

ACUTE LIVER FAILURE

● Treatment

● Supportive care/Medical Management

● LIVER TRANSPLANT – 60% survival rate

CRITERIA FOR SELECTION OF PATIENTS MOST LIKELY TO BENEFIT FROM

LIVER TRANSPLANTATION

● ACETAMINOPHEN TOXICITY

● PH< 7.3 regardless of grade of encephalopathy

● PT > 100 sec (INR >6.5) & creatinine > 300

umol/L (in patients with grade 3-4

encephalopathy

● VIRAL HEPATITIS/DRUG REACTION

● PT > 100 sec (INR >6.5 regardless of grade of

encephalopathy)

● or....

CRITERIA FOR SELECTION OF PATIENTS MOST LIKELY TO BENEFIT FROM

LIVER TRANSPLANTATION

VIRAL HEPATITIS/DRUG REACTION ● Any 3 of the following regardless of the grade of

encephalopathy)

1. age <11 & >40● 2. duration of jaundice before the onset of

encephalopathy> 7 days

● 3. cause : non-HepA, non-HepB, halothane

hepatitis, idiosyncratic drug reaction

● 4. PT > 50 sec (INR > 3.5)

● 5. serum bilirubin > 300 umol/L (> 17.5 mg/dl)

CHRONIC LIVER FAILURE

CIRRHOSIS

● Hepatic fibrosis

● Nodular regeneration

● Etiology

● Pathogenesis

● Clinical manifestations

CIRRHOSIS

Cirrhosis & portal hypertension negativeimpact on the outcomes of nontransplant

surgical procedures

ULTRASOUND

● Coarsened

echotexture

● Enlarged Left lobe

CHILD TURCOTTE PUGH CLASSIFICATION

CHILD-TURCOTTE-PUGH CLASSIFICATION

CHILD TURCOTTE PUGH

CHILD-TURCOTTE-PUGH

CLASSIFICATION

PORTAL HYPERTENSION

WHVP or direct portal venous pressure that is>5 mmHg greater than the inferior vena cava(IVC) pressure,

a splenic pressure of >15 mmHg,● or a portal venous pressure measured at

surgery of >20 mmHg

● A portal pressure of >12 mmHg is necessary for

varices to form and subsequently bleed.

Etiology

Pathophysiology

Cli i l if t ti

Clinical manifestations

● Cruveilhier-Baumgarten murmur

● Veins of Retzes- retroperitoneal

SURGICAL CONCERNS

● Encephalopathy

Ascites

● Variceal bleeding

VARICEAL BLEEDING

VARICEAL BLEEDINGPrevention of bleeding

improvement of liver function (i.e., abstention fromalcohol),

● avoidance of aspirin and NSAIDs,

● propranolol or nadolol (nonselective beta blockers)

● prophylactic endoscopic variceal ligation (EVL)-

– medium to large varices,

– every 1 to 2 weeks until obliteration,

● Esophagogastroduodenoscopy (EGD) 1 to 3 monthslater

● Surveillance EGD every 6 months

VARICEAL BLEEDINGManagement of bleeding

● ICU for resuscitation

● Blood resuscitation to a hemoglobin level of ~ 8 g/dL. Overreplacment of

packed red blood cells and the overzealous administration of saline →

rebleeding and increased mortality.

● fresh-frozen plasma and platelets

● short-term prophylactic antibiotics : ceftriaxone 1 g/day IV is often given.

● Vasopressin, administered IV at a dose of 0.2 to 0.8 units/min,

● Somatostatin and its analogue octreotide (initial bolus of 50 g IV followed bycontinuous infusion of 50 g/h) also cause splanchnic vasoconstriction.

● EGD & EVL

Even when aggressive pharmacologic and endoscopic therapies are

initiated and these treatment options are maximized, 10 to 20% of

patients with variceal bleeding will continue to bleed. Shunt therapy,

with either surgical shunts or TIPS, has been shown to control

refractory variceal bleeding in >90% of treated individuals. Shuntsurgery usually is considered only in patients with preserved hepatic

function (i.e., CTP class A); TIPS is used in patients with

decompensated liver disease (i.e., CTP class B or C). However, the use

of these treatment options is dependent on local expertise.

Balloon tamponade using a Sengstaken-Blakemore tube will control

refractory variceal bleeding in >80% of patients. However, its

application is limited due to the potential for complications, whichinclude aspiration and esophageal perforation. Therefore, use of a

Sengstaken-Blakemore tube should be limited to short-term therapy

(<24 hours) in those patients awaiting definitive care.

TRANSJUGULAR INTRAHEPATIC

PORTOSYSTEMIC SHUNT● Control variceal bleeding in

>90% refractory to medical

treatment

● Complications : bleeding,

infection, renal failure,

decreased hepatic function,

hepatic encephalopathy

PORTOCAVAL SHUNT

Eck fistula

● high incidence of

hepatic

encephalopathy

● decreased liver

function

makes subsequenthepatic transplantation

much more technically

difficult

MESOCAVAL SHUNT

● technically easier

● does not adversely

affect subsequent

hepatictransplantation.

● higher incidence of

shunt thrombosis and

rebleeding

DISTAL SPLENORENAL (WARREN)

● Used most often

● lower rate of hepatic

encephalopathy and

decompensation,

● not interfering with

subsequent hepatic

transplantation

DISTAL SPLENORENAL (WARREN)

● Used most often

● lower rate of hepatic

encephalopathy and

decompensation,

● not interfering with

subsequent hepatic

transplantation

SUGIURA PROCEDURE

● In patients withextrahepatic portal

vein thrombosis

and refractoryvariceal bleeding

BENIGN SOLID LIVER TUMORS

CYSTIC DISEASES OF THE LIVER

● Congenital cysts

● Biliary cystadenoma

Polycystic liver disease● Caroli's disease

LIVER INFECTIONS

● Pyogenic liver abscess

● Amoebic liver abscess

Hydatid Disease● Ascariasis

● Schistosomiasis

● Viral hepatitis

● The most common source of liver abscess is the biliary tree in

patients with cholecystitis choledocholithiasis or cholangitis

patients with cholecystitis, choledocholithiasis, or cholangitis

● Less common sources include other intra-abdominal processes,

such as appendicitis or diverticulitis, and hematogenous spread from

sources such as an infected heart valve or the oral cavity a the

vascular route is associated with multiple abscesses

● The right hepatic lobe is affected more than twice as frequently as

the left, due to vascular anatomy

● Aspiration of abscess fluid and subsequent culture guide antibiotic

choice

● Failure to culture pathogenic organism(s) may be due to prior

antibiotic treatment or inadequate anaerobic culture

● Treatment includes antibiotics and often either percutaneous or

surgical drainage/debridement, depending on the size, number, and

complexity of the abscess(es)

● Less common sources include other intra-abdominal processes such as

● Less common sources include other intra abdominal processes, such as

appendicitis or diverticulitis, and hematogenous spread from sources such as an

infected heart valve or the oral cavity

Amebic liver abscess should be considered in endemic areas or patients whohave been to the tropics

● Fungal microabscesses are seen primarily in patients with compromised

immune systems

● Rarely, liver abscess may be due to trauma, secondary infection from an

amebic abscess or a necrotic malignant hepatic tumor, or direct extension from

local structures

● Common pathogens include Streptococcus spp., Escherichia coli, Klebsiella,

and Bacteroides spp. Polymicrobial infections occur in 15% to 20% of patients;

approximately the same percentage have multiple abscesses

● Amebic liver abscess follows vascular spread of Entamoeba histolytica

from the colon in patients with the intestinal infection amebiasis. Amebic

abscesses may be very large; they contain aspirate with 'anchovy-sauce'

color and consistency

● Liver abscess in a child suggests immunocompromise

● A single abscess is the most common presentation; spread to the liver via

the vascular route is associated with multiple abscesses

● The right hepatic lobe is affected more than twice as frequently as the

left, due to vascular anatomy

● Aspiration of abscess fluid and subsequent culture guide antibiotic

choice

● Failure to culture pathogenic organism(s) may be due to prior antibiotictreatment or inadequate anaerobic culture

● Treatment includes antibiotics and often either percutaneous or surgical

drainage/debridement, depending on the size, number, and complexity of

the abscess(es)

MALIGNANT LIVER TUMORS

3rd most common cancer mortality

● Risk factors : Hep B, Hep C, Cirrhosis, aflatoxins, flukes

● Inc serum AFP in 55-95%

● Resection if :

● Single lesion < 5 cm, up to 3 lesions each < 3 cm

● Childs A & B

● No portal hypertension

● Tumor recurrence : 70% at 5 years

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