Liver anatomy and physiology medicine

7/17/2019 Liver anatomy and physiology medicine

http://slidepdf.com/reader/full/liver-anatomy-and-physiology-medicine 1/73

LIVER

ODESSA BACUD

-

TIANGCO, MD



ANATOMY



HEPATIC VEIN

● Small

short

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




uncojugated




conjugated



BILE

● 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

LIVER



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



CIRRHOSIS

● Hepatic fibrosis

● Nodular regeneration

● Etiology

● Pathogenesis

● Clinical manifestations



CIRRHOSIS

Cirrhosis & portal hypertension negativeimpact on the outcomes of nontransplant

surgical procedures



ULTRASOUND



ULTRASOUND

● Coarsened

echotexture

● Enlarged Left lobe




6

CHILD TURCOTTE PUGH CLASSIFICATION



CHILD-TURCOTTE-PUGH CLASSIFICATION

CHILD TURCOTTE PUGH



CHILD-TURCOTTE-PUGH

CLASSIFICATION



PORTAL HYPERTENSION



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



Pathophysiology

Cli i l if t ti



Clinical manifestations



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



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



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



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

Liver anatomy and physiology medicine

Documents

Transcript of Liver anatomy and physiology medicine