surgery seminar 2014

8/13/2019 Surgery Seminar 2014

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SEMINAR HEPATO BILLARYSURGERY

BY, Kadhiravan

ThayabalaCaisha


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PORTAL HYPERTENSION

S. Kadhiravan


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Hepatic portal circulation carries blood from GI tract (i.e.from the distal esophagus to anorectal junction) to the liver.

Portal venous blood drain into liver venous sinusoids andhence in to the hepatic veins.

Introduction


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Portal hypertension develop when there is elevation of portalpressure is greater than 12 mmHg, while normal portal

pressure is 5

10mmHg.

Decrease or reverse portal blood flow to the liver promotethe development/formation of portal-systemic collaterals,

shunting of portal blood flow to systemic circulationbypassing the liver

PortalHypertension


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Portosystemic anastomosis occurs in junctional areas ofvenous drainage.

The main sites of the collaterals are at the gastro-oesophageal junction,

the rectum,

the left renal vein,

the diaphragm,

the retroperitoneum

anterior abdominal wall via the umbilical vein.


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Child Pug Classification Of PortalHypertension


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Pre Hepatic:

1- Congenital portal atresia

2- Portal vein thrombosis (Neonatal sepsis)

3- Phlebitis of portal vein (abdominal infection)

4- Trauma or thrombosed porto caval shunt.

Hepatic:

1- Cirrhosis (alcoholic most frequently)

2- Chronic Active hepatitis

3- Parasitic diseases (Schiatosomiasis)

Causes Of Portal Hypertension


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Post Hepatic:

1- Budd Chiari syndrome (Hepatic venous thrombosis)

2- Constrictive pericarditis3- Tricuspid valve incompetence


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Surgical Implications

Upper GI bleed from oesophageal varices

Ascites due to liver cell dysfunction

Congestive splenomegaly


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Physical Examination

General examination

Level of consciousness

Vital parameters

Signs of hepatocellular failure :-

Ascites, Jaundice, Gynaecomastia, Spider angiomas, Palmer

erythema, Asterixis, Foetor hepaticus.


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Investigation

Laboratory

Cbc

Lft

Coagulation profile

Hepatitis markers (HbsAg)

Serum levels of BUN,creatinine,electrolytes

Blood grouping and cross matching


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Investigation

Endoscopy

Oesophageal varices

Blood clot over the varix

Varix over varix

Cherry red spots

Salmon patches

Fundic varices

Gastritis

Chronic duodenal ulcer


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Investigation

Radiology

USG - Status of liver

Status of spleen

Free fluid Portal cavernoma

Duplex doppler

Venous phase of superior mesenteric angiogram

Barium oesophagogram

Splenoportogram

Barium oesophagogram

CT CSAN


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General resuscitation

Anti coagulation for Budd Chiari syndrome

Treatment of hepatic cause

Treatment Of Chronic Complication such as Esophageal gastric varices:

1- Beta blocker (propranolol or nadolol), reduce portal venouspressure.

2- Repeated injection sclerotherapy or variceal ligation

3- Elective porto

systemic shunt (spleno

renal anastomosis)4- Liver transplant may be considered for treatment if associated with

severe liver diseases.

Treatment


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Acute Variceal Bleeding


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Initial Evaluation & Stabilization

1. Assessment of intravascular volume status

2. Fluid resuscitation

3. Endotracheal intubation prior to endoscopy for:

Uncontrolled bleeding

Altered mental status, severe agitation

Respiratory distress or depression


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Pharmacologic

Radiologic shuntTIPSS

Surgical Shunt

Balloon

Tamponade

Pharmacologic andendoscopic therapy

are the usual 1stand2ndinterventions

Endoscopic

Treatment forAcute Variceal Bleeding


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1. Octreotide

Synthetic analogue of somatostatin

Decreases portal pressure and azygos blood flow

Stops variceal bleed in 80% of the cases

Efficacy is similar to endoscopic sclerotherapy and betterthan vasopressin

Pharmacologic Therapy


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2. Vasopressin

Reduces portal pressure but causes myocardial andmesenteric ischemia (more side effects)

Control approximately 50% of acute episodes


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3. Terlipressin

Efficacy similar to endoscopic sclerotherapy and as effectiveas balloon tamponade when used with nitroglycerin


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Endoscopic Therapy

Sclerosant injection

Band ligation

Became a standard form of therapy in acute varicealbleeding

Initial control of hge in 70 95%

Re-bleeding 20 50%


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5% sodium morrhuate

5% ethanolamine oleate

Intravariceally : to obliterate the varix

Paravariceally : induce submucus fibrosis

Sclerotherapy achieved better initial hge control

Fewer episodes of rebleeding Improved long-term survival

Sclerotherapy


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Alternative to sclerotherapy

Fewer rebleeding episodes

Fewer endoscopic interventions

Lower procedure related mortality and over all mortality

Band Ligation


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Balloon positioning


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Direct temponade therapy is 90% effective in controllingthe bleeding

50% rebleeding after removal

Serious potential complications (mortality 20%)


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Creating an intrahepatic portosystemic fistula todecompress the portal hypertension

First performed in 1982

(non- selective side to side portosystemic shunt)

Transjagular IntrahepaticPortosystemic Shunting (TIPS)


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1. Cannulating the Rt hepatic vein via internal jagular vein

2. Passing needle through liver parenchyma to portal vein branch

3. Guide wire

4. Balloon dilatation


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5stenting the tract


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1. Contraindications:

R side heart failure

Polycystic liver

Portal vein thrombosis

2. Complication

Intraperitoneal bleeding due to perforation of the hepaticcapsule, hepatic, or portal veins

TIPS embolization

Acute right heart failure due to increased venous return to rightheart


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Most effective method in controlling portal hypertension and recurrent

bleeding

1 Portosystemic shunt procedures

2 Esophagogastric devascularization

3 Orthotopic liver transplantation

Surgical Therapy


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1Non selective Shunts

1. End to side portocaval (Eck'sfistula):

Higher rate of encephalopathyamong operative shunting

groups

Better control of rebleeding thanmedical treatment

Eck fistula medical therapy same incidence of

encephalopathy


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2. Side to Side portocavalshunt:

Maintain the anatomiccontinuity of the portal vein

Encephalopathy rate : nodifference

Decompress the sinusoidalpressure better ascitis

control

Recommended for BuddChiari Syndrome

More difficult than end toside


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. Interpositionesocaval Shunt:

Prosthetic autogennous vien

Avoid hilar dissection(future transplant)

Shunt ligation inrefractory post-op

encephalopathy

Drawback thrombosis(35%)


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4. Proximal Spleno-Renal Shunt:

Splenectomy +

anastomosing proximalSplenic vein to Lt Renalvein

Divert all portal flowinto renal vein non

selective

Shunt occlusion 18%


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Coronary

Caval Shunt:

Described in Japan in1984

Interposition graftbetween L Gastricand inferior vena cava


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Esophagogastric Devascularization

The most effectivenon-shunt operationfor preventing varicealbleeding:

Devascularization+ transection +splenectomy

Sugiura procedure

O th t i Li


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Orthotopic LiverTransplantation

The most definitive form oftherapy for complications of portalhypertension

Selective patients:

CoastUnavailability

Immunosuppresion


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Understanding the natural history of portal hypertension PH and due to other etiologies may have significant

implications in choosing the appropriate interventionand predicting the outcome.

Conclusion


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ACS Surgery : Principles and Practice 2004 Web,MD

Schwartz Principles of Surgery 7thEdition

Johns Hopkins Gastroenterology & Hepatology ResourceCenter (http://hopkins-gi.nts.jhu.edu)

References


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CHOLEDOLITHIASIS


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ACUTE CHOLECYSTITIS


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ACUTE CHOLECYSTITISETIOLOGY:

Mostly associated withCholelithiasis.

In 95% gall stone is foundimpacted In cystic duct.


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Types of Gall stones:

1) Mixed stones commonest

2) Pure cholesterol stones

3) Pigment stones

black & brown


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Common organisms grown are:

E.Coli , Klebsiella & Streptococcus fecalis.

Rarely Bacteroides & Clostridia may be

found (gas seen in gall bladder).

Acute Cholecystitis may occur as a

complication of Typhoid & perforation can

occur.


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Pathophysiology:

(1) cystic duct obstruction with GBdistension & ischemia,

(2) Mechanical (stone) injury to mucosa

(3) bacterial infection.


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Gall stones (by causing obstruction

to bile flow & GB distension) &lysolecithin in bile which damages

the mucosa play a part in the

pathology.Added to this is secondary

bacterial infection.


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Perforation of gall bladder- usually

occurs in fundus (due to ischemia) orat neck (due to pressure necrosis).

It may form a localised abscess or

diffuse peritonitis (mortality rate 50%).


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Clinical features:

Sudden onsetPain in hypochondrium

Nausea & vomiting

Pyrexia >38oC

Neutrophilia

Tenderness & guarding in hypochondrium


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Sometimes a mass may be

felt. Boasssign- an area of

hyperesthesia between 9th&

11thribs posteriorly on the

side.

Murphys sign- holdingbreath on hypochondrial

palpation.


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Signs of sepsis, shock &generalised peritonitis may

be present in elderly patients

or in a case of perforation.


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Diagnosis:Plain X-ray chest & abdomen

Ultrasonography

Radionuclide cholescintigraphyusing Tc99m isotope scan

ERCP or PTC if other tests do not

reveal the diagnosis.


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PLAIN XRAY OF ABDOMEN

Plain abdominal radiograph in a49-year-old diabetic womanshows air within the gallbladder

lumen due to emphysematouscholecystitis (arrow).


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Treatment:

Initially conservative followed byCholecystectomy.

Nil by mouth, naso-gastric aspiration,

analgesics & antibiotic cover will tide over the

crisis.


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Cholecystectomy performed 2-3 days after acute

phase subsides.

If the patient does not improve or perforation issuspected then emergency laparotomy is

performed.

Cholecystostomy is done in debilitated cases.


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Dissection of Cystic duct


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Clips applied to Cystic duct


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Cystic artery being dissected


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Gall bladder dissected from liver

bed
http://localhost/var/www/apps/conversion/tmp/Downloads/Laparoscopic%20Cholecystectomy.mp4


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Q2. Prophylactic cholecystectomy isnot recommended for

a) Heart transplant receipients

b) Diabetes Mellitus c) Incidental gallstones on laparotomy


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Q3. Which of the following is not anultrasonic finding in acute cholecystitis

a) Absence of gallstomes

b) Gallbladder wall thickness morethan 6 mm

c) Pericholecystic fluid

d) Sonographic Murphy's sign


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Q4. Which of the following is not apremalignant condition of gallbladder?

a) Porcelain gallbladder

b) Adenomyomatosis of gallbladder c) Salmonella infection

d) Phrygian cap

Q5 Which of the following is not true regarding


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Q5. Which of the following is not true regardinggallbladder cancer following cholecystectomy

a) Subsequent treatment depends on many

factors including stage of disease, surgicalmargins, spillage etc

b) For T1 and T2 lesions cholecystectomy issufficient

c) The term extended cholecystectomy ispreferred to radical cholecystectomy

d) Common Bile Duct (CBD) excision is notrequired in all cases

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