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Liver

By: Prof.G.R.Arbab

Embryology
Hepatic Endodermal bud arises from the distal end of the foregut.This divides into Rt. And Lt. Branch that grows into the mesoderm and forms the liver . From the hepatic endodermal bud a solid out growth of the cell;the end of this out growth expands and forms the Gall Bladder and the proximal portion changes into the Cystic Duct.Later it cannulises.

Test Serum Albumin 3.5-4.6 g/dL Total Proteins 6.0-7.4 g/dL Cholesterol 135-300 g/dL Alkaline Phosphate 24-100 IU/dL Serum Glutamic Oxalacetic Transaminase(AST) 10-36units/dL Serum Glutamic Pyruvic Transaminase(ALT) 10-48units/dL Gamma Glutamyl Transferase(GGT) (males) 0-48units/dL (females) 4-26units/dL Lactic Acid Dehydrogenase(LD) 180-225units/dL Prothrombin Time 90-100%of lab.control Fibrinogen 200-400 mg/dL Blood Ammonia Serum Bilirubin: Total Direct 10-63 mg/dL less than 1.4 mg/dL less than 0.3 mg/dL

Normal Values-Hepatic Function Tests: Values

Liver Injury
Relative Frequency of Visceral Injury from Blunt Trauma: Viscera Involved I Spleen Intestine Liver Kidneys Bladder Others(inclu. Diaphragm, Pancreas &Mesentry) Total 56 14 6 8 11 46 141 Series II 20 3 9 25 9 8 74 III 53 27 45 IV 37 13 5 V VI 20 4 14 26 4 7 38 19 19 27 25 91 8

not incl. not incl. 8 183 39

124 72 200

Aetiology
Blunt Injury Abdomen Penetrating Wounds Spontaneous:
1.Primary Carcinoma 2.Benign Hepatic Adenoma 3.Toxemia of pregnancy 4.Postmature infants at the time of

delivery.

Pathology
Classification:
I: Transcapsular: Rupture extends through the Glissons Capsule. II: Subcapsular: Capsule remains intact. III: Central: Interruption of Parenchyma.

Blunt Injuries:
-Usually involves the anteroposterior position and emboli may arise from parenchyma.

Penetrating Injuries:
-Rt.Lobe Dome is usually involved. -Rt. To Lt. Lobe ratio 7:1 -Penetrating injury to hilar region is usually fatal.

Clinical Manifestation
Signs,Symptoms of shock. Abdominal pain. Spasm & Rigidity.

Diagnosis
History Examination Examination WBC Count Mild elevation of serum Bilirubin on 3-4 day Peritoneal tapping US CT Celiac Angography

Treatment
Observation: -in haemodynamically stable patient. Surgical Procedures, directed at:
-Control of Hemorrhage
Pringle Maneuver Argon Coagulator Fibrin Glue Tamponade with packs Selective Hepatobiliary Resection sub-lobar debridement

-Removal of necrotic devitalized tissue -Establishment of external closed drainage

Complications
Hemorrhage
-Primary -Recurrent

Intra Abdominal Sepsis Haematobilia

Haematobilia
Occurs within a few days or after a period of weeks Triad:
-Abdominal injury -Gastrointestinal Haemorrhage -Colicky pain(diagnosis by angiography)

Treatment
-Resection of lesion -Debridement -Unroofing -Ligation of the contributing hepatic artery

Investigations
Scintillography CT Scan US Scan Angiography

Hepatic Abscesses
By: Prof.G.R.Arbab

Pyogenic Abscess
0.36% of autopsies 6th- 7th decade Male= Female Single= Multiple

Etiology
Ascending Biliary Infection Haematogenous Spread,via portal venous system Generalized septicemia, via hepatic artery circulation Direct extension Post hepatic trauma

Cause
Most common: Ascending cholangitis Second common: Generalized septicemia Third common : Portal Vein Routes,i.e:
-Ac. Appendicitis 0.05% -Perforated appendicitis 3% increasing incidence in immuno-comprised patients.

Pathogenesis
Mixed isolated 50% E.Coli 33% Staphylococcus aureus Streptococcus haemolyticus Proteus Klebsiella Bacteriodes

Clinical Manifestations
Fever Chills Profuse Sweating Nausea Vomiting Anorexia RT.HQ Pain Hepatomegaly 30-60% Jaundice-uncommon

Diagnostic Studies
Leukocytosis 18000-20000 Low HB Blood Cultures positive 40% Blood Serum alkaline phosphatase Hypalbuminaemia Immobility/restriction-RT.dome of Diaphragm Obliteration of RT.Cardiophrenic angle on PA Chest film Air fluid levels in gas forming microorganism US 99m Tc Sulfur Colloid Scan

Treatment
Antibiotics
- i/v 2 weeks - oral 1 month - Persutaneous drainage under US or CT Control - Transthroacic surgical drainage - Transabdominal surgical drainage - Surgical resection multiple abscesses in one lobe

Amaebic Abscess
Incidence:
-E. -Predominant in middle age -Male:Female 9:1

Pathology:
-Amaebic reach the liver by way of the portal venous system from a focus ulceration in the wall. -Usually single thin walled, containing reddish brown Anchovy paste.

Clinical Manifestations
Liver Pain: 88% Fever Chills Sweating Tenderness Bulge and pitting oedema of s/c tissue 30-40% have h/o antecedent diarrhea

Diagnosis
Leukocytosis Anemia 15% stool containing amoeba Indirect haemagglutination test Radiographic finding same as in pyographic abscess Scintillography US Angiography 30% abcess fluid contain amoeba

Complications: -Secondary infection 22% -Pleuropulmanary complications 20% -Rupture Treatment: -Amoebicidal drugs -Aspiration -Surgical drainage Prognosis: -Uncomplicated cases less than 5% -Complicated cases 43%

Liver Cysts
Types:
-Parasitic Cysts -Non Parasitic Cysts

Parasitic (Hydatid) Cyst


Hydatid disease is caused by Ecchinococcus Is spread worldwide Intermediate hosts: sheep,pigs and cattle Unilocular cysts -Echinococcus granulous Multilocular cysts - Echinococcus multilocularis 70% in liver 25-35% multiple 85% Rt.lobe is involved Usually superficial Two layers: inner-germinal & outer-adventitious Fluid is colorless,opalescent,alkaline,with high pressure of about 33ml of water Alveolar type are without capsule and metastises

Diagnostic Studies
Radiology calcified cysts Gas is seen in infected and in intrabiliary rupture US CT Eosinophilia 25% Indirect agglutination test 85% Compliment fixation test Casonis skin test 90%

Clinical Manifestations
Usually asymptomatic Painless Rt.HQ mass When symptomatic they are usually due to pressure on adjacent viscera Acute abdominal pain due to:
-Torsion -Intracystic hemorrhage -Intraperitoneal rupture

Clinical Manifestations
Asyptomatic:
-Symptoms from pressure on adjacent organs -Pain and tenderness -Palpable mass 70% -Diffuse hepatomegally -Hydatid thrill and fremitus-rare

Secondary Infection:
-Tender hepatomegally,chills,spiking temperature,urticaria and erthema due to anaphylactic reaction (contd)

Clinical manifestations #2

Biliary Rupture:
-Biliary Colic -Jaundice -Urticaria -Hydatidemesia -Hydatidenteria

Intra Thoracic Rupture:


-Shoulder Pain -Productive cough -Sputum contains blood -Bile and membranes 80%

Complications
Infection Intrabiliary rupture Intraperitoneal rupture Pleural cavity Extension Empyema and Broncho Pleural Fistula

Treatment
Small calcified cysts with negative serological tests need no treatment.

Surgical Treatment:
-Excision (germinal layer) -Marsupilization -Total excision of both germinal and adventitial layers

-Management of remaining cavity:


-Capsuloraphy -Capsuloraphy with extra peritoneal drainage -Marsupilization(closed) -Marsupilization(open) -Omentoplasty

Non-Parasitic Cysts
Maybe single,multiple,diffused,localized,unilocular or multilocular. Types:
-Blood and Degenerative Cysts -Dermoid Cysts -Lymphatic Cysts -Endothelial Cysts -Retention Cysts:
*Solitary *Multiple (polycystic disease)

-Proliferative disease(cystadenoma) -Post Traumatic Cyst

Pathology
Solitary:
Cysts contents are clear,watery with characteristically low internal pressure.

Polycystic:
Polycystic Disease of liver is associated with cystic involvement of kidney lesions.

Traumatic:
Traumatic cysts usually contain bile without any epithelial lining.

Cystadenomas:
Cystadenomas are usually smooth,encapsulated.lobular and contains a mucoid material.

Treatment
Asymptomatic:
No treatment indicated

Symptomatic:
-When superficial:
complete extiration resection

-With purulent fluid:


unroofing cyst external drainage marsupilization

Tumors of Liver
Benign:
-Hanartoma -Adenoma -Focal Nodular Hyperplasia -Haemangioma

Malignant:
-Primary Carcinoma -Sarcoma -Mesenchymoma -Infantile Haemangio Endothelioma -Angiosarcoma

Metastatic Neoplasm:

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