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D e e p P a t e l
J X U T C M
w a n d e r v e s t e r @ g m a i l . c o m
Liver abscess &
HEPATOCELLULAR
CARCINOMA
• Caused by
Streptococcus
milleri and
Escherichia
coli(common)
Streptococcus
faecalis,
Klebsiella
Proteus vulgaris
mixed growths
• Treatment
• antibiotics and ultrasound-
guided aspiration.
• First-line antibiotics
• penicillin,
• aminoglycoside and
metronidazole
• cephalosporin and
metronidazole.
Pyogenic liver
abscess • m/c type of liver abscess
• present in 5th and 6th decay and common in alcoholic males
• Routs of infections
1.Bile duct /biliary tract
• Cbd stones
• Cbd cholangiocarcinoma
• Cbd strictures
• Lft abnormality
2.Portal vein
• Appendicular
perforation or
diverticularis
3.Hepatic artery
• Clinical features
• fever with chills
and rigor
• Abdominal pain
• Anorexia
• Fatigue
• 20-25%cases
with jaundice
• Investigations
• Lab
ALP(m/c LFT abnormality)
GGT
• Imaging
USG- choice of
investigation
Ct- to rule out necrotic
neoplasm
Culture – reconfirm
• Caused by
entamoeba
histolytica
• Treatment
metronidazole
(400– 800mg t.d.s. for 7–10
days)
Amoebic liver
abscess • Affects male
• most commonly present with dysentery
• Routs of infections
Feco-oral
• Clinical features
• Abdominal pain
• Anorexia
• fever
• Fatigue
• Jaundice is rare
• Investigations
• Lab
Inc PT
Stool antigen
• Imaging
USG- choice of
investigation
Culture – Amoebic
serology(elisa)
 constant cycle of damage and repair are the
biggest culprits
genetic mistakes or mutations, potentially leading to
carcinogenesis or development of cancer cells.
Examples
alcoholic hepatitis and cirrhosis
hereditary hemochromatosis,
primary biliary cirrhosis,
alpha-1 antitrypsin deficiency,
and others
Hepatic malignancy commonly diagnosed in presence of chronic liver disease
What exactly causes
the mutation in the
hepatocyte though?
RISK FACTORS
▪Hepatitis B/C infection, coinfection with
hepatitis D
▪Hereditary hemochromatosis
▪Cirrhosis
▪Smoking; frequent alcohol consumption
▪Obesity
▪Alpha-1 antitrypsin deficiency
▪Gallstones
▪Chronic exposure to aflatoxin(mycotoxin
found in peanuts, soybeans, corn)
▪male
Signs
&symptoms
Often no
symptoms aside
from those of
chronic liver
disease
▪Epigastric pain;
appetite, weight
loss
▪Palpable
abdominal mass;
manifestations of
decompensated
cirrhosis (e.g.
splenomegaly,
ascites, jaundice);
hepatic bruit
COMPLICATIONS
▪Paraneoplastic syndrome: watery
diarrhea, hypoglycemia, hypercalcemia,
erythrocytosis; cutaneous lesions
(e.g. pemphigus foliaceus)
▪Extrahepatic metastasis: commonly
lymph nodes, lungs, adrenal gland
DIAGNOSTIC IMAGING
Triple phase CT chest/abdomen/pelvis and MRI
(standard)
▪Tumour visualization, histopathological analysis,
grading, TNM staging, potential for resection
MRI angiography
▪3D characterization of lesion, hepatic circulation
An abdominal CT scan in the axial
plane demonstrating a massive
hepatocellular carcinoma.
Histological appearance of a
hepatocellular carcinoma. The
cells show high nuclear variation,
thickened nuclear envelopes and
occasional prominent nucleoli.
The cells also have abundant
eosinophilic cytoplasm.
LAB RESULTS
▪Elevated aminotransferases, alkaline phosphatase,
gamma-glutamyl transpeptidase; hyperbilirubinemia;
hypoalbuminemia
▪Elevated alpha-fetoprotein (most common serum marker)
Staging of hepatocellular carcinoma
• The staging of liver cancer is determined only after the results of the pathology test. There are no defined stages for liver cancer;
however, T/N/M and the Barcelona Clinic Liver Cancer staging system (BCLC) are the most common. According to the Barcelona Clinic
Liver Cancer staging system (BCLC), there are four liver cancer stages-
OTHER INTERVENTIONS
▪Radiofrequency ablation
▪Percutaneous ablation with ethanol/acetic acid
▪Trans arterial chemoembolization
▪Cryoablation
▪Radiation therapy; stereotactic body radiation therapy
MEDICATIONS
▪Chemotherapy
▪Systemic molecularly targeted
therapy; sorafenib, nivolumab
SURGERY
▪Partial hepatectomy
▪Liver transplant
Treatment
Liver transplantation
• first described by
Mazzaferro in 1996,
• Liver transplantation for
HCC offers the advantage
of not only definitively
treating the tumor but also
removing the diseased
hepatic parenchyma
• Milan criteria are now
considered the benchmark
indications for
transplantation for HCC
1.Incision
2.Evaluation of the abdomen for abnormalities that would preclude liver
transplantation (for example: undiagnosed infection or malignancy)
3.Mobilization of the native liver (dissection of the liver attachments to the
abdominal cavity)
4.Isolation of important structures (the inferior vena cava above, behind,
and below the liver; the portal vein; the common bile duct; the hepatic
artery)
5.Transection of the above mentioned structures and removal of the
native, diseased liver.
6.Sewing in the new liver: First, venous blood flow is re-established by
connecting the donor's and the recipient's inferior vena cava and portal
veins. Next, arterial flow is re-established by sewing the donor's and
recipient's hepatic arteries. Finally, biliary drainage is achieved by sewing
the donor's and recipient's common bile ducts.
7.Ensuring adequate control of bleeding
8.Closure of the incision
Steps
• First falciform ligament is divided along
anteroposterior surface of liver towards supra
hepatic IVC
• Then the left triangular ligament is divided by
using swab in front of esophagogastric junction,
• the right triangular ligament is by retraction of
diaphragm away from right lobe
• This leads to exposure of bare area ,IVC is seen as
it passes behind liver, here the slung Bove renal
veins below the liver and at the level of main
hepatic vein sliver separation from IVC is achieved
by lifting liver anteriorly to expose inferior hepatic
veins(multiple small veins) passing b/w liver
parenchyma & IVC
• They are suture ligated(suture of vessel done first
than ligation of them done) to ensure hemostasis.
MOBILISATION OF
LIVER
DISSECTION OF THE HILUM
• peritoneum overlying hilum is divided
• CBD exposure on free edge of lesser omentum is
facilitated by ligation
• cystic duct & artery is divided & than removal of GB
occur exposure of common hepatic artery &
dissection of the main right & left branches is done by
slinging cbd with elastic sling.
• they are again slung to allow remaining lymphatic
tissue surrounding the portal vein to be ligated &
divided.
• possibility of a replaced right hepatic artery is sought
arising from superior mesenteric artery & lying
posterior to bile duct and accessory left hepatic artery
from left gastric artery in lesser omentum
• Dissection of hilar bile ducts careful retraction on
segment 4 of liver(as 4 and 1 segment are closely
related & 1 has dual drainage)
Hepatocellular carcinoma

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Hepatocellular carcinoma

  • 1. D e e p P a t e l J X U T C M w a n d e r v e s t e r @ g m a i l . c o m Liver abscess & HEPATOCELLULAR CARCINOMA
  • 2. • Caused by Streptococcus milleri and Escherichia coli(common) Streptococcus faecalis, Klebsiella Proteus vulgaris mixed growths • Treatment • antibiotics and ultrasound- guided aspiration. • First-line antibiotics • penicillin, • aminoglycoside and metronidazole • cephalosporin and metronidazole. Pyogenic liver abscess • m/c type of liver abscess • present in 5th and 6th decay and common in alcoholic males • Routs of infections 1.Bile duct /biliary tract • Cbd stones • Cbd cholangiocarcinoma • Cbd strictures • Lft abnormality 2.Portal vein • Appendicular perforation or diverticularis 3.Hepatic artery • Clinical features • fever with chills and rigor • Abdominal pain • Anorexia • Fatigue • 20-25%cases with jaundice • Investigations • Lab ALP(m/c LFT abnormality) GGT • Imaging USG- choice of investigation Ct- to rule out necrotic neoplasm Culture – reconfirm
  • 3. • Caused by entamoeba histolytica • Treatment metronidazole (400– 800mg t.d.s. for 7–10 days) Amoebic liver abscess • Affects male • most commonly present with dysentery • Routs of infections Feco-oral • Clinical features • Abdominal pain • Anorexia • fever • Fatigue • Jaundice is rare • Investigations • Lab Inc PT Stool antigen • Imaging USG- choice of investigation Culture – Amoebic serology(elisa)
  • 4.  constant cycle of damage and repair are the biggest culprits genetic mistakes or mutations, potentially leading to carcinogenesis or development of cancer cells. Examples alcoholic hepatitis and cirrhosis hereditary hemochromatosis, primary biliary cirrhosis, alpha-1 antitrypsin deficiency, and others Hepatic malignancy commonly diagnosed in presence of chronic liver disease What exactly causes the mutation in the hepatocyte though? RISK FACTORS ▪Hepatitis B/C infection, coinfection with hepatitis D ▪Hereditary hemochromatosis ▪Cirrhosis ▪Smoking; frequent alcohol consumption ▪Obesity ▪Alpha-1 antitrypsin deficiency ▪Gallstones ▪Chronic exposure to aflatoxin(mycotoxin found in peanuts, soybeans, corn) ▪male
  • 5. Signs &symptoms Often no symptoms aside from those of chronic liver disease ▪Epigastric pain; appetite, weight loss ▪Palpable abdominal mass; manifestations of decompensated cirrhosis (e.g. splenomegaly, ascites, jaundice); hepatic bruit COMPLICATIONS ▪Paraneoplastic syndrome: watery diarrhea, hypoglycemia, hypercalcemia, erythrocytosis; cutaneous lesions (e.g. pemphigus foliaceus) ▪Extrahepatic metastasis: commonly lymph nodes, lungs, adrenal gland
  • 6. DIAGNOSTIC IMAGING Triple phase CT chest/abdomen/pelvis and MRI (standard) ▪Tumour visualization, histopathological analysis, grading, TNM staging, potential for resection MRI angiography ▪3D characterization of lesion, hepatic circulation An abdominal CT scan in the axial plane demonstrating a massive hepatocellular carcinoma. Histological appearance of a hepatocellular carcinoma. The cells show high nuclear variation, thickened nuclear envelopes and occasional prominent nucleoli. The cells also have abundant eosinophilic cytoplasm. LAB RESULTS ▪Elevated aminotransferases, alkaline phosphatase, gamma-glutamyl transpeptidase; hyperbilirubinemia; hypoalbuminemia ▪Elevated alpha-fetoprotein (most common serum marker)
  • 7. Staging of hepatocellular carcinoma • The staging of liver cancer is determined only after the results of the pathology test. There are no defined stages for liver cancer; however, T/N/M and the Barcelona Clinic Liver Cancer staging system (BCLC) are the most common. According to the Barcelona Clinic Liver Cancer staging system (BCLC), there are four liver cancer stages-
  • 8. OTHER INTERVENTIONS ▪Radiofrequency ablation ▪Percutaneous ablation with ethanol/acetic acid ▪Trans arterial chemoembolization ▪Cryoablation ▪Radiation therapy; stereotactic body radiation therapy MEDICATIONS ▪Chemotherapy ▪Systemic molecularly targeted therapy; sorafenib, nivolumab SURGERY ▪Partial hepatectomy ▪Liver transplant Treatment
  • 9. Liver transplantation • first described by Mazzaferro in 1996, • Liver transplantation for HCC offers the advantage of not only definitively treating the tumor but also removing the diseased hepatic parenchyma • Milan criteria are now considered the benchmark indications for transplantation for HCC 1.Incision 2.Evaluation of the abdomen for abnormalities that would preclude liver transplantation (for example: undiagnosed infection or malignancy) 3.Mobilization of the native liver (dissection of the liver attachments to the abdominal cavity) 4.Isolation of important structures (the inferior vena cava above, behind, and below the liver; the portal vein; the common bile duct; the hepatic artery) 5.Transection of the above mentioned structures and removal of the native, diseased liver. 6.Sewing in the new liver: First, venous blood flow is re-established by connecting the donor's and the recipient's inferior vena cava and portal veins. Next, arterial flow is re-established by sewing the donor's and recipient's hepatic arteries. Finally, biliary drainage is achieved by sewing the donor's and recipient's common bile ducts. 7.Ensuring adequate control of bleeding 8.Closure of the incision Steps
  • 10. • First falciform ligament is divided along anteroposterior surface of liver towards supra hepatic IVC • Then the left triangular ligament is divided by using swab in front of esophagogastric junction, • the right triangular ligament is by retraction of diaphragm away from right lobe • This leads to exposure of bare area ,IVC is seen as it passes behind liver, here the slung Bove renal veins below the liver and at the level of main hepatic vein sliver separation from IVC is achieved by lifting liver anteriorly to expose inferior hepatic veins(multiple small veins) passing b/w liver parenchyma & IVC • They are suture ligated(suture of vessel done first than ligation of them done) to ensure hemostasis. MOBILISATION OF LIVER DISSECTION OF THE HILUM • peritoneum overlying hilum is divided • CBD exposure on free edge of lesser omentum is facilitated by ligation • cystic duct & artery is divided & than removal of GB occur exposure of common hepatic artery & dissection of the main right & left branches is done by slinging cbd with elastic sling. • they are again slung to allow remaining lymphatic tissue surrounding the portal vein to be ligated & divided. • possibility of a replaced right hepatic artery is sought arising from superior mesenteric artery & lying posterior to bile duct and accessory left hepatic artery from left gastric artery in lesser omentum • Dissection of hilar bile ducts careful retraction on segment 4 of liver(as 4 and 1 segment are closely related & 1 has dual drainage)