Pyogenic and amebic liver abscesses can develop from a variety of causes. Ultrasound or CT imaging are used to identify abscesses, which appear as hypoechoic or low attenuation areas on scans. Treatment involves intravenous antibiotics along with drainage of larger abscesses via needle aspiration or catheter placement. For pyogenic abscesses, antibiotics are chosen based on culture results and typically include combinations targeting common bacteria. Amebic abscesses are generally treated with metronidazole or other nitroimidazole antibiotics, sometimes along with drainage or other antiparasitic drugs. Complications can arise if abscesses rupture or spread beyond the liver.

1. HEPATIC ABSCESS

2. DR.SYED UBAID
M.S(KEM MUMBAI)
FMAS
LAPAROSCOPIC AND GENERAL
SURGEON
ASSOCIATE PROFESSOR OF SURGERY
IIMSR,JALNA

3. LIVER ABSCESS
Occurs when bacteria/protozoa destroy
hepatic tissue, produces a cavity which fills up
with infective organisms, liquefied cells &
leucocytes. Necrotic tissue then falls off the
cavity from rest of the liver.

4. Pyogenic Liver Abscess
• Male preponderance
• Average age – between 43 & 60 years
• Kupffer cells act as a filter for the clearance of
microorganisms in the liver. These organisms
reach the liver via the bloodstream, the biliary
tree, or by direct extension.

5. Etiology

6. Disease of the biliary system
1. Malignancy.
2. Intrahepatic stones and biliary stricture
3. Manipulation of the biliary tree
cholangiography, percutaneous transhepatic
stents, endoscopic stent placement, and
biliary-enteric anastomoses

7. Intestinal pathology
Transient bacteremia due to bacterial
translocation or frank gastrointestinal perforation
cause overwhelming numbers of microorganisms
to spread via the portal venous system to the
liver.
 Appendicitis
Diverticulitis
Perforated colon cancers
Abscesses elsewhere in the abdomen and pelvis
remain common causes of pyogenic liver
abscesses.

8. Contiguous extension
1. Gangrenous cholecystitis,
2. Perforated ulcers,
3. Subphrenic abscesses.
4. Percutaneous drains
5. Trauma to the liver causes parenchymal
necrosis and clot, which creates an ideal milieu
for the seeding and proliferation of
microorganisms and subsequent abscess
formation.

9. Arterial embolization of bacteria via
the hepatic artery
1. Intravenous drug abuse
2. hepatic artery chemoembolization
3 umbilical artery catheterization
4. Arterial embolization can also occur from
distant infection in the heart, lungs, kidneys,
bones, ears, and teeth.

10. Predisposing Factors for Pyogenic Liver
Abscesses
Children
Chronic granulomatous disease Complement deficiencies
Leukemia Malignancy
Sickle cell anemia Inflammatory bowel
disease
Polycystic liver disease Congenital hepatic fibrosis
Posttransplant liver failure Necrotizing enterocolitis
Chemotherapy steroid therapy
AIDS

11. Predisposing Factors for Pyogenic Liver
Abscesses
Adults
Diabetes mellitus Cirrhosis
Chronic pancreatitis Peptic ulcer
disease
Inflammatory bowel disease Jaundice
Pyelonephritis Malignancy
Leukemia and lymphoma Chemotherapy
and steroid therapy AIDS

12. Pathology & Bacteriology
• Portal, traumatic, and cryptogenic hepatic
abscesses are solitary and large, while biliary
and arterial abscesses are multiple and small.
Fungal abscesses are usually multiple,
bilateral, and miliary.
• Gram-Negative Aerobes 50–70 % of Patients
Escherichia coli, Klebsiella species,
enterococci, and Pseudomonas species are the
most common

13. MULTIPLE LIVER ABSCESS

14. Clinical Presentation
• The classic triad of fever, jaundice, and right
upper quadrant tenderness
• SYMPTOM
Fever Weight loss
Pain Nausea and vomiting
Malaise Chills
Anorexia Cough or pleurisy
Pruritus Diarrhea

15. Clinical Presentation
• SIGN
Right upper quadrant tenderness
Hepatomegaly
Jaundice
Right upper quadrant mass
Ascites
Pleural effusion or rub

16. Clinical Presentation
Laboratory Evaluation
 Leukocytosis
 Elevated alkaline phosphatase
 An elevated bilirubin and transaminases
 Anemia, hypoalbuminemia,
and prolonged prothrombin time

17. Radiology
• X ray chest
elevated right hemidiaphragm,
a right pleural effusion,
right lower lobe atelectasis.
• Abdominal films may show
hepatomegaly,
air-fluid levels in the presence of gas-forming
organisms, or portal venous gas if pylephlebitis
is the source

18. Elevated right hemidiaphragm

19. Ultrasound
• Ultrasound will distinguish solid from cystic
lesions and is cost effective and portable.
Ultrasound (US) is 80–95% sensitive but has
limited utility in the morbidly obese and in
lesions that are located under the ribs or in an
inhomogeneous liver.

20. Hypoechoic fluid filled area

21. Hypoechoic fluid filled area in liver

22. Computed tomography
• Computed tomography (CT) is more sensitive
(95–100%) than US in detecting hepatic
abscesses. On CT examination, an abscess is of
lower attenuation than the surrounding liver,
and the wall of the abscess may enhance with
intravenous contrast administration. Lesions
are detectable to around 0.5 cm. CT and US
may also be used to evaluate and potentially
treat the source of infection by percutaneous
drainage.

23. CT/MRI
Fluid Collection w/ surrounding stranding,
edema, and inflammation

24. low attenuation area in liver
(a spot that appears on a radiographic image as less dense than the
surrounding healthy tissue in that specific organ of the body)

25. Treatment
• Treatment of the abscess itself,
• concomitant treatment of the source.
• Steps in management include
 Antibiotic administration,
 Radiologic confirmation by US or CT,
 Drainage.
Exceptions to this strategy include multiple small
abscesses and miliary fungal abscesses. These
abscesses are treated with intravenous antibiotics and
antifungals respectively, without a drainage procedure.

26. Antibiotics
• After confirmatory imaging with US or CT, abscesses
are aspirated, blood cultures are drawn, and broad-
spectrum intravenous antibiotics are administered until
sensitivities allow a more selective antibiotic choice.
• Classic antibiotic regimens include an aminoglycoside,
clindamycin, and either ampicillin or vancomycin.
Fluoroquinolones can replace aminoglycosides, and
metronidazole can be used instead of clindamycin,
especially if an amebic source is suspected.
• Treatment used to be given for 4–6 weeks;

27. Antibiotics
• In the setting of multiple abscesses <1.5 cm in
size and no concurrent surgical disease, patients
may be treated with IV antibiotics alone.
• However, multiple small abscesses frequently
imply biliary tract disease and may require biliary
drainage for source control. Similarly, fungal
abscesses are miliary in nature and not amenable
to percutaneous or surgical drainage. Prolonged
systemic antifungals are the preferred treatment
for fungal abscesses.

28. TREATMENT
TO DRAIN OR NOT TO DRAIN:
• <5cm, single abscess- needle aspiration or catheter
• >5cm- catheter
• Also: Surgery, ERCP
• Amoeba: drainage not usually required
• Exceptions:
• Verge of rupture
• Abx not working
• Imminent need to exclude other dx

29. Needle Aspiration of liver abscess

30. Percutaneous Catheter Drainage

32. Needle Aspiration And Percutaneous
Catheter Drainage
• Needle aspiration is less invasive, less expensive,
and avoids all of the complications associated
with catheter care.
• Patients in whom percutaneous drainage is not
appropriate include those patients with
(1) multiple large abscesses;
(2) a known intra-abdominal source that requires
surgery;
(3) an abscess of unknown etiology;
(4) ascites

33. Surgical drainage
• Abscesses were drained extraperitoneally via a 12th-rib resection to
avoid contamination of the peritoneal cavity.
• With the advent of systemic antibiotics, transperitoneal surgical
exploration also was considered a safe surgical approach.
• The transperitoneal approach has the advantages of the ability to:
(1) Treat the inciting pathology in the remainder of the
abdomen/pelvis;
(2) Gain access and exposure of the entire liver for evaluation and
treatment; and
(3) Access the biliary tree for cholangiography and bile duct
exploration.

34. Extraperitoneal drainage via a 12th-rib resection

35. Open Surgical drainage

36. laparoscopic drainage

37. Complications
 Generalized sepsis
 Pleural effusions
 Empyema
 Pneumonia.
 Abscesses may also rupture intraperitoneally,
which is frequently fatal. Usually, however, the
abscess does not rupture, but develops a
controlled leak resulting in a perihepatic abscess.
Pyogenic abscesses also can cause hemobilia and
hepatic vein thrombosis

38. Amebic liver abscess

39. Life cycle ENTAMEBA. histolytica

40. Etiology
 E. histolytica is responsible for all forms of invasive
disease.
 The life cycle involves cysts, invasive trophozoites, and
fecally contaminated food or water to initiate the
infection.
 Fecal-oral transmission occurs; the cyst passes through
the stomach into the intestine unscathed, and then
pancreatic enzymes start to digest the outer cyst wall.
 The trophozoite is then released into the intestine and
multiplies there. Normally, no invasion occurs, and the
patient develops amebic dysentery alone or becomes
an asymptomatic carrier.

41. Etiology
 In a small number of cases, the trophozoite
invades through the intestinal mucosa, travels
through the mesenteric lymphatics and veins,
and begins to accumulate in the hepatic
parenchyma, forming an abscess cavity.
 Liquefied hepatic parenchyma with blood and
debris gives a characteristic "anchovy paste"
appearance to the abscess.

42. Pathology
 90% of people that become infected with E. histolytica are
asymptomatic.
 These cysts are resistant to the effects of gastric acid pH,
but become stimulated to form trophozoites in the alkaline
pH of the bowel.
 Trophozoites are found in the colon and in the feces of
humans and mammals.
 Humans become reservoirs, and transmission occurs by
ingesting food and water contaminated with amebic cysts,
or occasionally through person-to-person contact.
 Incubation takes 1–4 weeks. Left untreated, asymptomatic
individuals may shed cysts for many years.

43. Pathology
• Invasive amebiasis can include anything from
amebic dysentery to metastatic abscesses. The
most common form of the invasive disease is
colitis. The majority (70–80%) of patients
experience a gradual onset of symptoms with
worsening diarrhea, abdominal pain, weight loss,
and stools consisting of blood and mucus.
Trophozoites invade and induce apoptosis in
colonic mucosa resulting in "buttonhole" ulcers
with undermined edges. Trophozoites are actually
found in the edge of the ulcers.

44. Pathology
• The most common extraintestinal site of
amebiasis is the liver, occurring in 1–7% of
children and 50% of adults (usually males) with
invasive disease.Trophozoites reach the liver
through the portal system, causing focal necrosis
of hepatocytes and multiple micro-abscesses that
coalesce into a single abscess. The central cavity
of the lesion contains a homogenous thick liquid
that is typically red/brown and yellow in color
and similar to anchovy paste in consistency.

46. Clinical Presentation
SYMPTOM
 Pain 90%
 Fever 87%
 Nausea and vomiting 85%
 Anorexia 50%
 Weight loss 45%
 Malaise 25%
 Diarrhea 25%
 Cough or pleurisy 25%
 Pruritus 1%

47. Clinical Presentation
SIGN
 Hepatomegaly 85%
 Right upper quadrant
tenderness 84%
 Pleural effusion or rub 40 %
 Right upper quadrant mas 12%
 Ascites 10 %
 Jaundice 5 %

48. Clinical Presentation
LABORATORY DATA
 Increased alkaline phosphatase
 WBC count >10,000/mm3
 Hematocrit <36%
 Albumin <3 g/dL
 Bilirubin >2 mg/dL

49. Distinguishing Clinical Characteristics
of Patients with Hepatic Abscesses
Amebic Pyogenic
Age <50 years Age >50 years
Male:female ratio 10:1 Male:female ratio 1:1
Hispanic descent No ethnic predisposition
Recent travel to
endemic area Malignancy
Pulmonary dysfunction High fevers
Abdominal pain Pruritus
Diarrhea Jaundice
Abdominal tenderness Septic shock
Hepatomegaly Palpable mass

50. Radiology
Chest radiographs frequently show
• Pleural effusion, infiltrates, or an elevated
hemidiaphragm
• Single abscess is present and in the right lobe,
10% are in the left lobe, and the rest are multiple.
• The mean resolution time is 7 months, and 70%
have findings that persist for more than 6
months. Eventually, resolution may be complete
or result in a small residual cystic cavity that
resembles a simple cyst of the liver.

51. X ray chest
elevated right hemidiaphragm,
a right pleural effusion,
right lower lobe atelectasis.

52. ULTRASOUND

53. COMPUTERIZED TOMOGRAPHY

54. Treatment
Antibiotics
 Noninvasive infections can be treated with
paromomycin.
 Nitroimidazoles, especially metronidazole, are
the mainstays of treatment for invasive
amebiasis.
 Metronidazole reaches high concentrations in the
liver, stomach, intestine, and kidney. This
antibiotic crosses the placenta and blood-brain
barrier and is contraindicated in the first
trimester of pregnancy.

55. Treatment
Antibiotics
 Nitroimidazoles with longer half-lives
(secnidazole, tinidazole, and ornidazole) are
better tolerated and can be given for shorter
periods of time.
 Parasites persist in the intestine in up to 40–60%
of patients who get a nitroimidazole; thus
nitroimidazole treatment should be followed with
paromomycin or diloxanide furoate to cure
luminal infection or risk relapse from residual
infection in the intestine.

56. Therapeutic Aspiration
• Therapeutic aspiration may occasionally be
required as an adjunct to antiparasitic
treatment. Drainage should be considered in
patients that have no clinical response to drug
therapy within 5–7 days or those with a high
risk of abscess rupture defined as having a
cavity >5 cm in diameter or by the presence of
lesions in the left lobe.

57. Percutaneous Drainage
• Image-guided percutaneous treatment (aspiration or
catheter drainage) has replaced surgical intervention as the
procedure of choice for decreasing the size of an abscess.
• Percutaneous drainage remains most useful for treating
pulmonary, peritoneal, and pericardial complications. The
high viscosity of amebic abscess fluid, however, requires a
large diameter catheter for adequate drainage, and this
may cause more discomfort for the patient.
• Secondary infections related to the indwelling catheter are
always a risk of this intervention.

58. Complications
• Complications from amebic abscesses occur
secondary to rupture of the abscess into the
peritoneum, pleural cavity, or pericardium .
• Extrahepatic sites also have been described in
the lung, brain, skin, and genitourinary tract,
presumably from hematogenous spread.

60. Thank You