Liver abcess

liver abscess for medical students

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

31. 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

32. 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.

33. Extraperitoneal drainage via a 12th-rib resection

34. Open Surgical drainage

35. laparoscopic drainage

36. 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

37. Amebic liver abscess

38. Life cycle ENTAMEBA. histolytica

39. 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.

40. 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.

41. 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.

42. 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.

43. 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.

44. 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%

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

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

47. 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

48. 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.

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

50. ULTRASOUND

51. COMPUTERIZED TOMOGRAPHY

52. 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.

53. 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.

54. 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.

55. 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.

56. 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.

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