A concise revision on the pathology and current management of liver hepatic cysts and abscesses. Being a copy of seminar presentation I for the HepatoPancreaticoBiliary Unit of the Division of General Surgery, Ahmadu Belllo University Teaching Hospital, Zaria.

1. LIVER CYSTS AND ABSCESSES
BY Kabir, Abdulkareem

2. LIVER CYSTS

3. OUTLINE
• INTRODUCTION
• SURGICAL ANATOMY
• EPIDEMIOLOGY
• CLASSIFICATION/FORMS
• AETIOPATHOGENESIS
• CLINICAL FEATURES AND COMPLICATIONS
• INVESTIGATIONS
• TREATMENT

4. INTRODUCTION
• A cyst is a fluid filled cavity lined by epithelial
membrane
• Liver cysts are thin-walled sacs filled with air, fluids, or
semi-solid material
• Liver cysts occur in approximately 5% of people.
• The majority of cysts are benign

5. Liver Gross Anatomy
• 2 surfaces:
– Diaphragmatic
– Visceral
• Lobes:
– Right lobe
– Left lobe
• Divided by:
– Falciform ligament on diaphragmatic
surface
– Fissure on the visceral surface
– Quadrate lobe
– Caudate lobe
• Both part of left lobe and visceral
surface

6. EPIDEMIOLOGY
• The precise prevalence and incidence of liver cysts are not known,
• because are asymptomatic
• Estimated to occur in 5% of the population.
• No more than 10-15% of these patients have symptoms.
• Hepatic cysts are usually found as an incidental finding on imaging or
at the time of laparotomy.
• Most series in the literature are relatively small, reporting fewer than
50 patients each

7. CLASSIFICATION
LIVER CYSTS
PARASITIC
LIVER CYSTS
HYDATID CYST
NON PARASITI
LIVER CYSTS
NEOPLASTIC MULTIPLE SIMPLE TRAUMATIC

8. AETIOPATHOGENESIS
•SIMPLE CYSTS
•The cause of simple liver cysts is not known,
•They are believed to be congenital in origin.
•The cysts are lined by biliary-type epithelium
•May form from progressive dilatation of biliary
micro hamartoma

9. •Multiple cysts
•They are congenital cysts seen in Adult Polycystic
Liver Disease (AD-PCLD)
•Usually associated with autosomal dominant
polycystic kidney disease (AD-PKD) in 40%.
•Mutations in these patients have been identified in
PKD1 and PKD2 genes.

10. •Neoplastic cysts
•Neoplastic liver cysts are rare.
•They are usually cystadenoma and
cystadenocarcinoma
•The cause is unknown,
•But they may represent proliferation of abnormal
embryonic analogs of the gallbladder or biliary
epithelium.

11. TRAUMATIC LIVER CYST
•It is an acquired cyst of liver after liver injury in a
blunt abdominal trauma.
•Cyst is pseudocyst in liver without an epithelial
lining.
•It may present months or years after trauma

12. HYDATID CYST
• Hydatid cysts are caused by infestation by Echinococcus granulosus.
• The parasite is found worldwide, but is particularly common in areas
of sheep and cattle farming.
• The adult tapeworm lives in the digestive tract of carnivores, such as
dogs or wolves.
• Eggs are released into the stool and are inadvertently ingested by the
intermediate hosts, such as sheep, cattle, or humans.

13. • The egg larvae invade the bowel wall and mesenteric vessels of the
intermediate host, allowing circulation to the liver.
• In the liver, the larvae grow and become encysted.
• The hydatid cyst develops:
• An outer layer of inflammatory tissue and
• An inner germinal membrane that produces daughter cysts.
• When carnivores ingest the liver of the intermediate host, Thus
completing the life cycle of the worm

14. Life cycle of Echinococus

15. Adult Echinococcus

16. CLINICAL FEATURES & COMPLICATIONS
•Simple cysts
•Simple cysts generally cause no symptoms
•May produce dull right-upper-quadrant pain if large
in size.
•Patients with symptomatic simple liver cysts may
also report abdominal bloating and early satiety.
•Occasionally, a cyst is large enough to produce a
palpable abdominal mass.

17. •Complications
•Bile Duct Obstruction Jaundice (rare)
•Cyst torsion presenting as acute abdomen seen
usually in a mobile cyst
•Cyst Rupture  secondary infection, 
presentation similar to a hepatic abscess

18. • Polycystic liver disease
• Polycystic liver disease (PCLD) rarely arises in
childhood.
• Observed at the time of puberty and increase in
adulthood.
• They occur as part of a congenital disorder associated
with polycystic kidney disease (PKD).
• Women are more commonly affected.

19. • Usually they are asymptomatic
• However, patients may present with abdominal pain
as the cysts enlarge.
• Hepatomegaly may be prominent, and patients
occasionally progress to hepatic fibrosis, portal
hypertension, and liver failure.
• Complications (e.g, rupture, hemorrhage, and
infection) are rare.

20. •Neoplastic cysts
•Cystadenoma most often occurs in middle-aged
women.
•However, cystadenocarcinoma equally affects both
men and women.
•Most patients are asymptomatic or have vague
abdominal complaints of bloating, nausea, and
fullness.

21. •Hydatid cysts
• like those with simple cysts, are most often
asymptomatic,
• Pain may develop as the cyst grows.
• Larger lesions typically cause pain
• More likely to develop complications than simple cysts.
• At presentation, patients generally have a palpable mass
in the right upper quadrant.

22. • COMPLICATION
• Cyst rupture is the most serious complication of hydatid
cysts.
• Cysts may rupture into;
• The biliary tree,  jaundice or cholangitis
• Through the diaphragm into the chest,
• Or freely into the peritoneal cavity.  anaphylactic
shock
• May develop secondary infection and subsequent hepatic
abscesses.

23. INVESTIGATIONS
• Laboratory investigations:
• Liver function test (LFT) results, are usually normal or just mildly
abnormal,
• Bilirubin, prothrombin time (PT), and activated partial
thromboplastin time (aPTT) are usually within the reference range.
• Serum E,U, Cr are usually normal
• In the presence of hydatid cysts,
• eosinophilia is noted in approximately 40% of patients,
• Echinococcal antibody titers are positive in nearly 80% of patients

24. • Carbohydrate antigen (CA) 19-9 levels are elevated in cystic tumors

25. • Radiological Investigations:
• Ultrasonography is readily available, noninvasive, and highly sensitive.
• CT is also highly sensitive and is easier for most clinicians to interpret,
particularly for treatment planning
• Simple cysts are thin-walled with a homogenous low-density interior.
• Hydatid cysts can be identified by the presence of daughter cysts
within a thick-walled main cavity

30. TREATMENT
• Treatment of polycystic liver disease (PCLD) or solitary nonparasitic
cysts of the liver is indicated only in symptomatic patients.
• Asymptomatic patients do not require therapy,
• because the risk of developing complications related to the lesion is lower
than the risk associated with treatment.

31. • Simple cysts
• Ultrasound Guided Percutaneous Aspiration combined with sclerosis
with alcohol or other agents can be used for symptomatic cysts
• Successful sclerosis depends on complete decompression of the cyst
and apposition of the cyst walls.
• This is not possible if the cyst wall is thickened or if the cyst is large.
• Laparoscopic deroofing

32. Laparoscopic Deroofing of a simple liver cyst

33. • Polycystic liver disease/neoplastic cysts
• For PCLD, treatment is directed at symptomatic patients only
• Involves combination of unroofing and fenestration or resection
• for Neoplastic cysts, surgical resection of the affected segment is
advocated

35. • Hydatid cysts
•Medical therapy with antihydatid agents
(albendazole and mebendazole) is relatively
ineffective
•Surgery is thus the main stay
•This involves excision of the cyst and management
of residual hepatic dead space.
•Laparoscopic Deroofing
•PAIR (Punture, Aspiration, Injection &
Reaspiration)

36. LIVER ABSCESSES

37. OUTLINE
• Introduction
• Epidemiology
• Classification/Forms
• Aetiopathogenesis
• Management
• Prognosis
• Conclusion

38. INTRODUCTION
• It is a localized collection of pus within the liver parenchyma.
• Hepatic abscesses are uncommon yet potentially lethal clinical
entities.
• Because of the non-specific nature of the disease, high index of
suspicion is necessary for prompt diagnosis and treatment.
• If prompt diagnosis and treatment are not accomplished, the
condition is uniformly fatal.

39. EPIDEMIOLOGY
• The incidence of liver abscess remains low.
• Annual incidence 3.6/100000 in U.S & U.K and ranges from 8-15 cases
per 100,000 hospital admission.
• Incidence considerably higher in developing countries.
• Most cases of amoebic abscess occur in central & south America,
Africa and Asia.
• The incidence increases with age
- usually 4th-6th decade of life
• Male : Female- 2 : 1 ( 9:1 in amoebic abscess)

40. CLASSIFICATION
Three(3) major forms based on aetiology
I. Pyogenic abscess
-accounts for 80% of cases
- often polymicrobial
II. Amoebic abscess
-accounts for 10%
- Entamoeba histolytica
III. Fungal abscess
-accounts for <10%
-usually due to Candida spp.

41. PYOGENIC LIVER ABSCESS
Pyogenic liver abscesses divided into 2 categories;-
Macroscopic abscesses
- usually affect 1 lobe
- usually single or confluent
- subacute presentation
- may require some form of primary drainage
Microscopic abscesses
- affects both lobes
- multiple
- presents acutely
- require primarily medical therapy

42. AETIOPATHOGENESIS
The sources of liver abscess include:
1. Biliary disease
- 21-30% of cases
- extrahepatic biliary obstruction- ascending cholangitis  abscess
formation
- usually associated with choledocholithiasis, benign and malignant
tumours, biliary strictures, e.t.c
2. Infection via the portal system(portal pyemia)
- accounts for 20% of cases
- infectious process originates in the abdomen and reaches the liver by
embolization or seeding of the portal vein.

43. - seen in amoebiasis, appendicitis, pylephlebitis, acute diverticulitis,
inflammatory bowel disease.
3. Hematogenous(via hepatic artery)
- Results from seeding of bacteria into the liver in cases of
systemic bacteremia from UTI, bacterial endocarditis, intravenous
drug abuse.
4. Post-traumatic
- Blunt/penetrating trauma hepatic necrosis/intrahepatic
hemorrhage/intraparanchymal bile extravasation abscess
formation.

44. 5. Direct extension of infection
- Infections of the gallbladder, subphrenic space or subpleural
space.
- Disease processes in which gallbladder, gastric or intestinal
perforation occur directly into the liver.
6. Cryptogenic/miscellaneous
- Aetiology remains unknown in 5% cases.
- Increase incidence(of secondary infection) in;-
polycystic liver disease, hepatoma, Hydatic dx, amoebic abscess.

45. MICROBIOLOGY
• Polymicrobial infection occur in 22-64% of cases,
• Frequently are of gastrointestinal or biliary origin.
• Gastrointestinal flora accounts for >75% of abscesses.
• The most common organisms isolated are:-
- E. coli - Streptococcal spp.
- Klebsiella pneumoniae -Staphylococcus aureus
- Bacteroides spp.

46. Unusual causes(bacterial)
- Salmonella spp. - Yersinia enterocolitica
- Campylobacter -Listeria monocytogen
- Mycobacterium - Brucella spp.
Parasitic infection
- Entamoeba histolytica
- Schistosomiasis, ascariasis, toxocariasis increase risk of liver abscess
Candida spp.

47. MANAGEMENT
• HISTORY
Biodata
- Age: 4th-6th decade of life. Younger in amoebic abscess.
- Sex: commoner in males
 presentation
- Fever: in 87-100% of patients. Usually associated chills(infrequent in amoebic
abscess).
- Abdominal Pain: Occur in 90% of patients.
- Right lobe abscesspain right upper quadrant & lower intercostal
spaces.
- Superiorly placed abscess pain referred to the right shoulder.
- Left lobe abscess pain in epigastrium

48. - Abdominal swelling- Localized or generalized
- Anorexia, nausea, vomiting, malaise & weight loss occur in varying
frequency.
- Chest symptoms- cough, pleuritic chest pain.
 Previous history of amoebic colitis
History suggestive of the primary disease
Predisposing factors
- Alcoholism - Diabetes mellitus
- Malnutrition - Cytotoxic chemotherapy
- Physical exhaustion - malignancy

49. PHYSICAL EXAMINATION
General
• Acute/ chronic ill looking
• Febrile- >38 degree Celcius
• Jaundice
- In 1/3rd of patients with pyogenic abscess
- Rare in amoebic abscess
- pedal oedema may be present
Abdomen
- Abdominal distension- localized or generalized
- Tenderness and guarding in RUQ – absent in 1/3rd
- Hepatomegaly in 60% of cases

50. Chest
- Bulging, tenderness and pitting oedema of right
lower intercostal spaces.
- Signs of pleural effusion may be present.

51. INVESTIGATIONS
 Radiologic
 Abdominal Ultrasonography
- Imaging study of first choice.
- Sensitivity- 85-95%
- Shows hypoechoic lesion and may have heterogenous
echotexture and a well defined wall.
- Shows the site, size, number and nature of the abscess.
- May reveal an intraabdominal precipitating cause of liver
abscess.

52. Computerized Tomography( CT ) Scan:
- CT is more sensitive in detecting even small abscesses in liver.
- Sensitivity: 95-100%
- Expensive with risk of contrast nephropathy.
- Image: A hypodense lesion with low attenuation areas and an
enhancing rim.

55. CXR:
• May show:
• Elevation of right
hemidiaphragm
- Blunting of Right
costophrenic angle
• Fluid levels below
diaphragm in case of
gas forming
organisms

56.  Blood culture
- Positive in 33-65% of cases.
 Culture of abscess fluid
- Positive in 73-100% of cases.
 Serological Tests; To detect E. histolytica
- Indirect haemagglutination test, ELISA, Gel diffusion precipitative
test.
Stool Microscopy
- Amoebae trophozoites or cysts may be seen in 15% of cases.

57.  Full Blood Count
- Anaemia of chronic disease
- Neutrophilic leucocytosis ( eosinophilia in amoebic abscess)
- Raised ESR
 Liver function test
- Elevation of alkaline phosphatase
- Hypoalbuminemia
- Elevated transaminases and bilirubin occasionally.
 Proctoscopy and sigmoidoscopy
- Characteristic ulcers may be seen.

58. DIFFERNTIALS
• Hydatid cyst
• Subphrenic abscess
• Hepatoma
• Viral or alcoholic hepatitis
• Acute cholecystitis
• Lobar pneumonia(rt)
• Empyema

59. TREATMENT
PYOGENIC ABSCESS
The treatment must consider both the abscess and the underlying
cause.
treatment modalities include;
1. Percutaneous needle aspiration and antibiotic therapy.
2. Percutaneous catheter drainage and antibiotic therapy.
3. Laparoscopic drainage with antibiotic therapy.
4. Laparotomy with intraoperative drainage and antibiotic therapy.

60. Percutaneous aspiration and antibiotic
therapy
• Percutaneous aspiration is the first surgical 0ption
• Involves as complete as possible drainage of abscess cavity under USS
or CT guidance.
• Point of maximum tenderness or 9th or 10th intercostal space between
ant. & post. Axillary line is used.
• Aspirate is sent for culture
• May be repeated if needed
• Failure rate- 3-20% of cases.

61. Percutaneous catheter drainage
• Using a modified seldinger technique, catheter is placed into the abscess
cavity at most dependent part, under USS or CT guidance.
• Indications
- Persistence of sepsis or worsening of clinical features.
- Failed aspiration
• Contraindication
- Coagulopathy
- Lack of safe access route
- Multiple macroscopic abscesses
• Failure rate- 10-15% of cases.

62. OPERATIVE DRAINAGE
• Indication
- Patients who require laparotomy for the underlying problem
- Failed percutaeous catheter drainage.
- Patient with contraindications to percutaneous drainage.
• Midline or subcostal incision used
• Intraoperative USS and needle aspiration is used to localize the
abscess
• Hepatotomy is then performed
• Drain should be placed into the abscess cavity

63. TREATMENT OF UNDERLYING CAUSE
• Biliary ductal obstruction Sphincterotomy, biliary-enteric bypass
• Cholycystitis Cholecystectomy
• Portal vein dessimination Focus (appendicitis,diverticulitis) should
be managed accordingly
• Hepatic artery bacteremia identify focus and treat
• Trauma haematoma evacuation/debridement.

64.  AMOEBIC ABSCESS
 Drug therapy
- Metronidazole
- Chloroquine
- Emetine hydrochloride
 Surgical treatment
Indications
- Failure of medical therapy
- Clinical/radiological evidence of residual abscess
- Suspected pyogenic abscess
- Large/left sided abscess

65.  Fungal abscess
• Systemic antifungal agents should be commenced if fungal abscess
is suspected.
• Amphotericin B- First line drug
• Fluconazole
• Drainage if needed.

66. COMPLICATIONS
• Rupture into the lungs
• Empyema
• Generalized peritonitis
• Cardiac temponade
• Septicemia
• Liver failure
• Endophthalmitis

67. PROGNOSIS
• Depends on
- Virulence of the organism
- Density of infection/infestation
- Multiplicity of abscesses
- Host resistance
- Alcholism
- Stage of presentation/delay in diagnosis
- Presence of jaundice ( Bilirubin >3.4mg/dl )

68. CONCLUSION
• Despite their low occurrences, liver cysts & abscesses
can be encountered in clinical practice.
• Though liver cysts are largely innocuous, liver
abscesses are associated with a relatively high
mortality rate and several serious complications.
• For these reasons, prompt recognition is important in
instituting effective management and achieving good
outcomes

69. THANK YOU FOR LISTENING

70. REFERENCES
1. Marianna GM, Marco M, and George YW. The Evolving Nature of
Hepatic Abscess: A Review. J Clin Transl Hepatol. 2016 Jun 28; 4(2):
158–168. Published online 2016 Jun 15. doi
10.14218/JCTH.2016.00004
2. Prashanth R, Tagore S, Jeffrey PR. An updated review of cystic
hepatic lesions. Clin Exp Hepatol. 2019 Mar; 5(1): 22–29. Published
online 2019 Feb 20. doi: 10.5114/ceh.2019.83153
3. Ruben P. Hepatic Abscess. Medscape Article. Updated Jun 2018
4. Robert EG. Hepatic Cysts. Medscape Article. Updated Jun 2018
5. Baja’s. Principles and Practice of Surgery In the Tropics. 2015