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MANAGEMENT

LIVER ABSCESS

dr. Samuel Sampetoding, SpB-KBD

Department of Surgery Faculty of Medicine, Universitas Hasanuddin,

Wahidin Sudirohusodo Hospital, Makassar

LIVER ABSCESS?

is an encapsulated collection of suppurative

material within the liver parenchyma,

infected by bacterial, fungal, and/or

parasite

pyogenic liver

abscess

(PLA)

amebic liver

abscess

(ALA)

Beal E. Schackelford's Surgery of the Alimentary Tract Vol.2 (2019). 1430-1445

Figure 1. Liver Abscess Huston CD. Sleisenger and Fordtran's Gastrointestinal and Liver Disease (2016)|133

LIVER ABSCESS?

Abses Hepar

Pyogenik

(PLA)

Abses Hepar

Amoebik

(ALA)


10th

century

20th

century over the past 100 years has

seen fairly dramatic changes

in demographics, etiology,

diagnosis, and treatment.

↑ immunosuppression

↑ Liver Abscess

incidence

2.3 - 275.4 cases per 100.000

TYPES OF ABSCESS

Fig. 1. The gray areas. Depicts a comparison of the sub-groups of HA and also delineates the areas of overlap between them. Journal of

Clinical and Translational Hepatology 2016 vol. 4 | 158–168

ETIOPATHOGENESIS

Fig. 2. Routes of infection. Journal of Clinical and Translational Hepatology 2016 vol. 4 | 158–168

PLA ALA Pathogen:

• Escherichia coli

• Klebsiella pneumonia DM

• Streptococcus constellatus

immunocompetent

Pathogen:

• Entamoeba hystolitica

• Related to nutritional

status & poor sanitation


Infectious Abscess

Figure 2. Organisms isolated from all positive cultures.

Serraino et al. Medicine (2018) 97:19

ETIOPATHOGENESIS


Tabel 1 Etiology of PLA

RISK FACTORS Table 1. Risk factors for development of hepatic abscess (HA) and

increased mortality from HA

Increased risk of

developing HA

Increased mortality

from HA

Diabetes mellitus Malignancy

Liver cirrhosis Diabetes mellitus

Immune-compromised

state Liver cirrhosis

Use of PPI Male gender

Advanced age19 Multiorgan failure16

Male gender*16 Sepsis

Infection with mixed

organisms

HA rupture

Abscess size > 5 cm

Respiratory distress

Hypotension

Jaundice

Extrahepatic involvement16

*Diabetes mellitus, liver cirrhosis and male gender are risk factors for both

development and increased mortality of HA.

Journal of Clinical and Translational

Hepatology 2016 vol. 4 | 158–168

CLINICAL PRESENTATION


1

Early presentation non spesific

predormal symptomps: weight

loss, fever, fatigue, malaise, anorexia, and myalgia.

2

Classic triad

• right upper quadrant pain

• fever or chills

• generalized malaise

3 Others

• hepatomegaly • jaundice

1 Asymptomatic >>>

2

Sub-acute

• mild diarrhea to severy dystery

• abdominal pain

3 Others

• high grade fever • RUQ pain

• History of gastroenteritis

• Jaundice (uncommon)

PLA ALA

CLINICAL PRESENTATION


Tabel 2 Clinical Presentation of PLA

DIAGNOSIS (PLA)


it's non-spesific • WBC↑

• Hypoalbuminemia

• Transaminase &

alkaline phospate ↑ • Bilirubin ↑

Lab

Table 3 Laboratorium of PLA

DIAGNOSIS


• elevated right

diaphgrama

• air fluid level w/ gas

forming

subdiaphragmatica

• pleular effusion

• athelectasis

CXR

2

USG

3

• hypoechoic and

varying degrees of

internal echogenicity

• low opacity, reveal rim

and internal

septations

enhancement

CT

Scan

3

MRI

4

• hyperintense on T2-

weighted images and

hypointense on

noncontrast T1-

weighed images, by

gadolinium

demonstrate similar

enhancement on CT

RADIOLOGIC

DIAGNOSIS

Journal of Clinical and Translational Hepatology 2016

vol. 4 | 158–168

3.

4.

Figure 3. Ultrasound (US). A. US demonstrates a hypoechoic abscess with heterogeneous echogenicity centrally consistent with

septations and internal debris (blue arrow). B. Color Doppler US demonstrates peripheral hypervascularity surrounding the abscess

cavity.

DIAGNOSIS

Journal of Clinical and Translational Hepatology

2016 vol. 4 | 158–168 4.

Figure 4 Dynamic contrast-enhanced computed tomography (CT). A. Late arterial phase CT demonstrates hypervascular, peripheral enhancement of the abscess seen in Figure 4 (blue arrow). B. Portal venous phase CT demonstrates conspicuity of internally enhancing septations (blue star), likely representing intervening hepatic

parenchyma. Note the multilocular nature of the abscess, which has implications for potential treatments (blue arrows).

DIAGNOSIS

Journal of Clinical and Translational Hepatology 2016 vol. 4 | 158–

168

4.

Figure 5. Magnetic resonance imaging (MRI).

A. T2-weighted image demonstrates multiple (at least six) small hyperintense abscess cavities

in the right hepatic lobe (blue arrows). Note the hyperintense, edematous hepatic

parenchyma (blue star). B. Noncontrast T1-weighted fat-sat image demonstrates varying

degrees of T1 hyperintensity in the abscess cavities consistent with proteinaceous debris.

C. Postcontrast T1- weighted fat-sat image demonstrates peripheral or rim enhancement

around each of the abscesses.

TREATMENT

4.

Fig. 10. Treatment strategies*. *Adapted from Hope WW, Vrochides DV, Newcomb WL, Mayo-Smith WW, Iannitti DA. Optimal treatment of hepatic abscess. Am Surg

2008;74:178-182.

Journal of Clinical and Translational Hepatology 2016 vol. 4 | 158–168

DRUG THERAPY FOR PLA

4. Beal E. Schackelford's Surgery of the Alimentary Tract Vol.2 (2019). 1430-1445

1 Effective for small abscesses, < 3–5 cm in diameter and smaller abscesses in

difficult anatomical positions

2 Soon as blood obtained for identification of organisms, usually

accomplished a third-generation cephalosporin plus metronidazole or

piperacillin/tazobactam

3 Recommendation: empiric coverage for gram-negative bacilli, gram-

positive cocci, as well as anaerobic

• 3 weeks IV followed 1–2 months PO, or

• 2–3 weeks IV followed 1–2 weeks PO

4 Treatment duration depends on response, as determined by repeat US, and

resolution of fever and leukocytosis

DRUG THERAPY FOR ALA


1 Effective for uncomplicated amebic hepatic abscess

2

3

Both amebic colitis and liver abscess—nitroimidazole derivatives (e.g., metronidazole)

Amebic colitis—luminal agents such as paromomycin, diloxanide furoate,

iodoquino

PERCUTANEOUS DRAINAGE


1 PD is most common first-line treatment by 16-18 Ga needle aspiration or insertion of 8-14 F pigtail catheter drain under US or CT guidance

2 Benefits: minimally invasive procedure, no need for GA, lower risk of

adhesion formation, contamination, and lower cost in comparing with surgical

3 Failures: multiloculated, catheter blockage by viscous fluid and necrotic

tissue, hypoalbuminemia significant risk

4 Complications: haemorrhage and biliary fistula

5 PD indication for ALA: deterioration in clinical condition despite adequate

treatment, bacterial superinfection, abscess with high risk of rupture

CURRENT UNIT PROTOCOL FOR THE MANAGMENT OF DRAINS PLACED

Liver abscess: contemporary presentation and management in a Western population 23rd February 2018, Volume 131 Number 1470

SURGICAL


1 Indication:

• rupture peritonitis difficult access

• co-existing pathology requiring surgery

• larger abscesses (> 3–5 cm)

2

3

Approach: controversy

Type: surgical drainage or resection

(hepatectomy)

Fig. 9. Large solid-cystic multiloculate septate liver abscess in the right lobe

Pais-Costa SR, Araujo SLM, Figueiredo VN. Hepatectomy for pyogenic liver

abscess treatment: exception approach? ABCD Arq Bras Cir Dig.

2018;31(3):e1394.

COMPLICATION


Developed

in

15.7% of patients

Septic metastasis leading to extrahepatic complications:

endopthalmitis, septic

pulmonary embolism, infection

of lungs, CNS, and eyes

Abscess rupture: spontaneous

(6.1%), incidence of abscesses by Klebsiella > other bacteria

Erode diaphragm:

causing pleural effusion,

empyema, pneumonia,

pericarditis,

bronchopleural fistulas, or duodenobronchofistulas

MOF

THANKS FOR WATCHING

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