Pyogenic liver abscesses also occur as a result of impaired biliary drainage, hematogenous infection arising from sources such as
IV drug abuse and teeth cleaning, and local spread of infection (diverticulitis or Crohn's disease). Pyogenic hepatic abscesses may be single or multiple and are more frequently found in the right lobe of the liver.41 The
abscess cavities are variable in size and, when multiple, may coalesce to give a honeycomb appearance. Approximately 40% of abscesses
are monomicrobial, an additional 40% are polymicrobial, and 20% are culture negative. The most common infecting agents are gramnegative
organisms. Escherichia coli is found in two thirds, and Streptococcus faecalis, Klebsiella, and Proteus vulgaris are also common.
Anaerobic organisms such as Bacteroides fragilis are also seen frequently. Staphylococcus and Streptococcus are more common in patients
with endocarditis and infected indwelling catheters
Patients usually are symptomatic with right upper quadrant pain and fever. Jaundice occurs in up to one third of affected patients. A
thorough history and physical examination are necessary to attempt to localize the primary causative site. Leucocytosis, an elevated
sedimentation rate, and an elevated alkaline phosphatase (AP) level are the most common laboratory findings. Significant abnormalities in
the results of the remaining liver function tests are unusual. Blood cultures reveal the causative organism in approximately 50% of cases.
Ultrasound examination of the liver reveals pyogenic abscesses as round or oval hypoechoic lesions with well-defined borders and a variable
number of internal echoes. CT scan is highly sensitive in the localization of pyogenic liver abscesses. The abscesses are hypodense and may
contain air-fluid levels indicating a gas-producing infectious organism as well as peripheral enhancement (Fig. 31-19). MRI of the abdomen
also can detect pyogenic abscesses with a high level of sensitivity but plays a limited role because of its inability to be used for imageguided
diagnosis and therapy.
The current cornerstones of treatment include correction of the underlying cause, needle aspiration, and IV antibiotic therapy. On
presentation, percutaneous aspiration and culture of the aspirate may be beneficial to guide subsequent antibiotic therapy. Initial antibiotic
therapy needs to cover gram-negative as well as anaerobic organisms. Aspiration and placement of a drainage catheter is beneficial for only
a minority of pyogenic abscesses, because most are quite viscous and drainage is ineffective. Antibiotic therapy must be continued for at
least 8 weeks. Aspiration and IV antibiotic therapy can be expected to be effective in 80 to 90% of patients. If this initial mode of therapy
fails, the patients should undergo surgical therapy, including laparoscopic or open drainage.
Amebic Abscess
Entamoeba histolytica is a parasite that is endemic worldwide, infecting approximately 10% of the world's population. Amebiasis is most
common in subtropical climates, especially in areas with poor sanitation. E. histolytica exists in a vegetative form and as cysts capable of
surviving outside the human body. The cystic form passes through the stomach and small bowel unharmed and then transforms into a
trophozoite in the colon. Here it invades the colonic mucosa forming typical flask-shaped ulcers, enters the portal venous system, and is
carried to the liver. Occasionally, the trophozoite will pass through the hepatic sinusoid and into the systemic circulation, which results in
lung and brain abscesses.
Amebae multiply and block small intrahepatic portal radicles with consequent focal infarction of hepatocytes. They contain a proteolytic
enzyme that also destroys liver parenchyma. The abscesses formed are variable in size and can be single or multiple. The amebic abscess is
most commonly located in the superior-anterior aspect of the right lobe of the liver near the diaphragm and has a necrotic central portion
that contains a thick, reddish brown, pus-like material. This material has been likened to anchovy paste or chocolate sauce. Amebic
abscesses are the most common type of liver abscesses worldwide.
Ultrasound and CT scanning of the abdomen are both very sensitive but nonspecific for the detection of amebic abscesses.41 CT scanning
also is useful in detecting extrahepatic involvement. Amebic abscesses usually appear as well-defined low-density round lesions that have
enhancement of the wall. They also usually appear somewhat ragged in appearance with a peripheral zone of edema. The central cavity
may have septations as well as fluid levels.
Metronidazole 750 mg tid for 7 to 10 days is the treatment of choice and is successful in 95% of cases. Defervescence usually occurs in 3 to
5 days. The time necessary for the abscess to resolve depends on the initial size at presentation and varies from 30 to 300 days.41 Both
ultrasound and CT of the liver can be used as follow-up after the initiation of medical therapy. Aspiration of the abscess is rarely needed
and should be reserved for patients with large abscesses, abscesses that do not respond to medical therapy, abscesses that appear to be
superinfected, and abscesses of the left lobe of the liver that may rupture into the pericardium.
Hydatid disease is due to the larval or cyst stage of infection by the tapeworm Echinococcus granulosus, which lives in the dog.42 Humans,
sheep, and cattle are intermediate hosts. The dog is infected by eating the viscera of sheep that contain hydatid cysts. Scolices, contained in
the cysts, adhere to the small intestine of the dog and become adult taenia, which attach to the intestinal wall. Each worm sheds
approximately 500 ova into the bowel. The infected ova-containing feces of the dog contaminate grass and farmland, and the ova are
ingested by sheep, pigs, and humans. The ova have chitinous envelopes that are dissolved by gastric juice. The liberated ovum burrows
through the intestinal mucosa and is carried by the portal vein to the liver, where it develops into an adult cyst. Most cysts are caught in
the hepatic sinusoids, and 70% of hydatid cysts form in the liver. A few ova pass through the liver and are held up in the pulmonary
capillary bed or enter the systemic circulation, forming cysts in the lung, spleen, brain, or bones.
The uncomplicated cyst may be silent and found only at autopsy or
incidentally. Occasionally, the affected patient presents with dull right upper quadrant pain or abdominal distention. Cysts may become
secondarily infected, involve other organs, or even rupture, which leads to an allergic or anaphylactic reaction.
The diagnosis of hydatid disease is based on the findings of an enzyme-linked immunosorbent assay (ELISA) for echinococcal antigens, and
results are positive in approximately 85% of infected patients.42 The ELISA results may be negative in an infected patient if the cyst has not
leaked or does not contain scolices, or if the parasite is no longer viable. Eosinophilia of >7% is found is approximately 30% of infected
patients. Ultrasonography and CT scanning of the abdomen are both quite sensitive for detecting hydatid cysts. The appearance of the cysts
on images depends on the stage of cyst development. Typically, hydatid cysts are well-defined hypodense lesions with a distinct wall. Ringlike
calcifications of the pericysts are present in 20 to 30% of cases. As healing occurs, the entire cyst calcifies densely, and a lesion with
this appearance is usually dead or inactive. Daughter cysts generally occur in a peripheral location and are typically slightly hypodense
compared with the mother cyst. MRI of the abdomen may be useful to evaluate the pericyst, cyst matrix, and daughter cyst characteristics.
Unless the cysts are small or the patient is not a suitable candidate for surgical resection, the treatment of hydatid disease is surgically
based because of the high risk of secondary infection and rupture. Medical treatment with albendazole relies on drug diffusion through the
cyst membrane. The concentration of drug achieved in the cyst is uncertain but is better than that of mebendazole, and albendazole can be
used as initial treatment for small, asymptomatic cysts. For most cysts surgical resection involving laparoscopic or open complete cyst
removal with instillation of a scolicidal agent is preferred and usually is curative. If complete cystectomy is not possible, then formal
anatomic liver resection can be used.
Ascariasis
Ascaris infection is particularly common in the Far East, India, and South Africa. Ova of the roundworm Ascaris lumbricoides arrive in the
liver by retrograde flow in the bile ducts. The adult worm is 10 to 20 cm long and may lodge in the common bile duct, producing partial bile
duct obstruction and secondary cholangitic abscesses. The ascaris may be a nucleus for the development of intrahepatic gallstones. The
clinical presentation in an affected patient may include any of the following: biliary colic, acute cholecystitis, acute pancreatitis, or hepatic
abscess.43 Plain abdominal radiographs, abdominal ultrasound, and endoscopic retrograde cholangiography (ERCP) all can demonstrate the
ascaris as linear filling defects in the bile ducts. Occasionally worms can be seen moving into and out of the biliary tree from the duodenum.
Treatment consists of administration of piperazine citrate, mebendazole, or albendazole in combination with ERCP extraction of the worms.
Failure of endoscopic extraction warrants surgical removal of the áscaris.
Schistosomiasis
Schistosomiasis affects >200 million people in 74 countries. Hepatic schistosomiasis is usually a complication of the intestinal disease,
because emboli of schistosomiasis ova reach the liver via the mesenteric venous system. Eggs excreted in the feces hatch in water to
release free-swimming embryos, which enter snails and develop into fork-tailed cercariae. They then re-enter human skin during contact
within infected water. They burrow down to the capillary bed, and at that point there is widespread hematogenous dissemination. Those
entering the intrahepatic portal system grow rapidly, and a granulomatous reaction occurs. The degree of resultant portal fibrosis is related
to the adult worm load.
Schistosomiasis has three stages of clinical symptomatology: the first includes itching after the entry of cercariae through the skin; the
second includes fever, urticaria, and eosinophilia; and the third involves hepatic fibrosis followed by presinusoidal portal hypertension.
During this third phase the liver shrinks, the spleen enlarges, and the patient may develop complications of portal hypertension while
hepatic function is maintained. Active infection is detected by stool examination. Serologic tests indicate past exposure without specifics
regarding timing. A negative serologic test result rules out schistosomal infection. Serum levels of transaminases are usually normal, but the
AP level may be mildly elevated. A decreased serum albumin level is usually the result of frequent GI bleeds and decreased nutrition.
Medical treatment of schistosomiasis includes education regarding hygiene and the avoidance of infected water. Treatment with praziquantel
40 to 75 mg/kg as a single dose is the treatment of choice for all forms of schistosomiasis and produces few side effects. GI bleeding
usually is controlled by endoscopic variceal ligation. However, in a patient with refractory GI portal hypertensive bleeding, distal splenorenal
shunt or gastric devascularization and splenectomy need to be considered.
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