Invasive liver abscess syndrome is defined by K. pneumonia, which is isolated from the abscess aspirate or blood of a patient with imaging findings consistent with a liver abscess in the absence of underlying hepatobiliary disease .
In Taiwan, the serotypes K1 and K2 of K. pneumoniae are accompanied with presence of the magA and rmpA genes, which contribute to the virulence of hypermuco-viscosity and resistance to in vitro phagocytic uptake by neutrophils as risk factors for metastatic infection [7–10]. Risk factors include patients with impaired host defenses (eg, diabetes mellitus, alcoholism, malignancy, chronic obstructive pulmonary disease, and glucocorticoid therapy). The most common manifestations of metastatic infection are endophthalmitis, meningitis and brain abscess. Other manifestations include lumbar or cervical spondylitis and discitis, septic pulmonary emboli, lung abscess, splenic abscess, necrotizing fasciitis, neck abscess, cerebral abscess, purulent meningitis, otitis media, osteomyelitis, arthritis, prostate abscesses, pylephlebitis and psoas muscle abscesses [11–13].
Diabetes is a frequent underlying illness in reports of K. pneumoniae liver abscess, but our patient lacked that putative risk as well. The risk factors in our patient included liver cirrhosis, previous liver abscess and urethral calcification.
Previous liver abscess denote that the liver structure or hepatobiliary system blood flow may be partially destructed which impairs the Kupffer’s cells and renders invasive liver abscess syndrome. Six independent risk factors have been proposed predicting severe complications of K. pneumoniae liver abscess including: thrombocytopenia (<100,000/mm3), alkaline phosphatase >300 U/L, gas formation in the abscess, APACHE III score >40, use of cefazolin (instead of extended spectrum cephalosporin), and delayed drainage. The initial platelet count in our patient was 51,000/mm3 with alkaline phosphatase of 231 U/L, and use of cefazolin initially along with delayed drainage contributed to progression of the invasive liver abscess syndrome.
Relapse of K. pneumoniae liver abscess after adequate treatment is rare.
The K1 serotype and rmpA gene in our patient might play important roles as predominant virulent factors which leading to phagocytic resistance .
The liver has dual blood supply: sterile arterial blood from the hepatic artery and venous blood from the gut where transient bacteremia of the portal system is not unusual. The high relapse rate of K. pneumoniae related liver abscess in our case is probably due to the calcified urethra, which rendered the bacteria colonization.
Except for empiric antibiotic treatment, pigtail catheter drainage is the major treatment strategy for liver abscess unless multiple micro-abscess are present, in which case, fine needle aspiration is satisfactory for both diagnosis and treatment. The patient’s clinical course is usually uneventful if successful pigtail catheter drainage is combined with a 3-week course of parenteral antimicrobial treatment. Pigtail catheter drainage is usually continued for 1–2 weeks, and the drain is removed when culture of the liver abscess become sterile with daily drainage amount <5 mL for several days, and defervescence occurs even after the drainage tube is clamped. Oral antimicrobial treatment for 1–2 months after discharge from the hospital will consolidate the effect of treatment . Our patient declined aggressive intervention and successfully recovered with conservative antibiotic treatment.