Clin J Gastroenterol (2012) 5:136–140 DOI 10.1007/s12328-012-0293-6
CASE REPORT
Successful hepatectomy for intraperitoneal rupture of pyogenic liver abscess caused by Klebsiella pneumoniae Kazuhiko Morii • Asako Kashihara • Sho Miura • Hiroaki Okuhin • Takanori Watanabe Shiso Sato • Koichi Uesaka • Shiro Yuasa
•
Received: 10 November 2011 / Accepted: 29 February 2012 / Published online: 25 March 2012 Ó Springer 2012
Abstract Klebsiella pneumoniae (KP) is the most common cause of pyogenic liver abscess in eastern Asia. KP liver abscess commonly presents as a single large abscess with a predominantly solid consistency. It is sometimes unsuitable for percutaneous catheter drainage because of the poorly liquefied contents. Antibiotic therapy alone may raise a probability of treatment failure and occurrence of complications such as abscess rupture. Hepatic or portal venous thrombosis, hematogenous spread, and spontaneous rupture also occur frequently. We report a case of KP liver abscess with a typical solid appearance, complicated by disseminated intravascular coagulation, spontaneous rupture, and pyogenic spondylitis. Keywords Liver abscess Klebsiella pneumoniae Rupture Hepatic venous thrombosis Pyogenic spondylitis
Introduction Klebsiella pneumoniae (KP) is the most common causative pathogen of pyogenic liver abscess in eastern Asian countries [1, 2]. A shift from Escherichia coli to KP as the
K. Morii (&) H. Okuhin Department of Hepatology, Japanese Red Cross Society Himeji Hospital, 1-12-1 Shimoteno, Himeji, Hyogo 670-8540, Japan e-mail: [email protected]
causative pathogen of pyogenic liver abscess may also have occurred in the United States [3]. KP liver abscess is often cryptogenic and does not show any clear association with peritoneal sources of infections, such as hepatobiliary obstruction, pancreatitis, enterocolitis, or malignant diseases [4]. KP liver abscess is usually monomicrobial, whereas other pyogenic liver abscesses are often polymicrobial [3]. Compared with other pyogenic liver abscesses, monomicrobial KP liver abscess commonly presents as a single large unilobar abscess with a solid or multilocular appearance, complicated by thrombophlebitis [5]. Computed tomography (CT) images of KP liver abscess show the characteristic signs of ‘septal breakage’, ‘turquoise sign’, and ‘no rim enhancement’, which reflect the pathological features [6]. KP liver abscess sometimes does not lend itself suitable for percutaneous catheter drainage because of the poorly liquefied contents of the abscess. However, antibiotic therapy alone may be associated with the risk of treatment failure and certain complications, such as abscess rupture [7]. KP liver abscess is also associated with a high likelihood of hematogenous spread and distant metastatic infections [8]. We report a case of KP liver abscess in which percutaneous catheter drainage could not be performed because of the solid nature of the abscess and the complicating disseminated intravascular coagulation (DIC). The abscess ruptured spontaneously in spite of the administration of effective antibiotics, necessitating urgent hepatectomy. The postoperative course was remarkable for the development of pyogenic spondylitis.
A. Kashihara S. Miura K. Uesaka S. Yuasa Department of Internal Medicine, Japanese Red Cross Society Himeji Hospital, Himeji, Japan
Case report
T. Watanabe S. Sato Department of Gastroenterological Surgery, Japanese Red Cross Society Himeji Hospital, Himeji, Japan
A 69-year-old woman without a history of diabetes mellitus was referred to our hospital because of abdominal pain and
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fever. Eight days earlier, the patient had begun to suffer from abdominal pain and loose stools. Four days earlier, she saw her family physician and was prescribed anti-indigestion tablets for presumed enterocolitis. One day before this evaluation, laboratory examination had revealed leukocytosis and thrombocytopenia. She was referred to our hospital for further evaluation. On physical examination, mild icterus was noted. The abdomen was mildly distended and tender to deep palpation in the right upper quadrant, without any guarding or rebound tenderness. The liver was palpable approximately 5 cm below the right costal margin. White blood cell count was 16,000/lL with a shift to the left, red blood cell count was 424 9 104/lL, hemoglobin 13.3 g/dL, hematocrit 38.2 %, and platelet count 1.6 9 104/lL. Prothrombin time was 91 %, activated partial thromboplastin time 27.0 s, serum fibrinogen 848 mg/dL, serum fibrin degradation products 14 lg/mL (reference range 0–5), serum D-dimer 7.34 lg/mL (reference range 0–1), and serum antithrombin III 79 % (reference range 82–132). Serum total bilirubin was 3.3 mg/dL, serum direct bilirubin 2.3 mg/dL, serum aspartate aminotransferase 38 IU/L, serum alanine aminotransferase 96 IU/L, serum alkaline phosphatase 969 IU/L (reference range 115–359), serum gamma-glutamyltranspetpitase 113 IU/L, serum lactate dehydrogenase 349 IU/L (reference range 119–229), and serum C-reactive protein (CRP) 22.2 mg/dL (reference range 0–0.3). Tests for hepatitis A virus, hepatitis C virus, and human immunodeficiency virus were negative. The test for hepatitis B surface antigen was negative. Examination of stool specimens for ova and parasites, leukocytes, and occult blood were negative. Serum tumor marker levels (a-fetoprotein, CEA, and CA19-9) were all within the normal ranges. Blood culture grew KP susceptible to universal cepholosporins and aminoglycosides. Abdominal ultrasonography (Fig. 1) and CT with intravenous administration
Fig. 1 Oblique ultrasonographic image of the right hepatic lobe shows a large ill-defined abscess, which is predominantly solid. The lesion does not have cystic components or an apparent capsular structure
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of contrast material (Fig. 2) revealed a large non-enhancing heterogeneous mass in the liver, located just under the diaphragm. The mass was[10 cm in diameter and occupied the 7th and 8th subsegments of the liver, with thrombotic occlusion of the right hepatic vein. The mass had a thin wall and complex internal configurations composed of necrotic debris and broken septa, referred to as ‘septal breakage’ and ‘turquoise sign’ [6]. There was no rim enhancement or gas bubbles. There was no hepatobiliary obstruction or associated intra-abdominal pathological findings. Ascitic fluid was present, as well as right-sided pleural effusion, suggesting contiguous spread across the diaphragm. The diagnosis of a pyogenic liver abscess with DIC was made. The solid nature of the abscess and the complicating DIC precluded percutaneous catheter drainage of the abscess. Sulbactam/cefoperazone (SBT/CPZ) was administered with treatment to control the DIC. On the fourth day, the patient complained of worsening of the right upper abdominal pain with dyspnea. The abdomen was firm and tender to palpation with guarding and rebound tenderness. The platelet count increased to 10.8 9 104/lL, and the serum CRP worsened to 28.9 mg/dL. A repeat abdominal CT scan (Fig. 3) revealed increased ascitic fluid of higher density than before, consistent with intraperitoneal hemorrhage from the liver abscess. The right pleural effusion had significantly worsened with right basal atelectasis. The patient underwent an emergency laparotomy. Exploration of the abdomen showed the ruptured abscess located in the liver surface, and dense pus mixed with blood in the subphrenic space (Fig. 4). Partial hepatectomy of the 7th and 8th subsegements was performed, followed by cleaning of the abdominal cavity with sufficient
Fig. 2 CT scan obtained with contrast injection shows a large nonenhancing liver abscess measuring [10 cm in diameter. The characteristic CT appearances of the abscess are called ‘turquoise sign’. ‘Septal breakage’ are also seen (small arrow). Note the thrombotic occlusion of the right hepatic vein (arrow) and right-sided pleural effusion (arrowhead)
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Fig. 3 CT scan without contrast material shows an enlarged liver abscess with increased right-sided pleural effusion (arrow). Left-sided pleural effusion is also present (small arrow). Note the high density ascitic fluid, indicative of intraperitoneal hemorrhage (arrowhead)
Fig. 4 Exploration of the abdomen showed the ruptured abscess bulging out from the liver surface. The abscess is predominantly composed of solid necrotic tissues, with dense pus mixed with blood in the crevices
amounts of saline. The abscess was predominantly composed of solid necrotic tissues entangled with dense pus without sufficient liquefaction (Fig. 5). Histological examination showed neutrophilic infiltration, hemorrhage, and necrosis with massive thrombosis in the central vein (Fig. 6). Cultures of the intraperitoneal pus grew KP. Gentamicin (GM) was administered in addition to SBT/ CPZ until 3 weeks after the operation. The postoperative course was generally satisfactory, with return of the body temperature to normal. At 4 weeks after the operation, however, the patient became febrile again, and complained of lumbago. Lumbar magnetic resonance imaging revealed evidence of pyogenic spondylitis extending from the 3rd to
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Fig. 5 The abscess was predominantly composed of solid necrotic tissues (arrow) entangled with dense pus (small arrow). The necrotic tissue was poorly liquefied. A scale bar indicates 1 cm
Fig. 6 Histological examination of the liver abscess shows neutrophilic infiltrations (I), hemorrhage (H), and necrosis (N). Inflammation and necrosis are more prominent around the central area with massive thrombosis in the central vein (C). Borderlines of the abscess are entangled geographically with residual hepatic parenchyma (B). A scale bar indicates 500 lm (H&E stain)
the lumbar vertebrae (Fig. 7). Fine-needle aspiration of the lumbar abscess and washing with saline were performed. Administration of SBT/CPZ and GM was resumed. Cultures of the lumbar abscess grew no organisms. At 4 weeks after the aspiration, the patient was transferred to a rehabilitation hospital. Finally, the patient made a satisfactory recovery.
Discussion KP liver abscess has several characteristic CT findings, such as ‘septal breakage’ and the ‘turquoise sign’, which describe
Clin J Gastroenterol (2012) 5:136–140
Fig. 7 Axial reconstruction magnetic resonance imaging shows high T2-weighted signal intensity in lesions from the 3rd to 5th lumbar vertebrae (arrow), consistent with pyogenic spondylitis
complex intracavitary structures. ‘Septal breakage’ probably reflects invasion and destruction of the hepatic parenchyma by inflammation and tissue necrosis. On the contrary, non-KP liver abscess is seldom associated with septal breaks. Spiculate or arborizing patterns of septa, combined with no enhancement of the rim represent the ‘turquoise sign’, similar to the unique pattern of the turquoise [6]. Complete or partial obstruction of the hepatic vein has been reported to occur frequently (35 % of cases) around a liver abscess [9]. The diagnosis of hepatic venous thrombosis can be challenging, because the radiologic features of a liver abscess with vascular thrombosis may mimic those of hepatocellular carcinoma with vascular invasion [10]. Acute occlusion of the hepatic vein can induce hypoattenuation in the affected parenchyma, probably because of arterioportal shunting occurring at the presinusoidal level. Septic thrombosis of the hepatic vein may predispose to the spread of bacteria into the systemic circulation [11]. Thrombosis of the hepatic vein may also induce localized congestion of the hepatic parenchyma around an abscess [9]. However, it is not certain whether the congestion may lead to an increase of the internal pressure of the abscess and consequently its rupture. Spontaneous rupture of pyogenic liver abscess is a rare complication [3, 12, 13]. Lee et al. [14] reported that among 140 patients with KP liver abscess, 8 (5.7 %) developed spontaneous rupture of the liver abscess, and 20 (14.3 %) developed metastatic foci. To our surprise, all of their patients with ruptured liver abscess were successfully treated by immediate surgical interventions without any mortality. The risk factors for spontaneous rupture in pyogenic liver abscess are diabetes mellitus, large abscess size, gas-
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forming abscess, and left lobe involvement. Liver abscesses with a maximal diameter of [8 cm show a tendency to rupture. The bigger the abscess, the higher the internal pressure, and theoretically, the abscess is more likely to rupture [1]. Currently, percutaneous catheter drainage is the preferred treatment procedure for pyogenic liver abscess over surgical intervention. However, our patient was not a suitable candidate for percutaneous catheter drainage, because the abscess was predominantly solid. KP liver abscess tends to be poorly liquefied and predominantly solid, unlike other pyogenic liver abscesses, and contains only a small quantity of pus obtained at the initial aspiration [15]. KP has a predisposition to rapidly invade and destroy the parenchyma, without allowing enough time for the tissues to break down and liquefy into homogeneous pus [16]. In terms of the difficulty in its treatment by percutaneous catheter drainage, KP liver abscess may resemble pyogenic liver abscess in patients with chronic granulomatous disease, a rare inherited primary immunodeficiency in which phagocytes cannot destroy catalasepositive bacteria and fungi. The pyogenic liver abscess in patients with chronic granulomatous disease cannot usually be treated by percutaneous drainage and should be managed by aggressive surgical intervention, because abscesses are dense, septate masses containing inspissated fluid [17]. We must never forget that patients treated with antibiotics alone are at a higher risk of treatment failure and certain complications, such as abscess rupture [7]. Surgical intervention should be attempted if adequate clinical response is not obtained within a reasonable period [3]. Diffuse abdominal pain and/or septic shock are important predictors of spontaneous rupture of a liver abscess [2]. It is not easy, however, to decide surgical hepatectomy in such a critical patient like ours with concomitant DIC. In cases of emergency, the decision whether surgery is feasible or not should be based on a different criterion from that of a planned case. We considered that hepatectomy could be performed if the following conditions were fulfilled. First, a platelet count [5 9 104/lL, a prothrombin time [50 %, and a fibrinogen concentration [50 mg/dL should be maintained [18–20]. In patients with more profound thrombocytopenia or coagulopathy, transfusion should be performed for invasive procedures. Second, the operation should be able to eliminate the main focus of the disease. In any patient with DIC, it is definitely important to remove its underlying trigger. Third, the patient should not have another liver disease, or at least, portal hypertension; such patients will not usually decompensate after hepatic resection [21, 22]. Fourth, no other less invasive methods with the same therapeutic effect would be attainable. And finally, resection should be conducted by an experienced surgical team who could accurately trace the range of the
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abscesses and excise them in accordance with the anatomical systems of the hepatic subsegments. Such refined procedures will diminish surgical hemorrhage and allow sufficient hepatic reserve after surgery [23, 24]. Continuous close observation is warranted, even after successful surgical intervention for KP liver abscess. There is serious concern about the high incidence of bacteremia and the distant spread of infection from KP liver abscess [3, 5, 8]. An effective cephalosporin should be administered for 2–3 weeks even after resolution of the fever. In addition, a few doses of an aminoglycoside are recommended during the initiation of therapy, which can rapidly eradicate organisms in the bloodstream and prevent metastatic complications [3].
Conclusions KP is the most common causative pathogen of pyogenic liver abscess in eastern Asian countries and the United States. KP liver abscess has the distinct characteristics of a large-sized, unilobar, and relatively solid abscess as compared with other pyogenic liver abscesses. Spontaneous rupture of the abscess may complicate KP liver abscess at a higher frequency than other pyogenic liver abscesses. It is crucial to watch for signs of impending rupture in patients with KP liver abscess and to carry out immediate surgical intervention if necessary. This case underscores the need to recognize the unique clinicopathological features of KP liver abscess. Conflict of interest of interest.
The authors declare that they have no conflict
References 1. Chang FY, Chou MY. Comparison of pyogenic liver abscesses caused by Klebsiella pneumoniae and non-K. pneumoniae pathogens. J Formos Med Assoc. 1995;95:232–7. 2. Okano H, Shiraki K, Inoue H, Kawakita T, Yamamoto N, Deguchi M, Sugimoto K, Sasaki T, Ohmori S, Murata K, Nakano T. Clinicopathological analysis of liver abscess in Japan. Int J Mol Med. 2002;10:627–30. 3. Lederman ER, Crum NF. Pyogenic liver abscess with a focus on Klebsiella pneumonia as a primary pathogen: an emerging disease with unique clinical characteristics. Am J Gastroenterol. 2005;100:322–31. 4. Wang JH, Liu YC, Lee SS, Yen MY, Chen YS, Wang JH, Wann SR, Lin HH. Primary liver abscess due to Klebsiella pneumoniae in Taiwan. Clin Infect Dis. 1998;26:1434–8. 5. Alsaif HS, Venkatesh SK, Chan DSG, Archuleta A. CT appearance of pyogenic liver abscesses caused by Klebsiella pneumoniae. Radiology. 2011;260:129–38.
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6. Kim SB, Je BK, Lee KY, Lee SH, Chung HH, Cha SH. Computed tomographic differences of pyogenic liver abscesses caused by Klebsiella pneumoniae and non-Klebsiella pneumoniae. J Comput Assist Tomogr. 2007;31:59–65. 7. Cheng DL, Liu YC, Yen MY. Pyogenic liver abscess: clinical manifestations and value of percutaneous catheter drainage treatment. J Formos Med Assoc. 1990;89:571–6. 8. Cheng DL, Liu YC, Yen MY, Liu CY, Wang RS. Septic metastatic lesions of pyogenic liver abscess. Their association with Klebsiella pneumoniae bacteremia in diabetic patients. Arch Intern Med. 1991;151:1557–9. 9. Lee KH, Han JK, Kim YJ, Lee HJ, Park SH, Choi BI. Hepatic attenuation differences associated with obstruction of the portal or hepatic veins in patients with hepatic abscess. Am J Roentgenol. 2005;185:1015–23. 10. Brown KT, Gandhi RT, Covey AM, Brody LA, Getrajdman GI. Pylephlebitis and liver abscess mimicking hepatocellular carcinoma. Hepatobiliary Pancreat Dis Int. 2003;2:221–5. 11. Syed MA, Kim TK, Jang HJ. Portal and hepatic vein thrombosis in liver abscess: CT findings. Eur J Radiol. 2007;61:513–9. 12. Chou FF, Sheen CSM, Lee TY. Rupture of pyogenic liver abscess. Am J Gastroenterol. 1995;90:767–70. 13. Lee KT, Sheen PC, Chen JS, Ker CG. Pyogenic liver abscess: multivariate analysis of risk factors. World J Surg. 1991;15: 372–7. 14. Lee CH, Leu HS, Wu TS, Su LH, Liu JW. Risk factor for spontaneous rupture of liver abscess caused by Klebsiella pneumoniae. Diagn Micro Infect Dis. 2005;52:79–84. 15. Hui JYH, Yang MKW, Cho DHY, Li T, Loke TKL, Chan JCS, Woo PCY. Pyogenic liver abscesses caused by Klebsiella pneumoniae: US appearance and aspiration findings. Radiology. 2007;242:769–76. 16. Lee NK, Kim S, Lee JW, Jeong YJ, Lee SH, Heo J, Kang DH. CT differentiation of pyogenic liver abscesses caused by Klebsiella pneumoniae vs non-Klebsiella pneumoniae. Br J Radiol. 2011;54: 518–25. 17. Lublin M, Bartlett DL, Danforth DN, Kauffman H, Gallin GI, Malech HL, Shawker T, Choyke P, Kleiner DE, Schwartzentruber DJ, Chang R, DeCarlo ES, Holland SM. Hepatic abscess in patients with chronic granulomatous disease. Ann Surg. 2002;235:383–91. 18. Stephan F, Hollande J, Richard O, et al. Thrombocytopenia in a surgical ICU. Chest. 1999;115:1363–70. 19. Schiffer CA, Anderson KC, Benett CL, et al. Platelet transfusion for patients with cancer: clinical practice guidelines of the American society of clinical oncology. J Clin Oncol. 2001;19: 1519–38. 20. O’Shaughnessy DF, Atterbury C, Maggs PB, et al. Guidelines for the use of fresh-frozen plasma, cryoprecipitate and cryosupernatant. Br J Haematol. 2004;126:11–28. 21. Llovet JM, Fuster J, Bruix J. Intention-to-treat analysis of surgical treatment for early hepatocellular carcinoma: resection versus transplantation. Hepatology. 1999;30:1434–40. 22. Bruix J, Sherman M. Management of hepatocellular carcinoma: an update. Hepatology. 2011;53:1020–2. 23. Torzilli G, Minagawa M, Takayama T, et al. Accurate preoperative evaluation of liver mass lesions without fine-needle biopsy. Hepatology. 1999;30:889–93. 24. Ishizawa T, Hasegawa K, Aoki T, et al. Neither multiple tumors nor portal hypertension are surgical contraindications for hepatocellular carcinoma. Gastroenterology. 2008;134:1908–16.
CASE REPORT
Successful hepatectomy for intraperitoneal rupture of pyogenic liver abscess caused by Klebsiella pneumoniae Kazuhiko Morii • Asako Kashihara • Sho Miura • Hiroaki Okuhin • Takanori Watanabe Shiso Sato • Koichi Uesaka • Shiro Yuasa
•
Received: 10 November 2011 / Accepted: 29 February 2012 / Published online: 25 March 2012 Ó Springer 2012
Abstract Klebsiella pneumoniae (KP) is the most common cause of pyogenic liver abscess in eastern Asia. KP liver abscess commonly presents as a single large abscess with a predominantly solid consistency. It is sometimes unsuitable for percutaneous catheter drainage because of the poorly liquefied contents. Antibiotic therapy alone may raise a probability of treatment failure and occurrence of complications such as abscess rupture. Hepatic or portal venous thrombosis, hematogenous spread, and spontaneous rupture also occur frequently. We report a case of KP liver abscess with a typical solid appearance, complicated by disseminated intravascular coagulation, spontaneous rupture, and pyogenic spondylitis. Keywords Liver abscess Klebsiella pneumoniae Rupture Hepatic venous thrombosis Pyogenic spondylitis
Introduction Klebsiella pneumoniae (KP) is the most common causative pathogen of pyogenic liver abscess in eastern Asian countries [1, 2]. A shift from Escherichia coli to KP as the
K. Morii (&) H. Okuhin Department of Hepatology, Japanese Red Cross Society Himeji Hospital, 1-12-1 Shimoteno, Himeji, Hyogo 670-8540, Japan e-mail: [email protected]
causative pathogen of pyogenic liver abscess may also have occurred in the United States [3]. KP liver abscess is often cryptogenic and does not show any clear association with peritoneal sources of infections, such as hepatobiliary obstruction, pancreatitis, enterocolitis, or malignant diseases [4]. KP liver abscess is usually monomicrobial, whereas other pyogenic liver abscesses are often polymicrobial [3]. Compared with other pyogenic liver abscesses, monomicrobial KP liver abscess commonly presents as a single large unilobar abscess with a solid or multilocular appearance, complicated by thrombophlebitis [5]. Computed tomography (CT) images of KP liver abscess show the characteristic signs of ‘septal breakage’, ‘turquoise sign’, and ‘no rim enhancement’, which reflect the pathological features [6]. KP liver abscess sometimes does not lend itself suitable for percutaneous catheter drainage because of the poorly liquefied contents of the abscess. However, antibiotic therapy alone may be associated with the risk of treatment failure and certain complications, such as abscess rupture [7]. KP liver abscess is also associated with a high likelihood of hematogenous spread and distant metastatic infections [8]. We report a case of KP liver abscess in which percutaneous catheter drainage could not be performed because of the solid nature of the abscess and the complicating disseminated intravascular coagulation (DIC). The abscess ruptured spontaneously in spite of the administration of effective antibiotics, necessitating urgent hepatectomy. The postoperative course was remarkable for the development of pyogenic spondylitis.
A. Kashihara S. Miura K. Uesaka S. Yuasa Department of Internal Medicine, Japanese Red Cross Society Himeji Hospital, Himeji, Japan
Case report
T. Watanabe S. Sato Department of Gastroenterological Surgery, Japanese Red Cross Society Himeji Hospital, Himeji, Japan
A 69-year-old woman without a history of diabetes mellitus was referred to our hospital because of abdominal pain and
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fever. Eight days earlier, the patient had begun to suffer from abdominal pain and loose stools. Four days earlier, she saw her family physician and was prescribed anti-indigestion tablets for presumed enterocolitis. One day before this evaluation, laboratory examination had revealed leukocytosis and thrombocytopenia. She was referred to our hospital for further evaluation. On physical examination, mild icterus was noted. The abdomen was mildly distended and tender to deep palpation in the right upper quadrant, without any guarding or rebound tenderness. The liver was palpable approximately 5 cm below the right costal margin. White blood cell count was 16,000/lL with a shift to the left, red blood cell count was 424 9 104/lL, hemoglobin 13.3 g/dL, hematocrit 38.2 %, and platelet count 1.6 9 104/lL. Prothrombin time was 91 %, activated partial thromboplastin time 27.0 s, serum fibrinogen 848 mg/dL, serum fibrin degradation products 14 lg/mL (reference range 0–5), serum D-dimer 7.34 lg/mL (reference range 0–1), and serum antithrombin III 79 % (reference range 82–132). Serum total bilirubin was 3.3 mg/dL, serum direct bilirubin 2.3 mg/dL, serum aspartate aminotransferase 38 IU/L, serum alanine aminotransferase 96 IU/L, serum alkaline phosphatase 969 IU/L (reference range 115–359), serum gamma-glutamyltranspetpitase 113 IU/L, serum lactate dehydrogenase 349 IU/L (reference range 119–229), and serum C-reactive protein (CRP) 22.2 mg/dL (reference range 0–0.3). Tests for hepatitis A virus, hepatitis C virus, and human immunodeficiency virus were negative. The test for hepatitis B surface antigen was negative. Examination of stool specimens for ova and parasites, leukocytes, and occult blood were negative. Serum tumor marker levels (a-fetoprotein, CEA, and CA19-9) were all within the normal ranges. Blood culture grew KP susceptible to universal cepholosporins and aminoglycosides. Abdominal ultrasonography (Fig. 1) and CT with intravenous administration
Fig. 1 Oblique ultrasonographic image of the right hepatic lobe shows a large ill-defined abscess, which is predominantly solid. The lesion does not have cystic components or an apparent capsular structure
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of contrast material (Fig. 2) revealed a large non-enhancing heterogeneous mass in the liver, located just under the diaphragm. The mass was[10 cm in diameter and occupied the 7th and 8th subsegments of the liver, with thrombotic occlusion of the right hepatic vein. The mass had a thin wall and complex internal configurations composed of necrotic debris and broken septa, referred to as ‘septal breakage’ and ‘turquoise sign’ [6]. There was no rim enhancement or gas bubbles. There was no hepatobiliary obstruction or associated intra-abdominal pathological findings. Ascitic fluid was present, as well as right-sided pleural effusion, suggesting contiguous spread across the diaphragm. The diagnosis of a pyogenic liver abscess with DIC was made. The solid nature of the abscess and the complicating DIC precluded percutaneous catheter drainage of the abscess. Sulbactam/cefoperazone (SBT/CPZ) was administered with treatment to control the DIC. On the fourth day, the patient complained of worsening of the right upper abdominal pain with dyspnea. The abdomen was firm and tender to palpation with guarding and rebound tenderness. The platelet count increased to 10.8 9 104/lL, and the serum CRP worsened to 28.9 mg/dL. A repeat abdominal CT scan (Fig. 3) revealed increased ascitic fluid of higher density than before, consistent with intraperitoneal hemorrhage from the liver abscess. The right pleural effusion had significantly worsened with right basal atelectasis. The patient underwent an emergency laparotomy. Exploration of the abdomen showed the ruptured abscess located in the liver surface, and dense pus mixed with blood in the subphrenic space (Fig. 4). Partial hepatectomy of the 7th and 8th subsegements was performed, followed by cleaning of the abdominal cavity with sufficient
Fig. 2 CT scan obtained with contrast injection shows a large nonenhancing liver abscess measuring [10 cm in diameter. The characteristic CT appearances of the abscess are called ‘turquoise sign’. ‘Septal breakage’ are also seen (small arrow). Note the thrombotic occlusion of the right hepatic vein (arrow) and right-sided pleural effusion (arrowhead)
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Fig. 3 CT scan without contrast material shows an enlarged liver abscess with increased right-sided pleural effusion (arrow). Left-sided pleural effusion is also present (small arrow). Note the high density ascitic fluid, indicative of intraperitoneal hemorrhage (arrowhead)
Fig. 4 Exploration of the abdomen showed the ruptured abscess bulging out from the liver surface. The abscess is predominantly composed of solid necrotic tissues, with dense pus mixed with blood in the crevices
amounts of saline. The abscess was predominantly composed of solid necrotic tissues entangled with dense pus without sufficient liquefaction (Fig. 5). Histological examination showed neutrophilic infiltration, hemorrhage, and necrosis with massive thrombosis in the central vein (Fig. 6). Cultures of the intraperitoneal pus grew KP. Gentamicin (GM) was administered in addition to SBT/ CPZ until 3 weeks after the operation. The postoperative course was generally satisfactory, with return of the body temperature to normal. At 4 weeks after the operation, however, the patient became febrile again, and complained of lumbago. Lumbar magnetic resonance imaging revealed evidence of pyogenic spondylitis extending from the 3rd to
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Fig. 5 The abscess was predominantly composed of solid necrotic tissues (arrow) entangled with dense pus (small arrow). The necrotic tissue was poorly liquefied. A scale bar indicates 1 cm
Fig. 6 Histological examination of the liver abscess shows neutrophilic infiltrations (I), hemorrhage (H), and necrosis (N). Inflammation and necrosis are more prominent around the central area with massive thrombosis in the central vein (C). Borderlines of the abscess are entangled geographically with residual hepatic parenchyma (B). A scale bar indicates 500 lm (H&E stain)
the lumbar vertebrae (Fig. 7). Fine-needle aspiration of the lumbar abscess and washing with saline were performed. Administration of SBT/CPZ and GM was resumed. Cultures of the lumbar abscess grew no organisms. At 4 weeks after the aspiration, the patient was transferred to a rehabilitation hospital. Finally, the patient made a satisfactory recovery.
Discussion KP liver abscess has several characteristic CT findings, such as ‘septal breakage’ and the ‘turquoise sign’, which describe
Clin J Gastroenterol (2012) 5:136–140
Fig. 7 Axial reconstruction magnetic resonance imaging shows high T2-weighted signal intensity in lesions from the 3rd to 5th lumbar vertebrae (arrow), consistent with pyogenic spondylitis
complex intracavitary structures. ‘Septal breakage’ probably reflects invasion and destruction of the hepatic parenchyma by inflammation and tissue necrosis. On the contrary, non-KP liver abscess is seldom associated with septal breaks. Spiculate or arborizing patterns of septa, combined with no enhancement of the rim represent the ‘turquoise sign’, similar to the unique pattern of the turquoise [6]. Complete or partial obstruction of the hepatic vein has been reported to occur frequently (35 % of cases) around a liver abscess [9]. The diagnosis of hepatic venous thrombosis can be challenging, because the radiologic features of a liver abscess with vascular thrombosis may mimic those of hepatocellular carcinoma with vascular invasion [10]. Acute occlusion of the hepatic vein can induce hypoattenuation in the affected parenchyma, probably because of arterioportal shunting occurring at the presinusoidal level. Septic thrombosis of the hepatic vein may predispose to the spread of bacteria into the systemic circulation [11]. Thrombosis of the hepatic vein may also induce localized congestion of the hepatic parenchyma around an abscess [9]. However, it is not certain whether the congestion may lead to an increase of the internal pressure of the abscess and consequently its rupture. Spontaneous rupture of pyogenic liver abscess is a rare complication [3, 12, 13]. Lee et al. [14] reported that among 140 patients with KP liver abscess, 8 (5.7 %) developed spontaneous rupture of the liver abscess, and 20 (14.3 %) developed metastatic foci. To our surprise, all of their patients with ruptured liver abscess were successfully treated by immediate surgical interventions without any mortality. The risk factors for spontaneous rupture in pyogenic liver abscess are diabetes mellitus, large abscess size, gas-
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forming abscess, and left lobe involvement. Liver abscesses with a maximal diameter of [8 cm show a tendency to rupture. The bigger the abscess, the higher the internal pressure, and theoretically, the abscess is more likely to rupture [1]. Currently, percutaneous catheter drainage is the preferred treatment procedure for pyogenic liver abscess over surgical intervention. However, our patient was not a suitable candidate for percutaneous catheter drainage, because the abscess was predominantly solid. KP liver abscess tends to be poorly liquefied and predominantly solid, unlike other pyogenic liver abscesses, and contains only a small quantity of pus obtained at the initial aspiration [15]. KP has a predisposition to rapidly invade and destroy the parenchyma, without allowing enough time for the tissues to break down and liquefy into homogeneous pus [16]. In terms of the difficulty in its treatment by percutaneous catheter drainage, KP liver abscess may resemble pyogenic liver abscess in patients with chronic granulomatous disease, a rare inherited primary immunodeficiency in which phagocytes cannot destroy catalasepositive bacteria and fungi. The pyogenic liver abscess in patients with chronic granulomatous disease cannot usually be treated by percutaneous drainage and should be managed by aggressive surgical intervention, because abscesses are dense, septate masses containing inspissated fluid [17]. We must never forget that patients treated with antibiotics alone are at a higher risk of treatment failure and certain complications, such as abscess rupture [7]. Surgical intervention should be attempted if adequate clinical response is not obtained within a reasonable period [3]. Diffuse abdominal pain and/or septic shock are important predictors of spontaneous rupture of a liver abscess [2]. It is not easy, however, to decide surgical hepatectomy in such a critical patient like ours with concomitant DIC. In cases of emergency, the decision whether surgery is feasible or not should be based on a different criterion from that of a planned case. We considered that hepatectomy could be performed if the following conditions were fulfilled. First, a platelet count [5 9 104/lL, a prothrombin time [50 %, and a fibrinogen concentration [50 mg/dL should be maintained [18–20]. In patients with more profound thrombocytopenia or coagulopathy, transfusion should be performed for invasive procedures. Second, the operation should be able to eliminate the main focus of the disease. In any patient with DIC, it is definitely important to remove its underlying trigger. Third, the patient should not have another liver disease, or at least, portal hypertension; such patients will not usually decompensate after hepatic resection [21, 22]. Fourth, no other less invasive methods with the same therapeutic effect would be attainable. And finally, resection should be conducted by an experienced surgical team who could accurately trace the range of the
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abscesses and excise them in accordance with the anatomical systems of the hepatic subsegments. Such refined procedures will diminish surgical hemorrhage and allow sufficient hepatic reserve after surgery [23, 24]. Continuous close observation is warranted, even after successful surgical intervention for KP liver abscess. There is serious concern about the high incidence of bacteremia and the distant spread of infection from KP liver abscess [3, 5, 8]. An effective cephalosporin should be administered for 2–3 weeks even after resolution of the fever. In addition, a few doses of an aminoglycoside are recommended during the initiation of therapy, which can rapidly eradicate organisms in the bloodstream and prevent metastatic complications [3].
Conclusions KP is the most common causative pathogen of pyogenic liver abscess in eastern Asian countries and the United States. KP liver abscess has the distinct characteristics of a large-sized, unilobar, and relatively solid abscess as compared with other pyogenic liver abscesses. Spontaneous rupture of the abscess may complicate KP liver abscess at a higher frequency than other pyogenic liver abscesses. It is crucial to watch for signs of impending rupture in patients with KP liver abscess and to carry out immediate surgical intervention if necessary. This case underscores the need to recognize the unique clinicopathological features of KP liver abscess. Conflict of interest of interest.
The authors declare that they have no conflict
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