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A Case of Portal Venous Gas After Extracorporeal Shockwave Lithotripsy and Obstructive Pyelonephritis
Case Report A Case of Portal Venous Gas After Extracorporeal Shockwave Lithotripsy and Obstructive Pyelonephritis Abbas A. Rana, Patricia Sylla, David C. Woodland, and Daniel L. Feingold The presence of gas in the portal venous system is considered an ominous sign often mandating immediate exploratory laparotomy; however, there are numerous reports of benign incidences of this finding. This report describes a case of portal venous gas after extracorporeal shockwave lithotripsy. The patient had the rare complication of obstructive pyleonephritis that progressed to sepsis and subsequently underwent a negative exploratory laparotomy. It is suggested that the radiographic finding of portal venous gas should be correlated with the likely cause and overall clinical picture. UROLOGY 71: 546.e5–546.e7, 2008. © 2008 Elsevier Inc.
P
ortal venous gas (PVG) is considered to be an ominous sign with associated mortality as high as 90% and often mandates laparotomy.1 However, benign occurrences of PVG exist that can be managed nonoperatively. Therefore, this radiographic finding must be correlated with the clinical picture. Herein, we present a case of benign PVG after extracorporeal shockwave lithotripsy that resulted in a negative laparotomy.
CASE REPORT A 63-year-old man presented to the emergency department with severe, diffuse right-sided abdominal pain, fever, and vomiting. One day before presentation, he underwent right-sided extracorporeal shock-wave lithotripsy (ESWL) for treatment of nephrolithiasis, receiving 2500 shocks in the prone position under general anesthesia at 16 kV from a Dornier DoLi 50 lithotriptor (Dornier Medical Systems, Inc, Marietta, Ga). Respiratory gating was not used, and the instrument was focused and maintained according to institution protocol. Preprocedure laboratory tests and examinations showed no abnormalities suggestive of infection. On presentation, temperature was 102.9°F and other vital signs were unremarkable. The examination reproduced mild tenderness in the right upper quadrant and right flank without peritoneal signs. A compete blood count showed white blood count (WBC) of 5.4 (109/L), and urine analysis demonstrated 2⫹ leukocyte esterase with 43 white blood cells/hpf. Noncontrast computed From the Department of Surgery, Columbia University College of Physicians and Surgeons, New York, New York; and Columbia University College of Physicians and Surgeons, New York, New York Address correspondence to: Abbas A. Rana, M.D., Columbia University Surgery P&S 17-514, 630 West 168th Street, New York, NY 10032. E-mail: [email protected] Submitted: February 6, 2007, accepted (with revisions): October 26, 2007
© 2008 Elsevier Inc. All Rights Reserved
tomograph (CT) of the abdomen and pelvis (Fig. 1) revealed (1) portal and mesenteric venous gas with inflammatory changes of the ascending colon and hepatic flexure suggesting infectious versus ischemic colitis and (2) right hydronephrosis and hydroureter from an obstructing stone with fat stranding, suggesting pyelonephritis. No evidence of retrorenal colon was seen. Repeat blood work showed WBC count of 21.8 (109/L), creatinine of 4.2 (mg/dL), bicarbonate of 12 (mmol/L), and lactate of 3.6 (mEq/L). Surgery was consulted after the CT was obtained. At this time, the patient became hypotensive and tachycardic requiring high-dose norepinephrine drip. An exploratory laparotomy was then performed because of the clinical deterioration and PVG, suggesting the possibility of ischemic bowel. No abdominal disease was noted. A urologic physician was consulted intraoperatively and a stent was placed in the right ureter that drained frank pus. After a brief stay in the intensive care unit, the patient recovered. Blood and urine cultures grew Escherichia coli on postoperative day 2.
COMMENT The pathogenesis of PVG is thought to result from gas entering the portal venous circulation from either the bowel lumen or secondary to bacterial production. Factors predisposing to PVG formation are mucosal alteration (associated with ischemic insult, irritable bowel disorder [IBD], or ulcers), bowel distention with increased intraluminal pressure (obstruction, ileus, iatrogenic dilatation, blunt trauma, and barotrauma), and infection (necrotic bowel following ischemia, abscess, appendicitis, diverticulitis, cholangitis, and septicemia). Two or three of these factors are often present concurrently.2 Most cases of PVG are related to mesenteric ischemia with associated bowel necrosis and fatality. Outcomes 0090-4295/08/$34.00 546.e5 doi:10.1016/j.urology.2007.10.067
Figure 1. Noncontrast computed tomograph of the abdomen and pelvis with sections at (A) the level of the liver and (B) the level of the right renal pelvis.
depend on extent of infarction through the bowel wall and time between diagnosis and surgical exploration.3 This has created the perception that PVG is an ominous sign requiring urgent surgical intervention. With increasing use of more sensitive imaging devices, more cases of PVG are attributed to nonischemic causes, which, for the most part, are benign and do not require surgery.4 This distinction between critical, ischemic PVG that demands surgery and benign, nonischemic PVG that can be medically managed is essential and can only be made based on the clinical context. In this case, the patient’s decompensation was thought to be caused by urosepsis. PVG was a benign finding with 1 of 2 possible causes: mucosal damage secondary to ESWL and obstructed pyelonephritis. ESWL safety has been extensively documented. Rare complications do exist and can be divided into infectious complications (bacteremia, urosepsis, or perinephric abscess formation), fragment-related complications (incomplete fragmentation, residual fragments, steinstrasse, and obstruction), secondary tissue effects (renal injury, car546.e6
diovascular complications, and gastrointestinal (GI) injury), and effects on pregnancy (reports of spontaneous miscarriage).5 GI injuries are known to occur in patients who receive ESWL ranging in severity from asymptomatic damage to ulceration and perforation.6 Two studies focusing on preprocedure and postprocedure GI evaluation showed evidence of new mucosal erosion on upper GI endoscopy in 80% of patients and conversion of stool guaiac in 3.7%.7,8 No cases of benign PVG secondary to ESWL have been reported to date, and 1 study that used CT imaging before and 1 day after ESWL in 50 patients found no changes in the liver.9 Still, given the known factors predisposing to PVG formation and the GI mucosal erosions observed with ESWL, we believe this case may represent an occurrence of benign PVG caused by mucosal damage from ESWL. This would be similar to reported cases of benign PVG caused by colonoscopy and blunt trauma.2,6 Because the PVG was a benign finding, no ESWL precautions need to be taken. The second possible cause of the benign PVG is pyelonephritis with urosepsis. PVG after pyelonephritis has never been reported. Colitis secondary to inflammatory tracking from pyelonephritis has been reported in very limited cases but never with concomitant PVG.10 Three cases of benign PVG in the setting of generalized sepsis have also been reported11,12; however, this is an extremely rare finding given the high incidence of sepsis. It is essential the radiographic finding of PVG be correlated with the clinical picture so that emergent, ischemic cases can be separated from benign, nonischemic cases. ESWL is the likely cause for this case of benign PVG although pyelonephritis with urosepsis cannot be definitively ruled out as a potential cause.
References 1. Brown MA, Hauschildt JP, Casola G, et al: Intravascular gas as an incidental finding at US after blunt abdominal trauma. Radiology 210: 405– 408, 1999. 2. Sebastia C, Quiroga S, Espin E, et al: Portomesenteric vein gas: pathologic mechanisms, CT findings, and prognosis. Radiographics 20: 1213–1226, 2005. 3. Hong JJ, Gadaleta D, Rossi P, et al: Portal vein gas, a changing clinical entity: report of 7 patients and review of the literature. Arch Surg 132: 1071–1075, 1997. 4. Hou SK, Chern CH, How CK, et al: Hepatic portal venous gas: clinical significance of computed tomography findings. Am J Emerg Med 22: 214 –218, 2004. 5. Skolarikos A, Alivizatos G, and Rosette J: Extracorporeal shock wave lithotripsy 25 years later: complications and their prevention. Eur Urol 50: 981–990, 2006. 6. Maker V, and Layke J: Gastrointestinal injury secondary to extracorporeal shock wave lithotripsy: a review of the literature since its inception. J Am Coll Surg 198: 128 –135, 2004.
UROLOGY 71 (3), 2008
7. Al Karawi MA, Mohamed AR, el Etaibi KE, et al: Extracorporeal shock wave lithotripsy (ESWL)-induced erosions in upper GI tract: prospective study in 40 patients. Urology 30: 224 –227, 1987. 8. Bauer J, Finger M, Heidenberg H, et al. Incidence of stool guaiac conversion following extracorporeal shock wave lithotripsy. Urology 50: 192–194, 1997. 9. Rubin JI, Arger PH, Pollack HM, et al: Kidney changes after extracorporeal shock wave lithotripsy: CT evaluation. Radiology 162: 21–24, 1987.
UROLOGY 71 (3), 2008
10. Burck I, Yeh BM, Joe BN, et al: Pyelonephritis mimicking colitis on CT: case report. Abdom Imaging 30: 105–107, 2005. 11. Chevallier P, Peten E, Souci J, et al: Detection of portal venous gas on sonography, but not on CT. Eur Radiol 12: 1175–1178, 2002. 12. Wiesner W, Mortelé KJ, Glickman JN, et al: Portal-venous gas unrelated to mesenteric ischemia. Eur Radiol 12: 1432–1437, 2002.
546.e7
P
ortal venous gas (PVG) is considered to be an ominous sign with associated mortality as high as 90% and often mandates laparotomy.1 However, benign occurrences of PVG exist that can be managed nonoperatively. Therefore, this radiographic finding must be correlated with the clinical picture. Herein, we present a case of benign PVG after extracorporeal shockwave lithotripsy that resulted in a negative laparotomy.
CASE REPORT A 63-year-old man presented to the emergency department with severe, diffuse right-sided abdominal pain, fever, and vomiting. One day before presentation, he underwent right-sided extracorporeal shock-wave lithotripsy (ESWL) for treatment of nephrolithiasis, receiving 2500 shocks in the prone position under general anesthesia at 16 kV from a Dornier DoLi 50 lithotriptor (Dornier Medical Systems, Inc, Marietta, Ga). Respiratory gating was not used, and the instrument was focused and maintained according to institution protocol. Preprocedure laboratory tests and examinations showed no abnormalities suggestive of infection. On presentation, temperature was 102.9°F and other vital signs were unremarkable. The examination reproduced mild tenderness in the right upper quadrant and right flank without peritoneal signs. A compete blood count showed white blood count (WBC) of 5.4 (109/L), and urine analysis demonstrated 2⫹ leukocyte esterase with 43 white blood cells/hpf. Noncontrast computed From the Department of Surgery, Columbia University College of Physicians and Surgeons, New York, New York; and Columbia University College of Physicians and Surgeons, New York, New York Address correspondence to: Abbas A. Rana, M.D., Columbia University Surgery P&S 17-514, 630 West 168th Street, New York, NY 10032. E-mail: [email protected] Submitted: February 6, 2007, accepted (with revisions): October 26, 2007
© 2008 Elsevier Inc. All Rights Reserved
tomograph (CT) of the abdomen and pelvis (Fig. 1) revealed (1) portal and mesenteric venous gas with inflammatory changes of the ascending colon and hepatic flexure suggesting infectious versus ischemic colitis and (2) right hydronephrosis and hydroureter from an obstructing stone with fat stranding, suggesting pyelonephritis. No evidence of retrorenal colon was seen. Repeat blood work showed WBC count of 21.8 (109/L), creatinine of 4.2 (mg/dL), bicarbonate of 12 (mmol/L), and lactate of 3.6 (mEq/L). Surgery was consulted after the CT was obtained. At this time, the patient became hypotensive and tachycardic requiring high-dose norepinephrine drip. An exploratory laparotomy was then performed because of the clinical deterioration and PVG, suggesting the possibility of ischemic bowel. No abdominal disease was noted. A urologic physician was consulted intraoperatively and a stent was placed in the right ureter that drained frank pus. After a brief stay in the intensive care unit, the patient recovered. Blood and urine cultures grew Escherichia coli on postoperative day 2.
COMMENT The pathogenesis of PVG is thought to result from gas entering the portal venous circulation from either the bowel lumen or secondary to bacterial production. Factors predisposing to PVG formation are mucosal alteration (associated with ischemic insult, irritable bowel disorder [IBD], or ulcers), bowel distention with increased intraluminal pressure (obstruction, ileus, iatrogenic dilatation, blunt trauma, and barotrauma), and infection (necrotic bowel following ischemia, abscess, appendicitis, diverticulitis, cholangitis, and septicemia). Two or three of these factors are often present concurrently.2 Most cases of PVG are related to mesenteric ischemia with associated bowel necrosis and fatality. Outcomes 0090-4295/08/$34.00 546.e5 doi:10.1016/j.urology.2007.10.067
Figure 1. Noncontrast computed tomograph of the abdomen and pelvis with sections at (A) the level of the liver and (B) the level of the right renal pelvis.
depend on extent of infarction through the bowel wall and time between diagnosis and surgical exploration.3 This has created the perception that PVG is an ominous sign requiring urgent surgical intervention. With increasing use of more sensitive imaging devices, more cases of PVG are attributed to nonischemic causes, which, for the most part, are benign and do not require surgery.4 This distinction between critical, ischemic PVG that demands surgery and benign, nonischemic PVG that can be medically managed is essential and can only be made based on the clinical context. In this case, the patient’s decompensation was thought to be caused by urosepsis. PVG was a benign finding with 1 of 2 possible causes: mucosal damage secondary to ESWL and obstructed pyelonephritis. ESWL safety has been extensively documented. Rare complications do exist and can be divided into infectious complications (bacteremia, urosepsis, or perinephric abscess formation), fragment-related complications (incomplete fragmentation, residual fragments, steinstrasse, and obstruction), secondary tissue effects (renal injury, car546.e6
diovascular complications, and gastrointestinal (GI) injury), and effects on pregnancy (reports of spontaneous miscarriage).5 GI injuries are known to occur in patients who receive ESWL ranging in severity from asymptomatic damage to ulceration and perforation.6 Two studies focusing on preprocedure and postprocedure GI evaluation showed evidence of new mucosal erosion on upper GI endoscopy in 80% of patients and conversion of stool guaiac in 3.7%.7,8 No cases of benign PVG secondary to ESWL have been reported to date, and 1 study that used CT imaging before and 1 day after ESWL in 50 patients found no changes in the liver.9 Still, given the known factors predisposing to PVG formation and the GI mucosal erosions observed with ESWL, we believe this case may represent an occurrence of benign PVG caused by mucosal damage from ESWL. This would be similar to reported cases of benign PVG caused by colonoscopy and blunt trauma.2,6 Because the PVG was a benign finding, no ESWL precautions need to be taken. The second possible cause of the benign PVG is pyelonephritis with urosepsis. PVG after pyelonephritis has never been reported. Colitis secondary to inflammatory tracking from pyelonephritis has been reported in very limited cases but never with concomitant PVG.10 Three cases of benign PVG in the setting of generalized sepsis have also been reported11,12; however, this is an extremely rare finding given the high incidence of sepsis. It is essential the radiographic finding of PVG be correlated with the clinical picture so that emergent, ischemic cases can be separated from benign, nonischemic cases. ESWL is the likely cause for this case of benign PVG although pyelonephritis with urosepsis cannot be definitively ruled out as a potential cause.
References 1. Brown MA, Hauschildt JP, Casola G, et al: Intravascular gas as an incidental finding at US after blunt abdominal trauma. Radiology 210: 405– 408, 1999. 2. Sebastia C, Quiroga S, Espin E, et al: Portomesenteric vein gas: pathologic mechanisms, CT findings, and prognosis. Radiographics 20: 1213–1226, 2005. 3. Hong JJ, Gadaleta D, Rossi P, et al: Portal vein gas, a changing clinical entity: report of 7 patients and review of the literature. Arch Surg 132: 1071–1075, 1997. 4. Hou SK, Chern CH, How CK, et al: Hepatic portal venous gas: clinical significance of computed tomography findings. Am J Emerg Med 22: 214 –218, 2004. 5. Skolarikos A, Alivizatos G, and Rosette J: Extracorporeal shock wave lithotripsy 25 years later: complications and their prevention. Eur Urol 50: 981–990, 2006. 6. Maker V, and Layke J: Gastrointestinal injury secondary to extracorporeal shock wave lithotripsy: a review of the literature since its inception. J Am Coll Surg 198: 128 –135, 2004.
UROLOGY 71 (3), 2008
7. Al Karawi MA, Mohamed AR, el Etaibi KE, et al: Extracorporeal shock wave lithotripsy (ESWL)-induced erosions in upper GI tract: prospective study in 40 patients. Urology 30: 224 –227, 1987. 8. Bauer J, Finger M, Heidenberg H, et al. Incidence of stool guaiac conversion following extracorporeal shock wave lithotripsy. Urology 50: 192–194, 1997. 9. Rubin JI, Arger PH, Pollack HM, et al: Kidney changes after extracorporeal shock wave lithotripsy: CT evaluation. Radiology 162: 21–24, 1987.
UROLOGY 71 (3), 2008
10. Burck I, Yeh BM, Joe BN, et al: Pyelonephritis mimicking colitis on CT: case report. Abdom Imaging 30: 105–107, 2005. 11. Chevallier P, Peten E, Souci J, et al: Detection of portal venous gas on sonography, but not on CT. Eur Radiol 12: 1175–1178, 2002. 12. Wiesner W, Mortelé KJ, Glickman JN, et al: Portal-venous gas unrelated to mesenteric ischemia. Eur Radiol 12: 1432–1437, 2002.
546.e7