S.M.A.R.T. NITINOL STENT SYSTEM
Report
- Report Number
- 9616099-2015-00339
- Event Type
- Injury
- Date Received
- July 31, 2015
- Date of Event
- April 1, 2013
- Report Date
- July 16, 2015
- Manufacturer
- CORDIS CORPORATION
- Product Code
- FGE
- Adverse Event
- Yes
- Report Source
- Manufacturer report
- Reporter Location
- MO, US
- Reporter Occupation
- HEALTH PROFESSIONAL
Narratives
CONCOMITANT PRODUCTS: TWO 12X60MM SELF-EXPANDING STENTS (WALLSTENT; BOSTON SCIENTIFIC/MEDITECH, (B)(4)) ONE 11 MMX10CM COVERED STENT-GRAFT (VIABAHN; FORMERLY HEMOBAHN; GORE, (B)(4)) WAS DEPLOYED IN THE INFERIOR VENA CAVA. TWO 10X60 MM STENTS (WALLSTENT). ONE 10 F, 30 CM VASCULAR SHEATH (UNKNOWN) FOR SUPPORT. ONE ANGLED GUIDEWIRE (TERUMO, (B)(4)). ONE 5F, 0.038 IN MULTIPURPOSE CATHETER (MPA; CORDIS, JOHNSON AND JOHNSON, (B)(4)). ONE 0.014 IN GUIDEWIRE (HI-TORQUE FLEX T; PERIPHERAL SYSTEM. (B)(4) -SERUM PANCREATIC ENZYME LEVELS INCREASE. THIS ARTICLE WAS FOUND DURING A RECENT CLINICAL EVALUATION REVIEW/LITERATURE SEARCH OF THIS DEVICE. PLEASE NOTE THAT THE DEVICE IS A SMART NITINOL STENT BUT THE CATALOG AND LOT NUMBERS ARE NOT AVAILABLE. THE CITATION IS AS FOLLOWS: KLEIN ET AL PANCREATICOPORTAL FISTULA AND DISSEMINATED FAT NECROSIS AFTER REVISION OF A TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT; CARDIOVASCULAR AND INTERVENTIONAL RADIOLOGY (2013), 549-553;. A COPY OF THE PUBLICATION IS ATTACHED TO THIS REPORT. AS REPORTED BY KLEIN ET AL PANCREATICOPORTAL FISTULA AND DISSEMINATED FAT NECROSIS AFTER REVISION OF A TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT; CARDIOVASCULAR AND INTERVENTIONAL RADIOLOGY (2013), 549-553; A (B)(6) MAN WITH ALCOHOL RELATED CIRRHOSIS AND PORTAL HYPERTENSION WAS REFERRED FOR TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT (TIPS) TO TREAT HIS REFRACTORY ASCITES. TEN YEARS LATER, TWO SEQUENTIAL TIPS REVISIONS WERE PERFORMED FOR SHUNT STENOSIS AND RECURRENT ASCITES. IN A SETTING OF ACUTE THROMBOSIS OCCLUSION, THROMBECTOMY WAS PERFORMED. AFTER THESE REVISIONS, HE RETURNED WITH INCREASED SERUM PANCREATIC ENZYME LEVELS AND DISSEMINATED SUPERFICIAL FAT NECROSIS; AN IATROGENIC PANCREATICOPORTAL VEIN FISTULA CAUSED BY DISRUPTION OF THE PANCREATIC DUCT WAS SUSPECTED. THE BARE AREA OF THE TIPS WAS SUBSEQUENTLY LINED WITH A COVERED STENT-GRAFT, AND SERUM ENZYME LEVELS RETURNED TO BASELINE. IN THE INTERVAL FOLLOW-UP PERIOD, THE PATIENT HAS CLINICALLY IMPROVED. PRE-TIPS LIVER ULTRASOUND SHOWED RECANALIZATION OF THE UMBILICAL VEIN AND PATENCY OF THE PORTAL VEIN WITH HEPATOPETAL FLOW. THE PATIENT UNDERWENT TIPS CREATION IN STANDARD FASHION WITH PLACEMENT OF TWO 12X60 MM SELF-EXPANDING STENTS (WALLSTENT; BOSTON SCIENTIFIC/MEDITECH, (B)(4)), WHICH WERE BALLOON EXPANDED TO 12 MM IN DIAMETER. THE INITIAL PORTOSYSTEMIC PRESSURE GRADIENT MEASURED 24 MM HG, AND THE FINAL GRADIENT AFTER TIPS MEASURED 8 MM HG. BASELINE DUPLEX ULTRASOUND EVALUATION THE NEXT MORNING REVEALED COMPLETE THROMBUS OCCLUSION OF THE SHUNT NECESSITATING EARLY TIPS REVISION. A VIABAHN COVERED STENT-GRAFT (11 MMX10 CM; FORMERLY HEMOBAHN; GORE, (B)(4)) WAS DEPLOYED ACROSS THE PARENCHYMAL TRACT SPANNING FROM JUST INTO THE MAIN PORTAL VEIN TO THE HEPATIC VEIN¿INFERIOR VENA CAVA CONFLUENCE. DUE TO EARLY RESTENOSIS, A SECOND TIPS REVISION WAS ULTIMATELY NEEDED THE NEXT WEEK WITH ADDITIONAL PLACEMENT OF TWO WALLSTENTS (10X60 MM) AND ONE SMART NITINOL STENT (10X40 MM; CORDIS ENDOVASCULAR, (B)(4)) AFTER ANGIOPLASTY OF A SEGMENTAL STENOSIS IN THE EXISTING TIPS. THE ADDITIONAL STENTS WERE AGAIN POSITIONED JUST INTO THE PORTAL VEIN. AFTER THESE EARLY REVISIONS, THE PATIENT WAS HEPARINIZED AND PLACED ON THERAPEUTIC-LEVEL ENOXAPARIN FOR ANTICOAGULATION. DURING THE NEXT 9 YEARS, THE PATIENT CLINICALLY IMPROVED AND RETURNED FOR REGULAR-INTERVAL FOLLOW-UP VISITS WITH DUPLEX ULTRASOUND TO CONFIRM SHUNT PATENCY. WITHIN THIS TIME PERIOD, ANTICOAGULATION WAS DISCONTINUED, AND HIS SYMPTOMS OF ASCITES RESOLVED. HE REPORTED NO SIGNS OF GASTROINTESTINAL BLEEDING AND NO SYMPTOMS OF ENCEPHALOPATHY. IN (B)(6) 2011, THE PATIENT RETURNED WITH MODERATE ASCITES AND INCREASED TIPS VELOCITIES INDICATING SHUNT RESTENOSIS. BECAUSE HE HAD NOT REQUIRED PARACENTESIS IN MANY YEARS AND INITIALLY RESPONDED WELL TO INCREASED DIURETICS, A SHORT COURSE OF WATCHFUL MONITORING WAS ELECTED. HOWEVER, BY (B)(6) 2011 HIS ASCITES HAD PROGRESSED, WAS POORLY CONTROLLED, AND WAS NOW REFRACTORY TO MEDICAL MANAGEMENT. HE REQUIRED REGULAR-FREQUENCY LARGE-VOLUME PARACENTESIS. AT THIS POINT, SHUNT REVISION WAS DEEMED WARRANTED. USING A 10 F, 30 CM VASCULAR SHEATH FOR SUPPORT, A CATHETER WAS ADVANCED INTO THE TIPS. IMMEDIATE DIFFICULTY, HOWEVER, WAS ENCOUNTERED WITH ATTEMPTS TO CROSS INTO THE PORTAL VEIN. CONTRAST VENOGRAPHY REVEALED A NEAR TOTAL OCCLUSION AT THE PORTAL VEIN ENTRY WITH INFLOW THROUGH THE TIPS THAT WAS REROUTED BY WAY OF A NEST OF TRANSFORMED PORTAL VENOUS COLLATERALS. USING AN ANGLED GLIDEWIRE (TERUMO, (B)(4)) AND 5F, 0.038 INCH MULTIPURPOSE CATHETER (MPA; CORDIS, JOHNSON AND JOHNSON, (B)(4)), WE WERE ABLE TO ENTER THE SPLENIC VEIN THROUGH A SIDE-BRANCH COLLATERAL CHANNEL. OVER-THE-WIRE CONTRAST INJECTION USING A HI-TORQUE FLEX T (0.014 INCH; PERIPHERAL SYSTEMS GROUP) GUIDEWIRE, CONFIRMED OUR POSITION AND ENSURED THAT WE HAD NOT RUPTURED THE VEIN DURING PROBING. CONTRAST INJECTION FAILED, HOWEVER, TO OPACIFY THE SUPERIOR MESENTERIC VEIN (SMV), WHICH WE BELIEVED WAS LIKELY DUE TO THE COLLATERAL SIDE-BRANCH BYPASSING THE MAIN SMV SPLENIC VEIN CONFLUENCE. USING A VARIETY OF CATHETERS AND GUIDEWIRES, WE THEREFORE MADE SEVERAL ADDITIONAL ATTEMPTS TO GAIN A MORE DIRECT ROUTE INTO THE PORTAL VEIN BEFORE REVISING THE TIPS. WITHOUT A DIRECT ROUTE ACROSS THE TIPS INTO THE PORTAL VEIN, WE DECIDED TO EXTEND THE SHUNT THROUGH THE COLLATERAL SIDE-BRANCH. A TOTAL OF THREE BARE METAL STENTS (ONE WALLSTENT [12X60 MM] AND TWO SMART STENTS [ONE 12X60 MM AND ONE 10X40 MM]) WERE TELESCOPED IN AN OVERLAPPING FASHION TO EXTEND THE TIPS INTO THE SPLENIC VEIN. BARE STENTS WERE USED BECAUSE OF OUR UNCERTAINTY AS TO WHERE THE SMV CAME IN AND CONCERN WITH CAUSING A MESENTERIC OCCLUSION. A WIRE WAS POSITIONED DOWN THE INFERIOR MESENTERIC VEIN TO MARK THE LANDING ZONE OF THE SPLENIC-END STENT. AFTER STENT DEPLOYMENT, SIGNIFICANT RESISTANCE WAS ENCOUNTERED DURING SERIAL BALLOON DILATATION OF THE STENTS TO 8 AND 12 MM, RESPECTIVELY. COMPLETION PORTAL VENOGRAPHY, HOWEVER, SHOWED EXCELLENT FLOW THROUGH THE TIPS.TWO WEEKS AFTER TIPS REVISION, THE PATIENT RETURNED WITH PERSISTENT ASCITES AND SONOGRAPHIC EVIDENCE OF SHUNT REOCCLUSION. IN THE SETTING OF ACUTE THROMBUS OCCLUSION, TIPS 550 S. J. KLEIN ET AL.: PANCREATICOPORTAL FISTULA AND DISSEMINATED FAT NECROSIS 123 RECANALIZATION WAS PERFORMED USING THE ANGIOJET THROMBECTOMY SYSTEM (POSSIS, (B)(4)). THIS WAS FOLLOWED BY OVERNIGHT INFUSION OF TISSUE PLASMINOGEN ACTIVATOR AT 1 MG/H THROUGH A 30CM INFUSION CATHETER. THE NEXT DAY, THE PERCUTANEOUS THROMBECTOMY DEVICE WAS USED FOR MECHANICAL THROMBECTOMY OF THE INFLOW VEINS (PORTAL AND SPLENIC), AND A SINGLE 10X68MM WALLSTENT WAS DEPLOYED AND THE BALLOON DILATED TO 10MM IN DIAMETER. THE STENT WAS POSITIONED ACROSS A KINK IN THE EXISTING TIPS EXTENSION INTO THE SPLENIC VEIN, RESULTING IN A PORTO-SYSTEMIC GRADIENT OF 5MM HG. COMPLETION VENOGRAPHY AFTER THROMBOLYSIS AND SHUNT RECANALIZATION VERIFIED TIPS PATENCY, AND THE PATIENT WAS DISCHARGED HOME ON WEIGHT-BASED THERAPEUTIC DOSAGE OF ENOXAPARIN FOR ANTICOAGULATION. DURING THE NEXT MONTH, THE PATIENT RETURNED TO HIS PRIMARY MEDICAL DOCTOR WITH A CHIEF COMPLAINT OF PAINFUL SUBCUTANEOUS NODULES DISTRIBUTED ALONG HIS MID TO LOWER ABDOMEN AND LEGS OF APPROXIMATELY 4 WEEKS¿ DURATION. HE DENIED ASSOCIATED FEVER, ARTHRALGIAS, OR SIGNIFICANT ABDOMINAL PAIN. PHYSICAL EXAMINATION REVEALED MULTIPLE TENDER ERYTHEMATOUS NODULES WITHOUT EVIDENCE OF SKIN ULCERATION. CORTICOSTEROIDS WERE STARTED UNDER THE PRESUMPTION THAT THE SKIN CHANGES WERE RELATED TO THE ENOXAPARIN. REFRACTORY TO THIS MANAGEMENT, HOWEVER, HE WAS SOON ADMINISTERED A TREATMENT COURSE OF INTRAVENOUS VANCOMYCIN AND THEN ERTAPENEM. ABSENT OF ANY SIGNIFICANT RESPONSE, THE LESIONS WERE BIOPSIED AND CULTURED, AND THE LARGER NODULES WERE INCISED AND DRAINED BECAUSE THEY WERE SUSPECTED TO BE MULTIPLE ABSCESSES. THE PATIENT WAS TRANSFERRED TO OUR TERTIARY CARE CENTER FOR FURTHER MANAGEMENT. ON PRESENTATION, THE PATIENT¿S SERUM AMYLASE AND LIPASE LEVELS WERE MARKEDLY INCREASED ([3000 AND [4000 U/L, RESPECTIVELY). DIAGNOSTIC PARACENTESIS WAS PERFORMED, WHICH ALSO SHOWED INCREASED AMYLASE AND LIPASE LEVEL [300 AND[200 U/L, RESPECTIVELY), ALTHOUGH THESE WERE MILD COMPARED WITH THE SERUM LEVELS. CONTRAST COMPUTED TOMOGRAPHY (CT) SCAN REVEALED A PATENT TIPS AND NO RADIOGRAPHIC EVIDENCE OF ACUTE OR CHRONIC PANCREATITIS. IN THE ABSENCE OF CLINICAL EVIDENCE OR IMAGING FEATURES TO SUPPORT UNDERLYING PANCREATITIS, A DIAGNOSIS OF DISSEMINATED FAT NECROSIS WAS MADE BASED ON NEW DERMATOLOGIC FINDINGS, AN EARLIER SOFT-TISSUE BIOPSY SPECIMEN SHOWING FAT NECROSIS, AND MARKEDLY INCREASED SERUM PANCREATIC ENZYMES. GIVEN THE TIME COURSE OF THESE LESIONS, I.E., THEY DEVELOPED SOON AFTER TIPS REVISION, WE SUSPECTED AN IATROGENIC PANCREATIC DUCT INJURY. FURTHERMORE, IN THE SETTING OF DISCREPANT PANCREATIC ENZYME LEVELS BETWEEN SERUM AND ASCITES, WE FAVORED A PANCREATIC DUCT FISTULA TO THE PORTAL VEIN AND TIPS. CT CONFIRMED THE PROXIMITY OF THE COLLATERAL STENTED CHANNEL TO THE PANCREATIC HEAD, FURTHER LEADING US TO BELIEVE THAT DILATING THIS VESSEL HAD LIKELY TORN SOME ADJACENT PANCREATIC TISSUE. AT THIS POINT, WE REQUESTED AN ENDOSCOPIC RETROGRADE CHOLANGIOPANCREATOGRAM (ERCP) TO CONFIRM THE DIAGNOSIS; HOWEVER, THE RISK OF CAUSING OF CAUSING ERCP-INDUCED PANCREATITIS WAS BELIEVED BY THE ENDOSCOPISTS TO OUTWEIGH THE BENEFIT AND UNLIKELY TO ALTER THE NEXT STEP IN MANAGEMENT. THE PATIENT WAS BROUGHT BACK FOR REPEAT TIPS REVISION, WITH A PLAN TO COVER THE BARE AREA OF THE TIPS ACROSS THE STENTED COLLATERAL VEIN IN THE REGION OF THE PANCREATIC HEAD. THREE FLUENCY COVERED STENTS (BARD PERIPHERAL VASCULAR, (B)(4)) WERE DEPLOYED IN AN OVERLAPPING MANNER WITHOUT DIFFICULTY. AFTER TIPS REVISION WITH COVERED STENT GRAFTS, THE PATIENT¿S SERUM ENZYME LEVELS RETURNED PROMPTLY TO BASELINE. UNFORTUNATELY, WE WERE UNABLE TO PLOT THE EXACT TIME COURSE OF SERUM ENZYME ELEVATION EARLY ON IN HIS PRESENTATION. BETWEEN THROMBOLYSIS AND RECANALIZATION OF THE COLLATERAL TIPS INFLOW AND PLACEMENT OF COVERED STENT GRAFTS, SERUM LIPASE LEVELS INCREASED FROM NORMAL TO[8000 U/L. DURING THIS TIME, THE PATIENT MANIFESTED SUBCUTANEOUS NODULES; HOWEVER, HIS SERUM ENZYME LEVELS WERE NOT DRAWN TO CORRELATE WITH THESE CLINICAL CHANGES. AFTER TIPS REVISION WITH COVERED STENT-GRAFTS AND A COURSE OF OBSERVATION AND WOUND CARE, THE PATIENT WAS DISCHARGED. HE SHOWED NO EVIDENCE OF DISEASE PROGRESSION OR NEW AREAS OF FAT NECROSIS. AT 1-MONTH FOLLOW-UP, THE PATIENT REPORTED A SIGNIFICANT DECREASE IN ASCITES AND IMPROVED WOUND HEALING. FOLLOW-UP DUPLEX ULTRASOUND CONFIRMED SHUNT PATENCY AND TIPS VELOCITIES IN THE NORMAL RANGE.¿ THERE IS ALSO EVIDENCE THAT A PANCREATIC DUCT SIDE-BRANCH WAS LACERATED DURING THE PROCESS OF REVISING THIS PATIENT¿S TIPS. FIRST, A PORTAL VEIN COLLATERAL WAS SELECTED AS THE MAIN INFLOW THROUGH WHICH TO EXTEND THE TIPS. ITS PROXIMITY TO THE PANCREATIC HEAD SERVED AN ANATOMIC BASIS WITH WHICH TO LOCALIZE THE SITE OF INJURY. SECOND, THE TIPS OCCLUDED ALMOST IMMEDIATELY AFTER REVISION. IT IS LIKELY THAT A SMALL SIDE-BRANCH PANCREATIC DUCT INJURY, DIRECTLY COMMUNICATING TO THE TIPS, RESULTED IN EARLY THROMBUS OCCLUSION THE PRODUCTS REMAIN IMPLANTED AND ARE THUS NOT AVAILABLE FOR ANALYSIS. A REVIEW OF THE MANUFACTURING RECORDS COULD NOT BE CONDUCTED WITHOUT A LOT NUMBERS. RESTENOSIS IS A KNOWN POTENTIAL ADVERSE EVENT ASSOCIATED WITH IMPLANTING STENTS AND IS OFTEN ASSOCIATED WITH THE PROGRESSION OF ARTERIAL DISEASE. PANCREATIC FISTULAS ARE USUALLY CAUSED BY DISRUPTION OF THE PANCREATIC DUCT IN THE SETTING OF TRAUMA OR SURGERY OR IN ASSOCIATION WITH PANCREATITIS. THE MAJORITY OF THESE FISTULAS COMMUNICATE EXTERNALLY TO THE SKIN, ALTHOUGH INTERNAL PANCREATIC FISTULAS HAVE BEEN DESCRIBED. WHEN PRESENT, AN INTERNAL PANCREATIC DUCT FISTULA TO AN ADJACENT ORGAN (E.G., PERITONEAL CAVITY OR BOWEL) IS USUALLY A SECONDARY COMPLICATION OF CHRONIC PANCREATITIS. THE FORMATION OF A PANCREATIC DUCT FISTULA TO THE PORTAL VEIN, RESULTING IN WIDELY DISSEMINATED SUPERFICIAL FAT NECROSIS, HAS NOT BEEN REPORTED AS A DIRECT COMPLICATION OF TIPS REVISION. LACERATION OF A VESSEL IS A POTENTIAL COMPLICATION OF THIS TYPE OF PROCEDURE. THE PHYSICAL MANIPULATION INHERENT IN THE STENT IMPLANTATION PROCEDURE INTENTIONALLY DISRUPTS THE VESSEL PLAQUE AND INTIMA IN AN EFFORT TO RECONSTRUCT VIABLE PATENT VASCULATURE AND TREAT THE DISEASE PROCESS. IT IS LIKELY THAT A SMALL SIDE-BRANCH PANCREATIC DUCT INJURY, DIRECTLY COMMUNICATING TO THE TIPS, RESULTED IN EARLY THROMBUS OCCLUSION. PORTAL VEIN THROMBOSIS IS A WELL-DESCRIBED PROTECTIVE PHYSIOLOGIC RESPONSE IN THE SETTING OF PANCREATITIS AND PANCREATICOPORTAL FISTULA. WITHOUT THE LOT NUMBERS TO CONDUCT DHR REVIEWS, IT IS NOT POSSIBLE TO DETERMINE IF THE REPORTED EVENTS COULD BE RELATED TO THE MANUFACTURING PROCESS. THEREFORE NO CORRECTIVE AND PREVENTIVE ACTIONS WILL BE TAKEN AT THIS TIME. THIS IS ONE OF 3 PRODUCTS INVOLVED WITH THE REPORTED EVENT AND ARE ASSOCIATED MANUFACTURER REPORT NUMBERS 9616099-2015-00337, 9616099-2015-00338 AND 9616099-2015-00339.
AS REPORTED BY KLEIN ET AL PANCREATICOPORTAL FISTULA AND DISSEMINATED FAT NECROSIS AFTER REVISION OF A TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT; CARDIOVASCULAR AND INTERVENTIONAL RADIOLOGY (2013), 549-553; A (B)(6) MAN WITH ALCOHOL RELATED CIRRHOSIS AND PORTAL HYPERTENSION WAS REFERRED FOR TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT (TIPS) TO TREAT HIS REFRACTORY ASCITES. TEN YEARS LATER, TWO SEQUENTIAL TIPS REVISIONS WERE PERFORMED FOR SHUNT STENOSIS AND RECURRENT ASCITES. IN A SETTING OF ACUTE THROMBOSIS OCCLUSION, THROMBECTOMY WAS PERFORMED. IN ADDITION, A THERE WAS EVIDENCE THAT A PANCREATIC DUCT SIDE-BRANCH WAS LACERATED DURING THE INITIAL PROCESS OF REVISING THE TIPS. AFTER THESE REVISIONS, HE RETURNED WITH INCREASED SERUM PANCREATIC ENZYME LEVELS AND DISSEMINATED SUPERFICIAL FAT NECROSIS; AN IATROGENIC PANCREATIC PORTAL VEIN FISTULA CAUSED BY DISRUPTION OF THE PANCREATIC DUCT WAS SUSPECTED. THE BARE AREA OF THE TIPS WAS SUBSEQUENTLY LINED WITH A COVERED STENT-GRAFT, AND SERUM ENZYME LEVELS RETURNED TO BASELINE. IN THE INTERVAL FOLLOW-UP PERIOD, THE PATIENT HAS CLINICALLY IMPROVED. PRE-TIPS LIVER ULTRASOUND SHOWED RECANALIZATION OF THE UMBILICAL VEIN AND PATENCY OF THE PORTAL VEIN WITH HEPATOPETAL FLOW. THE PATIENT UNDERWENT TIPS CREATION IN STANDARD FASHION WITH PLACEMENT OF TWO 12X60 MM SELF-EXPANDING STENTS (WALLSTENT; BOSTON SCIENTIFIC/(B)(4)), WHICH WERE BALLOON EXPANDED TO 12 MM IN DIAMETER. THE INITIAL PORTOSYSTEMIC PRESSURE GRADIENT MEASURED 24 MM HG, AND THE FINAL GRADIENT AFTER TIPS MEASURED 8 MM HG. BASELINE DUPLEX ULTRASOUND EVALUATION THE NEXT MORNING REVEALED COMPLETE THROMBUS OCCLUSION OF THE SHUNT NECESSITATING EARLY TIPS REVISION. A VIABAHN COVERED STENT-GRAFT (11 MMX10 CM; FORMERLY HEMOBAHN; GORE, FLAGSTAFF, AZ) WAS DEPLOYED ACROSS THE PARENCHYMAL TRACT SPANNING FROM JUST INTO THE MAIN PORTAL VEIN TO THE HEPATIC VEIN¿INFERIOR VENA CAVA CONFLUENCE. DUE TO EARLY RESTENOSIS, A SECOND TIPS REVISION WAS ULTIMATELY NEEDED THE NEXT WEEK WITH ADDITIONAL PLACEMENT OF TWO WALLSTENTS (10X60 MM) AND ONE SMART NITINOL STENT (10X40 MM; CORDIS ENDOVASCULAR, (B)(4)) AFTER ANGIOPLASTY OF A SEGMENTAL STENOSIS IN THE EXISTING TIPS. THE ADDITIONAL STENTS WERE AGAIN POSITIONED JUST INTO THE PORTAL VEIN. AFTER THESE EARLY REVISIONS, THE PATIENT WAS HEPARINIZED AND PLACED ON THERAPEUTIC-LEVEL ENOXAPARIN FOR ANTICOAGULATION. DURING THE NEXT 9 YEARS, THE PATIENT CLINICALLY IMPROVED AND RETURNED FOR REGULAR-INTERVAL FOLLOW-UP VISITS WITH DUPLEX ULTRASOUND TO CONFIRM SHUNT PATENCY. WITHIN THIS TIME PERIOD, ANTICOAGULATION WAS DISCONTINUED, AND HIS SYMPTOMS OF ASCITES RESOLVED. HE REPORTED NO SIGNS OF GASTROINTESTINAL BLEEDING AND NO SYMPTOMS OF ENCEPHALOPATHY. IN (B)(6) 2011, THE PATIENT RETURNED WITH MODERATE ASCITES AND INCREASED TIPS VELOCITIES INDICATING SHUNT RESTENOSIS. BECAUSE HE HAD NOT REQUIRED PARACENTESIS IN MANY YEARS AND INITIALLY RESPONDED WELL TO INCREASED DIURETICS, A SHORT COURSE OF WATCHFUL MONITORING WAS ELECTED. HOWEVER, BY (B)(6) 2011 HIS ASCITES HAD PROGRESSED, WAS POORLY CONTROLLED, AND WAS NOW REFRACTORY TO MEDICAL MANAGEMENT. HE REQUIRED REGULAR-FREQUENCY LARGE-VOLUME PARACENTESIS. AT THIS POINT, SHUNT REVISION WAS DEEMED WARRANTED. USING A 10 F, 30 CM VASCULAR SHEATH FOR SUPPORT, A CATHETER WAS ADVANCED INTO THE TIPS. IMMEDIATE DIFFICULTY, HOWEVER, WAS ENCOUNTERED WITH ATTEMPTS TO CROSS INTO THE PORTAL VEIN. CONTRAST VENOGRAPHY REVEALED A NEAR TOTAL OCCLUSION AT THE PORTAL VEIN ENTRY WITH INFLOW THROUGH THE TIPS THAT WAS REROUTED BY WAY OF A NEST OF TRANSFORMED PORTAL VENOUS COLLATERALS. USING AN ANGLED GLIDEWIRE (TERUMO, (B)(4)) AND 5F, 0.038 INCH MULTIPURPOSE CATHETER (MPA; CORDIS, JOHNSON AND JOHNSON, (B)(4)), WE WERE ABLE TO ENTER THE SPLENIC VEIN THROUGH A SIDE-BRANCH COLLATERAL CHANNEL. OVER-THE-WIRE CONTRAST INJECTION USING A HI-TORQUE FLEX T (0.014 INCH; PERIPHERAL SYSTEMS GROUP) GUIDEWIRE, CONFIRMED OUR POSITION AND ENSURED THAT WE HAD NOT RUPTURED THE VEIN DURING PROBING. CONTRAST INJECTION FAILED, HOWEVER, TO OPACIFY THE SUPERIOR MESENTERIC VEIN (SMV), WHICH WE BELIEVED WAS LIKELY DUE TO THE COLLATERAL SIDE-BRANCH BYPASSING THE MAIN SMV SPLENIC VEIN CONFLUENCE. USING A VARIETY OF CATHETERS AND GUIDEWIRES, WE THEREFORE MADE SEVERAL ADDITIONAL ATTEMPTS TO GAIN A MORE DIRECT ROUTE INTO THE PORTAL VEIN BEFORE REVISING THE TIPS. WITHOUT A DIRECT ROUTE ACROSS THE TIPS INTO THE PORTAL VEIN, WE DECIDED TO EXTEND THE SHUNT THROUGH THE COLLATERAL SIDE-BRANCH. A TOTAL OF THREE BARE METAL STENTS (ONE WALLSTENT [12X60 MM] AND TWO SMART STENTS [ONE 12X60 MM AND ONE 10X40 MM]) WERE TELESCOPED IN AN OVERLAPPING FASHION TO EXTEND THE TIPS INTO THE SPLENIC VEIN. BARE STENTS WERE USED BECAUSE OF OUR UNCERTAINTY AS TO WHERE THE SMV CAME IN AND CONCERN WITH CAUSING A MESENTERIC OCCLUSION. A WIRE WAS POSITIONED DOWN THE INFERIOR MESENTERIC VEIN TO MARK THE LANDING ZONE OF THE SPLENIC-END STENT. AFTER STENT DEPLOYMENT, SIGNIFICANT RESISTANCE WAS ENCOUNTERED DURING SERIAL BALLOON DILATATION OF THE STENTS TO 8 AND 12 MM, RESPECTIVELY. COMPLETION PORTAL VENOGRAPHY, HOWEVER, SHOWED EXCELLENT FLOW THROUGH THE TIPS. TWO WEEKS AFTER TIPS REVISION, THE PATIENT RETURNED WITH PERSISTENT ASCITES AND SONOGRAPHIC EVIDENCE OF SHUNT REOCCLUSION. IN THE SETTING OF ACUTE THROMBUS OCCLUSION, TIPS 550 S. J. KLEIN ET AL.: PANCREATICOPORTAL FISTULA AND DISSEMINATED FAT NECROSIS 123 RECANALIZATION WAS PERFORMED USING THE ANGIOJET THROMBECTOMY SYSTEM (POSSIS, (B)(4)). THIS WAS FOLLOWED BY OVERNIGHT INFUSION OF TISSUE PLASMINOGEN ACTIVA.R AT 1 MG/H THROUGH A 30CM INFUSION CATHETER. THE NEXT DAY, THE PERCUTANEOUS THROMBECTOMY DEVISE WAS USED FOR MECHANICAL THROMBECTOMY OF THE INFLOW VEINS (PORTAL AND SPLENIC), AND A SINGLE 10X68MM WALLSTENT WAS DEPLOYED AND THE BALLOON DILATED TO 10MM IN DIAMETER. THE STENT WAS POSITIONED ACROSS A KINK IN THE EXISTING TIPS EXTENSION INTO THE SPLENIC VEIN, RESULTING IN A PORTO-SYSTEMIC GRADIENT OF 5MM HG. COMPLETION VENOGRAPHY AFTER THROMBOLYSIS AND SHUNT RECANALIZATION VERIFIED TIPS PATENCY, AND THE PATIENT WAS DISCHARGED HOME ON WEIGHT-BASED THERAPEUTIC DOSAGE OF ENOXAPARIN FOR ANTICOAGULATION. DURING THE NEXT MONTH, THE PATIENT RETURNED TO HIS PRIMARY MEDICAL DOCTOR WITH A CHIEF COMPLAINT OF PAINFUL SUBCUTANEOUS NODULES DISTRIBUTED ALONG HIS MID TO LOWER ABDOMEN AND LEGS OF APPROXIMATELY 4 WEEKS¿ DURATION. HE DENIED ASSOCIATED FEVER, ARTHRALGIAS, OR SIGNIFICANT ABDOMINAL PAIN. PHYSICAL EXAMINATION REVEALED MULTIPLE TENDER ERYTHEMATOUS NODULES WITHOUT EVIDENCE OF SKIN ULCERATION. CORTICOSTEROIDS WERE STARTED UNDER THE PRESUMPTION THAT THE SKIN CHANGES WERE RELATED TO THE ENOXAPARIN. REFRACTORY TO THIS MANAGEMENT, HOWEVER, HE WAS SOON ADMINISTERED A TREATMENT COURSE OF INTRAVENOUS VANCOMYCIN AND THEN ERTAPENEM. ABSENT OF ANY SIGNIFICANT RESPONSE, THE LESIONS WERE BIOPSIED AND CULTURED, AND THE LARGER NODULES WERE INCISED AND DRAINED BECAUSE THEY WERE SUSPECTED TO BE MULTIPLE ABSCESSES. THE PATIENT WAS TRANSFERRED TO OUR TERTIARY CARE CENTER FOR FURTHER MANAGEMENT. ON PRESENTATION, THE PATIENT¿S SERUM AMYLASE AND LIPASE LEVELS WERE MARKEDLY INCREASED ([3000 AND [4000 U/L, RESPECTIVELY). DIAGNOSTIC PARACENTESIS WAS PERFORMED, WHICH ALSO SHOWED INCREASED AMYLASE AND LIPASE LEVEL [300 AND[200 U/L, RESPECTIVELY), ALTHOUGH THESE WERE MILD COMPARED WITH THE SERUM LEVELS. CONTRAST COMPUTED TOMOGRAPHY (CT) SCAN REVEALED A PATENT TIPS AND NO RADIOGRAPHIC EVIDENCE OF ACUTE OR CHRONIC PANCREATITIS. IN THE ABSENCE OF CLINICAL EVIDENCE OR IMAGING FEATURES TO SUPPORT UNDERLYING PANCREATITIS, A DIAGNOSIS OF DISSEMINATED FAT NECROSIS WAS MADE BASED ON NEW DERMATOLOGIC FINDINGS, AN EARLIER SOFT-TISSUE BIOPSY SPECIMEN SHOWING FAT NECROSIS, AND MARKEDLY INCREASED SERUM PANCREATIC ENZYMES. GIVEN THE TIME COURSE OF THESE LESIONS, I.E., THEY DEVELOPED SOON AFTER TIPS REVISION, WE SUSPECTED AN IATROGENIC PANCREATIC DUCT INJURY. FURTHERMORE, IN THE SETTING OF DISCREPANT PANCREATIC ENZYME LEVELS BETWEEN SERUM AND ASCITES, WE FAVORED A PANCREATIC DUCT FISTULA TO THE PORTAL VEIN AND TIPS. CT CONFIRMED THE PROXIMITY OF THE COLLATERAL STENTED CHANNEL TO THE PANCREATIC HEAD, FURTHER LEADING US TO BELIEVE THAT DILATING THIS VESSEL HAD LIKELY TORN SOME ADJACENT PANCREATIC TISSUE. AT THIS POINT, WE REQUESTED AN ENDOSCOPIC RETROGRADE CHOLANGIOPANCREATOGRAM (ERCP) TO CONFIRM THE DIAGNOSIS; HOWEVER, THE RISK OF CAUSING OF CAUSING ERCP-INDUCED PANCREATITIS WAS BELIEVED BY THE ENDOSCOPISTS TO OUTWEIGH THE BENEFIT AND UNLIKELY TO ALTER THE NEXT STEP IN MANAGEMENT. THE PATIENT WAS BROUGHT BACK FOR REPEAT TIPS REVISION, WITH A PLAN TO COVER THE BARE AREA OF THE TIPS ACROSS THE STENTED COLLATERAL VEIN IN THE REGION OF THE PANCREATIC HEAD. THREE FLUENCY COVERED STENTS (BARD PERIPHERAL VASCULAR, TEMPE, AZ) WERE DEPLOYED IN AN OVERLAPPING MANNER WITHOUT DIFFICULTY. AFTER TIPS REVISION WITH COVERED STENT GRAFTS, THE PATIENT¿S SERUM ENZYME LEVELS RETURNED PROMPTLY TO BASELINE. UNFORTUNATELY, WE WERE UNABLE TO PLOT THE EXACT TIME COURSE OF SERUM ENZYME ELEVATION EARLY ON IN HIS PRESENTATION. BETWEEN THROMBOLYSIS AND RECANALIZATION OF THE COLLATERAL TIPS INFLOW AND PLACEMENT OF COVERED STENT GRAFTS, SERUM LIPASE LEVELS INCREASED FROM NORMAL TO[8000 U/L. DURING THIS TIME, THE PATIENT MANIFESTED SUBCUTANEOUS NODULES; HOWEVER, HIS SERUM ENZYME LEVELS WERE NOT DRAWN TO CORRELATE WITH THESE CLINICAL CHANGES. AFTER TIPS REVISION WITH COVERED STENT-GRAFTS AND A COURSE OF OBSERVATION AND WOUND CARE, THE PATIENT WAS DISCHARGED. HE SHOWED NO EVIDENCE OF DISEASE PROGRESSION OR NEW AREAS OF FAT NECROSIS. AT 1-MONTH FOLLOW-UP, THE PATIENT REPORTED A SIGNIFICANT DECREASE IN ASCITES AND IMPROVED WOUND HEALING. FOLLOW-UP DUPLEX ULTRASOUND CONFIRMED SHUNT PATENCY AND TIPS VELOCITIES IN THE NORMAL RANGE.¿IN RETROSPECT, THERE IS EVIDENCE THAT A PANCREATIC DUCT SIDE-BRANCH WAS LACERATED DURING THE PROCESS OF REVISING THIS PATIENT¿S TIPS. FIRST, A PORTAL VEIN COLLATERAL WAS SELECTED AS THE MAIN INFLOW THROUGH WHICH TO EXTEND THE TIPS. ITS PROXIMITY TO THE PANCREATIC HEAD SERVED AN ANATOMIC BASIS WITH WHICH TO LOCALIZE THE SITE OF INJURY. SECOND, THE TIPS OCCLUDED ALMOST IMMEDIATELY AFTER REVISION. IT IS LIKELY THAT A SMALL SIDE-BRANCH PANCREATIC DUCT INJURY, DIRECTLY COMMUNICATING TO THE TIPS, RESULTED IN EARLY THROMBUS OCCLUSION.
Devices
| Seq | Brand | Generic | Product Code | Manufacturer | Model | Lot | UDI-DI |
|---|---|---|---|---|---|---|---|
| 499960 | S.M.A.R.T. NITINOL STENT SYSTEM | SELF EXPANDING STENTS (FGE) | FGE | CORDIS CORPORATION | NA |
Patients
| Seq | Age | Sex | Outcome | Treatment |
|---|---|---|---|---|
| 1 | 69 YR | Hospitalization| L| R |