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454 M. A. Mauro and S. E. Black
https://t.me/med1917
A B
FIGURE 35-13. Dialysis catheters. A: Radiograph of a dual-lumen dialysis catheter placed via the left internal jugular vein (IJV)
and tunneled over the clavicle onto the chest wall. IJV.
Straight white arrows:
system placed via the right IJV and tunneled onto the chest wall. A, tip of arterial catheter at RA/SVC junction V, tip of venous catheter 4 cm lower in the right atrium.
catheter within subcutaneous tunnel on the chest wall. B: Radiograph of the dual Tesio dialysis catheter
Curved arrows:
Straight black arrow:
sites of right IJV access.
tip of catheter in RA.
Straight arrows:
Curved black arrow:
parallel tunnels onto the chest wall.
access site in left
■ Catheter Management and Removal
In addition to device selection and insertion, the inter­ventional radiologist must become familiar with post­procedural catheter care, patient follow-up, diagnosis, and management of catheter-related complications and, finally, device removal. A specialized nursing team for patient education and supervision of routine catheter care will help in significantly reducing the frequency of catheter-related thrombosis and infections.
46
Adherence to strict sterile techniques while accessing these devices, routine dressing changes, and proper catheter heparini­zation cannot be overemphasized. Nurses who are spe­cialized in infusion management also are trained in catheter repair using commercially available repair kits. Radiologists involved in this service should have these kits available and become familiar with their use.
Device removal is the responsibility of the service that initially places that device. Nontunnelled catheters are simply removed following release of the tape or sutures. Before a tunnelled catheter is removed, the catheter and tunnel are thoroughly prepared and draped. The skin site and the area around the cuff are infiltrated with a local anesthetic. Gentle blunt dissection is performed around the cuff using a hemostat. The catheter then is removed with steady traction. The cuff usually is dislodged from the subcutaneous tissues along with the catheter. If the cuff is not dissected free, it may be left behind. The retained cuff could be a continued nidus of infection in cases of sepsis or a tunnel infection. In these cases, the cuff should be removed. When the cuff is initially positioned within 1 to 2 cm from the exit site (as is our standard practice), it usually can be dissected free and removed with the cathe-
ter. When the cuff is located some distance from the exit site and requires removal, a separate incision over the cuff parallel to the tunnel is required for its removal.
Removal of a subcutaneous port requires a sterile site preparation analogous to its insertion. A surgical cutdown also is used to provide the adequate tools. For removal, the skin incision is made overlying the prior incision. Fol­lowing dissection, a white sheath is identified surround­ing the device and catheter, which will need to be incised and dissected free. The port will easily slide from this pocket. External pressure is applied for hemostasis. A two­layer closure is preferred. When needed, additional deep sutures should be placed to eliminate only any dead space that could lead to subsequent hematoma or seroma for­mation and an increased risk of infection.
■ Complications
Procedural complications
Access failure and catheter malposition constitute minor procedural complications. Blinded percutaneous access failure occurs in 5 to 8.9% of cases compared with less than 2% when radiologic guidance techniques are
8,15,16,21,47
used. to 2.5% incidence of catheter malposition immediately following placement. catheter malposition is immediately detected and cor­rected. A patient should not leave the suite with a malpo­sitioned catheter.
Major procedural complications include hematomas, pneumothorax, air embolism, and nerve injury.
Similarly, blind placement results in a 1.2
21,47,48
With radiologic guidance,
35
Hema-
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tomas typically result from an inadvertent arterial needle puncture or bleeding within the subcutaneous tunnel or pocket. The use of a 21-gauge needle, image guidance (ultrasound, fluoroscopy), and a peripheral puncture has virtually eliminated a significant hematoma resulting from an inadvertent arterial puncture.
8,15,21
Contrast in­jection or careful observation of the 0.018-inch guidewire will always confirm venous entry. Tunnel and subcutane­ous pocket hematomas occur more commonly in patients with a coagulopathy. Any coagulation and platelet abnor­mality should be corrected before tunneled or buried devices areplaced. If necessary,a temporary nontunneled device may be placed until the patient’s coagulation status is normalized.
Image guidance also has reduced the pneumothorax
rate to less than 1%.
8,15,21
In addition, the pneumothorax secondary to a 21-gauge needle is typically small and will resolve spontaneously. If not, it is easy to place a small catheter percutaneously in the apex through the second anterior intercostal space and to place it to an under­water seal.
An air embolism may occur if the patient inspires when the peel-away is open to the atmosphere. In a study of percutaneously placed large-bore hemodialysis catheters, air embolism occurred in 0.8% of cases, with no se­quelae.
42
The air accumulates in the pulmonary outflow tract and main pulmonary artery. Oxygen should be ad­ministered, and the patient should be observed. The air will dissipate in several minutes.
Long-term complications
Long-term or delayed complications include mechanical, thrombotic, and infectious complications. The interven­tional radiologist must be familiar with the detection and management of these complications.
Mechanical complications
Delayed catheter migration into the internal jugular vein, azygous vein, or contralateral innominate vein is caused by head or arm motion and a short catheter. A forceful injection of saline or placement of a guidewire or a trans­femoral relocation can correct the malposition. catheter migration recurs, the device should be ex­changed for a longer catheter.
Catheter fragmentation is caused by the mechanical stress on the catheter when it pierces the subclavius mus­cle and the costoclavicular ligament as it courses through the clavicle/first rib space (“pinch-off” syndrome). The fragment may lie anywhere from the subclavian vein to the pulmonar y arteries. The average time between insertion and fragmentation is 6.5 months. mentation is discovered, the remaining device is removed and the free fragment is retrieved by using conventional
36–38
23
When frag-
22,23,49
intravascular foreign-body retrieval techniques. This po­tential complication can be eliminated with venous entry lateral to the clavicle/first rib space.
The repeated use of external catheters may cause fa­tigue and fracture of the hubs and external tubing. Re­pair kits are commercially available for their repair. A severely damaged device must be replaced.
Thrombotic complications
Catheter-related thrombosis is a general term that may in­clude thrombus within the catheter lumen and thrombus within the vein and the fibrin sheath that surrounds the catheter. The reported incidence varies greatly, depend­ing on whether the diagnosis is made clinically or by some diagnostic test. The incidence of catheter-related thrombus varies from 3 to 70%. malignancies or who are in hypercoagulable states and those that are receiving caustic solutions (chemotherapy, hyperalimentation) are particularly susceptible to throm­botic complications. Clinical signs and symptoms of catheter-related thrombosis include ipsilateral swelling of the neck and arm, venous distention, and nonspecific pain in the neck and anterior chest wall.
The inability to aspirate blood is often the first indica­tion of problems relating to thrombus or a fibrin sheath. A fibrin sleeve develops around all catheters in place for longer than a week.
50
When the sleeve reaches the tip of the catheter, it will cause dysfunction. Contrast injection will show a stream of contrast that tracks back along the catheter and even extravasate from the venous entry site. Passing a guidewire through the catheter breaking the fibrin sleeve at the tip may restore function. Fibrin strip­ping using a transfemorally placed loop snare has been used successfully in maintaining catheter function. The snare is placed over the catheter, tightened, and pulled down, stripping the sleeve. Simple catheter ex­change over a guidewire through the same tunnel (for tunnelled catheters) also will restore function and will avoid a new puncture; the patient will be able to leave immediately after the procedure. The relationships of this fibrin sleeve and catheter thrombosis and infection are not well understood. Inability to aspirate blood can also occur when the catheter tip is against the vein wall,
If
a problem often corrected by a change in head or arm position or a Valsalva maneuver.
Treatment of luminal or vein thrombosis involves com­binations of intracatheter thrombolytic therapy, antico­agulation, venous thrombolysis, and catheter removal. Lu­minal thrombotic occlusion is treated with a low-dose thrombolytic regimen. A bolus is injected into the catheter and aspirated after a30-min dwelltime. If this is unsuccess­ful, an infusion may be used for 6 to 12 hr. restored in more than 95% of cases. Treatment of venous thrombosis depends on the severityof symptoms,the need
50–52
Patients who have
5,42
53,54
Patency is
456 M. A. Mauro and S. E. Black
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for access, and the availability of other sites. In patients with long-term need and limited access, heparinization followed by coumadin is used with the catheter left in place. For particularly symptomatic patients, venous thrombolytic therapy with urokinase also will be
50,55,56
used.
Symptomatic patients withlong-term need but with other available sites simply may be treated with cathe­ter removal, new catheter placement, and anti­coagulation. Signs of septic thrombophlebitis require im­mediate catheter removal and appropriate antibiotic treatment. Long-term low-dose (1 mg daily) coumadin and even full anticoagulation have been used to prevent thrombosis.
57
Infectious complications
Catheter-related infections occur at the catheter exit site, within the subcutaneous tunnel or pocket or systemically as catheter related bacteremia (or sepsis). infections often present with erythema and tenderness at the exit sitein additionto an exudate. A tunnel or subcuta­neous pocket infection is more serious and is charac­terized by erythema and tenderness along the tunnel or over the pocket. Pus may be expressed from the tunnel by “milking” the tract. Catheter-related bacteremias present with fever and a leukocytosis and often are used as a diag­nosis of exclusion in a patient with no other apparent source of sepsis. Clinicalevidence implicatingthe catheter as a source of sepsis includes (a) an exit-site or tunnel infection caused by the same organism isolated from the blood, (b) clinical sepsis refractory to antibiotics but re­solves followingcatheter removal, (c) positive quantitative catheter culture with isolation of the same organism from bloodstream, and (d) a differential quantitative blood cul­ture greater than 10-fold colony count of organisms iso­lated from blood obtained through the catheter and from blood obtained from a peripheral site. lated infections arise fromcontamination at the skin inser­tion site, colonization of the catheter hub, hematogenous seeding of the catheter, and infusate contamination. Catheter-related infections occur in 10 to 30% of patients with a rate of 0.2 episodes per 100 days at risk. rate compares favorably to surgical reports.
Local (exit site or subcutaneous) infections must be detected early and aggressively treated to save the device. Gram stain and culture of any drainage should be per­formed. Most (50–70%) of these infections are caused by skin flora. Gram-positive organisms are effectively treated with a 10- to 14-day course of intracath vancomycin hydro­chloride.
42,50
Early erythema withdrainage may be treated with oral antibiotics. If the condition does not improve or worsens on therapy, the device is removed immediately and new cultures are obtained. Even with treatment, the device is salvaged in only 25% of patients with tunnel infections and 70% with exit site infections.
58–60
58,61
Catheter-re-
50,59
Exit-site
42,59,60
58–60
This
Catheter-related bacteremias are treated with intrave­nous antibiotics according to culture and sensitivity stud­ies. If, however, no improvement has occurred in 48 to 72 hr, the device must be removed. Even when the device is salvaged, there is a 20% chance the bacteremia will recur compared with a 3% risk of recurrence if the device is removed.
58
■ Conclusion
The need for central venous access is expanding rapidly. This service can be provided economically and expedi­tiously by an interventional radiologist. Most cases can be completed within 45 to 60 min. The devices can be placed safely, and the late infectious and thrombotic complica­tions seen with these procedures are comparable to those seen when the devices are placed within an operating room. The skills and technology available to interven­tional radiologists place them in a unique position to deliver this service.
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3. Niederhuber JE, Ensminger W, Gyves J, et al. Totally implanted venous and arterial access system to replace external catheters in cancer treatment. Surgery 1982;92:706–712.
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16. Kahn MO, Barboza RB, Kling GA, et al. Initial experience with percutaneous placement of the P.A.S. port implantable venous ac­cess device. J Vasc Interv Radiol 1992;3:459–461.
17. Stalter KA, Stevens GF, Sterling WA. Late stenosis of the subclavian vein after hemodialysis catheter injury. Surgery 1986;100:924–927.
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19. Selby JB, Tegtmeyer CJ, Amodeo C. Insertion of subclavian hemo­dialysis catheters in difficult cases: value of fluoroscopy and angiog­raphic techniques. AJR Am J Roentgenol 1989;152:641–643.
20. Jaques PF, Campbell WE, Dumbleton S, et al. The first rib as a fluoroscopic marker for subclavian vein access. J Vasc Interv Radiol 1995;6:619–622.
21. Lameris JS, Post PJM, Zonderland HM, et al. Percutaneous place­ment of Hickman catheters: comparison of sonographically guided and blind techniques. AJR Am J Roentgenol 1990;155:1097–1099.
22. Hinke DH, Zandt-Stastny DA, Goodman LR, et al. Pinch-off syn­drome: a complication of implantable subclavian venous access devices. Radiology 1990;177:353–356.
23. Lafrenirre R. Indwelling subclavian catheters and a visit with the “pinch-off” syndrome. J Surg Oncol 1991;47:261–264.
24. Jaques PF, Mauro MA, Keefe B. Ultrasonographic guidance for vascular access. J Vasc Interv Radiol 1992;3:427–430.
25. Andrews JC, Walker-Andrews SC, William DE. Long-term central venous access with a peripherally placed subcutaneous infusion port: initial results. Radiology 1990;176:45–47.
26. Bonn J. Venous access: peripherally inserted central catheters, SCVIR Program. San Diego: Society of Cardiovascular and Inter­ventional Radiology, 1994:204–210.
27. Denny DF, Dorfman GS, Greenwood LH, et al. Translumbar infe­rior vena cava Hickman catheter placement for total parenteral nutrition. AJR Am J Roentgenol 1987;148:621–622.
28. Denny DF, Greenwood LH, Morse SS, et al. Inferior vena cava: translumbar catheterization for central venous access. Radiology 1989;170:1013–1014.
29. Kaufman JA, Greenfield AJ, Fitzpatrick GF. Transhepatic cannula­tion of the inferior vena cava. J Vasc Interv Radiol 1991;2:321–334.
30. Robertson LJ, Jaques PF, Mauro MA, et al. Percutaneous inferior vena cava placement of tunnelled Silastic catheters for prolonged vascular access in infants. J Pediatr Surg 1990;25:596–598.
31. Lund GB, Lieberman RP, Haire WD, et al. Translumbar inferior vena cava catheters for long-term venous access. Radiology 1990; 174:31–35.
32. Azizkhan RG, TaylorLA, Jaques PF, et al.Percutaneous translumbar and transhepatic inferior vena cava catheters for prolonged vascu­lar access in children. J Pediatr Surg 1992;27:165–169.
33. Andrews JC. Percutaneous placement of a Hickman catheter with use of an intercostal vein for access. J Vasc Inter v Radiol 1994;5: 859–861.
34. Dick L, Mauro MA, Jaques PF, et al. Radiologic insertion of Hick­man catheters in HIV-positive patients: infectious complications. J Vasc Inter v Radiol 1991;2:327–329.
35. Lund GB. Complications from long-term tunnelled venous access catheters: a review. Semin Interv Radiol 1994;2:340–348.
36. Carasco CH, RichliWR, Chusilp C, et al. Technical note: reposition­ing misplaced central venous catheters. Cardiovasc Interv Radiol 1987;10:234–236.
37. Lois JF, Gomes AS, Pussey R. Non-surgical repositioning of central venous catheters. Radiology 1987
38. Olcott EW, Gordon RL, Ring EJ. The injection technique for repo-
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sitioning central venous catheters: technical note. Cardiovasc Inter v Radiol 1989;12:292–293.
39. Andrews JC, Marx MV, Williams DM, et al. The upper arm ap­proach for placement of peripherally inserted central catheters for protracted venous access. AJR Am J Roentgenol 1992;158:427–429.
40. Brant-Zawadzki M, Anthony M, Mercer EC. Implantation of P.A.S. port venous access device in the forearm under fluoroscopic guid­ance. AJR Am J Roentgenol 1993;160:1127–1128.
41. Foley MJ. Radiologic placement of long-term central venous pe­ripheral access system ports (PAS port): results in 150 patients. J Vasc Inter v Radiol 1995;6:255–262.
42. Lund GB, Trerotola SO, Scheel PF, et al. Outcome of tunneled hemodialysis catheters placed by radiologists. Radiology 1996;198: 467–472.
43. Tesio F, De Baz H, Panarello G, et al. Double catheterization of the internal jugular vein for hemodialysis: indication, techniques, and clinical results. Artif Organs 1993;18:301–304.
44. Ganaud B, Beraud JJ, Joyeux H, et al. Internal jugular vein cannula­tion using 2 silastic catheters: anew, simple andsafe long-termvascu­lar access for extracorporeal treatment. Nephron 1986;43:133–138.
45. Canaud B, Beraud JJ, Joyeux H, et al. Internal jugular cannulation with two silicone rubber catheters: a new and safe temporary vascu­lar access for hemodialysis: thirty months’ experience. Artif Organs 1986;10:397–403.
46. Keohane PP, Attrill H, Northover J. Effect of catheter tunnelling and a nutrition nurse on catheter sepsis during parenteral nutri­tion. Lancet 1983;17:1388–1390.
47. Takasugi JK, O’Connell TX. Prevention of complications in perma­nent central venous catheters. Surg Gynecol Obstet 1988;167:6–11.
48. DelmoreJE,Horbelt DV. Jack BI, etal. Experiencewith thegroshong long-term central venous catheter. Gynecol Oncol 1989; 34:215–218.
49. Rubenstein RB, Alberty RE, Michels LG, et al. Hickman catheter separation. JPEN 1985;9:754–757.
50. Lowell JA, Bothe A Jr. Venous access preoperative, operative, and postoperative dilemmas. Surg Clin North Am 1991;71:1231–1246.
51. Haire WD, Lieberman RP, Lund GB, et al. Thrombotic complica­tions of silicone rubber catheters during autologous marrow and peripheral stem cell transplantation: prospective comparison of Hickman and groshong catheters. Bone Marrow Transplant 1991;7: 57–59.
52. Anderson AJ, Krasnow SH, Boyer MW, et al. Thrombosis: the major Hickman catheter complication in patients with solid tumor. Chest 1989;95:71–75.
53. Crain MR, Mewissen MW, Ostrowski GJ, et al. Fibrin sleeve stripping for salvage of failing hemodialysis catheters: technique and initial results. Radiology 1996;198:41–44.
54. Hosal VL, Ause RG,Hoskins PA. Fibrin sleeve formation on indwell­ing subclavian central venous catheters. Arch Surg 1971;102:353–
358.
55. Moss JF, Wagman LD, Riihimaki DU, et al. Central venous throm­bosis related to the silastic Hickman-Broviac catheters in an on­cologic population. J Parenter Enteral Nutr 1989;13:397–400.
56. Gray WJ, Bell WR. Fibrinolytic agents in the treatment of throm­botic disorder. Semin Oncol 1990;17:228–237.
57. Bern MM, Lokich JJ, Wallach SR, et al. Very low doses of warfarin can prevent thrombosis in central venous catheters. Ann Intern Med 1990;112:423–428.
58. Raad II, Bodey GP. Infectious complications of indwelling vascular catheters. Clin Infect Dis 1992;15:197–210.
59. Clarke DE, Raffin TA. Infectious complications of indwelling long­term central venous access catheters. Chest 1990;96:966–972.
60. Press OW, Ramsey PG, Larson EB, et al. Hickman catheter infec­tions in patients with malignancies. Medicine 1984
61. Weightman NC, Simpson EM, Speller DCE, et al. Bacteremia re­lated to indwelling central venous catheters: prevention, diagnosis, and treatment. Eur J Clin Microbiol Infect Dis 1988;7:125–129.
;63:189
–200.
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A.C. Roberts and J. E. SilberzweigHemodialysis Access Management
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36
■■■
Hemodialysis Access Management
ANNE C. ROBERTS AND JAMES E. SILBERZWEIG
Dialysis is defined as the removal of blood elements by diffusion through a semipermeable membrane. The pur­pose of dialysis is to remove metabolic waste products and maintain fluid and electrolyte balance. The hemodialysis machine functions as an “artificial kidney.” Blood is drawn from the patient at a rate of 300 to 500 mL per minute, passed through the dialysis machine, and then returned to the patient. Patients with end-stage renal disease typically require hemodialysis three times per week for 3 to 4 hours. The rapid circulation of blood between patient and hemodialysis machine requires a conduit that is durable, has a low infection rate, and is easily accessible. Peritoneal dialysis is an alternative form of dialysis in which dialysate is instilled into the perito­neal cavity, periodically drained, and replaced with fresh solution via a catheter. The peritoneal membrane acts as the dialyzing surface in peritoneal dialysis.
Alternatives for access to the patient’s blood circula­tion for hemodialysis include the use of a central venous catheter, a surgically created arteriovenous fistula, or a prosthetic graft interposed between an artery and vein. Central venous catheters have one lumen for drawing blood from the patient into the hemodialysis machine (arterial ) and one lumen for blood return to the patient from the hemodialysis machine (venous ). Access to a prosthetic graft or the venous outflow of a surgically cre­ated fistula is made with two 14- to 16-gauge needles.
Renal transplantation is the treatment of choice for many patients with end-stage-renal disease. Because of limited organ availability, however, dialysis is the primary therapy for most of these patients. More than 280,000 persons in the United States require chronic dialysis.
1
For
these patients, functioning dialysis accessis their“lifeline,” and maintenance of this access is critical. Hemodialysis access maintenance represents one of the most challeng­ing problems for interventional radiologists. Thrombosis is the most common cause of hemodialysis access graft loss and usually is related to stenoses in the venous outflow. The goal of hemodialysis access maintenance is to detect and treat access dysfunction prior to access thrombosis and to salvage thrombosed grafts.
■ Arteriovenous Graft
Most patients requiring chronic hemodialysis have an up­per-extremity arteriovenous graft (AVG) constructed of 6-mm-diameter polytetrafluoroethylene (PTFE) tubular graft material. Typical upper-extremity grafts include a loop graft with anastomoses at the brachial artery and basilic vein or cephalic vein and a straight graft with anasto­moses at the distal radial artery and the basilic or cephalic vein near the antecubital fossa. The graft is tunneled sub­cutaneously and is easily accessible by percutaneous nee­dle puncture. A lower-extremity loop graft extending from the common or superficial femoral artery to the saphenous vein is constructed when upper-extremity veins are no longer usable for graft construction. The most common complication associated with PTFE hemo­dialysis access grafts is the development of stenosis at the venous anastomosis or venous outflow of the graft result­ing in graft thrombosis. Patency rates at 1 year range from 55 to 75%, estimated to be less than 2 years.
2,4,5
and the life span of the average graft is
6
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■ Brescia–Cimino Fistula
The preferred access for hemodialysis is an endogenous arteriovenous fistula because it provides the greatest chance for long-term function. A Brescia–Cimino arte­riovenous fistula is usually constructed with a side-to-side anastomosis of the cephalic vein and radial artery at the wrist. A fistula also can be placed at the antecubital fossa with an anastomosis of the brachial artery and cephalic vein. Brescia–Cimino fistulas are less likely to thrombose than a PTFE graft because a fistula has a single anasto­mosis with multiple potential areas of venous outflow.
After an arteriovenous fistula is created, thepatient can­not undergo dialysis using this access until fistula matura­tion occurs. Maturation involves vein-wall thickening and dilatation, which facilitates vein puncture with large-bore needles and accommodates arterial blood flow required for dialysis. The maturation process typically takes 1 to 4 months. Fistulas are ideally placed several months prior to anticipated use to ensure adequate maturation.
Unfortunately, Brescia–Cimino fistulas have a high early failure rate, usually as a result of inadequate venous size or runoff. When the fistula is established and used successfully for hemodialysis, late failure is rare. In about 20 to 30% of cases, the fistula will never mature.
2–4
problem.
9
Occasionally, no underlying anatomic lesion can be found. It has been postulated that these grafts may have thrombosed due to excessive postdialysis graft com­pression at the needle puncture sites, hypotension, hypo­volemia, compression of the graft due to sleeping posi­tion, or a hypercoagulable state.
10
The development of venous stenoses appears to be caused by neointimal hyperplasia. The cause of this hy­perplasia is not well understood. A variety of theories have been proposed to explain the development of neointimal hyperplasia. One mechanism of hyperplasia is a response to turbulent blood flow and vibration result­ing from placement of the graft.
11
Other factors such as the transition between the relatively noncompliant graft material and the compliant vein, stretching of the vein at the anastomosis,
12
or angulation and
13
may be impor­tant. Whatever the cause, these stenoses inevitably recur after intervention because the underlying pathophysiol­ogy is unchanged. This is the cause for the ongoing requirement for repeated angioplasty and thrombolysis of the dialysis grafts. Until the pathophysiology of intimal hyperplasia is understood and techniques are developed to prevent intimal hyperplasia, there will be a need for the mechanical treatment of venous stenoses.
■ Causes of Graft Dysfunction
Thrombosis is the most common cause of hemodialysis access graft loss and usually is related to stenoses in the venous outflow. If thrombosis occurs in the first few weeks after placing the access, there is often a technical prob­lem related to the graft. Technical problems include graft kinking, narrow arterial or venous anastomoses, or pre­existing arterial inflow or venous outflow disease (Fig.
7
36-1). nous outflow stenosis after graft insertion.
Occasionally, there is rapid development of ve-
8
Thrombosis that occurs after 2 to 3 months is usually due to the development of stenosis in the venous outflow. Arterial inflow stenosis may occur, but it is a much less frequent
FIGURE 36-1. Kinking of this newly placed hemodialysis graft near the venous anastomosis ( sion.
arrow
) required surgical revi-
■ Treatment of the Poorly
Functioning Graft
The sites available for hemodialysis access are limited; therefore, it is important to extend the life of each access for as long as possible. Treatment of grafts prior to throm­bosis is more cost- and time-effective than treatment of thrombosed grafts. Long-term patency of grafts is im­proved if stenoses are treated prior to thrombosis as opposed to undertaking angioplasty or surgical revision after thrombosis has occurred; however, this requires identifying functioning grafts that are at risk for throm­bosis. If the developing stenosis can be identified and treated with angioplasty, the risk and cost of thrombolysis can be avoided.
A number of signs may identify developing graft stenoses, including elevated venous pressure, with needle placement, increased bleeding following needle removal, extremity edema, dilatation of collateral veins over the upper extremity or chest, of the normal graft thrill to a pulse. refers to the pressure measured by the dialysis machine as blood is returned to the patient. Venous return pres­sure greater than 150 mm Hg at a blood flow of 200 mL per minute is indicative of a venous outflow stenosis. Recent studies showed that Doppler ultrasound may be useful in the evaluation for stenoses.
19,20
Angiographic evaluation of a hemodialysis access graft should include the arterial anastomosis, graft, venous
8,14
15
and conversion
16,17
Venous pressure
difficulty
18
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anastomosis, and the entire venous outflow. This can be done easily by using a dialysis needle, which can be left in place following a dialysis session or using standard Seldin­ger technique. If a stenosis is identified, angioplasty can be performed immediately and the patient discharged following completion of the procedure (Fig. 36-2).
Early correction of venous stenoses prolongs access viability. A recent study followed up on 106 grafts sus­pected on clinical examination to have a venous steno-
21
sis.
The grafts were studied angiographically, and any venous stenosis was treated with balloon angioplasty. The technical success for angioplasty was 98%. The primary patency at 1 year was 23% for PTFE grafts. Repeated angioplasty improved the patency rate to 68% at 1 year and 51% at 2 years (primary assisted patency rate). A combination of thrombolysis and repeated angioplasty improved patency further, with secondary patency rates at 1 year of 82% and at 2 years of 65%.
21
Recurrence of stenoses should not be considered a failure of the procedure but rather an expression of the underlying pathophysiology. Redilatations allow easy and safe maintenance for months and even years.
17
Gaining added months of patency through redilatations could be of great value for dialysis patients. In contrast to a surgical graft revision, loss of central veins does not occur with angioplasty. Because angioplasty and surgical techniques may have similar secondary patency, the loss of future access sites becomes an important issue.
The treatment of a poorly functioning Brescia–Cimino fistula is less likely to involve thrombolysis and more likely to require angioplasty of a venous stenosis. In patients with Brescia–Cimino fistulas, most stenoses occur in the anastomotic and postanastomotic area before the punc­ture area for dialysis.
22
These fistulas are difficult to evalu­ate because of the number of outflow veins that become opacified with angiographic evaluation. This is particu­larly apparent when a stenosis in the main outflow and development of collateral veins occur. The collateral veins may overlie and obscure the venous stenosis, and angiography in multiple projections may be required to demonstrate an abnormality.
■ The Thrombosed Graft
The traditional therapy for failing hemodialysis access has been surgical thrombectomy with or without revision of the venous anastomosis. Thrombectomy alone is usu­ally not successful because thrombectomy does not ad­dress the cause of graft failure, and replacement is not a realistic option because the possible access sites would be exhausted rapidly.
During the past 10 to 15 years, percutaneous tech­niques have become widely used for dialysis access sal­vage. Graft thrombolysis and balloon angioplasty of sten­oses are the essence of percutaneous therapy for clotted hemodialysis access grafts. The thrombolysis portion of the procedure can be performed by several methods, including a combination of clot-dissolving medications and mechanical “declotting” devices.
A hemodialysis graft has unique characteristics that make it particularly amenable to percutaneous therapy. The graft is easy to access percutaneously, contains fresh clot responsive to thrombolytic agents, and is a closed system with only a single inflow and outflow, keeping the thrombolytic agent from diffusing into the systemic circu­lation.
The percutaneous approach to a thrombosed dialysis graft allows not only for thrombolysis but also for angio­graphic evaluation of the graft. The entire graft, includ­ing the arterial inflow and the complete venous outflow, can be evaluated easily. The venous anastomotic stenosis that is often encountered can be treated with balloon angioplasty.
The percutaneous graft declotting and angioplasty pro­cedure is performed in a single session and usually is performed on an outpatient basis. Following the conclu­sion of the procedure, the patient can be discharged to a dialysis unit or home. The graft is functional for dialysis immediately following percutaneous therapy, unlike after surgical revision or new graft insertion. This is crucial because successful percutaneous therapy obviates the need for the insertion of a temporary central venous hemodialysis catheter. Avoidance of the use of temporary
A B
FIGURE 36-2. Arteriovenous shunt stenosis. Venous anastomotic stenosis. (A). Before the 7-mm balloon angioplasty. (B). After angioplasty.
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jugular or femoral central venous dialysis catheters de­creases expenses and eliminates the risk of complications from these catheters, such as central venous stenosis and infection.
■ Patient Selection
Usually, thrombosis of a recently (within a few weeks) constructed graft is due to a surgical technical problem. Sometimes thrombolysis is performed to identify the cause of the problem, which may allow a focused surgical repair. There is some increased risk of bleeding from recent anastomotic sites; however, if this does occur, it is usually controlled easily with manual pressure. Balloon angioplasty of the anastomosis of a recently placed graft, however, is at increased risk for rupture and should be avoided.
Some patients should not undergo thrombolysis. Crite­ria that would exclude a patient with a thrombosed dialy­sis graft are the same for other thrombolytic procedures. Absolute contraindications to thrombolysis are active gas­trointestinal bleeding and recent neurologic processes, including intracranial bleeding, stroke, or neurologic surgery. Relative contraindications include major surgery or organ biopsy within 2 weeks; recent serious trauma; preexisting coagulation defects; uncontrolled, severe hy­pertension; pregnancy or the immediate postpartum pe­riod. The use of a mechanical thrombectomy device may be ideal for patients at increased risk for bleeding.
A contraindication to percutaneous graft thrombolysis is the presence of a graft infection. Lysis of infected clot may precipitate bacteremia and lethal sepsis.
23
Also an infected clot is relatively resistant to thrombolysis. Deter­mining the presence of infection in a graft is often diffi­cult. The classic signs of infection, such as redness, ten­derness, warmth, swelling, and fever, are often blunted in patients with uremia. Purulent discharge or skin break­down around the graft are obvious signs of infection, but these sign are uncommon. Needle aspiration of the graft clot for Gram stain and culture or of perigraft fluid col­lections found on ultrasound evaluation may be helpful in diagnosing graft infections.
24
Infection of the graft mandates treatment with antibiotics and referral for sur­gical removal of the graft.
Grafts that have undergone attempts at access just prior to the thrombolytic procedure are more likely to develop bleeding from the puncture sites during the thrombolytic procedure. It is worthwhile to develop a policy with the referring dialysis center so that if a patient presents with a pulseless graft, no attempts will be made to cannulate the graft, and the patient is immediately referred for percutaneous recanalization. Bleeding occa­sionally develops from puncture sites that are several days old, particularly if the puncture was traumatic. Usually
bleeding is not a serious problem. Bleeding can be man­aged by manual compression over the site and by rapid relief of the outflow stenosis by angioplasty that will de­crease the pressure within the graft. On occasion, it is not possible to control the bleeding site while continuing to recanalize the graft. In this situation, surgical therapy may be required.
■ Graft Recanalization Technique
Graft access
The crossed-catheter technique is the basis of the ap­proach to the thrombosed graft (Fig. 36-3 and Table
25–27
36-1). and venous ends of the graft simultaneously. A standard single-wall entry needle or a Micropuncture Introducer set (Cook, Bloomington, IN, U.S.A.) is used to access the graft. The first puncture is made in the graft at the junc­tion of the proximal and middle third of the graft (the arterial end of the graft) directed toward the venous end of the graft. The graft can be accessed most successfully if it is fixed between the thumb and index finger and held firmly while the puncture is being made. As the graft wall is punctured, there is a “popping” sensation. This sensa-
Graft
FIGURE 36-3. Initial catheter access for declotting of an up-
per-extremity hemodialysis loop graft using the crossed cathe­ter technique.
This approach allows access to both the arterial
Vein
Catheter
Artery
Catheter
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TABLE 36-1. Hemodialysis Graft Declotting Procedure
1. Obtain antegrade access to the graft near the arterial anastomosis.
2. Cross the venous anastomosis with diagnostic catheter.
3. Obtain pullback venogram of central veins and graft outflow.
4. Angioplasty/stent central venous stenosis/occlusion.
5. Obtain retrograde access to the graft near the venous anastomosis.
6. Insert infusion catheters and inject thrombolytic agent or perform mechanical thrombectomy.
7. Angioplasty venous anastomotic stenosis/occlusion.
8. Remove residual clot at the arterial anastomosis by passing a deflated Fogarty or occlusion balloon catheter through the graft into the inflow artery. Inflate the balloon with contrast and pull back into the graft.
9. Macerate residual clot with the angioplasty balloon.
10. Perform completion angiogram of the inflow artery, graft, and outflow veins.
11. Exchange vascular sheaths for temporary hemodialysis catheters and transfer patient to hemodialysis unit.
12. Remove catheters after hemodialysis.
tion can be blunted in an older graft because scar tissue builds up around the graft after many punctures. The graft is thrombosed; thus, there will be no pulse within the graft and usually no return of blood when the lumen is entered. When the graft is entered, the guidewire usu­ally passes easily through the lumen, even in the presence of clot. In some cases, a small amount of dark blood returns through the needle.
If the wire does not pass easily and coils in the soft tissues, as seen on fluoroscopy, the needle should be repositioned until it is within the graft lumen. If the patient complains of pain when the wire is advanced, this is an indication that the guidewire is not within the graft. On the other hand, the patient may not complain of pain when the wire is in the soft tissues, and so fluoroscopy and “feel” are extremely important. When the puncture is difficult, it is tempting to inject contrast to determine whether the graft has been entered. This temptation should be resisted. If the needle is not in the graft and contrast is injected into the soft tissues, the appearance may be misleading. At first, it may appear that the graft has been entered, as the injection continues, it will be­come evident that the contrast is not within the graft. At this point, however, the graft is often obscured and will remain obscured for the remainder of the procedure. Although it can be difficult to do so, it is best to rely on observing the wire following the course of the graft as evidence of correct placement of the needle within the graft.
After the guidewire has been placed correctly into the graft, avascular sheath is placed over the guidewire,which then must be passed through the venous anastomosis and into the venous outflow. If difficulty is encountered in passing the venous anastomosis or the stenosis that is often in the same vicinity, an angled Glidewire (Terumo,
Boston Scientific, Natick, MA, U.S.A.) may be useful. It is crucial to confirm passage of the wire into the venous outflow before proceeding. If the venous outflow stenosis cannot be passed, thrombolysis should not be performed. If venous outflow is not reestablished and blood flow is reestablished, bleeding will occur from previous puncture sites or from around the catheters. If the venous anasto­mosis cannot be crossed, surgical thrombectomy and revi­sion of the venous anastomosis are the most appropriate therapy.
When the guidewire can be passed beyond the venous anastomosis, a catheter is placed into the outflow vein. An outflow venogram then is performed to evaluate for any central venous stenosis and the presence of thrombus within the outflow vein.
The second vascular sheath in the cross-catheter tech­nique is placed by puncturing the graft at the junction of the middle one third and the distal one third of the graft (the venous end of the graft). The guidewire is directed toward the arterial end of the graft. The catheter and wire manipulations at the arterial end of the graft should be done gently. Vigorous movement of the wire or forceful contrast injections can cause embolization of clot from the arterial anastomosis into the artery (Fig. 36-4).
■ Thrombolysis/Thrombectomy
Thrombolysis
The tissue plasminogen activator (tPA) (Activase, Genen­tech, South San Fransisco, CA, USA; Retauase, Centoeor, Malvern, PA, USA) has become the thrombolytic agent of choice following the recall of Urokinase in 1999.
Several methods to deliver the thrombolytic agent are available, including endhole, coaxial, and multi-sidehole catheter infusions and forced intrathrombic injections (pulse-spray) with use of tip-occluded multi-sidehole and multislit-type catheters. Prolonged thrombolytic infusion,
FIGURE 36-4. Arterial embolus. A rare complication of hemo­dialysis declotting is arterial embolization. The embolus to the bifurcation of the brachial artery ( moved with the use of a Fogarty balloon catheter.
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) was successfully re-