CHAPTER 20 THE USE OF VENOUS ACCESS DEVICES

CHAPTER 20 THE USE OF VENOUS ACCESS DEVICES
Williams Hematology

CHAPTER 20 THE USE OF VENOUS ACCESS DEVICES

McDONALD K. HORNE
DONNA JO MAYO
ALISON G. FREIFELD

Basic Designs
Selection of a Venous Access Device
Placement and Removal of Devices
Catheter Maintenance
Complications of Venous Access Devices

Catheter Occlusion

Venous Thrombosis

Infections
Chapter References

Venous access devices are important in the management of advanced hematologic diseases. Several designs, including tunneled and nontunneled devices, are available, and the choice should be individualized to the needs of the patient. Careful maintenance of devices is required to prevent occlusion, thrombus formation, or infection. The latter may be confined to the catheter exit site or the tunnel, or it may include bacteremia or septicemia. Both thrombotic and infectious complications are common and require specific therapeutic interventions.

Acronyms and abbreviations that appear in this chapter include: PICC, peripherally inserted central catheter; VAD, venous access device.

Central venous access is essential in the management of advanced hematologic diseases requiring intensive therapy. Repeatedly catheterizing central veins, however, is impractical and hazardous. Therefore, VADs have been developed to provide a continuous portal to the central veins for extended periods of time. These devices are silicone rubber or plastic tubes that have been engineered to maximize their longevity.
BASIC DESIGNS
Although a variety of devices are available, there are a few basic designs (Table 20-1).1 Tunneled devices pass through the subcutaneous tissues of the anterior chest wall or neck for several centimeters before entering a central vein. Their exterior end either exits through the skin (Figure 20-1) or terminates in a reservoir (a port) that is buried beneath the skin (Figure 20-2). Because of this feature, ports can only be entered by a percutaneous puncture with a noncoring needle. Externalized devices have a fibrous cuff that anchors them in the tunnel as the insertion wound heals. Ports are secured by sutures in their subcutaneous pouches.

TABLE 20-1 COMMON VENOUS ACCESS DEVICES

FIGURE 20-1 Schematic illustration of an external catheter in place. (a) Exit site and end of subcutaneous tunnel. (b) Dacron cuff in subcutaneous tunnel, traditional placement. (c) Midsubcutaneous tunnel; optimal placement for cuff to minimize accidental dislodgement. (d) Subclavian vein insertion site. Tip should be placed as close as possible to the superior vena cava—right atrial junction. (Used with permission from Alexander HR, Lucas A: Long-term venous access catheters and implantable ports, in Vascular Access: The Cancer Patient. Lippincott, Philadelphia, 1994.)

FIGURE 20-2 Photograph of standard and low-profile ports. The low-profile port is suitable for younger or aesthenic patients with little subcutaneous tissue. (Used with permission from Alexander HR, Lucas A: Long-term venous access catheters and implantable ports, in Vascular Access: The Cancer Patient. Lippincott, Philadelphia, 1994.)

Nontunneled devices are inserted directly into a peripheral arm vein (PICCs) or a subclavian vein (central catheters).2 They are secured to the skin with tape or sutures.
Catheters are manufactured with one to three lumens of differing internal diameters (0.5–2.6 mm). The number and size of the lumens determines the external diameter of the catheter, which is measured in French (one French equals 0.33 mm). The catheter tips may be continuously open (e.g., Hickman or Broviac type) or fitted with a valve that opens with positive or negative pressure (e.g., Groshong type).
SELECTION OF A VENOUS ACCESS DEVICE
In order to minimize intravenous obstruction and trauma, the external diameter of the devices should be as small as possible while still providing the needed access. The choice of lumen diameter depends on the viscosity and desired flow rates of the fluids to be administered. When the catheter is intended only for standard chemotherapy and fluids, for example, small lumens are adequate, whereas apheresis procedures require large-bore devices.
The length of time that the catheter will be needed is also important. Tunneled catheters are more likely to function well for months to years, whereas the nontunneled varieties are more appropriate for short-term use.
Patient preferences should also be considered, since external devices present cosmetic problems and may restrict activities. Furthermore, all catheters require continuous care, which may be impossible for a patient to provide for themselves.
PLACEMENT AND REMOVAL OF DEVICES
Before an attempt is made to insert a catheter, a careful history and physical examination are required to determine whether the candidate vein has been previously catheterized or is likely to be compressed by a tumor mass. These circumstances suggest the possibility of distorted venous anatomy that may preclude placement of the device.3 A venogram may be required to assess the situation.
Tunneled devices should be placed by a surgeon or interventional radiologist in an operating suite under local anesthesia. Removal of a tunneled percutaneous catheter is complicated by the need to dissect the subcutaneous cuff, while removal of a port requires a more extensive procedure. PICCs, in contrast, can usually be inserted and removed by trained nurses in an outpatient setting, greatly reducing the cost and inconvenience of establishing central venous access.
The tip of the catheter should be placed in the superior vena cava, just outside the right atrium. If the tip resides inside the right atrium a right atrial thrombus may develop. If the tip is left in a subclavian or innominate vein there is an increased chance of catheter occlusion or venous damage from sclerosing infusates.
CATHETER MAINTENANCE
Immediately following insertion of a venous access device, surgical wound care is necessary. PICCs often cause sterile phlebitis in the upper arm or shoulder, but this usually resolves spontaneously or with the help of warm compresses.
Long-term maintenance of devices consists principally of periodic flushes to promote patency. Because of their locations nontunneled catheters are very difficult for patients to care for alone, whereas self-care is much easier for devices implanted in the chest wall. The optimal flushing program has never been established for any of the catheters. The routine programs have been rather arbitrarily developed and based largely on convenience. The lumens of open-ended devices constantly communicate with the blood. These are typically flushed daily with heparinized saline, unless they have a port buried beneath the skin. Then they are flushed monthly. The incidence of catheter occlusion is about the same whether the flushes are daily or monthly and regardless of whether they contain heparin or only saline.4,5
COMPLICATIONS OF VENOUS ACCESS DEVICES
CATHETER OCCLUSION
Reduced flow is a common problem.22 If fluid can neither be infused nor withdrawn easily, the catheter is probably kinked or pinched by a suture or is defective. However, it may have become blocked with lipid or with precipitates of drugs or of calcium phosphate. These occlusions can sometimes be cleared with instillations of 0.1 N hydrochloric acid or 70% ethanol.
A more common type of occlusion is limited to withdrawal only. This not only interferes with blood sampling but also suggests the possibility that the catheter tip has migrated into a small vein and lodged against the vessel wall. Concentrated chemotherapeutic agents infused through such a catheter will not be quickly diluted and may damage the small vein. Therefore, withdrawal occlusion should be relieved or investigated before the catheter is used. The problem can often be remedied by having the patient change body position or perform a Valsalva maneuver in order to move the tip of the catheter. If this does not resolve the problem, an occlusive fibrin sheath may be present.
Virtually all devices become coated with fibrin within a few days of insertion. If this coating progresses to involve the catheter tip, it may block the lumen when negative pressure is applied. One or two milliliters of urokinase (5000 units/ml) injected into the catheter and permitted to remain in the lumenal arm for up to 30 min will relieve most fibrin occlusions. If this treatment fails, the obstruction should be evaluated radiologically.
A chest x-ray may reveal that the catheter tip has migrated into a small vessel. If this is not the case a small amount of x-ray contrast material should be injected through the catheter under fluoroscopy. If an occlusive fibrin sheath is present the flow of dye will be diverted or may move retrograde along the outside of the catheter.6 In extreme cases the sheath may extend from the catheter tip to the insertion site in the vein, where contrast material extravasates. If sclerosing medications are infused through the catheter they may follow the same path and damage extravascular tissues.
Fibrin sheaths that are refractory to urokinase instillations can often be lysed by continuous infusions of urokinase through the occluded lumen. An effective and safe regimen is to infuse 5000 units/ml of urokinase at 8 ml/h.7* The occlusion may be relieved within a few hours. If more than 12 h of treatment is needed, it is unlikely to be successful.
VENOUS THROMBOSIS
The reported incidence of mural thrombi associated with venous access devices varies greatly, from virtually 0 to almost 40 percent.3,4,8 Thrombi tend to occur at the site where the catheter enters the vein or near the catheter tip, particularly if it is not properly placed in the vena cava.3,7 Usually these thrombi are asymptomatic because they only partially obstruct flow and/or because collateral veins rapidly develop.3 However, they may enlarge and cause pain and swelling of the ipsilateral arm or supraclavicular fossa and dilatation of the subcutaneous veins.
In the management of thrombi associated with venous access devices, several issues should be considered. If central venous access is still needed, the device should not be removed except in extreme cases. Symptomatic relief is often achieved by arm elevation. Full heparinization followed by chronic oral anticoagulation is recommended.9 Although pulmonary emboli have been reported in up to 15 percent of patients with access-device–related thrombi, the risk appears to be much lower with newer silicone catheters.9,10 There is also the fear that emboli will break off of a thrombus when the device is removed. Radiographically this has been shown to happen, but serious clinical events related to these emboli are unusual.6 Therefore, there is no established role for a course of anticoagulation prior to removing a device through a thrombus.
Chronic symptoms are reported to persist in 23 percent of the cases of device-associated thrombosis.11 However, they are usually tolerable and obscured by events related to the patient’s primary disease. Another long-term concern for many patients is future venous access, since a thrombosed vein rarely recanalizes sufficiently to admit another device if needed. If restoring venous patency is a high priority, thrombolytic agents are usually necessary.
Systemically administered agents generally bypass the clot by going through collateral veins. Regional delivery of thrombolytic drugs is much safer and more effective. If the tip of the catheter is lodged in a thrombus, infusion of urokinase through the device itself will deliver the drug where it is needed. The same urokinase protocol recommended for fibrin sheaths can be used, although longer treatment may be required and heparin may be needed if local venous flow is stagnant.
If the mural thrombus is peripheral to the catheter tip, the patient must be heparinized and the thrombus injected with urokinase or tissue plasminogen activator delivered through a different catheter.* Unless the thrombus is several weeks old or the vein has become stenotic or compressed by extravascular structures, such treatment is usually both safe and successful.12
PROPHYLACTIC ANTICOAGULATION
Prophylactic anticoagulation to prevent catheter-related thrombosis may be warranted in high-risk patients. One milligram of warfarin/day or a daily injection of low molecular weight heparin is reported to be effective.8,13
INFECTIONS
Ten to 40 percent of long-term tunneled devices become infected, and the rate is generally even higher for nontunneled catheters.14,23 In most studies, totally implanted infusion ports appear to be less prone to infection than externally tunneled catheters.14,15
The least serious of these complications is an exit site infection, which is an area of cellulitis within 2 cm of where the catheter penetrates the skin. Systemic symptoms are unusual. Sterile inflammation can sometimes also present in this manner and may be distinguished from infection by a semiquantitative culture of the area.15,16
An infection of the tunnel track or the pocket of a subcutaneously implanted catheter is more serious. It presents as cellulitis extending more than 2 cm into the catheter tunnel. Tenderness and erythema along the track of the catheter are prominent. Fever is common, and bacteremia occurs in nearly half of the cases.15
Catheter-related septicemia typically presents with fever, chills, and constitutional symptoms, often following an intravenous infusion or flush through the catheter. In some cases, however, intermittent fever may be the only sign that the catheter lumen is infected.
The patient’s own cutaneous flora represents the major source of contamination. Accordingly, the most common pathogens in catheter-related infections are coagulase-negative staphylococci and Staphylococcus aureus. Coagulase-negative staphylococci are particularly adept at adhering to polymer surfaces, where they encase themselves in a polysaccharide slime that allows them to avoid host defense mechanisms.17 Candida species and enterococci, including vancomycin-resistant strains, are increasingly common causes of bacteremia in patients with catheters.15
The management of catheter-related infections requires two decisions: which antibiotics to use and whether to remove the catheter. In most cases exit site infections can be treated with antibiotics and local care alone without catheter removal. The exceptions are exit site infections with Pseudomonas species and atypical mycobacteria, which do require device explantation. Tunnel and pocket infections, which are usually caused by S. aureus, also require catheter removal, as well as intravenous antibiotics for 10 to 14 days.16,18
Catheter-related septicemia, in contrast, can usually be managed without removing the device.14,17 Coagulase-negative staphylococci, the most common etiologic agents, are rapidly cleared with vancomycin administered for 7 to 10 days through the infected catheter. Many infections with gram-negative bacilli can also be managed with antibiotics given through the catheter, provided that the patient remains hemodynamically stable and blood cultures taken through all catheter lumens are negative 48 hours after the initiation of treatment. Pseudomonas and S. aureus infections are the exceptions and usually require catheter removal in order to clear the bacteremia and avoid recurrence.16
Although catheter removal was once considered essential for bloodstream infections due to Candida species, it appears that uncomplicated catheter-related candidemia can be treated with 10 to 14 days of amphotericin B or fluconazole. High-grade or complicated candidemia or persistence of positive blood cultures after 48 hours of therapy, however, requires that the catheter be removed.16
Urokinase infusions have been studied as an adjunct to antibiotics for treatment of intraluminal infections with the intent to dissolve thrombi that harbor bacteria. In randomized studies, however, urokinase did not improve the outcome.19
Antiseptic and antibiotic impregnated cuffs reduce infections of short-term central venous catheters, but this may not be the case for long-term or tunneled devices.20,21 Prophylactic vancomycin plus heparin flushes have also been shown to decrease rates of gram-positive infections, but this practice is discouraged because of the risk that resistant bacteria will emerge.
The most effective tactic to prevent catheter-related infections is to establish an experienced team devoted to the insertion and maintenance of all catheters within an institution.16
*Neither urokinase nor tissue plasminogen activator has been approved for this purpose by the U.S. Food and Drug Administration at the time of publication.
CHAPTER REFERENCES

1.
Ryder M: Device selection: a critical strategy in the reduction of catheter-related complications. Nutrition 12:143, 1996.

2.
Ng PK, Ault MJ, Ellrodt AG, Maldonado L: Peripherally inserted central catheters in general medicine. Mayo Clin Proc 72:225, 1997.

3.
Horne MK, Mayo DJ, Alexander HR, et al.: Venographic surveillance of tunneled venous access devices in adult oncology patients. Ann Surg Oncol 2:174, 1995.

4.
Mueller BU, Skelton J, Callender DPE, et al.: A prospective randomized trial comparing the infectious and noninfectious complications of an externalized catheter versus a subcutaneously implanted device in cancer patients. J Clin Oncol 10:1943, 1992.

5.
Smith S, Dawson S, Hennessey R, Andrew M: Maintenance of the patency of indwelling central venous catheters: is heparin necessary? Am J Pediatr Hem/Onc 13:141, 1991.

6.
Brismar B, Hardstedt C, Jacobson S: Diagnosis of thrombosis by catheter phlebography after prolonged central venous catheterization. Ann Surg 194:779, 1981.

7.
Horne MK, Mayo DJ: Low-dose urokinase infusions to treat fibrinous obstruction of venous access devices in cancer patients. J Clin Oncol 15:2709, 1997.

8.
Bern MM, Lokich JJ, Wallach SR, et al.: Very low doses of warfarin can prevent thrombosis in central venous catheters. Ann Intern Med 112:423, 1990.

9.
Gould JR, Carloss HW, Skinner WL: Groshong catheter-associated subclavian venous thrombosis. Am J Med 95:419, 1993.

10.
Monreal M, Raventos A, Lerma R, et al.: Pulmonary embolism in patients with upper extremity DVT associated to venous central lines—a prospective study. Thromb Haemost 72:548, 1994.

11.
Becker DM, Philbrick JT, Walker FB: Axillary and subclavian venous thrombosis. Arch Intern Med 151:1934, 1991.

12.
Chang R, Horne MK, Mayo DJ, Doppman JL: Pulse-spray treatment of subclavian and jugular venous thrombosis with recombinant tissue plasminogen activator. JVIR 7:845, 1996.

13.
Monreal M, Alastrue A, Rull M, et al.: Upper extremity deep venous thrombosis in cancer patients with venous access devices—prophylaxis with a low molecular weight heparin (fragmin). Thromb Haemost 75:251, 1996.

14.
Groeger JS, Lucas AB, Thaler HT, et al.: Infectious morbidity associated with long-term use of venous access devices in patients with cancer. Ann Intern Med 119:1168, 1993.

15.
The Hospital Infection Control Panel Advisory Committee: Guideline for prevention of intravascular device-related infections. Am J Infect Control 24:262, 1996.

16.
Raad II, Bodey GP: Infectious complications of indwelling vascular catheters. Clin Infect Dis 15:197, 1992.

17.
Peters G, Locci R, Pulverer G: Adherence and growth of coagulase-negative staphylococci on surfaces of intravenous catheters. J Infect Dis 146:479, 1982.

18.
Newman KA, Reed WP, Schimpff SC, et al.: Hickman catheters in association with intensive cancer chemotherapy. Support Care Cancer 1:92, 1993.

19.
Atkinson JB, Chamberlin K, Boody BA: A prospective randomized trial of urokinase as an adjuvant in the treatment of proven Hickman catheter sepsis. J Pediatr Surg 33:714, 1998.

20.
Veenstra DL, Saint S, Saha S, et al: Efficacy of antiseptic-impregnated catheters in preventing catheter-related bloodstream infection. JAMA 281:261, 1999.

21.
Daroucche RO, Raad II, Heard SO, et al: A comparison of two antimicrobial impregnated central venous catheters. New Engl J Med 340:1, 1999.

22.
Cobos E, Dixon S, Keung Y-K: Prevention and management of central venous catheter thrombosis. Curr Opin Hematol 5:355, 1998.

23.
Sotir MJ, Lewis C, Bisher EW, et al: Epidemiology of device-associated infections related to long-term implantable vascular access device. Inf Cont Hosp Epidemiol 20:187, 1999.
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Copyright © 2001 McGraw-Hill
Ernest Beutler, Marshall A. Lichtman, Barry S. Coller, Thomas J. Kipps, and Uri Seligsohn
Williams Hematology