Long
Term Central Venous Catheters: Issues for Care
Rita Wickham, MS, RN; Sandra Purl,
MS, RN; and Diane Welker MS, RN
From the College of Nursing and Section of Medical
Oncology, Rush Presbyterian St. Luke's Medical Center,
Chicago, IL; and Harley Medical Center, Flint, MI.
Seminars in Oncology Nursing l996;8,2(May):133-147.
Long-term central venous catheters (hereafter referred
to as catheters) have become a fact of life for a
significant number of persons with cancer and for their
caregivers. The placement of a catheter in most instances
allows the safe administration of chemotherapy, blood and
blood products, total parenteral nutrition (TPN), fluids,
and other medications. The use of central venous
catheters has led to increased patient comfort as well as
enhanced therapeutic options such as continuous
intravenous (IV) infusions of vesicant agents and
ambulatory continuous IV therapy. Despite their benefits,
at least 10% of patients will experience problems
secondary to catheter placement and/or use.1
Although the risk of certain complications, may be
greater with one type of device over another, some risk
exists for every person who has a catheter. Thus, the
health care team must practice preventative measures,
recognize early signs and symptoms of complications and
provide adequate care should complications occur. This
article will focus on the major catheter complications
including fibrin sleeve and mural thrombus formation,
infection, catheter occlusion, extravasation, and
catheter malposition, and will examine current
recommendations for their management, particularly as it
relates to the nurse's role.
Top
Overview of Long-Term Central Venous Catheter
Three general types of long-term catheters are
available: nontunneled, tunneled, and implanted ports. Table 1 depicts different types of
catheters and specific features.2-5
All catheters have a radiopaque strip so they can be
visualized on chest radiograph or fluoroscope after
placement to document the position of the catheter tip.
The optimal catheter tip location is in the superior vena
cava (SVC) at or above the junction of the right atriums.6
Top
Extraluminal Catheter Occlusion
Extraluminal occlusion involves either fibrin sleeve
or thrombus formation, which may present similar clinical
findings but are entirely different processes.
Fibrin Sleeve
Fibrin sleeves, which do not adhere to the venous
intima beyond their point of origin or to the catheter
surface, develop in the majority of silicone catheters in
as little as 48 hours or up to several months after
placement.7 8
The sleeve originates at the point of venous entry and
forms as a consequence of exposure of the catheter
surface to blood. Platelets and fibrin are deposited
along the catheter in a tubelike fashion and over time
extend to the distal catheter tip and even beyond it.
Once the sleeve extends beyond the catheter tip,
withdrawal occlusion may occur, in which the catheter can
be easily flushed but blood cannot be aspirated.
Instructing the patient to change positions or to perform
the Valsalva maneuver may allow blood to be withdrawn.
Administering 5,000 to 10,000 units of urokinase through
the catheter and allowing it to dwell within the device
for more than 1 hour more reliably lyses the sleeve to
restore blood sampling capability.9
l0 Lack of blood return in
and of itself does not mean a catheter cannot be used for
infusions unless withdrawal occlusion results from other
complications (i.e., catheter occlusion or displacement).
Thrombus Formation
Catheter-induced thrombosis is most likely
multifactorial. Catheterization itself causes endothelial
injury of the vessel wall from the catheter tip,
catheter, or introducer during cannulation.ll
12 This injury induces the
release of thromboplastic substances and causes platelets
to aggregate at the site of injury. The initial damage
may progress to small thrombi that arise from and adhere
firmly to the vessel wall (mural thrombi), and ultimately
to large veno-occlusive thrombi, which may propagate
retrograde and/or antegrade into the superior and/or
inferior vena cava and/or right atrium.l3
Although stiff catheters (i.e., polyvinyl chloride) are
most likely to damage the venous intima, polyurethane and
silicone catheters are also implicated in thrombosis.l4 Larger bore catheters are
associated with a greater risk for thrombosis as is
catheterization from the left side.l6
The catheter within the vein alters laminar blood flow
and maximizes contact of blood cells with the venous
intima, inducing a cycle of the release of thromboplastic
substances and platelet aggregation at the basement
membrane of the damaged areas.l5
l7 l8
Normally, the body's fibrinolytic system becomes
activated to lyse the clot, but this requires an intact
intima. Other factors, such as sclerosing chemotherapy
agents, venous compression by mediastinal tumor, or
bacterial colonization may initiate or aggravate this
process.l8-22
Hypercoagulability, associated with malignancies
including mucin-secreting adenocarcinomas of the lung,
gastrointestinal tract, pancreas and ovary, promyelocytic
leukemia, and myeloproliferative disorders could also
exacerbate thrombosis.l7 23
Patients with adenocarcinomas experience a higher rate
of catheter related thrombi than do those with squamous
cell tumors.l9
Signs and symptoms of thrombosis. Rates of
thrombosis of 3.7% to 10% have been documented.24 25
Signs and symptoms of thrombosis may be subtle and
delayed until complete occlusion of the vein occurs.13 l6
24 Physical findings relate
to impeded venous return and may include edema of the
neck, chest, or affected extremity as well as prominent
superficial collateral veins on the ipsilateral chest (Fig. 1).26
Mild to moderate neck pain that may radiate down the arm
or to the back, numbness and tingling of the ipsilateral
extremity, skin temperature changes, or skin
discoloration are later symptoms. Diagnosis is usually
made when the patient has symptoms of complete occlusion,
that is facial swelling, neck vein distention, and
infusional difficulties.27
Nurses should document and communicate progressive
symptoms, as lytic therapy is more likely to be
successful if initiated early before calcification of the
clot occurs.15
Thrombus location is usually confirmed by venogram
through the catheter as well as through an ipsilateral
peripheral vein.23 28 Duplex venous scans, doppler
ultrasonography, and computed tomography (CT) have been
used to visualize thrombi.29
30
Management of extraluminal thrombus. Management
depends on the severity of the symptoms, the need for the
catheter, and other associated complications (i.e.,
infected thrombus). Studies have confirmed that low-dose
warfarin (1 mg/day) can significantly reduce the rate of
thrombus development without causing bleeding states.3l 32
However, therapy is more commonly initiated when symptoms
of occlusive thrombus occur.
Symptomatic catheter-related thrombi are treated with
anticoagulants, thrombolytic agents, and rarely surgical
removal of the thrombus.30
Although some clinicians recommend removing the catheter
before anticoagulant therapy, this decision depends on
the severity of symptoms, the availability of peripheral
access, risk for pulmonary emboli, and previous history
of thrombosis.33
Heparin prevents further propagation of the thrombus
and allows the formation of venous collaterals.15 Continuous IV thrombolytic
therapy, either streptokinase or urokinase, has
successfully lysed extraluminal thrombi in some cases.34 35
There are no standard doses or methods of administering
fibrinolytic therapy. Fraschini et al35
recommend treating catheter tip thrombi directly with an
infusion through the device and mural thrombi by
peripheral infusion, using a vein as close to the
thrombus as possible.
Streptokinase and urokinase activate the fibrinolytic
system, so they can potentially induce hemorrhage.25 Nursing management thus
includes identification of high-risk patients who would
probably not receive this therapy, including those who
have active internal bleeding, a recent history of
cerebral vascular accident, intracranial or intraspinal
surgery, or blood dyscrasias.36
Urokinase is derived from human kidney cells and
streptokinase from bacteria. Streptokinase is much less
expensive than urokinase but is more antigenic, and in
rare instances causes fever, urticaria, nausea and
vomiting, headache, and flushing.37
38 Patients receiving
streptokinase are pretreated with acetaminophen,
diphenhydramine, and hydrocortisone to minimize side
effects. The only laboratory value that relates to
bleeding complications in patients receiving fibrinolytic
therapy is serum fibrinogen, which is maintained at 80 to
100 mg/dL by titration of the fibrinolytic agent.35
Fig 1.
Physical findings of venous thrombosis include enhanced
superficial collateral veins on the ipsilateral chest
wall.
Table 1. Overview of Catheter
Features
|
| Catheter Type |
Catheter Materials |
Number of Lumens |
Lumen Sizes |
Comments/ Distinguishing Features |
|
| Nontunneled catheter Centrasil
(Baxter, Deerfield, IL)
C-PICS (Cook, Bloomington, IN)
Per-Q-Cath (Gesco, San Antonio, TX )
|
Silicone
Silicone elastomer
Polyurethane |
Single
Double
Triple |
23 gauge to 16 gauge (ID) |
Available as centrally inserted
subclavian lines and peripherally inserted PICC
models (exit at antecubital space). These
catheters are generally inserted into a vein <1 inch from exit site. |
|
| Tunneled catheter Hickman
Broviac (Davol/Bard, Salt Lake City, UT)
Reaf (Quinton, Seattle, WA)
Groshong (Davol/Bard)
|
Silicone |
Single
Double
Triple |
1.0-3.2 mm (OD)
0.6-1.5 mm (ID) |
Tunneled for several inches
beneath skim from exit site to vein. Usually exit
between nipple and sternum (catheters inserted
into the IVC exit in the lower abdomen or groin).
All have a dacron cuff 1 to 2 inches proximal to
exit site to secure catheter and minimize risk of
infection. |
|
| Implanted Port Port-A-Cath
(Pharmacia Deltec, St. Paul, MN)
Infuse-A-Port (Strato, Beverly, MA)
S.E.A. Port (Harbor Medical, Jaffrey, NH)
OmegaPort (Norfolk Medical, Skokie, IL)
P.A.S. Port (Pharmacia Deltec)
|
Silicone
Polyurethane |
Single
Double |
1.5-4.6 mm (OD)
1.0-1.6 mm (ID) |
Silicone septum enclosed in
plastic, stainless steel, or titanium port.
Available for top, side or all direction access.
Central and peripheral models available. Accessed
with deflected tip (Huber) needles to prevent
coring with subsequent leaking. |
|
Abbreviations: OD, outer diameter; ID, inner diameter;
IVC, inferior vena cava; PICC percutaneously inserted
central catheter.
Top
Acknowledgement
The authors acknowledge the generous educational grant
from Pharmacia Deltec that made the printing of the color
prints possible.
[NOTE: The balance of this article will be reprinted
in a future issue of Meditheses.]
Reprinted by permission of Seminars in Oncology
Nursing.
References
- Collins JL: Central venous
catheter complications. Oncol Nurs Forum
18:819-820, 1991 (letter)
- Camp-Sorrell D: Advanced central
venous access. Selection, catheters, devices, and
nursing management. J Intravenous Nurs
13:361-370, 1990
- Winters V, Peters B, Coila S, et
al: A trial with a new peripherally implanted
vascular access device. Oncol Nurs Forum
17:891-896, 1990
- Masoorli S. Angeles T: PICC
lines: The latest home care challenge. RN
53(1):44-50, 1990
- Goodman MS, Wickham R: Venous
access devices: An overview. Oncol Nurs Forum
11(5):16-23, 1984
- Reed WP, Newman KA, de Jongh C:
Prolonged venous access for chemotherapy by means
of the Hickman catheter. Cancer 52:185-192, 1983
- Brismar B. Hardstedt C, Jacobson
S: Diagnosis of thrombosis by catheter
phlebography after prolonged central venous
catheterization. Ann Surg 194:779-783, 1981
- Williams EC: Catheter-related
thrombosis: Clin Cardiol 13:V134-V136, 1990
- Petersen FB, Clift RA, Hickman
RO, et al: Hickman catheter complications in
marrow transplant recipients. JPEN 10:58-62, 1986
- Schneider TC, Krzywda E, Andris
D, et al: The malfunctioning silastic
catheter-radiologic assessment and treatment.
JPEN 10:70-73, 1986
- Ahmed N. Payne RF: Thrombosis
after central venous cannulation. Med J Aust
1:217-220, 1976
- Cervera M, Dolz M, Herraez JV,
et al: Evaluation of the elastic behaviour of
central venous PVC, polyurethane and silicone
catheters. Phys Med Biol 34:177-183, 1989
- Reed WP, Newman KA, Tenney JH,
et al: Autopsy findings after prolonged
catheterization of the right atrium for
chemotherapy in acute leukemia. Surg Gynecol
Obstet 160:417-420,1985
- Hadaway LC: Evaluation and use
of advanced IV technology. Part 1: Central venous
access devices. J Intravenous Nurs 12:73-83, 1989
- Horattas MC, Wright DJ, Fenton
AH, et al: Changing concepts of deep venous
thrombosis of the upper extremity-report of a
series and review of the literature. Surgery
104:561-567, 1988
- Brown-Smith JK, Stoner MH,
Barley ZA: Tunneled catheter thrombosis: Factors
related to incidence. Oncol Nurs Forum
17:543-549,1990
- Luzzatto G, Schafer Al: The
prethrombotic state in cancer. Semin Oncol
17:147-159, 1990
- Donayre CE, White GH, Mehringer
SM, et al: Pathogenesis determines late morbidity
of axillosubclavian vein thrombosis. Am J Surg
152:179-184,1986
- Anderson AJ, Krasnow SH, Boyer
MW, et al: Thrombosis: The major Hickman catheter
complication in patients with solid tumor. Chest
95:71-75, 1989
- Pithie A, Soutar JS, Pennington
CR: Catheter tip position in central vein
thrombosis. JPEN 12:613-614, 1988 (brief
communication)
- Slagle DC, Gates RH: Unusual
case of central vein thrombosis and sepsis. Am J
Med 81:351-354, 1986
- Levine MN, Gent M, Hirsh J. et
al: The thrombogenic effect of anticancer drug
therapy in women with stage II breast cancer. N
Engl J Med 318:404-407, 1988
- Lokich JJ, Becker B: Subclavian
vein thrombosis in patients treated with infusion
chemotherapy for advanced malignancy. Cancer
52:1586-1589,1983
- Moss JF, Wagman LD, Riihimaki
DU, et al: Central venous thrombosis related to
the silastic Hickman-Broviac catheter in an
oncologic population. J Parenter Enteral Nutr
13:397-400, 1989
- Gray WJ, Bell WR: Fibrinolytic
agents in the treatment of thrombotic disorders.
Semin Oncol 17:228-237, 1990
- Lokich JJ, Bothe A, Benotti P.
et al: Complications and management of implanted
venous access catheters. J. Clin Oncol 3:710-717,
1985
- Beers TR, Burnes J, Fleming CR:
Superior vena caval obstruction in patients with
gut failure receiving home parenteral nutrition.
JPEN 14:474-479, 1990
- Haire WD, Lieberman RP, Edney
J, et al: Hickman catheter-induced thoracic vein
thrombosis. Cancer 66:900-908, 1990
- Kaufman J, Demas C, Stark K, et
al: Catheter-related septic central venous
thrombosis-current therapeutic options. West J
Med 145:200-203, 1986
- Levine M, Hirsh J: The
diagnosis and treatment of thrombosis in the
cancer patient. Semin Oncol 17:160-171, 1990
- Bern MM, Bothe A, Bistrian B.
et al: Prophylaxis against central venous
thrombosis with low-dose warfarin. Surgery
99:216-221, 1986
- Bern MM, Lokich JJ, Wallach SR,
et al: Very low doses of warfarin can prevent
thrombosis in central venous catheters. Ann
Intern Med 112:423-428, 1990
- Hill SL, Berry RE: Subclavian
vein thrombosis: A continuing challenge. Surgery
108:1-9, 1990
- Smith NL, Ravo B, Soroff HS, et
al: Successful fibrinolytic therapy for superior
vena cava thrombosis secondary to long-term total
parenteral nutrition. JPEN 9:55-57, 1985
- Fraschini G, Jadeja J, Lawson
M, et al: Local infusion of urokinase for the
lysis of thrombosis associated with permanent
central venous catheters in cancer patients. J
Clin Oncol 5:672-678, 1987
- Donovan BC: How to give
thrombolytic therapy safely. Chest 95:290S-292S,
1989
- Marder VJ: The use of
thrombolytic agents: Choice of patient, drug
administration, laboratory monitoring. Ann Intern
Med 90:802-808, 1979
- Kessler CM: Anticoagulation and
thrombolytic therapy. Practical consideration.
Chest 95:245S-255S, 1989
|