Chapter 52: Venous Catheter-Related Thrombosis

Roy E. Smith

INTRODUCTION

Incidence^1,2,3,4,5

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Incidence

Central Venous Catheter (CVCs)

Peripherally Inserted Central Catheters (PICCs)

Symptomatic DVT

1–10%

1–4%

Asymptomatic DVT (documented by venography)

~30%

~20%

Catheter occlusion (without DVT)

~10%

Evaluation^5,6,7

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Evaluation

Differential diagnosis:

Cellulitis
Fluid retention
Local vein compression by tumor

Upper extremity DVT predication score⁸

Parameter Category

Point Designation

Presence of catheter or access device in a subclavian or jugular vein or a pacemaker

Unilateral pitting edema in catheterized extremity

Localized pain in catheterized extremity

Another diagnosis at least as plausible

−1

Probability Category (Prevalence)

Risk Score

Low (9–13%)

−1 or 0

Intermediate (20–38%)

High (64–70%)

Imaging procedures:

Ultrasound: Use for jugular, axillary, and subclavian veins (sensitivity and specificity 80%)
Venography: Use for more central veins including innominate and vena cava, and when high clinical suspicion despite negative ultrasound

Complications of Upper Limp DVT⁵

Pulmonary embolism (PE): The incidence of clinical overt PE is estimated at 12%; the incidence of PE in persons with cancer is higher at 15–25%
Postphlebitic syndrome occurs in ~15%

Risk Factors Associated with Central Venous Catheter-Related Thromboembolism Among Patients with Cancer⁹

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Risk Factors Associated with Central Venous Catheter-Related Thromboembolism Among Patients with Cancer

Technical

Thrombogenicity of catheter material (polyethylene > polyurethane or silicone)

Large catheter diameter and number of lumens

Malpositioned catheter tip

Percutaneous insertion > cut down

More than 1 insertion attempt

Prior CVC insertion

Left-sided placement

Subclavian vein insertion > internal jugular insertion

Patient and Vascular

Catheter-associated infection

Fibrinous catheter lumen occlusion

Extrinsic vascular compression (enlarged cervical and/or mediastinal lymph nodes, etc)

Factor V Leiden mutation (and perhaps other thrombophilias)

Prior venous thromboembolism

Ovarian cancer

Treatment-Related

Asparaginase

Estrogens and/or progesterone

Growth factors (ie, epoetin, GM-CSFs, G-CSFs)

Aldesleukin (IL-2)

Thalidomide

Lenalidomide

Heparin-induced thrombocytopenia and thrombosis (HIT, HITT)

Chemical irritation

Treatment of Catheter-Related Venous Thrombosis^10,11,12,13

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Treatment of Catheter-Related Venous Thrombosis

If a CVC is functioning and does not appear to be infected, there is no imperative to remove it
If CVC removal is planned, consider full anticoagulation with unfractionated or low-molecular-weight heparin for 5–7 days prior to removal to reduce the risk embolization with device extraction
Clinicians should keep in mind patients with active malignancy may require prolonged anticoagulation after catheter removal should it be determined that the event occurred independent of the presence of CVC (eg, an additional thrombotic event distant to catheter site)
Catheter-related thrombosis occurring in patients with HIT/HITT is a special circumstance. These patients should receive a direct thrombin inhibitor or fondaparinux for acute anticoagulation with a transition to warfarin or fondaparinux for a total of 3 months of anticoagulation, or for as long as a catheter remains in place

Acute Care

Subacute Care

CVC-related DVT; restoring patency is not imperative

Standard doses of unfractionated heparin:

Loading dose: 80 units/kg by IV injection

Maintenance dose: 18 units/kg per hour by continuous IV infusion for 5–7 days, or

a low-molecular-weight heparin (LMWH) enoxaparin 1 mg/kg subcutaneously every 12 hours for a total of 5–7 days, or An alternative LMWH

Warfarin orally to maintain an INR of 2–3 for a total duration of anticoagulation of 3 months, or for as long as the catheter is in place, or

(a LMWH) Enoxaparin 1 mg/kg subcutaneously once daily for a total duration of 3 months, or for as long as the catheter is in place

CVC-related DVT; restoring patency is imperative

Alteplase (tPA) by direct injection into a clot under fluoroscopic guidance, or
Urokinase by direct injection into a clot under fluoroscopic guidance
Standard doses of unfractionated heparin

Loading dose: 80 units/kg by IV injection

Maintenance dose: 18 units/kg per hour by continuous IV infusion for 5–7 days, or

Enoxaparin 1 mg/kg subcutaneously every 12 hours for a total of 5–7 days, or

An alternative LMWH

Warfarin orally to maintain an INR of 2–3 for 3 months, or

Enoxaparin 1 mg/kg subcutaneously once daily (or an alternative LMWH) for 3 months

SVC thrombosis

Alteplase by direct injection into a clot under fluoroscopic guidance
Urokinase by direct injection into a clot under fluoroscopic guidance
Standard doses of unfractionated heparin

Loading dose: 80 units/kg Maintenance dose: 18 units/kg per hour for 5–7 days, or

Enoxaparin 1 mg/kg subcutaneously every 12 hours for a total of 5–7 days, or

An alternative LMWH

Warfarin orally to maintain an INR of 2–3 for 3 months, or

Enoxaparin 1 mg/kg subcutaneously once daily (or an alternative LMWH) for 3 months

Internal jugular vein thrombosis

Apply heat topically
Systemic antiinflammatory agents
If symptoms are severe or progressive, standard doses of unfractionated heparin

Loading dose: 80 units/kg

Maintenance dose: 18 units/kg per hour for 5–7 days, or

Enoxaparin 1 mg/kg subcutaneously every 12 hours for a total of 5–7 days, or An alternative LMWH

If treatment with heparin is required then

Warfarin orally to maintain an INR of 2–3 for 3 months, or

Enoxaparin 1 mg/kg subcutaneously once daily (or an alternative LMWH) for 3 months

Peripheral vein thrombophlebitis

Apply heat topically
Oral and/or topical antiinflammatory agents
VAD removal is almost always indicated

Patients at risk for the development of deep vein thrombosis (superficial phlebitis close to a deep vein or the presence thrombophilia) and patients with proximal basilic or cephalic thrombosis who remain symptomatic

Full-dose anticoagulation can be considered
The duration of anticoagulation should be individualized based upon the risk of bleeding and improvement in symptoms

IV, intravenous; VAD, vascular access device

^✫Urokinase is not available in the United States

Prevention of Catheter-Related Venous Thrombosis^{3,14,15,16,17,18}

Randomized controlled studies have not established the efficacy of prophylaxis with low-molecular-weight heparin or low-dose warfarin (1 mg/day). The 8th Annual American College of Chest Physicians Practice Guidelines for Antithrombotic and Thrombolytic Therapy do not recommend the use of prophylactic anticoagulation in this setting
If used, it is likely that therapeutic or near-therapeutic levels of anticoagulation and close monitoring will be required for the successful prevention of catheter-associated incident thrombosis and reduction of bleeding risk
When considering pharmacologic prophylaxis, clinicians must take into consideration an individual patient's risk for developing catheter-related thrombosis. Some experts have suggested that thromboprophylaxis should be considered for patients believed to be at high risk

Notes

Common Venous Access Devices¹⁹

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Design

Use

Duration of Use

Routine Flush^†

Blood Draw

IV Fluid

Blood Product^✫

Tunneled

Open-ended (eg, Hickman)

+ + + +

Weeks to years

Daily

Valved^‡ (eg, Groshong)

+ + + +

Weeks to years

Weekly

Ports (open or valved end)

+ + + +

Months to years

Monthly

Nontunneled

Peripheral (PICC, open or valved)

+ + + +

<3 months

Daily or weekly

Midline

+ + + +

<6 weeks

Daily

Central

+ + + +

<3 months

Daily

^✫The ability to administer packed red blood cells depends on the internal diameter of a catheter lumen

^†Either unfractionated heparin or 0.9% sodium chloride injection may be used. Heparin is contraindicated in patients with a history of heparin allergy or heparin-induced thrombocytopenia

^‡Valved catheters reduce or eliminate the need for heparinization and the risk of air embolism and blood reflux

Contraindications for the Placement of Central Venous Access Devices²⁰

Absolute:

An uncooperative patient
Availability of appropriate alternative peripheral insertion site
Significant coagulopathy in a stable patient
Obstruction of target vein (eg, venous thrombosis, anatomical defect, external compression)

Relative:

Infection or burn at insertion site
Sepsis (unless blood cultures were deemed sterile during prior 36–48 hours)
Significant coagulopathy in an unstable patient
Decreased platelet count associated with an increased bleeding risk (ie, platelets <50,000/mm³)

Incidence of Complications of Venous Access Devices²¹

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Arrhythmia

13%

Arterial puncture

2.8–3.8%

Inappropriately positioned reservoir

Pneumothorax

1–1.8%

Wound dehiscence

1.5%

Hemorrhage

1.1–1.2%

Failure of insertion

1.2%

Optimal Catheter Placement

The catheter tip should be in the mid-superior vena cava, just outside the right atrium. Opinions differ about the risks and benefits of placing the tip within the right atrium

Management of Catheter Tip occlusion with a Fibrin Sheath^{4,22,23,24,25}

Mechanism:

Accumulation of a fibrin coating (sheath) at the tip of a catheter, forming a one-way valve that blocks withdrawal from the CVC but allows infusion

Differential diagnosis:

Catheter migration out of the superior vena cava into a smaller vein where it abuts the vein wall more easily
Perpendicular abutment of the catheter tip against the wall of the superior vena cava
Catheter compression by kinking or a suture
Catheter lumen occlusion with precipitated salts or lipid

Evaluation:

Reposition the patient to relieve a reversible malposition of the catheter tip
Obtain chest x-ray to identify catheter tip location
Inject x-ray contrast material through the occluded lumens to identify pericatheter backtracking indicative of a fibrin sheath, and to rule out an extensive fibrin sheath that could lead to extravasation of infused fluids

Treatment:

If an occlusive fibrin sheath is identified but there is no evidence that infused fluid will extravasate, the catheter can be used for infusion
To restore the ability to withdraw (aspirate) fluid through a catheter: Instill alteplase 2 mg (2 mL of a 1-mg/mL solution) (Cathflo Activase, Genentech, Inc., South San Francisco, CA) into each occluded lumen and allow it to dwell for 2 hours. If this does not restore lumen patency, the same alteplase treatment may be repeated once
If available, urokinase offers another alternative. Doses ranging from 5000 units in each affected lumen with a dwell time of 15–60 minutes, which may be repeated for a second instillation if patency was not restored after a single instillation. Urokinase 10,000-unit boluses up to 2 times have been successful. Also, for refractory occlusions, slow infusions of urokinase (diluted to 5000 units/mL) 40,000 units (8 mL)/hour for 6–12 hours may restore function^26,27,28,29

REFERENCES

Chemaly RF et al. Venous thrombosis associated with peripherally inserted central catheters: a retrospective analysis of the Cleveland Clinic experience. Clin Infect Dis 2002;34:1179–1183 [PubMed: 11941543]

Horne MK et al. Venographic surveillance of tunneled venous access devices in adult oncology patients. Ann Surg Oncol 1995;2:174–178 [PubMed: 7728573]

Kuriakose P et al. Risk of deep venous thrombosis associated with chest versus arm central venous subcutaneous port catheters: a 5-year single-institution retrospective study. J Vasc Interv Radiol 2002;13:179–184 [PubMed: 11830624]

Stephens LC et al. Are clinical signs accurate indicators of the cause of central venous catheter occlusion? JPEN J Parenter Enteral Nutr 1995;19:75–79 [PubMed: 7658605]

Verso M et al. Venous thromboembolism associated with long-term use of central venous catheters in cancer patients. J Clin Oncol 2003;21:3665–3675 [PubMed: 14512399]

Baarslag HJ et al. Prospective study of color duplex ultrasonography compared with contrast venography in patients suspected of having deep venous thrombosis of the upper extremities. Ann Intern Med 2002;136:865–872

Haire WD et al. Limitations of magnetic resonance imaging and ultrasound-directed (duplex) scanning in the diagnosis of subclavian vein thrombosis. J Vasc Surg 1991;13:391–397

Constans J et al. A clinical prediction score for upper extremity deep venous thrombosis. Thromb Haemost 2008;99:202–207

Linenberger ML. Catheter-related thrombosis: risks, diagnosis, and management. J Natl Compr Canc Netw 2006;4:889–901 [PubMed: 17020667]

10.

Becker DM et al. Axillary and subclavian venous thrombosis. Prognosis and treatment. Arch Intern Med 1991;151:1934–1943 [PubMed: 1929680]

11.

Chang R, Horne MK 3rd, Mayo DJ, Doppman JL. Pulse-spray treatment of subclavian and jugular venous thrombi with recombinant tissue plasminogen activator. J Vasc Interv Radiol 1996;7:845–851 [PubMed: 8951751]

12.

Gould JR et al. Groshong catheter-associated subclavian venous thrombosis. Am J Med 1993;95:419–423 [PubMed: 8213875]

13.

Mayo DJ et al. Superior vena cava thrombosis associated with a central venous access device: a case report. Clin J Oncol Nurs 1997;1:5–10 [PubMed: 9410647]

14.

Agnelli G, Verso M. Is antithrombotic prophylaxis required in cancer patients with central venous catheters? No. J Thromb Haemost 2006;4:14–15

15.

Bern MM et al. Very low doses of warfarin can prevent thrombosis in central venous catheters. A randomized prospective trial. Ann Intern Med 1990;112:423–428 [PubMed: 2178534]

16.

Cunningham MS et al. Primary thromboprophylaxis for cancer patients with central venous catheters–a reappraisal of the evidence. Br J Cancer 2006;94:189–194 [PubMed: 16404436]

17.

Hirsh J et al. American College of Chest P: Antithrombotic and thrombolytic therapy: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th edition). Chest 2008;133:110S–112S [PubMed: 18574260]

18.

Monreal 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 1996;75:251–253 [PubMed: 8815570]

19.

Horne MK, Mayo DJ, Freifeld AG. In: Beutler E, Lichtman MA, Coller BS, Kipps TJ, Seligsohn U, eds. Williams Hematology, 6th ed. New York: McGraw-Hill, 2001:887–898

20.

Bishop L et al. Guidelines on the insertion and management of central venous access devices in adults. Int J Lab Hematol 2007;29:261–278 [PubMed: 17617077]

21.

Kuter DJ. Thrombotic complications of central venous catheters in cancer patients. Oncologist 2004;9:207–216 [PubMed: 15047925]

22.

Crain MR et al. Fibrin sheaths complicating central venous catheters. AJR Am J Roentgenol 1998;171:341–346 [PubMed: 9694448]

23.

Mayo DJ et al. Chemotherapy extravasation: a consequence of fibrin sheath formation around venous access devices. Oncol Nurs Forum 1995;22:675–680 [PubMed: 7675669]

24.

Semba CP et al. Treatment of occluded central venous catheters with alteplase: results in 1,064 patients. J Vasc Interv Radiol 2002;13:1199–1205 [PubMed: 12471182]

25.

Tschirhart JM, Rao MK. Mechanism and management of persistent withdrawal occlusion. Am Surg 1988;54:326–328 [PubMed: 3377325]

26.

Haire WD et al. Urokinase versus recombinant tissue plasminogen activator in thrombosed central venous catheters: a double-blinded, randomized trial. Thromb Haemost 1994;72:543–547 [PubMed: 7878629]

27.

Haire WD et al. Recombinant urokinase for restoration of patency in occluded central venous access devices. A double-blind, placebo-controlled trial. Thromb Haemost 2004;92:575–582 [PubMed: 15351854]

28.

Haire WD, Lieberman RP. Thrombosed central venous catheters: restoring function with 6-hour urokinase infusion after failure of bolus urokinase. JPEN J Parenter Enteral Nutr 1992;16:129–132 [PubMed: 1556806]

29.

Monturo CA et al. Efficacy of thrombolytic therapy for occlusion of long-term catheters. JPEN J Parenter Enteral Nutr 1990;14:312–314 [PubMed: 2112649]

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Chapter 52: Venous Catheter-Related Thrombosis

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Updated chapter to come.

INTRODUCTION

Notes

REFERENCES

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