Dysfunction and Thrombotic Complications of Vascular Access DevicesFrom the General Surgery, Head, Intestinal Rehabilitation Program, Nutrition Support and Vascular Access Department, Cleveland Clinic Foundation, Cleveland, Ohio Correspondence: Ezra Steiger, MD, CNSP, 24959 Letchworth Road, Beachwood, OH 44122. Electronic mail may be sent to steigee{at}ccf.org. Catheter dysfunction occurs frequently in patients receiving home parenteral nutrition (HPN). Catheter-associated thrombosis can be life threatening and limit future vascular sites. Both of these complications can be minimized and treated by proper catheter placement and being aware of preventative and therapeutic measures. Catheter dysfunction is the inability to withdraw blood or freely infuse fluids or both through a vascular access catheter or device. Catheter dysfunction may be due to thrombotic causes such as a blood clot in the lumen of the catheter, or nonthrombotic causes due to mineral precipitates or mechanical causes. Catheter-associated thrombosis, on the other hand, is deep venous thrombosis (DVT) that is associated with presence of a catheter or vascular access device. In this review, common causes of catheter dysfunction and their management and prevention will be presented. Similarly, the etiologies, treatment, and prevention of catheter-related thrombosis will be analyzed. In a recent analysis of over 50,000 patients and 2.8 million catheter-days, the complication rates per 1000 catheter-days were noted by Moureau et al.1 They noted that catheter dysfunction occurred 0.83 times per 1000 catheter-days, and its etiology was nonthrombotic in 0.6 of the 0.83 times per 1000 days and was thrombotic 0.23 times per thousand catheter-days. In this review, the prevalence of catheter dysfunction was greater than catheter-site or bloodstream infections. Further analysis of their data showed a difference in dysfunction outcomes between peripherally inserted central catheters (PICCs), Hickman catheters, and subcutaneous port devices. The incidence of thrombotic and nonthrombotic dysfunction was significantly greater in those patients who had PICC lines in place.
Mechanical complications, rather than an occluding thrombus, probably cause a significant number of dysfunctional catheters.2 Theses include a kinked catheter, a tight retaining suture, inadvertent clamping of the catheter, or catheter pinch-off at the junction of the first rib and clavicle.3 Catheter pinch-off occurs in catheters placed by the percutaneous subclavian vein approach.4 When a catheter is inserted too far medially on the chest wall into the subclavian vein, it will lie in the narrow space between the clavicle and the first rib. Movement of the clavicle against the first rib can compress the catheter in the subclavian vein. When this occurs, the vascular access device intermittently functions, depending on the position of the patient's arm. With the patient's arm elevated, the clavicle is lifted off the first rib and the compression of the catheter is relieved, reestablishing catheter patency. The ability of the patients to restore free flow through the catheter by shrugging their shoulders or elevating their arms should alert one to the possibility of catheter pinch-off occurring. Andris et al5 prospectively studied 1457 tunneled Silastic catheters placed by the percutaneous subclavian vein approach. Pinch-off was identified in 16 patients (1.1%) by x-ray and in 15 of those patients clinically by positional obstruction. Fractured catheters occurred in 3 patients who presented with shoulder pain and clavicular area swelling. Catheter pinch-off can be avoided by inserting the catheter more laterally when using the percutaneous subclavian approach or by using a different access vein, such as the internal jugular vein. When diagnosed, the catheter should be replaced before catheter fracture and distal migration of the catheter tip occur. Catheter occlusion can be due to blood, lipid, or mineral and drug precipitates. Usually, tissue plasminogen activator (tPa) is very effective in lysing thrombus from the tip of the catheter and restoring catheter function. If the patient presents with the history of just having had lipid infusions and develops occlusion, then 70% ethanol might dissolve that lipid occlusion. Medication or calcium phosphorous precipitates can sometimes be dissolved by instilling 0.1-N hydrochloric acid into the catheter lumen. It should be noted that fibrin blockage at the tip of the catheter can be readily dissolved within the first 7 days. However, this thrombus material is gradually converted into fibrous connective tissue that cannot be dissolved by thrombolytic agents after the first week or so.6,7 The "fibrin" sheath around the catheter that interferes with normal functioning is usually not lysed by tPa, but it may be stripped off of the catheter tip by an interventional radiologist with a transfemoral vein stripping device. Even after successful stripping, a recurrent fibrin sheath usually redevelops, necessitating repeated stripping. Merport et al8 published a prospective randomized trial of catheter stripping vs catheter exchange for hemodialysis catheters that had developed decreased flow rates, a form of catheter dysfunction. They noted that catheter exchange rather than stripping allowed for greater patency at 1 and 4 months and was significantly less expensive. For these reasons, it is generally recommended that if sheaths form over the catheter tips that interfere with catheter function, then strong consideration be given to catheter exchange rather than stripping.
Scolapio et al9 noted that of the 20 patients in their series of home parenteral nutrition (HPN) patients who died of HPN causes, 2 deaths (10%) were associated with venous thrombosis. In addition, venous thrombosis may be responsible for loss of vascular access and is a relative indication for considering small-bowel transplantation in HPN patients.10 The frequency of central vein thrombosis is felt to be 0.027 episodes per catheter-year, according to Howard and Ashley.11 The predisposing factors that lead to venous thrombosis were described by Virchow in 1856 and include stasis, altered coagulation, and local trauma. Risk factors for developing DVT include older age, immobility, heart failure, malignancy, estrogen therapy, previous DVT, antithrombin 3 deficiency, protein C deficiency, and protein S deficiency.12 In considering the merits of screening for coagulation disorders, Joffe and Goldhaber noted13 that patients with a family history of DVT, those with recurrent unexplained pregnancy losses, or a personal history of DVT should be screened. They do not, however, believe that routine screening is cost-effective. Additional factors that place the patient at risk for DVT include traumatic catheter insertion, history of a previous central catheter, dehydration, catheter malposition, and catheter size and composition. In a study of 86 consecutive patients with the central venous catheters who developed DVT, Monreal et al14 noted that 13 out of 86 patients developed a pulmonary embolus, and 2 of those patients died. They noted that pulmonary emboli were more common in patients with polyvinyl or polyethylene catheters as opposed to patients who had polyurethane or silicone catheters. Signs and symptoms of catheter-related thrombosis of the upper extremity include swelling of the neck and arm, the appearance of superficial veins on the anterior chest wall on the side of a catheter, tenderness in the axilla when pressing on the axillary vein, and discoloration of the arm even in the absence of marked swelling. Thrombosis of the superior vena cava (SVC) may present as facial and neck swelling and fullness, rhinorrhea, tearing, shortness of breath, sore throat, and chest pain. The diagnosis of DVT in a patient with a vascular access device is usually made by ultrasound or by venography. Fibrinogen assay or the D-dimer test has a high negative predictive value of 97%–99%.15 Magnetic resonance angiography16 has also been used for those patients where the thrombosis is in the central chest area behind bony structures and otherwise difficult to see by ultrasound or conventional angiography. The presence of collateralization on a venogram, even in the absence of being able to delineate the exact site of thrombosis, is diagnostic of a major thrombosis. The treatment options for upper-extremity DVT include the use of heparin, low-molecular-weight heparin, warfarin, systemic thrombolysis, catheter-directed thrombolysis, percutaneous mechanical thrombectomy, surgical thrombectomy, and SVC filter.17 Patients having a stenosed segment of a major central vein may have patency of the vein restored by dilating and stenting the involved venous segment.
Thrombosis prophylaxis in patients with central venous catheters on parenteral nutrition (PN) showed a nonsignificant trend in favor of adding heparin to PN solutions according to 5 randomized prospective studies that were analyzed by Klerk et al.18 In addition, there were no increases in bleeding events noted. In that same review in patients with cancer and a central venous catheter, there were 2 randomized prospective studies that were analyzed to show that 1 mg of warfarin or 2500 international units of low-molecular-weight heparin both showed an important and statistically significant reduction in the incidence of thrombosis and no increase in bleeding events. The position of the vascular access device tip is a risk factor for catheter-related DVT. Luciani et al19 did monthly Doppler ultrasounds on 145 patients with silicon ports and noted that there were 13 instances of asymptomatic thromboses and 4 instances of symptomatic thromboses. Of those patients with a distally placed tip, near the junction of the SVC and right atrium (RA), the incidence of thrombosis was 5.7% vs 46% in patients whose catheter tip was in the upper SVC. In another study, Petersen et al20 noted that the closer the tip location was to the junction of the RA and SVC, the more likely the catheter would function normally. Those catheters that were >6 cm above the junction of the SVC RA had an 87.5% malfunction rate, whereas those catheters that were at or below the junction of the RA SVC had a 2.3% catheter malfunction rate. Cadman et al21 and Laboreve et al22 both noted a higher incidence of venous thrombosis in their patients whose catheter tip was positioned in the upper SVC. A group of patients who developed chest pain on infusion of their PN solution, reported by Passaro et al,23 was noted to have a normal cardiac workup. The only abnormalities noted on their evaluation was a chest x-ray showing tip malposition pointing against the side wall of the SVC. When the catheter tips were repositioned or new catheters placed, the chest pain on infusion disappeared. Symptoms of pain or discomfort associated with infusion through a vascular access device should prompt the clinician to obtain a posterior to anterior (PA) and lateral chest x-ray to rule out catheter malposition. In a systematic review of central venous catheter complications, Ruesch et al24 noted that catheter malposition was less likely to occur when catheters are placed via the internal jugular vein rather than through the subclavian vein.
Maintaining prolonged vascular access is an important part of the success of a HPN program. Preventing, diagnosing, and treating vascular access device malfunction and thrombosis can prolong the life of the vascular access device, and prolong safe vascular access for the patient in need of HPN. Clinicians caring for HPN patients should be aware of these complications and how to prevent, diagnose, and manage them in order to improve the quality and quantity of life receiving HPN. Received for publication March 2, 2005. Accepted for publication October 3, 2005.
Journal of Parenteral and Enteral Nutrition, Vol. 30, No. 1 suppl,
S70-S72 (2006) This article has been cited by other articles:
|
|
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
 |
|
|
 |
|
Top
Vascular Access Device...
Catheter-Related Central Venous...
