Complications
During LTCVA Device Insertion
Complications during LTCVA device placement are generally related to the method of insertion and the experience of the operator.
Pneumothorax
Pneumothorax is the most common complication of the percutaneous insertion technique, especially via the subclavian vein approach. The incidence of pneumothorax has been reported in most series to be approximately 1% to 5%. It appears to be seen more frequently in nutritionally compromised and emaciated patients. Its incidence has also been thought to be related to the number of attempts required to access the vein and to the experience of the operator. Use of venous ultrasound to guide placement of the venipuncture needle into the initial point of entry of the subclavian vein or the internal jugular vein during the percutaneous venipuncture approach may reduce the risk of pneumothorax. A venous cutdown approach eliminates the risk of pneumothorax.
Pneumothorax is usually recognized on a post-procedural upright chest x-ray. The ability to detect a small pneumothorax on a chest x-ray can be aided by performing an expiratory film. Delayed pneumothorax can develop several hours to several days after an attempted percutaneous venipuncture approach to LTCVA device placement. If the pneumothorax is small (< 5%), the patient can be followed with subsequent chest x-rays, and the air occupying the pneumothorax can be left in place to be physiologically reabsorbed. Use of 100% oxygen can aid in reabsorption of a pneumothorax. Patients with a larger pneumothorax are generally treated by placement of a chest tube that is connected to a closed suction system or a Heimlich valve (one-way valve).
Iatrogenic arterial puncture
Iatrogenic arterial puncture occurs most frequently with the percutaneous internal jugular vein approach and less frequently with the percutaneous subclavian vein approach. Pulsatile flow confirms an arterial puncture. In this instance, the venipuncture needle should be removed and the vessel compressed for 5 to 10 minutes. If an arterial puncture is initially unrecognized and the guidewire is passed into the vessel, a position of the guidewire to the left of the thoracic spine on fluoroscopy should alert the operator to the suspicion of the occurrence of this complication. In a patient with a persistent left superior vena cava, the guidewire will also be seen to the left of the thoracic spine on fluoroscopy. Standard contrast venography performed at the time of attempted LTCVA device placement can be very helpful to confirm this diagnosis.
Hemothorax as a result of injury to major vessels
Hemothorax as a result of injury to major vessels is seen less than 1% of the time, but when it occurs it can be life-threatening. During the percutaneous venipuncture approach, injury to one of the major vessels with the venipuncture needle, guidewire, or dilator and peel-away introducer sheath may result in a hemothorax. Careful attention to insertion technique, the use of fluoroscopy, and the selective use of standard contrast venography can all help to prevent this complication. Use of a venous cutdown approach is much less likely to injure a major vessel than is a percutaneous venipuncture approach.
Most patients who develop a hemothorax can be treated with a large-bore, laterally placed chest tube connected to a closed suction system. Many of these closed suction systems have a blood re-infusion collecting system. Thoracotomy may be indicated in certain circumstances (in patients with ongoing bleeding [> 500 mL/hour] or with a massive hemothorax [> 1,500 mL]).
Local subcutaneous hematomas
Local subcutaneous hematomas can occur more frequently in thrombocytopenic patients or coagulopathic patients. They are best treated by local compression over the area of the subcutaneous hematoma. Adequate replacement of platelets and clotting factors prior to LTCVA device placement can help to prevent these complications.
Catheter tip malposition
Catheter tip malposition is usually recognized and corrected at the time of catheter placement by the use of peri-procedural fluoroscopy. However, under fluoroscopy catheters situated in the azygos vein or the right internal mammary vein can look strikingly similar to catheters situated in the superior vena cava in an anterior-posterior projection. Frequently, these catheters do not withdraw blood easily and the catheter tip does not move with the cardiac rhythm. Lateral rotation of the fluoroscope and utilization of standard contrast venography during LTCVA catheter placement can help to differentiate this sometimes subtle finding.
Other Device-Related Complications
Catheter compression, fracture, and embolization
Catheter compression, fracture, and embolization can occur when a central venous catheter placed by the percutaneous subclavian vein approach is inserted too medially along the clavicle at the medial costoclavicular ligament. In such cases, the catheter may become chronically compressed between the clavicle and the first rib. This can be recognized radiographically as a "pinch-off sign." Chronic compression of the catheter may result in structural fatigue of the catheter wall that may eventually cause fracturing and distal embolization of the central venous catheter. This can be prevented by ensuring that the percutaneous venipuncture site is selected more laterally on the clavicle, as well as 1 cm to 2 cm below the clavicle. If this problem is recognized during central venous catheter placement, the catheter should be removed and then replaced through a different percutaneous venipuncture site.
Device malfunction
Device malfunction can be divided into two types: (1) inability to withdraw blood from a LTCVA device; and (2) inability to infuse into a LTCVA device. Inability to withdraw blood from a device, despite retaining the ability to infuse into the device, is most frequently caused by a fibrin sheath at the tip of the catheter that produces a one-way valve effect. Less frequently, it is due to a catheter tip being positioned against the side wall of the venous structure within which it resides. In patients with this problem, a Valsalva maneuver or repositioning of the patient (eg, lying supine vs lying lateral decubitus vs sitting upright) can sometimes result in successful blood withdrawal.
Inability both to withdraw blood from and to infuse into a LTCVA device can have many mechanical causes, such as catheter tip malposition, catheter kinking, catheter lumen thrombosis, intraluminal precipitation of medications, or venous thrombosis. A chest x-ray may identify some of these mechanical causes. Standard contrast venography, venous duplex Doppler ultrasonography, and CT and MR venography can all potentially be useful for evaluating a patient with this problem.
Thrombolytic therapy, using tissue plasminogen activator (tPA) or alteplase(Drug information on alteplase) (recombinant tPA), can help to restore the ability to withdraw blood from a device or to clear a device from intraluminal thrombosis or intraluminal precipitation of medications. Usually, 1 mg to 2 mg of tPA in 1 mL to 2 mL of sterile water is instilled into the device, left in place for 1 to 2 hours, and then aspirated. Alternatively, 2.5 mL aliquots (diluted to 1 mg/mL) of alteplase can be used in a similar fashion. This may be repeated daily for several days until total patency is restored. Likewise, chemical occlusion of a device resulting from precipitation of chemotherapeutic agents, poorly soluble salts (calcium, magnesium, or phosphates), or antibiotics (amikacin [Amikin], vancomycin(Drug information on vancomycin)) can be successfully treated with instillation of 0.2 mL to 1 mL of 0.1 N hydrochloric acid. The solution is irrigated in and out of the device for 2 minutes, left in place for 1 hour, and then aspirated. This may be repeated daily for several days until total patency is restored. Hydrochloric acid at these doses has not been associated with side effects or metabolic acidosis.
External catheter damage
The external portion of a percutaneous tunneled external catheter can be damaged at the site of an attached plastic clamp or at a suture site. Use of needleless connections for infusions and irrigations should prevent needle damage to external portions of the catheter. The external portion of a percutaneous tunneled external catheter should never be grasped and occluded with a surgical hemostatic clamp. Most external catheters have repair kits to replace any damaged external portion of the catheter.
Drug extravasation
Drug extravasation into the subcutaneous tissues can occur with subcutaneous implanted ports when there is inappropriate placement or accidental dislodgment of the percutaneous noncoring (Huber) access needle from the reservoir of the subcutaneous implanted port. This may result in chemical cellulitis, tissue necrosis, and loss of soft tissues in the area of extravasation. Clinical signs of extravasation include pain, burning, soft-tissue swelling, skin erythema, and skin vesicle formation at the infusion site. If drug extravasation is suspected, the infusion should be stopped and the percutaneous non-coring (Huber) access needle should be immediately withdrawn and removed from the subcutaneous implanted port. Management depends on the type of drug infused, the amount of drug extravasated, and the degree/severity of resultant skin/tissue damage.
Venous thrombosis
Venous thrombosis secondary to CVA catheter placement occurs more commonly than is thought, since venous thrombosis may be present without the occurrence of any visible signs or symptoms (especially in those instances in which the evidence of venous thrombosis is nonocclusive). The incidence of venous thrombosis varies across multiple studies, ranging from 0% to 65%. Several risk factors have been identified for the development of central venous catheter–associated thrombosis. The incidence of venous thrombosis is higher in patients in whom the catheter tip is placed less centrally (eg, in the innominate vein or proximal superior vena cava), as compared with more central placement within the distal superior vena cava/right atrial junction. Ideally, the catheter tip should be positioned at the superior vena cava/right atrial junction and should be free-floating. The incidence of venous thrombosis is higher in patients with multiple-lumen catheters than in those with single-lumen catheters. Venous thrombosis also occurs at a higher incidence when the device is placed percutaneously rather than via a venous cutdown approach. Peripherally placed central venous access devices have been shown to be associated with a significant risk of upper-extremity deep vein thrombosis. Preexisting hypercoagulable states predispose patients to development of venous thrombosis. A history of having multiple prior central venous access devices placed and a documented history of previous upper-extremity deep vein thrombosis and/or previous intrathoracic central venous thrombosis are additional risk factors for development of future central venous catheter–associated thrombosis.
Early retrospective studies have suggested that antithrombotic prophylaxis reduces the risk of central venous catheter–associated thrombosis in cancer patients. However, three more recent double-blind, placebo-controlled, randomized clinical trials assessing antithrombotic prophylaxis have subsequently failed to show any such risk reduction within the time frame of those studies.
In 2005, Verso et al evaluated enoxaparin(Drug information on enoxaparin), a low molecular weight heparin(Drug information on heparin) (LMWH) agent. Patients undergoing central venous catheter placement received either 6 weeks of a 60 mg daily dose of subcutaneous enoxaparin or 6 weeks of a daily subcutaneous placebo, and with the first dose administered 2 hours before catheter placement. The incidence of central venous catheter–associated thrombosis was assessed with venography at the time of suspected catheter-related complications or at completion of the study medication. The incidence of venography-proven thrombosis was not significantly different in the two groups, with 14.2% (22/155) in the enoxaparin group and 18.1% (28/155) in the placebo group. Symptomatic thrombosis was observed in 1% of the enoxaparin group and in 3.1% of the placebo group.
In 2005, Couban et al evaluated low-dose warfarin(Drug information on warfarin). Patients undergoing central venous catheter placement received either 9 weeks of a 1-mg daily oral dose of warfarin or 9 weeks of a daily oral placebo, and starting within 4 days after catheter placement. The incidence of central venous catheter–associated thrombosis was assessed clinically, as defined as symptomatic central venous catheter–associated thrombosis. All symptomatic cases were then confirmed radiographically, first by compression ultrasonography, and then by venography, if ultrasonography results were normal. There was no statistically significant difference in the incidence of symptomatic central venous catheter–associated thrombosis between the two groups, with a 4.6% (6/130) incidence in the low-dose warfarin group and a 4% (5/125) incidence in the placebo group.
In 2006, Karthaus et al evaluated dalteparin, another LMWH agent. Patients undergoing central venous catheter placement received either 16 weeks of a 5,000 IU daily dose of subcutaneous dalteparin or 16 weeks of a daily subcutaneous placebo, randomized in a 2:1 ratio of dalteparin to placebo, and starting within 5 to 7 days of catheter placement. The incidence of central venous catheter–associated thrombosis was assessed with venography or ultrasound at the time of suspected catheter-related complications or at completion of treatment with the study medication. There was no statistically significant difference in the incidence of symptomatic central venous catheter–associated thrombosis between the two groups, with a 3.7% (11/294) incidence in the dalteparin group and a 3.4% (5/145) incidence in the placebo group.
In 2009, De Cicco et al evaluated the oral anticoagulant agent acenocumarine vs the subcutaneous LWMH agent dalteparin vs no anticoagulant treatment in a non-blind, placebo-controlled, randomized clinical trial in patients undergoing LTCVA device placement. Patients undergoing LTCVA device placement received either acenocumarine (1 mg oral daily dose for 3 days before and then for 8 days after central venous catheter placement), or dalteparin (5,000 IU sc daily dose at 2 hours before and then for 8 days after central venous catheter placement), or no anticoagulant treatment. All patients were assessed for central venous catheter–associated thrombosis by venography performed on days 8 and 30 after central venous catheter placement or at the time of suspected catheter-related complications. The incidence of nonocclusive, occlusive, and overall total cases of central venous catheter–associated thrombosis in the three study groups was assessed on day 8 and day 30 after LTCVA device placement. Both acenocumarine and dalteparin sigificantly reduced the incidence of both the overall total cases of central venous catheter–associated thrombosis (acenocumarine, 24/114 [21.1%] at 8 days and 25/114 [21.9%] at 30 days; dalteparin, 46/120 [38.3%] at 8 days and 48/120 [40%] at 30 days; no anticoagulation, 60/114 [52.6%] at 8 days and 30 days) and the cases of nonocclusive central venous catheter–associated thrombosis (acenocumarine, 23/114 [20.2%] at 8 days and 24/114 [21.1%] at 30 days; dalteparin, 43/120 [35.8%] at 8 days and 44/120 [36.7%] at 30 days; no anticoagulation, 60/114 [52.6%] at 8 days and 58/114 [50.9%] at 30 days), as compared with patients who did not receive anticoagulant treatment. In this regard, acenocumarine was significantly more effective than dalteparin. However, specifically regarding cases of occlusive central venous catheter–associated thrombosis, there were no significant differences observed between the three study groups (acenocumarine, 1/114 [0.9%] at 8 days and 30 days; dalteparin, 3/120 [2.5%] at 8 days and 4/120 [3.3%] at 30 days; no anticoagulation, 0/114 [0%] at 8 days and 2/114 [1.89%] at 30 days). They concluded that antithrombotic prophylaxis may be considered for selected cancer patients with risk factors for development of central venous catheter–associated thrombosis.
As a last point with regard to low-dose warfarin antithrombotic prophylaxis in cancer patients with central venous catheters, data have also shown a high incidence of INR (international normalized ratio) abnormalities in patients receiving fluorouracil(Drug information on fluorouracil) (5-FU)-based chemotherapy regimens who were maintained on 1 mg/day of warfarin, as noted in 55 of 427 patients (12.8%) reported by Magagnoli et al in 2005. In this regard, the authors recommended that such cancer patients should undergo periodic monitoring of the prothrombin time and INR if they are maintained on low-dose warfarin antithrombotic prophylaxis.
Treatment of venous thrombosis secondary to placement of CVA catheters should be directed toward prevention of pulmonary embolism, avoidance of clot propagation, prevention of the postphlebitic syndrome, and preservation of the LTCVA device, if possible. With these objectives in mind, the LTCVA device should be removed only if it is no longer necessary or if initial therapy for venous thrombosis fails and the patient's symptoms progress. The patient can be treated initially with systemic heparinization or subcutaneous LMWH, and this can be followed by conversion to oral anticoagulation with warfarin or continuation with subcutaneous LMWH. The LTCVA device may be kept in place as long as the patient with previous symptomatic central venous catheter–associated thrombosis stabilizes and improves, and if there are no contraindications to anticoagulation therapy. According to NCCN guidelines for venous thromboembolic disease: (1) when the decision is made to keep the CVA device in place, anticoagulant therapy should be continued for a minimal duration of at least 3 months or for the duration of the life of the CVA device; and (2) when the decision is made to remove the CVA device, anticoagulant therapy should be continued for a minimal duration of at least 3 months after device removal.
Device-Related Infections
Please see the section "Catheter-associated infections" in the "Infectious complications" chapter.
