Ventricular tachycardia secondary to Port-a-Cath® fracture and embolization

Introduction 

In 1984, Aitken and Minton were the first to document a case of catheter fracture and embolization secondary to a pinching effect between the clavicle and the first rib (1). Of 48 patients who had Hickman catheter placement for chemotherapy, four developed catheter obstruction and one developed catheter fracture and embolization into the right pulmonary artery. This fragment was removed transcutaneously. Since that time, several cases have been reported with minimal or no symptoms 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22.

We report a case of a potentially life-threatening complication from an implanted venous access device. We review the clinical presentation and management of reported cases and discuss prevention and risk factors for developing this rare complication.

Case report 

A 52-year-old man presented to the Emergency Department (ED), University of Washington Medical Center, complaining of palpitations of 1 or 2 h duration that began while doing daily activities at home. The patient described this feeling as an “irregular heart beat,” and he denied feeling a fast heart rate. He noticed it more when he moved. These palpitations had been present on and off for the past 2 days. He denied chest pain, shortness of breath, lightheadedness, nausea or sweating. He had many episodes of palpitations in the past, which he believed were due to panic disorder. He also reported increased stress secondary to marital difficulties in the recent past. He stated that he felt anxious, but believed that these palpitations were “different” from his normal panic attacks. The patient denied any medical or surgical history except for Hodgkin’s disease 3 years previously that was treated with chemotherapy through an implanted intravenous access device in the left subclavian vein. He denied any allergies. He also denied the use of medicines, herbal supplements, tobacco or illicit drugs. He did admit to drinking about four beers per day. Cardiac risk factors included only his age and sex.

Physical examination revealed a mildly obese, well-hydrated man who appeared somewhat anxious. He had the following vital signs: blood pressure 133/93 mm Hg, pulse 92 beats/min, respirations 20 breaths/min, temperature 37.5°C, and a pulse oximetry of 98% on room air. There was no jugular venous distention. The chest was clear. Cardiac auscultation revealed a regular rate and rhythm, with frequent ectopy, no murmurs, gallops or rubs with a normal S1 and S2. The implanted venous access device was present in the left upper pectoral region underneath a well-healed incision. The overlying skin was non-tender and non-erythematous. The abdomen was benign. Extremities were without edema. The pulse examination revealed a regular rhythm with frequent episodes of fast and irregular beats.

The patient was then placed in a monitored bay. The initial electrocardiogram (EKG) revealed normal sinus rhythm without ectopy, but subsequent telemetry and rhythm strips demonstrated a frequently changing rhythm, ranging from normal sinus rhythm to polymorphic ventricular tachycardia (Figure 1). Interestingly, the ectopy increased when the patient changed position. The patient continued to have frequent, polymorphic runs of wide complex beats that appeared to be emanating from at least four different foci. Lidocaine was given (75 mg bolus, 1 mg/min drip) with no effect on the tachydysrhythmia. A portable chest X-ray study showed normal lung fields, normal cardiac silhouette, and a shortened left subclavian Port-a-Cath® (Figure 2). We were unable to visualize the distal segment of the Port-a-Cath® even with improved PA and lateral chest X-ray studies. Assuming that the distal portion of the Port-a-Cath® had to be in the circulation, we made a presumptive diagnosis of catheter fracture and embolization causing ventricular ectopy.

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Figure 1. EKG revealing some of the ectopy recorded during the initial evaluation.

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Figure 2. Initial portable chest radiograph revealing the shortened Port-a-Cath® in left subclavian vein. Repeat portable and PA/lateral chest radiographs with removal of overlying chest leads failed to visualize the distal segment of the catheter.

After consultation with cardiology and radiology, the decision was made to confirm the diagnosis under fluoroscopy and to attempt fluoroscopically guided transvenous retrieval of the embolized fragment by Interventional Radiology (Figure 3). The 10-cm distal portion of the Port-a-Cath® was located in the right ventricle and successfully removed through a right femoral vein approach (Figure 4).

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Figure 3. Distal segment of catheter seen under fluoroscopy in the inferior vena cava after removal from the right ventricle.

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Figure 4. Distal 10-cm segment of the catheter after percutaneous removal.

Discussion 

Intravenous catheter fracture and embolization has been discussed in the literature since the early 1950s 23, 24, 25. Most of the cases before the mid-1970s involved peripherally inserted lines and iatrogenic cutting of the catheter with the end of the needle at the time of insertion 26, 27. Over 200 cases were reported in the 20 years before 1974. Adverse events from catheter emboli were so common, in fact, that some authors published cases to “help discourage the routine use of intravenous catheters” (28). From these data, there were no deaths reported in the patients who underwent removal of the embolized catheter. Nearly 25% of patients with the catheter left in, however, died from perforation, embolus, thrombosis, dysrhythmia, endocarditis, or sepsis. Another 20% had major non-fatal complications including dysrhythmia, thrombosis, embolus, and endocarditis (27). Since that time, the number of cases reported in the literature has decreased dramatically. This decrease may be due to lack of reporting, improved technology, and the widespread use of the Seldinger technique.

Aitken and Minton proposed a new etiology of catheter fracture and embolization in 1984 (1). They proposed that mechanical compression between the clavicle and first rib could lead to catheter fracture. At least 42 cases have been reported in the surgery, radiology and oncology literature since the initial discovery. Review of these case reports reveals a surprisingly subtle typical clinical presentation when compared to the morbidity data presented earlier (Table 1). Only two cases (5%) presented with what was described as “chest discomfort” in one case and “sudden onset of bilateral chest pain” in the other 2, 3. Another 7% complained of palpitations, which were described as frequent PVCs in one case and not characterized in the other two cases 4, 5, 6. The authors did not discuss the presenting complaint in another 5% of cases 7, 8. In the other 83% of cases, the presentations were benign. Thirty-six percent were asymptomatic, 29% experienced mild pain or swelling in the infra/supra clavicular region, 5% pectoral swelling, 12% shoulder pain, and 2% a “swishing sound” during medication or fluid infusions. The catheter fractures and embolization in the asymptomatic patients were found by routine chest radiographs or chest radiographs that were completed due to inability to flush or draw from the catheter (Table 2). In contrast, our patient presented with a potentially lethal dysrhythmia probably secondary to the mechanical irritation of the myocardium by the embolized catheter.

Table 1. Review of 42 Cases of Central Venous Catheter Fracture

	Symptoms (Number of Cases)	References/Number of Cases
	Chest pain (2)	Carr 1989, (2)/2*
		Prager & Hertzberg, 1987 (3)/1
	Palpitations (3)	Rubenstein et al., 1985 (4)/1
		Debets et al., 1995 (5)/1
		McMenamin, 1993 (6)/1
	NR (2)	Hinke et al., 1990 (7)/1
		Stanislav et al., 1987 (8)/1
	Asymptomatic (15)	Rubenstein et al., 1985 (4)/2
		McMenamin 1993, (5)/1
		Monsuez et al., 1997 (9)/3
		Roggla et al., 1993 (10)/1
		Bauch et al., 1992 (11)/1
		Brincker & Saeter, 1986 (12)/1
		Noyen et al., 1987 (13)/1
		Nace & Ingle, 1993 (14)/1
		Klotz et al., 1996 (15)/1
		Vadlamani et al., 1998 (16)/3
	Infra/supraclavicular swelling or pain (12)	Aitken & Minton, 1984 (1)/1
		Rubenstein et al., 1985 (4)/2
		Nace & Ingle, 1993 (14)/3
		Klotz et al., 1996 (15)/1
		Coles et al., 1998 (17)/1
		Franey et al., 1988 (18)/1
		Kirvela & Satokari, 1989 (19)/1
		Lafreniere, 1991 (20)/1
		diCarlo et al., 2000 (21)/1
	Pectoral swelling (2)	Rubenstein et al., 1985 (4)/2
	Shoulder pain (5)	Debets et al., 1995 (5)/2
		McMenamin, 1993 (6)/1
		Nace & Ingle, 1993 (14)/1
		Ramsden et al., 1995 (22)/1
	Swishing sound (1)	Rubenstein et al., 1985 (4)/1

* One case of catheter separation (not fracture) at infusion port with embolization to heart (right upper quadrant pain). NR = Not reported.

Table 2. Diagnosis of Asymptomatic Catheter Fracture and Embolization

	Reference/Number of Cases	Diagnosed by
	Rubenstein et al., 1985 (4)/2	Routine CXR (2)
	McMenamin, 1993 (6)/1	Routine chest CT (1)
	Monsuez et al., 1997 (9)/3	Routine catheter removal (1)
		Catheter removal for “resistant blockade” (2)
	Roggla et al., 1993 (10)/1	Routine CXR (1)
	Bauch et al., 1992 (11)/1	Routine CXR (1)
	Brincker & Saete, 1986 (12)/1	NR
	Noyen et al., 1987 (13)/1	Routine CXR (1)
	Nace & Ingle, 1993 (14)/1	Routine CXR (1)
	Klotz et al., 1996 (15)/1	CXR for inability to aspirate (1)
	Vadlamani et al., 1998 (16)/3	Routine CXR (1)
		CXR for inability to aspirate (1)
		CXR for “nonfunctional” catheter (1)

CXR = chest radiograph; CT = computed tomography; NR = Not reported.

The new etiology of this rare complication seems to be a pinching of the catheter as it passes between the clavicle and the first rib, rather than the historically described cutting of the catheter with the needle at the time of insertion. Over time, this pinching may lead to catheter fracture and embolization of the distal segment into the heart and great vessels. Potentially life-threatening dysrhythmias may result. Aitken and Minton first described the “pinch-off sign” on chest radiographs of patients with indwelling subclavian catheters as a narrowing of the catheter as it passes between the clavicle and first rib (1). The angle between the clavicle and the rib is wide in the supine position. If the catheter is inserted too medially, then it may transverse this angle outside of the vessel lumen. In the upright position, the angle narrows, pinching the catheter. Mechanical stress and time may then lead to catheter fracture. By inserting the catheter from a more lateral position, the catheter will enter the vein before the angle between the clavicle and rib. In this location, the risk of catheter pinching is minimized because the space is wider.

In 1990, Hinke et al. described 11 cases of catheter pinch-off syndrome in a review of 987 patients with implanted central venous access devices through the subclavian vein (7). They graded the severity of pinch-off by radiographic criteria with grade 1 defined as an abrupt change in catheter direction without luminal narrowing, grade 2 defined as luminal narrowing and grade 3 as complete catheter fracture. They found that in two of five cases in which Grade 2 compression was present and the catheter was left in place for more than 3 weeks, catheter fragmentation was present on removal. In one case, there was complete transection and distal embolization. In the other, the catheter was fragmented, but not completely transected. Based on these cases, they recommended prompt removal of catheters from patients with radiographic evidence of catheter compression. Inspection of the end of the catheter in our case revealed an elliptical shape with irregular edges consistent with a compression mechanism of fracture. Unfortunately, we were unable to locate any prior chest radiographs containing the Port-a-Cath® and, therefore, we cannot determine if the pinch-off sign was present before fracture.

In terms of catheter fracture, clinical presentations might vary from those patients with embolus and significant symptoms, to those with embolus and minimal symptoms, to those at risk for embolus with no symptoms.

The minority of patients with catheter embolus may present with significant symptoms including chest pain, palpitations, dysrhythmias, and unstable vital signs. Several cases of ventricular perforation and death from tamponade have been reported in early literature 24, 28. An EKG and chest X-ray study are essential. The key to the diagnosis is the chest radiograph. It is especially important to evaluate the position and length of any long-term intravenous access catheters. It may not be possible to see the distal fragment of the catheter, and catheter shortening may be the only clue to the diagnosis.

Catheter embolus is an uncommon entity but it may be seen in patients with significant comorbidity, and historically it has a high mortality and morbidity. Long-term intravenous access catheters are placed in patients needing extended antibiotic therapy, chemotherapy, hemodialysis, and hyperalimentation. Many of these patients have concomitant chronic diseases including diabetes, renal failure, emphysema and cancer. These disease states place the patient at high risk for pulmonary emboli, myocardial infarction, pericardial effusion, pericarditis, pneumothorax, and electrolyte disorders that can all present with symptoms similar to catheter embolus.

Catheter-related history should be asked in any patient with a long-term access device to determine the reason for the indwelling catheter, the length of time it has been in place, and any recent difficulty with accessing the device. Any history of recent difficulty aspirating or accessing the intravenous line should be evaluated with a chest X-ray study. Many of the asymptomatic catheter emboli in the reviewed cases were discovered in this manner (Table 2). One should also evaluate for catheter compression at the level of the first rib and clavicle and, if available, compare to prior radiographs. Hinke et al. recommend prompt removal of any catheter with radiographic evidence of compression to prevent embolization (7). Catheter-related physical examination should include inspection and palpation of the overlying skin and subcutaneous tunnel, searching for evidence of infection, as well as evaluation of the chest radiograph with specific attention given to the catheter length.

Once catheter embolus is diagnosed the definitive management is removal of the catheter. Although experience in the literature is lacking, electricity and anti-dysrhythmic therapy will likely be unsuccessful due to the mechanical nature of the myocardial irritation. In the unstable patient, however, we recommend following ACLS guidelines while arranging definitive management through Interventional Radiology, Cardiology and Cardiothoracic Surgery.

Nearly all recent cases of catheter embolus have been successfully managed with transcutaneous retrieval through a femoral vein approach. This may necessitate transfer to a higher level of care from institutions without specialists capable of this intravascular technique. Although uncommon now, thoracotomy was once used as a primary means of retrieval of centrally embolized catheters (28).

Summary 

Catheter fracture and distal embolization to the heart is a rare but potentially life-threatening complication of implanted central venous access catheters. The most important risk factor for developing this complication is the catheter pinch-off sign on chest radiography. Although the recent literature shows that catheter fracture typically presents subtly without dramatic dysrhythmias, it may be prudent to remove catheters with radiographic evidence of luminal narrowing as described by Hinke et al. (7).