Paradoxical emboli after central venous catheter removal

Annals of Oncology 11: 885-886, 2000. © 2000 Kluwer Academic Publishers. Primed in the Netherlands.

Clinical case Paradoxical emboli after central venous catheter removal R. Zuha,1 T. Price,1 R. Powles1 & J. Treleaven2 Departments of 'Medical Oncology,2Haematology, The Royal Marsden NHS Trust, Sutton, Surrey, UK

Summary

Central venous catheters are widely used in intensive medicine to provide blood product, nutritional and antibiotic support. A 45-year-old man with an unsuspected patent foramen ovale underwent a bone marrow allograft for poor-risk acute lymphoblastic leukaemia. His venous line was removed because of probable infection, and he simultaneously sustained a myocardial infarct and a cerebrovascular accident. He made a

Central venous catheters are widely used in intensive medicine to provide blood product, nutritional and antibiotic support. They may be used either transiently or for more protracted periods in patients with chronic problems such as an on-going requirement for blood products. There are many recognised complications associated with their use, and these relate chiefly to infection, thrombosis or trauma caused by their insertion. A comprehensive list of catheter-associated problems is given in [1]. Large vessel thrombosis is said to occur in 8%-63% of patients with indwelling central venous catheters [2-4], and clots have been found in 30% of samples taken from heparinised lines [5]. Right atrial thrombi have been described [6], on occasion large enough to obstruct the tricuspid valve [7, 8]. The problem may be enhanced in the bone marrow transplant population as some chemotherapeutic agents degrade catheter surfaces, predisposing to platelet adherence and thrombus formation [9]. Encasement of the endovascular catheter shaft by a fibrin sheath occurs in 75% of catheters as early as 48 hours post-insertion [10, 11], and is probably present on all catheters by 5-7 days [12], and this may propagate from sites of intimal damage. We describe the unusual complication of multiple arterial embolisation occurring secondary to a previously undiagnosed patent foramen ovale. Case history A 45-year-old man with poor prognosis acute lymphoblastic leukaemia underwent an allogeneic bone marrow transplant from his HLA-compatible sister. His past medical history and baseline cardiovascular examina-

Key words: bone marrow allograft, central venous catheter, cerebrovascular accident, myocardial infarction, paradoxical embolus

tion and investigations were unremarkable, including an electrocardiogram (ECG) and chest X-ray (CXR). Apart from the anticipated mucositis, febrile neutropenia and grade 2 graft-vemw-host disease, he tolerated the procedure without major problems and attained a neutrophil count >0.5 x 109/l on day 12 and an unsupported platelet count of 20 x 109/l on day 14. He had had a Hickman line in situ throughout his transplant, and this was removed without problems after recovery of his blood count, because of probable infection. On day 18 post-transplant, a right internal jugular venous catheter was inserted due to poor peripheral access.The tip of the line was sited in the superior vena cava, five centimetres above the right atrium as was confirmed by chest X-ray. On day 25, after the infusion of 2 ml of a trial immunosuppressive agent (CLF 08-0299), he became acutely short of breath, although physical examination, electrocardiogram and chest X-ray were normal. The infusion was stopped, but he recovered after an hour and it was recommenced without further problems. Twenty four hours later, the central venous catheter was removed, and during removal he again became acutely short of breath with a marked cough. His symptoms again resolved after approximately one hour, but three hours later he suddenly lost consciousness while moving his bowels. He remained haemodynamically stable, with a Glasgow coma score of three, and an ECG now revealed acute STwave elevation anteriorly, and CPK levels were elevated a few hours later. Computer tomography (CT) of his brain was normal. He received rTPA (recombinant tissue plasminogen activator) with partial resolution of the ECG changes but remained unconscious with generalised and focal right-sided seizures. Repeat CT 18 hours later remained normal. Examination of his cerebrospinal fluid showed: WBC I/mm3, RBC 5/mm3, protein 0.63 g/1, glucose 3.7 mmol/1

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Introduction

good recovery from both, but subsequently died of relapsed disease. Appropriate pre-transplant screening investigations are discussed, and the differential diagnosis of this complication in the bone marrow transplant setting.

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Discussion Since it is well recognised that clot or fibrin commonly accumulate in or around venous catheters, it is likely that either these or other debris within the central line were dislodged at removal. These then embolised first via the right heart to the lungs, causing the initial episope of cough and shortness of breath, and subsequently through the patent foramen ovale into the arterial system causing the ensuing cerebral and coronary artery occlusions. The latter event possibly occured secondary to raised right heart pressure and an ensuing Valsava effect caused by straining at stool. Patent foramen ovale is said to be present in up to 35% of people [13, 14] and is a well-recognised cause of stroke. Paradoxical embolic events, including air emboli, have been documented to occur in association with Hickman line presence or at insertion [15, 16], as has a paradoxical embolus leading to lower limb ischemia [17]. However, we believe that this is the first documented case of removal of a CVC leading to simultaneous coronary and cerebral vessel occlusion. In view of the frequency of thrombotic complications in catheterised veins when mural thrombi are seen in 38% of post mortem studies [7], and the recognised incidence of PFOs of up to 1:4 individuals, it is may be expedient to carry out routine pre-transplant echocardiograms so that patients with PFOs can be identified and heparin cover given prior to CVC removal. However, this is unlikely to be cost-effective. To assess need for routine screening, unexplained embolic events man-

ifesting within hours of CVC removal should meanwhile be reported to lead haemato-oncology centres or transplant registries.

References 1. Nightingale C, Filshie J. Venous access in bone marrow transplantation. In Barrett AJ, Treleaven JG (eds): The Clinical Practice of Stem-Cell Transplantation, Chapter 28. Oxford, UK: Isis Medical Media 1998; 419-33. 2. Anderson AJ, Krasnow SH, Boyer MW, Cuder DJ. Thrombosis: The major Hickman catheter complication in patients with solid tumour. Chest 1989; 95: 71-5. 3. Haire WD, Lieberman RP, Lund GB et al. Thrombotic complications of silicone rubber catheters during autologous marrow and peripheral stem-cell transplantation: Prospective comparison of Hickman and Groshong catheters. Bone Marrow Transplant 1990; 7: 57-9. 4. Wagman LD, Kirkemo A, Johnston R. Venous access: A prospective, randomised study of the Hickman catheter. Surgery 1984; 95: 303-8. 5. Anderson AJ, Krasnow SH, Boyer MW, Raucheisen ML. Hickman catheter clots: A common occurrence despite daily heparin flushing. Cancer Treat Rep 1987; 71: 651-3. 6. Reed WP, Newman K. Tenney J. Autopsy findings after prolonged catheterisation of the right atrium for chemotherapy in acute leukaemia. Surg Gynaecol Obstet 1985; 160: 417-20. 7. Chakravarthy A, Edwards WO, Fleming CR. Fatal tricuspid valve obstruction due to a large infected thrombus attached to a Hickman catheter. J Am Med Assoc 1987; 257: 801-3. 8. Benbow EW, Love EM, Love HG, MacCallum PK. Massive right artrial thrombus associated with a Chiari network and a Hickman catheter. Am J Clin Pathol 1987; 88: 243-8. 9. Ranchere JY, Tabone E, Latour JF. Polyurethene catheters and antineoplastic chemotherapy. An experimental study. Ann Franchises Anaesth Reanimat 1988; 7: 517-9. 10 Wagman LD, Neifeld JP. Experience with the Hickman catheter: Unusual complications and suggestions for their prevention. J Parenteral Enteral Nutrit 1986; 10: 311-5. 11. Riella MC, Scribner BH. Five years' experience with a right atrial catheter for prolonged parenteral nutrition at home. Surg Gynaecol Obstet 1976; 143: 205-8. 12. Crain MR, Mewissen MW, Ostrowski GJ et al. Fibrin sleeve stripping for salvage of failing hemodialysis catheters: Technique and initial results. Radiology 1996; 198: 41^t. 13. Fisher DC, Fisher EA, Budd JH et al. The incidence of patent foramen ovale in 1,000 consecutive patients. Chest 1995; 107 (6): 1504-9. 14. Penther P. Patent foramen ovale: An anatomical study. Apropos of 500 consecutive autopsies. Arch Mai Coeur Vaiss 1994; 87 (1): 15-21. 15. Yu AS, Levy E. Paradoxical cerebral air embolism from a hemodialysis catheter. Am J Kidney Dis 1997; 29 (3): 453-5. 16. Elejalde Guerra JI et al. Paradoxal air embolism caused by a central venous catheter. An Med Intern 1998; 15 (10): 562-3. 17. Lagattolla NR, Sandison AJ, Smith K et al. Acute limb ischaemia due to paradoxical embolism from a long-term central venous catheter. Eur J Vase Endovasc Surg 1998; 16 (4): 365-6. Received 22 March 1999; accepted 6 April 1999.

Correspondence to: Dr J. Treleaven Department of Haematology Royal Marsden Hospital Downs Road Sutton, Surrey SM2 5PT UK

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(serum 12.3 mmol/1), no blasts on cytology, and polymerase chain reaction for herpes simplex virus negative. Bone marrow aspirate showed good trilineage engraftment and complete remission. In view of a drop of 3 g in his haemoglobin, a fall in platelet count and presence of neurological symptoms, a diagnosis of thrombotic thrombocytopenic purpura (TTP) was considered. A three litre plasma exchange was undertaken but the pheresis product was entirely normal in colour indicating that no significant red cell fragmentation was taking place; this was confirmed by inspection of the blood film. Four days later, the patient regained consciousness and a dense right-sided hemiplegia was noted. Further investigations including magnetic resonance imaging (MRI) of the brain now revealed multiple small infarcts in both cerebral hemispheres with a larger infarct in the left motor cortex. A transoesophageal echocardiogram showed a patent foramen ovale (PFO) with a right to left shunt on Valsalva. Magnetic resonance angiography of the carotid arteries was normal. Four weeks later, the patient had regained grade three power in the lower limb, with minimal movement in the upper limb. He continued physiotherapy and low molecular weight heparin, but sadly his underlying disease relapsed aggressively two months after the allograft and he died from progressive disease.