Totally implantable intravascular devices-related complications: effectiveness of insertion by trained team

Totally implantable intravascular devices-related complications: effectiveness of insertion by trained team

248 Letters to the Editor Totally implantable intravascular devices-related complications: effectiveness of insertion by trained team Sir, The comfo...

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248

Letters to the Editor

Totally implantable intravascular devices-related complications: effectiveness of insertion by trained team Sir, The comfort and quality of chemotherapy have improved with the use of long-term vascular access devices. The use of totally implantable intravascular devices (TIDs) instead of peripherally inserted or tunnelled central venous catheters aims to reduce the risk of catheter-related complications (infection, thrombosis and extrusion).1 However, infection remains the most frequent complication and is associated with increased morbidities and mortalities, prolonged hospitalization and increased medical costs.2,3 In our oncology unit, TIDs were inserted by 12 different surgeons, of whom one (surgeon A) has focused his activity on TID insertion, whereas others (surgeon group B) only occasionally perform TID insertions. During a period of 18 months, 145 patients requiring TIDs were studied. The median follow-up was eight months for catheters placed by surgeon A and nine months for surgeon group B. Before TID insertion, the skin was prepared using the same protocol with povidone iodine as an antiseptic. The position of the TIDs was checked by chest radiograph. No prophylactic antibiotic was administered. After TID placement, patients were re-admitted to the oncology unit and catheter care was identical for all patients. Failure was defined as catheter removal for infection, thrombosis or dislodgement. TID infection was defined as (1) bacteraemia diagnosed by isolation of the same micro-organism in at least two blood cultures and culture of the same micro-organism in the catheter and/or (2) presence of pus at the TID implantation site associated with local signs of inflammation (erythema, warmth, swelling and tenderness). Thrombosis was suspected on clinical presentation (pain and oedema with or without collateral circulation on the neck or on the arm of same side than the catheter) and confirmed by imaging. Statistical analysis was performed using

the Fisher’s exact test. Twenty-three (15.9%) catheter-failures occurred during the period of study (Table I). TID insertion by the more experienced surgeon A was associated with a complication rate (5.9%) lower than that observed in the group of less experienced surgeons (24.7%; P ¼ 0:002). Thrombosis occurred less commonly when TID insertion was performed by surgeon A ðP ¼ 0:01Þ: The small sample number may be the reason that the difference in infection rate, even though four times less for surgeon A (Table I), did not reach statistical significance. Micro-organisms responsible for infection were Staphylococcus aureus ðN ¼ 2Þ; Staphylococcus epidermidis ðN ¼ 3Þ; Pseudomonas aeruginosa ðN ¼ 2Þ; Klebsiella oxytoca ðN ¼ 1Þ; Serratia marcescens ðN ¼ 1Þ and Candida tropicalis ðN ¼ 1Þ: All except one were associated with bacteraemia. The overall rate of infection in our study was higher (6.9%) than that previously reported (around 4%), but was lower (2.9%) for surgeon A. It was previously demonstrated that insertion and maintenance by inexperienced staff might increase the risk of catheter colonization,4 and that teams specifically trained for placement and maintenance of intravascular devices have a lower complication rate.5 Management of TIDs by a trained team has now been recommended by Centers for Disease Control and Prevention under the guidelines for prevention of intravascular device-related infections (category II recommendation).2 As a result of our study only experienced surgeons now insert TIDs for patients on our oncology unit.

References 1. Groeger JS, Lucas AB, Thaler HT, et al. Infectious morbidity associated with long-term use of venous access devices in patients with cancer. Ann Intern Med 1993;119:1168—1174. 2. Pearson ML. Guideline for prevention of intravascular devicerelated infections. Am J Infect Control 1996; 24:262—277. 3. Raad I, Hohn DC, Gilbreath BJ, et al. Prevention of central venous catheter-related infections by using maximal sterile barrier precautions during insertion. Infect Control Hosp Epidemiol 1994;15:231—238.

Table I Occurrence of complications according to surgeons responsible for TID insertion Surgeon group A TID insertion ðN ¼ 145Þ Median follow-up (months) Infection ðN ¼ 10Þ Thrombosis ðN ¼ 10Þ Dislodgment ðN ¼ 3Þ Overall complications ðN ¼ 23Þ

2 1 1 4

68 8 (2.9%) (1.5%) (1.5%) (5.9%)

Surgeon group B 77 9 8 (10.4%) 9 (11.7%) 2 (2.6%) 19 (24.7%)

P ¼ 0:07 P ¼ 0:01 P ¼ 0:002

Letters to the Editor

4. Armstrong CW, Mayhall CG, Miller KB, et al. Prospective study of catheter replacement and other risks factors for infection of hyperalimentation catheters. J Infect Dis 1986;154: 808—816. 5. Tomford JW, Hershey CO, Mc Laren CE, Porter DK, Cohen DI. Intravenous therapy team and peripheral venous catheterassociated complications. A prospective control study. Arch Intern Med 1984;144:1191—1194.

A. Boulamery-Vellya, C. Merciera, F. Duffauda, R. Favrea, L. Diguea, B. La Scolab,* a ´dicale, Ho ˆpital de la Service d’oncologie Me ˆpitaux de Timone, Assistance Publique-Ho Marseille, Marseille, France b ´ des Rickettsies, CNRS UPRESA 6020, Faculte ´ Unite ´decine, Universite ´ de la Me ´diterrane ´e, 27 de Me Boulevard Jean Moulin, 13385 Marseille cedex 05, France E-mail address: [email protected] *Corresponding author. Tel.: þ33-4-9138-55-17; fax: þ33-49183-03-90 doi:10.1016/j.jhin.2003.12.013

SARS in a hospital visitor and her intensivist Sir, Severe acute respiratory syndrome (SARS) is a novel infectious disease in humans caused by a coronavirus that was first recognized in Southeast Asia in late February 2003.1 The World Health Organization (WHO) has issued definitions for probable and suspected cases.2 Most transmissions occurred by close hospital or household contact with infected individuals suggesting a predominant droplet mode of spread.3 Widespread use of personal protective equipment (PPE) including N95 respirators is thought to have been instrumental in controlling the epidemic. We report a patient who had had no direct contact with SARS patients and who subsequently transmitted the infection to her intensivist who was wearing standard PPE during a bronchoscopy. A 43-year-old woman was admitted to our hospital with a respiratory and systemic illness of 1-week duration. She had had no direct contact with any patients suffering from SARS, but had visited a friend with hepatitis in hospital who was at least two cubicles (approximately 10 m) away from a patient later confirmed to have SARS. On examination, she was tachypnoiec and febrile.

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Chest radiography revealed bilateral basal consolidations and the white blood cell count was 19.3 £ 109/L (polymorphs 90%, lymphocytes 4%). Community-acquired pneumonia was diagnosed and the patient was isolated in a single room with negative pressure and started on intravenous antibiotics. The following day, she required endotracheal intubation and mechanical ventilation. Over the next four days, she developed multisystem organ failure and adult respiratory distress syndrome requiring haemofiltration and vasopressor support and died on the eighth day of admission. Cultures of blood, urine and bronchoalveolar lavage (BAL) were negative for micro-organisms including fungi and mycobacteria. Three days after the bronchoscopy, the intensivist (K.-H.L.) who performed the procedure developed fever and myalgia and was subsequently diagnosed as having SARS with pneumonia, despite wearing a N95 mask, glasses, gown, and gloves throughout the procedure. He required admission to intensive care unit and mechanical ventilation, and survived the episode. The patient’s serology was positive for SARS by a dot-blot immunoassay using a viral lysate in a postmortem analysis of a serum sample taken on day three of admission. Her intensivist was also seropositive 4 weeks after hospitalization. Our patient met the revised WHO criteria2 for SARS except that she did not ‘care for, live with, or have had direct contact with respiratory secretions and body fluids of a person with SARS,’ as the WHO defines close contact.2 Her serology was only found to be positive at post-mortem. To our knowledge, fomite spread has not been well documented for SARS, although it has been demonstrated experimentally for other respiratory viral pathogens, and is the probable route of transmission for our patient. Environmental contamination is the most likely route of transmission in Hotel M, which triggered off the worldwide outbreak of SARS1 and in the large Amoy Gardens outbreak.4 Transmission to a bronchoscopist has not, to our knowledge, been documented before. During the procedure the doctor wore an N95 mask, glasses, gloves, footwear and disposable gown. However, he was not using specific eye protection and a powered air purifying respirator (PAPR) hood, which has become common practice since then. This case suggests that if the viral load is high the N95 mask may not offer sufficient protection during high-risk procedures, including bronchoscopy, nebulizer therapy or intubation. This is similar to the experience in Canada in which transmission of SARS to protected healthcare workers occurred during a difficult intubation.5 We believe that