Non-pulmonary Critical Care - part 9 ppsx

of the patients are on antibiotics at the time of diagnosis. 77 Infection is excluded by the absence of a pathogeninBALfluidandbythelackofclinical response to antimicrobial therapy. DAH and periengraftment respiratory distress syndrome (PERDS) also fulfill the diagnostic criteria of IPS. 78,79 Despite over- lap in the clinical features of IPS, DAH, and PERDS, their responses to treatment and clinical courses are different. 78 In our diagnostic approach to patients with suspected IPS, we perform BAL and, if there are no contraindications, transbronchial lung biopsy. We pro- ceed to video-assisted thoracoscopic lung biopsy if transbronchial lung biopsy is contraindicated or if the transbronchial specimen is inadequate. Lung biopsies of patients with IPS may show diffuse alveolar damage, organizing or acute pneumonia, and interstitial lymphocytic inflammation. 77,80 TREATMENT There have been no randomized clinical trials address- ing the treatment of IPS. Despite case reports of patients with IPS responding to treatment with corticosteroids, studies with larger sample sizes have not shown any outcome benefit. 77,80,81 Currently, management consists of supportive care and p revention and treatment of infection. There is a report of three cases of HSCT recipients with IPS whose lung function improved following the administration of etanercept. 76 This observation awaits further confirmation by clinical trial. CLINICAL COURSE AND PROGNOSIS The clinical course of HSCT recipients with IPS is usually complicated by viral and fungal infections as well as pneumothorax, pneumomediastinum, subcutaneous emphysema, pulmonary fibrosis, and autoimmune polyserositis. 13 The overall mortality of IPS is 74%, with a reported range between 60 and 86%. 13 The 1 year survival rate is less than 15%. 77,81 For those who require mechanical ventilation, the hospital mortality exceeds 95%. 77 Diffuse Alveolar Hemorrhage EPIDEMIOLOGY DAH represents an important subset of IPS. It occurs in 5% of HSCT recipients, in both al lo- and autotrans- plants, with a ran ge of 2 to 21%. 13 Risk factors for DAH include age > 40 years, intensive chemotherapy, total body irradiation, the presence of inflammatory cells in BAL fluid, mucositis, and acute GVHD. 13 There are no associations between the development of DAH and prolonged prothrombin or partial thromboplastin time or low platelets. DAH is not corrected with platelet transfusion. 82 CLINICAL FINDINGS AND DIAGNOSTIC EVALUATION Symptoms of DAH typically include dyspnea, fever, and cough. 82 Hemoptysis is reported in fewer than 20% of patients. 78,83 The onse t of DAH is usually within the first 30 (median between 11 and 24) days following HSCT. Arterial blood gas studies show hypoxemia. Chest radiographs usually show alveolar and interstitial infiltrates involving middle and lower lung zones. 84 The early radiographic changes may be subtle, unilateral, or asymmetrical. 84 CT of the chest has a limited role in the diagnosis. Criteria for the diagnosis DAH include (1) signs and symptoms of pneumonitis, (2) no evidence of infection, and (3) BAL showing progressively bloodier return from separate subsegmental bronchi, or > 20% hemosiderin-laden alveolar macrophages. 13,78 Lung tis- sues in DAH show diffuse alveolar damage. 59,82 TREATMENT Based on retrospective studies, HSCT recipients with DAH are treated with systemic corticosteroids. 78,83 We commonly use methylprednisolone, 1 g daily in four divided doses for 5 days, followed by 1 mg/kg for 3 days, tapering off over 2 to 4 weeks. 78 There are case reports of allogeneic HSCT recipients with DAH successfully treated with recombinant factor VIIa. 85,86 CLINICAL COURSE AND PROGNOSIS The majority of HSCT recipients with DAH require mechanical ventilation. 78,83 The reported mortality rate of DAH ranges between 48 and 100%. 78,83 The two most common reported causes of death had been multiple organ failure and sepsis. 87,88 However, in a recent study, respiratory failure was the immediate cause of death in the majority of HSCT recipients with DAH. 83 Periengraftment Respiratory Distress Syndrome EPIDEMIOLOGY PERDS occurs in 5% of autologous HSCT recipients. 79 About one third of DAH occurs during the periengraftment period and about one third of patients with PERDS have DAH. 79,83 CLINICAL FINDINGS AND DIAGNOSTIC EVALUATION PERDS is a subset of IPS characterized by acute lung injury during the neutrophil periengraftment period. It represents the pulmonary component of the engraftment syndrome, which may also present with diarrhea and skin rash. 79,89,90 ThediagnosticcriteriaofPERDS include the presence of fever and evidence of pulmonary injury in the form of hypoxia (SaO 2 < 90%) and/or COMPLICATIONS FOLLOWING HEMATOPOIETIC STEM CELL TRANSPLANTATION/AFESSA, PETERS 303 pulmonary infiltrates on chest radiograph, in the absence of cardiac dysfunction or infection, within 5 days of neutrophil engraftment. 79 The m edian time to onset of PERDS is 11 days (range, 4 to 25 days) after transplant. 79 BAL may show neutrophilic alveolitis. 79 Trans- bronchial lung biopsy is usually contraindicated because of thrombocytopenia. Surgical lung biopsy is rarely necessary but may show diffuse alveolar damage. 79 TREATMENT/PROGNOSIS High-dose corticosteroid therapy often leads to rapid clinical improvement. 79 Unlike DAH and IPS, only about one third of HSCT recipients with PERDS require intensive care unit admission and mechanical ventilation. 79 The reported mortality rate of PERDS is 26%. 79 Bronchiolitis Obliterans EPIDEMIOLOGY About 45% of long-term survivor allogeneic HSCT recipients develop chronic GVHD. 91 Bronchiolitis obliterans (BO) is a severe mani festation of chronic GVHD characterized by airflow limitation. 92 The overall frequency of BO in allogeneic HSCT recipients is 3.9%. 13 Risk factors for BO include GVHD, older donor and recipient age, myeloablative conditioning, methotrexate use, antecedent respiratory infection, and serum immunoglobulin deficiency. 13 CLINICAL FINDINGS AND DIAGNOSTIC EVALUATION The pathogenesis of BO in HSCT recipients is not well understood. BO usually occurs between 2 months and 9 years after transplantation. 13 The clinical presentation includes dry cough and dyspnea in most, wheezing in 40%, and antecedent cold symptoms in 20%. 13 Twenty percent of the patients with BO had no respiratory symptoms at the time of the abnormal pulmonary function testing. 93 The diagnostic evaluation should include organs likely to be affected by GVHD, including the liver, sinuses, and esop hagus. 13 PFT shows irreversible airway obstruction. The chest radiograph may be normal or show hyperinfla- tion. 13 HRCT of the chest may show decreased lung attenuation, bronchial dilatation, centrilobular nodules, and expiratory air trapping. 13 BAL may show either or both neutrophilic and lymphocytic inflammation. 94 Transbronchial lung biopsy is usually non- diagnostic. Video-assisted thoracoscopic l ung biopsy, showing fibrinous obliteration of the small airway lumen, provides a definitive histologic diagnosis of BO. 13 However, surgical biopsies are rarely indicated because the diagnosis can usually be made clinically by the presence of irreversible airflow obstruction and the exclusion of other causes of this functional abnormal- ity in allogeneic HSCT recipients with chronic GVHD. 13,95 TREATMENT The treatment of BO usually consists of corticosteroids and augmented immunosuppression, targeting chronic GVHD. However, only a minority show clinical improvement. 13 In a recent study, Khalid and colleagues reported eight HSCT recipients with BO whose PFT improved after treatment with azithromycin. 96 Randomized clinical trials are warranted to define the role of macrolide therapy for BO. Prophylaxis for PCP and Streptococcus pneumoniae should be provided. In selected HSCT recipients with respiratory failure secondary to BO, lung transplantation may be an option. 97 CLINICAL COURSE AND PROGNOSIS The airflow limitation in HSCT recipients with BO improves in only 8 to 20%. 13 The overall case fatality rate is 59%, with a reported range of 14 to 100%. 13 In a recent study, the 5 year survival rate of 47 HSCT recipients with BO was 10%, compared with 40% for those without BO. 98 Bronchiolitis Obliterans Organizing Pneumonia EPIDEMIOLOGY The published medical literature on bronchiolitis obliterans organizing pneumonia (BOOP) in HSCT recipients is limited to case reports with a maximum number of five patients. 13 Although BOOP has been reported mostly in allogeneic HSCT recipients with GVHD, it also occurs in autologous transplant. 99 CLINICAL FINDINGS AND DIAGNOSTIC EVALUATION HSCT recipients with BOOP present with dry cough, dyspnea, and fever, usually at 1 month to 2 years after transplant. 13 PFT shows a restrictive defect, decreased diffusing capacity for c arbon monoxide, normal airflow flow, and hypoxemia. 13 Chest radiographs and HRCT show patchy air space consolidation, ground-glass attenuation, and nodular opacities. Although usually bilateral, radiographic abnormalities can be unilateral. 99 Exhaled nitric oxide concentration is increased in HSCT recipients with BOOP and decline in response to treatment. 100 The diagnosis of BOOP in the HSCT recipient requires lung biopsy, occasionally transbronchial but usually surgical. 101 The histologic hallmark is patchy intraluminal fibrosis consisting of polypoid plugs of immature fibroblasts resembling granulation tissue, ob- literating the distal airways, alveolar ducts, and peribron- chial alveolar spaces. 102 304 SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE/VOLUME 27, NUMBER 3 2006 TREATMENT AND PROGNOSIS Approximately 80% of HSCT recipi ents with BOOP respond favorably to treatment with corticosteroids. 13 Radiographic abnormalities usually clear within 1 to 3 months of initiating corticosteroid therapy. A favor- able outcome has been observed in one allogeneic HSCT recipient with BOOP following the use of erythromycin in conjunction with corticosteroids. 103 The case fatality rate of BOOP in HSCT recipients is 19%. 13 Delayed Pulmonary Toxicity Syndrome EPIDEMIOLOGY In the 1990s, many patients with breast cancer were treated with autologous HSCT following chemotherapy with cyclophosphamide, cisplatinum, and bischloroethy- linitrosurea (BCNU). 104 Delayed pulmonary toxicity syndrome (DPTS) developed in up to 72% of these patients. 105–107 Currently, DPTS is uncommon because the use of HSCT for metastatic breast cancer has not been shown to be of benefit. 108 CLINICAL FINDINGS AND DIAGNOSTIC EVALUATION Patients with DPTS present with cough, dyspnea, and fever, 2 weeks to 4 months after transplant. 106,107,109 In the appropriate clinical setting, DPTS is diagnosed by demonstration of a decline in carbon monoxide diffu- sion capacity and exclusion of infectious causes. 106,109 CT of the chest may be normal but usually shows ground-glass opacities, linear or nodular opacities, and consolidation. 109 TREATMENT AND PROGNOSIS DPTS responds to corticosteroid therapy. 106,107,109 One case of DPTS refractory to steroid was treated successfully with interferon-gamma. 110 Inhaled fluticasone may be used to prevent DPTS. 111 No death has been attributed to DPTS. 105–107,109 Pulmonary Cytolytic Thrombi Pulmonary cytolytic thrombi (PCT) occurs exclusively in allogeneic HSCT recipients, typically in the setting of GVHD. Most of the reported PCT cases were from a single institution and were under age 18. 112,113 The median onset of PCT is 72 days after transplantation. 113–115 All patients are febrile and some have cough at presentation. 113–115 Chest CT may show multiple peripheral pulmonary nodules. 115 The diagnosis of PCT requires surgical lung biopsy, showing occlusive vascular lesions and hemorrhagic infarcts due to thrombi consisting of intensely basophilic, amorphous material that may extend through the vascular wall. 112 The treatment of PCT is not well defined. There have been no reported deaths attributed to PCT. CONCLUSIONS HSCT recipients are at risk for multiple complications. Their immune defect and recovery follow a predictable course. Knowledge of their immune status at the various phases following transplant is essential to focus on the most likely complications. 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Autologous hematopoietic stem cell transplantation for breast cancer in Europe: critical evaluation of data from the European Group for Blood and Marrow Transplantation (EBMT) Registry 1990–1999. Bone Marrow Transplant 2003;32:489–494 105. Bhalla KS, Wilczynski SW, Abushamaa AM, et al. Pul- monary toxicity of induction chemotherapy prior to standard or high- dose chemotherapy with autologous hematopoietic support. Am J Respir Crit Care Med 2000;161:17–25 106. Cao TM, Negrin RS, Stockerl-Goldstein KE, et al. Pulmonary toxicity syndrome in breast cancer patients undergoing BCNU-containing high-dose chemotherapy and autologous hematopoietic cell transplantation. Biol Blood Marrow Transplant 2000;6:387–394 107. Chap L, Shpiner R, Levine M, Norton L, Lill M, Glaspy J. Pulmonary toxicity of high-dose chemotherapy for breast cancer: a noninvasive approach to diagnosis and treatment. Bone Marrow Transplant 1997;20:1063–1067 108. Stadtmauer EA, O’Neill A, Goldstein LJ, et al. Conven- tional-dose chemotherapy compared with high-dose chemotherapy plus autologous hematopoietic stem-cell transplantation for metastatic breast cancer. Philadelphia 308 SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE/VOLUME 27, NUMBER 3 2006 Bone Marrow Transplant Group. N Engl J Med 2000;342: 1069–1076 109. Wilczynski SW, Erasmus JJ, Petros WP, Vredenburgh JJ, Folz RJ. Delayed pulmonary toxicity syndrome following high-dose chemotherapy and bone marrow transplantation for breast cancer. Am J Respir Crit Care Med 1998;157:565– 573 110. Suratt BT, Lynch DA, Cool CD, Jones RB, Brown KK. Interferon-gamma for delayed pulmonary toxicity syndrome resistant to steroids. Bone Marrow Transplant 2003;31:939– 941 111. McGaughey DS, Nikcevich DA, Long GD, et al. Inhaled steroids as prophylaxis for delayed pulmonary toxicity syndrome in breast cancer patients undergoing high-dose chemotherapy and autologous stem cell transplantation. Biol Blood Marrow Transplant 2001;7:274–278 112. Gulbahce HE, Pambuccian SE, Jessurun J, et al. Pulmonary nodular lesions in bone marrow transplant recipients: impact of histologic diagnosis on patient management and prognosis. Am J Clin Pathol 2004;121:205–210 113. Morales IJ, Anderson PM, Tazelaar HD, Wylam ME. Pulmonary cytolytic thrombi: unusual complication of hematopoietic stem cell transplantation. J Pediatr Hematol Oncol 2003;25:89–92 114. Gulbahce HE, Manivel JC, Jessurun J. Pulmonary cytolytic thrombi: a previously unrecognized complication of bone marrow transplantation. Am J Surg Pathol 2000;24:1147– 1152 115. Woodard JP, Gulbahce E, Shreve M, et al. Pulmonary cytolytic thrombi: a newly recognized complication of stem cell transplantation. Bone Marrow Transplant 2000;25:293– 300 COMPLICATIONS FOLLOWING HEMATOPOIETIC STEM CELL TRANSPLANTATION/AFESSA, PETERS 309 Infection Control and the Prevention of Nosocomial Infections in the Intensive Care Unit Gonzalo M.L. Bearman, M.D., M.P.H., 1 Cindy Munro, Ph.D., R.N., A.N.P., 2 Curtis N. Sessler, M.D., 3 and Richard P. Wenzel, M.D., M.Sc. 4 ABSTRACT Nosocomial infections continue to be signi ficant causes of morbidity, mortality, and added costs in the health care setting. Half of all life-threatening nosocomial bloodstream infections and pneumonias occur in intensive care units (ICUs), despite ICUs representing only 15 to 20% of all hospital beds. Thus an efficient focus for prevention and control of life-threatening health care–associated infections should be in ICUs. Further, growing antibiotic resistance complicates the therapy of serious infections. Meticulous infection control practice with continued attention to hand hygiene is of paramount importance. Strict adherence to evidence-based catheter insertion and main- tenance policies reduces nosocomial bloodstream infections. Evidence-based prevention strategies for ventilator-associated pneumonia, including management of respiratory equipment according to published guidelines and maintaining backrest elevation at 30 to 45 degrees, are effective. For greatest risk reduction, multifaceted programs ensuring maximal adherence with evidence-based infection control guidelines are needed. KEYWORDS: Nosocomial infections, bloodstream infections, ventilator-associated pneumonia, infection control Nosocomial infections add significant morbidity, mortality, and costs to those expected from the patient’s underlying conditions alone. The concep t of attributable mortality has been championed 1 to examine the direct contribution to mortality due to the infection, after accounting for the impact of the patient’s baseline illnesses. When examining the attributable mortality from nosocomial bloodstream infections (BSIs) alone, Wenzel and Edmond showed that they are equivalent to the eighth leading cause of death in the United States. 2 Furthermore, with conservative assumptions nosocomial BSIs annually lead to over 250,000 years of life lost. 2 Therefore, current data are compelling that lives can be extended by preventing BSIs occurring in hospitals. The crude mortality (all cause) for nosocomial BSIs is 25 to 30%, 3 and most studies of pathogen- specific, nosocomial BSIs show that the attributable mortality is at least half of the crude mortality ( 15% on average conservatively). 4–7 Furthermore, the crude and attributable mortality figures for nosocomial pneumonias are  30% and 10%, respectively. The data imply that one third of all pneumonia-related deaths are due directly to the lung infection. Importantly, half of all life-threatening nosocomial BSIs and pneumonias occur 1 Divisions of Quality HealthCare and Infectious Diseases, 2 School of Nursing, 3 Division of Pulmonary and Critical Care Medicine, 4 Department of Internal Medicine, Virginia Commonwealth Univer- sity Medical Center, Richmond, Virginia. Address for correspondence and reprint requests: Gonzalo M.L . Bearman, M.D., M.P.H., Divisions of Quality HealthCare and Infectious Diseases, P.O. Box 980019, V irginia Commonwealth University Medical Center, Richmond, VA 23298-0019. E-mail: gbearman@vcu.edu. Non-pulmonary Critical Care: Managing Multisystem Critical Illness; Guest Editor, Curtis N. Sessler, M.D. Semin Respir Crit Care Med 2006;27:310–324. Copyright # 2006 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel: +1(212) 584-4662. DOI 10.1055/s-2006-945534. ISSN 1069-3424. 310 in critical care units, usually representing 15 to 20% of all hospital beds. Thus an efficient focus for prevention and control of life-threatening health care–associated infections shou ld be in ICUs. Complicating the therapy of serious ICU-related infections is the problem of antibiotic resistance, a global issue with wide country to country variation. 8,9 Consider the leading causes of nosocomial BSIs (proportion of all nosocomial BSIs) in the United States: coagulase negative Staphylococci (31%), S. aur eus (20%), Enterococci (9%), and Candida species (9%) in rank order. In the United States, over 90% of coagulase negative Staph- ylococci and half of all S. aureus nosocomial bloodstream isolates are resistant to methicillin. 3 Approximately 30% of enterococcal isolates are resistant to vancomycin, and over 10% of Candida species are resistant to first-generation triazoles. The crude mortality of BSIs for each species, respectively, is 21%, 25%, 34%, and 39%. 3 Surely the challenge for clinicians is to treat early with appropriate antibiotics in the ICU because inappropriate therapy in the first 24 hours doubled the expected mortality (62% vs 29%) in one study. 10 Furthermore, in the same study, after accounting for the impact of the underlying diseases in a multivariable analysis, the au- thors showed that the adjusted odds ratio for death if the patients were given inappropriate therapy was 6.9. 10 It is clear that the modern clinician in the ICU must not only anticipate the likely organisms and the antibiograms but also treat early. In examining the reasons for prescribing inadequate therapy for ICU BSIs, Ibrahim and colleagues showed that failure to treat for Candi da BSIs had an adjusted odds ratio of 52. 10 This observation suggests that clinicians still fail to recognize the high likelihood of Candida as a cause of serious ICU-related BSIs and thus do not give antifungal therapy empirically. This is an especially important issue because BSIs with Candida independently predict death in analyses that account for the underlying diseases 11 and have a very high attributable mortality. 5,12 Additionally, the modern clinician must be aware of species differences because all of C. krusei, 10 to 20% of C. glabrata, and up to 10% of C. albicans are resistant to first-generation triazoles. 13 Recently, an argument has been made to use easily identified risk factors to target only high risk ICU patients for anti-Candida prophylactic therapy. The model as- sumed a necessary 33% threshold of risk of candidemia for preventive treatment and a 65% efficacy for the drug to be given to prevent candidemia. With the assumptions, the number needed to treat (NNT) to prevent a Candida- related death would be only seven patients. 14 A major concern since 2002 has been the emergence of fully vancomycin-resistant isolates of S. aureus acquired in the health care setting. So far, four cases have been reported, and fortunately no transmission has occurred. In two patients, diabetes mellitus, peripheral vascular disease, and chronic renal insufficiency have been common. In three patients, an extremity had been the site of the soft tissue or bone infection. In all patients, the substrate organism was methicillin-resistant S. aureus (MRSA), and the mechanism of resistance was plasmid transfer of a mec A gene from a co-coloniz- ing Enterococcus (vancomycin resistant enterococci) to the MRSA strain. Earlier it had been shown that 30% of identified patients colonized with vancomycin-resistant enterococci are also colonized with MRSA. 15 Thus the opportunities to see the continual emergence of fully vancomycin-resistant strains are increasing. For the time being, therefore, clinicians have another reason to control MRSA: the reduction of a risk of selecting for vancomycin-resistant S. aureus. With respect to gram-negative rod BSIs, the fifth through ninth leading causes of nosocomial BSIs, in order, are Escherichia coli, Klebsiella species, Pseudomonas aeruginosa, and Enterobacter species. Their respective crude mortality rates are 22%, 28%, 38%, and 27%. 3 It should be pointed out that among patients with hospital-acquired BSIs, P. aeruginosa independently predicts death, 11 and in the United States, 15% of isolates reported in 2003 were resistant to imipenam. 9 Thus a recognition of their frequency and the antibiogram in the ICU is key to effective therapy and prevention of death. In summary, nosocomial BSIs alone are equivalent to the eighth leading cause of death in the United States. Along with nosocomial pneumonias, these life- threatening infections can be found disproportionately in critical care units, where increasing levels of antibiotic resistance are prevalent. Astute clinicians need to know the likely pathogens and treat early with appropriate antibiotics empirically to minimize mortality. The prevention of these infections will have a huge impact on morbidity, mortality, and costs of health care. NOSOCOMIAL BLOODSTREAM INFECTIONS IN THE ICU BSIs are among the most common and most deadly nosocomial infections encountered. 16 Intravascular catheterization ranks as the strongest independent risk factor for nosocomial bacteremia, 17 and the vast majority of primary bacteremias (those not clearly associated with another defined site of infection) are related to vascular catheters. Catheter-related BSI (CRBSI) is associated with prolonged ICU and hospital length of stay, associated added costs, and attributable mortality. 7,18–21 Because an estimated 5 million central venous catheters (CVCs) are inserted in the United States annually, 22 and BSI accompanies 3to 5% of these catheters, as many as 250,000 CRBSI might occur annually in the United States alone. 23 Accordingly, strategies to prevent these common and costly infections are critically important. 22,24–27 INFECTION CONTROL AND PRE VENTION IN THE ICU/ BEARMAN ET AL 311 The principal mechanism by which infections develop is via colonization of the skin surrounding the catheter insertion site followed by migration of pathogens along the su bcutaneous catheter tract and external catheter surface. A second important mechanism that becomes more prevalent with longer catheter duration is the colonization of stopcocks and catheter hubs with subsequent contamination of luminal surfaces and catheter infection. An important intermediary step is accu- mulation of biofilm on the luminal surface. Additional less common mechanisms for CRBSI include hematog- enous seeding from distant foci, and rarely, infusate contamination. Strategies for prevention of CRBSI focus prin- cipally on various measures designed to prevent colonization of external and luminal catheter surfaces with microorganisms. An expert panel convened by the U.S. Centers for Disease Control and Prevention (CDC) identified the following as major areas of emphasis for prevention of catheter-related infection: (1) educating and training health care providers who insert and maintain catheters, (2) using maximal sterile barrier precautions during CVC insertion, (3) using a 2% chlorhexidine preparation for skin antisepsis, (4) avoid- ing routine replacement of CVCs as a strategy to prevent infection, and (5) using antiseptic/antibiotic- impregnated short-term CVCs if the rate of infection is high despite adherence to other strategies. 24 These recommendations are based largely upon clinical trial evidence. Raad and coworkers 28 demonstrated maximum barrier precautions (large sterile drape on the patient and sterile gown and gloves, mask and cap worn by operators) to be a cost-effective approach associated with reduced catheter-related infections. Two percent chlorhexidine is superior to povidone-iodine for skin disinfectant preparation prior to CVC insertion, based upon a meta- analysis of eight randomized, controlled trials that demonstrated lower rates of CRBSI for all catheters (risk ratio ¼ 0.49, 95% confidence interval 0.28 to 0.88) and for CVC (RR ¼ 0.51, 95% CI ¼ 0.27 to 0.97) specifi- cally. 29 Scheduled replacement of CVC or balloon flota- tion pulmonary artery catheters was not found to reduce infectious and mechanical complications when compared with an as needed approach, 30 nor supported in a meta- analysis of eight studies 31 ; thus scheduled replacement is not endorsed. Educational programs and the role of antibacterial/antiseptic-impregnated catheters will be discussed. The CDC working group 24 made additional level I recommendations regarding CVC insertion that include practicing proper hand hygiene, selecting the subclavian vein insertion site to avoid infection whenever feasible upon considering the risk for mechanical complications, and using a sterile gauze or sterile transparent semipermeable dressing to cover the insertion site. The site of CVC insertion has been the subject of debate and personal preference for years. There are meta-analyses of nonrandomized trials, 32 and risk factor analysis from nonrandomized trials, 33 that suggest the subclavian vein approach has fewer CRBSIs than the internal jugular approach vein. Nonrandomized studies 34 and a single randomized trial 35 demonstrate higher rates of catheter- related infections with the femoral vein approach, although some large, nonrandomized case series show only trends for higher CRBSI rates with the femoral approach. 36–38 Accordingly, insertion of a CVC at the subclavian vein site is preferred and the femoral vein site avoided in comprehensive strategies to reduce CRBSI rates. 39–41 The availability of two-dimensional ultrasound (2-D US) may also influence site selection because use of 2-D US is associated with lower rates of both failed CVC insertion and CVC complications, with the most convincing data for the internal jugular site. 42,43 Additional simple measures that have been associated with reduced infection rates in prospe ctive studies include use of proper hand hygiene and a structured approach to achieve high compliance with sterile technique through checklists, consolidated bedside CVC supply carts, and nursing empowerment to stop proce- dures in which violations have occurred. 41 Although these strategies focus primarily on optim izing technique during catheter insertion, equal emphasis must be placed on the timely removal of the catheter, including formal questioning of the continued need for the catheter on daily ICU rounds. 41 Additionally, because hub colonization can occur during frequent manipulation, disin- fection with chlorhexidine/alcohol should be performed when hubs are accessed. 44 Organized strategies that focus on either or both education and improving the process of catheter insertion and care have been shown to produce sustained reductions in rates of CRBSI. 39–41,45–48 Major compo- nents of these and other programs, and recommendations from recent reviews are outli ned in Table 1. Most approaches focus on educating and modifying the be- havior of ICU caregivers, including physicians and nurses; however, some educational programs also target medical students. 49,50 In the event that CRBSI rates remain unaccept- ably high despite implementing strategies such as those already described, experts recommend considering the use of antiinfective catheters. 24 Catheters coated with chlorhexidine and silver sulfadiazine (CSS) have been most widely studied and were demonstrated in a 1999 meta-analysis to be associated with reduced rates of CRBSI compared with uncoated catheters. 51 However, this catheter was found to be inferior to a minocycline- rifampin (MR)-impregnated catheter for preventing CRBSI in a head to head multicenter, randomized, controlled trial (RCT). 52 Both catheters have been modified and current products have coatings of both external and luminal surfaces. The newer CSS catheter 312 SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE/VOLUME 27, NUMBER 3 2006 [...]... all ICU patients. 89 Backrest elevation reduces risk of gastroesophageal reflux and aspiration90 ,91 and risk of VAP .92 ,93 However, backrest elevation has been underutilized .94 97 Although patient positioning is a nursing activity, a written physician order for backrest elevation may increase time spent at 30 to 45 degrees .98 In 2005, the Joint Commission on the Accreditation of Healthcare Organizations... cause of morbidity and mortality in critically ill adults A recent meta-analysis examining 89 VAP research studies published since 199 0 concluded that VAP occurs in 10 to 20% of patients receiving more than 48 hours of mechanical ventilation.70 VAP doubles the mortality risk of critically ill patients, lengthens ICU and hospital stay, and increases hospital costs Early-onset VAP (diagnosed on or before... catheters can be cost-effect if baseline CRBSI rate is sufficiently high.58 Additional technology-based or invasive approaches to insertion of short-term CVCs in ICU patients include use of a chlorhexidine-impregnated sponge dressing, 59 catheter hub ‘‘lock’’ with solutions containing alcohol, heparin, and/or vancomycin,60,61 use of heparin-coated CVCs,62 and subcutaneous tunneling of short-term CVCs.63,64... cost of medical care, trigger the use of unnecessary antimicrobials, and provide a nosocomial reservoir of drug-resistant pathogens.68 As such, nosocomial urinary tract infections are of epidemiological importance The majority of catheter-associated urinary tract infections derive from the patient’s own periurethral and perineal flora or from cross-transmission via the hands of health care workers during... unnecessary catheterizations A recent paper by Maki and Tambyah 69 suggested that urinary catheter use should be limited to patients requiring relief of urinary obstruction, patients undergoing surgical repair of the genitourinary tract, 313 314 SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE/VOLUME 27, NUMBER 3 critically ill or post-operative patients requiring adequate measurement of urine output,... increasing the pool of gastric organisms that serve as a source of VAP pathogens Despite much research (including seven meta-analyses since 199 1),110 a consensus regarding recommendations for prophylaxis with histamine-2 receptor antagonists versus sucralfate, balancing risk of stress-bleeding with risk of VAP, has not yet emerged Acidification of gastric feedings has also been proposed as a method to reduce... femoral sites (2.3/1000 CVC days).65 CATHETER-ASSOCIATED URINARY TRACT INFECTIONS Urinary catheters are inserted into more than 5 million patients in both acute care hospitals and extended care facilities Nosocomial bacteriuria predictably occurs in 25% of patients requiring urinary catheterization for greater than 7 days.66,67 Several studies suggest that catheter-associated urinary tract infections, although... pneumoniae, Staphylococcus aureus), whereas late-onset VAP (diagnosed after day 5 of intubation) is more frequently associated with aerobic gram-negative bacteria (Pseudomonas aeruginosa or Acinetobacter species) and MRSA.71–75 Additional risk factors for VAP with antibiotic-resistant organisms include recent antibiotic use and recent admission to a health care facility.75 Patients with pneumonia caused... expanded use of PICCs 5 Consider use of anti-infective catheter if institutional CRBSI rates remain excessive despite careful attention to conventional infection control issues Catheter insertion and care 1 Confirm that CVC is really needed 2 Select insertion site based upon CVC indication, patient risk factors for complications, patient anatomy, and availability of two-dimensional ultrasound Use subclavian... focus of VAP prevention efforts While implementation of a comprehensive oral-hygiene program is recommended for those at risk for VAP, evidence-based oral care protocols have not been published Oral chlorhexidine gluconate (0.12%) rinse begun prior to cardiac surgery in adults and continued until extubation decreased VAP108,1 09 and is now recommended, but because only limited data are available for ICU . 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