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Biomedical subjects

Craig M Coopersmith

Publications and source records attributed to Craig M Coopersmith.

35 records · Page 2Linked to original sources
PubMed2004

The impact of bedside behavior on catheter-related bacteremia in the intensive care unit.

HYPOTHESIS: The success of an educational program in July 1999 that lowered the catheter-related bloodstream infection (CRBSI) rate in our intensive care unit (ICU) 3-fold is correlated with compliance with "best-practice" behaviors. DESIGN: Before-after trial. SETTING: Surgical ICU in a referral hospital. PATIENTS: A random sample underwent bedside audits of central venous catheter care (n = 187). All ICU admissions during a 39-month period (N = 4489) were prospectively followed for bacteremia. INTERVENTIONS: On the basis of audit results in December 2000, a behavioral intervention was designed to improve compliance with evidenced-based guidelines of central venous catheter management. MAIN OUTCOME MEASURES: Compliance with practices known to decrease CRBSI. Secondary outcome was CRBSI rate on all ICU patients. RESULTS: Multiple deficiencies were identified on bedside audits 18 months after the previous educational program. After the implementation of a separate behavioral intervention in July 2001, a second set of bedside audits in December 2001 demonstrated improvements in documenting the dressing date (11% to 21%; P<.001) and stopcock use (70% to 24%; P<.001), whereas nonsignificant trends were observed in hand hygiene (17% to 30%; P>.99) and maximal sterile barrier precautions (50% to 80%; P =.29). Appropriate practice was observed before and after the behavioral intervention in catheter site placement, dressing type, absence of antibiotic ointment, and proper securing of central venous catheters. Thirty-two CRBSIs occurred in 9353 catheter-days 24 months before the behavioral intervention compared with 17 CRBSIs in 6152 catheter-days during the 15 months after the intervention (3.4/1000 to 2.8/1000 catheter-days; P =.40). CONCLUSIONS: Although a previous educational program decreased the CRBSI rate, this was associated with only modest compliance with best practice principles when bedside audits were performed 18 months later. A behavioral intervention improved all identified deficiencies, leading to a nonsignificant decrease in CRBSIs.

Adult↗
PubMed2004

Treatment of hypophosphatemia using a protocol based on patient weight and serum phosphorus level in a surgical intensive care unit.

BACKGROUND: Hypophosphatemia may cause organ derangements in the surgical intensive care unit. The purpose of this study was to determine the impact of a repletion protocol for hypophosphatemia based on admission weight and phosphorus level. STUDY DESIGN: All patients who presented to an 18-bed surgical intensive care unit with a serum phosphorus level of 2.2 mg/dL or less or who received phosphorus supplementation despite having normal levels were identified. In the preintervention phase between January and June 2001, 137 patients were retrospectively identified who met these criteria. A protocol was then designed giving a single intravenous dose of phosphorus based on weight and serum phosphorus. Repletion was given with sodium or potassium phosphorus based on presupplementation levels. After protocol implementation 141 patients met these criteria between September 2001 and February 2002, and treatment and postrepletion levels were followed prospectively. RESULTS: A total of 47 patients were repleted before the intervention with adequate followup and 22 (47%) attained a normal level. Supplementation success was 53% in moderate hypophosphatemia (2.2 mg/dL or less) and 27% in severe hypophosphatemia (less than 1.5 mg/dL). After protocol implementation, 111 patients were repleted with 84 (76%) correcting to a normal level (p = 0.002 compared with retrospective patients). Success was 78% in moderate hypophosphatemia and 62% in severe hypophosphatemia. Inappropriate supplementation of normal phosphorus levels decreased from 51 to 16 patients after protocol implementation. CONCLUSIONS: A protocol based on weight and serum levels successfully treated both moderate and severe hypophosphatemia in the majority of critically ill patients. Protocol implementation also decreased unnecessary supplementation of normal phosphorus levels.

Adult↗
PubMed2004

High-dose exogenous iron following cecal ligation and puncture increases mortality rate in mice and is associated with an increase in gut epithelial and splenic apoptosis.

OBJECTIVES: Despite having dysregulated iron metabolism, critically ill patients may receive exogenous iron for the treatment of anemia. Iron is associated with increased tissue apoptosis and may facilitate bacterial growth. We hypothesized that exogenous iron administration given after the onset of sepsis would lead to increased mortality rate. To discriminate between elevated cell death and bacterial overgrowth as potential mediators of mortality, we examined gut epithelial and lymphocyte apoptosis and systemic bacterial counts in animals given iron supplementation after the onset of sepsis. DESIGN: Prospective, randomized, controlled study. SETTING: Animal laboratory in a university medical center. SUBJECTS: Male C57BL/6 mice, 6-10 wks old. INTERVENTIONS: C57BL/6 mice were subjected to cecal ligation and puncture (CLP), a well-accepted model of intra-abdominal sepsis, followed by daily subcutaneous injections of either 1 mL of iron dextran (5 mg/mL) or 0.9% NaCl for a total of five doses. Animals (n = 78) were followed for survival for 8 days. Separate cohorts (n = 76) were killed 24 or 48 hrs after cecal ligation and puncture or sham laparotomy and were assayed for gut epithelial and splenic apoptosis as well as for quantitative blood cultures. MEASUREMENTS AND MAIN RESULTS: Eight-day survival was 7% in animals that received iron and 26% in mice that received 0.9% NaCl (p < .005). Iron supplementation after cecal ligation and puncture increased apoptosis by both active caspase 3 and hematoxylin and eosin staining in both the intestinal epithelium and spleen at 24 hrs (p < .05). Iron supplementation after sham laparotomy did not cause mortality or elevated apoptosis. Quantitative blood cultures revealed no detectable differences between septic animals that received iron and those that received 0.9% NaCl. CONCLUSIONS: High-dose iron supplementation with iron dextran after the onset of sepsis significantly increases mortality rate in this animal model. Iron-induced mortality may be mediated by an increase in gut epithelial and splenic apoptosis, whereas severity of bacteremia does not appear to play a causative role.

Anemia, Iron-Deficiency↗
PubMed2004

Antibiotics improve survival in sepsis independent of injury severity but do not change mortality in mice with markedly elevated interleukin 6 levels.

Genetically identical mice have a heterogeneous response to antibiotic therapy in sepsis, with only a subset deriving therapeutic benefit. We sought to determine whether the severity of a septic insult correlates with the survival benefit conferred by antibiotics. We also sought to determine whether antibiotics given 12 h after injury alter survival in animals predicted to die based upon high interleukin (IL)-6 levels drawn 6 h earlier. Adult male ND4 mice (n = 363) were subjected to double-puncture cecal ligation and puncture (CLP) with a 19-, 21-, or 23-gauge needle. Animals were randomized to receive imipenem or 0.9% NaCl every 12 h after CLP for 5 days. Ten-day survival was 16%, 26%, and 52%, respectively, for untreated animals. Antibiotics decreased the absolute risk of death 17% to 23% regardless of injury severity. In a separate cohort, mice (n = 37) were subjected to single or double-puncture CLP with a 21-gauge needle. IL-6 levels were assayed 6 h postoperatively and mice were followed for survival. Levels greater than 14,000 pg/mL were identified as predicting a 100% mortality (7/7 animals dead). A third set of mice (n = 94) then underwent double-puncture CLP with either 21-, 23-, or 25-gauge needle and had IL-6 levels measured in a similar fashion. Animals were randomized to receive imipenem or 0.9% NaCl beginning 12 h postoperatively (6 h after IL-6 levels were drawn) and continued for 5 days or until death. Although antibiotics decreased mortality overall, all animals with IL-6 levels greater than 14,000 pg/mL (n = 13) died, regardless of whether they received antibiotics or the gauge of needle used. These results indicate that antibiotics improve outcome in murine sepsis, regardless of injury severity. Furthermore, there is a threshold IL-6 level that can be identified 6 h after sepsis above which animals are destined to die, and antibiotic treatment does not alter their outcome.

Animals↗
PubMed2004

Sequence makes a difference: paradoxical effects of stress in vivo.

In vitro studies have shown that induction of heat shock before an inflammatory stimulus is cytoprotective, whereas induction of heat shock after an inflammatory stimulus can lead to apoptosis (the "heat shock paradox"). We sought to determine whether induction of the heat shock response in vivo caused similar, order-dependent effects on survival, and if so, by what mechanism. ND4 and C57BL/6 mice were used to calibrate the response to hyperthermia at 41.5 degrees C via induction of inducible heat shock protein 70. Sequences of heat shock and septic stresses were studied in murine models of hyperthermia (41.5 degrees C for 20 min) and cecal ligation and puncture (CLP), respectively. Previous heat shock to 41.5 degrees C did not protect CLP mice when compared with control CLP animals heated to 37 degrees C, but heat shock increased mortality when activated after CLP compared with controls. This effect of heat shock on CLP mortality was strain independent, and did not involve alterations in CLP-induced thymus, spleen, or intestinal apoptosis. We conclude that the heat shock paradox can occur in vitro and in vivo, and that the negative effects of heat shock on survival after CLP appeared to be strain independent. Furthermore, the stress of general anesthesia and warming also altered CLP mortality unexpectedly. The cellular mechanisms responsible for these "stressor" paradoxes in vivo are not known, but do not involve altered sepsis-induced apoptosis.

Animals↗
PubMed2004

Age disproportionately increases sepsis-induced apoptosis in the spleen and gut epithelium.

Both aging and sepsis independently increase splenic and gut epithelial apoptosis. Sepsis-induced apoptosis in either cell type is also associated with increased mortality in young mice. We sought to determine whether age alters sepsis-induced splenic and gut epithelial cell death. Young (2 months) and aged (22 months) male ND4 mice were subjected to either single-puncture cecal ligation and puncture (CLP) with a 23-gauge needle or sham laparotomy. Apoptosis was assessed 24 hours later in the spleen and gut epithelium by active caspase 3 and hematoxylin and eosin staining. Aged septic mice had increased splenic apoptosis compared with either young septic animals or aged sham animals (15 vs. 7 vs. 5 apoptotic cells/high-powered field, P < 0.05). Similarly, aged septic animals had an elevation in gut epithelial cell death compared with either young septic or aged sham mice (33 vs. 16 vs. 6 apoptotic cells/100 contiguous crypts, P < 0.05). Elevated intestinal cell death was not associated with changes in either gut proliferation or cell division. To verify that the increase in splenic apoptosis seen in septic aged animals was not strain specific, double-puncture CLP with a 25-gauge needle or sham laparotomy was performed on young (4 months) or aged (24 months) C57BL/6 male mice. Similar to results seen in outbred animals, aged septic animals in this inbred strain had increased splenic apoptosis compared with either young septic animals or aged sham animals (23 vs. 7 vs. 4 apoptotic cells/ high powered field, P < 0.05). These results indicate that although infection and aging each independently cause an increase in splenic and gut epithelial apoptosis, their combination leads to a disproportionate increase in cell death in these rapidly dividing cell populations,and potentially plays a role in the marked increase in mortality seen with aging in sepsis.

Aging↗
PubMed2003

Effects of age on mortality and antibiotic efficacy in cecal ligation and puncture.

The incidence and mortality of sepsis increase with age, consequently, 80% of the clinical mortality from sepsis occurs in patients over age 65. Despite this aged clinical population, most research models of sepsis use 6- to 16-week-old mice as patient surrogates. This age range of mice corresponds to human ages 10 to 17 years. To assess the influence of age on rodent CLP and on antibiotic therapy, we studied young (4 month), mature (12 month), and aged (24 month) mice. Male C57BL/6 mice (n = 27-30 in each age group) were subjected to cecal ligation and puncture (CLP), two punctures with a 25-gauge needle. Mice were observed untreated for 10 days. Young mice had 20% mortality, mature mice had 70% mortality (P = 0.0013 vs. young), and aged mice had 75% mortality (P = 0.0001 vs. young). To assess the effects of age on antibiotic therapy, mice were subjected to CLP as above (n = 38-40 in each age group). Mice were then randomized to treatment with intraperitoneal injections of ceftriaxone and metronidazole or normal saline. Therapy was initiated 12 h after CLP, and injections were repeated every 12 h for 7 days. Young mice saw a 56% decrease in mortality from CLP with antibiotic therapy (P = 0.001), and mature mice had a 30% decrease in mortality (P = 0.06). Aged mice saw no benefit from antibiotic therapy. We also compared plasma cytokine levels between young and aged mice after CLP. When compared with young mice, aged mice had higher levels of IL-6 and TNF-alpha 24 h after CLP. However, high IL-6 was predictive of mortality at any age. Mice appear to have age-dependent responses to intra-abdominal sepsis and to appropriate therapy.

Age Factors↗
PubMed2003

Role of intestinal epithelial apoptosis in survival.

PURPOSE OF REVIEW: To outline evidence that suggests increased intestinal epithelial apoptosis (programmed cell death) plays an important role in critical illness of infectious and noninfectious origin. RECENT FINDINGS: Both human and animal studies demonstrate that the gut epithelium has increased levels of cellular death in sepsis and noninfectious inflammation. Importantly, gut apoptosis appears to be detrimental to survival in sepsis. Transgenic mice that overexpress the antiapoptotic protein Bcl-2 in their gut epithelia have increased survival compared with wild-type littermates in murine models of ruptured appendicitis and Pseudomonas aeruginosa pneumonia. SUMMARY: These animal studies offer a possible new mechanism underlying the gut's role as the "motor" of the systemic inflammatory response syndrome and suggest that intestinal epithelial apoptosis may be a novel therapeutic target in future critical care research.

Animals↗
PubMed2003

Sepsis from Pseudomonas aeruginosa pneumonia decreases intestinal proliferation and induces gut epithelial cell cycle arrest.

OBJECTIVES: To evaluate whether the up-regulation in sepsis-induced gut epithelial apoptosis is balanced by an increase in intestinal proliferation and to assess mechanisms affecting the gut's regenerative response to overwhelming infection. DESIGN: Prospective, randomized, controlled study. SETTING: Animal laboratory in a university medical center. INTERVENTIONS: Mice were subjected to intratracheal injection of Pseudomonas aeruginosa and killed between 1.5 and 24 hrs after induction of pneumonia-induced sepsis to assess for gut epithelial proliferation and cell division and for apoptosis. Animals were compared with sham-operation controls, septic transgenic mice that overexpress Bcl-2 throughout their small intestinal epithelium, and septic p53-/- mice. MEASUREMENTS AND MAIN RESULTS: Proliferation and cell division were assessed by measuring S-phase and M-phase cells in intestinal crypts. The number of S-phase cells showed a progressive decline at all time points measured, with a 5-fold decrease in proliferation between control animals and septic mice 24 hrs after intratracheal injection of pathogenic bacteria (p <.0001). In contrast, cells in M-phase remained constant for the first 12 hrs after the onset of sepsis, but increased nearly 50% at 24 hrs after instillation of P. aeruginosa (p <.005). Both the decrease in S-phase cells and the increase in M-phase cells were partially suppressible in Bcl-2 overexpressors, but cellular proliferation and division were similar between septic p53-/- and p53+/+ mice. Crypt apoptosis was increased at all time points, with maximal death occurring between 12 and 24 hrs. CONCLUSIONS: Sepsis from P. aeruginosa pneumonia induces a p53-independent decrease in gut epithelial proliferation. Despite an increase in sepsis-induced intestinal apoptosis, there is no compensatory increase in intestinal epithelial proliferation, and there is evidence of a cell cycle block with an accumulation of cells in M-phase. Decreasing gut apoptosis by overexpression of Bcl-2 is associated with a partial reversal of the effect of sepsis on the cell cycle.

Animals↗
PubMed2003

Antibiotics improve survival and alter the inflammatory profile in a murine model of sepsis from Pseudomonas aeruginosa pneumonia.

Differing antibiotic regimens can influence both survival and the inflammatory state in sepsis. We investigated whether the addition and/or type of antimicrobial agent could effect mortality in a murine model of Pseudomonas aeruginosa pneumonia-induced sepsis and if antibiotics altered systemic levels of cytokines. FVB/N mice were subjected to intratracheal injection of pathogenic bacteria and were given gentamicin, imipenem, or 0.9% NaCl 2 h after surgery, which continued every 12 h for a total of six doses. Survival at 7 days (n = 24 in each group) was 100% for mice given gentamicin, 88% for mice given imipenem, and 8% for sham mice treated with 0.9% NaCl (P < 0.0001). Systemic interleukin (IL) 6 levels were assayed 6 h postoperatively on all mice to see if they were predictive of outcome. Plasma IL-6 levels above 3,600 pg/mL were associated with a 100% mortality, levels under 1,200 pg/mL were associated with a 100% survival, and levels between 1,200 and 3,600 pg/mL had no utility in predicting mortality. In a separate experiment, mice were sacrificed at 3, 6, 12 or 24 h after instillation of P. aeruginosa and were assayed for levels of TNF-alpha, IL-6, IL-10, and IL-12. Significant alterations in the proinflammatory cytokines TNF-alpha and IL-6 were present at all time points except 3 h between mice treated with antibiotics and sham controls. In contrast, statistically significant differences in the anti-inflammatory cytokine IL-10 were present between the groups only at 6 h, and levels of IL-12 were similar at all time points. These results indicate that both gentamicin and imipenem increase survival at least 10-fold in a model of pneumonia-induced monomicrobial sepsis, and this is predominantly associated with a down-regulation of proinflammatory cytokines.

Animals↗
PubMed2003

Bcl-2 inhibits gut epithelial apoptosis induced by acute lung injury in mice but has no effect on survival.

Gut epithelial apoptosis is increased in human studies and animal models of noninfectious inflammation and sepsis. Elevated intestinal cell death appears to be physiologically significant in sepsis. Previous studies demonstrate that overexpression of the antiapoptotic protein Bcl-2 in the gut epithelium of transgenic mice is associated with improved survival from Pseudomonas aeruginosa pneumonia and cecal ligation and puncture. The functional significance of elevated gut apoptosis in noninfectious inflammation has not been examined. We hypothesized that intestinal apoptosis would be detrimental to survival in noninfectious critical illness. To address this issue, acute lung injury (ALI) was induced with intratracheal injection of lipopolysaccharide (LPS, 800 microg) in wild-type (WT) FVB/N mice and transgenic mice that overexpress Bcl-2 in their intestinal epithelium. Guts were harvested at 12, 24, 48, and 72 h and assessed for apoptosis by both hematoxylin and eosin and active caspase-3 staining in 100 contiguous crypts. ALI increased gut epithelial apoptosis 12 h after LPS instillation compared with shams (P < 0.01), whereas overexpression of Bcl-2 decreased intestinal apoptosis compared with WT animals with ALI when assayed by active caspase-3 (P < 0.05). Plasma levels of tumor necrosis factor alpha, interleukin (IL)-6, and IL-10 were similar between WT and transgenic animals with ALI, both of which had elevated IL-10 levels at 12 h and elevated IL-6 levels at 24 h compared with sham animals. In a separate experiment, transgenic and WT animals with ALI were followed for mortality to determine whether gut overexpression of Bcl-2 conferred a survival advantage. Survival at 10 days was 73% in WT animals (n = 33) and 65% in Bcl-2 animals (n = 23, P = ns). These results indicate that while gut epithelial apoptosis is elevated in multiple models of critical illness, prevention of intestinal cell death by overexpression of Bcl-2 is associated with a disparate survival effect between sepsis and noninfectious inflammation.

Administration, Inhalation↗
PubMed2002

Inhibition of intestinal epithelial apoptosis and survival in a murine model of pneumonia-induced sepsis.

CONTEXT: Increased intestinal epithelial apoptosis is present in both human autopsy studies and animal models of sepsis. Whether altering gut apoptosis decreases mortality in sepsis induced by pathogenic bacteria outside the gut is unknown. OBJECTIVE: To determine if decreasing levels of intestinal cell death improves survival in a murine model of Pseudomonas aeruginosa pneumonia-induced sepsis. DESIGN AND MATERIALS: Prospective study in which transgenic mice that overexpress the antiapoptotic protein Bcl-2 in their intestinal epithelium (n = 25) and control littermates (n = 26) were subjected to intratracheal injection of P aeruginosa. MAIN OUTCOME MEASURES: Survival at 7 postoperative days, compared between the 2 groups. Secondary outcomes included quantification of gut epithelial apoptosis. RESULTS: Survival in transgenic mice that overexpress Bcl-2 in the intestinal epithelium was 40% (10/25) compared with 4% (1/26) in control littermates 7 days after intratracheal injection of P aeruginosa (P =.001), with differences in survival noted within 24 hours of surgery. Overexpression of Bcl-2 was associated with a decrease in gut epithelial apoptosis demonstrated by active caspase 3 staining, the terminal deoxynucleotidyltransferase-mediated dUTP nick end-labeling assay, and hematoxylin-eosin staining. CONCLUSIONS: In this murine model, inhibiting gut epithelial apoptosis by overexpression of Bcl-2 was associated with a survival advantage in P aeruginosa pneumonia-induced sepsis. These results suggest that intestinal epithelial apoptosis may play a role in sepsis-related mortality.

Animals↗
PubMed2002

Effect of an education program on decreasing catheter-related bloodstream infections in the surgical intensive care unit.

OBJECTIVE: The purpose of the study was to determine whether an education initiative aimed at improving central venous catheter insertion and care could decrease the rate of primary bloodstream infections. DESIGN: Pre- and postintervention observational study. SETTING: Eighteen-bed surgical/burn/trauma intensive care unit (ICU) in an urban teaching hospital. PATIENTS: A total of 4,283 patients were admitted to the ICU between January 1, 1998, and December 31, 2000. INTERVENTIONS: A program primarily directed toward registered nurses was developed by a multidisciplinary task force to highlight correct practice for central venous catheter insertion and maintenance. The program consisted of a 10-page self-study module on risk factors and practice modifications involved in catheter-related infections as well as a verbal in-service at staff meetings. Each participant was required to take a pretest before taking the study module and an identical test after its completion. Fact sheets and posters reinforcing the information in the study module were also posted throughout the ICU. MEASUREMENTS AND MAIN RESULTS: Seventy-four primary bloodstream infections occurred in 6874 catheter days (10.8 per 1000 catheter days) in the 18 months before the intervention. After the implementation of the education module, the number of primary bloodstream infections fell to 26 in 7044 catheter days (3.7 per 1000 catheter days), a decrease of 66% (p < .0001). The estimated cost savings secondary to the decreased infection rate for the 18 months after the intervention was between $185,000 and $2.808 million. CONCLUSIONS: A focused intervention primarily directed at the ICU nursing staff can lead to a dramatic decrease in the incidence of primary bloodstream infections. Educational programs may lead to a substantial decrease in cost, morbidity, and mortality attributable to central venous catheterization.

Catheterization, Central Venous↗
PubMed2002

Overexpression of Bcl-2 in the intestinal epithelium improves survival in septic mice.

OBJECTIVES: The aim of this study was to determine whether decreasing intestinal epithelial apoptosis in sepsis would alter mortality rates. The roles of the antiapoptotic protein Bcl-2 and the "executioner" protease caspase-3 in sepsis-induced gut cell death also were evaluated. DESIGN: Prospective, randomized, controlled trial. SETTING: Animal laboratory in an academic medical center. INTERVENTIONS: Transgenic mice that overexpress Bcl-2 throughout the small intestinal epithelium (n = 23) and littermate controls (n = 27) were subjected to cecal ligation and puncture (CLP) and followed for 8 days to assess survival. A second group of transgenic (n = 15) and littermate animals (n = 15) were subjected to CLP and were killed between 16 and 48 hrs postoperatively to assess for intestinal apoptosis and active caspase-3 staining. MEASUREMENTS AND MAIN RESULTS: Survival of transgenic animals was 83% 8 days after CLP compared with 44% for littermate controls (p < .005). Survival curves between the two groups of animals began diverging within 24 hrs. Overexpression of Bcl-2 was associated with a significant decrease in apoptosis between 16 and 24 hrs post-CLP (p < .05) as well as decreased staining for active caspase-3. CONCLUSIONS: Decreasing intestinal epithelial cell death via overexpression of Bcl-2 improves survival in septic mice. The gut may play a central role in the pathophysiology of sepsis.

Animals↗
PubMed2002

Effect of an education program aimed at reducing the occurrence of ventilator-associated pneumonia.

OBJECTIVE: The purpose of the study was to determine whether an education initiative could decrease the hospital rate of ventilator-associated pneumonia. DESIGN: Pre- and postintervention observational study. SETTING: Five intensive care units in Barnes-Jewish Hospital, an urban teaching hospital. PATIENTS: Patients requiring mechanical ventilation who developed ventilator-associated pneumonia between October 1, 1999, and September 30, 2001. INTERVENTIONS: An education program directed toward respiratory care practitioners and intensive care unit nurses was developed by a multidisciplinary task force to highlight correct practices for the prevention of ventilator-associated pneumonia. The program consisted of a ten-page self-study module on risk factors and practice modifications involved in ventilator-associated pneumonia, inservices at staff meetings, and formal didactic lectures. Each participant was required to take a preintervention test before the study module and identical postintervention tests following completion of the study module. Fact sheets and posters reinforcing the information in the study module were also posted throughout the intensive care units and the Department of Respiratory Care Services. MEASUREMENTS AND MAIN RESULTS: One hundred ninety-one episodes of ventilator-associated pneumonia occurred in 15,094 ventilator days (12.6 per 1,000 ventilator days) in the 12 months before the intervention. Following implementation of the education module, the rate of ventilator-associated pneumonia decreased to 81 episodes in 14,171 ventilator days (5.7 per 1,000 ventilator days), a decrease of 57.6% (p <.001). The estimated cost savings secondary to the decreased rate of ventilator-associated pneumonia for the 12 months following the intervention were between $425,606 and $4.05 million. CONCLUSIONS: A focused education intervention can dramatically decrease the incidence of ventilator-associated pneumonia. Education programs should be more widely employed for infection control in the intensive care unit setting and can lead to substantial decreases in cost and patient morbidity attributed to hospital-acquired infections.

Cost-Benefit Analysis↗