Biomedical subjects

J Jason Hoth

Publications and source records attributed to J Jason Hoth.

17 recordsLinked to original sources

PubMed2007

Thoracic trauma: when and how to intervene.

Trauma is the leading cause of death in patients younger than 40 years of age. Thoracic injuries are common and often can be managed by tube thoracostomy. In many patients, however, the thoracic injuries must be repaired surgically in one of three time periods: immediate, urgent, or delayed thoracotomy. In this article, we describe the general approach to effectively managing thoracic trauma patients. We review common injuries and scenarios that may be encountered by the surgeon and discuss the considerations and variables that enter into the decision-making process for operative intervention.

Aorta, Thoracic↗

PubMed2006

Interleukin-10 suppresses natural killer cell but not natural killer T cell activation during bacterial infection.

Interleukin (IL)-10 is an anti-inflammatory cytokine known to modulate the outcome of sepsis by decreasing pro-inflammatory cytokine production, including IL-12, a main activator of natural killer (NK) cells. We hypothesized that neutralization of IL-10 would increase NK and natural killer T (NKT) cell activation through increased IL-12 in a mouse model of bacterial peritonitis. NK and NKT cell activations were measured by CD69 expression on NK1.1+/CD3- and NK1.1+/CD3+ cells after cecal ligation and puncture (CLP). NK cells were significantly more activated in mice treated with anti-IL-10 antibodies, whereas no such effect was observed in NKT cells. Similarly, intracellular interferon gamma (IFN-gamma) levels were increased in NK cells of anti-IL-10-treated mice, but not in NKT cells. IL-12 and IL-18 levels were increased in both CLP groups, but in anti-IL-10-treated mice, early IL-12 and late IL-18 levels were significantly higher than in controls. Survival at 18 h after CLP was lower in anti-IL-10 mice, which was associated with increased liver neutrophil accumulation. In summary, these data show an activating effect of IL-10 on NK, but not on NKT cells after CLP, which corresponded with decreased survival, higher IFN-gamma production, and increased remote organ neutrophil accumulation. These effects were not mediated by IL-12 and IL-18 alone, and reinforce a role for NK cells in remote organ dysfunction following peritonitis.

Animals↗

PubMed2006

A practical application of practice-based learning: development of an algorithm for empiric antibiotic coverage in ventilator-associated pneumonia.

BACKGROUND: Development of practice-based learning (PBL) is one of the core competencies required for resident education by the Accreditation Council for Graduate Medical Education, and specialty organizations including the American College of Surgeons have formed task forces to understand and disseminate information on this important concept. However, translating this concept into daily practice may be difficult. Our goal was to describe the successful application of PBL to patient care improvement with development of an algorithm for the empiric therapy of ventilator-associated pneumonia (VAP). METHODS: The algorithm development occurred in two phases. In phase 1, the microbiology and timing of VAP as diagnosed by bronchoalveolar lavage was reviewed over a 2-year period to allow for recognition of patterns of infection. In phase 2, based on these data, an algorithm for empiric antibiotic coverage that would ensure that the large majority of patients with VAP received adequate initial empiric therapy was developed and put into practice. The period of algorithm use was then examined to determine rate of adequate coverage and outcome. RESULTS: : In Phase 1, from January 1, 2000 to December 31 2001, 110 patients were diagnosed with VAP. Analysis of microbiology revealed a sharp increase in the recovery of nosocomial pathogens on postinjury day 7 (19% < day 7 versus 47% > or = day 7, p = 0.003). Adequate initial antibiotic coverage was seen in 74%. In Phase 2, an algorithm employing ampicillin- sulbactam for coverage of community- acquired pathogens before day 7 and cefipime for nosocomial coverage > or =day 7 was then employed from January 1, 2002 to December 31, 2003. Evaluation of 186 VAP cases during this interval revealed a similar distribution of nosocomial cases (13% < day 7 versus 64% > or = day 7, p < 0.0001). Empiric antibiotic therapy was adequate in 82% of cases or =day 7: overall accuracy improved to 83% (p = 0.05). Mortality from phase 1 to phase 2 trended toward a decrease (21% versus 13%, p = 0.1). CONCLUSIONS: Application of the concept of PBL allowed for identification of local patterns of infection and development of an institution specific treatment algorithm that resulted in >80% adequate initial empiric coverage for VAP with a trend toward decreased mortality. PBL allows for alteration in practice based on local patterns and outcomes and has the potential to improve patient care.

Algorithms↗

PubMed2006

Validation of stroke work and ventricular arterial coupling as markers of cardiovascular performance during resuscitation.

BACKGROUND: Resuscitation regimens based on stroke work index (SWI) and ventricular-arterial coupling (VAC) are controversial. The Signal Interpretation and Monitoring (SIMON) system continuously collects and stores physiologic intensive care unit (ICU) bedside data at 3- to 5-second intervals. The purpose of this study was to demonstrate the capabilities of a completely automated data management system by further evaluating SWI-based resuscitation. METHODS: This study was a retrospective review of all severely injured patients requiring a pulmonary artery catheter (PAC) for acute postinjury resuscitation. Patients with a severe head injury were excluded. Hemodynamic (HD) data (21 million datapoints) were densely acquired and archived by SIMON. Mean values of HD variables were compared between survivors and nonsurvivors. Receiver operator characteristic (ROC) curves were constructed for HD variables. Threshold values which maximized sensitivity and specificity were determined. RESULTS: Eighty-eight patients over a 19-month time period met criteria and were included in the analysis. SWI was significantly greater in survivors versus nonsurvivors (4421 +/- 1278 versus 3163 +/- 1066 mm Hg . mL/m, p = 0.0008). VAC was quantified by the ratio (RATIO) of afterload (Ea) to contractility (Ees). RATIO (Ea/Ees) in survivors was significantly better than in nonsurvivors (1.9 +/- 1.1 vs. 2.9 +/- 1.0, p = 0.002). ROC curves identified threshold values of 3250 mm Hg x mL/m for SWI and 2.1 for RATIO (AUC = 0.78 and 0.82, respectively). CONCLUSION: Previous work demonstrating the use of SWI and VAC as resuscitation guidelines was supported through the use of a powerful ICU data management system (SIMON). The emergence of these "new vital signs" may change the way injured patients are evaluated and resuscitated in the ICU.

Adult↗

PubMed2006

The pathogenesis of pulmonary contusion: an open chest model in the rat.

BACKGROUND: Chemokines direct leukocytes to areas of inflammation or injury. In general, CC chemokines (MCP-1, MIP-1alpha, RANTES) are chemoattractants for mononuclear cells and CXC (CINC-1, MIP-2alpha) for polymorphonuclear cells (PMNs). Herein we describe an open chest model of pulmonary contusion (PC) in a rodent (rat) and have identified a possible role for CC and CXC chemokines in the pathogenesis of PC. METHODS: Sprague-Dawley rats (350 g) underwent thoracotomy. The exposed lung was struck with a piston at 5.2 m/s (150 J/M2). Blood, bronchoalveolar lavage (BAL), and lung tissue were collected at 3 hours and 24 hours after injury. PaO2/FiO2 (P/F) ratio was calculated at 15-minute intervals for 3 hours after contusion. Serum was evaluated for cytokine and chemokine expression using ELISA. Cell count/differential was performed on BAL, and lung tissue was obtained for histologic analysis, protein expression and wet to dry weights. Data are reported as pg/mL +/- SE. Data were analyzed using Student's t test to identify significant differences (p < or = 0.05 significant) between sham and injured animals. RESULTS: Piston impact caused PC based upon morphologic and histologic criteria. BAL cell count and lung wet to dry weights were increased and P/F ratio was decreased after PC. Systemic levels of IL-ra, MCP-1, and the CXC chemokines MIP-2alpha and CINC-1 were significantly elevated at 3 hours when sham and injured animals were compared. All chemokines were found to be significantly elevated at 24 hours, consistent with the early PMN and subsequent mononuclear infiltration observed in the contused lung. Pulmonary expression of TNF-alpha, IL-1beta, CINC-1, MIP-2alpha, ICAM-1, and elastase were increased and activated systemic neutrophils showed increased CD-11b. CONCLUSION: A model of PC is described in which innate inflammation is activated locally and systemically. Systemic levels of CC and CXC chemokines are increased after PC. This correlates with elevated PMN CD-11b expression, enhanced pulmonary ICAM-1 expression, and mononuclear and PMN infiltration into the lung and alveolar space. Elevated levels of CC and CXC chemokines are seen after PC and may be involved in the lung's inflammatory response to injury.

Animals↗

PubMed2005

Injury-associated hypothermia: an analysis of the 2004 National Trauma Data Bank.

Severe injury and shock are frequently associated with abnormalities in patient body temperature. Substantial increases in mortality have been associated with profound hypothermia, especially below 35 degrees C. The purpose of this study was to further characterize the impact of hypothermia in a large dataset of trauma patients. This study was a retrospective analysis of the 2004 version of the National Trauma Data Bank (NTDB), which contains approximately 1.1 million patients from over 400 trauma centers. Admission temperature was analyzed with respect to mortality, injury severity score (ISS), base deficit (BD), Glasgow Coma Score (GCS), and hospital outcomes. The NTDB contained 701,491 patients with temperatures recorded upon trauma center admission. Of these, 11,026 patients had admission temperatures <35 degrees C, and 802 had temperatures <32 degrees C. Comparison of core temperature versus mortality revealed that as temperature decreased, the mortality rate increased, reaching approximately 39% at 32 degrees C, and remained constant at lower temperatures. Surprisingly, 477 patients (59.5%) survived with temperatures <32 degrees C. Similarly, BD increased as hypothermia worsened until body temperature reached 31 degrees C, below which there was little further increase. Patients with admission temperatures less than 35 degrees C had significantly greater mortality (25.5% vs. 3.0%, P < 0.001) and BD (7.8 vs. 3.7, P < 0.001) when compared with patients with temperatures >or=35 degrees C. In survivors, average ventilator days and intensive care unit (ICU) days were 14.4 and 12.8, respectively, for patients with temperatures <35 degrees C as opposed to more normothermic patients who demonstrated an average of 9.5 ventilator days and 9.1 ICU days (P < 0.001). When grouped by individual ISS, BD level, and GCS motor score, mortality was significantly greater when admission temperature was below 35 degrees C (ISS mean difference = 11.4%, BD mean difference = 22.8%, and GCS motor mean difference = 9.85%). Logistic regression revealed that hypothermia remains an independent determinant of mortality after correction for confounding variables (odds ratio = 1.54, 95% confidence interval 1.40-1.71). Admission hypothermia is associated with greater mortality, increased injury severity, more profound acidosis, and prolonged ICU/ventilator courses. However, although mortality at <32 degrees C is high, patients with temperatures this low do survive. As temperatures drop below 32 degrees C, mortality rates remain constant, which may indicate a threshold below which physiologic mechanisms are unable to correct body temperature regardless of injury severity. Although shock severity is highly indicative of outcome, hypothermia independently contributes to the substantial mortality associated with severe injury.

Adolescent↗

PubMed2005

Development of a finite element-based injury metric for pulmonary contusion part I: model development and validation.

Pulmonary contusion is the most commonly identified thoracic soft tissue injury in an automobile crash and after blunt chest trauma and affects 10-17% of all trauma admissions. The mortality associated with pulmonary contusions is significant and is estimated to be 10-25%. Thus, there is a need to develop a finite element model based injury metric for pulmonary contusion for the purpose of predicting outcome. This will enable current and future finite element models of the lung to incorporate an understanding of how stress and strain may be related to contusion injuries. This study utilizes 14 impacts onto male Sprague-Dawley rats. In 5 of these tests, a calibrated weight (46 g) is dropped from a height of 44 cm directly onto the lungs of intubated, anesthetized rats in situ. Contused volume is estimated from MicroPET scans of the lung and normalized on the basis of liver uptake of 18F-FDG. The lungs are scanned at 24 hours, 7 days, and 28 days (15 scans), and the contused volume is measured. In addition, 9 controlled mechanical tests on in situ rat lung are used for model development and validation. Identical impacts are performed on a finite element model of the rat lung. The finite element model is developed from CT scans of normal rat and scaled to represent average rat lung volume. First principal strain is chosen as a candidate injury metric for pulmonary contusion. The volume of contused tissue at the three time points measured using PET is compared to the strain level achieved by a corresponding volume in the finite element model. For PET scans (n=5 scans per time point), the average contusion volume was 4.2 cm3 at 24 hours, 2.8 cm3 at 7 days, and 0.39 cm3 at 28 days. These volumes were used to identify threshold peak first principal strain levels measured by the finite element model. Maximum first principal strain from the finite element model for the three volume levels (4.2, 2.8, and 0.39 cm3) was 3.5%, 8.8%, and 35% strain, respectively. Furthermore, the lung model exhibited exponential decay in principal strain threshold as more of the lung volume was considered, correlating to the precise and well defined volume of the contusion as it healed. The results of this study may be used to establish an injury metric to predict pulmonary contusion due to an impact to the lungs. The results may be used to improve finite element models of the human body, which may then be used to tune stiffnesses of interior components of automobiles and tune safety systems for maximum mitigation of this serious injury.

Journal Article↗

PubMed2004

Genetic background influences natural killer cell activation during bacterial peritonitis in mice, and is interleukin 12 and interleukin 18 independent.

Some mouse strains produce strong pro-inflammatory, T-helper (Th)1 responses (e.g. C57BL/6), or strong anti-inflammatory, Th2 responses (e.g. BALB/c). The exact mechanisms for development of distinct immune responses to infection are not completely understood, although cytokines such as interleukin (IL)-12, IL-18 and IL-4 are known to play roles. Natural killer T (NKT)/natural killer (NK) cells are important regulators of immune responses in infection and non-infection models, and NKT/NK activation is also regulated by IL-12 and IL-18 in many models. We investigated the role of IL-12/IL-18 in NKT/NK activation in murine bacterial peritonitis, as well as differential NKT and NK cell activation in C57BL/6 and BALB/c mice. No differences in NKT or NK cell activation or intracellular interferon (IFN)-gamma were determined between mice given control, anti-IL-12 or anti-IL-18 antibodies or in NKT/NK cell activation in STAT4-/- mice (deficient in IL-12 signaling) or wild type controls. However, there were significant differences in the activation of NKT and NK cells between C57BL/6 mice and BALB/c mice, with NKT/NK cytokine production following Th1 or Th2 lines dependent on strain. This suggests a role for NKT and NK cell activation in the development of Th1 and Th2 responses during bacterial infection independently of IL-12 or IL-18.

Animals↗

PubMed2004

Non-helmeted motorcyclists: a burden to society? A study using the National Trauma Data Bank.

INTRODUCTION: Helmet laws remain controversial. Opponents believe negative findings are a result of biased statistical analyses that fail to account for the impact of alcohol and drugs. In this study, we evaluated the effect that helmet use had upon injury severity, outcome controlling for alcohol or drug use, resource utilization, and financial burden using the National Trauma Data Bank (NTDB). METHODS: Two groups of patients, helmeted and non-helmeted motorcyclists, were identified using the NTDB over an 8-year period. Group differences were compared using nonparametric Wilcoxon tests for continuous variables and Fisher's exact test for dichotomous outcomes. To evaluate the effect that alcohol or drug use had on mortality, logistic regression models were created. RESULTS: A total of 9,769 patients were identified by the NTDB of which 6756 (69.2%) were helmeted and 3013 (30.8%) were non-helmeted. Helmet use was associated with lower injury severity, mortality, and resource utilization. Non-helmeted motorcyclists accrued greater hospital charges and were significantly less likely to have health insurance. When controlling for alcohol or drug use, mortality continued to be significantly associated with non-helmet use. CONCLUSION: Non-helmeted motorcyclists have worse outcomes than their helmeted counterparts independent of the use of alcohol or drugs. Furthermore, they monopolize more hospital resources, incur higher hospital charges, and as non-helmeted motorcyclists frequently do not have insurance, reimbursement in this group of patients is poor. Thus, the burden of caring for these patients is transmitted to society as a whole.

Accidents, Traffic↗

PubMed2004

Leukotriene B4 receptor (BLT-1) modulates neutrophil influx into the peritoneum but not the lung and liver during surgically induced bacterial peritonitis in mice.

Leukotriene B4 (LTB4) is a rapidly synthesized, early neutrophil chemoattractant that signals via its cell surface receptor, BLT-1, to attract and activate neutrophils during peritonitis. BLT-1-deficient (BLT-1(-/-)) mice were used to determine the effects of LTB4 on neutrophil migration and activation, bacterial levels, and survival after cecal ligation and puncture (CLP). Male BLT-1(-/-) or wild-type (WT) BALB/c mice underwent CLP. Tissues were harvested for determination of levels of bacteria, myeloperoxidase (MPO), LTB4, macrophage inflammatory protein 2 (MIP-2), and neutrophil (polymorphonuclear leukocyte [PMN]) numbers at 4 and 18 h after CLP. PMN activation was determined by an assessment of phagocytosis ability and CD11b expression. Survival was also determined. BLT-1(-/-) mice had decreased numbers of PMNs in the peritoneum at both 4 and 18 h after CLP but increased numbers of PMNs in the blood at 18 h compared with WT mice. Liver and lung MPO levels were significantly higher in BLT-1(-/-) mice at both 4 and 18 h after CLP, with increased bacterial levels in the blood, the liver, and peritoneal fluid at 4 h. Bacterial levels remained higher in peritoneal fluid at 18 h, but blood and liver bacterial levels at 18 h were not different from levels at 4 h. PMN phagocytosis and CD11b levels were decreased in BLT-1(-/-) mice. LTB4 levels were similar between the groups before and after CLP, but MIP-2 levels were decreased both locally and systemically in BLT-1(-/-) mice. Survival was significantly improved in BLT-1(-/-) mice (71%) compared with WT mice (14%) at 48 h post-CLP. Thus, LTB4 modulates neutrophil migration into the mouse peritoneum, but not the lung or liver, after CLP. Despite higher bacterial and PMN levels at remote sites, there was increased survival in BLT-1(-/-) mice compared to WT mice. Decreased PMN activation may result in less remote organ dysfunction and improved survival.

Animals↗

PubMed2004

Laryngotracheal injuries: does injury mechanism matter?

Laryngotracheal injuries are potentially lethal injuries whose diagnosis can be difficult. The purpose of this study was to delineate the effect of injury mechanism on the types of injury sustained and patient outcome. Patient records during a 7-year period were reviewed for injury mechanism, patient demographics, clinical presentation, patient evaluation, injury location, associated injuries, operative interventions, and outcome. Fifteen patients with laryngotracheal injuries were studied. Blunt injuries were more common (60%). Patient demographics, mortality, average length of stay, and Injury Severity Score were similar for both groups. Prevalent physical findings on examination included subcutaneous air (53%), hoarseness (47%), stridor (20%), and neck tenderness (27%). Diagnosis was confirmed by CT scan of the neck (66% blunt, 33% penetrating) or bronchoscopy (44% blunt, 66% penetrating). Injury location, patient disposition, and associated injures were the same for both groups. The most frequent operative intervention performed for both groups consisted of a primary airway repair via a collar incision within 8 hours of injury. Only patients with a laryngeal injury required concomitant tracheostomy regardless of mechanism. Blunt and penetrating neck injuries resulted in similar types of tracheal and laryngeal injuries. Anatomic location of the injury determined the need for tracheostomy. Regardless of mechanism, the overall outcome for patients with laryngotracheal injuries is good when injuries are recognized and treated expeditiously. A high level of suspicion must be maintained when evaluating all potential laryngotracheal injury patients irrespective of the mechanism of injury.

Adult↗

PubMed2003

A novel model of pneumonia from intraperitoneal injection of bacteria.

BACKGROUND: Pneumonia remains a major clinical problem in the surgical patient. Experimental modeling by intratracheal injection of bacteria is not consistently reproducible. In an attempt to produce peritonitis by Klebsiella, we found evidence of pneumonia on autopsy and further developed this approach as a new experimental model. METHODS: Male Swiss Webster mice were given intraperitoneal (IP) injections of Klebsiella pneumoniae serotype 2 in different doses and this was compared with similar doses given intravenously (IV). A dose dependent survival curve was generated. Subsequently, 10(3) colony forming units (CFU) of bacteria were used in further experiments. Blood, peritoneal fluid and lung tissue were collected at time points up to 72 hours after injection and were cultured for levels of bacteria. Lung weights and myeloperoxidase levels were also measured. RESULTS: Intraperitoneal administration of Klebsiella was uniformly lethal with as few as 10(2) bacteria. Lung weight increased after IP Klebsiella, and all animals became bacteremic within 24 hours correlating with high bacterial levels in the lung. Conversely, most animals (72%) survived IV injection of bacteria, and were able to clear bacteria from the blood and lung. CONCLUSIONS: We found that this model produced no clinically apparent peritonitis after 48 hours, but uniformly resulted in histopathologic changes of pneumonia by 24 hours. Survival time was related to initial dose of Klebsiella and there was a linear correlation between bacterial levels in the blood and lung. This model is reproducible, simple to perform, and the severity is easy to manipulate.

Animals↗

PubMed2003

Trauma alters alveolar effector cell apoptosis.

BACKGROUND: The lung's immune response to trauma is biphasic with an initial proinflammatory and a subsequent anti-inflammatory cytokine response that alters cell function. Apoptosis, programmed cell death, is regulated by cytokines, and alteration of this important cellular function has been associated with end-organ dysfunction. We hypothesize that the lung's immune response to trauma alters alveolar inflammatory cell apoptosis and may contribute to posttrauma pulmonary dysfunction. METHODS: Bronchoalveolar lavage specimens were obtained from trauma patients with an injury severity score of 16 or more compared with patients who underwent elective surgery. Interleukin (IL)-8 and IL-10 were measured in the supernatant. Apoptosis and HLA-DR expression were measured in the cellular content, and Pao(2)/Fio(2) ratios were calculated as a measure of pulmonary function. RESULTS: After trauma, the alveolar inflammatory cell population was composed primarily of neutrophils. Apoptosis was suppressed initially after injury but increased to control levels by 72 hours after injury in parallel to alveolar concentrations of IL-10. Levels of IL-8 remained elevated, and HLA-DR expression remained suppressed throughout the study period. Pao(2)/Fio(2) ratios demonstrated pulmonary dysfunction by 72 hours. CONCLUSION: The lung's biphasic cytokine response to injury significantly alters both alveolar inflammatory cell apoptosis and HLA-DR expression. The alteration of alveolar inflammatory cell apoptosis may be dependent on the local production of IL-10. A reduction in apoptosis immediately preceded the onset of clinically significant pulmonary dysfunction.

Adult↗

PubMed2003

Tertiary care centers: a strategy for fiscal survival.

BACKGROUND: Managed care organizations use a variety of payment strategies to contract for high-end tertiary services with academic healthcare centers. We assessed the financial outcome of these strategies and attempted to identify those that maintain a balance between cost and reimbursement. METHODS: Patients admitted with an Injury Severity Score > or =16, hospital charges > or =$100,000, and a managed care organization as the payer were evaluated. RESULTS: A fixed reimbursement contract decreased reimbursement by 28% and negatively impacted the margin by 215%. The addition of a stop-loss provision to a fixed reimbursement contract is the best strategy to share the risk between payer and provider. If the fixed reimbursement strategy continued, the negative impact to the margin would have been $36,984 per patient. CONCLUSIONS: Fixed reimbursement strategies shift all the risk to the academic healthcare center. If volume, severity of illness, or cost is not controlled, they negatively affect the financial outcomes. The addition of a stop loss at $100,000 of charges paid at 40% of the entire claim most equitably distributes risk between the academic healthcare center and the managed care organization. It also excludes the negative impact of increasing severity of illness and volume and should induce cost control.

Academic Medical Centers↗

PubMed2003

Pathogenesis of posttraumatic empyema: the impact of pneumonia on pleural space infections.

BACKGROUND: Thoracic empyema may result either from primary pneumonic sources or intraabdominal sources of infection that seed the pleural space secondarily. In patients with thoracostomy tubes, empyema may result when blood in the pleural space becomes contaminated during tube insertion. To elucidate the cause of posttraumatic empyema, preoperative bronchoalveolar lavage (BAL)/sputum cultures obtained from patients with posttraumatic empyema were compared with cultures obtained at the time of decortication. MATERIALS AND METHODS: A retrospective study was conducted of trauma patients who developed empyema and underwent either video-assisted thoracoscopy or thoracotomy with decortication following blunt or penetrating trauma. At our level I trauma center, we studied all empyema cases diagnosed from November, 1998 to July, 2001. Data collection included patient demographics, injuries sustained, preoperative BAL/sputum cultures, and culture data obtained at the time of decortication. All BAL/sputum cultures were performed no more than 5 days prior to decortication. RESULTS: Thirty-seven patients (26 blunt/11 penetrating) were identified. No patients had concurrent intra-abdominal sources of infection. All patients had at least one chest tube placed prior to decortication. Preoperative respiratory cultures (BAL/sputum) were obtained in 34 patients. The most common organisms isolated were Staphylococcus aureus in six patients (18%) and Hemophilus influenzae in six patients (18%). Intraoperative cultures were obtained in all 37 patients, with the most common organism being S. aureus isolated in 22 patients (60%). Interestingly, a correlation between preoperative BAL/sputum and intraoperative cultures was found in only seven of the 34 patients (21%) who had concomitant respiratory and pleural cultures. Cultures positive for S. aureus were isolated from five patients, Streptococcus pneumoniae from one patient, and Pseudomonas aeruginosa from one patient. CONCLUSION: Little correlation existed between preoperative BAL/sputum cultures and intraoperative cultures in this series of patients with posttraumatic empyema. This suggests that the causation is most often not a parapneumonic process. Furthermore, since S. aureus was the most common organism recovered from empyema, the source was more likely from inoculation of the pleural space by the injury itself or by tube thoracostomy.

Adolescent↗

PubMed2003

Prophylactic antibiotics adversely affect nosocomial pneumonia in trauma patients.

BACKGROUND: Little data are available regarding the impact that prolonged prophylactic antibiotic use (>48 hours) has on the development of nosocomial pneumonia. This retrospective study was conducted to assess the effect that prolonged prophylactic antibiotic use has on the development of nosocomial pneumonia and antibiotic use complications. METHODS: The records of patients who contracted nosocomial pneumonia during mechanical ventilation were retrospectively reviewed. These patients then were classified into two groups: those who received prolonged prophylactic antibiotics before the diagnosis of pneumonia and those who did not receive antibiotics. RESULTS: For the patients who received prolonged prophylactic antibiotics, the first pneumonia was diagnosed later, the causative organisms were more likely to be resistant or Gram-negative bacteria, and the incidence of antibiotic complications were two times greater than for patients who did not receive extended antibiotic prophylaxis. CONCLUSION: Justification for the use and duration of prolonged (>48 hours) prophylactic antibiotics requires careful reevaluation because this practice is associated with significant clinical complications that lead to increased use of patient resources, lengthened hospital stay, and higher cost.

Adult↗

PubMed2003

Natural killer cell activation primes macrophages to clear bacterial infection.

Natural killer (NK) cells are major cytokine producers during bacterial sepsis, but their precise role is undefined. This study investigates the effect of NK cell depletion with and without prior activation on macrophage function and bacterial clearance during cecal ligation and puncture. Two different NK cell-depleting antibodies were used: anti-asialo-GM1 (GM1), a nonactivating antibody, and anti-NK1.1 (NK1.1), an NK cell-activating antibody. C57BL/6 mice were NK depleted with either GM1 or NK1.1 by intraperitoneal injection 7 and 3 days before experimentation. Control animals received isotype immunoglobulin G. Depletion was confirmed by flow cytometry. Bacterial levels in peritoneal washout, blood, and liver were determined 4 hours after cecal ligation and puncture. Macrophage activation was measured by phagocytosis ability and by production of nitric oxide and interleukin-6. Depletion with GM1 resulted in significantly higher bacterial levels at 4 hours, whereas depletion with NK1.1 had the opposite effect of significantly decreasing bacterial levels. Macrophage phagocytosis ability was significantly increased in mice depleted with NK1.1 compared with those mice depleted with GM1. We conclude that activation of NK cells improves bacterial clearance by priming macrophages to help clear a subsequent bacterial challenge. Macrophages are less able to clear bacteria when NK cells are depleted without activation. NK cells are therefore important in bacterial clearance through interactions with macrophages.

Animals↗