Brain abscess caused by dental peri-implantitis.

We report the case of a patient presenting with severe headache and progressive aphasia due to a large brain abscess. End-stage peri-implantitis on a dental implant in the upper jaw with contact to the maxillary sinus floor causing maxillary and frontal sinusitis could be identified as the source of infection. Multidisciplinary treatment included broad-spectrum antibiotics, craniotomy for abscess drainage, sinus surgery, and the removal of the implant. Despite all the care taken, the patient died, underlining the importance of oral hygiene and a frequent recall in patients with dental implants. To the best of our knowledge, this is the first report of a brain abscess caused by peri-implantitis in the literature.

[Practices' evaluation of missed miscarriage diagnosis in gynecologic emergency service in Tours CHU]. / Évaluation des pratiques de diagnostic de grossesse évolutive aux urgences gynécologiques du CHU de Tours.

INTRODUCTION: In the gynecology emergency departments, a pregnancy of uncertain viability is diagnosed in 29% of all first-trimester pregnancy medical consultations that require an ultrasound. The question of pregnancy viability is therefore common in our medical practice and comes along with human implications. In 2014, the French National College of Obstetricians and Gynecologists (CNGOF) promulgated clear guidelines regarding missed early miscarriage diagnosis and treatment. We wanted to evaluate our level of compliance with the diagnosis dimension of those guidelines and assess their optimization level since they were published. MATERIALS AND METHODS: This retrospective and descriptive study is based on all missed early miscarriage that were taken care of within the gynecology emergency department at the CHU in Tours (France) over the course of three non-consecutive years. The year 2013 has been considered - before the guidelines were promulgated, 2015 - just after the guidelines were promulgated and lastly, 2018 in order to have the necessary distance for the interpretation. The following criteria was assessed for each year: the diagnostic ultrasound criteria; when relevant, the monitoring ultrasound deadlines; and the details regarding any patient management errors if errors were made. Secondarily, the uterine evacuation treatment procedures were examined. RESULTS: The study population includes 297 women. The non-compliance with the guidelines affected 20% of the women in 2013, 12% in 2015 and 15% in 2018 (p = 0.25 when comparing the pre-guideline and post-guideline periods). An ultrasound performed too early is the most common error made each year even though its frequency has decreased (p = 0.03). The least experienced sonographers tend to be rather cautious, performing additional unnecessary examinations and scheduling excessive additional monitoring ultrasound deadlines. Only 13% of the medication-based therapies made uterine evacuation successful. If the initial use of prostaglandin substances was not successful, no additional dose of medication enabled any women patient to avoid surgery. CONCLUSION: The compliance with the guidelines regarding pregnancies of uncertain viability is not optimal. Partial improvements in our own patient care management have been made since the publication of the guidelines; however, the main risk at stake is to terminate the evolution of a normal pregnancy due to some remaining medical misjudgments. The introduction of quality scores for clinical ultrasound images would be an interesting topic to discuss.

Midazolam plasma concentration after anesthesia premedication in clinical routine - an observational study : Midazolam plasma concentration after anesthesia premedication.

BACKGROUND: Midazolam is commonly used as a pre-anesthesia anxiolytic. It`s elimination may not be fast enough for short procedures. In orally premedicated patients we obtained midazolam plasma concentrations at the end of surgical procedures and compared those to concentrations at anesthesia induction. METHODS: The study was conducted prospectively with consent of the local ethics committee (Ethikkomission Kanton Thurgau, Switzerland) and carried out with written informed consent of each patient. Female patients aged 20 to 60 years undergoing elective procedures with general anesthesia were included, and were divided in two groups according to the planned surgical time: group S (<30 min) and group L (90-120 min), respectively. All patients received 7.5 mg Midazolam po as premedication. Blood samples were drawn at anesthesia induction, and at the end of surgery. Data were compared with t-test (independent samples; significance level p <0.05). RESULTS: Twenty-five patients per group were included. Four patients were excluded from analysis, since midazolam was not detectable in any samples. Time of premedication to the 1st blood sample was not statistically different between groups, neither were Midazolam plasma levels at this time point (p = 0.94). None of the patients from group L (n = 24), but five patients in group S (n = 22) did have a higher plasma level of Midazolam at the end of the case compared to the beginning. CONCLUSIONS: The elimination half-life of oral Midazolam can lead to higher plasma levels at the end of a short procedure compared to those at induction of anesthesia. TRIAL REGISTRATION: German Clinical Trials Register (Deutsches Register Klinischer Studien), DRKS00005429 ; date of registration 3rd January 2014.

[Lesions of the oral mucosa : Differential diagnostic approach from the maxillofacial surgeon's perspective]. / Schleimhauterkrankungen : Differenzialdiagnostischer Zugang aus kieferchirurgischer Sicht.

A detailed medical history and a careful clinical examination are the basis for developing a list of possible differential diagnoses in lesions of the oral mucosa. On this basis, it can be decided whether a lesion can be observed for 14 days after removal of possible causes or the start of a trial treatment, or whether a biopsy for histological examination must be taken immediately. An excisional biopsy is performed for small and presumably benign lesions, an incisional biopsy for large and presumably malignant lesions. If an autoimmune blistering disease is suspected, a second sample for examination by immunofluorescence is taken. Depending on the results of the histological examination further treatment steps are planned or regular appointments for follow-up are arranged.

Myeloid PTEN deficiency impairs tumor-immune surveillance via immune-checkpoint inhibition.

Tumor-host interaction is determined by constant immune surveillance, characterized by tumor infiltration of myeloid and lymphoid cells. A malfunctioning or diverted immune response promotes tumor growth and metastasis. Recent advances had been made, by treating of certain tumor types, such as melanoma, with T-cell checkpoint inhibitors. This highlights the importance of understanding the molecular mechanisms underlying the crosstalk between tumors and their environment, in particular myeloid and lymphoid cells. Our aim was to study the contribution of the myeloid PI3K/PTEN-signaling pathway in the regulation of tumor-immune surveillance in murine models of cancer. We made use of conditional PTEN-deficient mice, which exhibit sustained activation of the PI3K-signaling axis in a variety of myeloid cell subsets such as macrophages and dendritic cells (DCs). In colitis-associated colon cancer (CAC), mice deficient in myeloid PTEN showed a markedly higher tumor burden and decreased survival. We attributed this observation to the increased presence of immune-modulatory conventional CD8α(+) DCs in the spleen, whereas other relevant myeloid cell subsets were largely unaffected. Notably, we detected enhanced surface expression of PD-L1 and PD-L2 on these DCs. As a consequence, tumoricidal T-cell responses were hampered or redirected. Taken together, our findings indicated an unanticipated role for the PI3K/PTEN-signaling axis in the functional regulation of splenic antigen-presenting cells (APCs). Our data pointed at potential, indirect, tumoricidal effects of subclass-specific PI3K inhibitors, which are currently under clinical investigation for treatment of tumors, via myeloid cell activation.

[3-Tesla MRI of rare large cystic prostate carcinoma]. / 3-Tesla-MRT von seltenen zystisch imponierenden Prostatakarzinomen.

Magnetic resonance imaging of rare cystic prostate cancers using multiparametric MRI (mp-MRI, 3 Tesla) shows, especially in solid tumor masses, the criteria of ESUR-MR classification with a PI-RADS >3 ("probably malignant"). In association with additional morphological evidence of intracystic hemorrhage and evidence of villous tumor nodules and irregular septa on the cyst wall, further malignancy criteria are met. MRI complementary to TRUS may be useful for targeted biopsy in solid tumor areas.

Expression patterns of CD44 and CD44 splice variants in patients with rheumatoid arthritis.

OBJECTIVES: It has been suggested that CD44 is involved in the pathogenesis of rheumatoid arthritis (RA). By alternative splicing, numerous CD44 isoforms can be generated which may play different roles the inflammatory process. We therefore studied the expression of various CD44 splicevariants in the circulation and synovial tissue of patients with RA and correlated expression with clinical features. METHODS: Expression of distinct CD44 splice variants was analysed by FACS in peripheral monocytes of 46 RA patients and 36 healthy controls. Expression of CD44 splice variants in synovial tissue of RA and OA patients was analysed by immunohistochemistry and the effects of blocking CD44v4 on RA-fibroblast like synoviocytes (FLS) were studied. RESULTS: On monocytes, the expression of CD44 and CD44v3 was significantly lower in patients with erosive disease than in those without radiographic progression (p<0.05 for CD44 and p<0.01 for CD44v3). CD44v6 on monocytes was significantly associated with the clinical disease activity index (r=0.34, p<0.05) and CRP-levels (r=0.37, p<0.02). Immunhistochemical analyses revealed that most variants were expressed to a significantly higher extent in RA than in OA synovial membranes. Particularly the variants CD44v4, CD44v6 and CD44v7-8 were highly expressed in the RA lining and also abundantly in the endothelium. Blocking CD44v4 in RA-FLS reduced the proliferation to 68±8% (p<0.02) when compared to control experiments and led to a reduction in IL-1ß mRNA expression (p<0.05). CONCLUSIONS: Expression of CD44 splice variants is generally increased in the synovial lining of RA patients when compared to OA. The inverse association of CD44v3 expression on monocytes with the development of erosive disease and the functional impacts of CD44v4 blockade in RA-FLS suggests a pathogenetic role of this splice variants which needs to be further investigated.

Concentration of hospital care for acute sickle cell disease-related visits.

BACKGROUND: Sickle cell disease (SCD) is characterized by frequent disease-related events that require acute care. It is unknown to what extent patients utilize multiple hospitals for acute care. We examined the continuity pattern of acute care visits to the hospital or emergency department. We hypothesized that among patients with multiple SCD related acute care visits, children experience more concentrated hospital care than adults and privately insured patients experience more concentrated hospital care than publicly insured patients. PROCEDURE: We conducted a retrospective cohort study using data from the 2005 and 2006 Healthcare Cost and Utilization Project State Inpatient Databases and State Emergency Department Databases. Subjects included patients with SCD ≥ 1 year of age. The primary outcome was proportion of patients with multiple acute care visits to a single hospital. RESULTS: A total of 13,533 patients made ≥ 2 acute SCD-related visits. Of the 5,030 children, 77.3% went to the same hospital for all visits. In contrast, of the 8,503 adults, only 51.3% visited the same hospital. Adolescents were more likely than adults to go to one hospital [adjusted relative risk (ARR) 1.40, confidence interval (CI) 1.35-1.45]. Those with public insurance and the uninsured had a decreased probability of using one hospital (ARR 0.96, CI 0.94-0.99, and ARR 0.83, CI 0.79-0.88, respectively). CONCLUSIONS: Adults and patients with public insurance or no insurance are more likely to use multiple hospitals for acute care. By receiving acute care at multiple hospitals, patients with SCD experience dispersed and fragmented care potentially leading to decreased care quality.

Cancer-associated alteration of pericentromeric heterochromatin may contribute to chromosome instability.

Many tumors exhibit elevated chromosome mis-segregation termed chromosome instability (CIN), which is likely to be a potent driver of tumor progression and drug resistance. Causes of CIN are poorly understood but probably include prior genome tetraploidization, centrosome amplification and mitotic checkpoint defects. This study identifies epigenetic alteration of the centromere as a potential contributor to the CIN phenotype. The centromere controls chromosome segregation and consists of higher-order repeat (HOR) alpha-satellite DNA packaged into two chromatin domains: the kinetochore, harboring the centromere-specific H3 variant centromere protein A (CENP-A), and the pericentromeric heterochromatin, considered important for cohesion. Perturbation of centromeric chromatin in model systems causes CIN. As cancer cells exhibit widespread chromatin changes, we hypothesized that pericentromeric chromatin structure could also be affected, contributing to CIN. Cytological and chromatin immunoprecipitation and PCR (ChIP-PCR)-based analyses of HT1080 cancer cells showed that only one of the two HORs on chromosomes 5 and 7 incorporate CENP-A, an organization conserved in all normal and cancer-derived cells examined. Contrastingly, the heterochromatin marker H3K9me3 (trimethylation of H3 lysine 9) mapped to all four HORs and ChIP-PCR showed an altered pattern of H3K9me3 in cancer cell lines and breast tumors, consistent with a reduction on the kinetochore-forming HORs. The JMJD2B demethylase is overexpressed in breast tumors with a CIN phenotype, and overexpression of exogenous JMJD2B in cultured breast epithelial cells caused loss of centromere-associated H3K9me3 and increased CIN. These findings suggest that impaired maintenance of pericentromeric heterochromatin may contribute to CIN in cancer and be a novel therapeutic target.

[Atopic dermatitis and psoriasis: what is the benefit of in-patient high altitude climate therapy?]. / Neurodermitis und Psoriasis: Was bringt die stationäre Therapie im Hochgebirgsklima mehr?

Atopic dermatitis as well as psoriasis are characterized as common, chronic, often long lasting disorders of the cutis. In case of (a) a refractory out-patient therapy, (b) an acute severe exacerbation of skin lesions, (c) functional impairment of hands and feet, (d) suberythroderma or erythroderma, (e) complex topical as well as systemic treatment modalities, (f) complicating somatic or psychological co-morbidity, a referral to in-patient treatment at high altitude must be considered. The therapy at the Hochgebirgsklinik Davos (1,560 m above sea level) is characterized by application of natural-borne UV radiation all year round, missing house dust mite allergen, massive reduction of pollens and mycotic spores, improvement of skin perfusion as well as a reduction in itching (as compared to low altitude regions). Last but not least, silence and distance from home and company may show benefits for psychological and cutaneous well-being the 24-hour daily presence of dermatology experts, a broad armamentarium of topical and systemic treatment modalities as well as wide range of up-to-date diagnostic and therapeutic tools have to be further mentioned.

Systemic lupus erythematosus patients exhibit functional deficiencies of endothelial progenitor cells.

OBJECTIVE: SLE is characterized by an increased cardiovascular risk. Since endothelial progenitor cells (EPCs) have been described to serve as a biomarker for the CV risk and are known to be depleted in various diseases, we were interested if SLE would also be associated with altered peripheral EPC levels or functional abnormalities of these cells. METHODS: EPCs were quantified in 31 female SLE patients with different disease activity and in age-matched healthy controls (HCs) by FACS analysis and by colony forming unit (CFU) assay. Furthermore, EPC adhesion and migration capacity were tested. RESULTS: EPC levels were similar in HC and SLE when assessed by FACS (0.045 +/- 0.006% vs 0.036 +/- 0.007% within the lymphocyte gate) and by the CFU assay (18 +/- 3 vs 15 +/- 2 colonies/well). No correlation with disease activity could be observed, but SLE patients treated with chloroquine exhibited significantly decreased EPC levels (0.058 +/- 0.005% without vs 0.024 +/- 0.008% with chloroquine, P < 0.05). Addition of chloroquine to in vitro cultures also led to a decreased colony formation in SLE and in HC. When testing the adhesion and migration capacity of EPC on human umbilical vein endothelial cells (HUVEC), cells from SLE patients had reduced adhesion (19.2 +/- 3.5% vs 36.6 +/- 5.2% EPC/high power field, P < 0.02) and migratory activity (56 +/- 6 cells/random microscopic field in SLE vs 121 +/- 28 in controls, P < 0.02). CONCLUSION: The data reveal that EPCs are significantly affected in SLE. While circulating EPC levels are in the range of HC, they exhibit functional deficiencies that may lead to impaired tissue availability.

Healthcare providers' sun-protection promotion and at-risk clients' skin-cancer-prevention outcomes.

BACKGROUND: This study aims to determine whether healthcare providers' (HCPs') communication dealing with sun-protection (i.e., counseling) is associated with clients' skin-cancer-related prevention practices, detection self-efficacy, and knowledge. METHODS: Secondary analysis of two surveys of 1,469 randomly sampled farmers and soccer participants from southeast and coastal Georgia. RESULTS: Farmers and soccer participants who report ever having been counseled by a HCP about how to protect their skin from the sun report being more likely to wear sunscreen (P < 0.05), get clinical exams of their skin (P < 0.001), be certain that they can recognize unhealthy changes in their skin (P < 0.001), be certain that they know how to perform a skin exam (P < 0.001), and be knowledgeable about skin cancer prevention (P < 0.05 and P < 0.001, respectively); soccer participants are additionally more likely to wear protective headgear (P < 0.05) and perform monthly self-exams of their skin (P < 0.001). All analyses incorporated three control variables: participants' prior history of skin cancer, age, and non-HCP-derived skin-cancer awareness. CONCLUSIONS: Findings suggest that HCPs' counseling can positively shape skin-cancer-related prevention practices, detection self-efficacy, and knowledge. Additional research is needed on HCPs' actual communication about skin cancer and sun protection and its influence on client outcomes.

TNFalpha mediates susceptibility to heat-induced apoptosis by protein phosphatase-mediated inhibition of the HSF1/hsp70 stress response.

TNFalpha uniquely combines proinflammatory features with a proapoptotic potential. Activation of HSF1 followed by induction of hsp70 is part of a stress response, which protects cells from apoptosis. Herein, the effects of TNFalpha on the hsp70 stress response were investigated. TNFalpha caused transient downregulation of HSF1 activation and hsp70 synthesis, leading to increased sensitivity to heat-induced apoptosis. Blockade of TNF-R1, but not TNF-R2, as well as inhibition of protein phosphatases PP1/PP2a and PP2b completely blocked this effect. In contrast, blockade of MAPK/SAPK-, NF-kappaB (NF-kappaB)-, and PKC- pathways as well as the caspase cascade did not prevent downregulation of HSF1/hsp70. These data demonstrate that TNFalpha transiently inhibits the hsp70 stress response via TNF-R1 and activation of protein phosphatases. The price of inhibition of an essential cellular stress response is increased sensitivity to apoptotic cell death.

Increased bioactive TNF in human systemic lupus erythematosus: associations with cell death.

In systemic lupus erythematosus (SLE) serum TNF is increased and correlates with its soluble receptors and with disease activity. We therefore investigated (i) whether the TNF in SLE serum is bioactive, (ii) whether SLE cells react to TNF and (iii) whether there are associations with cell death, which is regarded as pathogenic in SLE. Sera from active SLE patients induced an increase in fibroblast CD54, which was abolished by blocking antibodies against TNF, suggesting TNF bioactivity. SLE lymphocytes had a similar surface expression of TNF-RI as healthy lymphocytes, their expression of TNF-RII was slightly increased. Recombinant TNF induced cell death in PBMC of SLE patients, suggesting functional receptors. Serum levels of sTNF-RII (as a surrogate marker for TNF activity) correlated with sTNF-RI and disease activity, as expected, and also correlated with the percentage of dying lymphocytes and with lymphocytic CD95. SLE sera contain increased amounts of biologically active TNF. Peripheral blood lymphocytes of SLE patients express functional TNF receptors. Finally, associations with cell death and CD95 receptors suggest that TNF may be pathogenic in SLE.

Outpatient mastectomy: clinical, payer, and geographic influences.

OBJECTIVE: To determine (1) the use of outpatient services for all surgical breast procedures for breast cancer and (2) the influence of payer and state on the use of outpatient services for complete mastectomy in light of state and federal length-of-stay managed care legislation. DATA SOURCES: Healthcare Cost and Utilization Project representing all discharges from hospitals and ambulatory surgery centers for five states (Colorado, Connecticut, Maryland, New Jersey, and New York) and seven years (1990-96). STUDY DESIGN: Longitudinal, cross-sectional analyses of all women undergoing inpatient and outpatient complete mastectomy (CMAS), subtotal mastectomy (STMAS), and lumpectomy (LUMP) for cancer were employed. Total age-adjusted rates and percentage of outpatient CMAS, STMAS, and LUMP were compared. Independent influence of state and HMO payer on likelihood of receiving an outpatient CMAS was determined from multivariate models, adjusting for clinical characteristics (age < 50 years, comorbidity, metastases, simple mastectomy, breast reconstruction) and hospital characteristics (teaching, ownership, urban). PRINCIPAL FINDINGS: In 1993, 1 to 2 percent of CMASs were outpatient in all states. By 1996, 8 percent of CMASs were outpatient in Connecticut, 13 percent were outpatient in Maryland, and 22 percent were outpatient in Colorado. In comparison, LUMPs were 78 to 88 percent outpatient, and by 1996, 43 to 72 percent of STMASs were outpatient. In 1996, women were 30 percent more likely to receive an outpatient CMAS in New York, 2.5 times more likely in Connecticut, 4.7 times more likely in Maryland, and 8.6 times more likely in Colorado compared to New Jersey. In addition, women with Medicare, Medicaid, or private commercial insurance were less likely to receive an outpatient CMAS compared to women with an HMO payer. CONCLUSIONS: LUMP is an outpatient procedure, and STMAS is becoming primarily outpatient. CMAS, while still primarily inpatient, is increasingly outpatient in some states. Although clinical characteristics remain important, the state in which a woman receives care and whether she has an HMO payer are strong determinants of whether she receives an outpatient CMAS.

Serum interleukin-15 is elevated in systemic lupus erythematosus.

OBJECTIVE: To investigate if interleukin-15 (IL-15) (rather than IL-2) is increased in systemic lupus erythematosus (SLE) and might be responsible for immunological abnormalities of SLE such as the increased lymphocytic expression of Bcl-2 and CD25. METHODS: Serum IL-15, IL-2 and tumour necrosis factor (TNF) levels of 65 SLE patients, 20 healthy persons and 10 rheumatoid arthritis (RA) patients were measured by enzyme-linked immunosorbent assay (ELISA). For 25 SLE patients, the percentage of CD25 + lymphocytes and the lymphocytic Bcl-2 levels were simultaneously determined by fluorocytometry. Peripheral blood mononuclear cells (PBMC) of 15 SLE patients were incubated with or without recombinant IL-15 and the influence on Bcl-2 and CD25 was determined. RESULTS: IL-15 was found to be elevated in 25 SLE sera (38%), but in none of the 20 healthy sera (P = 0.0005) and none of the 10 RA sera. Both lymphocyte CD25 and Bcl-2 expression significantly correlated with serum IL-15 and were increased by recombinant IL-15. CONCLUSION: Serum IL-15 may in part be responsible for the immunological abnormalities seen in active SLE.

Overexpression of transcription factor Ets-1 in rheumatoid arthritis synovial membrane: regulation of expression and activation by interleukin-1 and tumor necrosis factor alpha.

OBJECTIVE: To investigate the expression of the transcription factor Ets-1 in synovial tissue and cultured synovial fibroblasts from patients with rheumatoid arthritis (RA) and osteoarthritis (OA) and to study the regulation of Ets-1 expression and activation in synovial fibroblasts by proinflammatory cytokines. METHODS: In situ expression of Ets-1 in synovial tissue from RA and OA patients was examined by double immunohistochemistry. The effects of interleukin-1 (IL-1) or tumor necrosis factor alpha (TNFalpha) on Ets-1 expression and activation (DNA binding) in cultured synovial fibroblasts were analyzed by Western blotting and DNA gel shift assay, respectively. In addition, the intracellular location of Ets-1 in synovial fibroblasts was determined by immunofluorescence. RESULTS: Pronounced expression of Ets-1 was detected in synovial tissues from all RA patients evaluated, particularly in the synovial lining layer and the sublining areas. Ets-1 was expressed by both fibroblasts and macrophages as well as by endothelial cells, while only a few T cells stained positive for Ets-1. In synovial specimens from OA patients, Ets-1 expression was much less frequently observed and was largely restricted to vascular cells. Ets-1 was expressed to a similar degree in cultured synovial fibroblasts from RA and OA patients, as demonstrated by reverse transcriptase-polymerase chain reaction and Western blotting. Both IL-1 and TNFalpha induced pronounced up-regulation of Ets-1 in synovial fibroblasts. Moreover, binding of Ets-1 to its specific DNA binding site was induced by both cytokines, although with different time courses. Immunofluorescence staining revealed a dominant nuclear localization of Ets-1 in IL-1- or TNFalpha-stimulated synovial fibroblasts. CONCLUSION: The overexpression of Ets-1 observed in RA synovial tissue appears to be caused by TNFalpha and IL-1, suggesting that Ets-1 may be an important factor in the cytokine-mediated inflammatory and destructive cascade characteristic of RA.

Predictors of acquiring a nosocomial bloodstream infection on extracorporeal membrane oxygenation.

PURPOSE: The aim of this study was to identify independent predictors of acquiring a nosocomial bloodstream infection (BSI) during extracorporeal membrane oxygenation (ECMO). METHODS: This retrospective cohort consisted of 202 neonates treated with ECMO from 1989 to 1998 at the author' institution. Data collected included patient demographics, primary and secondary diagnoses, white blood cell counts, antibiotic usage, presence of central lines, operative procedures, and outcome. Surveillance blood cultures were drawn daily from the circuit using sterile technique to identify acquired pathogens. Statistical analyses included logistic regression, Cox proportional regression analysis, and discriminate analysis. RESULTS: There were 1,245 blood cultures drawn on 202 patients (6.2 cultures per patient), and a nosocomial BSI was identified in 7 patients (3.4%) during this 10-year span. These were infections that were neither present nor incubating on admission. Pre-ECMO diagnoses of patients who had a nosocomial BSI while on bypass included group B beta-hemolytic streptococcal sepsis (n = 2), herpes simplex viral sepsis (n = 1), congenital diaphragmatic hernia (n = 2), persistent pulmonary hypertension (n = 1), and congenital heart disease (n = 1). The median time on ECMO before obtaining a positive culture was 390 hours. The infectious agents responsible for these BSIs included Staphylococcus epidermidis (n = 5), Staphylococcus aureus (n = 1), and Escherichia coli (n = 1). The major factor associated with acquiring a nosocomial BSI on ECMO was the duration of bypass (391 v 141 hours, P =.002). Additionally, patients in the BSI group were more likely to have had an arterial catheter in place (16 v 7 days, P =.009) and to have received more screening blood cultures (16 v 6 cultures, P < 001). White blood cell counts, absolute neutrophil counts, and immature/total (I/T) ratios were not useful in predicting a nosocomial BSI. Of the 31 patients who required ECMO for more than 10 days, 7 (23%) had a positive blood culture, and 5 of these 7 infants (71%) died (P =.03). CONCLUSIONS: The only predictor of acquiring a nosocomial BSI on ECMO was the duration of support for greater than 10 days. Because classical predictors of infection are unreliable while the patient is on ECMO, the authors suggest that obtaining daily surveillance blood cultures beginning on the tenth day should be performed with prolonged ECMO courses. The authors confirmed previous reports of the association between a prolonged ECMO course and a high mortality rate. However, the authors speculate that, in actuality, the primary diagnosis leads to the prolonged course of support and is the major factor in the infant' demise.