Eliminating sternal wound infections: Why every cardiac surgery program needs an I hate infections team.

Objectives: The majority of studies examining deep sternal wound infection (DSWI) prevention focus on ameliorating 1 variable at a time. There is a paucity of data regarding the synergistic effects of combining clinical and environmental interventions. This article describes an interdisciplinary, multimodal approach to eliminate DSWIs at a large community hospital. Methods: We developed a robust, multidisciplinary infection prevention team to evaluate and act in all phases of perioperative care to achieve a cardiac surgery DSWI rate of 0, named: the I hate infections team. The team identified opportunities for improved care and best practices and implemented changes on an ongoing basis. Results: Patient-related interventions consisted of preoperative methicillin-resistant Staphylococcus aureus identification, individualized perioperative antibiotics, antimicrobial dosing strategies, and maintenance of normothermia. Operative-related interventions involved glycemic control, sternal adhesives, medications and hemostasis, rigid sternal fixation for high-risk patients, chlorhexidine gluconate dressings over invasive lines, and use of disposable health care equipment. Environment-related interventions included optimizing operating room ventilation and terminal cleaning, reducing airborne particle counts, and decreasing foot traffic. Together, these interventions reduced the DSWI incidence from 1.6% preintervention to 0% for 12 consecutive months after full bundle implementation. Conclusions: A multidisciplinary team focused on eliminating DSWI identified known risk factors and implemented evidence-based interventions in each phase of care to ameliorate risk. Although the influence of each individual intervention on DSWI remains unknown, use of the bundled infection prevention approach reduced the incidence to 0 for the first 12 months after implementation.

Paradoxical effects of cigarette smoke and COPD on SARS-CoV-2 infection and disease.

BACKGROUND: How cigarette smoke (CS) and chronic obstructive pulmonary disease (COPD) affect severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) infection and severity is controversial. We investigated the effects of COPD and CS on the expression of SARS-CoV-2 entry receptor ACE2 in vivo in COPD patients and controls and in CS-exposed mice, and the effects of CS on SARS-CoV-2 infection in human bronchial epithelial cells in vitro. METHODS: We quantified: (1) pulmonary ACE2 protein levels by immunostaining and ELISA, and both ACE2 and/or TMPRSS2 mRNA levels by RT-qPCR in two independent human cohorts; and (2) pulmonary ACE2 protein levels by immunostaining and ELISA in C57BL/6 WT mice exposed to air or CS for up to 6 months. The effects of CS exposure on SARS-CoV-2 infection were evaluated after in vitro infection of Calu-3 cells and differentiated human bronchial epithelial cells (HBECs), respectively. RESULTS: ACE2 protein and mRNA levels were decreased in peripheral airways from COPD patients versus controls but similar in central airways. Mice exposed to CS had decreased ACE2 protein levels in their bronchial and alveolar epithelia versus air-exposed mice. CS treatment decreased viral replication in Calu-3 cells, as determined by immunofluorescence staining for replicative double-stranded RNA (dsRNA) and western blot for viral N protein. Acute CS exposure decreased in vitro SARS-CoV-2 replication in HBECs, as determined by plaque assay and RT-qPCR. CONCLUSIONS: ACE2 levels were decreased in both bronchial and alveolar epithelial cells from COPD patients versus controls, and from CS-exposed versus air-exposed mice. CS-pre-exposure potently inhibited SARS-CoV-2 replication in vitro. These findings urge to investigate further the controversial effects of CS and COPD on SARS-CoV-2 infection.

Paradoxical effects of cigarette smoke and COPD on SARS-CoV2 infection and disease.

INTRODUCTION: How cigarette smoke (CS) and chronic obstructive pulmonary disease (COPD) affect severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and severity is controversial. We investigated the protein and mRNA expression of SARS-CoV-2 entry receptor ACE2 and proteinase TMPRSS2 in lungs from COPD patients and controls, and lung tissue from mice exposed acutely and chronically to CS. Also, we investigated the effects of CS exposure on SARS-CoV-2 infection in human bronchial epithelial cells. METHODS: In Cohort 1, ACE2-positive cells were quantified by immunostaining in FFPE sections from both central and peripheral airways. In Cohort 2, we quantified pulmonary ACE2 protein levels by immunostaining and ELISA, and both ACE2 and TMPRSS2 mRNA levels by RT-qPCR. In C57BL/6 WT mice exposed to air or CS for up to 6 months, pulmonary ACE2 protein levels were quantified by triple immunofluorescence staining and ELISA. The effects of CS exposure on SARS-CoV-2 infection were evaluated after 72hr in vitro infection of Calu-3 cells. After SARS-CoV-2 infection, the cells were fixed for IF staining with dsRNA-specific J2 monoclonal Ab, and cell lysates were harvested for WB of viral nucleocapsid (N) protein. Supernatants (SN) and cytoplasmic lysates were obtained to measure ACE2 levels by ELISA. RESULTS: In both human cohorts, ACE2 protein and mRNA levels were decreased in peripheral airways from COPD patients versus both smoker and NS controls, but similar in central airways. TMPRSS2 levels were similar across groups. Mice exposed to CS had decreased ACE2 protein levels in their bronchial and alveolar epithelia versus air-exposed mice exposed to 3 and 6 months of CS. In Calu3 cells in vitro, CS-treatment abrogated infection to levels below the limit of detection. Similar results were seen with WB for viral N protein, showing peak viral protein synthesis at 72hr. CONCLUSIONS: ACE2 levels were decreased in both bronchial and alveolar epithelial cells from uninfected COPD patients versus controls, and from CS-exposed versus air-exposed mice. CS-pre-treatment did not affect ACE2 levels but potently inhibited SARS-CoV-2 replication in this in vitro model. These findings urge to further investigate the controversial effects of CS and COPD on SARS-CoV2 infection.

Enhanced recovery after cardiac surgery program to improve patient outcomes.

This article details the obstacles of implementing a cardiac-specific enhanced recovery after surgery (ERAS) program in a 919-bed not-for-profit community-based health system and the benefits of ERAS programs for different patient populations.

Tollip SNP rs5743899 modulates human airway epithelial responses to rhinovirus infection.

BACKGROUND: Rhinovirus (RV) infection in asthma induces varying degrees of airway inflammation (e.g. neutrophils), but the underlying mechanisms remain unclear. OBJECTIVE: The major goal was to determine the role of genetic variation [e.g. single nucleotide polymorphisms (SNPs)] of Toll-interacting protein (Tollip) in airway epithelial responses to RV in a type 2 cytokine milieu. METHODS: DNA from blood of asthmatic and normal subjects was genotyped for Tollip SNP rs5743899 AA, AG and GG genotypes. Human tracheobronchial epithelial (HTBE) cells from donors without lung disease were cultured to determine pro-inflammatory and antiviral responses to IL-13 and RV16. Tollip knockout and wild-type mice were challenged with house dust mite (HDM) and infected with RV1B to determine lung inflammation and antiviral response. RESULTS: Asthmatic subjects carrying the AG or GG genotype (AG/GG) compared with the AA genotype demonstrated greater airflow limitation. HTBE cells with AG/GG expressed less Tollip. Upon IL-13 and RV16 treatment, cells with AG/GG (vs. AA) produced more IL-8 and expressed less antiviral genes, which was coupled with increased NF-κB activity and decreased expression of LC3, a hallmark of the autophagic pathway. Tollip co-localized and interacted with LC3. Inhibition of autophagy decreased antiviral genes in IL-13- and RV16-treated cells. Upon HDM and RV1B, Tollip knockout (vs. wild-type) mice demonstrated higher levels of lung neutrophilic inflammation and viral load, but lower levels of antiviral gene expression. CONCLUSIONS AND CLINICAL RELEVANCE: Our data suggest that Tollip SNP rs5743899 may predict varying airway response to RV infection in asthma.

Dendritic cell-derived tumor necrosis factor α modifies airway epithelial cell responses.

Mucosal dendritic cells (DC) are intimately associated with the airway epithelium and thus are ideally situated to be first responders to pathogens. We hypothesize that DC drive innate immune responses through early release of tumor necrosis factor (TNF) α, which drives airway epithelial cell responses. In a mouse model, TNFα release was significantly increased following a single exposure to German cockroach (GC) frass, an event independent of neutrophil recruitment into the airways. While lung epithelial cells and alveolar macrophages failed to release TNFα following GC frass exposure, bone marrow-derived DC (BMDC) produced substantial amounts of TNFα suggesting their importance as early responding cells. This was confirmed by flow cytometry of pulmonary myeloid DC. Addition of GC frass-pulsed BMDC or conditioned media from GC frass-pulsed BMDC to primary mouse tracheal epithelial cells (MTEC) or MLE-15 cells induced chemokine (C-C) motif ligand (CCL) 20 and granulocyte macrophage (GM) colony-stimulating factor (CSF), both of which are important for DC recruitment, survival and differentiation. Importantly, DC do not produce CCL20 or GM-CSF following allergen exposure. Blocking TNFα receptor 1 (TNFR1) completely abolished chemokine production, suggesting that BMDC-derived TNFα induced airway epithelial cell activation and enhancement of the innate immune response. Lastly, blocking TNFR1 in vivo resulted in significantly decreased CCL20 and GM-CSF production in the lungs of mice. Together, our data strongly suggest that DC-derived TNFα plays a crucial role in the initiation of innate immune responses through the modification of airway epithelial cell responses.

Analysis of tasks performed by certified ophthalmic medical personnel.

BACKGROUND: Proper delegation of routine tasks to trained personnel might increase cost efficiency by freeing the physician to concentrate on the medical and judgmental aspects of patient care. In ophthalmology, certified ophthalmic medical personnel (OMP) assist the physician by performing many tasks. The Joint Commission on Allied Health Personnel in Ophthalmology (JCAHPO) selected 77 specific tasks performed by OMP and conducted a task analysis survey to determine the importance of these tasks to ophthalmic practice. Individual and practice demographics were surveyed simultaneously to compare the effect of individual and practice differences on task importance. METHODS: Certified OMP and their sponsoring ophthalmologists were surveyed independently. Each group was asked to rate the importance of the 77 selected tasks using a five-point scale of importance. Importance ratings from each survey group were used independently to generate a rank order listing of tasks. RESULTS: Only 3 of the 77 tasks differed significantly in importance between ophthalmologists and OMP. The same five tasks were rated as most important by both groups, whereas the second group of the five most important tasks varied only by +/-4. CONCLUSIONS: The similarity in task importance rankings indicates a common perception between ophthalmologists and OMP concerning the role played by OMP in ophthalmic eye care.

Light and scanning electron microscopy of greenbug aphid damage in wheat using the same section.

A method has been developed to enable correlative light microscopy (LM) and scanning electron microscopy (SEM) on the same section of wheat (Triticum aestivum L.) leaves infested by greenbug aphids (Schizaphis graminum Rondani). Segments of infested leaf tissue were fixed, embedded in paraffin, sectioned, and affixed to slides by standard histological techniques. Serial sections were viewed by LM as temporary mounts in xylene. Sections of interest were identified and re-embedded in fingernail polish, affixed to aluminum stubs, freed of polish with ethyl acetate or acetone, and sputter-coated for SEM. SEM of re-embedded leaf sections showed excellent preservation of leaf anatomy. The same aphid tracks and regions of cell damage identified by LM were visible. SEM increased resolution and provided a much clearer sense of the three-dimensional relations involved in the interaction between plant and insect.

Combined cataract and strabismus surgery.

A patient with cataracts and congenital exotropia underwent combined cataract and strabismus surgery OU. A lateral rectus recession plus an extracapsular cataract extraction with intraocular lens implantation was done OD first; three months later, this procedure was repeated OS. The patient's postoperative course was benign in both cases, and her strabismus resolved after the second operation. A combined surgical approach to cataracts and strabismus (where only a single muscle is involved) was safe and useful in restoring this patient's vision, binocularity, and appearance.

Intraoperative discovery of a neurofibroma during routine ptosis surgery.

A noncosmetic blepharoplasty with levator tuck was planned to repair a congenital ptosis presumed to be caused by levator maldevelopment. During surgery a mass was found in the lid, revealing the ptosis to be mechanical in nature. Biopsy and subsequent pathological exam revealed this to be a plexiform neurofibroma in a reportedly undiagnosed patient.

Angle closure glaucoma following a combined blepharoplasty and ectropion repair.

This paper reports an occurrence of angle closure glaucoma following a combined blepharoplasty and ectropion repair. We are unaware of any previous reports of such an incident. Specific to this case was the coexistence of a cataract that contributed to the narrowing of the anterior chamber. This condition, along with pupil dilation secondary to the anesthetic, precipitated a phacomorphic angle closure glaucoma attack, necessitating emergency cataract surgery. Because other procedures involve pupillary dilation as a potential side effect, we recommend an increased awareness of this potential postoperative complication.