Improvement in Multidisciplinary Provider Rounding (Surgical Rounds) in the Pediatric Cardiac ICU: An Application of Lean Methodology.

OBJECTIVES: Provider-only, combined surgical, and medical multidisciplinary rounds ("surgical rounds") are essential to achieve optimal outcomes in large pediatric cardiac ICUs. Lean methodology was applied with the aims of identifying areas of waste and nonvalue-added work within the surgical rounds process. Thereby, the goals were to improve rounding efficiency and reduce rounding duration while not sacrificing critical patient care discussion nor delaying bedside rounds or surgical start times. DESIGN: Single-center improvement science study with observational and interventional phases from February 2, 2021, to July 31, 2021. SETTING: Tertiary pediatric cardiac ICU. PARTICIPANTS: Cardiothoracic surgery and cardiac intensive care team members participating in daily "surgical" rounds. INTERVENTIONS: Implementation of technology automation, creation of work instructions, standardization of patient presentation content and order, provider training, and novel role assignment. MEASUREMENTS AND MAIN RESULTS: Sixty-one multidisciplinary rounds were observed (30 pre, 31 postintervention). During the preintervention period, identified inefficiencies included prolonged preparation time, redundant work, presentation variability and extraneous information, and frequent provider transitions. Application of targeted interventions resulted in a 26% decrease in indexed rounds duration (2.42 vs 1.8 min; p = 0.0003), 50% decrease in indexed rounds preparation time (0.53 vs 0.27 min; p < 0.0001), and 66% decrease in transition time between patients (0.09 vs 0.03 min; p < 0.0001). The number of presenting provider changes also decreased (9 vs 4; p < 0.0001). Indexed discussion duration did not change (1 vs 0.98 min; p = 0.08) nor did balancing measures (bedside rounds and surgical start times) change (8.5 vs 9 min; p = 0.89 and 38 vs 22 min; p = 0.09). CONCLUSIONS: Lean methodology can be effectively applied to multidisciplinary rounds in a joint cardiothoracic surgery/cardiac intensive care setting to decrease waste and inefficiency. Interventions resulted in decreased preparation time, transition time, presenting provider changes, total rounds duration indexed to patient census, and anecdotal improvements in provider satisfaction.

Secondary neoplasms of the urinary bladder-clinical management and oncological outcomes.

BACKGROUND: Secondary neoplasms of the bladder account for 4.5% of all bladder neoplasms however there is limited literature reporting management and survival. This is the largest single centre series presented in current literature with long term oncological follow up. METHODS: This is a single institutional, retrospective cohort study of patients with a histological diagnosis of a secondary bladder neoplasm from January 2007 to December 2017 (n=40). Prognostic variables examined included age at diagnosis, histology, disease free survival and treatment. Kaplan-Meier analysis was used to calculate survival. We used multiple regression analysis to identify the most significant treatments for each population group in terms of their survival. RESULTS: Twenty-one patients were male (53%) with a median age of 68 and 19 were female (47%) with a median age of 64. The most common secondary neoplasms and their median survival were prostate [12 patients (30%), 446 days], colorectal [9 patients (23%), 403 days], ovarian [5 patients (13%), 369 days], cervical [4 patients (10%), 148 days], breast [3 patients (8%), 241 days], lymphoma [3 patients (8%), 145 days], gastric [2 patients (5%), 66 days], and renal [2 patients (5%), 854 days]. Those receiving treatment following a secondary diagnosis demonstrated statistical significance in survival for colorectal (surgery P=0.013), prostate (radiotherapy P=0.0012 and hormonal therapy P=0.004) and ovarian cancer (chemotherapy P=0.00002). CONCLUSIONS: Prognosis and treatment depends upon the primary neoplasm. There is some survival benefit in well selected patients receiving treatment following a diagnosis of a bladder secondary.

Impact of Primary Percutaneous Coronary Intervention on Complete Atrioventricular Block With Acute Inferior ST-Elevation Myocardial Infarction.

Background and aims Complete atrioventricular block (CAVB) is associated with poor clinical outcomes in ST-elevation myocardial infarction (STEMI). This study determined the frequency and outcomes of primary percutaneous coronary intervention (PPCI) in patients with CAVB with acute inferior STEMI. Methods We conducted an observational, prospective study and enrolled 151 patients who were diagnosed with inferior STEMI. All patients received PPCI. The clinical outcomes were compared in patients with and without CAVB. The data was recorded on a collection form and analyzed on Statistical Package for Social Sciences (SPSS) software. Descriptive statistics were applied. For quantitative variables, standard deviation and mean were obtained, and statistical tests were also applied. Results Baseline characteristics were homogeneous in all patients. Half of the study population was either diabetic or hypertensive. Out of 151 participants, 21 (13.9%) developed CAVB. Two-thirds of the patients, who had developed heart block, reverted after PPCI. After a follow-up of two weeks, in-hospital mortality did not differ between the groups. Conclusion We conclude that PPCI can improve outcomes of CAVB-complicated acute inferior STEMI and suggest that primary PCI should be the preferred reperfusion therapy in patients with CAVB with STEMI.

Microbial Resistance in Urinary Tract Infections.

Objective To determine the pattern of microbes responsible for urinary tract infections and their susceptibility to antimicrobial agents. Methods This was a prospective, observational study conducted at Benazir Bhutto Hospital, Rawalpindi, Pakistan. The urine samples of 440 patients were collected and sent for culture and sensitivity analysis. The results were recorded on a proforma. The data were analyzed using IBM Statistical Package for Social Sciences (SPSS) version 22 (IBM Corp., Armonk, NY). Descriptive statistics were used to describe the data. Chi-square test was applied to determine the significance of the difference between gender and microorganisms as well as microorganism and antimicrobial sensitivity. P-value of less than 0.05 was considered significant. Results Out of 440 urine samples, 144 culture-positive samples had been obtained from male participants and 296 culture-positive samples had been obtained from female participants. The most common organism on analysis was Escherichia coli. There were more rates of resistance in males. The organisms were most susceptible to fosfomycin and imipenem (p = 0.01). The organisms were resistant to ceftazidime (p = 0.01). Conclusion In Pakistan, most patients with resistance present with mild symptoms instead of severe clinical manifestations. Therefore, there is a need to reduce the over-prescription of antibiotics for urinary tract infections, especially in cases when other non-antimicrobial agents can be used.

Atypical presentation of ventricular tachycardia.

Cardiac syncope and epileptic seizure are two very similar presentations and difficult to differentiate without a proper history, physical examination and investigations. In a former study, 10 out of 22 episodes of induced ventricular tachycardia or fibrillation can result in stereotypical tonic-clonic movement with varied electroencephalography changes. We present a case which was diagnosed as ventricular tachycardia from seizure-like attack. It is to emphasise the importance of including ventricular tachycardia among other differential diagnoses of seizure-like activity in a patient with cardiovascular risks.

Two cases of severe Purtscher-like retinopathy demonstrating recurrence and progression to neovascularization and vitreous hemorrhage.

PURPOSE: To report the clinical course of two cases with Purtscher-like retinopathy (PLR), associated with peritoneal dialysis (PD), demonstrating disease recurrence and progression to neovascularization and vitreous hemorrhage. OBSERVATIONS: Case 1 (45-year old woman) experienced acute bilateral vision loss. Medical history included hypertension, end-stage renal failure (ESRF), PD, and obstructive sleep apnea. Visual acuity (VA) was 20/100 OD, 20/80 OS. Fundus findings were pathognomonic for PLR and included white streaks within arterioles. Nine months later, repeat imaging demonstrated disease recurrence and progression, including increased ischemia and new retinal neovascularization. The patient was managed with pan-retinal photocoagulation, sleep apnea treatment, and oral corticosteroids. Four months later, VA remained stable without additional progression.Case 2 (74-year old woman) experienced acute bilateral vision loss. Medical history included hypertension, ESRF, and PD, complicated by peritonitis. VA was 20/25 OD, 20/32 OS. Fundus findings were pathognomonic for PLR and included white streaks within arterioles. Three months later, further acute vision loss occurred, coinciding with recurrent peritonitis. Repeat imaging revealed disease recurrence and progression, including severely increased retinal ischemia. The PD catether was removed and the patient converted to hemodialysis. Bilateral vitreous hemorrhage later complicated the course. CONCLUSIONS AND IMPORTANCE: PLR can occur in association with PD, particularly in acute peritonitis. Contrary to classical descriptions, PLR may take a chronic and progressive course, with increasing ischemia and progression to neovascularization or vitreous hemorrhage. Increased surveillance for complications is recommended and treatment of neovascularization may be required.

Chemokine (C-C Motif) Receptor-Like 2 is not essential for lung injury, lung inflammation, or airway hyperresponsiveness induced by acute exposure to ozone.

Inhalation of ozone (O3), a gaseous air pollutant, causes lung injury, lung inflammation, and airway hyperresponsiveness. Macrophages, mast cells, and neutrophils contribute to one or more of these sequelae induced by O3 Furthermore, each of these aforementioned cells express chemokine (C-C motif) receptor-like 2 (Ccrl2), an atypical chemokine receptor that facilitates leukocyte chemotaxis. Given that Ccrl2 is expressed by cells essential to the development of O3-induced lung pathology and that chemerin, a Ccrl2 ligand, is increased in bronchoalveolar lavage fluid (BALF) by O3, we hypothesized that Ccrl2 contributes to the development of lung injury, lung inflammation, and airway hyperresponsiveness induced by O3 To that end, we measured indices of lung injury (BALF protein, BALF epithelial cells, and bronchiolar epithelial injury), lung inflammation (BALF cytokines and BALF leukocytes), and airway responsiveness to acetyl-ß-methylcholine chloride (respiratory system resistance) in wild-type and mice genetically deficient in Ccrl2 (Ccrl2-deficient mice) 4 and/or 24 hours following cessation of acute exposure to either filtered room air (air) or O3 In air-exposed mice, BALF chemerin was greater in Ccrl2-deficient as compared to wild-type mice. O3 increased BALF chemerin in mice of both genotypes, yet following O3 exposure, BALF chemerin was greater in Ccrl2-deficient as compared to wild-type mice. O3 increased indices of lung injury, lung inflammation, and airway responsiveness. Nevertheless, no indices were different between genotypes following O3 exposure. In conclusion, we demonstrate that Ccrl2 modulates chemerin levels in the epithelial lining fluid of the lungs but does not contribute to the development of O3-induced lung pathology.

Plasminogen activator inhibitor-1 does not contribute to the pulmonary pathology induced by acute exposure to ozone.

Expression of plasminogen activator inhibitor (PAI)-1, the major physiological inhibitor of fibrinolysis, is increased in the lung following inhalation of ozone (O3), a gaseous air pollutant. PAI-1 regulates expression of interleukin (IL)-6, keratinocyte chemoattractant (KC), and macrophage inflammatory protein (MIP)-2, which are cytokines that promote lung injury, pulmonary inflammation, and/or airway hyperresponsiveness following acute exposure to O3 Given these observations, we hypothesized that PAI-1 contributes to the severity of the aforementioned sequelae by regulating expression of IL-6, KC, and MIP-2 following acute exposure to O3 To test our hypothesis, wild-type mice and mice genetically deficient in PAI-1 (PAI-1-deficient mice) were acutely exposed to either filtered room air or O3 (2 ppm) for 3 h. Four and/or twenty-four hours following cessation of exposure, indices of lung injury [bronchoalveolar lavage fluid (BALF) protein and epithelial cells], pulmonary inflammation (BALF IL-6, KC, MIP-2, macrophages, and neutrophils), and airway responsiveness to aerosolized acetyl-ß-methylcholine chloride (respiratory system resistance) were measured in wild-type and PAI-1-deficient mice. O3 significantly increased indices of lung injury, pulmonary inflammation, and airway responsiveness in wild-type and PAI-1-deficient mice. With the exception of MIP-2, which was significantly lower in PAI-1-deficient as compared to wild-type mice 24 h following cessation of exposure to O3, no other genotype-related differences occurred subsequent to O3 exposure. Thus, following acute exposure to O3, PAI-1 neither regulates pulmonary expression of IL-6 and KC nor functionally contributes to any of the pulmonary pathological sequelae that arise from the noxious effects of inhaled O3.

Resistin deficiency in mice has no effect on pulmonary responses induced by acute ozone exposure.

Acute exposure to ozone (O3), an air pollutant, causes pulmonary inflammation, airway epithelial desquamation, and airway hyperresponsiveness (AHR). Pro-inflammatory cytokines-including IL-6 and ligands of chemokine (C-X-C motif) receptor 2 [keratinocyte chemoattractant (KC) and macrophage inflammatory protein (MIP)-2], TNF receptor 1 and 2 (TNF), and type I IL-1 receptor (IL-1α and IL-1ß)-promote these sequelae. Human resistin, a pleiotropic hormone and cytokine, induces expression of IL-1α, IL-1ß, IL-6, IL-8 (the human ortholog of murine KC and MIP-2), and TNF. Functional differences exist between human and murine resistin; yet given the aforementioned observations, we hypothesized that murine resistin promotes O3-induced lung pathology by inducing expression of the same inflammatory cytokines as human resistin. Consequently, we examined indexes of O3-induced lung pathology in wild-type and resistin-deficient mice following acute exposure to either filtered room air or O3. In wild-type mice, O3 increased bronchoalveolar lavage fluid (BALF) resistin. Furthermore, O3 increased lung tissue or BALF IL-1α, IL-6, KC, TNF, macrophages, neutrophils, and epithelial cells in wild-type and resistin-deficient mice. With the exception of KC, which was significantly greater in resistin-deficient compared with wild-type mice, no genotype-related differences in the other indexes existed following O3 exposure. O3 caused AHR to acetyl-ß-methylcholine chloride (methacholine) in wild-type and resistin-deficient mice. However, genotype-related differences in airway responsiveness to methacholine were nonexistent subsequent to O3 exposure. Taken together, these data demonstrate that murine resistin is increased in the lungs of wild-type mice following acute O3 exposure but does not promote O3-induced lung pathology.

Effect of antigen sensitization and challenge on oscillatory mechanics of the lung and pulmonary inflammation in obese carboxypeptidase E-deficient mice.

Atopic, obese asthmatics exhibit airway obstruction with variable degrees of eosinophilic airway inflammation. We previously reported that mice obese as a result of a genetic deficiency in either leptin (ob/ob mice) or the long isoform of the leptin receptor (db/db mice) exhibit enhanced airway obstruction in the presence of decreased numbers of bronchoalveolar lavage fluid (BALF) eosinophils compared with lean, wild-type mice following antigen (ovalbumin; OVA) sensitization and challenge. To determine whether the genetic modality of obesity induction influences the development of OVA-induced airway obstruction and OVA-induced pulmonary inflammation, we examined indices of these sequelae in mice obese as a result of a genetic deficiency in carboxypeptidase E, an enzyme that processes prohormones and proneuropeptides involved in satiety and energy expenditure (Cpe(fat) mice). Accordingly, Cpe(fat) and lean, wild-type (C57BL/6) mice were sensitized to OVA and then challenged with either aerosolized PBS or OVA. Compared with genotype-matched, OVA-sensitized and PBS-challenged mice, OVA sensitization and challenge elicited airway obstruction and increased BALF eosinophils, macrophages, neutrophils, IL-4, IL-13, IL-18, and chemerin. However, OVA challenge enhanced airway obstruction and pulmonary inflammation in Cpe(fat) compared with wild-type mice. These results demonstrate that OVA sensitization and challenge enhance airway obstruction in obese mice regardless of the genetic basis of obesity, whereas the degree of OVA-induced pulmonary inflammation is dependent on the genetic modality of obesity induction. These results have important implications for animal models of asthma, as modeling the pulmonary phenotypes for subpopulations of atopic, obese asthmatics critically depends on selecting the appropriate mouse model.

Early repair of large infant ventricular septal defect despite respiratory syncytial virus-induced respiratory failure with postrepair chylous pericardial effusion requiring pleuropericardial window: a case report and review of the literature.

The surgical correction of congenital cardiac lesions that are complicated by intercurrent respiratory syncytial virus (RSV) pneumonitis has traditionally been deferred for at least 6 to 8 weeks. The presumption is that using cardiopulmonary bypass will increase the risk of postoperative pulmonary complications. We present an infant who developed acute respiratory failure related to RSV pneumonitis and required urgent mechanical ventilation. Cardiac evaluation revealed a large nonrestrictive ventricular septal defect (VSD), aortic arch hypoplasia, normally functioning bicuspid aortic valve, and hemodynamic instability associated with markedly increased pulmonary blood flow. Separation from mechanical ventilation was unsuccessful preoperatively. He underwent VSD repair with cardiopulmonary bypass less than 4 weeks after initial RSV infection. He was extubated successfully within 72 hours of VSD repair. Approximately 6 weeks postoperatively, he developed a circumferential chylous pericardial effusion of unclear etiology--an exceedingly rare complication of VSD repair in early infancy in a non-Down syndrome patient. The chylous effusion was initially managed unsuccessfully with Portogen/Monogen and a percutaneously placed pericardial drain. Two weeks later, he underwent creation of a pleuropericardial window with successful resolution of the chylous effusion. It is of interest to pediatricians to be able to correctly time the repair of congenital heart disease lesions after RSV infection to minimize post-bypass pulmonary complications and yet avoid morbidity from undue delays in repair. In addition, chylopericardium can occur in infants after VSD repair, and dietary modification and catheter drainage may not be adequate.