Length of Stay and Hospital Cost Reductions After Implementing Bedside Percutaneous Ultrasound Gastrostomy (PUG) in a Critical Care Unit.

Background: Critical care patients receive 50% of gastrostomy tubes placed in the United States. Several gastrostomy placement methods exist, however care processes remain variable and often lack health system cost effectiveness. No data exists on efficiency or cost impact of performing bedside percutaneous ultrasound gastrostomy (PUG) on patients with ventilator-dependent respiratory failure. This study's objective was to determine if implementing bedside PUG would positively impact efficiency and cost outcomes in intensive care unit (ICU) patients compared to usual care gastrostomy. Design and Methods: This is a retrospective cohort study of patients with ventilator-dependent respiratory failure who received a gastrostomy consult or procedure in the ICU. Patients received PUG or usual care gastrostomy, determined by the presiding attending's skillset, and both groups were compared across patients' demographics, clinical characteristics and outcomes. Primary outcomes were length of stay (LOS) and total hospital costs. Results: A total of 88 patients were included in the analysis, 45 patients in the PUG group and 43 in the usual care gastrostomy group. No differences were observed in demographic and clinical characteristics. Patients who received PUG had a significantly shorter mean ICULOS and hospital LOS, with reductions of 5.0 and 8.7 days, respectively. Total hospital costs were significantly reduced in the PUG group, with a cost savings of US $26,621 per patient. No differences in mortality or discharge disposition were observed. PUG patients received concomitant percutaneous dilatation tracheostomy (PDT) and PUG ("TPUG") 70% of the time, whereas no usual care patients received concomitant procedures. Off-hour procedures occurred in 53.3% of PUG and 4.6% of usual care gastrostomy. Conclusions: This study demonstrates bedside PUG leads to decreased LOS and total hospital costs in patients with ventilator-dependent respiratory failure. Hospital costs were significantly reduced with a per patient savings of $26,621 compared to usual care gastrostomy.

Mitochondrial dysfunction and pulmonary hypertension: cause, effect, or both.

Pulmonary hypertension describes a heterogeneous disease defined by increased pulmonary artery pressures, and progressive increase in pulmonary vascular resistance due to pathologic remodeling of the pulmonary vasculature involving pulmonary endothelial cells, pericytes, and smooth muscle cells. This process occurs under various conditions, and although these populations vary, the clinical manifestations are the same: progressive dyspnea, increases in right ventricular (RV) afterload and dysfunction, RV-pulmonary artery uncoupling, and right-sided heart failure with systemic circulatory collapse. The overall estimated 5-yr survival rate is 72% in highly functioning patients, and as low as 28% for those presenting with advanced symptoms. Metabolic theories have been suggested as underlying the pathogenesis of pulmonary hypertension with growing evidence of the role of mitochondrial dysfunction involving the major proteins of the electron transport chain, redox-related enzymes, regulators of the proton gradient and calcium homeostasis, regulators of apoptosis, and mitophagy. There remain more studies needed to characterize mitochondrial dysfunction leading to impaired vascular relaxation, increase proliferation, and failure of regulatory mechanisms. The effects on endothelial cells and resulting interactions with their microenvironment remain uncharted territory for future discovery. Additionally, on the basis of observations that the "plexigenic lesions" of pulmonary hypertension resemble the unregulated proliferation of tumor cells, similarities between cancer pathobiology and pulmonary hypertension have been drawn, suggesting interactions between mitochondria and angiogenesis. Recently, mitochondria targeting has become feasible, which may yield new therapeutic strategies. We present a state-of-the-art review of the role of mitochondria in both the pathobiology of pulmonary hypertension and potential therapeutic targets in pulmonary vascular processes.

A Woman in Her 60s With Lung Adenocarcinoma Presents With Copious Watery Sputum and Respiratory Failure.

CASE PRESENTATION: A woman in her 60s presented with 1 month of progressive dyspnea, watery rhinorrhea, and paroxysmal cough productive of clear, watery sputum. She was diagnosed with epidermal growth factor receptor (EGFR) mutation-positive lung adenocarcinoma at another institution 1 week prior to presentation and 3 weeks after the onset of symptoms. She was a never-smoker. She denied fevers and had completed a course of antibiotics for presumed pneumonia, without clinical improvement. She presented to the hospital due to increasing severity of her shortness of breath.

Complexity of macrophage migration inhibitory factor (MIF) and other angiogenic biomarkers profiling in pulmonary arterial hypertension.

Macrophage migration inhibitory factor (MIF) and 22 a priori selected biomarkers were measured from pulmonary arterial hypertension (PAH) patients. Significant positive correlations were found between MIF and several angiogenic factors suggesting a possible MIF regulation role in PAH angiogenesis and pathobiology, but simultaneously highlighting the biomarkers profiling complexity in PAH.