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1.
Cureus ; 16(2): e54701, 2024 Feb.
Article in English | MEDLINE | ID: mdl-38524021

ABSTRACT

Intraoperative acute cardiac tamponade associated with iatrogenic intracardiac perforation from percutaneous interventional cardiac procedures is a rare but potentially catastrophic complication. We report a case of intraoperative acute hemopericardium caused by a left atrial (LA) perforation resulting in cardiac tamponade in a patient undergoing a baffling procedure for the correction of two anomalous pulmonary veins draining into her superior vena cava (SVC) that required continuous pericardiocentesis with autologous blood transfusion via the femoral vein and an emergency intraoperative transfer from the interventional cardiology cath lab to the cardiac operating room for an open sternotomy and primary repair. An 86-year-old female with known right-ventricular (RV) failure with preserved ejection fraction (left ventricular ejection fraction (LVEF): 50-55% on transesophageal echocardiography (TEE) one week prior) and atrial fibrillation was admitted for her third heat failure exacerbation in two months despite being adherent to her aggressive diuresis medication regimen. Upon her readmission and due to her symptomatic and seemingly refractory heart failure, the patient underwent a cardiac computer tomography (CT) with 3D reconstruction that showed previously undiagnosed partial anomalous pulmonary venous return (PAPVR) of two of her four pulmonary veins aberrantly draining into the SVC. This anatomic pathology was deemed to be the likely etiology of her repeated episodes of recurring heart failure exacerbations, shortness of breath, peripheral edema, and fatigue. The patient was counseled and consented to a percutaneous baffle of the two anomalous veins to redirect more of the returning pulmonary venous blood away from the SVC and to the LA. While under general endotracheal anesthesia (GETA) with a TEE in place during the procedure, the patient suddenly developed acute hypotension, tachycardia, and a reduction in expired carbon dioxide (EtCO2) was noted quickly followed by evidence of a rapidly accumulating hemopericardium on TEE. Cardiothoracic surgery was urgently consulted to the interventional cardiology cath lab while the patient underwent an emergency pericardiocentesis that momentarily alleviated her hemodynamic instability, cardiac tamponade physiology, and deteriorating overall clinical picture. While performing continuous pericardiocentesis with autologous return of the aspirated blood via femoral venous access the patient was urgently transported to the cardiac operating room and prepped for emergency sternotomy for primary repair of the LA. Following primary repair via sternotomy, multiple drains were placed and the thoracic cavity was closed with wires. The patient was immediately transported to the surgical intensive care unit (SICU) intubated, mechanically ventilated, and sedated. During this time, the patient progressively required additional vasoactive and inotropic agents to support her mean arterial pressure (MAP), and following a multidisciplinary discussion with the patient's family regarding her goals of care, the decision was made to withdraw further resuscitation efforts and the patient expired four hours later.

2.
Am J Crit Care ; 32(4): 302-306, 2023 07 01.
Article in English | MEDLINE | ID: mdl-37391367

ABSTRACT

BACKGROUND: Open intensive care unit (ICU) visitation policies facilitate communication between clinicians and patients' families. Restrictive visitation policies (eg, during a pandemic) may reduce families' comprehension of information. OBJECTIVES: To determine whether written communication increased awareness of medical issues among ICU families and whether the effect size depended on the visitation policies in place when participants were enrolled. METHODS: Families of ICU patients were randomly assigned to receive usual care with or without daily written patient care updates from June 2019 to January 2021. Participants were asked whether patients had experienced 6 ICU problems at up to 2 time points during the ICU stay. Responses were compared with the study investigators' consensus. RESULTS: Of 219 participants, 131 (60%) were restricted from visiting. Participants in the written communication group were more likely than participants in the control group to correctly identify shock, renal failure, and weakness and were just as likely as participants in the control group to correctly identify respiratory failure, encephalopathy, and liver failure. Participants in the written communication group were more likely than participants in the control group to correctly identify the patient's ICU problems when all 6 were grouped as a composite outcome, with the adjusted odds ratio of correct identification tending to be higher among participants enrolled during restricted versus open visitation periods: 2.9 (95% CI, 1.9-4.2; P < .001) vs 1.8 (95% CI, 1.1-3.1; P = .02), P = .17 for difference. CONCLUSIONS: Written communication helps families correctly identify ICU issues. The benefit may be enhanced when families cannot visit the hospital. ClinicalTrials.gov Identifier: NCT03969810.


Subject(s)
Critical Care , Intensive Care Units , Humans , Communication , Consensus , Policy
4.
eNeuro ; 8(4)2021.
Article in English | MEDLINE | ID: mdl-34193510

ABSTRACT

In the central and peripheral nervous systems, the myelin sheath promotes neuronal signal transduction. The thickness of the myelin sheath changes during development and in disease conditions like multiple sclerosis. Such changes are routinely detected using electron microscopy through g-ratio quantification. While g-ratio is one of the most critical measurements in myelin studies, a major drawback is that g-ratio quantification is extremely laborious and time-consuming. Here, we report the development and validation of MyelTracer, an installable, stand-alone software for semi-automated g-ratio quantification based on the Open Computer Vision Library (OpenCV). Compared with manual g-ratio quantification, using MyelTracer produces consistent results across multiple tissues and animal ages, as well as in remyelination after optic nerve crush, and reduces total quantification time by 40-60%. With g-ratio measurements via MyelTracer, a known hypomyelination phenotype can be detected in a Williams syndrome mouse model. MyelTracer is easy to use and freely available for Windows and Mac OS X (https://github.com/HarrisonAllen/MyelTracer).


Subject(s)
Myelin Sheath , Software , Animals , Axons , Disease Models, Animal , Mice , Microscopy, Electron , Optic Nerve
5.
Blood ; 135(19): 1696-1703, 2020 05 07.
Article in English | MEDLINE | ID: mdl-32107559

ABSTRACT

There are unresolved questions regarding the association between persistent leukocytosis and risk of thrombosis and disease evolution in polycythemia vera (PV), as much of the published literature on the topic does not appropriately use repeated-measures data or time-dependent modeling to answer these questions. To address this knowledge gap, we analyzed a retrospective database of 520 PV patients seen at 10 academic institutions across the United States. Taking hematologic laboratory data at ∼3-month intervals (or as available) for all patients for duration of follow-up, we used group-based trajectory modeling to identify latent clusters of patients who follow distinct trajectories with regard to their leukocyte, hematocrit, and platelet counts over time. We then tested the association between trajectory membership and hazard of 2 major outcomes: thrombosis and disease evolution to myelofibrosis, myelodysplastic syndrome, or acute myeloid leukemia. Controlling for relevant covariates, we found that persistently elevated leukocyte trajectories were not associated with the hazard of a thrombotic event (P = .4163), but were significantly associated with increased hazard of disease evolution in an ascending stepwise manner (overall P = .0002). In addition, we found that neither hematocrit nor platelet count was significantly associated with the hazard of thrombosis or disease evolution.


Subject(s)
Leukemia, Myeloid, Acute/pathology , Leukocytosis/physiopathology , Myelodysplastic Syndromes/pathology , Polycythemia Vera/complications , Primary Myelofibrosis/pathology , Adult , Aged , Aged, 80 and over , Female , Follow-Up Studies , Humans , Leukemia, Myeloid, Acute/etiology , Male , Middle Aged , Myelodysplastic Syndromes/etiology , Polycythemia Vera/pathology , Primary Myelofibrosis/etiology , Prognosis , Retrospective Studies , Survival Rate , Thrombosis , Young Adult
6.
Biochem J ; 475(3): 561-569, 2018 02 09.
Article in English | MEDLINE | ID: mdl-29170160

ABSTRACT

The purpose of the present study was to determine the effects of prolonged hyperinsulinemia on mitochondrial respiration and uncoupling in distinct adipose tissue depots. Sixteen-week-old male mice were injected daily with placebo or insulin to induce an artificial hyperinsulinemia for 28 days. Following the treatment period, mitochondrial respiration and degree of uncoupling were determined in permeabilized perirenal, inguinal, and interscapular adipose tissue. White adipose tissue (WAT) mitochondria (inguinal and perirenal) respire at substantially lower rates compared with brown adipose tissue (BAT). Insulin treatment resulted in a significant reduction in mitochondrial respiration in inguinal WAT (iWAT) and interscapular BAT (iBAT), but not in perirenal WAT (pWAT). Furthermore, these changes were accompanied by an insulin-induced reduction in UCP-1 (uncoupling protein 1) and PGC-1α in iWAT and iBAT only, but not in pWAT or skeletal muscle. Compared with adipose tissue mitochondria in placebo conditions, adipose tissue from hyperinsulinemic mice manifested a site-specific reduction in mitochondrial respiration probably as a result of reduced uncoupling. These results may help explain weight gain so commonly seen with insulin treatment in type 2 diabetes mellitus.


Subject(s)
Adipose Tissue, Brown/metabolism , Diabetes Mellitus, Type 2/metabolism , Insulin/pharmacology , Mitochondria/drug effects , Adipose Tissue, Brown/drug effects , Adipose Tissue, White/drug effects , Adipose Tissue, White/metabolism , Animals , Diabetes Mellitus, Type 2/drug therapy , Diabetes Mellitus, Type 2/genetics , Diabetes Mellitus, Type 2/pathology , Humans , Hyperinsulinism/genetics , Hyperinsulinism/metabolism , Hyperinsulinism/pathology , Insulin/metabolism , Mice , Mitochondria/pathology , Mitochondrial Uncoupling Proteins/genetics , Muscle, Skeletal/drug effects , Muscle, Skeletal/metabolism , Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/genetics , Respiration/drug effects , Uncoupling Protein 1/genetics
7.
Int J Mol Sci ; 18(5)2017 May 20.
Article in English | MEDLINE | ID: mdl-28531105

ABSTRACT

We have previously found that cigarette smoke disrupts metabolic function, in part, by increasing muscle ceramide accrual. To further our understanding of this, we sought to determine the role of the cytokine high-mobility group box 1 (HMGB1), which is increased with smoke exposure, in smoke-induced muscle metabolic perturbations. To test this theory, we determined HMGB1 from lungs of human smokers, as well as from lung cells from mice exposed to cigarette smoke. We also treated cells and mice directly with HMGB1, in the presence or absence of myriocin, an inhibitor of serine palmitoyltransferase, the rate-limiting enzyme in ceramide biosynthesis. Outcomes included assessments of insulin resistance and muscle mitochondrial function. HMGB1 was significantly increased in both human lungs and rodent alveolar macrophages. Further testing revealed that HMGB1 treatment elicited a widespread increase in ceramide species and reduction in myotube mitochondrial respiration, an increase in reactive oxygen species, and reduced insulin-stimulated Akt phosphorylation. Inhibition of ceramide biosynthesis with myriocin was protective. In mice, by comparing treatments of HMGB1 injections with or without myriocin, we found that HMGB1 injections resulted in increased muscle ceramides, especially C16 and C24, which were necessary for reduced muscle mitochondrial respiration and compromised insulin and glucose tolerance. In conclusion, HMGB1 may be a necessary intermediate in the ceramide-dependent metabolic consequences of cigarette smoke exposure.


Subject(s)
Ceramides/biosynthesis , HMGB1 Protein/metabolism , Lung/metabolism , Muscle Fibers, Skeletal/metabolism , Nicotiana/adverse effects , Smoke/adverse effects , Smoking/metabolism , Animals , Cell Respiration , Ceramides/antagonists & inhibitors , Ceramides/genetics , Fatty Acids, Monounsaturated/pharmacology , HMGB1 Protein/blood , HMGB1 Protein/pharmacology , Humans , Insulin/metabolism , Insulin Resistance , Lung/pathology , Macrophages, Alveolar/metabolism , Male , Mice , Mitochondria/metabolism , Phosphorylation , Proto-Oncogene Proteins c-akt/metabolism , Reactive Oxygen Species/metabolism , Serine C-Palmitoyltransferase/metabolism
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