BACKGROUND:

People with chronic obstructive pulmonary disease (COPD) are sedentary but the extent of the problem is not fully understood.

PURPOSES:

This study examines sedentary time and physical activity (PA) and the relative effects of demographic and clinical characteristics on sedentary time and PA in a population-based sample of people with COPD and a comparison group from the general population.

METHODS:

Subjects were drawn from the National Health and Nutrition Examination Survey dataset (2003-2006). Physical activity was measured by accelerometry.

RESULTS:

People with COPD were sedentary and spent less time in most levels of PA. Age, gender, race, level of education, working status, shortness of breath, self-reported health, and body mass index were significantly associated with sedentary time or level of PA.

CONCLUSION:

Findings emphasize the need to decrease sedentary time and increase PA in people with COPD.

INTRODUCTION:

Omega-3 polyunsaturated fatty acids (PUFA) have demonstrated to have antiarrhythmic properties. However, randomized studies have shown inconsistent results.

OBJECTIVE:

We aimed to analyze the effect of omega-3 PUFA on preventing potentially fatal ventricular arrhythmias and sudden cardiac death.

METHODS:

Randomized trials comparing omega-3 PUFA to placebo and reporting sudden cardiac death (SCD) or first implanted cardioverter-defibrillator (ICD) event for ventricular tachycardia or fibrillation were included in this study. A meta-analysis using a random effects model was performed and results were expressed in terms of Odds Ratio (OR) and 95% Confidence Interval (CI) after evaluating for interstudy heterogeneity using I(2). The reported data were extracted on the basis of the intention-to-treat principle.

RESULTS:

A total of 32,919 patients were included in nine trials; 16,465 patients received omega-3 PUFA and 16,454 received placebo. When comparing omega-3 PUFA to placebo, there was nonsignificant risk reduction of SCD or ventricular arrhythmias (OR = 0.82 [95% CI: 0.60-1.21], p = 0.21 I(2) = 49.7%).

CONCLUSION:

Dietary supplementation with omega-3 PUFA does not affect the risk of SCD or ventricular arrhythmias.

The administration of iodinated contrast medium may lead to excess free thyroid hormone release and cause thyroid storm. A woman presented to the emergency department with dyspnea, hemoptysis, and intermittent bilateral lower extremities edema. Physical examination revealed mildly enlarged thyroid. Patient underwent a computed tomography scan of the chest with intravenous iodinated contrast medium to rule out pulmonary embolism, the patient developed a thyroid storm second to iodinated contrast medium injection. Proper treatment was provided and the patient had a good outcome. We present this case of an unusual presentation of a thyroid storm with cardiac arrest. This case illustrates that evaluating thyroid function tests in patients with an enlarged thyroid prior to the administration of iodinated contrast medium could prevent the development of thyroid storm.

We present an unfortunate case of a previously healthy woman who suffered an out-of-hospital cardiac arrest in the setting of severe emotional distress, likely due to apical ballooning syndrome. This case highlights the fact that although patients with apical ballooning syndrome typically do well following recovery from transient left ventricular dysfunction, they should be monitored closely in the acute setting due to the potential for life-threatening arrhythmias.

OBJECTIVES:

Pulmonary nocardiosis is an uncommon opportunistic infection affecting mainly immunocompromised patients. We herein present a case of nocardiosis without profound underlying immunodeficiency.

BACKGROUND:

A female, 84-years' old patient with stage IV chronic obstructive pulmonary disease (COPD) is presented. No profound causes of immunodeficiency existed, such as HIV infection, diabetes mellitus, malignancy, alcoholism, chemotherapy or previous corticosteroid intake. The patient recovered after treatment with trimethoprim/sulfamethoxazole for 6 months.

RESULTS:

One year after infection resolution, stimulation of the patient's blood monocytes with Nocardia antigens revealed defective production of tumor necrosis factor-alpha, interleukin (IL)-6 and IL-17.

CONCLUSION:

We provide preliminary evidence for a link between defective innate immune responses and predisposition for Nocardia infections. Further studies must be conducted in order to fully investigate this mechanism of infection acquisition.

A 56-year-old woman with a history of paraplegia and chronic pain due to neuromyelitis optica (Devic's syndrome) was admitted to a spinal cord injury unit for management of a sacral decubitus ulcer. During the hospitalization, she required emergency transfer to the intensive care unit (ICU) because of progressive deterioration of respiratory muscle function, severe respiratory acidosis, obtundation and hypotension. Upon transfer to the ICU, arterial blood gas revealed severe acute-on-chronic respiratory acidosis (pH 7.00, PCO2 120 mm Hg, PO2 211 mm Hg). The patient was immediately intubated and mechanically ventilated. Intravenous fluid boluses of normal saline (10.5 L in about 24 h) and vasopressors were started with rapid correction of hypotension. In addition, she was given hydrocortisone. Within 40 min of initiation of mechanical ventilation, there was improvement in acute respiratory acidosis. Sixteen hours later, however, the patient developed life-threatening hypokalemia (K(+) of 2.1 mEq/L) and hypomagnesemia (Mg of 1.4 mg/dL). Despite aggressive potassium supplementation, hypokalemia continued to worsen over the next several hours (K(+) of 1.7 mEq/L). Urine studies revealed renal potassium wasting. We reason that the recalcitrant life-threatening hypokalemia was caused by several mechanisms including total body potassium depletion (chronic respiratory acidosis), a shift of potassium from the extracellular to intracellular space (rapid correction of respiratory acidosis with mechanical ventilation), increased sodium delivery to the distal nephron (normal saline resuscitation), hyperaldosteronism (secondary to hypotension plus administration of hydrocortisone) and hypomagnesemia. We conclude that rapid correction of respiratory acidosis, especially in the setting of hypotension, can lead to life-threatening hypokalemia. Serum potassium levels must be monitored closely in these patients, as failure to do so can lead to potentially lethal consequences.

Clinical trials exploring optimal sedation management in critically ill pediatric patients are urgently needed to improve both short- and long-term outcomes. Concise operational definitions that define and provide best-available estimates of sedation-related adverse events (AE) in the pediatric population are fundamental to this line of inquiry.To perform a multiphase systematic review of the literature to identify, define, and provide estimates of sedation-related AEs in the pediatric ICU setting for use in a multicenter clinical trial.In Phase One, we identified and operationally defined the AE. OVID-MEDLINE and CINAHL databases were searched from January 1998 to January 2012. Key terms included sedation, intensive and critical care. We limited our search to data-based clinical trials from neonatal to adult age. In Phase Two, we replicated the search strategy for all AEs and identified pediatric-specific AE rates.We reviewed 20 articles identifying sedation-related adverse events and 64 articles on the pediatric-specific sedation-related AE. A total of eleven sedation-related AEs were identified, operationally defined and estimated pediatric event rates were derived. AEs included: inadequate sedation management, inadequate pain management, clinically significant iatrogenic withdrawal, unplanned endotracheal tube extubation, post-extubation stridor with chest-wall retractions at rest, extubation failure, unplanned removal of invasive tubes, ventilator-associated pneumonia, catheter-associated bloodstream infection, Stage II+ pressure ulcers and new tracheostomy.Concise operational definitions that defined and provided best-available event rates of sedation-related AEs in the pediatric population are presented. Uniform reporting of adverse events will improve subject and patient safety.