1182

Abstract

Introduction: Redundant diaphragm describes a condition, usually resulting from bilateral phrenic nerve palsy, leading to the inability of the diaphragm to contract during respiration. It has also been described as a result of post-surgical, iatrogenic injuries where mediastinal shifts from paradoxical diaphragm movement can worsen respiratory distress. In the latter group, early recognition and treatment with surgical diaphragm plication reduces the duration of mechanical ventilation, morbidity, and ICU stay especially in pediatric patients. Redundant diaphragm has been hypothesized in advanced Chronic Obstructive Pulmonary Disease (COPD). There is conflicting literature on prevalence of diaphragm dysfunction attributed to direct effect on lung volume changes on diaphragm. Possible mechanisms for redundant diaphragm in COPD include phrenic neuropathy from chronic steroid use or direct muscle changes from chronic hyperinflation. Studies have shown myofibre atrophy, impaired fiber contractility with remodeling in the diaphragm in advanced COPD. Use of muscle ultrasound has made bedside visualization of the diaphragm possible in critically ill patients. Ultrasound can be used to evaluate diaphragm thickness, change in thickness with respiration, excursion amplitude and paradoxical movements with respiration. Feasibility of expeditious bedside ultrasound is uncovering unique phenomenon that may help understand natural history of diaphragm changes seen in COPD. We present a case of redundant diaphragm visualized using ultrasound in a patient with advanced COPD. An 88-year old female with chronic kidney disease was admitted with right basal ganglia and temporal lobe infarcts. On hospital day 2, the patient had acute respiratory failure from aspiration, requiring intubation. Patient was noted to have tachypnea (Rate 35)and acutely increased work of breathing using accessory muscles while on ventilator settings SIMV, FiO2 100%, PEEP 8 cm H2O. Chest x-ray showed pulmonary edema with hyperinflation, suggesting severe COPD. Bedside diaphragm ultrasound in mid axillary line in the zone of apposition showed visible diaphragm separating the thorax and abdomen, with lack of thickening during respiration. Fasciculations were seen in diaphragm muscle but descending lung shadows were not visualized corresponding to diaphragm movements signifying passive movements of diaphragm with positive pressure changes during mechanical ventilation. Abnormal attachment of the diaphragm was visualized on both liver and spleen windows with adhesions seen at the zone of apposition. Ineffective movements were also suspected based on fluttering of diaphragm around incidental splenic accessory lobe without any splenic movements seen. All changes were captured on video using ultrasound. Her hospital course was complicated by worsening hypoxia and hypotension and evolution of septic and cardiogenic shock, leading to her death on hospital day 4. The emerging interest in the use of bedside ultrasonography in real time in critically ill patients may uncover unique phenomena like a redundant diaphragm. Visualization of the diaphragm for changes in thickness and pattern of movements in acute respiratory distress can help uncover natural history of disease and help provide newer perspectives to pathophysiology of respiratory muscle dysfunction in critical illness.