RESUMO
The diaphragm is the essential respiratory muscle, and damage can significantly impede a human's capacity for blood oxygenation. During inspiration, the diaphragm domes permit the pleural cavity to expand. Whenever this process is disrupted, it results in decreased thoracic expansion and, as a result, hypoventilation. The phrenic nerve innervates the diaphragmatic muscle via the cervical nerve roots C3, C4, and C5. Diaphragmatic paralysis is a multifactorial consequence caused by trauma, neurogenic diseases, infections, inflammatory responses, and chest operative surgery, with the last being the most prevalent causative factor. Here, we are describing the case of a 52-year-old male patient who has had ongoing dyspnea for months after contracting COVID-19 in December 2021, despite the remission of his previous COVID-19 pneumonia in 2020. An X-ray of the chest revealed no diaphragm elevation, whereas electromyography verified diaphragm impairment. On the conservative treatment plan, he reported persistent dyspnea following a period of pulmonary rehabilitation. To a lesser extent, it is advised to wait at least one year to see if there is any reinnervation, which could benefit his lung capacity. COVID-19 has been linked to many systematic diseases. As a result, COVID-19 will not be restricted to its inflammatory effect on the lungs. In other words, it is a multi-organ systematic syndrome. One of these effects is diaphragm paralysis, which should be considered a post-COVID-19 disease. However, there is a need for more literature to support physicians as guidelines for neurological conditions related to COVID-19 infection.
RESUMO
BACKGROUND: The volume-outcome relationship associated with intensive care unit (ICU) experience with managing acute myocardial infarction (AMI) remains inadequately understood. METHODS AND RESULTS: Within a multicenter clinical ICU database, we identified patients with a primary ICU admission diagnosis of AMI between 2008 and 2010 to evaluate whether annual AMI volume of an individual ICU is associated with mortality, length-of-stay, or quality indicators. Patients were categorized into those treated in ICUs with low-annual-AMI volume (≤50th percentile, <2 AMI patients/month, n=569 patients) versus high-annual-AMI volume (≥90th percentile, ≥8 AMI patients/month, n=17 553 patients). Poisson regression and generalized estimating equation with negative binomial regression were used to calculate the relative risk (95% CI) for mortality and length-of-stay, respectively, associated with admission to a low-AMI-volume ICU. When compared with high-AMI-volume, patients admitted to low-AMI-volume ICUs had substantially more medical comorbidities, higher in-hospital mortality (11% versus 4%, P<0.001), longer hospitalizations (6.9±7.0 versus 5.0±5.0 days, P<0.001), and fewer evidence-based therapies for AMI (reperfusion therapy, antiplatelets, ß-blockers, and statins). However, after adjustment for baseline patient characteristics, low-AMI-volume ICU was no longer an independent predictor of in-hospital mortality (relative risk 1.17 [0.87 to 1.56]) or hospital length-of-stay (relative risk 1.01 [0.94 to 1.08]). Similar findings were noted in secondary analyses of ICU mortality and ICU length-of-stay. CONCLUSIONS: Admission to an ICU with lower annual AMI volume is associated with higher in-hospital mortality, longer hospitalization, and lower use of evidence-based therapies for AMI. However, the relationship between low-AMI-volume and outcomes is no longer present after accounting for the higher-risk medical comorbidities and clinical characteristics of patients admitted to these ICUs.
