Association of abnormal pulmonary vasculature on CT scan for COVID-19 infection with decreased diffusion capacity in follow up: A retrospective cohort study.

BACKGROUND: Coronavirus Disease 2019 (COVID-19) is a respiratory viral illness causing pneumonia and systemic disease. Abnormalities in pulmonary function tests (PFT) after COVID-19 infection have been described. The determinants of these abnormalities are unclear. We hypothesized that inflammatory biomarkers and CT scan parameters at the time of infection would be associated with abnormal gas transfer at short term follow-up. METHODS: We retrospectively studied subjects who were hospitalized for COVID-19 pneumonia and discharged. Serum inflammatory biomarkers, CT scan and clinical characteristics were assessed. CT images were evaluated by Functional Respiratory Imaging with automated tissue segmentation algorithms of the lungs and pulmonary vasculature. Volumes of the pulmonary vessels that were ≤5mm (BV5), 5-10mm (BV5_10), and ≥10mm (BV10) in cross sectional area were analyzed. Also the amount of opacification on CT (ground glass opacities). PFT were performed 2-3 months after discharge. The diffusion capacity of carbon monoxide (DLCO) was obtained. We divided subjects into those with a DLCO <80% predicted (Low DLCO) and those with a DLCO ≥80% predicted (Normal DLCO). RESULTS: 38 subjects were included in our cohort. 31 out of 38 (81.6%) subjects had a DLCO<80% predicted. The groups were similar in terms of demographics, body mass index, comorbidities, and smoking status. Hemoglobin, inflammatory biomarkers, spirometry and lung volumes were similar between groups. CT opacification and BV5 were not different between groups, but both Low and Normal DLCO groups had lower BV5 measures compared to healthy controls. BV5_10 and BV10 measures were higher in the Low DLCO group compared to the normal DLCO group. Both BV5_10 and BV10 in the Low DLCO group were greater compared to healthy controls. BV5_10 was independently associated with DLCO<80% in multivariable logistic regression (OR 1.29, 95% CI 1.01, 1.64). BV10 negatively correlated with DLCO% predicted (r = -0.343, p = 0.035). CONCLUSIONS: Abnormalities in pulmonary vascular volumes at the time of hospitalization are independently associated with a low DLCO at follow-up. There was no relationship between inflammatory biomarkers during hospitalization and DLCO. Pulmonary vascular abnormalities during hospitalization for COVID-19 may serve as a biomarker for abnormal gas transfer after COVID-19 pneumonia.

Veno-arterial extracorporeal membrane oxygenationas a bridge to cytolytic therapy.

We describe a case of successful use of veno-arterial (VA) extracorporeal membrane oxygenation (ECMO), as a bridge to cytoreductive therapy, in a patient with large mediastinal mass due to T cell lymphoblastic leukemia, complicated by acute cardiorespiratory compromise from mechanical compression and pulmonary embolism.

Use of positional therapy when incorporated into a diagnosis-treatment algorithm for obstructive sleep apnea.

PURPOSE: Positional obstructive sleep apnea (OSA) is prevalent. We hypothesized that by incorporating positional therapy into a diagnosis-treatment algorithm for OSA it would frequently be prescribed as an appropriate first-line therapy. METHODS: Fifty-nine members (45 males, 49±9 yrs, BMI 35.2±5.6 kg/m2) of the Law Enforcement Health Benefits (LEHB), Inc. of Philadelphia with clinically suspected OSA were evaluated. Patients completed an Epworth Sleepiness Scale (ESS) questionnaire and a home sleep test (HST). Patients diagnosed with positional OSA (non-supine apnea-hypopnea index [AHI] < 5 events/hr) were offered positional therapy. A cost comparison to continuous positive airway pressure (CPAP) therapy was performed. RESULTS: Fifty-four (92%) of the patients (43 males, 49±9 yrs, BMI 35.2±5.3 kg/m2) had OSA on their HST (AHI 24.2±20.1 events/hr). Sixteen (30%) patients had positional OSA. Compared to non-positional patients, patients with positional OSA were less heavy (32.4±5.1 vs. 36.4±5.1 kg/m2, respectively [p=0.009]), less sleepy (ESS 8±5 vs. 12±5, respectively [p=0.009]), and had less severe OSA (AHI 10.4±4.3 vs. 30.0±21.3 events/hr, respectively [p<0.001]). Thirteen of the 16 patients with positional OSA agreed to positional therapy and 31 non-positional OSA patients agreed to CPAP therapy. Based on initial costs, incorporating positional therapy ($189.95/device compared to CPAP therapy at $962.49/device) into the treatment algorithm resulted in a 24% cost savings compared to if all the patients were initiated on CPAP therapy. CONCLUSION: With the high prevalence of positional OSA, using a diagnosis-treatment algorithm that incorporates positional therapy allows it to be more frequently considered as a cost effective first-line therapy for OSA.

Effect of Emphysema Severity on the Apnea-Hypopnea Index in Smokers with Obstructive Sleep Apnea.

RATIONALE: The presence of obstructive sleep apnea (OSA) in patients with chronic obstructive pulmonary disease (COPD) is referred to as the OSA-COPD overlap syndrome. While lung inflation has been shown to be an important factor in determining upper airway stability, its role in determining OSA severity in smokers, including those with emphysema, has not been evaluated. OBJECTIVES: To evaluate the importance of lung inflation on OSA severity (apnea-hypopnea index [AHI]) in smokers with suspected OSA. METHODS: Fifty-one smokers (18 males; mean [±SD] age, 59 ± 9 yr; body mass index [BMI], 32 ± 9 kg/m(2)) who were part of the Genetic Epidemiology of COPD (COPDGene) project were studied. Patients underwent a full-night polysomnography for suspected OSA. Other testing included spirometry and volumetric chest computed tomography (CT) for quantitative measurement of CT-derived percent emphysema and CT-derived percent gas trapping. MEASUREMENTS AND MAIN RESULTS: For the group overall, there was evidence of obstructive airway disease by spirometry (FEV1, 1.4 ± 0.5 L, 58 ± 14% predicted) and emphysema by quantitative CT (CT-derived percent emphysema, 11 ± 13%; CT-derived percent gas trapping, 31.6 ± 24.1%). Twenty-nine (57%) of the patients had OSA (AHI, 18 ± 12 events/h). Patients with OSA had a higher BMI but were younger than those without OSA (BMI, 35 ± 9 kg/m(2) vs. 29 ± 7 kg/m(2), respectively [P = 0.007]; age, 56 ± 8 yr vs. 62 ± 9 yr, respectively [P = 0.01]). There was an inverse correlation between the AHI and the CT-derived percent emphysema and CT-derived percent gas trapping, both for the entire group (r = -0.41 [P < 0.01] and r = -0.44 [P < 0.01], respectively) and when just those patients with OSA were evaluated (r = -0.43 [P = 0.04] and r = -0.49 [P = 0.03], respectively). Multiple linear regression revealed that, in addition to CT-derived percent emphysema and CT-derived percent gas trapping, sex and BMI were important in determining the AHI in these patients. CONCLUSIONS: In smokers with OSA, increased gas trapping and emphysema as assessed by CT are associated with a decreased AHI. Along with sex and BMI, these measurements may be important in determining the severity of OSA in patients with COPD and may offer a protective mechanism in patients with more advanced disease.

Update on parasomnias: a review for psychiatric practice.

Parasomnias, defined as undesirable behavioral, physiological, or experiential events that accompany sleep, are common in the general population. As a rule, they occur more frequently in children than in adults with the exception of REM sleep behavior disorder (RBD), which is more common in men over 50. No longer considered to be invariably a sign of psychopathology, parasomnias are currently understood as clinical phenomena that arise as brain transitions between REM sleep, non-REM sleep, and wakefulness. This paper presents a clinical approach to diagnosing and treating parasomnias in the general population and in psychiatric patients.

Sleep-disordered breathing: in depression and schizophrenia.

Sleep disorders are becoming more prevalent. There is an overlap of symptoms related to obstructive sleep apnea syndrome (OSAS) and many psychiatric conditions. Complaints of excessive sleepiness, insomnia, cognitive dysfunction, and depressive symptoms can be related to both disease states. Obstructive sleep apnea syndrome is characterized by repetitive disruption of sleep by cessation of breathing and was first described in the 19th century by bedside observation during sleep. Physicians observed this cessation of breathing while the patient slept and postulated that these episodes were responsible for subsequent complaints of sleepiness. OSAS can coexist with major depressive disorder, exacerbate depressive symptoms, or be responsible for a large part of the symptom complex of depression. Additionally, in schizophrenia, sleep apnea may develop as a result of chronic neuroleptic treatment and its effect on gains in body weight, a major risk factor for the development of OSAS.It is important to recognize the signs and symptoms of sleep apnea, namely excessive daytime sleepiness, snoring, and witnessed apneas. Recognition of the existence of sleep apnea, prompt referral to a sleep specialist, and ultimately treatment of an underlying sleep disorder, such as OSAS, can ameliorate symptoms of psychiatric disease.