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Introduction and Objectives: Limited healthcare access and resource inequities pose significant barriers to care, all of which have been amplified during the COVID-19 pandemic. DFUs represent an especially challenging medical problem to prevent and treat due to the resource intensive care required. We sought to evaluate the feasibility of multidisciplinary, mobile, DFU outreach clinics to improve access to care. Method(s): Our clinic model focused on creating mobile diabetic foot clinics staffed by volunteer clinical providers who specialize in Vascular Surgery, Diabetes, and Podiatry. We recruited volunteer healthcare providers from an academic medical center. We partnered with local community centers with established programs providing services to unhoused individuals. Result(s): Between June 2020 and August 2022, a total of 130 unhoused individuals were seen at four mobile clinics set up at different locations. Diabetic foot care was provided by volunteers from seven departments: Endocrinology/Diabetes, Vascular Surgery and Vascular Lab, Podiatry, Addiction Medicine, Smoking Cessation, and Financial. On average, 32 healthcare provider volunteers participated at each clinic. Services provided include: vitals, blood glucose, HgA1c, lipid panel testing, ankle-brachial index, podiatric exam, wound care, medical education, COVID vaccination/booster, insurance enrollment, and new socks and shoes. Of 130 unhoused patients, 29% had hypertension (38), 34% had abnormal ABI (44), and 14% had diabetes (18). Fifteen patients were further identified as high risk for developing DFU-associated amputation (12%) and were provided with ambulatory follow-ups. Conclusion(s): In our pilot experience, it is feasible to provide consistent comprehensive DFU care through mobile outreach clinics. By using the infrastructure of partner organizations and healthcare expertise of an academic center, our clinics could integrate into existing community services. [Formula presented]Copyright © 2022
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The arrangement of natural and physical features on the earth's surface are a few among the countless items that govern the airborne acoustic transmission at boundary layers. In particular, if the acoustic waves are attributes of live concerts at open-air theatres, without losing the sheen and quality, the audience should certainly receive the unbroken depth of the performance. Hence, at all times, it is advisable to analyse the auditory receptiveness, particularly in all intended recreational spaces. The current pandemic circumstances and the mandated COVID-19 prevention protocols encourage gatherings in naturally ventilated outdoor regions than confined indoors. This work predicts and quantifies the acoustic experience at the naturally carved amphitheatre at SAINTGITS, an autonomous institution at the down South-West of the Indian Subcontinent. The entire recreational space at SAINTGITS AMPHI was separately modelled as a Base case and Advanced case, and were analysed using the acoustic modelling module of EASE Focus, a renowned simulation freeware, which is in strict adherence with the International standards. The variation in loudness received at the nearest and farthest ends of the amphitheatre was between 67 to 80 dB. Though the Zero frequency SPL (Z-weighting) exhibited the loudness in the range of 81 to 85 dB and could maintain a safer auditory level for any human ear, it was confined to a hemispherical region near the sound source. A vertical beam angle of -4.0 degrees was found to be effective throughout. The procedures and analyses will certainly help the future organizers and stakeholders to effectively plan the resources to reap rich acoustic experience at terrain-centric locales. The surface topography and contours were plotted with another set of freeware, the CADMAPPER and the QUIKGRID, to compare terrain gradient with the known data. Furthermore, this interdisciplinary research exhibits the extensive simulation capability of both EASE Focus and QUIKGRID and demonstrates the modelling versatility and deliverable potential of these freeware to benefit the budding architects and researchers.
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Mucormycosis is fungal disease caused by fungus Mucor. It has been seen as a life-threatening complication of disease Covid-19. It has 70 times higher prevalence rate in India as compared to the world, having only few but expensive treatment options. The triggers of Mucor infection in Covid-19 patients are immune deficiency and hyperglycaemia caused by the use of corticosteroid, which favours Mucorales tissue Penetration. Mucormycosis has mainly six different types viz pulmonary, rhino-orbital-cerebral, gastrointestinal, widely disseminated, cutaneous, & miscellaneous infection, the commonest clinical presentation is rhino-orbito-cerebral in Covid-19 pandemic. Ayurveda though an ancient science of healing, has strength to treat newer diseases from several decades. Mucormycosis disease is not mentioned in Ayurveda text directly, it is Un uttered disease (Anukta Vyadhi) but it can be treated with help of basic principles of Ayurveda. By understanding the pathogenesis, it can be stated that, it is an Abhishangaja Vyadhi (diseased caused by Virus/ Bacteria/ Parasite) and categorised as Raktapitta Pradhan Tridoshaja Vyadhi (disease caused by vitiation of all three humors with rakta pitta predominance). Prevention of Mucormycosis can be achieved by following daily (Dincharya) and seasonal (Ritucharya) regimens. The treatment protocol include Krimighna (Antimicrobial), Tridoshashamak (normalise all three humors) and Raktashodhaka / Pittashamak (blood purifier), Agnideepak (improve digestion) & Aampachak (improve metabolism), Pramehhar (treatment of diabetes/hyperglycaemia) and Rasayana (Rejuvenation) drugs.
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Despite the devastating impact of COVID-19 on all domains of health, very few studies focus on epigenetics-based approaches to target both the viral-host immune responses and central nervous system involvement in COVID-19. Hospitalized COVID-19 patients experience a wide array of neurological symptoms ranging from convulsions to strokelike syndrome and anosmia. None of the pipeline antiviral drugs has been shown to penetrate the blood-brain barrier to exert neurotrophic actions to counteract the COVID-19 damage to the brain. We have identified curcumin extracted from Turmeric (Curcuma longa) exhibiting dual properties: to disrupt viral attachment and hijacking host-viral immune response and to target epigenetics pathway regulating oxidative stress and inflammation responses underlying COVID-19 syndrome. We recruit nanotechnology to formulate liposome-based curcumin: Lipocurc, and completed Phase I study showing very favorable safety and efficacy in Parkinson disease model. We propose to translate the findings to COVID-19 syndrome and exploit the antidepressant and cognitive enhancing properties to accelerate recovery from COVID-19 through navigating brain pathways regulating mood, behavioral control, and cognition within the context of acute and postacute COVID-19 syndrome. © 2021 Elsevier Inc.
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Case Report While the COVID-19 pandemic killing millions world-wide, definitive therapy is not yet available. However, vaccines were shown to effectively reduce COVID-19 related mortality. Side effects of COVID vaccination include thrombosis. Most of the vaccine-related thrombosis took place after the Oxford-AstraZeneca and Johnson & Johnson vaccines. Our case, however, developed thrombosis after receiving the Moderna mRNA vaccine. A 62 y/o female with hypertension and paroxysmal atrial fibrillation had retroperitoneal hematoma thought to be due to an aneurysm posterior to the pancreatic head and underwent embolization. Following this, she developed bilateral pulmonary embolism (PE) secondary to iliac vein thrombosis which was thought to be a direct result of compression from the hematoma. She was started on anticoagulation (rivaroxaban) at that time and monitored closely for possible bleeding. Unfortunately, she stopped rivaroxaban after one month due to financial reasons. A year later, the patient presented to the hospital with chest tightness for 3 days, one week after she took her 2nd dose of Moderna vaccine. 2 days later, she started having left-sided chest tightness and dizziness. She has no family history of clotting disorder, recent surgery, and has no known malignancy. On admission, she was hemodynamically stable with normal oxygen saturation in room air. Blood work showed normal platelet count and coagulation panel. CT angiogram of the chest showed PE in the right middle lobe segmental branch without right ventricular strain. She did not have troponin elevation or EKG changes. Apixaban was initiated through a financial assistance program on discharge. Although vaccine-related thrombosis remains at the top of the differential diagnosis for our patient, a history of prior thromboembolic event a year earlier and lack of adherence to anticoagulation may have enhanced this lady's resurgence of thrombosis. Having a high degree of suspicion following COVID vaccination is always important to make an early diagnosis and prevent serious consequences of thromboembolism. It is possible that the immune-modulatory effects of the mRNA vaccines can enhance the recurrence of thrombosis in persons with previous history of the condition.
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Case Report Hypercoagulability in the setting of COVID 19 infection is well known, but data about arterial thrombosis in this context is limited. There have also been rare instances of aortic thrombosis in the setting of acute pancreatitis. We present the case of a 64-year-old female who was admitted for acute hypoxic respiratory failure due to COVID pneumonia. A few days earlier, the patient was admitted for a bout of acute pancreatitis that was medically managed but left the hospital against medical advice. During this admission, she was found to be covid positive but was asymptomatic. Chest imaging showed bilateral interstitial opacities. The patient was readmitted due to worsening hypoxia and received dexamethasone, antibiotics and prophylactic heparin on admission. The patient didn't receive remdesivir due to acute kidney injury. Oxygen requirements increased over the next 2 days. On hospital day 3 , the patient developed right lower limb pain not relieved with analgesics with symptoms suggestive for acute limb ischemia. CT angiography of the abdominal aorta and lower extremities revealed significant clot burden in infrarenal aorta and acute occlusion of bilateral popliteal arteries and right profunda femoral artery likely due to aortic clot emboli. Vascular surgery was consulted and proceeded with thrombectomy in the infrarenal aorta, bilateral common iliac arteries and bilateral lower extremity arteries with compartment fasciotomy of the lower extremities. Unfortunately, the patient developed severe septic shock and passed away a few hours after the surgery. Although rare, there have been a few other case reports where aortic thrombosis was caused by COVID 19 or acute pancreatitis. In our patient, both pancreatitis and COVID 19 likely have played a role in aortic thromboembolism leading to critical limb ischemia. Once diagnosed, arterial occlusion is a medical emergency and needs urgent attention and immediate intervention! Physicians should be aware of the possibility of arterial occlusion in the context of Covid 19, especially if acute pancreatitis preceded Covid 19 infection.
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Introduction: Myocarditis is an important cause of sudden cardiac death in competitive athletes. There have been reports of myocardial inflammation on cardiovascular magnetic resonance (CMR) in athlete and nonathlete populations after SARS-CoV-2 infection;however, their clinical and functional significance is not known. We sought to investigate the relationship between left ventricular (LV) strain and other CMR markers suggestive of myocardial inflammation or fibrosis. Hypothesis: Reduced myocardial strain is associated with the presence of CMR abnormalities suggestive of inflammation, fibrosis, or necrosis in athletes recovering from SARS-CoV-2 infection. Methods: Collegiate athletes (N = 123) underwent a comprehensive CMR exam including strain encoded (SENC) imaging. We analyzed LV global longitudinal strain (GLS) across five groups defined by the presence or absence of late gadolinium enhancement (LGE), and T1 or T2 abnormalities. Myocarditis diagnosis on CMR required both abnormal T1 or LGE, and abnormal T2, in the same LV segment. Results: We enrolled 11 COVID negative control athletes (Group 1). Among COVID positive athletes, 42 had no abnormalities on CMR (Group 2), 31 had isolated right ventricular insertion point (RVIP) LGE (Group 3), 28 had LGE beyond RVIP (Group 4), and 11 athletes had myocarditis (Group 5). GLS was significantly lower in Groups 3, 4, and 5 compared with negative controls (p<0.05, Figure 1). There was a deterioration in GLS as CMR abnormalities progressed from control athletes to those with LGE and myocarditis. There was no significant difference in LV ejection fraction between the 5 groups. Conclusions: In conclusion, SARS-CoV-2 infection in collegiate athletes leads to subtle abnormalities in cardiac function detected by GLS that correlate with abnormal mapping and LGE suggestive of myocardial inflammation and fibrosis. The clinical significance of these abnormalities remains to be determined.
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Objective: Extracorporeal Membrane Oxygenation (ECMO) has been used to support patients with severe ARDS. Bleeding and thrombosis are common complications and have been linked to a hyperinflammatory state. To better understand the coronavirus disease 2019 (COVID-19) associated procoagulant and anticoagulant pathophysiology, we examined our experience with COVID-19 patients supported with venovenous (VV) ECMO. Study Design: retropsective study Settings: Tertiary care institution Patients: During the study period extending from April 1, 2020, to January 1, 2021, we included all patients with confirmed COVID-19 who have been supported with VV ECMO for severe ARDS. Intervention: None Measurements and Main Results: Data captured include patient demographic characteristics, comorbidities, ECMO support variables, and ECMO associated complications, inflammatory and coagulation markers, and therapeutic interventions specific for COVID-19. The ECMO nonsurvivors experienced higher rates of bleeding (72.7%), thrombotic events such as digital ischemia (36.3%), and secondary infection (63.6%). Mean lactate dehydrogenase (LDH) levels were markedly elevated in the ECMO non-survivors vs. survivors (1031.00 [IQR 801.50, 1684.50] vs. 609.00 [455.75, 896.00], p = 0.026). Also, platelet dysfunction as reflected by the low Maximum Amplitude (MA) was worse in the non-survivors (65.25 [IQR 60.68, 67.67] vs. 74.80 [73.10, 78.40], p = 0.012). Finally, we found prominent interaction between both coagulation and inflammation in the non-survivors group in comparison to the survivor group. Conclusion: The strong correlation between inflammation and coagulation in the non-survivors supported with VV ECMO could be indicative of dysregulated inflammatory response and associated with worse clinical outcomes. More studies are warranted to confirm our findings.
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Rationale: Venovenous extracorporeal membrane oxygenation (VVECMO) has recently been shown to have acceptable outcomes for refractory COVID-19-related ARDS. Whether the duration of symptoms before the commencement of ECMO impact the outcomes is unknown. Objectives: The study investigated the impact of symptoms duration on VV-ECMO support for COVID-19 acute respiratory failure. Methods: retrospective analysis of VV ECMO patients treated in our institution through the study period from April 2020 through December 2020. Measurement and Main Results: There were 32 COVID-19 patients were supported with VV ECMO for severe acute respiratory distress syndrome (ARDS). The majority of our patients were Hispanic (62.5%), male (68.8%), with a median age of 43.5 (IQR = 27-64). The prevalent co-morbidities are hypertension (62.5%) followed by Diabetes Mellitus (37.5%). Sixteen (50%) patients survived the hospital discharge. The median duration of symptoms before ECMO initiation was 18 days (SD = 5.7) in the ECMO survivors and the non-survivors 12 days (SD = 7) (p = 0.17). Conclusion: Our study suggests that the duration of clinical symptoms has no impact on the patient outcome if they were supported by VV-ECMO. More studies are needed to confirm our findings.
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Objective: There is a high rate of bleeding and thrombosis in coronavirus disease 2019 (COVID-19) patients. This is attributed to the hyperinflammatory state induced by the COVID-19 infection. The aim of our study is to highlight the interaction of both coagulation and inflammation in COVID-19 patients supported by venovenous (VV) Extracorporeal membrane oxygenation (ECMO) for acute respiratory failure Methods: An observational study was done in high volume ECMO center and included patients who received VV-ECMO from the beginning of the pandemic till 10/31/2020. Inflammatory markers collected include peak LDH, peak IL-6, nadir WBC, peak Troponin, peak CRP, peak ESR, peak Ferritin and peak Procalcitonin. Coagulation markers collected include Thromboelastography (TEG), INR, aPTT, Anti-Xa, Platelet count and Fibrinogen. Results: Among coagulation markers, TEG Maximum Amplitude (MA) was significantly different between ECMO survivors and non-survivors, 74.8% for survivors, 65.2% for non-survivors (p-value = 0.012), all other coagulation markers were not statistically different between groups. Correlation between inflammatory markers and coagulation profile showed correlation between Troponin peak and Fibrinogen nadir (r 0.58, p-value 0.001), peak Troponin with INR (r 0.76, p-value < 0.0001), MA and peak ferritin (r -0.72, p-value < 0.0001). All other correlations were not found to be statistically significant. Conclusions: Inflammatory markers seem to correlate with coagulation profile abnormalities in COVID-19 patients, larger studies need to be done to confirm the relationship.