 Hello everyone, today's my paper presentation topic is thromboembolic events as a complication of COVID-19. I, Dr. Dheeraj Ganeshgiri, junior resident, present this topic under the guidance of Dr. Yogendra Sathdev sir, professor and HOD department of radio diagnosis, Pravara Rural Hospital Lone, aim to evaluate the thromboembolic events as a complication of COVID-19. Coronavirus disease 2019 is a viral illness caused by a novel coronavirus, severe acute respiratory syndrome coronavirus 2 SARS-CoV-2. It has been rapidly spreading throughout the world, causing a pandemic involving more than 188 countries, more than 24 million cases and 8,40,000 deaths, SARS-CoV-2 enters through the angiotensin-converting enzyme 2 ACE2 receptors, which are present in type 2 alveolar cells of the lungs, myocardium and proximal nanotubules. COVID-19 manifestation can range from asymptomatic infection to organ failure to death. The respiratory system is involved in almost all cases in both proven COVID-19 and COVID like illness, fever, curve, dyspnea, chest pain and oxygen desaturation upon exertion are observed and these symptoms have been associated with increased D-dimer levels and pulmonary micro angiopathy on necropsy. The kidneys can be involved with a similar pathophysiology presenting with a hematuria and rapidly progressive renal failure with oliguria and death. There are various and diverse complications associated with SARS-CoV-19 infection. Current data doesn't provide adequate information about the use of anticoagulants and management of thrombolic events. Many authors suggest that a patient with high risk for development of thrombolic state should be started with empirical anticoagulant treatment whereas some authors say that the use of full dose anticoagulant should be done only in cases of confirmed thrombolism. Inclusion criteria, patient giving consent for study. Patients refer to radiology department with symptoms of fever, curve, malaise and breathlessness. Exclusion criteria, patient not giving consent for study. Materials and methods. Five patients were studied for the assessment of patients were done by using a Siemens Sam somatom perspective 64 rise 128 slice machine, pathogenesis and risk factors. COVID-19 shows rising pro and anti-inflammatory cytokines. There is evidence of complement activation in COVID-19 by direct endothelial infection which includes release of anaphylatoxine C5A. Experiment activation as seen in COVID-19 not only drives neutrophil dysfunction leading to susceptibility to secondary infection but also activates the coagulation system thereby propagating a pro thrombotic state. Coagulability associated with COVID-19 may be explained by the two-way activation theory as seen by thrombocytopenia in critically ill patients and the encompassing inflammatory and micro thrombogenic responses that occur when endothelial insert takes place. While the inflammatory pathway release cytokines, the activation of micro thrombotic pathway is mediated by release of a large polymers of 1-villain bird factor. In the phase of sepsis induced endothelial injury, this reaction is aggravated causing enhanced platelet activation and consumption thrombocytopenia. In contrast to the typical consumptive coagulophathy and disseminated intravascular coagulation profile observed in a sepsis patient with COVID-19 typically have relatively normal coagulation and platelet profiles. Progression to a DIC in a minority of patients rarely developing in a survivor's. Therefore, it seems that in keeping with virtuous triad, thrombosis is driven both by the activation of coagulation factors and endothelium. In situ, immune thrombosis plays a key role to be unifying mechanism explaining the micro and micro thrombotic manifestation of the disease. It should, however, be emphasized that in situ, micro thrombosis has also been demonstrated in pulmonary and systemic tissue beds in ARDS and sepsis and therefore may not necessarily be unique to the population. In addition to the factors mentioned above, these patients have additional risk factor for increased thrombosis most notable among those being hypoxia, immobility made worse by frequent use of prone positioning, although not systematically assess reduced staffing coupled with isolation precautions which limit frequent position changes and mobility may further predispose patient to a pro-thrombotic state. Now Case 1. This is a case of a 32-year female patient who was referred from outside to our hospital for a CT scan of abdomen and pelvis, plane and contrast with acute pain in abdomen to rule out the intestinal perforation. The patient did not have a fever, curve, cold, malaise and orbitlessness since the beginning. The patient did not pass tools since four days. HRCT was done for the same patient as a few ground glass opacities were noted in the visualized lung section during the abdomen scan. These are the ground glass opacities on HRCT findings where multiple sublural and intrapulmonary ground glass opacities with interstitial septal thickening involving bilateral lung feeds. It was a typical for a COVID-19 Quarads 5 score, Quarads 5 and CTs where it is score was 12 by 25. Now, same patient CTs abdomen and pelvis, plane and contrast, waist shape, non-enhancing hypodensities are noted in upper pole and interpolar region of spleen. A hypodense feeling defect is noted in a splenic artery which suggests thrombosis with splenic infarct. In this scan image shows the splenic infarct and the renal infarct which is hypodense. In this image, we can see a Jejunal wall thickening with intramural air foci, with intramural air foci, with poor wall enhancement on post-contrast study. Treatment for this patient, the patient was referred to different hospital after the scan where the patient was given antithrombotics. Now case 2, this is a case of 57 year female patient who came for MRI brain with complaints of right sided weakness since morning, she was a known case of COVID-19 15 days ago. Investigation done in the hospital is MRI brain reveal a multiple impact in left frontal parietal temporal region. It is an axial section on diffusion, the infarct is seen in left frontal parietal temporal region. It gives a diffusion restriction. Now case 3, a case of 30 year female patient who came for CT abdomen and pelvis plane and contrast with complaints of pain in right flank and iliac process since 15 to 20 days. Then HRCT thorax of the same patient was done as she also had a complaint of fever and cough since 15 days. Other investigation also done, blood investigation WBC count is 14,460 increase, CRP is 70, increase urine analysis, urine appearance is clear, deposits are absent, RBC is 2 to 3 deciliter and WBC is 3 to 4,000. Then the same patient CT abdomen and pelvis plane and contrast images. The CT scan reveal a hypodense non-enhancing area involving the cortex and the medulla of upper and mid polar region of the left kidney. HRCT thorax reveal a multiple sublural and intra pulmonary, multiple sublural and intra pulmonary ground glass opacities in bilateral lung fields with the CT scan where it is core is 5. Now case 4, this is a case of 81 year old female patient with the history of COVID-19 10 days back the patient came with complaint of left sided weakness and disorientation. There was no known comorbidity documented. The patient came for MRI brain, here the diffusion and ADC images of the brain suggesting that the right side secondary to thromboembolic effect of COVID-19 infection, this is the in fact seen in the right side. Now case 5, this is a case of 42 year male patient with the history of COVID-19 infection. The patient came with a complaint of right sided weakness since one day no known comorbidity is where documented. The patient came for MRI brain to rule out in fact, here are the diffusion and ADC images of the patient representing the left sided in fact. The patient was started with thrombolatics immediately after the MRI. This is the axial image diffusion wetted image. This is low ADC values seen in fact. Now the protocol for the treatment of thromboembolic event in a COVID-19 patient, patient with a COVID-19, obtain baseline prothrombine time D dimer fibronogen platelet count. Low assess the bleeding risk if low or acceptable then encourage mobilization and initiate the thrombosis profile access with a UFH or LMWHH. Consider a higher dosing for the patient at higher risk who base malignancy immobility surgery or spontaneous eco. Then active routine screening for a venous or arterial thrombosis cutaneous pulmonary deep venous stroke line thrombosis acute coronary syndrome then clinical radiological surveillance titled D dimer. Then consider the therapeutic anticoagulation with either UFH or LMWHH titled to APTT then reassess the bleeding risk routinely then transition to a vitamin K antagonist or UFH or direct oral anticoagulant on discharge. Now second side. Obtain baseline prothrombine time D dimer fibrogen or platelet count. Assess bleeding risk then we assess the bleeding risk if it is high then encourage mobilization plus sequential compression device when not abulating then hold thrombo profile axis. After that active routine screening for venous arterial thrombosis then clinical radiological surveillance then screen positive on very high clinical suspicion of acute microthrombosis then consider the therapeutic anticoagulation then transition to a vitamin K antagonist UFH direct oral anticoagulant on discharge. Then management of anticoagulation the optimal approach to the management of anticoagulation when these patients remains unclear remains unclear in absence of well conducted trial. There remains a major uncertainty in the optimal management of immune thrombosis as commonly seen in a COVID-19. In asymptomatic and mildly symptomatic patients who do not require hospital admission ambulation should continue to be a mainstream of thromboprofile axis. It is advisable to institute at minimum prophylactic anticoagulation in admitted patient without clinical contraindication. Unfractionated heparin and low molecular weight heparin have been successfully used in these patients both prophylactically and threpartically. Higher doses should be considered for those with higher risk patient that is obese, active, malignancy, prolonged morbidity or recent surgery. As a caveat it must be noted a high incidence of VTE has been noted even on a patient on either a prophylactic and a therapeutic anticoagulant which makes routine surveillance extremely important. Then in addition to the usual indication such as obesity or active malignancy where higher intensity dosing of prophylactic anticoagulation may be warranted patients with COVID-19 who demonstrate ACC on surveillance imaging may be considered for augmented dosing although high quality data to support routine use of this strategy is currently unavailable. Although some retrospective studies have demonstrated systemic anticoagulation to be associated with improved outcomes in a hospitalized patient it is advisable to institute at minimum profile active anticoagulation is in admitted patient without clinical contraindication. Now on conclusion systemic thrombosis is frequently associated with critically ill COVID-19 patients and may lead to a fatal outcomes if not diagnosed and managed appropriately. Thrombotic risk commonly persists despite initiation of anticoagulation until more information is available providers should consider prophylactic versus therapeutic anticoagulation based on a combination of patient specific criteria including laboratory result, imaging, clinical suspicion and a care for balance of thrombotic and bleeding risk. Routine active surveillance guided by a clinical and a radiological assessment is recommended to either pre-empt or aid from diagnosis of macrothrombotic events which may be beneficial in guiding anticoagulation strategies larger well-designed prospective studies are urgently needed to further illustrate optimal management strategies to mitigate the thrombotic risk associated with COVID-19. Now these are the reference. Thank you everyone.