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Hello and welcome everyone to this talk on Pulmonary embolisms, also known as P ES. This talk is inspired by the M and A content map and is being presented by the Sheffield Radiology Society in association with Ir Juniors. Pulmonary embolism is defined as the partial or complete occlusion of the pulmonary artery and or one of its branches. The most common cause of occlusion is a thrombus. Um and other non thrombotic causes include gas tumors, fluid and fat. However, the term pe is commonly used synonymously with occlusion secondary to an embolus of a blood clot. It is considered a venous thromboembolic disease. Occlusion of one or more of the pulmonary arteries leads to the absence of perfusion in that area of the lung. This causes a ventilation perfusion, mismatch or a VQ mismatch. This VQ mismatch may lead to hypoxia and clinical features of breathlessness. The area of the lung may undergo infarction but is usually prevented by the bronchial circulation. The VQ mismatch can lead to elevated pulmonary artery pressure, artola collapse, worsening hypoxemia and also a reduction in cardiac output. Risk factors for developing a pe include modifiable causes such as obesity, hormone replacement therapy with estrogen immobility and also long distance sedentary travel, but also non modifiable risk factors such as recent surgery, pregnancy, malignancy, polycythemia, systemic lupus, erythematosus and thrombo failure. Presentation of A pe can vary. Patients may be asymptomatic or only have one symptoms and some patients may have quite a few symptoms. Patients to look out for include new onset dyspnea, which may be present in up to 50% of patients with a pe pruritic chest pain, which means pain on chest pain on inhalation, um which may be present in up to 39% of patients with a pe patients may also present with a cough and this cough may also um be productive of blood um which is hemoptysis. Patients may also have syncope or presyncope and leg pain and swelling. Um may suggest that the origin of the thrombus could be a DVT in terms of clinical signs when it comes to pe the refute to look out for tachypnea, which is an elevated respiratory rate may be present in between 21 to 39% of patients with a pe patients may also have a tachycardia. They may have a low grade fever. They may be hypoxic, their BP might be low and they may have an elevated jugular venous pressure. This diagram shows the investigation pathway for hemodynamically stable patients which are suspected to have a pe. The most common diagnostic test of choice for pe is CT pulmonary angiograms baseline bloods include full blood count, U and ES to assess renal function. LFT S coagulation studies. And these are done before starting any anticoagulants. Other investigations which are done are chest x rays and EC GS. These are mainly to rule out um differential diagnosis, diagnoses with similar presentations and also to monitor for any complications from pe such as right ventricular failure, which an echo may be done if um there's clinical suspicion of that. Two main alternative diagnostic tests for pe are pulmonary angiography, which is the gold standard and VQ scans, which are equally diagnostic as C TPA, pulmonary pulmonary angiography. Although the gold standard is invasive and not as widely available. VQ scans are more preferable for those who. The contrast which is used in C TPA is contraindicated such as patients with severe renal failure. Um but it cannot be used to make an alternative diagnosis. If pe is excluded by the VQ scan for pregnant patients, that may also have a DVT with pe symptoms doing lower limb compression, venous ultrasound scans can show DVT if shown, then treatment can be started without doing a C TPA. Straight away. The main risk scores used for different patients are the pe rule out criteria, which means the patient needs to not meet any criteria to be excluded from having a pe the two level well score um where patients are classified into likely and unlikely pe and this determines whether they need immediate C TPA or D dimer first, as shown in the diagram, if patients have to wait for a C TPA or the DA results won't be back in four hours. An interim dose of anticoagulant is started um which is usually one that can be continued once um the pe is confirmed. Another risk score is the year's criteria which is used using D dimer levels. It's used for pregnant patients and it either rules out pe or indicates the need for further imaging. Likely C TPA chest x rays are done largely to help rule out differential conditions like pneumothorax, which can have similar presentation to pe. There can be no significant findings or nonspecific changes within findings. Pleural effusion is one of the more common ones in pe cases and this will most likely be exudate and not directly related to infarction. Nonspecific changes show atelectasis, consolidation and pleural effusion all due to a pulmonary infarction. The three images of the bone of the slide shows three signs that may appear in a patient with pe. Here we have a short section of an axial ct pa with contrast in the arterial phase, meaning the contrast is are pacifying the pulmonary arteries. And ideally the aorta should be darker. In the example, you can see multiple filling defects that is across the bifurcation of the pulmonary trunk in both left and right pulmonary arteries and further segments as well. In this case, this was a patient POSTOP which is a risk factor for pe do not that there are non thrombotic calls for pe and there needs to be correlation with other investigations mentioned to differentiate between the two. The main management for P ES are anticoagulants, direct oral anticoagulants also known as Dox and now increasingly used as opposed to low molecular weight heparin as low molecular weight heparin will typically be switched to either warfarin which requires I NR monitoring or dabigatran or dox band, which requires at least five days of lead in therapy with parenteral anticoagulants for ongoing management. After acute treatment, starting with Apixaban in the initial phase means that the patient can just continue and may be safer in terms of major bleed. Further management for stable patients can be guided by the pe severity index score or the pe E score. Low risk patients can be considered for early discharge and treated as outpatients high to intermediate risk patients are those with the two listed here being present and raised. These patients need close monitoring and if they deteriorate will be considered for reperfusion, intermediate to low risk patients are those with only one fulfilled or neither and they will be admitted for obs observation. Right. Ventricular dysfunction can be assessed using the C CPA or an echo if available from diagnostics for management of hemodynamically unstable patients. An A to B assessment is performed and critical care and senior support must be involved. A C TPA should be used to confirm the pe um which will lead to the patient being treated by A C TPA is unavailable or the patient is too well to tolerate C TPA. An echo should be done to check the signs of right ventricular dysfunction. And if these signs are present, the p the patient will be treated for a pe. So treatment to not be delayed, um early anticoagulants if there are no contraindications. So this may be IV unfractionated heparin and this has started before diagnosis and is continued after thrombolysis but stops within 24 hours. Urgent primary reperfusion. If there is no contraindications include thrombolysis, um which may be done with alpl streptokinase or urokinase. First line is systemic thrombolysis which is done into the peripheral veins. And there are other alternatives to consider if um thrombolysis is not tolerated, supportive treatment includes fluids. If the systolic BP is below 90 you also monitor for signs of heart failure and if the systolic BP is still below 90 with fluids and thrombolysis, you may consider vasopressors. Um adrenaline and oxygen support may be used if needed in terms of ongoing management and prevention. All patients should continue the anticoagulants for at least three months in patients with no known risk factors for pe it's referred to as an unprovoked pe and typically would at least continue anticoagulants an extra three months totaling six months in total. Some patients may take them longer or may have them life long, um the regime is personalized and based on VT E and bleed risk, all patients should be followed up in a pe clinic and in patients with recurring P ES, the dosage and type of anticoagulant can be changed if already optimized IVC filters may be considered if recurrence is DVT related. And now we have a case presentation. So you are an F one working in the A&E department and a 65 year old female patient presents with dyspnea for three days, an unproductive cough and new onset chest pain on her right side. So some differentials you might think of. Um if you think using the surgical sieve vascular, maybe angina M I pe pericarditis infection could be pneumonia, trauma, potentially thinking about pneu pneumothorax and rib fractures and neoplastic as well, maybe thinking of lung cancer. So you clock the patient in Ed and you on her observations only her heart rate is a bit elevated at 100 and eight BPM history wise. Um, she has a past medical history of osteoarthritis hypertension and type two diabetes. She's currently taking Metformin, Simvastatin and amLODIPine. She hasn't had any previous DVTs or P ES and she recently returned from holiday in Morocco last week on examination. The patient looks short of breath but is well perfused and has a strong pulse on auscultation. Her chest sounds clear as well and there are no signs of DVT. You decide to order an E CG and a chest X ray. And the E CG shows a sinus rhythm with a rate of 100 and 10 BPM with no ST or T changes on chest X ray, the film is unremarkable compared to a previous chest X ray done two years ago, which was also normal. Her bloods have also come back normal. So going through the pathway, the patient is hemodynamically stable. So we're using this pathway for hemodynamically stable patients. There's a high clinical suspicion of a pe. Um so we do the well score and on her well score, there are no signs or symptoms of DVT. Um but she does score for pe being the highest differ differential and her heart rate being over 100. So she scores 4.5 which is over four. So she's given Apixaban as she awaits um C TPA. And once the CT P confirms the diagnosis of pe um she's continued on the Apixaban and due to her Pezzi score being low risk, um the patient is discharged kept on Apixaban for three months and reviewed in the pe clinic. Hi, all this is Ir Juniors with some further ir content for you. Nice guidelines suggest considering an IR procedure called an IVC filter in patients with DVT or PE for whom anticoagulation is contraindicated or patients who have a pe whilst already on anticoagulants after steps for assessing treatment failure have been taken, it is an endovascular device placed in the infrarenal inferior vena cava initial vascular access is achieved using ultrasound. And from there, the procedure is fluoroscopically guided contrast is injected into the IVC intraprocedurally to assess the size and anatomy of the IVC location of the renal veins and to check the position of the filter. After deployment, the filter traps emboli to prevent them from traveling to pulmonary arteries. However, the filter should be removed at the earliest possible safe opportunity to reduce risk of complications. This slide shows images from a real life case of an IVC filter being deployed, percutaneous thrombectomy for pe percutaneous thrombectomy is not currently part of the mainstream guidelines for P it is currently rarely performed and only in patients with high risk pe who are unsuitable for regular treatment or regular treatment options have failed. It involves the endovascular insertion of a catheter into the pulmonary arteries and removing the emboli through methods such as vacuum, suction, syringe, aspiration, mechanical removal devices or a combination of methods. The procedure could potentially have a lower risk of bleeding compared to thrombolysis in some patients. So just a quick summary on the presentation. Today, we covered the MLA presentations, mainly the symptoms that people may get when they present with a pe. We touched on the pathophysiology of pulmonary embolism. We discussed risk factors for developing a pe, we discussed the investigations that you would do when um pulmonary embolism is suspected. We touched on the risk scores. Um The well score, the perk score, um the Pezzi score as well. And we also discuss management of pe and how management varies, depending on whether the patient um is stable, unstable and where when things are contraindicated as well.