Pulmonary Embolism.

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Presentation transcript:

Pulmonary Embolism

DVT – Epidemiology and Etiology Annual incidence of venous thromboembolism (VTE) is 1/1000 DVT accounts for over one half of VTE Carefully evaluated, up to 80% of patients with VTE have one or more risk factors Majority of lower extremity DVT arise from calf veins but ~20% begin in proximal veins About 20% of calf-limited DVTs will propagate proximally

DVT – VTE Risk Factors Malignancy Surgery Trauma Pregnancy Oral contraceptives or hormonal therapy Immobilization Inherited thrombophillia Presence of venous catheter Congestive failure Antiphospholipid antibody syndrome Hyperviscosity Nephrotic syndrome Inflammatory bowel disease

An Introduction to Pulmonary embolus Pulmonary embolism is a life-threatening condition that occurs when a clot of blood or other material blocks an artery in the lungs.  This is an extremely common and highly lethal condition that is a leading cause of death in all age groups. One of the most prevalent disease processes responsible for in-patient mortality (30%) Overlooked diagnosis.

Pulmonary Blood Flow Pulmonary embolism is a life-threatening condition that occurs when a clot of blood or other material blocks an artery of the lungs

Pulmonary Embolism back ground Prompt diagnosis and treatment can dramatically reduce the mortality and morbidity rate. Majority of the cases are unrecognised clinically. One third of the patients who survive an initial PE die of a future embolic episode. Many patients who die of PE have not had any diagnostic workup nor have they received any prophylaxis for the disease. In most cases the CLINICIANS have not even considered the diagnosis of PE.

Pathophysiology of pulmonary embolism It is often a fatal complication of underlying venous thrombosis. Normally microthrombi (RBC,Platelets and Fibrin) are formed and lysed with in the venous circulatory system. Under pathological condition these microthrombi may escape and propagate and will block the pulmonary blood vessels causing PE

Predisposing factors Patients on prolonged bed rest for > a week. Prolonged immobilization. Patients in ICU, CCU. After bypass surgery or any surgery. All trimesters of pregnancy and puerperium. Older patients – Age no bar still.

Predisposing factors 5-MI. 6-Obesity. 7-Old age. 8-Malignancy. 1-CCF. 2-Fractures. 3-Oral Contraceptives. 4-Drug abuse. 5-MI. 6-Obesity. 7-Old age. 8-Malignancy. 9-Catheters

Patient presentation Haemoptysis, Dyspnoea and Chest pain – (Virchows Triad) Back pain, Abdominal pain, wheezing, SOB, Seizures, Productive cough, Hiccoughs, Fever…… Can be asymptomatic.

Diagnostic Modalities in PE ECG*** D Dimer assay test Plain film radiography Radionuclide imaging (VQ Scan) CT Angiography Pulmonary angiography Echocardiography Ultrasound(DVT)*** MRI & MRA

D-Dimer Assays Gainfully employed to select patients for further radiological imaging. It is a cross linked fibrin degradation product and a plasma marker of fibrin lysis. Serum level less than 500ng/L excludes PE with 90-95% accuracy. Unfortunately a positive test is non specific (specificity only 25 – 67% and occurs in about 40 – 69% of the patients

Plain film radiography Chest X-ray Initial CxR always NORMAL

Plain film radiography Chest X-ray Initial CxR always NORMAL. May show – Collapse, consolidation, small pleural effusion, elevated diaphragm. Pleural based opacities with convex medial margins are also known as a Hampton's Hump

Plain film radiography Chest X-ray Initial CxR always NORMAL. May show – Collapse, consolidation, small pleural effusion, elevated diaphragm. Westermark sign – Dilatation of pulmonary vessels proximal to embolism along with collapse of distal vessels, often with

Embolism without Infarction Most PEs (90%) Frequently normal chest x-ray Pleural effusion Westermark’s sign “Knuckle” sign abrupt tapering of an occluded vessel distally Elevated hemidiaphragm

Embolism with Infarction Consolidation Cavitation Pleural effusion (bloody in 65%) No air bronchograms “Melting” sign of healing Heals with linear scar

Ventilation-perfusion scanning V/Q Scanning Single most important diagnostic modality for detecting PE. Always indicated when PE is suspected and there is no other diagnosis. 1 in every 25 pts sent home after a normal V/Q scan actually has a PE that has been MISSED

Ventilation-perfusion scanning V/Q Scanning

Ventilation-perfusion scanning V/Q Scanning Radiological procedure which is often used to confirm or exclude the diagnosis of pulmonary embolism. It may also be used to monitor treatment. The ventilation part of the scan is the inhalation of Krypton 81m, which has a short half life and is a pure gamma emitter. Ventilation is assessed under a gamma camera.

Ventilation-perfusion scanning V/Q Scanning The perfusion part of the scan is achieved by injecting the patient with technetium 99m, which is coupled with macro aggregated albumin (MAA). This molecule has a diameter of 30 to 50 micrometres, and thus sticks in the pulmonary capillaries. An embolus shows up as a cold area when the patient is placed under a gamma camera. The MAA has a half life of about 10 hours

Spiral CT HRCT (spiral) CT with CT angiography is a promising technique. CT unlikely to miss any lesion. CT has better sensitivity, specificity and can be used directly to screen for PE. CT can be used to follow up “non diagnostic V/Q scans.

Pulmonary Angiogram Positive angiogram provides 100% certainty that an obstruction exists in the pulmonary artery. Negative angiogram provides > 90% certainty in the exclusion of PE. Catherterisation of the Subclavian vein – Superior vena cava – right atrium – right ventricle – main pulmonary artery

Pulmonary Angiogram

Pulmonary Angiogram Westermark sign – Dilatation of pulmonary vessels proximal to embolism along with collapse of distal vessels, often with a sharp cut off.

Treatment of pulmonary embolism Emergency treatment and hospitalization are necessary. In cases of severe, life-threatening pulmonary embolism, definitive treatment consists of dissolving the clot with thrombolytic therapy. Anticoagulant therapy prevents the formation of more clots and allows the body to re-absorb the existing clots faster.

Treatment of pulmonary embolism Thrombolytic therapy (clot-dissolving medication) includes streptokinase, urokinase, or t-PA. Anticoagulation therapy (clot-preventing medication) consists of heparin by intravenous infusion initially, then oral warfarin (Coumadin). Subcutaneous low-molecular weight heparin is often substituted for intravenous heparin in many circumstances

Treatment of pulmonary embolism In patients who cannot tolerate anticoagulation therapy, an inferior vena cava filter (IVC filter) may be placed. This device, placed in the main central vein in the abdomen, is designed to block large clots from traveling into the pulmonary vessels.

PE – Assigning Pretest Probability