قراءة
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Venous thromboembolism VTE and Pulmonary embolism PE

د.خلدون العباﮂﭽي- كلية طب نينوى- المرحلة الرابعة

Objectives

Focus your attention on the following:
1. It is a serious medical condition and may prove fatal.
2. Deep vein thrombosis is the main source.
3. Risk factors
4. Ventilation-perfusion mismatch.
5. Grades: mild, moderate, severe.
6. PE can cause acute and chronic pulmonary hypertension.
7. Dyspnea is the main symptom.
8. Colour doppler and CT pulmonary angiography are the mainstay of
diagnosis.
9. Management: Suspect the diagnosis and suspect the diagnosis!, give
heparin urgently before you confirm the diagnosis.
10. Core therapy: O2, heparin, warfarin, thrombolytic therapy.
11. Principles of anticoagulant use, their side effects and indication of
thrombolytic therapy.


Introduction
-VTE: common disease, responsible for 5% of hospital deaths.
- Most common cause of death in pregnancy.
- 75% of PE arises from lower limb deep vein thrombosis DVT.
- Rare types of emboli: amniotic fluid, placenta, air, fat, and septic emboli.
Risk factors
1. Surgery: pelvic, hip.
2. Pregnancy and peurperium.
3. Cardiopulmonary: COPD, heart failure.
4. Lower limb problems: fracture, varicose veins, stroke.
5. Malignancy
6. Drugs: contraceptive pills, chemotherapy.
7. Others: aging, previous VTE, immobility, trauma, thrombotic disorders.
Pathophysiology
1. Ventilation- perfusion mismatch V/Q. If moderate to severe PE→hypoxia and normo or hypocapnea.
2. Acute: mild-moderate PE leads to pulmonary infarction effusion.
Severe→ acute right ventricular (RV) failure.
3. Chronic→ pulmonary hypertension and RV failure.

Clinical features

1. It depends on severity of embolism and co-morbidity.
Small embolus→minor haemodynamic compromise and few symptoms.
Large embolus→major haemodynamic compromise and may prove fatal.
2. Symptoms: anxiety, apprehension, palpitation, breathlessness, chest pain (pleuritic or central), fainting, collapse, haemoptysis.
3. Signs: tachycardia, hypotension, chest crackles, pleural rub, signs of pleural effusion, low grade fever, collapse and cyanosis, right sided heart failure (↑JVP, RV gallop, split S2).


Investigations
1. Chest X-ray: either normal or may show: pulmonary opacities (any size or shape, may be linear or wedge shaped due to pulmonary infarction), pleural effusion, lung oligaemia, enlarged pulmonary artery and elevated hemidiaphragm.
2. ECG: tachycardia is the most common, T wave and ST segment changes, right heart strain as S1T3Q3 pattern, right bundle branch block RBBB.
3. Arterial blood gas: may be normal or reveals ↓PaO2, normal or low PaCO2. If severe leads to metabolic acidosis.
4. D.dimer: fibrinolysis of fibrin in clot liberates D.dimer into blood, assessed by ELISA. If low <500ng/ml it carries a high negative predictive value (nearly excludes VTE), high value is non-specific and may occur in myocardial infarction, pneumonia and sepsis and is of limited value in the diagnosis. Normal value in the context of suggestive features of PE warrants further investigations to exclude it.
5. Imaging
A. Ventilation-perfusion scan: Confirms PE by using radiolabelled xenon and albumin. Normal V/Q scan excludes PE. High probability scan with suggestive clinical picture establishes the diagnosis of PE. Majority (70%) of scans are indeterminate due to COPD and heart failure.
B. Helical CT pulmonary angiography CTPA: widely used, gives a clear picture of PE. By this imaging PE can be excluded and an alternative diagnosis can be given.
C. Colour doppler: investigation of choice for DVT of the legs.
6. Echocardiography: Very helpful in the differential diagnosis of PE. In massive PE it shows acute dilation of right heart and thrombus may be visible. It can exclude LV failure, aortic dissection and pericardial effusion, it also determines pulmonary artery pressure in pulmonary hypertension and excludes mitral stenosis.
7. Pulmonary angiography: using contrast, is the gold standard test for PE diagnosis, but it is invasive and done for severe cases of PE that need intervention and has been largely superseded by CTPA.

Differential diagnosis

Heart failure Pneumonia Pneumothorax Myocardial infarction
Pericarditis and pericardial effusion Aortic dissection

Management

1. Suspicion of diagnosis and confirmation of diagnosis may be life saving.
2. O2 for dyspnea and hypoxia aiming at O2 saturation of >90%.
3. Opiates for pain, but used with great caution in hypotensive patients.
4. Avoid diuretics and vasodilators.
5. External cardiac massage CPR may be successful in moribund patients by breaking up large central embolus.
6. Anticoagulation: should be given immediately in patients with high or intermediate probability.
- Low molecular weight heparin SC: as effective as i.v unfractionated heparin, dose according to body weight, no need for coagulation blood tests. Heparin reduces mortality by reducing the propagation of clot and the risk of further pulmonary embolism, given for at least 5 days.
- Warfarin: for continuation of anticoagulation after heparin, heparin should not be stopped until INR >2.
- Duration of warfarin:
▪ for life for those with prothrombotic risk or history of previous emboli.
▪ 3 month therapy for those with reversible risk factors.
▪ 6 months for idiopathic DVT.
7. Thrombolytic therapy: for severe PE with shock, risk of intracranial bleeding.
8. Caval filters: indicated in:
▪ Recurrent PE despite adequate anticoagulation.
▪ Anticoagulation is contraindicated.
Prognosis
1. Recurrent rate is low in PE embolism after operation or those with reversible risk factors.
2. Right ventricular dysfunction in echo is a risk for cardiogenic shock.
3. Persistence of pulmonary hypertension and right ventricular dysfunction 6 weeks after PE is a risk for developing RV failure over the next 5 years.










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رفعت المحاضرة من قبل: Ehab ALbyate
المشاهدات: لقد قام 10 أعضاء و 135 زائراً بقراءة هذه المحاضرة








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