قراءة
عرض

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
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.
ECG
tachycardia is the most common, T wave and ST segment changes, right heart strain as S1T3Q3 pattern, right bundle branch block RBBB.
Arterial blood gas
may be normal or reveals ↓PaO2, normal or low PaCO2. If severe leads to metabolic acidosis.
D.dimer
Of limited value, as it maybe raised in a variety of other conditions, including myocardial infarction, pneumonia and sepsis. However, low levels, particularly in the context of a low clinical risk, have a high negative predictive value and further investigation is usually unnecessary.
Serum troponin I
may be elevated, reflecting right heart strain.
Imaging
A. CT pulmonary angiography CTPA: is the first-line diagnostic test. It has the advantage of visualising the distribution and extent of the emboli or exclude an alternative diagnosis, such as consolidation, pneumothorax or aortic dissection.

B. Ventilation-perfusion scan: In CTPA Contrast may be nephrotoxic or may cause iodine hypersensitivity.In these cases, either V̇ /Q̇ scanning or ventilation/perfusion single photon emission computed tomography (V̇/Q̇ SPECT) may be considered.
.
C. Colour doppler: investigation of choice for DVT of the legs.

7. 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 tamponade, it also determines pulmonary artery pressure in pulmonary hypertension and excludes mitral stenosis.

8. Pulmonary angiography: useful in selected settings or for the delivery of catheter-based therapies.


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. Circulatory shock should be treated with intravenous fluids or plasma expander,
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.
- Alternatively, patients may be treated with a DOAC ( directly acting oral anticoagulant). Rivaroxaban and apixaban may be used immediately from diagnosis without the need for LMWH, while the licences for dabigatran and edoxaban include initial treatment with LMWH for a minimum of 5 days before commencing the DOAC.
Thrombolytic therapy: for severe PE with shock, risk of intracranial bleeding.
Surgical pulmonary embolectomy may be considered in selected patients but carries a high mortality.
8. Caval filters: indicated in:
▪ Recurrent PE despite adequate anticoagulation.
▪ Anticoagulation is contraindicated.
Prognosis
Immediate mortality is greatest in those with echocardiographic
evidence of right ventricular dysfunction or cardiogenic shock.
Once anticoagulation is commenced, however, the risk of
mortality rapidly falls.
The risk of recurrence is highest in the
first 612 months after the initial event, and at 10 years around
one-third of individuals will have suffered a further event.










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رفعت المحاضرة من قبل: Omar The-Czar
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