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Pulmonary Embolism (Diagnostic tests (cardiac troponin (limited role in…
Pulmonary Embolism
Diagnostic tests
- Anamnesis, physical examination, gas analysis
- ECG
sinus tachycardia
supraventricular arrhytmias (atrial fiblillation, atrial flutter)
RV overload:
incomplete / complete RBBB, QR pattern in V1
negative T-wave in V1-V4, S-wave>0.15mV in I and aVL
- Chest X-ray:
Heart enlargement, Pleuritis, Elevated diaphragm, Atelectasis, Pulmonary oedema, Diminished vascular outline (Westermark sign), Pulmonary infarction (Hampton hump), pleural effusion
, prominent central pulmonary artery
In 30% of cases chest X-ray is normal
- D-dimer testing:
+Elevated plasma D-dimer levels:
venous thromboembolism (DVT, PE)
inflammation, infection, sepsis
after trauma, operation, cancer
acute coronary syndrome, DIC
pregnancy, increase with with age
+D-dimer level increases with age
< 50 years of age: upper level < 500 μg/l
≥ 50 years of age: upper level < age x 10 μg/l
+if this is undetectable, it excludes a diagnosis of pulmonary embolism.
+most sensitive test for thromboembolic disease.
- Compression venous USG:
sensitivity 90%, specificity 95% for proximal DVT
Reveals DVT in 30-50% of PE patients
Proximal DVT in a patient with suspected PE is enough to apply anticoagulation without further examinations
- Perfusion Scintigraphy
Scintygraphy result could be :
normal (excludes PE)
high probability of PE
non-diagnostic (30-50%)
Scintigraphy is an examination of high sensitivity and low specificty
- Computed tomographic pulmonary angiography (CT): „gold standard”
Enables visualization of the pulmonary arteries down to at least segmental level (or sub-segmental when multi-detector CT)
PE confirmation – when PE within at least segmental arteries (or larger arteries)
- Pulmonary angiography:
Previously the „gold standard” of diagnosis, nowadays totally replaced by CT
Always should be preceeded by echocardiography (to exclude right heart thrombi)
Indispensable when surgical embolectomy is planned
- Echocardiography:
right ventricular dysfunction
RV enlargement
RV diameter / LV diameter > 0.9-1.0
↑ maximal velocity of tricuspid insufficiency
inter ventricular septal bulging into the LV
dilated proximal pulmonary arteries
cardiac troponin
- limited role in decision making
- released due to right ventricular muscle damage in acute right heart strain in massive (>70% of one lung is involved) PE
-
TREATMENT
- Give oxygen and start heparin immediately before the diagnosis is confirmed and
while the diagnostic workup is being completed.
- Anticoagulation
• unfractionated heparin (UFH)
• low molecular weight heparin (LMWH)
• fondaparynux
• rivaroxaban (Xarelto), apixaban (Eliquis), dabigatran (Pradaxa)
• warfarin, acenocoumarol
- Thrombolysis (streptokinase, urokinase, rt-PA)
- Embolectomy
• surgical
• percutanous (catheter directed)
- Venous filters
in patients with absolute anticoagulant contraindications
in patient with recurrent VTE despite adequate anticoagulant treatment
indicated after surgical embolectomy
- When PE is probable, but without shock or hypotension
Direct anticoagulation:
First 5-10 days: use LWMH, UFH or fondaparynux
Within the first 5-10 days add VKA: warfarin or acenocoumarol
Stop LWMH, UFH or fondaparynux treatment when INR > 2.0 in 2 consecutive days
Anticoagulation – for at least 3 months (often longer)
- High-risk:
thrombolysis (urokinase, streptokinase, alteptase)
embolectomy (contraindications to thrombolytic)
anticoagulant (unfractionated heparin (UFH), LMWH, Fondaparinux – selective factor Xa inhibitor)
Pathophysiology
- ↑ RV afterload --> RV dilation --> TV insufficiency --> ↑ RV wall tension --> neurohormonal activation --> Myocardial inflammation --> ↑ RV O2 demand --> RV ischemia --> ↓ RV contractility --> ↓ RV output --> ↓ LV pre-load --> ↓ CO --> ↓ systemic BP --> RV coronary perfusion --> ↓ RV O2 delivery --> cariogenic shock ---> Death
- more than 50% of the pulmonary circulation is obstructed, the clinical signs become dominated
TREATEMENT of VTE
- newer oral anticoagulants (NOAC) are preferred to VKA (warfarin) in acute and chronic treatment of PE and DVT (similar efficacy to VKA, but significantly less risk of bleeding)
Rivaroxaban (Xarelto)
Apixaban (Eliquis)
Dabigatran (Pradaxa)
-
-
VTE predisposing factors
- Patient-related (constant): old age, previous VTE, cancer, Thrombophilia, neurological disease with peripheral paralysis, oral contraceptives
- Situation-related (transient): surgery, trauma, pregnancy, APL Ab syndrome
- inherited: Factor V leiden, Prothrombin gene mutation, Low protein C, protein S, antithrombin III
- 30-50% of patients have no risk factors (idiopathic PE or DVT)
Virchow triad
- alterations in blood flow,
immobilization (after surgery), injury, pregnancy (also procoagulant), obesity (also procoagulant), Cancer (also procoagulant)
- factors in the vessel wall
surgery (knee replacement carries a 70% risk), catheterizations causing direct injury
- factors affecting the properties of the blood
estrogen-containinghormonal contraception
genetic thrombophilia
acquired thrombophilia
cancer (due to secretion of pro-coagulants)
criteria to diagnose PE
-
In US
Wells’ Criteria
• Symptoms of DVT (3 points)
• No alternative illness that explains symptoms (3 points)
• Immobilization (≥3 days) or surgery in the previous 4 weeks (1.5 points)
• Prior history of DVT or PE (1.5 points)
• Presence of hemoptysis (1 point)
• Presence of malignancy (1 point)
• Score <2 = low probability of PE
• Score ≥2 but <6 = mean moderate probability of PE
• Score >6 = high probability of PE
Symptoms
Dyspnoea > Chest pain ( commonly Pleuritic) > Symptomatic DVT (leg swelling, pain) > Cough > Hemoptysis, Syncope , Unilateral leg pain, Fever (> 38.5), jugular venous pressure (JVP) is raised
- closure or narrowing of the pulmonary artery or its branches by embolic material - usually a thrombus
- Sporadically:
amniotic fluid, fat tissue after long bone fracture, tumour mass
- clinical manifestations of venous thromboembolism (VTE):
pulmonary embolism (PE) and deep vein thrombosis (DVT)
Proximal (from popliteal fossa and above) deep vein thrombosis is a common source of embolic material or rarely in the right heart (<10% of cases)
- Epidemiology:
30-day mortality – 6% DVT; 12% – PE
If anticoagulant therapy is stopped in patients with VTE, the risk of recurrence is about 10% at 1 year and 30% at 5 years
Chronic thromboembolic pulmonary hypertension (CTEPH) occurs in 2-4% of patients with PE (complication)
50% of patients with proximal DVT have PE (asymptomatic)
70% of patients with PE have DVT of the lower extremities
