33. Deep venous thrombosis and pulmonary embolism. Diagnostics and treatment

Page created on October 18, 2021. Last updated on October 19, 2021 at 12:29

Venous thromboembolism

Definition and epidemiology

Venous thromboembolism (VTE) refers to deep vein thrombosis (DVT) and/or pulmonary embolism (PE).

DVT are venous thromboses which occur in deep veins, most commonly in the legs or groin. Its main importance is the risk of the deep venous thrombosis dislodging and traveling to the lungs, causing pulmonary embolism. DVT mostly affects the distal deep veins, but may affect the larger, proximal veins as well, including the iliac, femoral, or popliteal veins. PE is a serious complication which can lead to death in 30 – 60% of cases, and is more common in case of proximal DVT.

PE is classified into three different types, nonmassive, submassive, and massive PE. Massive pulmonary embolism refers to PE which causes obstructive shock and haemodynamic instability, usually because of a saddle-thrombus (thrombus at the pulmonary trunk bifurcation). Submassive PE causes RV dysfunction but not haemodynamical instability. Nonmassive PE causes neither.

VTE is a major source of mortality and morbidity, and its incidence is increasing. In the US alone it causes > 200 000 deaths annually, more than HIV, motor vehicle accidents, and breast cancer combined. VTE is preventable, and a major cause of preventable death. Many patients with VTE develop recurrent VTE later.

Etiology

VTE occurs due to Virchow’s triad, three categories of factors which contribute to thrombosis:

  • Stasis (alteration in normal blood flow)
  • Hypercoagulability (alteration in the constitution of blood predisposing to thrombosis)
  • Endothelial injury

There are many risk factors for VTE, which we can categorise according to Virchow’s triad:

  • Stasis
    • Old age
    • Recent immobility (especially after surgery or trauma)
    • Heart failure
    • Paralysis
    • Obesity
    • Varicose veins
  • Hypercoagulability
    • Cancer
    • Smoking
    • High oestrogen state
    • Pregnancy
    • Thrombophilia
    • Sepsis
  • Endothelial damage
    • Surgery
    • Previous VTE
    • Trauma

Deep vein thrombosis

Clinical features

DVT presents as a unilaterally swollen leg which is warm and erythematous. The leg may be tender or painful. Homans sign refers to calf pain on dorsiflexion of the foot, which may be positive. In distal DVT, symptoms are confined to the calf. Proximal DVT may cause symptoms of the whole leg. limb ischaemia.

Upper extremity DVT is rare and usually due to central catheters or cancer.

Diagnosis and evaluation

When DVT is suspected, we calculate the pre-test probability of DVT to determine how to proceed. The pre-test probability of DVT can be calculated with the Wells score:

Item Points
Active or recent cancer + 1
Paralysis or recent cast + 1
Recent bed rest or surgery + 1
Pain on palpation of deep veins + 1
Swelling of entire leg + 1
Diameter difference compared to other calf of > 3 cm + 1
Pitting oedema on affected side only + 1
Dilated superficial veins on affected side + 1
Alternative diagnosis at least as probably as DVT (cellulitis, Baker cyst, etc.) – 2

If the Wells score is 0, the pre-test probability is low (3%). If 1 – 2, the probability is intermediate (17%). If 3 or more, the probability is high (> 50%). The Wells score is then used to guide further evaluation.

  • Wells score 0
    • -> measure D-dimer
      • D-dimer negative: DVT excluded
      • D-dimer positive: perform ultrasound
  • Wells score 1 – 2
    • -> perform ultrasound
      • Ultrasound negative: measure D-dimer
      • Ultrasound positive: diagnostic of DVT

D-dimer is a fibrin degradation product. It’s level in the blood correlates with the activity of coagulation and fibrinolysis. It’s highly sensitive for VTE and DIC, in which case the level is increased., D-dimer is not specific. It can be elevated due to other conditions, like pregnancy, cancer, infection, kidney disease, surgery, etc. Thus, D-dimer is used to rule out VTE (if the pre-test probability is low), rather than diagnose it. If D-dimer is normal, VTE is effectively ruled out (high negative predictive value). It should not be measured in those with conditions known to cause positive D-dimer.

Ultrasound is important in the evaluation of DVT. It may show the thrombus as a hyperechoic mass in the venous lumen. When applying pressure to the vein with the ultrasound probe, an obstructed vein will not be compressible. Doppler imaging may show absent blood flow. If these findings are present, the diagnosis of DVT is made.

If D-dimer and ultrasound are inconclusive, venography with CT or MRI may be used.

Patients with VTE without clear risk factors, especially if recurrent, should be considered for screening for a hypercoagulable state (thrombophilia) and malignancy.

Treatment

DVT should be treated with anticoagulants for 3 months, preferably DOACs like rivaroxaban or apixaban. Very low-risk patients with distal DVT may be managed with regular surveillance rather than anticoagulants, but in almost all cases patients with DVT should receive anticoagulant therapy.

After three months, the patient should be reassessed for whether they require longer therapy. If the underlying risk factor(s) which are suspected to have caused the DVT are irreversible, indefinite anticoagulant therapy may be appropriate. If the risk factor(s) was reversible and is now reversed, anticoagulant therapy should be stopped after these three months.

If anticoagulants are contraindicated, IVC filters may be used. These filters are placed in the IVC and aim to prevent embolisms from reaching the heart and lungs.

Complications

  • Pulmonary embolism
  • Post-thrombotic syndrome (see topic B29 of surgery-traumatology)
  • Phlegmasia cerulea dolens

Phlegmasia cerulea dolens is a severe form of DVT where all veins of one extremity is obstructed, leading to necrosis. It’s an emergency with high mortality, which causes severe swelling, pain, cyanosis, and pulselessness. It requires emergency thrombectomy surgery to prevent shock, gangrene, and limb loss.

Pulmonary embolism

Clinical features

Pulmonary embolism has no specific symptoms and can be difficult to recognise clinically. Symptoms occur acutely. The most common symptoms include dyspnoea, pleuritic chest pain, dizziness, and cough. Other possible symptoms include tachypnoea, haemoptysis, and jugular vein distension. Symptoms of DVT may be present. Massive PE gives syncope or haemodynamic instability.

Diagnosis and evaluation

When PE is suspected, we calculate the pre-test probability of PE to determine how to proceed, as for DVT. The pre-test probability of PE can be calculated with the Wells score for PE (which is different from the one for DVT), or the revised Geneva score.

  • Low or intermediate pre-test probability for PE
    • -> measure D-dimer
      • D-dimer negative: PE excluded
      • D-dimer positive: perform CTPA
  • High pre-test probability for PE
    • -> perform CTPA

In patients with low pre-test probability, the pulmonary embolism rule-out criteria (PERC) may be applied. If all these eight criteria are fulfilled, PE is excluded, and D-dimer testing is not necessary.

Pulmonary embolism causes a sudden increased load on the right ventricle, which may manifest on the ECG. These ECG findings are not specific for PE, but most people with PE have one or more ECG abnormality. Some of the possible signs include:

  • Sinus tachycardia
  • SIQIIITIII-pattern (S-wave in I, Q-wave in III, and T inversion in III)
  • RBBB

Echocardiography is useful in PE, as it allows for ruling out other differential diagnoses (tamponade, myocardial ischaemia, valvular disease, etc.), and in case of massive PE right ventricular strain may be visible.

Arterial blood gas may show hypocapnia and hypoxaemia. Troponins and NT-proBNP may be positive due to the strain on the heart.

The gold standard for PE diagnosis is CT pulmonary angiography (CTPA), a rapid sequence with IV contrast. The scan itself takes only seconds, but the whole procedure including administration of contrast and set-up takes up to 10 minutes. And alternative to CTPA is V/Q scan.

Treatment

If the patient is haemodynamically unstable, they must be stabilised first. These patients often require ventilation and fluid resuscitation.

Once the patient is stabilised, definitive treatment must be initiated. Patients with massive PE should be managed with anticoagulation as well as thrombolysis or embolectomy. Thrombolysis involves administration of a tPA like alteplase via a peripheral IV catheter or directly into the pulmonary circulation to dissolve the clot. Embolectomy refers to physical removal of the clot, with a catheter or surgery.

Patients with nonmassive PE should be anticoagulated with LMWH or UFH, or given IVC filter is anticoagulation is contraindicated. Anticoagulation should also be initiated in patients at high suspicion for PE, even if the diagnosis isn’t made yet, as long as there are no contraindications.

After the first 5 – 10 days of anticoagulation, we may switch to oral anticoagulants, preferably DOACs. After three months, the patient is reassessed as described for DVT.

Complications

  • Obstructive shock
  • Death

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