Thromboembolism is a spectrum of conditions in which a fragment of a blood clot (embolus) originating from one blood vessel, vein or artery, travels to another vessel thereby occluding it.
The typical symptoms and signs of symptomatic DVT are the pain, swelling, warmth, and redness of the calf or thigh. Cellulitis may complicate the clinical picture. Additionally, thrombosis at the site of the iliac bifurcation produces bilateral leg edema. Patients may have signs of PE prior to diagnosis of DVT.
While the symptomology of PE may be non-specific, the clinical picture is characterized by dyspnea, pleuritic or retrosternal chest pain, cough, and hemoptysis . Patients can become anxious and agitated while suffering from mental status changes. Moreover, these patients may exhibit signs of a DVT.
Remarkable findings on the physical exam include cyanosis, tachycardia, tachypnea, and fever. Cardiovascular features such as elevated jugular venous pressure may develop. Chest auscultation reveals abnormal sounds such as a gallop rhythm, a widely split S2, and a tricuspid valve regurgitant murmur .
The clinical assessment consists of the patient's history including risk factors for VTE, a physical exam, and the appropriate studies.
An arterial blood gas (ABG) test will reveal hypoxemia. There is an increased alveolar-arterial oxygen gradient in PE patients. Additionally, a D-dimer test is done when there is high suspicion for DVT. Note that a positive result is not specific and should warrant further testing. A coagulation panel should be obtained if indicated.
Doppler ultrasonography is the initial test used for detection of a venous clot. Other modalities include but are not limited to venography and plethysmography.
Pulmonary angiography, the long-standing criterion standard for diagnosis of PE, displays the pulmonary vessels and demonstrates absent blood flow to embolized segment(s). Another useful study is the spiral computed tomography (CT) scan with IV contrast, which provides visualization of the pulmonary vasculature. Furthermore, the commonly employed ventilation-perfusion scan assesses the airflow and blood circulation throughout the lungs. Finally, a chest x-ray yields mostly normal results in PE patients although it can depict an enlarged pulmonary artery, reduced vascularity, and other similar findings.
Electrocardiogram (EKG) is performed to evaluate the patient for myocardial infarction. Findings suggestive of PE may include sinus tachycardia, right axis deviation, inverted T waves in leads V1 to V3, and a right bundle branch block. The "classic" S1Q3T3 pattern is present in only 20% of PE patients.
Another useful test is the echocardiogram which can indicate right heart strain.
There should be aggressive and prompt evaluation and treatment of DVT and PE since PE can be rapidly fatal. Also, clinicians should consult guidelines when choosing the medication(s), duration of treatment, and prophylaxis. Crucial details that must be considered include preexisting diseases, inherited thrombophilias, underlying malignancies, and high-risk situations such as recent surgery.
Standard anticoagulants used to treat acute episodes include unfractionated heparin (UFH), low molecular weight heparin (LMWH), and fondaparinux. Patients on these agents are transitioned to warfarin therapy early. Furthermore, target specific agents such as rivaroxaban and dabigatran may be used as well. First-time events should be treated with anticoagulation for at least 3 months and therapy is extended if there is an underlying disease.
Patients who cannot take anticoagulants are candidates for vena cava filter placement, which serves as the treatment and secondary prophylaxis. In rare cases, embolectomy may be necessary for large clots in the lungs.
Note that there are contraindications and serious complications associated with these medications. Therefore, thorough knowledge about the various agents and the patient's medical history is paramount to help reduce and prevent adverse outcomes.
The outcome of a major episode of PE depends on the size of the embolus and the preexisting cardiopulmonary status . Specifically, the prognosis of patients with PE is stratified by the Pulmonary Embolism Severity Index (PESI), which categorizes the mortality risk following PE.
DVT is fatal when it is associated with massive PE, which accounts for as much as 300,000 deaths in the US every year . One European study reported that 34% of VTE-related deaths were sudden fatal PE .
Patients with small PE exhibit a recurrence rate that is below 5% during the anticoagulation period but this increases to 30% a decade later . Another major long-term complication is post-phlebitic syndrome.
The cause of DVT and PE is explained by the Virchow's triad, which consists of venous stasis, vessel wall injury, and hypercoagulability . These factors threaten the tightly regulated coagulation system that normally ensures a blood clot formation in the presence of vessel wall injury .
Risk factors for DVT include a recent surgery or trauma especially of the pelvis, hip or lower extremity, malignancy, recent hospitalization, underlying illness, inherited thrombophilias, etc .
The incidence of DVT in the general population is 1 in 2000 individuals annually . In the United States, it is estimated that there were approximately 550,000 hospitalizations with VTE in patients 18 years of age or greater between 2007 and 2009 , with a slight predilection for females. Additionally, advanced age is a significant risk factor. With regards to race, thromboembolism occurs more commonly in African Americans than Caucasians.
A blood clot is formed by fibrin, platelets, and red blood cells due to obstruction, hypercoagulability, or damage to the endothelial cells of the vessel wall. The mass may then separate or propagate and embolize to the pulmonary arteries. Consequently, the pulmonary embolus triggers a series of mechanisms that ultimately alter the hemodynamics of the pulmonary circulation such as increasing the pulmonary vascular resistance. The resultant right ventricular dysfunction and failure may finally cause cardiogenic shock, which can be fatal.
There are guidelines to help clinicians and patients to make appropriate decisions regarding prophylaxis. There are also risk stratification measures to identify which patients should be treated prophylactically. Ambulation, compression stockings, and possibly early prophylaxis are used in post-surgical patients.
Thromboembolism may affect the venous or arterial vasculature. With regards to venous thromboembolism (VTE), it is comprised of two interrelated processes known as deep venous thrombosis (DVT) and pulmonary embolism (PE), in which an embolus originating from a deep vein circulates to the pulmonary vessels. In arterial thromboembolism, an embolus arising from the heart could impact in arteries leading to the brain, gut, kidneys, spleen and lower extremities .Thromboemboli originating from common carotid arteries impact in arteries of the brain, while those originating from the abdominal aorta frequently end in arteries of the kidneys and lower extremities.
This article will focus on DVT and PE. As with all vascular events, it is imperative to establish a prompt diagnosis and initiate early treatment.
What is thromboembolism?
The most typical example is venous thromboembolism (VTE). It is made up of two conditions: deep venous thrombosis (DVT) and pulmonary embolism (PE). DVT is a blood clot that forms in deep veins of the lower extremities which separate and travels as an embolus to the lungs to form a PE.
What are the signs and symptoms?
DVT can be asymptomatic but its typical signs are:
How is it diagnosed?
The clinician will obtain the patient's history, perform a physical exam, and order the appropriate blood tests and imaging studies such as :
How is it treated?
Meyer G, Planquette B, Sanchez O. Long-term outcome of pulmonary embolism. Curr Opin Hematol. 2008;15(5):499-503.