300 Deep Venous Thrombosis and Pulmonary Thromboembolism Flashcards
(45 cards)
Nr. of deaths in the states for pulmonary embolism.
100,000 to 180,000 deaths annually from PE
Postthrombotic syndrome
damages the venous valves of the leg and causes ankle or calf swelling and leg aching, especially after prolonged standing. In its most severe form, postthrombotic syndrome causes skin ulceration
What are the two most common thrombophilic autosomal dominan genetic mutations?
factor V Leiden and prothrombin
Most common acquired cause of thrombophilia
Antiphospholipid antibody syndrome
Name the 5 pathophysiologic abnormalities in PE.
pathophysiologic abnormalities include:
- Increased pulmonary vascular resistance
- Impaired gas exchange
- Alveolar hyperventilation
- Increased airway resistance
- Decreased pulmonary compliance
Massive PE accounts for which % of cases?
5–10%
Submassive PE accounts for which % of patients?
20–25%
Low-risk PE constitutes which % of cases.
70–75%
Clinical presentation of Massive and Submassive PE?
Dyspnea, syncope, hypotension, and cyanosis are hallmarks of massive PE. Patients with massive PE may present in cardiogenic shock and can die from multisystem organ failure.
Submassive PE is characterized by RV dysfunction despite normal systemic arterial pressure. The combination of right heart failure and release of cardiac biomarkers indicates an increased likelihood of clinical deterioration.
Relation between leg DVT and arm DVT?
Leg DVT is about 10 times more common than upper
extremity DVT.
Nonthrombotic PE etiologies
Fat embolism after pelvic or long bone fracture, tumor embolism, bone marrow and air embolism. Cement embolism and bony fragment embolism in total hip or knee replacement. Intravenous drug users
may inject themselves with hair, talc, and cotton. Amniotic fluid embolism.
What is the sensitivity of the d-dimer test?
The sensitivity of the d-dimer is more than 80% for DVT (including isolated calf DVT) and more than 95% for PE.
Diseases that can elevate D-Dimers?
Myocardial infarction, pneumonia, sepsis, cancer, and the postoperative state and those in the second or third trimester of pregnancy.
What is the ECG abnormality more specific por PE?
In addition to sinus tachycardia, is the S1Q3T3 sign
Changes in the ultrasonography of DVT?
Ultrasonography of the deep venous system relies on loss of vein compressibility as the primary criterion for DVT. The thrombus can be visualized, it appears homogeneous and has low echogenicity. The vein itself often appears mildly dilated, and collateral channels may be absent.
Changes in the chest x-ray of PE?
focal oligemia (Westermark’s sign), a peripheral wedged-shaped density above the diaphragm (Hampton’s hump), and an enlarged right descending pulmonary artery (Palla’s sign)
What is the principal imaging test for the diagnosis of PE?
CT of the chest with intravenous contrast.
VPP of Lung scanning for PE?
About 90% certain in patients with high-probability scans
False negatives of Lung scanning for PE?
As many as 40% of patients with high clinical suspicion for PE.
What is the use of MR pulmonary angiography in PE?
May detect large proximal PE but is not reliable for smaller segmental and subsegmental PE.
McConnell’s sign
hypokinesis of the RV free wall with normal or hyperkinetic motion of the RV apex.
Definitive diagnosis of PE in Pulmonary Angiography?
Visualization of an intraluminal filling defect in more than
one projection. Secondary signs of PE include abrupt occlusion (“cutoff”) of vessels, segmental oligemia or avascularity, a prolonged arterial phase with slow filling, and tortuous, tapering peripheral vessels.
open vein hypothesis postulate
patients who receive primary therapy will sustain less long-term damage to venous valves, with consequent
lower rates of postthrombotic syndrome. Still not confirmed.
Alternatives for effective anticoagulation.
(1) parenteral therapy “bridged” to warfarin, (2) parenteral therapy “bridged” to a novel oral anticoagulant such as dabigatran (a direct thrombin inhibitor) or edoxaban (an anti-Xa agent), or (3) oral anticoagulation with rivaroxaban or apixaban (both are anti-Xa agents) with a loading dose followed by a maintenance dose as monotherapy without parenteral anticoagulation.
