300 Deep Venous Thrombosis and Pulmonary Thromboembolism Flashcards
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.
Dosage of UFH
target activated partial thromboplastin time (aPTT) of 60–80 s. The most popular nomogram uses an initial bolus of 80 U/kg, followed by an initial infusion rate of 18 U/kg per h.
Warfarin Dosage
Requires 5–10 days of administration to achieve effectiveness as monotherapy (Unfractionated heparin, low-molecular-weight heparin, and fondaparinux
are the usual immediately effective “bridging agents” used when initiating warfarin)
Usual start dose is 5 mg
Titrate to INR, target 2.0–3.0
Continue parenteral anticoagulation for a minimum of 5 days and until two sequential INR values, at least 1 day apart, achieve the target INR range
Approved treatment for PE and DVT?
Rivaroxaban, a factor Xa inhibitor, is approved
for treatment of acute DVT and acute PE as monotherapy, without a parenteral “bridging” anticoagulant. Apixaban is likely to receive similar approval for oral monotherapy. Dabigatran, a direct thrombin inhibitor, and edoxaban, a factor Xa inhibitor, are likely to be approved for treatment of VTE after an initial course of parenteral anticoagulation.
What is the most serious adverse effect of anticoagulation?
hemorrhage
What are the two principal indications for insertion of an IVC filter?
(1) active bleeding that precludes anticoagulation and (2) recurrent venous thrombosis despite intensive anticoagulation.
1st therapeutic measure in patients with massive PE and hypotension?
500 mL of normal saline
Action of fibrinolytic therapy?
(1) dissolving much of the anatomically obstructing pulmonary arterial thrombus, (2) preventing the continued release of serotonin and other neurohumoral factors that exacerbate pulmonary hypertension and (3) lysing much of the source of the thrombus in the pelvic or deep leg veins, thereby decreasing the likelihood of recurrent PE.
What is the preferred fibrinolytic regimen?
100 mg of recombinant tissue plasminogen activator (tPA) administered as a continuous peripheral intravenous infusion over 2 h. The sooner thrombolysis is administered, the more effective it is.
what is the overall major bleeding rate with alteplase 100 mg/2 h? And the risk of intracranial hemorrhage?
overall major bleeding rate is about 10%, including a 1–3% risk of intracranial hemorrhage.
Is there a benefit to using thrombolytic agent tenecteplase?
Death or hemodynamic collapse within 7 days of randomization was reduced by 56% in the tenecteplase group. However, hemorrhagic stroke occurred in 2% of tenecteplase patients versus 0.2% in patients who only received heparin.
% of patients with acute PE that develop chronic thromboembolic pulmonary hypertension?
2–4%
What is the mortality rate of pulmonary thromboendarterectomy?
approximately 5%
Computerized reminder systems can increase the use of preventive measures and, at Brigham and Women’s
Hospital, have reduced the symptomatic VTE rate by how much?
more than 40%
What is the ongoing trial novel oral anticoagulant for extended-duration VTE prophylaxis?
betrixaban
How long is prophylaxis for patientes with hip replacement or extensive cancer surgery?
the duration of prophylaxis is usually at least 1 month
% of patients that will develop a disease very similar
clinically and pathologically to PAH after resection of the proximal thrombus in group IV of PH?
10-15%
Name other diseases that causa PH.
Sarcoidosis; sickle cell disease and schistosomiasis
What are the available pharmacologic therapies for PH?
prostacyclin analogues, phosphodiesterase-5 inhibitors, a soluble guanylyl cyclase stimulator, and endothelin receptor antagonists
Available prostanoids?
Epoprostenol delivered as a continuous intravenous infusion (6 min.); Treprostinil subcutaneous (4 h); Inhaled iloprost and treprostinil
Available Phosphodiesterase-5 (PDE5) inhibitors for PH?
Sildenafil, tadalafil. Recently, the oral soluble guanylyl cyclase stimulator, riociguat, was approved for the treatment of both PAH and CTEPH.
What is the median survival for a person with PAH?
It is only 5–6 years.
