Definitions for Thrombo-Veno-Embolism
DVT: Deep vein thrombosis
A blood clot develops in the deep veins of the legs (femur),
but may arise in the arms, or on pacemaker lines or other intra
vascular devices.
The primary condition located in the systemic deep veins
usually the legs or pelvic veins.
Pulmonary Embolism (PE)
A DVT dislodges and is swept into the lungs where it
causes occlusion of a or more pulmonary arteries
A complication of DVT and
May be fatal if large enough or occur repeatedly
Thrombus in situ of pulmonary arteries
is thought very rare, but may be important among
patients with severe pulmonary hypertension in
whom customary to recommend AC treatment
Pulmonary infarct (i.e. ischemic necrosis of the lung), Is rare; does not change management.
Chronic thrombo-veno-embolism a complication
of recurrent PE with development of (severe)
pulmonary hypertension
What are the vessels that provide oxygen to the lung parenchyma?
The bronchial vessels
The airways
The pulmonary circulation
Mortality of VTE
Within 30 days of diagnosis:
among all patients: 11.4%
among treated patients: 9.2%
among untreated patients: 25.2
What are the components of Virchow’s triad?
Local trauma to the vessel wall:
Past DVT, fracture, trauma, surgery.
Stasis in the circulation:
pregnancy, pelvic tumor, operation of abdomen or pelvic
areas, immobilization, prolonged bed rest, congestive
heart failure.
Hyper-coagulability and increasing
viscosity of the blood
Congenital:
protein S - C deficiency, factor V Leiden factor,
Acquired:
anti-phospholipid syndrome, Troussseau syndrom
What are the consequences of pulmonary emobolism and mechanical blockade of pulmonary arterial vascular bed
Increase pressure proximal to embolus causing increase in pulmonary vascular resistance.
A decrease/ cessation of blood flow distal to
embolus causing loss of surfactant, causing hemorrhage.
The cardiac index will fall only if there is a massive embolism occluding more than 50% of the pulmonary vascular bed.
What is the effect of atelectasis of the alveoli?
loss of surfactant (due to reduced perfusion) and
alveolar hemorrhage due to occluded pulm artery
Causes of hypoxemia in pulmonary embolism
V/Q inequality - mainly
Shunt
Increased dead space
Diffusion impairment in areas with high
flow (reduced transit time)
Opening up of latent pulmonary artery-vein
anastomoses d/t high pulm artery pressure
Blood flow infarcted areas
Humoral factors of pulmonary embolism
Vasoconstriction and Bronchostriction.
Platelets in the emboli release – serotonin, prostatagladins, histamine and more
Reflex vasoconstriction d/t sympathetic nervous system
Prevention of DVT/PE
Medically:
sc clexan (low molecular weight heparin (LMWH)) (40 mg/1 d)
Pro/con: once daily, expensive, (no antidote)
sc low dose heparin (5000 units X 2-3/d)
Pro/con: Cheap, but 2-3x /day, (antidote available).
Mechanically:
early mobilization,
treadmill in bed,
elastic stockings
Clinical Presentation of Pulmonary Embolism
Also: hypocapnia/alkalosis, CT scan abnormal
Difficult to diagnose, use probability and ruling out others (negative D-dimers, normal V/Q scan, etc)
Therapy for Pulmonary Embolism
If high risk of death:
For recent hemorrhagic CVA, eye surgery or neurosurgical operation, give FEX. Can also consider filter in IVC but will have pooling in legs.