Vascular Thromboembolic Disease Flashcards
Hemostasis
the physiologic process by which bleeding stops
Thrombosis
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Thrombus
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Embolization
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Emboli
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Key Pathologic Consequence of clot
REDUCTION IN or CESSATION OF BLOOD FLOW
Underlying Inciting Event in several Clinical Diseases
TIA/CVA, MI, DVT, PE, etc.
Substances that can embolize
Air Amniotic Fluid Foreign Bodies Parasitic Eggs Septic Emboli Tumor Cell MOST COMMON: Thrombus
Location of Thromboembolism
can occur anywhere in Cardiovascular System
Purpose of Hemostatic System
Prevent blood loss due to vascular Injury
Thrombus: A leading cause of morbidity and mortality
Epidemiology
US: cause of death in ~1 million individuals per year
Annual Incidence: ~1 case/1000 individuals
Components of hemostatic system
Formed Elements: Cells (Platelets, Monocytes, RBCs) &
Plasma Proteins (Clotting Factors, Fibrinolytic Factors, Inhibitors)
Vessel Wall: Epithelium, vonWillibrand Factor (vWF), Collagen, Tissue Factor
Hemostasis- Vascular Injury
will expose VW factor, collagen matrix, etc. and when this is exposed that’s when coagulation occurs
Primary Hemostasis
formation of platelet plug
Secondary Hemostasis
Clotting Cascade: Activate Fibrin (form meshwork that binds everything together)
Hemostasis- Fibrinolysis and Regulation
once clot is formed, further clot formation is prevented and clot starts to breakdown
Arteries
Higher Pressure
More smooth muscle
Atherosclerosis
Veins
More Distensible
Capacitance Vessels
Valves
Virchow’s Triad
Arterial Thromboembolism may cause
Arterial Occlusive Disease Myocardial Infarction Ischemic Cerebrovascular Accident Mesenteric Ischemia Vasculitides
Venous Thromboembolism (VTE) may cause
PE DVT Superior Vena Cava Obstruction Chronic ThromboEmbolic Pulmonary HTN (CTEPH) Dural Sinus Thrombosis Portal Vein Thrombosis Vasculitis-Bechet’s, Granulomatosis with polyangiitis Mesenteric Vein Occlusion
Pulmonary venous thromboembolism (AKA PE)
3rd leading cause of death among hospital pts
Often not recognized ante mortem
Thrombus description
- Most common etiology of emboli
- Most Common Site of Origin is Deep Veins of the Lower extremities
- Found in 50-70% of pts with symptomatic PE
- Can Form AnywhereThrombus
Diagnosis of VTE (venous thrombolytic embolism)
- NOTORIOUSLY DIFICULT DIAGNOSIS
- Findings depend of size of embolus and preexisting cardiopulmonary disease
- Common signs and symptoms are not specific
Signs & Symptoms of VTE
*Dyspnea
*Pain on inspiration
*Tachypnea
Cough
Hemoptysis
Leg Pain
Tachycardia
Palpitations
Crackles
Homan’s Sign- Dorsiflex foot and have calf tenderness (may be indication of DVT)
DIFFERENTIAL DIAGNOSIS for VTE
Pneumonia Lung Cancer MI COPD Asthma Traumatic Injury Muscle Strain Costochondritis Inhalation Injury Aortic Aneurysm Congestive Heart Failure
Virchow’s Triad- 3 things that promote coagulability
Stasis, Hypercoagulability, Endothelial injury
Description of Stasis (part of Virchow’s triad)
Stasis Prolonged immobility post orthopedic surgery, Low Cardiac Output Pregnancy Post CVA Travel (Air, Car)
Description of Hypercoagulability (part of Virchow’s triad)
Hypercoagulability
Medications: Oral Contraception, Hormone Replacement
Malignancy
Genetic: Factor V Leiden, Protein C/S/antithrombin III deficiency/dysfunction, prothrombin gene mutation, hyperhomcysteinemia, antiphospolipid antibodies
Description of Endothelial Injury (part of Virchow’s triad)
Traumatic Injury
Recent Surgery
Previous Thrombosis
EKG findings of VTE
- Abnormal in about 70% of pts with PE
- Most Common Finding: Sinus Tachycardia & Nonspecific SR and T wave changes
- Right Heart Strain: RBBB, Right Axis Deviation, S1Q3T3
- Prominent S wave (lead 1), Prominent Q wave (lead 3) and Inverted T wave (lead 3) –>this may also indicate PE
Arterial Blood Gas findings of VTE
- Usually Respiratory Alkalosis
- Abnormal pO2 and Alveolar-arterial O2 gradient
- NOT DIAGNOSTIC
- ->Profound Hypoxia with Normal Chest X-ray THINK PE
D-dimer
- *Indicative of general clot formation (not specific)**
- Fibrin Degradation product
- Can be elevated in trauma, always elevated with inflammation
- Positive D-dimer DOES NOT INDICATE a PE
- Sensitivity 95-97%, Specificity 45%
- NO diagnostic threshold established for positive result
- BEST INFORMATION WHEN NEGATIVE (indicates NO clot has formed)
- Negative
Other Lab findings of VTE
- Serum Troponins, BNP typically elevated in PE
- Indicative of R heart strain/R heart failure
- Not Useful in diagnosis, correlate with adverse outcomes
Findings of Chest Xray with VTE
- Useful to rule out other etiologies
- Most Frequent findings: Atelectasis, Parenchymal Infiltrates, Pleural Effusion
Uncommon Findings of Chest Xray with VTE
Westermark Sign: prominent central pulmonary artery with local oligemia; Absence of vascular markings distal to engorged central pulmonary vein
Hampton’s Hump: pleural based areas of increased opacity representing intraparenchymal hemorrhage (may represent pulmonary infarct as well)
LOOK UP PICTURES
Gold standard for diagnosing VTE
CT angiography (WITH CONTRAST)
Very sensitive for large central pulmonary arteries and veins; may see saddle embolus indicated by lack of contrast (filling defect)
With VTE, primary and secondary findings of CT angiography are
- Requires IV contrast dye
- Primary finding suggestive of PE: Intravascular filling defect, Very sensitive for central vascular filling defects
- ~80% sensitive, 96% specific
- 15-20% false negative rate (high)
*Secondary Findings suggestive of PE: Abrupt arterial cutoff, asymmetrical blood flow, prolonged or slowed filling
Normal CT chest requires
initiation of empiric therapy (high pretest probability) or further testing (V/Q scan, etc.)
Ventilation Perfusion (V/Q) scan
- Perfusion assessed by injection of radiolabeled albumin injected into venous circulation
- Ventilation assessed by records distribution of inhaled radiolabeled gas
- The two mages are compared, looking for defects
Ventilation Perfusion (V/Q) scan and probability of VTE
- Criteria for assessment are complex, confusing and not standardized
- Reported in terms of probability: low, intermediate, and high
- PIOPED1; If low, 14% probability of PE. Combined with low pretest probability , lowers risk to 4%
- If indeterminate, low or intermediate probability, further testing required (if pretest is low, further testing is required)
-Lower extremity doppler may be used to see if there is a blood clot
Venous Ultrasonography: positive and negative tests are indicated by ________
- Positive Test: Incompressibility of common femoral or popliteal veins
- In a patient with appropriate symptoms (unilateral swelling, erythema of one limb vs. another) –> Positive predictive value 97% (more likely, probably present)
- Negative Test: Full compressiblity at both vessels
- Negative Predictive value 98% (less likely, probably no there)
- Less accurate in distal thrombi, recurrent thrombi, and asymptomatic patients
Integrated Approach to PE Diagnosis: Wells Criteria
Wells Criteria: scoring systems to assess PE Risk
- Clinical Signs and symptoms of DVT: Unilateral edema, and pain with palpation 3 pts
- Alternative Diagnosis Less likely than PE (if you’re not suspecting another diagnosis like muscle cramping, traumatic injury, etc) 3 pts
- Pulse >100bpm 1.5 pts
- Immobilization >3days in past 4 wks 1 pt
- Previous DVT/PE 1 pt
- Hemoptysis 1 pt
- Cancer (With Tx w/in past 6 mo. or Palliation) 1 pt
Total >4pts: Imaging warranted
Total
People who are HIGH RISK for PE/DVT
DVT/PE ARE preventable
Surgical patients, Major orthopedic procedure/arthroplasty, Abdominal/pelvic cancer undergoing surgery, recent spinal cord injury or major trauma w/in previous 90days,
>3 intermediate criteria
People who are INTERMEDIATE RISK for PE/DVT
DVT/PE ARE preventable
Ambulation 30, OCP/HRT use, Immobilization >72hrs, Hypercoagulable state, nephrotic syndrome, burns, cellulitis, varicose veins, paresis, Systolic Heart Failure, COPD exacerbation
People who are LOW RISK for PE/DVT
DVT/PE ARE preventable
Minor procedures, age
Interventions for DVT/PE
Sequential Compression Devices
Medication: Heparin, Lovenox
Treatment for Pulmonary VTE
Heparin or Catheter directed tPA
