Aortic Dissection/Venous Thromboembolism Flashcards
Cases per year of aortic dissection? What allows this to happen?
• Approximately 5000 cases per year • Intimal tear allows hematoma to form between intima and adventitia (Cystic medial necrosis) • 10-15% vaso vasorum rupture causes intramural hematoma
Explain the Stanford Classification?
• Stanford classification • Type A involves ascending aorta and originates at the aortic valve level (2/3 of cases) • Type B involves descending aorta and originates at ligamentum arteriosum
DeBakey Classification?
• DeBakey classification • Type I Ascending and descending • Type II Ascending only • Type III Descending only
Causes of Aortic Dissection?
• Marfan’s syndrome • Ehlers-Danlos syndrome • Hypertension • Trauma (blunt or iatrogenic) • Pregnancy (half of women cases under age 40) • Bicuspid aortic valve independent of stenosis gradient • Age 50-70 • Male to female 2:1 • 90% of acute cases of ascending dissection have no recognized substrate
Physical symptoms of Aortic dissection?
• Sudden onset of intrascapular pain that radiates to extremities more likely descending aorta • Chest pain through to back more likely ascending aorta • Pleuritic chest pain may represent pericardial effusion • Abdominal pain if involves mesenterics • Neurological changes involving cerebral distribution
Imaging for Aortic stenosis?
• CXR (sensitivity 67%) • EKG non specific most common • CT Scan gold standard now with new scanners • TEE excellent sensitivity and specificity • MRI lack of availability and length of scan • History and physical exam
Physical exam findings of Aortic dissection?
• Water Hammer Pulse-created by widened pulse pressure—- boards. • Aortic Insufficiency diastolic murmur • Differential blood pressure between arms • Gallop rhythm S3 or S4 due to rapid ventricular filling and possible myocardial infarction- this is super advanced probably won’t come up ever.
Aortic Dissection mortality rates?
Mortality 1-2% per hour in first 24 hours
50% first week
75% first month
90% first year
Management of Aortic Dissection?
- Blood pressure control to a mean arterial pressure of 60-75 desirable
- Sodium nitroprusside with a beta blocker (esmolol, labetalol) first line therapy
- IV cardizem/diltiazem second line with combined decreased blood pressure and inotropic effect
- Refractory hypertension consider renal artery involvement
- Surgical intervention required for ascending disease
- Medical therapy for descending dissection
Ascending vs. descending super important.
Risk factors for Aortic Dissection?
Aortic Dissection
• Advanced age
- Aneurysm leak
- Concominant CAD
- Renal Failure
- Pericardial effusion/tamponade
- Shock
Most Venous thromboembolism are? Incidence? Mortality?
- Venous thromboembolism (VTE) • Most common are deep vein thrombosis (DVT) and pulmonary embolism (PE)
- Incidence of VTE is about 1/1,000 in the US
- Death occurs within one month of an episode in about 6% of those with DVT and 10% of those with PE • Mortality rate for pulmonary embolism approaches about 30% • There is also significant morbidity • Post-thrombotic disorder • Pulmonary hypertension
What is Virchow’s Triad? This is a must know.
- Hypercoagubility • Surgery • Cancer • Inherited disorders
- Stasis (IE immobility or anatomical factors reducing blood flow) • May-Thurner
- Endothelial injury
Risk factors for Venous thromboembolism?
- More than half of patients presenting with VTE have three or more of the following six risk factors present at the time of VTE
- >48 hours of immobility in the preceding month;
- hospital admission
- Surgery
- malignancy,
- infection in the past three months
- current hospitalization
Hemostasis process?
- Formation of the platelet plug
- Adhesion, aggregation, secretion, propagation (platelet factors)
- Initiation of clotting cascade
- exposure to collagen/TF and interaction with Factor VII
- TF and VIIa activates Factor X
- Factor Xa and Va convert prothrombin to thrombin
- Thrombin activates Factors V, VIII, IX, Fibrinogen Fibrin Thrombosis
DVT should be suspected in patients with what features?
- DVT should be suspected in patients who present with leg swelling, pain, warmth, and erythema • Swelling or edema – 97 (sensitivity) and 33 percent (specificity) • Pain – 86 and 19 percent • Warmth – 72 and 48 percent
- Assess for risk factors of VTE (discussed previously)
- Personal and family history of VTE
Pulmonary embolism presenting features?
- Pulmonary embolism (PE) has a wide variety of presenting features, ranging from no symptoms to shock or sudden death
- Most common presenting symptom is dyspnea (73% of patients) and this is usually rapid in onset
- Other common features include chest pain (classically pleuritic in nature), cough, and symptoms of deep venous thrombosis
- Syncope can also be the presenting symptom, though this is not common (210% of patients with PE)
Physical findings of DVT? PE?
- Leg swelling, warmth, erythema • Degree of swelling dependent on size and location of DVT • Proximal DVT could have entire leg involvement • Bilateral swelling is uncommon
- For pulmonary embolism • Tachycardia • Tachypnea • Hypoxia • JVD • Lung sounds generally normal • Loud P2 component of heart sounds • Fever (~3% of patients)
EKG findings of PE?
- Most common finding = sinus tachycardia_ BOARDS!!!!!!!!!!!
- Other findings are generally non-specific and insensitive. Finding of “S1Q3T3” is fairly specific for right ventricular strain and is present in a minority of PE.
Right heart strain on EKG is characterized by? Seen in what conditions?
- ST depression and T wave inversion in the leads corresponding to the right ventricle • Inferior leads and V1-V3
- Can be seen with PE, pulmonary hypertension, cor pulmonale, or mitral stenosis
Labs and tests for PE?
- Chest Xray generally normal • Hampton’s hump and Westermark’s sign (next slides)
- ABG will show hypoxia with a high A-a gradient
- BNP and troponin can be elevated
- D-dimer elevated
What does this chest X-ray show?
Hampton’s Hump:
Shallow, hump-shaped opacity in the periphery of the lung, with its base against the pleural surface and hump towards the hilum
What does this Chest X-ray show?
Westermark’s Sign:
Demonstration of a sharp cut-off of pulmonary vessels with distal hypoperfusion in a segmental distribution within the lung
Explain Ultrasound for DVTs? which veins can be assessed?
- Duplex venous ultrasound is the test of choice for confirming diagnosis of DVT
- Presence of thrombus is diagnosed by demonstrating noncompressibility of the imaged vein.
- Veins that can be assessed for compressibility are the proximal (eg, the common femoral, femoral, and popliteal veins) and distal veins (eg, peroneal, posterior and anterior tibial, and muscular veins)
- Iliac veins often cannot be assessed for compressibility
- May be limited depending on body habitus of patient
What are the deep veins in the legs?
Superficial femoral vein is also a deep vein (trick question on boards). This is also called “femoral vein”
Best imaging modality for PE?
- CT is Imaging modality of choice to confirm PE
- Filling defects within the pulmonary vasculature with acute pulmonary emboli
- Can also see right ventricular strain (dilation) on CT
What is a v/q scan?
- Alternative diagnostic modality
- Less radiation (so sometimes used in pregnancy)
- Alternative if contrast cannot be used (IE allergy or AKI/CKD)
- Baseline CXR should be normal or there will be ventilation defects that impede interpretation
- Atelectasis or pneumonia may cause perfusion/ventilation mismatch
- Often non-diagnostic or “intermediate” probability
- Diagnostic test of choice for chronic thromboembolic disease (CTEPH)
- Can also be positive if there is extrinsic compression of PA from a tumor or in the presence of radiation therapy
What is a Provoked DVT? Proximal DVT? Renal impairment? Unprovoked DVT or PE?
- Provoked DVT or PE: DVT or PE in patients with recent occurrence of major clinical risk factor for VTE
- Proximal DVT: DVT in popliteal vein or above
- Renal impairment: eGFR of less than 90 ml/minute/1.73 m2 (see notes)
- Unprovoked DVT or PE: DVT or PE in patients with no recently occurring major clinical risk factors for VTE
How do we evaluate DVT?
- Diagnostic evaluation should be based on pretest probability
- Well’s score for DVT
- If DVT is unlikely (<2 points on Wells) • Perform D-dimer testing • If D-dimer negative, no further testing required
- If DVT likely (>2 points on Wells) • Perform duplex venous ultrasound
Evaluation of PE?
- If PE is unlikely (4 points or less) • D dimer. If negative, then no further testing
- If PE is likely (more than 4 points) • Immediate CT for PE if able • Interim anticoagulation if immediate CT not available
- If PE is very likely (6 points or more) • Immediate anticoagulation followed by confirmatory testing
- If pregnant, consider V/Q scan (less radiation) or scan legs. If DVT present, no need to proceed to CT or V/Q • A positive US “rules in” PE in high risk patient • A negative D-dimer “rules out” low risk patients • A negative D-dimer does not rule out high risk patients
How to evaluate hemodynamic status in PE?
• ”Massive” PE = hemodynamic compromise • Hypotension or persistent hypoxia • Does not necessarily correlate to size of PE on imaging • IE “saddle embolism” • These patients should receive urgent thrombolytics in the absence of a contraindication
Treatment of DVT?
- Consider location and symptoms
- All proximal DVTs should be treated
- Symptomatic DVTs should be treated (if distal or proximal)
- Distal DVT do not require treatment with anticoagulation if: • Asymptomatic • No prior history of DVT • Isolated to only one vein • Non extensive (<5cm) • Not in close proximity to a proximal vein • Absence of an irreversible risk factor (cancer, prolonged immobility)
- If an observation strategy is undertaken (IE no anticoagulation), then serial ultrasounds should be performed • Weekly ultrasound for 2 weeks • If clot resolves, then can stop monitoring • If clot extends, then anticoagulate • If remains stable, then continue surveillance (every 2 weeks) • If symptoms develop, then anticoagulate
consider catheter directed thrombolytic therapy when?
- Consider catheter-directed thrombolytic therapy for patients with symptomatic iliofemoral DVT who have:
- symptoms of less than 14 days’ duration and
- good functional status and
- a life expectancy of 1 year or more and
- a low risk of bleeding.
Inferior vena cava filters?
- Temporary inferior vena cava filters to patients with proximal DVT or PE who cannot have anticoagulation treatment
- Remove the inferior vena cava filter when the patient becomes eligible for anticoagulation treatment
- Ensure a plan is in place for filter retrieval
- There are other indications where IVC filters are considered, but these are controversial
- Presence of a large PE and proximal DVT
- Presence of a very proximal DVT that extends into IVC
Treatment of a Pulmonary Embolism?
- Identify patients with hemodynamic compromise for thrombolytic therapy • Systemic thrombolytics are preferred (faster than catheter directed) • Bleeding rates are close to the same for catheter directed and systemic
- Consider thrombolytics in patients who are hemodynamically stable with evidence of right ventricular strain or failure • Younger patient with few comorbid conditions • No contraindication to lytics present • Catheter directed lytics may be helpful to prevent long-term complications (RV failure and pulmonary hypertension).
- Mechanical thrombectomy is an option if contraindication to lytics exist
Anticoagulation in VTE?
- Anticoagulation is mainstay of treatment for VTE
- Initial treatment is often parenteral
- Unfractionaed heparin with dose adjustment based on aPTT levels
- LMWH (enoxaparin) injected once or twice daily subcutaneously
- Oral anticoagulation
- For minimally symptomatic DVT or symptomatic distal DVT, this can be started immediately and followed outpatient
- For low-risk patients with PE, these can be started initially and followed outpatient
- No hypoxia, resolution of chest pain, no evidence of RV strain, no arrythmia, etc
- Patients can be risk stratified and sent home from ER on OAC or LMWH based on the simplified PESI score. Score of 0 is required to take this approach
What are the methods of anticoagulation?
- Vitamin K Antagonists (Warfarin)
- Heparin and LMWH (activate antithrombin)
- Direct Thrombin Inhibitors • Hirudin analogs (leperudin, bivalirudin, etc) • Argatroban • Dabigatran
- Indirect Factor Xa Inhibitors (Fundaparinux - subcutaneous)
- Direct Factor Xa Inhibitors (Rivaroxaban, Apixiban)
Explain warfarin?
- Act on Vitamin K dependent clotting factors (II, VII, IX, and X), and Proteins C&S by inhibiting gamma carboxylation
- Anticoagulant effect is seen 36-72 hours after dosing once the normal (carboxylated/activated) factors are cleared
- Plasma half-life of Factor II is 3 days
- Require “bridging” of therapy with parenteral UFH or subQ LMWH for at least 72 hours
- Metabolism: CYP2C9- many interactions, many genetic variations
- Rarely used any more
- Benefit: cost
Explain Heparin and its analoges?
- Unfractionated heparin and low molecular weight heparin (enoxaparin)
- Indirect thrombin inhibitor
- Complexes to antithrombin, which then inactivates thrombin and Xa
- Heparin requires frequent blood draws for monitoring of aPTT
- aPTT levels are often not therapeutic
- LMWH (enoxaparin) has much more predictably pharmacokinetics and does not require monitoring
- LMWH dosing for therapeutic anticoagulation is 1mg/kg BID -or- 1.5mg/kg daily
- Much lower risk of heparin induced thrombocytopenia with LMWH
- No reversal agents for LMWH (versus heparin which has a reversal agent, protamine, and whose action is short lived once infusion is stopped)
Explain the direct factor 10 inhibitors?
- Rivaroxaban (xarelto) and apixiban (eliquis)
- Eliquis was shown to be superior to warfarin for treatment of DVT/PE
- Rivaroxaban Dose: 20mg/day for three weeks, then15mg bid
- Clcr >50 mL/minute: No dosage adjustment necessary.
- Clcr 15-50 mL/minute: 15 mg once daily • Clcr <15 mL/minute: Avoid use
- Apixiban dose: 10mg BID for 7 days followed by 5mg BID
- Not recommended in patients with CKD and CrCl of <15, limited data for CrCl of 15-29
Explain Dabigatran?
- Direct Thrombin inhibitior
- Requires a minumum of 5 days of parenteral anticoagulation prior to use for VTE
- Dose: 150mg BID
- There is a specific reversal agent available: idarucizumab aka praxibind
- Monoclonal antibody specific for dabigatran
Duration of therapy and special considerations for therapy in VTE?
- Provoked DVT, first occurrence = 3 months
- Unprovoked or if first occurrence was “life threatening” = lifelong
- Patient’s with malignancy = until malignancy is cured or lifelong • These patients should receive LMWH
- Pregnant patients should receive LMWH
- Discontinue 24 hours prior to delivery if delivery time known (induction or C-section)
- Continue 12 hours after delivery
- Warfarin is safe for breast feeding
Should we test for Hypercoagulability disorders?
- Generally NOT recommended
- Does not change treatment or affect duration of anticoagulation
- Most cannot be reliably tested during an acute thrombosis
- Can be pursued for • Recurrent VTE • VTE in unusual locaiton (IE protal vein thrombosis) • Arterial thrombosis
- A search for occult malignancy is not recommended, except for the usual ageappropriate screening or if presentation suggests an underlying malignancy
What is the most common heritable hypercoaguble state? Others? Hypercoaguable state with most risk of recurrent VTE?
- Most common heritable hypercoaguble state = Factor V Leiden
- Hypercoaguble state with most risk of recurrent VTE = antiphospholipid syndrome
- Other disorders • Antithrombin III deficiency • Protein C/S deficiency • Prothrombin gene mutation
Anticoagulation reversal with warfarin?
- Reverse with any evidence of severe bleeding
- Severe bleeding in patient on warfarin should be managed with proothrombin complex concentrates (PCC).
- Vitamin K (oral, subQ, or IV) takes 24-48 hours for effect so too slow for acute bleeding
- FFP does work, but must be cross-matched and thawed and should only be given if PCC not available
- For supratherapeutic INR <9 and no evidence of bleeding, just hold warfarin and monitor. If INR >9 without bleeding, hold warfarin and give vitamin K
Oral Anticoagulant reversal?
- Rivaroxaban and apixaban (As well as edoxaban) now have reversal agent • Andexanet alfa is specific reversal agent for Xa inhibitors
- Otherwise, 4-factor prothrombin complex concentrates can be given • Tranexamic acid has also been used and is recommended for lifethreatening bleeding in addition to the above
- Activated Factor VII concentrates have also been used, but are not recommended on a routine basis.
