Aortic Dissection/Venous Thromboembolism Flashcards

1
Q

Cases per year of aortic dissection? What allows this to happen?

A

• 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

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2
Q

Explain the Stanford Classification?

A

• 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

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3
Q

DeBakey Classification?

A

• DeBakey classification • Type I Ascending and descending • Type II Ascending only • Type III Descending only

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4
Q

Causes of Aortic Dissection?

A

• 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

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5
Q

Physical symptoms of Aortic dissection?

A

• 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

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6
Q

Imaging for Aortic stenosis?

A

• 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

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7
Q

Physical exam findings of Aortic dissection?

A

• 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.

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8
Q

Aortic Dissection mortality rates?

A

 Mortality 1-2% per hour in first 24 hours

 50% first week

 75% first month

 90% first year

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9
Q

Management of Aortic Dissection?

A
  • 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.

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10
Q

Risk factors for Aortic Dissection?

A

Aortic Dissection
• Advanced age

  • Aneurysm leak
  • Concominant CAD
  • Renal Failure
  • Pericardial effusion/tamponade
  • Shock
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11
Q

Most Venous thromboembolism are? Incidence? Mortality?

A
  • 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
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12
Q

What is Virchow’s Triad? This is a must know.

A
  • Hypercoagubility • Surgery • Cancer • Inherited disorders
  • Stasis (IE immobility or anatomical factors reducing blood flow) • May-Thurner
  • Endothelial injury
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13
Q

Risk factors for Venous thromboembolism?

A
  • 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
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14
Q

Hemostasis process?

A
  • 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
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15
Q

DVT should be suspected in patients with what features?

A
  • 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
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16
Q

Pulmonary embolism presenting features?

A
  • 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)
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17
Q

Physical findings of DVT? PE?

A
  • 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)
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18
Q

EKG findings of PE?

A
  • 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.
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19
Q

Right heart strain on EKG is characterized by? Seen in what conditions?

A
  • 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
20
Q

Labs and tests for PE?

A
  • 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
21
Q

What does this chest X-ray show?

A

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

22
Q

What does this Chest X-ray show?

A

Westermark’s Sign:

Demonstration of a sharp cut-off of pulmonary vessels with distal hypoperfusion in a segmental distribution within the lung

23
Q

Explain Ultrasound for DVTs? which veins can be assessed?

A
  • 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
24
Q

What are the deep veins in the legs?

A

Superficial femoral vein is also a deep vein (trick question on boards). This is also called “femoral vein”

25
Q

Best imaging modality for PE?

A
  • 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
26
Q

What is a v/q scan?

A
  • 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
27
Q

What is a Provoked DVT? Proximal DVT? Renal impairment? Unprovoked DVT or PE?

A
  • 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
28
Q

How do we evaluate DVT?

A
  • 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
29
Q

Evaluation of PE?

A
  • 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
30
Q

How to evaluate hemodynamic status in PE?

A

• ”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

31
Q

Treatment of DVT?

A
  • 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
32
Q

consider catheter directed thrombolytic therapy when?

A
  • 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.
33
Q

Inferior vena cava filters?

A
  • 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
34
Q

Treatment of a Pulmonary Embolism?

A
  • 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
35
Q

Anticoagulation in VTE?

A
  • 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
36
Q

What are the methods of anticoagulation?

A
  • 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)
37
Q

Explain warfarin?

A
  • 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
38
Q

Explain Heparin and its analoges?

A
  • 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)
39
Q

Explain the direct factor 10 inhibitors?

A
  • 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
40
Q

Explain Dabigatran?

A
  • 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
41
Q

Duration of therapy and special considerations for therapy in VTE?

A
  • 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
42
Q

Should we test for Hypercoagulability disorders?

A
  • 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
43
Q

What is the most common heritable hypercoaguble state? Others? Hypercoaguable state with most risk of recurrent VTE?

A
  • 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
44
Q

Anticoagulation reversal with warfarin?

A
  • 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
45
Q

Oral Anticoagulant reversal?

A
  • 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.