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PE and bleeding and clotting, oh my!

Dr. Salazar presents a post-op patient with a 1 day history of shortness of breath that is progressively worsening, ultimately diagnosed with a pulmonary embolism.


1. Diagnosis of pulmonary embolism:


EKG findings, although common with suspected PE, are non-specific. The most common findings are tachycardia and nonspecific ST-segment and T-wave changes (in about 70% of cases).


Abnormalities more suggestive of PE (S1Q3T3 pattern, RV strain, new incomplete RBBB) only appear in less than 10% of cases.


EKG can help with prognosis. Those associated with poor prognosis include:

  • Atrial arrhythmias - atrial fibrillation

  • Bradycardia (<50) or tachycardia (>100)

  • New RBBB

  • Inferior Q waves (leads II, III, and aVF)

  • Anterior ST-segment changes and T-wave inversion

  • S1Q3T3 pattern

For most patients with suspected PE, CTPA is the first-choice testing. It is most sensitive and specific for the diagnosis of PE. This radiology protocol uses thin (</= 2.5 mm) slices after a bolus administration of IV contrast that is timed for maximal enhancement of pulmonary arteries. The patient may need to hold their breath for approximately 30 seconds. A CT chest w/ contrast that is NOT performed with PA protocol may incidentally detect a PE, but is not adequate for exclusion of a PE.


 

2. What is the role for obtaining an echo?

An echo is not sensitive or specific for diagnosis of PE. In a hemodynamically unstable patient with suspected PE, it may demonstrate clot or new R heart strain that could quickly justify the use of thrombolytic therapy.


Although limited diagnostically, echo can be very useful prognostically in a patient with confirmed PE. 30-40% of patients with PE have echo findings of RV strain or pressure overload. Data does support that the extent of RV dysfunction correlates to the degree of perfusion defects on lung scans.


Findings to suggest RV dysfunction:

  • Increased RV size

  • Decreased RV function

  • Tricuspid regurgitation

  • Abnormal septal wall motion

  • McConnell's sign: regional wall motion abnormalities that spare the RV apex (insensitive - 77%, but can be used to differentiate between acute PE and pulmonary HTN, which has more global dyfunction)


Additional findings that are worrisome:

  • RV thrombus

  • Pulmonary artery thrombus


 

3. Management depends on hemodynamic stability.

---> Hemodynamically stable:



---> Hemodynamically unstable:



Takaway points from studies reviewed by Dr. Salazar:

  • When using thrombolytics, there was seen to be less hemodynamic decompensation at 7 days with fibrinolysis, however also noted increased bleeding.


 

4. What does the data say about post-orthopedic surgery DVT prophylaxis?

-At baseline, hip/knee arthroplasty, hip fracture surgery, and pelvic fracture surgery are considered high risk of thrombosis (baseline risk for 35 days pos-op is 4.3%, highest risk in first 7-14 days).

-If patients are low bleeding risk, recommend pharmacologic prophylaxis - preferring LMW heparin or DOACs (rivaroxaban or apixaban), UFH if patient has renal insufficiency. Aspirin should not be used as sole initial agent for VTE ppx, but can be switched to after a short course (5 days) of rivaroxaban

-For patients with contraindications to ppx or at high risk off bleeding, recommend IPC

-Per ACCP - minimum recommended duration is 10-14 days, but if the pt doesn't have increased bleeding risk, extended-duration ppx up to 35 days is preferred

-Recommends against the routine placement of IVC filter for VTE ppx, recommend against routine surveillance for VTE with venous compression US



Caprini score only validated in patients undergoing non-orthopedic surgery.


The orthopedic literature is slightly different. They have a decent amount of studies demonstrating efficiency of Aspirin in DVT/PE prophylaxis

  • Pooled rate of DVT was 1.2%

  • Pooled rate of PE was 0.6%

  • Rates of major bleeding episodes is low, only 0.3%

  • There have been non-inferiority trials - demonstrating aspirin only did not have higher risk of subsequent VTE than did patients who received anticoagulants

  • Evidence still is of limited quality and has been heterogenous in regards to dosage and duration

  • Warfarin ppx has demosntrated a higher risk of complications - needs for transfusion, hemorrhage, etc

further reading:



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