Explore the complex diagnosis and management of acute pulmonary embolism, where subtle symptoms can lead to serious outcomes. Learn about the critical risk factors, from recent surgeries to genetic predispositions, and the importance of precise risk stratification. The hosts delve into various presentation signs, treatment protocols, and advanced resuscitation techniques. Discover the role of biomarkers and imaging methods in assessing patient conditions. Plus, get insights into outpatient management and key takeaways for effective care.
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question_answer ANECDOTE
Missed Anticoagulation Caused Massive PE
A 70-year-old woman had ROSC after collapse and CTA showed a large saddle PE with severe right heart strain.
Family later revealed an inherited hypercoagulable disorder and interrupted apixaban therapy.
insights INSIGHT
Scope And Origins Of Pulmonary Embolism
PE usually originates from proximal lower extremity DVTs but can be tumor, air, or fat emboli.
Incidence in the USA is roughly 300–370k cases yearly with 60–100k deaths.
volunteer_activism ADVICE
Recognize High-Risk Presentations Quickly
Look for dyspnea, pleuritic chest pain, hemoptysis, syncope, and abnormal vitals when assessing for PE.
Activate PERT and treat emergently if systolic BP <90 for >15 minutes, need vasopressors, or signs of shock.
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Definition: Obstruction of pulmonary arteries, usually from a DVT in the proximal lower extremity veins (iliac/femoral), but may be tumor, air, or fat emboli.
Incidence & Mortality: 300,000–370,000 cases/year in the USA, with 60,000–100,000 deaths annually.
Mantra: “Don’t anchor on the obvious. Always risk stratify and resuscitate with precision.”
Risk Factors: Broad, including older age, inherited thrombophilias, malignancy, recent surgery/trauma, travel, smoking, hormonal use, and pregnancy.
Clinical Presentation and Risk Stratification
Presentation: Highly variable, showing up as anything from subtle shortness of breath to collapse.
Acute/Subacute:Dyspnea (most common), pleuritic chest pain, cough, hemoptysis, and syncope. Patients are likely tachycardic, tachypneic, hypoxemic on room air, and may have a low-grade fever.
Chronic: Can mimic acute symptoms or be totally asymptomatic.
Pulmonary Infarction Signs: Pleuritic pain, hemoptysis, and an effusion.
High-Risk Red Flags: Signs of hypotension (systolic blood pressure < 90 mmHg for over 15 minutes), requirement of vasopressors, or signs of shock → activate PERT team immediately.
History/Scoring: Ask about prior clots, recent surgeries, hospitalizations, travel. Use Wells/PERC criteria to assess pretest probability.
Labs:
D-dimer: A good test to rule out PE in a patient with low probability. If suspicion is high, proceed directly to imaging.
Troponin/BNP: Act as RV stress gauges. Elevated levels are associated with increased risk of a complicated clinical course (25-40%).
Lactate: Helpful in identifying patients in possible cardiogenic shock.
EKG: Most common finding is sinus tachycardia. Classic RV strain patterns (S1Q3T3, T-wave changes/inversions) are nonspecific.
Imaging:
CXR: Usually normal, but quick and essential to rule out other causes.
CTPA: The usual standard and gold standard for stable patients. High sensitivity (> 95%) and can detect RV enlargement/strain.
V/Q Scan: Option for patients with contraindications to contrast (e.g., severe contrast allergies).
POCUS (Point-of-Care Ultrasound): Useful adjunct for unstable patients.
Bedside Echo: Can show signs of RV strain (enlarged RV, McConnell sign).
Lower Extremity Ultrasound: Can identify a DVT in proximal leg veins.
Treatment & Management
Resuscitation (Reviving the RV):
Oxygenation: Give supplementally as needed (nasal cannula, non-rebreather, high flow).
Intubation:Avoid if possible; positive pressure ventilation can worsen RV dysfunction.
Fluids:Be judicious; even the smallest amount can worsen RV overload.
Vasopressors:Norepinephrine is preferred as first-line for hypotension/shock.
Anticoagulation (Start Immediately):
Initial choice is UFH or LMWH (Lovenox).
Lovenox is preferred for quicker time to therapeutic range, but is contraindicated in renal dysfunction, older age, or need for emergent procedures.
DOACs can be considered for stable, low-risk patients as an outpatient.
Escalation for High-Risk PE
Systemic Thrombolytics: Consider for very sick patients with shock/cardiac arrest (e.g., Alteplase 100 mg over two hours or a bolus in cardiac arrest). High risk of intracranial hemorrhage; weigh risks versus benefits.
PERT Activation: Engage multidisciplinary teams (usually including ICU, CT surgery, and interventional radiology).
Interventions: Consult specialists for catheter-directed thrombolysis or suction embolectomy. Surgical embolectomy can also be considered.
Bridge to Care: Activate the ECMO team early for unstable patients to buy valuable time.
Prognosis & Disposition
Mortality: Low risk < 1%; intermediate 3-15%; high risk 25-65%.
Complications: 3-4% of patients develop Chronic Thromboembolic Pulmonary Hypertension (CTEPH). Others may have long-term RV dysfunction and chronic shortness of breath.
Recurrence: ∼ 30% chance in the next few weeks to months, if not treated correctly.
Disposition:
ICU: All high-risk and some intermediate-high risk patients.
Regular Floor: Intermediate-low risk patients.
Outpatient Discharge:Low-risk patients can be sent home on anticoagulation. Use PSI or HESTIA scores to risk stratify suitability, typically starting a DOAC.
Shared Decision-Making: Critical to ensure care is safe and consistent with the patient’s wishes.