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Pulmonary Embolism

Acute pulmonary embolism (PE) is a serious condition characterized by obstruction of the pulmonary artery, often arising from deep vein thrombosis. Diagnosis is complicated due to nonspecific symptoms and requires consideration of various risk factors, clinical decision tools, and imaging modalities. Treatment involves anticoagulation strategies, advanced therapies for high-risk cases, and careful monitoring to manage complications and long-term outcomes.

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0% found this document useful (0 votes)
83 views12 pages

Pulmonary Embolism

Acute pulmonary embolism (PE) is a serious condition characterized by obstruction of the pulmonary artery, often arising from deep vein thrombosis. Diagnosis is complicated due to nonspecific symptoms and requires consideration of various risk factors, clinical decision tools, and imaging modalities. Treatment involves anticoagulation strategies, advanced therapies for high-risk cases, and careful monitoring to manage complications and long-term outcomes.

Uploaded by

Kailash rana
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Pulmonary Embolism

Acute pulmonary embolism (PE) is a form of venous thromboembolism (VTE) that is


common and sometimes fatal.
The clinical presentation of PE is variable and often nonspecific making the diagnosis
challenging.
Pulmonary embolus (PE) refers to obstruction of the pulmonary artery or one of its
branches by material (eg, thrombus, tumor, air, or fat) that originated elsewhere in the
body.

Pathophysiology:

Pathogenesis hinges on Virchow's triad modifications: endothelial injury (surgery, trauma),


hypercoagulability (malignancy, thrombophilia), and venous stasis (immobility, heart failure)

Deep vein thrombosis (DVT) serves as the embolic source in 70-90% of PE cases, with pelvic
and proximal lower extremity veins constituting high-risk origins

Non-thrombotic emboli (amniotic fluid, tumor cells) represent <2% of incidents but require
distinct management pathways.
Symptomatology Spectrum
PE manifests along a clinical continuum:

Low-risk PE: Dyspnea (73%), pleuritic pain (66%), cough (37%)


Submassive PE: Tachycardia (>100 bpm), hypotension (SBP 90-100 mmHg), elevated
jugular venous pressure
Massive PE: Syncope, circulatory collapse (SBP <90 mmHg), cardiac arrest.

Classification:

The temporal pattern of presentation (acute, subacute, or chronic) – Patients with PE can
present acutely, sub-acutely, or chronically.
The presence or absence of hemodynamic stability (hemodynamically unstable or stable)
The anatomic location (saddle, lobar, segmental, subsegmental)
The presence or absence of symptoms (symptomatic or asymptomatic)

PRE-DISPOSING FACTORS FOR VENOUS THROMBOEMBOLISM

STRONG FACTORS (OR> 10)


Fracture of lower limb
Hospitalization for heart failure or atrial fibrillation/flutter (within previous 3 months)
Hip or knee replacement
Major trauma
Myocardial infarction (within previous 3 months)
Previous VTE
Spinal cord injury

MODERATE RISK FACTORS (OR 2-9)

Arthroscopic knee surgery


Autoimmune diseases
Blood transfusion
Central venous lines
Intravenous catheters and leads
Chemotherapy
Congestive heart failure or respiratory failure
Erythropoiesis-stimulating agents
Cancer (highest risk in metastatic disease, pancreatic cancer, haematological
malignancies, lung cancer, gastric cancer, and brain cancer carry the highest risk)
Hormone replacement therapy (depends on formulation)
In vitro fertilization
Oral contraceptive therapy
Post-partum period
Infection (specifically pneumonia, urinary tract
infection, and HIV)
Inflammatory bowel disease
Paralytic stroke
Superficial vein thrombosis
Thrombophilia

WEAK RISK FACTORS (OR < 2)

Bed rest >3 days


Diabetes mellitus
Arterial hypertension
Immobility due to sitting (e.g. prolonged car or air travel)
Increasing age
Laparoscopic surgery (e.g. cholecystectomy)
Obesity
Pregnancy
Varicose veins

ECG CHANGES:

Electrocardiogram (ECG) abnormalities, although common in patients with suspected PE,


are nonspecific.
The most common findings are tachycardia and nonspecific ST-segment and T-wave
changes (70 percent).
ECG abnormalities that are associated with a poor prognosis in patients diagnosed with PE
include:
Atrial arrhythmias (eg, atrial fibrillation)
Bradycardia (<50 beats per minute) or tachycardia (>100 beats per minute)
New right bundle branch block
Inferior Q-waves (leads II, III, and aVF)
Anterior ST-segment changes and T-wave inversion
S1Q3T3 pattern
CHEST X RAY:

Nonspecific abnormalities on chest radiography are common (eg, atelectasis, effusion) in


PE, but a normal chest radiograph can be seen in 12 to 22 percent of patients.
Fleischner sign: enlarged pulmonary artery (20%)
Hampton hump: peripheral wedge of airspace opacity and implies lung infarction (20%)
Westermark sign: regional oligemia and highest positive predictive value (10%)
Pleural effusion (35%) - pleural effusions in pulmonary embolism
Palla sign : enlarged right descending pulmonary artery
Chang sign : dilated right descending pulmonary artery with sudden cut-off

2D-ECHO (TTE): Look for Right Ventricular pressure Overload


SCORES (clinical decision rules):
GENEVA SCORE- ORIGINAL AND SIMPLIFIED

WELL’S SCORE

Regardless of the score used, the proportion of patients with confirmed PE can be expected
to be
10% in the low-probability category,
30% in the moderate-probability category,
65% in the high-probability category.
When the two-level classification is used, the proportion of patients with confirmed PE is
12% in the PE-unlikely category and 30% in the PE-likely category.

D-Dimer Testing
Quantitative ELISA assays demonstrate 95% sensitivity when combined with low clinical
probability (Wells ≤4 or Geneva ≤5).
Age-adjusted cutoffs (age × 100 ng/mL for patients >50 years) reduce false positives without
compromising safety (YEARS)

troponin testing indicated for right heart strain.

Imaging Modalities

Modality Sensitivity Specificity Radiation (mSv)


CTPA 98% 94% 4-20
V/Q scan 77% 98% 2-5
MRPA 78% 99% 0

CT pulmonary angiography (CTPA) remains first-line for hemodynamically stable patients, while
ventilation-perfusion (V/Q) scanning preserves utility in renal insufficiency or contrast allergies.
Emerging MR pulmonary angiography (MRPA) techniques show promise for pregnant patients
despite longer acquisition times
STEP 1: Suspect PE ion patients with Dyspnea, Shock, Cardiac Arrest, Syncope, Hemoptysis,
Chest Pain, others

STEP 2: Look for factors with high and moderate risk for VTE

STEP 3: Use Clinical Decision Tools (Wells/Geneva)


STEP 4: Send D-Dimers in moderate risk (or PE unlikely group as per 2 level Wells) and CT-PA
or other imaging for high risk.

STEP 5: Use PERC rule for low risk group to rule out PE (send d-dimer if PERC positive)

STEP 6: Confirm Diagnosis and Treat Or rule out PE

TREATMENT

Therapeutic Management Protocols


Anticoagulation Strategies
Initial Phase (0-7 days):

Parenteral overlap: Enoxaparin 1 mg/kg BID with warfarin (INR 2-3)


DOAC monotherapy: Apixaban 10 mg BID ×7 days then 5 mg BID

Maintenance Phase (3-6 months):

Agent Dose Renal Adjustment


Rivaroxaban 20 mg OD CrCl <30: Avoid
Apixaban 5 mg BID CrCl <25: 2.5 mg BID
Edoxaban 60 mg OD CrCl 15-50: 30 mg OD

Advanced Therapies for High-Risk PE


1. Systemic Thrombolysis: Alteplase 100 mg over 2 hours (Mortality RR 0.53 vs heparin)
2. Catheter-Directed Therapy: Ultrasound-assisted thrombolysis (20 mg tPA over 15 hours)
3. Surgical Embolectomy: Reserved for contraindications to thrombolysis with RV
dysfunction

Risk Stratification Frameworks


Pulmonary Embolism Severity Index (PESI)
This 11-variable model stratifies 30-day mortality risk

Class Points Mortality


I ≤65 1.1%
Class Points Mortality
II 66-85 3.1%
III 86-105 7.9%
IV 106-125 14.5%
V >125 24.5%

Simplified PESI (sPESI)


A pragmatic adaptation retaining prognostic accuracy

1. Age >80 (+1)


2. History of cancer (+1)
3. Chronic cardiopulmonary disease (+1)
4. Heart rate ≥110 (+1)
5. SBP <100 mmHg (+1)
6. Arterial O₂ saturation <90% (+1)

≥1 point indicates intermediate-high risk (3-15% mortality) warranting advanced monitoring.

Discharge Criteria and Follow-Up Monitoring


Outpatient Management Eligibility
4. sPESI 0
5. Normal RV function (TTE RV/LV ratio <1.0)
6. Absence of hypoxia (SpO₂ ≥95% room air)
7. No active bleeding or renal impairment (CrCl >30 mL/min)

Post-Discharge Surveillance
Weekly clinical assessment ×4 weeks
D-Dimer at 3 months (predicts recurrence risk)
CT follow-up at 6 months for residual thrombosis

Complications and Long-Term Sequelae


Acute Complications
Complication Incidence Management
Recurrent PE 4-6% Switch to LMWH if DOAC
failure
Major Bleed 2-4% Idarucizumab for dabigatran
reversal
Chronic Thromboembolic Pulmonary 0.5-3.9% Pulmonary endarterectomy
Hypertension (CTEPH)

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