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PULMONARY EMBOLISM
Deep venous thrombosis (DVT)
clottingof blood in a deep vein of an
extremity (usually calf or thigh) or the
pelvis.
DVT is the primary cause of pulmonary
embolism. DVT results from conditions
that impair venous return, lead to
endothelial injury or dysfunction, or
cause hypercoagulability.
PATHOPHYSIOLOGY
VIRCHOWS TRIAD
Stasis of blood
Vessel damage
Increased blood coagulability
Variable Score
Age >65 1
Previous DVT or PE 1
Surgery or fracture within 1 month 1
Active malignancy 1
Unilateral lower limb pain 1
Hemoptysis 1
Pain on deep vein palpation of
1
lower limb and unilateral edema
Heart rate 75 to 94 bpm 1
Heart rate greater than 94 bpm +1
Score of less than 2 is low probablility for PE, score of less than 2 plus a
negative D-dimer results in a likelihood of PE of 3%
DIAGNOSTIC
PATHWAYS
Diagnostic Algorithm
Algorithm for Diagnosis of Pulmonary Embolism
Clinical sign & symptoms
of PE
Wells Score
Start heparin if >6, Perform D-dimer
test
PE less likely PE likely
Perform
D-dimer CTPA
R/w clinical probability & D dimer Diagnosis of
results PE
VTE Treatment
PE less likely & PE likely & - PE likely algorithm
+ D dimer D dimer with + D
results results dimer results
Perform Ultrasou
Risk of PE is low.
duplex nd
Consider other
ultrasound of results?
diagnosis
the leg
Venous Thromboembolism Treatment Algorithm
Diagnosis of DVT/PE
No
Complicated thromboembolism of
comorbidities?
LMWH , UFH/
Fondaparinex
Warfarin
Outpatient
OP treatment appropriate? protocol
Patient
Inpatient education
treatment
Other Complication
Therapies during therapies
Anticoagulation
Cnt. Anticoagulation with Failure?
followup & secondary
DIAGNOSTIC TESTS
ABG
Usually shows hypoxia, hypocapnia, respiratory
alkalosis
A-a gradient:
Normal 7-14 depending on age
Increases with age, FiO2 and supine posture
Estimate of normal for age:
Age/4 +4
A-a gradient = (FiO2 x713 pCO2/0.8) PaO2
If A-a gradient normal, PaO2 <80, Pa CO2 >45
then hypoventilation accounts for hypoxia
Increased A-a gradient occurs in V/Q
mismatch, shunting and any kind of barrier to
diffusion (e.g. pulmonary edema)
BUT can be normal and still have PE!
D-dimer
It specific degradation product of cross-linked fibrin.
Non-pharmacological
These include lifestyle changes like
Avoid smoking
Eating a healthy balanced diet
Getting regular exercise and
Maintaining ahealthy weight or losing weight if patient
obese
Leg Raising:This reduces the pressure in the calf veins
ANTICOAGULANTS
40
42
Low-Molecular-Weight Heparins
43
Successful fibrinolytic therapy rapidly reverses right heart failure and may
result in a lower rate of death and recurrent PE by
(1) dissolving much of the anatomically obstructing pulmonary arterial
thrombus
(2) preventing the continued release of serotonin and other neurohumoral
factors that exacerbate pulmonary hypertension
(3) lysing much of the source of the thrombus in the pelvic or deep leg
veins, thereby decreasing the likelihood of recurrent PE.
The preferred fibrinolytic regimen is 100 mg of recombinant tissue
plasminogen activator (tPA) administered as a continuous peripheral
intravenous infusion over 2 hours. Patients appear to respond to
fibrinolysis for up to 14 days after the PE has occurred.
Contraindications to fibrinolysis include intracranial disease, recent
surgery, and trauma. The overall major bleeding rate is about 10%,
including a 13% risk of intracranial hemorrhage.
The only FDA-approved indication for PE fibrinolysis is massive PE
Surgical Options
52
Pulmonary Embolectomy :
The risk of intracranial hemorrhage with fibrinolysis has prompted a
renaissance of surgical embolectomy. More prompt referral before the onset of
irreversible cardiogenic shock and multisystem organ failure and improved
surgical technique have resulted in a high survival rate. A possible alternative
to open surgical embolectomy is catheter embolectomy. P
Pulmonary Thromboendarterectomy :
Chronic thromboembolic pulmonary hypertension occurs in 24% of acute PE
patients. Therefore, PE patients who have initial pulmonary hypertension
(usually diagnosed with Doppler echocardiography) should be followed up at
about 6 weeks with a repeat echocardiogram to determine whether pulmonary
arterial pressure has normalized. Patients impaired by dyspnea due to chronic
thromboembolic pulmonary hypertension should be considered for pulmonary
thromboendarterectomy, which, if successful, can markedly reduce, and at
times even cure, pulmonary hypertension. The operation requires median
sternotomy, cardiopulmonary bypass, deep hypothermia, and periods of
hypothermic circulatory arrest. The mortality rate at experienced centers is
approximately 5%.
Methods of DVT Prophylaxis
Mobilization
Graduated compression stockings
Intermittent pneumatic compression
Aspirin
Unfractionated heparin 5000 s.c TDS
Low-molecular weight heparins
Enoxaparin(0.4cc), Dalteparin(5000 U daily)
Vitamin K antagonists
Warfarin, acenocoumarol, phenindione, & dicoumarol