1. Deep Vein Thrombosis & Pulmonary Embolism

2. Deep Vein Thrombosis Etiology: According to Virchow’s triad
Changes in the vessel wall (endothelial damage)
Changes in the blood flow (stasis)
Changes in blood composition (hypercoagulation)

3. Clinical Presentation:
Asymptomatic
Pain, redness, swelling with difficulty in walking
Features of pulmonary embolism may be the presenting feature in 30% of the patients

4. On examination: Pitting oedema of the ankle, Dilated surface veins,
A stiff calf
Tenderness.
Homans’ sign
A low-grade pyrexia may be present
Signs of pulmonary embolism or pulmonary hypertension

5. Investigations: D-dimer measurement Duplex ultrasound
Ascending and descending venography

6. Prophylaxis:
Low risk: young, with minor illnesses, who are to undergo operations lasting 30 min or less.
Moderate risk: over 40 or with a debilitating illness or are to undergo major surgery.
High risk: over 40 who have serious medical conditions, or undergoing major surgery with an additional risk factor.

7. Methods of prophylaxis:
Mechanical methods:
graduated elastic compression stockings
external pneumatic compression
passive foot movement (foot paddling machine)
simple limb elevation
Pharmaceutical methods:
low molecular weight heparin
unfractionated heparin
warfarin

8. Graduated elastic compressive stocking

9. External pneumatic compression

10. Foot Paddling Machine

11. Treatment: Medical conservative treatment: Surgical treatment Bed rest
Elevation
Bandage
anticoagulation
Thrombolytic therapy (phlegmasia cerulea dolens )
Surgical treatment
Venous thrombectomy
IVC filter

12. Pulmonary embolism ½ times as common as MI
3 times more common than CVA
3rd most common cause of death
Majority are silent
Acute major PE  15-20%
die within 48 hours

13. Pathophysiology: Hemodynamic effect depends on
the size of the embolus,
the degree of PA obstruction
the pre-embolus pulmonary function
The degree of PA obstruction depends on
Mechanical obstruction
Hormonal obstruction
50-60% of PA obstructed  symptoms
PA obstruction  RV failure   Cardiac output

14. Clinical presentation:
Minor Pulmonary Embolism:
Tachycardia, rales, low-grade fever, pleural rub.
Heart sounds and systemic blood pressure are often normal.
ABG are normal.
Pulmonary angiograms: less than 30% occlusion of the pulmonary arterial vasculature

15. Major (submassive) Pulmonary Embolism:
Dyspnea, tachypnea, dull chest pain, ± syncope
Tachycardia, mild to moderate hypotension, and elevation of central venous pressure.
Adequate cardiac output.
ABG: moderate hypoxia, and mild hypocarbia.
Echocardiograms may show right ventricular dilatation.
Pulmonary angiograms indicate that 30–50% of the pulmonary vasculature is blocked

16. Massive pulmonary embolism:
Dyspnea, tachypnea, sweating ± loss of consciousness
Urine output falls, and peripheral pulses are poor
Tachycardia, hypotension, CVP with distended neck veins
Low cardiac output and cardiac arrest may occur
ABG: severe hypoxia, hypocarbia, and acidosis
Echo.; Dilated RV and RV failure
Pulmonary angiography: more than 50% occlusion of pulmonary vasculature

17. Investigations: ECG: tachycardia and nonspecific changes.
CXR oligemia or linear or triangular consolidation,
Ventilation–perfusion (V/Q) areas of normal ventillation with poor perfusion.
Pulmonary angiograms: filling defects or obstruction of pulmonary arterial branches.
Echocardiography

22. Medical treatment: Supplementary O2 Mechanical ventilation
Invasive cardiac monitoring
Pharmaceutical myocardial support, mechanical myocardial support
Immediate anticoagulation with i.v. heparin
Consider thrombolysis in patients with major-to-massive pulmonary embolism.

23. Surgical treatment: Emergency pulmonary embolectomy is indicated in
Critical hemodynamic instability or severe respiratory distress
thrombolytic or anticoagulation therapy is contraindicated,
The presence of a large clot trapped within the right atrium or ventricle

29. Thank You