1. Deep Venous Thrombosis ROSENS EM MAJIDI ALIREZA RESIDENT OF EM SBMU

2. Pathophysiology of Thrombosis
VTE represents the end product of imbalanced
clot formation versus clot breakdown.
Factors that enhance fibrin
formation include systemic inflammation (which
includes almost all so-called acquired states of hypercoagulability
sluggish blood flow in large
veins permits the process of fibrin deposition.

3. Hypercoagulable states:
Three generic factors promote clotting
Hypercoagulable states:
Cancer
Nephrotic syndrome
Sepsis
Inflammatory conditions:
Ulcerative colitis
Increased estrogen:
Pregnancy
Oral contraceptives
Antiphospholipid syndrome
Protein S, C, and antithrombin III deficiencies, Factor V Leiden, prothrombin gene mutations, others
Stasis:
Prolonged bed rest
Immobility (such as from a cast)
Long plane, car or train ride
Neurologic disorders with paralysis
Congestive heart failure
Obesity
Vascular damage:
Trauma
Surgery
Central lines:
Especially with upper extremity DVT
Multifactorial issues:
Advancing age:
Prior DVT or PE

4. Pathophysiology of Thrombosis
Virchow,
triad of venous injury, slow blood flow, and hypercoagulability
as the cardinal factors that the clinician
should use to classify a patient as at risk for excessive
fibrin deposition relative to fibrin removaL'

5. Pathophysiology of Thrombosis
DVT represents a disease spectrum ranging from a minimally
symptomatic isolated calf vein thrombosis to
a limb-threatening iliofemoral venous obstruction.

6. Anatomy calf veins deep venous system includes the anterior
The venous anatomy of the lower extremity can be
divided into the deep and superficial systems
deep venous system includes the anterior
tibial, posterior tibial, and peroneal veins,
calf veins
Proximal DVT refers to clot in the
popliteal vein or higher, whereas distal clot refers to an isolated calf vein thrombosis

7. Clinical Presentation
The initial symptoms of DVTcan be as subtle and nonspecific
as a mild cramping sensation or sense of fullness
in the calf, without objective swelling, and may be
difficult to differentiate clinically

8. Clinical Presentation
6 mo
recent
;,3 days
tenderness
3 cm larger
Pitting edema
Alternative

9. Diagnosis Estimation of the pretest probability of DVT is the
initial step in the diagnostic strategy.
Contrast venography has been considered the gold
standard in the evaluation of DVT and has the advantage
of being able to differentiate between acute and
chronic thrombus

10. Diagnostic Tests for DVT tintinali

11. Diagnosis hours. Venous duplex ultrasonography has
a sensitivity and specificity of approximately 95% for
proximal DVT and is the diagnostic test of choice in most centers
plasma concentration indicates the presence of clot
formed somewhere in the body within the past 72
hours.

12. Diagnosis D-Dimer concentration is elevated with any condition
fibrin deposition, including malignancy,
pregnancy, advanced age, prolonged bed rest,
recent surgery, infection, inflammation, new indwelling
catheters, stroke, and myocardial infarction

13. Diagnosis a negative D-dimer result excludes
the diagnosis ofDVT only in patients with a low pretest
probability of disease.

14. Diagnosis Magnetic resonance imaging (MRI) can image the
pelvic vasculature and vena cava,
Impedance plethysmography and strain-gauge plethysmography
measure changes in venous outflow
from the extremities to diagnose DVT.

15. Differential Diagnosis

16. Treatment
When the diagnosis of DVT has been established, anticoagulation
should be initiated, unless contraindicated
un fractionated heparin (80 U/kg
intravenous bolus followed by 18 U/kg/h infusion)
enoxaparin,
1 mg/kg subcutaneously every 12 hours)
Treatment
requires anticoagulation with warfarin for
at least 3 months.
6- or 8-hour delay

17. Treatment starting with
a dose of 10 mg of warfarin sodium in most adults
achieves a therapeutic effect faster and without
increase in bleeding complications."

18. Superficial Thrombophlebitis
many patients with clinically suspected superficial
thrombophlebitis have a synchronous DVT
Patients
with clot in the greater saphenous vein thatextends
above the knee are at risk for progression to DVT via the saphenous-femoral junction and should be considered for anticoagulation.

19. Superficial Thrombophlebitis
superficial thrombophlebitis should be
treated symptomatically with nonsteroidal antinflammatory
drugs, heat, and graded compression stockings
(fitted to exert 30 to 40 mm Hg of pressure on the
extremity). Increased ambulation and elevation of the
extremity above the level of the heart while at rest help
to decrease venous stasis. Routine anticoagulation is
not indicated for superficial thrombophlebitis

20. Isolated Calf or Saphenous Vein Thrombosis
saphenous, tibial or peroneal veins remains controversial.
Longitudinal studies subsequently
found that approximately 25% of isolated calf vein
thromboses propagate proximally, prompting many
experts to recommend treatment with anticoagulation
as for DVT.
healthy, ambulatory patient with an
isolated calf thrombus and no other indication for anticoagulation
is to prescribe anti platelet therapy with
aspirin (325 mg/day

21. Phlegmasia Cerulea Dolens (Painful Blue Leg)
Massive iliofemoral occlusion results in swelling of the
entire leg with extensive vascular congestion and associated
venous ischemia producing a painful, cyanotic
extremity.
arterial spasm
resulting in phlegmasia alba dolens (painful white leg
or milk leg), which may mimic an acute arterial occlusion.

22. Upper Extremity Venous Thromboses
associated most often with
central venous catheters, pacemakers, and malignancies
Upper extremity DVT can cause PE, and all
patients with upper extremity DVT require definitive
treatment.B.'
Anticoagulation usually is indicated, and
thrombolysis should be considered to treat apparent
phlegmasia cerulea dolens of the arm.

23. Complications fatal PE chronic venous varicose veins
insufficiency, resulting in disabling pain and swelling
varicose veins
skin changes
nonhealing ulcers

24. Pathophysiology of Thrombosis
Aging leads to venous valvular incompetence, which
impairs venous return, and causes blood stasis; aging
also increases the probability of an acquired hypercoagulability,
such as malignancy. Older patients have
more cumulative effects of inflammatory damage to
venous endothelium and are more likely to be exposed
to the independent risk factor of surgery. Older patients
may be predisposed to dehydration, which probably
accelerates clot deposition. Older patients are more
likely to have heart and lung disease,

25. Discharge Criteria 5-minute
Outpatient treatment with a LMWH:
No serious concomitant disease that requires hospitalization
Patient has means of communication and transportation to return to the hospital if needed.
Patient (or family member) is willing and able to inject the medication.
Patient needs hematocrit, platelet count, and international normalized ratio (INR) checked in two to three days.
aPTT does not need to be checked.
Heparin-induced thrombocytopenia is less common with the LMWH but still occurs.
INR needs to be checked at about day three.
Patients with superficial or distal thrombophlebitis can be discharged with close follow-up.