Dr. Balbaa
By
Mohammad Ashraf Balbaa, MD
Associate Professor of Surgery
Intrinsic pathway
HMW kininogen
XII
Prekallikerin
XIIa
HMW kininogen
XI
Extrinsic pathway
XIa
TPL
IX
VIIa
IXa
PL
VIII
Ca++
PL
VIIIa
Ca++
X
Xa
TPL
PL
Ca++
V
Prothrombin
Va
Thrombin
Fibrinogen
XIII
VII
XIIIa
Fibrin
Ca++
Dr. Balbaa
Definition:
 A venous thrombus is the formation of a
semi-solid coagulum within flowing blood in
the venous system.
Dr. Balbaa
Types:
 Superficial Thrombophlebitis
 Deep vein thrombosis
Dr. Balbaa
Dr. Balbaa


The term “Superficial Thrombophlebitis” is
customarily applied to any kind of
thrombotic process in the superficial venous
system.
However, it implies existence
inflammatory component, which
always present.
of an
is not
Dr. Balbaa
Definition:
 Localized inflammation of the vein wall
+
thrombus formation in the lumen
Dr. Balbaa
Etiology:
 Direct trauma.


A direct blow over a superficial vein can result in
phlebitis.
Venous intimal damage
Infusion of hypertonic solutions, injurious compounds
as antibiotics & chemotherapeutic agents and I.V. drug
abuse.
 Cannula insertion.


N.B. Traumatic thrombophlebitis can be put to
clinical use in the form of sclerotherapy.
Dr. Balbaa
Dr. Balbaa
Clinical Picture:
 The vein becomes painful, tender, firm &
cord-like.
 The overlying skin becomes dusky &
edematous.
Dr. Balbaa
Clinical Picture:
 Embolization is rare as the thrombus is firmly
adherent
 Sometimes, it is accompanied with DVT,
especially if there is marked edema that can
not be explained by simple or superficial
Dr. Balbaa
phlebitis alone.
Dr. Balbaa
Dr. Balbaa
Treatment:
 Prevention:

The best R/ for traumatic thrombophlebitis is
prevention by:
 Rotating IV sites every 3 days & changing IV tubing
regularly under sterile conditions
 Diluting irritant infusions.
Dr. Balbaa
Treatment:
 Conservative Measures :


Rest & elevation + elastic bandage.
Warm
compresses
+
non-steroidal
antiinflammatory drugs (NSAIDs) or aspirin. 
antibiotics.
Dr. Balbaa
Treatment:
 Surgical Measures:


If the thrombus propagates e.g. in the long
saphenous vein above the knee  ligation of the
sapheno-femoral junction, under local anesthesia.
Excision, in recurrent & symptomatizing phlebitis.
Dr. Balbaa
Types:
 Superficial Thrombophlebitis
 Deep vein thrombosis
Dr. Balbaa
INCIDENCE:
 Prevalence
 Site
 Side
•Occurs for the first time in about 100
persons per 100,000 each year in the
United States. This incidence increases
with increasing age.
•The
recurrence
rate
with
anticoagulation has been noted to be
6% to 7% in the ensuing 6 months.
Dr. Balbaa
INCIDENCE:
 Prevalence
 Site
 Side
Upper limb:
Axillary vein thrombosis.
Lower limb:
•venous plexus calf vein
thrombosis.
•Ilio-femoral thrombosis
(phlegmasia alba dolens PAD).
•Ilio-frmoral thrombosis + deep
pelvic vien thrombosis (phegmasia
cerulae dolans PCD).
Dr. Balbaa
INCIDENCE:
 Prevalence
 Site
 Side
Ilio-femoral thrombosis occurs on
the left side > right (3:1) due to:
•It is more liable to be
compressed by the overlying
right common iliac artery
against L5
•Left iliac vein is longer than
the right.
Dr. Balbaa
Dr. Balbaa
Etiology
A triad (posited by Virchow in 1856):
 Stasis
 Intimal damage
 Hypercoagulability
Dr. -1902
Balbaa
1821
Etiology
A triad (posited by Virchow in 1856):
 STASIS
 Intimal damage
 Hypercoagulability
Dr. Balbaa
STASIS:
 Stasis in the lower limb is associated with:

Immobilization during anesthesia, after trauma
and fractures, post operative recumbency &
serious illness.

Diminished cardiac function (heart failure).

Previous DVT: cannot maintain uni-directional
venous flow due to valvular incompetence.
Dr. Balbaa
Etiology
A triad (posited by Virchow in 1856):
 Stasis
 INTIMAL DAMAGE
 Hypercoagulability
Dr. Balbaa
INTIMAL DAMAGE
 It caused by:



Trauma & fractures.
Infusions.
Infection & toxemia.
Dr. Balbaa
Etiology
A triad (posited by Virchow in 1856):
 Stasis
 Intimal damage
 HYPERCOAGULABILITY
Dr. Balbaa
HYPERCOAGULABILITY
 1ry or familial causes:


Anti-thrombin III deficiency
Protein S or C deficiency
Dr. Balbaa
HYPERCOAGULABILITY
 2ry or acquired causes:

Malignancy, dehydration, toxemia and sepsis,
polycythemia, D.M., smoking, pregnancy &
post partum state.
Dr. Balbaa
RISK FACTORS


Patient factors
Disease or surgical
procedure
•Age ≥ 60 yr
•Obesity
•Immobility
•Pregnancy
•Puerperium
•High-dose estrogen therapy
•Previous deep vein thrombosis
or pulmonary embolism
Dr. Balbaa
RISK FACTORS


Patient factors
Disease or surgical
procedure
•Trauma or surgery, especially of
procedure pelvis, hip and lower limb
•Malignancy,
•Heart failure
•Paralysis of lower limb(s)
•Polycythaemia
Dr. Balbaa
PATHOGENESIS
1ry platelet thrombus
Mural Coralline thrombus
Occluding thrombus
Consecutive clot
Propagated clot
Dr. Balbaa
PATHOGENESIS
1ry platelet thrombus
Mural Coralline thrombus
Occluded thrombus
Consecutive clot
Propagated clot
Dr. Balbaa
PATHOPHYSIOLOGY
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Point of Difference
1. Major cause:
2. Clinical
Presentation:
Thrombophlebitis
Inflammation of the vein
wall
Pain
+
signs
of
inflammation
Phlebothrombosis
Stasis
&
hypercoagulability
Silent  few signs &
symptoms
3. Size of propagated Short & fixed
Large & easy detachable
clot:
liable
to
4. Emboli:
Less liable to embolization. More
embolization.
Dr. Balbaa

CONSEQUENCES OF THROMBOSIS
Dr. Balbaa



Locally
Distally
Proximally
Dr. Balbaa
LOCALLY
 Lysis:


Organization and fibrosis:


Results from fibrinolytic action of blood
→ retraction  post-phlebitic leg (CVI),
i.e. recanalization with valve destruction
Infection:

High virulence
emboli.
organisms
→
septic
Dr. Balbaa
Distally:
 A varying degree of edema after
which
venous
collateral
circulation soon opens up 
tortuous superficial veins, i.e. 2ry
VV.
 Phlegmasia alba and cerula.
 Post-phlebetic syndrome
Dr. Balbaa
Proximally:
 Detachment

pulmonary
embolism  pulmonary infarction
up to death.
Dr. Balbaa

CLINICAL PICTURE
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CLINICAL PRESENTATION
 DVT can be completely asymptomatic in
about 30-50% of cases.
Passed unnoticed
 Detectable PE, which may be sometimes fatal.
 Low grade fever which fails to settle after
operation.


By the occurrence of local signs of in the limb.
Dr. Balbaa

Swelling the extent of which depends on the
site of the thrombus → (frog-leg position):


Leg is externally rotated
The knee is flexed)
Dr. Balbaa


Aching pain and heaviness on moving the
calf and thigh.
Tenderness on pressure on the instep of the
sole of the foot and along the affected veins.
Dr. Balbaa


Increase warmth of the affected limb.
Varicose veins due to distension of the
superficial veins (late sign).
Dr. Balbaa
Certain tests:
 Homan's sign:

Dorsiflexion of the foot → resistance or pain of the
calf muscles to forcible dorsiflexion – is not
discriminatory and should be abandoned.
Dr. Balbaa
Certain tests:
 Pratt's sign:


Compression of the calf against tibia → pain.
Moses's sign:

Compression of the calf from side to side → pain.
Dr. Balbaa

Phlegmasia alba (white) dolens (pain)
(White Leg; Milk Leg)

Phlegmasia cerulae (blue) dolens
Dr. Balbaa
Dr. Balbaa
Dr. Balbaa

COMPLICATIONS
Dr. Balbaa

2ry varicose veins:


Venous gangrene:


2ry collaterals develop when the deep system is
occluded.
In PCD.
Pulmonary embolism:

When a thrombus becomes dislodged form its
attachment to the venous wall & is carried into the
pulmonary arteries
Dr. Balbaa
INVESTIGATIONS:
Dr. Balbaa
NON INVASIVE INVESTIGATIONS
 Doppler Ultrasonography
 Duplex Imaging
 Doppler Color Flow.
 Magnetic Resonance Venography (MRV)
Dr. Balbaa
NON INVASIVE INVESTIGATIONS
 Blood Tests

Breakdown products of complexed fibrin (fibrin
acted on by factor XIII) generated during
physiologic fibrinolysis (D-Dimer).

A negative D-dimer test in patients with suspected
DVT has a high negative predictive value. A
normal D-dimer reliably excludes DVT.
Dr. Balbaa
MANAGEMENT :
 Prophylaxis of DVT
 Treatment of established DVT


Conservative (non-operative) treatment
Operative surgical treatment
Dr. Balbaa
PROPHYLAXIS OF DVT
 Preoperative measures:

Mechanical prophylaxis:
 Elastic compression stockings.
 Intermittent pneumatic compression (IPC) devices:
Dr. Balbaa
PROPHYLAXIS OF DVT
 Preoperative measures:

Pharmacologic prophylaxis:
 Low-dose unfractionated heparin:
 5000 unites, CS, beginning 2 hours preoperatively
 Low-molecular weight heparin (LMWH):
 Dose is drug dependent, SC, twice daily, no monitoring
or dose adjustment.
Dr. Balbaa
Dr. Balbaa
PROPHYLAXIS OF DVT
 Operative measures:

Reduction of trauma to the calf muscles during
surgery; the operating table should be well padded
to decrease the pressure on the buttocks, calves and
heel.

Elevation and massage of the leg at the end of the
operation is a good plan.
Dr. Balbaa
PROPHYLAXIS OF DVT
 Postoperative measures:
Early ambulation after surgery.
 Maintenance of adequate hydration.
 Pharmacologic prophylaxis.
 Daily examination of the calves & feet for local
signs of thrombosis & on suspicion or history,
anticoagulants should be considered.

Dr. Balbaa
MANAGEMENT :
 Prophylaxis of DVT
 Treatment of established DVT


Conservative (non-operative) treatment
Operative surgical treatment
Dr. Balbaa




Bed rest and foot elevation
Anti-coagulants
Thrombolytic (fibrinolytic) & defibrinating
agents
Post treatment compression to control leg
edema:
Dr. Balbaa
Dose
duration
1. Parentral (Heparin)
and  5000-10,000 units/6 hours,
7 days, in calf thrombosis
and for 14 days in
Iliofemoral thrombosis.
 Low dose MW: 1 mg/kg/12
hrs.
2. Oral (Dendivan)
3 tablets/day reduced to 2 tabs,
then one tab for 6 months, started
before we stop heparin by 3 days
(as it takes 3 days to start its
action)
Dr. Balbaa




Bed rest and foot elevation
Anti-coagulants
Thrombolytic (fibrinolytic) & defibrinating
agents
Post treatment compression to control leg
edema:
Dr. Balbaa
Tissue palsmingen activators :
streptokinase & human urokinase.
Dr. Balbaa

Indications:


Most effective when given to thrombi of 5-7 days
duration.
For patients whose clot extends proximally beyond
the origin of the deep femoral vein.
Dr. Balbaa
Dr. Balbaa