DVT pdf - D. Ahmed - Muhadharaty

VENOUS DISORDERS

Deep Vein Thrombosis

Etiology

According to Virchow:-

1-Stasis
2-The Hypercoagulable State

3-Endothelial damage

Risk Factors for Venous Thromboembolism

Acquired

Advanced age

Hospitalization/immobilization

Hormone replacement therapy and oral contraceptive use

Pregnancy and puerperium

Prior venous thromboembolism

Malignancy

Major surgery

Obesity

Nephrotic syndrome

Trauma or spinal cord injury

Long-haul travel (>6 h)

Varicose veins

Antiphospholipid antibody syndrome

Myeloproliferative disease

Polycythemia

Inherited

Factor V Leiden

Prothrombin 20210A

Antithrombin deficiency

Protein C deficiency

Protein S deficiency

Factor XI elevation

Dysfibrinogenemia

Mixed Etiology

Homocysteinemia

Factor VII, VIII, IX, XI elevation

Hyperfibrinogenemia

Activated protein C resistance without factor V Leiden

Other factors associated with venous thrombosis include traditional cardiovascular risk factors (obesity,
hypertension, diabetes), and there is a racial predilection for whites and African Americans, compared with Asians and
Native Americans.

Pathology

The thrombotic process initiating in a venous segment can, in the absence of
anticoagulation or in the presence of inadequate anticoagulation, propagate to involve
more proximal segments of the deep venous system, thus resulting in edema, pain, and

VENOUS DISORDERS

immobility. The most serious sequel to acute DVT is that of pulmonary embolism, a
condition of potentially lethal consequence. The late consequence of DVT may be post-
thrombotic syndrome, as a result of valvular dysfunction in the presence of luminal
obstruction & venous hypertension.

Clinical features

Swelling, pain, tenderness, hotness & dilated superficial veins of affected extremety.
Massive DVT of the major deep veins of the extremity with relative sparing of collateral
veins causes a condition called

phlegmasia alba dolens

. This condition is characterized by

blanching due to arterial spasm. There is no associated cyanosis. When the thrombosis
extends to the collateral veins, the condition is known as

phlegmasia cerulea dolens

Investigations

Duplex Ultrasound

It's now the most commonly performed test for the detection of infrainguinal DVT, both
above and below the knee, and has a sensitivity and specificity of >95% in symptomatic
patients.

The primary method of detecting DVT with ultrasound is demonstration of the lack of
compressibility of the vein with probe pressure.

If any segment of the venous system

being examined fails to demonstrate augmentation on compression, venous thrombosis
is suspected. In addition, the chronicity of the thrombus can be evaluated.

Prophylaxis

The patient who has undergone either major abdominal surgery or major orthopedic
surgery, has sustained major trauma, or has prolonged immobility (>3 days) represents
an elevated risk for the development of venous thromboembolism.

Effective methods of VTE prophylaxis involve:-

Mechanical methods

include

leg elevation

early ambulation, intermittent pneumatic

compression

and

graduated compression stockings

Pharmacologic agents

include

low-dose UFH

LMWH

 Low-dose unfractionated heparin.

The dose is 5000 units of subcutaneous

unfractionated heparin every 12 hours.

 Low-molecular-weight heparin (LMWH)

. LMWH has a longer plasma half-life and

has  significantly  higher  bioavailability.  No  laboratory  monitoring  is  necessary
because  the  partial  thromboplastin  time  (PTT)  is  unaffected.  LMWH  results  in
equivalent,  if  not  better,  efficacy  with  significantly  less  bleeding  complications.  The
dose is 100 I.U./Kg/day.

VENOUS DISORDERS

Treatment

The goals of treatment are the prevention of pulmonary embolism and the postphlebitic
syndrome.

Anticoagulant

nfractionated heparin or low molecular weight heparin is

initiated & continued for at

least  5  days,  while  oral  vitamin  K  antagonists  (  warfarin  )  are  being  simultaneously
administered.  The  initial  therapy  typically  is  discontinued  when  the  international
normalized ratio (INR) is  ≥ 2.0.

 Unfractionated heparin therapy

is most commonly administered with an initial IV bolus

of 80 units/kg or 5000 units. The initial bolus is followed by a continuous IV drip, initially
at 18 units/kg per hour or 1300 units per hour.

 Low molecular weight heparin

The dose is 100 I.U./ Kg /12 hours subcutaneously

with no need for monitoring.

 Direct-thrombin inhibitors

include recombinant

hirudin

argatroban

, and

bivalirudin

These antithrombotic agents bind to thrombin, inhibiting the conversion of fibrinogen to
fibrin as well as thrombin-induced platelet activation. The direct thrombin inhibitors
should be reserved for patients with HIT.

 Vitamin K antagonists

, which include warfarin

Oral administration of anticoagulants is begun shortly after initiation of heparin therapy.

The treatment time of (6) months is advocated in most cases. If, however, the patient
has a known hypercoagulable state or has recurrent DVT, then lifetime anticoagulation
is required.

Systemic and Catheter-Directed Thrombolysis

Patients  with  extensive  proximal  DVT  may  benefit  from  systemic  thrombolysis  or
catheter-directed  thrombolysis,  which  can  potentially  reduce  acute  symptoms  more
rapidly  than  anticoagulation  alone.  These  techniques  also  preserve  venous  valves  and
may  decrease  the  development  of  postthrombotic  syndrome.  Several  thrombolysis
preparations are available, including

streptokinase

urokinase

alteplase

reteplase

, and

tenecteplase

. All these agents share the ability to convert plasminogen to plasmin, which

leads to the degradation of fibrin.

Inferior Vena Caval Filters

Indications for a Vena Cava Filter

Recurrent thromboembolism despite adequate anticoagulation

DVT in a patient with contraindications to anticoagulation

Chronic pulmonary embolism and resultant pulmonary hypertension

Propagating iliofemoral venous thrombus in anticoagulated patient.

VENOUS DISORDERS

Operative Venous Thrombectomy

In patients with acute iliofemoral DVT, surgical therapy is generally reserved for patients
who worsen with anticoagulation therapy and those with phlegmasia cerulea dolens and
impending venous gangrene.
Other measures like analgesia, good hydration, bed rest, elevation of affected limb,
crape bandage can be applied on the affected limb from the dorsum of foot and up to
above knee joint or even to the groin, etc…

DEEP VENOUS THROMBOSIS OF THE UPPER EXTREMITY

Upper extremity DVT is much less common than lower extremity DVT & can be divided
into two categories:

- Primary etiologies

 Paget-Schroetter syndrome

It develops due to repetitive motion of upper extremity, such as swimming, which
causes repetitive extrinsic compression of the subclavian vein in a patient with
thoracic outlet syndrome.

 Idiopathic upper extremity DVT.

It's sometimes attributed to an occult malignancy,



Secondary etiologies



Indwelling central venous catheter



Pacemaker



Thrombophilia



Malignancy

Clinical features, investigations & treatment

The same as for lower extremity DVT.

Superficial Thrombophlebitis

Predisposing  risk  factors  are  recent  surgery,  recent  childbirth,  venous  stasis,  varicose
veins,  or  intravenous  drug  use  and  indwelling  catheter.  Patients  who  deny  any  of  the
aforementioned  factors  may  be  classified  with  idiopathic  thrombophlebitis.  In  these
cases,  care  must  be  taken  to  ensure  that  the  patient  does  not  harbor  an  occult
hypercoagulable state or an occult malignancy.
Treatment of localized, noncomplicated thrombophlebitis involves conservative therapy,
which consists of anti-inflammatory medication and compression stockings.