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Deep Vein Thrombosis: A Complete Overview


There are two basic types of veins in the leg:

a) Superficial – just under the skin in the subcutaneous fat.
b) Deep – surrounded by the deep muscles of the leg.

Deep vein thrombosis (DVT) concerns the deep veins of the leg. Typically divided into above knee (AK) and below knee (BK) DVT due to treatment differences.


Public records indicate:

• DVT in children is rare – about 1:100,000 annually.
• DVT is adults is relatively common 1:1,000 annually.
• DVT is frequent in the elderly 1:100 annually.
• Kahn SR et al, Lancet Dec 2013, reported no difference >2 years in post-thrombotic leg syndrome (PTLS) after DVT from wearing compression hose v sham compression hose.
• 2 million DVTs occur in the US annually, 30 day mortality rises from 1% to 6% as age advances even with effective treatment.

Any condition promoting immobility increases the incidence of DVT in all populations: surgery, trauma, childbirth, certain medications also increase the DVT occurrence probability. DVT is 10-15% more common during winter months v summer months.

History of Deep Vein Thrombosis

First recorded case noted in the Sanskrit dated between 600-900 BC (Sushruta – India).

Causes of DVT

(Virchow 1856)

The German pathologist described Virchow’s triad:

• Abnormal endothelium (blood vessel lining)
• Thick, hyper-coagulable blood (typical in venous blood v arterial blood)
• Slow flow (typical in venous flow)
• Inflammatory response

Must consider DVT as a cause of swollen painful lower extremity in: cancer pts, recent trauma, recent childbirth, immobility for any reason, positive past history, known pro-thrombotic syndromes such as Leiden Factor V deficiency, oral contraceptives, existing central venous catheter are well known DVT promoters.

• Common nonspecific promoters: age > 40 (59%), obesity (28%), recent major surgery (23%).


• Hospitalization $7,000-$10,000 initial visit.
• Follow up costs 3-6 months and 1 year: $5,000, $10,000, and $33,000 respectively.
• Overall DVT cost in the US lies between $5-$8 billion annually.

Diagnosis – clinical:

• Sudden onset lower extremity pain and swelling, warmth, tenderness – sometimes superficial veins are distended.
• Not infrequent following recent surgery or trauma. (Spinal and hip surgery).
• Lower extremity discoloration – DVT leg often rather swollen and bluish.
• Less common in Asiatic races.
• Rule out in elderly and cancer.

Diagnosis – nonclinical

• Non-clinical diagnosis is made by Duplex ultrasound – followed with duplex ultrasound and Doppler color flow monitoring.
• Venography and CT venogram or MR venogram can also make the diagnosis. But are more expensive tests.
• Older tests are now historical.

Typical image of DVT L common femoral vein by deep venous duplex ultrasound

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Microbiology cause:

Both the endothelium (internal blood vessel lining) and platelets normally secrete PGI2 (Prostacyclin) on surfaces. The chemical (PGI2) maintains the blood vessel wall surface and platelet surface potential at ~-120mV. Those two similar charges repel each other and normally prevent DVT. Platelets are unable to approach the endothelium due to the similar electrostatic surface charges. That is nature’s way of reducing the incidence of DVT.

When injured, vein wall PGI2 production falls (trauma inflammation etc), the endothelial static charge rises from ~-120mV to zero, whereas the platelets remain at ~-120mV. That results in a positive (vein wall) negative (platelet) situation and the platelets now activate, this is associated with platelet mitochondrial alpha degranulation, the platelet now becomes sticky and develops external projections; this mitochondrial reaction releases low affinity platelet factor-4 (LAPF-4), which can be measured in blood. The platelets migrate outward, and quickly adhere to the zero potential vein wall by electrostatic attraction and the DVT soon expands. It soon changes from a ‘white’ thrombus to a ‘red’ thrombus as red blood cells accumulate and grow the DVT. At this time there is risk of proximal propagation and early treatment is indicated. LAPF-4 release triggers release of TXA2 (thromboxane A2 – liver), which on passing through the lungs (Type 1 pneumocyte) converts to TXB2 by cleaving off two peptides. TXB2 is a putative vasoconstrictor. This powerful local vasoactive response tries to limit blood flow into the DVT and thus limit the DVT growth and limit DVT propagation.

Treatment of Deep Vein Thrombosis

• BK DVT usually compression hose + aspirin. If calf very swollen and painful then consider anticoagulation.

i) Medical compression hose + Lovenox followed by Heparin and Coumadin. Coumadin needs INR>2 monitoring q 2 weekly (blood tests). Alternative drugs
ii) Xeralto – rivaroxaban – Factor Xa inhibitor
iii) Pradaxa – dabigtran – anti-thrombin agent.

• In most situations pt will need weekly duplex monitoring

The newer blood thinners do not have reliable reversible medications in the event of a major bleed. The physician must evaluate risk benefit analysis. Both have about 24-hr therapeutic effect. Pt may need replacement/supportive blood transfusion if a major bleed develops. Sometimes Factor VII (Novo-7) transfusion may help.

The DVT is then monitored q2 weekly by DVUS. Once the DVT resolved the anticoagulants may be withdrawn. Typically ~6 months.

• If the leg is grossly swollen and very painful in selected situations either catheter directed thrombolysis or mechano-chemolysis may be considered these treatments require hospitalization. Typical procedures may include IV tPA or Urokinase and/or a Trellis Procedure.


• Usually immediate intervention with anticoagulants will resolve the DVT (98%) and in most, recovery approaches 100% without complications. Note anticoagulation medications do NOT dissolve the DVT they simply prevent further clot formation.
Clot elimination is under the management of naturally produced Plasmin (serine protease). Lytic therapy mimics plasmin.

• When the diagnosis is missed then complications can be mild or catastrophic. Diagnostic tools of PE: VQ scan, thin slice high resolution CT scan, pulmonary angiogram. The most serious complications are:

i) Pulmonary embolus (PE). In PE fragments of the DVT break off and embolise first to the IVC then the heart and then the lung. Once in the lung they become trapped. If the clots become trapped in the main pulmonary artery as it divides into the R and L lungs that is called a ‘saddle’ embolus and is often rapidly fatal. More typical the emboli will migrate out toward the lung periphery. The general rule of thumb: if 600,000 DVTs occur annually, 60,000 will embolise, 6,000 are fatal. VTE or PE (venous thromboembolism) may be acute, acute on chronic or chronic >6 weeks). If the patient has a PFO (patent foramen ovale the patient can sustain a paradoxical embolus and sustain a stroke, or some similar systemic infarction event.
ii) IVC Filter. Most cases of DVT involving pulmonary embolus, meet criteria for insertion of an IVC filter placed below the renal veins.
iii) Pulmonary infarction often associated with pleuritic pain on breathing. if not treated it can result in pulmonary hemorrhage, pulmonary infection with abscess formation and ultimately necrosis and liquefaction of the lung. Necessitating high than normal risk pulmonary resection.
iv) Pulmonary thromboendarterectomy. (PTE) Once the PE is considered chronic patient long term issues may involve pulmonary hypertension, breathlessness and right heart failure. Pt may be a candidate for pulmonary thromboendarterectromy.
v) Pulmonary embolectomy. In less common situations with a ‘saddle’ embolus or main branch pulmonary embolus if instantly life threatening, some might consider emergency pulmonary embolectomy either without the heart lung assistance if ultra urgent with a failing right ventricle (Trendelenberg Procedure) with pump assistance (Modified Trendelenberg Procedure). Can be life saving, but uncommon procedure, usually early anticoagulation is sufficient.
vi) Post phlebitic leg syndrome. Once the DVT has resolved by plasmin effects, the plasmin is not programmed to distinguish clots from valve tissue and 10-15% of DVT patients the valves in the CFV are reabsorbed. That permits reflux in the common femoral vein and is variably called deep venous insufficiency or (chronic) DVI.

That in turn results in chronic venous congestion in the lower extremity and can result in discoloration, heavy legs that tire easily and may result in skin pigmentation and ulceration.


Screen Shot 2014-03-07 at 10.40.43 AM26 months later . . .

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For more information on treating deep vein thrombosis, give us a call today and set up a consultation.