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9.9 Thrombus Resolution
andVein Wall Remodeling
The thrombus resolution process is complex
and its mechanism is not fully understood.
Natural brinolysis breaks thrombi at variable
rates. The thrombus resolution process, which
involves pro- brotic growth factor, the deposition of collagen, and the activation of matrix
metalloproteinases, resembles wound healing.
Leucocytes are involved in the thrombus in a
specic sequence. The rst cell type to be
involved is the neutrophil, while monocytes are
one of the most important cells for later resolution. Recent data suggest that inhibition of the
inammatory response can decrease vein wall
brosis. Vein wall brosis can promote recurrent thrombosis.
9.10 Clinical Aspects
Prompt and accurate diagnosis of DVT prevents
morbidity. However, the clinical diagnosis of
DVT is misleading in roughly 50% of cases
(Fig.9.2) [10, 11]. Formerly, an ascending contrast venogram was the gold standard for DVT
diagnosis, but duplex ultrasound has now
replaced venography. The availability, non-invasive nature, and relative ease of use of ultrasound
has increasingly led to its use in providing early
and accurate diagnosis [12].
Virchow’s DVT triad of: stasis, changes in
vessel walls, and thrombogenic changes in blood
is now thought of differently. Stasis may not be a
direct cause of DVT. Recent thinking shows a
shift in the causal balance toward systemic infection and systemic inammation promoting
thrombotic pathways.
Apart from endogenous causes, extrinsic
venous obstructions such as tumors, hematomas,
cysts, aneurysms, and changes in the musculoskeletal structure are now included in the thinking on stasis.
Deep vein thrombosis is a signicant cause
of morbidity and mortality; acute pulmonary
embolism (PE) and chronic pulmonary hypertension are the best examples of conditions
associated with DVT morbidity and mortality.
Untreated DVT or incompletely treated DVT
can cause chronic venous disease, mainly in
terms of secondary varicose veins, post-thrombotic syndrome (PTS), chronic stasis ulcerations, and secondary lymphedema; the
socioeconomic burden of these diseases is considerable [13].
Fig. 9.2 Swollen limb
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High risk factors for DVT are age above
40years; a past history of DVT; orthopedic surgery; and the presence of malignancy, trauma,
spinal cord injury, or a hypercoaguable state
(thrombophilia).
9.11 Clinical Examination
Acute pain and swelling of the limb that is uniformly spread from groin to toes or from knee to
toes is the primary observation. Tender calf and
tender femoral vein in the inguinal region are
important signs. Mild cyanosis of the toes may be
present. Many signs and maneuvers described
earlier do not have proven clinical accuracy
[14–16].
In the event of associated infection, the
extreme peripheral venules can be seen to be
thrombosed, with the surrounding tissue showing
signs of acute inammation.
Extreme swelling may be seen in phlegmasia
cerulea dolens or phlegmasia alba dolens. If the
limb is enlarged and associated with varicose
veins or spider veins and acute pain, recurrent
DVT with chronic venous insufciency should be
suspected. The varicosity in the vein can be primary or secondary, owing to previous DVT [17].
9.12 Doppler Ultrasound
Examination
Doppler ultrasound is the mainstay of DVT diagnosis. During ultrasound examination, the salient
features of suspected unilateral DVT are
observed, along with the features of a normal
limb. A normal vein is compressible with an
ultrasound probe, while a thrombosed vein is not
compressible. Careful examination may demonstrate a thrombus head. The vein should be traced
from the tibial vein up to the inferior vena cava
(IVC). The iliac vein and IVC require a convex
probe and the compressibility test may be difcult; however, color ow imaging and compression of the opposite normal side help to secure
the diagnosis (Fig.9.3).
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Fig. 9.3 Thrombus on venography
9.13 Acute Versus Chronic
Thrombus
An acute (fresh) thrombus seen in a dilated vein
is hypoechoic, homogenous, and slightly compressible and may sometimes be oating. In color
mode, a gentle proximal compression may show
some color ow between the thrombus and the
vein wall. The vein wall is thin, smooth, and
echolucent.
A chronic thrombus is hyperechoic, heterogeneous, non-compressible, and rmly adherent to
the vein wall. The vein wall is thick and irregular.
In color mode, multiple intra-thrombus channels
may be seen. The channels may be reuxing. There
may be dilated, collateral, or multiple reuxing
tributaries, particularly in the inguinal region.
9.14 Supercial Vein Thrombosis
Supercial vein thrombosis, also known as supercial vein phlebitis, can occur in any vein of the
extremities. In the current era of medical practice
the presence of peripheral and central lines can
cause thrombosis owing to sensitivity to infused
drugs. Cracks in the feet may carry infection and
cause thrombophlebitis. Recurrent eeting
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thrombophlebitis may indicate a hidden malignancy. Varicose veins can become thrombosed.
Coagulation abnormalities in the form of a hypercoagulable state can promote supercial vein
thrombosis. Supercial vein thrombosis can
progress to the deep veins, resulting in DVT and
even in PE [18].
9.15 Upper Extremity DVT
Upper extremity DVT is uncommon in comparison to that in the lower extremities. Primary
upper extremity DVT, or spontaneous thrombosis
of the axillary subclavian vein, accounts for up to
24% of all upper extremity DVTs. Upper extremity DVTs are mostly associated with unusual
hyperabduction activity such as that occurring
during painting. Other factors associated with the
occurrence of these DVTs are venous thoracic
outlet syndrome, chronic atriovenous stula created for dialysis, axillary lymph node dissection
(postoperatively), the use of crutches in lower
limb amputees, traumatic fracture of the clavicle,
and effort thrombosis. Upper extremity DVTs
caused by effort thrombosis tend to affect young
healthy adults who participate in sporting
activities.
9.17 Acute DVT: Pathophysiology
andNatural History
A complication of acute DVT, VTE, is the most
common and most preventable cause of sudden
death owing to DVT.Improvements in our understanding of the coagulation and brinolytic systems, of the vascular endothelium in thrombosis
and hemostasis, and of newly identied prethrombotic conditions, have changed the scenario. A new area of investigation is the tissue
response to prothrombosis and how this response
leads to thrombus augmentation. This tissue
response occurs through the convergence of several risk factors against the background of an
imbalance between coagulation and brinolysis.
Non-invasive diagnostic methods have been an
asset in recognizing and observing the progress
of treatment [5].
9.17.1 Epidemiology
Whites have a lower incidence of VTE than do
African Americans (104 versus 141 per 100,000)
and the inhabitants of all the Asian Pacic islands
(104 versus 21 per 100,000); in the year [19], the
total number of new VTE cases in the United
States was more than 275,000.
9.16 Thrombosis at Other Sites
Thrombosis can occur at other sites, such as
cavernous sinus thrombosis (intracranial), mesenteric and portal vein thrombosis, thrombosis
of the dorsal vein of the penis, and isolated renal
vein thrombosis. Superior vena cava (SVC)
thrombosis can occur in patients on renal dialysis that is carried out via upper extremity vessels. Radiation over the chest and intrathoracic
tumors causing external compression can also
cause thrombosis. Inferior vena cava (IVC)
thrombosis may be a result of retroperitoneal
brosis. While the thrombosis in the hepaticrenal- atrial valves could also be a cause of IVC
thrombosis.
9.17.2 Population Aected
Individuals at risk for DVT have been less well
studied. The incidence of VTE is directly related
to and the use of thromboprophylaxis, the intensity of screening, and the accuracy of the diagnostic test used. For example, in acute spinal cord
injury patients who were studied with venography, DVT was demonstrated in 81%. However,
DVT was diagnosed in 64% of these patients after
discharge from the intensive care unit (ICU).
Thirty percent of these patients experienced recurrence in a 10-year time span. In another study,
there was a 1% incidence of PE and a 0.36% incidence of death from PE in all hospitalized patients.
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9.18 Risk Factors forDVT
In patients with DVT with an absence of risk factors the condition is termed primary or idiopathic.
Some investigators have found the risk of acute
DVT to be signicantly higher only for those
with three or more independent risk factors.
9.19 Independent Risk Factors
forVTE
9.19.1 Age
A population-based study [20] has shown the
incidence of VTE to increase exponentially with
age. The relative risk increases by 1.9 for each
10-year increase between the age groups of 20
and 80 years. Changes in the venous system associated with increased stasis and increased levels
of thrombin activation markers, leading to an
acquired prothrombotic state, are some of the
multiple factors associated with age.
VTE in children is almost always associated
with recognizable thrombotic risk factors.
Multiple risk factors are often required to precipitate thrombosis. The risk factors are hospitalization, hospitalization in the ICU, spinal cord
injury, and prolonged immobilization owing to
orthopedic procedures . DVT may occur in as
many as 3.7% of pediatric patients immobilized
in halo-femoral traction for the preoperative
treatment of scoliosis [21]. Local infection with
trauma; an inherited hypercoagulable state; the
use of femoral venous catheters; and the presence
of concomitant severe respiratory, oncological,
and infectious diseases are precipitating causes
of DVT.
9.19.2 Geographic Dierences
The postoperative incidence of DVT is reported
to be higher in Europeans than in Asians. The
presence of genetic risk factors such as blood
group and factor V Leiden mutation varies in
geographic areas and this could be associated
with the incidence of DVT [22–25].
9.19.3 Immobilization
Stasis in the soleal veins and behind the valve
cusps is exacerbated by advancing age and inactivity of the calf muscle pump. In autopsy studies
DVT was found to have paralleled the duration of
bed rest, with an increase during the rst 3days
of connement and a rapid rise to very high levels after 2weeks [26–28].
The incidence of lower extremity thrombosis
prior to prophylaxis use was noted to increase
within 3days of bed rest. Also, the incidence rapidly rose to 15%, 77%, and 94% after 1, 2, and
4 weeks of connement, respectively. Bilateral
thrombosis is frequent following bed rest,
whereas unilateral thrombosis is associated with
stroke conned to the paralyzed limb.
9.19.4 Travel
DVT has also been called “economy class syndrome”. After a meeting in 2001, the World
Health Organization published a consensus statement [29], in which it was observed that, over a
period of 8years, 56 of 135.3 million airline passengers had severe PE.The frequency in those
who traveled more than 5000km was 150 times
higher than the frequency in those who traveled
less than 5000km. A history of previous VTE,
recent trauma, the presence of varicose veins,
obesity, immobility during ight, and cardiac disease were predisposing risk factors.
9.19.5 Recurrent Thromboembolism
Recurrent thromboembolism develops in 1 of
every 11–50 persons with a previous episode of
thromboembolism. Recurrent thromboembolism occurs as a result of disordered venous
hemodynamics and the resultant damage.
Heterozygous factor V Leiden and impaired
brinolysis are correlated in recurrent thromboembolism. A higher incidence of thromboembolism was noted in patients with irreversible
thrombotic risk factors than in those with idiopathic DVT [30, 31].
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9.19.6 Malignancy
The hypercoagulable state in malignancy has been
well studied and is multifactorial. Venous compression secondary to tumor growth, cancerassociated thrombocytosis, an indwelling central
line, chemotherapy, and radiotherapy are causes of
primary importance in the development of VTE.
However, the systemic prothrombotic
response seen in malignancy is mediated by cytokines, inhibitors of brinolysis, and procoagulants. These cytokines initiate hemostasis through
the expression of TF. Normally TF is not
expressed on the resting vascular endothelium;
its expression is induced by chemicals and mediated during times of inammation or vessel damage. This will bind to factors VII and VIIa and
activate factor X.It has been detected in 81% of
cancer patients. The platelet adhesion molecules
glycoprotein Ib and glycoprotein IIb/IIIa have
also been identied on tumor cells. Cytokines
such as vascular endothelial growth factor, tumor
necrosis factor-alpha, and IL-1 contribute to the
prothrombotic potential and their action is mediated through the induction of TF on the vascular
endothelium, monocytes, and leukocytes is classically associated with mucinous gastrointestinal
tumors. In othermalignancies and carcinoma of
the lung may be associated with DVT in 19–30%
of cases. Of all patients presenting with idiopathic thrombosis, 3–23% develop a malignancy
within 2 years, probably owing to the activation
of coagulation, mediated by TF, cancer procoagulants, and macrophage-associated cytokines.
fulminans and warfarin skin necrosis are also
associated with protein C deciency. Patients
with conditions associated with acute thrombotic
events, such as liver disease, renal disease, disseminated intravascular coagulation, hemolyticuremic syndrome, chemotherapy with
L-asparaginase, thrombotic thrombocytopenic
purpura, and acute infection, can also have an
acquired protein C deciency.
9.19.8 Protein S
Protein S is a vitamin K-dependent cofactor for
the protein C-mediated inactivation of factor Va
and factor VIIIa. Deciency of protein S—which
is autosomal dominant in nature—is more common than protein C deciency. The incidence of
protein S-associated VTE has been reported to be
5–7%, with the prevalence in the general population being 0.13%. There are more than 130 types
of protein S mutation and these can be grouped
into three categories. Type I deciency is quantitative, type II deciency is qualitative, and type
III deciency is caused by a mutation that
increases the afnity of protein S for C4b-binding
protein [33].
9.19.9 Antithrombin
The incidence of VTE associated with antithrombin
deciency has been reported to be 0.5–3%, with a
prevalence of 0.2% in the general population.
9.19.7 Protein C
An increase in thrombotic risk is associated with
an acquired or an inherited reduction in protein C
activity. Autosomal-dominant inherited deciency of protein C is classied as type I protein
C deciency, and is characterized by a reduction
in both antigenic and functional levels, while in
type II protein C deciency, antigen levels are
normal. In a study conducted on VTE, 3.2% of
2132 patients were found to have protein C deciency [32]. In addition to VTE, neonatal purpura
9.19.10 Other Inherited
Thrombophilias
Dysbrinogenemia, manifested by elevated levels of factors VIII, IX, and XI, has been demonstrated to be an independent risk factor for VTE.
9.19.11 Pregnancy
The incidence of VTE in the pregnant population
is six to ten times greater than that in non-
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pregnant controls. The occurrence of thrombosis
is equally distributed throughout all three
trimesters.
Impaired venous outow occurs secondary to
uterine compression, and up to 97% of reported
thromboses have been isolated to the left leg.
There is a transient hypercoagulable state because
of increases in the levels of brinogen; vWF; and
factors II, VII, VIII, and X. Additionally, the
development of acquired functional resistance to
APC is seen in pregnant patients. Furthermore,
protein S levels are decreased by 50–60% early in
pregnancy. The brinolytic system is also altered
in pregnancy, with decreased levels of tPA and
increased levels of PAI-1 and PAI-2. Inherited
thrombophilia is an additional risk factor.
Worldwide, VTE is the second most common
cause of death associated with pregnancy, the
most common being abortion [34]. An acquired
pre- thrombotic state impairs venous outow. The
incidence of VTE worldwide is 0.75 per 1000
deliveries. Factor V Leiden mutation and suppression of lactation tend to be two to three times
higher in patients with postpartum DVT than in
those with no DVT.
9.19.14 Inammatory Bowel Disease
DVT may complicate inammatory bowel disease in 1.2–7.1% of cases [36, 37]. Thromboses
occur in young patients, and are more common in
those with active disease and in areas such as the
cerebral veins. Active inammation is associated
with the activation of coagulation, possibly mediated by endotoxin-induced monocyte activation.
9.19.15 Systemic Lupus
Erythematosus (SLE)
SLE may be complicated with an underlying syndrome of arterial and venous thrombosis, recurrent abortion, thrombocytopenia, and neurological
disease and by the presence of anti-phospholipid
antibodies. Patients with SLE who have lupus
anticoagulant have a sixfold higher risk of VTE.
9.20 Anatomic Risk Factors
VTE and anatomic anomalies or syndromes are
congenital risk factors for DVT.
9.19.12 Oral Contraceptives
andHormonal Therapy
Estrogen in pharmacological doses is associated
with alterations in the coagulation system that
may contribute to VTE.Such alterations include
decreases in PAI-1 and increases in blood viscosity, brinogen, plasma levels of factors VII
and X, and platelet adhesion and aggregation.
Increases in factor VIIa levels, as well as
depressed AT and protein S activity, are associated with pharmacological doses of estrogen.
The calculated absolute risk of VTE is approximately 3.3 per 1000 regular users of oral contraceptives [35].
9.19.13 Blood Group
The prevalence of DVT is higher in people with
blood group A.
9.20.1 Iliac Vein Compression
May-Thurner syndrome is a classical example of
venous compression by surrounding structures.
In this syndrome the right common iliac artery
compresses the left iliac vein against the sacral
promontory. Whether the condition is congenital
or acquired is a matter of debate, but clinical
observations show that DVT occurs more commonly on the left side.
9.20.2 Popliteal Vein Entrapment
Popliteal vein entrapment occurs because of anatomic anomalies of the medial head of the gastrocnemius; it occurs either alone or together
with the artery in 10% of cases of DVT.Venous
entrapment has been reported to occur almost
70% of the time in femaleswith DVT [38].
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9.20.3 Inferior Vena Caval Anomalies
Congenital hypoplasia or absence of the IVC
presents another anatomic risk factor for DVT.
9.20.4 Surgery
Risk factors causing DVT are preoperative
immobilization, activated coagulation, and transient depression of brinolysis; increases in
thrombin activation, as well as elevated levels of
PAI-1, are also risk factors for DVT.
9.20.5 Trauma
Blood transfusion; surgery; fracture of the pelvis,
femur, or tibia; spinal cord injury; and femoral
venous catheters are all risk factors for
DVT.Virchow’s triad and all its components are
also regarded as risk factors in trauma.
9.21 Primary Hypercoagulable
State
Certain thrombophilic conditions form a genetic
basis for DVT. Recently described abnormalities
are substantially more common than those previously described [39]. In 20% of DVT cases factor
V Leiden mutation is present. In approximately 6%
of those with DVT and this mutation, the condition
is associated with a point mutation in the 3’region
of the prothrombin gene, at nucleotide position
20,210; this is associated with increased plasma
levels of prothrombin. Hyperhomocysteinemia is
another inherited hypercoagulable state that is an
independent risk factor.
9.22 Other Risk Factors
factors provide insight into the underlying pathophysiology, blood ow abnormalities, and vessel
wall injury. Abnormalities of blood coagulation
and brinolysis result in imbalances within the
coagulation and brinolytic systems.
9.23 Newer Thinking inVenous
Thrombogenesis
There is little evidence that either microscopic or
gross endothelial injury plays a signicant role in
venous thrombogenesis, exceptions being direct
venous trauma, hip arthroplasty, and the presence
of a central venous catheter. It is biologic injury
to the endothelium that plays a major role [6].
The venous endothelium is normally antithrombotic. It produces prostaglandin i-2, TM,
tPA, and glycosaminoglycan, which are
antithrombogenic cofactors. The endothelium
may become prothrombotic, producing TF, vWF,
and bronectin in favorable conditions. A procoagulant state that occurs because of endothelial
hypoxia is caused by endothelial leukocyte adhesion during stasis. Thus, stasis can be a permissive factor for the events required for
thrombosis.
An imbalance in the activation of the coagulation system is one of the most important factors
underlying many episodes of acute DVT.There is
continuity in the hemostatic system: it shows a
precise balance between inhibitors and activators
of brinolysis and coagulation, and connes
thrombus formation to sites of local injury.
A prothrombotic state may result from activation exceeding antithrombotic capacity. This
state is facilitated by the thrombin-T complex.
Factors such as age, presence of malignancy, surgery, trauma, a primary hypercoagulable state,
and oral contraceptive use can cause an imbalance in coagulation.
Obesity, cardiac disease, systemic hypercoagulability, and congestive heart failure are other
important risk factors for DVT [7, 8].
However, thrombotic risk is not uniformly dis-
tributed in the population. The associated risk
9.24 Treatment ofDVT
Duplex ultrasound has been the most important
development in characterizing the natural history
of venous thrombi in humans. Valvular incompe-
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tence and persistent venous obstruction are the
most important chronic manifestations of acute
DVT [40].
Thrombosis in the venous bloodstream (systemic and pulmonary) is addressed by, rstly,
prevention and, secondly, treatment of a thrombosis that has occurred.
Most of the drugs trialed and their clinical
applications are in relation to the prophylaxis of
VTE, and DVT is discussed in this context.
However, a preventive/prophylactic approach
and the treatment of an established DVT may be
quite different.
Established acute DVT may be present in the
most peripheral veins and may not have progressed to the main bloodstream. The aim is to
evacuate the thrombus from the system, either by
lysing it or by surgically removing it.
Very small thrombi will be treated by the body
mechanism for natural lysis. When the thrombus
load increases to a point whereupon the body
mechanism nds it difcult to clear, other
approaches come into play. Untreated DVT may
progress to PE, or the thrombus may adhere to
the vein wall in such a way that free fragmentation does not occur. Therefore, the natural outcome could be PE followed by chronic pulmonary
hypertension or death due to PE [9] or PTS.
An adherent deep vein thrombus may resolve
partially, resulting in valve destruction and
chronic venous hypertension in the affected limb
or organ. Or the thrombus may be completely
lysed and leave behind a normal venous bloodstream. The outcome depends on the thrombus
load in the system and the various factors
described above.
The treatment centers on the prevention of PE,
thereby preventing a life-threatening situation,
while also preventing the development of chronic
status, such as PTS, and preventing the imposition
of a lifelong socioeconomic burden on the patient.
Three modalities are used to treat established
acute DVT: heparin therapy, CDT, and surgical
thrombectomy. All three modalities are followed
by the long-term use of various anticoagulants.
9.25 Unfractionated Heparin
Heparin is available in unfractionated form and
as fractionated low molecular weight heparin
(LMWH).
Heparin, with a molecular weight of
10–16 kDa, is a pentasaccharide that inhibits
thrombin and factor Xa by binding to antithrombin II (ATIII). Also, heparin catalyses the
inactivation of thrombin by cofactor II.Other
effects of heparin include the release of TF
pathway inhibitors that bind to platelet proteins, endothelial cells, and leucocytes. Heparin
increases vascular permeability. A therapeutic
level of heparin achieved in the rst 24h after
the diagnosis of venous thrombosis reduces the
risk of recurrence; failure to reach this level
entails a 23.3% risk of recurrence [41]. Heparin
can cause bleeding (greater risk in those who
are underweight and those aged above 65; independent risk factors), thrombocytopenia, and
osteoporosis. Recent surgery, trauma, peptic
ulcer, malignancy, liver disease, and hemostatic
defects pose particular risks in the use of
heparin.
9.25.1 LMWH
The molecular weight of LMWH is 4–5kDa.
Various LMWHs are prepared by different processes. A true comparison between the various
varieties is still inconclusive and therefore the
doses of different LMWHs are not comparable.
LMWH, compared with heparin, is claimed to
have better bioavailability, a prolonged halflife, and predictable clearance, resulting in
twice- daily doses; also, it does not need laboratory monitoring. It has the capacity to inactivate
platelet- bound Xa and to vascular permeability
(leading to fewer hemorrhagic events).
Repeated venographic studies have shown
LMWH to be as effective as heparin in preventing thrombus extension and in increasing
thrombus resolution.
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9.25.2 Catheter-Directed
Thrombolysis (CDT) (Fig.
The best agent with which to lyse a thrombus is a
tPA.With a tPA: plasminogen is activated to plasmin and plasmin degrades the brin in the clot.
The maximum action of plasmin occurs when the
tPA is directly sprayed on brin complexes.
Therefore, systemic infusion and even use
through a peripheral vein that drains into a thrombus do not have the maximum desired effect on
clot lysis. To achieve the best result, the tPA
should be delivered into the thrombus.
9.4)
9.25.3 Rationale forUse ofCDT
Extensive DVT, particularly in the ilio-femoropopliteal segment of the vein, will have a massive
thrombus load and will cause a painfully swollen
extremity, and if not treated aggressively by
thrombolysis will result in venous hypertension
and loss of both valve function and deep vein
reuxes. The outcome will be severe PTS [42].
Persistent obstruction increases the severity of
PTS.Early lysis preserves valvular function. Two
prospective studies have shown that patients who
received thrombolytic therapy were free of PTS
as compared with those who received anticoagulation alone [43, 44].
9.25.4 CDT Technique
Under ultrasound guidance, the posterior tibial
vein and or popliteal vein is punctured with a
needle and a 5fr or 8fr sheath is advanced over a
wire. A catheter with multiple side holes is parked
intra-thrombus and the preferred tPA is slowly
infused, using a pump delivery system.
Venograms for approximately 12-h checks are
obtained, and the multihole catheter is advanced/
repositioned as required. The most terminal portion is the common iliac vein and the help of a
pigtail catheter may be needed. At the completion
of thrombolysis if the check venogram shows any
stenotic or occlusive lesion this is treated by balloon dilation or by the deployment of a stent—
the choice depends on the patient’s age and
underlying disease. DVT of the upper limb and
IVC can be treated similarly. Post-procedure,
heparin cover is given for 48h and a switch over
to oral anticoagulant is then done. The newer
anticoagulants—rivaroxaban and dabigatran—
are now being used in place of drugs of the warfarin group. These newer oral anticoagulants
Fig. 9.4 Catheter-directed thrombolysis
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Damage to
vessel wall
Endothelial
disruption
Release of tissue factor
(cell membrane protein)
Extrinsic pathway
activation
VII VIIa + TF complex
++
Ca
XXa
IX IXa
V
Va
101
Exposure of
sub endothelial
collagen
Activation of platelets
Changes in shape
Contains receptors for
Va
fibrinogen VWF ADP
VIIIa
Fig. 9.5 Coagulation cascade
have obviated the need for repeated international
normalized ratio (INR) checking.
The currently available literature and my personal experience support CDT as the preferred
approach in patients with ilio-femoral DVT,
axillo-subclavian DVT, SVC DVT, and IVC
DVT.If there is any contraindication to this therapy, or if CDT fails, then venous thrombectomy
may be considered.
9.25.5 Surgical Treatment ofAcute
Ilio-Femoral DVT
Prior to the endovascular era, massive DVT was
treated surgically; the initial procedure in the
treatment of this condition was ligation of the
femoral vein or iliac vein. The aim was to prevent PE and to prevent reux after re-canalization [45].
The newer surgical approach is in the form of
exposure of the common femoral vein at the level
of the inguinal ligament and its control. A venous
Fogarty catheter technique is used to evacuate
ilio-femoral thrombi after transverse venotomy.
The thrombus load from the calf and lower thigh
is evacuated by rm massage from calf to thigh,
Release of
-ve charge
adhesion
Platelet plug
Platelet - Fibrinogen complex
VWF
GPllb/lla receptors
Release of prothrombotic
platelet granules
Collagen
which will expel the thrombi from the venotomy.
The sequence may have to be repeated several
times before good evacuation occurs.
In patients with phlegmasia cerulea dolens a
calf fasciotomy may be needed [46].
An IVC or a renal thrombus may need a retroperitoneal laparotomy or a subcostal retroperitoneal approach (Fig.9.5).
Conclusion
DVT is a common phenomenon in hospital
settings and may be a cause of sudden death
because of PE.The aim should be to prevent
the DVT, and if it occurs, to perform the
required therapy, in terms of anticoagulation,
thrombolysis, or thrombectomy.
References
1. Criado E, Passman MA. Physiological assessment
of the venous system. In: Rutherford RB, editor.
Vascular surgery. 3rd ed. Philadelphia: WB Saunders;
1989. p.175–7.
2. Hjelmstedt A.The pressure in the veins of the dor-
sum of the foot in quiet standing and during exercise
in limbs without signs of venous disorder. Acta Chir
Scand. 1968;134:235–44.
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