3 : 31
venous thromboembolism- indian perspective
Overview of Venous Thromboembolism
Venous Thromboembolism consists of deep vein thrombosis
(DVT) and pulmonary embolism (PE). The true incidence of VTE
is hard to estimate because of the often silent nature of the
condition. In the western world, the incidence is one case of DVT
and 0.5 cases of PE per 1000 population / year.Hospitalized patients
are especially at risk for VTE as most have multiple risk factors.
Autopsy studies have shown the incidence of VTE in hospitalized
patients to be as high as 34.7% with fatal pulmonary embolism in
9.4% of cases1.VTE contributes substantially to patient morbidity,
mortality and cost of management. PE accounts for 5-10% of
death in hospitalized patients, making VTE the most common
preventable cause of inhospital death2. It has been estimated
that between 5 Lakh and 2 million VTE cases including PE occur
annually in USA3.
DVT and PE are distinct but related aspects ofVTE.Approximately
one third of patients with symptomatic VTE manifest PE, whereas
two thirds manifest DVT alone.VTE is often silent and difficult to
diagnose because approximately 80% of all DVTs are asymptomatic
and even symptoms do occur they may be nonspecific. Silent VTE
may develop into PE which may be unrecognized. PE is often
asymptomatic and even when symptoms do appear they may be
difficult to recognize. Consequently less than half of all cases of
fatal PE are detected prior to death4.
It is perceived by many that thromboses in the deep veins proximal
to the knee (Proximal DVT) are associated with an increased risk
for PE and thromboses of calf vein (Calf DVT) are associated with
post thrombotic syndrome. Studies shows that 15 – 25% of calf
DVT propagate and converts into proximal DVT. Such “proximal
conversion” renders a calf DVT just as dangerous as any proximal
DVT and this occurs within initial 2 weeks after diagnosis31.
The risk of early death among patients with symptomatic PE is
18 fold higher compared to patients with DVT alone. PE is an
independent predictor of reduced survival for upto 3 motnhs after
onset. For almost 25% of PE patients the initial clinical presentation
is sudden death5. In untreated patients death from PE occurs most
frequently within 24 – 48 hours of initial presentation. All cause
mortality in treated patients with PE is 11% at 2 weeks and 17%
at 3 months3. VTE is a chronic disease with episodic recurrence.
About 30% of patients develop recurrence within next 10 years
Gandharba Ray, Manoranjan Behera, Cuttack
and is highest within first 6 to 12 months of presentation5.
VTE predominantly a disease of old age.The overall age adjusted
incidence rate is higher for men (114 per 100,000) than women
(105 per 100,000). Male to female sex ratio is 1.2 : 1.4
Pathophysiology and Risk Factors
The factors that predispose to venous thrombosis have been
originally described by virchow in 1859. These include (i)
circulatory Stasis (ii) Hypercoagulability (iii) Vascular wall injury4.
Venous thrombi are intravascular deposits composed of cellular
material (RBC,WBC and Platelets) enmeshed with fibrin strands.
Typically, these thrombi are belived to start in areas of slow or
turbulent venous flow such as large venous sinuses or venous valve
cusps or in areas of direct venous trauma. Hypercoagulability or
activation of blood coagulation can be initiated by many factors
such as tissue or vascular injury and inflammation. Vascular wall
injury occurs as a result of mechanical or chemical trauma, which
subsequently stimulates an inflammatory response known as
“Phlebitis”. Circulatory stasis may be due to a reduced or altered
blood flow through the deep veins of the lower limb which impairs
clearing of clotting factors allowing them to concentrate locally,
further favouring activation of blood coagulation.
Endothelial injury can expose collagen causing platelet aggregation
and tissue thromboplastin release. Tissue thromboplastin forms
thrombin and fibrin that traps RBCs and propagates proximally
as a red or fibrin thrombus. More than 95% of pulmonary emboli
originate as thrombi from deep veins of lower extremeties4.
Important risk factors are shown in Table 1. Other risk factors
include air travel (more than 8 hours), varicose vein, heavy smoking
etc4. Most hospitalized patients have one or more risk factor
for VTE. These risk factors are generally cumulative. Recent
family – based studies indicate that VTE is highly heritable and
follows a complex mode of inheritance involving environmental
interaction. Inherited reduction in plasma natural anticoagulants
(e.g. antithrombin, protein C or S) are uncommon but potent
risk factors for VTE. Recent discoveries of impaired down
regulation of the procoagulant system (e.g. activated protein – C
resistance, factor – V – Leiden), increased plasma concentrations
 Medicine Update 2010  Vol. 20
Table 1 : Risk factors for VTE
Surgery
Trauma (major trauma or lower – extremity injury)
Immobility, lower – extremity paresis
Cancer (active or occult)
Cancer therapy (hormonal, chemotherapy, angiogenesis inhibitors, radio-
therapy)
Venous compression (tumor, hematoma, arterial abnormality)
Previous VTE
Increasing age
Pregnancy and the postpartum period
Estrogen-containing oral contraceptives or hormone replacement therapy
Selective estrogen receptor modulators
Erythropoiesis-stimulating agents
Acute medical illness
Inflammatory bowel disease
Nephrotic syndrome
Myeloproliferative disorders
Paroxysmal nocturnal hemoglobinuria
Obesity
Central venous catheterization
Inherited or acquired thrombophilia
Source : American College of Chest Physicians evidence based clinical
practice guidelines (8th Edition), Chest 2008 : 133 : 381S – 453S.
of procoagulant factors (Fibrinogen, prothrombin, factor VIII, IX,
XI), increased basal procoagulant activity, impaired fibrinolysis and
increased basal innate immunity activity and reactivity predisposes
to thrombosis (thrombophilia). Inherited thrombophilias interact
with clinical risk factors (eg. Pregnancy, hormone therapy, surgery)
to increase the risk of incident thromboembolism. Genetic
interaction increases the incidence of incident and recurrentVTE5.
Western Scenario
VTE among whites is 108 per 100,000 person-years with about
250,000 incident cases occurring annually among US whites. The
incidence appears to be similar or higher among Blacks and lower
among ASIAN and Native Americans. The incidence among US
– Blacks is about 78 per 100,000, suggesting that about 27000
incident VTE cases occur annually among US Blacks. Recent data
suggests that more than 900 000 incident or recurrent, fatal and
non fatal VTE occur in the US annually. The incidence of VTE has
not changed significantly over the last 25 years5.
Indian Scenario
The prevailing belief that VTE in the ASIAN population is less
than in the western population has been disproved by recent
studies and there appears no reason to believe that it should
be any different in India. The incidence of VTE in India is highly
underestimated because of lack of adequate studies highlighting
the incidence of VTE especially in medical patients, existence of
a few but conflicting studies in post surgical patients and paucity
of data from autopsied patients as autopsy is being done in very
few institutions in India.
330
Jain et al6 conducted a prospective study in post – surgical
patients with total knee (26 patients) and hip arthroplasty (45
patients), and showed a very low incidence (2/71) of DVT. They
concluded that the incidence of DVT in Indian patients is very
low in comprasion to west and emphasized the fact that no
thromboprophylaxis is needed in Indian patients undergoing total
Hip / Knee arthroplasty if they have no known risk factors for
DVT.Vijayraghavan et al7 did a retrospective study on DVT in the
South Indian population and showed an incidence of 1.79 / 1,000
population.Agarwal et al8 conducted a study in patients undergoing
total hip / knee arthroplasty and revealed an overall incidence of
DVT in 60% cases in the non prophylaxis group. This data was
comparable to the date from other parts of Asia and West and
emphasized the need of thromboprophylaxis. The Smart Study
Group9 conducted a prospective observational study on Asian
patients (2420 Patients) undergoing major orthopaedic surgery
without thromboprophylaxis and revelaed symptomatic VTE in
2.3% patients and sudden death in 1.2% patients. Prospective
registry on venous thromboembolic events (PROVE)10 conducted
in 19 countries enrolled 3526 patients with symptomatic DVT, out
of which 667 were from India. DVT was found proximally and in
the calf in 54% of Indian patients which is comparable to western
date. Sharma et al11 in a prospective study of 112 patients who
underwent surgery for fractures around hip joint found a 19.6%
of incidence of DVT. A prospective study conducted in PGIMER
, Chandigarh by Nagi et al12, revealed 8% incidence of DVT after
major orthopaedic surgery.
Bhan et al 13, in a multicentric study, found an incidence of 23.34% of
DVT in the nonprophylaxis group as compared to nil in the group
which received mechanical prophylaxis. Lee et al14 conducted
a retrospective study in CMC Vellore from (1996-2005) to
determine the incidence of VTE among hospitalized patients and
showed an overall incidence of confirmed DVTs to be 17.46
per 10,000 admissions with 64% being non surgical non trauma
patients. PE was diagnosed in 14.9% of the study patients. Mortality
in those with confirmed PE was 13.5%.A recently published study
from Dept. of Medicine, AIIMS, New Delhi by Pandey et al15, 75%
of the patients admitted to Medicine ward and medicine ICU had
the highest risk for DVT and PE. Only 12.5% had DVT prophylaxis
within first two days of admission. They emphasized the need to
aggressively implement DVT risk stratification strategy in medical
patients and provide prophylaxis unless contraindicated. Shead et
al16 found a 28% incidence of post operative DVT in 50 paients
above 50 years of age in South India.
Autopsy provides the final diagnosis of PE. Shead et al16 showed
major PE to have occurred in 1.9% cases in a retrospective
analysis of autopsy examination performed on 432 patients dying
postoperatively and stressed on the disproportion between
the frequent occurrence of post operative DVT and the low
incidence of PE at autopsy. In the study by Kakkar and Vasishta17
the overall incidence of PE in medical autopsies (all three groups
– fatal, contributory and incidental) was 15.9%. Incidence of PE
contributing significantly to the death of the patient (fatal and
contributory) was 12.6% . Thus PE very significantly contributed
 Venous Thromboembolism- Indian Perspective
Table 2 : Wells Prediction Rule for Diagnosing DVT :
Clinical Evaluation Table for Predicting Pretest Prob-
ability of DVT*.
Clinical Characteristics
Active cancer (treatment ongoing, within previous 6 months, or
palliative)
Paralysis,paresis, or recent plaster immobilization of the lower
extremities
Recently bedridden >3 days or major surgery within 12 weeks
requiring general or regional anesthesia.
Localized tenderness along the distribution of the deep venous
system
Entire leg swollen
Calf swelling 3 cm larger than asymptomatic side (measured 10 cm
below tibial tuberosity)
Pitting edema confined to the symptomatic leg
Collateral superficial veins (nonvaricose)
Alternative diagnosis at least as likely as deep venous thrombosis
* Clinical probability : low, <0; intermediate, 1-2 high, >3. In patients with
symptoms in both legs, the more symptomatic leg is used. Reprinted from.
Wells PS, Anderson DR, Bormanis J, et al.Value assessment of pretest prob-
ability of deep-vein thrombosis in clinical management. The lancet 1997;
351 : 1795-8.
to death in 79.24% (126/159) of above group of patients. Bergqvist
and Lindblad18 found an incidence of 23.6% PE at autopsy in surgical
patients half of whom were not operated upon. Rubenstein et al19
found an incidence of 3.4% (Fatal and contributory) at autopsy
in medical patients. Stein et al20 found an incidence of 0.23% of
acute pulmonary embolism in tertiary care general hospital but
a previous study by Datta et al21 from the same institute found
an incidence of 3.1% at autopsy, but their study was purely based
on gross morbid anatomical analysis only. Antemortem diagnosis
of PE has been poor in various studies carried out in different
parts of the world22,23. Kakkar and Vasistha17 found that PE affected
younger population as 79.87% of the overall patients, 66.67% of
the fatal group and 73% of combined group. This is incontrast
to western studies where young adults or adolescents were
occasionally affected.
Diagnosis of VTE & PE
It is difficult to establish an accurate diagnosis of VTE because of
its nonspecific history, and clinical findings and the lack of simple,
conclusive, low cost , low risk test for establishing a diagnosis.
Major PE remains undiagnosed in around 40 – 70% cases because
of such reasons. A clinical practice guideline from the American
Academy of Family Physicians and the American College of
Physicians summarize, the current approaches for the diagnosis
of VTE / PE 24.
Recommendation 1: Validated clinical prediction rules should be
used to estimate pretest probability of VTE, both DVT and PE and for
the basis of interpretation of subsequent tests.
Recommendation 2 : In appropriately selected patients with
Table 3 : Wells Prediction Rule for Diagnosing Pulmo-
nary Embolism : Clinical Evaluation Table for Predicting
Pretest Probability of Pulmonary Embolism*
Score Clinical Characteristics Score
1 Previous pulmonary embolism or deep venous thrombosis +1.5
Heart rate > 100 beats per minute + 1.5
1 Recent surgery or immobilization +1.5
Clinical signs of deep venous thrombosis +3
1 Alternative diagnosis less likely than pulmonary embolism +3
Hemoptysis +1
1 Cancer +1
* Clinical probability of pulmonary embolism : low, 0-1; intermediate, 2-6;
1
high, >7, Reprinted from Am J. Med. 2002; 113 : Chagnon I, Bounameaux H,
1
Aujesky D, et al, Comaprision of two clinical prediction rules and implicit
assessment among patients with suspected pulmonary embolism 269-275.
1
1 low pretest probability of DVT or PE, obtaining a high sensitivity D-dimer
-2 is a reasonable option, and if negative indicate a low likelihood of VTE.
Recommendation - 3 :Ultrasound is recommended for patients
with intermediate to high pretest probability of DVT in the lower
extremeties.
Recommendation-4 : Patients with intermediate or high pretest
probability of PE require diagnostic imaging studies.
Thromboprophylaxis : Almost all hospitalized patients have
at least one risk factor forVTE, and approximately 40% have three
or more risk factors.Without thromboprophylaxis, the incidence
of objectively confirmed, hospital acquired DVT is shown in
Table -425. The mortality, acute and long term morbidities and
resource utilization related to unpreventedVTE strongly supports
for effective preventive strategies at least for moderate to high
risk patients25. Evidence based consensus guideline for VTE
prophylaxis have been available for more than 15 years, despite
which VTE prophylaxis remains under-used globally2.According to
ENDORSE Study2 of hospitals from 32 countries worldwide,about
65% of surgical patients and 42% of medical patients were found
to be at risk of VTE, however only 59% of surgical and less than
half (40%) of medically ill patients received thromboprophylaxis.
In India, while a comparable portion (45%) of medical in- patients
were found to be at risk, only 19% received thromboprophylaxis.
There is increased use ofVTE thromboprophylaxis among surgical
patients than medical patients worldwide because of several
reasons.According to Pandey et al15 from AIIMS, New Delhi, 75% of
the patients admitted to the medicine ward and medical ICU had
the highest risk of DVT & PE but only 12.5% had DVT prophylaxis
within first two days of admission.Within two weeks of admission,
30.8% of patients were discharged, and 16.2% died. 72.6% of the
patients still in the wards belonged to the highest risk category.
Rationale for Thromboprophylaxis :
The rationale for use of thromboprophylaxis is based on solid
principles and scientific evidences (Table 5)25.
331
 Medicine Update 2010  Vol. 20
Table 4 : Approximate Risk of DVT in Hospitalized
Patients*
Patient Group DVT Prevalence, %
Medical patients 10 – 20
General Surgery 15 – 40
Major gynecologic surgery 15 – 40
Major urologic surgery 15 – 40
Neurosurgery 15 – 40
Stroke 20 – 50
Hip or knee arthroplasty, HFS* 40-60
Major trauma 40-80
SCI* 60-80
Critical Care patients - 80
Rates based on objective diagnostic screening of asymptomatic DVT in
patients not receiving thromboprophylaxis.
* HFS: Hip fracture surgery, * SCI : Spinal cord Injury.
Thromboembolism risk Stratification :
There are two general approaches in making thromboprophylaxis
decission . One is “individualized” risk stratification and other is
“group-specific” risk stratification.At present American College of
Chest Physicians recommends “group specific risk stratification”25
8th ACCP Guidelines for
Thromboprophylaxis25
According to the guidelines issued by 8th American College of
Chest Physicians (ACCP) consensus on Antithrombotic and
thrombolytic therapy.
i. For every general hospital, a formal active strategy that ad-
dresses the prevention of VTE be developed (Grade IA).
ii. Mechanical methods of thromboprophylaxis be sued pri-
marily in patients at high risk for bleeding (Grqade IA) or
possible an adjunct to anticoagulant - based thrombopro-
phylaxis (Grade 2A).
iii. For acutely ill medical patients admitted to hospital with
CHF or severe respiratory disease or who are confined to
bed and have one or more additional risk factors includ-
ing active cancer, previous VTE, sepsis, acute neurologic dis-
ease, or inflammatory bowel disease, thromboprophylaxis
with low molecular weight heparin - LMWH (Grade IA),
low dose unfractionated heparin- LDUH (Grade –IA), or
fondaparinux (Grade IA) is recommended for patients hav-
ing contraindication to anticoagulant prophylaxis, the opti-
mal use of mechanical thromboprophylaxis with graduated
compression stocking (GCS) or Intermittent pneumatic
compression (IPC) is recommended (Grade IA).
iv. For patients admitted to a critical care unit, routine assess-
ment for VTE risk and routine thromboprophylaxis in most
is recommended. (Grade IA). Patients at moderate risk of
VTE thromboprophylaxis using LMWH or LDUH is rec-
ommended (Grade IA).
332
Table 5 : Rationale of Thromboprophylaxis in Hospital-
ized Patients
High prevalence of VTE
Almost all hospitalized patients have one or more risk factors for VTE
DVT is common in many hospitalized patient groups.
Hospital – acquired DVT and PE are usually clinically silent
It is difficult to predict which at – risk patients will develop
Symptomatic thromboembolic complications.
Screening at –risk patients using physical examination or
Noninvasive testing is neither cost-effective nor effective
Adverse consequences of unprevented VTE
Symptomatic DVT and PE
Fatal PE
Cost of investigating symptomatic patients
Risk and costs of treating unprevented VTE
Increased future risk of recurrent VTE
Chronic postthrombotic syndrome
Efficacy and effectiveness of thromboprophylaxis
Thromboprophylaxis is highly efficacious at preventing DVT and
proximal DVT
Thromboprophylaxis is highly effective at preventing Symptomatic
VTE and fatal PE
The prevention of DVT also prevents PE
Cost effectiveness of thromboprophylaxis has repeatedly been dem-
onstrated.
v. Patients who are at higher risk, thromboprophylaxis using
LMWH is recommended (Grade IA). Patients who are at
high risk for bleeding, optimal use of mechanical thrombo-
prophylaxis with GCS and / or IPC at least until the bleeding
risk decreases is recommended (Grade IA). When bleed-
ing risk decreases, pharmacologic thromboprophylaxis be
substituted for or added to mechanical thromboprophylaxis
(Grade I C)
vi. Use of aspirin alone as thromboprophylaxis against VTE for
any patient group is not recommended (Grade I A)
vii. Hence, for Indian patients it is advisable to follow the ACCP
recommendations for VTE prophylaxis. However, in re-
source limited settings UFH is likely to be more cost effec-
tive than LMWHs.
8th ACCP Guidelines for Antithrombotic
Therapy for VTE26
1. For patients with objectively confirmed DVT /PE, antico-
agulant therapy with SC LMWH, monitored IV or SC UFH,
unmonitored weight based SC UFH or SC fondaparinux
is recommended (all Grade IA). For patients with a high
clinical suspicion of DVT / PE treatment with anticoagu-
lants while awaiting the outcome of diagnostic tests (Grade
IC). For patients with confirmed PE early evaluation of the
risk to benefits of thrombolytic therapy is recommended
(Grade IC). For those with haemodynamic compromise
short course thrombolytic therapy is recommended (grade
I B) and for those with non-massive PE use of thrombolytic
 Venous Thromboembolism- Indian Perspective
therapy is not recommended (Grade IB).
2. In acute DVT /PE, initial treatment with LMWH, UFH, or
Fondaparinux for at least 5 days rather than a shorter
period is recommended (grade I C) and initiation of vita-
min K antagonists (VKAs) together with LMWH, UFH, or
fondaparinux on the first treatment day and discontinua-
tion of these heparin preparations when the INR is > 2.0
for at least 24 hrs (Grade IA).
3. For patients of DVT / PE secondary to a transient risk factor
(reversible), treatment with a Vit K antagonist for 3 months
is recommended (Grade IA) and then all patients are evalu-
ated for the risks to benefits of indefinite therapy (Grade
IC). Indefinite anticoagulation therapy is recommended for
first unprovoked proximal DVT or PE and low risk of bleed-
ing when this is consistent with patients preference (Grade
IA) and for most patients with a second unprovoked DVT
(Grade IA).
4. Dose of VKA be adjusted to maintain a target INR of 2.5
(INR range 2.0 – 3.0) for all treatment durations (Grade IA)
5. For prevention of post thrombotic syndrome (PTS) after
proximal DVT, use of an elastic compression stocking is rec-
ommended (Grade IA).
6. For DVT of upper extremity, similar treatment as for DVT
of leg is recommended (Grade IC).
7. Selected patients with lower extremity (Grade 2B) and up-
per extremity (Grade 2 C) DVT, thrombus removal using
catheter based thrombolytic techniques may be considered.
8. For extensive superficial vein thrombosis, treatment with
prophylactic or intermediate doses LMWH or intermediate
doses UFH for 4 weeks is recommended (Grade IB).
ROLE OF STATINS IN PREVENTION OF VTE27:
Jupiter trial, a randomized trial reveals that rosuvastatin (20mg
/ day) was associated with a significant reduction in the risk of
VTE, an independent benefit of statin use. During a median follow
up period of 1.9 years (maximum 5 years) the rates of VTE were
0.18 and 0.32 events per 100 person – years in rosuvastatin and
placebo groups respectively. The rates of PE were 0.09 and 0.12
events per 100 person years in the rosuvastatin and placebo
groups respectively. Rosuvastatin apart from its favourable lipid
profile and anti-inflammatory properties inhibits isoprenylation of
signalling proteins, reduces tissue factor expression and thrombin
generation, attenuates fibrinogen cleavage and activation of factor
V &VII. Statins augment the activity of transcription factor Kruppel
- like factor 2 (KLF-2) promoting thrombomodulin expression on
endothelial cells, thereby enhancing the activity of the protein-C
– anticoagulant pathway.
CONCLUSION
VTE is a major public health issue globally. Incidence of VTE in the
333
Indian sub-continent is underestimated. Indian scenario is very
much like that of the western scenario. Despite solid scientific
evidences, VTE prophylaxis remain under- used even in premier
institutes. Hospital wide strategies to assess patients’ VTE risk
should be implemented, together with measures that ensure that
at-risk patients receive appropriate VTE prophylaxis.
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