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pschycotherapy for the treatment of pelvic congestion , Br J Obstet
https://t.me/med1917
Gynaecol. 1989 . 96 : 1153–1162.
16. Reginald PW , Beard RW , Kooner JS , etal. Intravenous dihydroer­gotamine to relieve pelvic congestion with pain in young women , Lancet. 1987 . 330 ( 8555 ): 351–353.
17. Beard RW , Kennedy RG , Gangar KE , et al. Bilateral oophorec­tomy and hysterectomy in the treatment of intractable pelvic pain associated with pelvic congestion , Br J Obstet Gynaecol. 1991 . 98 : 988–992.
18. Gomez ER , Villavicencio JL , Conaway CW , et al.  e manage­ment of pelvic varices by combined retroperitoneal ligation and sclerotherapy (Abstract). European American Venous Symposium, Washington, DC,  1987 .
19. Richardson GD , Beckwith TC , Mykytowycz M , Lennox AF . Pelvic congestion syndrome: Diagnosis and treatment , ANZ J Phlebol. 1999 . 3 ( 2 ): 51–56.
20. Scott J , Huskisson EC . Graphic representation of pain , Pain . 1976 . 2 : 175–184 .
21. Edwards RD , Robertson IR , McLean AB , Hemingway AP . Case report:Pelvic pain syndrome:Successful treatment of a case by ovar­ian vein embolization , Clin Radiol. 1993 . 47 : 429–431.
22. Sichlau MJ , Yao JST , Vagelzang RL . Transcatheter embolotherapy for the treatment of pelvic congestion syndrome , Obstet Gynecol. 1994 . 83 : 892–896.
23. Boomsma J , Potocky V , Kievit C , Vertrulsdonek J , Gooskens V , Weemhof R . Phlebography and embolization in women with pelvic vein insu ciency , MedicaMundi. 1998 . 42 ( 2 ): 22–29.
24. Cordts P , Eclavea A , Buckley P , DeMaioribus C , Cockerill M , Yeager T . Pelvic congestion syndrome:Early clinical results a er transcath­eter ovarian vein embolisation , Vasc Surg. 1998 . 5 : 862–868.
25. Richardson GD , Driver B . Ovarian vein ablation:Coils or surgery?, Phlebology. 2005 . 21 ( 1 ): 16–23 .
258 • PRIMARY SUPERFICIAL VENOUS INSUFFICIENCY
P A R T  I I I
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VENOUS THROMBOEMBOLISM
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33.
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THE EPIDEMIOLOGY OF VENOUS THROMBOEMBOLISM
IN THE COMMUNITY
IMPLICATIONS FOR PREVENTION AND MANAGEMENT
J o h n A .  H e i t
INTRODUCTION
 e epidemiology of venous thromboembolism (VTE) in the community has important implications for prevention and management.  is chapter describes the incidence, sur­vival, recurrence, complications, and risk factors for deep vein thrombosis of the leg, pelvis, or arm, and its complica­tion, pulmonary embolism.  e epidemiology of thrombo­sis a ecting other venous circulations (e.g., cerebral sinus, mesenteric, renal, hepatic, portal) is beyond the scope of this review. Since population-based studies of venous thromboembolism epidemiology are most generalizable to the reader’s individual patients, this chapter focuses on data provided from studies that included the complete spectrum of the disease from well-described populations.
THE INCIDENCE OF DEEP VEIN
THROMBOSIS AND PULMONARY
EMBOLISM
 e average annual incidence rates of venous thromboem­bolism among white Americans during the 25-year period 1966 to 1990 (age- and sex-adjusted to the 1980 US white
1
population), was 117 per 100,000 person-years.
 e venous thromboembolism incidence over the 7-year period 1991 to 1997 (117.7 per 100,000; similarly adjusted, but to the 2000 US white population), had not changed signi cantly compared with the 10-year period 1981 to 1990 (116.7 per 100,000; see Figure33.1). Based on the 1991–1997 rates, 249,000 incident venous thromboembolism cases occur annually among US whites.  e incidence appears to be sim­ilar or higher among African Americans and lower among
2–6
Asian Americans and Native Americans.
Assuming that the 1991 to 1997 age- and sex-speci c venous thromboem­bolism incidence among blacks (black or African American alone) is comparable to whites, and adjusting for the di er­ent age and sex distribution of black Americans, the overall age- and sex-adjusted venous thromboembolism incidence was 77.6 per 100,000. Based on this incidence, 27,000
incident venous thromboembolism cases occur annually among US blacks, for a total of over 275,000 new venous thromboembolism cases per year in the United States.
Venous thromboembolism is predominantly a disease
1,7,8
of older age. or thrombophilia, to late adolescence.
In the absence of a central venous catheter 9
10
venous thromboembolism is rare prior
1,11
 e age- and sex-adjusted venous
thromboembolism incidence rate for persons age 15years
1
or older is 149 per 100,000.
Incidence rates increase exponentially with age for both men and women and for both deep vein thrombosis and pulmonary embolism (see
1,8
Figures33.2 and 33.3).
 e overall age-adjusted incidence
rate is higher for men (130 per 100,000) than women (110
1
per 100,000; male:female sex ratio is 1.2:1).
Incidence rates are somewhat higher in women during the childbearing years, whereas incidence rates a er age 45years are gener­ally higher in men. Pulmonary embolism accounts for an increasing proportion of venous thromboembolism with
1
increasing age for both genders.
SURVIVAL AFTER DEEP VEIN
THROMBOSIS AND PULMONARY
EMBOLISM
Survival a er venous thromboembolism is worse than expected, and survival a er pulmonary embolism is much worse than a er deep vein thrombosis alone (see
12–14
Table 33.1).
 e risk of early death among patients with symptomatic pulmonary embolism is 18-fold higher compared with patients with deep vein thrombosis
12
alone.
Pulmonary embolism is an independent predic­tor of reduced survival for up to 3 months. For almost one-quarter of pulmonary embolism patients, the initial clinical presentation is sudden death. Independent pre­dictors of reduced early survival a er venous thrombo­embolism include increasing age, male gender, lower body mass index, con nement to a hospital or nursing home at venous thromboembolism onset, congestive heart failure, chronic lung disease, serious neurological disease, and
261
250
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200
150
100
100,000
50
Adjusted annual incidence/
0
1966 1970 1975 1980
All DVT or PE PE ± DVT DVT alone
1985 1990
Ye ar
Figure33.1 Age- and sex-adjusted annual incidence of all venous thromboembolism, deep vein thrombosis (DVT) alone, and pulmonary embolism with or without deep vein thrombosis (PE ±DVT).
Reference1)
(From
Table33.1 SURVIVAL %AFTER DEEP VEIN THROMBOSIS VERSUS PULMONARY EMBOLISM
TIME DEEP VEIN
THROMBOSIS ALONE
0days 7days 14days 30days 90days 1year 2years 5years 8years
(From Reference12)
97.0
96.2
95.7
94.5
91.9
85.4
81.4
72.6
65.2
PULMONARY
EMBOLISM
76.5
71.1
68.7
66.8
62.8
57.4
53.6
47.4
41.5
1,200
1,000
800
600
400
200
Annual incidence/100,000
0
0–14
15–19
20–24
Male Female
25–29
30–34
35–39
40–44
45–49
50–54
Age group
55–59
60–64
65–69
70–74
75–79
80–84
85 +
Figure33.2 Annual incidence of venous thromboembolism by age and gender.
(From Reference1)
1,200
1,000
800
600
400
200
Annual incidence/100,000
0
0–14
15–19
20–24
25–29
30–34
35–39
40–44
45–49
50–54
Age group
55–59
60–64
All DVT or PE
65–69
70–74
DVT alone
75–79
80–84
PE ± DVT
85 +
Figure33.3 Annual incidence of all venous thromboembolism, deep vein thrombosis (DVT) alone, and pulmonary embolism with or without deep vein thrombosis (PE ± DVT) byage.
active malignancy.
8,12,13
Additional clinical predictors of
(From Reference1)
poor early survival a er pulmonary embolism include syn-
15
cope and arterial hypotension.
Evidence of right heart
failure based on clinical examination, plasma markers (e.g.,
16,17
cardiac troponin T, brain natriuretic peptide),
13
cardiography
predicts poor survival among normoten-
or echo-
sive pulmonary embolism patients. Pulmonary embolism patients with these characteristics should receive aggressive anticoagulation therapy, and possibly thrombolytic therapy
18,19
in selected cases.
VENOUS THROMBOEMBOLISM
RECURRENCE
Venous thromboembolism recurs frequently; about 30% of patients develop recurrence within the next 10years (see
20
Table33.2, Figure33.4).
 e hazard of recurrence var­ies with the time since the incident event and is highest within the  rst 6 to 12months. However, even at 10years the hazard of recurrent venous thromboembolism never falls to zero. Although active therapeutic anticoagulation
21–23
is e ective in preventing recurrence,
the duration of anticoagulation does not a ect the risk of recurrence once primary therapy for the incident event is stopped.
24–26
 ese data suggest that for a subset of patients, venous thromboembolism is a chronic disease with episodic recur­rence; inde nite secondary prophylaxis may be warranted for this patient subset.
21–23,26,27
recurrence include male gender,
Independent predictors of
20,28,29
increasing patient age and body mass index, neurological disease with extrem­ity paresis, and active malignancy (see Table33.3).
8,20,30–33
Additional predictors include “idiopathic” venous throm-
22,24,33
boembolism, lipid antibody,
Table33.2 CUMULATIVE INCIDENCE AND HAZARD OF VENOUS THROMBOEMBOLISM RECURRENCE
VENOUS THROMBOEMBOLISM RECURRENCE
TIME TO
RECURRENCE
0days 7days 30days 90days 180days 1year 2years 5years 10years
(From Reference20)
a lupus anticoagulant or antiphospho-
22,34
antithrombin, protein C or protein
CUMULATIVE
RECURRENCE
%
0.0
1.6
5.2
8.3
10.1
12.9
16.6
22.8
30.4
HAZARD OF RECURRENCE
PER 1,000
PERSONDAYS ±SD
0 170 (30) 130 (20)
30 (5) 20 (4) 20 (2) 10 (1)
6 (1) 5 (1)
262 • VENOUS THROMBOEMBOLISM
40
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30
20
10
Cumulative recurrence (%)
0
012345678910
Figure33.4 Cumulative incidence of  rst venous thromboembolism recurrence (—), and the hazard of  rst recurrence per 1000 person-days (---).
(From Reference20)
Yea r s
200
Hazard rate/1,000 person-ddays
150
100
50
0
S de ciency, 35 and possibly persistent residual deep vein
36
thrombosis.
Prolonged secondary prophylaxis with anti­coagulation therapy should be considered for patients with these characteristics. Although the incident event type (deep vein thrombosis alone vs. pulmonary embolism) is not a predictor of recurrence, patients with recurrence are signi cantly more likely to recur with the same event
37,38
type as the incident event type.
Because the 7-day case fatality rate is signi cantly higher for recurrent pulmonary embolism (34%) compared to recurrent deep vein throm-
38
bosis alone (4%),
prolonged anticoagulation should be considered for incident pulmonary embolism, especially for patients with chronically reduced cardiopulmonary f u n c t i o n a l r e s e r v e .
COMPLICATIONS OF VENOUS
THROMBOEMB OLISM
 e major complications of venous thromboembolism are venous stasis syndrome (e.g., postthrombotic syndrome, including dependent leg swelling and pain, stasis pigmenta­tion and dermatitis, and dermatoliposclerosis) and venous ulcer, and chronic thromboembolic pulmonary hyperten­sion.  e overall incidence of venous stasis syndrome and venous ulcer is 76.1 and 18.0 per 100,000 person-years,
Table33.3 INDEPENDENT PREDICTORS OF VENOUS THROMBOEMBOLISM RECURRENCE
CHARACTERISTIC HAZARD
Age* Body Mass Index† Neurologic Disease with Extremity
Paresis Active Malignancy Malignancy with Chemotherapy Malignancy without Chemotherapy
*per decade increase inage. †per 10kg/m (From Reference20)
2
increase in body massindex.
RATIO
1.17
1.24
1.87
4.24
2.21
95% CI
1.11, 1.24
1.04, 1.47,
1.28, 2.73
2.58, 6.95
1.60, 3.06
39
respectively. a 17-fold increased risk of venous stasis syndrome.
Venous thromboembolism patients have
39
 e 20-year cumulative incidence of venous stasis syndrome a er venous thromboembolism and a er proximal deep vein thrombosis are about 25% and 40%, respectively.
32,40
Risk factors for venous stasis syndrome include the venous thromboembolism event type (deep vein thrombosis, with or without pulmonary embolism) and deep vein thrombo­sis location (proximal deep vein thrombosis).  e 20-year
40
cumulative incidence of venous ulcer is 3.7%.
 e risk for
venous ulcer is increased 30% per decade of age at the inci-
40
dent venous thromboembolism.
Venous thromboembo-
lism accounts for about 12% of all venous stasis syndrome
39
occurring in the community.
 e incidence of chronic thromboembolic pulmonary
hypertension over the 21-year period 1976 to 1996 was 6.5
41
per million person-years.
Over this same time period, the incidence of acute pulmonary embolism was 485.6 per mil­lion person-years.  us, the vast majority of acute pulmo­nary emboli do not progress to chronic thromboembolic pulmonary hypertension. Applying these incidence rates to the 2000 US white population, approximately 1,367 new chronic thromboembolic pulmonary hypertension cases occur in the United States annually.
RISK FACTORS FOR VENOUS
THROMBOEMB OLISM
In order to improve survival, avoid recurrence, prevent com­plications, and reduce health care costs, the occurrence of venous thromboembolism must be reduced. To accomplish this, persons at risk for venous thromboembolism  rst must be identi ed. Independent risk factors for venous throm­boembolism include patient age, surgery, trauma, hospital or nursing home con nement, active malignant neoplasm with or without concurrent chemotherapy, central vein catheterization or transvenous pacemaker, prior super ­cial vein thrombosis, varicose veins among the young, and neurological disease with extremity paresis; patients with chronic liver disease have a reduced risk (see Table33.4).
42,43
 e incidence of venous thromboembolism increases signif­icantly with age for both idiopathic and secondary venous thromboembolism, suggesting that the risk associated with advancing age may be attributable to the biology of aging rather than simply an increased exposure to venous throm-
44
boembolism risk factors with advancing age.
Compared to residents in the community, hospitalized residents have over a 150-fold increased incidence of acute venous throm-
45
boembolism.
Hospitalization and nursing home resi­dents together account for almost 60% of incident venous thromboembolism events occurring in the community.
46
 us, hospital con nement provides an important oppor­tunity to signi cantly reduce venous thromboembolism incidence. Of note, hospitalization for medical illness and
THE EPIDEMIOLOGY OF VENOUS THROMBOEMBOLISM IN THE COMMUNITY • 263
Table33.4 INDEPENDENT RISK FACTORS FOR DEEP
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VEIN THROMBOSIS OR PULMONARY EMBOLISM
BASELINE CHARACTERISTIC ODDS RATIO 95% CI
Institutionalization with or without
recent surgery
Institutionalization without
recent surgery
Institutionalization with
recentsurgery Tr auma No malignancy Malignancy without chemotherapy Malignancy with chemotherapy Prior central venous catheter or
transvenous pacemaker Prior super cial vein thrombosis Neurologic disease with extremity
paresis Serious liver disease
(From Reference 42)
7.98
21.72
12.69
1.0
4.05
6.53
5.55
4.32
3.04
0.10
4.49, 14.18
9.44, 49.93
4.06, 39.66
1.93, 8.52
2.11, 20.23
1.57, 19.58
1.76, 10.61
1.25, 7.38
0.01, 0.71
hospitalization for surgery account for almost equal pro­portions of venous thromboembolism (22% and 24%, respectively), emphasizing the need to provide prophylaxis to both of these risk groups. Nursing home residents inde­pendently account for over one-tenth of all venous throm-
46
boembolism disease in the community.
 e risk among surgery patients can be further strati ed
based on patient age, type of surgery, and the presence of
47,48
active cancer. boembolism increases with advancing patient age, cially for surgery patients that are 65years of age or older.
 e risk of postoperative venous throm-
49
espe-
48
High-risk surgical procedures include neurosurgery; major orthopedic surgery of the leg ; thoracic, abdominal, or pelvic surgery for malignancy; renal transplantation; and cardio-
48
vascular surgery.
Obesity
of Anesthesiology physical status
49–51
and poor American Society
51
are risk factors for venous thromboembolism a er total hip arthroplasty. Other inde­pendent risk factors for venous thromboembolism a er major surgery (a er controlling for active cancer) include intensive care unit (ICU) length of stay greater than 6days,
49
immobility, and infection.
 e risk from surgery may be
less with neuraxial (spinal or epidural) anesthesia compared
52
to general anesthesia.
Risk factors for venous thromboem­bolism among patients hospitalized for acute medical illness may include active cancer and prior venous thromboembo-
53
A er controlling for active cancer, additional inde-
lism. pendent risk factors include increasing patient age and body mass index, prior super cial vein thrombosis, chronic renal disease, neurological disease with extremity paresis, fracture
54
and immobility,
and possibly infection. 53
Active cancer accounts for almost 20% of incident
venous thromboembolism events occurring in the commu-
46
 e risk appears to be higher for patients with pan-
nity. creatic cancer, lymphoma, malignant brain tumors, cancer of the liver, leukemia, and colorectal and other digestive
55,56
cancers.
Cancer patients receiving immunosuppressive
or cytotoxic chemotherapy are at even higher risk for venous thromboembolism,
42
including therapy with
L-asparaginase, thalidomide, or tamoxifen.
A central venous catheter or transvenous pacemaker
now accounts for 9% of incident venous thromboembolism
46
occurring in the community.
Prior super cial vein throm­bosis is an independent risk factor for subsequent deep vein thrombosis or pulmonary embolism remote from the
42
episode of super cial thrombophlebitis.
 e risk of deep
vein thrombosis imparted by varicose veins is uncertain and
42
appears to vary by patient age.
Long-haul (>6 h) air travel is associated with a slightly increased risk for venous throm­boembolism that is preventable with elastic stockings. Coenzyme Areductase inhibitor (statin) therapy may pro­vide a 20 to 50% risk reduction for venous thromboembo-
58
However, the risk associated with atherosclerosis, or
lism. other risk factors for atherosclerosis, remains uncertain. Body mass index, current or past tobacco smoking, chronic obstructive pulmonary disease, and renal failure are not inde­pendent risk factors for venous thromboembolism a er con­trolling for other risk factors (e.g., surgery, hospitalization,
42
trauma). independent of hospitalization, is low.
 e risk associated with congestive heart failure,
42,43
Among women,
additional risk factors for venous thromboembolism include
62
oral contraceptive use and hormone therapy
and therapy
with the selective estrogen receptor modulator, raloxifene,
43,63
and pregnancy and the postpartum period.
Compared to nonpregnant women of childbearing age, the venous throm­boembolism risk among pregnant women is increased over four-fold.
64
 e annual venous thromboembolism incidence is  ve-fold higher among postpartum compared to pregnant women (511.2 versus 95.8 per 100,000), and the incidence of deep venous thrombosis is three-fold higher than pulmo­nary embolism (151.8 versus 47.9 per 100,000). Pulmonary embolism is relatively uncommon during pregnancy com­pared to postpartum (10.6 versus 159.7 per 100,000).
Other conditions associated with venous thromboem­bolism include heparin-induced thrombocytopenia, myelo­proliferative disorders (especially polycythemia rubra vera and primary thrombocythemia), intravascular coagulation and  brinolysis/disseminated intravascular coagulation (ICF/DIC), nephrotic syndrome, paroxysmal nocturnal hemoglobinuria, thromboangiitis obliterans (Buerger’s dis­ease), thrombotic thrombocytopenic purpura, Bechet’s syn­drome, systemic lupus erythematosus, in ammatory bowel disease, Wegener’s granulomatosis, homocystinuria, and
65,66
possibly hyperhomocysteinemia.
T H E G E N E T I C
EPIDEMIOLOGY OF VENOUS
THROMBOEMB OLISM
Recent family-based studies indicate that venous thrombo­embolism is highly heritable and follows a complex mode
59–61
57
264 • VENOUS THROMBOEMBOLISM
of inheritance involving environmental interaction.
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67–69
Inherited reductions in plasma natural anticoagulants (e.g., antithrombin, protein C, or protein S) have long been rec­ognized as uncommon but potent risk factors for venous
70,71
thromboembolism.
More recent discoveries of impaired
downregulation of the procoagulant system (e.g., acti-
72–74
vated protein C resistance, Factor V Leiden),
increased plasma concentrations of procoagulant factors (e.g., factors I [ brinogen], II [prothrombin], VIII, IX, and XI),
80–82
increased basal procoagulant activity,
83
nolysis,
and altered innate immunity 84 have added new
impaired  bri-
75–79
paradigms to the list of inherited or acquired disorders predisposing to thrombosis (thrombophilia).  ese plasma hemostasis-related factors or markers of coagulation activa­tion both correlate with increased thrombotic risk and are
85–89
highly heritable.
Inherited thrombophilias interact with
such clinical risk factors (e.g., environmental risk factors) as
90
oral contraceptives,
93
surgery
to increase the risk of incident venous thrombo-
pregnancy, 91 hormone therapy, 92 and
embolism. Similarly, genetic interaction increases the risk of incident
94
and recurrent venous thromboembolism.
95–99
 ese  ndings support the hypothesis that an acquired or familial thrombophilia may predict the subset of exposed persons who actually develop symptomatic venous thrombo­embolism. Although the clinical utility of diagnostic testing for an inherited or acquired thrombophilia remains contro­versial, such studies hold the potential for further identify­ing individual patients at high and low risk for incident and recurrent venous thromboembolism, targeting prophylaxis to those who would bene t most, and, ultimately, reducing the occurrence of venous thromboembolism.
R E F E R E N C E S
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Melton LJ III. Trends in the incidence of deep vein thrombosis and pulmonary embolism:A25-year population-based study , Arch Intern Med . 1998 . 158 : 585–593 .
2. White RH , Zhou H , Romano PS . Incidence of idiopathic deep
venous thrombosis and secondary thromboembolism among ethnic groups in California , Ann Intern Med . 1998 . 128 : 737–740 .
3. Klatsky AL , Armstrong MA , Poggi J . Risk of pulmonary embolism
and/or deep venous thrombosis in Asian-Americans, Am J Card . 2000 . 85 ( 11 ): 1334–1337 .
4. Stein PD , Kayali F , Olson RE , Milford CE . Pulmonary thromboem-
bolism in Asians/Paci c Islanders in the United States , Am J Med . 2004 . 116 : 435–442 .
5. Hooper WC , Holman RC , Heit JA , Cobb N . Venous thromboem-
bolism hospitalizations among American Indians and Alaska Natives ,  romb Res . 2002 . 108 ( 5–6 ): 273–278 .
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Venous thromboembolism according to age:Impact of an aging pop­ulation , Arch Intern Med . 2004 . 164 : 2260–2265 .
8. Cushman M , Tsai AW , White RH , etal. Deep vein thrombosis and
pulmonary embolism in two cohorts: e Longitudinal Investigation of  romboembolism Etiology , Am J Med . 2004 . 117 : 19–25 .
9. Massicote MP , Dix D , Monagle P , Adams M , Andrew M . Central venous catheter related thrombosis in children: Analysis of the Canadian Registry of Venous  romboembolic Complications , J Pediatr . 1998 . 133 : 770–776 .
10. Tormene D , Simioni P , Prandoni P , etal.  e incidence of venous thromboembolism in thrombophilic children:Aprospective cohort study , Blood . 2002 . 100 ( 7 ): 2403–2405 .
11. van Ommen CH , Heijboer H , Büller HR , Hirasing RA , Heijmans HSA , Peters M . Venous thromboembolism in childhood:Aprospec­tive two-year registry in  e Netherlands , J Pediatr . 2001 . 139 : 676–681 .
12. Heit JA , Silverstein MD , Mohr DN , Petterson TM , O’Fallon WM , Melton LJ III. Predictors of survival a er deep vein thrombosis and pulmonary embolism:Apopulation-based cohort study , Arch Intern Med . 1999 . 159 : 445–453 .
13. Goldhaber SZ , Visani L , De Rosa M . Acute pulmonary embo­lism:Clinical outcomes in the International Cooperative Pulmonary Embolism Registry (ICOPER) , Lancet . 1999 . 353 : 1386–1389 .
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