Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:

Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3953_Библиотеки_им_академика_М_И_Перельмана

.pdf
Скачиваний:
0
Добавлен:
12.10.2026
Размер:
6 Мб
Скачать
☆
40. Levine MN, Gent M, Hirsh J, et al. The thrombogenic effect of anticancer drug therapy in
women with stage II breast cancer. N Engl J Med 1988; 318:404–407.
41. Wall JG, Weiss RB, Norton L, et al. Arterial thrombosis associated with adjuvant
chemotherapy for breast cancer: a cancer and leukemia group B study. Am J Med 1989;
87:501–504.
42. Fisher B, Redmond C, Legault-Poisson S, et al. Postoperative chemotherapy and tamoxifen
compared with tamoxifen alone in the treatment of positive node breast cancer patients aged
50 years and older with tumours responsive to tamoxifen: results from the national surgical
adjuvant breast and bowel project B16. J Clin Oncol 1990; 8:1005–1018.
43. Saphner T, Tormey DC, Gray R. Venous and arterial thrombosis in patients who received
adjuvant therapy for breast cancer. J Clin Oncol 1991; 9:286–294.
44. Clahsen PC, Van de Velde CJH, Julien JP, Floiras JL, Mignolet RH. Thromboembolic
complications after perioperative chemotherapy in women with early breast cancer: a
European Organization for Research and Treatment of breast cancer cooperative group study.
J Clin Oncol 1994; 12:1266–1271.
45. Rifkin SE, Green S, Metch B, et al. Adjuvant CMFVP versus tamoxifen versus concurrent
CMFVP and tamoxifen for postmenopausal node positive and estrogen receptor positive
breast cancer patients: a Southwest Oncology group study. J Clin Oncol 1994; 12:2078–2085.
46. Pritchard KI, Paterson AH, Paul NA, Zee B, Fine S, Pater J. Increased thromboembolic
complications with concurrent tamoxifen and chemotherapy in a randomized trial of adjuvant
therapy for women with breast cancer. J Clin Oncol 1996; 14:2731–2737.
47. Tempelhoff GF, Dietrich M, Hommel G, Heilmann L. Blood coagulation during adjuvant
epirubicin/cyclophosphamide chemotherapy in patients with primary operable breast cancer.
J Clin Oncol 1996; 14:2560–2568.
48. Orlando L, Colleoni M, Nole F, et al. Incidence of venous thromboembolism in breast cancer
patients during chemotherapy with vinorelbine, cisplatin, 5-fluorouracil as continuous
infusion (ViFuP regimen): is prophylaxis required? Ann Oncol 2000; 11:117–118.
49. Goodnough LT, Saito A, Manni A, Jones PK, Pearson OH. Increased incidence of
thromboembolism in stage IV breast cancer patients treated with a five-drug chemotherapy
regimen: a study of 159 patients. Cancer 1984; 54:1264–1268.
50. Pritchard KI, Paterson AH, Paul NA, Zee B, Fine S, Pater J. Increased thromboembolic
complication with concurrent tamoxifen and chemotherapy in a randomized trial of adjuvant
therapy for women with breast cancer. J Clin Oncol 1996; 14:2731–2737.
51. Deitcher SR, Gomes MPV. The risk of venous thromboembolic disease associated with
adjuvant hormone therapy for breast carcinoma. Cancer 2004; 101:439–449.
52. Verso M, Agnelli G. Venous thromboembolism associated with long-term use of central
venous catheters in cancer patients. J Clin Oncol 2003; 21:3665–3675.
53. Bern MM, Lokich JJ, Wallach SR, et al. Very low dose of warfarin can prevent thrombosis in
central venous catheters. A prospective trial. Ann Intern Med 1990; 112:423–428.
54. Monreal M, Alastrue A, Rull M, et al. Upper extremity deep venous thrombosis in cancer
patients with venous access devices- prophylaxis with a low molecular weight heparin
(fragmin). Thromb Haemost 1996; 75:251–253.
55. Levine MN, Lee AY, Kakkar AK. From Trousseau to targeted therapy: new insights and
innovations in thrombosis and cancer. J Thromb Haemost 2003; 1:1456–1463.
56. Geerts WH, Pineo GF, Heit JA, et al. Prevention of venous thromboembolism: the Seventh
ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 2004;
126:338S–400S.
57. Bergqvist D, Burmark US, Flordal PA, et al. Low molecular weight heparin started before
surgery as prophylaxis against deep vein thrombosis: 2500 versus 5000 XaI units in 2070
patients. Br J Surg 1995; 82:496–501.
58. Enoxacan Study Group. Efficacy and safety of enoxaparin versus unfractionated heparin for
prevention of deep vein thrombosis in elective cancer surgery: a double-blind randomized
multicentre trial with venographic assessment. Br J Surg 1997; 84:1099–1103.
Prandoni et al.168
59. McLeod RS, Geerts WH, Sniderman KW, et al. Subcutaneous heparin versus low-molecular-
weight heparin as thromboprophylaxis in patients undergoing colorectal DVT prophylaxis
trial: a randomized, double-blind trial. Ann Surg 2001; 233:438–444.
60. Agnelli G, Bergqvist D, Cohen AT, Gallus AS, Gent M. Randomized clinical trial of
postoperative fondaparinux versus perioperative dalteparin for prevention of venous
thromboembolism in high-risk abdominal surgery. Br J Surg 2005; 92:1212–1220.
61. Rasmussen MS, Jorgensen LN, Wille-Jorgensen JP, et al. Prolonged prophylaxis with low
molecular weight heparin (dalteparin) after major abdominal surgery: the Fame study.
Programs and Abstracts of the XIX Congress of the International Society on Thrombosis and
Haemostasis, Birmingham, England, July 12–18, 2003. Malden, Mass: Blackwell Publishing,
2003, abstract (computer disk).
62. Wells PS, Lensing AWA, Hirsh J. Graduated compression stockings in the prevention of
postoperative venous thromboembolism: a meta-analysis. Arch Intern Med 1994; 154:67–72.
63. Nurmohamed MT, van Riel AM, Henkens CM, et al. Low molecular weight heparin and
compression stockings in the prevention of venous thromboembolism in neurosurgery.
Thromb Haemost 1996; 75:233–238.
64. Agnelli G, Piovella F, Buoncristiani P, et al. Enoxaparin plus compression stockings
compared with compression stockings alone in the prevention of venous thromboembolism
after elective neurosurgery. N Engl J Med 1998; 339:80–85.
65. Levine MN, Hirsh J, Gent M, et al. Double-blind randomized trial of very-low-dose warfarin
for prevention of thromboembolism in stage IV breast cancer. Lancet 1994; 343:886–889.
66. Bern MM, Bothe A, Jr., Bistrian B, Champagne CD, Keane MS, Blackburn GL. Prophylaxis
against central vein thrombosis with low-dose warfarin. Surgery 1986; 99:216–221.
67. Couban S, Goodyear M, Burnell M, et al. A randomized, double-blind, placebo-controlled
study of low-dose warfarin for the prevention of symptomatic central venous catheter-
associated thrombosis in patients with cancer. Blood 2002; 100:70a.
68. Heaton DC, Han DY, Inder A. Minidose warfarin as prophylaxis for central vein catheter
thrombosis. Intern Med 2002; 32:84–88.
69. Reichardt P, Kretzschrnar A, Biakhov M, et al. A phase III double-blind,.placebo-controlled
study evaluating the efficacy and safety of daily low-molecular-weight heparin (dalteparin) in
preventing catheter-related complications in cancer patients with central venous catheters.
Clin Oncol 2002; 21:1474a.
70. Klerk CP, Smorenburg SM, Buller HR. Thrombosis prophylaxis in patient populations with
a central venous catheter. A systematic review. Arch Intern Med 2003; 163:1913–1921.
71. Prandoni P, Lensing AWA, Cogo A, et al. The long-term clinical course of acute deep venous
thrombosis. Ann Intern Med 1996; 125:1–7.
72. Hansson PO, Sorbo J, Eriksson H. Recurrent venous thromboembolism after deep vein
thrombosis. Incidence and risk factors. Arch Intern Med 2000; 1260:769–774.
73. Heit JA, Mohr DN, Silverstein MD, Petterson TM, O’Fallon WM, Melton LJ, III. Predictors
of recurrence after deep vein thrombosis and pulmonary embolism. A population-based
cohort study. Arch Intern Med 2000; 160:761–768.
74. Hutten B, Prins M, Gent M, Ginsberg J, Tijsen JGP, Buller HR. Incidence of recurrent
thromboembolic and bleeding complications among patients with venous thromboembolism
in relation to both malignancy and achieved international normalized ratio: a retrospective
analysis. J Clin Oncol 2000; 18:3078–3083.
75. Palareti G, Legnani C, Agnes L, et al. A comparison of the safety and efficacy of oral
anticoagulation for the treatment of venous thromboembolic disease in patients with or
without malignancy. Thromb Haemost 2000; 84:805–810.
76. Prandoni P, Lensing AWA, Piccioli A, et al. Recurrent venous thromboembolism and
bleeding complications during anticoagulant treatment in patients with cancer and venous
thrombosis. Blood 2002; 100:3484–3488.
77. Lee AY, Levine MN, Baker RI, et al. Low-molecular-weight heparin versus a coumarin for
the prevention of recurrent venous thromboembolism in patients with cancer. N Engl J Med
2003; 349:146–153.
Venous Thromboembolism and Malignant Diseases 169
78. Meyer G, Marjanovic Z, Valcke J, et al. Comparison of low-molecular-weight heparin and
warfarin for the secondary prevention of venous thromboembolism in patients with cancer.
Arch Intern Med 2002; 162:1729–1735.
79. Zacharski LR, Henderson WG, Rickles FR, et al. Effect of warfarin anticoagulation on
survival in carcinoma of the lung, colon, head and neck, and prostate. Cancer 1984;
53:2046–2052.
80. Dolovich LR, Ginsberg JS, Douketis JD, Holbrook AM, Cheah G. A meta-analysis comparing
low-molecular-weight heparins with unfractionated heparin in the treatment of venous
thromboembolism. Arch Intern Med 2000; 160:181–188.
81. Zacharski LR. Anticoagulants in cancer treatment: malignancy as a solid phase coagulopathy.
Cancer Lett 2002; 186:1–9.
82. Klerk CPW, Smorenburg SM, Buller HR. Antimalignant properties of antithrombotic agents.
In: Lugassy G, Falanga A, Kakkar AK, Rickles FR, eds. Thrombosis and Cancer. London:
Taylor & Francis Group, 2004:207–222.
83. Kakkar AK, Levine MN, Kadziola Z, et al. Low molecular weight heparin, therapy with
dalteparin, and survival in advanced cancer: The Fragmin Advanced Malignancy Outcome
Study. J Clin Oncol 2004; 22:1944–1948.
84. Klerk CPW, Smorenburg, SM, Otten, HYM, et al. The effect of low-molecular-weight
heparin on survival in patients with advanced malignancy. J Clin Oncol 2005; 23:2130–2135.
85. Altinbas M, Coskun HS, Er O, et al. A randomized clinical trial of combination chemotherapy
with and without low-molecular-weight heparin in small cell lung cancer. J Thromb Haemost
2004; 2:1266–1271.
86. Schulman S, Lindmarker P. Incidence of cancer after prophylaxis with warfarin against
recurrent venous thromboembolism. N Engl J Med 2000; 342:1953–1958.
87. Taliani MR, Agnelli G, Prandoni P, et al. Incidence of cancer after a first episode of idiopathic
venous thromboembolism treated with 3 months or 1 year of oral anticoagulation. J Thromb
Haemost 2003; 1:1730–1733.
88. Rege KP, Jones S, Day J, Hoggarth CE. In proven deep vein thrombosis, a low positive
D-Dimer score is a strong negative predictor for associated malignancy. Thromb Haemost
2004; 91:1219–1222.
89. Aderka D,Brown A, Zelikovski A, Pinkhas J. Idiopathic deep vein thrombosis in an apparently
healthy patient as a premonitory sign of occult cancer. Cancer 1986; 57:1846–1849.
90. Prandoni P, Lensing AWA, Bu
¨
ller HR, et al. Deep-vein thrombosis and the incidence of
subsequent symptomatic cancer. N Engl J Med 1992; 327:1128–1133.
91. Ahmed Z, Mohuddin Z. Deep vein thrombosis as a predictor of cancer. Angiology 1996;
47:261–265.
92. Monreal M, Fernandez-Llamazares J, Perandreu J, Urrutia A, Sahuquillo JC, Contel E. Occult
cancer in patients with venous thromboembolism: which patients, which cancers. Thromb
Haemost 1997; 78:1316–1318.
93. Hettiarachchi RJK, Lok J, Prins MH, Bu
¨
ller HR, Prandoni P. Undiagnosed malignancy in
patients with deep vein thrombosis. Cancer 1998; 83:180–185.
94. Rajan R, Levine M, Gent M, et al. The occurrence of subsequent malignancy in patients
presenting with deep vein thrombosis: results from a historical cohort study. Thromb Haemost
1998; 79:19–22.
95. Bura A, Cailleux N, Bienvenu B, et al. Incidence and prognosis of cancer associated with
bilateral venous thrombosis: a prospective study of 103 patients. J Thromb Haemost 2004;
2:441–444.
96. Sorensen HT, Mellemkjaer L, Steffensen H, Olsen JH, Nielsen GL. The risk of a diagnosis of
cancer after primary deep-venous thrombosis or pulmonary embolism. N Engl J Med 1998;
338:1169–1173.
97. Baron JA, Gridley G, Weiderpass E, Nyren G, Linet M. Venous thromboembolism and
cancer. Lancet 1998; 351:1077–1080.
98. Murchison JT, Wylie L, Stockton DL. Excess risk of cancer in patients with primary venous
thromboembolism: a national, population-based cohort study. Br J Cancer 2004; 91:92–95.
Prandoni et al.170
99. Sorensen HT, Mellemkjaer L, Olsen JH, Baron JA. Prognosis of cancers associated with
venous thromboembolism. N Engl J Med 2000; 343:1846–1850.
100. Monreal M, Lensing AWA, Prins MH, et al. Screening for occult cancer in patients with acute
deep vein thrombosis or pulmonary embolism. J Thromb Haemost 2004; 2:876–881.
101. Piccioli A, Lensing AWA, Prins MH, et al. Extensive screening for occult malignant disease
in idiopathic venous thromboembolism. J Thromb Haemost 2004; 2:884–889.
Venous Thromboembolism and Malignant Diseases 171
14
Venous Thrombosis Prophylaxis
Joseph A. Caprini
Feinberg School of Medicine, Northwestern University, Chicago, Illinois;
Evanston Northwestern Healthcare, Evanston, Illinois; and
Glenbrook Hospital, Glenview, Illinois, U.S.A.
Dereck W. Wentworth
U.S. Medical Affairs, New York, New York, U.S.A.
INCIDENCE AND MAGNITUDE OF THE PROBLEM
Venous thromboembolism (VTE) is a leading cause of mortality in the United States
and causes more deaths than AIDS, breast cancer, and motor vehicle crashes combined.
Pulmonary embolism (PE) is responsible for up to 200,000 fatalities annually in the United
States, while in 2002 AIDS-related deaths were seen in 14,095 individuals (1). Breast
cancer-related fatalities for the year 2002 were estimated to be 41,883 patients (2), while
U.S. highway fatalities that same year were 44,065 individuals (3). The in-hospital case
fatality rate attributed to venous thromboembolic disease is 10–25% in the United States.
Elderly patients suffering pulmonary emboli have a case fatality rate of 15% at 28 days,
while cancer patients have a 25% fatality rate at 28 days. By one year elderly VTE victims
suffered a mortality rate of 21% and cancer patients 39% (1,4,5). Most of these studies
underestimate the incidence of VTE because of low autopsy rates of 10–20%, outpatient
cases were not counted, and long-term care facility data were not considered. The actual
mortality from VTE is probably higher, but unfortunately, unlike breast cancer and AIDS,
the National Center for Health Statistics does not track deaths due to VTE.
Surgical patients have been well-studied and their risk for VTE is known. In patients
undergoing total hip replacement who do not have additional risk factors and do not
receive prophylaxis, the incidence of fatal PE is 0.2% to 0.5%. Patients who undergo
surgery for fractured hips and do not receive prophylaxis may suffer a 2.5% to 7.5%
incidence of fatal PE (6). Risk factors associated with acute inpatient mortality following
orthopedic surgery were evaluated in 43,215 patients. Conditions identified preoperatively
related to mortality included chronic renal failure, congestive heart failure, cancer with
bone metastasis, COPD, atrial fibrillation, and age over 70 years. Procedural factors
influencing mortality were found to be surgery for trauma or hip fracture, with a mortality
rate five times higher than other procedures. Mortality rates from postoperative complica-
tions were 27.6% from renal failure, 19.3% from pulmonary embolus, 19.3% from
myocardial infarction, and 8.6% each for cerebrovascular accidents and pneumonia (7).
One of the important lessons learned from this study is that mortality from surgical
173
procedures is frequently caused by pulmonary embolism, certain surgical procedures are
higher risk than others, and preoperative patient factors also affect risk of VTE. This
indicates that the choice of VTE prophylaxis should take into account all of these factors.
Surgical patients are not the only ones at risk for VTE. The incidence of thrombosis
in patients admitted to the hospital on the medical service averages 10% to 20% overall.
Patients admitted with stroke have up to a 56% incidence of DVT and those admitted to the
medical intensive care unit have a rate of DVT between 28% and 33% (8–10). Patients at
risk are those who have COPD, CHF, pneumonia, and inflammatory bowel disease. Large
randomized prospective trials in the medical population have been done and consistently
demonstrate an incidence of DVT between 10% to 20% in patients who receive no
prophylaxis (11,12).
Patients undergoing colorectal surgery have a high incidence of VTE due in part
to the long duration of surgery, pelvic resection, and the presence of cancer and/or
inflammatory bowel disease. In a series of 20,000 patients in this category, 1.8% died of
fatal pulmonary embolism despite receiving low-dose unfractionated heparin prophylaxis.
The risk of PE in untreated patients is approximately 5% (13). The incidence of DVT in
12 general surgical trials was 22% in untreated surgical subjects, while it was seen in 29%
of patients undergoing colorectal procedures (14).
There are a number of important reasons to provide thrombosis prophylaxis to
patients who are at risk for VTE, as seen in Table 1. Prandoni and others have provided
data regarding the long-term clinical course of acute DVT. In approximately 5% of
patients, DVT will recur within three months, in 18% at two years, and by eight years
following the acute event, about 30% of individuals will suffer a second DVT (15–17).
The post-thrombotic syndrome (PTS) is estimated to occur in about 25% of patients
following a first episode of DVT. This syndrome is characterized by the development of
leg swelling, skin pigmentation, rashes, and in approximately 4% of individuals, an open
ulcer. PTS can develop in patients with asymptomatic DVT, while recurrent ipsilateral
DVT and proximal DVT will increase the risk of developing the syndrome. PTS also takes
time to develop, with only 23% of post-thrombotic cases presenting within two years
of the acute DVT (16). After such a long time, symptoms of recurrent VTE and PTS are
not often attributed to a previous operative procedure or hospitalization for illness.
One startling fact about the post-thrombotic syndrome is that 7% of patients are disabled
by this condition and if a person develops recurrent DVT, the risk of the post-thrombotic
syndrome is increased by six-fold (18).
Table 1 Rationale for VTE Prophylaxis
Prevent fatal pulmonary emboli
1–5% incidence in patients with O4 risk factors
16.7% mortality at 3 months
Prevent clinical venous thromboembolism
Morbidity—months of anticoagulation, tests, hose, changes in lifestyle
Prevent silent venous thromboembolism
Risk of subsequent event double that of control population (Borrow)
Prevent embolic stroke in those with patent foramen ovale
20–30% PFO rate; 50% disabled; 20% die; 30% recover
Prevent the post-thrombotic syndrome
25% incidence following DVT and 7% severe
May not be evident for 2–5 years
Abbreviations: VTE, venous thromboembolism; PFO, patent foramen ovaie; DVT, deep vein thrombosis.
Caprini and Wentworth174
The American Venous Forum has published an excellent classification of venous
problems called the CEAP score, which helps classify the severity of changes in individual
patients. Figure 1 shows a woman with severe post-thrombotic changes combined with
lymphedema. This is a very difficult picture as far as treatment is concerned and is
definitely a permanent problem. It has been estimated that in the United States 2 million
workdays are lost annually and 15 million Americans suffer from this problem (19). The
cost of care for these problems in the United Kingdom is estimated at 400 million pounds
annually and $300 million in the United States (8). The syndrome represents one of the
most compelling arguments for effective thrombosis prophylaxis in all medical and
surgical patients at risk, as it is much easier to prevent VTE than it is to treat PTS.
Another problem that is poorly recognized and very difficult to assess is the
incidence of recurrent thromboembolism in patients who have had a subclinical event and
later are at risk because of an operation or medical illness. Borow reported on 500 patients
who underwent surgical procedures lasting an hour or more, were over the age of 40 years,
and were studied postoperatively with fibrinogen scans and confirmed with contrast
venography (20). He found that 66% of patients who had a history of venous thrombosis
developed thrombosis postoperatively. He also reported that 50% of the patients with
a significant medical history, including previous abdominal or leg surgery, trauma to the
lower abdomen, or long bone fracture, developed postoperative venous thrombosis.
Table 2 is a list of various signs, symptoms and clinical findings that may be associated
with a venous thromboembolic event. Obviously, all of these problems do not end with
a fatality but that does not diminish the importance of the presence of these abnormalities
as a clue to signal a possible VTE event.
We frequently encounter successful, busy clinicians who dispute the above data,
usually saying that “in our practice we just don’t see these problems.” We would
emphasize that in this modern era, autopsies are difficult to obtain; without them, the true
incidence of venous thromboembolic problems associated with clinical fatalities is
impossible to calculate. Another modern problem in the United States is delivery of health
Figure 1 An example of severe post-thrombotic syndrome (PTS) post–hip arthroplasty. This
woman demonstrates lymphedema, discoloration, pain, ulceration, and obviously is severely
debilitated by her condition. Source: Adapted from Ref. 34. (See color insert.)
Venous Thrombosis Prophylaxis 175
care. When patients are discharged from the hospital after surgery or acute medical illness,
they often may not be readmitted to the same hospital to treat a post-discharge VTE event.
If these people develop venous thromboembolic complications, how is the busy clinical
practitioner able to find out about these problems unless the patients’ activities and
whereabouts following discharge are carefully documented? We would remind those
clinicians who are skeptical about the incidence and clinical significance of venous
thromboembolic problems that the data are real and have been derived from hundreds of
references. The thrombosis prophylaxis chapter in the latest Chest Consensus Conference
on Antithrombotic Therapy contains 797 references that are the scientific basis for the
incidence, morbidity and mortality associated with venous thromboembolic disease (6).
RISK ASSESSMENT
Some of us feel that the single most important aspect of thrombosis prophylaxis in medical
and surgical patients is a careful, detailed risk analysis of each individual patient, being
careful not to miss any important risk factors. One might say that this process is the
medical equivalent of the preflight cockpit checklist for a commercial airliner. It would be
unthinkable to fly without checking every possible item on the list to ensure the safety of
the passengers and crew. We are indebted to the Chest Consensus Conference Guidelines
that now have been published for the seventh time and give us clear direction regarding
risk factors and their importance in the prevention of VTE. A number of formal risk
assessment models are available for this purpose (21,22). Many feel that these are
cumbersome and have not been adequately validated (6). Furthermore, clinicians find
them cumbersome to implement in their routine practice. The consensus group suggests a
simplified approach, categorizing patients into four different categories depending on their
age, type of surgery, and presence of additional risk factors (Table 3). This is intended
to provide a uniform approach to a population of patients; however, we encounter daily
situations where a low-risk procedure is performed on a patient at very high risk for VTE.
It is true that in these very-high-risk individuals maximum prophylaxis will be used, so one
could ask why all risk factors must be listed. There is considerable literature to suggest
that patients with large numbers of risk factors may be at enormous risk for developing
a postoperative venous thromboembolic event (6,8,23,24). If the patient is undergoing
a quality-of-life procedure and falls into this category, we feel that part of the preoperative
informed consent process should be to advise the patient of the degree of risk so the patient
can decide on the importance of the procedure given the risks involved as assessed.
Table 2 Nonspecific Signs and Symptoms of VTE
Leg pain Leg swelling
Chest pain Shortness of breath
Transient orthostatic hypotension Narcotic excess
Fainting spell Hypoxia
Patient readmission 90 days postoperatively Postoperative pneumonia
Patient death 90 days postoperatively Sudden death
Suspected MI Death without autopsy
Patent foramen ovale Post-thrombotic syndrome 5 years
postoperatively
Postoperative stroke Failure to thrive
Abbreviations: VTE, venous thromboembolism; MI, myocardial infarction.
Caprini and Wentworth176
For example, if a patient with a heterozygous Factor V Leiden defect also has a protein C
or S defect, the incidence of thrombosis may be as high as 70% to 90% (25). That may be
too much of a chance to take for an elective quality-of-life procedure. Even with proper
prophylaxis, VTE may still occur (the event rate is not zero), or they might experience
excessive bleeding requiring withdrawal of prophylaxis, thus exposing the patient to
a high risk of severe or fatal events. Without a complete preoperative risk assessment, how
would one know which patients are in this category and need this extra counseling and
decision-making analysis preoperatively?
We have developed a risk assessment form that has been used in our clinic for more
than 15 years and is provided in Table 4. It consists of a point system linking the patient to
the risk factor schema proposed by the Chest Consensus Guidelines (see Table 3). The use
Table 3 Risk of VTE and Therapy Recommendations
DVT (%) PE (%)
Recommended
therapyLevel of patient risk Calf Proximal Symptomatic Fatal
Low
Age under 40 yr 2 0.4 0.2 0.002 Aggressive
mobilization
Minor surgery
No other RF
Moderate
Minor surgery and
additional RF
10–20 2–4 1–2 0.1–0.4 LDUFH q12 h,
LMWH, GCS,
IPC
Minor surgery, 40–60 yr
and no additional RF
Major surgery, !40 yr
with no additional RF
High
Minor surgery in
patients O60 yr or
w/additional RF
20–40 4–8 2–4 0.4–1.0 LMWH, LDUFH
q8 h, IPC
Major surgery in
patients O40 yr or
w/additional RF
Very high
Major surgery in
patients O40 yr plus
prior VTE, cancer, or
hypercoaguable state
40–80 10–20 4–10 0.2–5 LMWH, fondapari-
nux, oral VKA,
adjusted UFH,
IPC/GCSC
LDUFH/LMWH
Hip or knee arthroplasty,
hip fracture surgery
Major trauma, spinal
cord injury
Abbreviations: GCS, graduated compression stockings; IPC, intermittent pneumatic compression; LDUFH, low
dose unfractionated heparin; LMWH, low molecular weight heparin; RF, risk factors; VKA, Vitamin K
antagonists.
Source: Adapted from Ref. 6.
Venous Thrombosis Prophylaxis 177