Добавил:
Sekretar
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_3938_Библиотеки_им_академика_М_И_Перельмана
.pdf
108 Negative Pressure Dressings in Venous Ulcers
took until approximately day 11 to achieve the same results with wet-dry
dressings.
5
WOUND BED DEFORMATION
Another explanation for the potential benefi ts of topical negative pres-
sure dressing in accelerated wound healing is the fact that the open
cell sponge induces mechanical deformations of the wound base when
negative pressure is applied. The walls of each open cell anchor portions
of the wound bed, while the intervening segments are not anchored in the
same way. Topical negative pressure then stretches and deforms these
intervening areas. This induces deformation of the cells and stimulates
cellular proliferation and migration.
2,11
This is similar to the cellular pro-
liferation that occurs with the use of tissue expanders in plastic surgery
and also is present with the use of bone distraction devices in orthopedics
and oral surgery.
11
In vitro studies have revealed that cells allowed to
stretch tend to proliferate, while unstretched cells are less likely to
divide.
11
This effect is thought to be modulated through cytoskeletal and indirect
connections between the cell wall and the nucleus. These connections
transfer mechanical forces that the cell has experienced to the nucleus,
leading to a series of events resulting in expression of growth factor, protein
formation, and gene expression, which induces cellular conformational
changes and increases cellular proliferation.
2
DIRECT WOUND CLOSURE
The direct effect of negative pressure on the wound and wound edges
also exerts a constant effect on the wound edges contracting the ulcer. This
effect directly decreases the size of the wound independent of any cellular
proliferation that may be occurring.
7
WOUND HEALING ENVIRONMENT
One of the mainstays of therapy through time has been wet-to-dry dress-
ings. It is well known that a moist wound healing environment in the wound
bed is benefi cial in the wound healing process. The moist wound environ-
ment creates an environment that stimulates angiogenesis, encourages
expression of normal growth factors, and increases fi brinolysis.
14
Typica lly,
wet-to-dry dressings are changed multiple times throughout the day. The
theory is that moistened dressings slowly dry out during the intervening
https://t.me/med1917
Negative Pressure Dressings in Venous Ulcers 10 9
time period, and when removed, there is mechanical debridement of any
necrotic tissue from the wound bed; however, there is also the potential for
removal of healthy granulation tissue.
Other modalities are also employed, which further maintain a moist
wound healing environment. In addition to simple saline gauze, various
hydrocolloid gels as well as occlusive dressings are used to maintain a moist
wound healing environment. A properly used topical negative pressure
dressing will maintain a moist wound healing environment. It should,
however, be noted that when a topical negative pressure dressing has a
large persistent air leak, the wound may desiccate, which will be detrimen-
tal to wound healing.
8
WOUND HYPOXIA
The direct effects of negative pressure on the wound bed lead to a local-
ized decrease in the partial pressure of the oxygen within the wound. This
may stimulate the formation of new blood vessels and further result in
improvement in the granulation bed.
12
This results in a healthier microen-
vironment within the wound bed.
ADJUNCT TO ASSISTED CLOSURE
Despite continued progress in the management of wounds, some wounds
continue to prove extremely diffi cult to heal with standard techniques and
often require other surgical modalities such as fl ap closure and skin graft-
ing in order to obtain fi nal coverage. The topical negative pressure dress-
ing, through promotion of an adequate granulation bed, increases success
of local fl ap closures. Because this type of dressing decreases overall wound
size, the extent of defi nitive procedures may also be lessened.
2
The topical negative pressure dressing may be effective in bolstering
split thickness skin grafts after they are placed on a granulating wound
bed. The negative pressure aids in the removal of excess fl uid from the
wound bed, thus allowing for good apposition of the split thickness skin
graft to the granulation tissue. It also accentuates angiogenesis, which
would also potentially lead to improvements in the outcomes from split
thickness skin grafting. The even negative pressure applied through the
open cell design allows for even apposition of the skin over the wound
surface. When topical negative pressure dressing is used for split thickness
skin graft coverage, it is most often recommended that subatmospheric
pressure be utilized at –50 to –75 mmHg instead of –125 mmHg. Most
individuals recommend placement of a nonadherent barrier between the
open cell sponge and the split thickness skin graft to avoid ingrowth of
https://t.me/med1917
110 Negative Pressure Dressings in Venous Ulcers
healthy tissue into the sponge and inadvertent damage to the graft with
dressing changes. The dressing is left in place for up to approximately 4
days prior to removal. When used to bolster a split thickness skin graft,
the negative pressure is usually applied in a continuous, not intermittent,
fashion.
6
INDICATIONS AND CONTRAINDICATIONS
Some of the common indications for use of the topical negative pressure
dressing as approved by the FDA include “diabetic foot wounds, pressure
ulcers, chronic wounds, acute and traumatic wounds, dehisced surgical
wounds, partial-thickness wounds, fl aps and grafts” (VAC® Therapy
Guidelines). Contraindications for use of the topical negative pressure
dressing include “Malignancy in the wound, untreated osteomyelitis, non-
enteric and unexplored fi stula, necrotic tissue and eschar presenting the
wound, exposed organs and blood vessels” (VAC® Therapy Guidelines).
There are few reported complications attributed to the use of topical nega-
tive pressure dressings. The most common reported complications are
pain, typically resolved when the negative pressure is decreased, and exces-
sive tissue ingrowths into the dressing sponge.
8
This may lead to bleeding
when the dressings are changed. Other reported complications have
included erysipelas, damage to surrounding skin, and failure to heal
ulcers.
13
CONCLUSION
In conclusion, although the exact mechanism of action for topical nega-
tive pressure dressing in the management of chronic venous wounds is
unknown, numerous theories exist. The utility of a topical negative pres-
sure dressing may be as simple as removal of chronic wound fl uid, increas-
ing local blood fl ow; decrease in wound bacterial burden; effects of
mechanical deformation of the wound bed; decrease in interstitial edema;
and the maintenance of a moist wound healing environment. Some of these
processes, all of these processes, or a combination of them may account
for the topical negative pressure dressing’s benefi cial effects.
In a search of the literature completed by Shirakawa,
7
six randomized
controlled trials were found to have been completed comparing topical
negative pressure dressings with standard dressings. The six studies
were for a wide variety of wound types; only one trial included venous
wounds and this was a subgroup of a diverse wound population. Five of
the six studies indicated that there may be some benefi t to utilizing
topical negative pressure dressings, though, as the authors note, only three
of the studies showed a statistically signifi cant improvement in wound
https://t.me/med1917
Negative Pressure Dressings in Venous Ulcers 111
healing, and two showed a trend that was not found to be statistically
signifi cant. All the studies could be questioned secondary to methodologi-
cal fl aws.
7
In a recent study by Vuerstaek et al., the topical negative pressure
dressing was evaluated for effi cacy in the healing of chronic leg ulcers.
This randomized controlled study compared topical negative pressure
dressings to standard wound dressings in the healing of venous, combined
venous/arterial, and arteriolosclerotic leg ulcers. All groups were evalu-
ated for wound bed preparation time and then for time to complete wound
healing following grafting. The authors found that topical negative pres-
sure therapy resulted in a shorter wound healing time in all subgroups,
though statistical signifi cance could not be demonstrated in the combined
venous/arterial subgroup. The authors also noted a trend for fewer ulcer
recurrences in the topical negative pressure group when compared to
the standard dressing group, though no statistical signifi cance was found.
One limitation of this study was that all patients were treated in the
inpatient setting.
13
Further well-designed studies will be needed to more defi nitively defi ne
the utility of the topical negative dressing as well as to elucidate the mecha-
nism or mechanisms by which the potential benefi ts are gained.
REFERENCES
1. Valencia IC, Falabella A, Krisner RS, Eaglstein WH. Chronic venous insuffi ciency and
venous leg ulceration. J Am Acad Dermatol. 2001;44:401–421.
2. Andros G, Armstrong DG, Attinger C, et al. Consensus statement on negative pressure
wound therapy for the management of diabetic foot wounds. Vasc Dis Manage
2006(Suppl, July).
3. Emmanuella J, Hamori CA, Bergman S, Roaf E, Swann NF, Anastasi GW. A prospec-
tive, randomized trial of vacuum-assisted closure versus standard therapy of chronic
nonhealing wounds. Wounds. 2000;12(3):60–67.
4. Thomas S. World wide wounds: An introduction to the use of vacuum-assisted closure.
2001. Available at: http://www.worldwidewounds.com/2001/may/Thomas/Vacuum-
Assisted-Closure.html.
5. DeFranzo AJ, Argenta LC, Marks MW, et al. The use of vacuum-assisted closure
therapy for the treatment of lower extremity wounds with exposed bone. Plast Reconstr
Surg. 2001;108(5):1184–1191.
6. Argenta LC, Morykwas M. Vacuum-assisted closure: A new method for wound control
and treatment: Clinical experience. Ann Plastic Surg. 1997;38:563–577.
7. Shirakawa M, Isseroff RR. Topical negative pressure devices: Use for enhancement of
healing chronic wounds. Arch Dermatol. 2005;141:1449–1453.
8 . Morykwas M, Faller B, Pea rce D, Argenta L. Effects of varying levels of subatmospheric
pressure on the rate of granulation tissue formation in experimental wounds in swine.
Ann Plast Surg. 2001;47(5):547–551.
9. Morykwas M, Argenta LC, Shelton-Brown EI, McGuirt W. Vacuum-assisted closure: A
new method for wound control and treatment: Animal studies and basic foundation.
Ann Plast Surg. 1997;38(6):553–562.
https://t.me/med1917
112 Negative Pressure Dressings in Venous Ulcers
10. Moues CM, Vos MC, Van Den Bemd GJCM, Stijnen T, Hovius SER. Bacterial load in
relation to vacuum-assisted closure wound therapy: A prospective randomized trial.
Wound Repair and Regeneration. 2004;12(1):11–17.
11. Saxena V, Hwang CW, Huang S, Eichbaum Q, Ingber D, Orgill DP. Vacuum-assisted
closure: Microdeformations of wounds and cell proliferation. Plast Reconstr Surg.
2004;114(5):1086–1096.
12. Kirby F. Ward S, Sanchez O, Walker E, Mellett MM, Maltz SB, Lerner TT. Novel uses
of a negative-pressure wound care system. J Trauma. 2002;53(1):117–121.
13. Vuerstaek J, Vainas T, Wuite J, Nelemans P, Neumann MHA, Veraart JCJM. State-of-
the-art treatment of chronic leg ulcers: A randomized controlled trial comparing
vacuum-assisted closure (V.A.C.) with modern wound dressings. J Vasc Surg.
2006;44(5):1029–1038.
14. Field K. Overview of wound healing in a moist environment. J Surg. 1994;167(1A):
2s–6s.
https://t.me/med1917
113
10
Deep Vein Thrombosis
and Prevention of
Post-Thrombotic
Syndrome
Joseph A. Caprini
INTRODUCTION
Deep vein thrombosis (DVT) refers to the formation of a thrombus in
one of the deep veins of the body, usually in the leg, resulting in leg pain,
tenderness, and swelling. The clinical course of DVT may be complicated
by the potentially fatal conditions of pulmonary embolism (PE), recurrent
DVT, and in the long term by the emergence of post-thrombotic syndrome
(PTS). In its presentation, PTS is typifi ed by a variety of symptoms and
signs that can be systematically assessed, including edema, skin induration,
hyperpigmentation, pain, pruritus, and paresthesia (Table 10-1). The most
severe form of the syndrome will manifest as venous ulcers.
1
As both a frequent and chronic complication of DVT, PTS interferes
with patients’ daily life, function, and health. The syndrome can have a
profoundly adverse effect on quality of life, limiting physical activity, inter-
fering with work and social activities, causing psychological distress, and
changing patients’ health perceptions.
2
Furthermore, PTS carries a high
cost of medical care, with costs amounting to about 75% of the cost of a
primary DVT.
3
There are currently limited options for treating PTS, and most are
aimed at the prevention or treatment of leg ulcers.
4
Indeed, the treatment
of established PTS is described as frustrating for patients and physicians
alike, with current therapies and management only able to improve or sta-
bilize symptoms in around half of all patients.
4,5
Despite extensive study of DVT and its prevention and treatment in
recent years, PTS has received little attention from clinicians and research-
Venous Ulcers
Copyright © 2007 by Academic Press, Inc.
All rights of reproduction in any form reserved.
https://t.me/med1917
114 Deep Vein Thrombosis and Prevention of Post-Thrombotic Syndrome
ers.
4
The syndrome has rarely been included as an outcome measure in
DVT trials and continues to be an underdiagnosed, underappreciated, and
often overlooked morbid consequence of DVT. There is poor appreciation
of the burden posed by PTS and a prevailing perception that the condition
is an inevitable and untreatable consequence of DVT.
4
Prophylaxis with anticoagulant therapy is known to reduce the rate of
DVT and its recurrence, and consensus guidelines on the prevention of
venous thromboembolism have been formulated based on a strong body
of evidence.
6,7
The prevention of DVT in the fi rst place may therefore offer
the best opportunities for optimal patient care and avoidance of PTS and
venous ulcers.
RISK OF VENOUS THROMBOEMBOLISM,
RECURRENCE, PTS, AND VENOUS ULCERS
Venous thromboembolism (VTE) is a major health problem. Recent
estimates suggest that the total annual number of nonfatal, symptomatic
VTE events in the United States exceeds 600,000, more than half of which
are DVT.
8
Individual risk for DVT varies according to clinical situation,
as shown in Table 10-2,
6
and potential of additional VTE risk factors
including an acute infectious disease, cancer, age greater than 75 years,
stroke, immobilization, and previous history of VTE.
9,10
TABLE 10 -1 Clinical Scale for Post-Thrombotic
Syndrome (PTS) According to Villalta et al.
1
PTS Symptoms
Pain
Cramps
Heaviness
Pruritus
Paresthesia
PTS Signs
Edema
Skin induration
Hyperpigmentation
Ectasia
Redness
Pain during calf compression
PTS Score*
0– 4 No PTS
5–14 Mild PTS
≥15, or presence of ulcer
Severe PTS
* PTS score is based on the cumulative rating of the fi ve
symptoms and six signs, with each rated as 0 (absent),
1 (mild), 2 (moderate), or 3 (severe).
https://t.me/med1917
Deep Vein Thrombosis and Prevention of Post-Thrombotic Syndrome 11 5
Data from a population-based cohort study in the United States reveal
that the risk for VTE recurrence after a fi rst episode is high. As many as
5% of patients with a fi rst VTE experience a recurrent event within
30 days, around 17% have a recurrence within 2 years, and 30% within
10 years.
11
The hazard of recurrence is highest in the fi rst 6–12 months
after the initial event, with hazard rate per 1,000 person-days ranging from
30 recurrent VTE events at 7 days, to 50 events at 30 days, and 10 at 6
months and 1 year.
11
In a group of 335 consecutive patients who experienced symptomatic
thrombosis, PTS occurred in 23% within 2 years of the VTE event, with
a strong association between the development of ipsilateral recurrent DVT
and risk for PTS.
12
Severe cases of PTS had manifested in 9% of patients
after 5 years.
12
A recent meta-analysis has also shown that in patients in
whom postoperative DVT was asymptomatic, the relative risk of develop-
ing PTS is 1.58 times (95% confi dence interval [CI] 1.24–2.02) the risk in
patients without evidence of DVT (P < 0.0005).
13
This highlights that even
silent DVT predisposes the patient to the later threat of chronic PTS and
risk for venous ulceration.
To date, specifi c patient risk factors for developing PTS have not been
clearly established, but it has emerged that many patients with chronic
venous ulceration have unsuspected PTS.
14,1 5
Several risk factors have been
put forward, of which only recurrent DVT has clearly been identifi ed as
increasing the risk of PTS as much as 6-fold (Table 10-3).
4
The annual incidence of venous ulceration is estimated to be at least
0.3%, of which around one-quarter of cases can be linked to a DVT
history.
16,17
Both clinical and subclinical VTE appear to be signifi cant pre-
TABLE 10 -2 Risk of Deep Vein Thrombosis (DVT) in Different Patient Populations
6
Probability of DVT without Prophylaxis (%)
Surgical
Elective hip replacement 51 (48–54)
Total knee replacement 47 (42–51)
Hip fracture 44 (40–47)
General surgery 25 (24–26)
Gynecological surgery (malignancy) 22 (17–26)
Gynecological surgery (benign disease) 14 (11–17)
Medical
General medical 12 (10–14)
Stroke 56 (51–61)
Myocardial infarction 22 (16–28)
Spinal cord injury 35 (31–39)
Medical intensive care 25 (19–32)
95% confi dence intervals in parentheses.
https://t.me/med1917
116 Deep Vein Thrombosis and Prevention of Post-Thrombotic Syndrome
disposing factors for the development of chronic venous insuffi ciency and
venous ulcers.
18–2 0
Indeed, patients with a DVT history have been shown
to be 2.4-fold (95% CI 1.7–3.2) more likely to develop venous stasis with
its associated risk for venous ulcer formation.
19
THROMBOPROPHYLAXIS: REDUCING THE
INCIDENCE OF VTE AND LONG-TERM
COMPLICATIONS
There is a compelling body of evidence that the incidence of VTE, and
thereby its long-term complications, can be drastically reduced by provid-
ing effective thromboprophylaxis to patients at known risk for VTE.
6,7
Many studies of VTE prophylaxis have focused more on surgical rather
than medical patients because of the very high risk of VTE following major
surgical procedures. However, the absolute numbers of potentially at-risk
patients reveal high numbers of medical patients who are candidates for
VTE prophylaxis in accord with current guidelines on VTE prevention.
6,7,21
TABLE 10 -3 Proposed Risk Factors for Post-Thrombotic Syndrome (PTS)
4
Proposed Risk Factor Association with PTS
Recurrent DVT
Clearly identifi ed risk factor, up to 6-fold increase
Asymptomatic DVT
Identifi ed risk factor, 1.6-fold increase
Characteristics of the initial
DVT; distal DVT
Distal DVT appears to be associated with PTS, although
some studies suggest that the site of the initial thrombus
is not predictive, or that the risk is higher in patients
with proximal rather than distal DVT
Patient characteristics
Factors predictive of PTS (as identifi ed in retrospective
studies):
• Increasing age
• Female gender
• Hormone therapy
• Varicose veins
• Abdominal surgery
• Increased body mass index
Factors not predictive of PTS (as identifi ed in prospective
studies):
• Gender
• Delay in initiating treatment for DVT
• Risk factors for thrombosis
• Family history of thrombosis
• Intensity of warfarin anticoagulation
DVT = deep vein thrombosis.
https://t.me/med1917
Deep Vein Thrombosis and Prevention of Post-Thrombotic Syndrome 11 7
Of an estimated 13.4 million U.S. residents who meet the current Ameri-
can College of Chest Physicians (ACCP) guideline defi ned risks for VTE
each year, 7.6 million (57%) are medical patients.
21
Despite internationally recognized guideline recommendations and
government-backed initiatives in support of wider adoption of VTE pro-
phylaxis in at-risk groups, the reality is that prophylaxis for VTE continues
to be underutilized in clinical practice in both surgical and medical patient
groups.
6,7,22–24
A recent multicenter study in Canada revealed that while
most patients hospitalized for medical illness had indications for thrombo-
prophylaxis, only 16% received prophylaxis deemed appropriate to reduce
the risk of VTE.
24
In a Spanish study, it was noted that appropriate adher-
ence to all guideline recommendations on VTE prophylaxis was observed
in only 42% of patients with risk factors, with dosage of thromboprophy-
laxis often inappropriate according to patients’ relative risk.
23
Reasons for underprophylaxis of hospitalized patients may relate to an
underestimation of VTE risk, since VTE events often arise after hospital
discharge and VTE is often clinically silent, or to emergence of symptoms
that are not immediately detected or detectable during patient follow-up.
Inadequate levels of prophylaxis not only increase the risk of occurrence
of thrombosis, but also increase the risk of PTS and, in this way, venous
ulceration.
4
The key to optimal VTE prevention lies in better assessment
of patient risk and appropriate intervention. Indeed, in the United
States, the National Quality Forum (NQF) identifi es VTE risk assessment
among its 30 practices for improving patient safety, highlighting the need
to evaluate all patients for VTE risk on hospital admission and stressing
the need for appropriate methods to prevent VTE, a recommendation
supported by the Agency for Healthcare Research and Quality (AHRQ)
as well.
22
RISK ASSESSMENT MODEL (RAM)
There is a body of literature and evidence regarding VTE risk factors
and guidance on patient risk assessment to support clinicians and surgeons
in identifying patients at risk of VTE in daily practice. The ACCP guide-
lines approach to risk assessment is to defi ne patients as belonging to one
of four broad categories of VTE risk: low, moderate, high, and highest risk.
7
However, the ACCP approach of broad risk categories and its lack of
specifi cation of what constitutes “other risk factors” does not provide an
immediately accessible model for application in clinical practice, and there
have therefore been attempts to develop more practical risk assessment
models and tools.
For example, using a computerized alert program, it is possible to
encourage greater and more successful use of prophylaxis among at-risk
patients.
25
In a study conducted at a large U.S. hospital, an alert system
https://t.me/med1917
Соседние файлы в папке Библиотека им академика М.И. Перельмана