Phẫu Thuật Tạo Hình Grabb & Smith’s (Bản Cập Nhật – Kevin C. Chung)

Secondary Lymphedema
Secondary lymphedema is an acquired dysfunction of the lymphatic system from disruption by extrinsic
factors. Disruption of the lymphatic system may be secondary to infection, malignancy, or as a
consequence of tissue trauma most commonly from proximal lymph node dissection. The most common
form of secondary lymphedema worldwide is caused by infection with Wuchereria bancrofti, a filarial
nematode parasite that invades and obstructs lymphatic channels. The global burden of lymphatic
filariasis is between 120 and 250 million people, largely affecting populations in low-income countries. 13
In middle and high-income countries, the most common cause of secondary lymphedema is tissue
trauma from surgical procedures. 2 In the United States, the greatest burden of noninfectious secondary
lymphedema is among the breast cancer patient population (breast cancer-related lymphedema (BCRL))
due to the relatively higher incidence of the disease compared to other solid malignancies. However,
patients with other malignancies who undergo dissection of lymph node basins, including gynecological
and genitourinary tumors, sarcomas, and melanoma, are also at risk for secondary lymphedema. 2,6,14
Among breast cancer patients, the risk of BCRL is strongly associated with axillary procedures. 15,16 The
incidence of lymphedema following sentinel lymph node biopsy is between 5% and 7%. 16,17 The incidence
for patients who undergo axillary lymphadenectomy is approximately 20% and that for patients who
undergo a combination of axillary lymphadenectomy and radiation therapy reaches 25% to 40%. 16-19
Clearly, it appears that a higher degree of axillary intervention results in a higher risk of secondary
lymphedema. Lymphedema incidence and prevalence data are not as robust for other solid malignancies.
However, several large series in the gynecological patient population report up to 10% to 15% prevalence
of clinically diagnosed secondary lymphedema. 2,9,14,20 Similar to the breast cancer population, pelvic
lymphadenectomy and radiation treatments put patients at higher risk of lower limb lymphedema. 14,20
Finally, there is a long list of widely debated risk-reducing behaviors proposed for patients at risk of
developing secondary lymphedema. The most commonly cited of these risk-reducing behaviors include
avoidance of venipuncture, blood-pressure monitoring, and resistance exercise involving at-risk limbs.
The plurality of evidence has thus far not shown these risk-reducing behaviors as credible. 21 Moreover,
there is evidence that both aerobic and resistance exercise, in addition to not increasing the risk of
lymphedema, provide strength and physical function benefits. 21-23 The best evidence supported and
widely acknowledged risk factors for secondary lymphedema include obesity, infections, radiation, and
genetic predisposition. 24 Of these factors, obesity is perhaps the best recognized with robust evidence of
its association with secondary lymphedema and equally good evidence that weight loss interventions can
ameliorate symptoms of secondary lymphedema. 25 Thus, obesity and infections are potentially
controllable risk factors that should be acted upon by clinicians who encounter high-risk patients.
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Natural History and Pathophysiology
The natural history of primary lymphedema is widely variable within each of the currently defined
categories (congenital, praecox, and tarda). The reason for this is that natural history perhaps depends
more on underlying causal mutations and their penetrance rather than time of onset. Moreover,
classification by underlying mechanism necessitates consideration of other associated features such as
vascular anomalies and limb growth disturbances that manifest in several primary lymphedema
phenotypes and can influence natural history. 11,12
Patients who develop BCRL typically present an average of 8 to 12 months after surgery. 26 Up to 77% of
patients who will develop BCRL do so by the third year after surgery and then the risk is approximately
1% per year. 27 Hence, some patients develop BCRL even decades after surgery. Most patients with lower
limb secondary lymphedema have been treated for gynecological and genitourinary tumors. 2 Data from
several large series showed that up to 75% of these patients who developed secondary lymphedema did
so within the first year of surgery. 2,14,20 In the absence of interventions, secondary lymphedema is
generally a progressive disease. However, the rate of disease progression is widely variable with some
patients rapidly developing debilitating disease and others having an indolent course for several years.
With sustained disruption of lymphatic function by intrinsic defect or secondary influence, there is
accumulation of protein-rich fluid within the affected tissues. The accumulated protein-rich ultrafiltrate
triggers a pathological cytokine activation cascade that incites a profound inflammatory response. 1
Inflammatory cells, fibroblasts, keratinocytes, and adipocytes taxi to the involved tissues in response to
proinflammatory messaging. The incoming cells induce a chronic inflammatory state, increased collagen
deposition, fibrosis of skin and subcutaneous tissues, and excess adipose deposition. 1 The clinically overt
manifestation of lymphedema begins with pitting edema that correlates with interstitial accumulation of
protein-rich ultrafiltrate. Eventually, with fibrosis of lymphatic vessels, skin, and subcutaneous tissues,
the edema is wooden and does not resolve with elevation. With these tissue changes, skin breakdowns
and bouts of erysipelas are common and underlie a significant aspect of the morbidity of the disease.
Lastly, severe limb hypertrophy and dysmorphia with a hyperkeratotic verrucous appearance otherwise
known as elephantiasis ensues with further extracellular fibrosis and adipogenesis 10 (Figure 98.2).
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FIGURE 98.2 A patient with bilateral lower extremity elephantiasis characterized by severe limb hypertrophy and verrucous
hyperkeratosis
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Diagnosis
Lymphedema is a clinical diagnosis that depends mostly on thorough history gathering and physical
examination. Secondary lymphedema patients will have a history of antecedent trauma to the lymphatic
system and report common symptoms such as limb swelling and heaviness, aching, fatigue, numbness,
stiffness, and impaired mobility. Primary lymphedema patients in contrast, generally will not have an
antecedent injury to the lymphatic system, will most likely be female, and may allude to a family history
of idiopathic limb swelling. Clinicians must also consider that patients can present with a mixed picture
of primary and secondary lymphedema.
Patient-reported outcome (PRO) instruments are increasingly gaining ground as part of the subjective
assessment of lymphedema, especially in BCRL as this makes up a large proportion of secondary
lymphedema population. 6 Data from PROs, as a complement to clinical symptoms, add information
about functional impairment and psychosocial impact to capture a fuller picture of the patient’s
experience with lymphedema. The upper limb lymphedema-27 (ULL-27) questionnaire is currently the
only validated condition-specific PRO for BCRL; however, most studies to date use generic functional,
cancer and symptom-specific PRO instruments . 6,28 Regardless of the PRO instrument used, several
studies demonstrate that lymphedema patients have poorer health-related quality of life with decreased
physical functioning, psychological, and social well-being. 3-6,28
In conjunction with the information gathered from the subjective history, patient-reported symptoms,
and physical examination, objective measurements improve the accuracy and reliability of lymphedema
diagnosis. Objective measurements also provide a means of interval assessments to track disease
progression or the effects of interventions. There are several contemporary objective measurements used
in clinical practice including bioimpedance spectroscopy, perometry, skin tonometry, tissue dielectric
constant, water displacement, and circumferential measurement. 29 Ideally, an objective measure is easy
to use, noninvasive, hygienic, cost-effective, reliable, reproducible, and quantifiable, and each of the
above listed measures have merits and demerits with regards to these criteria. Water displacement
(volume of water a limb displaces when immersed) is considered the most accurate measurement because
of its high reliability. 29-31 However, significant challenges limit its use in clinical practice. For instance,
water displacement cannot be used in patients with open wounds for hygiene reasons, and it cannot be
used for severe lower limbs that do not fit in the water tanks. Circumferential measurements are the most
commonly used measure in clinical practice and if properly performed meet the desired criteria outlined
earlier. 29,31 The measurement is performed with nonelastic tape beginning from a fixed point on the limb
and repeated at intervals. Using anatomical landmarks (e.g., radial styloid and elbow) as part of the
intervals decreases measurement error. Lastly, having baseline measurements of ipsilateral and
contralateral limbs are vital to account for potential differences between dominant and nondominant
limbs. A 2 cm or greater increase in circumference is widely accepted as the definition of lymphedema.
29,31
Radiographic tests also play a role in the objective assessment of lymphedema. Lymphoscintigraphy, the
most commonly used radiographic test in lymphedema assessment, is a qualitative test based on
detection of peripherally injected radiolabeled Technetium-99m colloid uptake by proximal nodal basins
31 Historically, lymphoscintigraphy has been mostly useful as a simple qualitative confirmatory test for
lymphatic dysfunction. However, there is no standard protocol for quantifying radiocolloid uptake and
transit time, making it difficult to standardize quantification of disease severity across centers and
studies. Near-infrared fluorescence lymphography with indocyanine-green (ICG) has gained wider use,
also as a qualitative test of lymphatic function. It shows superficial (up to 12 mm depth) lymphatic flow
in real time, including the pattern of flow, that is, a linear pattern or various backflow patterns (splash,
stardust and diffuse) that can be correlated with the severity of disease. Additionally, the ability to see
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flow in real time with this test is useful for intraoperative navigation in microsurgical lymphatic
reconstruction. 32,33
Finally, surveillance on at-risk patients is a new paradigm in the assessment of secondary lymphedema.
29,31,34 This paradigm originates in the knowledge that all modes of lymphedema treatment are palliative
and not curative, thus making prevention the most effective intervention. Current surveillance guidelines
propose preoperative and standardized interval postoperative subjective (patient-reported outcomes) and
objective (e.g., circumferential measurement) assessments of ipsilateral and contralateral limbs for 3 to
5 years after surgery. 29,34 Lymphatic stasis and accumulation of protein-rich fluid trigger the cascade
leading to disease progression. Hence, the objective of surveillance is to detect subclinical interstitial fluid
accumulation manifested by as little as 3% to 5% limb volume changes. 34 Early detection permits time for
implementing interventions to ameliorate fluid accumulation before the cascade of inflammation, fibrosis,
and adipocytosis associated with chronic edema ensue.
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Staging
Although there is no universally accepted scheme, the most widely used staging classification for
lymphedema is the International Society of Lymphology (ISL) staging system, which is based on the
progression of clinical features of the disease 24 (Table 98.1). In this classification, early-stage disease is
described as latent or subclinical edema. From latency, the disease progresses to clinically overt but
reversible edema with or without pitting. Irreversible edema follows and finally, elephantiasis which is
characterized by severe limb hypertrophy and dysmorphia with acanthotic hyperkeratosis and a cobble-
stone appearance of the skin. However, more recently proposed staging schemes are based on the
premise that objective results including imaging and limb circumference measurements are useful
adjuncts to ISL staging to clarify diagnosis and disease severity. The MD Anderson classification defines
stages of lymphedema based on flow patterns observed on ICG lymphography 33 (Figure 98.3). In this
scheme, the severity of stages depends on a combination of the extent of patent linear lymphatic channels
and extensiveness of dermal backflow seen on ICG lymphangiography. Cheng’s lymphedema grading
system in contrast bases its five-grade scheme on differential circumference at distinct anatomic
landmarks (e.g., 10 cm above and below the elbow joint in upper limbs) between the affected limb and
uninvolved contralateral limb 35 (Table 98.2).
TABLE 98.1
International Society of Lymphology Lymphedema Staging Classification
Stage
Description
Pathophysiology
Clinical Features
0
Subclinical
Impaired lymph 
 transport
Swelling not evident
I
Spontaneously
reversible
Early lymph accumulation
Swelling relieved by limb elevation
Pitting may be present
II
Not spontaneously
reversible
Fat hypertrophy and 
 deposition with tissue 
 fibrosis
Swelling not improved by limb
elevation
Pitting edema present with fibrosis
III
Lymphostatic
elephantiasis
Chronic lymphatic 
 stasis and inflammation, 
 further fibrosis and
fatty deposition
Swelling not improved by limb
elevation
Edema nonpitting and wooden
Hyperkeratotic and verrucous skin
changes
From International Society of Lymphology. The diagnosis and treatment of peripheral lymphedema: 2016
consensus document of the International Society of Lymphology. Lymphology. 2016;49(4):170-184.
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FIGURE 98.3 Lymphedema classification based on extent of patent lymphatics and lymphatic obstruction seen on indocyanine
lymphography. A. Stage 1: many patent lymphatic vessels, with minimal, patchy dermal backflow. B. Stage 2: moderate
number of patent lymphatic vessels, with segmental dermal backflow. C. Stage 3: few patent lymphatic vessels, with extensive
dermal backflow. D. Stage 4: no patent lymphatic vessels seen, with severe dermal backflow involving the entire arm and
extending to the dorsum of the hand.
(Reproduced with permission from Chang, DW, Suami, H, Skoracki, R. A prospective analysis of 100 consecutive lymphovenous bypass cases for treatment
of extremity lymphedema. Plast Reconstr Surg. 2013;132(5):1305-1314.)
TABLE 98.2
Cheng’s Lymphedema Grading System
Grade
Symptoms
Circumferential Differentiation
Lympho-
 scintigraphy
0
Reversible
<9
Partial occlusion
I
Mild
10–19
Partial occlusion
II
Moderate
20–29
Total occlusion
III
Severe
30–39
Total occlusion
IV
Very 

severe
>40
Total occlusion
Reprinted by permission from Springer: Patel, KM, Lin, CY, Cheng, MH. A prospective evaluation of
lymphedema-specific quality-of-life outcomes following vascularized lymph node transfer. Ann Surg
Oncol. 2015;22(7):2424-2430. Copyright © 2014 Society of Surgical Oncology.
Circumference differentiation: circumference of the lesioned limb subtracted from the circumference of the healthy limb and divided by the
circumference of the healthy limb, which is measured at 10 cm above and below the elbow, 15 cm above and below the knee, and 10 cm
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above the ankle.
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Treatment and Outcomes
Nonsurgical Treatment
Generally, lymphedema treatment is palliative and not curative; therefore, the main objectives are
preventing disease progression and ameliorating symptoms. Nonsurgical treatments are first line,
including in situations when subclinical limb swelling is identified on lymphedema surveillance.
Nonsurgical treatments also play an adjunctive role to preserve outcomes from surgical treatment of
lymphedema. Finally, patient education is a crucial element of lymphedema care. Patients at risk of
secondary lymphedema should be made aware of their lifetime risk, and they should be educated on
early signs and symptoms to recognize. Additionally, clinicians should educate patients on practical and
evidence-based risk-reducing strategies such as skin care, exercise, and weight loss. 24,29,31,34
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Complete Decongestive Therapy
Complete decongestive therapy (CDT) is considered the first line in lymphedema management. It is a
multimodal approach that incorporates manual lymphatic drainage (MLD), compression bandaging,
exercise, and skin care. This treatment involves a reductive phase (phase I) and a maintenance phase
(phase II). In phase I, patients see a lymphedema specialist five times a week for up to 8 weeks and
undergo MLD, compression therapy, and physiotherapy to achieve limb volume reduction. Phase II is
largely patient-directed and includes meticulous skin and nail care, wearing compression garments or
sleeves, self-lymph drainage massage and exercise to preserve gains in limb volume reduction. The
drawbacks of CDT are that it is labor intensive, expensive, and time-consuming, making patient
noncompliance an issue. Hence, a number of randomized trials have examined the effectiveness of less-
intensive treatments such as compression bandaging alone and physiotherapy alone compared to CDT
with mixed results. In 2015, the Cochrane Library published a systematic review of MLD for
lymphedema treatment. 36 In that review, two similarly conducted trials comparing MLD with
compression bandaging to compression bandaging alone reported equivalent additional volume
reduction in favor of MLD and compression bandaging, especially for patients with mild to moderate
disease. 37,38 However, other trials comparing MLD with compression to compression alone or
compression with physiotherapy have shown no significant differences in volume reduction and
subjective quality-
 of-life metrics. 36 Thus, in the absence of incontrovertible evidence that less-intensive
therapy is superior or noninferior, CDT remains the first-line treatment for lymphedema.
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Surgical Treatment
Surgical treatments are indicated when first-line conservative measures fail and when patients present
with late-stage disease. There are two main categories of surgical treatment: excisional and physiologic
procedures. Excisional procedures are essentially a surgical reduction of excess fibroadipose tissue in the
affected limb whereas physiologic procedures reconstruct the lymphatic system to improve physiologic
drainage. The goals of surgical treatment are to decrease the load of lymph production by excisional
procedures or liposuction: to increase the drainage of the lymph by bypassing the lymph into subdermal
venule or transfer of robust vascularized lymph node flap to restore the lymphatic drainage function.
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Excisional Procedures
Liposuction
Chronic lymphedema induces excess adipose deposition in the subcutaneous tissues with subsequent
limb hypertrophy and associated morbidities including limb heaviness, limited mobility, functional
impairments, and cosmetically unappealing appearance. In patients with later stage disease who have
failed conservative treatment and present with limb hypertrophy and nonpitting edema, liposuction
combined with controlled compression therapy has been shown to be a safe and effective technique for
significantly reducing limb volume. 39 Studies have also shown sustained limb volume reduction with
this technique up to 15 years after surgery. 40 Albeit, postoperative care involves permanent use of
compression garments and mandatory close follow-up to refit the garments periodically to maintain
volume reduction gains from the procedure. 39,40
Liposuction should be performed with tumescent technique and under tourniquet control to minimize
blood loss and the need for transfusions. Moreover, fluid monitoring is imperative for patients who
undergo large volume liposuction (>5 L), and these patients should be admitted for postoperative
monitoring. Contraindications to liposuction include metastatic disease, open wounds, medical history of
coagulopathy, patients unfit for surgery, or patients deemed unreliable to adhere to postoperative
compressive therapy. 40 Complications of liposuction are generally minor and include small wound-
healing problems, paresthesia, and contour irregularities. Rapid recurrence occurs if the patient is
noncompliant with postoperative compressive therapy. 40
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Direct Excision
Direct excision techniques are not widely used and are generally reserved for patients with severe
refractory lymphedema suffering significant morbidity with no other surgical options. For these patients,
direct excision techniques offer limb debulking to improve function; however, outcomes are generally not
ideal. The Charles procedure is one such technique for severe lower limb lymphedema. The Charles
procedure resects skin and subcutaneous tissue to the level of the deep fascia 41 (Figure 98.4A). Split or
full thickness skin grafts harvested from the resected specimen are then used as coverage for the open
wounds. The procedure is fraught with risks including blood loss requiring transfusion, substantial skin
graft failure necessitating reoperations or prolonged wound care, acute infections, recurrence of
lymphedema, contour irregularities, and unaesthetic appearance of the limb in the long term. Another
direct excision technique applies staged elliptical excisions of skin and subcutaneous tissues 42 (Figure
98.4B). Excisions may be targeted to specific sites to limit the morbidity of the operation; however,
patients remain at significant risk of infections, delayed wound healing, contour irregularities,
unaesthetic appearance, loss of limb function, and recurrence of lymphedema.
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FIGURE 98.4 Excisional procedures for lymphedema. A. The Charles procedure: excision with skin grafting. B. Elliptical
excision and primary closure.
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Physiological Procedures
Over the past century, surgeons have devised several techniques to treat lymphedema aimed at restoring
the physiologic drainage function of the lymphatic system. The general basis of these techniques are
bypassing lymph into venous system or using transferred tissue containing normal lymph nodes to
reestablish functional drainage. Contemporarily, lymphovenous anastomosis (LVA) and vascularized
lymph node transfer (VLNT) are the most commonly used physiological procedures in clinical practice.
Advances in imaging and surgical techniques have contributed immensely to the popularization of LVA
and VLNT. Near-infrared fluorescence lymphography with ICG converted identifying patent lymphatic
channels, for bypass techniques, from a somewhat speculative to a more precise process. Additionally,
ICG lymphography has enhanced instructional studies on the function of the lymphatic system, patterns
of obstruction underlying different stages of the disease, and lymphatic system response to surgical
techniques. 32,33 The introduction of supermicrosurgery techniques that made it possible to perform
anastomoses between submillimeter diameter lymphatic vessels and subdermal venules has also
contributed immensely to the contemporary popularization of LVA. 43
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Lymphovenous Anastomosis
Peripheral collectors return lymphatic fluid to the venous circulation centrally via the thoracic duct. In
lymphedema patients, the function of peripheral collectors is progressively impaired due to stasis-
induced lymphatic channel fibrosis. LVA restores lymphatic fluid return to the venous circulation but
does so peripherally with anastomosis of patent lymphatic channels to adjacent subdermal venules, to
bypass lymph to the venous system (Figure 98.5). Although there are no clear evidence-based guidelines
on indications for LVA, there is effectively wide agreement on conditions favorable to LVA. LVA is
considered by most authors to be appropriate for patients with early-stage lymphedema. These patients
generally exhibit partial lymphatic obstruction with residual patent lymphatic vessels on
lymphoscintigraphy and ICG lymphography; moreover, they have not developed extensive fibrosis and
adipose hypertrophy. 33,44
FIGURE 98.5 A patent lymphovenous anastomosis. Isosulfan blue dye passes through the anastomosis from the lymphatic
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vessel into the venule.
(Reproduced with permission from Chang, DW, Suami, H, Skoracki, R. A prospective analysis of 100 consecutive lymphovenous bypass cases for treatment
of extremity lymphedema. Plast Reconstr Surg. 2013;132(5):1305-1314.)
ICG lymphography obviates the need for extensive dissection to find patent lymphatic channels. It
enables intraoperative lymphatic mapping to identify target lymphatic collectors suitable for
anastomoses. The ICG dye is injected intradermally in the webspaces of the hand or foot and binds to
proteins transported in lymphatic fluid. Near-infrared light from an imaging source detects the ICG thus
enabling real-time visualization of lymphatic fluid clearance. 32,33 Identifying patent collectors that
demonstrate distal to proximal dynamic directional flow without dermal stasis is key to success of the
anastomosis. 33,44
A tourniquet is not necessary for a bloodless field if the surgical site is infiltrated locally with dilute
epinephrine for vasoconstriction. A small transverse incision (2–3 cm) just through the dermis is all that is
required, and dissection is performed in the superficial subcutaneous plane to isolate the lymphatic
vessels identified on fluorescence lymphography. Injecting patent blue dye distal to the incisions helps
with identifying otherwise clear lymphatic channels in situ. After identifying a suitable subdermal vein
and collecting lymphatic vessel, end-to-end or side-to-end anastomosis is made and the passage of patent
blue dye across the anastomosis serves an immediate patency test. Additionally, the passage of
indocyanine green fluorescence across the anastomosis confirms anastomotic patency. Most authors
advocate several anastomoses to increase the likelihood of success with LVA. However, the basis of this
practice is largely theoretical, as there is no evidence associating a threshold number of anastomoses with
likelihood of success. 44
Most LVA outcomes studies are small retrospective case series with significant flaws in design. Study
populations are often heterogeneous due to notable differences in criteria for patient selection for surgery,
and because patients with distinctly different conditions (e.g., primary and secondary lymphedema) are
often mixed. This heterogeneity does undoubtedly confound findings. Moreover, variations in surgical
technique(s) and adjunctive treatments, duration and adequacy of follow-up, and both objective and
subjective outcome measurements used make high-level evidence difficult to obtain. 45
With these shortcomings in mind, several reviews to date report objective limb volume reduction and
subjective patient-reported symptom improvement after LVA. 45 In one of the larger and oft-cited case
series consisting of 100 patients, Chang et al. demonstrated that 96% of patients who underwent upper
limb LVA procedure reported symptom improvement. 33 Quantitatively, mean volume reduction varied
depending on lymphedema stage. International Society of Lymphology classification stage I and stage II
lymphedema patients had an average of 61% reduction in volume at 12 months, and stage III patients had
only 17% volume reduction at 12 months. In another large series, Campisi et al. followed 843 LVA
patients postoperatively (5–15 y) and reported that 73% had over 75% volume reduction and 24% had
over 50% volume reduction. 46 In summary, LVA is a minimally invasive procedure that involves a low
risk of morbidity to patients. 43,46 Although more rigorously conducted studies are necessary to establish
LVA outcomes and better delineate patients who would most benefit from the procedure, a considerable
plurality of current evidence demonstrates objective and subjective benefit for patients with early-stage
lymphedema potentially eliminating the need for continued use of compression garments. 43,45,46
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Vascularized Lymph Node Transfer
VLNT is a transfer of lymphatic tissue including lymph nodes from one of several possible donor sites to
proximal or distal recipient beds in the affected limb. There are two prevailing theories posited for the
mechanism by which VLNT works. The first theory proposes that the transferred physiologically normal
lymph nodes, through the action of growth factors and cytokines, induce reconstitution of lymphatic flow
within the recipient bed. 47 The other theory is that vascularized lymph nodes behave like the motor of a
pump, taking up interstitial fluid and subsequently diverting the fluid into the peripheral venous
circulation. There is an accompanying catchment effect whereby the decrease in subcutaneous interstitial
pressure in the lymphedematous limb due to the pump-like action further directs lymph from
surrounding tissues into the transferred lymph nodes. 48
Vascularized lymph node flaps can be transferred to proximal or distal recipient sites in the affected limb.
However, by the pump theory, the gravity effect resulting in interstitial fluid accumulating distally in
lymphedematous limbs would maximize the drainage efficiency of flaps transferred to distal recipient
sites. Other benefits of using a distal recipient site include an unscarred and nonoperated area with
available recipient vessels. Lastly, the number of vascularized lymph nodes in the transferred flap is
positively correlated with the degree of limb volume reduction. Therefore, choosing a flap with a high
number of viable lymph nodes within it increases the chance of a successful outcome. 49
There are a few donor sites described for VLNT, each with potential merits and risks. 44,50 The groin is the
most commonly used donor site for lymph node harvest. Groin lymph node flaps offer the benefit of a
concealed scar and the option to combine as a chimeric flap with abdominally based flaps for breast
reconstruction. Groin lymph node flaps may be based on the superficial circumflex iliac, superficial
inferior epigastric, or the deep inferior epigastric artery if combined with autologous breast
reconstruction. Reverse lymphatic mapping and avoiding dissection below the inguinal crease improves
the chances of including lymph nodes that drain the abdominal wall while leaving behind those that
drain the lower limb to avoid iatrogenic lower limb lymphedema. The submental lymph node flap, based
on the submental artery, includes lymph nodes from level Ia and Ib in the neck (Figure 98.6). Drawbacks
of this flap include the potential for injury to the marginal mandibular branch of the facial nerve that can
be avoided with dissection under microscope for better visualization. The merits of the submental lymph
node flap are that it has a substantial number of lymph nodes that have been correlated with better
outcomes with VLNT. Additionally, there is no risk of iatrogenic lymphedema. The supraclavicular flap
is based on the transverse cervical artery and branches of the external jugular vein. This flap is commonly
reported to have a variable blood supply and an inconsistent skin paddle (if required) and also leaves a
visible scar. In the lateral thoracic lymph node flap, axillary level I lymph nodes (inferior to lateral border
of pectoralis minor) are harvested based on the lateral thoracic or thoracodorsal vessels. Harvesting these
nodes carries the risk of iatrogenic upper limb lymphedema. Lastly, the omentum is a rich source of
lymphatic tissue and can be harvested in open or laparoscopic fashion. The risks of omentum harvest
include intra-abdominal solid and hollow viscus injuries and adhesions. 44
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FIGURE 98.6 A. Design of the vascularized submental lymph node flap with a 2.5-cm elliptical skin paddle. B. The donor site
was primarily closed and located below the mandibular edge, which allows the scar to be hidden. C. Sizable lymph nodes are
evident at the base of the flap (yellow arrows) along the course of the submental artery (red arrow). A facial vein (blue arrows)
was separated from the facial artery. D. Minimal donor site morbidity with an inconspicuous scar after the vascularized
submental lymph node flap transfer at the 24-month follow-up.
(Courtesy of Ming-Huei Cheng, MD.)
VLNT is the most recent of surgical treatments for extremity lymphedema (Figure 98.7). Although studies
are accumulating, there are yet no consistent objective and quality-of-life outcomes data from which to
draw definitive conclusions on efficacy. 50 However, the principal theories underlying the mechanism by
which VLNT works are backed by clinical and laboratory evidence that offer a foundation with which to
establish appropriate indications and produce higher level objective and subjective outcomes evidence of
efficacy.
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FIGURE 98.7 A. A 60-year-old woman with breast cancer-related lymphedema of the right upper extremity. B. She underwent
left vascularized groin lymph node flap transfer to the right wrist. C. The skin paddle in the wrist was de-epithelialized, and the
left upper medial arm was subjected to liposuction at 14 and 27 months. At the 36-month follow-up, the reduction rates of the
affected limb circumference were 40% and 38% above the elbow and below the elbow, respectively, without the use of a
compression garment. The improvements in circumferential difference were 25% and 18% above the elbow and below the
elbow, respectively.
(Courtesy of Ming-Huei Cheng, MD.)
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Questions
1. In using circumferential measurement as an objective diagnostic test, what is the minimum
increase in limb circumference used to define lymphedema?
a. 1 cm
b. 2 cm
c. 3 cm
d. 5 cm
e. 10 cm
2. Which of the following is not a risk factor for secondary lymphedema?
a. Cellulitis
b. Resistance exercise
c. Radiation
d. Overweight
3. A 45-year-old woman is suspected to have developed lymphedema of the right lower extremity
7 months after pelvic node dissection and radiation for uterine cancer treatment. Which of the
following is the most appropriate diagnostic imaging test?
a. Magnetic resonance imaging
b. Lymphoscintigraphy
c. Fluorescence lymphography
d. Lymphangiography
4. A 52-year-old woman presents with swelling, heaviness, and soreness of the left upper extremity
that began 12 months ago. Two years ago, she underwent bilateral mastectomies with right axillary
lymph node sampling. You suspect secondary lymphedema. Which of the following is the most
appropriate treatment?
a. Compression therapy
b. LVA
c. Diuretics
d. CDT
5. A 39-year-old woman describes a 20-year history of unilateral lower extremity swelling. She thinks
her grandmother had a similar problem. On exam, her left lower extremity is severely enlarged with
nonpitting wooden edema and verrucous hyperkeratosis. Which of the following is not an
appropriate surgical option?
a. Excision
b. Vascularized lymph node transplant
c. Amputation
d. LVA
1. Answer: b. Circumferential limb measurement is one of the most commonly used objective tools in
lymphedema diagnosis generally, because it is inexpensive and convenient to use in clinical settings.
The reliability of the test is high if it is administered properly: obtaining multiple circumference
points along the limb using nonelastic tape measure. A 2 cm increase in limb circumference is most
commonly used to define lymphedema.
2. Answer: b. Venipuncture, blood-pressure monitoring, and resistance exercise involving at-risk
limbs are a few of several factors that have been largely discredited as risk factors for lymphedema.
There also is robust evidence that both aerobic and resistance exercise, in addition to not increasing
the risk of lymphedema, provide strength and physical function benefits. All of the other options are
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recognized risk factors for lymphedema. Radiation impairs lymphatic transport with fibrosis of
lymphatic channels. Although the mechanism is not well understood, patients with
overweight/obesity (BMI >25) have a higher incidence of lymphedema after exposure to risk (e.g.,
lymph node dissection). Moreover, excess adipose deposition is a key element of lymphedema
pathophysiology. Cellulitis and other soft tissue infections also increase the risk of developing
lymphedema. Overweight/obesity and soft tissue infections are potentially controllable risk factors.
3. Answer: b. Lymphoscintigraphy is the standard diagnostic test for lymphedema. The test requires
injecting radiolabeled colloid into the dermis at the distal limb and observing the transit and
proximal uptake of colloid in the nodal basin. Magnetic resonance imaging may show changes in the
skin and subcutaneous tissues secondary to lymphedema; however, it is not a standard imaging
technique used in diagnosis of lymphedema. In fluorescence lymphangiography, indocyanine green
is injected in the dermis at the distal limb and a near-infrared light source is used to observe
lymphatic drainage. It is a useful adjunct to lymphoscintigraphy for diagnosis and surgical planning
for physiologic procedures but it is not the recognized gold standard diagnostic test.
Lymphangiography involves injection of contrast dye directly into a lymphatic vessel to visualize the
lymphatic system under fluoroscopy. Lymphangiography is not widely used because of concerns
that the inflammatory reaction to intraluminal injection of contrast can damage lymphatic vessels.
4. Answer: d. CDT is the first-line treatment for lymphedema. It comprises several elements
including MLD, compression therapy, and skin care, which in combination are effective in
decreasing limb swelling and bouts of skin infections. Compression therapy is one of the elements of
CDT, and several studies have compared its effectiveness as a lone measure, to CDT so far with
mixed results. Hence, CDT remains the standard treatment for lymphedema. LVA is a surgical
option for treating lymphedema in patients who have failed conservative treatments. Diuretics are
not effective as primary treatment for lymphedema.
5. Answer: c. Staged elliptical excisions or excision of diseased tissue followed by wound coverage
with skin grafts are surgical options for patients who present with late-stage lymphedema and
elephantiasis causing functional limitations. Amputation is not a primary treatment for lymphedema
and unnecessarily subjects the patient to significant loss of limb function. Vascularized lymph node
transplant and LVA are surgical options to reconstruct the lymphatic system. These options are most
appropriate in patients with earlier stage lymphedema (International Society of Lymphology stage I
or II) with partial lymphatic obstruction and no severe hypertrophic limb changes.
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References
Jiang, X, Nicolls, MR, Tian, W, et al. Lymphatic dysfunction, leukotrienes, and lymphedema. Annu Rev Physiol. 2018;80:49-70.
Cormier, JN, Askew, RL, Mungovan, KS, et al. Lymphedema beyond breast cancer: a systematic review and meta-analysis of cancer-related
secondary lymphedema. Cancer. 2010;116(22):5138-5149.
Gärtner, R, Jensen, MB, Kronborg, L, et al. Self-reported arm-lymphedema and functional impairment after breast cancer treatment – a
nationwide study of prevalence and associated factors. Breast. 2010;19(6):506-515.
Fu, MR, Ridner, SH, Hu, SH, et al. Psychosocial impact of lymphedema: a systematic review of literature from 2004 – 2011. Psychooncology.
2013;22(7):1466-1484.
Heiney, SP, McWayne, J, Cunningham, JE, et al. Quality of life and lymphedema following breast cancer. Lymphology. 2007;40(4):177-184.
Pusic, AL, Cemal, Y, Albornoz, C, et al. Quality of life among breast cancer patients with lymphedema: a systematic review of patient-
reported outcome instruments and outcomes. J Cancer Surviv. 2013;7(1):83-92.
Basta, MN, Fox, JP, Kanchwala, SK, et al. Complicated breast cancer-related lymphedema: evaluating health care resource utilization and
associated costs of management. Am J Surg. 2016;211(1):133-141.
Boyages, J, Xu, Y, Kalfa, S. Financial cost of lymphedema borne by women with breast cancer. Psychoocology. 2017;26(6):849-855.
Rockson, SG, Rivera, KK. Estimating the population burden of lymphedema. Ann N Y Acad Sci. 2008;1131:147-154.
Szuba, A, Rockson, SG. Lymphedema: classification, diagnosis and therapy. Vasc Med. 1998;3(2):145-156.
Mortimer, PS, Rockson, SG. New developments in clinical aspects of lymphatic disease. J Clin Invest. 2014;124(3):915-921.
Connell, F, Gordon, K, Brice, G, et al. The classification and diagnostic algorithm for primary lymphatic dysplasia: an update from 2010 to
include molecular findings. Clin Genet. 2013;84(4):303-314.
Lymphatic filariasis. World Health Organization. Available at
Accessed April 1, 2018.
Beesley, V, Janda, M, Eakin, E, et al. Lymphedema after gynecological cancer treatment. prevalence, correlates, and supportive care needs.
Cancer. 2007;109(12):2607-2614.
McLaughlin, SA, Wright, MJ, Morris, KT, et al. Prevalence of lymphedema in women with breast cancer 5 years after sentinel lymph node
biopsy or axillary dissection: patient perceptions and precautionary behaviors. J Clin Oncol. 2008;26(32):5220-5226.
DiSipio, T, Rye, S, Newman, B, Hayes, S. Incidence of unilateral arm lymphoedema after breast cancer: a systematic review and meta-
analysis. Lancet Oncol. 2013;14(6):500-515.
Yen, TW, Fan, X, Sparapani, R, et al. A contemporary, population-based study of lymphedema risk factors in older women with breast
cancer. Ann Surg Oncol. 2009;16(4):979-988.
Ashikaga, T, Krag, DN, Land, SR, et al. Morbidity results from the NSABP B-32 trial comparing sentinel lymph node dissection versus
axillary dissection. J Surg Oncol. 2010;102(2):111-118.
Ververs, JM, Roumen, RM, Vingerhoets, AJ, et al. Risk, severity, and predictors of physical and psychological morbidity after axillary lymph
node dissection for breast cancer. Eur J Cancer. 2001;37(8):991-999.
Ki, EY, Park, JS, Lee, KH, et al. Incidence and risk factors of lower extremity lymphedema after gynecologic surgery in ovarian cancer. Int J
Gynecol Cancer. 2016;26(7):1327-1332.
McLaughlin, SA, DeSnyder, SM, Klimberg, S, et al. Considerations for clinicians in diagnosis, prevention and treatment of breast cancer-
related lymphedema, recommendations from an expert panel: part 2: preventive and therapeutic options. Ann Surg Oncol.
2017;24(10):2827-2835.
Schmitz, KH, Ahmed, RL, Troxel, AB, et al. Weight lifting for women at risk for breast-cancer-related lymphedema. JAMA. 2010;304(24):2699-
2705.
Kolden, GG, Strauman, TJ, Ward, A, et al. A pilot study of group exercise training (GET) for women with primary breast cancer: feasibility
and health benefits. Psychooncology. 2002;11(5):447-456.
International Society of Lymphology. The diagnosis and treatment of peripheral lymphedema: 2013 consensus document of the International
Society of Lymphology. Lymphology. 2013;46(1):1-11.
Shaw, C, Mortimer, P, Judd, PA. A randomized controlled trial of weight reduction as a treatment for breast cancer-related lymphedema.
Cancer. 2007;110(8):1868-1874.
Norman, SA, Localio, AR, Potashnik, SL, et al. Lymphedema in breast cancer survivors: incidence, degree, time course, treatment and
symptoms. J Clin Oncol. 2009;27(3):390-397.
Petrak, JA, Senie, RT, Peters, M, et al. Lymphedema in a cohort of breast carcinoma survivors 20 years after diagnosis. Cancer.
2001;92(6):1368-1377.
Launois, R, Alliot, F. Quality of life scale in upper limb lymphoedema – a validation study. Lymphology. 2000;33(suppl):266-274.The study
describes the construction and validation of the Upper Limb Lymphedema—27 Questionnaire, currently the only condition-specific, quality-

of-life,
patient-reported outcome measure for upper extremity lymphedema. It improves the opportunity to design outcomes studies that provide informative
conclusions about the effectiveness of lymphedema treatments.
McLaughlin, SA, Staley, AC, Vicini, F, et al. Considerations for clinicians in the diagnosis, prevention, and treatment of breast cancer-related
lymphedema: recommendations from a multidisciplinary expert ASBrS panel part 1: definitions, assessments, education, and future
directions. Ann Surg Oncol. 2017;24(10):2818-2826.
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Chen, YW, Tsai, HJ, Hung, HC, et al. Reliability study of measurements for lymphedema in breast cancer patients. Am J Phys Med Rehabil.
2008;87(1):33-38.
Armer, JM, Hulett, JM, Bernas, M, et al. Best practice guidelines in assessment, risk reduction, management, and surveillance for post-breast
cancer lymphedema. Curr Breast Cancer Rep. 2013;5(2):134-144.
Ogata, F, Narushima, M, Mihara, M, et al. Intraoperative lymphography using indocyanine green dye for near-infrared fluorescence labeling
in lymphedema. Ann Plast Surg. 2007;59(2):180-184.This study introduced near-infrared lymphography with indocyanine green (ICG) for
intraoperative lymphatic mapping during microsurgical lymphatic reconstruction. The practice obviates the need for extensive dissection to find patent
lymphatics, essentially making LVA an easier minimally invasive procedure.
Chang, DW, Suami, H, Skoracki, R. A prospective analysis of 100 consecutive lymphovenous bypass cases for treatment of extremity
lymphedema. Plast Reconstr Surg. 2013;132(5):1305-1314.
International Society of Lymphology. The diagnosis and treatment of peripheral lymphedema: 2016 consensus document of the International
Society of Lymphology. Lymphology. 2016;49(4):170-184.
Patel, KM, Lin, CY, Cheng, MH. A prospective evaluation of lymphedema-specific quality-of-life outcomes following vascularized lymph
node transfer. Ann Surg Oncol. 2015;22(7):2424-2430.
Ezzo, J, Manheimer, E, McNeely, ML, et al. Manual lymphatic drainage for lymphedema following breast cancer treatment. Cochrane Database
Syst Rev. 2015;21(5):CD003475.
Johansson, K, Albertsson, M, Ingvar, C, et al. Effects of compression bandaging with or without manual lymph drainage treatment in
patients with postoperative arm lymphedema. Lymphology. 1999;32(3):103-110.
McNeely, ML, Magee, DJ, Lees, AW, et al. The addition of manual lymph drainage to compression therapy for breast cancer related
lymphedema: a randomized controlled trail. Breast Cancer Res Treat. 2004;86(2):95-106.
Brorson, H, Svensson, H. Liposuction compared with controlled compression therapy reduces arm lymphedema more effectively than
controlled compression therapy alone. Plast Reconstr Surg. 1998:102(4);1058-1067.
Brorson, H. Liposuction in lymphedema treatment. J Reconstr Microsurg. 2016;32(1):56-65.
Dumanian, GA, Futrell, JW. The Charles procedure: misquoted and misunderstood since 1950. Plast Reconstr Surg. 1996;98(7):1258-1263.
Salgado, CJ, Mardini, S, Spanio, S, et al. Radical reduction of lymphedema with preservation of perforators. Ann Plast Surg. 2007;59(2):173-
179.
Koshima, I, Inagawa, K, Urushibara, K, et al. Supermicrosurgical lymphaticovenular anastomosis for treatment of lymphedema in the upper
extremities. J Reconstr Microsurg. 2000;16(6):437-442.In the evolution of LVA using larger caliber cutaneous veins, patency was a concern primarily
because of backflow from the higher pressure cutaneous venous system. This study described supermicrosurgical LVA using subdermal venules with
more favorable pressures, potentially improving patency rates.
Allen, RJ, Cheng, MH. Lymphedema surgery: patient selection and an overview of surgical techniques. J Surg Oncol. 2016;113(8):923-931.
Scaglioni, FM, Fontein, BYD, Arvanitakis, M, et al. Systematic review of lymphovenous anastomosis (LVA) for the treatment of lymphedema.
Microsurgery. 2017;37(8):947-953
Campisi, C, Davini, D, Bellini, C, et al. Lymphatic microsurgery for the treatment of lymphedema. Microsurgery. 2006;26(1):65-69.
Shesol, BF, Nakashima, R, Alvavi, A, et al. Successful lymph node transplantation in rats, with restoration of lymphatic function. Plast
Reconstr Surg. 1979;63(6):817-823.The authors demonstrated, in laboratory experiments, that vascularized transplanted nodes established connections
with local, open lymphatic channels after lymphadenectomy. This four-decade old finding forms a basis of contemporary VLNT techniques.
Cheng, MH, Huang, JJ, Wu, CW, et al. The mechanism of vascularized lymph node transfer for lymphedema: natural lymphaticovenous
drainage. Plast Reconstr Surg. 2014;133(2):192e-198e.
Lin, CH, Ali, R, Chen, SC et al. Vascularized groin lymph node transfer using the wrist as a recipient site for management of postmastectomy
upper extremity lymphedema. Plast Reconstr Surg. 2009;123(4):1265-1275.
Pappalardo, M, Patel, KM, Cheng, MH. Vascularized lymph node transfer for treatment of extremity lymphedema: an overview of current
controversies regarding donor sites, recipient sites and outcomes. J Surg Oncol. 2018;117(7):1420-1431.
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C H A P T E R 9 9
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Pressure Injuries
Christi M. Cavaliere and Rachel E. Aliotta
Key Points
When external pressure exceeds capillary bed pressure (32 mm Hg), perfusion is impaired and
results in ischemic tissue and pressure-related injuries.
Relieving pressure over a bony prominence for 5 minutes every 2 hours will allow adequate
perfusion and reduce the risk of soft tissue breakdown.
Pressure injury resolution can only occur if infection is treated, pressure is relieved, and exacerbating
spasms or contractures are controlled.
Medical and nutrition optimizations are critical before reconstruction should be attempted.
Because of the high risk of recurrence, the choice of soft tissue closure should always anticipate the
need for future reoperations.
Successful pressure injury treatment depends on multidisciplinary team efforts employing both
medical and surgical management in a team-based approach.
Unrelieved prolonged pressure, commonly over a bony prominence such as the sacrum, can result in
localized soft tissue injury. Although historically referred to as bed sores, or decubitus ulcers, these wounds
can occur anywhere on the body when there is increased pressure or friction, shearing forces, or limb
spasticity. 1 Constant and attentive repositioning is essential for prevention and healing of pressure-
induced wounds. Wound management begins with identifying and aggressively managing the
modifiable factors that contribute to pressure injury development such as positioning, incontinence,
spasticity, nutrition, equipment, and medical comorbidities. Early interventions include dressing care and
cleaning of the wound as well as appropriate support surfaces. Bedside debridement of nonviable or
infected tissue may be appropriate in some cases; however, surgical management may be necessary in
more severe cases or to promote patient comfort. Preoperative medical optimization, thorough
debridement, and tension-free soft tissue coverage for closure of these defects remain the fundamental
pillars of pressure injury management. 2 With increasingly complex patient populations suffering from
these often-debilitating wounds, multidisciplinary specialty team care is essential for long-term success.
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Epidemiology
An estimated 2.5 million pressure injuries are treated annually in the United States. 3 These patients are
more likely to have increased hospital admissions and longer length of stay, and they are more likely to
be discharged to a skilled nursing facility on discharge. 4 With costs over $11 billion, pressure injuries
pose a significant burden to the health-care system. 5 The cost to treat one hospital-acquired pressure
injury is estimated to be over $100,000. 6,7 Moreover, pressure-related injuries are now considered among
the eight preventable conditions identified by the Centers for Medicare and Medicaid Services in 2008 as,
never events. By this designation, the cost of treatment is no longer reimbursable for hospitals, no matter
the inevitability or attempts made to prevent their occurrence. 8,9
Certain populations have been identified as high risk for developing pressure-related injuries 2 :
Patients with hip fracture or spinal cord injury (SCI)
Patients with lower extremity trauma resulting in bone or soft tissue injury with fixation and casting
Elderly patients with immobility and/or cachexia
Intensive care unit (ICU) patients
The risk is even more pronounced in the SCI population, in which there is an estimated incidence of 20%
to 30% in paraplegic and quadriplegic patients. 10 Patients may also present with more complicated risk
factors, such as long-term use of pain medications, suicidal behavior, history of incarceration, smoking,
and substance abuse. 2,11
Multiple pressure injury risk assessment tools have been developed to stratify patient risk and may be
used to guide prevention interventions, such as the Braden, Waterlow, and Norton scales. Patient
characteristics are included in the scales, such as mobility, nutrition, incontinence, and mental status. 12–14
Predictive value of these scales is fair, but there is no significant effect of implementation of the scales on
reducing the incidence of pressure injuries. 15
The National Pressure Injury Advisory Panel is the authoritative voice for pressure injury prevention,
treatment, and outcomes in the United States. In 2016 the National Pressure Injury Advisory Panel
updated the pressure injury staging system. Although there are some clinical exceptions, in general stage
1 and 2 pressure injuries are treated nonoperatively. Stage 3 and 4 may require operative intervention to
ameliorate. Proper staging may require initial debridement of any overlying nonviable tissue if the extent
of injury is indeterminate on initial clinical examination (Table 99.1).
TABLE 99.1
National Pressure Ulcer Advisory Panel Staging System for Pressure Injuries16
Description
Treatment
Stage 1
Nonblanching erythema
Pressure relief
Stage 2
Partial-thickness loss of dermis
Pressure relief, wound care
Stage 3
Full-thickness loss; subcutaneous tissue visible (but no muscle or bone)
Pressure relief, wound care, possible surgical
debridement
Stage 4
Full-thickness loss with exposed bone, tendon, or muscle
Pressure relief, wound care, possible surgical
debridement
Unstageable
Full-thickness loss, unknown depth due to eschar or slough
Wound care, removal of devitalized tissue for
proper staging, possible surgical debridement
Deep tissue
pressure
injury
Purple/maroon colored intact skin with unknown true depth, or
epidermal separation revealing dark wound bed or blood filled blister
Pressure relief, monitor wound over time, may
go on to need surgical debridement
Mucosal
membrane
Found on mucous membranes with a history of a medical device used
at the location. These are not staged.
The economics of pressure injuries and prevention are astounding. Pressure-related injuries account for
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the second-most common hospital billing claim, and are estimated to cost $70,000 to $150,000 per patient
for stage 3 or 4 injuries, at times resulting in over $250,000 in legal settlements. 6,17,18 Therefore,
understanding common clinical situations and appropriate documentation and coding is essential in
clinical practice management.
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Pathophysiology
Pressure
Pressure injures are caused by unrelieved mechanical pressure to soft tissue, most commonly over a
weight-bearing bony prominence such as the sacrum, ischium, heel, or trochanter (Figure 99.1). When
external pressure exceeds capillary bed pressure (32 mm Hg), perfusion is impaired resulting in both
ischemic tissue injury and pressure-related injury. Relieving pressure over a bony prominence for
5 minutes every 2 hours will generally allow adequate perfusion and reduce the risk of soft tissue
breakdown 19 (Figure 99.2). When the pressure exerted on the soft tissue becomes higher than that of the
supplying blood vessels, edema and ischemia occur, metabolic waste products and free radicals
accumulate, and with time permanent tissue destruction leads to significant defects 20 . Perhaps
counterintuitively, the clear relationship between pressure and time is seen pathologically first in the
muscle overlying the bone, followed by the superficial soft tissues and lastly the skin. 21 This distribution
with less visible injury at the surface and the more extensive tissue injury deep, adjacent to the bone, is
referred to as the tip of the 

iceberg (Figure 99.3).
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FIGURE 99.1 Common sites of pressure on the human body when seated, prone, and supine.
(Reprinted with permission of Cleveland Clinic Center for Medical Art & Photography ©2018. All rights reserved.)
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FIGURE 99.2 The inverse relationship between time and pressure in the formation of pressure injuries.
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FIGURE 99.3 Tip of the iceberg cone-shape pattern of pressure-related injury from unrelieved pressure affecting the deepest
structures adjacent to the bone with the greatest injury.
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Inflammation
Inflammation plays a key role in tissue injury, repair, and regeneration. Dynamic reciprocity, or the
ongoing bidirectional interaction between cells and their surrounding environment, is an integral process
in wound healing. 22 The lack of objective quantifiable biochemical and physiologic markers that can be
used to assess wound status is still a major hurdle in the progress of improved treatment regimens.
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Edema
Increased applied pressure leads to plasma extravasation and edema. Inflammatory mediators (e.g.,
prostaglandin E2) are released in response to compression and cause leakage through cell membranes,
which increases the amount of interstitial fluid. With local denervation there is a loss of sympathetic tone
to area vasculature, leading to vasodilation and vessel engorgement. This is exacerbated by circulatory
disease (i.e., heart or renal failure, venous insufficiency) and further increases edema in dependent areas.
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Other Factors
Additional factors contributing to or exacerbating soft tissue loss include friction, shearing forces,
malnutrition, moisture, and neurologic injury. Perspiration, wound drainage, and incontinence can lead
to an increased coefficient of friction between the wound and dressing or bed linens. This further
potentiates contact damage and tissue breakdown. 23 Despite this, there is no known direct evidence
linking urinary or fecal incontinence with the direct formation of pressure-related injuries themselves.
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Clinical Prevention and Management
Control Extrinsic Factors
Behavioral modification: The mainstay of pressure injury prevention is the even distribution of
pressure across the body in contact with any surface.
Mobilize and/or reposition
Avoid prolonged sitting
Encourage smoking cessation
Manage excess perspiration in and around wound and skin folds with appropriate dressings
and clothing
Establish effective toileting routine to reduce/prevent soilage and maceration
Pressure relief: No single specific device has been proven superior for prevention relative to others. 24
Minimize head-of-bed elevation to reduce sacral shear forces (<45°)
Reposition every 2 hours, encourage mobility (if able)
Adjunct pressure offloading devices (i.e., foam wedge, pillows, boots)
In the operating room: float heels, intermittent scalp massage, pressure points padded
Pressure-relieving mattresses or seating surfaces (eg. Foam, low-air loss, or air-fluidized)
Consider prophylactic foam dressings on high-risk surfaces
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Control Intrinsic Factors
Medical optimization
Optimize other underlying medical comorbidities; congestive heart failure, respiratory failure,
and complicated diabetes are the most common diagnoses in patients with pressure injuries. 25
Optimize kidney function
Manage urinary and fecal incontinence—modify bowel routine or divert
Manage uncontrolled fistulas
Optimize blood glucose control, HgbA1c to <6%
Correct anemia
Nutrition: Malnutrition correlates with development of primary injuries and poor wound healing.
Consult nutritionist for assessment and dietary modifications to meet caloric goals for wound
healing (e.g., tube feed, high-calorie shakes).
Laboratory test results: serum albumin, prealbumin, and micronutrients: Zn, Ca, Fe, Cu, Vit A
and C
Optimize healing potential with serum albumin ideal goal >3.0 g/dL before operating. Goal is to
provide adequate protein for positive nitrogen balance.
Track inflammatory markers in conjunction with nutritional laboratory results (erythrocyte or
Westegren sedimentation rate, or C-reactive protein) as inflammation may artificially suppress
albumin and prealbumin levels.
May need colorectal diversion for wound hygiene, as well as to improve diet and nutritional
health
Swallow evaluation with or without feeding tube
Infection management
Septicemia, pneumonia, and urinary tract infections are the most common infection diagnoses in
patients with pressure injuries. 25
Laboratory test results: evaluate markers of inflammation and infection (white blood cell count,
erythrocyte sedimentation rate, C-reactive protein)
Avoid bedside swab of wounds due to contamination; intraoperative deep cultures are superior
for antibiotic tailoring (22%–36% concordance between superficial swab versus intraoperative
cultures reported). 26,27
Treat with pathogen-directed antibiotics when indicated
MRI may be indicated to evaluate extent of osteomyelitis (97% sensitive, 89% specific). 28
Bone biopsy is gold standard for diagnosis.
Neurologic spasm and contracture management
Especially SCI: Incidence of spasm varies with level of SC injury (proximal lesion = higher
incidence)
Spasm and contracture create shear forces contributing to pressure injury development
Common in hip and knee joints
Antispasmodic pharmacotherapy: baclofen, diazepam, dantrolene
Botulinum toxin improves function and reduces limb spasticity with minimal side effects.
Procedural intervention if severe, after failed medical management
Peripheral nerve block, epidural stimulator, baclofen pump, rhizotomy
Surgical release of joint contracture or in severe cases amputation
Consider medical rhizotomy (phenol)
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Wound Care
Make clinical assessment before choosing appropriate wound care dressing regimens for each patient and
each wound. Be sure to diagram, use photographs, and document a comprehensive physical examination
of all affected areas, including:
Dimensions (length × width × depth)
Presence of undermining, position (clock face location)
Indicators of infection and/or systemic symptoms of infection
Drainage, amount, and character
Odor, possible source, or cause
Deepest visible layer affected or seen in base of wound
Condition of periwound skin (such as bruising or maceration)
Vascular assessment of surrounding tissue or affected
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Nonoperative Management
Dressings
Based on patient and wound assessment, select a dressing that will support a moist healing environment
for the wound. Appropriate wound-healing agents include hydrocolloids, alginates and hydrofibers,
hydrogels, paraffin gauze dressings, and many other dressings and topical agents. 29 However, there is
little clinical evidence to aid the choice between different dressings. In general, the consensus opinion
favors hydrogels during the debridement stage, foam and low-adherence dressings for the granulation
stage, and hydrocolloid and low-adherence dressings for the epithelialization stage. Packing the wound
cavity with moist gauze may be appropriate in some circumstances. Ultimately, the dressing chosen
should be best suited to manage the moisture level in and around the wound.
Preventive: A recent consensus panel recommendation concluded multilayered silicone dressing was
effective as an adjunct for reducing pressure-related injuries to sacrum, buttocks, and heels in high-
risk environments (the OR, ICU) when combined with traditional preventative measures. Silicone is
elastic and therefore able to absorb the shear forces and reduce skin deformation. 30
For dry wounds, create a moist healing environment. Many are dressings appropriate.
Traditional wet to moist saline dressing, typically should be changed one or two times per day,
depending on wound debridement needs.
Use sodium hypochlorite solution or bleach-based solution if infection is suspected, particularly
Pseudomonas. Diluted sodium hypochlorite solution has been shown to be bactericidal with fibroblast
preservation.
Hydrogels—Used as tube of gel or sheet; water-based, nonadherent; changed daily
Hydrocolloid dressing has been associated with almost three times more complete healing compared
with the use of saline gauze alone. 31 There is no evidence to support superiority of topical collagen
versus hydrocolloid for pressure injury healing, and it is more costly. 32
Honey—variable gel thickness and composition, minimal risk, and low cost, with possible autolytic
and antimicrobial properties. 33
Studies on sustained silver-releasing dressing demonstrated a tendency for reducing the risk of
infection and promoting faster healing, but sample sizes have been too small for statistical analysis to
draw formal conclusions. 34
For wounds with large amount of drainage, use dressings that are absorbent.
Alginates (derived from seaweed) or synthetic hydrofibers. These dressings have a dry, felt-like
texture and absorb several times their weight in moisture. There is evidence the use of alginates
with hydrocolloid results in significantly greater reduction in the size of stage 3 and 4 pressure
injuries compared to hydrocolloid alone. 35
Hydrocolloid gel forming polymers
Foam dressings—can be used alone or as a cover dressing. Gentle on skin but can be more
costly.
Wicking systems or salt-impregnated gauze
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Negative-Pressure Wound Therapy
Negative-pressure wound therapy (NPWT), as well as NPWT systems with automated instillation
capabilities and dwell time, is gaining popularity in the wound care armamentarium. In addition to the
benefits of negative-pressure therapy the cyclic instillation and dwelling of topical wound solutions aided
cleaning and granulation tissue formation. The proposed benefits include removal of infectious materials,
36 reduced risk of compromise due to contamination, the ability to solubilize necrotic tissue, reduced
volume of exudate, increased granulation tissue, and decreased wound size. 37 However, the use of
negative-pressure systems should be considered in light of the effect it may have on patient mobility and
ambulation, as well as cost-to-benefit ratio given clinical and social scenario of each individual patient.
Contraindications to the use of NPWT include exposed vessels or organs, nonenteric and unexplored
fistulas, malignancy, and untreated osteomyelitis. 38
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Hyperbaric Oxygen Therapy
Hyperbaric oxygen therapy (HBOT) has been used as an adjunct to treat wounds for decades, proving to
be safe and beneficial for selected patients. HBOT increases oxygen transport to the wound area,
facilitates angiogenesis, reduces inflammation and swelling, improves lymphatic circulation, reduces
infection by increasing the capacity of the leukocyte, and may relieve some pain. 39 A pressure injury itself
is not an indication for HBOT; however, HBOT may be used as adjunctive treatment for chronic
refractory osteomyelitis within a pressure injury or a failed graft or flap. 40
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Biologic Therapies
The efficacy of platelet-derived growth factors, fibroblast growth factor, and granulocyte macrophage
colony stimulating factor in improving complete pressure injury healing has not been well established.
There is limited low-quality evidence on skin matrix and 
 tissue-engineered skin equivalents, with
insufficient evidence to draw conclusions. 34
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Other Therapies
There is some evidence that electrotherapy 41 and whirlpool therapy 42 may help reduce the size and
surface area of stage 2 to 4 pressure injuries. However, the efficacy of other therapy modalities such as
electromagnetic therapy, low-level laser therapy, cold lasers, light therapy, or ultrasound therapy has not
been found to promote superior healing of pressure injuries at present. 34
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Surgical Management
Indications
Necrotizing infection
Need for significant debridement
Biopsy for malignancy, deep cultures
Bone and/or hardware exposure
Vasculature exposure
Organ exposure
Retained foreign body (i.e., packing)
Small skin opening with area of large undermining
Necessity due to medical complexity
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Debridement and Wound Optimization
Soft Tissue
Infected and necrotic wounds require early and aggressive debridement of any infected or devitalized
tissue. Goals are the following:
Remove necrotic tissue
Decrease the bacterial count and biofilm
Convert a chronic wound to an acute wound
Bedside debridement may be limited by patient comfort and ability to secure hemostasis in both sensate
and insensate patients. Consider the patient’s risk of autonomic dysreflexia (AD) with pain stimulus.
Intraoperatively, consider painting wound borders with methylene blue to ensure removal of the entire
cavity. Send deep tissue for culture to tailor antibiotic choice because this has been shown superior to
superficial swabs, which tend to have high rate of misdiagnosis and may lead to antibiotic over
treatment. 26 Initiate wound care following debridement.
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Bone
Some institutions advocate taking bone biopsy only in conjunction with soft tissue debridement as
needed, as to avoid seeding deep bone with any overlying infectious processes. 2 There is a high reported
rate of osteomyelitis, with 56% of primary injuries and 79% of recurrent injuries having positive bone
biopsies for osteomyelitis. 43 Remove as minimal bone as possible. Avoid radical ostectomy for bony
prominences, as this can lead to skeletal instability, excessive bleeding, and pressure point redistribution
(as seen with unilateral ischiectomy with contralateral injury formation).
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Contracture Release and Management of Spasticity
These strategies are important to optimize positioning before attempted final reconstruction.
Peripheral nerve blocks, epidural stimulator, baclofen pumps, rhizotomy
Consider medical rhizotomy (phenol) or surgical
Tenotomy for limb contracture. Avoid hip release in wheelchair-
 bound patients because this will
interfere with transfers if flail extremity occurs.
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Reconstruction
When considering flap reconstruction, it is essential to take into account that flap coverage does not
address the root cause of the pressure injury (i.e., the complex interplay between ischemia, nutrition,
infection, and overall health of the patient). Careful patient selection with flap choice tailored to the
individual patient is the most critical step in improving overall patient outcomes in these difficult cases.
Avoid primary closure of pressure injuries due to high rates of breakdown and dehiscence.
Skin grafts will likely fail in this area because of lack of adequate tolerance to repeated pressure and
shear.
There is no reported difference in success using myocutaneous compared to fasciocutaneous flaps
44,45 (Figure 99.4).
Despite the use of risk assessment tools and preventative risk reduction practice, complications and
recurrence rates for flap coverage are high. 46,47
FIGURE 99.4 Considerations using myocutaneous versus fasciocutaneous flaps.
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Management by Pressure Injury Location
Ischium
These defects common in patients seated for prolonged periods (i.e., wheelchair-bound patients).
High recurrence rates may be due to pressure and tension across joint while sitting. Recurrence rates
of 19% to 33% have been reported for ischial pressure injuries after flap reconstruction. 47,48
Ischial flap design should take into consideration:
Ambulatory status
Possibility of future flaps due to high rate of recurrence
Avoid placing incisions over weight-bearing prominences
Consider flaps that can be readvanced subsequently: for example gluteal rotation or V-Y hamstring.
Avoid tension with these closures, as hip flexion can cause dehiscence.
Tensor fascia lata (TFL) may be considered, but it may be too thin distally.
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