44-56_OWM0108_Fife-Carter.qxd
1/4/08
4:12 PM
Page 44
FEATURE
A
TE
Lymphedema in the Morbidly
Obese Patient: Unique Challenges
in a Unique Population
Caroline E. Fife, MD; and Marissa J. Carter, PhD
U
PL
IC
The population of morbidly obese patients, along with the incidence of lymphedema and massive localized lymphedema associated with this condition, is increasing. A 5-year retrospective review of data (2000–2005) shows that the percentage of patients
>350 lb in the authors’ clinic population increased from approximately 7% to 11% and 75% of their morbidly obese patients (body
mass index >40) had or have lymphedema. After a differential diagnosis between lipedema and lymphedema (primary or secondary) has been made, lymphedema management options include compression bandaging, manual lymphatic drainage, and
localized surgeries. The treatment of morbidly obese lymphedema patients requires additional staff time and specialized equipment to move or position them and may be confounded by other conditions (eg, heart failure and venous insufficiency) that contribute to edema. Lymphedema treatments have been found to be useful, providing patients are able to follow treatment guidelines, especially with regard to weight control. In the authors’ experience, massive localized lymphedema will recur unless the primary issue of obesity is addressed. Establishing clear criteria and patient participation guidelines before initiating a comprehensive localized lymphedema program will improve outcomes.
D
KEYWORDS: morbid obesity, lymphedema, massive localized lymphedema, manual lymphatic drainage, compression bandaging
T
Ostomy Wound Management 2008;54(1):44–56
n the majority of US states, 20% to 24% of the population — approximately 40 million individuals — is
considered obese (20% over the ideal body weight).1
Morbid obesity is defined as weighing >100 lb more than
ideal body weight or having a body mass index (BMI) of
>40; its prevalence increased from 2.9% in 1988 to 1994
to 4.7% in 1999 to 2000.2 The healthcare costs for morbidly obese patients are nearly double those of normal
weight patients due to the additional costs of obesitylinked chronic health conditions, such as diabetes, hypertension, and cardiovascular disease.3 Moreover, results
from Fontaine et al’s4 epidemiological research study
D
O
N
O
I
using National Health and Nutrition Examination
Survey I and II cohort data (N = 14,407 and 9,282,
respectively) show that morbidly obese Caucasian men
and women ages 20 to 30 years are estimated to lose 13
and 8 years, respectively, from their life expectancies. For
young African American men, this figure is even higher
at 20 years. Conservative estimates based on two
prospective studies5,6 of morbidly obese bariatric surgery
candidates and a comparative retrospective study7
approximate that 75% of morbidly obese people have at
least one comorbid condition that may explain the
observed risk of premature death.
Dr. Fife is Associate Professor, Department of Anesthesiology, University of Texas Health Science Center, and the Memorial Hermann
Center for Lymphedema Management, Houston, TX. Dr. Carter is President, Strategic Solutions, Inc., Cody, Wyo. Please address correspondence to: Caroline E. Fife, MD, 6411 Fannin, Houston, TX 77030; email: [email protected].
44
OstomyWound Management
Page 45
Figure 1. Lymphedema clinic patients weighing >350 lb:
2000–2005; N = 1,464.
U
PL
Lymphedema is one comorbid condition that has
not been studied extensively in morbidly obese
patients. In general populations, lymphedema is a relatively rare and serious disorder of the lymphatic system with a reported crude prevalence rate of 0.13%8
that tends to be associated with older female patients.
However, information from wound clinic data submitted through the Intellicure (The Woodlands, Tex)
Research Consortium (IRC), a repository of de-identified electronic medical records (EMR) of approximately 15,000 patients from 17 wound centers in both
urban and rural areas of 18 US states, show a 74%
crude prevalence of lymphedema in morbidly obese
patients. This is a very high prevalence rate compared
to the reported rate in the general population. The
prevalence of lymphedema among morbidly obese
people has been referred to by some lymphologists as
an “epidemic hidden in plain sight.” The purpose of
this article is to educate clinicians regarding the features and treatment of lymphedema in the context of
the morbidly obese.
TE
4:12 PM
A
1/4/08
IC
44-56_OWM0108_Fife-Carter.qxd
Obesity Data
N
O
T
D
To determine the accuracy of the authors’ clinical
perception that the actual weight of lymphedema
patients had increased over the years, a total of 1,463
electronic patient records from 2000 to 2005 were analyzed. Data were available for 575 men (39.2%) and
889 women (60.8%) with lymphedema. Without corresponding height data, BMI cannot be determined;
however, by evaluating only patients (all races) weighing more than 350 lb, a trend toward increasing weight
among patients presenting for treatment was noted
during the 5-year period surveyed (see Figure 1).
Figure 2. Dilated superficial lymphatics in a patient with congestive heart failure. The buttock is on the right and the crease of the
leg is seen vertically in the picture. The lymphatics are attempting to move fluid caudally back to the heart (to the left).
action. Thus, the lymphatic system represents an
alternative circulatory system, a kind of “storm
sewer” system for the tissues, which generally receives
little consideration until it is unable to manage the
volume of fluid with which it is presented. Like
Edema and Obesity
D
O
Because the body’s rich capillary network is
designed to be “leaky,” filtered capillary fluid can
remove the waste products of the extracellular space
due to the slight pressure imbalance resulting from
Starling forces, as long as the lymphatic system functions normally. At least 8 liters of lymph containing
approximately 240 g of protein9 is collected from the
extracellular spaces and carried back to the heart
each day.10,11 The lymphangions propel lymph fluid
via an intrinsic, unidirectional, pulsatile pumping
Ostomy Wound Management 2008;54(1):44–56
KEY POINTS
• The diagnosis and treatment of lymphedema in
•
patients who are morbidly obese requires careful
planning and consideration.
The authors describe and illustrate the physiology,
diagnosis, and treatment options of lymphedema
in this group of patients.
January 2008 Vol. 54 Issue 1
45
1/4/08
4:12 PM
Page 46
IC
A
TE
44-56_OWM0108_Fife-Carter.qxd
PL
Figure 4. A morbidly obese patient who has developed secondary lymphedema due to a combination of venous disease and
obesity. Note the hemosiderin deposits extending to the thighs,
an unusual finding.
U
Lymphedema
is
diagnosed as primary
or secondary on the
basis of etiology.14
Primary lymphedema
affects a small minority
of patients born with
defects in the lymphconducting pathways
(see Figure 5). The estimated incidence of primary lymphedema in
the US is one in 6,000
or
approximately
50,000 individuals.15
Secondary lymphedema results from extrinsic damage or obstruc- Figure 5. A 13-year-old girl with prition of the lymphatics. mary lymphedema, which caused
dramatic changes to the left foot.
The most common Primary lymphedema usually
examples of secondary affects the feet first and is usually
lymphedema include asymmetrical or unilateral.
filiariasis, a major
problem in some developing countries (geographically associated with the life cycle of its mosquito vector),
and arm lymphedema that results from trauma
induced by axillary dissection or radiation therapy
associated with breast cancer surgery.
Figure 3. A 48-year-old man with liver failure resulting in volume
overload and pitting bilateral leg edema.
D
O
N
O
T
D
domestic drainage systems, overflow can be caused
by obstruction in the movement of normal volumes
of fluid (mechanical insufficiency) or by excessive
volumes of fluid that exceed the system’s transport
capacity. Examples of the latter include congestive
heart failure, hepatic failure, and hypoproteinemia
due to chronic renal insufficiency or ascites (see
Figure 2).10 When overflow occurs, fluid accumulates in the superficial tissues, usually resulting in
bilateral leg swelling (see Figure 3). Increased capillary filtration results in low-viscosity, protein-poor
interstitial fluid (pitting edema); lymphatic dysfunction produces a protein-rich fluid, initiating a
cascade of inflammation that leads to dramatic
changes in the skin and subcutaneous tissue.12 An
additional consideration is venous insufficiency
(VI), characterized by hemosiderin staining due to
the deposition of iron oxide from extravasation of
red blood cells into the tissues from venous hypertension. Over time, the inflammation associated
with VI can lead to secondary lymphedema (see
Figure 4). Morbidly obese patients are commonly
observed to have both VI and lymphedema.13
46
OstomyWound Management
44-56_OWM0108_Fife-Carter.qxd
1/4/08
4:12 PM
Page 47
D
O
N
O
T
D
U
PL
IC
A
TE
on the history and physical examination and
can include a serum creatinine, albumin, electrolytes, thyroid panel, liver functions, or complete blood count. In patients whose physical
findings or history are suggestive of cardiac
disease, an echocardiogram should be obtained
to assess the cardiac ejection fraction before
initiating compression bandaging to ensure the
heart is able to tolerate the increased work load
of fluid mobilized from the legs.
Ironically, overuse of diuretics also can
worsen lymphedema.17,18 As the patient
becomes dehydrated, tissue osmolality increases, resulting in the extravascular movement of
fluid into the tissue compartment. Patients for
whom diuretics are prescribed to control
hypertension do not need to discontinue this
medication; however, patients who have been
prescribed diuretics solely for the purpose of
edema reduction almost universally report this
Figure 6a,b. “Stemmer’s Sign” is a diagnostic sign for lymphedema. A positive treatment is ineffective and will likely feel betStemmer’s sign is the inability to pinch a fold of skin at the base of the toes.
This 37-year-old woman has primary lymphedema. Her Stemmer’s is positive on ter after diuretics are discontinued once approthe left foot (b) but negative on the right (a). Note the creases from compres- priate compression measures are initiated.17,18
sion stockings on her left ankle and the loss of vascular markings, all indicative
Primary lymphedema should be suspected
of subtle lymphedema.
any time a patient presents with chronic unilateral extremity swelling — ie, edema that
does not improve with bedrest. A medical history also
Differential Diagnosis: Lymphedema
will provide a number of clues. For example, primary
and Lipedema
lymphedema is typically identified during one of three
Lymphedema. During the initial presentation,
timeframes: at birth (congenital), in later adolescence
lymphedema and lipedema may be confused because
(16 to 18 years of age; lymphedema praecox), or at
both present with the appearance of additional girth
about age 35 years (lymphedema tarda). If the patient
in the lower body. The best screening tool is a thorhas ipsilateral arm edema and a history of breast canough medical, social, and family history including the
cer treatment (surgery or radiation therapy), secondclinical course of edema onset in relation to medicaary lymphedema is likely the cause.19,20
tions and/or other medical problems. Because many
morbidly obese patients have low exercise tolerance
Features. Skin inflammation, a basic feature of
and many are not able to lay supine for non-cardiac
lymphedema, can cause chronic pain, functional
reasons, differentiating cardiac disease from non-carimpairment, and recurrent cellulitis. The diagnosis of
diac factors can be challenging. Physical examination
lymphedema in the lower extremities starts with the
should include determining edema sites (eg,
appearance of “Stemmer’s Sign” — the inability to
abdomen, hands and face), the presence of ascites or
pinch a fold of skin at the base of the toes (see Figure
jaundice, and features of myxedema (eg, hair loss, pale
6a,b).10 The dorsum of the foot also can appear
mucus membranes, or heart murmur). Paradoxically,
squared-off. Dermal changes that follow include dry
morbidly obese individuals can be malnourished and
or flaky skin, hyperkeratosis, skin creases, fibromas,
more prone to unhealthy forms of dieting than normal
lymphangiomas, and papillomas (see Figures 7 to 10);
weight individuals.16 Laboratory testing should be based
these will be evident on physical examination when
January 2008 Vol. 54 Issue 1
47
1/4/08
4:12 PM
Page 48
Confirmation of lymphedema is best obtained
through MRI, which is considered superior to CT,12 or
through lymphoscinctigraphy. Differentiating chronic
VI from lymphedema via lymphoscinctigraphy is not
always possible in the early stages because the former
can cause the latter and will show unusually delayed
lymph drainage;22,23 hence, quantitative lymphoscinctigraphy, which involves measurement of
radiotracer accumulation in regional lymph nodes, is
a viable option.24
Lipedema. Lipedema, a syndrome often mistaken
for lymphedema,25 is a genetically mediated disease
that involves the pathological accumulation of fat on
the lower body. It is most commonly seen in women.
One of the most definitive features is that the feet initially are spared — leg enlargement affects the ankle
and lower leg in a “pantaloon” distribution (see Figure
11); whereas, in (primary) lymphedema, the feet are
commonly the first area affected (ie, the “Stemmer’s
Sign”). Furthermore, in lipedema, both legs are symmetrically affected. In later life, fatty depositions can
occlude the lymphatic system, which can lead to secondary lymphedema; this “lipolymphedema” is apparent in Figure 7. In later life, morbidly obese patients
who may have had only lipedema can develop secondary lymphedema and other complications such as
recurrent cellulitis (which further worsens lymphatic
obstruction) or heart failure with volume overload
(due to sleep apnea from obesity). Late in life, when
many sequelae of obesity have presented, determining
whether edema problems began with primary or secondary lymphatic malfunction is almost impossible
(see Figure 7).
The typical appearance of various edema syndromes (primary lymphedema, secondary lipolymphedema, venous insufficiency, and edema due to
heart or renal failure — see Table 1) — are illustrated
in Figures 3, 4, 5, 7, and 11. Common causes of chronic, bilateral edema include heart failure, renal insufficiency, hypoalbuminemia (which can be due to a protein-losing enteropathy, malabsorption, or malnutrition), myxedema, abdominal tumors, liver failure, or
various drugs.12
Although a person with primary lymphedema also
may be obese, lymphedema in most morbidly obese
patients is due to the obesity. Whether lymphedema
PL
IC
A
TE
44-56_OWM0108_Fife-Carter.qxd
N
O
T
D
U
Figure 7. Lipolymphedema. Note the pantaloon distribution of
fat near the ankle and the relative sparing of the feet, which indicate that primary lymphedema was probably not the original
problem. However, on the left leg, the patient has fibromas and
massive distortion after recurrent bouts of cellulitis, consistent
with secondary lymphedema.
O
Figure 8. A 65-year-old woman with morbid obesity, cellulitis, lymphedema, sleep apnea, and congestive heart failure. She might
have originally have had lipedema or primary lymphedema.
D
lymphedema is more advanced. Extreme lymphedema manifests as elephantiasis. The International
Society of Lymphology 21 has determined three
stages of lymphedema: Stage I represents a
reversible condition (mild, pitting edema), Stage II
introduces fibrotic conditions (pitting often stops),
and Stage III involves elephantiasis.
48
OstomyWound Management
1/4/08
4:12 PM
Page 49
A
TE
44-56_OWM0108_Fife-Carter.qxd
IC
Figure 10. A 54-year-old man weighing 620 lb; estimated pannus
weight = 300 lb. Note the hemosiderin and “cobblestone” changes
due to inflammation on the dependent aspect of the abdomen. The
pannus drags on the ground during his brief periods of ambulation.
PL
Figure 9. A morbidly obese (530-lb) 19-year-old man with massive localized lymphedema (MLL). When surgically removed, the
collection of fat and dilated lymphatics weighed more than 50 lb.
N
O
T
D
U
results from chronic VI (secondary lymphedema), a
form of lipolymphedema, other obesity complications
such as congestive heart failure (CHF), immobility,
the loss of the calf muscle pump, associated sleep
apnea, obstruction from overhanging pannus, or all of
these factors, the fact is that obesity-related lymphedema is a direct result of the obesity and cannot be
addressed separately. Equally as important, the clinician must ensure that neither the lymphedema nor the
weight problems are due to undiagnosed conditions
such as thyroid disease.26
Unique Obesity-Related Problems
D
O
Massive localized lymphedema (MLL) is an
extreme example of the subcutaneous fat deposits
pathognomonic of lymphedema. Although the literature27 describes MLL as “rare,” it is a common occurrence among morbidly obese individuals with lymphedema in the authors’ clinic. Massive localized lymphedema is characterized by a benign overgrowth of
lymphoproliferative tissue, composed of fibrotic and
edematous fibroadipose tissue.27 Due to its large size
and similarity to sarcoma, this tissue mass often is
termed a pseudosarcoma.28 These massive overgrowths
commonly involve the thigh, popliteal fossa, scrotum,
suprapubic and inguinal regions, and abdomen (see
Figures 8, 9, 12). Histologically, the overgrowths
exhibit vascular ectasia, mononuclear cell infiltrates,
Figure 11. Lipedema in a morbidly obese patient. Note the symmetrical distribution of fatty deposits, the “pantaloon” distribution of fat above the ankles, and the relative sparing of the feet.
fibrosis, edema between collagen fibers, and ischemic
changes, such as infarction and fat necrosis.26 In the
authors’ experience, patients with this condition seek
treatment when the size of the tissue mass starts to
interfere with their daily activities or when excoriation
or skin breakdown occurs.
Skin changes are inevitable with lymphedematous
conditions because macrophages acquire adipose tissue,
January 2008 Vol. 54 Issue 1
49
44-56_OWM0108_Fife-Carter.qxd
1/4/08
4:12 PM
Page 50
Primary Lymphedema
Lipolymphedema
Unilateral or bilateral Asymmetrical (unilateral,† Usually bilateral
or one leg affected
more than the other)
Venous Insufficiency
Chronic Heart
Failure/Renal Failure
Usually bilateral (might Bilateral†
be worse on one side)
A
Attribute
TE
TABLE 1
COMPARISON OF THE CHARACTERISTICS OF CHRONIC LOWER-EXTREMITY SWELLING
CAUSED BY PRIMARY LYMPHEDEMA AND LIPOLYMPHEDEMA WITH MORBID OBESITY
Aching can be present† Aching can be present
from skin stretching
None in the early stages† Aching dysesthesia
Onset and course
Usually presents by the
age of 35;*† unrelieved
by elevation†
Presents in adulthood;
initially improves with
elevation until fibrosis
occurs
Area affected
Feet typically affected
first (Stemmer’s Sign)*;
can include genitalia;
massive localized lymphedema (MLL) does
not occur
When severe goes from
Feet spared initially;
Affects ankles and
feet to groin, including
“pantaloon distribucalves; feet spared
tion of fat; usually
unless secondary lym- abdomen
only knee to ankle;
phedema develops
MLL can occur in morbidly obese
Skin changes
Inflammation always
present
Inflammation present
IC
Pain
D
U
PL
Presents in adulthood†; Presents in association
improves with elevation with other organ diseases; improves with
elevation
Hemosiderin deposits
on legs/ankles†; visible varicosities often
present
Pitting almost always
present†
T
Adapted from: *Williams10; † Ely JW, Osheroff JA, Chambliss ML, Ebell MH12
O
N
O
causing permanent deposits of subcutaneous fat.
Although usually seen on the lower extremities, skin
changes also can occur in an overhanging abdominal
pannus, giving rise to abdominal lymphedema (see
Figures 9 and 10) and sometimes chronic, draining
abdominal wounds. In such dramatic cases, surgery to
remove the entire pannus or MLL is necessary.
However, persistent edema and patient issues limit
surgical success.
D
Initial Treatment of Lymphedema
An aggressive and coordinated regimen (commonly called complete decongestive therapy
[CDT)]29) of manual lymph drainage (MLD), compression bandaging, and skin care is required to
reduce the volume of the affected extremities to a
near normal level. This is an internationally recognized
50
OstomyWound Management
standard of care for lymphedema treatment18 that is
also successful for lymphedema arising from breast
cancer treatment.30
Rather than long stretch bandages (eg, Ace wraps
or cohesive bandages), CDT utilizes washable,
reusable cotton bandages that provide little elasticity when maximum tension is applied. This feature
permits the bandage to act as a resistive shell against
which muscles can contract, giving rise to the high
working but low resting pressure concept.31 Layers
of foam and viscose-cotton or polyester padding are
applied to protect bony protuberances and skin under
the bandages.32 Wrapped in a distal to proximal gradient33 and worn continually in the initial stages, compression bandaging for lymphedema often extends
from the toes to the groin in the lower extremities and
from the fingers to the axillae for arm bandages.34 Such
44-56_OWM0108_Fife-Carter.qxd
1/4/08
4:12 PM
Page 51
Lymphedema and Wound Healing
PL
IC
A
TE
In general, wounds are managed by controlling
bioburden, debriding nonviable tissue, and managing
drainage. Similar to VI,35 wounds usually are not likely to heal if the edema is not controlled but controlling
edema is challenging. Serious regional oxygen deficiency followed by reperfusion periods can occur in
lymphedematous tissue36 as well as in ulcerated edematous limbs37 but it is not clear whether the reduced
oxygen levels are entirely responsible for the compromised wound healing in this situation or to what
extent the amount of edema present influences the
course of events.
Integrating compression into wound management
requires careful planning. Dressings must be chosen
according to their performance under sustained compression (ie, preventing rubbing, irritation, or leaving
marks on the skin) and whether they have sufficient
absorptive properties, odor control, and other practical attributes, including cost.
Figure 12. A customized Legassist (Compression Design, Zeeland,
Mich) for a patient with a large MLL.
D
O
N
O
T
D
U
wrapping is far more
extensive than the compression bandaging used in
venous disease.
Although compression
garments constitute the
mainstay
lymphedema
treatment, most obese
patients with lymphedema
are not able to wear garments due to limb distortion
and abdominal girth that
prohibits use of such garments. However, semirigid
™
Figure 13. An example of a devices, such as the Circaid
knee-high Farrow wrap (CircAid Medical Products
(Farrow Medical Innovations, Inc, San Diego, Calif),
Bryan, Tex). These semi-cusArmassist or Legassist™
tom devices can be manufacDesign,
tured with straps measured (Compression
to fit the limb circumference. Zeeland, Mich), or Farrow
wrap (Farrow Medical
Innovations, Bryan, Tex) can be useful in the morbidly
obese (see Figures 12 and 13). Medicare does not cover
garments for patients who do not have wounds so any
type of garment or device for lymphedema management
is non-reimbursable for Medicare beneficiaries. Other
payors have covered this important equipment if clinicians write letters of medical necessity.
Skin Care and Wound Prevention
Skin care and prevention of even minor tissue trauma must be emphasized. The National Lymphedema
Network38 recommends several practices to reduce the
risk of infection and skin breakdown. First, the skin
must be kept clean, dry, and moisturized to prevent
chaffing. Low-pH moisturizers can be used to reduce
microbial growth.39 Next, protective clothing such as
gloves should be worn while engaging in activities that
might cause skin injury; likewise, insect repellent to
prevent insect bites and sunscreen to prevent sunburn
are prudent precautions. Razors should be used carefully to prevent nicks and cuts to the skin and injections or blood tests should be minimized to reduce the
number of occasions for opportunistic infection.
Finally, if a cut or skin puncture occurs, the wound
should be carefully cleansed and antibiotic cream
applied. Patients also are advised to contact their primary care healthcare provider if obvious signs of
infection (eg, rashes, itching, redness, increased skin
temperature, or fever) occur.
For patients with more advanced lymphedema who
exhibit fissured, keratinified skin, lactic acid products
can be helpful in addressing desquamation and
Olivamine™-containing formulations (eg, Remedy
January 2008 Vol. 54 Issue 1
51
1/4/08
4:12 PM
Page 52
providing them with increased social opportunities,
these devices can worsen their condition by making
ambulation unnecessary.
Transfer. Patients with morbid obesity also have
serious transfer problems.43 A treatment table
obtained by the authors was certified to sustain high
weight but required three therapists to counterbalance
large patients ascending the table in order to prevent it
from tipping over. Thus, selecting equipment only on
the basis of weight-bearing capability can be inadequate when attempting to provide a safe environment
for patients (see Figure 14).
Position. Morbidly obese patients may be unable to
lay supine. Sometimes, this may be due to CHF but
more commonly relative to obstructive apnea, severely limiting the benefits of MLD. Some patients can be
so short of breath due to cardiac or respiratory factors
that MLD therapy is not safe.
Compression application. The physical challenges
of applying compression bandages to large patients
are well known to therapists. Often, two or three awkwardly positioned therapists are required to accommodate the mobility limitations of obese patients (see
Figure 15) and the required additional bandaging
materials and more staff time cannot be recouped by
increasing billed charges. Even if compression bandaging can be applied, the application process might well
be futile, because the lack of movement does not provide the necessary “muscle-pump” activity for certain
bandages to work properly.44
Equipment. Ten years ago, no patients >500 lb
came to the authors’ clinic for treatment. Now, seeing
500- or 600-lb patients is not uncommon. Waiting
room furniture at the authors’ clinic is now wider and
sturdier and chairs without armrests have been added.
In addition, special scales that can weigh patients up to
800 lb and are wide enough to allow patients to stabilize themselves on the scale were purchased.
Patients who do not have their own transport
devices usually cannot be safely accommodated in
wheelchairs that are pushed manually. After the wheels
on an extra-wide manual chair collapsed while in use
by a large patient and subsequent to a petite transportation technician losing control of a heavy patient
on a descending ramp, the authors’ clinic purchased
an electronic, extra-wide wheelchair that is rated to
U
PL
IC
A
TE
44-56_OWM0108_Fife-Carter.qxd
D
Figure 14. Two therapists kneel on a treatment table to counterbalance a 650-lb patient. The treatment table is capable of sustaining a weight up to 750 lb but will tip over if the weight is not
evenly distributed.
O
N
O
T
Skin Care, Medline Industries, Inc., Mundelein, Ill)
can help reduce superficial inflammation.
Obesity is implicated in a wide spectrum of dermatological diseases, including acanthosis nigricans,
acrochordons, keratosis pilaris, striae distensae, adiposis dolorosa, plantar hyperkeratosis, skin tags, and
candidal intertrigo.40,41 Therefore, morbidly obese
patients who also have lymphedema are at risk for
additional skin disorders. The authors have found that
a new product, Interdry Ag+ (Coloplast, Minneapolis,
Minn), a fabric that wicks away moisture and reduces
bioburden, may be useful in patients with multiple,
redundant skin folds.
D
Lymphedema Therapy and Equipment
Challenges
Exercise. Exercise is a lynchpin of edema treatment42 but because morbidly obese patients have
ambulation problems, their ability to exercise is
limited. Moreover, such patients frequently become
dependent on electronic transport devices. While
52
OstomyWound Management
44-56_OWM0108_Fife-Carter.qxd
1/4/08
4:12 PM
Page 53
IC
A
TE
1. Absence of diseases that affect the safety of
MLD therapy (eg, uncontrolled congestive
heart failure)
2. Must be able to safely and with minimal assistance transfer on and off the MLD table
3. Patient weight cannot exceed MLD table
weight limit
4. Must be ambulatory, even if minimally
5. Must not have a BMI >70 (eg, 5'2" woman
weighing 380 lb)
6. Must commit to maintaining a constant
weight, or preferably losing weight, during the
course of treatment.
Weight Control
PL
Bariatric surgery has been shown to have many
beneficial and even life-saving results among the morbidly obese. Long-term follow-up studies45-51 of
bariatric surgery involving morbidly obese patients
have started to appear in the literature and the results
are illuminating. The procedures require that patients
follow a detailed set of guidelines in order for weight
loss to be successful; postoperative complications can
occur.46,47 Increasingly, bariatric surgery programs
include counseling48-50 in order to moderate the potentially unrealistic expectations and anxiety found to be
associated with the significant issue of non-adherence
to guidelines.51
What is most interesting is that adherence to follow-up in a series of cognitive behavioral therapy programs designed to treat obesity was found to be
inversely proportional to the severity of the obesity.52
These results mirror the authors’ experience. The psychosocial factors that interact to produce a morbidly
obese individual are complex and poorly understood
but clearly affect participation in, and benefits derived
from, lymphedema treatment. In the authors’ experience, patients who gain weight respond poorly to
edema treatment; conversely, patients who maintain
or lose weight achieve benefit. Although they should
occur concurrently, specific counseling programs are
not offered at the authors’ facility; instead, patients
“contract” for continued care by exhibiting positive
behaviors regarding weight loss, attendance at
bariatric support groups, Weight Watchers®, or other
beneficial practices. Morbidly obese patients who
Figure 15. Two therapists bandage the left thigh of a morbidly
obese patient with lymphedema.
O
N
O
T
D
U
750 lb and operated by a toggle switch in the back.
This chair cost in excess of $10,000 in 1998; at the
time, the purchase was controversial. Administrators
questioned the need to allocate a substantial percentage of the equipment budget for a “transportation
device.” Now in its tenth year of use, the chair is in
constant demand by departments all over the hospital.
Extra-wide potty chairs, bariatric hospital beds, lifting chairs, and other equipment that might be needed
for obese patients represent an increasing proportion
of hospital budgets across the country. These costs are
usually not borne by third-party payors. Nevertheless,
patients expect facilities to be prepared to meet their
needs. A patient comment from one of the authors’
clinic feedback cards sums up the problem: “Don’t you
know that the number of overweight people is on the
rise and the need is here now to help us?”
D
Memorial Hermann Guidelines
Participation in the MLD Program
for
Many obese patients can participate and benefit
from lymphedema therapy. However, the authors
found the need to establish consistent criteria to
ensure consistency and patient and staff safety. The
program criteria for MLD therapy include these
patient requirements:
January 2008 Vol. 54 Issue 1
53
44-56_OWM0108_Fife-Carter.qxd
1/4/08
4:12 PM
Page 54
References
1. Finkelstein EA, Fiebelkorn IC, Wang G. State-level
estimates of annual medical expenditures attributable to obesity. Obesity Res. 2004;12(1):18–24.
2. Flegal KM, Carroll MD, Ogden CI, Johnson CL.
Prevalence and trends in obesity among US adults,
1999–2000. JAMA. 2002;288(14):1723–1727.
3. Arterburn DE, Maciejewski ML, Tsevat J. Impact of
morbid obesity on medical expenditures in adults.
Int J Obes (Lond). 2005;29(31):334–339.
4. Fontaine KR, Redden DT, Wang C, Westfall AO,
Allison DB. Years of life lost due to obesity. JAMA.
2003;289(2):187–193.
5. Solga SF, Clark JM, Alkhuraishi AR, et al. Race and
comorbid factors predict nonalcoholic fatty liver disease histopathology in severely obese patients. Surg
Obes Relat Dis. 2005;1(1):6–11.
6. Sugerman H, Windsor A, Bessos M, Wolfe L. Intraabdominal pressure, sagittal abdominal diameter
and
obesity
comorbidity. J
Int
Med.
1997;241(1):71–79.
7. Scott SK, Rabito FA, Price PD, et al. Comorbidity
among the morbidly obese: a comparative study of
2002 U.S. hospital patient discharges. Surg Obes Relat
Dis. 2006;2(2):105–111.
8. Moffatt CJ, Franks PJ, Doherty DC, et al.
Lymphoedema: an underestimated health problem.
Q J Med. 2003;96(10):731–738.
9. Levick JR. Changing perspectives on microvascular
fluid exchange. In: Jordan D, Marshall J (eds).
Cardiovascular Regulation. London, UK: Portland
Press; 1999:127–152.
10. Williams A. An overview of non-cancer related
chronic oedema—a UK perspective. Worldwide
Wounds 2003. Available at: www.worldwidewounds.com/2003/apr il/Williams/ChronicOedema.html. Accessed December 7, 2006.
11. Levick JR. Capillary filtration-absorption balance
reconsidered in light of dynamic extravascular factors. Exp Physiol. 1991;76(6):825–857.
12. Ely JW, Osheroff JA, Chambliss ML, Ebell MH.
Approach to leg edema of unclear etiology. J Am
B
N
O
T
D
U
PL
IC
A
A
TE
is a life-or-death decision but patients often focus
more on the treatment of an obesity symptom — ie,
edema — than the underlying problem that will
shorten their life.3 Treatment of lymphedema must be
linked to the treatment of obesity if long-term success
is to be achieved. When the clinician and patient
develop a collaborative approach to care, lymphedema
in morbidly obese patients can be managed with good
results (see Figure 16 a,b). - OWM
Figure 16a and 16b. a) Before complete congestive therapy
(CDT) in a morbidly obese woman. Note draining sores on her
legs; b) after a program of CDT, including exercise, manual lymph
drainage, and bandaging.
O
ignore the condition that predisposed them toward
lymphedema are unlikely to have a good prognosis
with lymphedema treatment.
D
Conclusions
Based on clinician observation and experience,
management of the morbidly obese patient with lymphedema requires that the obesity be addressed in a
frank and supportive way. Many morbidly obese
patients exhibit a strong element of denial regarding
the disease of obesity. Obtaining treatment for obesity
54
OstomyWound Management
Page 55
22. Tiwari A, Cheng KS, Button M, Myint F, Hamilton
G. Differential diagnosis, investigation, and current
treatment of lower limb lymphedema. Arch Surg.
2003;138(2):152–161.
23. Bull RH, Gane JN, Evans JE, Joseph AE, Mortimer
PS. Abnormal lymph drainage in patients with
chronic venous leg ulcers. J Am Acad Dermatol.
1993;28(4):585–590.
24. Szuba A, Shin WS, Strauss HW, Rockson S. The third
circulation: radionuclide lymphoscintigraphy in the
evaluation of lymphedema. J Nucl Med.
2003;44(1):43–57.
25. Rudkin GH, Miller TA. Lipedema: a clinical entity
distinct from lymphedema. Plast Reconstr Surg.
1994:94(6):841–847; discussion, 848–849.
26. Wu D, Gibbs J, Corral D, Intengan M, Brooks JJ.
Massive localized lymphedema: additional locations
and association with hypothyroidism. Hum Pathol.
2000;31(9):1162–1168.
27. Goshtasby P, Dawson J, Agarwal N. Pseudosarcoma:
massive localized lymphedema of the morbidly
obese. Obes Surg. 2006;16(1):88–93.
28. Farshid G, Weiss S. Massive localized lymphedema in
the morbidly obese: a histologically distinct reactive
lesion simulating liposarcoma. Am J Surg Pathol.
1998;22(10):1277–1283.
29. Foldi E. The treatment of lymphedema. Cancer.
1998;83(12 suppl American):2833–2835.
30. Ramos SM, O’Donnell LS, Knight G. Edema volume,
not timing, is the key to success in lymphedema
D
O
N
O
T
D
U
PL
Board Fam Med. 2006;19(2):148–160.
13. Alexander JW, Rowan L, Cafiero M, et al. Roundtable
discussion: does skin care for the obese patient
require a different approach? Bariatr Nurs Surg
Patient Care. 2006;1:157–165.
14. Mortimer PS. ABC of arterial and venous disease.
Swollen lower limb—2: lymphoedema. BMJ.
2000;320(7248):1527–1529.
15. Swirsky J, Sakett Nannery D. Coping with
Lymphedema. Garden City Park, NY: Avery
Publishing Group;1998:12.
16. Charlesbois D, Wilmoth D. Critical care of patients
with obesity. Crit Care Nurse. 2004;24(4):19–27.
17. Mortimer PS. Therapy approaches for lymphedema.
Angiology. 1997;48(1):87–91.
18. National Lymphedema Network. Position statement
of the National Lymphedema Network. Topic: treatment.
Available
at:
www.lymphnet.org/pdfDocs/nlntreatment.pdf.
Accessed September 2, 2006.
19. Deo SVS, Ray S, Rath GK, et al. Prevalence and risk
factors for development of lymphedema following
breast cancer treatment. Indian J Cancer.
2004;41(1):8–12.
20. Erickson VS, Pearson ML, Ganz PA, Adams J, Kahn
KL. Arm edema in breast cancer patients. J Natl
Cancer Inst. 2001;93(2):96–111.
21. International Society of Lymphology. The diagnosis
and treatment of peripheral lymphedema. Lymphol.
2003;36(2):84–91.
TE
4:12 PM
A
1/4/08
IC
44-56_OWM0108_Fife-Carter.qxd
January 2008 Vol. 54 Issue 1
55
Page 56
41. Hahler B. An overview of dermatological conditions
commonly associated with the obese patient. Ostomy
Wound Manage. 2006;52(6):34–40.
42. Ko DS, Lerner R, Klose G, Cosimi AB. Effective treatment of lymphedema of the extremities. Arch Surg.
1998;133(4):452–458.
43. Grant P, Newcombe M. Emergency management of
the morbidly obese. Emerg Med Australas.
2004;16(4):309–317.
44. Clarke-Moloney M, Godfrey A, O’Connor V, et al.
Mobility in patients with venous leg ulceration. Eur J
Vasc Endovasc Surg. 2007;33(4):488–493.
45. Livingston EH. Obesity, mortality, and bariatric surgery death rates. JAMA. 2007;298(20):2406–2408.
46. Suter M, Calmes JM, Paroz A, Giusti V. A 10-year
experience with laparoscopic gastric banding for
morbid obesity: high long-term complication and
failure rates. Obes Surg. 2006;16(7):829–835.
47. Elkins G, Whitfield P, Marcus J, Symmonds R,
Rodriguez J, Cook T. Noncompliance with behavioral recommendations following bariatric surgery.
Obes Surg. 2005;15(4):546–551.
48. Clark MM, Balsiger BM, Sletten CD, et al.
Psychosocial factors and 2-year outcome following
bariatric surgery for weight loss. Obes Surg.
2003;13(5):739–745.
49. Buddeberg-Fischer B, Klaghofer R, Sigrist S,
Buddeberg C. Impact of psychosocial stress and
symptoms on indication for bariatric surgery and
outcome in morbidly obese patients. Obes Surg.
2004;14(3):361–369.
50. Wolf AM, Kortner B, Kuhlmann HW. Results of
bariatric surgery. Int J Obes Relat Metab Disord.
2001;25(suppl 1):S113–S114.
51. Poole NA, Al Atar A, Kuhanendran D, et al.
Compliance with surgical after-care following
bariatric surgery for morbid obesity: a retrospective
study. Obes Surg. 2005;15(2):261–265.
52. Melchionda N, Besteghi L, Di Domizio S, et al.
Cognitive behavioural therapy for obesity: one-year
follow-up in a clinical setting. Eat Weight Disord.
2003;8(3):188–193.
D
O
N
O
T
D
U
PL
treatment. Am J Surg. 1999;178(4):311–315.
31. Leduc O, Peeters A, Bourgeois P. Bandages: scintigraphic demonstration of its efficacy on colloidal
protein reabsorption during muscular activity. In:
Nishi M, Uchino S, Yabuki S, (eds). Progress in
Lymphology XII. Exerpta Medica, International
Congress series 887. Amsterdam, The Netherlands:
Elsevier;1990(12):421–423.
32. Williams AF, Keller M. Practical guidance on lymphoedema bandaging of the upper and lower limbs.
In: Calne S, Moffatt C, Mortimer P, et al. Euro Wound
Manage Assoc Focus Document: Lymphoedema
Bandaging in Practice. London, UK: MEP
Ltd;2005;10–14.
33. Lawrence D, Kakkar VV. Graduated, static, external
compression of the lower limb. Br J Surg.
1980;67(2):119–121.
34. Casley-Smith JR, Boris M, Weindorf S, Lasinski B.
Treatment for lymphedema of the arm—the CasleySmith method. Cancer. 1998;83(12 suppl
American):2843–2860.
35. Treiman GS, Copland S, McNamara RM, et al.
Factors influencing ulcer healing in patients with
combined arterial and venous insufficiency. J Vasc
Surg. 2001;33(6):1158–1164.
36. Siems WG, Brenek R, Beier A, Grune T. Oxidative
stress in chronic lymphedema. Q J Med.
2002;95(12):803–809.
37. Nemeth AJ, Falanga V, Alstadt SP, Eaglstein WH.
Ulcerated edematous limbs: effect of edema removal
on transcutaneous oxygen measurements. J Am Acad
Dermatol. 1989;20(2 Pt 1):191–197.
38. National Lymphedema Network. 18 steps to prevention revised. Lymphedema risk-reduction practices.
Available
at:
www.lymphnet.org/lymphedemaFAQs/riskReductio
n/riskReduction.htm. Accessed July 16, 2007.
39. Vaillant L. Infectious complications of lymphedema.
Rev Med Interne. 2002;23(suppl 3):403–407.
40. Yosipovitch G, DeVore A, Dawn A. Obesity and the
skin: skin physiology and skin manifestations of obesity. J Am Acad Dermatol. 2007;56:901–916.
TE
4:12 PM
A
1/4/08
IC
44-56_OWM0108_Fife-Carter.qxd
56
OstomyWound Management