Erysipelas
Article Last Updated: Feb 11,
2008
AUTHOR
AND EDITOR INFORMATIONS
Authors and Editors Introduction Clinical
Differentials Workup Treatment Medication Follow-up
Multimedia
References
Author:
Loretta Davis, MD, Professor, Department of Internal Medicine, Division of
Dermatology, Medical
College of Georgia
Loretta Davis is a
member of the following medical societies: American Academy of
Dermatology
Coauthor(s): John A Cole, BS, Medical College of Georgia;
Keith Benbenisty, MD, Consulting Staff, Associates in
Dermatology,
MDs, PA
Editors: Robert A Schwartz, MD, MPH, Professor and Head of
Dermatology, Professor of Medicine, Professor of
Pediatrics,
Professor of Pathology, Professor of Preventive Medicine and Community Health,
UMDNJ-New
Jersey Medical School; Michael J Wells, MD, Associate
Professor, Department of Dermatology, Texas Tech
University Health
Sciences Center; Christen M Mowad, MD, Assistant Professor, Department of
Dermatology,
Geisinger Medical Center; Glen H Crawford, MD,
Assistant Clinical Professor, Department of Dermatology,
University
of Pennsylvania School of Medicine; Chief, Division of Dermatology, The
Pennsylvania Hospital; Dirk
M Elston, MD, Director, Department of
Dermatology, Geisinger Medical Center
Author and
Editor Disclosure
Synonyms and related keywords: non-necrotizing
dermohypodermitis, acute bacterial dermohypodermitis
INTRODUCTION
Authors and Editors Introduction Clinical Differentials Workup Treatment
Medication
Follow-up Multimedia
References
Background
Erysipelas is a superficial bacterial skin
infection that characteristically extends into the cutaneous lymphatics.
This disease has been traced back to the Middle Ages where it was
referred to as "St Anthony's Fire,"
named after an Egyptian healer
who was known for successfully treating the infection. Historically, this
infection occurred on the face and was caused by Streptococcus
pyogenes. However, a shift in the
distribution and etiology of the
disease has occurred, with most erysipelas infections now occurring on the
legs and with non–group A streptococci sometimes being identified as
the etiologic agents.
Pathophysiology
Bacterial inoculation into an
area of skin trauma is the initial event in developing erysipelas. Thus, local
factors, such as venous insufficiency, stasis ulcerations,
inflammatory dermatoses, dermatophyte infections,
insect bites, and
surgical incisions, have been implicated as portals of entry. The source of the
bacteria in
facial erysipelas is often the host's nasopharynx, and
a history of recent streptococcal pharyngitis has been
reported in
up to one third of cases. Other predisposing factors include diabetes, alcohol
abuse,1 HIV
infection, nephrotic syndrome, other immunocompromising
conditions, and vagrant lifestyle.
The infection rapidly invades and
spreads through the lymphatic vessels. This can produce overlying skin
"streaking" and regional lymph node swelling and tenderness. Immunity
does not develop to the inciting
organism.
Frequency
United States
Isolated cases are
the rule with erysipelas, although epidemics have been reported. The incidence
of
erysipelas declined throughout the mid-20th century, possibly
due to antibiotic development, improved
sanitation, and decreased
virulence. The change in distribution from the face to the lower extremities is
most
likely related to an aging population with risk factors such
as lymphedema. Approximately 85% of cases
occur on the legs rather
than the face.
International
Erysipelas is somewhat more common in
European countries. Isolated cases are still the rule, and
distribution and etiology remain similar to that in the United
States.
Mortality/Morbidity
The most common complaints during the
acute infection include tenderness of the involved area, fever, chills,
and swelling. Death as a direct result of erysipelas is exceedingly
rare. Predisposed patients often develop
local recurrence, and this
can lead to disfiguring and disabling healing reactions, such as elephantiasis
nostras
verrucosa. This chronic warty, edematous condition is caused
by lymphatic destruction from repeated
infection.
Race
Erysipelas infections affect all
races.
Sex
Erysipelas has been reported to be more common in females,
but occurring at an earlier age in males
because of their more
aggressive activities. Other studies indicate that predisposing factors, rather
than
gender, account for any male/female differences in
incidence.
Age
Cases of erysipelas have been reported in all age
groups, but it does appear that infants, young children, and
elderly patients are the most commonly affected groups. The peak
incidence has been reported to be in
patients aged 60-80 years,
especially in patients who are considered high-risk and immunocompromised or
those with lymphatic drainage problems (eg, after mastectomy,
pelvic surgery, bypass grafting).
CLINICALSection 3 of 10
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History
Patients often cannot recall an inciting
event, but there may be a history of recent trauma or pharyngitis.
Prodromal symptoms, such as malaise, chills, and high fever, often
begin before the onset of the skin lesions
and usually are present
within 48 hours of cutaneous involvement. Pruritus, burning, and tenderness are
typical complaints.
Physical
Erysipelas begins as a small
erythematous patch that progresses to a fiery-red, indurated, tense, and shiny
plaque. The lesion classically exhibits raised sharply demarcated
advancing margins. Local signs of
inflammation, such as warmth,
edema, and tenderness, are universal. Lymphatic involvement often is
manifested by overlying skin streaking and regional lymphadenopathy.
More severe infections may exhibit
numerous vesicles and bullae
along with petechiae and even frank necrosis. With treatment, the lesion often
desquamates and can resolve with pigmentary changes that may or may
not resolve over time.
Causes
Streptococci are the primary cause of
erysipelas. Most facial infections are attributed to group A
streptococci, with an increasing percentage of lower extremity
infections being caused by non–group A
streptococci.
Streptococcal toxins are thought to contribute to the brisk inflammation that
is pathognomonic
of this infection. No clear proof has emerged that
other bacteria cause typical erysipelas, although they
clearly
coexist with streptococci at sites of inoculation. Recently, atypical forms
reportedly have been caused
by Streptococcus pneumoniae, Klebsiella
pneumoniae, Haemophilus influenzae, Yersinia enterocolitica, and
Moraxella species, and they should be considered in cases refractory to
standard antibiotic therapy.
The role of Staphylococcus aureus, and
specifically methicillin-resistant S aureus, remains controversial. No
conclusive evidence demonstrates a pathogenic role for staphylococci in
typical erysipelas. The infection's
predictable response to
penicillin, even when S aureus is present, argues against S aureus as an
etiologic
agent. However, analogous to what occurs in bullous
impetigo or staphylococcal scalded skin syndrome,
exotoxins from
coexisting S aureus may account for the clinical presentation of bullous
erysipelas.2
DIFFERENTIALSSection 4 of 10 Authors and Editors
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Erythema Annulare
Centrifugum
Other Problems to be Considered
Erysipelas can be
differentiated from cellulitis by its characteristically raised advancing edges
and sharply
demarcated borders, reflecting its more superficial
nature. Cellulitis has no lymphatic component and exhibits
indiscreet margins.
WORKUPSection 5 of 10 Authors
and Editors Introduction Clinical Differentials Workup Treatment
Medication Follow-up Multimedia References
Lab
Studies
In classic erysipelas, no laboratory workup is required for
diagnosis or treatment.
Routine blood and tissue cultures are not
cost-effective because they have an extremely low yield and results
have a minimal impact on management. Cultures are perhaps best reserved
for very immunosuppressed
hosts in whom an atypical etiologic agent
might be more likely.3
Bacterial cultures from the portal of entry may be
most helpful in persons with atypical clinical presentations.
Imaging
Studies
Imaging studies are not usually indicated and are of low yield.
MRI and bone scintigraphy are helpful when
early osteoarticular
involvement is suspected. In this setting, standard radiographs are typically
normal.
Histologic Findings
The histologic hallmarks of erysipelas
are marked dermal edema, vascular dilatation, and streptococcal
invasion of lymphatics and tissues. This bacterial invasion results in
a dermal inflammatory infiltrate consisting
of neutrophils and
mononuclear cells. The epidermis is often secondarily involved. Rarely,
bacterial invasion
of local blood vessels may be
seen.
TREATMENTSection 6 of 10 Authors and Editors
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Medication
Follow-up Multimedia References
Medical Care
Elevation and
rest of the affected limb are recommended to reduce local swelling,
inflammation, and pain.
Saline wet dressings should be applied to ulcerated
and necrotic lesions and changed every 2-12 hours,
depending on the
severity of the infection.
Streptococci cause most cases of erysipelas;
thus, penicillin has remained first-line therapy.4 Penicillin
administered orally or intramuscularly is sufficient for most cases of
classic erysipelas and should be given for
10-20 days.
A
cephalosporin or macrolide, such as erythromycin or azithromycin, may be used
if the patient has an
allergy to penicillin. Cephalosporins may
cross-react with penicillin first-generation cephalosporins and
should not be used in patients with a history of severe penicillin
allergy, urticarial reactions, or anaphylaxis.
Hospitalization for close
monitoring and intravenous antibiotics is recommended in severe cases and in
infants, elderly patients, and patients who are
immunocompromised.
Coverage for S aureus is not usually necessary for
typical infections, but it should be considered in patients
who do
not improve with penicillin or who present with atypical forms of erysipelas,
including bullous
erysipelas. Some authors believe that facial
erysipelas should be treated empirically with a penicillinase-
resistant antibiotic, such as dicloxacillin or nafcillin, to cover
possible S aureus infection, but supporting
evidence for this
recommendation is lacking.2
Two drugs, roxithromycin and pristinamycin, have
been reported to be extremely effective in the treatment
of
erysipelas. Several studies have demonstrated greater efficacy and fewer
adverse effects with these drugs
compared with penicillin.5
Currently, the Food and Drug Administration has not approved these drugs in the
United States, but they are in use in Europe.
Patients with
recurrent erysipelas should be educated regarding local antisepsis and general
wound care.
Predisposing lower extremity skin lesions (eg, tinea
pedis, stasis ulcers) should be treated aggressively to
prevent
superinfection. Use of compression stockings should be encouraged for as long
as 1 month in
previously healthy patients and for the long-term in
patients with preexisting lower extremity edema. Long-
term
prophylactic antibiotic therapy generally is accepted, but no true guidelines
are available. Treatment
regimens should be tailored to the
patient. One reported regimen is benzathine penicillin at 2.4 MU
intramuscularly every 3 weeks for up to 2 years.6
Surgical
Care
Debridement is necessary only in severe infections with necrosis or
gangrene.
Consultations
Most patients with erysipelas respond very
well to conventional antibiotic therapy. However, in atypical
infections that are unresponsive to first- and second-line agents, an
infectious disease consult may be useful.
Activity
Patients with
acute infections involving the extremities should be encouraged to limit their
activity and keep
the limb elevated to decrease
swelling.
MEDICATIONSection 7 of 10 Authors and Editors
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Follow-up Multimedia References
The objective of pharmacotherapy is
to reduce morbidity and to prevent complications.
Drug Category:
Antibiotics
Penicillin is the standard therapy for typical erysipelas,
although coverage for S aureus should be considered
in the
appropriate setting.
Drug Name Penicillin (Wycillin,
PenVeeK)
Description Penicillin G procaine (Wycillin) and penicillin VK
(PenVeeK) currently are recommended as
first-line agents, indicated
for the treatment of moderately severe infections of skin and skin structure.
In
adults, administer penicillin G procaine by deep IM injection
only into upper, outer quadrant of buttock. In
infants and small
children, the midlateral aspect of the thigh may be a better site for
administration.
Adult Dose Penicillin G procaine: 0.6-1.2 million U IM bid
for 10 d
Penicillin VK: 250-500 mg PO qid for 10-14 d
Pediatric Dose
Penicillin G procaine:
<30 kg: 300,000 U/d
>30 kg: Administer as in
adults
Penicillin VK:
<12 years: 25-50 mg/kg/d PO divided tid/qid; not
to exceed 3 g/d
>12 years: Administer as in adults
Contraindications
Documented hypersensitivity
Interactions Increases risk of bleeding when
administered concurrently with warfarin; ethacrynic acid,
aspirin,
indomethacin, and furosemide may compete with penicillin G for renal tubular
secretion, increasing
penicillin serum concentrations; probenecid
can increase effects; coadministration of tetracyclines can
decrease effects; may increase methotrexate toxicity; may decrease
contraceptive efficacy; may interfere
with immunological response
to live typhoid vaccine; concurrent administration with aminoglycoside therapy
may result in inactivation of aminoglycoside (amikacin appears to
possess greatest stability in presence of
penicillins; in treatment
of severely ill patients requiring both penicillin and aminoglycoside therapy,
amikacin
is aminoglycoside of choice)
Pregnancy B - Fetal risk
not confirmed in studies in humans but has been shown in some studies in
animals
Precautions Never use IV route to administer penicillin G
procaine; administer >10 d to eliminate organism
and to prevent
such complications as endocarditis and rheumatic fever.
Drug Name
Dicloxacillin (Dycill, Dynapen)
Description Treatment of infections caused
by penicillinase-producing staphylococci. Penicillinase-resistant
penicillin that will cover for S aureus.
Adult Dose 125-500 mg PO qid
for 10 d
Pediatric Dose <40 kg: 12.5 mg/kg/d PO q6h
>40 kg: 125 mg
PO q6h
Contraindications Documented hypersensitivity
Interactions
Probenecid may increase effect of penicillins; tetracyclines may decrease
effect of penicillins
with concurrent use
Pregnancy B - Fetal
risk not confirmed in studies in humans but has been shown in some studies in
animals
Precautions Renal impairment; cross-sensitivity to other
penicillin derivatives; breastfeeding; caution in
impaired renal
function
Drug Name Nafcillin (Unipen)
Description Initial therapy
for suspected penicillin G-resistant streptococcal or staphylococcal
infections.
Use parenteral therapy initially in severe infections. Change to
oral therapy as condition warrants.
Because of thrombophlebitis,
particularly in elderly patients, administer parenterally only for short term
(1-2
d); change to PO as clinically indicated.
Adult Dose 1-2 g
IV qid for 7 d
Infection due to S aureus, penicillinase-producing: 500 mg IV
q4h; alternatively, 500 mg IM q4-6h
Severe infection: 1000 mg IV or IM
q4h
Pediatric Dose 0-4 kg: 10 mg/kg IM bid
4-40 kg: 25 mg/kg IM bid;
alternatively, 100-200 mg/kg/d IV/IM in 4-6 divided doses
Children: 50
mg/kg/d PO divided qid
Contraindications Documented hypersensitivity;
hypersensitivity to corn or corn products; dextrose solutions
may
precipitate an allergic reaction
Interactions Associated with warfarin
resistance when administered concurrently; effects may decrease with
bacteriostatic
action of tetracycline derivatives; concomitant penicillin and aminoglycoside
therapy reported
to result in inactivation of aminoglycoside both
in vivo and in vitro; nafcillin appears to decrease cyclosporine
serum concentrations or interfere with cyclosporine assay
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some
studies in animals
Precautions Renal impairment; cross-sensitivity to
other penicillin derivatives; breastfeeding; >10 d treatment
to
eliminate infection and prevent sequelae (eg, endocarditis, rheumatic fever);
adverse reactions include
hypokalemia and interstitial nephritis;
history of significant allergies or asthma; increased risk for allergic
reaction; diarrhea subsequent to nafcillin may be indicative of
overgrowth of Clostridium difficile resulting in
pseudomembranous
colitis
Reports of proteinuria associated with high doses of nafcillin
indicate this pseudoproteinuria is result of
interaction between
nafcillin and/or metabolites and quantitative reagents used in TCA
(trichloroacetic acid)
and sulfosalicylic acid method of urine
protein analysis (semiquantitative dipstick technique for estimation of
urinary protein [primarily albumin] does not produce this interaction);
antibiotics that possess bacterial
activity against Salmonella
typhi organisms may interfere with immunological response to live typhoid
vaccine
(allow 24 h or more to elapse between administration of last
dose of antibiotic and live typhoid vaccine)
Drug Name Erythromycin
(E-mycin, E.E.S., Eryc)
Description Macrolide used for penicillin-allergic
individuals. Inhibits bacterial growth, possibly by blocking
dissociation of peptidyl t-RNA from ribosomes causing RNA-dependent
protein synthesis to arrest. For
treatment of staphylococcal and
streptococcal infections.
In children, age, weight, and severity of
infection determine proper dosage. When bid dosing is desired, half
total daily dose may be taken q12h. For more severe infections, double
the dose.
Adult Dose 250-500 mg PO qid for 10 d
Pediatric Dose 30-50
mg/kg/d (15-25 mg/lb/d) PO divided q6-8h; double dose for severe
infection
Contraindications Documented hypersensitivity; hepatic
impairment
Interactions Coadministration may increase toxicity of
theophylline, digoxin, carbamazepine, and
cyclosporine; may
potentiate anticoagulant effects of warfarin; coadministration with lovastatin
and
simvastatin increases risk of rhabdomyolysis
Pregnancy B -
Fetal risk not confirmed in studies in humans but has been shown in some
studies in animals
Precautions Caution in liver disease; estolate
formulation may cause cholestatic jaundice; GI adverse effects
are
common (give doses pc); discontinue use if nausea, vomiting, malaise, abdominal
colic, or fever occur;
hepatotoxicity or skin rash may occur;
caution in breastfeeding
FOLLOW-UPSection 8 of 10
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Complications
The most common complications of
erysipelas include abscess, gangrene, and thrombophlebitis. Less
common complications (<1%) are acute glomerulonephritis,
endocarditis, septicemia, and streptococcal
toxic shock syndrome.
Rare osteoarticular complications involve joints contiguous with the erysipelas
plaques and include bursitis, osteitis, arthritis, and
tendinitis.7
Prognosis
The prognosis for patients with
erysipelas is excellent. Complications of the infection usually are not life
threatening, and most cases resolve after antibiotic therapy without
sequelae. However, local recurrence has
been reported in up to 20%
of patients with predisposing conditions.
MULTIMEDIASection
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REFERENCESSection 10 of 10 Authors and
Editors Introduction Clinical Differentials Workup
Treatment
Medication Follow-up Multimedia References
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Erysipelas excerpt
Article Last Updated:
Feb 11,
2008
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Pain
syndromes
Q. I have just been diagnosed with shingles (very painful) and
they are spreading toward my lymphedema side. I
have been managing
my LE for two years, but I m frightened that this could aggravate the LE. I am
treating with
w/Famvir and patience. The clinic analyzing the
shingles did not seem knowledgeable about a possible impact on
LE.
Can you help me with this?
A. I have treated several patients who developed
shingles either before or after CLT treatment, often on the trunk
on the lymphedematous side. In some patients, the inflammation did
worsen the swelling temporarily, but with a
bit of extra care, this
swelling was resolved. Those who were maintaining good reduction prior to the
shingles
found that they were able to continue this, or regain
their reduction fairly quickly as the shingles resolved.
Prevention
of secondary infection is the most important thing for you now. I would
recommend applying
antibiotic ointment to any lesions that are open
and oozing to help prevent this. Monitor your skin very carefully. If
there is any sign of even a local infection, consult with your physician about starting systemic antibiotics to avoid
a local infection from
progressing rapidly into a more serious systemic infection.
Q. I recently
ran across an article that mentioned the medication "Daflon" in the treatment
of lymphedema. I am
always searching for new information and have
never heard of this. Can you tell me a little about this medication
and how it is used?
A. Daflon has been used for varicose veins and
other conditions, and is available in many countries. It works
much
the same way as the benzopyrones, i.e. by enhancing the macrophage activity and
increasing the numbers
(this has been well established in
experimental models).
Daflon has been successfully tested in clinical
trials for the treatment of lymph-edema, but optimal dosages are still
undecided. At this point in the trials, the higher dose has been more
successful. (Pecking [France]; Ciucci
[Argentina]) We think that
probably the dose should be at least 2gm per day, but 900mg taken cautiously
should
help. I suggest you contact Servier Laboratories, the
manufacturer, directly for further info. Director of Research,
Institut de Recherches Internationales Servier (I.R.I.S.) 6, Place des
Pleiades - 92415 Courbevoie Cedex
FRANCE. Tel: (33 1) 46 41 60 00.
email: [email protected].
Daflon
Shingles
Menstration and LE
Q: I
am 40 years old and have secondary lymphedema of both legs from injuries
sustained in a car accident in
1993. I notice that when it is time
for my monthly period, no matter what I do or how much I use my lymphatic
pump (Wright Linear Pump, which usually helps a great deal), I swell up
so extremely the fluid even moves into
the pelvis and abdomen, and
my right leg is in excruciating pain. After my period the swelling in my
abdomen
subsides. FYI: My right leg developed lymphedema from
cellulitis after the accident (from glass puncture wounds)
and
there is a constant nagging ache. My left leg does not hurt. What do you know
of the connection between the
two?
A: As you know, most women
accumulate fluid before and during their monthly period. But patients with
lymphedema particularly have problems and often feel extremely bloated
during this time. Clearly, the affected
limb, and often the rest of
the body, feels extremely uncomfortable, and the compression garment becomes
too
tight. My advice is: lower your salt intake even more during
this time; drink lots of water to dilute and improve the
circulation and increase urination, and maybe wear a larger
garment.
Patients who have had severe cellulitis often end up with
persistant subclinical inflammations resulting in ongoing
pain/discomfort. You might try prophylactic antibiotics for a period of
3 months ( Pen VK 250mg one tbl. day).
How to get your doctor to listen
about le
Q: How do you get your doctor to listen to your concerns about
lymphedema, especially if s/he doesn't think it is a
serious
problem?
A: Contact the NLN office and request a copy of the Consensus
document: The Diagnosis and Treatment of
Peripheral Lymphedema
written by the Executive Committee of the International Society of Lymphology
(Lymphology 28[1995] 113-117). Bring this to your doctor's
attention and make sure he or she reads it. It's an
excellent first
step to educating your physician and other health care providers and,
hopefully, getting the care you
need.
Compression garments
without therapy first
Q: If you can't afford Manual Lymph Drainage, is it
safe to buy and use a CircAid or Reid Sleeve? Do you have to
use
both of them or, if you can only afford one, which one should you use?
A:
You can use both of them or only one. The Reid sleeve can be used as a
maintenance garment after the limb
has been decongested and usually
is worn throughout the night instead of bandaging. The CIRCAID is used during
the day and worn over the thigh-high compression stocking (the
below -the-knee CircAid). This also is available in
a full-length
style which is worn during the night to replace bandaging. Both the Reid sleeve
and the CircAid
devices are extremely effective and many patients
use both. If you can only afford one, consider purchasing the
one
that will bring the most simplicity to your daily self-care
program.
Indeed, Manual Lymph Drainage can be expensive or often
insurance companies will not reimburse for this
treatment. I highly
recommend investing in the Self-Care videotape designed by JoAnn Rovig, LMT for
patients
who have no therapist in their area or who cannot afford
treatment. Many patients and clinics are using this video
and the
feedback has been excellent. The video instructs viewers in the educational and
self-management aspects
of lymphedema. (The video is available
through the NLN, please consult the Reprints List.).
--------------------
Article Last Updated: Feb 11,
2008
AUTHOR
AND EDITOR INFORMATIONS
Authors and Editors Introduction Clinical
Differentials Workup Treatment Medication Follow-up
Multimedia
References
Author:
Loretta Davis, MD, Professor, Department of Internal Medicine, Division of
Dermatology, Medical
College of Georgia
Loretta Davis is a
member of the following medical societies: American Academy of
Dermatology
Coauthor(s): John A Cole, BS, Medical College of Georgia;
Keith Benbenisty, MD, Consulting Staff, Associates in
Dermatology,
MDs, PA
Editors: Robert A Schwartz, MD, MPH, Professor and Head of
Dermatology, Professor of Medicine, Professor of
Pediatrics,
Professor of Pathology, Professor of Preventive Medicine and Community Health,
UMDNJ-New
Jersey Medical School; Michael J Wells, MD, Associate
Professor, Department of Dermatology, Texas Tech
University Health
Sciences Center; Christen M Mowad, MD, Assistant Professor, Department of
Dermatology,
Geisinger Medical Center; Glen H Crawford, MD,
Assistant Clinical Professor, Department of Dermatology,
University
of Pennsylvania School of Medicine; Chief, Division of Dermatology, The
Pennsylvania Hospital; Dirk
M Elston, MD, Director, Department of
Dermatology, Geisinger Medical Center
Author and
Editor Disclosure
Synonyms and related keywords: non-necrotizing
dermohypodermitis, acute bacterial dermohypodermitis
INTRODUCTION
Authors and Editors Introduction Clinical Differentials Workup Treatment
Medication
Follow-up Multimedia
References
Background
Erysipelas is a superficial bacterial skin
infection that characteristically extends into the cutaneous lymphatics.
This disease has been traced back to the Middle Ages where it was
referred to as "St Anthony's Fire,"
named after an Egyptian healer
who was known for successfully treating the infection. Historically, this
infection occurred on the face and was caused by Streptococcus
pyogenes. However, a shift in the
distribution and etiology of the
disease has occurred, with most erysipelas infections now occurring on the
legs and with non–group A streptococci sometimes being identified as
the etiologic agents.
Pathophysiology
Bacterial inoculation into an
area of skin trauma is the initial event in developing erysipelas. Thus, local
factors, such as venous insufficiency, stasis ulcerations,
inflammatory dermatoses, dermatophyte infections,
insect bites, and
surgical incisions, have been implicated as portals of entry. The source of the
bacteria in
facial erysipelas is often the host's nasopharynx, and
a history of recent streptococcal pharyngitis has been
reported in
up to one third of cases. Other predisposing factors include diabetes, alcohol
abuse,1 HIV
infection, nephrotic syndrome, other immunocompromising
conditions, and vagrant lifestyle.
The infection rapidly invades and
spreads through the lymphatic vessels. This can produce overlying skin
"streaking" and regional lymph node swelling and tenderness. Immunity
does not develop to the inciting
organism.
Frequency
United States
Isolated cases are
the rule with erysipelas, although epidemics have been reported. The incidence
of
erysipelas declined throughout the mid-20th century, possibly
due to antibiotic development, improved
sanitation, and decreased
virulence. The change in distribution from the face to the lower extremities is
most
likely related to an aging population with risk factors such
as lymphedema. Approximately 85% of cases
occur on the legs rather
than the face.
International
Erysipelas is somewhat more common in
European countries. Isolated cases are still the rule, and
distribution and etiology remain similar to that in the United
States.
Mortality/Morbidity
The most common complaints during the
acute infection include tenderness of the involved area, fever, chills,
and swelling. Death as a direct result of erysipelas is exceedingly
rare. Predisposed patients often develop
local recurrence, and this
can lead to disfiguring and disabling healing reactions, such as elephantiasis
nostras
verrucosa. This chronic warty, edematous condition is caused
by lymphatic destruction from repeated
infection.
Race
Erysipelas infections affect all
races.
Sex
Erysipelas has been reported to be more common in females,
but occurring at an earlier age in males
because of their more
aggressive activities. Other studies indicate that predisposing factors, rather
than
gender, account for any male/female differences in
incidence.
Age
Cases of erysipelas have been reported in all age
groups, but it does appear that infants, young children, and
elderly patients are the most commonly affected groups. The peak
incidence has been reported to be in
patients aged 60-80 years,
especially in patients who are considered high-risk and immunocompromised or
those with lymphatic drainage problems (eg, after mastectomy,
pelvic surgery, bypass grafting).
CLINICALSection 3 of 10
Authors and Editors Introduction Clinical Differentials Workup Treatment
Medication Follow-up Multimedia
References
History
Patients often cannot recall an inciting
event, but there may be a history of recent trauma or pharyngitis.
Prodromal symptoms, such as malaise, chills, and high fever, often
begin before the onset of the skin lesions
and usually are present
within 48 hours of cutaneous involvement. Pruritus, burning, and tenderness are
typical complaints.
Physical
Erysipelas begins as a small
erythematous patch that progresses to a fiery-red, indurated, tense, and shiny
plaque. The lesion classically exhibits raised sharply demarcated
advancing margins. Local signs of
inflammation, such as warmth,
edema, and tenderness, are universal. Lymphatic involvement often is
manifested by overlying skin streaking and regional lymphadenopathy.
More severe infections may exhibit
numerous vesicles and bullae
along with petechiae and even frank necrosis. With treatment, the lesion often
desquamates and can resolve with pigmentary changes that may or may
not resolve over time.
Causes
Streptococci are the primary cause of
erysipelas. Most facial infections are attributed to group A
streptococci, with an increasing percentage of lower extremity
infections being caused by non–group A
streptococci.
Streptococcal toxins are thought to contribute to the brisk inflammation that
is pathognomonic
of this infection. No clear proof has emerged that
other bacteria cause typical erysipelas, although they
clearly
coexist with streptococci at sites of inoculation. Recently, atypical forms
reportedly have been caused
by Streptococcus pneumoniae, Klebsiella
pneumoniae, Haemophilus influenzae, Yersinia enterocolitica, and
Moraxella species, and they should be considered in cases refractory to
standard antibiotic therapy.
The role of Staphylococcus aureus, and
specifically methicillin-resistant S aureus, remains controversial. No
conclusive evidence demonstrates a pathogenic role for staphylococci in
typical erysipelas. The infection's
predictable response to
penicillin, even when S aureus is present, argues against S aureus as an
etiologic
agent. However, analogous to what occurs in bullous
impetigo or staphylococcal scalded skin syndrome,
exotoxins from
coexisting S aureus may account for the clinical presentation of bullous
erysipelas.2
DIFFERENTIALSSection 4 of 10 Authors and Editors
Introduction Clinical Differentials Workup
Treatment Medication
Follow-up Multimedia References
Erythema Annulare
Centrifugum
Other Problems to be Considered
Erysipelas can be
differentiated from cellulitis by its characteristically raised advancing edges
and sharply
demarcated borders, reflecting its more superficial
nature. Cellulitis has no lymphatic component and exhibits
indiscreet margins.
WORKUPSection 5 of 10 Authors
and Editors Introduction Clinical Differentials Workup Treatment
Medication Follow-up Multimedia References
Lab
Studies
In classic erysipelas, no laboratory workup is required for
diagnosis or treatment.
Routine blood and tissue cultures are not
cost-effective because they have an extremely low yield and results
have a minimal impact on management. Cultures are perhaps best reserved
for very immunosuppressed
hosts in whom an atypical etiologic agent
might be more likely.3
Bacterial cultures from the portal of entry may be
most helpful in persons with atypical clinical presentations.
Imaging
Studies
Imaging studies are not usually indicated and are of low yield.
MRI and bone scintigraphy are helpful when
early osteoarticular
involvement is suspected. In this setting, standard radiographs are typically
normal.
Histologic Findings
The histologic hallmarks of erysipelas
are marked dermal edema, vascular dilatation, and streptococcal
invasion of lymphatics and tissues. This bacterial invasion results in
a dermal inflammatory infiltrate consisting
of neutrophils and
mononuclear cells. The epidermis is often secondarily involved. Rarely,
bacterial invasion
of local blood vessels may be
seen.
TREATMENTSection 6 of 10 Authors and Editors
Introduction Clinical Differentials Workup Treatment
Medication
Follow-up Multimedia References
Medical Care
Elevation and
rest of the affected limb are recommended to reduce local swelling,
inflammation, and pain.
Saline wet dressings should be applied to ulcerated
and necrotic lesions and changed every 2-12 hours,
depending on the
severity of the infection.
Streptococci cause most cases of erysipelas;
thus, penicillin has remained first-line therapy.4 Penicillin
administered orally or intramuscularly is sufficient for most cases of
classic erysipelas and should be given for
10-20 days.
A
cephalosporin or macrolide, such as erythromycin or azithromycin, may be used
if the patient has an
allergy to penicillin. Cephalosporins may
cross-react with penicillin first-generation cephalosporins and
should not be used in patients with a history of severe penicillin
allergy, urticarial reactions, or anaphylaxis.
Hospitalization for close
monitoring and intravenous antibiotics is recommended in severe cases and in
infants, elderly patients, and patients who are
immunocompromised.
Coverage for S aureus is not usually necessary for
typical infections, but it should be considered in patients
who do
not improve with penicillin or who present with atypical forms of erysipelas,
including bullous
erysipelas. Some authors believe that facial
erysipelas should be treated empirically with a penicillinase-
resistant antibiotic, such as dicloxacillin or nafcillin, to cover
possible S aureus infection, but supporting
evidence for this
recommendation is lacking.2
Two drugs, roxithromycin and pristinamycin, have
been reported to be extremely effective in the treatment
of
erysipelas. Several studies have demonstrated greater efficacy and fewer
adverse effects with these drugs
compared with penicillin.5
Currently, the Food and Drug Administration has not approved these drugs in the
United States, but they are in use in Europe.
Patients with
recurrent erysipelas should be educated regarding local antisepsis and general
wound care.
Predisposing lower extremity skin lesions (eg, tinea
pedis, stasis ulcers) should be treated aggressively to
prevent
superinfection. Use of compression stockings should be encouraged for as long
as 1 month in
previously healthy patients and for the long-term in
patients with preexisting lower extremity edema. Long-
term
prophylactic antibiotic therapy generally is accepted, but no true guidelines
are available. Treatment
regimens should be tailored to the
patient. One reported regimen is benzathine penicillin at 2.4 MU
intramuscularly every 3 weeks for up to 2 years.6
Surgical
Care
Debridement is necessary only in severe infections with necrosis or
gangrene.
Consultations
Most patients with erysipelas respond very
well to conventional antibiotic therapy. However, in atypical
infections that are unresponsive to first- and second-line agents, an
infectious disease consult may be useful.
Activity
Patients with
acute infections involving the extremities should be encouraged to limit their
activity and keep
the limb elevated to decrease
swelling.
MEDICATIONSection 7 of 10 Authors and Editors
Introduction Clinical Differentials Workup
Treatment Medication
Follow-up Multimedia References
The objective of pharmacotherapy is
to reduce morbidity and to prevent complications.
Drug Category:
Antibiotics
Penicillin is the standard therapy for typical erysipelas,
although coverage for S aureus should be considered
in the
appropriate setting.
Drug Name Penicillin (Wycillin,
PenVeeK)
Description Penicillin G procaine (Wycillin) and penicillin VK
(PenVeeK) currently are recommended as
first-line agents, indicated
for the treatment of moderately severe infections of skin and skin structure.
In
adults, administer penicillin G procaine by deep IM injection
only into upper, outer quadrant of buttock. In
infants and small
children, the midlateral aspect of the thigh may be a better site for
administration.
Adult Dose Penicillin G procaine: 0.6-1.2 million U IM bid
for 10 d
Penicillin VK: 250-500 mg PO qid for 10-14 d
Pediatric Dose
Penicillin G procaine:
<30 kg: 300,000 U/d
>30 kg: Administer as in
adults
Penicillin VK:
<12 years: 25-50 mg/kg/d PO divided tid/qid; not
to exceed 3 g/d
>12 years: Administer as in adults
Contraindications
Documented hypersensitivity
Interactions Increases risk of bleeding when
administered concurrently with warfarin; ethacrynic acid,
aspirin,
indomethacin, and furosemide may compete with penicillin G for renal tubular
secretion, increasing
penicillin serum concentrations; probenecid
can increase effects; coadministration of tetracyclines can
decrease effects; may increase methotrexate toxicity; may decrease
contraceptive efficacy; may interfere
with immunological response
to live typhoid vaccine; concurrent administration with aminoglycoside therapy
may result in inactivation of aminoglycoside (amikacin appears to
possess greatest stability in presence of
penicillins; in treatment
of severely ill patients requiring both penicillin and aminoglycoside therapy,
amikacin
is aminoglycoside of choice)
Pregnancy B - Fetal risk
not confirmed in studies in humans but has been shown in some studies in
animals
Precautions Never use IV route to administer penicillin G
procaine; administer >10 d to eliminate organism
and to prevent
such complications as endocarditis and rheumatic fever.
Drug Name
Dicloxacillin (Dycill, Dynapen)
Description Treatment of infections caused
by penicillinase-producing staphylococci. Penicillinase-resistant
penicillin that will cover for S aureus.
Adult Dose 125-500 mg PO qid
for 10 d
Pediatric Dose <40 kg: 12.5 mg/kg/d PO q6h
>40 kg: 125 mg
PO q6h
Contraindications Documented hypersensitivity
Interactions
Probenecid may increase effect of penicillins; tetracyclines may decrease
effect of penicillins
with concurrent use
Pregnancy B - Fetal
risk not confirmed in studies in humans but has been shown in some studies in
animals
Precautions Renal impairment; cross-sensitivity to other
penicillin derivatives; breastfeeding; caution in
impaired renal
function
Drug Name Nafcillin (Unipen)
Description Initial therapy
for suspected penicillin G-resistant streptococcal or staphylococcal
infections.
Use parenteral therapy initially in severe infections. Change to
oral therapy as condition warrants.
Because of thrombophlebitis,
particularly in elderly patients, administer parenterally only for short term
(1-2
d); change to PO as clinically indicated.
Adult Dose 1-2 g
IV qid for 7 d
Infection due to S aureus, penicillinase-producing: 500 mg IV
q4h; alternatively, 500 mg IM q4-6h
Severe infection: 1000 mg IV or IM
q4h
Pediatric Dose 0-4 kg: 10 mg/kg IM bid
4-40 kg: 25 mg/kg IM bid;
alternatively, 100-200 mg/kg/d IV/IM in 4-6 divided doses
Children: 50
mg/kg/d PO divided qid
Contraindications Documented hypersensitivity;
hypersensitivity to corn or corn products; dextrose solutions
may
precipitate an allergic reaction
Interactions Associated with warfarin
resistance when administered concurrently; effects may decrease with
bacteriostatic
action of tetracycline derivatives; concomitant penicillin and aminoglycoside
therapy reported
to result in inactivation of aminoglycoside both
in vivo and in vitro; nafcillin appears to decrease cyclosporine
serum concentrations or interfere with cyclosporine assay
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some
studies in animals
Precautions Renal impairment; cross-sensitivity to
other penicillin derivatives; breastfeeding; >10 d treatment
to
eliminate infection and prevent sequelae (eg, endocarditis, rheumatic fever);
adverse reactions include
hypokalemia and interstitial nephritis;
history of significant allergies or asthma; increased risk for allergic
reaction; diarrhea subsequent to nafcillin may be indicative of
overgrowth of Clostridium difficile resulting in
pseudomembranous
colitis
Reports of proteinuria associated with high doses of nafcillin
indicate this pseudoproteinuria is result of
interaction between
nafcillin and/or metabolites and quantitative reagents used in TCA
(trichloroacetic acid)
and sulfosalicylic acid method of urine
protein analysis (semiquantitative dipstick technique for estimation of
urinary protein [primarily albumin] does not produce this interaction);
antibiotics that possess bacterial
activity against Salmonella
typhi organisms may interfere with immunological response to live typhoid
vaccine
(allow 24 h or more to elapse between administration of last
dose of antibiotic and live typhoid vaccine)
Drug Name Erythromycin
(E-mycin, E.E.S., Eryc)
Description Macrolide used for penicillin-allergic
individuals. Inhibits bacterial growth, possibly by blocking
dissociation of peptidyl t-RNA from ribosomes causing RNA-dependent
protein synthesis to arrest. For
treatment of staphylococcal and
streptococcal infections.
In children, age, weight, and severity of
infection determine proper dosage. When bid dosing is desired, half
total daily dose may be taken q12h. For more severe infections, double
the dose.
Adult Dose 250-500 mg PO qid for 10 d
Pediatric Dose 30-50
mg/kg/d (15-25 mg/lb/d) PO divided q6-8h; double dose for severe
infection
Contraindications Documented hypersensitivity; hepatic
impairment
Interactions Coadministration may increase toxicity of
theophylline, digoxin, carbamazepine, and
cyclosporine; may
potentiate anticoagulant effects of warfarin; coadministration with lovastatin
and
simvastatin increases risk of rhabdomyolysis
Pregnancy B -
Fetal risk not confirmed in studies in humans but has been shown in some
studies in animals
Precautions Caution in liver disease; estolate
formulation may cause cholestatic jaundice; GI adverse effects
are
common (give doses pc); discontinue use if nausea, vomiting, malaise, abdominal
colic, or fever occur;
hepatotoxicity or skin rash may occur;
caution in breastfeeding
FOLLOW-UPSection 8 of 10
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References
Complications
The most common complications of
erysipelas include abscess, gangrene, and thrombophlebitis. Less
common complications (<1%) are acute glomerulonephritis,
endocarditis, septicemia, and streptococcal
toxic shock syndrome.
Rare osteoarticular complications involve joints contiguous with the erysipelas
plaques and include bursitis, osteitis, arthritis, and
tendinitis.7
Prognosis
The prognosis for patients with
erysipelas is excellent. Complications of the infection usually are not life
threatening, and most cases resolve after antibiotic therapy without
sequelae. However, local recurrence has
been reported in up to 20%
of patients with predisposing conditions.
MULTIMEDIASection
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REFERENCESSection 10 of 10 Authors and
Editors Introduction Clinical Differentials Workup
Treatment
Medication Follow-up Multimedia References
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J
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Samonis G, Maniatakis P, Georgala S, Tosca A. Bullous erysipelas: clinical
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Dermatology. 2006;212(1):31-5. [Medline].
Leppard BJ, Seal DV, Colman G,
Hallas G. The value of bacteriology and serology in the diagnosis of
cellulitis
and erysipelas. Br J Dermatol. May 1985;112(5):559-67. [Medline].
Bishara J,
Golan-Cohen A, Robenshtok E, Leibovici L, Pitlik S. Antibiotic use in patients
with erysipelas: a
retrospective study. Isr Med Assoc J. Oct
2001;3(10):722-4. [Medline].
Bernard P, Plantin P, Roger H, Sassolas B,
Villaret E, Legrain V, et al. Roxithromycin versus penicillin in the
treatment
of erysipelas in adults: a comparative study. Br J Dermatol. Aug
1992;127(2):155-9. [Medline].
Sjöblom AC, Eriksson B, Jorup-Rönström C,
Karkkonen K, Lindqvist M. Antibiotic prophylaxis in
recurrent
erysipelas. Infection. Nov-Dec 1993;21(6):390-3. [Medline].
Coste N, Perceau
G, Léone J, Young P, Carsuzaa F, Bernardeau K, et al. Osteoarticular
complications
of erysipelas. J Am Acad Dermatol. Feb
2004;50(2):203-9. [Medline].
Bisno AL, Stevens DL. Streptococcal infections
of skin and soft tissues. N Engl J Med. Jan 25 1996;334(4):
240-5.
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Bonnetblanc JM, Bédane C. Erysipelas: recognition and
management. Am J Clin Dermatol. 2003;4(3):
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Bratton RL, Nesse RE. St. Anthony's Fire: diagnosis and
management of erysipelas. Am Fam Physician.
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[Medline].
Chartier C, Grosshans E. Erysipelas. Int J Dermatol. Sep
1990;29(7):459-67. [Medline].
Chartier C, Grosshans E. Erysipelas: an
update. Int J Dermatol. Nov 1996;35(11):779-81. [Medline].
Elston DM.
Epidemiology and prevention of skin and soft tissue infections. Cutis. May
2004;73(5 Suppl):3-
7. [Medline].
Grosshans EM. The red face:
erysipelas. Clin Dermatol. Apr-Jun 1993;11(2):307-13. [Medline].
Hammar H,
Wanger L. Erysipelas and necrotizing fasciitis. Br J Dermatol. Apr
1977;96(4):409-19.
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Schewach-Millet M, Modan M. Erysipelas. Changing faces. Int J Dermatol. Apr
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Erysipelas excerpt
Article Last Updated:
Feb 11,
2008
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Pain
syndromes
Q. I have just been diagnosed with shingles (very painful) and
they are spreading toward my lymphedema side. I
have been managing
my LE for two years, but I m frightened that this could aggravate the LE. I am
treating with
w/Famvir and patience. The clinic analyzing the
shingles did not seem knowledgeable about a possible impact on
LE.
Can you help me with this?
A. I have treated several patients who developed
shingles either before or after CLT treatment, often on the trunk
on the lymphedematous side. In some patients, the inflammation did
worsen the swelling temporarily, but with a
bit of extra care, this
swelling was resolved. Those who were maintaining good reduction prior to the
shingles
found that they were able to continue this, or regain
their reduction fairly quickly as the shingles resolved.
Prevention
of secondary infection is the most important thing for you now. I would
recommend applying
antibiotic ointment to any lesions that are open
and oozing to help prevent this. Monitor your skin very carefully. If
there is any sign of even a local infection, consult with your physician about starting systemic antibiotics to avoid
a local infection from
progressing rapidly into a more serious systemic infection.
Q. I recently
ran across an article that mentioned the medication "Daflon" in the treatment
of lymphedema. I am
always searching for new information and have
never heard of this. Can you tell me a little about this medication
and how it is used?
A. Daflon has been used for varicose veins and
other conditions, and is available in many countries. It works
much
the same way as the benzopyrones, i.e. by enhancing the macrophage activity and
increasing the numbers
(this has been well established in
experimental models).
Daflon has been successfully tested in clinical
trials for the treatment of lymph-edema, but optimal dosages are still
undecided. At this point in the trials, the higher dose has been more
successful. (Pecking [France]; Ciucci
[Argentina]) We think that
probably the dose should be at least 2gm per day, but 900mg taken cautiously
should
help. I suggest you contact Servier Laboratories, the
manufacturer, directly for further info. Director of Research,
Institut de Recherches Internationales Servier (I.R.I.S.) 6, Place des
Pleiades - 92415 Courbevoie Cedex
FRANCE. Tel: (33 1) 46 41 60 00.
email: [email protected].
Daflon
Shingles
Menstration and LE
Q: I
am 40 years old and have secondary lymphedema of both legs from injuries
sustained in a car accident in
1993. I notice that when it is time
for my monthly period, no matter what I do or how much I use my lymphatic
pump (Wright Linear Pump, which usually helps a great deal), I swell up
so extremely the fluid even moves into
the pelvis and abdomen, and
my right leg is in excruciating pain. After my period the swelling in my
abdomen
subsides. FYI: My right leg developed lymphedema from
cellulitis after the accident (from glass puncture wounds)
and
there is a constant nagging ache. My left leg does not hurt. What do you know
of the connection between the
two?
A: As you know, most women
accumulate fluid before and during their monthly period. But patients with
lymphedema particularly have problems and often feel extremely bloated
during this time. Clearly, the affected
limb, and often the rest of
the body, feels extremely uncomfortable, and the compression garment becomes
too
tight. My advice is: lower your salt intake even more during
this time; drink lots of water to dilute and improve the
circulation and increase urination, and maybe wear a larger
garment.
Patients who have had severe cellulitis often end up with
persistant subclinical inflammations resulting in ongoing
pain/discomfort. You might try prophylactic antibiotics for a period of
3 months ( Pen VK 250mg one tbl. day).
How to get your doctor to listen
about le
Q: How do you get your doctor to listen to your concerns about
lymphedema, especially if s/he doesn't think it is a
serious
problem?
A: Contact the NLN office and request a copy of the Consensus
document: The Diagnosis and Treatment of
Peripheral Lymphedema
written by the Executive Committee of the International Society of Lymphology
(Lymphology 28[1995] 113-117). Bring this to your doctor's
attention and make sure he or she reads it. It's an
excellent first
step to educating your physician and other health care providers and,
hopefully, getting the care you
need.
Compression garments
without therapy first
Q: If you can't afford Manual Lymph Drainage, is it
safe to buy and use a CircAid or Reid Sleeve? Do you have to
use
both of them or, if you can only afford one, which one should you use?
A:
You can use both of them or only one. The Reid sleeve can be used as a
maintenance garment after the limb
has been decongested and usually
is worn throughout the night instead of bandaging. The CIRCAID is used during
the day and worn over the thigh-high compression stocking (the
below -the-knee CircAid). This also is available in
a full-length
style which is worn during the night to replace bandaging. Both the Reid sleeve
and the CircAid
devices are extremely effective and many patients
use both. If you can only afford one, consider purchasing the
one
that will bring the most simplicity to your daily self-care
program.
Indeed, Manual Lymph Drainage can be expensive or often
insurance companies will not reimburse for this
treatment. I highly
recommend investing in the Self-Care videotape designed by JoAnn Rovig, LMT for
patients
who have no therapist in their area or who cannot afford
treatment. Many patients and clinics are using this video
and the
feedback has been excellent. The video instructs viewers in the educational and
self-management aspects
of lymphedema. (The video is available
through the NLN, please consult the Reprints List.).
--------------------