12th State of Georgia Lymphedema Awareness Day

State of Georgia Lymphedema Awareness Program

.

Lighthouse Lymphedema Network

.

THERE IS STILL TIME TO GET THOSE REGISTRATIONS IN

.

An educational and awareness conference for patients, caregivers and professionals!

.

Where?

.

Saint Joseph Hospital Auditorium 5665 Peachtree Dunwoody Road, NE Atlanta, GA 30342

.

When?

.

Saturday, October 24, 2009 7:30 am - 5:00 pm

.

Click here for Registration Form

.

Schedule

.

7:30-8:15am Registration – Continental Breakfast – Exhibits 8:15-8:30am Welcome .

Plenary Session:

.

8:30-10:00am Moderator: Elaine Gunter, MT (ASCP)

.

Nicole Stout, PT, MPT, CLT-LANA Will discuss her studies on early intervention for breast cancer including the anatomy, reconstruction, breast cancer surgeries, truncal and other upper extremity lymphedema

.

10:00-10:30am Break Exhibits

.

10:30-12:00 Charles McGarvey, PT, DPT, MS, FAPTA

.

Lymphedema Secondary to Pelvic Cancer Treatment: A Review of Literature and Clinical Practice

.

12:00 – 1:30pm Lunch Exhibits

.

1:00-2:15pm Teen (only) Networking -Parent Networking (parents of children with lymphedema)

.

Separate sessions

.

Plenary Session:

.

1:30-2:15pm Daniel Beless, MD, Director of Wound Care at Saint Joseph Hospital Wound Care and the lymphedema patient

.

2:15-3:00pm DeCourcy Squire, PT, CLT-LANA

Research updates from the International Society of Lymphology of Lymphedema Diagnosis and Treatment

.

3:00-3:30pm Break Exhibits

.

3:30-4:30pm Panel Discussion

All speakers will participate in this question and answer discussion

.

4:30-5:00pm Closing Remarks

New Lymphedema Treatment Clinic - Myrtle beach, South Carolina

It gives me great pleasure to announce a new lymphedema treatment clinic in the Myrtle Beach, South Carolina area:

Tom Kincheloe, OTR/L, CLT
Founder/Clinical Director
RIVERTOWN LYMPHEDEMA CLINIC AND REHAB, LLC.
100 Prather Park Drive, Suite A
Myrtle Beach, SC 29588-7910
Bus. Phone: (843) 742-5701
Bus. Fax: (843) 742-5704
Cell: (843) 957-2422
Email: erivertownlymph@sc.rr.com

I know Tom personally and two things strike me about him.

First, is his real concern/compassion for his patients.

Secondly is his knowledge of lymphedema.

A winning combination! So if you live in his area and are looking for lymphedema help, give him a call.

Pat

Angiosarcoma consecutive to chronic lymphoedema: a Stewart-Treves syndrome

.

Lymphangiosarcoma referred to as angiosarcoma or Stewart Treves Syndrome is a possible complication

of long term (chronic) lymphedema. It has always been reported as rare, but ironically in the groups I participate in there

have been several members over the last couple years that have come down with it.

Historically, it was though that this mostly effected breast cancer survivors, but now is being recognized as something

that is possible for all chronic LE patients. Indeed, every one of the members who got it were not breast cancer patients.

A couple had other types of cancer and another two were primary lymphedema.

Also, it needs to be mentioned that in every case our members had bruises that didn't heal. When they were biopsied, it

turned out to be lymphangiosarcoma. it is critical that we keep check on our limbs that are effected and don't assume

any change is simply a discoloration cause by the LE.

In my own case, I had a small perfectly round spot on the calf of my left leg. It continued to grow until it reached

the size of a quarter. For me, it turned out to be mixed b-cell lymphoma.

So pay attention and report to your doctor when these spots arise.

Pat

Angiosarcoma consecutive to chronic lymphoedema: a Stewart-Treves syndrome

Rev Med Liege. 2009 Jul-Aug

Gonne E, Collignon J, Kurth W, Thiry A, Henry F, Jerusalem G, Gennigens C.

Université de Liège, Belgique.

The Stewart-Treves Syndrome is defined as an angiosarcoma (very aggressive malignant tumor originating from endothelial cells) appearing in a specific clinical setting. This tumor develops in patients suffering from chronic lymphedema of the upper limb following mastectomy and axillary lymph node dissection for breast cancer. The diagnosis relies on medical history, clinical examination and a histological assesment (biopsy or resection). This syndrome represents a rare clinical entity. Unfortunately, the prognosis is poor. A large surgical resection is the treatment of choice if the patient is a candidate for a surgical resection with a curative intent Radiotherapy is sometimes used as a palliative local treatment. Chemotherapy is only used in more advanced cases, not curable by surgery alone.

Pub Med

For further information, please refer to our pages:

LYMPHANGIOSARCOMA

and

Stewart Treves Syndrome

Lighthouse Lymphedema Network

I wanted to make a special announcement that the Lighthouse Lymphedema.Network is now on Facebook.

.

You can join by going to:

.

Lighthouse Facebook

.

.

There is also an area where you can post and participate. AND - don't forget our upcoming program in October.

.

We will be having both a parenting network and a teen network this year....be there or be square!

.

see the details for that at:

Lighthouse Lymphedema Network

.

**yes, I'm on it too :-)

.

Pat

The CEAP-L classification for lymphedemas of the limbs: the Italian experience.

The CEAP-L classification for lymphedemas of the limbs: the Italian experience.
Int Angiol. 2009 Aug

Gasbarro V, Michelini S, Antignani PL, Tsolaki E, Ricci M, Allegra C.
Unit of Vascular and Endovascular Surgery, Department of Surgical, Anesthesiological and Radiological Sciences, Sant'Anna University Hospital, University of Ferrara, Ferrara, Italy allegra@mclink.it.

AIM: A method to classificate lymphedema has been needed to gather all the important information on the clinical evolution of the disease using a common language and an easy clinical applicability.

METHODS: The proposal for a new classification of the limb lymphedema was inspired by the C.E.A.P. classification for chronic venous insufficiency of the lower limb. The classification adopts the acronym C.E.A.P. by adding the letter L to underline the aspect ''lymphedema'' and is based on clinical data such as extension of lymphedema, presence of lymphangitis, leg ulcers and loss of functionality of the limb and instrumental criteria that permit to confirm and precise diagnosis. The Clinical classification is based on the most objective sign in these patients, the edema which is subdivided into 5 classes depending on the clinical manifestations. The etiological aspect considers 2 types of alterations of the lymphatic system: congenital and acquired. The anatomic is aimed to locate the anatomical structures involved. Pathophysiological conditions are gathered into 5 groups: agenesia or hypoplasia, hyperplasia, reflux, overload, obstruction.

RESULTS: The classification has already been appraised after 4 years of activity at the unit of Vascular and Endovascular Surgery of Ferrara, at the S. Giovanni Battista Hospital in Rome, at the Umberto I Ancona Hospital and at the S. Giovanni- Addolorata Hospital in Rome.

CONCLUSIONS: The proposal for a new classification of lymphedema C.E.A.P. L was developed in order to categorize patients with definite and objective marks, creating clinical reports with a common vocabulary, clear to all clinicians, permitting to stage the disease, evaluate treatment and finally obtain epidemiological and statistical data.

PubMed

Adverse effects of compression in treatment of limb lymphedema.]

Adverse effects of compression in treatment of limb lymphedema.

J Mal Vasc. 2009 Aug 18

Vignes S, Arrault M.

Unité de lymphologie, centre national de référence des maladies vasculaires rares, hôpital Cognacq-Jay, 15, rue Eugène-Millon, 75015 Paris, France.

INTRODUCTION: Limb lymphedema, whether primary or secondary, is a chronic disease. Compression is the cornerstone of therapy and includes multilayer low-stretch bandages and elastic garments. Compression is usually well-tolerated. The aim of our study was to identify all the different types of adverse effects of compression.

MATERIALS AND METHODS: Since January 2005, we have recorded all adverse events occurring in outpatients and inpatients consulting in a single lymphology department, spontaneously reported by patient during consultations or physical examinations, and noted the type of compression material used.

RESULTS: Adverse effects were secondary to poor choice of therapeutic material, excessive pressure or contact dermatitis. For the arms, an elastic garment stopping at the wrist can be responsible for lymphedema of the hand and fingers. Rubbing of sleeve seams may cause pain and even ulcers between the thumb and forefinger. Open-toed elastic stockings may exacerbate digital lymphedema, leading to the formation of oozing lymph vesicles. Hyperpressure may cause severe pain localized to the first and fifth toes, overlapping toes, interdigital corns and/or ingrown toenails. Silicone-banded soft-fit elastic garments may cause painful phlyctena, urticaria or eczematiform lesions. Elastic bandages may induce pain or purpuric lesions.

CONCLUSION: Compression can be responsible for adverse effects, sometimes severe, requiring treatment change or withdrawal. Further studies are needed to precisely determine their frequency to improve prescriptions and currently available products.

EMConsulte

Massive Localized Lymphedema - A Review

Massive localised lymphoedema: a clinicopathological study of 22 cases and review of the literature.

J Clin Pathol. 2009 Sep;

Manduch M, Oliveira AM, Nascimento AG, Folpe AL.
Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota 55905, USA.

BACKGROUND: Massive localised lymphedema (MLL) is a rare, relatively recently described pseudosarcoma most often occurring in morbidly obese patients.

AIM: To perform a retrospective review of all cases diagnosed as MLL.

METHODS AND RESULTS: Clinical information was obtained. 22 morbidly obese adults (mean patient weight 186 kg) presented with unilateral, large soft tissue lesions of longstanding duration. Most lesions involved the thigh, but also occurred in the posterior calf and lower leg. Clinically, most lesions were regarded as representing benign processes, including pedunculated lipoma, lymphocoele or recurrent cellulitis, although soft tissue sarcoma was also suspected in two cases. Grossly, all masses showed markedly thickened skin with a "cobblestone" appearance, and were ill-defined, unencapsulated, lobulate, and very large (mean size 31 cm, range 15-61.5 cm, mean weight 3386 g, range 1133-10,800 g). Histologically, all 22 cases showed striking dermal fibrosis, expansion of the fibrous septa between fat lobules with increased numbers of stromal fibroblasts, lymphatic proliferation and lymphangiectasia. Multinucleated fibroblastic cells, marked vascular proliferation, moderate stromal cellularity and fascicular growth raised concern among referring pathologists for atypical lipomatous tumour/well differentiated liposarcoma, angiosarcoma, and a fibroblastic neoplasm such as fibromatosis in 10, 2 and 1 case, respectively.

CONCLUSION: The diagnosis of MLL continues to be challenging, in particular for pathologists. Awareness of this entity, clinical correlation and gross pathological correlation are essential in the separation of this distinctive pseudosarcoma from its various morphological mimics.

British Medical Journal

For further information on Massive Localized Lymphedema and Tretments available click here: Massive Localized Lymphedema

Georgia Lymphedema Education and Awareness Program

11th Annual Lymphedema Education & Awareness Program

An educational and awareness conference for patients, caregivers and professionals!

Where?

Piedmont Hospital

Piedmont Hospital

Richard H. Rich Auditorium

1968 Peachtree Road, NW, Building 77

Atlanta, Georgia

When?

Saturday, October 18, 20087:30 am - 5:30 pm

Program includes

What to expect of tissue after radiation?

What is the physiology response of radiation?

What does radiation do to the lymph nodes? - Peter Rossi, MD

How does vascular flow affect the lymphatics? - Ken Harper, MD

Expectations of surgery. - Christopher Hart, MD, FACSThe Lymphatic System, Wound Care,

Infections and Treatment - Paula Stewart, MDParent Networking

Aquatic Exercises

The Connection of obesity and increased swelling in people with lymphedema and lipedema.and more.

Additional information and registration form - Home website - Lighthouse Lymphedema Network

See you there - Pat

Podoconiosis - non-filarial geochemical elephantiasis - a neglected tropical disease?

Podoconiosis - non-filarial geochemical elephantiasis - a neglected tropical disease?

J Dtsch Dermatol Ges. 2009 May

Nenoff P, Simon JC, Muylowa GK, Davey G.
Laboratory for Medical Microbiology, Mölbis, Germany.

Summary

Podoconiosis or mossy foot is a form of non-filarial lymphedema. This geo-chemical elephantiasis is a disabling condition caused by the passage of microparticles of silica and aluminum silicates through the skin of people walking barefoot in areas with a high content of soil of volcanic origin. Podoconiosis is widespread in tropical Africa, Central America and North India, yet it remains a neglected and under-researched condition. The disabling effects of podoco-niosis cause great hardship to patients. It adversely affects the economic (reduced productivity and absenteeism), social (marriage, education, etc.) and psychological (social stigma) well-being of those affected. Podoconiosis can be prevented; the main primary preventive measure is protective footwear. Secondary measures include a strict hygiene regimen and compression therapy, which can reverse initial lesions. Tertiary approaches include surgical management, such as shaving operations to reduce hyperplastic and verru-cous elephantiasis.

WileyInterScience

Pole walking for patients with breast cancer-related arm lymphedema

Pole walking for patients with breast cancer-related arm lymphedema
Physiother Theory Pract. 2009 Apr

Jönsson C, Johansson K.
Lymphedema Unit, Lund University Hospital, Lund, Sweden. charlotta.jonsson@skane.se

Arm lymphedema is a well-known side effect of breast cancer treatment. Studies of the effect of physical exercise on arm lymphedema are very rare. The purpose of this study was to investigate the influence of pole walking on breast cancer-related arm lymphedema when using a compression sleeve. Twenty-six women with unilateral arm lymphedema took part in a clinical study of pole walking on one occasion, 4 kilometers for 1 hour. Measurements were made before, immediately after, and 24 hours later. Results revealed no changes in total arm volume of the swollen arm, measured with water displacement method, or in subjective assessments of heaviness and tightness in the affected arm using visual analogue scale. Immediately after pole walking, a temporary increase in total arm volume of the healthy arm (P=0.037) was found. Twenty-four hours later, no differences were found compared to the measurements before walking. The median for perceived exertion immediately after pole walking, measured with Borg scale, was 11 ("fairly light"). The results suggest that a controlled, short-duration pole-walking program can be performed by patients with arm lymphedema, using a compression sleeve, without deterioration of the arm lymphedema.

InformaWorld

Antibiotic Preventative Therapy for LE Related Cellulitis

Antibiotic Preventative Therapy for LE Related Cellulitis

May 11, 2009

The protocol I use and recommend comes directly from all my doctors over thelast forty years including infectious disease doctors, so it isn't just alayman's suggestion. It is also supported by several of our well known LE doctors that I have discussed it with.

You can not treat cellulitis in an individual as if it was just a simple infection.

One must remember

(1) A lymphedema limb is a immuno-compromised limb.

(2) As such any infection must be treat immediately to prevent spread anddditional lymphatic damage and complications such as gangrene and/or sepsis. Because of the limb being immuno-compromised the infection WILL spread rapidly without immediate care.

(3.) When you do go to the doc, they will look at the leg and prescribe sometype of antiibiotic. And...guess what????? When they do so, they don't have aclue as to the specific bacteria that is causing the infection.

There are only two ways you can tell the specifics. First, if you took anactual biopsy/culture of the infected area. This is almost never done anymore and is absolutely not what a LE patient needs to have - an open wound in the midst of infected tissue.

The second way is to do a blood culture. But, the only way you can identify thebacterium in a blood culture is if you are already septic or rather if the infection has become systemic. You must in no uncertain terms wait for this to happen.

Finally, time is absolutely essential here. Here's the scenario about waitingthat so many have expressed.

You call your doctor. Generally, they will/might say that can't see you today -perhaps tomorrow - perhaps whenever. To wait is not acceptable.

Or - they do tell you to come in and they prescribe an antibiotic as I said previously without identifying the bacteria. Or - they will say go to the ER. Here's the problem with that. In a leadingCanadian hospital, they found that cellulitis was incorrectly diagnosed andimproperly treated in 30% of the ER cases in their distinguished hospital. Thisis just my opinion - but that isn't a record I frankly would want to put my life on the line for.

Then you wait, possible again for hours. Then, more and more they give you abag of cancomycin and send you home.

This is bad for two reasons:

(1) Vanco should be used as a last line antibacterial defense. Use of it as an immediate frontline med is what is truely helping create the super duper bugs. Bacterial infections fall into two broad groups. What is called gram-positive or what isreferred to as gram-negative. What most doctors would do is presribe a longer term broad spectrum antibiotic that is capable of hitting both types of bacteria.

(2) Giving you one bag of Vanco and sending you home very well could be aprescription for disaster. Most cellulitis is simply not going to be eliminatedby one bag of super antibiotic.

Why?

Well, first if you have fibrosis, this is going to make it very very hardfor the antibiotic to penetrate to areas where the bacterial may be hiding. One"hit" may not do the job.

Secondly, we are talking about limbs that are greatly enlarged with a lot ofextra fluid - greatly diluting the antibiotic.

Quantitative bioimpedance spectroscopy for the assessment of lymphedema

Quantitative bioimpedance spectroscopy for the assessment of lymphoedema

Breast Cancer Res Treat. 2008 Dec

Ward LC, Czerniec S, Kilbreath SL.
School of Molecular and Microbial Sciences, University of Queensland, St Lucia, Brisbane, QLD, 4072, Australia, l.ward@uq.edu.au.

The aim was to make bioimpedance spectroscopy (BIS) quantitative for assessment of lymphoedema. Apparent resistivity coefficients were determined for the intra- and extracellular water of arms in a control cohort of women (n = 66). These coefficients were used to predict water volumes in the arms of women with lymphoedema (n = 23) and a separate control group without lymphoedema (n = 13) and to compare these with total arm size measured by perometry. Total arm volume was highly correlated (r = 0.80-0.90) with arm fluid volumes predicted by BIS and the proportional increase in arm size predicted by BIS was not significantly different to that measured by perometry. BIS predicted that the increased volume in the women with lymphoedema was predominantly (60%) due to increase in extracellular fluid. BIS is capable of quantifying the volume increase in limb size seen in lymphoedema.

SpringerLink

Lymphedema in systemic juvenile arthritis: a rare extraarticular feature

Lymphedema in systemic juvenile arthritis: a rare extraarticular feature
Acta Reumatol Port. 2008 Oct-Dec

Ambrósio C, Abreu P, Alexandre M, Malcata A.
Serviço de Reumatologia dos Hospitais da Universidade de Coimbra.

Extraarticular features are usually found in rheumatological diseases sometimes with no correlation with the disease's activity in that moment. Lymphoedema is one of these manifestations and it's defined as a tissue fluid accumulation with gradual onset of swelling of a limb. Because it is an unusual finding, the physiopatological explanation of this feature is still difficult to understand. We describe a case report of lymphoedema on left upper arm, in a patient with systemic juvenile arthritis, with no identified cause and with no associated systemic signs or symptoms.

PMID: 19107091 [PubMed - in process]

Supplemental surgical treatment to end stage (stage IV-V) of chronic lymphedema.

Supplemental surgical treatment to end stage (stage IV-V) of chronic lymphedema.

*Note - I am posting this for information and it shuld not be taken as an endorsement for the surgical treatment of lymphedema. It is critical that ALL efforts be made to treat and manage lymphedema through manual decongestive therapymanual lymphatic drainage (MLD, CDT) before any attempt at any surgery.

The results from MLD can be remarkable, even with limbs that would otherwise look hopeless.

Pat

Supplemental surgical treatment to end stage (stage IV-V) of chronic lymphedema.

Int Angiol. 2008 Oct

Lee BB, Kim YW, Kim DI, Hwang JH, Laredo J, Neville R.
Department of Surgery, Georgetown University, Washington DC, USA.

AIM: When the lymphedema reaches to its end stages, the complex decongestive therapy (CDT) and/or compression therapy become less effective and increased risk of systemic/general sepsis to become potentially life threatening condition.

METHODS: To improve its clinical management, excisional surgery was performed on 22 patients for their 33 limbs in the end stage of lymphedema as a supplemental therapy, and its efficacy was retrospectively analyzed. Diagnosis was made by radionuclide lymphoscintigraphy and basic laboratory studies (e.g. ultrasonography, magnetic resonance imaging). Twenty-two patients (mean age: 46 years; 3 male and 19 female; 5 primary and 17 secondary) submitted to the excisional surgery on 33 limbs (unilateral: 11; bilateral: 22). Surgery was indicated by further progression of the disease with recurrent sepsis despite adequate antibiotics therapy. A modified Auchincloss-Homan's operation was used to excise grotesquely disfigured soft tissue with advanced dermato-lipo-fibrosclerotic change. The normal limb contour was re-established to allow proper postoperative therapy. Postoperative CDT and compression therapy were mandatorily implemented in all cases.

RESULTS: A postoperative assessment of the treatment results, at 12 months showed an overall improvement in 28 of the 33 limbs: substantial improvement on the condition of limb function and quality of life (QOL), and local and/or systemic sepsis. Eighteen patients with good compliance to maintain the postoperative CDT showed much improved clinical results and QOL through the first interim assessment (24 months).

CONCLUSION: Excisional surgery at the end stage of lymphedema seems to provide substantial improvement of clinical condition and QOL only when mandated postoperative CDT/compression therapy is well kept.

PMID: 18974701 [PubMed - in process]

Do Bone Fractures Cause Lymphedema?

Do Bone Fractures Cause Lymphedema?
Over the past few years, there have been several members of my various groups who have reported lymphedema triggered by bone breaks. These cases involve both arm lymphedema and leg lymphedema.

This is highly unusual and even many lymphedema experts are unaware this can occur.

If we start with the premise that some people are born with an already “at risk” lymph system and then understand the exact mechanisms of the lymphatic system response to trauma and the changes within the lymph nodes, then it becomes clear that this is in fact a possibility.

I need to remind readers that I am not a medical professional nor have I ever had formal medical training and/or education. What is presented is a combination of my fifty-five years of living with lymphedema and from the research that I have undertaken.

Pat

Effect of lymphedema on the recovery of fractures

J Orthop Sci. 2007 Nov;
Arslan H, Uludağ A, Kapukaya A, Gezici A, Bekler HI, Ketani A. Department of Orthopedic and Trauma Surgery, University of Dicle, School of Medicine, Diyarbakir, Turkey.

BACKGROUND: Lymphedema delays the healing of any wound by negatively affecting its inflammatory period. Whether it affects bone healing in a similar negative manner is unknown. Therefore, we experimentally investigated the effect of lymphedema on fracture recovery.

METHODS: We used thirty 200- to 250-g Sprague-Dawley rats for the experiment. The rats were randomly divided into two groups of 15 rats each for the experimental lymphedema and control groups. Lymphedema development was confirmed by measuring the circumference and diameter of the extremities together with lymphoscintigraphy. Twenty days after the development of lymphedema, a fracture model was created in both groups in the right tibia with mid-diaphyseal osteotomy and fixing with an intramedullary Kirschner wire. After 6 weeks, all rats were sacrificed and the callus tissue that formed along the osteotomy was compared between groups with respect to radiographic, histological, and biomechanical characteristics.

RESULTS: The three-point bending test yielded an average stiffness value of 1227 N/mm (n = 6) in the control group and 284 N/mm (n = 7) in the experimental lymphedema group (P <>

CONCLUSIONS: Lymphedema negatively affected bone healing in rats. However, the mechanism of this negative effect and its occurrence in humans are still unknown. Further experimental and clinical studies are needed to support and extend our findings.

Springerlink

The healing of tibial fracture and response of the local lymphatic system

Szczesny G, Olszewski WL, Gewartowska M, Zaleska M, Górecki A. Department of Surgical Research and Transplantology, Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland. g.szczesny@cmdik.pan.pl

BACKGROUND: Damage of tissues by mechanical injury and inflammation is followed by reaction of the regional lymphoid tissue, lymphatics, and lymph nodes. In our previous lymphoscintigraphic studies, we showed that closed fractures of a lower limb cause reaction of the local lymphoid tissue. There was dilation of lymphatics draining the site of the fracture and enlargement of inguinal lymph nodes. These changes persisted even after clinical healing of the fracture. In the long-lasting nonhealing fractures, the lymphoscintigraphic pictures were different. The draining lymphatics became obliterated, and the lymph nodes disappeared.

METHODS: In this study, we tried to correlate the lymphoscintigraphic images, reflecting the immune events at the fracture site, with the immunohistochemical observations of the biopsy specimens obtained during corrective operations from the healing and nonhealing fracture gaps. Thirty-eight patients with closed fracture of the tibia without traumatic skin changes were studied.

RESULTS: We confirmed that closed tibial fracture evokes response of the regional lymphatic system. Normal fracture healing with immune cell infiltrates and foci of ossification was accompanied by dilated lymphatics and enlarged lymph nodes. Prolonged nonhealing fracture with lack of cellular reaction in the gap proceeded with decreased mass of lymph nodes.

CONCLUSION: This study provides evidence for existence of a functional axis between wound of bone and surrounding soft tissue and the local lymphatic (immune) system. We hypothesize that the fast healing is regulated by influx into the wound of lymph node regulatory cells, whereas prolonged healing causes gradual exhaustion of the regional lymph node functional elements, and reciprocally impairment in sending regulatory cells to the fracture gap.

Journal of Trauma

Limb lymph node response to bone fracture.

Lymphat Res Biol. 2004;
Szczesny G, Olszewski WL, Zaleska M. Department of Surgical Research and Transplantology, Medical Research Centre, Polish Academy of Sciences, 02-106 Warsaw, Poland. g.szczesny@cmdik.pan.pl

In previous clinical studies, dilation of afferent lymphatics and enlargement of inguinal lymph nodes (LN) were observed in lymphoscintigrams from patients with persistent posttraumatic edema of lower extremities after fractures and trauma of soft tissues. In this study, changes in rat popliteal and iliac lymph nodes draining lymph from the site of tibial fracture and adjacent soft tissue injury were investigated. The observed parameters were lymph node weight, cell number, phenotype frequency, cell cytokine expression, and reactivity to mitogens. The key observations included: a) increase in the weight and total cell number of the lymph nodes; b) increased autotransformation rate and responsiveness of lymph node cells to mitogen; c) decreased frequency of ED1 macrophages and activated OX8 cytotoxic cells in flow cytometry analysis; d) high expression of OX6 class II-positive, OX7 (stem cells), OX62 (migrating dendritic cells), ED1 (macrophages), and OX12 (B cells) on immunohistochemical sections of LNs with some few HIS48 (granulocytes); e) high expression of NOS3 and TGF beta by lymph node lymphocytes and endothelial cells.

In summary, local lymph nodes reacted to internal wounds, such as bone fracture and injury to adjacent tissues, through mobilization of cells from the blood circulation, along with activation of cellular subsets. The molecular mechanism that provides the signal for this reaction remains unknown. The absence of major changes in the frequency of lymph node cell subpopulations indicates that lymph nodes are constitutively prepared for influx of antigens from damaged tissues and react only with increase in cell number and cell activation. The nature of the reaction, including lack of immunization against autoantigens, remains unclear. Further elucidation will require studies on the mechanism of cross-tolerance to self-antigens during wound healing.

Liebertonline

Lymphedema of the Hand and Forearm Following Fracture of the Distal Radius

By David A. Kasper, DO, MBA; Menachem M. Meller, MD, PhD ORTHOPEDICS 2008; 31:172

February 2008

Lymphedema of the hand following a fracture of the distal radius is a rare complication resulting from abnormal protein-rich fluid accumulation in the affected area. Although lymphedema affects approximately 2.5 million Americans and frequently is associated with breast cancer treatment, its occurrence in the context of a commonplace injury to the wrist is virtually nonexistent.1

The etiology of lymphedema development following fracture care is poorly understood and has been attributed to psychogenic causes. Only one case of lymphedema following a Colles fracture has been reported in the literature.2 In that report, the patient was a 42-year old man who presented with lymphedema after a fall while accidentally being pulled by a chain. After closed reduction of the fracture and immobilization, the patient reported intense pain without swelling. Immediately after removal of the patient’s final cast, his hand began to swell, and he underwent intense physiotherapy, numerous sympathetic nerve blocks, and hospitalization with no improvement. The authors suggested the pathogenesis of the patient’s lymphedema after his fracture was self-induced and psychogenic in nature.

This article presents a case of Colles fracture complicated by nonpitting edema in a 62-year-old woman in whom psychogenic causes were not identified.

Case Report

A 62-year-old right hand-dominant woman fell down a few steps at work onto her outstretched right hand. Evaluation in the emergency room indicated a fracture of the distal radius, and the patient underwent closed reduction (Figure 1) under general anesthesia without a tourniquet.
This resulted in excellent restoration of the skeletal alignment. She was placed in a well-padded short arm cast.

At a routine follow-up visit 10 days later, the patient had complete loss of position, with the fracture reverting to the presurgical misalignment sustained immediately following the injury. She subsequently underwent open reduction and internal fixation using a dorsal plate. Both the surgery and postoperative course were uneventful.

The patient’s history included controlled hypertension, mitral valve prolapse, gastroesophageal reflux disease, rheumatic fever, scarlet fever, and a prior arthroscopic knee procedure. She reported no prior malignancies, and she was compliant with routine general medical care.
Psychological profiling was normal.

Following cast removal, the patient began occupational and physical therapy. Two months postoperatively, the swelling persisted, and she developed increasing asymmetry. She also had progressive nonpitting edema. The patient reported having no pain, hypersensitivity, or other symptoms. She also reported she did not develop any other illnesses or malignancies during this time.

The patient underwent an extensive workup that included electrodiagnostic studies and radiographs of the cervical spine, right shoulder, and right wrist (Figure 2). Computed tomography and magnetic resonance imaging revealed prominent edema adjacent to the capsule (Figure 3). An intravenous Doppler study ruled out deep vein thrombosis of the right upper extremity. A Duplex arterial scan and technetium bone scan revealed no pathological findings other than the fractured wrist.

Her fracture healed satisfactorily without additional loss of position. However, the function of her right hand was limited by the edema (Figure 4). Traditional treatments, such as a Jobst gauntlet (BSN-Jobst, Inc, Charlotte, North Carolina), Kinesio taping (Kinesio, Albuquerque, New Mexico), massage, elevation, and Isotoner gloves (Totes Isotoner Corp, Cincinnati, Ohio) supplemented by home exercises failed to relieve her symptoms.

Treatment subsequently was prescribed with the NormaTec PCD (pneumatic compression device; NormaTec, Newton Center, Massachusetts), and the patient initially used it at home for 4 hours daily. Within 2 weeks, her massive forearm edema dramatically diminished, and her wrist and hand motion normalized. She was able to bring her fingertips down to the proximal palmar crease with good grip, pinch, and opposition.

To inhibit the recurrence of the edema and hand stiffness, the patient has continued to use the device at home approximately 1 hour per week. She requires no compression garments and has not had any episodes of cellulitis (Figure 5).

Discussion

Although lymphedema is a common and severely disabling medical condition, it has not been described following orthopedic injuries such as a Colles fracture. The only previously published case report describing this injury combination attributed the lymphedema to psychogenic causes.2 In our patient, psychogenic causes were not identified.

Lymphedema results when the lymphatic volume in tissue exceeds the lymphatic transport system’s capabilities to clear the fluid. Increased hydrostatic pressure or decreased plasma oncotic pressure creates gradients across the capillary membranes, which causes the excess fluid to spill and accumulate in the interstitial space. Possible causes of this excess fluid production include local inflammation, surgery, infection, cancer, lymphatic obstruction (ie, due to scarring), and trauma.3 Although all body tissues are bathed in interstitial fluid, the lymph circulation still remains a complex, dynamic, and incompletely understood process.4

Lymphedema can be classified into two types: primary and secondary. Primary lymphedema is associated with hypoplastic, hyperplastic, missing, or impaired lymph vessels. Other presentations are classified further by age of onset. However, causes of primary lymphedema are generally unknown and cannot be linked to any specific traumatic event. The most common cause of primary lymphedema is lymphangiodysplasia.

Secondary lymphedema can be attributed to trauma to the lymph nodes or the lymphatic vessels themselves. Secondary lymphedema frequently is seen in surgical patients and is attributed to lymphatic obstruction.3 Speculations suggest secondary lymphedema associated with trauma is a consequence of an infectious or inflammatory process.3

Mechanical injury of the soft tissues and bones of the extremities usually is followed by edema distal to the site and at the site itself but not proximal to it. Patients usually present with a sensation of fullness and pain in the affected area, induration, edema, hyperkeratosis, and xerosis. Functional limitations include decreased range of motion, joint inflexibility, decreased mobility (if the lower limb is affected), and decreased activities of daily living (eg, grooming and dressing).3

For several decades, treatments to relieve lymphedema and traumatic or postoperative edema included manual massage, gradient compression stockings and sleeves, bandaging, taping, and pneumatic compression devices previously referred to as lymphedema pumps. All of these treatments used external compression, but none produced consistently good clinical outcomes.

Additionally, these treatments used static compression strategies, with compression applied and held constant for varying lengths of time. Most of the lymphedema pumps were poorly bioengineered, and their designs lacked understanding of the optimum parameters for noninvasive compression.

Recently, the concept of pneumatic medicine was developed to more clearly characterize and advance the science of external compression strategies. As defined by Avery et al,5 pneumatic medicine is the use of noninvasive, dynamic compression to treat the array of peripheral vascular disorders, including arterial insufficiency, chronic wounds, venous insufficiency, and lymphedema.

The NormaTec PCD uses a multi-cell sleeve or boot that is placed on the affected limb and pneumatically inflated and deflated via a unique Peristalic Pulse dynamic compression strategy. The patented Peristalic Pulse pneumatic waveform consists of a “pulse, gradient hold, release” compression cycle, simulating normal physiology. It incorporates three major physiological concepts: dynamic pulsing compression as seen in the muscle pump of a normal limb, directionality of flow similar to the venous and lymphatic one-way valves, and the effective movement of fluids created by peristalsis. The parameters of the NormaTec PCD are programmed by the physician, and the patient then uses the device independently at home.
A full functional outcome for our patient, who had chronic, clinically significant symptoms, was achieved in a brief period of time after numerous other treatments failed. The Peristalic Pulse compression strategy dynamically decongested the edematous tissues, and her hand and wrist range of motion improved markedly. Our patient has continued to use the device approximately 1 hour per week as maintenance therapy to prevent the return of edema and upper extremity stiffness. No compression garment is required, and compliance with the treatment program has been excellent.

A pathological anomaly that may have been a causative agent in our patient’s proximal edema following reduction of her Colles fracture is complex regional pain syndrome. According to the literature, the incidence of patients with Colles fractures who develop complex regional pain syndrome, albeit controversial, ranges between 2% and 37%.6 Although the pathogenesis is poorly understood, complex regional pain syndrome commonly is triggered by minor injuries such as fractures, crush injuries, peripheral nerve injuries, and other precipitating events that involve abnormal sympathetic nervous system activity.

Complex regional pain syndrome is characterized by pain and tenderness that is described as burning or aching in nature and usually occurring at a distal extremity. Patients with complex regional pain syndrome may develop rapid bony demineralization, trophic skin changes, and vasomotor instability that also are disproportionate to the underlying injury.

Complex regional pain syndrome progresses through three clinical phases. The first phase is characterized by an intense burning pain, edema, warmth, and tenderness of a distal extremity, especially noted around the joints. The joints become stiff, and pain is reproduced on passive and active motion of the joint. During the second phase (3 to 6 months), the patient’s skin becomes thin, cool, and shiny. In the third phase (another 3 to 6 months), the skin becomes atrophic and dry, with progression to flexion contractures and palmar fibromatosis.3

To aid in the diagnosis of complex regional pain syndrome, plain radiographs of patients with fractures may exhibit spotty rarefaction (Sudeck atrophy). Other tests used to substantiate this diagnosis include thermography, bone scan, and sympathetic blockade.

The key component to successful conservative treatment is early diagnosis within 6 to 8 weeks. Conservative treatment modalities include heat, elevation, and desensitization. Chronic disability occurs when the diagnosis and subsequent treatment is delayed. However, some authors have suggested there is no correlation among age, adequacy or number of reductions, or severity of fracture in patients who present with complex regional pain syndrome.3 In our patient, we ruled out complex regional pain syndrome because electromyography, nerve conduction study, radiographs, intravenous Doppler study, duplex arterial scan, and technetium bone scan revealed no pathologic findings other than the fractured wrist.

Some patients present with this syndrome after age 40 years, with the highest incidence in the sixth decade of life. Some patients also present with this anomaly after requiring repeated fracture reductions. Itzchaki et al2 suggested there may be a psychogenic component to this syndrome. Emotional instability was identified in one third of patients with this syndrome.2
Other causes of lymphedema were evaluated extensively in our patient. Local, regional, and metastatic causes such as breast cancer and Pancoast tumor were ruled out as were mechanical dysfunctions such as thoracic outlet syndrome and Milroy disease. Neurological involvement also was ruled out based on normal electroencephalographic readings and nonpathological clinical and physical findings.

The surgical procedure in our patient was uncomplicated and thus lymphedema secondary to any vascular injury was ruled out. Questions that need to be addressed are whether the lymphedema was locally or systemically mediated, or whether the onset of the fracture induced an avascular anastomosis that led to the lymphedema. Our conclusions led us to believe the development of lymphedema of the distal radius following Colles fracture was idiopathic in our patient.

References

Norton S. Managing lymphedema. Advance. 2000; 11(10):1-6. Itzchaki M, Ben-Hur N, Ashur H. Lymphedema of the hand following a fracture of the distal radius. Int Surg. 1978; 63(1):29-30. Patel AT. Lymphedema. In: Frontera WR, Silver JK, eds. Essentials of Physical Medicine and Rehabilitation. 1st ed. Philadelphia, PA: Hanley and Belfus; 2002:575-577. St Louis JD, McCann RL. Lymphatic System. In: Townsend CM, ed. Sabiston Textbook of Surgery. 16th ed. Philadelphia, PA: WB Saunders Co; 2001:1446-1450. Avery KB, Solomon AD, Weber RB, Jacobs LF. Treatment of congenital lymphoedema with sequential intermittent pneumatic compression therapy. The Foot. 2000; 10(4):210-215. Stern PJ, Derr RG. Non-osseous complications following distal radius fractures. Iowa Orthop J. 1993; 13:63-69. Authors Drs Kasper and Meller are from the Department of Orthopedic Surgery, Veterans Hospital, University of Pennsylvania, Philadelphia, Pennsylvania.

Drs Kasper and Meller have no relevant financial relationships to disclose.

Correspondence should be addressed to: Menachem M. Meller, MD, PhD, Department of Orthopedic Surgery, Veterans Hospital, University of Pennsylvania, 424 Stemmler Hall, Philadelphia, PA 19104-6081.

OrthoSuperSite