Solaris vest denied, going to appeal

Tina, so they won't cover head and neck and groin LE??

I know when Binney has been faced with this, she sends over NLN guidelines, and on the SUSO site for truncal/breast LE, there's a very graphic article that I'd send over in full color

http://www.stepup-speakout.org/breast_chest_trunckal_lymphedema.htm

Yesterday, I reviewed the UptoDate page on LE, and it has good references: it's subscriber only, but you can use it to educate the doctor

:Lymphedema: Etiology, clinical manifestations, and diagnosis
Authors
Emile R Mohler, III, MD
Tammy E Mondry, DPT, MSRS, CLT-LANA
Section Editor
Julie R Gralow, MD
Deputy Editors
Diane MF Savarese, MD
Susan E Pories, MD, FACS

Disclosures
Last literature review version 19.2: May 2011 | This topic last updated: April 27, 2011

INTRODUCTION - Edema is defined as a palpable swelling produced by expansion of the interstitial fluid volume. A variety of common clinical conditions are associated with the development of edema, including heart failure, cirrhosis, nephrotic syndrome, and renal failure (table 1).

A less common form of edema is lymphedema, which is due to an abnormality in the lymphatic system, often involves one limb, and is generally irreversible (table 2). The most common cause is interruption of the axillary lymphatic system by surgery and/or radiation therapy in women with breast cancer, resulting in the development of arm edema.

The etiology, clinical manifestations, and diagnosis of lymphedema will be reviewed here, beginning with a summary of the anatomy of the lymphatic system and its role in the maintenance of fluid balance. Prevention and treatment of lymphedema and an overview of the pathophysiology and etiology of edema are presented separately. (See "Lymphedema: Prevention and treatment" and "Pathophysiology and etiology of edema in adults".)

PHYSIOLOGY OF LYMPH FLOW - The normal capillary circulation has a small gradient favoring filtration across the capillary wall into the interstitium that varies in magnitude in different organs. There is also a variable permeability to proteins, resulting in some protein movement into the interstitium. (See "Pathophysiology and etiology of edema in adults", section on 'Capillary hemodynamics'.)

The filtered, protein-enriched fluid that does not reenter the capillaries is returned to the systemic circulation by the lymphatic system [1-3]. Unlike the high pressures in the systemic circulation, lymph flow takes place in a low pressure system. Uptake of interstitial fluid begins in initial lymphatic vessels (lymphatic capillaries and precollectors) that abut the interstitial space. This process is facilitated by local arterial pulsation, skeletal muscle contraction, and unidirectional valves that prevent backward flow. The initial lymphatics merge into vessels of increasing caliber that become equipped with a smooth muscle coat that, via contraction, promotes peristaltic movement of the lymph fluid.

In the extremities, there is a superficial lymphatic system that drains the skin and subcutaneous tissue and a deep system that drains subfascial structures such as muscle and bone [2,4]. The two systems of the upper extremities merge in the axilla and the two systems of the lower extremities merge in the pelvis.

The major lymph vessels eventually drain into the central venous circulation. The lymph draining from both lower extremities, the gastrointestinal tract, and the left upper body (upper extremity, chest wall, upper back, shoulder, and breast) enter the venous circulation through the thoracic duct, which opens into the left venous angle between the left subclavian vein and left internal jugular vein (figure 1) [2]. The lymph draining from the right upper body drains into the right venous angle via the right lymphatic duct.

PATHOGENESIS

Edema - Edema results from an imbalance between the rate of lymph production (which reflects fluid movement out of the capillary) and the rate of return of the lymphatic fluid to the systemic circulation [1]. In the common edematous states, such as heart failure, cirrhosis, nephrotic syndrome, and renal failure, the primary problem is increased fluid movement out of the capillary due to increased venous pressure, hypoalbuminemia, or, less often, enhanced capillary permeability. In addition, enhanced capillary filtration due to increased venous pressure is responsible for localized edema due to chronic venous disease. Lymphatic flow and contractility increase in the presence of tissue edema, which then leads to removal of some of the excess interstitial fluid. (See "Pathophysiology and etiology of edema in adults", section on 'Edema formation' and "Pathophysiology and etiology of edema in adults", section on 'Safety factors' and "Clinical evaluation of lower extremity chronic venous disease".)

Lymphedema - In contrast, the major defect in most patients with lymphedema is impaired lymphatic transport due to lymphatic obliteration, as occurs with primary (hereditary) lymphatic malformations and after cancer treatments such as lymph node dissection and radiation therapy (RT) [1,3,5]. As a result, some of the filtered fluid that does not reenter the capillaries cannot be returned to the systemic circulation by the lymphatic vessels and accumulates in the interstitium. The rate of capillary filtration is normal in patients with lymphedema, not increased as in the generalized edema states [3].

ETIOLOGY AND RISK FACTORS - The major causes of lymphedema are generally classified as primary (hereditary) or secondary (acquired), which are much more common (table 2) [1-6].

Causes of secondary lymphedema - There are a number of acquired causes of lymphedema including axillary or inguinal lymph node dissection and/or radiation, malignant obstruction, and infection. Lymph node dissection and/or radiation for breast cancer and melanoma is the most common cause in developed countries, while filariasis is the most common cause worldwide.

The increasing prevalence of lymphedema in developed countries is largely due to lymph node dissection and/or radiation therapy for malignant disease [1,4,6-8]. In a review from the Stanford Lymphedema Center, which sees approximately 200 new cases of lymphedema per year, approximately 75 percent were due to malignancy or its therapy, one-half of which were related to breast cancer surgery [4].

The likelihood of developing lymphedema after axillary or inguinal node dissection is related to several factors including the number of lymph nodes removed, the extent of surgery, tumor location, local radiation therapy, delayed wound healing, postoperative infection, the development of hematoma or seroma, and obesity [8]. Examples include a swollen arm occurring after lymph node dissection for breast cancer, swollen limbs following lymph node dissection or radiation in the pelvic region for gynecologic and urologic malignancies, and face and neck swelling after treatment of head and neck cancer. Lymphedema may also result from a tumor causing lymphatic obstruction or from progressive obliteration of lymphangioles due to chronic inflammation. (See "Classic Kaposi's sarcoma: Clinical features, staging, diagnosis, and treatment", section on 'Skin lesions' and "Complications of gynecologic surgery", section on 'lymphedema and lymphocyst'.)

Breast cancer therapy - The major cause of secondary lymphedema in developed countries is interruption of the axillary lymphatic system by surgery and/or RT in women with breast cancer, resulting in the development of ipsilateral arm edema [1,7].

The overall rate of arm edema is approximately 20 to 25 percent in women undergoing breast cancer surgery [7]. However, the rate varies substantially with the lymph node procedure that is performed and whether RT is used, but does not appear to differ between mastectomy versus breast conserving surgery [9]. The rate can be reduced by limiting the use and extent of axillary lymph node dissection (ALND) and the performance of sentinel lymph node biopsy (SLNB) to identify women who do not need a full ALND [7,10-16].

The potential reduction in lymphedema with SLNB was illustrated in a randomized trial in which 298 patients with early breast cancer who were clinically node negative were assigned to ALND or to SLNB (followed by ALND if subsequently positive) [13]. At one year, the SLNB group had a significantly smaller increase in arm volume (14 versus 56 mL) and were significantly less likely to develop subjective lymphedema (odds ratio 0.36, 95% CI 0.15-0.86). There was a greater reduction in the likelihood of developing subjective lymphedema in the node-negative SLNB patients who did not undergo ALND (odds ratio 0.20, 95% CI 0.03-0.75).

The incidence of lymphedema is also significantly lower in patients who undergo SLNB alone compared to those who undergo SLNB followed by ALND (7 versus 14 percent in a randomized trial) [14,15]. In a multicenter American College of Surgeons Oncology Group trial in which the procedure was performed by a wide range of surgeons, the rate of lymphedema after SLNB alone is also low [17]. Similar findings have been noted in other studies [14-16].

The timing of the completion ALND in patients with a positive SLNB (during the SLNB or delayed in another procedure) does not appear to affect the incidence of lymphedema [18].

The rate of lymphedema is increased when axillary lymph node surgery is combined with axillary RT [7,10]. In a 2001 literature review, lymphedema was much more likely in women who underwent surgery followed by axillary RT compared to surgery alone (average 41 versus 17 percent) [7]. The rate is highest in patients who underwent full ALND plus axillary RT (38 and 55 percent in two series) [19,20]. However, the field of RT is also important, with less lymphedema developing in women treated with breast irradiation than those treated with breast and axillary RT, for example [21,22].

The incidence of arm edema increases over time, which in part reflects chronic inflammatory changes that produce both subcutaneous and lymph vessel fibrosis. In one report, for example, the incidence of lymphedema in patients who underwent full ALND plus axillary radiation was 36 percent at one year and 55 percent at two years [20]. Older age, obesity, supraclavicular irradiation, and extremity injury, such as inflammatory arthritis, also appear to increase the risk of developing lymphedema and the risk of it progressing [23-25]. (See 'Inflammatory arthritis' below and 'Obesity' below.)

The ipsilateral breast and trunk are also at risk for the development of secondary lymphedema. The incidence rate for breast lymphedema is 6 percent with lumpectomy alone, 23 percent when SLNB and RT are combined, and 6 to 48 percent when both ALND and RT are performed [26].

Melanoma therapy - Lymphedema is a problem after axillary or inguinal lymph node dissection in patients with melanoma [8]. Avoiding deep groin dissection, if possible, can markedly reduce the incidence of lymphedema. However, even sentinel lymph node biopsy has been associated with the development of lymphedema, occurring in 5 of 235 patients (1.7 percent) in one series [27]. (See "Evaluation and treatment of regional lymph nodes in melanoma", section on 'Extent of dissection and morbidity'.)

Infection - Infectious causes of lymphedema are more common in tropical and subtropical regions. Lymphedema in developing countries is most often related to lymphatic obstruction from parasitic infections, with filariasis being the most common cause worldwide [3,6]. Lymphedema may be a complication of recurrent erysipelas in patients with contact dermatitis [28]. (See "Epidemiology, pathogenesis, and clinical features of lymphatic filariasis", section on 'Lymphedema' and "Cellulitis and erysipelas", section on 'Recurrent cellulitis'.)

Inflammatory arthritis - Upper or lower extremity lymphedema, sometimes bilateral, is a rare extra-articular manifestation of inflammatory joint disease, most often rheumatoid arthritis or psoriatic arthritis [29-35]. The mechanism of lymphedema is not known, but inflammatory synovitis leading to fibrosis of lymph vessels has been proposed [36]. In some patients, the lymphedema improves with effective treatment of the arthritis [34-36]. (See "Overview of the systemic and nonarticular manifestations of rheumatoid arthritis", section on 'Lymphatic obstruction' and "Clinical manifestations and diagnosis of psoriatic arthritis".)

A similar clinical appearance in the absence of lymphoscintigraphic evidence of impaired lymphatic function may be caused by extensive tenosynovitis in patients with psoriatic arthritis [33].

Obesity - Obesity may be associated with massive localized lymphedema and also can exacerbate breast cancer related lymphedema (figure 2) [37-39].

Causes of primary lymphedema - There are three categories of primary lymphedema that are classified by their age at onset: congenital lymphedema (less than one year), lymphedema praecox (1 to 35 years), and lymphedema tarda (more than 35 years) [3,40,41]. The estimated prevalence is 1:6000 to 1:10,000 live births [1].

Congenital lymphedema and VEGFR-3 - Congenital lymphedema is a rare disorder that is characterized by lymphatic malformation at birth. One cause is Milroy disease (also called congenital hereditary lymphedema, primary congenital lymphedema, or hereditary lymphedema type I), which may also be associated with intestinal lymphangiectasia and cholestasis. It is transmitted as an autosomal dominant trait.

The defect in most families with congenital hereditary lymphedema involves the gene (located at 5q35.3) that encodes for vascular endothelial growth factor receptor-3 (VEGFR-3, FLT4) [42-44]. VEGFR-3 is expressed in the lymphatic endothelium, plays an important role in lymphatic development, and is activated after binding to VEGF-C and VEGF-D. The importance of this pathway is illustrated by the observation that in transgenic mice that express soluble VEGFR-3, an inhibitor of VEGF signaling, lymphangiogenesis is impaired and lymphedema results [45]. In humans, missense mutations of VEGFR-3 prevent normal lymphatic growth [44].

The VEGFR-3 pathway also may play an important role in tumor lymphangiogenesis and subsequent metastasis [46-48]. As an example, VEGF-C is overexpressed in some breast cancer cells, promoting both intratumoral lymphangiogenesis and metastases to the regional lymph nodes and lungs [46]. In one study, VEGF-C expression was detectable in some node-positive breast cancers but not in node-negative tumors [48]. In contrast, VEGF ligands to VEGFR-2 do not stimulate lymphangiogenesis [47].

In addition to Milroy disease, congenital lymphedema can also occur in a variety of other hereditary disorders with variable modes of transmission [1]. These include:

X-linked - Turner syndrome in which lymphedema is the key to diagnosis in girls presenting in infancy [49,50]. Turner syndrome should be considered if two or more of the following dysmorphic features are present: webbed neck, nail dysplasia, high palate, and short fourth metacarpal [49]. (See "Clinical manifestations and diagnosis of Turner syndrome (gonadal dysgenesis)".)
Autosomal dominant - Noonan syndrome, which is characterized by dysmorphic features, proportionate short stature, and heart disease, most commonly pulmonic stenosis and hypertrophic cardiomyopathy [51]. (See "Clinical manifestations and diagnosis of pulmonic stenosis", section on 'Etiology'.)

Lymphedema praecox - Lymphedema praecox describes primary lymphedema that typically becomes clinically apparent at or near puberty, although the age at presentation ranges from 1 to 35 years [3]. Meige disease is an autosomal dominant disorder that usually has an onset at or around puberty, and mostly affects the lower limbs [52-55]. The lymphedema-distichiasis syndrome, in which pubertal-onset primary lymphedema is associated with aberrant eyelashes (distichiasis), and some other lymphedema phenotypes appear to result from mutations in the forkhead transcription factor, FOXC2 gene (located at 16q24.3), which encodes for a transcription factor [55-57].

The impairment in lymphatic function with FOXC2 mutations results from agenesis of lymphatic valves that normally prevent lymphatic backflow and from enhanced recruitment of vascular mural cells to lymphatic capillaries that may also impair lymphatic flow [58]. FOXC2 is also highly expressed in venous valves, which could explain why approximately one-half of patients with lymphedema-distichiasis also have venous insufficiency and incompetent venous valves [59].

Lymphedema tarda - Lymphedema tarda has, by definition, an onset after 35 years of age [3]. Occasional families with hereditary lymphedema present at this time, with some patients developing lymphangiosarcoma [60]. (See 'Lymphangiosarcoma' below.)

CLINICAL MANIFESTATIONS - The clinical manifestations of lymphedema are different in secondary and primary lymphedema. Secondary lymphedema typically involves a single limb (ie, unilateral edema), while more widespread involvement may be seen in primary lymphedema.

Secondary lymphedema - Secondary lymphedema, as with lymph node dissection and/or radiation, is typically characterized by slowly progressive ipsilateral swelling of an arm following axillary node dissection or a leg following inguinal node dissection [4]. The swelling may first be apparent only in the proximal portion of the limb, or it can affect only a portion of the distal limb including the digits.

Among women with breast cancer, there may also be swelling over the ipsilateral breast and/or upper chest wall. Other manifestations include a feeling of heaviness, tightness, aching or discomfort in the limb, and restricted range of motion.

Secondary lymphedema in other disorders may involve more than a single limb. In rheumatoid arthritis, for example, involvement of a single limb may be most common, but both the upper and lower limbs may be affected and cases of symmetrical swelling have been reported [29-31]. Similar findings have been described with psoriatic arthritis [35]. (See "Overview of the systemic and nonarticular manifestations of rheumatoid arthritis", section on 'Lymphatic obstruction'.)

The onset of secondary lymphedema is usually insidious. Affected patients may initially experience aching pain at the affected area and a sense of heaviness or fullness of the limb. At this stage, lymphedema is typically soft and pitting in nature. Over time, the skin becomes dry and firm with less pitting and is fibrous to palpation. (See 'Classification' below.)

The clinical hallmark of more severe lymphedema is the presence of cutaneous and subcutaneous thickening, as manifested by cutaneous fibrosis, peau d'orange, and a positive Stemmer sign, which refers to the examiner being unable to tent (ie, lift) the skin at the base of the upper surface of the digits, usually the second toe or finger, in the affected extremity (figure 3) [1]. These findings as well as localized involvement are clearly different from those in generalized edematous states, such as heart failure and the nephrotic syndrome (table 3). (See "Clinical manifestations and diagnosis of edema in adults".)

Primary lymphedema - The primary forms of lymphedema have a relative lack of fibrosis that permits greater amounts of edema to form than in secondary disease [61]. (See 'Causes of primary lymphedema' above.)

The sites of involvement in primary lymphedema vary with the cause:

Congenital lymphedema tends to involve one or both lower extremities, but can also involve the upper extremities, and even the face [3,55].
Lymphedema praecox is usually confined to the lower extremities (particularly the foot and calf); however, involvement limited to one upper extremity has been described [3,53,55].
Lymphedema tarda most often involves both lower extremities [62,63].

Classification - Several groups have developed classification schemes to describe the severity of lymphedema [2,5,64,65]. The classification scheme of the International Society of Lymphology involves two criteria to diagnose and classify lymphedema: the "softness" or "firmness" of the limb (reflecting fibrotic soft tissue changes); and the outcome after 24 hours of elevation [5].

Pitting is variable in patients with lymphedema. Pitting reflects movement of the excess interstitial water in response to pressure. Testing for pitting involves applying firm pressure to the edematous tissue for at least five seconds. If an indentation remains after the pressure is released, pitting edema is present.

Stage I - Stage I is characterized by the accumulation of fluid that has a relative high protein content (in comparison with "venous" edema) and that subsides with 24-hour limb elevation (figure 4). The appearance is that of soft edema that may pit, with no fibrosis. This is sometimes called reversible edema.
Stage II - In stage II (also called spontaneously irreversible lymphedema), 24-hour limb elevation alone rarely reduces soft tissue swelling (figure 5). Late in stage II, the limb may not pit as fibrosis progresses.
Stage III - Stage III is characterized by lymphostatic elephantiasis, where pitting is absent, and by trophic skin changes such as fat deposits, acanthosis, and warty overgrowths (figure 3).

Within each stage, severity based upon volume differences can be assessed as minimal (<20 percent increase), moderate (20 to 40 percent increase), or severe (>40 percent increase). (See 'Limb circumference and volume' below.)

An increasing number of lymphologists recognize an earlier stage of lymphedema, termed stage 0, which refers to a subclinical or latent condition where swelling is not evident despite impaired lymphatic transport [2,5]. Most patients are asymptomatic, but some report a feeling of heaviness in the limb. Stage 0 may exist for months or years before the onset of overt lymphedema [5].

The American Physical Therapy Association (APTA) uses girth as an anthropometric measurement to classify lymphedema. The maximum girth difference between the affected and unaffected limb is used to determine the class of lymphedema. Mild lymphedema is a maximum girth difference of less than 3 centimeters (cm); moderate lymphedema is 3 to 5 cm differential; and severe lymphedema is a differential of greater than 5 cm [66].

Another classification scheme, the National Cancer Institute Common Terminology Criteria for Adverse Events (CTCAE), is based upon both the response to limb elevation and the presence of functional impairment [67].

Complications - The clinical manifestations of lymphedema may be affected by confounding conditions such as venous insufficiency, morbid obesity, and occult trauma [5]. In addition, cellulitis and lymphangiosarcoma are potential complications and psychosocial morbidity is common.

Skin infection - Lymphedematous skin is at risk for breakdown and subsequent infection, which may be recurrent and due in part to the protein-rich lymph providing a medium for bacterial growth. The types of infection include cellulitis, erysipelas, and lymphangitis [3,68-72].

Cellulitis is a well described complication of lymphedema, particularly in patients who have undergone axillary or inguinal lymph node dissection. The development of cellulitis is related to impaired lymphatic function, and lymphedema (even if subclinical) is a risk factor [73,74]. Typical manifestations include erythema, pain, and tenderness; systemic signs, such as fever, may not be present. In addition, lymphedema can masquerade as infectious cellulitis [75].

The range of motion of the infected limb may become restricted and interfere with lifestyle. The texture of the skin may also change and become hyperkeratotic with verrucous and vesicular skin lesions. These lesions are characteristically associated with elephantiasis.

Lymphangiosarcoma - A rare secondary malignant tumor, called lymphangiosarcoma, can occur in patients with chronic lymphedema, usually those with massive and protracted edema [76]. It is classically seen in the postmastectomy, lymphedematous arm (Stewart-Treves syndrome) [77-79]. It has also been described with primary lymphedema and chronic filarial lymphedema [60,80,81].

The tumor originates in vascular endothelial cells within chronic lymphedema, not the lymphatic vessels [78]. It may initially appear as blue-red or purple skin lesions with a macular or papular shape. Multiple lesions are common and subcutaneous nodules may appear. Such skin lesions should be carefully evaluated in patients with chronic lymphedema. (See "Pathogenetic factors in soft tissue and bone sarcomas" and "Breast sarcomas".)

Quality of life - Lymphedema results in psychological morbidity and a reduced quality of life including aspects of emotional, functional, physical and social well being [82,83]. Psychological problems seen in women with chronic lymphedema after treatment for breast cancer include anxiety, depression, sexual dysfunction, social avoidance, and exacerbation of existing psychiatric illness.

DIAGNOSIS

General principles - The diagnosis of lymphedema is largely based upon the history and physical examination. Careful measurements are necessary since patients often perceive a greater degree of lymphedema than detected by direct measurement [15,84].

In adults, the presence of secondary lymphedema is usually suggested by the following findings:

Localized rather than generalized edema. The edema is typically characterized by slowly progressive ipsilateral (unilateral) swelling of an arm following axillary node dissection or a leg following inguinal node dissection [4]. Other causes of localized limb swelling, such as deep vein thrombosis, malignancy (which may obstruct proximal lymphatic vessels), and infection should be evaluated with appropriate studies. Patients in endemic areas should be tested for filarial infection. (See "Diagnosis, treatment, and prevention of lymphatic filariasis".)
A history of a trauma or cancer treatment, such as axillary or inguinal lymph node dissection and/or RT, and the absence of a cause of generalized edema (eg, heart failure, nephrotic syndrome). (See 'Secondary lymphedema' above.)
A positive Stemmer sign in which the examiner is unable to lift the skin, or has difficulty lifting the skin of the dorsum of the fingers or toes as compared to the contralateral limb. It is possible to have a false negative Stemmer sign, but there cannot be a false positive sign. A positive Stemmer sign is always indicative of lymphedema [85].
A unique finding in lymphedema is the presence of cutaneous and subcutaneous thickening which are not present in patients with stage I and early stage II disease [1]. (See 'Clinical manifestations' above and 'Classification' above.)

The edema should be classified as pitting or nonpitting. Pitting reflects movement of the excess interstitial water in response to pressure. Testing for pitting involves applying firm pressure to the edematous tissue for at least five seconds. If an indentation remains after the pressure is released, pitting edema is present.

Nonpitting edema is suggestive of lymphedema or venous insufficiency. However, the presence of pitting does NOT exclude lymphedema since, as noted above, pitting is present in lymphedema patients with stage I disease and in some with stage II disease. (See 'Classification' above and "Clinical manifestations and diagnosis of edema in adults", section on 'Venous insufficiency or thrombosis' and "Clinical manifestations and diagnosis of edema in adults", section on 'Nonpitting edema'.)

Occasional patients have both lymphedema and generalized edema, such as breast cancer patients who have undergone axillary lymph node dissection and have heart failure as a result of treatment with cardiotoxic agents (trastuzumab or doxorubicin). In this setting, concurrent lymphedema is suggested by more prominent swelling in the ipsilateral arm. (See "Cardiotoxicity of trastuzumab" and "Cardiotoxicity of anthracycline-like chemotherapy agents".)

Limb circumference and volume - Measurements of limb circumference and volume are common methods used for the diagnosis of limb edema and for monitoring during and after therapy, particularly arm edema in patients with breast cancer [5]. Arm volume can be measured by the water displacement method or estimated by taking several circumferential measurements at standard distances [9,86,87].

Circumferential measurements, at the same points on the affected and contralateral arm, are a simple and inexpensive method to estimate edema. Measurements in the arm are made at four points: the metacarpal-phalangeal joints, the wrists, 10 cm distal to the lateral epicondyles, and 15 cm proximal to the lateral epicondyles [88]. A difference of more than 2 cm between the affected and contralateral arm is considered clinically significant. Changes in arm circumference may be more difficult to detect in obese women and are subject to variation related to differences in muscle mass due to hand dominance (which can be avoided by taking circumferential measurements of both arms at baseline) and shifting of fluid proximally or distally due to arm positioning and/or compression.

Water displacement detects changes in arm volume of less than 1 percent, and a volume difference of 200 mL or more between the affected and opposite arms is typically considered as a cutoff point to define lymphedema [9,19,87]. Standard model water displacement arm volumeters are large, prone to leaks, and expensive. An alternative, home-made, and smaller device has been developed that is as accurate and is suitable for home or office use (figure 6 and table 3) [89].

Measurement of arm volume rather than arm circumference has been used in some of the clinical trials that tested treatment strategies for arm edema. However, it is not clear if there is an advantage to following arm volume rather than arm circumference. Although there is some evidence that measurement of arm volume is a more accurate diagnostic test, particularly with leg edema, circumferential measurements have shown a high correlation with the water displacement method [9,86,87].

Imaging - Imaging of the lymphatic system is usually not necessary to confirm the diagnosis of lymphedema if the diagnosis is obvious. If imaging is performed to distinguish lymphedema from nonlymphatic causes of edema, lymphoscintigraphy (radionuclide imaging) is the preferred test [4,90-92] and has largely replaced lymphangiography, which is more invasive and technically difficult [4,92].

Lymphoscintigraphy - With lymphoscintigraphy, radioactive tracers are injected subcutaneously or intradermally in the web space of the upper or lower extremities [4]. Imaging is performed at 30 to 60 minutes after injection. The patient then performs a stress activity (such as walking, massage, or squeezing a ball for about 20 minutes), which is followed by repeat imaging. Criteria for impaired lymphatic function include delayed, asymmetric, or absent visualization of the regional lymph nodes and dermal backflow [4].

The protocol for lymphoscintigraphy is not standardized and differs among major centers. Quantitation of regional lymph node accumulation of the tracer appears to be more sensitive than qualitative lymphoscintigraphy (100 versus 70 percent in a series of 219 patients with secondary or primary lymphedema) [92]. All cases missed with qualitative lymphoscintigraphy were mild grade I disease. (See 'Classification' above.)

MRI and CT - Other imaging techniques, such as magnetic resonance imaging and computerized tomography, may complement information obtained via lymphoscintigraphy [1]. Such imaging provides anatomic and nodal detail that is otherwise not available. These techniques are most helpful in ruling out obstructive causes of lymphedema, such a cancer recurrence in a nodal region.

Bioimpedance spectroscopy - Bioimpedance spectroscopy is a reliable and accurate tool to determine arm volume by comparing the composition of fluid compartments using resistance to electrical current [93-96]. It has been mostly used to evaluate arm edema in patients with breast cancer [97], but impedance ratio thresholds for lymphedema of the legs have also been established [98].

Although BIS has not been widely used, at least in the US, the US FDA has approved BIS for lymphedema assessment and the procedure has received a category III CPT code. It remains to be seen whether BIS will now receive wider clinical application.

Optoelectronic volumetry - Volume measurements can also be assessed utilizing an infrared optoelectronic assessment. This is a computerized analysis that uses infrared beams to scan the limb and calculate a volume. The optoelectronic volumetry method has been found to have better reliability than water displacement volumetry in the measurement of upper extremity lymphedema [99,100].

INFORMATION FOR PATIENTS - UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Beyond the Basics topics (see "Patient information: Lymphedema after breast cancer surgery")

SUMMARY - Lymphedema is caused by impaired lymphatic transport due to lymphatic obliteration, which occurs with lymphatic malformations, lymphatic surgery or radiation, and certain infections such as filariasis. These mechanisms are different from the mechanisms of edema in generalized edematous states such as heart failure, cirrhosis, and nephrotic syndrome.

There are two types of lymphedema: primary (or hereditary) and secondary (or acquired).

Primary lymphedema is classified by age of onset and includes congenital lymphedema, lymphedema praecox, and lymphedema tarda. (See 'Causes of primary lymphedema' above.)
The major cause of secondary lymphedema in developed countries is interruption of the lymphatic system by surgery and/or radiation in the treatment of breast cancer and melanoma. Other causes of secondary lymphedema include obstruction by tumor, infection (filariasis), recurrent cellulitis, and connective tissue disease. (See 'Causes of secondary lymphedema' above.)
The risk of developing lymphedema in women undergoing treatment for breast cancer can be minimized by limiting the use and extent of axillary lymph node dissection (ALND) and axillary radiation therapy (RT). The incidence of lymphedema with sentinel lymph node biopsy (SLNB) is significantly lower than with ALND. (See 'Breast cancer therapy' above.)
The diagnosis of lymphedema is largely based upon the history and physical examination. In adults, the presence of secondary lymphedema is usually suggested by localized rather than generalized edema, the presence of cutaneous and subcutaneous thickening, a positive Stemmer sign, and a history of an appropriate cause. (See 'Clinical manifestations' above and 'Diagnosis' above.)
The measurement of limb circumference is a common method used for the diagnosis of lymphedema in women with breast cancer. Imaging of the lymphatic system is usually not necessary if the diagnosis is obvious. (See 'Diagnosis' above.)

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Binney innudates with data--also, maybe call Solaris, they should be able to help.

Kira

Tina, Bob Weiss has researched the issue of saving overall for initial investment in therapy and garments and has a lot of documentation about it. If it would help you approach the insurance people, do get in contact with him. He's very responsive.

Tina, I'm so sorry about the appeal denial. No, I'm angry. This should not be so difficult!

Big hugs, and Kay has brownies she's giving away today -- help yourself!
Binney

Tina~

I've had a couple of tests done by Mayo that were denied by Anthem-Blue Cross, Blue Shield that I went on to appeal. 

The first time my doctor sent the letter of recommendation, etc. to the insurance company.  Of course they claimed it never was sent.  My doctor's assistant kept trying to call and even did a 3-way conference call with me on it to show that they kept leaving messages and no one would return calls.  I was so sick of the hassle and after nine month, I said screw it.

The next time; however, I did the appeal process myself.  My doctor sent me a letter of medical necessity, I wrote my opinion on why it should be covered.  I followed all the instructions on the back of the EOB for the appeal process.

I sent it to BCBS via certified mail, so I had proof that they received it.  Then I received a letter from an appeals representative letting me know the status and her contact info.  I picked up the phone and called the rep immediately.   I very nicely let her know that I would be fighting it to the end and would take it on to the State if appeal was denied.  They have to complete the appeals process and respond back to you with the answer within 60 or 90 days (I have to check that again). 

Anyway, I won my last appeal !!!  Of course, they waited until the very last day to call me to let me know.

It was the most ridiculous bullshit I've ever dealt with because the test they denied was so obviously necessary, a Mayo doc is giving a thorough letter of necessity, and the time and money the insurance company spent to deny a $300 test was much more than the cost of the test!!!  I swear they randomly just deny things and hope the patients just pay it.  It is a freakin' hassle.

I have a 3-ring notebook that I meticulously track all my EOBs, itemized statements, invoices, etc.  I even have a tab for "Appeals." 

I wish you much luck with your appeal -- and please don't give up -- but try not to get too stressed out over it either.

When I get my BCBS EOBs in the mail, I have to BREATHE before I open them. 

Tina, I'm assuming that's the "retail" cost of the vest, the insurance company will "allow" a lesser amount.

The garment manufacturers mark up their products by 100%--wholesale to the supplier is half the amount quoted. 

Excellent point from LisaAlissa!

Kira

If you ladies are interested, there's a write-to-Washington effort organized by some women on another thread. The idea is to send a letter to the president, speaker Boehner, your senator, your representative, etc.--whoever you would like to 'talk' to, on a topic of your choice, related to your interests as a breast cancer survivor. Monday is the target mailing date, with letters ideally being sent in a pink envelope, just as an attention grabber.  You could certainly lobby for more sane healthcare payment systems/methods/coverages.  Consensus on any topic or position is not an objective, and the goal is simply to put our collective interests on the political radar screen.  I am participating and have a letter ready to go.  Hard to say that anything tangible will come of it, but for a few minutes' time and a few pennies for postage, it does feel good to vent in some official manner.

Tina, coverage issues specific to LE are a great topic for capturing in a story at www.lymphedemaspeaks.com.  That is, if you have time and heart to package your story up for the advocacy story site.  You must be feeling very discouraged.  Pinkheart and garnet, you too.  Paying for life-saving and other necessary health care sure can mess up a life plan.  I am sure sorry that anyone has to take these kinds of financial sucker punches.  Just. Not. Right.

Carol

Tina, and they pay for all sorts of unproven surgeries--knee surgery for osteoarthritis, without batting an eyelash.

this is flat out ridiculous.

There is no research, because there's no funding. That's the limit of of evidence based medicine, either garbage in/garbage out or lack of study. So go with clinical knowledge and the best care of the patient.....

Kira

Tina, Your tenacity is really spectacular here!  I love it that you are are able to turn frustration into motivation to keep on pushing.  Keep us posted on your progress.  I admire you so much!  --Carol

Tina, it's really criminal that this process is so overwhelming.  And it sure is wonderful that Mr. Weiss is willing and can find the time to be such an amazing advocate.  You still have had to do your part, though.  Not everyone would have the organization and patience to provide him with the amount of information I bet you had to collect so he could document his presentation.  But you are right...we all owe him a huge 'thank you' for his help. As Binney said, it benefits us all.

I know you said that the research articles are practically zip.  I am building a library of LE -related articles on all manner of topics.  If you have links to any of the articles you located, can you put them in a post? 

Carol 

Thank you, Tina.  That would be great.

Tina, wow! They caved! I'm happy for you and for all of us. THANK YOU!
Binney

mmmmm....brownies!