Manual Lymph Drainage in a Patient with Congestive Heart Failure: A Case Study

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Ostomy Wound Management 2015;61(10):38–45
Madeline M. Vaassen, PT, DPT, GCS, CLT

Abstract

A variety of conditions result in lower extremity edema, such as deep vein thrombosis, cellulitis, venous stasis insufficiency, and congestive heart failure (CHF). A case study is presented to illustrate the dynamics of the lymphatic system, the pathology of CHF, the importance of obtaining a pretreatment differential diagnosis, and how to implement a safe treatment plan.

The patient was a 69-year-old overweight woman with bilateral lower extremity lymphedema of almost equal volume (~9,100 mL) of >2 months’ duration. She had 11 draining wounds and a reported history of chronic obstructive pulmonary disease (COPD) but no cardiac dysfunction. Treatment consisted of 6 sessions of manual lymph drainage (MLD), remedial exercises, and compression wrapping and weekly volumetric measurements over a period of 3 weeks. A 4-L decrease in lower extremity edema volume was noted, but fatigue and shortness of breath increased markedly. Treatment was discontinued and the patient was referred back to her physician for cardiac evaluation and treatment. The literature suggests patients, as well as health care professionals, do not always distinguish CHF symptoms from COPD. Proper assessment, monitoring, and lymphedema treatment adjustments are paramount to providing safe care for patients with signs and symptoms of COPD and suspected CHF. More research to elucidate best practice approaches in patients with lymphedema and concurrent CHF/COPD before the start of MLD treatment is warranted.

 

Lymphedema is an accumulation of protein-rich fluid that can be present for a number of reasons, including damage to the lymphatic network as a result of trauma, removal of lymph nodes, and genetics, as in the case of some primary lymphedema syndromes.1 A patient with lymphedema may have swelling in the trunk, face/neck, genitals, or extremities as a result of compromised lymphatic flow pursuant to lymph node removal, trauma, or a possible genetic predisposition.

As of 2002, a literature review of more than 1,900 references to determine the incidence of both primary and secondary types of the condition in the United States Medicare age group (65+) showed lymphedema affected upwards of 6.8 million individuals.2 Research, by literature review, is underway to determine the incidence in the nonMedicare-age group population, specifically persons with breast cancer, trauma, and primary lymphedema, but currently collection of these data by an online website forum2 is not complete.

According to the Position Statement of the National Lymphedema Network (NLN),3 a qualified health care professional should help determine the diagnosis of lymphedema in the earliest possible stage for more effective treatment. Patients referred for lymphedema treatment can have a variety of diagnoses; therefore, it is important to obtain a thorough patient and cardiovascular/pulmonary systems history, integumentary review, musculoskeletal and neuromuscular assessment, and determination of communication capabilities and to conduct a physical therapy examination to diagnose the cause of lower extremity swelling. The physical therapist (PT) or the health care professional who is differentially diagnosing patients with lower extremity swelling needs to know the duration, distribution, and accompanying symptoms of the leg edema in order to render an effective differential diagnosis.4 Five diagnostic tests necessary to properly diagnose lymphedema include magnetic resonance imaging (MRI), computed tomography scan (CT), lymph vessel imaging, volumetric measurements, and assessment of changes in biomechanical or electrical properties of the fluid.

According to the NLN3 and a literature review by Young,5 swelling distribution (bilateral versus unilateral) is important in determining pathology, and bilateral leg edema is usually an indication of a systemic process.4 The PT/health care provider needs to have full knowledge of patient medication and reports of pain, trauma, and surgery to help determine the cause of edema. Any accompanying symptoms, such as dyspnea with exertion, orthopnea, and/or paroxysmal nocturnal dyspnea, most likely are indicative of congestive heart failure (CHF).4 Physical examination to determine the presence of heart failure such as distended neck veins, listening for ventricular gallop, and conducting echocardiography4 are also an important part of the evaluation process. Determining what diagnostic tests have been performed on the patient is essential. For example, the PT should obtain, if possible, previous medical records on the patient and have ongoing communication with the referring physician to order appropriate laboratory tests.

Ciocon et al4 conducted a review of the literature on the differential diagnosis of leg edema. Their review showed increased peripheral venous pressure is the most common cause of leg swelling. Chronic venous insufficiency (CVI) is the most common condition resulting from increased venous pressure4 and can result in extravasation of large molecules and red blood cells to the dermis and cause inflammation and possibly ulceration.6

According to Lampe’s7 literature review on lower extremity chronic venous disease, the pathogenesis of venous disease can have many origins, including venous failure, venous reflux, and venous hypertension. Lampe’s review7 also explains CVI may occur as a result of long-term vein malfunction, potentially leading to ulceration. Venous hypertension along with increased capillary hydrostatic pressure can lead to fluid leakage into the interstitial space, which essentially is one of the causes of secondary lymphedema.1,7 According to Bolton et al’s8 literature review on the global efforts to address wounds and lymphedema, the estimated prevalence of chronic ulcers in patients >60 years old with venous insufficiency is 1% to 3%. Bolton et al concluded saving limbs and lives requires correct diagnosis, addressing the cause of skin breakdown early, and managing the wound well. Lampe7 stresses adequate edema assessment is necessary. Recent soft pitting edema may indicate trauma or early stages of venous insufficiency, and hard/indurated or brawny tissue is related to longstanding venous hypertension and venous insufficiency.

Due to the progressive nature of lymphedema, early intervention will lead to more effective treatment. According to a consensus document of the International Society of Lymphology,1 manual lymph drainage (MLD) in combination with remedial exercises and compression, termed complete decongestive therapy, is the standard treatment approach for patients seeking lymphedema management.

MLD. MLD is a standard treatment approach to peripheral lymphedema that involves a specific type of light touch massage. This gentle, light, superficial massage technique stimulates the lymphatic system to allow proficient uptake and movement of lymphatic fluid. This therapy typically is performed by either a PT or occupational therapist who is a Certified Lymphedema Therapist (CLT).1

CHF. According to the consensus document of the International Society of Lymphology,1 the second most significant diagnosis that results in leg edema is CHF. Each year, 660,000 individuals are newly diagnosed with CHF.9 It is imperative that patients and health care providers be familiar with the signs and symptoms of CHF. The presence of CHF can dramatically change the treatment approach for the patient. For example, the health care provider will need to closely monitor the patient’s vital signs and symptoms throughout treatment sessions to make sure the heart is not being overworked. A baseline assessment of all vital signs will help determine if the patient is progressing and tolerating the treatment in a stable manor without adverse effects. A literature review by Frese et al10 discusses blood pressure (BP) guidelines for PTs; the BP measurement gives the PT information on how the patient is responding to treatment/exercise and guides exercise prescription or when to potentially stop treatment. This is critical when performing MLD therapy, because additional fluid is moved toward the heart. Being able to recognize signs and symptoms of CHF as a health care provider and as a patient is important in the diagnostic process.

Albert et al9 investigated patients’ perceptions of signs and symptoms of heart failure before an ambulatory visit/hospitalization. Using a convenience sample of 276 patients with systolic heart failure, researchers had participants complete a 1-page checklist of signs and symptoms. The authors found patients may not report their signs and symptoms to health care providers because they do not perceive them as indicative of a heart-related problem and may cope by ignoring or denying such symptoms. The authors also found 100% of participants in their study reported shortness of breath (SOB), while less than half (126 out of 276) reported edema/swelling.

Many patients seeking lymphedema treatment as a result of lower extremity swelling have comorbidities that may produce SOB, profound fatigue, and/or generalized weakness. In the study by Albert et al,9 patients documented these symptoms without realizing they are symptoms of CHF and the incidence of lower extremity edema in that patient population was 46%. This finding is relevant, considering many patients seeking lymphedema treatment may have underlying symptoms of CHF but are not aware that they actually have CHF; therefore, it is important for the health care provider to perform a complete history/screen.9

Theories about the origin of CHF abound. Based on their literature review of the development of dyspnea and edema symptoms, Churchouse and Thomas11 theorized the development of CHF is a result of right ventricular failure occurring secondary to severe left ventricular failure. The cardiac lymphatic system also plays a role in the development of leg edema when anatomical and/or functional abnormalities of the lymphatic vasculature are present that can lead to lymph flow impairment, a known cause of edema.11

Primary functions of the lymphatic system are to maintain fluid homeostasis and to provide a route for large protein molecules.12 Cui’s12 literature review investigated the connection between the cardiac system and the lymphatic system; evidence indicates blocking the cardiac lymph flow may contribute to several forms of cardiac injury. This review also reported lymphatic fluid drains passively into the heart, relying completely on powerful cardiac muscular contraction and relaxation. In other tissues, active lymphatic pumping has been found to be an important lymphatic fluid draining mechanism.12

Because these systems are intimately linked, the PT must be cautious not to overload the heart with the fluid that is being moved from the extremity to the thoracic duct when applying MLD to persons with CHF. Depending on the stage of CHF, movement of fluid toward the heart could be life-threatening. It is intuitive to stop MLD when a patient is showing classic signs of CHF, but research that states at what stage of CHF MLD is contraindicated is lacking.

To investigate the consequences of thoracic duct drainage in CHF patients, Witte et al13 focused on patients (N = 12) with severe CHF in whom a cannula was inserted in the thoracic duct to relieve symptoms. These researchers found initial high lymph flow pressure before cannulation and the presence of edema, indicating the flow of the unvented lymphatic system, was unable to keep pace with the rate of lymph formation. The investigators also found 4 of the 12 participants experienced significant CHF symptom relief within a few hours following insertion of the cannula into the thoracic duct. These changes included relief in dyspnea, orthopnea, and abdominal discomfort. It is important to note cannulation is a dangerous procedure that was fatal in 5 of the 12 patients. Although the study sample size was small, the morbidity rate suggests MLD must be considered a potentially dangerous treatment in patients with active acute heart failure.

An awareness of the relationship between the lymphatic system and the cardiac system will allow the PT a better understanding of the risks involved in treating patients with mild CHF symptoms, especially because patients seeking MLD may be unaware of signs and symptoms of CHF. On initial examination, a complete checklist of CHF signs and symptoms will help complete a thorough screening.

The basics of examining a patient with lymphedema and concurrent circulation and integumentary concerns are described in the Guide to Physical Therapist Practice.14 Examination of the patient, per the Guide, should include 3 main components: patient/client history, systems review, and tests and measures. The patient/client history is a systematic gathering of past and current information from the client/family regarding why this patient is seeking the services of physical therapy.14 The systems review is a brief examination of physiological status of the cardiovascular/pulmonary systems; for this patient, that involves collection of vital signs, including heart rate, respiratory rate, blood pressure, and edema assessment, as well as integumentary assessment that addresses measurement of any wounds, odor, or drainage and overall skin integrity/texture. Systems review also includes musculoskeletal and neuromuscular assessment. The final part of the systems review is assessment of the patient’s ability to communicate, his/her affect, cognition, language, and learning style. Appropriate standardized tests and measures are selected by the PT as part of the examination and may include aerobic capacity/endurance, edema/girth measurements, balance testing, and functional tasks such as the ability to transfer out of bed safely and independently.

The purpose of this case report is to illustrate the principles of care and potential complications of treating lower extremity edema in a patient with COPD/CHF.

Case Report

Patient background. Ms. K is a 69-year-old woman who was referred to a PT for the treatment of bilateral lower extremity lymphedema. She presented with weeping wounds on both distal anterior lower extremities. At the time of examination, no wound measurements or photographs were taken. The patient was married and worked full time as a Medicare insurance consultant.

History and symptom review. At the time of examination, Ms. K reported symptoms of bilateral lower extremity swelling and her wounds had been present for at least 2 months. She was asked about her cardiac history and denied any past or current significant cardiac problems, past cardiac procedures, and/or past medical history of CHF. She was observed to have mild dyspnea with exertion. When questioned about this symptom, she reported a history of emphysema and asthma that caused SOB as opposed to any past history of CHF.

Ms. K was asked about any past or present kidney problems/voiding, and she denied any issues with her urinary system. She was seen by a physician for the evaluation of her bilateral lower extremity edema and SOB and was referred to physical therapy for management of her lower extremity lymphedema. No tests were performed or ordered to screen for cardiac conditions. The lower extremity tissues felt hard and fibrotic. She was observed to be overweight for her height, but no body mass index was calculated. Her cardiac/pulmonary status at rest exhibited normal respiratory and heart rates; however, she developed SOB with minimal exertion.

Tests and measures. Tests and measurements for the patient with lymphedema include functional mobility, volumetric measurements, and other standardized testing customized to the client (eg, a specific balance test such as the Berg Balance test or a test for fall risk, such as the Timed Up and Go test14). Unfortunately, no baseline functional cardiac/endurance tests, such as the 6-minute walk test (a test developed by Enright15 commonly performed and indicated for patients with COPD, heart failure, and/or with the elderly to determine baseline cardiac functional ability and to determine exercise prescription), were performed on initial examination by the examining PT. Baseline volumetric measurements were taken every 4 cm with a tape measure using a mathematical formula to calculate total volume, a technique acceptable according to the NLN.4 Leg volumes were almost equal bilaterally, with the right lower extremity measuring 9,107.62 mL and the left lower extremity 9,176.64 mL. This provided the therapist with a baseline volume that was reevaluated on a weekly basis to determine the effectiveness of interventions. All weekly circumferential measurements, reported as volume, performed from the initial examination until discharge were taken by the same PT (see Table 1). OWM_Vaassen_Table1

Functional limitations included the inability to bend over due to poor mobility and obesity; her distended abdomen prevented her from physically reaching her lower legs to don/doff stockings/socks. Transfers required minimal assistance: the increased weight of the lower extremities made them difficult to lift onto the bed. Ms. K’s gait was slow, and she manifested a slight trunk lean from side-to-side due to chronic bilateral hip pain. She did not require an assistive device for safety or stability. Based on these evaluative findings, Ms. K’s problem list was prioritized: 1) lymphatic overload in bilateral lower extremities; 2) functional transfer limitations from sit to supine as a result of increased fluid/weight of her legs; 3) infection risk due to open, draining wounds; and 4) bilateral hip pain with activity rated at 8 out of 10 (visual analog scale) that interfered with her ability to function at work and at rest that at times kept her awake at night.

It was determined that addressing lymphatic overload would help resolve all other problems on the list; with decreased volume and pressure in her lower extremities, transfers would become easier, wound fluid would diminish and the wounds would heal, and she would have less pain with functional mobility.

Differential diagnosis. A differential diagnosis of venous stasis-induced lymphedema was made based on the onset of the patient’s symptoms, the location of the edema, and the fibrosis present in bilateral lower extremities.

Treatment. According to the Guide to Physical Therapist Practice,14 Ms. K could fall into in 2 practice patterns: 1) Practice pattern 6H, Impaired Circulation and Anthropometric Dimensions Associated with Lymphatic System Disorders; and 2) Practice 232 Pattern 7A, Primary Prevention/Risk Reduction for Integumentary Disorders. Based on prognosis and expected range of number of visits in the Guide, the therapist anticipated approximately 9 visits in 30 days (approximately twice a week for 4 weeks) were appropriate based on Ms. K’s mild lymphedema classification.14 The focus of intervention was to address her edema, strength, and functional limitations and to relieve pressure on the lymphatic system. Short-term and long-term goals addressed her pain, wound healing, functional limitations, ability to perform self-massage, and assistance with donning and doffing compression wraps/garments (see Table 2). OWM_Vaassen_Table2

Interventions. Before interventions, Ms. K provided consent for treatment. Interventions began with patient education, which specifically addressed what lymphedema is, what might be causing the problem in this particular case, and how the planned interventions were anticipated to help heal the wounds and improve functional mobility.

Ms. K was educated on the function and purpose of the lymphatic system and the problems that typically occur when the system is compromised. She also was informed that MLD facilitates movement of the fluid to the thoracic duct and to the heart. She also was instructed on the importance of self-monitoring her breathing and SOB using the Borg Scale of Perceived Exertion,16 a subjective measure of physical activity intensity. Based on the physical sensations experienced during exercise, the person assesses respiration, breathing, sweating, heart rate, and muscle fatigue. The scale ranges from 6 to 20 (6 being no exertion at all to a 20 being maximum exertion); the number reported from the patient correlates highly with the actual heart rate. Ms. K also was asked to monitor urinary output to make sure voiding was at or above what was typical for her; decreased urinary output (voiding less than her usual amount) would lead the therapist to suspect fluid might be moving elsewhere in the body and not being excreted through the kidneys.

Ms. K understood her treatment would consist of MLD massage and remedial exercises and that compression wraps (1-way stretch) to stimulate the lymphatic system and allow efficient fluid movement would be applied after massage was completed. The amount of pull/pressure applied with the wraps would be a graduated level of compression, with more pressure applied distally. Her spouse was given a printed handout detailing how to wrap Ms. K’s legs; in addition, the therapist provided a demonstration of the wrapping procedure. Ms. K was instructed to wear the wraps 23 out of 24 hours. She was further instructed to wash her legs in the hour off with an antibacterial soap and water and to apply lotion to the areas on her legs where she did not have weeping wounds. Instructions were given to rewrap her legs immediately if at any time the wraps became loose (due to volume reduction) or if they bunched uncomfortably and thus restricted circulation or fluid movement. Ms. K and her spouse demonstrated understanding of all instructions.

MLD was started during the first visit and instruction on basic remedial lower extremity exercises to encourage more fluid movement was provided during the second MLD session 5 days later. Following MLD massage, a light compression stockinette (10 mm Hg) was applied along with moderately dense foam around the areas with the greatest fibrosis and 3 rolls of 1-way stretch compression wraps to both lower extremities. Rolls are of various widths, with the smaller width over the foot (8 cm) and increasing width (10 cm to 12 cm) wrapping up the leg depending on the size of the extremity. No chemical applications were placed on the wounds for the treatment of the leg ulcers; however, a basic ABD pad was applied to absorb drainage and placed directly on the wound.

Outcomes. Ms. K’s fluid volume in her lower extremities was reassessed with circumferential measurements on the second visit (see Table 1). She experienced large amounts of fluid loss in her legs (Table 1), but her breathing at rest was becoming progressively more difficult. She was advised to pay close attention to any symptoms of SOB with minimal exertion because this may be a potential sign of CHF; she also was advised to monitor her urine output, although no issues were apparent at this time. At the third visit (week 2), the therapist contacted the physician office because Ms. K’s symptoms indicated potential onset of CHF. At this point, Ms. K was told that if her breathing worsened at any time of the day or night, she should remove her compression wraps; she also was advised to weigh herself daily to monitor fluid retention. An appointment with her physician was made for late in the following week.

On visit 4, <2 weeks from initiation of treatment, the patient’s SOB had worsened slightly; a Borg rate of perceived exertion was not obtained. Despite the loss of lower extremity fluid (see Table 1), Ms. K reported no significant increase in urine output or change in weight. She indicated she was scheduled for an echocardiogram at the same time as the physician recheck. 

At the fifth visit, approximately 2-and-a-half weeks from the initial examination, Ms. K continued to lose fluid volume in her legs, for a total loss of 4,104.19 mL (approximately 4L) between both lower extremities. Her wounds were closed and no longer draining, and no redness was present. She expressed satisfaction with the volume reduction in her lower extremities; however, her SOB with any functional mobility had become intolerable. Echocardiogram results were not available, but she was advised to discontinue her compression wraps. Removal of the compression wraps was projected to decrease pressure on the thoracic duct and the heart.

Her volumetric measurements at the sixth visit (third week) increased due to the discontinuation of her compression wraps at the previous visit (see week 3 increase from week 2 on Table 1).  Her wounds remained healed. At this last visit, Ms. K’s treatment options were discussed at length, with particular reference to her complicated medical condition. The therapist strongly recommended discontinuing lymphedema treatment as a means of ensuring Ms. K’s safety, and she was discharged from physical therapy due to the progressive nature and symptoms of the CHF and returned to the care of her physician. Any further MLD/compression treatment was contraindicated. She was educated with regard to this fact and was comfortable with the discharge plan.

Discussion

Reflecting on the management and outcomes of this case, therapists can appreciate the intimate connection between the cardiac and lymphatic systems and how important it is to educate patients about the signs and symptoms of CHF.

In examining the differential diagnosis of this patient, a concerning question remains regarding the patient symptoms of asthma, COPD, and the further connection this may have with her developing heart failure. The pathogenesis of COPD and CHF are similar, with overlapping signs and symptoms.17,18 Practitioners examining and following these patients should collaborate in order to facilitate the differential diagnosis process. Inadequate assessment can lead to improper treatment if the patient has both COPD and CHF,17 which is the case with Ms. K. She and her referring physician were not able to recognize her COPD symptoms coincided with her CHF symptoms, resulting a less-than-optimal outcome for the patient.

Laboratory tests that would have been valuable for this and other patients include plasma level of natriuretic peptides (NP).18 These levels are a fast and sensitive biomarker for heart failure in patients with COPD.15 B-type natriuretic peptide (BNP) levels ranging from 100 pg/mL to 500 pg/mL in COPD patients may indicate cor pulmonale, moderate left ventricular heart failure, or both.18 The Diez et al18 literature review of these laboratory values goes into more specific detail and references several other authors confirming their findings. Diez et al18 supported the fact if the BNP level is below 100 pg/mL, it is unlikely the patient has heart failure; however, levels above 500 pg/mL are suggestive of acute heart failure in COPD patients.18 Other tests such as echocardiography, which is a reference test for detection and diagnosis of CHF, are limited in obese patients or persons with COPD because of the poor echocardiographic window and pulmonary hyperinflation. In these cases, an MRI is a better choice to evaluate the right ventricle.18 Hawkins et al’s17 literature review on the relationship between heart failure and COPD and the pitfalls of differential diagnosing suggests testing all patients suspected of having CHF and COPD should include an echocardiograph and pulmonary function test. These are tests that could be performed in the differential diagnosis process to help confirm the appropriate pathway of treatment. 

Albert et al9 noted patients may not report signs or symptoms to their health care providers because the provider does not ask appropriate questions or because the patient is not aware these signs/symptoms are related to impaired heart function. This may explain why Ms. K associated her symptoms of dyspnea and fatigue with a chronic lung condition rather than CHF. She was not provided a complete checklist of signs and symptoms of CHF on the initial patient/history questionnaire. The treatment approach was cautious, and she was educated about recognizing symptoms that would indicate active CHF and necessitate cessation of wrapping and self-massage. Churchouse and Thomas11 mention leg massage and remedial lower extremity exercises and elevation are helpful in the management of peripheral leg edema. Future investigation of other safe options for the treatment of lower extremity edema in patients with CHF is necessary.

Additional studies address this concern. Roberts’19 outcomes study with 21 subjects of various comorbidities with both CHF and lower extremity lymphedema noted a decrease in CHF symptoms and weight loss and increased diuresis by initiating the low-sodium diet that comprises 900 mg of sodium, 70 g of protein, 20 g of fat, 3.5 g of potassium, 250 mg of magnesium, and substantial amounts of essential vitamins and minerals consumed daily. Educating patients with lymphedema on this diet combination or insisting on dietitian referral may be an essential part of their treatment plan. In addition to diet, Pierce and McLeod,20 as part of their pilot prospective clinical study, incorporated plantar micro-mechanical stimulation to the calf muscle for 30–60 minutes per day for peripheral edema in 6 patients with CHF. Lean mass of the legs decreased an average of 0.5 kg with no significant changes in health after 1 month of calf muscle pump stimulation. A limitation of this study was the short duration/dosage of the muscle pump stimulation.  These early research results are encouraging because they indicate safe treatment options to reduce peripheral edema in CHF patients are being tested.

Similarly, Leduc et al21 investigated the hemodynamic parameters of 9 patients with heart failure who received MLD. They observed it was safe to perform MLD on patients with confirmed CHF but not in conjunction with compression wraps, garments, or pumps. The study sample size limits the ability to draw firm conclusions but does provide some evidence for a safe approach and guidance for CLTs.

The inherent limitations of case studies also apply to this case report of a patient with lymphedema and symptoms of CHF/COPD. However, the outcome observed is consistent with currently available literature and illustrates the importance of obtaining a differential diagnosis before treating patients with bilateral lymphedema.

Conclusion

The literature related to managing lymphedema in patients who also present with symptoms of heart failure suggests it is imperative to obtain a differential diagnosis before treating the lymphedema. This case study illustrates and confirms the importance of that recommendation. Further research is needed to obtain more outcomes data and define optimal interdisciplinary collaboration requirements among cardiologists, pulmonologists, and CLTs to facilitate optimal patient outcomes. 

References

1.         Consensus Document of the International Society of Lymphology. The diagnosis and treatment of peripheral lymphedema. Lymphology. 2003;36(2):84–91. 

2.         Weiss R. The Incidence of Lymphedema. Available at: www.lymphnotes.com/article.php/id/401/ Updated 2007. Accessed February 23, 2011.

3.         NLN Medical Advisory Committee. The Diagnosis and Treatment of Lymphedema; 396 Position Statement of the National Lymphedema Network. Updated February 2011. Available at: www.lymphnet.org/resources/nln-position-paper-the-diagnosis-and-398 treatment-of-lymphedema. Accessed September 30, 2014.

4.         Cicocon JO, Fernandez BB, Cicocon DG. Leg edema: clinical clues to the differential diagnosis. Geriatrics. 1993;48(5):34–45.

5.         Young JR. The swollen leg. Clinical significance and differential diagnosis. Cardiol Clin. 1991;9(3):443–456.

6.         Simon EB. Leg edema assessment and management. Medsurg Nurs. 2014;23(1):44–53. 

7.         Lampe KE. Lower extremity chronic venous disease. Cardiopulm Phys Ther. 2004;15(1):13–22.

8.         Bolton LL, Macdonald J, Geyer MJ. Global efforts address wounds and lymphedema. Ostomy Wound Manage. 2010;56(5):6–8.

9.         Albert N, Trochelman K, Li J, Lin S. Signs and symptoms of heart failure: are you asking the right questions? Am J Crit Care. 2010;19(5):443–452.

10.       Frese E, Fick A, Sadowsky HS. Blood pressure measurement guidelines for physical therapists. Cardiopulm Phys Ther. 2011;22(2):5–12.

11.       Churchouse W, Thomas E. Dyspnoea and oedema in chronic heart failure. Pract Nurs. 2010;39(9):35–41. 

12.       Cui Y. The role of lymphatic vessels in the heart. Pathophysiology. 2010;17(4):307–314.

13.       Witte MH, Dumont AE, Clauss RH, Roder B, Levine N, Breed ES. Lymph circulation in congestive heart failure. Effect of external thoracic duct drainage. Circulation. 1969;39:723–733.

14.       American Physical Therapy Association (APTA). Guide to Physical Therapist Practice, 2nd ed. Phys Ther. 2001;81:9-744.

15.       Enright PL. The six-minute walk test. Respir Care. 2003;48(8):783–785.

16.       Center of Disease Control and Prevention. Perceived Exertion. (Borg Rating of 422 Perceived Exertion Scale). Updated. March 30, 2011. Available at: www.cdc.gov/physicalactivity/everyone/measuring/exertion.html. Accessed May 29, 2015.

17.       Hawkins NM, Petrie MC, Jhund PS, Chalmers GW, Dunn F, McMurry JJ. Heart failure and chronic obstructive pulmonary disease: diagnostic pitfalls and epidemiology. Eur J Heart Fail. 2009;11(2):130–139.

18.       de Miguel Diez J, Chancafe Morgan J, Jimenez Garcia R. The association between COPD and heart failure risk: a  review. Int J Chron Obstruct Pulmon Dis. 2013;8:305–312.

19.       Roberts H. Use of a low-sodium formula as an improved Karell diet, with emphasis upon the outpatient management of heart failure and lymphedema. Am Heart J. 1963;65:32–49.

20.       Pierce C, McLeod KJ. Feasibility of treatment of lower limb edema with calf muscle pump stimulation in chronic heart failure. Eur J Cardiovasc Nur. 2009;8(5):345–348.

21.       Leduc O, Crasset V, Leleu C, et al. Impact of manual lymphatic drainage on hemodynamic parameters in patients with heart failure and lower limb edema. Lymphology. 2011;44(1):13–20. 

 

Potential Conflicts of Interest: none disclosed

 

Dr. Vaassen is Assistant Professor of Physical Therapy, Clarke University, Dubuque, IA. Please address correspondence to: Madeline M. Vaassen, PT, DPT, GCS, CLT, Physical Therapy, Clarke University, 1550 Clarke Drive, Dubuque, IA  52001; email: mimi.vaassen@clarke.edu.

 

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