Pathophysiology Of Lymphedema Research Articles

Current concepts in lymphedema management.

To provide physicians and nurses with an overview of the pathophysiology, assessment and diagnosis, and treatment of lymphedema. This continuing education activity is intended for physicians and nurses with an interest in managing patients with lymphedema. After reading the article and taking the test, the participant will be able to: 1. Describe the pathophysiology of lymphedema and the difference between transient and chronic lymphedema. 2. Describe the assessment and diagnosis of lymphedema. 3. Identify treatment options and teaching considerations for patients with lymphedema.

Lymphologie 2002.Du diagnostic au traitement des lymphœdèmes

Lymphedema are primary (lower limb) or secondary for the upper limb after treatment of breast cancer. Genetic research allows to explain better pathophysiology of lymphedema. Lymphoscintigraphy is the main imaging technique for lymphedema. Venous or compressive etiologies may be first excluded. Treatment of lymphedema includes decongestive physiotherapy: manual lymph drainages, bandages, elastic stockings, exercises, skin care to avoid infections. Other treatments may be associated: weight loss, drugs (procyanidolic oligomers), surgery for genital lymphedema, pneumatic compression pumps for lymphovenous insufficiency.

Lymphoedema following surgery for breast cancer.

Lymphoedema is a common complication of breast cancer treatment, affecting approximately a quarter of patients. Those affected can have an uncomfortable, unsightly and sometimes functionally impaired limb prone to episodes of superficial infection. The aetiology, pathophysiology and management of these patients is poorly understood. This is a systematic review of all published literature on lymphoedema following treatment for breast cancer, using the Medline and Cinahl databases with cross-referencing of major articles on the subject up to the end of 1999. The aetiology and pathophysiology of lymphoedema in patients with breast cancer appear to be multifactorial and are still not fully understood. Although conservative treatment techniques can be very successful in controlling symptoms, they do not afford a cure. The place of surgical and pharmacological therapy remains unclear. Improved understanding of the pathophysiology may assist in reducing the incidence of this condition, or help to identify those at greatest risk, in whom early initiation of conservative treatment measures may prove effective.

Lymphedema: anatomy, physiology and pathogenesis.

The authors review the current understanding of lymphatic anatomy and physiology, and the pathophysiology of lymphedema. The skin lymphatic system consists of the initial lymphatics, which converge into lymphatic precollectors, collectors and lymphatic ducts; these in turn convey the lymph to the regional lymph nodes. Interstitial fluid and particles enter the initial lymphatics through interendothelial openings and by vesicular transport. Lymphatic uptake is enhanced by external compression. Lymphatic transport depends greatly on contraction of lymphangions, which generate the suction force that promotes absorption of interstitial fluid and expels lymph to collecting ducts. In lymphedema, various types of congenital and acquired abnormalities of lymphatic vessels and lymph nodes have been observed. These often lead to lymphatic hypertension, valvular insufficiency and lymphostasis. Accumulation of interstitial and lymphatic fluid within the skin and subcutaneous tissue stimulates fibroblasts, keratinocytes and adipocytes eventuating in the deposition of collagen and glycosaminoglycans within the skin and subcutaneous tissue together with skin hypertrophy and destruction of elastic fibers.

Flow velocity of cutaneous lymphatic capillaries in patients with primary lymphedema.

For the first time measurements of lymph flow velocities in cutaneous microlymphatics of patients with lymphedema were performed and compared with healthy subjects. Flow velocity in single lymphatic skin capillaries was measured using fluorescence video microscopy after subepidermal microinjection of FITC-dextran 150,000 in 15 healthy volunteers and 16 patients with primary lymphedema. Initial filling of the lymphatic capillary network was fast with significantly higher mean velocities in patients with primary lymphedema than in healthy controls (890 +/- 43 vs. 550 +/- 390 microns/s, p < 0.05). The resting velocities were not significantly different between controls and patients (10.3 +/- 4.1 vs. 16.6 +/- 13.9 microns). In 12 out of the 16 lymphedema patients cutaneous backflow of the fluorescent contrast medium from deeper invisible lymphatics was observed. In 4 of these patients rhythmic reflux with a mean frequency of 1.4 +/- 0.5 cycles/min was measured by video densitometry in microlymphatics with a significantly (p < 0.01) enhanced diameter. Mean flow velocity (Vp) in these precollectors was significantly increased compared to the resting velocities (p < 0.01). On the basis of these results the hypothesis is advanced that rhythmic cutaneous backflow originates from intrinsic contractions of deeper lymph collector segments and is transmitted to the superficial microlymphatics through incompetent connecting channels. This newly recognized mechanism appears to be an important factor for the pathophysiology of lymphedema.

Physiology of Lymphatic Oedema

Objective: To describe the physiological mechanisms implicated in lymph formation and drainage, and the pathophysiology of lymphoedema. Design: Historical steps leading to the current understanding of the physiology and pathophysiology of lymph formation. Data extraction: Selection of relevant articles from the literature. Data synthesis: After a summary of the anatomical structures involved in the lymphatic system, the physiology of lymph formation and transport is described with special emphasis on recent hypotheses. The pathophysiology of lymphoedema is explained based on a combination of two factors: protein content and fluid movements within the lymphatic system. Conclusion: The pathophysiology of lymphoedema is currently better understood, even if some aspects remain unclear. This can lead to an improved therapeutic management of lymphoedema.

The Effect of Acute Inflammatory Episodes (Cellulitis) on the Treatment of Lymphoedema

Lymphoedema is a chronic, progressive condition which affects a significant number of patients following treatment for cancer. AcutelnflammatoryEpisodes(AIE),commonlyknown as cellulitis, may be a complication, or causative factor, in the development of lymphoedema, and has a detrimental effect on the management of lymphoedema. This paper reviews the literature regarding the pathophysiology oflymphoedema and its treatment using conservative treatment measures. The prevention and treatment of AlE is addressed, highlighting the importance of identifying those patients at risk of developing lymphoedema, and consequently AlE. The role of the nurse in patient education is discussed. INTRODUCTION The literature cites several factors which play a role in the developmentoflymphoedema. Of particular interest is the role of cellulitis, both in the development, and as a complication, of secondary lymphoedema related to cancer and its treatment This paper focuses on the physical effects of lymphoedema, and reviews the pathophysiology of lymphoedema. The development of AlE and its effect on current conservative lymphoedema treatments will be discussed with reference to the treatment and prophylaxis of AlE. The role of the nurse in the education of the patient will be outlined, with suggestions for future development Prior to commencing this review, two objectives were identified: 1) To achieve greater personal understanding of the patho-physiology of lymphoedema, its treatment and the role of AlE. 2) To provide a theoretical background (through this literature review) for the development of a controlled clinical study into the prophylaxis of AlE related to lymphoedema. For the purpose of this paper, the term 'nurse' will be used to describe those members of the multi-disciplinary team (whether they be nurse, physiotherapist, occupational therapist or surgical appliance officer) who are involved in the provision of care to patients with lymphoedema. PATHOPHYSIOLOGY OF LYMPHOEDEMA Lymphoedema is commonly referred to as a chronic swelling resulting from a failure of the lymph drainage system, with the consequent accumulation of protein-rich interstitial fluid 1•2•3•• 5 • 6 • 7 • 8 • One or more limbs may be affected, and sometimes the adjacent quadrant of the trunk • To achieve an understanding of the problems that may occur whenthelymphaticsystemfails,itisfirstnecessarytounderstand the basic pathophysiology of the lymphatic system. The lymphatic system The lymphatics serve two major purposes: the regulation of tissue homeostasis, and an immunological function • 9•• It comprises a complex network of vessels which provide an accessory one-way drainage route by which fluid can flow from the interstitial spaces, carrying macromolecules (including protein and bacteria) back into the bloodstream. It has also been likened to the route taken by a river from its source (tissues) to the sea (bloodstream) • The blood and lymph systems complement each other, providing a fine balance between filtration and reabsorption 11 • Fluid leaves the capillaries and enters the tissues under the compulsion of hydrostatic pressure, which is greater at the arterial end of the capillary. Proteins act as the vehicles in the blood transport system, carrying oxygen and nutrients to the cells of the tissues. At the venous end of the capillary, osmotic pressure (exerted by the plasma proteins remaining in the bloodstream) draws the fluid back into the capillaries. However, macromolecules such as protein and bacteria are unable to return directly to the bloodstream, and must exit via the lymphatic route • Approximately 90% of the tissue fluid returns via the venous system, and the other 10% enters the lymphatic capillaries to combine with plasma proteins, cell debris, organic matter, foreign bodies and fat (from the intestine) to form lymph. The rate of lymph flow is influenced by three major factors: changes in interstitial fluid pressure; muscular activity; and the continual rhythmic contraction of the lymphatic vessels • •• The development of lymphoedema Lymphoedema can be classified into two types: primary and secondary. Primary lymphoedema arises from a congenital abnormality of the lymphatics (which will not be specifically discussed), whereas secondary lymphoedema results from obstruction or damage to the lymphatic vessels 2•5• The literature describes several factors which reduce the transport capacity of the system (Fig 1), and precipitate the presentation of lymphoedema. Currently there has been no work to suggest the degree of risk attached to each factor. The literature describes several factors which reduce the transport capacity of the system: Axillary or groin dissection .s·••• Axillary radiotherapy 1.s·8•15 Tumour Post-operative wound infection•••.ZO Venous complications Radiodermatitis•

The lymphedema chaos: a lancet.

Pathophysiology of lymphedema is not an enigma. It is caused by a low-output failure of the lymph vascular system in combination with an inadequate scavenging of stagnating plasma protein by macrophages. Axillary venous diseases alone never cause chronic postmastectomy edema. In the diagnosis of lymphedema, invasive methods (i.e., direct lymphography and venography) are not only unnecessary but are potentially harmful and do not give any information of therapeutic relevance. Lymphedema of the limbs without reflux of lymph or chyle is not a surgical disease. It can be treated successfully by the skillful application of specific physiotherapeutic measures free of any side effect. The results of this therapy can be maintained if the patient's compliance is good.