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School of Medicine and PharmacyDOC I
GROUP V
CARDIOVASCULAR SYSTEM MODULE
Topic: Pathophysiology and clinical manifestation of lymphedema
November 21, 2016
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Reg. number Names Surnames
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214002211 BIZIMANA Arlette 215023224 GACUTI Benissa215002409 GIRIMPUHWE Rodrigue 215006227 HATANGIMANA Patrick 215001051 HATEGEKIMANA Vincent 215004257 HATEGEKIMANA Vincent 215005303 IRADUKUNDA Robert 215011253 ISANGANO Samuel 215003362 ISHIMWE Pascal 215002765 ISHIMWE Belyse 215009404 ISHIMWE Celine
216351480 ITUZE Ange Marie215019414 IYAMUREMYE Protogene 215007216 KANKINDI Alice 215007804 KWIZERA JEAN Raymond 215001058 MBABAZI Prince 215003549 MUGABIRE Prudence 215003736 MUSONI Venuste 216351146 MWIZERO Aria Genaelle215002734 NDAYISHIMA Patrick 215004113 NGIZWENAYO William 215005137 NISHIMWE Raymond 215001845 NSENGIMANA Sosthene 216352126 NTADOHOKA Ariella 215007309 NTAMBARA Sabiniane215005290 NTEZIYAREMYE BALINDA Vicky Oni215004445 NTIBASHIRAKANDI Pilote 215003134 NTIRENGANYA Yves Parfait215003295 NYIRABAHIZI Clarisse 215004658 RAFIKI Etienne 215008534 RWANDARWACU VICTOR Pacifique 215019725 SHYAKA Wilson 215001849 SIMBI SANGWA Leandre 215012932 SINABUBARAGA Vincent 215013483 TUYISHIME Yannick 215003122 TUYISHIMIRE Brigitte 215004762 UWAMAHORO Angelique215005003 UWAMBAYINGABIRE Angelique 215019331 UWIZEYIMANA Anastase
1. DEFINITION
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Lymphedema is build up of excess protein-rich lymph fluid in body tissues due to lymphatic insufficiency or obstruction of lymphatic drainage back into the blood stream. The affected area can become swollen and distorted in shape. This can result in pain, heaviness, discomfort, impairment of movement and it impact on daily activities.
They are classified into two classes: primary and secondary lymphedema
Primary lymphedema is related to congenital malformation of the lymphatic channels.
Secondary lymphedema results from illness or treatments that obstruct lymphatic drainage. Cancer related lymphedema can occur due to the physical location of a tumor, or as a result of investigations or treatment e.g.: lymph node excision or radiation.
2. PATHOPHYSIOLOGY OF LYMPOEDEMAa. Normal physiology
The normal function of the lymphatics is to return proteins, lipids, and water from the interstitium to the intravascular space; 40-50% of serum proteins are transported by this route each day. High hydrostatic pressures in arterial capillaries force proteinaceous fluid into the interstitium, resulting in increased interstitial oncotic pressure that draws in additional water. Interstitial fluid normally contributes to the nourishment of tissues.
About 90% of the fluid returns to the circulation via entry into venous capillaries. The remaining 10% is composed of high-molecular-weight proteins and their oncotically associated water, which are too large to readily pass through venous capillary walls. This leads to flow into the lymphatic capillaries, where pressures are typically subatmospheric and can accommodate the large size of the proteins and their accompanying water. The proteins then travel as lymph through numerous filtering lymph nodes on their way to join the venous circulation.
b. Disease-related changes in lymphatic flow and their effects
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In a diseased state, the lymphatic transport capacity is reduced. Consequently, the normal volume interstitial fluid formation exceeds the rate of lymphatic return, resulting in the stagnation of high-molecular-weight proteins in the interstitium. This usually occurs after flow has been reduced by 80% or more. The result, as compared with forms of edema that have much lower concentrations of protein, is high-protein edema, or lymphedema, with protein concentrations of 1.0-5.5 g/mL.
This high oncotic pressure in the interstitium favors the accumulation of additional water. Accumulation of interstitial fluid leads to massive dilatation of the remaining outflow tracts and valvular incompetence that causes reversal of flow from subcutaneous tissues into the dermal plexus. The lymphatic walls undergo fibrosis, and fibrinoid thrombi accumulate within the lumen, obliterating much of the remaining lymph channels. Spontaneous lymphovenous shunts may form.
Lymph nodes harden and shrink, losing their normal architecture. In the interstitium, protein and fluid accumulation initiates a marked inflammatory reaction. Macrophage activity is increased, resulting in destruction of aelastic fibers and production of fibrosclerotic tissue. Fibroblasts migrate into the interstitium and deposit collagen. The result of this inflammatory reaction is a change from the initial pitting edema to the brawny nonpitting edema characteristic of lymphedema. Consequently, local immunologic surveillance is suppressed, and chronic infections, as well as malignant degeneration to lymphangiosarcoma, may occur.
The overlying skin becomes thickened and displays the typical peau d'orange (orange skin) appearance of congested dermal lymphatic. Chronic lymphedema causes fissuring and impairment of the epidermis, allowing bacteria to enter and grow, and leading to lymphorrhea, the leakage of lymph onto the surface of the skin. With chronic lymphedema, the development of verrucous, cobblestone plaques, a condition known as elephantiasis nostra verrucosa (ENV), can occur.
Protein composition in lymphedema a theory has also been proposed that chronic lymphedema changes the protein composition of lymph in affected areas. A decrease in alpha-2 globulin levels and an increase in the albumin-to-globulin ratio have been reported. This change in proteins and the resultant slowing of transport to the lymphoid tissue have been suggested to play a role in diminishing the
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effectiveness of immune surveillance and to prevent early detection of tumor-specific antigens. Additionally, repeat episodes of chronic ulceration and healing may stimulate the proliferation of keratinocytes, which may contribute to neoplastic transformation.
3. CLINICAL MANIFESTATIONS OF LYMPHOEDEMA Onset of the onset of 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. Over time, the skin becomes dry and firm with less pitting and is fibrous to palpation.
Laterality Two-thirds of cases of lymphedema are unilateral, although the laterality depends on the precipitating event. For example, an axillary node dissection will increase the risk of lymphedema in the ipsilateral arm while a pelvic node dissection increases the risk of bilateral lower extremity edema.
Swelling At onset, swelling in the affected limb is typically characterized as “soft” and “pitting”. Pitting is variable in patients with lymphedema and reflects
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movement of the excess interstitial water in response to pressure. It is generally absent with progressive lymphedema, reflecting the evolution of fibrosis and adipose tissue deposition.
For patients who had previously undergone a lymph node dissection and/or radiation, lymphedema is typically characterized by slowly progressive ipsilateral swelling of an arm following axillary node dissection or a leg following inguinal node dissection. 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 patients 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.
Skin changes with worsening lymphedema, dermal thickening becomes clinically apparent, which is manifested by cutaneous fibrosis. The overlying skin of the affected limb also becomes hyperkeratotic, which can lead to verrucous and vesicular skin lesions.
Discomfort which is a feeling of heaviness, tightness, aching or discomfort in the affected limb commonly accompanies swelling.
Restricted range of motion with later stages of lymphedema, patients may develop restricted range of motion in the affected limb as a result of the increased weight, which may limit their ability to perform activities of daily living (ADLs).
REFERENCE
www.uptodate.com
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