Lecture 6: Lymphatic System Flashcards
Lymphatic System
- part of circulatory system
- network of organs, lymph nodes, lymph ducts and lymph vessels
- make and move clear fluid called lymph from tissues to bloodstream directionally toward heart
- regional system that moves fluid from periphery to central circulation
- major part of immune system
- maintains fluid balance in tissues; fights infection; and helps remove cellular debris and waste products
- lymph nodes are soft, small, round structures: usually cannot be seen or easily felt; located in clusters in various parts of body, such as neck, armpit, groin, and inside center of chest and abdomen
- pressure driven system based on principles of osmotic diuresis
Initial Lymphatics
- endothelium of lymphatics in direct contact with microfilaments of surrounding connective tissue
- microfilaments pull endothelial cell junction open when tissue pressure rises: allows movement of fluid through
- without changes in tissue pressure, fluid cannot enter lymphatics and fluid will accumulate in interstitium leading to edema
Vessels
- deeper vessels contain smooth muscles and valves
- one way vessel system that drains the 10% excess tissue fluid volume and plasma proteins that remain in the interstitium after normal capillary perfusion/filtration has taken place and returns it to subclavian veins; increased number of plasma proteins in interstitium pulls water in and leads to edema
- all lymph passes through lymph nodes before going back into venous circulation
Starling’s Theory of Fluid Dynamics
- plasma hydrostatic pressure: comes from capillaries and pushes into tissues
- tissue hydrostatic pressure: pushes fluid into capillaries
- plasma colloidal osmotic pressure: fluid pulled into capillary
- tissue colloidal osmotic pressure: fluid pulled out of capillary
- fluid at arterial end of capillary will tend to flow into tissue spaces (filtration): due to plasma hydrostatic pressure and pushes fluid from capillary into tissue
- fluid on venous end of capillary tends to flow back into vessel (reabsorption): due to plasma colloidal pressure and pulls fluid from tissue into capillary
- 10% of fluid does not get back into venous circulation and is taken up by lymphatics: lymphatic drainage occurs when fluid and proteins are not reabsorbed into capillary
Flow of Lymphatics
-pre-collectors –> collecting lymphatics –> lymph trunks –> thoracic duct and right lymphatic duct –> left and right subclavian veins
Lymph Nodes
- act as filters: cleanses lymph of waste products and cellular debris
- vessels distal to nodes are called afferent lymph vessels
- proximal to nodes are efferent lymph vessels
- produce lymphocytes and macrophages
Lymphatic Territories and Watersheds
- lymph drainage territories called lymphotomes: bordered and separated by watershed areas (separates fluid going to different parts of body)
- trunk divided into 4 quadrant lymphotomes: L and R thoracic and L and R abdominal
- thoracic drain into ipsilateral axilla
- UE’s drain into ipsilateral axilla
- abdominal drain into superficial inguinal nodes
- LE’s drain into ipsilateral superficial inguinal nodes
Lymphedema
- swelling of soft tissues that results from accumulation of protein rich fluid in extracellular spaces
- most common in extremities
- classification: primary (idiopathic) and secondary (acquired)
Stages of Lymphedema Using International Society of Lymphology’s Scale
- stage 0 or latent lymphedema: lymph transport impaired, no edema; may have early S&S (achiness, limb pain, and sensation of heaviness)
- stage I: soft, pits on pressure, reverses with elevation
- stage II: nonpitting and does not reduce on elevation, clinical fibrosis, skin changes present, ma get recurrent bacterial and fungal infections
- stage III: lymphostatic elephantitis, severe nonpitting, fibrotic edema connective scar tissue, atrophic skin changes (thickened, leathery, keratotic skin, skin folds with tissue flaps, warty protrusions-papillomas-leaking lymph fistulae
Etiologic Factors of Primary Lymphedema
- unknown
- 3 types of malformations
- aplasia: nearly absent lymph collectors
- hypoplasia: less than normal lymph collectors; most common
- hyperplasia: grossly dilated and enlarged lymph collectors
Etiologic Factors of Secondary Lymphedema
- filariasis (most common): parasitic infection carried by mosquitoes, can grow to 20 cm long and 1-2 cm in diameter, adult male has tale that whips, damaging endothelium, after worm death foreign proteins cause severe local inflammatory reactions: blocks larger lymph collectors
- invasive procedures used in diagnosis and treatment of cancer: surgery and local radiation
- bacterial or viral infection
- multiple abdominal surgeries
- repeated pregnancies
- liposuction
- crush injuries, compound fractures, severe lacerations, paralysis, lipedema, AIDS
Pathogenesis of Lymphedema
- normal lymph load, but transport is inadequate
- increased lymph load and inadequate transport
- chronic inflammation exists in lymphedematous tissue
- chronic inflammation leads to progressive tissue fibrosis
- increased tissue channel size leads to increased distance for oxygen to travel leading to hypoxia
Structural Impairments from Lymphedema
- aging or damaged vessels have fibrin physically narrowing or blocking tissue channels
- hypoplasia of collecting lymphatics
- growth spurt and increase in tissue mass causes body to outgrow or outstrip capacity of lymphatic system
- incompetent valves of initial lymphatics
- gaps and tears in initial lymphatic walls associated with trauma and inflammation: integrity of lymph system not in tact
- physical obstruction of collecting lymphatics associated with fibrosis, radiation therapy, tumor growth, surgical excision of lymphatics during tumor removal, and torn anchoring filaments associated with acute edema
- in filariasis the adult worm blocks the vessels-damage due to constantly motile adult worm and toxic effects of parasite secretory/excretory products
Functional Impairment of Lymphedema
- anything that causes a lac of variation in total tissue pressure causes lymphedema
- bed rest, paralysis, prolonged immobility, spasm of collecting lymphatics, paralysis of collecting lymphatics and impaired contraction
Clinical Manifestations of Lymphedema
- secondary lymphedema can develop immediately postoperative, weeks, months, or years after surgery
- S&S: full sensation, skin tightness, decreased flexibility in hand, wrist, ankle, difficulty fitting into clothing
- physical impairments: increased circumferential limb girth, postural changes, discomfort, neuromuscular deficits, integumentary complications
- healing time increased
- risk of injury increased and oxygenation and metabolism of waste and cellular debris decreased
- atrophic skin changes can occur: loss of hair and sweat glands, formation of keratotic patches on skin, development of papillomas
Complications of Lymphedema
- dermal layer of skin thickens, skin dries and cracks and ulcerations develop
- ulcers do not heal
- folds/flaps become breeding grounds for fungal and bacterial infections
- chronic fungus (tinea) is common in foot/toes, groin, under breast
- difficult to treat topically
- pathogenic alterations in gait pattern and decreases in functional ROM and strength caused by fatigue and inactivity; tactile sensation and kinesthetic awareness impaired
- balance may be impaired and may no longer be able to shower or bathe independently; hygiene becomes a problem
Diagnosis of Primary Lymphedema
-stemmer’s sign, a thickened cutaneous fold of skin over second toe
Diagnosis of Secondary Lymphedema
- detailed medical history
- doppler study to rule out thrombus and recurrence of cancer firmly ruled out
- lymphedema may be first sign of cancer recurrence
- lymphoscintigram: outlines major lymphatic trunks in region and provides functional description of how much tracer material is moved, how far, and in what unit of time, compared with “normal” values of a person of similar height and weight; subcutaneously injecting radioactive tracer then take serial radiographs
Treatment of Lymphedema
- first treat cancer then manage lymphedema
- undergo treatment without guilt or fear that it will worsen lymphedema
- CDT (complete decongestive therapy)
- benzopyrones (not approved by FDA in US) have some effect on increasing proteolysis and increasing macrophage activity (degrade protein and decrease fluid retention)
- increased proteolysis helps to reduce interstitial protein concentration (can therefore absorb more ECF) and have shown to soften fibrotic tissue and increase healing
- diuretics do not help lymphedema (do work on sodium retention edema)
- of surgical approaches, none have been clinically successful
- prognosis: lifelong, chronic condition but can be effectively managed
SIFTT of Lymphedema
- components of intervention modified according to each individual client’s needs
- manual lymphatic drainage
- short-stretch compression bandaging
- exercise
- compression garments
- education (anatomy, skin and nail care, self-massage, self-bandaging, garment care, infection management), compression pumps, psychological and emotional support
Lymphadentits
- when lymph nodes become overwhelmed with infection, lymph node itself can become infected
- in acute, lymph nodes are enlarged, tender and reddened
- in chronic, lymph nodes are scarred with fibrous tissue (nodes enlarged and firm to palpation, but not warm and tender)
- management is treatment of underlying disorder
Lymphangitis
- acute inflammation of subcutaneous lymphatic channels usually occurs as result of streptococci or staphylococci or both entering lymphatic channels
- red streak, radiating from infection site in direction of regional lymph nodes: may be easily overlooked, especially in dark-skinned people
- systemic manifestations include fever, chills, malaise, and anorexia
Medical Management of Lymphatic System Infection in Intact Lymphatic System for Lymphangitis
- dx: differential diagnosis of superficial thrombophlebitis
- red streak radiating toward regional lymph nodes
- doppler and ultrasound to rule out DVT
- laboratory tests may include blood culture, culture and sensitivity studies on wound exudate or pus
- tx and prognosis: prompt parenteral antibiotic therapy
Medical Management of Lymphatic System Infection in Impaired Lymphatic System: Individual at Risk and Individual with Lymphedema
- dx: cellulitis/lymphangitis often triggers development of lymphedema in individual who is at risk but has no clinical signs of edema
- not acceptable for these people to wait and see and call physician in a day or two
- must be seen and evaluated by physician immediately to rule out thrombosis vs. cellulitis/lymphangitis and initiate appropriate treatment immediately
- tx and prognosis: no head applied for those with or at risk of developing lymphedema
- rest and immobilization of involved areas
- cold applied to relive pain
- original area of redness outlined to check on progress or regression of infection
Lipedema: Overview and Etiologic Factors
- symmetrical “swelling” of both legs, extending from hips to ankles, caused by deposits of subcutaneous adipose tissue
- not a disorder of lymphatic system
- occurs almost exclusively in women
Stages of Lipedema
- stage I: skin is soft and regular, but nodular changes can be felt on palpation
- no color changes, spongy feel
- stage II: subcutaneous tissue becomes more nodular and tough; large fatty lobules
- pitting edema is common
- skin changes color in lower leg
Medical Management of Lipedema
- dx: often are told they’re fat and should just lose weight to resolve problem
- fatty tissue accompanying condition cannot be significantly decreased by diet
- clinical differences between lipedema and bilateral primary lymphedema: feet are not involved in lipedema, stemmer’s sign negative in lipedema, lipedema swelling is symmetrical, subcutaneous tissues rubbery
- 90% of lipedema cases have accompanying diagnoses of hormonal disturbances
- bilateral LE lymphedema in morbidly obese individuals are seen
- obesity does not cause lipedema
- tx and prognosis: no effective medical treatment available, prognosis is guarded