Chap 65-67 Lymphedema

Question 0

What is the difference b/w high-input and low-output failure?
Give e.g. of each.

Answer 0

high-input
increased lymph prod > transport capacity even if lymph conduits normal. e.g. venous edema
low-output
pathologic condition compromises lymph flow
eg. hypoplasia/aplasia, abnormal valves

Question 1

What is lymphedema?

Answer 1

various disease states characterized by the interstitial accumulation of protein-enriched fluid

Question 2

What is the major classification of lymphedema?

Answer 2

Primary and secondary

Question 3

What is a sub-clssification of primary?

Answer 3

congenital
   non-familial
   familial (milroy's)
Praecox (age 1-35)
  non-familial
  familial (meige's disease)
Tarda (age >35)

Question 4

What is a sub-clssification of secondary?

Answer 4

filariasis
lymph node excision
tumor invasion
infection
trauma

Question 5

What condition can congenital lymphedema be associated too?

Answer 5

turner, klingelters, trisomy 21, noonans

Question 6

what is most common/rare form of primary?

Answer 6

praecox common
tarda rare (10%)

Question 7

what is most common secondary?

Answer 7

filariasis followed by breast cancer

20-30% of breast cancer patients

Question 8

What is the morphological classification of lymphedema?

Answer 8

aplasia–absence of collecting vessels
hypoplasia–diminished number
numerical hyperplasia–increased number
hyperplasia–increased number and valve incompetence

Question 9

What is most common parasite associated with filariasis lymphedema? How transmitted?

Answer 9

Wuchereria bancrofti (90%)
mosquito and poor sanitation

Question 10

How do you diagnose filariasis?

Answer 10

Eosinophilia found in periph blood smear, microfilaria in peripheral nocturnal blood, centrifuged urine sediment, lymphatic fluid

Question 11

How do you stage lymphedema?

Answer 11

Latent phase: Excess fluid accumulates and fibrosis occurs around the lymphatics, but no edema is apparent clinically.


Grade I: Edema pits on pressure and is reduced largely or completely by elevation; there is no clinical evidence of fibrosis.



Grade II: Edema does not pit on pressure and is not reduced by elevation; moderate to severe fibrosis is evident on clinical examination.


Grade III: Edema is irreversible and develops from repeated inflammatory attacks, fibrosis, and sclerosis of the skin and subcutaneous tissue. This is the stage of lymphostatic elephantiasis.

Question 12

What are associated skin chafes with lymphedema?

Answer 12

stemeners sign-square toes from edema
buffalo humb-dorsum of foot
feet may take woody texture
pinkish/red, warm
long-standing-thick, hyperkeratosis, peau d’orange
lymphorrhea–vesicles drain clear fluid
primary-yellow nail syndrome, clubbing and friability of nails

Question 13

Is pain a symptom of lymphedema?

Answer 13

No. if painful suspect infection

Question 14

what is most common complication of lymphedema?
why does it happen?
most common sources?

Answer 14

infection (31% of patients)

accumulation of fluid and protein god substrate for bacterial growth
lymph dysfunction impairs local immune responses

group A strep, staph species

Question 15

What are other complications?

Answer 15

malnutrition from protein loss
immunodeficiency
Cancer

Question 16

What are most common cancers associated with lymphedema?

Answer 16

lymphangiosarcoma (usually 2ary)
multicentric lesions with bluish nodules, sclerotic plaques or bullous changes

sarcoma

Question 17

What modalities can you use to diagnose lymphedema?

Answer 17

Lymphoscintigraphy
CT/MRI
direct contrast lymphagiography

Question 18

what is appearance of lymphedema on CT/MRI?

how is this different then venous edema and lipedema?

Answer 18

Lymphedema—honeycomb distributon of edema win epifascial structures, thickening of the skin
Venous edema, epi and subfascial compartements affected
Lipedema fat accumulation without fluid

Question 19

What is differential diagnosis for lymphedema?

Answer 19

Systemic
Cardiac failure
Hepatic failure
Renal failure
Hypoproteinemia
Hyperthyroidism (myxedema)
Allergic disorders
Idiopathic cyclic edema
Hereditary angioedema

Drugs 
Antihypertensives: methyldopa, nifedipine, hydralazine
Hormones: estrogen, progesterone
Anti-inflammatory drugs: phenylbutazone
Monoamine oxidase inhibitors

Local
Chronic venous insufficiency
Lipedema
–depostition of fatty tissue in subcu layers)
0besity

Congenital vascular malformation
 (usually has larger limb, bruit
Arteriovenous fistula
Trauma
Snake or insect bite
Infection, inflammation
Hematoma
Dependency
Rheumatoid arthritis
Post-revascularization edema
Soft tissue tumor
Hemihypertrophy

Question 20

Describe preventative treatments for lymphedema?

Answer 20

skin hygiene
clothing precautions
trauma avoidance
fungal/bacterial control

Question 21

Describe non-surgical treatments for lymphedema?

Answer 21

limb elevation
exercise
diet 
pressure avoidance
compression
massage

Question 22

What is ideal compression strength for lymphedema?

Answer 22

30-40mmHg or 40-50mmhg if really bad and chronic

Question 23

How does subcutaneous fibrosis occur in lymphedema?

Answer 23

Insuff lymph transport leads to accumulation of hyaluronan and glycoproteins in extracellular space
Increase in fibroblast, keratinocytes, macs
Leads to increased collagen deposition and CT in skin and subcut

Question 24

What abnormalities on lymphoscintigraphy are common for lymphedema?

Answer 24

Dermal backflow
Absent or delayed transport of tracer
Crossover filling with retrograde backflow
Absent or delayed visualization of lymph nodes
Obliterated channels

Question 25

What are surgical techniques for lymphedema?

Answer 25

Lymph grafting
Lymphovenous anastomosis
Liposuction