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Cardiovascular > Peripheral Venous & Lymphatic Vessel Disease > Flashcards

Peripheral Venous & Lymphatic Vessel Disease Flashcards

1
Q

Dilated, tortuous superficial veins in the legs
Asymptomatic or aching discomfort/pain
Often hereditary
Increased frequency after pregnancy

these are indicative of which dx?

A

Varicose Veins

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2
Q

Varicose veins develop in the lower extremities due to ?

A

periods of high venous pressure

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3
Q

contributing factors of varicose veins

A

Postpartum women (highest incidence)
Prolonged standing
Heavy lifting

Varicosities develop in over 20% of all adults

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4
Q

what is the hallmark of chronic venous disease

A

Combination of progressive venous reflux and venous hypertension

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5
Q

venous valve does not close appropriately leading to backward blood flow into lower extremities

A

Venous reflux

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6
Q

increased venous pressure as a result of reflux

A

Venous hypertension

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7
Q

varicose veins MC affects which vein

A

great saphenous and its tributaries
Short saphenous vein in posterior leg may also be affected

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8
Q

Distention of the veins further prevents valve leaflet closure resulting in ?

A

valve incompetence and reflux

Vein segments below the defective valves distend and progressively fail as well

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9
Q

secondary varicosities may result from obstructive changes and valve damage in the deep venous system following ?

A

thrombophlebitis

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10
Q

causes of secondary varicosities

A
  • Rarely a result of proximal venous occlusion due to neoplasm or fibrosis
  • congenital or acquired arteriovenous fistulas or venous malformations, especially if present in young patients
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11
Q

presentation of varicose vein

A
  • Dull, aching heaviness or a feeling of fatigue of the legs following periods of standing is MC complaint
  • Itching from venous eczema may occur either above the ankle or directly overlying large varicosities
  • severity not correlated with the number and size of the varicosities - may have no pain but numerous varicosities
  • Dilated, tortuous veins of the thigh and calf are visible and palpable - esp when standing
  • Long standing varicose veins may progress to chronic venous insufficiency - ankle edema, brownish skin hyperpigmentation, and chronic skin induration or fibrosis
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12
Q

dx eval for varicose veins

A
  • No diagnostic testing needed for the diagnosis of varicose veins
  • If there is a suspected obstruction, imaging warranted
  • If surgical intervention is planned, imaging is a necessary aid - Duplex ultrasonography is the test of choice for planning therapy
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13
Q

management for varicose veins

A
  1. nonsurgical - compression stockings (20-30 mmHg pressure), leg elevation (PM)
    - Effective for sx management
    - Should be worn during waking hours
    - Helpful for elderly or wishing to avoid surgery
  2. sclerotherapy
  3. endovenous laser therapy (EVLA)
  4. endovenous radiofrequency ablation (EVRFA)
  5. vein stripping (last resort)
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14
Q

what is sclerotherapy

A
  • Direct injection of a sclerosing agent → permanent fibrosis and obliteration of the target veins
  • Recurrence rate >50% if underlying reflux is not managed
  • Complications: phlebitis, tissue necrosis, or infection may occur
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15
Q

what is Endovenous Laser Therapy (EVLA)

A
  • Performed with local anesthesia
  • The laser heats up the small vein and destroys it
  • Could result in heat-induced thrombosis, requiring prolonged anticoagulation
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16
Q

which intervention is better for significant varicose veins with signs of venous insufficiency or for long varicosities

A

Endovenous Radiofrequency Ablation (EVRFA)

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17
Q

what is vein stripping

A

last resort
Involves removing the part of the vein that is torturous

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18
Q
  • History of prior DVT or leg injury
  • Edema, (brawny) skin hyperpigmentation, subcutaneous lipodermatosclerosis in the lower leg
  • Venous ulcers characterized by ulcerations at or above the medial ankle

what is this dx?

A

Chronic Venous Insufficiency

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19
Q

A severe manifestation of venous hypertension

A

Chronic Venous Insufficiency

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20
Q

causes of Chronic Venous Insufficiency

A
  • Prior deep venous thrombophlebitis (MC)
  • Progressive superficial venous reflux
  • History of leg trauma or surgery
  • Other: congenital or neoplastic obstruction of the pelvic veins or a congenital or acquired arteriovenous fistula
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21
Q

what is a complicating factor for patients with chronic venous insufficiency

A

obesity

22
Q

how does chornic venous insufficiency happen and its result?

A
  1. Insufficiency → valve leaflets do not close bc they are thickened and scarred (post-thrombotic syndrome) or are functionally inadequate due to vein dilation
  2. Chronic thrombus/scarring = proximal venous obstruction, worsening the problem
  3. Venous reflux ensues leading to blood back up in the lower leg/foot
  4. The leg develops venous HTN and an abnormally high hydrostatic force is transmitted to the subcutaneous veins and tissues of the lower leg
  5. result = edema
23
Q

pathologic changes of chronic venous insufficiency

A
  1. Muscle bx: interstitial space changes
    - Enlargement and fibrosis - High levels of fibrinogen and fibrin
    - Edema and inflammation = local hypoxia and malnutrition
  2. Increase in the number of capillaries in the subcutaneous tissue
  3. Peri-capillary fibrosis - subcutaneous thickening and induration
  4. Hemosiderin deposits resulting from erythrocyte lysis
24
Q

clinical manifestations of chronic venous insufficiency

A
  • Primary sx: progressive pitting edema of the lower leg
  • Secondary changes in the skin and subcutaneous tissues develop over time - Stasis dermatitis
  • Other common sx: itching, a dull discomfort made worse by periods of standing, and pain if an ulceration is present
  • Secondary lymphedema - Progressive sclerosis of lymph channels
  • Taut, shiny skin at ankle - edema
  • hemosiderin staining
  • loss of skin integrity with ulceration - secondary cellulitis - dx by blanching erythema with pain
  • fixation of the ankle joint secondary to tissue fibrosis
  • Lipodermatosclerosis (panniculitis)
  • Atrophie Blanche
  • Corona Phlebectatica
  • Venous Ulcers
25
Q

leg is described having
Skin induration
Increased pigmentation
Swelling
Redness
“Inverted champagne bottle” or “bowling pin” appearance

what could this be?

A

Lipodermatosclerosis

26
Q

Star-shaped or polyangular, ivory-white depressed atrophic plaques
Prominent red dots within the scar due to enlarged capillary blood vessels
Surrounding hyperpigmentation

what is this sign?

A

Atrophie Blanche

27
Q

Characterized by abnormally dilated veins around the ankle

what is this sign

A

Corona Phlebectatica

28
Q

dx eval for chornic venous insufficiency

A
  • No diagnostic testing needed for dx
  • If suspected obstruction = imaging
  • If surgery planned, imaging is a necessary - Duplex US
  • Multidetector computed tomographic (MDCT) venography and magnetic resonance (MR) venography could be considered - Used if doppler US nondiagnostic; Requires injection of IV dye; $$
29
Q

tx for chronic venous insufficiency

A
  1. 1st line - Fitted, graduated compression stockings (20–30 mm Hg pressure or higher) from foot to just below knee during AM and PM
  2. Patient education
    - Avoidance of long periods of sitting or standing
    - Intermittent elevations of the involved leg
    - Sleeping with the legs elevated
  3. pneumatic compression for refractory cases
  4. Unna Boot - Provides both compression and topical therapy; 3 layer dressing, changed weekly
  5. vein tx
    - significant saphenous reflux - ablation
    - ulcers - monitored by wound care team
30
Q

Defined as inflammation of a superficial vein, which typically results in a clot
MC a result of a recent venous catheter placement (IV)

A

Superficial Venous Thrombophlebitis

  • IV sites should be evaluated daily for signs and should be removed if present
  • May lead to thrombotic or septic complications if ignored
  • Other causes: Varicose veins, Spontaneous in pregnant or postpartum women, Trauma, Hypercoagulable states
31
Q

MC pathogen of SVT

A

staph

32
Q

SVT typically affects mainly where but can also develop in other sites such as?

A
  • lower extremities - great saphenous vein
  • penis, breast
33
Q

presentation of SVT

A
  1. Localized redness, induration, and tenderness along a superficial vein
  2. pain, fever, and chills
  3. If spontaneous, MC involves great saphenous vein
  4. A palpable cord may be present for several weeks, even after initial inflammatory reaction is past
34
Q

complications of SVT

A
  • Extension into the deep venous system
  • Hyperpigmentation over the affected vein
  • Persistent, firm nodule in subcutaneous tissues at the site of the affected vein
  • suppurative thrombophlebitis
35
Q

complications of suppurative phlebitis

A

Metastatic abscess formation
Septicemia
Septic emboli

36
Q

dx eval for SVT

A
  • clinical dx requiring no testing - hypercoagulable state testing if spontaneous thrombophlebitis
  • elevated WBC -
  • Venous doppler US - only if involves proximal LE or if pt has mixed picture
37
Q

mangement for SVT

A
  1. Mild, localized: mild analgesics (ASA/NSAIDs) + elastic support - Patients are encouraged to continue their usual daily activities
  2. More severe, larger: elevate extremity + hot, wet compresses
    - >5 cm: prophylactic Fondaparinux/LMWH/ Rivaroxaban x 45 d
    - Rapidly progressing or extension into deep system → full dose anticoagulation
  3. cannula/catheter: device removed and cx
  4. septic state: Vanc + Ceftriaxone + Heparin/Fondaparinux
38
Q

Red streaking from wound or cellulitis towards regional lymph nodes, which are typically enlarged and tender; Inflammation of the lymphatic channels

Chills, fever, malaise may be present

A

Lymphangitis

39
Q

MC pathogen of lymphangitis

A

MC cutaneous inoculation of hemolytic streptococci or S. aureus that invades lymphatic vessels and spread toward regional LN

40
Q

pathogenesis of lymphangitis

A
  • Pseudomonas species
  • strep pneumo → uncommon
  • Pasteurella multocida → dog and cat bites
  • G- rods, G- bacilli, and fungi → cellulitis and resultant lymphangitis in immunocompromised
  • Aeromonas hydrophila → can contaminate wounds that occur in freshwater
  • Wuchereria bancrofti → filarial nematode; major cause of acute lymphangitis WW; leads to a chronic Filariasis resulting in subsequent lymphedema with thickening of skin and subcutaneous tissue
41
Q

painful or painless nodular subcutaneous swellings along the course of the lymphatic channels

A

Nodular lymphangitis

42
Q

Lymphangitis can occur in the setting of ____ (neoplastic lymphangitis or lymphangitis carcinomatosa)

A

malignancy

Breast, lung, stomach, pancreas, rectal, and prostate cancers are the most common tumors

43
Q

presentation of lymphangitis

A
  • Hx abrasion or trauma distal to site of infection
  • F, chills, myalgias, and malaise, esp children
  • N, anorexia, and HA may also be present
  • erythematous and irregular linear streaks - tender and warm, extending from the primary infection site toward draining regional nodes, Primary site may be an abscess, an infected wound, or an area of cellulitis
  • Swollen and tender LN
  • Febrile and tachycardic
44
Q

diagnostic eval/work-up for lymphangitis

A
  1. CBC w/ diff and blood cx
  2. Wound culture, abscess I&D if possible
  3. Consult infectious disease to assist in the diagnostic workup
  4. Imaging - define anatomic abnormalities (rarely useful for dx of infectious etiologies)
    - Lymphangiography & lymphoscintigraphy have been used to evaluate for lymphedema and/or lymphatic obstruction
45
Q

management for lympahngitis

A
  1. abx covering for GABHS
    - Dicloxacillin, Cephalexin, Cefazolin, Cefuroxime, Ceftriaxone, Clindamycin, Nafcillin, Trimethoprim and sulfamethoxazole (TMP/SMZ) are all good options
  2. Oral outpatient therapy - for nontoxic, are afebrile, and not immunocompromised
    - Otherwise, consider inpatient parenteral therapy
  3. Analgesics and/or anti-inflammatories for pain
  4. Hot, moist compresses
  5. Elevate & immobilize affected areas to reduce swelling, pain, and the spread of infection if possible
  6. abscess - surgical drainage
  7. Nodular lymphangitis - surgical intervention
46
Q

what is the primary form of lymphedema

A

congenital hypoplastic or hyperplastic proximal or distal lymphatics
Pelvic or lumbar lymph channel and node obstruction present when the disease is extensive and progressive

47
Q

what is the secondary form of lymphedema

A

involves inflammatory or mechanical lymphatic obstruction from trauma, regional lymph node resection/irradiation, or malignant disease or filariasis
May occur following surgical removal of the lymph nodes in the groin or axilla

48
Q

this result can occur in both forms of lymphedema, which leads to incompetence of valve system, poor lymphatic fluid flow, and results in progressive stasis of a protein-rich fluid

Can result in episodes of acute and chronic inflammation, worsening the edema

A

secondary dilation of the lymphatics

49
Q
  • Painless limb hypertrophy - Markedly thickened and fibrotic skin and subcutaneous tissue
  • Pt typically w/o ulceration, varicosities, or stasis pigmentation

what is this dx?

A

lymphedema

50
Q

how to dx lymphedema

A
  • clinical dx
  • MRI - identify lymphatics and proximal obstructing masses
  • Lymphangiography and radioactive isotope - identify focal defects in lymph flow but are of little value in planning therapy
51
Q

management for lymphedema

A
  1. No cure for lymphedema
  2. Control lymphedema and allow nml function
  3. Common treatment strategies
    - Edema control - leg elevation, esp while sleeping (foot of bed elevated 15–20 degrees), Constant use of graduated elastic compression stockings, Massage toward the trunk (either by hand or with pneumatic pressure devices designed)
    - Referral to wound care centers
    - Stress good hygiene and tx of secondary infection
    - Intermittent use of diuretics is rarely helpful
    - lymphangiosarcoma - Amputation (rare)

Cardiovascular (24 decks)

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