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Integumentary > Vascular wound management > Flashcards

Vascular wound management Flashcards

1
Q

Vascular wounds are…

A

interruption in blood flow in any one or more vessels can cause pahtology resulting in

  • integumentary changes
  • wounds
  • impaired healing
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2
Q

vascular wounds

causes from arterial system

A
  • peripheral artery disease
  • ischemia
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3
Q

vascular system

venous system causes

A
  • venous HTN
  • chronic venous insufficiency
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4
Q

Arterial dysfunction

A

arterial occulsion can occur in

  • macro-circulation: named arteries
  • micro-circulation: arterioles/capillaries <0.5mm (not perfusing correctly)

peripheral arterial disease: symptoms include

  • fatigue, heaviness
  • claudication
  • resting pain - related to positional elevation
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5
Q

Describe the phases of ischemia

A
  • first critical phase: collateral circulation is insufficient to meet metabolic needs; wounds heal more slowly or become infected and dont heal
  • second critical phase: exercise/activity cause ischemia and pain
  • third critical phase: resting pain, gangrene, non- healing wounds
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6
Q

PAD vs lumbar spinal stenosis

A
  • symptoms are similar: pain in calf/thigh
  • PAD/ischemia; symptoms will decrease with cessation of activity
  • spinal stenosis pain: symptoms will decrease only with change of position; stand to sit or sit to supine
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7
Q

Arterial mircosystem

A
  • superficial and deep arterioles, venules, and capillaries present ithin the dermis, cutaneous branches
  • capillary loop allow filtration in the arterial end and absorption in the venous end. each papillae usually contains a capillary loop
  • increased pressure at either end, leads to increased interstitial edema or shunting of blood to other areas
  • defects in capillary loop mechanism occur in patient with diabetes along with micro sclerosis (hard to test for)
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8
Q

Arterial micro dysfunction

A
  • clinical signs are more subtle than macro circulation dysfunction
  • re-development of necrotic tissue within 24 hours of debridement
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9
Q

characterisitics of arterial ulcers

A
  • pain: can be severe, increased with elevation
  • location: distal toes (fingers), dorsal foot, areas of trauma, less frequently, distal tibia, distal ischemia
  • tissue: pale granulation (if any), dry necrotic of slough, may progress to gangrene, little/no drainage
  • wound edges: punched out lesion
  • exudate: none unless infected (dry)
  • peri-wound: dry, hairless, thin, skiny skin, loss of hair, ducky or cynanotic
  • pulses: decreased or absent
  • temperature: decreased
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10
Q

mangement of arterial ulcers

A
  • local wound care
  • prevent infection (increased risk)
  • debride carefully: remember that there is ischemia
  • maximize prefusion: avoid noxious stimuli/smoking
  • exercise: gait/mobility; aerobic/progressive walking (claudication guidelines)
  • surgical revascularization if ABI < 0.4: bypass, percutaneous balloon angioplasty
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11
Q

Local wound care

A
  • protects surrounding skin: moisturize, avoid adhesives, reduce friction between toes, pad to protect ischemic tissue (so edges can grow)
  • wound bed: moist wound, debride cautously, prevent maceration
  • maximize circulation: positioning, avoid compression, proper footwear to accommodate for bandages and decrease stress to wound; keep limb warm (prevent further vasoconstriction)
  • education: wound etiology, intervention strategies, risk factor modifcation, foot care guidelines
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12
Q

Gangrene risk factors

A
  • obesity
  • DM
  • smoking
  • hyperlipidemia
  • IV drug use
  • surgery
  • trauma
  • alchololism
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13
Q

subtypes of gangrene

dry gangrene

A
  • arterial obstruction following long-standing peripheral artery disease or vasculitis in the lower extremities of diabetic patients
  • features of black eschar located on the distal extremities: (clear demarcated, hard, dry, foul order, painful)
  • skin is atrophic, shiny, free of hair,
  • limb is pale cold and pulseless
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14
Q

subtypes of gangrene

wet gangrene

A
  • necrotizing soft tissue infection usually caused by invasion of bacteria into site of local trauma or skin breaches
  • edematous, moist appearing skin characterized by: cyanosis, blistering, foul odor painful
  • patient may also present with systemic signs and symptoms
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15
Q

subtypes of gangrene

gas gangrene

A
  • severe pain with evidence of gas (crepitus) on palpation
  • fourneir’s gangrene: life-threatening necrotiing fasciitis involving the gential or perineal regions
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16
Q

Management of dry gangrene

A
  • risk reduction strategies (smoking cessation, diet, exercise and routine foot exam)
  • revascularization
  • amputation/debridement once blood flow is optimized
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17
Q

management of

wet/gas gangrene

A
  • agressive surgical debridement
  • systemic broad-spectrum antibiotics
  • wet: carbapenem + MRSA agen + clindmycin
  • gas: clindamycin + piperacillin-tazbactam
18
Q

venous system

A
  • superficial veins: greater and lesser saphenous
  • deep veins: paired with each corresponding artery (femoral, popliteal, tibial)
  • perforator veins: conduits BTW superficial and deep systems
  • communicating veins: connect veins in same systems

damage to any can cause blood to pool typically starts in superficial veins

19
Q
A
20
Q

chronic venous insufficiency

A
  • slow healing and recurrence is common
  • ulcers from CVI: referred to as venous stasis, venous HTN is root cause
  • small trauma to skin leads to open wounds (impaired vascular system)
21
Q

what is venous HTN caused by

A
  • insufficient valves
  • from deep communicating or superficial veins
  • obstruction of LE veins, ex: pregnancy, obseity, clotting/thrombus
  • insufficient calf muscle pump (soleus and gastroc = enough ROM?)
  • prolonged standng (esp. no walking)
  • neuromuscular/MSK disease of LE
  • immobilization of LE
22
Q

Venous HTN

A
  • results in elevated capillary pressure
  • leak fluid, molecules, RBC into interstitial space
  • leakded RBC release forms hemosiderin in skin
23
Q

Venous dysfunction: CEAP classification system

A
  • Clinical signs: varicose veins, edema, pigmentation, healed or active ulcers
  • Etiology: congenital, primary, secondary causes
  • Anatomic: superficial, deep, perforator veins
  • Pathophysiology: reflux, obstruction, both
24
Q

CEAP classification: clinical

A

C0: no visible or palpable sings of venous disease
C1: telangioctases or reticular veins
C2: varicose veins
C3: edema
C4b: lipodermatosclerosis or atrophie blanche
C5: healed venous ulcer
C6: active venous ulcer

25
Q

CEAP: etiologic

A

Ec: congential
Ep: primary
Es: secondary (post thrombotic)
En: no venous cause identified

26
Q

CEAP: anatomic

A

As: superficial veins
Ap: perforator veins
Ad: deep veins
An: no venous location identified

27
Q

CEAP: pathophysiologic

A

Pr: reflux
Po: obstruction
Pr,o: refulx and obstruction
Pn: no venous pathophyiology identifiable

28
Q

characteristics of venous ulcers

A
  • pain: mild to moderate, decreased with compression or elevation
  • location: medial malleolus, medial lower leg, usually lower 3rd of LE
  • tissue: irregular shape, ruddy wound bed, fibrous yellow or glossy coating over wound bed, varies but may be copious
  • peri-wound: edema, cellulitis, hemisiderin staining, lipodermatosclerosis
  • pulses: normal or decreased from edema (hard to find)
  • temperature: normal to mild warmth
29
Q

Management of venous ulcer

A
  • local wound care: similar to other chronic wounds; absorptive dressing, control bacteria, protect peri-ound skin with barrier for skin, moisturize dry scaly skin
  • compression therapy: start low and gradually increase elevation to enhance venous return; assess to be sure no PAD
  • ablation of saphenous vein: reduce recurrence but not overall healing
30
Q

exercise indicated for..

with patients with vascular and integumentary disorders

A
  • increase strength (esp. muscle pump)
  • increase joint ROM
  • improve QOL perceptions
  • Increase blood flow to extremities
  • increase calf pump activity
  • prevent pressure ulcers
  • enhance effects of bandaging
31
Q

Exercise: aerobic exercise

A
  • enhances effect of respiratory pump
  • can help with calf pump
  • assist with weight loss for patients who are obese
  • assist with blood sugar control with patient with DM
32
Q

Exercise: mobility training for patients with vascular and integmentary issues

A
  • improves independence and safety
  • increase perception of mobility
  • enhance patient’s sense of well-being
33
Q

tests and measures for vascular wounds

A
  • PMH: specific vascular related events, smoking history, symptoms of claudication, resting pain, limb fatigue
  • inspection: size, symmpetry (to other limb), cyanosis, clubbing, edema, assess all visible wounds
34
Q

Pitting edme scale

A

1+ barely percepitble depression
2+ easily identified depression (skin rebounds to its original controu within 15 seconds)
3+ ID; skin rebounds to its original contour within 15 seconds
4+ EID (rebound >30 sec)

35
Q

Pulses: scale 0-3+

A
  • 0: absent pulse
  • 1+: Diminished pulses
  • 2+ normal pulses
  • 3+ pathologically prominent pulses of severe aortic insufficiency or if the artery is aneurysmal
36
Q

pulses: scale 0-4+

A

0: no palpable pulse
1+: faint but detectable pulse
2+ diminished pulse
3+ normal pulse
4+ bound pulse

37
Q

circulation testing

A
  • capillary refill: pressing on end of toe or skin just proxiumal to wound; normal = < 3 seconds

ankle brachial index:

    • < 0.5 = severe ischemia w/ resting pain refer to specialist
  • 0.5-0.8 = moderate PAD refer to vascular intermitten claudication
  • < 0.6 = compression contraindiciated
  • 0.6-0.8 = modified compression
  • 0.8-1- mild PAD compression safe to use
  • 1-1.2 = normal
  • > 1.2 = refer to specialist calcified vessles in DM
38
Q

Other tests

A
  • rubor of dependency = arterial perfusion: arterial insufficiency foot will blanch hen elevated and take >30 seconds to return pink or turn bright red
  • venous filling time: venous insufficiency = < 5 seconds, nomral 5-15 second, arterial insufficiency = > 20 seconds
  • venous patency: percussion test, trendeleburg test
  • homans sign
39
Q

Non-invasive arterial testing

A
  • dopplar US
  • segmental and digital plethysmography
  • arterial duplex scanning
  • transcutaneous oxygen measurements (normal 60-90 mmHg, < 30 = wound can be debrided, 20-30: healing expected but delayed, < 20 = poor prognosis to heal
  • MRA
  • comuted tomography angiography
40
Q
A

Integumentary (4 decks)

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