Vascular wound management Flashcards
Vascular wounds are…
caused by what and result in what
interruption in blood flow in any one or more vessels can cause pathology resulting in
- integumentary changes
- wounds
- impaired healing
can be arterial or venous
vascular wounds
causes from arterial system
- peripheral artery disease
- ischemia
vascular system
venous system causes
- venous HTN
- chronic venous insufficiency
Arterial dysfunction
- arterial occulsion can occur where?
- PAD symptoms
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
Describe the phases of ischemia related to PAD
- first critical phase: decreased blood flow; 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
PAD vs lumbar spinal stenosis
- 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
Arterial mircosystem
describe
- superficial and deep arterioles, venules, and capillaries present within 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)
Arterial micro dysfunction
clinical signs
- clinical signs are more subtle than macro circulation dysfunction
- re-development of necrotic tissue within 24 hours of debridement
characterisitics of arterial ulcers
- Pain
- location
- tissue
- wound edges
- exudate
- periwound
- pulses
- temp
- 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, nectoric, slough, gangrene,
- wound edges: punched out lesion
- exudate: none unless infected (dry)
- peri-wound: dry, hairless, thin, skiny skin, loss of hair, dusky or cynanotic
- pulses: decreased or absent
- temperature: decreased
mangement of arterial ulcers
- 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
Local wound care
describe parts of local wound care of arterial wounds
- protects surrounding skin: moisturize, avoid adhesives, reduce friction between toes, pad to protect ischemic tissue (so edges can grow)
- wound bed: moisture, debride cautiously, prevent maceration
- maximize circulation: positioning, avoid compression, keep limb warm (prevent further vasoconstriction)
- education: wound etiology, intervention strategies, risk factor modifcation, foot care guidelines
Gangrene risk factors
- obesity
- DM
- smoking
- hyperlipidemia
- IV drug use
- surgery
- trauma
- alchololism
subtypes of gangrene
dry gangrene
- arterial obstruction following PAD or vasculitis in the lower extremities
- 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
subtypes of gangrene
wet gangrene
- necrotizing soft tissue infection usually caused by bacteria into site of wound
- edematous, moist appearing skin characterized by: cyanosis, blistering, foul odor painful
- patient may also present with systemic signs and symptoms
subtypes of gangrene
gas gangrene/fourneir’s gangrene
- severe pain with evidence of gas (crepitus) on palpation
- fourneir’s gangrene: life-threatening necrotiing fasciitis involving the gential or perineal regions
Management of dry gangrene
- risk reduction strategies (smoking cessation, diet, exercise and routine foot exam)
- revascularization
- amputation/debridement once blood flow is optimized
management of
wet/gas gangrene
- aggressive surgical debridement
- systemic broad-spectrum antibiotics
- wet: carbapenem + MRSA agent + clindmycin
- gas: clindamycin + piperacillin-tazbactam
venous system
- 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
chronic venous insufficiency
how does this cause wounds
- 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)
what is venous HTN caused by
- 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
Venous HTN
what happens as a result of this
- results in elevated capillary pressure
- leak fluid, molecules, RBC into interstitial space
- leaked RBC release forms hemosiderin in skin
Venous dysfunction: CEAP classification system
- Clinical signs: varicose veins, edema, pigmentation, healed or active ulcers
- Etiology: congenital, primary, secondary causes
- Anatomic: superficial, deep, perforator veins
- Pathophysiology: reflux, obstruction, both
CEAP classification: clinical signs
C0: no visible or palpable signs 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
classification
CEAP: etiologic
Ec: congential
Ep: primary
Es: secondary (post thrombotic)
En: no venous cause identified
CEAP: anatomic
As: superficial veins
Ap: perforator veins
Ad: deep veins
An: no venous location identified
CEAP: pathophysiologic
Pr: reflux
Po: obstruction
Pr,o: refulx and obstruction
Pn: no venous pathophyiology identifiable
characteristics of venous ulcers
- Pain
- location
- tissue
- wound edges
- exudate
- periwound
- pulses
- temp
- 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
Management of venous ulcer
- 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
exercise indicated for..
with patients with vascular and integumentary disorders
- 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
What does
Exercise: aerobic exercise do for patients with vascular conditions/wounds
- 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
what does Exercise and mobility training do for patients with vascular and integmentary issues
- improves independence and safety
- increase perception of mobility
- enhance patient’s sense of well-being
tests and measures for vascular wounds
- 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
Pitting edme scale
1+ barely percepitble depression (2mm)
2+ 4mm (skin rebounds to its original contour within 15 seconds)
3+ 6mm skin rebounds to its original contour within 15-30 seconds
4+ 8mm (rebound >30 sec)
Pulses: scale 0-3+
- 0: absent pulse
- 1+: Diminished pulses
- 2+ normal pulses
- 3+ pathologically prominent pulses of severe aortic insufficiency or if the artery is aneurysmal
pulses: scale 0-4+
0: no palpable pulse
1+: faint but detectable pulse
2+ diminished pulse
3+ normal pulse
4+ bound pulse
circulation testing
capillary refill and ABI: numbers
- 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
Other tests
- 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
Non-invasive arterial testing
- 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
- commuted tomography angiography
