wounds (art and ven insuff, p ulcers, lower extrem ulcers, diabetic food and leg) Flashcards
wht is a pressure ulcer
what is the initial sig of P ulcer
how does this progress to P ulcer
- P ulcers are localized areas of infracted soft tissue that occur when P applied to skin over time is greater than normal capillary closure P (25-32mm Hg. Critically ill pts have lower cap closure P and are more at risk)
- Initial sign is erythema d/t reactive hyperaemia (normally gone in an hr)
- First cutaneous tissue destr, then destr and necrosis of underlying soft tissueP ulcer thats painful and slow to heal
because immoblity is risk of P ulcer and If P occurs long enough small vein thrombosis and tissue necrosis occur
…this is most likely to occur where?
Bony prominences most likely site as only covered by skin and sm amounts of subcut tissue eg sacrum, coccygeal area, ischial tuberosistis, greater trochanter, heel, knee, malleolus, medial condyle of tibia, fibular head, scapula, elbow
how is adipose risk of P ulcer
Obese have lg amounts of poory vascularised adipose which is susceptibe to breakdown
what nutritional def could promote wound dev
what is good ndicator of protein levels?
which vit and minerals nec for repair
- Pts with nutrional def of low protein (good indicator is albumin. Low levels assoc with hypoalbuminemic tissue edema and inc risk of P ulcer) or negative nitrogen balance have tissue wasting and inhibited tissue repair.
- Anemic pts have dec O2 carrying capacity. Metb disorders canP ulcers. Vitamin c and trace minerals like zinc nec for tissue maint and repair
what is shear and what parts of body are most at risk of it
what is friction
- Shear is created by gravitational forces and friction. When it occurs, tissue layers slide over one another, blood vessels stretch and twist and microcirc to skin and subcut tissue is disrupted. Sacrum and heals are most at risk of shear
- Friction=resistance to movement that occurs when two surfaces are moved across each other
what is maceration and how does this affect ehaling
• Prolonged contact w moisture leads to maceration (softening) of skin
why are elderly so at risk of P ulcer dev
o Dec elasticity, dec collagen, muscle/tissue atrophy, polypharmacy, comorbidities all affect wound healing and inc risk of breakdown. Dec inflm response, decsubcut padding, dec intake
what factors do you assess for risk of pt dev P ulcer
o To assess risk of P ulcer dev assess: Mobility, sensory perception, cog abilities, tissue perfusion, nutritional, friction and shear, sources of moisture on skin, age
how often do you assess someones skin if they have risk of P ulcer
what do if pt has erythema
what labs are you checking
2x daily
check erythema for blanching
hgb, hct, lytes, albumin, transferrin, creatinine),
!! you have a pt with a stage 2 ulcer but it is healing. how do you document this
what if you had a stage 1 that is getting worse
o Ulcers can be upgraded eg stage 1 to 3 but not downgraded. Instead we say it is healing stage 3 ulcer or healed.
how many stages of P ulcers are there
I-IV
stage I P ulcer
these are NPUAP american ulcer categories..not sure what we use.. we need to know assessments of chronic wounds…
• Area of erythema that doesn’t blanch with P
• Inc skin temp
• Tissue swollen and congested
• Pt complains of discomfort
• Erythema progresses to dusky blue-grey
o Darkly pigmented skin may not have visibe blanching but colour may be different than surrounding area. Can be warmer or cooler than surrounding area.
stage II P ulcer
Stage II: skin breaks, abrasion, blister, or shallow crater, edema persists, ulcer drains, infect may dev
-Partial thickness loss of dermis.
-Presents as shallow open ulcer with red pink wound bed with no slough or
-as open/ruptured serum-filled or serosanguineous filled blister.
Presents as shiny or dry shallow ulcer without slough or bruising (bruising indicates deep tissue injury).
Dont use to describe skin tears, tape burns, incontinence assoc dermatitis, maceration or excoriation.
stage III P ulcer
Stage III: ulcer extends to subcut, infection dev, necrosis and drainage continue
o Full thickness tissue loss.
Subcut fat can be visible but no tendon muscle bone. Can have slough that doesn’t obscure depth of tissue loss.
May have undermining and tunnelling.
Depth varies
stage IV P ulcer
Stage IV: ulcer extends to muscle and bone, deep pockets of infect dev, necrosis and drainage continue
o Full thickness tissue loss. Osteomyelitis or osteitis likely.
o The bridge of nose, occiput and malleolus have no subcut adipose. These areas can have shallow ulcers
which stage can you first have tunneling
when can bruising appear
when tendon appears what stage is it
III=tunneling
not until III=bruising
tendon=IV
pt has nonblanching erythema and the skin is broken, which stage
you can see bridge of pts nose (bone) what stage
II ( one is nonblanching erythema but broken skin=2)
since theres little subcut tissue it is stage IV
!!do you want to have venous insufficiency raised above heart or arterial and why
venous to promote VR.
arterial should be below heart to use gravity to promote flow to extremities
you have pt with arterial insuff how can you inc their blood flow
o Moderate + isometric exercises to help blood flow + dev of collateral circ
o Enc moderate amount of walking until the point of pain, rest until pains gone, then walk again to inc endurance (and increases collateral circ). The pain shows lack of O2 to tissue.
interventions to promote vasodilation and prevent vascular compression
\:maint warm temp and avoid chilling. Discourage tobacco (causes vasospasm). Counsel to have stress mgmt and avoid emotional upset. Discourage constrictive clothes. Enc not to cross legs (venous stasis and compression) for >15min. Admin vasodilators (relax sm muscle) and adrenergic blocking agents (block SNS response and circulating catecholamines)
considerations with using heat on extremities of pt with arterial insufficiency
o A hot water bottle can be applied to pts abdm causing reflex vasodilation through lower extrem if pt is chilled (avoid hot water bottles and heating pads on extrem). Test temp of bath water. Even at low temps, trauma to the tissues can ocur in ischemic extrem. If pt has vasospastic disorder egRaynauds, heat that doesn’t exceed body temp can be applied to extrem.
o Excess heat may inc the metb rate of the extreme and inc need for O2 beyond that provided by dec arterial flow through diseased artery
if pt has severe art insuff is dilation possible
o Goal is to inc vasodilation in extremities but these patients, if arteries are severlysclerosed, inelastic or damaged, dilation is not possible
what is venous insuff
what veins can be involved
o Venous insuff results from obstr of venous valves in the legs or reflux of blood through the valves
o Both superficial and deep veins may be involved
o Resultant venous HTN can occur whenever theres been prolonged inc in venous P eg with DVT
o The thin walls of veins distend easily when venous P inc consistently. This stretches the valves and doesn’t let them close allt he way, causing backflow or reflux of blood in veins
maybe too specific of a wound not sure…
20-50% of pts post DVT get postthrombotic syndrome what is this
what kind of wound can result
how can it look
where is it
qaulity of the skin
risks
o PTS is characterized by chronic venous stasis, resulting in edem, alt pigmentation, pain, and stasis dermatitis
o Stasis ulcers dev d/t rupture of small skin veins and seubseq ulcerations. The RBCs degranulate in surrounding tissue which leaves brownish discolouration of the tissues. This pigmentation and ulceration usually occurs in lower parts of the extrem, in the area of malleolus of ankle. The skin gets dry, cracks and itches, subcut tissues fibrose and atrophy. The risk of injury and infect of the extreme is inc.
