Pressure Ulcers Flashcards
what is the pathophys behind pressure ulcers caused by presssure
unrelieved external pressure results in localized ischemia and/or necrosis of the underlying tissue
- tissue damage w/ high pressures for short time or low pressures for long time
note: “excess” pressure changes per tissue tolerance in each patient - average of capillary closing pressure in arterioles = 32 mmHg
- average of capillary closing pressure in venules = 12 mmHg
what is the pathophys behind pressure ulcers caused by shear forces
- acts parallel to skin’s surface, so skin is in fixed position but tissue underneath shifts, tearing the capillaries
- may contribute to undermining and/or sinus tracts
what is the pathophys behind pressure ulcers caused by heat and moisture
- moisture: causes maceration, which makes skin 5x more likely to breakdown than intact skin
- heat: 1 deg C in skin temp=10% INC in tissue metabolism, but cutaneous capillaries can’t dilate to dissipate heat since pressure causes occlusion (create tissue hypoxia and necrosis)
what are the general risk factors to develop PU’s
- decreased mobility
- diminished mental capacity
- incontinence (maceration)
- PMH of PU’s
- bed surfaces or tight clothing
- medical devices
what are intrinsic risk factors to develop PU’s
- malnutrition/dehydration since nutrients (calcium, vit C/A, zinc) are needed for collagen synthesis
- prealbumin
stage 1
intact skin w/ non-blanchable redness of a localized area
stage 2
partial thickness loss of dermis, shallow ulcer w/ red/pink wound bed and NO slough or serum-filled blister
painful
stage 3
full-thickness loss, with possible slough and may be able to see subcutaneous fat
stage 4
full-thickness tissue loss and exposed bone, tendon or muscle, slough and eschar present
deep tissue
purple or maroon localized area of discolored intact skin or blood-filled blister
-usually progress to stage 3 and 4
unstageable
full-thickness tissue loss in which the base of the ulcer is covered by slough and/or eschar in the wound bed, so you can’t see what’s at the base
what is the pathophys behind neuropathic ulcers
numerous alterations occur in the structure/fxn of the foot, which leads to changes in weight bearing, posture, and gait to elevate focal pressure
what is the pathophys behind Charcot neuropathic ulcers
- elevated BG from DM over long period of time cause this foot deformity
- leads to: ankle equinus causing mechanical stress, increased peripheral blood flow due to sympathetic denervation, osteolysis or osteopenia, loss of protective sensation
- cycle from fracture, healing and remodeling through a series of fractures due to perceived/unperceived trauma
what are the risk factors of neuropathic ulcers
- DM >10 years
- male
- uncontrolled BG
- peripheral neuropathy w/ loss of protective sensation
- altered biomechanics
- CV, retinal, or renal complications
what is a hallmark clinical sign of neuropathic ulcer
hyperkeratosis or callous formations
what is unique medical management of DFUs
- total contact casting
- confirm vascular supple
what is the pathophys of venous ulcers and where are they located
- above malleoli
- ambulation causes foot/calf muscle pumps to push venous blood up, which reduces venous pressure
- if calf pump fails to activate conduit veins, pressure increases in the veins and ulcers develop from inc. internal pressure
- venous thrombosis, obstruction, and hemorrhage all contribute as well
describe how venous thrombosis increases likelihood of venous ulcers
as platelets adhere to endothelial walls and lumen become occluded, valves become damaged which can INC internal pressure
describe how venous obstruction INC likelihood of venous ulcers
- when obstruction is in superficial veins, rarely form ulcer b/c collateral vessels compensate
- when obstruction is in deep veins, increase swelling and ulcer formation
what is key component of med management
- compression and calf muscle pump
- should heal w/l 1 mon
what is clinical presentation of venous ulcer
- distal medial third of leg
- swelling, aching, heavy
- pain worse in standing and better with elevation
- hemosiderin staining from blood leeking
what are med diagnostic tests for venous ulcers or arterial wounds
- ABI
- doppler US
- venography or arteriogram
what is the pathophys behind arterial insufficiency causing wounds
structure of arterial wall changes due to:
-lumen narrowed by lipid plaque (DM, smoking, HTN, older than 50)
-vasomotor diagnoses: Raynaud’s
structural changes cause lack of adequate perfusion, leading to ischemic skin changes and necrosis
how can progression of arterial wounds be slowed down
exercise promotes growth of collateral vessels in patients w/ intermittent claudication
-Contraindicated in patient’s w/ critical limb ischemia (ABI
what is the typical clinical presentation of arterial wounds
- pain w/ elevation
- diminished pulses
- pale, dry wound base w/ little drainage
- thin, shiny, and hairless skin
- hypertrophic nails
- ABI
what is the med management of arterial wounds
- angioplasty or stents
- limb protection techniques
- exercise if indicated
- thrombolytics
what is the pathophys of surgical wounds
risk factors for dehiscence (surgical wound re-opening):
- infected wound
- DM
- high dose steroids
- bacterial lvls
- mechanical stress from malnutrition, compromised perfusion, and ab incision w/ coughing or sternal incision w large breasts
what are the 2 different skin flap location in LE amputations? what are the 2 types of skin flaps?
- equal ant. and post. flaps
- longer post. flap
- myoplasty: muscle-to-muscle (agonist and antagonist) for stailization
- myodesis: muscle to bone for transtibial amps
how can you differentiate between superficial and deep wound infections
- superficial (NERDS): Non-healing, exudate increase, red/friable tissue, debris present, smells (topical therapy)
- deep (STONEES): size increasing, temperature increasing, osteomyelitis, new/satellite wounds, erythema, edema, and smell (systemic therapy, 3+ of either of these is indication)
how can you prevent surgical wound dehiscence
pre-op: no anti-coagulants, good diet, no smoking
post-op: blood volume, maintain warmth for vasodilation, BG
