Bennett Flashcards
Describe Peripheral vascular disease
- 4x more prevalent in diabetics
- arterial occlusion typically involves the tibial and peroneal arteries but, spares the dorsalis pedi artery
- CONTRIBUTING FACTORS
- Smoking
- HTN
- Hyperlipidemia
- elevated cholesterol or decreased HDL
- obesity and age
signs and symptoms of arterial occlusive disease
- claudication
- rest pain
- Atrophic, shiny skin
- diminished hair growth
- dependent rubor
- pallor on elevation
complications of peripheral neuropathy
- Sensory
- loss of protective sensation
- PAIN, PRESSURE, TEMPERATURE
- Motor
- Atrophy of the intrinisc muscles
- Flexion deformity (contraction of toes)
- Pressure at Met. Heads and toes
- Autonomic
- Dyshidrosis and dry skin
- AV shunting (increase in bone and skin perfusion)
Altered biomechanics
-associated with an increased risk of ulceration and amputation
–> increased plantar pressure
–> bony prominence
–> limited joint mobility
what are systemic factors that delay wound healing
- old age
obesity
chronic disease (diabetes, anemia etc)
malnutrition
vascular insufficiency
immunodeficiency
poor health
stress
what are local factors that delay wound healing
continued pressue
dessication and dehydration
trauma and edema
colonization or infection
lack of oxygen delivery
poor hygience
what are the phases of normal cutaenous wound healing
- Inflammation (3days)
- haemostasis
- cell migration
- Substrate phase (3-7 or 10 days)
- cell proliferation
- ECM synthesis
- angiogenesis
- maturation phase (day 10 –> 1 year) (becomes more organized adds strength)
- remodelling
- wound closure
- contraction and reorganization
What occurs for a stalled wound
- increased MMP (matric metallic proteases) or decreased TIMPs
–> kicks wound into high gear, if become too high its no longer beneficial
- exagerated inflammation and PAIN
- No trigger of acute tissue damage (need to debride)
- defiicency of growth factor receptors; destruct of GFs by MMPs
- fibroblasts become senescent (not really doing anything)
- increased bioburdon - biofil (greater risk of infection)
describe wagner grading system for diabetic feet
- Grade 0: no evidence of ulcer or infection.
- Grade 1: ulcers are superficial lesions, but suggest full thickness erosions of the epidermis; the dimensions of these, and all, lesions should be noted.
- Grade 2: ulcers may simply be considered deeper lesions that have penetrated to bone or a fascial plane (tracking).
- Grade 3: ulcers extend to bone, or have invaded a fascial plane and may be associated with abscess formation (infection or abscness)
- Grade 4: feet have gangrene of the forefoot, frequently requiring debridement or amputation.
- Grade 5: implies gangrene of the entire foot that will likely require amputation.
University of texas wound classification
DEPTH
– Grade O – Intact Skin, Pre or post ulcerative site
– Grade I – Ulcers are superficial wound through the epidermis/dermis
– Grade II – Through tendon or capsule
– Grade III – Through bone or into joints
COMORBIDITIES
– Stage A – Clean
– Stage B –Infection
– Stage C – Ischemic (poor circulation)
– Stage D – Ischemic and infected
Principles of ulcer management
- vascular supply
- debridement
- Infection
- Offloading
- wound management
- wound closure
- management of medical comorbidities (mgmt of diabetes)
- nutrition status (adequate PROTEIN)
What to look for on specific imaging techniques
- Plain radiographs can help identify bone destruction and gas in the soft tissues.
- Bone destruction seen on plain films or a computerized tomography scan (CT) may indicate osteomyelitis, but questionable cases may be resolved by nuclear imaging techniques such as bone scanning or leukocyte Indium scanning.
- Magnetic resonance imagine (MRI) may help evaluate for osteomyelitis, Charcot foot, or deep abscess formation in questionable cases.
Acute Osteomyelitis
Positive Tc-99m Scan
positive indium scan
Inactive chronic osteomyelitis
Acute cellulitis
charcot joint
Positive for Tc-99m Scan (phase 3 and 4)
- indium scan = negative
