Pressure sores, vascular disease, diabetes - & their wounds Flashcards
COMPARE UPPER VS LOWER MOTOR NEURON INJURY IN PARAPLEGIA
- Root (lower motor neuron)
- Pure root below L1
- Flaccid paralysis
- Loss of sensation
- Cord (upper motor neuron)
- Pure cord lesion above T10
- Spastic paralysis (local reflex activity)
- Loss of sensation
WHAT IS THE PATHOPHYSIOLOGY OF SPASTICITY IN UPPER MOTOR NEURON PARAPLEGIA/PARALYSIS?
- Increase in muscle tone due to hyperexcitable stretch reflex.
- Elimination of CNS suppression of spinal reflex arc leading to hypertonia and hyperreflexia
LIST MEDICAL MANAGEMENT OPTIONS FOR SPASTICITY
- Diazepam - ↑ GABA receptor at cord – presynaptic inhibition
- Baclofen – GABA agonist at cord level
- Dantrolene – ↓ Ca released from sarcoplasmic reticulum in skeletal muscle
- Tinzanadine (ZANFLEX) – central α2 agonist à inhibits pre-synaptic sensory afferents
- Botulinum toxin type A – Inhibits Ach release at NMJ and prevents docking and fusion of Ach at presynaptic membrane, sprouting of blocked nerves forms new NM jxn to overcome effect
- Other Meds: Clonidine, Lamotrigine, Gabapentin, Cannabinoids (nabilone, dronabilone)
LIST SURGICAL MANAGEMENT OPTIONS OF SPASTICITY
- Nerve block
- Transthecal baclofen pump
- Selective dorsal rhizotomy – L2 to S2 dorsal nerve roots transected thus interrupting reflex arch. Subarachnoid infiltration of phenol is a chemical method of rhizotomy.
- Contracture release – lengthening or release of muscle or tendon
- Osteotomies: to correct bone deformity secondary to contracture
Discuss RF for development of a pressure sore
- Braden scale helps to identify most important local & systemic factors:
- Nutrition
- Sensation
- Activity
- Mobility
- Moisture
- Friction & Shear
- Other important systemic factors: LOC/dementia, DM, smoking, vasculopathy, other RF associated w/ poor wound healing
- Other important local factors: inflammation, infection, edema, FB
describe pathophysiology of development of pressure sore
- Pressure
- Dependent on pressure intensity & duration; Inverse relationship btwn pressure / time needed to cause ulceration
- normal capillary pressure ~ 12-30mmHg; 2x end-capillary pressure (~70 mmHg) for as short as 2 hours can produce ischemia (@ 500mmHg < 5 min)
- Injury can be prevented if pressure relieved for as little as 5min
- Muscle ischemia first, skin last
- Progression can be affected / accelerated by
- Infection – Bacterial counts increase in compressed areas – Proposed mechanisms: impaired lymphatic & immune function, ischemia
- Inflammation – Imbalance between proinflammatory MMP & their inhibitors = chronic wound development
- Edema – vasodilation = plasma extravasation & edema à sebum dilution (↓ protection against infection)
- Moisture – causes skin breakdown and maceration, ↑ coefficient of friction (e.g. fecal/urinary incontinence)
- Malnutrition – Contributes to weight loss, negative nitrogen balance, immunosuppression
how do you classify pressure wounds?
- National pressure ulcer advisory panel – most commonly used
- Stage 1: non-blanchable erythema intact skin (usually resolves after 1 hour of relief)
- Stage 2: PT skin loss (erythema lasts > 36h)
- Stage 3: FT loss, superficial to fascia ± tunneling
- Stage 4: FT loss, deep to investing fascia, damage to muscle/bone/etc
- Limitations: infection, eschar (unstagable), pre/post debridement
describe your history and physical exam for pressure wound:
- History
- General – Age, general health, pre-ulcer functional and ambulatory capacity
- Characterization of RFs – systemic (DM, ESRD, CVD, PVD, Tobacco, steroids/immune-suppressants, radiation, nutrition) & local (Braden scale)
- Wound history – chronicity/recurrence, changes, other sites, previous work ups and evaluations, wound care management to date, recent changes (new chair), previous procedures for wound closure including flaps used
- Symptoms of acute infection
- Physical Exam
- General: mental status, nutritional status, positioning, contractures, spasticity, soilage
- Neurovascular status of tissues (ie pulses, sensation, bleeding bed)
- Location and tissues involved
- wound edge and wound base
- presence/absence granulation tissue; beefy red vs. pale; hyper granulation
- Measurements: Location, size, depth, undermining, exposed bone
- Odour, infected/necrotic tissue
- Presence/location of scars, osteotomies etc
why would imaging be indicated for a pressure sore?
To rule in/out:
§ osteomyelitis
§ joint involvement
§ sinus vs fistula tract
§ peri-anal/peri-rectal disease
Discuss principles of pressure sore management and patient optimization
- Primary treatment / Prevention is key
- Education – patient, family, health care team
- Optimize nutritional status
- protein intake (1.5-3.0g/kg/d), caloric intake, micronutrients and vitamins: Vit C, Fe, Cu, Ca++, Zn
- serum markers: albumin > 20g/dL; blood sugar management
- Pressure off-loading
- use Braden scale to determine who should have dynamic pressure off-loading
- static (position changes q2h, foams) vs. dynamic (alternate pressure / low pressure mattress, Roho cushion)
- Debridement of necrotic/infected tissue
- tissue culture / pathology
- Clean and moist wound
- ensure prompt changes in incontinent patients, use of barrier creams/sprays (pro shield)
- consideration to urinary/fecal diversion
- non-operative management with dressings
- Management of spasticity
- baclofen, dantrolene, diazepam, botox
Discuss indication for non-operative management, and what that entails
- For stage I/II +/- III
- Optimization strategies as above plus:
- Local wound care
- Inflammatory phase (infected, necrotic)
- Consider treat infection systemically
- Sharp debridement of infected/necrotic tissue
- Mechanical debridement with dressings and reduction in bioburden: OD/BID
- Saline / betadine / Dakin’s (0.025% sodium hypochlorite) / sulfamylon (eschar, pseudomonas)/ antibiotic solution: gent/flagyl
- Promote healing (diverting colostomies, foley etc)
- Proliferative phase (granulating wound bed, going for contraction)
- minimal to moderate exudate: duoderm, hydrogel, intrasite, foam, occlusives
- moderate to severe exudate: aliginates, hydrocolloids
- NPWT
Discuss favourable wounds, unfavourable wounds, and contraindications to NPWT
Indication for NPWT
Unfavorable – NPWT
Contraindications to NPWT
- Full-thickness pressure ulcers (Stage III & IV)
- Ulcer size large enough to allow foam contact with base of the wound
- Poor / inadequate granulation tissue
- Presence of undermining/tunneling
- Presence of edema
- Inadequately debrided, fibrotic or desiccated wound bed
- Ulcer size too small to allow foam contact with the base of wound
- Inadequate hemostasis/bleeding disorder
- Inadequate perfusion to support healing
- Intolerance of pain resulting from therapy despite altered technique
- Inability to maintain an airtight seal
- Necrotic tissue w/ eschar
- Malignancy in wound
- Untreated osteomyelitis
- Non-enteric and unexplored fistulas
- Presence of a fistula to an organ or cavity in proximity to wound
- Allergy/sensitivity to NPWT material
**Cannot place foam directly on blood vessels, anastamotic sites, nerves, organs**
list indications for operative intervention for pressure sore
o Reserved for stage III/IV ulcers in appropriate patients
o Compliant
o Optimized (above)
o Able to pressure off-load surgical site
Besides usual optimization strategies, what are other pre-operative considerations for patient with pressure sore going for surgery?
o Pre-op consults (Anesthesia, Ortho-bony resections/joint, GIM/ID)
o Counselling (patient/family) about recurrence (>30%)
o urinary/fecal diversion
o future surgical procedures, recurrence, readvancements
o multiple pressure sites: stage and pressure off-load separately
o management and duration of antibiotics for OM
what are surgical goals for pressure sore management?
· Prevention of progressive osteomyelitis/sepsis (only consider reconstruction on stable, optimized wound)
· Reduction of protein loss through wound
· Improve quality of life
· Lower rehabilitation costs
· Improve patient hygiene and appearance
