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PRESSURE SORES
EPIDEMIOLOGY
 Common, especially in 2 groups of patients:
1. paraplegics
2. the elderly and infirm
 prevalence:
1. 10% to 18% in the general acute care setting,
2. 2.3% to 28% in long-term care facilities
3. 0 to 29% in home care settings.
 highest incidence is seen in elderly patients with femoral neck fractures (66%) and in quadriplegic patients
(60%).
 2/3s of these patients will be >70 years of age.
 25-85% of paraplegics suffer at least one pressure ulcer.
 Pressure sores are the direct cause of death in 7-8% of paraplegics through complications such as
osteomyelitis or sepsis.
 1-year mortality rate of 50-70% among hospitalized patients after developing a pressure ulcer.
 Development of new pressure ulcers is not an independent risk factor for increased mortality, but rather an
indirect marker for coexisting illness, malnutrition, and decreased functional status.
 Chronicity of the lesion imparts great cost to their management.
 most common site of occurrence- sacrum (36%) followed by the heel (30%).
 Stage 1 ulcers accounted for 47% of lesions and stage 2 for 33%.
 In the early acute phase after spinal cord injury, the sacral area tends to be the most common site of pressure
ulcers as patients are stabilized and treated.
 In the subacute and chronic phases after spinal cord injury, the ischial area becomes the predominant site of
pressure ulcers as the patient begins to sit up in a wheelchair during rehabilitation.
AETIOLOGY
 three patient groups are at risk of developing pressure sores
1. the neurologically impaired
o immobility
2
o diminished sensation
2. the elderly
o poor wound healing – vessel disease, malnutrition
o incontinence
o thin skin prone to shearing
o immobility
3. the hospitalized.
o Immobility
o Reduces sensation (ie epidural)
o malnutrition
Multifactorial Hypothesis
 The current hypothesis in the mechanism of pressure sore formation is that they are multifactorial in aetiology
 Both extrinsic and intrinsic factors contribute to their cause. It is a complex process and cannot be attributed
to any one factor.
 Extrinsic Factors
1. pressure - perpendicular load exerted on a unit area;
2. shear - mechanical stress parallel to the plane;
3. friction - friction is the resistance of two surfaces moving across one another
 Intrinsic Factors
1. local ischemia or fibrosis

angiogenic response is dependent on anatomical location and is attenuated significantly in the lower,
as compared with upper, dorsum
2. diminished autonomic control - loss of the protective circulatory reflex responses (neuropathic theory)
3. infection
4. patient age
5. weight
6. sensory loss
7. impaired mobility
8. decreased mental status
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9. fecal or urinary incontinence
10. Predisposing diseases: arteriopathy, DM, collagen vascular diseases
11. anemia
12. hypoproteinemia.
Pressure
 The single most important factor in the aetiology of pressure sores.
 universally accepted that pressure begins the process
 In the supine position, the sacrum, buttocks, heels and occiput are subject to the greatest pressures, in the range
of 40-60 mmHg.
 In the prone position, the knees and chest are subject to 50mmHg
 In the sitting position, pressures of 100 mmHg can occur over the sacrum.
 But, how much pressure? For how long? Which tissues most susceptible?
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 Low pressures over a longer time have a greater propensity to cause pressure sores than high pressure
of short duration. Time factor more important than pressure intensity. The longer the duration of pressure
applied, the greater its effect.
 70 mmHg for 1-2 hrs will produce irreversible tissue damage.
 Arterial capillary pressure is 32 mmHg. Sustained pressure greater than this for any lengthy period will
produce a pressure sore. Effect of shearing will modify this pressure threshold
 Uninterrupted pressure is important in the formation of pressure sores.
 Pressures are greatest over the bone and decreases towards the periphery.
 The muscle is more susceptible to pressure than the skin - because of the higher metabolic requirements of
muscle. Muscle begins to necrose after 4 hours of ischemia whereas skin can withstand approximately 12
hours of ischemia before it begins to show signs of necrosis.
 Body weight is borne by superficial bony prominences which are not covered by muscle.
 So long as an applied load is evenly distributed over the whole body, human tissue can tolerate a high degree
of pressure – ie deep sea divers
 Thus, relates to duration of pressure, degree of pressure and site of pressure.
 Pressure is not the only factor in the development of pressure sores. For example, patients with cerebral palsy
have a lesser tendency to develop pressure sores than patients with neurol deficits of other cause.
2. Friction and shear
 Friction rubs off the epidermis
o increases transepidermal water loss and allows moisture to accumulate on the surface of the
body, which in turn raises the coefficient of friction and may cause adherence.
 Shear theory: shear (or stretch) of muscular perforators results in ischaemic necrosis.
3. Nutritional status
 Poor nutritional status plays a role in the development of pressure sores and leads to chronicity due to poor
healing
 no study has demonstrated that improvement in nutritional status can prevent pressure sore
4. Infection
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 Bacteria do not cause pressure sores, but they do contribute to tissue breakdown and delayed wound healing.
 Generalised sepsis leads to local infection at the site of pressure, abscess formation, extension of
inflammation, thrombosis and worse tissue necrosis.
 Septic sores usually enlarge and once the infection controlled, healing occurs.
 Washing with soap and water simply cleans pressure sores and reduces the bact load.
 In a prospective, double blind clinical trial examining topical therapy, silver sulphadiazine was found to be
better than povidone iodine which was better than saline in reducing bacterial load.
5. Paraplegia
 Why?
1) Restricted mobility
2) Loss of sensory “alarm system”
3) Faecal and urinary incontinence macerates skin, promotes tissue breakdown and infection.
 Denervation increases the susceptibility to pressure ulceration and especially infection.
 Occur more commonly in flaccid than spastic paraplegics (Controversial!).
 Flaccid paralysis occurs when the roots are divided (no local reflexes). Below T10.
 Spastic paralysis occurs when the cord is completely transected above the area allowing local feed back
reflexes but no inhibition from above. Sensation is absent as is central control of movement. (Above L1 vert).
Spasticity occurs in 40-54%. Spasticity more common in higher lesions.
 Above T10-cord only.
 T10-L1 -roots and cord.
 Below L1- roots only.
PATHOPHYSIOLOGY
Acute phase
 Pressure, erythema swelling, blistering, cyanosis
 The acute phase can be reversed by relieving the pressure and other measures.
 Can also progress or become secondarily infected.
Chronic phase
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 Further, deep destruction occurs to involve subcutaneous tissue, fascia, muscle, bone and joints. Often the
superficial extent of the necrotic area is small in comparison to the deeper layers.
 Osteitis or septic arthritis may occur as sequelae which can lead to pathological fractures and dislocations.
 With periods of repeated healing and breakdown, scar tissue becomes evident and the epithelium at the edges
thin, shiny and atrophic. Granulation tissue may be pale and purulent.
 The patient’s general condition deteriorates: malaise, protein deficiency, anaemia.
 Long sinus tracts can develop to deep seated cavities or joints.
 Genito-urinary problems, septicaemia and death can ensue.
 Amyloidosis with resultant renal failure is a common cause of death.
Pathophysiological Stages
Stage 1
Hyperaemia: Redness occurs after 30 minutes of pressure.
Relieved an hour after pressure removed.
Stage 2
Ischaemia:
Develops after 2-6 hours of continuous pressure.
Takes 36 hrs to resolve.
Stage 3
Necrosis:
Occurs after 6 hours of continuous pressure.
Prolonged period required to heal.
Stage 4
Ulceration:
Takes about 2 weeks to develop
RISK FACTORS
 Various scales and grading systems have been tried (eg, the modified Norton scale), but in prospective studies,
these have not been found to be of useful prognostic value.
 Braden scale for predicting pressure sore risk is one of the most widely used risk assessment tools. Composite
of six subscales:
1. sensory perception
2. skin moisture
3. activity
4. mobility
5. friction and shear
6. nutritional status
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 scale has a minimum value of 6 and a maximum value of 23. Score of 16 = threshold for pressure development
in tertiary care facilities.
SITES
 The vast majority (87%) occur in the lower half of the body
o 2/3 occur in the hip/buttock area
o 25-33% occur in the lower limb
 Can occur anywhere, even well padded soft areas.
 In paraplegics the frequency according to site is as follows:
Ischium
28%
Sacrum
17-27%
Trochanter
12-19%
Heel
9-18%
Malleoli
5-8%
Pretibial
4-5%
Patella
4%
Foot
3%
ASIS/crest
2%
Other sites:
costal margin, elbows, occiput, etc.
 Site of development dependent on whether patient bedridden, wheelchair bound or ambulatory and on whether
spastic or flaccid paralysis.
o Flaccid, bedridden patients  sacral, trochanteric, calcaneal, thoracic, occipital.
oSpastic patient, in addition, may develop medial knee or malleolus sores.
oWheelchair patients  ischial, thoracic, foot sores.
CLASSIFICATION
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 By the time the skin ulceration is seen, the underlying ulcer may already be quite deep. The skin changes are
merely the tip of the iceberg.
PREVENTION

Basic principles
1. Monitoring of pressure sites
2. Basic skin care
3. Control Spasticity
4. Pressure dispersion
5. Turning - alternating weight bearing sites
6. Good general condition: nutrition, anaemia, etc.
Skin care
1. Frequent cleansing with soap and water.
2. Prevent excessive skin moisture
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a. moisture can cause a fivefold increase in the risk of developing an ulcer.
b. Indwelling catheter and urinary/faecal diversion to prevent soiling
3. Keep the bed free of particulate matter.
4. Avoid excess moisture on the skin.
Control Spasticity


Nonoperative

muscle relaxants (diazepam, baclofen, botox)

intrathecal phenol

positioning
Operative

Neurosurgical ablation (cordotomy or rhizotomy)

Amputation

Contracture release
Pressure dispersion
1. Proper patient positioning
2. Seated patients must lift themselves or be lifted from their chairs for at least 10 seconds every 10 minutes,
and recumbent patients must be repositioned at least every 2 hours.
3. Wheelchair pads

Cushions for wheelchairs filled with gel, foam, air, or water are available to help relieve pressure.

typical wheelchair sling seat exerts a “hammocking” effect that can produce abnormal scoliotic posture
and pelvic obliquity. This in turn causes asymmetrical pressure on both trochanter and ischium that
requires specialized cushions for prevention.

Subcutaneous pressures decreased with thicker cushions, with the maximum effectiveness obtained with
an 8-cm cushion

Although wheelchair pads reduce pressure, they do not do so enough to prevent ischial sores.
4. Sophisticated beds

air mattresses
i. Low-airloss (LAL) beds
a. support the patient on multiple inflatable air-permeable pillows.
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b. LAL beds produce consistently less pressuresthan standard beds or water beds.
c. When LAL beds are adjusted properly, the pressures measured at the skin-surface interface are
comparable to those recorded with air-fluidized beds.
ii. Air-fluidized beds
a. patient floats on ceramic beads while warm, regulated air is forced through, helping to eliminate
excessive moisture from the skin.
b. the forced warm air may cause too much fluid loss and dehydration, particularly of large, open
wounds.
c. turning and repositioning in bed can be difficult

Matrress overlays
i. static pads - composed of high density foam-, gel-, water-, or air-filled sacs
ii. alternating air cell (AAC) mattresses

mattresses lose their ability to provide near-0 interface pressures when the head of the bed is elevated to
45 degrees or higher. Patients should avoid prolonged periods of sitting in this position while on these
mattresses.

No one device has been shown to be clearly superior over the others, but they all have been shown to
reduce tissue pressure over conventional hospital mattresses and wheelchair cushions.

Established pressure sores heal 3 times faster with low-air-loss beds. Although expensive, some authors
have found them to be cost effective.
Alternating weight-bearing surfaces
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1. Regular turning by nursing staff (2 hourly).
2. “Pressure conscious patient” Seated patients must lift themselves for 10 seconds every 10 minutes.
3. Stryker frame, ripple mattress, rotating and electric beds are all helpful.
4. Electrical stimulation of gluteal muscles sequentially alters its pressure bearing configuration and has been
shown to be useful.
TREATMENT
a) Medical
b) Surgical
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MEDICAL
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Multidisciplinary care
1.
Medical/spinal physician to optimise medical care
2.
Urologist - Renal tract ultrasound to exclude infection
3.
Orthopedic/spinal surgeon
4.
Microbiologist
5.
Wheelchair engineer/occupational therapist
6.
Physiotherapist
7.
Social worker
Principles
1. Avoid pressure (see above)
2. Keep clean, appropriate wound care
3. Debridement of dead tissue/slough
4. Control of infection (topical agents)
5. Relief spasms
6. Improve the general condition of the patient (nutrition, anaemia)
Protocol
1. Acknowledge that every patient with limited mobility is at risk for developing a sacral, ischial,
trochanteric, or heel ulcer
2. Daily assessment of the skin, particularly around the at-risk areas, including ischial, sacral, trochanteric,
and heel areas
3. Objective measurement of every wound by photography (at a minimum, weekly) and thorough
documentation of the wound's progress with a graph, recording the wound area, depth, and region and
degree of undermining
4. Immediate initiation of a treatment protocol upon recognition of a break in the skin
5. Mechanical debridement of all nonviable tissue
6. Effective wound-bed preparation and establishment of a moist wound-healing environment
7. Aggressive nutritional supplementation of all malnourished/undernourished patients
8. Pressure relief for the wound and other at-risk areas
9. Elimination of all drainage and cellulitis
10. Consideration of biological therapies for all patients with wounds not healing rapidly after initial
treatment
11. Physical therapy
12. Palliative care
 Above principles should be tried in all individuals
 Conservative measures result in healing in a variable number of patients (30-80%).
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 Which ulcers will heal and which will not is difficult to predict before hand.
 Healing usually is prolonged, taking around 3 months in those that do heal.
 In those with a tendency to recur, suspect noncompliance
 Grade I-II ulcers heal more readily than grade III-IV.
 The overall goals of treatment and the ethics of Mx must be considered.
Nutrition
 High protein, CHO and vitamin diet to restore a +ve N balance.
 Nutrition must be corrected early and the patient must be well nourished prior to surgery.
Anaemia
 Correction goes hand in hand with restoration of normal nutritional status.
 Iron, folate and blood transfusions if necessary
Relief of spasm
 Can make the sores worse and interfere with surgery.
Dressings
 Prolonged administration of topical antibiotics may impair wound healing and promote bacterial resistance.
 Occlusive – some have concerns that this worsens infections
 Semiocclusive - maintain a moist local wound environment by trapping moisture from the wound and holding
it at the surface while allowing gases (oxygen and carbon dioxide) to pass.
 goal of wound-bed preparation is to have well-vascularized granulation tissue without signs of local
infection, which includes drainage, cellulitis, and odor.
 Three topical treatments shown to enhance the wound-bed preparation are
1) Iodosorb, an efficient antiseptic that does not inhibit the healing process. Moberg found that Iodosorb
is more effective than normal saline dressings as treatment for decubitus ulcers.
2) the nanocrystalline silver-based dressings, such as Acticoat, Actisorb Silver 220 (, and Acquacel Ag
(Convatec, Princeton Junction, NJ), which are reported to minimize the potential of fungal infection,
thereby reducing some complications that delay wound healing
3) collagenase, which although designed as a chemical debriding agent, may also help prepare the wound
bed and stimulate local granulation tissue.
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 Healthpoint System (HP) consists of three FDA-approved gel products—Accuzyme, Iodosorb, and Panafil
1. Accuzyme, a papain–urea debridement ointment, is best suited for necrotic wounds.
2. Iodosorb gel and Iodoflex pads consist of 0.1 to 0.3 mm hydrophilic beads containing 0.9%
cadexomer iodine. Iodosorb is identical structurally to Iodoflex, the latter being indicated for larger,
deeper ulcers. When applied to an infected wound bed with liquefaction necrosis, the beads soak up
bacteria and cellular debris by capillary action, thus reducing inflammation, odor, and edema, while
concomitantly releasing iodine, which imparts antimicrobial properties to the dressing.
3. Panafil—a papain–urea–chlorophyllin–copper ointment—is ideal for clean, granulating wounds.
 Negative pressure wound therapy
o consists of an open-cell polyurethane or polyvinyl alcohol foam sponge with a pore size ranging
from 400–600 m in diameter.
o Benefits

removes interstitial fluid high in cytokines, collagenases, and elastases, which are
known to inhibit fibroblast development and proliferation.

Improves tissue perfusion -the interstitial fluid causes a mechanical occlusion of local
capillary blood flow.

increased granulation tissue,

decreased bacterial counts
o There are no published results that it is better
o contraindications
1.
fistula
2.
necrotic tissue
3.
haemorrhage
4.
active infection and osteomyelitis – relative, has been used for infected sternum
5.
cancer
 External tissue expansion using skin traction device (Br J Plast Surg Jul 2001)
o Used for patients with significant co-morbid conditions that, except for one wheelchair-bound
person,confined them to bed.
 decubitus direct current treatment (DDCT) electrostimulation - time needed for wound closure was 52%
longer in placebo group compared with treatment group (Arch Gerontol Geriatr 2005)
 Experimental
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o GM-CSF
o PDGF-BB
o Topical NGF
o Apligraf
SURGICAL
 Debridement usually required for grade III-IV sores.
 Reserve reconstruction for fit patients who have unstable wounds not responding to conservative
management
Goals of Surgery
1. improve hygiene and appearance
2. lower rehabilitation costs
3. reduce protein loss through the wound
4. prevent osteomyelitis and sepsis
5. avoid future Marjolin’s ulcer
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6. avoid progressive secondary amyloidosis and renal failure
Guidelines (Conway and Griffiths, 1956)
1. Excision of the ulcer, surrounding scar, underlying bursa and soft tissue calcification.
2. Radical removal of the underlying bone.
3. Padding of bone stumps and filling of dead space with muscle or fascial flaps.
4. Resurfacing with a large, regional, pedicled flap.
5. Haemostasis and suction drain.
6. Tension free closure or grafting the secondary defect with thick split skin.
Timing for reconstruction
 The patient must be in good general condition.
 The ulcer must be ready for surgery: no necrotic tissue or infection, healthy granulation tissue, improving
ulcer, ie advancing epithelial margin.
 Delay reconstruction if osteomyelitis suspected
o Confirm with bone scan or CT
o MRI preferred by some - more sensitive to marrow edema
o Best test is bone biopsy
o Give 6 weeks IV antibiotics
General peri-operative care
 Usually prone position for surgery. Pressure points well padded.
 Catheter - every attempt should be made to sterilize the urinary tract prior to surgery pending installation of an
indwelling catheter
 Pre-op bowel washout plus op site over the anus, or faecal diversion procedure. Low residue diets and codeine
may be useful in the patient with loose stools and soiling. Although colostomy may be useful, some are against
the procedure.
 Sedation of GA (often sedation sufficient)
 Good monitoring: often extensive blood loss d/t loss of sympathetic vasoconstrictory tone.
 The whole ulcer must be excised: mark the margin of undermining with a curved clamp and ink and it is often
useful to spread ink inside the ulcer.
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Flap design (Conway and Griffiths, 1956)
1. As large as possible.
2. Suture line away from the area of direct pressure.
3. The flap design should not violate adjacent flap territories so as to preserve options in the event of a recurrence
or breakdown.
Flap selection
 Based on a number of factors:
1. site of sore
2. previous ulceration or surgery
3. level of the lesion
4. rehab and ambulatory status/potential
5. daily habits
6. motivation and education
7. associated medical problems
 Bear in mind the tendency for pressure sores to recur.
 Safeguard as many options as possible.
 Options: skin, F-C, muscle + SSG, M-C, free flap.
Muscle
 Indications for using muscle are poorly defined. On the one hand, muscle is more prone to ischaemic necrosis
than either skin or subcutaneous tissue. Muscle necrosis has been noted despite intact skin. On the other
hand, in the rat model, when muscle was interposed between skin and bone, the incidence of ulceration
decreased from 100% to 69%. The muscle mass helps to diffuse the effects of pressure on the skin.
 Muscle is regarded as beneficial for the following reasons:
1. supplements vascularity
2. enhance perfusion and tissue coaptation in the depths of a pressure sore defect
3. eliminates dead space - eliminate dead space in a deep wound, assisting in hemostasis and preventing
subsequent fluid collection beneath the flap
4. provides a pad for wider dispersion of residual pressure (at least temporarily)
5. acts as a barrier for vertical spread of the infection.
 The use of muscle allows more rapid healing and fewer Cx (breakdown, infection, haematoma).
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 Muscle does tend to atrophy d/t interuption of reflex arcs, division of its tendon, possible devascularisation and
repeated pressure.
 No difference shown between M-C flap and muscle flap covered by SSG.
 Wong TC: Comparison of gluteal fasciocutaneous rotational flaps and myocutaneous flaps for the treatment
of sacral sores. Int Orthop. 2006 Feb
 The rate of healing of the sore, sore healing time and complication rate were comparable in the two
groups but the rate of recurrence was lower to a statistically significant extent in myocutaneous flap
patients. The authors suggest that both methods are comparable, good and safe in treating sacral sores;
myocutaneous flaps are more durable.
 Yamamoto Y: Long-term outcome of pressure sores treated with flap coverage. PRS Oct 1997
 45 ischial sores and 24 sacral sores in 53 paraplegic patients
 FC flaps resulted in less recurrences than myocutaneous or muscle flap for treatment of ischial and sacral
sores
Perforator flaps
 Koshima developed the superior gluteal artery perforator flap, which they used to cover trochanteric and
ischial pressure sores.
 not only preserve muscle, but also conserve future reconstructive options and adhere to the principle of placing
the suture line away from the area of direct pressure.
 muscle sparing should always be a goal in the ambulatory and sensate patient, as it may prevent some
functional loss and potentially reduce postoperative pain.
Free flaps
 Free flaps have been shown to have a role in pressure sore Mx.
 tensor fascia lata muscle skin unit as a free flap for lower trunk reconstruction with sensation is maintained by
including the lateral femoral cutaneous nerve in the neurovascular pedicle.
 Plantar skin (resilient skin pad) has been transferred as a free flap to successfully provide ischial padding.
Tissue Expansion
Controversial.
 Primary indication to cover shallow ulcers with no dead space to fill.
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 Usually reserved for difficult cases requiring additional tissue for coverage.
Proponents:
 Well tolerated in plegic patients.
 Especially useful for transferring sensate skin.
 Improved vascularity after expansion
 Despite the apparent contradiction of placing a TE in patients at high-risk for pressure induced dermal wounds,
the TE actually protects by distributing the forces evenly, instead of concentrating the pressure on a small area
of the bony prominence.
Critics:
 TE can be problematic:
a) a foreign body
b) inserted close to a contaminated pressure sore
a) especially if inserted into anaesthetic area.
RECONSTRUCTION BY ANATOMIC SITE
SACRAL SORES
for small sores:
1. Primary closure (after wide undermining)
2. SSG
3. Reverse dermal graft
4. Random skin flaps
Options for significant sores:
1. Gluteus maximus muscle or fasciocutaneous flaps (many ways to use it)
2. Lumbar artery perforator flap
3. Transverse lumbosacral back flap
a. based on the contralateral lumbar perforators
b. donor site is most commonly skin grafted.
4. Parasacral perforator based M-C flap
5. fasciocutaneous flaps
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6. Sensate flaps
a.
intercostal island flap
b. TFL flap with nerve graft from intercostal to LFCN
c. Has appeal in that it may reduce recurrence
Lumbar artery perforator flap (Kato BJPS 1999)
 four lumbar perforators on either side of the midline.
 second lumbar artery best choice as it was reliably present and had the largest caliber.
 medial border was 5 cm lateral to the midline, and the lateral margin extended over the midaxillary line.
 Advantages of this flap were:
1)no sacrifice of muscle
2)large rotational arc based on a single pedicle
3)donor site can be closed primarily
Modification by de Weerd and Weum (BJPS 2002)
 include 2nd anr 3rd lumbar artery perforators as well as the intermediate nerve to preserve protective sensation.
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Gluteus Maximus
 The gluteus maximus flap is the workhorse for sacral sore coverage.
 Traditionally, the upper half of the muscle is taken and transferred based on the superior gluteal vessels.
 Variations:
1) V-Y gluteus advancement flaps
 Preferably based on the superior half of the gluteus muscle to preserve overall muscle function.
 Sliding gluteal flap (Ramirez) – VY musculocutaneous flap based on IGA
2) Turnover gluteal flap
3) Bilateral gluteus advancement-rotation flaps
4) Gluteal fasciocutaneous flap
 Less reliable in obese patients – aim to include muscle
 Superior gluteal artery perforator flap most commonly used
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hatchet design VY advancement
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ISCHIAL SORES
for small sores:
1. Primary closure (after wide undermining)
2. SSG
3. Reverse dermal graft
4. Random skin flaps
Options for significant sores:
1. Posterior thigh flap (many ways)
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2. Posteromedial thigh flap
 Based on musculocutaneous perforators from either the gracilis or the adductor magnus muscle
3. Inferior gluteus flap (rotated from above and laterally down and medially).
4. IGAP (Blondeel BJPS 2002) – more ideal for ischial pressure sores
5. Anterolateral thigh
6. Gracilis
7. Hamstring (mainly biceps femoris)
8. TFL
9. Vastus lateralis
10. Transpelvic rectus abdominis
 Transferred through the retropubic space of Retzius to the perineum (separation of peritoneum from
the transversalis fascia over the bladder, extends from the muscular floor of the pelvis to the Arcuate
line).
 Because the rectus muscle initiates vertebral flexion and aids in respiration, urination, defecation, and
vomiting, the muscle is more important, and thus less expendable, in paraplegics than in
neuromuscularly intact patients.
 Used as a salvage
Foster RD: Ischial pressure sore coverage: a rationale for flap selection. Br J Plast Surg. 1997
 114 consecutive patients underwent flap coverage of 139 ischial pressure sores
 inferior gluteus maximus island flap and the inferior gluteal thigh flap had the highest success rates,
94% (32/34) and 93% (25/27), respectively, while the V-Y hamstring flap and the tensor fascia lata flap had
the poorest healing rates, 58% (7/12) and 50% (6/12), respectively.
 overall complication rate was 37%
 Flap success was not significantly affected by the age of the patient or the prior number of flaps used
Posterior Thigh Flap
 The posterior thigh flap, a fasciocutaneous flap based on the descending branch of the inferior gluteal artery, is
the workhorse.
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 The flap is centred over a vertical line down the back of the leg defined above as being halfway between the
ischial tuberosity and the greater trochanter and below halfway between the medial femoral condyle and the
posterior border of the fascial lata.
 a cutaneous branch of the inferior gluteal artery that accompanies the posterior femoral cutaneous nerve
between the semitendinosus and biceps femoris muscles
 In 30% of cases this branch of the inferior gluteal artery is said to be absent - —the flap can be elevate as a
superiorly based random fasciocutaneous unit supplied by multiple perforators from the cruciate anastomosis
of the fascial plexus.
 It can be used as a transposition, rotation, V-Y advancement or sliding flap and may or may not include biceps
femoris.
Gluteus Maximus
 SGAP flaps will not reach ischial sores
 inferior gluteal myocutaneous rotation flap donor site often leads to donor site problems thus IGAP (muscle
sparing) may be preferable
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Tensor fascia Lata
 Origin – 5-8cm of outer lip pf ASIS
 Insertion – iliotibial tract into lateral condyle tibia
 Nerve supply – superior gluteal nerve
 Blood supply
o Type 1
o Ascending branch of LCFA
o 10cm below ASIS
o Distal 1/3rd (8-10cm above knee) is supplied by the superior geniculate artery
The skin of an extended tensor fasciae latae flap can be thought of as
analogous to a fasciocutaneous flap with three vascular territories. The
subcutaneous plexus overlying the tensor fasciae latae muscle constitutes the
proximal vascular zone. The subcutaneous plexus comprising perforators of the
profunda femoris artery constitutes the middle vascular zone. The superior lateral
genicular artery is the predominant vessel supplying the distal zone of the
extended tensor fasciae latae flap. The watershed area between the middle and
distal zones is about 8 to 10 cm proximal to the knee joint, where the flap usually
becomes unreliable. FA, femoral artery;LCFA, lateral circumflex femoral
artery;PFA, profunda femoris artery;SLGA, superior lateral genicular artery.
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 Line drawn from ASIS to the lateral condyle of tibia represents the anterior extent
 Flap may be taken up to 10cm posterior to this line
 Distal extent is 20cm distal to ASIS but with delay, may extend to the knee
 Can be raised as an innervated flap via the lateral femoral cutaneous nerve
 A dog-ear deformity is usually caused by rotation of the proximal bulky muscle, which is esthetically
unpleasing and may interfere with wheelchair positioning for the paraplegic patient
 May be combined with a tangentially split vastus lateralis for added bulk and adds reliability to the distal
aspect of the skin paddle
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TFL+VL flap
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Hamstring Flaps
 Useful only in the nonambulatory patient
 Raised as VY advancements detaching origin and insertion
1. Biceps Femoris
o Type II
o Dominant artery –
i.
first perforating branch of profunda for long head
ii. Second or third perforating branch for short head
2. Semimembranosus
o Type II
i. first perforating branch of profunda
3. Semitendinosus
o Type II
i. first perforating branch of profunda
Trochanteric Sores
 Typically minimal skin involvement and extensive bursa formation.
 Bony resection of the greater trochanter should be done to create a smooth contour to the lateral surface.
Small defects
1.
Primary closure (after wide undermining)
2.
SSG
3.
Reverse dermal graft
4.
Random skin flaps
Options for significant sores
1.
TFL
2.
Vastus lateralis
3.
Posterior thigh flap
4.
Gluteus maximus or medius flaps
 Generally, trochanteric sores are closed with TFL or
vastus lateralis flaps.
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 TFL can be used as a muscle only, M-C, island flap, V-Y, bipedicle, sensate, free flap.
 Vastus lateralis can be used together with TFL (where greater bulk is required) or can be used independently.
 The posterior thigh flap also works well for trochanteric sores although it is probably best preserved for
coverage of ischial sores.
BONE RESECTION
 Excision of underlying bony prominences, reduces the frequency of recurrence.
 Bone removal, however, can add to post-op Cx.
 Also, the removal of bone, although it reduces the recurrence rate, it also changes the pressure distribution
areas and allows the development of pressure sores elsewhere.
Removal of Ischial tuberosity
 After ischial removal, weight bearing is transferred to perineum, pubic rami and proximal femur - sites at
which pressure sores can now develop. Urethral fistulae can occur (disaster).
 Perineal ulcers, urethrocutaneous fistulas, and perineourethral diverticula have been reported in up to 58% of
patients after complete bilateral ischiectomy.
 The endpoint of bony resection should be healthy bleeding bone, although osteopenia may cloud this end point
in plegic patients.
Proximal femorectomy (Girdlestone procedure)
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 Proximal femorectomy is indicated for recalcitrant trochanteric
sores with significant heterotopic ossification around the hip and
especially if there is a fistula into the hip and chronic sepsis
 Girdlestone arthroplasty with soft-tissue coverage is mandatory
for successful treatment of pressure sores with hip joint
involvement (Evans GR PRS Feb 1993)
 MRI very useful for detecting joint involvement by osteomyelitis
in patients with stage 4 trochanteric ulcers.
 3 step procedure:
1. Girdlestone procedure
2. transposition of the vastus lateralis muscle into the void that
was left by the removal of the femoral head and neck and the
acetabular wall
3. external fixation to prevent unrestrained motion(pistoning) of
the femoral shaft, which might damage the transposed muscle
 important to obliterate a large pseudoarthrosis cavity by
muscle transfer from the thigh using a hamstring or a vastus lateralis.
MULTIPLE OR RECURRENT SORES
 Not uncommon.
 Often associated with osteitis and septic arthritis.
 Proximal femorectomy causes shortening which may allow primary closure of sores.
 Usually these wounds can be closed by transposition of one or two of the local muscular flaps in the area.
 Amputate and hemicorporectomy reserved for extreme life threatening/uncurable cases.
Total thigh or leg flaps
 Occasionally massive defects will require closure with total thigh or leg flaps.
 These are massive procedures associated with the requirement for large transfusions and prone to post-op Cx.
 Problems of balance occur after amputation of one, and especially both, legs.
 The recurrence rate is high.
POST-OP CARE
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 Suction drain.
 Hb.
 ROS at 3 weeks.
 No weight on the flap for 4 weeks.
COMPLICATIONS
1. Haemorrhage (Commonest Cx. Often predisposes to others.)
2. Seroma (Leave drains in for 7-10 days)
3. Infection (Significant Cx)
4. Wound dehiscence (Poor general condition of patient and tension the main causes)
5. Flap breakdown (Caused by poor flap design and implementation)
6. Heterotopic calcification
7. Recurrence (Common: Some say 50% 4 year breakdown rate. Some say higher).
MALIGNANT DEGENERATION
 Marjolin’s ulcer - can occur, after about 10-15 years.
 Malignant change in pressure sores usually occurs after 20 years, whereas that occurring in burns or venous
ulcers usually have a latent period of 30 years.
 Heralded by increasing pain (although often not painful), discharge, odour, bleeding.
 Recent change of any kind is suspicious and warrants a biopsy.
 Tend to be highly aggressive, mets occur often and prognosis is poor.
 Require aggressive treatment, usually with LND.
HEALING ACCELERANTS
 Epidermal GF, PDGF and other substances have usually shown a beneficial effect although some trials have
shown the opposite.
 Cultured allogeneic keratinocyte grafts also help - ?mode of action:
a) temporary biological dressing
b) help in the delivery of GFs.
PSYCHOLOGICAL ASPECTS
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These are important in both flap formation (negative attitude) and flap management (rehab). Patients may often
harbour a residual anger and self destructive force that should be recognised and treated to obtain successful
pressures sore closure.
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