clinical case presentation

1. Sacral Pressure Sore: Case discussion
(PLASTIQUEST)
Presenter-
Dr Pratik Porwal (M.Ch 3rd Year Resident),
BJ Medical College, Ahmedabad
Plastiquest PG Mentor-
Prof Dr Palukuri Lakshmi
Osmania Medical College,
Hyderabad

2.  Institute Guide- Prof & Head Dr Jayesh P. Sachde, BJMC Ahmedabad
 Guest Faculty:- Dr. U.R. Nandakumar
Former Prof of Plastic Surgery,
Govt. Medical College, Kottayam.
Sr. Consultant Cosmopolitan Hospitals, Trivandrum
 Moderators: Dr. Sundeep Vijayaraghavan
Dr. G.S. Radhakrishnan

3. Chief Complaints
 64 year old female Geeta retired
Government employee by
occupation and belongs to Lower
socio economic class presented with
chief complaints of:
 Unable to move left side of body since 4
month
 Wound over lower back since 3 and
1/2month

4. History of present illness
 Patient had suffered from stroke associated with left side hemiplegia 4
month back after which she was admitted to intensive care unit of
neuromedicine department at our institute. The Patient is unable to
stand or walk and bedridden since then.
 Patient’s relative has noticed skin peeling 2 weeks after the admission
over lower back which gradually increased in size and developed in to
discharging open wound of present size. Wound is dressed daily once in
the morning. There is improvement in her symptoms of lower limb
weakness and sensation since last one month.

5.  Patient does not have bladder and bowel incontinence.
 She has been catheterized initially for a week for output monitoring
and uses diapers after that.
 Patient is on regular physiotherapy.
 No history of tightness or restriction in movement of any joint
(Spasticity)
 No history of development of any joint deformity (Contracture)
 No history of cough and fever at present
 No history of convulsion

6.  Treatment History:
 Patient managed conservatively by neuromedicine department.
 Patient is being taken care by the physiotherapist and her relatives
for general care.
 Past history:
 History of hypertension for last 10 years and history of diabetes for
last 8 years for which she was taking oral medication.
 No History of smoking/ Alcoholism/ asthma/ allergy/ Tuberculosis
 No history of any surgery for the same.

7. GENERAL EXAMINATION:
 Patient is alert, conscious, co-operative and well oriented to time, place
and person and moderate built and nourished.
 Attitude of patient: Patient is lying in bed in lateral position with hip and
knee in mid flexion and ankle in slight planter flexion.
 Afebrile
 Pulse 78/min.
 Blood pressure 140/86 mm of Hg in right arm in supine position.
 No Pallor, Icterus, Cyanosis, Clubbing, Edema, lymphadenopathy.

8.  Mid Arm Circumference is 20 cm
 Triceps skin fold thickness 15 mm.
 Skin and hair normal (No sign of vitamin deficiency)
 RS: Respiratory rate is 16/min, air entry bilateral equal, no foreign
sounds heard.
 CVS: S1, S2 present, no murmurs heard.
 P/A: Abdomen is soft, no Organomegaly present.
 CNS examination: GCS 15/15

9. LOCAL EXAMINATION:
 After taking consent patient is examined in front of
female attendant with adequate light & exposure.
Inspection:
 There is single, oval, approximately 6 x 7 cm in size
ulcer located over sacro-coccygeal region and
extending 3 cm from midline in both sides and 7 cm
vertically from the natal cleft.
 Margins are irregular, edges are undermined, floor
having unhealthy granulation, minimal seropurulent
discharge present, no active bleeding, and no redness
in surround skin.
 No surrounding Edema.
 Signs of secondary healing in the circumscribed area.

10. Palpation:
 On palpation, no local Warmth or
Tenderness.
 7 x 8 cm size oval ulcer extending 3 cm
right and 4 cm left to midline with 2cm of
undermining edges on left side.
 Ulcer based on sacral bone and having fixed
to underlined base.
 Distal peripheral pulses are palpable
 There is no lower limb length discrepancy .
 No palpable lymph nodes.
 No skin pockets in the surrounding area.

11. Musculoskeletal examination:
 Mid-thigh and Mid leg circumference is equal in both limb.
 Left lower limb:
Muscle tone is reduced
Power: Grade 1 power in left Lowe limb muscle
Sensory examination:
sensation to touch and pain present and slightly reduced on left side.
Reflexes: Deep tendon reflex increased,
Babinski positive ( extensor Planter response)
 No spasm or spasticity
 No Contracture in any joint
 No Trophic changes (Thin dry skin, sparse hair, brittle nails)

12. DIAGNOSIS:
 Sacral Pressure ulcer of grade IV National Pressure Ulcer Advisory
Panel (NPUAP) classification without complication in patient with
UMN type of recovering hemiplegia without spasticity.

13. INVESTIGATIONS:
 Wound evaluation: Swab C/S, Bone Biopsy, Bone Culture
 Routine blood investigations, ECG, CxR, S. Protein, S. transferrin, HbA1C
 X-ray local part, MRI (Rule out osteomyelitis).
MRI Protocol:
 Long standing pressure sore with suspected osteomyelitis in X ray
 MRI Accuracy of 97%, sensitivity of 98%, and specificity of 89%.
 It helps define the extent of infection, which may help limit the surgical
resection. MRI is superior to CT-Scan for detection of osteomyelitis

14. PROBLEMS AND APPROACH:
 All preventive measures to be started like weight redistribution for 5 min every
2 hours, keeping part away from moisture.
 Physiotherapy, nutritional improvement (correct anemia/ hypoproteinemia)
 Management of co-morbidities and Chronic medical conditions - such as
diabetes, cardiovascular disease.
 Control of infection, wound dressing until patient is fit for surgery
 Non surgical Debridement:
Mechanical: cleaning with high pressure water jet
newer modalities:- low frequency energy ultrasound waves
high powered continuous waves of CO2 Laser
Biological: maggots therapy

15. Goals of management for a patient with a pressure sore are:
(1) prevention of complications, particularly invasive infection, related to
the existing sore;
(2) preventing the existing sore from getting larger;
(3) preventing sores in other locations; and
(4) coverage of the wound

16. Dressings

17. Nutrition:
Requirement of
 1.5-3 g/kg/d protein
 25-35 kcal/kg/d of non-protein calories
 Daily intake of 135 gm of protein is recommended.
 S. Protein level above 6 gm/dl needed prior to surgery.

18. DEBRIDEMENT
 Removal of devitalised tissue
 In an operating room
 In adequately bright light
 Under assistance
 With facilities to control bleeding (like cautery)
 Under magnification
 Debridement of pressure ulcer is to be done as En block removal
known as Pseudo tumor excision.

19. Negative Pressure Wound therapy in Pressure sore
 Helps to promote granulation formation
 Applies controlled localized negative pressure to uniformly draw the
edges of ulcer that reduces the wound size
 Allows tissue decompression by removing interstitial fluid
 Removes infectious material
 Provides moist environment to promote healing
Pre debridement and VAC application Post VAC application

20. Gluteal rotation flap
 Flap of choice for this case.
 Multiple anastomosing branches from superficial
branches of superior and inferior gluteal artery
supply the overlying skin.
 Lateral limit of the flap is medial to the greater
trochanter.
 Tension free closure is recommended so as large
as possible flap is to be taken.
 Rotation of the flap is possible 2 to 3cm across
the midline to increase the reach of the flap a
back cut can be introduced to shift the pivot
point the flap.

21.  Superior gluteal artery
 The larger of the two vessels,
 leaves the pelvis above the piriformis
 Supply the superior half of the gluteus maximus,
gluteus medius and gluteus minimus muscles.
 The inferior gluteal artery
 Passes posterior to the piriformis muscle
 Supplies the inferior half of the gluteus maximus
muscle and a portion of the posterior thigh
 Usually the IGA is dominant over the SGA and supplies
approximately two-thirds of the muscle

22. Surface marking
The superior gluteal artery (5 mm)
1. Marked out by a point lying 1/3 on
the line joining the posterior superior
iliac spine and top of the greater
trochanter.
2. It exits from the pelvis approximately
5 cm inferior to the posterior superior
iliac spine and 5 cm lateral to the
midline of the sacrum.
The inferior gluteal artery (3.5 mm)
1. Marked out by a point lying 1/2 on
the line joining the posterior superior
iliac spine and Ischial tuberosity .
2. The inferior gluteal artery lies 3 cm
inferior to superior gluteal artery.

23. Unilateral Gluteal rotation flap: inferiorly based
fasiocutaneous or Musculocutaneous


24. Other Options for flap cover:
 Superior Gluteal Artery based perforator flap
 Limberg flap
 Propeller flap
 Unilateral Gluteas Maximus Myocutaneous rotation flap
 V – Y advancement flap: unilateral or bilateral
 Lumbosacral flap (fasiocutaneous)
 Island musculocutaneous flap
 Muscle transposition flap

25. Definition of Pressure Ulcer
 Pressure ulcer is defined as “an area of localized soft
tissue ischemic necrosis caused by prolonged pressure
higher than the capillary pressure which is 32 mm Hg with
or without shear, related to posture which usually occurs
over a bony prominence”.
 Now a days pressure ulcers are also known as Pressure
Injury.
 Low pressure for long period & high pressure over short
time also lead to pressure sore.

26. Classifications:
 National Pressure Ulcer Advisory Panel (NPUAP) classification:
 Stage 1: Non- blanchable erythema of intact skin
 Stage 2: Partial thickness skin loss involving epidermis/dermis (abrasion, blister, crater)
 Stage 3: Full thickness skin loss –damage of subcutaneous tissue but not through underlying
fascia
 Stage 4: Full thickness skin loss with extensive destruction, tissue necrosis or damage to
muscle, bone or supporting structure ( eg. tendon, joint capsule.)
 Shea classification:
 Stage I - Limited to epidermis, exposing dermis Includes a red area
 Stage II - Full thickness of dermis to the junction of subcutaneous fat
 Stage III - Fat obliterated, limited by the deep fascia undermining of skin
 Stage IV - Bone at the base of ulceration
 Stage V - Closed large cavity through a small sinus

27. RISK FACTORS FOR PRESSURE SORE
DEVELOPMENT
 Limited mobility.
 Prolonged bed rest.
 Decreased skin sensations.
 Moisture
 SKIN SHEARING & INJURY ( during transfer of patient )
 Spacticity

28. Risk factors FOR POOR HEALING
 Age . 65 yrs
 Diabetes
 Smoking
 Renal failure
 Wound infection
 Local irradiation
 Systemic infection
 Immunosuppressive agents
 Hemodynamic instability
 Prolonged hyperalimentation
 Low total proteins
 Bladder and bowel incontinence
 Decreased skin sensation
 Muscle spasticity
 Nutritional status
 Limited mobility & prolonged bed rest.
28

29. Pathophysiology of Pressure Sores
 Extrinsic (primary) factors:
 Pressure
 Shear
 Friction
 Moisture
 Intrinsic (secondary) factors:
 Neurological Injury
 Malnutrition
 Other Factors
29

30. Extrinsic (primary) factors
Pressure:
 Pressure is a perpendicular load exerted on a unit area.
 Pressure applied to soft tissue at a level higher than that
found in the blood vessels supplying that area for an
extended time period.
 Average capillary closing pressure is approx. 32 mmHg.
 Highest pressure were the sacrum, buttocks, heel and
occiput pressure measured were around 50-60 mmHg.
 In sitting pressures up to 100 mmHg were recorded over
the ischial tuberosity.
30

31. Common sites
31
Lying position
Prone position

32. Common sites
32
Lateral position Sitting position

34. Importance of uninterrupted pressure
 All soft-tissues are not
equally sensitive to the
effects of pressure.
 Muscle > skin.
 Time period to undergo
ischemic necrosis
 Muscle begins after 4
hours
 Skin begins after 12 hours.
34

35. Friction:
 Friction is the resistance of two surfaces moving
across one another.
 Friction acts directly on the epidermis by rubbing
off the outermost layer of skin.
 This increases trans-epidermal 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.
35

36. Shear :
 Shear develops when friction adheres skin and superficial tissues
to sheets or bedding which are then stretched tightly over deeper
structures.
 Shear forces causes stretching and compression of muscle-
perforating vessels to the skin, which leads to ischemic necrosis
of the adjacent tissues.
 Subcutaneous tissue in particular lacks tensile strength and is
particularly susceptible to shear stress.
 Patient movements like
 transfers,
 sliding or dragging the patient in bed,
 “ boosting “ patients up in bed
 allowing patients to elevate themselves in bed by pushing with
elbows and heels
 semi- Fowler’s position or sliding down in a wheelchair all cause
significant shear.
36

37. 37

38. Moisture:
 Excessive skin moisture can be secondary to
perspiration, urine, feces, or drainage from a
fistula or wound.
 Excessive moisture is not only a risk factor for
pressure sores, but may also result in separate
pathology inclusive of incontinence dermatitis,
perineal dermatitis, and moisture lesions.
 Moist skin has a higher coefficient of friction and is
prone to maceration and excoriation.
38

39. EDEMA:
 Approx. 80% of soft tissue mass is fluid.
 External pressure on soft tissue increases plasma
extravasation.
 Circulatory deficiencies, such as heart failure, renal failure,
and venous insufficiency are risk factors
 Molecular level
o Inflammatory mediators - prostaglandin E2 released in
response to the trauma of compression
o Leakage through the cell membranes.
o Interstitial fluid accumulation.
39

40. Intrinsic (SECONDARY) factors
Malnutrition:
 Patients who are chronically ill and debilitated
frequently have accompanying nutritional
deficiencies.
 The deleterious effects of poor nutrition includes:
 Weight loss
 Negative nitrogen balance
 Exacerbation of wounds
 Impairment of the immune system
 Retarded healing response
40

41.  Ascorbic acid and Vitamin A are essential for
wound healing.
 Serum Albumin level is maintained above 2.0
gm/dL.
 A diet with sufficient Protein is required for
optimal healing.
 Daily Protein requirement of 1.5 to 3.5g/kg/d
restores lost lean body mass.
41

42. Neurological Injury:
 Diminished autonomic control, sensory loss, impaired
mobility, fecal or urinary incontinence all contribute to
development of pressure sore.
 Patients with Spinal cord injury there is loss of
sympathetic tone which results in vasodilatation of
denervated tissues.
Spasticity:
 It is the key contributor in development of pressure sore as it
causes significant shear so it should be evaluated and if
needed controlled medically or surgically.
42

43.  Discussion with other specialty regarding the recovery of patient.
 Measure to rehabilitate socially.
 All surgical strategy discussed with patient and relatives, if patient is
willing for surgery, habit of prone positioning is started before surgery
as post-operative prone positioning required for 2-3 weeks.
 When patient is fit, debridement of wound under general anesthesia
(pseudo tumor excision: Necrotic & scarred soft tissue / bursa /
ostectomy) followed by flap cover.
 Biopsy is recommended for the excised part.

44. Newer research
 Supportive therapies to promote healing of pressure ulcers to aid
wound healing, still require further research to determine their
effectiveness:
Growth factors and cytokines
Hyperbaric oxygen (HBO) to increase tissue oxygen tension
Skin graft substitutes (bioengineered skin)
Connective tissue matrix.
Expanded epidermis.
Epidermal stem cells
Bone marrow (BM) or adipose tissue derived stem cell (ASC)
therapy

45.  Types of beds:
 Constant Low pressure (CLP) devices:
Low air loss (LAL) beds
Air Fluidized (AF) beds
 Alternating pressure (AP) devices

46. Superior Gluteal Artery based perforator flap
 Provide stable wound coverage
for large midline wound.
 Dissection is continued through
the upper incision under the
deep fascia till the perforator
is reached.
 Flap is advanced in V-Y manner
with minimal donor side
morbidity.

47. Limberg Flap

48.  INDICATIONS:
 Small pressure ulcers
 ANATOMY:
 Random pattern supply from the subdermal plexus
 Equilateral parallelogram – rhombus
 Length-width ratio 1:1
 60-120 degree
 Short diagonal
 Line of maximum extensibility
 4 potential flaps

49. Perforator flaps
 Plain fasciocutaneous flaps may suffice
 Muscle is preserved,
 May be spared for future reconstruction
 Higgins et al, muscle sparing should always be a goal in ambulatory
and sensate patients, as it may prevent some functional loss and
potentially reduce post operative pain

50. Musculocutaneous flap
 Advantage
 Decreased rate of skin ulceration, due to increased muscle bulk,
helps to diffuse the effects of pressure on skin
 To obliterate dead space
 To cover larger wounds
 Better local vascular supply
 Disadvantage
 Muscle is more susceptible to ischemic necrosis
 Gluteus Maximus is not an expandable muscle so can not use entire
muscle in patient with potential of recovery only superior or
inferior part of the muscle can be used.

51. V – Y advancement flap: unilateral or
bilateral

52. Muscle transposition flap

53. Island Musculocutaneous Flap
 Is technically simpler to elevate the superior half of the
gluteus maximus muscle and advance this to cover the sacral
defect.
 In ambulatory patients, maintaining the inferior half of the
gluteus maximus muscle intact preserves function and
restores normal buttock contour .
 When the sacral defect is less than 6 cm after debridement,
a unilateral superior gluteal island musculocutaneous flap is
usually adequate for closure. If the defect is larger, bilateral
flaps may be necessary for coverage.
 It is advisable to design the skin island 3 to 4 cm larger than
the defect to be covered to minimize tension.

54. • Superior half is detached from its Insertion on the
femur and iliotibial tract.
• Muscle with the island of skin and subcutaneous
tissue is elevated in a superomedial direction
• Then the origin of the superior half of the gluteus
muscle is detached, leaving the whole muscle and
skin paddle attached only by the superior gluteal
vessels.
• The flap is advanced to cover the defect.
• The donor site is closed in V-to-Y advancement
fashion

55. Tissue expansion
 Tolerated well
 Advantage of transferring sensate skin, helps to prevent future
pressure ulcers
 Helps in unstable wounds
 Pre-expansion of tensor fascia latae and lumbosacral
fasciocutaneous flaps may be done, allows primary closure of
donor sites, reduces mechanical shear, improves vascularity
 Problem of placing foreign body in a contaminated wound

56. Dermotaxis
 It is based on viscoelastic property of skin.
 It can be applied to small size pressure ulcer without involvement of
bone.
 If skin is stretched to a constant distance, it will expand and lead to a
decrease in the force or tension on the skin with time, a phenomenon
known as stress relaxation.
 If skin is stretched with a constant force, it will expand, a
phenomenon known as mechanical creep.
 In dermotaxis (Singh’s skin traction) method, two parallel Kirschner
wires (0.9 mm or 1 mm) are passed through the dermis on either side
1 cm away of the wound margins and interconnected by compression
device consisting of threaded rod having two blocks and compression
knob. Gradual compression was applied daily at the rate of 1 turn/12
h on both sides of the wound .

57.  Medical Management of spasticity
 Choice for spasticity and reflex spasms is Baclofen 15-
100 mg a y-amino butyric acid receptor agonist.
 Diazepam 10-40 mg & Dantrolene sodium 50-800mg
are effective alternatives/adjunctive treatments.
 Other:
Mephensin carbonate 3-15 mg
Dimethothiazine 300-500 mg
Orciprenaline 40 mg
Chemodenervation: Intrathecal phenol, Ethanol,
Botulinum

58. Surgical management of spasticity
 Baclofen Pump implantation
 Surgical release of flexion contractures
 Surgical means (i.e., Cordotomy or rhizotomy)
 Neurosurgical ablations (Myelotomy & T-Myelotomy)
 Amputation

59. References
Books
Case Discussion in Plastic Surgery 1st edition
Neligan 4th edition: Trunk and Lower Extremity
Text book of Plastic, Reconstructive, and Aesthetic Surgery: Pressure Ulcer… Dr
Karoon Agrawal
GRABB’S ENCYCLOPEDIA OF FLAPS
Articles
The Cause, Prevention, and Treatment of Pressure Sores: Robert M. Woolsey,
MD, and John D. McGarry

60. Thank You