Pressure Sore

1. Pressure Sore MarzouqAmarin. MD Plastic and Reconstructive Surgeon University of Jordan

2. PRESSURE SORE • Necrosis and ulceration of tissue from pressure • lesions caused by unrelieved pressure that results in damage to the underlying tissue. • these are the result of soft tissue compression between a bony prominence and an external surface for a prolonged period of time

3. Etiology/mechanism • Tissue ischemia from external pressures exceeding the closing pressure of nutrient capillaries (32 mmHg) for a prolonged duration • Pressures exceeding 70 mmHg for 2 hours result in irreversible ischemia

5. Shear forces can induce tissue ischemia: Vessel stretch leading to ischemia: Vessel stretch leading to thrombosis • Friction may cause epidermal injury (e.g., during transfers) • Excess moisture especially from incontinence: Skin maceration and increased pressure sore risk

6. Ischemia-reperfusion cycle has being implicated • Decreased autonomic control leading to spasm, loss of bladder and bowel control, and excessive sweating • Advanced age: Decreased skin tensile strength • Malnutrition: Important to supplement calories and vitamins • Sensory loss: Inability to experience discomfort or tissue ischemia

7. Other risk factors • a.  Cerebrovascular disease • b.  History of pressure sore • c.  Immobility (debility or paralysis) • d.  Poor nutritional statuse.  Low BMI • f.  End-stage renal disease • g.  Small vessel occlusive disease: Diabetes mellitus and smoking • H. Sensory loss • i.  Decreased level of consciousness

8. Epidemiology • Prevalence •   15% in general acute care setting •   15% in long-term care setting • 15% in home care setting • Incidence • 0.5% to 38% in general care settings • 2% to 24% in long-term care settings •  0% to 17% in home care settings • Over 60% of patients with pressure sores are >70 years of age

9. Surface anatomy • Depends on patient positioning, which depends on patient’s underlying condition • Supine: Sacral and heel sores most common • Seated: Ischial sores most common • Overall ischialtuberosities are the most common site (about 30%)

13. Diagnosis/Work-up

14. Stages defined by the National Pressure Ulcer Advisory Panel (NPUAP) • Stage I: • Nonblanchableerythema present for >1 hour after pressure relief. Skin intact. • Stage II: • Partial thickness skin loss • Stage III: • Full thickness skin loss into subcutaneous tissue but not through fascia • Stage IV: • Through fascia into muscle, bone, tendon, or joint • Unstageable: • If eschar is present, wound cannot be staged until fully debrided.

16. Muscle is more susceptible to ischemia than skin. • Muscle ischemia may have occurred with skin erythema as the only sign

18. Laboratory studies and imaging • a.  Complete blood cell (CBC) count with differential • b.  Glucose/hemoglobin A1c • c.  Albumin/pre-albumin • d.  Erythrocyte sedimentation rate (ESR)/C-reactive protein (CRP) • e.  MRI

19. Osteomyelitis (OM): Presence of bone infection must be determined. Initial studies include: • ESR, CRB, and CBC • MRI can identify OM and extent of disease. However, bone biopsy remains the gold standard for diagnosis. • Identify contractures and spasticity in paraplegic and quadriplegic patients: Patient may need physical medicine consult

20. Assess bowel/bladder routine and continence •  Assess motivation and support structure • Adherence to pressure relief protocols • Adherence to wound care routines • Maintenance of adequate nutrition, • Serum albumin <3.5 mg/dL is a risk factor for developing pressure sores • Participation in risk factor modification (e.g., smoking cessation)

21. Treatment • Overview • a.  Avoid invasive infection • b.  Contain size of existing wound • c.  Avoid new pressure sores • d.  Wound closure. Surgical closure is not attainable in all patients • Make management plan accordingly.

22. Management • a.  Debridement of nonviable tissues • b.  Wound care • c.  Antibiotic therapy • d.  Surgical closure when possible

23. Stage I and II wounds • Stage I: • Wound dressing to prevent dessication and protect tissue • i.  Pressure relief with frequent patient repositioning • ii.  Appropriate pressure dispersion • Stage II •  i.  Silver sulfadiazine ointment (Silvadene) to prevent bacterial invasion • ii.  Impregnated gauze (xeroform and petrolatum gauze) are useful alternatives for sulfa-allergic patients • Pressure relief with frequent patient repositioning

24.  Stage III and IV wounds • History and physical  • i.   Identify the specific etiology of the wound • ii.  Identify risk factors present • iii.  Assess current wound care regimen • iv.  Assess social circumstances (e.g., available help/support)  • v.  Assess level of activity and mobility

25. Vi.  Assess type of bed/wheelchair cushion • vii.  Investigate previous surgical and nonsurgical treatments • viii.  Assess wound characteristics (stage, size in three dimensions, palpable bone, tissue present in wound bed, presence of bacterial invasion, nature and volume of exudate, and integrity of tissue around the wound) • ix.  Assess history of wound and how it has been progressing with current dressing regimen

26. Modify risk factors  • i.  Treat spasticity when present • ii.  Eliminate excess moisture with bladder/bowel regimen or diversion (e.g., Foley catheter/diverting ostomy) • iii.  Eliminate pressure (specialty mattresses, cushions, and pressure relief protocols) • iv.  Optimize nutritional status

27. Assess for OM  • i.  CBC, CRP, and ESR (>100 is diagnostic for OM) • ii.  MRI (may conconfirm OM when ESR is 50 to 100, shows extent of disease for surgical and overall treatment planning) • iii.  Bone biopsy for culture and pathology is diagnostic standard

28. Surgical debridement  • i.  Excise devitalized tissue and bone • ii.  Resected bone is sent to microbiology and pathology • iii.  Wound care regimen initiated • iv.  Postdebridement 6-week outpatient IV antibiotic course: Initially broad-spectrum and then tailored when bone culture results available

29. Preparing for wound closure  • i.  Appropriate wound care regimen • ii.  Assessments of the wound to ensure healing is taking place (e.g., there is healthy granulation and wound shrinkage) • iii.  Consider becaplermin (Regranex); recombinant PDGF. Improves ability to achieve wound closure. Need 6-week course of treatment after antibiotic course. • Definitive closure •  i.  Use well-vascularized tissue • ii.  May allow wound to heal secondarily if reasonably small, healing well and aligns with patient preference

30. WOUND DRESSINGS (STAGE III/IV SORES) • Goals •  Achieve warm, moist, and clean environment for wound healing • a.  Desiccated wound needs hydration • b.  Wound with excess drainage needs absorbent • C.  Wound with necrosis needs debridement • d.  Infected wound needs antimicrobial

31.  Wet-to-moist dressing • 1.  With normal saline or silver sulfadiazine and mesh gauze • 2.  In clean wounds: Prevents desiccation for optimal fibroblast and keratinocyte development and epithelial migration • Debriding dressing • 1.  Chemical: Enzymatic agents such as collagenase.  Liquefy devitalized tissue • 2.  Autolytic: Hydrocolloids inner gel forming absorbent layer keeps wound moist • Moisture softens devitalized slough

32.  Antiseptic dressings • 1.  Oxychlorosene, Dakin’s solution, and dilute bleach • a.  Applied in wet-to-moist fashion • 2.  Used in heavily contaminated wounds to decrease bacterial counts • a.  Acetic acid thought to be effective in controlling Pseudomonas • 3.  Several of these agents have detrimental effects on wound healing (e.g., impair fibroblast proliferation). Switch to other dressings when wound is clean • Absorbent dressings, alginates • 1.  Hydrophilic gels with ability to absorb up to 20 times their weight • 2.  Have antimicrobial properties • 3.  Used in excessively exudative wounds

33. Negative pressure wound therapy •  No guidelines for role in pressure sore management •  Appropriate for stage III and IV wounds • Contraindicated with OM, necrotic tissue, malignancy, and fistulas

34. SOFT TISSUE INFECTIONS (STAGE III/IV SORES) • Local infections •  Cellulitis, a malodorous wound and purulent discharge •  Can lead to systemic infections with leukocytosis, fever, and sepsis • Obtain specimens after debridement for quantitative bacterial counts, culture, and sensitivity •  Staphylococcus, Streptococcus, Escherichia coli, and Pseudomonas are most common culprits •  Mixed aerobic/anaerobic infections not uncommon • Treat promptly with drainage, irrigation, debridement, and antibiotics guided by cultures

35. BONE INFECTIONS (OM) • Diagnosis • Exposed/palpable bone on initial evaluation: OM until proven otherwise • Bone biopsy: Gold standard for diagnosis •  Obtain bone biopsy during initial evaluation with a rongeur if patient is insensate • Bone scans: Not specific for diagnosing OM but can rule out OM if negative • MRI • a.  98% sensitivity and 88% specificity in diagnosis of OM • b.  Can also use to determine extent of disease • c.  Enhancement of bone and marrow in T2 signal

36. Treatment • Debridement of devitalized and infected bone • A 6-week IV antibiotic course tailored to causative organism • When resection is impossible (extension to acetabulum and pubic rami) • a.  Flap closure is contraindicated • b.  Management is chronic suppressive antibiotics and wound dressings indefinitely

37. PREOPERATIVE AND INTRA-OPERATIVE CONSIDERATIONS FOR WOUND CLOSURE •  Minimize risks of recurrence •  Recognize that not all patients are candidates for closure • a.  Patients who have not optimized conservative measures such as bowel and bladder regimens and contractures • b.  Patients with significant medical comorbidities • Optimize nutritional status: Serum albumin of ≥3.5 mg/dL • Optimize spasticity management

38. Optimize comorbidities management, • glycemic control in diabetics • No smoking • Optimize bladder/bowel regimen (prevent moisture/soilage): • Consider urinary and fecal diversion if bladder/bowel regimen cannot be optimized • Establish history of adherence to wound care regimen, pressure relief protocols • Motivated patient •  Mood disorders (not uncommon in pressure sore patients) are detrimental to motivation

39. Social support for the postoperative convalescence when restrictive regimens are in place to protect flap • Wound must demonstrate capacity to heal after debridement and treatment with systemic antibiotics. If no wound shrinkage after debridement/antibiotics, or if there are signs of invasive infection (increased drainage, malodor, soft tissue infection), • Halt plans for closure and reevaluate: CBC, ESR, CRP, bone biopsy, and MRI • Post debridement monitoring should include • a.  Weekly ESR and CRP and CBC during antibiotic treatment • b.  Evaluate the trend of these test results before embarking on closure to ensure ESR is not elevated or trending up.

40. Patient should be off antibiotics for at least 7 days before closure to get an accurate microbiological assessment of intra-op bone cultures • Intra-op • a.  Excise entire ulcer and bursa, scar tissue, and soft tissue calcifications • b.  Send tissue for quantitative counts, culture, and sensitivities • c.  Resect devitalized bone until bleeding bone is encountered • d.  Send bone to microbiology and pathology • e.  Be careful with partial ischiectomy: Overly radical ischiectomy increases risk of contralateral recurrence and perineal pressure sores

41. Other considerations for wound closure •  Need bulk to fill dead space and pad underlying bone with muscle, musculocutaneous flaps, or fasciocutaneousflaps • Preserve lower extremity function in ambulatory patients by using perforator flaps rather than myocutaneousflaps • Design large flap to prevent tension after closure and place suture line away from direct pressure • Do not violate adjacent flap territories to preserve options for recurrence or development of new pressure sores • Rotation and V–Y advancement flaps can be re-advanced if recurrence occurs •  If possible, bring sensate tissue into the wound for protective sensation • In OR, pad all pressure points appropriately: Do not give patient new pressure sore

42.  FLAPS AND OTHER PROCEDURES • Sacral pressure sores • Gluteal flaps (gluteus maximus): Muscle, musculocutaneous flaps, and fasciocutaneous flaps • a.  Musculocutaneous and fasciocutaneous flaps can be designed as rotation, V–Y advancement flaps (unilateral or bilateral) and island flaps • b.  Mathes type III muscle • c.  Blood supply: Superior and gluteal artery off of internal iliac • d.  *In ambulatory patients • preserve origin and insertion of gluteus maximus

44. Ischialpressure sores • Gluteal flaps (gluteus maximus): Include rotational musculocutaneous and island musculocutaneous flaps • a.  Inferior gluteal artery-based rotational musculocutaneousflap • f.  Preserve inferior gluteal artery and sciatic nerve • g.  Eliminate dead space • h.  *Not appropriate for ambulatory patients

45. Posterior/gluteal thigh flap • a.Fasciocutaneous flap based on descending branch of inferior gluteal artery • b.  May be designed as laterally based rotation flap or V–Y advancement flap • c.  Rotational posterior gluteal thigh flap  • Preserve posterior femoral cutaneous nerve and profundafemorisperforators • Rotate flap into the defect • May be used in ambulatory patients

47. Trochanteric pressure sores • Tensor fascia-lata (TFL) flap: Muscle and musculocutaneousflaps • a.  Musculocutaneous flap can be designed as rotation (transposition) or V–Y advancement flaps • b.  Muscle only flap will require STSG • c.  May need STSG to cover donor defect • d.  Mathes type I flap supplied by descending branch of lateral femoral circumflex artery (enters muscle 10 cm inferior to anterior superior iliac spine [ASIS])

50. NONOPERATIVE TREATMENT (STAGE III/IV)A • For patients with unresectable OM (extension to acetabulum and pubic rami) who are not surgical candidates