Wound Care

01 Wound Healing Physiology

Wound healing is a dynamic, highly orchestrated process involving the coordinated interaction of cells, growth factors, cytokines, and extracellular matrix components. Normal acute wound healing proceeds through four overlapping phases: hemostasis, inflammation, proliferation, and remodeling. Disruption at any phase leads to chronic non-healing wounds. Understanding this cascade is foundational to every clinical decision in wound care.

Phase 1 — Hemostasis (Seconds to Hours)

Immediately following tissue injury, vascular disruption triggers the coagulation cascade. Vasoconstriction occurs within seconds, mediated by thromboxane A2 and endothelin, reducing blood loss. Exposed subendothelial collagen activates platelets, which adhere via glycoprotein Ib-IX-V receptors and von Willebrand factor, then aggregate to form the initial platelet plug. The coagulation cascade (intrinsic and extrinsic pathways) converges on the common pathway producing thrombin, which converts fibrinogen to fibrin. The resulting fibrin clot serves as both a hemostatic barrier and a provisional matrix for migrating cells. Platelets degranulate, releasing platelet-derived growth factor (PDGF), transforming growth factor-beta (TGF-β), epidermal growth factor (EGF), and vascular endothelial growth factor (VEGF), which serve as chemotactic signals initiating the inflammatory phase.

Phase 2 — Inflammation (Hours to Days 4-6)

Vasodilation follows the initial vasoconstriction, mediated by histamine, prostaglandins, and complement fragments (C3a, C5a). Increased vascular permeability allows plasma proteins and leukocytes to enter the wound. Neutrophils are the first inflammatory cells to arrive (within 6-12 hours), reaching peak numbers at 24-48 hours. They phagocytose bacteria and debris, release reactive oxygen species (ROS) and proteolytic enzymes, and undergo apoptosis after 24-48 hours. Monocytes/macrophages arrive at 48-72 hours and are the most critical cell in wound healing — they debride devitalized tissue, kill bacteria, release growth factors (PDGF, TGF-β, FGF, VEGF, IL-1, TNF-α), and transition the wound from inflammation to proliferation. Macrophage depletion experiments result in severely impaired healing.

Macrophage Phenotype Switching

Macrophages exhibit remarkable phenotypic plasticity, and the transition between phenotypes is critical for normal wound healing. M1 macrophages (classically activated; pro-inflammatory) predominate during the early inflammatory phase — they produce TNF-α, IL-1β, IL-6, reactive oxygen species, and nitric oxide, serving primarily bactericidal and debris-clearing functions. M2 macrophages (alternatively activated; anti-inflammatory/reparative) gradually replace M1 cells as the wound transitions to the proliferative phase. M2 macrophages produce TGF-β, VEGF, IL-10, and arginase, promoting angiogenesis, fibroblast recruitment, collagen synthesis, and resolution of inflammation. In chronic wounds, this M1-to-M2 transition fails — macrophages remain locked in the M1 pro-inflammatory phenotype, perpetuating tissue destruction and preventing progression to proliferation. This concept has implications for emerging therapies targeting macrophage polarization as a wound healing strategy.

Phase 3 — Proliferation (Days 4-21)

This phase is characterized by three concurrent processes: granulation tissue formation, wound contraction, and epithelialization.

Granulation tissue formation: Fibroblasts migrate into the wound along the fibrin scaffold, proliferate under the influence of PDGF and FGF, and begin synthesizing type III collagen (the initial collagen deposited in wounds), proteoglycans, and glycosaminoglycans. New capillary buds sprout from existing vessels in a process called angiogenesis, driven primarily by VEGF and FGF-2. The resulting tissue — a rich bed of new capillaries, fibroblasts, and loose extracellular matrix — is clinically visible as beefy red, moist, granular tissue.

Wound contraction: Myofibroblasts (fibroblasts that have differentiated to express α-smooth muscle actin) generate centripetal force, pulling wound edges together. Contraction reduces the wound surface area by 40-80% in open wounds, is most effective in loose-skinned areas, and is the primary mechanism of closure in secondary-intention wounds.

Epithelialization: Keratinocytes at the wound edge and from residual hair follicle remnants lose their desmosomal attachments, express integrin receptors, flatten, and migrate across the wound bed in a process called epiboly. They advance as a monolayer over viable granulation tissue (not over necrotic tissue or eschar). Migration is contact-inhibited — cells stop when they meet other advancing keratinocytes. Subsequent proliferation and differentiation restore the multilayered epidermis. In partial-thickness wounds, epithelialization occurs from both wound edges and adnexal structures (hair follicles, sweat glands), explaining faster healing.

Phase 4 — Remodeling (Day 21 to 1-2 Years)

The longest phase of wound healing involves the progressive replacement of type III collagen with type I collagen (the predominant collagen in mature skin). Collagen fibers are cross-linked and reorganized along lines of mechanical stress by matrix metalloproteinases (MMPs) balanced by tissue inhibitors of metalloproteinases (TIMPs). Net collagen content peaks at approximately 3 weeks. The collagen III:I ratio gradually shifts from 30:70 in early wounds toward the normal skin ratio of 10:90.

MMP regulation is critical during remodeling. Key enzymes include MMP-1 (interstitial collagenase, cleaves fibrillar collagen), MMP-2 and MMP-9 (gelatinases, degrade denatured collagen and basement membrane components), MMP-3 (stromelysin, broad substrate specificity including proteoglycans and laminin), and MMP-8 (neutrophil collagenase, predominant in acute wounds). In normal healing, MMPs are tightly regulated by TIMPs (TIMP-1 through TIMP-4) maintaining a balanced MMP:TIMP ratio. In chronic wounds, this ratio is pathologically elevated — excess MMP activity degrades newly deposited collagen, growth factors, and provisional matrix faster than they can accumulate, perpetuating the non-healing state.

Extracellular matrix (ECM) remodeling: Beyond collagen turnover, the ECM undergoes compositional changes during maturation. Fibronectin, which serves as a provisional scaffold in early healing, is progressively replaced by more organized collagen bundles. Proteoglycan content shifts from hyaluronic acid (predominant in early healing, promoting cell migration and hydration) to dermatan sulfate and chondroitin sulfate (characteristic of mature dermis, providing structural integrity). Elastic fiber regeneration is minimal in scar tissue, contributing to the lack of elasticity in healed wounds compared to normal skin.

Key Growth Factors in Wound Healing

Chronic Wound Pathophysiology

In chronic wounds, the healing cascade is stalled — typically in a persistent inflammatory state. The chronic wound microenvironment is characterized by:

Elevated MMPs: MMP-2 and MMP-9 levels are 10-100x higher in chronic wound fluid compared to acute wound fluid. These proteases degrade not only necrotic tissue but also newly deposited collagen, fibronectin, growth factors (PDGF, VEGF, TGF-β), and their receptors, creating a self-perpetuating cycle of matrix destruction.

Deficient TIMPs: TIMP-1 and TIMP-2 levels are reduced, further tilting the protease-antiprotease balance toward degradation. This imbalance is a primary therapeutic target — collagen dressings act as "sacrificial substrates" to absorb excess MMP activity.

Senescent cells: Fibroblasts in chronic wounds exhibit a senescent phenotype with reduced proliferative capacity, diminished response to growth factor stimulation, and altered gene expression. These cells fail to synthesize adequate collagen and ECM components despite the presence of growth factor signals.

Biofilm: Present in 60-80% of chronic wounds, biofilms create a physical barrier to immune cell access, release enzymes that degrade host defenses, and maintain a persistent inflammatory stimulus that prevents transition to the proliferative phase. Biofilm bacteria are metabolically quiescent and protected by extracellular polymeric substance (EPS), rendering them 500-1000x more resistant to antibiotics than their planktonic counterparts.

Hypoxia: Chronic wounds are hypoxic (tissue pO2 often <20 mmHg vs 40-60 mmHg in normal tissue) due to impaired perfusion, edema, and increased metabolic demand. While transient hypoxia is a normal stimulus for angiogenesis (via HIF-1α and VEGF), persistent hypoxia impairs neutrophil oxidative killing, collagen synthesis (which requires O2 as a substrate for prolyl hydroxylase), and epithelialization.

02 Wound Assessment & Documentation

Accurate, reproducible wound assessment is the cornerstone of wound care practice. It drives treatment decisions, tracks healing trajectory, and provides medicolegal documentation. Every wound encounter requires systematic evaluation of wound dimensions, wound bed characteristics, exudate, periwound skin, and associated symptoms. The initial assessment must also include a comprehensive patient history: wound etiology and duration, prior treatments and their outcomes, relevant comorbidities (diabetes, PVD, venous disease, immunosuppression, malignancy), medications (especially steroids, anticoagulants, immunosuppressants), nutritional status, functional status, pain assessment, psychosocial factors (living situation, caregiver support, financial barriers), and patient goals of care (curative intent vs comfort-focused/palliative).

Wound Measurement

Linear measurement: Length × width × depth in centimeters. Length is measured as the longest dimension in the head-to-toe axis; width is the longest dimension perpendicular to the length. Depth is measured by inserting a sterile cotton-tipped applicator at the deepest point and marking at the wound edge. All measurements use the "clock face" method with 12 o'clock toward the patient's head. Consistency in measurement technique across clinicians is essential for reliable longitudinal tracking — even small variations in orientation or measurement points can create artifact that mimics improvement or deterioration.

Digital planimetry: Computerized wound measurement systems (e.g., WoundZoom, eKare InSight, Silhouette) use digital photography with calibration markers or 3D imaging to calculate wound area and volume with greater accuracy and reproducibility than manual ruler measurements. These systems reduce inter-rater variability and provide photographic documentation simultaneously. While more expensive than manual measurement, they improve data quality for clinical decision-making and research.

Undermining: Tissue destruction extending under intact skin at the wound edges. Documented by clock position and distance (e.g., "undermining 2.0 cm from 2 o'clock to 5 o'clock"). Assessed by inserting a probe under the wound edge and measuring the distance from the wound edge to the extent of undermining.

Tunneling (sinus tract): A narrow channel extending from the wound in one direction. Documented by clock position and depth (e.g., "tunnel 3.5 cm at 9 o'clock"). Suggests abscess, foreign body, or fistula.

Area and volume: Surface area (L × W) is the most commonly tracked metric. Wound planimetry (tracing on transparent film or digital planimetry) provides more accurate area measurement. Volume can be estimated by instilling saline and measuring the volume required to fill the wound.

Wound Bed Assessment

Document the percentage of each tissue type in the wound bed (e.g., "wound bed: 60% granulation, 30% slough, 10% eschar"). This quantification tracks debridement effectiveness and healing progress.

Exudate Assessment

Exudate amount is documented as none, scant, small, moderate, or large (copious). Excessive exudate in chronic wounds contains elevated levels of MMPs that degrade growth factors and extracellular matrix, impeding healing.

Periwound Skin Assessment

Evaluate the skin within 4 cm of the wound edge for: maceration (white, softened skin from excess moisture — indicates need for more absorptive dressing), erythema (redness extending >2 cm from wound edge suggests infection or cellulitis), induration (firmness indicating inflammation or infection), callus (hyperkeratosis common around DFUs — requires debridement), excoriation (denudation from adhesive or caustic drainage), edema, and temperature changes.

Validated Assessment Tools

Photography Standards

Wound photographs must include: patient identifier and date (label, not on patient), a disposable ruler or measuring guide in the field, consistent camera angle (perpendicular to wound surface), consistent distance and lighting, inclusion of an anatomic landmark for orientation, and the same background for serial photos. Photographs are part of the medical record and should be obtained at initial assessment and at least weekly or with significant changes.

Wound Healing Trajectory Monitoring

Calculating the percent area reduction (PAR) provides the most clinically meaningful measure of healing trajectory. PAR = [(initial area − current area) / initial area] × 100. A wound that does not achieve ≥40% area reduction by week 4 has a <10% probability of healing by week 12 with current therapy. This "4-week checkpoint" should trigger a comprehensive reassessment including: wound etiology confirmation (consider biopsy if atypical), vascular status, nutritional parameters, glycemic control, infection/biofilm evaluation, adherence to offloading/compression, medication review, and consideration of advanced therapies. Conversely, wounds achieving ≥50% PAR at 4 weeks have an ~80% probability of complete healing by 12 weeks, supporting continuation of the current treatment plan.

03 Terminology & Abbreviations

Wound care uses a specialized vocabulary shared across nursing, medicine, and surgical disciplines. Consistent terminology ensures clear communication, accurate documentation, and proper coding. Using standardized wound care terminology across all disciplines reduces ambiguity in treatment plans, facilitates care transitions between providers and settings (hospital to home health, wound clinic to primary care), and supports accurate data collection for quality improvement initiatives.

Essential Wound Care Terms

04 Pressure Injuries

Pressure injuries (formerly pressure ulcers or decubitus ulcers) result from sustained pressure or pressure combined with shear, typically over bony prominences. They represent the most common chronic wound in acute and long-term care settings, affecting up to 3 million Americans annually with an estimated cost of $9.1-$11.6 billion per year.

NPUAP/EPUAP Pressure Injury Staging System (2016 Revision)

Braden Scale for Predicting Pressure Injury Risk

The Braden Scale is the most widely validated risk assessment tool. It comprises six subscales, each scored 1-4 (except friction/shear scored 1-3). Lower scores indicate higher risk.

Prevention Strategies

Repositioning: Reposition every 2 hours in bed; every 1 hour in chair. Use the 30-degree lateral tilt position to offload the sacrum. Avoid positioning directly on the trochanter. Elevate heels off the bed using pillows or heel-suspension devices. Use draw/lift sheets to reposition (reduces shear). Post repositioning schedule at the bedside and document each turn.

Support surfaces: Use pressure-redistribution mattresses based on risk level. Group 1 (reactive/constant low pressure): foam overlays, alternating pressure pads, gel overlays — appropriate for Stage 1-2 or at-risk patients who can be repositioned. Group 2 (powered pressure redistribution): alternating pressure mattresses, low-air-loss mattresses — for Stage 3-4, multiple turning surfaces impractical, or failure to heal on Group 1 surface. Group 3 (air-fluidized): fluidized silicone bead beds (e.g., Clinitron) — for large Stage 3-4 pressure injuries, myocutaneous flap patients, or burns >40% TBSA. Do not use ring cushions ("donut" cushions) — they concentrate pressure at the ring edges and worsen ischemia.

Moisture management: Use incontinence briefs with superabsorbent polymers; apply barrier creams (dimethicone-based) to protect perianal skin. Implement structured incontinence care protocols (assessment, scheduled toileting, perineal cleansing, barrier application). Differentiate moisture-associated skin damage (MASD) from pressure injury — MASD presents as diffuse erythema conforming to moisture exposure area, not localized over a bony prominence.

Nutrition: Ensure adequate caloric (30-35 kcal/kg/day) and protein (1.25-1.5 g/kg/day) intake; supplement zinc and vitamin C. Consult dietitian for all patients with existing pressure injuries or Braden nutrition subscale score ≤2. Provide oral nutritional supplements (ONS) between meals for patients unable to meet caloric requirements through diet alone.

Skin inspection: Perform head-to-toe skin assessment at admission and daily, with particular attention to bony prominences (sacrum, heels, ischial tuberosities, trochanters, occiput). In darkly pigmented skin, non-blanchable erythema may not be visually apparent — assess for localized warmth, edema, induration, or pain compared to adjacent tissue. Use good lighting and palpation. Document findings and interventions at each assessment.

05 Diabetic Foot Ulcers

Diabetic foot ulcers (DFUs) affect approximately 15-25% of people with diabetes during their lifetime and precede 85% of diabetes-related lower-extremity amputations. The triad of peripheral neuropathy (present in 60-70% of DFU patients), peripheral arterial disease (present in 50%), and foot deformity creates the pathologic milieu for ulceration. Minor trauma or repetitive pressure on an insensate, ischemic, deformed foot leads to tissue breakdown.

Wagner Classification of Diabetic Foot Ulcers

University of Texas (UT) Classification

The UT system is a two-dimensional matrix combining wound depth (grade) with the presence of infection and/or ischemia (stage), providing superior prognostic value compared to Wagner alone.

IDSA/IWGDF Classification of Diabetic Foot Infections

Neuropathy Screening

Semmes-Weinstein 10-g monofilament: The standard screening test. The monofilament is applied perpendicular to the skin at 10 sites on each foot (plantar aspects of hallux, 1st, 3rd, and 5th metatarsal heads, plantar midfoot, heel, and dorsal first web space). Loss of sensation at ≥4 sites indicates clinically significant neuropathy. Sensitivity 66-91%, specificity 34-86%. 128-Hz tuning fork: Tests vibratory perception at the hallux dorsal interphalangeal joint. Loss of vibratory sense correlates with large-fiber neuropathy. Vibration perception threshold (VPT): Biothesiometry provides quantitative measurement; VPT >25 volts indicates high ulceration risk (7-fold increased risk). Ankle reflexes: Absent Achilles reflex suggests peripheral neuropathy. Michigan Neuropathy Screening Instrument (MNSI): Validated questionnaire + physical exam scoring system.

Vascular Assessment

Charcot Neuroarthropathy (Charcot Foot)

A progressive, destructive process affecting the bones, joints, and soft tissues of the foot and ankle in patients with peripheral neuropathy. The neurotraumatic and neurovascular theories explain the pathogenesis: repetitive unperceived trauma on an insensate foot with autonomic neuropathy-driven hyperemia leads to osteoclast activation (RANKL upregulation), microfractures, joint dislocation, and architectural collapse. The most commonly affected site is the tarsometatarsal (Lisfranc) joint complex (Sanders-Frykberg Type II, accounting for ~60% of cases), followed by the midfoot and hindfoot.

Offloading

Total contact cast (TCC): The gold standard for offloading neuropathic plantar DFUs. Achieves healing rates of ~90% at 12 weeks. Distributes pressure across the entire plantar surface, reduces shear, and ensures adherence (non-removable). Contraindicated in active infection, significant PAD, and extreme edema fluctuation. Irremovable walkers: Removable cast walkers (e.g., CAM boot) rendered irremovable with a cohesive bandage wrap have equivalent efficacy to TCC and may be preferred for ease of application. Other options: Therapeutic footwear (depth shoes with custom insoles), half shoes, healing sandals, felted foam, and accommodative padding for lower-risk ulcers.

06 Vascular Ulcers

Vascular ulcers account for approximately 70-80% of chronic lower-extremity wounds. They are divided into venous (60-80% of leg ulcers), arterial (15-25%), and mixed (15-30%) etiologies. Accurate differentiation is critical because treatment strategies differ fundamentally — compression for venous ulcers is contraindicated in severe arterial disease.

Venous Leg Ulcers

Venous ulcers result from sustained venous hypertension due to valvular incompetence in the superficial, deep, or perforator veins. Ambulatory venous pressure remains elevated (normally drops from ~100 mmHg at rest to ~20 mmHg with ambulation; in venous disease it remains >60 mmHg), causing capillary distension, fibrinogen leakage, pericapillary fibrin cuff formation, white blood cell trapping, and chronic inflammation.

Clinically they present as shallow, irregularly shaped ulcers in the gaiter area (medial lower leg between ankle and mid-calf), with surrounding hemosiderin staining (brown pigmentation from red blood cell extravasation and hemoglobin degradation), lipodermatosclerosis (woody induration of subcutaneous tissue from chronic fibrosis), varicose veins, stasis dermatitis (eczematous changes with pruritus), and edema. The wound bed is typically granular with heavy serous or serosanguineous exudate. Pain is variable — often described as a dull ache that improves with leg elevation (in contrast to arterial pain which worsens with elevation).

CEAP Classification of Chronic Venous Disease

The full CEAP classification also includes Etiology (Ec = congenital, Ep = primary, Es = secondary, En = no cause identified), Anatomy (As = superficial, Ap = perforator, Ad = deep), and Pathophysiology (Pr = reflux, Po = obstruction, Pr,o = both). Clinical class is further qualified as symptomatic (s) or asymptomatic (a) — for example, C2s indicates symptomatic varicose veins.

Compression Therapy for Venous Ulcers

Compression is the cornerstone of venous ulcer management. Target compression is 30-40 mmHg at the ankle, graduated (highest at ankle, decreasing proximally). Options include:

Multilayer compression bandaging: Four-layer bandage system (e.g., Profore) providing sustained compression for up to 7 days. Considered the gold standard for active venous ulcers. Unna boot: Zinc oxide-impregnated gauze bandage providing semi-rigid compression. Changed every 1-2 weeks. Well-suited for ambulatory patients. Compression stockings: Used primarily for maintenance after ulcer healing. 30-40 mmHg knee-high stockings reduce recurrence by approximately 50%. Adjustable compression wraps: Velcro-type wraps (e.g., CircAid) allowing patient self-adjustment. Intermittent pneumatic compression (IPC): Mechanical pump devices for patients unable to tolerate sustained compression or with refractory ulcers.

Pentoxifylline 400 mg TID is the only medication with Level 1 evidence for improving venous ulcer healing when combined with compression (NNT ~6 for complete healing). Its mechanism includes reducing blood viscosity, improving red blood cell deformability, decreasing platelet aggregation, and anti-inflammatory effects (reduces TNF-α and leukotriene production). It may be used even in patients who cannot tolerate compression. Common side effects include gastrointestinal upset (nausea, dyspepsia). Aspirin 300 mg daily has shown modest evidence of accelerating venous ulcer healing in some studies, though results are inconsistent. Micronized purified flavonoid fraction (MPFF/Daflon) 500 mg BID has evidence in European guidelines for venous ulcer healing as adjunctive therapy, though it is not FDA-approved for this indication in the US.

Venous Ulcer Recurrence Prevention

Venous ulcer recurrence rates are 30-70% within 12 months without ongoing compression. Lifelong compression therapy is the cornerstone of recurrence prevention. Patients who have healed a venous ulcer should wear 30-40 mmHg graduated compression stockings daily for life. Compliance is the major challenge — stockings should be replaced every 3-6 months as elasticity degrades. Stocking donning aids (e.g., Medi Butler, Doff N' Donner) improve independence and compliance for patients with limited hand strength or mobility. Additional recurrence prevention measures include: regular exercise (calf muscle pump activation), leg elevation when sedentary, weight management, skin care (emollients to prevent dryness and cracking), treatment of underlying venous reflux (endovenous ablation, sclerotherapy), and prompt wound care at the first sign of skin breakdown.

Arterial Ulcers

Arterial ulcers result from inadequate arterial perfusion (peripheral arterial disease). They present as well-demarcated, "punched-out" ulcers with pale or necrotic wound beds and minimal granulation tissue, located on the distal toes, dorsum of the foot, over the lateral malleolus, or at sites of trauma. Associated findings include absent pedal pulses, cool/pale extremity, dependent rubor (red-purple color with dependency that blanches on elevation), trophic changes (thin shiny skin, hair loss, thick dystrophic nails), and pain at rest (especially nocturnal, relieved by dependency).

Key diagnostic criteria: ABI <0.5 (severe PAD), rest pain, tissue loss. Treatment priority is revascularization first (endovascular angioplasty/stenting or surgical bypass), followed by wound care after adequate perfusion is established. Wound care without revascularization is futile in critical limb ischemia. Post-revascularization wound care follows standard moist wound healing principles. Post-procedure monitoring includes repeat ABI and clinical assessment to confirm improved perfusion before initiating definitive wound therapy.

Venous Ablation and Surgical Interventions

Correction of underlying venous reflux accelerates ulcer healing and reduces recurrence. Endovenous thermal ablation (radiofrequency or laser ablation of the great or small saphenous veins) and ultrasound-guided foam sclerotherapy are first-line interventions for superficial venous reflux. The EVRA trial demonstrated that early endovenous ablation (within 2 weeks of presentation) combined with compression resulted in faster ulcer healing compared to compression alone (median healing time 56 vs 82 days). Subfascial endoscopic perforator surgery (SEPS) addresses incompetent perforator veins. Deep venous reconstruction (valve repair, stenting for iliac vein obstruction) is reserved for refractory cases with documented deep venous pathology. All patients with venous ulcers should undergo duplex ultrasound assessment of the superficial and deep venous systems to identify correctable reflux.

Mixed Arterial-Venous Ulcers

Patients with concurrent venous insufficiency and moderate PAD (ABI 0.5-0.8). Management requires modified compression (reduced to 23-30 mmHg or short-stretch bandaging that provides high working pressure but low resting pressure) with vascular surgery consultation. Inelastic compression systems are preferred over elastic systems in mixed disease because they provide compression primarily during ambulation (muscle pump) with low resting pressure.

07 Moist Wound Healing & Dressing Categories

In 1962, George Winter demonstrated that wounds covered with an occlusive dressing epithelialized twice as fast as those left to dry in the air, establishing the principle of moist wound healing. A moist wound environment promotes cell migration (keratinocytes migrate faster over moist surfaces), growth factor activity, autolytic debridement, angiogenesis, and reduces pain. The goal is balanced moisture — enough to prevent desiccation but not so much as to cause maceration.

TIME Framework for Wound Bed Preparation

The TIME framework provides a systematic approach to removing barriers to healing:

Comprehensive Dressing Category Guide

Periwound Skin Protection

Protection of the periwound skin is as important as managing the wound bed itself. Periwound damage (maceration, excoriation, contact dermatitis) expands the wound margin and impairs healing. Strategies include:

Moisture barrier products: Dimethicone-based skin protectants (e.g., Cavilon, Critic-Aid) form a breathable, transparent barrier against wound exudate and incontinence. Apply to periwound skin at each dressing change. Petrolatum-based barriers (zinc oxide paste, A+D ointment) provide thicker protection but may interfere with adhesive dressing adherence. Cyanoacrylate-based skin protectants (e.g., Marathon liquid skin protectant) form a durable film lasting 48-72 hours that protects against adhesive stripping and moisture damage.

Window framing: Apply a hydrocolloid "frame" around the wound before placing the primary dressing. The hydrocolloid protects the periwound skin from adhesive trauma and exudate exposure while providing a secure adhesive surface for the secondary dressing.

Negative pressure considerations: When applying NPWT, ensure drape does not contact macerated skin directly. Apply skin prep or hydrocolloid under the drape margins to protect fragile periwound tissue.

Wound Cleansing

Proper wound cleansing removes surface contaminants, loose debris, and residual dressing material without damaging viable tissue. Normal saline (0.9% NaCl) is the traditional standard cleansing solution — isotonic, non-cytotoxic, and widely available. Tap water (potable) is equivalent to saline for wound cleansing in most settings (Cochrane review found no difference in infection rates). Antiseptic cleansers: Solutions containing PHMB with betaine surfactant (Prontosan) or hypochlorous acid (Vashe, Microcyn) provide antimicrobial wound cleansing with minimal cytotoxicity. These are preferred over traditional antiseptics (povidone-iodine, hydrogen peroxide, Dakin solution at full strength) which are cytotoxic to fibroblasts and keratinocytes at concentrations that kill bacteria.

Irrigation pressure: Optimal wound irrigation pressure is 4-15 psi (pounds per square inch). Pressures below 4 psi are insufficient to dislodge bacteria and debris. Pressures above 15 psi can drive bacteria into tissue and damage the wound bed. A 35 mL syringe with an 18-gauge angiocatheter delivers approximately 8 psi, which is the most commonly recommended bedside method. Commercially available irrigation systems (pulsed lavage devices) allow adjustable pressure settings for larger or deeper wounds.

08 Antimicrobial Dressings

Antimicrobial dressings play a critical role in managing the wound infection continuum, particularly at the level of critical colonization and local infection where systemic antibiotics are not indicated but bacterial burden impedes healing.

Wound Infection Continuum

Silver-Based Dressings

Ionic silver (Ag+): Released from silver-containing compounds (silver sulfadiazine, silver nitrate, silver chloride). Disrupts bacterial cell membranes and enzyme systems. Broad-spectrum activity against gram-positive and gram-negative bacteria, fungi, and some viruses. Available in multiple substrates (foam, alginate, hydrofiber, CMC). Examples: Aquacel Ag, Mepilex Ag. Nanocrystalline silver: Provides sustained release of silver ions from ultra-small silver crystals. Higher antimicrobial potency at lower silver concentrations. Acticoat (nanocrystalline silver on rayon/polyethylene mesh) is the prototype. Must be moistened with sterile water (NOT saline, which precipitates silver chloride and inactivates it). Can cause transient gray-blue skin discoloration (argyria-like) that resolves when discontinued.

Other Antimicrobial Agents

Cadexomer iodine: Starch microspheres containing 0.9% iodine. As the microspheres absorb exudate, they swell and release iodine slowly into the wound. Provides sustained antimicrobial activity, absorbs exudate, and facilitates debridement. Effective against biofilm. Contraindicated in thyroid disorders (Hashimoto, Graves), iodine allergy, pregnancy/lactation, lithium use, and large wounds (>150 cm²). Example: Iodosorb.

PHMB (polyhexamethylene biguanide): A synthetic antiseptic with broad-spectrum activity against bacteria, fungi, and viruses. Low cytotoxicity relative to other antiseptics. Available as wound irrigation solution (e.g., Prontosan) and impregnated dressings. Effective for biofilm disruption when combined with a surfactant (betaine).

Medical-grade honey (Manuka/Leptospermum): Multiple mechanisms of action: high osmolarity draws fluid and creates hostile environment for bacteria; low pH (3.5-4.5) inhibits bacterial growth; continuous low-level hydrogen peroxide production from glucose oxidase; methylglyoxal (MGO) in Manuka honey provides non-peroxide antibacterial activity rated by Unique Manuka Factor (UMF). Effective against MRSA and biofilm. Must be medical-grade (gamma-irradiated, standardized). Do not use food-grade honey on wounds.

Biofilm Management

Biofilms are present in 60-80% of chronic wounds and are a primary cause of healing failure. Biofilm bacteria are 500-1000x more resistant to antibiotics than planktonic (free-floating) bacteria. Biofilm management requires a combined approach: (1) sharp/mechanical debridement to physically disrupt and remove the biofilm, followed immediately by (2) topical antimicrobial dressing application (within the "therapeutic window" before biofilm reconstitutes in 24-72 hours). This "wound hygiene" approach should be repeated at each dressing change for chronic wounds with suspected biofilm. Biofilm reformation occurs within 24 hours of debridement, reaching mature biofilm status again within 72 hours if not suppressed.

09 Advanced Wound Products

Advanced wound therapies are indicated for chronic wounds that have failed to demonstrate adequate healing progress (≥40-50% area reduction) after 4 weeks of standard care including debridement, moisture balance, offloading/compression, infection management, and nutritional optimization.

Skin Substitutes & Tissue-Engineered Products

Growth Factors

Becaplermin (Regranex): Recombinant human PDGF-BB (rhPDGF-BB) 0.01% gel. The only FDA-approved growth factor for wound healing. Applied as a thin layer to a clean, debrided DFU daily, covered with saline-moistened gauze. Indicated for neuropathic DFUs extending into subcutaneous tissue or deeper. Demonstrated a 43% complete healing rate vs 35% with placebo gel at 20 weeks. Carries a black box warning for increased mortality from malignancy with ≥3 tubes used (post-marketing data; causality debated). Contraindicated in known neoplasm at application site.

Platelet-Rich Plasma (PRP)

Autologous platelet-rich plasma is prepared by centrifuging the patient's own blood to concentrate platelets (typically 3-5x baseline concentration) and their associated growth factors (PDGF, TGF-β, VEGF, EGF, IGF-1). The concentrated platelet preparation is applied directly to the wound bed or injected into the wound edges. PRP provides a supraphysiologic concentration of autologous growth factors at the wound site. Evidence supports use in chronic DFUs and venous ulcers refractory to standard care. Advantages include autologous origin (no rejection risk), relatively low cost, and point-of-care preparation. Limitations include lack of standardized preparation protocols (significant variability between devices and techniques), variable platelet concentrations, and limited high-quality RCT data.

Extracellular Matrix (ECM) Scaffolds

ECM-based products provide a three-dimensional scaffold that supports cellular ingrowth and modulates the wound microenvironment. Unlike simple collagen dressings, intact ECM scaffolds retain the complex structural and signaling molecules of the native tissue, including basement membrane components (laminin, type IV collagen), growth factors bound to the matrix, and glycosaminoglycans. These products undergo "constructive remodeling" — host cells infiltrate the scaffold, degrade it over time, and replace it with site-appropriate tissue rather than scar. Key products include porcine SIS (Oasis), porcine urinary bladder matrix (MatriStem), bovine pericardium (PriMatrix), and ovine forestomach matrix (Endoform). Application requires a clean, granulating wound bed free of necrotic tissue and active infection.

Collagen Dressings & ECM Products

Collagen-based wound dressings (bovine, porcine, equine, or avian sourced) serve as "sacrificial substrates" for excess MMPs in chronic wounds. Elevated MMP-2 and MMP-9 in chronic wound fluid degrade endogenous collagen and growth factors. Exogenous collagen preferentially binds and is degraded by these MMPs, protecting the wound's native repair molecules. Collagen also provides a scaffold for fibroblast migration and proliferation. Products are available as sheets, particles, gels, and pads (e.g., Promogran, Puracol Plus, Endoform).

Cellular and/or Tissue-Based Products (CTPs) — Coverage Criteria

10 Negative Pressure Wound Therapy

Negative pressure wound therapy (NPWT), also known as vacuum-assisted closure (VAC), applies sub-atmospheric pressure to a wound through a sealed dressing system. Since its introduction in the 1990s, NPWT has become one of the most widely used adjunctive wound therapies.

Mechanisms of Action

Macrodeformation: The negative pressure mechanically draws wound edges together, reducing wound volume and surface area. Microdeformation: At the foam-wound interface, the negative pressure creates microstrain on cells, stimulating cell proliferation, angiogenesis, and granulation tissue formation via mechanotransduction pathways (similar to the distraction osteogenesis principle). Fluid removal: Active removal of excess wound exudate decreases interstitial edema, reduces bacterial burden in the fluid, and removes inhibitory factors (MMPs, pro-inflammatory cytokines). Stabilization of the wound environment: The sealed dressing maintains moist wound healing, insulates the wound, and provides a barrier to external contamination.

Settings and Application

Indications

Acute and traumatic wounds, dehisced surgical wounds, chronic wounds (pressure injuries, DFUs, venous ulcers) failing standard therapy, flap and graft management (bolster dressing), open abdominal wounds (abdominal NPWT/wound VAC), preparation of wound bed for definitive closure, and reduction of edema in complex wounds.

Contraindications

Troubleshooting Common NPWT Problems

NPWT with Instillation (NPWTi-d)

NPWTi-d (negative pressure wound therapy with instillation and dwell time) combines standard NPWT with automated instillation of a topical wound solution (most commonly normal saline or dilute antiseptic such as 0.1% dakin solution or PHMB). The solution is instilled into the wound, held for a programmable dwell time (typically 10-20 minutes), then aspirated by the negative pressure. This cycle repeats every 2-4 hours. Indicated for infected wounds, wounds with heavy biofilm burden, and wounds requiring frequent irrigation. Evidence demonstrates reduced time to wound closure and decreased biofilm reformation compared to standard NPWT alone.

Portable and Disposable NPWT

Single-use, disposable NPWT systems (e.g., PICO, SNaP) provide a smaller, quieter, canister-free alternative to traditional NPWT. These battery-powered devices deliver continuous negative pressure through an absorbent multilayer dressing that manages exudate via evaporation rather than canister collection. Advantages include improved patient mobility and quality of life, ease of application in outpatient settings, and lower cost for smaller wounds. Typical settings are -80 mmHg continuous. Indicated for closed surgical incisions (prophylactic iNPWT), low-to-moderate exudate wounds, and wounds appropriate for transitioning from traditional NPWT to a lighter system as exudate decreases. Not appropriate for large, heavily exudating wounds or wounds requiring instillation therapy.

11 Debridement Methods

Debridement — the removal of devitalized tissue, debris, and biofilm from a wound — is the single most important intervention in chronic wound management. Necrotic tissue provides a medium for bacterial growth, obscures wound assessment, impedes granulation tissue formation, and prevents epithelialization. The method of debridement is selected based on wound characteristics, patient status, clinical setting, and clinician skill.

Debridement Methods Compared

Ultrasonic Debridement

Low-frequency ultrasonic debridement (LFUD) uses ultrasonic energy (typically 20-40 kHz) transmitted through a saline mist to the wound surface. The mechanical energy disrupts biofilm, loosens necrotic tissue, and promotes debridement while preserving viable tissue. Two modes of action are involved: (1) cavitation — formation and implosion of microscopic bubbles that mechanically disrupt cell membranes and biofilm matrix, and (2) acoustic microstreaming — fluid movement around the probe tip that facilitates debris removal and enhances drug penetration. Advantages over sharp debridement include reduced pain (can be performed without anesthesia in many patients), selective tissue removal, biofilm disruption at a depth sharp instruments cannot reach, and stimulation of growth factor release. Devices include contact (e.g., SonicOne) and non-contact (e.g., MIST Therapy) systems. LFUD is particularly useful for wounds with heavy biofilm burden, patients who cannot tolerate sharp debridement (anticoagulated, pain-sensitive), and as an adjunct to sharp debridement for biofilm management.

Hydrosurgical Debridement

Versajet is the primary hydrosurgical debridement device, delivering a high-pressure saline jet across a small window in a handheld tip. The Venturi effect created by the jet simultaneously cuts and aspirates tissue, allowing precise, controlled debridement of necrotic tissue while preserving viable structures. The power level is adjustable (1-10), allowing the operator to match the aggressiveness of debridement to the tissue type. Particularly useful for tangential debridement of burns (excision to viable dermis), removal of biofilm from large wound surfaces, and debridement around delicate structures (tendons, nerves). Requires training for safe and effective use.

Maintenance Debridement

The concept of maintenance debridement recognizes that a single debridement episode is insufficient for chronic wounds. Biofilm reconstitutes within 24-72 hours of disruption. Serial debridement at each wound visit (typically weekly) maintains a clean wound bed, disrupts biofilm reformation, removes senescent wound edge cells, and stimulates the acute wound healing response. Maintenance debridement is associated with improved healing rates in both DFUs and venous ulcers.

Wound Hygiene Protocol

The emerging concept of wound hygiene provides a structured approach to biofilm-based wound care at every dressing change. The four-step protocol includes:

Step 1 — Cleanse: Irrigate the wound and periwound skin with an antiseptic solution (PHMB with betaine surfactant or hypochlorous acid). Surfactant-based cleansers are more effective at disrupting biofilm EPS than saline alone. Extend cleansing to the periwound skin (at least 5 cm beyond the wound edge) to address the "biofilm penumbra" — bacteria extending into surrounding tissue beyond the visible wound margin.

Step 2 — Debride: Perform sharp debridement of the wound bed (remove slough, non-viable tissue, and biofilm) and wound edges (remove callus, rolled edges/epibole, and non-migrating epithelium). Debridement of the wound edge refreshes the epithelial front and stimulates keratinocyte migration.

Step 3 — Refashion wound edges: Sharp debridement of the wound perimeter removes the biofilm penumbra, senescent cells at the wound margin, and hyperkeratotic tissue. This step converts the non-advancing chronic wound edge back to an acute edge with renewed migratory potential.

Step 4 — Dress: Apply an antimicrobial dressing immediately after debridement to suppress biofilm reformation during the critical 24-72 hour window before biofilm reestablishes. Select the dressing based on wound bed characteristics, exudate level, and infection status.

12 Wound Infection Management

All chronic wounds contain bacteria; the clinical significance depends on the quantity, virulence, and host response. The wound infection continuum progresses from contamination through colonization, critical colonization (local infection), local infection, spreading infection, and systemic infection.

Clinical Signs of Wound Infection

Wound Culture Technique

Levine quantitative swab technique: The recommended method for wound culture. Cleanse the wound with saline, remove necrotic tissue. Rotate a sterile swab over a 1 cm² area of clean granulation tissue with sufficient pressure to express fluid from the wound tissue (not superficial exudate). Bacteria count >10⁵ CFU/g tissue (or per swab equivalent) indicates critical colonization/infection. This technique correlates well with tissue biopsy quantitative culture (the true gold standard).

Tissue biopsy: The gold standard for wound culture. Provides quantitative culture (CFU/g tissue) and identifies organisms within the tissue, not just surface contaminants. Reserved for wounds not responding to empiric therapy or when accurate speciation is critical.

"Z" swab technique: An older method where a swab is rotated across the wound bed in a zigzag pattern covering the entire wound surface. Less accurate than the Levine technique because it samples superficial exudate and contaminants rather than tissue-level organisms. Not recommended for clinical decision-making. Needle aspiration: Useful for sampling closed abscesses or deep fluid collections. A 10 mL syringe with 22-gauge needle is inserted through intact, prepped skin into the fluid collection; aspirated material is sent for aerobic and anaerobic culture. Avoid aspirating through the open wound surface.

Empiric Antibiotic Selection

Always obtain cultures before starting empiric antibiotics and narrow coverage when sensitivities return. Duration of therapy depends on severity: mild infections 1-2 weeks; moderate 2-3 weeks; severe 3-4 weeks (longer if osteomyelitis). Reassess at 48-72 hours — if not improving, broaden coverage, obtain imaging for abscess/osteomyelitis, and reconsider wound etiology.

Wound Infection in Special Populations

Immunocompromised patients (HIV/AIDS, organ transplant recipients, chemotherapy, chronic corticosteroids) may not exhibit classic signs of infection due to impaired inflammatory response. In these patients, subtle findings such as increasing wound size, new friable tissue, delayed healing, or increasing pain may be the only indicators of infection. Maintain a low threshold for culture and empiric antibiotic initiation. Patients with diabetes often have blunted inflammatory responses and impaired leukocyte function; up to 50% of diabetic foot infections lack fever, leukocytosis, or elevated inflammatory markers. Bite wounds (human and animal) have unique microbiology: Pasteurella multocida (cat/dog bites), Capnocytophaga canimorsus (dog bites in asplenic patients), Eikenella corrodens (human bites); empiric treatment with amoxicillin-clavulanate covers typical bite wound pathogens. Cat bites carry higher infection rates than dog bites due to deep puncture inoculation.

13 Osteomyelitis in Chronic Wounds

Osteomyelitis is a serious complication of chronic wounds, particularly diabetic foot ulcers and pressure injuries overlying bony prominences. Contiguous-spread osteomyelitis (from adjacent soft tissue infection to bone) is the predominant mechanism in wound-associated osteomyelitis, as opposed to hematogenous osteomyelitis seen in children and IV drug users.

Diagnosis

Probe-to-bone (PTB) test: A sterile blunt metal probe is inserted into the wound. If bone is palpable (hard, gritty surface felt at the wound base), the test is positive. In the context of a diabetic foot ulcer, a positive PTB test has a positive predictive value (PPV) of 89% for osteomyelitis. In low-prevalence settings, the negative predictive value is more useful. Combined with clinical suspicion (wound area >2 cm², wound depth >3 mm, ESR >70 mm/hr), the PTB test guides imaging decisions.

Laboratory markers: ESR >70 mm/hr has ~90% sensitivity for osteomyelitis in DFU. CRP is less specific but useful for monitoring treatment response. WBC count is often normal in chronic osteomyelitis. Procalcitonin is elevated in systemic infection but not reliable for localized osteomyelitis.

Imaging: Plain radiographs are the first-line study — findings include periosteal reaction, cortical destruction, and medullary lucency, but changes require 40-50% bone loss to become visible (2-4 week lag). MRI is the imaging gold standard for osteomyelitis (sensitivity 90%, specificity 83%) — shows bone marrow edema (low signal on T1, high signal on T2/STIR), cortical disruption, and soft tissue extent. Nuclear medicine scans (triple-phase bone scan, WBC-labeled scan) are used when MRI is contraindicated.

Bone biopsy and culture: The diagnostic gold standard. Provides definitive microbiologic identification and antibiotic sensitivity. Percutaneous bone biopsy or intraoperative sample obtained from a separate clean incision (avoid contamination from wound surface bacteria). Culture results guide targeted antibiotic therapy.

Cierny-Mader Classification of Osteomyelitis

Treatment

Antibiotic therapy: Culture-directed antibiotics for 6 weeks (standard duration for osteomyelitis). IV antibiotics traditionally used for at least the first 2-4 weeks, with transition to oral agents with high bioavailability (fluoroquinolones, rifampin combinations, linezolid) if appropriate. The OVIVA trial demonstrated non-inferiority of early switch to oral antibiotics at 1 week in selected patients. Surgical management: Debridement of infected/necrotic bone, curettage of medullary canal, resection to bleeding bone ("paprika sign"). Dead space management with antibiotic beads/spacers or muscle flaps. In DFU osteomyelitis, partial ray amputation or metatarsal head resection may be limb-preserving. Conservative (antibiotic-only) management may be appropriate for small areas of osteomyelitis in poor surgical candidates.

14 Surgical Wounds & Dehiscence

Surgical wounds are the most common acute wounds encountered in clinical practice. They are classified by the method of closure and the level of contamination.

Postoperative Wound Care Phases

Immediate postoperative (0-48 hours): Surgical incisions closed by primary intention should be covered with a sterile occlusive dressing for 24-48 hours. During this period, the wound is sealed by the fibrin clot and early epithelial cell migration begins. The dressing protects against external contamination during this vulnerable period. Gentle cleansing with saline or mild soap and water may begin after 48 hours for most clean surgical wounds. Subacute phase (48 hours to 2 weeks): Monitor for signs of infection (erythema >2 cm from incision, increasing pain, purulent drainage, fever). Sutures or staples are typically removed based on anatomic location: face 3-5 days, scalp 7-10 days, trunk/extremities 10-14 days, over joints 14 days. Steri-Strips may be applied after suture removal for additional support during the continued remodeling phase. Maturation phase (2 weeks to 1-2 years): Scar management includes silicone sheeting or gel (evidence-based for scar prevention and treatment), sun protection (UV exposure causes permanent hyperpigmentation of immature scars), and avoidance of excessive tension on the incision line.

Wound Closure Methods

CDC Surgical Site Infection (SSI) Classification

SSI Depth Classification

Superficial incisional SSI: Within 30 days of surgery; involves only skin and subcutaneous tissue; purulent drainage, positive culture, or deliberate opening by surgeon with signs/symptoms of infection. Deep incisional SSI: Within 30 days (or 90 days if implant in place); involves fascia and muscle layers; purulent drainage from deep incision, spontaneous dehiscence or deliberate opening with fever >38°C, localized pain/tenderness, or abscess on imaging. Organ/space SSI: Any part of the body deeper than the fascia/muscle that was opened or manipulated; abscess or infection identified involving organ/space.

Wound Dehiscence

Dehiscence is the partial or complete separation of wound edges after primary closure. Risk factors include obesity, diabetes, malnutrition, smoking, chronic steroid use, infection, poor surgical technique, increased abdominal pressure (coughing, vomiting, ileus), and radiation. Evisceration (protrusion of abdominal contents through a dehisced abdominal wound) is a surgical emergency requiring immediate coverage with sterile saline-moistened gauze, patient positioning (supine, knees bent), and urgent surgical intervention.

Management of non-evisceration dehiscence depends on depth, infection status, and patient factors: small superficial dehiscence may heal by secondary intention; deep dehiscence may require NPWT for wound bed preparation followed by delayed primary closure or skin grafting; infected dehiscence requires antibiotic therapy and source control.

Incisional NPWT (iNPWT)

Prophylactic application of negative pressure to closed surgical incisions reduces SSI rates, seroma formation, and dehiscence in high-risk patients (obese, revisional surgery, vascular surgery groin incisions, cesarean section in obese patients, joint arthroplasty). Applied in the OR immediately after closure. Devices include Prevena (KCI/3M) and PICO (Smith+Nephew). Standard treatment duration is 5-7 days (matching the period of highest SSI vulnerability). The mechanism involves lateral tissue approximation, reduced dead space, increased lymphatic drainage, reduced lateral tension on incision edges, and maintenance of a clean closed environment.

15 Burn Wound Management

Burns are tissue injuries caused by heat (thermal), electricity, chemicals, radiation, or friction. Burn wound management involves rapid assessment of burn depth and total body surface area (TBSA) to guide resuscitation, determine need for burn center referral, and select appropriate wound care.

Burn Depth Classification

TBSA Estimation

Rule of 9s (adults): Head/neck = 9%, each upper extremity = 9%, anterior trunk = 18%, posterior trunk = 18%, each lower extremity = 18%, perineum = 1%. Lund-Browder chart: More accurate, especially for children; adjusts proportions for age (children have proportionally larger heads and smaller extremities). Palm method: Patient's palm (including fingers) represents approximately 1% TBSA; useful for small or scattered burns. Note: superficial (first-degree) burns are NOT included in TBSA calculations for fluid resuscitation.

Fluid Resuscitation

Burn Center Referral Criteria (ABA)

Partial-thickness burns >10% TBSA; any full-thickness burn; burns involving face, hands, feet, genitalia, perineum, or major joints; chemical or electrical burns (including lightning); inhalation injury; burns in patients with preexisting medical conditions that could complicate management; burns with associated trauma where burn is the greater risk; burns in children at facilities without qualified pediatric care; burns requiring special social, emotional, or rehabilitative intervention.

Topical Burn Agents

Escharotomy

Full-thickness circumferential burns produce a rigid, inelastic eschar that cannot expand. As underlying tissue edema increases during resuscitation, compartment pressures rise, compromising distal perfusion and, in the case of thoracic burns, restricting ventilation. Escharotomy is an emergent bedside procedure involving longitudinal incision through the full thickness of the eschar (but not into subcutaneous fat) along the mid-lateral or mid-medial lines of the extremity, or along the anterior axillary lines for chest escharotomy. Because full-thickness burns are insensate, local anesthesia is typically not required. Immediate restoration of perfusion (palpable pulses, capillary refill, improved SpO2) or ventilatory compliance confirms adequate release. Fasciotomy may be required for deep electrical burns or when escharotomy alone fails to restore perfusion, as these injuries may involve muscle compartment pressure elevation.

Skin Grafting

Split-thickness skin graft (STSG): Harvested with a dermatome at 0.008-0.012 inches (epidermis + partial dermis). Can be meshed (1:1.5 to 1:6 expansion) for large wounds. Donor site heals by epithelialization in 10-14 days. Workhorse of burn surgery. Full-thickness skin graft (FTSG): Includes epidermis + full dermis. Better cosmetic result, less contracture; limited donor tissue availability; used for face, hands, and small defects. Donor site requires primary closure.

Graft take factors: Successful graft adherence ("take") requires: (1) well-vascularized recipient bed (clean granulation tissue), (2) close contact between graft and bed (no hematoma, seroma, or shear), (3) adequate immobilization (bolster dressings, NPWT, or splinting for 5-7 days), and (4) absence of infection. Causes of graft failure include hematoma/seroma beneath the graft (most common technical cause), infection (especially Pseudomonas and beta-hemolytic Streptococcus, which produce fibrinolysins that dissolve the fibrin attachment), shear/mechanical disruption, and inadequate recipient bed vascularity.

16 Skin Tears

Skin tears are traumatic wounds caused by shear, friction, or blunt force resulting in separation of the skin layers. They are the most common wound in elderly and neonatal populations, occurring primarily on the extremities (dorsal forearm and hands most common) due to age-related skin fragility (dermal thinning, decreased collagen, loss of rete ridges, decreased subcutaneous fat, increased capillary fragility).

ISTAP Classification (International Skin Tear Advisory Panel)

Payne-Martin Classification (Historical)

Category I: Skin tear without tissue loss. Ia: linear type (epidermis and dermis pulled apart in a straight line). Ib: flap type (epidermal flap that can cover the dermis). Category II: Skin tear with partial tissue loss. IIa: scant tissue loss (≤25% of flap lost). IIb: moderate to large tissue loss (>25% of flap lost). Category III: Skin tear with complete tissue loss (entire epidermal flap absent).

Prevention in the Elderly

Moisturize skin BID with emollient creams (not lotions — lotions evaporate and may further dry skin). Protect extremities with long sleeves and shin guards. Pad bed rails and wheelchair arms. Use gentle adhesives (silicone-based tapes such as Mepitac, paper tape). Remove adhesives with adhesive remover rather than peeling. Maintain adequate nutrition and hydration. Use proper transfer and turning technique (lift, do not slide). Apply skin protectant (dimethicone or cyanoacrylate barrier) to vulnerable areas.

Risk Factors for Skin Tears

17 Atypical Wounds

Atypical wounds are those whose etiology is not related to the common causes (pressure, neuropathy, venous/arterial insufficiency, or surgery). They should be suspected when a wound has an unusual appearance, location, or fails to respond to standard evidence-based treatment after 4-12 weeks. Biopsy of the wound edge is often required for diagnosis.

Pyoderma Gangrenosum (PG)

A neutrophilic dermatosis presenting as a rapidly progressive, painful ulcer with violaceous, undermined borders and a purulent/necrotic base. Key feature: pathergy — worsening with surgical debridement or trauma (new lesions at surgical sites). Associated with inflammatory bowel disease (ulcerative colitis > Crohn's), rheumatoid arthritis, hematologic malignancy (AML, myeloma), and monoclonal gammopathy. Diagnosis is clinical (no pathognomonic histology); must exclude mimics (infection, vascular, malignancy). Treatment: immunosuppression (systemic corticosteroids first-line, cyclosporine, infliximab, dapsone); local wound care (moist wound healing, NPWT with caution); avoid surgical debridement (pathergy risk).

Calciphylaxis (Calcific Uremic Arteriolopathy)

A life-threatening condition of systemic arteriolar calcification and skin necrosis, primarily affecting patients with end-stage renal disease (ESRD) on dialysis, though non-uremic calciphylaxis can occur in patients with normal renal function who have other risk factors. Presents as exquisitely painful, retiform (net-like) purpura progressing to necrotic ulcers, most commonly on the lower extremities, abdomen, and buttocks. Mortality is 60-80% at 1 year, primarily from sepsis secondary to wound infection.

Risk factors: ESRD (on hemodialysis or peritoneal dialysis), hyperparathyroidism (secondary or tertiary), elevated calcium-phosphorus product (>70 mg²/dL²), warfarin use (inhibits matrix Gla protein, a calcification inhibitor), obesity (BMI >30 — adipose tissue is preferentially affected), diabetes, female sex, hypoalbuminemia, and protein C or S deficiency.

Diagnosis: Skin biopsy shows pathognomonic findings of arteriolar medial calcification, intimal hyperplasia, thrombosis, and subcutaneous fat necrosis. Von Kossa staining highlights calcium deposits. However, biopsy carries risk of wound expansion and should be performed cautiously (use punch biopsy from the wound edge, avoid large excisional biopsies).

Treatment: Sodium thiosulfate (25 g IV three times weekly during dialysis — chelates calcium, antioxidant, vasodilator); intensify dialysis (daily or extended sessions to optimize phosphorus clearance); correct hyperparathyroidism (cinacalcet for medical management, parathyroidectomy for refractory cases); discontinue warfarin and calcium-based phosphate binders (switch to sevelamer or lanthanum); wound care with meticulous pain management (often requiring opioids); surgical debridement controversial (high morbidity, poor healing capacity in affected tissue); HBOT may be considered as adjunctive therapy. Multidisciplinary management with nephrology, wound care, pain management, and nutrition is essential.

Vasculitis Ulcers

Ulcers resulting from inflammation and destruction of blood vessel walls. Presentation varies by vessel size: small-vessel vasculitis (palpable purpura, petechiae, ulcers on lower legs), medium-vessel (livedo reticularis, nodules, deep ulcers), large-vessel (claudication, ischemic ulcers). Causes include autoimmune (SLE, RA, ANCA-associated vasculitis), infection (hepatitis B/C), drug-induced, and cryoglobulinemia. Diagnosis requires punch biopsy of the wound edge (including subcutaneous tissue for medium/large vessel) showing vessel wall inflammation and fibrinoid necrosis. Treatment: address underlying cause; immunosuppression (corticosteroids, cyclophosphamide, rituximab); local wound care.

Martorell Ulcer (Hypertensive Ischemic Ulcer)

A rare but frequently misdiagnosed ulcer caused by arteriolar narrowing and ischemia in patients with severe, often poorly controlled hypertension. Presents as an exquisitely painful ulcer on the lateral or posterolateral lower leg or Achilles tendon area — in contrast to the medial location of venous ulcers. The wound is typically well-demarcated with a necrotic base and violaceous borders. Arteriolar hyalinosis and subintimal fibrosis are seen on deep biopsy. Key differentiating feature from calciphylaxis: Martorell ulcers occur in patients with hypertension but normal renal function and normal calcium-phosphorus metabolism. Treatment includes aggressive blood pressure control, pain management (often requiring opioids), local wound care (moist wound healing, cautious debridement), and consideration of surgical closure with skin grafting once the wound bed is prepared.

When to Biopsy a Wound

Radiation Dermatitis & Radiation Ulcers

Acute radiation dermatitis occurs during radiation therapy and follows a predictable dose-dependent progression:

Late radiation injury (months to years post-treatment) presents as chronic non-healing ulcers in irradiated tissue with impaired vascularity, fibrosis, and poor healing potential. The underlying pathophysiology is obliterative endarteritis — progressive fibrosis and occlusion of small blood vessels in the radiation field, creating a hypoxic, hypocellular, hypovascular (the "3H" tissue) environment. Treatment: pentoxifylline + vitamin E (PENTOCLO protocol for radiation fibrosis); hyperbaric oxygen therapy (promotes angiogenesis in radiation-damaged tissue — approved indication; 40-60 sessions typically required); gentle wound care with moisture balance; surgical reconstruction with well-vascularized tissue (free flaps from outside the radiation field) for refractory ulcers.

Malignant Wounds (Fungating Tumors)

Wounds caused by primary skin cancer or metastatic cancer infiltrating the skin. Present as fungating (proliferative, cauliflower-like growth above the skin surface), ulcerating (crater-like erosion into tissue), or combined fungating-ulcerating lesions. Most common primary tumors causing fungating wounds include breast cancer (60-70%), head and neck cancers, and melanoma. Management is often palliative, focusing on:

Odor control: Malodor is caused by anaerobic bacteria colonizing necrotic tissue; treat with topical metronidazole gel 0.75% BID (directly targets anaerobes), activated charcoal dressings (adsorb volatile odor compounds), cadexomer iodine, or medical-grade honey. Environmental measures include room ventilation, charcoal filters, and scented products (used cautiously — some patients develop aversive associations with specific scents).

Bleeding management: Tumor neovascularization produces friable vessels prone to hemorrhage. Use atraumatic dressing changes with silicone contact layers (Mepitel), topical tranexamic acid (500 mg tablet crushed and dissolved in 5 mL saline, applied on gauze), alginate dressings for hemostasis, topical epinephrine (1:1000 on gauze), silver nitrate cautery sticks, or sucralfate paste. Avoid sharp debridement of actively vascularized tumor tissue. For catastrophic hemorrhage (erosion into major vessel), have dark-colored towels available to minimize visual distress, and ensure comfort measures are prioritized.

Exudate management: Superabsorbent dressings, hydrofiber or alginate primary layers, and frequent dressing changes. NPWT may be used cautiously if no exposed vessels. Pain management: Topical lidocaine 2-4% applied 15-20 minutes before dressing changes, topical morphine (mixed with hydrogel), systemic analgesics, and anxiolytics as needed. Psychosocial support: Fungating wounds cause significant body image distress, social isolation, and reduced quality of life; involve palliative care and psychosocial support services early.

18 Hyperbaric Oxygen Therapy

Hyperbaric oxygen therapy (HBOT) involves breathing 100% oxygen at pressures greater than 1 atmosphere absolute (ATA) in a pressurized chamber. The resulting supraphysiologic tissue oxygen tensions produce therapeutic effects that support wound healing in selected patients.

Mechanisms of Action

Hyperoxia: Tissue pO2 increases from normal ~40 mmHg to 200-400 mmHg during HBOT, creating an oxygen gradient that drives oxygen diffusion into hypoxic wound tissue. Angiogenesis: The oxygen gradient at the wound edge (high pO2 in healthy tissue, low pO2 in wound center) is the primary stimulus for VEGF release and new blood vessel formation. HBOT enhances this gradient. Bactericidal activity: Elevated oxygen tension directly kills obligate anaerobes and enhances oxidative killing by neutrophils (respiratory burst requires O2). Synergistic with aminoglycosides and fluoroquinolones (which require O2 for bacterial cell entry). Anti-inflammatory effects: Reduces neutrophil adhesion to endothelium, decreases edema, and modulates cytokine production. Stem cell mobilization: HBOT mobilizes bone marrow-derived stem/progenitor cells (CD34+) into the circulation, promoting vasculogenesis.

Approved Indications for HBOT (UHMS)

The Undersea and Hyperbaric Medical Society (UHMS) recognizes 14 approved indications for HBOT. Wound-related indications include:

Treatment Protocol

Standard wound healing protocol: 2.0-2.4 ATA for 90 minutes of oxygen breathing time per session (with air breaks every 20-30 minutes to prevent oxygen toxicity). Sessions are daily, 5 days per week. Total course: 30-60 sessions depending on indication and response. DFUs typically receive 30-40 sessions. Radiation injury may require 40-60 sessions.

Air breaks: Patients breathe air (not 100% O2) for 5 minutes after every 20-30 minutes of oxygen breathing. Air breaks reduce the cumulative oxygen dose to the lungs and CNS, significantly decreasing the risk of pulmonary and CNS oxygen toxicity without diminishing wound healing benefit. A typical 90-minute treatment session includes three 30-minute oxygen periods separated by two 5-minute air breaks.

Chamber Types

Monoplace chambers: Single-patient acrylic chambers pressurized entirely with 100% oxygen. The patient lies supine inside the chamber. Advantages include lower cost, smaller footprint, and simpler operation. Limitations include inability for staff to directly access the patient during treatment, claustrophobia risk, and the entire chamber atmosphere is oxygen (higher fire risk — all materials inside must be approved for oxygen-enriched environments; no electronics, no petroleum-based products). Multiplace chambers: Room-sized steel chambers accommodating multiple patients and an inside attendant (nurse or technician). Chamber is pressurized with compressed air; patients breathe 100% oxygen through a hood, mask, or endotracheal tube. Advantages include direct bedside patient care, ability to treat critically ill or ventilated patients, reduced claustrophobia, and lower fire risk (chamber atmosphere is air). Disadvantages include higher construction and operating costs and larger space requirements.

Complications of HBOT

Contraindications

Absolute: Untreated pneumothorax (risk of tension pneumothorax during decompression). Relative: Uncontrolled seizure disorder (oxygen toxicity lowers seizure threshold), concurrent bleomycin or cisplatin use (enhanced pulmonary toxicity), severe COPD with CO2 retention (loss of hypoxic drive concern — largely theoretical), untreated malignancy in the treatment field (concern for tumor growth — evidence limited), claustrophobia (monoplace chambers), active upper respiratory infection or inability to equalize middle ear pressure, pregnancy (theoretical teratogenicity at high O2 tensions — not well studied), and high fever (lowers seizure threshold synergistically with hyperoxia).

19 Offloading & Compression

Mechanical offloading (reducing pressure on the wound) and compression therapy (applying external pressure to the limb) are the foundational non-pharmacologic treatments for diabetic foot ulcers and venous leg ulcers, respectively. No wound product can overcome the continued mechanical insult of unaddressed pressure or venous hypertension.

Offloading for Diabetic Foot Ulcers

Offloading Special Situations

Heel ulcers: Heel offloading requires complete elimination of pressure on the heel (unlike forefoot offloading which redistributes pressure). Options include heel suspension devices (Prevalon boot, DH Pressure Relief Walker), pillows placed lengthwise under the calf to "float" the heel, or wedge-shaped foam devices. Elevating the heel off the bed surface is critical — pillows alone may shift, re-exposing the heel. Purpose-built devices with straps maintain position during sleep. Do not use ring-shaped ("donut") cushions under the heel, as they concentrate pressure at the ring edge and worsen ischemia.

Bilateral DFUs: Present a significant challenge as the patient requires offloading on both feet simultaneously. Wheelchair use may be necessary for plantar ulcers during the acute healing phase. Bilateral irremovable walkers are generally impractical due to fall risk. A combination of removable walkers (accepted lower healing rate) with intensive patient education, or wheelchair with heel-free positioning, may be required.

Charcot foot with ulceration: The deformity creates abnormal pressure points (bony prominences from midfoot collapse). TCC can accommodate the deformity during the acute phase. Once consolidated, custom-molded shoes with accommodative insoles (total contact inserts) are required for lifelong ulcer prevention.

Compression Therapy for Venous Disease

20 Nutrition & Systemic Optimization

Nutritional deficiency is among the most modifiable risk factors for impaired wound healing. Wound healing is an energy-intensive, anabolic process requiring adequate calories, protein, vitamins, minerals, and hydration. Systemic conditions (hyperglycemia, smoking, edema, immunosuppression) must also be addressed for optimal healing.

Macronutrient Requirements

Micronutrient Supplementation

Nutritional Screening Markers

Albumin (half-life 20 days): reflects long-term protein status; <3.5 g/dL indicates malnutrition; <2.5 g/dL is severe. However, albumin is a negative acute-phase reactant — it decreases in inflammation, infection, and fluid overload regardless of nutritional status. It is a prognostic marker for outcomes, not a direct treatment target. Prealbumin (transthyretin; half-life 2-3 days): more responsive to nutritional changes; <15 mg/dL suggests malnutrition; <11 mg/dL is severe. Useful for monitoring response to nutritional supplementation (check weekly). Also a negative acute-phase reactant.

Malnutrition Screening Tools

Malnutrition Universal Screening Tool (MUST): A five-step screening tool using BMI, unplanned weight loss, and acute disease effect. Score 0 = low risk, 1 = medium risk, ≥2 = high risk. Mini Nutritional Assessment (MNA): Validated for geriatric populations; includes dietary intake, weight loss, mobility, neuropsychological problems, and BMI. Score <17 = malnourished, 17-23.5 = at risk, ≥24 = well-nourished. Subjective Global Assessment (SGA): Clinician-administered tool combining history (weight change, dietary intake, GI symptoms, functional capacity) with physical examination (subcutaneous fat loss, muscle wasting, ankle/sacral edema). Rates patients as A (well-nourished), B (moderately malnourished or suspected malnutrition), or C (severely malnourished). All patients with chronic wounds should be screened for malnutrition on admission and at regular intervals; those identified as at-risk or malnourished require formal dietitian assessment and individualized nutrition care plans.

Systemic Optimization

Glucose control: Hyperglycemia impairs neutrophil function (chemotaxis, phagocytosis, and oxidative burst are all reduced at blood glucose >200 mg/dL), increases infection risk, glycosylates growth factors and their receptors reducing signaling efficacy, and impairs all phases of wound healing. Target HbA1C <8% for wound healing (some guidelines suggest <7%); avoid hypoglycemia. In the acute care setting, maintain blood glucose 140-180 mg/dL. Perioperative glucose >200 mg/dL doubles the risk of surgical site infection.

Smoking cessation: Nicotine causes vasoconstriction reducing tissue perfusion; carbon monoxide reduces oxygen-carrying capacity (shifts the oxyhemoglobin dissociation curve left); hydrogen cyanide inhibits oxidative metabolism. Smoking reduces wound oxygen tension by 30-40%. Cessation improves healing within 4 weeks. Even reduction in smoking frequency provides measurable benefit. Nicotine replacement therapy (patches, gum) is preferred over continued smoking, though nicotine itself has vasoconstrictive effects.

Edema management: Interstitial edema increases diffusion distance for oxygen and nutrients, compresses capillaries, and impairs cellular metabolism. Treat with compression, elevation, diuretics as indicated, and lymphedema therapy (complete decongestive therapy with manual lymphatic drainage and short-stretch bandaging for lymphedema component).

Medication review: Identify medications that impair healing and minimize or adjust when possible. Corticosteroids suppress inflammation, fibroblast proliferation, collagen synthesis, and immune function — vitamin A 25,000 IU daily for 10 days can partially reverse steroid-impaired healing. Immunosuppressants (methotrexate, mycophenolate, calcineurin inhibitors) impair cell proliferation and immune-mediated wound defense. Anticoagulants increase bleeding risk during debridement; warfarin specifically associated with calciphylaxis risk. Vasopressors reduce peripheral tissue perfusion. Chemotherapy suppresses bone marrow and cell proliferation. NSAIDs may impair the early inflammatory phase of healing, though evidence is mixed.

21 Wound Care Documentation

Complete and accurate wound care documentation serves clinical, legal, and reimbursement purposes. Every wound encounter must include a systematic assessment, treatment plan, and evidence of clinical decision-making.

Wound Assessment Documentation Template

Progress Tracking

Wound area reduction is the most important metric for predicting healing trajectory. Evidence demonstrates that wounds that achieve 40-50% area reduction at 4 weeks are highly likely to heal by 12 weeks, while those that do not are unlikely to heal with current therapy and require treatment reassessment. This "4-week rule" guides clinical decision-making about when to escalate therapy (advanced wound products, surgical intervention, HBOT, referral).

Additional metrics tracked longitudinally include: wound depth (decreasing = healing), exudate volume (decreasing = healing), wound bed tissue type progression (necrotic → slough → granulation → epithelial), periwound condition improvement, and pain trajectory.

CPT Coding for Wound Care

Additional CPT Codes for Wound Care

Medical Necessity Documentation

For advanced wound care products and HBOT, payers require documentation of: wound duration (>30 days), failure of standard care (debridement, moisture management, offloading/compression, infection treatment, nutritional optimization), absence of adequate vascular supply exclusion (ABI/TcPO2), wound measurements showing lack of progress (<40% area reduction at 4 weeks), absence of untreated infection, and patient adherence to treatment plan. Failure to document these elements results in claim denial.

ICD-10 Coding for Wound Care

Accurate ICD-10 coding captures wound etiology, laterality, and specificity. Key code families include: L89.xxx (pressure ulcers by site and stage), L97.xxx (non-pressure chronic ulcer of lower extremity by site, laterality, severity, and tissue involvement), E11.621 (type 2 diabetes with foot ulcer), I87.0xx (postthrombotic syndrome with ulcer), I83.0xx (varicose veins with ulcer), and T81.31xA (disruption of wound, initial encounter). Code to the highest specificity available: laterality (right/left), severity (limited to breakdown of skin, with fat layer exposed, with necrosis of muscle, with necrosis of bone), and chronicity (initial encounter, subsequent encounter, sequela). Use combination codes when available (e.g., E11.621 + L97 for diabetic foot ulcer site specificity).

22 Quality Metrics & Prevention Programs

Wound care quality is measured through standardized metrics, regulatory requirements, and evidence-based prevention programs. Hospitals and long-term care facilities face financial penalties for hospital-acquired pressure injuries (HAPI) under CMS value-based purchasing programs. A comprehensive wound care quality program integrates prevention, evidence-based treatment, outcome tracking, and continuous improvement processes.

Present on Admission (POA) Documentation

CMS requires hospitals to report whether diagnoses were present on admission (POA). Stage 3, Stage 4, and unstageable pressure injuries classified as hospital-acquired (not POA) are designated as hospital-acquired conditions (HACs) and are no longer eligible for higher DRG payment — the hospital absorbs the additional cost of treatment. Accurate POA documentation requires: complete skin assessment within hours of admission (ideally during the emergency department visit or within the first nursing assessment), photographic documentation of any existing wounds, staging and measurement of all identified pressure injuries, and clear documentation that the wound was present before hospitalization. If a comprehensive skin assessment is not completed within the admission window, any subsequently discovered pressure injury may default to hospital-acquired status.

CMS Quality Measures

NQF #0201 (PSI 03): Pressure ulcer rate (hospital-acquired Stage 3, 4, or unstageable pressure injuries per 1000 discharges). Publicly reported and linked to hospital reimbursement. NQF #0678: Percent of residents with new or worsened pressure ulcers in long-term care (MDS-derived). HAC Reduction Program: Hospitals in the worst-performing quartile for hospital-acquired conditions (including Stage 3/4 pressure injuries) receive a 1% payment reduction on all Medicare discharges.

Wound Care Certification

Skin Care Bundles for Prevention

Evidence-based prevention bundles reduce HAPI rates by 50-80% when implemented consistently. Components include: structured risk assessment on admission and daily (Braden Scale); skin inspection on admission and every shift; moisture management and incontinence care; pressure redistribution (support surfaces, repositioning schedule); nutritional assessment and supplementation; patient/family education; documentation compliance monitoring; and quality improvement data tracking with unit-level feedback.

SSKIN Bundle

A widely adopted pressure injury prevention framework:

Wound Care Team Structure

Comprehensive wound care programs utilize a multidisciplinary team approach: wound care nurse/CWOCN (direct wound assessment, treatment planning, product selection, education); physician/CWSP (medical management, debridement, HBOT supervision, surgical referral); podiatrist/DPM (DFU management, offloading, nail and callus care, Charcot management); vascular surgeon (revascularization assessment, ABI interpretation, compression clearance); physical/occupational therapy (mobility, offloading, edema management, functional optimization); registered dietitian (nutritional assessment, caloric and protein targets, supplement recommendations); social worker (insurance navigation, durable medical equipment procurement, adherence barriers, home care coordination); and orthotic/prosthetic specialist (custom footwear, offloading devices, prosthetics after amputation).

WOCN Society Guidelines

The Wound, Ostomy and Continence Nurses (WOCN) Society publishes evidence-based guidelines for pressure injury prevention and treatment, venous ulcer management, diabetic foot ulcer management, and ostomy care. These guidelines are updated periodically and serve as the standard of care in wound management. Key recommendations are graded by level of evidence (A = strong evidence, B = moderate evidence, C = expert opinion). The WOCN guidelines align with and complement international guidelines from EPUAP/NPIAP (pressure injuries), IWGDF (diabetic foot), and the Society for Vascular Surgery (venous disease), providing a comprehensive evidence framework for clinical practice and institutional policy development.

Key Performance Indicators (KPIs) for Wound Care Programs

Effective wound care programs track measurable outcomes including: HAPI incidence rate (new hospital-acquired pressure injuries per 1,000 patient-days), HAPI prevalence rate (point-prevalence survey data), average time to wound closure by wound type, percentage of wounds achieving ≥40% area reduction at 4 weeks, surgical site infection rates by procedure, debridement rates (percentage of wounds with necrotic tissue that receive timely debridement), compression therapy compliance rates for VLU patients, offloading compliance rates for DFU patients, amputation rates for diabetic foot patients, and patient-reported outcome measures (pain scores, quality of life). Benchmarking against national databases (NDNQI for pressure injuries, NSQIP for SSI) enables comparison with peer institutions.

Telehealth in Wound Care

Remote wound monitoring and telehealth consultations have expanded access to wound care expertise, particularly in rural and underserved settings. Store-and-forward (asynchronous) wound photography allows wound specialists to review images and provide treatment recommendations without synchronous visits. Real-time video consultations enable specialist guidance for bedside clinicians performing assessments and dressing changes. Requirements for effective telehealth wound care include: standardized photography protocols (consistent distance, lighting, angle, ruler in frame), calibrated digital measurement tools, structured assessment templates, and secure HIPAA-compliant platforms. Studies demonstrate comparable healing outcomes for telehealth-managed wounds versus in-person care, with improved access, reduced travel burden, and earlier specialist involvement.

Legal Considerations

Pressure injuries are the second most common claim in nursing malpractice litigation. Key documentation requirements for legal protection: evidence of risk assessment on admission, implementation of prevention interventions appropriate to risk level, regular reassessment and documentation of skin status, evidence that changes in wound status prompted treatment modifications, informed consent for debridement and advanced therapies, and documentation of patient/family education and adherence barriers. Facilities should maintain policies defining accountability for skin assessments, documentation timelines, escalation procedures when new pressure injuries are identified, root cause analysis processes, and staff competency validation in wound prevention and care.

23 Staging Systems Master Table

24 Dressing Selection Guide

This quick-reference table matches wound characteristics to the most appropriate dressing category with clinical rationale.

25 ABI Interpretation Table

26 TIME Framework Quick Reference

27 Common Wound Care Products by Category

28 Abbreviations Master List