Wound Care

01 Skin Anatomy & Wound Healing Physiology

Wound care as a specialty sits at the intersection of dermatology, vascular surgery, plastic surgery, endocrinology, infectious disease, and rehabilitation medicine. Before a scribe can document a wound encounter intelligently, they need a working knowledge of skin architecture and the biology of healing — because every dressing, debridement, and advanced therapy is chosen to correct a specific failure in that biology.

Skin Layers

The skin has three functional layers. The epidermis is the outer avascular layer composed primarily of keratinocytes; it is responsible for the water-barrier function and is replenished from the basal layer. The dermis lies beneath and contains the vascular supply, collagen, elastin, sensory nerves, hair follicles, sebaceous glands, and sweat glands. Beneath the dermis is the subcutaneous tissue (hypodermis), a fat-rich cushioning layer that houses larger blood vessels and nerves. Wounds are described by which layers they involve: partial-thickness wounds stop within the dermis, while full-thickness wounds extend through the entire dermis into subcutaneous tissue or deeper (muscle, tendon, bone).

The Four Phases of Wound Healing

Normal wound healing moves through four overlapping phases. Hemostasis begins within seconds of injury: vasoconstriction, platelet aggregation, and fibrin clot formation stop bleeding. Inflammation dominates days 1–4, as neutrophils and then macrophages clear debris and bacteria and release cytokines and growth factors. Proliferation takes over from day 4 through roughly week 3: fibroblasts lay down collagen, new capillaries form (angiogenesis), granulation tissue fills the wound bed, and keratinocytes migrate across the surface (epithelialization). Remodeling continues for months to years, as type III collagen is replaced by stronger type I collagen and the scar matures. A healed wound only regains about 80% of the tensile strength of uninjured skin.

Acute vs Chronic Wounds

An acute wound is one expected to progress through these phases on a predictable timeline. A chronic wound is any wound that fails to heal in an orderly manner within an expected time frame — conventionally defined as a wound that has not substantially improved in 4 weeks or fully healed in 8–12 weeks. Chronic wounds are typically stuck in a prolonged inflammatory phase, with elevated matrix metalloproteinases (MMPs), senescent fibroblasts, heavy bacterial bioburden, and biofilm formation that actively block progression into the proliferative phase. Your job as a scribe in a wound clinic is essentially documenting the physician's effort to diagnose why a wound is stuck and to move it forward.

02 Scribe Documentation Framework

Wound clinic notes are usually SOAP-formatted, but the Objective section is unusually dense compared with most specialties because every wound requires precise measurement, description, and staging at every visit. The note must answer three questions: (1) What does this wound look like today, in measurable detail? (2) Is it better or worse than last visit? (3) What did we do about it today, and what did we instruct the patient to do at home?

03 Wound Assessment & the TIME Framework Foundation

The TIME framework, endorsed by the Wound Healing Society and the World Union of Wound Healing Societies, is the universal mental model wound care physicians use when assessing any chronic wound. Every assessment you document should implicitly address all four domains, and most wound clinic templates are built around them.

Measuring the Wound

Standardized measurement is the only way to track healing trajectory. Length is measured head-to-toe, width is measured perpendicular (side-to-side), and depth is measured with a sterile cotton-tip applicator gently inserted into the deepest part of the wound. Undermining is tissue destruction under intact skin edges — documented as the depth and clock position (e.g., "undermining 1.5 cm from 2 to 5 o'clock"). Tunneling (also called sinus tract) is a narrow channel extending from the wound in a specific direction — documented as length and clock position.

04 Pressure Injuries Core Wound

A pressure injury (the term "pressure ulcer" was officially retired by the National Pressure Injury Advisory Panel in 2016) is localized damage to the skin and/or underlying soft tissue, usually over a bony prominence or related to a medical device, resulting from intense and/or prolonged pressure, often in combination with shear. The most common sites are the sacrum, coccyx, heels, ischial tuberosities, trochanters, and occiput. Device-related pressure injuries occur under oxygen tubing, nasogastric tubes, cervical collars, and endotracheal tube ties.

Pathophysiology

Sustained external pressure — particularly over a bony prominence — exceeds capillary closing pressure (~32 mmHg) and produces local ischemia. If pressure is not relieved, ischemia progresses to irreversible tissue necrosis. Shear forces (e.g., the sacral skin dragging against bed sheets as the head of bed is elevated) compound this by mechanically disrupting perfusion. Moisture, friction, malnutrition, immobility, incontinence, and reduced sensation all multiply the risk.

NPIAP / NPUAP Pressure Injury Staging

The 2016 NPIAP (formerly NPUAP) staging system is the universally used classification. Memorize every stage — you will chart this at every encounter.

Prevention & Management

Management follows the international NPIAP/EPUAP/PPPIA clinical practice guideline: pressure redistribution (turning every 2 hours, specialty mattresses, heel suspension), moisture management, nutrition optimization (protein 1.25–1.5 g/kg/day, vitamin C, zinc), and local wound care based on stage. Stage 3 and 4 wounds often need debridement, NPWT, and sometimes surgical flap closure. Unstageable wounds on heels with stable dry eschar are often not debrided — the eschar is left as a "biological cover" unless infection develops.

05 Diabetic Foot Ulcers (DFU) Core Wound

Diabetic foot ulcers are the single highest-volume diagnosis in most multidisciplinary wound clinics. Approximately 15–25% of patients with diabetes develop a foot ulcer in their lifetime, and DFU precedes roughly 85% of all diabetes-related lower-extremity amputations. The pathogenic triad is neuropathy, ischemia, and infection.

Pathophysiology

Peripheral neuropathy (sensory, motor, and autonomic) eliminates the protective sensation that normally prompts a person to shift weight off a painful area. The patient walks on a pressure point until the skin breaks down, then continues walking because they do not feel the wound. Motor neuropathy causes intrinsic foot muscle atrophy and toe clawing, shifting weight to the metatarsal heads. Autonomic neuropathy reduces sweating, producing dry, fissured skin. Concomitant PAD (especially tibial disease) compromises perfusion and healing. Hyperglycemia impairs neutrophil function, so infection spreads rapidly.

Clinical Presentation & Classification

DFUs are typically located at plantar pressure points (first and fifth metatarsal heads, great toe, heel) or at areas of footwear friction. Neuropathic ulcers have a surrounding callus ring; ischemic ulcers have pale, painful bases; neuro-ischemic ulcers combine both features. The two major classification systems are the Wagner system and the University of Texas (UT) system.

Diabetic Foot Infection (DFI)

The IWGDF/IDSA 2023 guidelines define infection severity by extent of inflammation and systemic involvement. This classification drives antibiotic selection and hospitalization decisions.

Management

The pillars of DFU care are offloading, debridement, infection control, vascular assessment, and glycemic control. Offloading with a total contact cast (TCC) is the gold standard for plantar neuropathic DFUs — it redistributes weight across the entire plantar surface and achieves healing rates above 80% in compliant patients. Alternatives include removable cast walkers, surgical shoes, and felted foam. Sharp debridement of callus and devitalized tissue is performed at nearly every visit. Every new DFU patient needs a vascular assessment (pulses, ABI/TBI) — if ischemia is present, revascularization precedes aggressive local wound care. Probe-to-bone (PTB) testing with a sterile blunt probe is a classic bedside test for osteomyelitis.

06 Venous Leg Ulcers (VLU) Core Wound

Venous leg ulcers account for the majority of lower extremity ulcers (~70%) and are the end-stage manifestation of chronic venous insufficiency (CVI). They are characteristically located in the gaiter area — the region between the mid-calf and the ankle, most commonly over the medial malleolus along the great saphenous vein territory.

Pathophysiology

Incompetent venous valves (primary or secondary to prior DVT) allow reverse flow and pooling of blood in the lower extremity veins. Ambulatory venous hypertension transmits pressure to the dermal capillaries, causing fibrinogen leakage, perivascular fibrin cuff formation, red blood cell extravasation (producing hemosiderin deposition), leukocyte trapping, and chronic inflammation. The skin becomes hyperpigmented, thickened, and fragile (lipodermatosclerosis), and minor trauma opens a wound that cannot heal in the hypertensive venous environment.

Clinical Features

VLUs are typically shallow with irregular borders, a granulating or sloughy wound bed, and moderate-to-heavy exudate. Surrounding skin shows hemosiderin staining (brown discoloration), lipodermatosclerosis ("inverted champagne bottle" leg), atrophie blanche (smooth white scarring), varicose veins, and pitting edema. Pain is typically dull, worse at the end of the day, and improved with leg elevation — the opposite of arterial pain.

CEAP Classification

The CEAP classification (2020 revision) stages chronic venous disease clinically, etiologically, anatomically, and pathophysiologically. The clinical "C" component is what scribes document most often.

Management

Compression therapy is the foundation. SVS/AVF CEAP-based guidelines and the ACP guideline on VLU recommend multilayer high-compression systems (30–40 mmHg at the ankle) in patients with an ABI ≥ 0.80. Options include multilayer bandaging systems (Profore, Coban 2), short-stretch bandages, Unna boots (zinc oxide paste), and compression stockings once healed. Pentoxifylline 400 mg TID is an evidence-supported oral adjunct. Treatment of underlying superficial reflux (endovenous ablation of the GSV or SSV) accelerates healing and reduces recurrence — the EVRA trial is the landmark evidence.

07 Arterial & Mixed Arterial-Venous Ulcers Core Wound

Arterial ulcers result from inadequate arterial perfusion — almost always from atherosclerotic PAD, less commonly from thromboembolism, vasculitis, or Buerger disease. They are typically located at the most distal points of perfusion (toes, heels, lateral malleolus), are painful, dry, pale-based, and have "punched-out" well-demarcated borders. The surrounding skin is cool, shiny, hairless, with dependent rubor and elevational pallor.

Mixed Arterial-Venous Ulcers

Approximately 15–20% of lower extremity ulcers have both arterial and venous components. These wounds present a therapeutic dilemma: compression (needed for the venous component) can worsen ischemia. An ABI of 0.50–0.80 defines the mixed category; modified compression (light, short-stretch) is used if tolerated. An ABI < 0.50 requires revascularization before compression can be safely applied.

Martorell Hypertensive Ischemic Leg Ulcer

A specific arteriolosclerotic ulcer seen in patients with long-standing poorly controlled hypertension (and often diabetes). Located on the lateral or posterior calf, it is extremely painful, has a necrotic black base with surrounding livedo racemosa, and is often misdiagnosed as pyoderma gangrenosum. Management includes aggressive BP control, debridement, and often skin grafting.

Sickle Cell Leg Ulcers

Patients with sickle cell disease develop chronic, painful ulcers of the medial or lateral malleolus in late adolescence and young adulthood. Pathogenesis involves microvascular occlusion, chronic inflammation, and venous stasis. Management combines hydroxyurea, compression (if perfusion adequate), topical wound care, and sometimes transfusion therapy for non-healing wounds.

08 Surgical Wound Dehiscence Acute Wound

Dehiscence is partial or complete separation of a previously approximated surgical incision. It usually occurs between postoperative days 5 and 14. Risk factors include obesity, diabetes, malnutrition, chronic cough, steroid use, smoking, infection, hematoma, and increased intra-abdominal pressure. Superficial dehiscence involves the skin and subcutaneous tissue only; deep dehiscence extends through the fascia and is a surgical emergency because of the risk of evisceration (abdominal contents protruding through the open wound). The "pink fluid sign" — serosanguinous drainage from an otherwise well-appearing abdominal wound 5–7 days postop — is the classic warning of impending fascial dehiscence.

Management depends on depth. Superficial dehiscence is typically opened, irrigated, packed, and allowed to heal by secondary intention, often with NPWT. Fascial dehiscence requires urgent operative closure. Chronic non-healing surgical wounds are one of the most common indications for outpatient wound clinic referral.

09 Traumatic Wounds & Skin Tears Acute Wound

Traumatic wounds include lacerations, abrasions, avulsions, crush injuries, and bites. In the wound clinic, the most common traumatic presentation is the skin tear — a separation of skin layers usually in elderly or corticosteroid-using patients whose fragile skin shears from minor trauma (bumping into furniture, removing adhesive tape). The ISTAP classification grades skin tears:

Management involves gentle cleansing, flap reapproximation if viable, non-adherent dressings (silicone contact layers, petrolatum gauze) to avoid re-tearing on removal, and arrow-labeling the dressing to show the direction of safe removal. Medical adhesive-related skin injury (MARSI) is a closely related diagnosis — skin damage from aggressive adhesive removal — prevented with silicone-based adhesives and adhesive remover wipes.

10 Burns (Acute and Chronic) Core Wound

Although acute major burns are managed at burn centers, outpatient wound clinics see small superficial burns, healed burns with contractures, and chronic burn-related wounds. Burns are classified by depth:

Burn surface area is estimated by the Rule of Nines (adult): head 9%, each arm 9%, each leg 18%, anterior trunk 18%, posterior trunk 18%, perineum 1%. Topical antimicrobials historically included silver sulfadiazine (Silvadene) — though now often replaced by silver-impregnated dressings or bacitracin on the face. Chronic burn wounds may need debridement, skin grafting, or scar contracture release.

11 Atypical & Inflammatory Wounds Atypical

Any wound that fails to respond to standard care, has unusual morphology, or arises in an atypical location should raise suspicion for an atypical etiology. Biopsy is indicated when a wound does not respond to 4–6 weeks of appropriate therapy.

12 Infected Wounds, Biofilm & Osteomyelitis Infection

Every chronic wound is colonized with bacteria; not every colonized wound is infected. The distinction matters clinically and drives antibiotic decisions.

Biofilm

Biofilm is a structured community of bacteria embedded in a self-produced extracellular polymeric matrix that is resistant to antibiotics, antiseptics, and host immunity. Biofilm is present in the majority of chronic wounds and is a major cause of stalling. Mechanical disruption (debridement) is the single most effective way to disrupt biofilm; antimicrobial dressings (silver, iodine, PHMB, methylene blue/gentian violet) provide adjunctive control.

Osteomyelitis

When a wound extends to bone, osteomyelitis becomes the concern. Bedside probe-to-bone (PTB) testing with a sterile blunt probe has high positive predictive value in high-prevalence populations (DFU). Workup includes inflammatory markers (ESR, CRP), plain radiographs (may lag 2–3 weeks behind disease), MRI (gold standard for soft tissue and early bone involvement), and bone biopsy for definitive diagnosis and culture. Treatment combines prolonged antibiotics (typically 6 weeks IV or bioequivalent oral) and surgical debridement of infected bone.

13 Moisture-Associated Skin Damage (MASD) Skin Injury

MASD is inflammation and erosion of the skin from prolonged exposure to urine, stool, sweat, wound drainage, or ostomy effluent. It is frequently mistaken for pressure injury but differs in mechanism and treatment. The four MASD subtypes:

Management is protective: barrier creams (dimethicone, zinc oxide, petrolatum), polymer-based skin protectants (3M Cavilon), superabsorbent briefs and wicking products, and treatment of underlying candidal overgrowth with topical antifungals (nystatin, clotrimazole, miconazole powder).

14 Lymphedema & Other Chronic Wound Settings Supporting

Lymphedema — protein-rich interstitial edema from impaired lymphatic drainage — is a major contributor to non-healing lower extremity wounds. Primary lymphedema is congenital; secondary lymphedema follows lymph node dissection, radiation, filariasis, recurrent cellulitis, or chronic venous insufficiency (phlebolymphedema). Skin changes include Stemmer sign (inability to pinch the skin at the base of the second toe), peau d'orange, papillomatosis, and lichenification. Management is complete decongestive therapy (CDT): manual lymphatic drainage, multilayer short-stretch compression bandaging, exercise, and meticulous skin care, followed by long-term compression garments or pneumatic compression devices.

Fistulas and Sinus Tracts

A fistula is an abnormal communication between two epithelialized surfaces (enterocutaneous, rectovaginal, urocutaneous). A sinus tract is a blind-ended tract leading from the skin to a deep cavity. Both produce complex wound management challenges — output containment (fistula bags, NPWT with fistula isolation), skin protection, and definitive surgical closure when possible.

15 Debridement Techniques Procedure

Debridement — the removal of non-viable tissue, debris, biofilm, and senescent cells — is the single most important wound clinic procedure. It converts a chronic wound into an acute-appearing wound and restores the proliferative phase. Debridement is billed by technique, depth, and surface area.

16 Negative Pressure Wound Therapy (NPWT) Procedure

Negative pressure wound therapy (NPWT; also called vacuum-assisted closure, "wound vac," KCI V.A.C., PICO) applies sub-atmospheric pressure to a sealed wound via an open-pore foam or gauze filler connected to a canister through tubing. Typical settings are −125 mmHg continuous or intermittent, though lower pressures (−75 mmHg) are used on fragile tissue.

Mechanism

NPWT works by (1) removing interstitial fluid and reducing edema, (2) increasing local perfusion, (3) applying mechanical forces (macro- and microstrain) that stimulate granulation tissue, (4) containing exudate, and (5) approximating wound edges. Dressings are changed every 2–3 days (3×/week is standard).

Indications and Contraindications

Indications: Chronic non-healing wounds, surgical dehiscence, traumatic wounds, flaps and grafts (to bolster take), pressure injuries Stage 3–4, diabetic foot ulcers, open abdomen, sternotomy dehiscence.

Contraindications: Untreated osteomyelitis, malignancy in the wound, exposed unprotected blood vessels or organs, necrotic tissue with eschar, enteric fistulas that are not isolated.

NPWT with Instillation (NPWTi-d)

NPWT with instillation and dwell time (V.A.C. VeraFlo) periodically instills a topical solution (typically normal saline or a wound cleanser like Prontosan) into the wound, allows it to dwell 10–20 minutes, then resumes negative pressure. Indicated for heavily colonized or infected wounds not amenable to immediate closure.

17 Advanced Therapies & Skin Substitutes Procedure

When a wound has failed 4–6 weeks of standard care (debridement, offloading/compression, moisture balance, infection control), advanced therapies are considered. These are generally billed under Medicare as cellular and/or tissue-based products (CTPs) or bioengineered cellular and tissue products (BCTPs).

Hyperbaric Oxygen Therapy (HBOT)

HBOT delivers 100% oxygen at > 1 atmosphere (typically 2.0–2.4 ATA) in a chamber. Indications accepted by the Undersea & Hyperbaric Medical Society include Wagner grade 3 or higher DFU that has failed 30 days of standard care, delayed radiation injury, compromised flaps/grafts, refractory osteomyelitis, and necrotizing soft tissue infection. Typical protocol: 2 hours daily, 5 days/week, 20–40 sessions.

Other Advanced Modalities

Growth factors: Becaplermin (Regranex) — topical recombinant PDGF-BB for neuropathic DFUs. Carries a boxed warning for malignancy with heavy use.

Platelet-rich plasma (PRP): Autologous concentrated platelets applied topically or injected into wound margins.

Skin grafting: Split-thickness skin grafts (STSG) are the workhorse for large granulating wounds; punch grafts are used for small VLUs; cultured epithelial autografts (Epicel) for extensive burns.

Flap reconstruction: Local, regional, or free tissue transfer for wounds with exposed critical structures or that fail all simpler closures (managed by plastic surgery).

18 Offloading & Compression Therapy Procedure

Offloading (DFU & Pressure Injury)

Compression (VLU & Lymphedema)

19 Dressings — A to Z Reference

The dressing decision is driven by the wound bed (dry vs wet), depth, infection status, and patient factors. The universal principle, articulated by Winter in 1962 and endorsed by every modern guideline, is that a moist wound bed heals faster than a dry one. Match the dressing to the wound, not the other way around.

20 Imaging, Labs & Diagnostics Diagnostics

Vascular Assessment

Every lower extremity wound needs a vascular assessment. Pulses (DP, PT), ankle-brachial index (ABI), toe-brachial index (TBI) (for diabetics/CKD with non-compressible vessels), transcutaneous oxygen measurement (TcPO2) (a TcPO2 < 40 mmHg predicts poor healing; > 40 mmHg is favorable), skin perfusion pressure (SPP), and duplex ultrasound for venous reflux or arterial stenosis mapping.

Imaging

Labs

CBC with differential, ESR, CRP, procalcitonin (sepsis), comprehensive metabolic panel (glucose, renal, liver), A1C, albumin and prealbumin (nutritional markers), vitamin D, zinc, vitamin C (healing cofactors), wound or deep tissue cultures (swab cultures of the wound surface are of limited value; tissue biopsy is preferred), and bone biopsy with culture for osteomyelitis.

21 Medications You Must Know Reference

Systemic Antibiotics

Topical Antimicrobials

Supportive and Adjunctive Medications

22 Classification Systems Reference

This section consolidates every grading and classification system referenced throughout the guide. Fully enumerated scales appear in their condition sections; this is a quick-reference map.

23 Physical Exam — The Wound Exam Reference

The wound-focused physical exam is performed at every visit and its findings populate discrete fields in the wound flow sheet. It is the most structured exam in clinical practice — essentially a checklist.

Beyond the wound itself, the lower extremity exam includes pulse grading, monofilament testing (10-g Semmes-Weinstein at 10 plantar sites for diabetic neuropathy screening), vibratory testing (128 Hz tuning fork), capillary refill, skin temperature, and Buerger test (elevational pallor and dependent rubor). For venous disease, document varicosities, hemosiderin staining, lipodermatosclerosis, atrophie blanche, and edema grading (1+ to 4+).

24 Abbreviations Master List Reference

Wound Types & Assessment

Procedures & Therapies

Vascular & Diagnostics

Guideline Bodies

25 Sample HPI Templates Reference

These templates demonstrate the rhythm and content of a strong wound clinic HPI. Pattern-match off them during your first weeks.

26 References & Sources

Clinical Practice Guidelines

Landmark Trials & Evidence

Diagram & Figure Sources