Integumentary System Disease Reference Cards

Basic Explanation of Cause

Acne is a chronic inflammatory disorder of the pilosebaceous unit (hair follicle + sebaceous gland). Four main factors cause acne:

• Excess sebum production: Sebaceous glands overproduce oil, triggered by androgens (hormones)
• Follicular plugging: Dead keratinocytes and sebum block the hair follicle opening
• Bacterial overgrowth: Cutibacterium acnes thrives in the oxygen-poor, oil-rich plugged follicle
• Inflammation: Immune response to bacteria creates red, painful lesions

Signs & Symptoms

Location:

• Face (especially T-zone), chest, upper back, shoulders
• Areas with highest concentration of sebaceous glands
• NOT on palms/soles (no hair follicles = no sebaceous glands)

Appearance:

• Non-inflammatory: Comedones (whiteheads/blackheads)
• Inflammatory: Red papules (bumps), pustules (pus-filled), nodules (large/deep/painful), cysts
• Post-inflammatory: Dark marks (hyperpigmentation), red marks, scars

Symptoms:

• Pain/tenderness (especially nodular acne)
• Oily skin
• Usually NOT itchy

First Line of Testing

Clinical diagnosis - No tests needed for typical acne

When to test:

• Hormonal workup if: Irregular periods, excessive facial/body hair, or severe jawline acne in women
  • Total/free testosterone, DHEA-S, LH/FSH (screen for PCOS)
• Pregnancy test before starting isotretinoin or spironolactone

Rule Out Secondary Causes

Acne is primary in most cases. Consider other conditions if atypical presentation:

• Rosacea: Facial redness, flushing, pustules but NO comedones, affects older adults
• Folliculitis: Bacterial infection of hair follicles, often after shaving
• Perioral dermatitis: Papules around mouth, associated with topical steroids
• Drug-induced acne: Corticosteroids, lithium, some anticonvulsants
• PCOS: If associated with irregular periods, hirsutism, weight gain

First Line Treatment

Mild to Moderate Acne:

• Topical retinoid (tretinoin, adapalene)
  • Increases cell turnover, prevents follicle plugging
  • Apply at night, start low concentration
  • Takes 8-12 weeks to work
• Benzoyl peroxide
  • Kills bacteria, mild exfoliation
  • 2.5-10% wash or gel
  • Can combine with retinoid
• Topical antibiotic + benzoyl peroxide (clindamycin/erythromycin + BP)
  • Reduces bacteria and inflammation
  • Never use antibiotic alone (causes resistance)

Second Line Treatment

Most commonly used for moderate to severe acne:

• Oral antibiotics (doxycycline, minocycline)
  • Kills bacteria, anti-inflammatory
  • Use for 3-6 months, then taper
  • Continue topical retinoid

Social & Emotional Impact

Impact on daily life:

• Avoiding eye contact, photos, social events
• Spending significant time and money on skincare/makeup to cover acne
• Missing school/work on "bad skin days"
• Declining activities where makeup might come off (swimming, sleepovers)
• Strained relationships due to self-consciousness
• Sleep disruption from treatment regimens

Basic Explanation of Cause

Primary focal hyperhydrosis is excessive sweating localized to specific body areas (palms, soles, axillae, face) that occurs independent of thermoregulatory needs.

Cause: Overactive eccrine sweat glands driven by excessive sympathetic nervous system stimulation

Key distinction: "Primary" = not secondary to another medical condition (like hyperthyroidism). "Focal" = specific areas, not whole body.

Signs & Symptoms

Location (focal areas):

• Palms (most common, most distressing)
• Soles of feet
• Axillae (underarms)
• Face (less common)
• Typically bilateral and symmetric

Characteristics:

• Sweating is visible and excessive - can drip from palms/soles
• Occurs independent of heat or exercise (though heat/stress worsen it)
• NOT present during sleep (key diagnostic feature)
• Starts in childhood or adolescence, persists into adulthood
• Emotionally triggered (stress/anxiety worsen it)

Associated symptoms:

• Maceration (skin breakdown) on soles
• Increased fungal infections (athlete's foot)
• Secondary social anxiety

First Line of Testing

Clinical diagnosis based on history and exam

Diagnostic criteria (must meet):

• Visible, excessive sweating for at least 6 months
• Focal (specific areas, not generalized)
• At least 2 of: bilateral/symmetric, impairs daily activities, ≥1 episode per week, age onset <25 years, family history, cessation during sleep

Objective test (rarely needed):

• Starch-iodine test (Minor's test): Apply iodine solution, dust with cornstarch - areas of sweating turn dark blue/black

Rule Out Secondary Causes

Only test if presentation is atypical (generalized sweating, night sweats, started in adulthood, unilateral):

• Hyperthyroidism: TSH, free T4
• Hypoglycemia: Glucose
• Infection/lymphoma: CBC
• Medication-induced: Review medications (beta-blockers, antidepressants, hormones)
• Menopause: Hot flashes with night sweats

First Line Treatment

Topical therapy (start here):

• Aluminum chloride antiperspirant (Drysol 20%, Certain Dri 12%)
  • Mechanism: Plugs sweat ducts
  • Apply to completely dry skin at bedtime, wash off in morning
  • 50-70% improvement for axillae; less effective for palms/soles
  • Side effects: Skin irritation, burning

If topical fails, move to systemic:

• Oral anticholinergics (glycopyrrolate, oxybutynin)
  • Mechanism: Block acetylcholine → prevent nerve signals to glands
  • 60-80% reduction in sweating
  • Side effects: Dry mouth (very common), dry eyes, constipation, blurred vision

Second Line Treatment

Most commonly used (highly effective):

• Botulinum toxin (Botox) injections
  • Blocks acetylcholine release → paralyzes sweat glands
  • 80-90% reduction in treated area
  • Lasts 6-12 months, then repeat needed
  • Very painful for palms/soles (nerve blocks recommended)
  • FDA-approved for axillae, off-label for palms/soles

Social & Emotional Impact

Impact on daily life:

• Difficulty with handshakes, fine motor tasks at work
• Avoiding social situations (handshakes, holding hands, dancing)
• Wearing only dark clothing to hide underarm sweat stains
• Can't use touch screens when palms are wet
• Paper, tools, phones slip from wet hands
• Constant worry about others noticing sweating

Basic Explanation of Cause

Eczema is a chronic inflammatory skin condition caused by epidermal barrier dysfunction.

Primary problem: Defective keratin production in the stratum corneum → "leaky" barrier

What happens:

• Defective stratum corneum can't hold water → dryness, cracking
• Allergens penetrate broken barrier → immune system reacts → inflammation
• Scratching damages barrier further → itch-scratch cycle

Signs & Symptoms

Location:

• Flexural areas: Inner elbows, behind knees, neck creases
• Face (especially in infants/children)
• Hands, wrists

Appearance:

• Red, dry, poorly defined patches
• Weepy, oozy during acute flares
• Lichenification (thickened, leathery skin from chronic scratching)
• Fissures (cracks) in severe cases

Symptoms:

• VERY ITCHY - this is the hallmark symptom
• Worse at night, disrupts sleep
• Worse in winter (low humidity)

Associated conditions (Atopic Triad):

• Asthma
• Allergic rhinitis (hay fever)
• Food allergies

First Line of Testing

Clinical diagnosis based on history, distribution, appearance

When to test:

• Patch testing: If suspected contact allergy contributing
• Skin biopsy: Rarely needed; shows spongiosis (fluid between epidermal cells)
• IgE levels, allergen testing: If considering food/environmental allergies

Rule Out Secondary Causes

• Contact dermatitis: Specific trigger (poison ivy, nickel, fragrances)
• Psoriasis: Thick silvery plaques on extensor surfaces, minimal itch
• Seborrheic dermatitis: Greasy, yellowish scales on scalp, face
• Scabies: Intense itch, burrows, worse at night, contagious
• Fungal infection: Ringworm has raised, scaly border

First Line Treatment

Goal: Repair barrier + reduce inflammation

• Aggressive moisturization (MOST IMPORTANT)
  • Thick ointments (petroleum jelly, CeraVe Healing Ointment, Aquaphor)
  • Apply multiple times daily, especially after bathing while skin damp
  • This compensates for defective keratin barrier
• Topical corticosteroids
  • Reduce inflammation during flares
  • Low-potency (hydrocortisone) for face/kids
  • Mid-potency (triamcinolone) for body
  • Apply twice daily for 1-2 weeks, then taper
  • Side effects: Skin thinning with long-term use
• Antihistamines
  • For itch relief, especially at bedtime (cetirizine, diphenhydramine)

Skincare tips:

• Short, lukewarm baths (not hot - dries skin)
• Gentle, fragrance-free cleansers
• Pat dry, don't rub
• Avoid triggers (harsh soaps, wool, stress)

Second Line Treatment

Most commonly used for moderate-severe eczema:

• Topical calcineurin inhibitors
  • Tacrolimus (Protopic), pimecrolimus (Elidel)
  • Suppress T-cell activation, reduce inflammation
  • Good for face/neck (no skin thinning like steroids)
  • Side effects: Burning/stinging initially

Social & Emotional Impact

Impact on daily life:

• Sleep disruption from intense nighttime itching → fatigue, irritability
• Avoiding activities where skin is visible (swimming, short sleeves, gym)
• Time-consuming skincare routines (frequent moisturizing, medications)
• Missing work/school due to flares or sleep deprivation
• Children: Social isolation, bullying about appearance
• Constant itch-scratch cycle affecting concentration

Basic Explanation of Cause

Psoriasis is a chronic autoimmune condition causing keratinocyte hyperproliferation.

Primary problem: T-cells mistakenly attack skin → release inflammatory cytokines → stratum basale goes into overdrive

What happens:

• Keratinocytes are rushed to surface before they can properly mature, flatten, and die
• Immature cells pile up in stratum corneum → thick, scaly plaques
• Stratum corneum becomes 10-20x thicker than normal

Signs & Symptoms

Location:

• Extensor surfaces: Outer elbows, outer knees (opposite of eczema!)
• Scalp (very common)
• Lower back, gluteal cleft
• Nails (pitting, thickening)

Appearance:

• Well-defined, raised plaques with sharp borders
• Thick silvery-white scales (immature keratinocytes)
• Red/pink base
• Auspitz sign: Pinpoint bleeding when scale is scraped off

Symptoms:

• Minimal to no itch (big difference from eczema!)
• May have mild burning or soreness
• Joint pain if psoriatic arthritis present (20-30% of psoriasis patients)

Associated conditions:

• Psoriatic arthritis (inflammatory arthritis)
• Metabolic syndrome, cardiovascular disease (inflammatory connection)

First Line of Testing

Clinical diagnosis based on appearance and distribution

When to test:

• Skin biopsy: If diagnosis uncertain
  • Shows acanthosis (thickened epidermis), parakeratosis (nuclei retained in stratum corneum - sign of rapid turnover), inflammatory infiltrate
• Joint evaluation: If joint pain/stiffness
  • X-rays, rheumatology referral

Rule Out Secondary Causes

• Eczema: Flexural surfaces, very itchy, poorly defined borders, weepy
• Seborrheic dermatitis: Greasy yellow scales, scalp/face, not as thick
• Tinea (fungal infection): Ringworm has raised scaly border, KOH prep positive
• Lichen planus: Purple, flat-topped papules, very itchy
• Cutaneous T-cell lymphoma: If atypical presentation, biopsy

First Line Treatment

Goal: Slow keratinocyte proliferation + suppress autoimmune response

Mild psoriasis (topical therapy):

• Topical corticosteroids
  • First-line for plaques
  • High-potency (clobetasol) for body
  • Apply once or twice daily
  • Reduces inflammation, slows cell division
• Vitamin D analogs
  • Calcipotriene (Dovonex)
  • Slows keratinocyte proliferation
  • Often combined with corticosteroid
• Coal tar
  • Shampoos, ointments
  • Slows cell turnover, reduces inflammation
  • Messy, smelly, but effective (especially for scalp)
• Salicylic acid
  • Keratolytic - helps remove thick scales

Second Line Treatment

Most commonly used for moderate to severe psoriasis:

• Biologic medications (highly effective!)
  • IL-23 inhibitors: Guselkumab (Tremfya), risankizumab (Skyrizi)
    • Newest class, blocks IL-23
    • Extremely effective - 80-90% clear skin
    • Injection every 8-12 weeks (least frequent dosing!)
    • Also treats psoriatic arthritis
  • Side effects: Increased infection risk, injection site reactions. Requires TB screening before starting.

Social & Emotional Impact

Impact on daily life:

• Avoiding activities where skin is visible (swimming, shorts, short sleeves)
• Difficulty finding barbers/hairdressers willing to work with scalp psoriasis
• Flaking scales on clothing, furniture causing embarrassment
• People avoid handshakes, refuse services due to misconception it's contagious
• If psoriatic arthritis present: Pain and stiffness limiting work and hobbies
• Chronic, relapsing nature requires ongoing treatment commitment

Basic Explanation of Cause

Vitiligo is an autoimmune condition in which melanocytes are destroyed, resulting in depigmented (white) patches of skin.

Cause: T-cells attack and kill melanocytes in the stratum basale

Signs & Symptoms

Location:

• Hands, wrists, fingers
• Around body openings (mouth, eyes, nose, genitals)
• Face
• Often symmetrical

Appearance:

• Milky-white patches (complete depigmentation)
• Sharp, well-defined borders
• Normal skin texture (no scaling, no thickening)
• More visible in darker skin types
• May affect hair (white patches of hair in affected areas)

Symptoms:

• NO physical symptoms - no pain, no itch, no texture change
• Purely cosmetic/pigmentary change
• Depigmented skin is vulnerable to sunburn (no melanin protection)

Progression:

• Unpredictable - may be stable, slowly progressive, or rapidly spreading
• Rarely spontaneously repigments

First Line of Testing

Clinical diagnosis based on appearance

• Wood's lamp examination: UV light makes vitiligo patches fluoresce bright white (confirms depigmentation)
• Skin biopsy (rarely needed): Shows absence of melanocytes
• Thyroid function tests (TSH, anti-thyroid antibodies): Vitiligo is associated with other autoimmune diseases, especially thyroid disease (Hashimoto's, Graves')

Rule Out Secondary Causes

• Tinea versicolor: Fungal infection, lighter patches but not completely white, fine scale, KOH prep positive
• Pityriasis alba: Pale patches (not completely white), common in kids, mildly scaly
• Post-inflammatory hypopigmentation: History of preceding rash/injury, usually temporary
• Chemical leukoderma: Depigmentation from exposure to chemicals (phenols, hydroquinone)
• Piebaldism: Genetic, present from birth, white forelock of hair

First Line Treatment

Goal: Suppress autoimmune attack on melanocytes, stimulate repigmentation

Honest expectation-setting: Vitiligo is difficult to treat. Results are slow and often incomplete. Treatment may take 6-12 months to see results.

• Topical corticosteroids
  • Mid-to-high potency (triamcinolone, clobetasol)
  • Suppress local immune attack
  • May help repigmentation in early/small patches (30-40% success)
  • More effective on face than hands/feet
• Topical calcineurin inhibitors
  • Tacrolimus (Protopic), pimecrolimus (Elidel)
  • Good for face (no skin thinning)
  • Similar efficacy to steroids
• Narrowband UVB phototherapy
  • 2-3x/week for months
  • Stimulates remaining melanocytes to proliferate and migrate
  • 50-70% see some repigmentation
  • Often combined with topicals
• Excimer laser
  • Targeted UVB to specific patches
  • Higher doses than phototherapy
  • Good for small, localized areas

CRITICAL: Sun protection

• Depigmented skin has ZERO melanin = ZERO UV protection
• SPF 50+ sunscreen, protective clothing, hats
• Risk of severe sunburn and skin cancer in affected areas

Second Line Treatment

Most promising newer option:

• Topical JAK inhibitors
  • Ruxolitinib cream (Opzelura) - FDA approved for vitiligo 2022
  • Blocks inflammatory signals driving melanocyte destruction
  • 30-50% repigmentation in studies
  • Applied twice daily to affected areas

Social & Emotional Impact

Impact on daily life:

• Time and expense on cosmetic camouflage (special makeup)
• Avoiding photos, social events due to self-consciousness
• Constant sun protection vigilance (depigmented areas burn easily, no melanin protection)
• Explaining condition to strangers who ask intrusive questions
• Unpredictable progression causing anxiety about new patches appearing
• More visible and stigmatizing in darker skin types

Basic Explanation of Cause

Melasma is hyperpigmentation (brown patches) on the face caused by melanocyte overproduction of melanin.

Triggers: Hormones + UV exposure + genetic predisposition

Signs & Symptoms

Location:

• Face only: Cheeks, upper lip ("mustache"), forehead, chin
• Symmetric distribution
• Sun-exposed areas

Appearance:

• Brown patches (light to dark brown)
• Irregular, blotchy borders (not sharp like vitiligo)
• Normal skin texture (no scaling, no elevation)
• Darkens with sun exposure, may lighten in winter

Symptoms:

• NO physical symptoms - purely cosmetic/pigmentary

Triggers/Risk factors:

• Pregnancy ("mask of pregnancy" or chloasma)
• Birth control pills, hormone replacement therapy
• Sun exposure
• Darker skin types (Fitzpatrick III-VI)
• Family history

First Line of Testing

Clinical diagnosis based on appearance and history

• Wood's lamp examination: Helps determine if melanin is in epidermis (enhances under Wood's lamp - better prognosis) vs. dermis (doesn't enhance - harder to treat)
• No biopsy needed (diagnosis is clinical)

Rule Out Secondary Causes

• Post-inflammatory hyperpigmentation: History of preceding acne, eczema, or injury
• Drug-induced hyperpigmentation: Certain medications (minocycline, antimalarials)
• Addison's disease: Generalized hyperpigmentation, includes non-sun-exposed areas, associated with fatigue, weight loss (check cortisol, ACTH)
• Tinea versicolor: Fungal infection, can cause hyperpigmented patches, KOH prep positive

First Line Treatment

Goal: Reduce melanin production + prevent worsening

CRITICAL: Sun protection (most important!)

• SPF 50+ broad-spectrum sunscreen daily (zinc oxide or titanium dioxide based)
• Wide-brimmed hat, avoid peak sun hours
• One day of sun can undo months of treatment

Topical treatments:

• Triple combination cream (GOLD STANDARD)
  • Hydroquinone 4% + Tretinoin 0.05% + Fluocinolone 0.01%
  • Hydroquinone: Inhibits tyrosinase (enzyme that makes melanin)
  • Tretinoin: Increases cell turnover, sheds pigmented cells
  • Fluocinolone: Mild steroid reduces inflammation
  • Apply nightly for 8-12 weeks
  • 50-70% improvement
• Hydroquinone alone (2-4%)
  • Lightening agent, inhibits melanin production
  • Apply twice daily for 2-4 months MAX
  • Don't use long-term (risk of ochronosis - paradoxical darkening)
• Azelaic acid (15-20%)
  • Inhibits tyrosinase, safe for long-term use
  • Good maintenance after hydroquinone
• Kojic acid, vitamin C, niacinamide
  • Over-the-counter lightening agents
  • Less effective than hydroquinone but safer for long-term

Second Line Treatment

Most commonly added for better results:

• Tranexamic acid
  • Oral: 250mg twice daily for 3-6 months
  • Interferes with melanin synthesis
  • Very effective - 50-70% improvement when added to topicals
  • Side effects: Minimal (small clot risk - avoid if history of DVT)

Maintenance therapy (lifelong):

• After initial treatment, switch from hydroquinone to azelaic acid for long-term maintenance
• Continue strict sun protection forever - one day of sun can undo months of treatment

Social & Emotional Impact

Impact on daily life:

• Spending significant money on makeup to cover facial patches
• Constant vigilance about sun exposure (hat, sunscreen, avoiding peak hours)
• Frustration when one day of sun exposure causes relapse
• If triggered by pregnancy: Feeling "marked" by childbearing, changes that don't resolve postpartum
• Chronic, relapsing nature requires lifelong management and sun protection
• Feeling judged for not "taking care of skin" (misconception it's poor hygiene)

Basic Explanation of Cause

A 2nd degree (partial thickness) burn is a thermal injury that destroys the entire epidermis and superficial dermis.

Cause: Heat, chemicals, electricity, or radiation damage skin layers

Healing timeline: 2-4 weeks if no infection

Signs & Symptoms

Appearance:

• Blisters filled with clear fluid (hallmark of 2nd degree)
• Red, moist, weepy wound base when blisters rupture
• Pink granulation tissue as healing progresses

Symptoms:

• VERY painful (nerve endings in dermis are exposed but intact)
• Swelling, inflammation

Progression through wound healing phases:

• Days 0-3 (Inflammatory): Red, swollen, blisters form, fibrin clot/scab
• Days 4-21 (Proliferative): Pink granulation tissue forms, re-epithelialization from edges and hair follicles
• Day 21+ (Remodeling): New epidermis complete but pink/red, scar tissue matures over months

First Line of Testing

Clinical diagnosis - assess burn depth and extent

Burn assessment:

• Depth:
  • 1st degree = epidermis only (red, painful, no blisters)
  • 2nd degree superficial = epidermis + superficial dermis (blisters, very painful, pink base)
  • 2nd degree deep = epidermis + deep dermis (blisters, white/mottled base, less painful)
  • 3rd degree = full thickness through dermis (white/brown/black, NO pain - nerves destroyed)
• Extent (% body surface area): Use Rule of Nines
  • Head/neck = 9%, each arm = 9%, each leg = 18%, front trunk = 18%, back trunk = 18%, genitals = 1%

When to hospitalize/refer burn center:

• 2nd degree >10% body surface area
• Burns to face, hands, feet, genitals, major joints
• 3rd degree burns of any size
• Electrical or chemical burns
• Inhalation injury

Rule Out Complications

• Infection: Increased pain, purulent drainage, foul odor, fever, spreading redness → wound culture, antibiotics
• Conversion to deeper burn: If inadequate care, ischemia can extend burn depth
• Compartment syndrome: Circumferential burns causing swelling → vascular compromise → escharotomy needed

First Line Treatment

Goal: Prevent infection, support natural healing phases, minimize scarring

Initial care (first 24-48 hours):

• Cool the burn: Cool (not ice) water for 10-20 minutes to stop heat damage
• Clean gently: Mild soap and water
• Leave blisters intact initially - they're a natural sterile dressing
• Pain control: Ibuprofen or acetaminophen

Days 0-3 (Inflammatory Phase):

• Topical antimicrobial: Silver sulfadiazine cream (prevents infection)
  • Apply 1-2x daily
  • Don't use on face (causes discoloration)
• Non-adherent dressing: Petroleum-impregnated gauze (prevents dressing from sticking to wound)
• Keep clean: Daily gentle washing
• Elevation: Reduce swelling

Days 4-21 (Proliferative Phase):

• Moist wound healing: Switch from silver sulfadiazine to petroleum jelly or Aquaphor
  • Keeps wound moist → faster re-epithelialization, less scarring
• Non-adherent dressing continues
• Monitor for infection
• Range of motion exercises if near joint (prevent stiffness)

Day 21+ (Remodeling Phase):

• Sun protection: SPF 50+ on healed burn (new epidermis has no melanocytes yet)
  • UV exposure causes permanent hyperpigmentation
• Moisturize: Keep scar tissue supple
• Scar management: Silicone gel sheets or silicone gel (apply daily 12+ hours)
  • Flattens and softens scars

Second Line Treatment

For extensive burns or complications:

• Scar management (months later):
  • Silicone gel sheets or silicone gel (apply daily 12+ hours)
  • Flattens and softens scars
  • Most effective when started early in remodeling phase

Social & Emotional Impact

Impact on daily life:

• Pain limits activities during healing (2-4 weeks)
• Dressing changes are time-consuming and uncomfortable
• Need to avoid sun on healing/healed burn for 6-12 months (prevents permanent pigment changes)
• Visible scars (especially on face, hands, arms) may cause self-consciousness
• If over joints: Range of motion exercises needed to prevent stiffness
• Scars are permanent but will mature and fade over 6-12 months

Basic Explanation of Cause

A chronic diabetic leg ulcer is a non-healing wound caused by multiple factors related to diabetes: neuropathy, vascular disease, and impaired immune function.

Why it won't heal (stuck in inflammatory phase):

• Neuropathy: Nerve damage → can't feel pain → continued trauma/pressure on wound
• Microangiopathy: Small blood vessel damage → inadequate oxygen and nutrient delivery → cells can't proliferate
• Venous insufficiency (often coexists): Blood pools in legs → edema → tissue hypoxia
• Hyperglycemia: High blood sugar impairs neutrophil/macrophage function → can't fight infection effectively
• Bacterial biofilm: Established bacterial communities resist antibiotics and keep wound in chronic inflammation

Definition of "chronic wound": Wound that hasn't healed after 4-6 weeks

Signs & Symptoms

Location:

• Feet (especially over pressure points: heels, metatarsal heads, toes)
• Lower legs (venous ulcers: medial malleolus area)

Appearance:

• Shallow to deep ulcer with irregular borders
• Wound bed: Patchy granulation tissue + yellow/gray slough (dead tissue) + possible exposed bone/tendon (severe)
• Wound edges: Rolled, thickened, callused
• Surrounding skin:
  • Brown discoloration (hemosiderin staining from venous disease)
  • Shiny, hairless (vascular insufficiency)
  • Edema (swelling)

Symptoms:

• Minimal to NO pain (due to neuropathy) - this is a RED FLAG (should hurt but doesn't!)
• Drainage (may be purulent if infected)
• Foul odor (if infected or necrotic tissue present)

Duration: Months to years without proper treatment

First Line of Testing

Wound assessment:

• Measure size, depth, photograph for tracking
• Probe for depth, tunneling, bone exposure (osteomyelitis risk)

Vascular assessment (CRITICAL):

• Ankle-brachial index (ABI): Compare ankle vs. arm blood pressure
  • Normal: 0.9-1.3
  • <0.9 = arterial insufficiency (poor inflow)
  • >1.3 = vessel calcification (common in diabetes, falsely elevated)
• Venous duplex ultrasound: Assess for venous insufficiency (valve incompetence)

Infection assessment:

• Wound culture: Deep tissue swab or tissue biopsy (not surface swab - gives false results)
• X-ray of foot/leg: Rule out osteomyelitis (bone infection)
• MRI: If suspect osteomyelitis or deep abscess

Diabetes control:

• HbA1c: Assess long-term glucose control (goal <7%)
• Fasting glucose: Current control

Rule Out Other Causes

• Arterial ulcer: Painful (intact nerves), distal toes, punched-out appearance, absent pulses, ABI <0.5
• Pure venous ulcer: Medial malleolus, shallow, irregular borders, heavy drainage, hemosiderin staining, edema
• Pressure ulcer: Over bony prominence (sacrum, heels), immobile patient
• Vasculitis: Multiple ulcers, systemic symptoms, biopsy shows vasculitis
• Malignancy: Non-healing ulcer, atypical appearance → biopsy

First Line Treatment

Goal: Address ALL barriers to healing (not just the wound itself!)

1. Optimize glucose control (MOST IMPORTANT systemic factor):

• Work with endocrinology to get HbA1c <7%
• Adjust diabetes medications, diet, lifestyle
• High glucose impairs immune function and healing

2. Debridement (remove dead tissue):

• Sharp debridement: Surgical removal of slough, necrotic tissue, callus (in clinic)
• Removes biofilm, stimulates wound bed, allows assessment of wound depth
• May need repeated debridement every 1-2 weeks

3. Infection control:

• If infected: Oral or IV antibiotics based on culture (often need 2-4 weeks)
  • Cover Staph, Strep, Gram-negatives, anaerobes
• Topical antimicrobials: Silver dressings, cadexomer iodine, honey dressings

4. Offloading (remove pressure from wound):

• Total contact cast or offloading boot for foot ulcers
• Crutches, wheelchair if needed
• Patient can't feel pain, so they'll walk on wound → prevents healing

5. Edema control (improve venous return):

• Compression therapy: Graduated compression stockings (20-30 mmHg) if ABI >0.8
  • DON'T compress if arterial insufficiency (ABI <0.8) - will worsen ischemia
• Leg elevation: Above heart level 30 min, 3-4x daily

6. Moist wound healing:

• Appropriate dressings based on wound characteristics:
  • Foam dressings for moderate drainage
  • Hydrocolloid for minimal drainage
  • Alginate for heavy drainage
• Change dressings per protocol (every 1-7 days depending on type)

Second Line Treatment

Most commonly used for refractory wounds:

• Negative pressure wound therapy (wound vac)
  • Sealed dressing + portable pump applies gentle suction
  • Removes excess fluid, increases blood flow, promotes granulation tissue
  • Patient wears pump 24/7, dressing changed 2-3x/week
  • Effective for jump-starting stalled healing

Social & Emotional Impact

Impact on daily life:

• Mobility severely limited by offloading requirements (special boot, crutches, wheelchair)
• Can't work if job requires standing/walking
• Frequent medical appointments (wound clinic 1-2x/week for months)
• Complex daily care routine (dressing changes, medications, compression, elevation)
• Odor and drainage causing social isolation and embarrassment
• Wearing wound vac 24/7 is cumbersome and limits activities
• Fear of amputation (diabetic foot ulcers precede 85% of amputations)
• Financial burden from lost work, frequent appointments, expensive dressings