• Galvanic current (direct, unidirectional) is used in iontophoresis (drug delivery through skin) and galvanic stimulation for denervated muscles.
• Faradic current (interrupted/alternating, ~50 Hz) is used in faradic muscle stimulation to contract innervated muscles.

Electrotherapy: Faradic vs. Galvanic Current

1. Faradic Stimulation (uses faradic/alternating current)

• Faradic current is a rapidly alternating (AC) current, with each pulse being less than 1 millisecond.
• Used to stimulate innervated muscles (muscles with intact nerve supply).
• Normal muscles respond briskly to faradic stimulation.
• In denervated muscles: no response to faradic stimulation - this is a hallmark finding in Reaction of Degeneration.

2. Galvanic Stimulation (uses galvanic/direct current)

• Galvanic current is a constant, direct current (DC), with pulse duration of several milliseconds.
• Used to stimulate denervated muscles (muscles that have lost nerve supply).
• In denervated muscles: weak galvanic response with reversal of polarity - the Anodal Closure Contraction (ACC) becomes stronger than Kathodal Closure Contraction (KCC), which is the reverse of normal.
• Also used in iontophoresis for transdermal drug delivery.

Reaction of Degeneration (RD) - The Classic Combined Test

"Denervated muscles will show 'reaction of degeneration', i.e. no response in Faradic stimulation and weak Galvanic response with reversal of polarity" - S Das, A Manual on Clinical Surgery, 13th Ed.

"The electrical pulse required is brief, less than a millisecond, and is most effectively induced by rapidly alternating (faradic) current. If there has been muscle denervation, an electrical pulse of several milliseconds induced by a constant electrical (galvanic) stimulus is required" - Adams and Victor's Principles of Neurology, 12th Ed.

Summary

• Faradic current - used in faradic/neuromuscular electrical stimulation (for innervated muscles)
• Galvanic current - used in galvanic stimulation and iontophoresis (for denervated muscles/drug delivery)
• Together, they form the basis of the Reaction of Degeneration test - the classic electrotherapy diagnostic modality that distinguishes between innervated and denervated muscle.

• Red electrode = Active (positive, anode)
• Black electrode = Passive/Indifferent (negative, cathode)

Active vs. Passive Electrode in Electrotherapy

Key Points

• Also called the "treatment electrode" or "working electrode"
• Smaller in size - produces more concentrated current density
• Placed directly over the motor point or area being treated
• In galvanic (DC) therapy: the positive pole (anode) = red
• Produces the desired therapeutic effect at the treatment site

• Also called the "indifferent electrode" or "dispersive electrode"
• Larger in size - disperses current over a wider area
• Placed at a distant, neutral site on the body
• In galvanic (DC) therapy: the negative pole (cathode) = black
• Completes the circuit without producing a focused effect

Important clinical note - Iontophoresis exception

• Positively charged drug - delivered from the red (positive/anode) electrode
• Negatively charged drug - delivered from the black (negative/cathode) electrode

Memory Aid

"Red = Active" - Think of red as the "action" color (like a red traffic light demanding attention), placed at the site of action.

Ultraviolet Radiation (UVR) for Wound Healing

What is UVR?

Mechanisms of Action in Wound Healing

• UVC and UVB destroy bacteria by damaging their DNA (thymine dimer formation)
• Effective against gram-positive and gram-negative organisms
• Useful for infected/sloughy wounds

• UVR stimulates keratinocyte proliferation and migration
• Accelerates re-epithelialization of wound surface
• Most effective in the proliferative phase of healing

• Causes localized erythema (vasodilation)
• Increased blood flow brings oxygen, nutrients, and immune cells to the wound

• Low doses stimulate the early inflammatory phase
• Promotes macrophage activity and growth factor release

• UVB triggers local Vitamin D3 production, which supports immune function and tissue repair

Dosimetry - The Minimal Erythema Dose (MED)

Indications for UVR in Wound Healing

• Chronic non-healing wounds (pressure sores, venous ulcers)
• Infected wounds / sloughy wounds
• Skin grafts (to prepare recipient site)
• Psoriatic plaques and dermatological conditions
• Stimulating granulation tissue formation

Treatment Protocol

1. Determine MED - test on a small unexposed skin area (inner forearm) 24 hours before treatment
2. Expose wound - remove dressings, clean the wound
3. Protect surrounding skin - cover peri-wound area with wet towels or zinc oxide paste
4. Distance - lamp held typically 45-60 cm from wound surface
5. Duration - calculated from MED and lamp output (mW/cm²)
6. Progression - increase dose by 25-50% each session as wound improves

Contraindications

• Acute inflammatory conditions
• Photosensitive patients (lupus, porphyria)
• Patients on photosensitizing drugs (tetracyclines, sulfonamides, phenothiazines)
• Over the eyes (must be shielded)
• Malignancy in the area
• Pulmonary tuberculosis

Key Clinical Summary

UVR for wound healing primarily exploits bactericidal (UVC > UVB) and epithelialization-stimulating (UVB) effects. Dosage is always calculated relative to the individual patient's MED, typically starting at E2-E3 doses for infected wounds and titrating based on wound response.

Grades/Stages of Ulcer

1. Wagner Classification - Diabetic Foot Ulcers (Most Common in Exams)

Campbell's Operative Orthopaedics, 15th Ed 2026, Table 91.1

2. Brodsky Depth-Ischemia Classification - Diabetic Foot Ulcers

Campbell's Operative Orthopaedics, 15th Ed 2026, Table 91.2

3. NPUAP Staging - Pressure Ulcers (Bedsores)

Dermatology 2-Volume Set, 5th Ed - Fig. 105.19

Quick Comparison Summary

Clinical Features and Complications of Diabetes Mellitus (DM)

CLINICAL FEATURES

Type 1 DM

• Typically lean, younger than 40 years at diagnosis
• Prone to ketosis
• Plasma insulin levels: absent to low; plasma glucagon levels: high
• Onset is abrupt with rapid development of:
  • Polydipsia (excessive thirst)
  • Polyuria (excessive urination)
  • Polyphagia (excessive hunger)
  • Weight loss
• May be heralded by diabetic ketoacidosis (DKA)
• Requires insulin therapy

Type 2 DM

• Typically middle-aged or older, overweight/obese (though 20% are non-obese)
• Normal to high insulin levels, but relatively deficient for glucose levels
• Onset is gradual - often diagnosed incidentally on routine blood work
• Hyperglycemia may be controlled with diet, oral hypoglycemic agents, or insulin
• Decompensation leads to HHS (Hyperosmolar Hyperglycemic State) rather than DKA

Classic Symptoms (both types)

ROSEN's Emergency Medicine - "The onset of symptoms may be abrupt, with polydipsia, polyuria, polyphagia, and weight loss developing rapidly"

COMPLICATIONS

ACUTE COMPLICATIONS

1. Diabetic Ketoacidosis (DKA)

• Mainly in Type 1 DM
• Triad: hyperglycemia + ketonemia + metabolic acidosis
• Precipitated by infection, missed insulin, stress
• Features: nausea/vomiting, abdominal pain, Kussmaul breathing, fruity breath, dehydration, altered consciousness

2. Hyperosmolar Hyperglycemic State (HHS)

• Mainly in Type 2 DM
• Extreme hyperglycemia (>600 mg/dL), severe dehydration, no significant ketosis
• High mortality (10-20%)
• Altered sensorium, seizures, focal neurological signs

3. Hypoglycemia

• Most common acute complication (especially with insulin/sulfonylurea therapy)
• Features: sweating, tremor, palpitations, confusion, seizures, coma

CHRONIC COMPLICATIONS

MICROVASCULAR COMPLICATIONS (directly related to hyperglycemia)

• Leading cause of new-onset blindness in ages 20-74
• Two stages:
  • Nonproliferative (NPDR): Microaneurysms, blot hemorrhages, cotton-wool spots, venous changes
  • Proliferative (PDR): Neovascularization near optic disc/macula → vitreous hemorrhage → fibrosis → retinal detachment
• Also: cataracts, glaucoma (occur earlier and more frequently in DM)
• Duration of DM and degree of glycemic control are the best predictors

Harrison's 22nd Ed: "DM is the leading cause of new cases of blindness between ages 20 and 74"

• 20-40% of patients with either type develop nephropathy
• Progression: microalbuminuria → macroalbuminuria → declining GFR → ESRD
• Kimmelstiel-Wilson nodular glomerulosclerosis is the classic pathological finding
• Hypertension accelerates progression

• Types:
  • Distal symmetric polyneuropathy (DPN): Most common; "stocking-glove" sensory loss, pain, paresthesias
  • Autonomic neuropathy: Orthostatic hypotension, gastroparesis, diabetic diarrhea, neurogenic bladder, erectile dysfunction, anhidrosis
  • Focal neuropathies: Mononeuropathies, cranial nerve palsies (CN III most common)
• DPN is responsible for 50-75% of non-traumatic amputations

Washington Manual: "Sensorimotor DPN is a major risk factor for foot trauma, ulceration, and Charcot arthropathy"

MACROVASCULAR COMPLICATIONS

• CHD, stroke, and PVD account for 80% of deaths in DM
• CAD occurs at a younger age with atypical presentations
• MI carries worse prognosis; angioplasty gives less satisfactory results
• Increased risk of both ischemic and non-ischemic heart failure

• Increased risk of both ischemic and hemorrhagic stroke
• Associated with hypertension and dyslipidemia

• Limb ischemia, claudication, non-healing ulcers
• Risk factors: insulin resistance, hyperglycemia, albuminuria, hypertension, dyslipidemia, smoking, obesity

• Combination of neuropathy + ischemia + infection
• Charcot arthropathy (neuropathic joint destruction)
• Non-healing ulcers → gangrene → amputation

OTHER COMPLICATIONS

Pathogenic Mechanisms of Chronic Complications

1. Formation of Advanced Glycation End-products (AGEs) - cross-link proteins, damage vessel walls
2. Activation of Protein Kinase C (PKC) - alters vascular permeability and growth factor expression
3. Disturbances in polyol pathways - sorbitol accumulation in lens (cataracts), nerves
4. Overload of hexosamine pathway - contributes to insulin resistance and endothelial dysfunction

Summary Table

Sources: Harrison's Principles of Internal Medicine 22nd Ed, Washington Manual of Medical Therapeutics, Robbins Pathologic Basis of Disease, ROSEN's Emergency Medicine, Goldman-Cecil Medicine