Inflammation & Wound Healing
Understand the inflammatory response from cellular mechanisms to clinical signs, differentiate acute from chronic inflammation, master inflammatory mediators and their pharmacologic targets, and learn the phases of wound healing.
Acute vs. Chronic Inflammation
Protective response vs. pathological process
Inflammation is a fundamental protective response to tissue injury or infection. Acute inflammation is rapid, self-limiting, and beneficial, it eliminates the threat and initiates repair. Chronic inflammation persists for weeks to years, causes ongoing tissue damage, and underlies many chronic diseases including atherosclerosis, rheumatoid arthritis, and cancer.
Acute Inflammation
Onset: Seconds to minutes. Duration: Hours to days. Primary cells: Neutrophils (first responders). Vascular changes: Vasodilation, increased permeability (exudate formation). Purpose: Eliminate the injurious agent, remove necrotic tissue, initiate repair. Outcomes: Complete resolution, abscess formation, or progression to chronic inflammation. Examples: Acute appendicitis, sprained ankle, bacterial pneumonia, surgical incision.
Chronic Inflammation
Onset: Gradual or follows unresolved acute inflammation. Duration: Weeks to years. Primary cells: Macrophages, lymphocytes, plasma cells. Tissue changes: Fibrosis, tissue destruction, angiogenesis occurring simultaneously. Purpose: Attempt to contain persistent threat, often causes more damage than the original insult. Examples: Rheumatoid arthritis, atherosclerosis, Crohn's disease, chronic hepatitis, tuberculosis.
The Five Cardinal Signs of Inflammation
The five cardinal signs of inflammation were first described by Celsus (rubor, calor, dolor, tumor) with functio laesa added by Virchow. Rubor (redness) results from vasodilation increasing blood flow to the area. Calor (heat) occurs from increased blood flow and metabolic activity. Dolor (pain) is caused by inflammatory mediators stimulating nerve endings and tissue swelling compressing nerves. Tumor (swelling) results from increased vascular permeability allowing fluid and proteins to leak into interstitial spaces. Functio laesa (loss of function) occurs as a protective mechanism, pain and swelling limit movement of the affected area, promoting healing.
Inflammatory Mediators & Pharmacologic Targets
Chemical signals that drive the inflammatory cascade
Understanding inflammatory mediators is essential because most anti-inflammatory medications work by targeting specific mediators or their pathways. Every NSAID, corticosteroid, antihistamine, and biologic drug connects back to these chemical signals.
Key Inflammatory Mediators
Inflammatory Mediators and Drug Targets
Inflammatory mediators are chemical signals that coordinate the inflammatory response. Histamine (from mast cells) causes immediate vasodilation and increased vascular permeability, this is why antihistamines reduce swelling and itching. Prostaglandins (produced via the COX pathway) cause pain, fever, and prolonged vasodilation, NSAIDs work by inhibiting COX enzymes. Cytokines (IL-1, IL-6, TNF-alpha) are signaling proteins that recruit immune cells, induce fever via the hypothalamus, and can trigger systemic inflammatory response syndrome (SIRS) when overproduced. Complement proteins create membrane attack complexes that lyse pathogens. Leukotrienes cause bronchospasm and are involved in asthma pathophysiology.
Fever Physiology & Immune Regulation
Understanding fever as a regulated immune response
Fever is not a malfunction, it is a deliberate upward resetting of the hypothalamic thermostat in response to pyrogens. It enhances immune function but can become dangerous at extreme levels. Understanding fever physiology helps nurses make evidence-based decisions about when to treat fever and when to let it serve its protective role.
Fever Mechanism
Exogenous pyrogens (bacteria, viruses) stimulate macrophages to release endogenous pyrogens (IL-1, IL-6, TNF-α). These act on the hypothalamus to increase prostaglandin E2 (PGE2) production, which raises the thermostat set point. The body then generates heat through shivering and vasoconstriction (chills) until the new set point is reached. Antipyretics (acetaminophen, NSAIDs) lower fever by inhibiting PGE2 synthesis, they reset the thermostat back to normal, causing vasodilation and sweating (defervescence).
Immune Overreaction vs. Immunosuppression
Overreaction (Hypersensitivity): The immune system attacks harmless substances (allergies, Type I), self-tissues (autoimmune diseases, Type II/III), or causes excessive cell-mediated responses (contact dermatitis, Type IV). In severe cases, systemic overreaction causes anaphylaxis or cytokine storm. Immunosuppression: Inadequate immune response, from HIV/AIDS, chemotherapy, corticosteroids, malnutrition, or extremes of age. Increases susceptibility to opportunistic infections. Both extremes require nursing vigilance for different complications.
Wound Healing Phases
From hemostasis through remodeling
Wound healing is a complex, overlapping process that depends on adequate nutrition (especially protein and vitamin C), oxygenation, moisture balance, and absence of infection. Nurses play a critical role in optimizing healing conditions and recognizing signs of impaired healing.
Four Phases of Wound Healing
Wound Healing Fundamentals
Wound healing proceeds through four overlapping phases. Hemostasis (seconds to hours): vasoconstriction, platelet plug formation, fibrin clot stabilization, stops bleeding. Inflammatory phase (1-6 days): neutrophils arrive first (within hours) to phagocytize bacteria, followed by macrophages (24-48 hours) that clear debris and release growth factors. Proliferative phase (4-21 days): fibroblasts produce collagen, angiogenesis creates new blood vessels, granulation tissue fills the wound, and epithelial cells migrate across the wound surface. Remodeling phase (21 days to 2 years): collagen reorganizes along stress lines, scar tissue matures and strengthens (reaching maximum 80% of original skin strength), and excess vasculature regresses.
Match the Inflammation Concept
Terms
Definitions
Inflammation & Wound Healing Quiz
1/20Which cells are the FIRST to arrive at an acute inflammatory site?
Pre-nursing comprehensive review
1/20Which organelle contains its own DNA and is inherited exclusively from the mother?