Pathophysiology · Musculoskeletal, Integumentary, and Reproductive Disorders

Integumentary Disorders, Burns, and Wound Complications

9 min read
Want it in plain words first? Jump to Eli explains — the same idea, no jargon.
On this page 7 sections
  1. In 30 seconds
  2. Why this matters
  3. The college version
  4. Eli explains
  5. Worked example
  6. Key takeaway
  7. Study tools

In 30 seconds

The skin is the body's largest organ and its first line of defense, protecting against water loss, microbes, chemicals, and temperature change. When injury — a burn, pressure, inflammation, or infection — breaches this barrier, the body loses that protection and must repair the damage through wound healing. Severe burns add a second problem: damaged capillaries leak fluid, shifting blood volume out of circulation and threatening circulation and temperature control. Complications arise when healing stalls, infection sets in, or a wound reopens.

Why this matters

Skin assessment is a core clinical skill: recognizing early (non-blanchable redness), estimating burn extent and depth, monitoring fluid balance and temperature after major burns, and observing wounds for signs of infection or reopening all depend on this pathophysiology. This knowledge informs prevention (turning and repositioning, moisture control, skin protection) and patient education about wound care, sun protection, and early reporting of spreading redness or fever. It is relevant to nursing, medical assisting, physical therapy, and pharmacy technician education. Lab values, wound-classification systems, burn-referral criteria, guidelines, and scope-of-practice vary by institution and jurisdiction and must be followed. Learning pathophysiology supports assessment and reasoning but does not replace clinical training, supervision, or provider evaluation.

The college version

1. Normal function first

The skin has three layers. The is the thin, outer, waterproof layer of tightly packed cells (keratinocytes) that constantly shed and renew. The below it holds collagen and elastin fibers, blood vessels, nerves, hair follicles, and sweat and oil glands. The subcutaneous (hypodermis) layer stores fat and anchors skin to deeper tissue. The skin's comes mainly from the epidermis: it prevents water loss, blocks entry of microbes and chemicals, and shields against ultraviolet light. The skin is also the body's main thermoregulation organ — blood vessels in the dermis widen (vasodilate) to release heat or narrow (vasoconstrict) to conserve it, while sweat evaporation cools the body.

2. What changes in disease

  • Pressure injuries: Sustained pressure on skin over a bony prominence compresses capillaries, starving tissue of oxygen. The damage starts deep and spreads outward, progressing from non-blanchable redness to open sores and, in severe cases, down to muscle and bone. Moisture, friction, and shearing (skin sliding one way while bone slides another) worsen it.
  • : Inflammation of the skin ("-itis" = inflammation, "derm-" = skin) from irritants, allergens, or other triggers. The epidermis becomes red, itchy, swollen, and sometimes blistered or cracked, weakening the barrier.
  • : A chronic condition in which skin cells multiply much faster than normal and the immune system drives inflammation, so thick, scaly, silvery plaques build up instead of shedding normally.
  • Skin infections: Bacteria (such as Staphylococcus or Streptococcus), viruses, or fungi invade when the barrier is breached, causing cellulitis, abscess, impetigo, or other local infection that can spread.
  • Burns: Thermal, chemical, electrical, or radiation injury destroys skin cells and damages the capillaries beneath. Burn-depth classification ranges from superficial (epidermis only, red and painful, heals without scarring) to partial-thickness (into the dermis, blistering) to full-thickness (through the dermis, may be painless because nerve endings are destroyed).
  • : In major burns, damaged capillaries leak plasma (fluid and protein) into surrounding tissue, causing massive swelling (edema) and a drop in circulating blood volume. This "third-spacing" peaks in the first day or two.
  • Infection risk: With the barrier gone and dead tissue present, bacteria colonize easily, and the body's immune defenses are impaired.
  • Thermoregulation loss: Burned skin cannot retain heat or sweat normally, so the person loses heat and fluid rapidly.
  • Wound and infection: A healing wound can split open (dehiscence) if tension is too high or healing is poor, and any open wound can become infected, delaying closure.
  • Scar formation: Healing by collagen deposition replaces normal tissue with — stronger but less flexible, without hair follicles or sweat glands, and sometimes overgrown (hypertrophic or keloid).

3. Why the changes matter

A broken barrier leads to fluid and heat loss, infection, pain, and impaired mobility or body-image distress. Major burns can cause hypovolemic shock from fluid shift, hypothermia, and sepsis from infection. Pressure injuries signal poor tissue perfusion and can progress silently to deep, hard-to-heal wounds. Chronic skin inflammation (dermatitis, psoriasis) impairs quality of life and raises infection risk through scratching and cracking. Understanding these patterns guides assessment: measuring burn size and depth, checking skin over pressure points, watching fluid balance and temperature, and monitoring wounds for the redness, warmth, swelling, or drainage that may indicate infection.

How it works

  1. Heat or another injury destroys skin cells and damages the small blood vessels in the dermis.
  2. Those damaged capillaries become leaky, so plasma and protein escape into surrounding tissue, producing swelling.
  3. Because that fluid left the bloodstream, the circulating blood volume falls, which can reduce blood pressure and delivery of oxygen to organs.
  4. The damaged skin can no longer hold heat or block microbes, so heat is lost and infection risk rises while the body simultaneously tries to heal the wound.

Common confusions

Do not confuseWithDifference
Superficial burnPartial-thickness burnSuperficial = epidermis only (no blisters, no scar); partial-thickness = into dermis (blisters, more pain)
Full-thickness burnPartial-thickness burnFull-thickness destroys nerves and may be painless; partial-thickness is very painful
Fluid shift (third-spacing)Simple local swellingFluid shift moves plasma out of the circulation itself, threatening blood pressure, not just puffiness
DehiscenceNormal scar formationDehiscence is a wound reopening; scar formation is the expected collagen repair

Memory aids

"Barrier, Blood flow, Bugs" — the three B's of skin. A wound loses the Barrier, the Blood flow (or leaks it out), and invites Bugs (infection). For burn depth, think "S-P-F": Superficial (pink/painful), Partial (blisters), Full (waxy/leathery, may be numb).

Quick review

Topic Recap

  • Skin is a layered, living barrier that manages water, microbes, and temperature.
  • Pressure injuries, dermatitis, and psoriasis each disrupt skin through ischemia, inflammation, or overproduction of cells.
  • Burns are classified by depth; major burns cause a life-threatening fluid shift, heat loss, and infection risk.
  • Wound healing replaces damaged tissue with scar; infection and dehiscence are the key local complications.

Knowledge Check

  1. Which layer of skin is primarily responsible for waterproofing and the microbial barrier?
  2. Why can a full-thickness burn be less painful than a partial-thickness burn?
  3. What is the fluid shift, and why is it dangerous after a major burn?
  4. Why do pressure injuries often show deeper damage than is visible on the surface?
  5. What is wound dehiscence, and what are two factors that increase its risk?

Answers and Rationales

  1. Answer: The epidermis. Why: Its tightly packed keratinocytes and intercellular lipids keep water in and microbes out; the dermis supports and supplies but is not the main barrier.
  2. Answer: Because a full-thickness burn destroys the nerve endings in the dermis, so sensation is lost. Why: Pain requires intact nerves; their destruction explains why the deepest burns can be numb while partial-thickness burns are intensely painful.
  3. Answer: Damaged capillaries leak plasma and protein out of the bloodstream into the tissues, lowering circulating blood volume. Why: This can progress to hypovolemic shock and poor organ perfusion if large enough.
  4. Answer: Pressure compresses the deep capillaries over the bone first, so tissue death begins below the surface and only later becomes visible on top. Why: The damage travels upward from the deep, compressed tissue.
  5. Answer: Dehiscence is the reopening of a wound along the healing line. Why: High tension on the wound and infection (or poor nutrition/perfusion) are common contributors that weaken the repair.
Eli, the EliExplains learning guide

Eli explains

The same idea, in plain words

Explain it like I’m 10

Think of your skin as a brick-and-mortar wall wrapped around your whole body. The surface cells are the bricks, and the oily material between them is the mortar — together they keep water in and germs out. Underneath, a basement of tougher tissue and blood vessels supports the wall and feeds it.

A burn is like a fire that damages part of the wall. A small burn chips the paint (surface layer); a deeper burn takes out bricks and even the support beams below. When a lot of wall is damaged at once, the pipes behind it start leaking fluid into the space between the wall and the body — that is the fluid shift, and it can leave the circulating blood volume low, like a house losing water pressure. Pressure injuries are what happens when one spot of the wall is squashed against the furniture for too long: the blood supply pinches off and that patch of wall dies. This wall comparison stops being exact because skin is alive and self-repairing, not dead brick — it heals by cells dividing and crawling across the wound, and burns affect the whole body (temperature, fluid, infection risk), not just the damaged spot.

Simple Example

A paper cut is a tiny hole in the wall: it leaks a little, scabs over, and the body patches it within days. A large burn is a hole in the wall big enough that heat escapes, water leaks out, and germs can walk straight in — the body has to fight on several fronts at once.

Worked example

  1. Predisposing factors or causes: Immobility, poor nutrition, and moisture (pressure injuries); irritant or allergen exposure (dermatitis); genetics and immune triggers (psoriasis); breaches in the barrier (infections); heat, flame, chemicals, electricity, or radiation (burns); poor wound perfusion or infection (dehiscence).
  2. Initial physiologic change: Capillaries under skin are compressed, the epidermis becomes inflamed, skin cells overproduce, microbes invade, or skin layers are destroyed and capillaries leak.
  3. Compensation or adaptation: The body shunts blood, mounts an inflammatory and immune response, and begins wound healing — clotting, inflammation, new tissue formation, and collagen remodeling.
  4. Progression or decompensation: In large burns, fluid shift drops blood pressure and organ perfusion; skin fails to regulate temperature; dead tissue provides a breeding ground for infection; pressure injury advances from redness to deep ulceration; wounds open or fail to close.
  5. Broad manifestations and possible complications: Edema and low blood volume, hypothermia, pain, infection and sepsis, delayed healing, scarring, contractures, and — in severe cases — multi-organ failure.

Key takeaways

  • High yield: The epidermis, not the dermis, provides most of the barrier and waterproofing.
  • High yield: Burn depth (superficial, partial-thickness, full-thickness) determines healing, scarring, and pain — full-thickness burns may be painless because nerves are destroyed.
  • High yield: The fluid shift after major burns is a loss of plasma from circulation into tissue ("third-spacing"), risking hypovolemic shock.
  • Pressure injuries begin deep and appear later on the surface; prevention (relieving pressure) is key.
  • Burned skin loses both thermoregulation and infection protection.
  • Wound dehiscence and infection are the main local complications that delay or reverse healing.

Keep learning

Ready to build on this? Continue to the next lesson.

Practice Pathophysiology

This lesson has no separate scored set. Practice draws from the subject’s question bank.

Study tools & related lessonsYou’ll learn to · Key vocabulary · Related

You’ll learn to

  • Describe the layered structure of skin and explain its barrier and thermoregulatory functions.
  • Explain how pressure injuries, dermatitis, and psoriasis disrupt skin structure and function.
  • Outline how burns are classified by depth and why major burns trigger a dangerous fluid shift.
  • Describe how wounds heal and why infection, dehiscence, and abnormal scarring complicate recovery.

Key vocabulary

Epidermis
Outer waterproof layer of skin
Dermis
Middle layer with vessels, nerves, and glands
Barrier function
Skin's ability to keep water in and germs out
Pressure injury
Tissue death from sustained pressure cutting off blood flow
Dermatitis
Skin inflammation from irritation, allergy, or other cause
Psoriasis
Excessively fast skin-cell turnover with immune inflammation
Partial-thickness vs. full-thickness burn
Burn into dermis vs. through dermis
Fluid shift
Leak of plasma from damaged capillaries into tissues
Dehiscence
A healing wound splitting back open
Scar tissue
Collagen replacement tissue after healing

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