Musculoskeletal & Integumentary
This last chapter covers the frame and the wrapping. The frame is the bones and joints that hold you up. The wrapping is the skin that keeps the world out. We start with broken bones and the dangers that follow. Then come the common joint diseases. Then we move to the skin: its own disorders, its infections, and the whole-body emergency of a bad burn.
By the end of this chapter you can
- Name the fracture types and the stages of bone healing.
- Spot compartment syndrome and fat embolism as emergencies.
- Tell osteoarthritis from rheumatoid arthritis, and spot gout and osteoporosis.
- Stage pressure injuries and spot melanoma with ABCDE.
- Judge how deep and how big a burn is, and name the first jobs.
Section 1Fractures & bone healing
Bone looks solid and fixed. In truth it is living tissue that rebuilds itself all the time. A hard outer shell of compact (cortical) bone wraps a spongy inner layer. The whole bone wears a thin skin called the periosteum, packed with blood vessels and nerves. Inside, two cell crews work in a lifelong team. Osteoblasts lay down new bone matrix. Osteoclasts break old matrix down. Because bone is full of vessels and nerves, a break bleeds and hurts a lot. A fracture is simply a break in the continuity of a bone. It happens when the force on the bone is more than the bone can soak up. The cause may be a fall, a crash, stress over and over, or a bone already weak from disease.
Types of fractures
The name of a fracture tells you what happened to the bone. That guides the care. The first question is always the same. Is the skin broken?
| Feature | Closed (simple) | Open (compound) |
|---|---|---|
| Skin | Whole over the break | Bone pokes through skin, or a wound reaches the bone |
| Infection risk | Lower | High. It is an orthopedic emergency |
| Priority | Line the bone up and hold it still | Keep infection out (osteomyelitis), then repair |
Next we name the break pattern. A complete fracture goes all the way through and splits the bone into pieces. An incomplete fracture cracks only part way. The classic one is a greenstick fracture. A soft child's bone bends and splinters on one side, like a young twig. Other patterns are easy to picture. Comminuted means the bone shatters into three or more pieces, often from a hard, fast hit. Transverse is a straight break across the shaft. Oblique is an angled line. Spiral comes from a twisting force, and it can be a red flag for abuse. Compression means the bone is crushed, which is typical in spine bones thinned by osteoporosis. Pathologic means the break runs through bone already weak from a tumor or disease. A stress fracture is a tiny crack from doing one thing over and over.
How bone heals
Bone is one of the few tissues that can heal with no scar. It rebuilds itself back into living bone. Healing moves through stages that overlap. The whole job takes weeks to months.
- Hematoma formation (first hours to days): torn vessels bleed, and a clot forms at the break. This fracture hematoma seals the bone ends. It also brings in cells that clean up debris. That is why the spot is swollen, warm, and sore early on.
- Soft callus (roughly days to 2-3 weeks): fibroblasts and chondroblasts build a soft bridge across the gap. The bridge is fibrous tissue and cartilage. It is weak, which is just why the bone must stay still now.
- Hard callus (about 3 weeks to several months): osteoblasts swap the soft bridge for woven bone. This lumpy but sturdy bony callus joins the pieces.
- Remodeling (months to years): osteoclasts and osteoblasts reshape the callus along the lines of stress. The bone gets its old strength and shape back.
Signs of a fracture, and why we line it up and hold it still
Think fracture when pain gets worse with movement. Look for swelling, bruising (ecchymosis), and clear deformity or a shorter limb. The part may also show loss of function. Sometimes you hear or feel crepitus, a grating as bone ends rub. Alignment (reduction) puts the pieces back where they belong. Then the callus bridges the gap in the right place and the limb heals straight. Immobilization with a cast, splint, or fixation holds that line so healing can go on. Just as important, it keeps sharp bone ends from tearing nearby nerves and vessels.
Why osteoporosis raises fracture risk
In a healthy adult, bone breakdown and rebuilding stay even. In osteoporosis, osteoclasts work faster than osteoblasts. Bone is taken away faster than it is put back. The result is low bone mass and deteriorated microarchitecture, which means a damaged inner structure. The bone is left porous and brittle. People call it a silent disease, since nothing hurts until a bone breaks. Falling estrogen after menopause is a big driver. Estrogen normally holds osteoclasts back. So postmenopausal women often get fragility fractures of the hip, wrist, and spine. These come from forces that would never break healthy bone, such as a small bump or even a hard cough.
The interactive figure lets you compare fracture patterns. You can also walk through the healing stages. Go explore it below.
- A fracture is a break in bone continuity. Describe it by the skin (open or closed) and by the pattern (complete, greenstick, comminuted, and others), since those details guide care.
- Healing runs hematoma, soft callus, hard callus, then remodeling. The soft callus stage is weak, which is why we hold the bone still.
- Classic signs are pain, swelling, deformity, loss of function, and crepitus. Always check nerves and blood flow with the 5 P's: pain, pulse, pallor, paresthesia, and paralysis, below (distal to) the injury. An abnormal check is the cue to move to the 6 P's.
- Reduction puts the bone back in line, and immobilization holds it there. The bone heals straight and nearby nerves and vessels stay safe.
- Osteoporosis tips the balance toward breakdown. Bone turns porous and brittle, and fragility fractures follow, above all in postmenopausal women.
Section 2Fracture complications
When a bone breaks, the body starts a well-ordered repair job. Blood pools at the break and clots into a hematoma. Cleanup cells clear the debris. A soft cartilage callus bridges the gap. Over weeks, hard bone replaces that callus, and then it is reshaped. For all this to work, the tissue around the break needs steady blood flow, oxygen, and room to swell. Most fracture complications start when one of those is lost. Pressure builds where it cannot escape. Clots or fat drops travel where they should not. Or the healing timeline stalls. Explore the interactive figure below as you read.
Compartment syndrome: pressure with nowhere to go
Muscles sit in compartments wrapped in tough fascia that does not stretch. After a fracture, often the tibia or forearm, bleeding and swelling raise the pressure in that closed box. The fascia will not give. So the thin-walled veins squash shut first, blood backs up, and swelling gets worse. Then the pressure squeezes the capillaries until tissue no longer gets oxygen. This is acute compartment syndrome, and it is a surgical emergency. Without a fast fasciotomy to open the compartment, muscle and nerve die within hours. That can cost the limb.
Work through the 6 P's. The earliest and most reliable is pain out of proportion to the injury. Pain when you gently stretch the fingers or toes is a strong clue. The rest are paresthesia (pins and needles, from nerve starved of blood), pallor, poikilothermia (a limb that drifts to room temperature), paralysis, and pulselessness. A tight, tense feel to the compartment goes with them, though it is not one of the six. Here is the key point. Pulselessness is a late sign. If you wait for the pulse to vanish, the muscle is already dying.
Fat embolism syndrome: droplets on the move
Long bones such as the femur hold fatty yellow marrow, and so does the pelvis. When they break, marrow fat can slip into torn venous channels. It travels to the lungs and sets off a storm of inflammation. Classic fat embolism syndrome (FES) shows up 24 to 72 hours after the injury as a triad. First comes respiratory distress: low blood oxygen (hypoxemia), fast breathing (tachypnea), and shortness of breath (dyspnea) as fat plugs lung capillaries. Second come neurologic changes: confusion, restlessness, and a drop in alertness. Third is a petechial rash across the chest, the armpits, and the eye linings (conjunctivae). Those tiny red spots are fairly specific, so watch for them. Care is mostly supportive with oxygen. The best medicine is prevention, which means fixing the fracture early.
Clots from lying still: DVT and PE
Lying still after a fracture ticks every box of Virchow's triad. There is venous stasis, since the calf muscles are not pumping. There is hypercoagulability, because the injury itself makes blood clot more easily. And there is endothelial injury, damage to the vessel lining. The result is a deep vein thrombosis (DVT), usually in the calf, with swelling, warmth, and tenderness in one leg. The feared next step is a piece breaking off and lodging in the lung. That is a pulmonary embolism (PE). It brings sudden shortness of breath (dyspnea), sharp chest pain with each breath (pleuritic pain), a fast heart rate (tachycardia), and low oxygen (hypoxia). Prevention is gold: get patients moving early, use sequential compression devices, and give prophylactic anticoagulation, which means blood thinners to head off clots.
| Feature | Fat embolism | Pulmonary embolism (from DVT) |
|---|---|---|
| Usual timing | 24 to 72 hours after the break | Days to weeks (from lying still) |
| What travels | Drops of marrow fat | A blood clot |
| Telltale sign | Petechiae plus confusion | Sudden sharp chest pain, DVT in the leg |
| Fracture link | Long bone or pelvis | Any, from lying still |
When healing stalls: delayed union, nonunion, and infection
Healing needs three things: blood supply, a steady hold, and bone ends that meet. Delayed union means healing is slower than expected but still moving. Nonunion means a fracture has stopped healing. Common reasons are poor blood flow, too much motion, a wide gap, or infection, and it usually needs surgery or a bone graft. Malunion means the bone healed crooked. Osteomyelitis is a bone infection. It is a special threat in open fractures, where broken skin lets bacteria reach bone straight away. It shows up as local pain, warmth, drainage, and fever, and it is famously hard to clear.
- Compartment syndrome is a surgical emergency. Pain out of proportion is the earliest sign and pulselessness is late. Treat with fasciotomy, and never ice or raise the limb above the heart.
- The 6 P's: pain, paresthesia, pallor, poikilothermia, paralysis, pulselessness.
- Fat embolism follows long bone or pelvic fractures at 24 to 72 hours, with trouble breathing, confusion, and petechiae. Prevent it by fixing the fracture early.
- Lying still (immobility) drives DVT and PE through Virchow's triad. Prevent them with early movement, SCDs, and blood thinners.
- Nonunion, malunion, and osteomyelitis stall recovery. Frequent neurovascular checks are the priority for catching trouble early.
Section 3Musculoskeletal disorders
Bone can feel like the most lifeless part of you. In truth it is living, changing tissue. Two crews work on it your whole life. Osteoblasts lay down new bone, and osteoclasts chew old bone away. This steady teardown and rebuild is called remodeling. While the two crews stay even, bone stays strong. Joints glide for another reason. The bone ends wear a slick cap of articular cartilage and float in synovial fluid. When that balance or that cushion fails, you get the disorders below. Explore the interactive figure below to see each one.
Osteoporosis: quietly losing bone
In osteoporosis, the osteoclasts outwork the osteoblasts. More bone is removed than replaced. The bone left behind has normal chemistry. There is simply less of it. Bone mineral density (BMD) drops, and the inner scaffold grows thin and porous. The result is fragility. Bones snap under loads a strong skeleton would shrug off. A minor fall, or even a hard cough, can cause a fragility fracture. The classic sites are the hip, wrist, and vertebrae. Crushed spine bones explain the lost height and the stooped upper back (kyphosis) seen in many older adults.
The scary part is that it is usually silent until something breaks. Patients feel nothing while density slips away. Risk climbs with age and with being female. Estrogen normally holds osteoclasts back, so density can drop sharply after menopause. Other risks are a small body frame, smoking, low calcium and vitamin D, and long-term corticosteroid use. Screening uses a DEXA scan, reported as a T-score. A value of -2.5 or lower usually means osteoporosis.
Osteoarthritis vs rheumatoid arthritis
Both get called "arthritis," but they are not the same problem at all. Osteoarthritis (OA) is a mechanical, wear-and-tear process. Over years, the articular cartilage that cushions a joint frays and thins, until bone rubs on bone. It targets the weight-bearing joints, which are the knees, hips, and spine. It also hits the small joints at the fingertips. The pain is use-related. It is worse after activity and at the end of the day, and better with rest. The damage is local and mechanical, so there are no systemic signs. No fever, no whole-body tiredness. Morning stiffness is brief, usually under 30 minutes.
Rheumatoid arthritis (RA) is an autoimmune disease. The immune system attacks the synovium, which is the joint lining. The lining swells into a damaging tissue called pannus that eats cartilage and bone from within. RA is symmetric, hitting both hands and both wrists. It favors the small joints of the hands and feet. Its hallmark is morning stiffness lasting longer than an hour. Because the whole immune system is at work, it brings systemic signs: tiredness, low-grade fever, and high inflammatory markers (ESR, CRP). Over time it can bend joints into set patterns, such as ulnar deviation.
| Feature | Osteoarthritis | Rheumatoid arthritis |
|---|---|---|
| Cause | Wear-and-tear cartilage loss | Autoimmune attack on the joint lining |
| Joints | Weight-bearing, often asymmetric (not matched side to side) | Small joints, symmetric (matched side to side) |
| Pain pattern | Worse with use, better with rest | Stiff after rest, eases with movement |
| Morning stiffness | Usually < 30 min | Usually > 1 hour |
| Systemic signs | None | Tired, fever, high ESR/CRP |
Gout: crystals in the joint
Gout comes from too much uric acid, which is waste from breaking down purines. When blood uric acid stays high (hyperuricemia), needle-shaped monosodium urate crystals form inside a joint. The immune system treats the crystals as invaders and attacks hard. The attack is sudden and severe, and it often starts overnight. The joint turns red, hot, and swollen. It gets so tender that even a bedsheet hurts. The classic first target is the big toe, at the first metatarsophalangeal joint, and that picture is called podagra. Attacks are often set off by red meat, shellfish, alcohol, or too little fluid.
Telling them apart
A few quick questions usually sort these out. Ask about tempo. Gout blows up in hours, while OA and RA build over years. Ask about pattern. OA hits big weight-bearing joints and gets worse with use. RA hits small joints symmetrically, on both sides, with long morning stiffness. Gout usually strikes one joint, classically the toe. Ask about the whole body. Tiredness and fever point toward RA, or toward a gout flare. OA stays purely local. And remember that osteoporosis sits in its own lane. It is painless until a fragile bone fractures.
- Osteoporosis is silent low bone density (osteoclasts > osteoblasts). It leads to fragility fractures of the hip, wrist, and spine, and a DEXA T-score makes the call.
- Osteoarthritis is mechanical cartilage wear in weight-bearing joints. It is worse with use, stiffness is brief, and there are no systemic signs.
- Rheumatoid arthritis is autoimmune synovitis: symmetric small joints, morning stiffness > 1 hour, and whole-body signs such as tiredness, fever, and high ESR/CRP.
- Gout is urate crystals in a joint. It causes a sudden, severe, single hot joint, classically the big toe (podagra).
- Sort by tempo, pattern, and systemic signs: hours or years, one joint or both sides, local or whole-body.
Section 4Skin conditions
Your skin is the largest organ you have. Its main job is to be a barrier, a smart wall that repairs itself, between your insides and the outside world. It keeps water in and germs out. It senses touch and heat, and it helps hold your body heat steady. Once you see that barrier job, most skin disease starts to make sense. These are the ways the wall goes wrong: it gets inflamed, overbuilt, broken down, or invaded.
Skin has three layers. The epidermis is the thin, tough top layer. It makes the waterproof keratin shell, and it sheds and regrows all the time. Under it, the dermis holds collagen, blood vessels, nerves, hair follicles, and sweat glands. Below that sits the subcutaneous (hypodermis) layer of fat and connective tissue, for insulation and padding. Damage that stays in the epidermis usually heals cleanly. Damage that reaches the dermis or deeper is where scars and serious injury begin.
Dermatitis (eczema) and psoriasis
Dermatitis is inflammation of the epidermis. In its atopic form it is often called eczema. The skin barrier leaks, so water escapes and irritants and allergens get in. The immune system overreacts. The skin turns red and itchy, and it may weep or crust. The problem is inflammatory and often allergic. So it flares with triggers like soaps, stress, and dry air. It gets better with moisturizers and with steroid creams that calm the inflammation.
Psoriasis looks different because the mechanism is different. Here the trouble is fast epidermal turnover. Skin cells that should take about a month to rise and shed do it in days. An overactive immune response (T cells) drives that speed. The cells pile up faster than they can mature. They form thick plaques topped with silvery scales, classically on the elbows, knees, and scalp. It is long-lasting and autoimmune in nature, so we manage it rather than cure it.
| Feature | Eczema/Dermatitis | Psoriasis |
|---|---|---|
| Core mechanism | Leaky barrier plus allergic inflammation | Fast cell turnover (autoimmune) |
| Look | Red, weepy, crusted, very itchy | Thick plaques with silvery scale |
| Typical sites | Flexural folds (skin creases), hands, face | Elbows, knees, scalp (extensor) |
Pressure injuries
A pressure injury used to be called a pressure ulcer or bedsore. It starts when steady pressure squeezes blood vessels shut. The spot is usually over a bone, such as the sacrum, the heels, or the hips. With no blood flow, tissue runs out of oxygen (ischemia) and starts to die. Shear and moisture make it worse. That is why patients who cannot move are at such risk, and why prevention is such a priority. Here is the standard staging:
- Stage 1: skin is still whole, with redness that does not blanch.
- Stage 2: partial-thickness loss into the dermis. You see a shallow open sore or a blister.
- Stage 3: full-thickness loss with fat in view.
- Stage 4: full-thickness loss with muscle, tendon, or bone in view.
- Unstageable means slough or eschar hides the base. Deep tissue injury means a lasting maroon or purple patch. Both are their own categories.
Prevention is all about taking the pressure off. Turn the patient, usually every 2 hours. Float the heels. Use support surfaces. Keep skin clean and dry. Keep food and fluids up, so tissue can repair.
Skin cancers and the ABCDE rule
Most skin cancer traces back to UV damage to DNA in epidermal cells. Those cells then grow out of control. The three big ones differ sharply in how dangerous they are.
- Basal cell carcinoma: the most common and the least aggressive. It starts in basal keratinocytes. It often looks like a pearly, pink, or waxy bump that may break open. It rarely spreads (metastasizes), but it does eat local tissue.
- Squamous cell carcinoma: starts in upper keratinocytes. It looks scaly or crusted, or like a firm red lump. It spreads more often than basal cell if it is ignored.
- Melanoma: the deadliest. It starts in melanocytes, the cells that make pigment. It grows and spreads fast, so catching it early saves lives.
Screen odd moles with ABCDE. Asymmetry means one half does not match the other. Border means a ragged edge. Color means more than one shade. Diameter means wider than about 6 mm, the size of a pencil eraser. Evolving means any change in size, shape, or color, or new bleeding or itching.
Take a look at the interactive figure below. It shows how these common skin conditions really appear.
- The skin's three layers (epidermis, dermis, subcutaneous) form a barrier. Most skin disease is that barrier inflamed, overbuilt, broken down, or invaded.
- Eczema is a leaky barrier with allergic inflammation, so the skin is red, weepy, and itchy. Psoriasis is fast autoimmune turnover, making thick, silvery plaques.
- Pressure injuries come from ischemia under steady pressure. They run from stage 1 (redness that will not blanch) to stage 4 (muscle or bone in view), and we prevent them with turning, offloading, skin care, and food.
- Basal cell cancer is common and stays local, squamous cell can spread, and melanoma is the deadliest because it spreads early.
- Use ABCDE, which is Asymmetry, Border, Color, Diameter >6 mm, and Evolving, to flag a lesion for a closer look.
Section 5Skin infections
Your skin is your body's largest organ and its first wall of defense. Two layers do the heavy lifting. The tough outer epidermis is waterproofed by a protein called keratin. The deeper dermis holds blood vessels, nerves, and hair follicles. On top of all this lives a healthy crowd of harmless bacteria and fungi, the normal skin flora. There is also an oily, slightly acidic film, the acid mantle, that keeps troublemakers in check. Infection happens when that barrier is breached. A cut, a scratch, cracked skin, a bug bite, or a weak immune system can do it. Then organisms slip past the wall and multiply faster than your defenses can clear them.
Bacterial infections: cellulitis, impetigo, and MRSA
Cellulitis is a deep infection of the dermis and the fat below it. It is usually caused by Streptococcus or Staphylococcus aureus. Bacteria enter through a break in the skin, and your immune system floods the area. That is exactly why you see the classic signs: redness, warmth, swelling, and pain. Those signs are not the bacteria. They are inflammation, with wide vessels bringing white blood cells and fluid. The border is often fuzzy and moving outward. The edge is often drawn with a pen and the time noted, so the team can see if it advances.
Impetigo is a surface infection of the epidermis, most common in young children. It makes oozing sores that dry into a signature honey-colored crust. It spreads very easily by touch, and scratching carries it further. MRSA stands for methicillin-resistant Staphylococcus aureus. It is not a different disease, it is a resistant strain. It shrugs off common penicillin-family antibiotics, because its penicillin-binding protein is altered. MRSA often looks like an angry, painful abscess or boil that patients swear was a "spider bite." It needs specific antibiotics, and an abscess must be drained.
Fungal infections: tinea and candida
Fungi love places that are warm, dark, and moist, which tells you exactly where to look. Tinea (dermatophyte infection) feeds on keratin in the dead outer skin. The fungus grows outward while the center clears. That makes a ring with a raised, scaly edge, and it is why we say ringworm. There is no worm involved. Tinea gets body-part names: tinea pedis (athlete's foot), tinea cruris (jock itch), and tinea capitis (scalp).
Candida is a yeast that normally lives on us quietly. It overgrows in skin folds, under the breasts, in the groin, and in diaper areas. It makes a beefy-red rash with satellite lesions, which are small separate spots near the edges. It thrives after antibiotics wipe out rival bacteria. It also thrives in patients with diabetes or a weak immune system. That is one reason high blood sugar and repeat yeast infections often travel together.
Viral infections: herpes simplex and herpes zoster
Herpes viruses share one signature trick. After the first infection they hide in nerve cells for life. Then they reactivate with stress, illness, sunlight, or a weak immune system. Herpes simplex virus (HSV) makes painful, grouped, fluid-filled vesicles. HSV-1 causes cold sores around the mouth, and HSV-2 causes genital sores.
Herpes zoster (shingles) is the chickenpox virus waking up. That virus, varicella-zoster, has lain dormant in a sensory nerve root (a dorsal root ganglion) since childhood. When it wakes, it travels down that single nerve. It erupts as a painful blistering rash in a dermatome, the strip of skin one nerve supplies. That is why shingles classically shows up as a stripe on one side of the body. The stripe stops short at the midline. Burning pain often comes before the rash, and the pain can linger for months as postherpetic neuralgia.
| Feature | Herpes simplex | Herpes zoster (shingles) |
|---|---|---|
| Virus | HSV-1 / HSV-2 | Varicella-zoster, woken up |
| Pattern | Grouped blisters, mouth or genitals | One dermatome, one side, stops at the midline |
| Comes back? | Yes, in the same place | Usually once, but the pain can last |
When skin infection turns dangerous: necrotizing fasciitis
Necrotizing fasciitis is sometimes called a "flesh-eating" infection. It is a surgical emergency. Fierce bacteria race along the fascia, the sheet beneath the skin and fat. They release toxins that kill tissue and clot off its blood supply. The telltale clue is pain out of proportion to what you see. The surface may look only mildly red while the patient is in agony. Later signs are fast spread, dusky or purple skin, and blisters. You may feel crepitus, a crackling from gas in the tissue, and the patient looks very sick. Treatment is urgent surgery to cut away dead tissue, plus IV antibiotics. Delay costs limbs and lives. Explore the infection types in the interactive figure below.
- Skin infection starts when the epidermal barrier is breached. Redness, warmth, and swelling are inflammation, not the microbe itself.
- Cellulitis is deep and spreading, so mark the border. Impetigo shows honey-colored crusts. MRSA is resistant staph, often a painful abscess.
- Fungi (tinea, candida) favor warm, moist areas. Candida overgrows after antibiotics and in diabetes.
- HSV and zoster hide in nerves and reactivate. Shingles follows a single dermatome and stops at the midline.
- Necrotizing fasciitis is a surgical emergency. Pain out of proportion to the exam is the warning sign.
Section 6Burns
Your skin is the largest organ you have, and it does a lot of quiet work you never think about. It holds fluid in and keeps germs out. It senses touch and heat, and it helps hold your body heat steady. A burn injures this barrier. Once enough of it is gone, the trouble reaches far beyond the skin itself. That is the single most important idea in burn care. A large burn is a whole-body emergency, not just a wound.
Burn depth: how deep did the injury go?
Skin has layers. The thin outer epidermis sits on top of the thicker dermis, which holds blood vessels, nerve endings, hair follicles, and sweat glands. Below that is fat under the skin, then muscle and bone. How deep a burn reaches sets how it looks, how much it hurts, and whether it can heal on its own.
| Feature | Superficial | Partial-thickness | Full-thickness |
|---|---|---|---|
| Layers involved | Epidermis only | Epidermis plus part of the dermis | All of the epidermis and dermis (may reach fat, muscle, bone) |
| Old name | First-degree | Second-degree | Third-degree |
| Appearance | Red, dry, no blisters | Red, moist, blisters, weeping | White, leathery, waxy, or charred, and dry |
| Pain | Painful | Very painful | Often painless in the deepest spots |
| Healing | Days, no scar | Weeks, may scar | Cannot heal alone, needs grafting |
The pain pattern surprises people. A superficial burn, such as a mild sunburn, hurts because the nerve endings are irritated but still alive. A full-thickness burn can be oddly painless in its center, because the sensory nerves there were destroyed. So a quiet, leathery, white patch is often worse than a screaming red blistered one. A deep full-thickness burn can also form eschar, a tight band of dead tissue that will not stretch. If it squeezes a limb or the chest, a surgeon may need to release it, in a procedure called an escharotomy.
Estimating burn size: the rule of nines
Depth tells you how bad the burn is. Size tells you how big the whole-body threat is. Clinicians estimate the total body surface area (TBSA) burned with the rule of nines. It splits the adult body into parts worth about 9% each, or multiples of 9. The head and neck are 9%. Each arm is 9%. The front of the torso is 18%, and the back is 18%. Each leg is 18%, and the genital area is 1%. For scattered small burns, the patient's own palm is roughly 1% TBSA. Children have larger heads for their size, so pediatric charts differ. TBSA matters because it drives the fluid math and the choice to send the patient to a burn center.
Why a big burn threatens the whole body
Once TBSA climbs past roughly 20-25%, the injury stops being local. Damaged tissue releases inflammatory mediators that make capillaries leaky everywhere. Plasma, protein, and fluid pour out of the bloodstream into the tissues. That causes massive third-spacing and edema. The result is burn shock, a form of hypovolemic shock. Blood volume drops even though total body water has not. Blood pressure falls, and organs are underperfused, so they do not get the blood they need. This is why we work the ABCs.
- Airway first. If someone was burned in a closed space, watch for inhalation injury. Clues include facial burns, singed nose hairs, soot in the mouth, a hoarse voice, and sooty (carbonaceous) sputum. Hot gases and swelling can close the airway fast. So the team often chooses early intubation, placing a breathing tube, before swelling makes it impossible.
- Breathing and circulation. With smoke exposure, suspect carbon monoxide poisoning and give high-flow oxygen. A pulse oximeter can read falsely normal, since it cannot tell oxygen from carbon monoxide.
- Fluid resuscitation. Large burns need aggressive IV fluids, usually lactated Ringer's. A formula such as the Parkland formula sets the starting rate. Then you titrate it, meaning you adjust it, to urine output, often about 0.5 mL/kg/hr in adults. Too little fluid deepens shock, and too much causes dangerous edema.
The delayed threat: infection
The burned skin barrier is gone. The burn wound is a warm surface rich in protein, which bacteria love. After the first day or two, infection and sepsis become the leading cause of death in major burns. That is why burn wounds get careful cleaning, topical antimicrobials (germ-killing creams), and strict aseptic technique. The immune system is also thrown off. Add the huge open surface, and these patients are very easy to infect.
- Depth runs from superficial (red, dry, painful) to partial-thickness (blistered, weeping, very painful) to full-thickness (white and leathery, often painless because the nerves are destroyed).
- The rule of nines estimates TBSA (head 9%, each arm 9%, front torso 18%, back 18%, each leg 18%, genitals 1%, palm about 1%). It drives fluid and transfer choices.
- Large burns cause leaky capillaries and third-spacing, which bring on hypovolemic burn shock even though total body water is unchanged.
- Priorities follow time. Airway first, for inhalation injury. Then fluid resuscitation with lactated Ringer's, titrated to urine output. Then prevention of infection and sepsis.
- A large burn is a whole-body emergency, not just a skin wound.
The chapter in one breath
- Fracture healing runs in order: hematoma, soft callus, hard callus, then remodeling. So pain, swelling, and deformity are the body walling off the break and rebuilding bone over weeks to months.
- Compartment syndrome is the fracture emergency you cannot miss. Pressure rises in a closed muscle compartment. You catch it EARLY by pain out of proportion to the injury and pain with passive stretch, with paresthesia as an early sensory sign. Pulselessness, pallor, paralysis, and poikilothermia (a cool limb) are LATE, grim signs that tissue is already dying. So even though the classic list is the 6 P's (pain, paresthesia, pallor, pulselessness, paralysis, poikilothermia), do not wait for the late P's. A pulse you can feel does not rule it out. It demands a fasciotomy before tissue dies.
- Fat embolism usually follows a long bone or pelvic fracture within 24 to 72 hours. Marrow fat lodges in the lungs and brain, so the classic picture is shortness of breath, confusion, and a petechial rash.
- Osteoporosis is silent low bone density, with bone resorption outpacing bone formation. So the first sign is often a fragility fracture of the hip, wrist, or a vertebra, rather than pain.
- Tell the arthritides apart. Osteoarthritis is wear-and-tear joint pain, often asymmetric (not matched side to side), and worse with use. Rheumatoid arthritis is symmetric autoimmune inflammation with long morning stiffness. Gout is monosodium urate crystals, causing a hot, red, intensely painful great-toe attack (podagra).
- Learn skin cancer by ABCDE (Asymmetry, Border, Color, Diameter >6 mm, Evolving). Melanoma is the deadliest because of early metastasis, meaning it spreads early, unlike the more common but rarely fatal basal and squamous cell carcinomas.
- Cellulitis is a deeper bacterial infection of the dermis and the fat below (often Staph or Strep). It is warm, red, swollen, and tender, with poorly defined borders, and it can turn systemic with fever.
- Estimate how much of the body burned with the rule of nines, and judge depth by tissue. Superficial burns redden and blanch. Partial-thickness burns blister and hurt intensely. Full-thickness burns are leathery, painless, and need grafting.
- For major burns the killer is hypovolemic (burn) shock from a massive capillary fluid leak. So fluid resuscitation (often the Parkland formula) comes first, along with watching the airway for inhalation injury.
ReferenceWords worth knowing
A quick list of the terms in this chapter. Skim it now, or come back any time a word trips you up.
- ABCDE rule
- A quick checklist for odd-looking skin spots. It prompts you to watch for Asymmetry, a ragged Border, uneven Color, a Diameter wider than about 6 mm, and any Evolving change in size, shape, or color over time.
- Callus
- The soft new woven bone and cartilage that forms a bridge around a healing fracture. The body later reshapes it into stronger, mature lamellar bone.
- Cellulitis
- A deeper bacterial skin infection, usually from Staphylococcus or Streptococcus. It spreads through the dermis and the tissue below, bringing warmth, redness, swelling, and tenderness with fuzzy edges.
- Compartment syndrome
- An emergency that can cost a limb. Swelling or bleeding inside a closed muscle compartment raises pressure high enough to cut off blood flow. The classic clue is pain out of proportion to the injury that gets worse with passive stretch.
- Fat embolism
- A complication seen most often after long bone or pelvic fractures. Fat globules from the marrow enter the blood and lodge in the lungs or brain. The usual result is shortness of breath, confusion, and a petechial rash.
- Fracture
- A break in the continuity of a bone. It ranges from a tiny hairline crack to a complete split, and it happens when force is greater than the bone can absorb.
- Gout
- An inflammatory arthritis caused by uric acid crystals settling in a joint, classically the big toe. It brings sudden severe pain, redness, warmth, and swelling.
- Herpes zoster
- Also called shingles. It is a painful blistering rash along a single dermatome, which breaks out when the sleeping varicella-zoster (chickenpox) virus wakes up in a nerve root.
- Melanoma
- The most dangerous skin cancer. It starts in melanocytes, the cells that make pigment, and it can spread (metastasize) early. It is often caught first by using the ABCDE rule on a changing mole.
- Osteoarthritis
- A wear-and-tear joint disease in which cartilage slowly breaks down. Pain and stiffness get worse with use and usually ease with rest.
- Osteoporosis
- Low bone mass with a weakened inner structure. Bones are left porous and fragile, which greatly raises the risk of fractures, above all in the hip, spine, and wrist.
- Partial-thickness burn
- A burn that damages the epidermis and part of the dermis. It usually looks red, moist, and blistered, and it stays painful because the sensory nerve endings are still alive.
- Pressure injury
- Damage to skin and the tissue under it, over a bony prominence, from sustained pressure that cuts off blood flow (ischemia). It often shows up in patients who cannot move, over the sacrum, heels, or hips.
- Psoriasis
- A long-lasting autoimmune skin disease in which skin cells turn over far too fast. They pile up into well-defined red plaques covered by silvery scales, often on the elbows, knees, and scalp.
- Rheumatoid arthritis
- A long-lasting autoimmune disease in which the body attacks the joint lining (synovium). It brings matched pain, swelling, and morning stiffness that usually gets better with movement.
- Rule of nines
- A fast way to estimate what percent of the body surface is burned. It splits the adult body into regions worth about 9% each, or multiples of nine, and it guides fluid resuscitation.
DrillFlashcards for this unit
These are the Week 14 cards. They are the same deck as the hub, pulled in here so you can review as soon as you finish reading. Tap a card to flip it, and hit Shuffle to mix them up. To grade yourself and track what you have mastered across the whole deck, open the full flashcards page.