Burns

A major burn patient can lose liters of plasma into interstitial spaces within hours — yet the fluid you give in the first 8 hours matters more than the next 16. Timing is everything.

Major burns trigger a massive systemic inflammatory response that produces three distinct phases. The emergent/resuscitative phase (0–48 hours) is defined by capillary leak: plasma shifts from intravascular to interstitial spaces, causing hypovolemia, hemoconcentration, and edema. Urine output — not blood pressure — is the primary indicator of adequate resuscitation, targeting 0.5–1 mL/kg/hr in adults (1 mL/kg/hr in children). The Parkland formula guides initial crystalloid replacement: 4 mL × body weight (kg) × %TBSA burned. Half of the calculated volume is infused in the first 8 hours from the time of injury (not from hospital arrival), and the remaining half over the next 16 hours using lactated Ringer's solution. During the acute/intermediate phase (beginning around 48 hours), capillary integrity begins to restore. Fluid shifts back into the vasculature, causing hemodilution and risk of fluid overload — watch for crackles, jugular vein distention, and rising CVP. The rehabilitative phase focuses on wound healing and functional recovery. Potassium is released from damaged cells during the emergent phase, creating hyperkalemia risk; as diuresis begins in the acute phase, hypokalemia becomes the concern.

Key Distinctions

The 8-hour window starts from time of burn injury, not ED arrival — students consistently get this wrong and miscalculate infusion rates. Don't confuse the emergent phase (hypovolemia, hemoconcentration, hyperkalemia) with the acute phase (hypervolemia, hemodilution, hypokalemia) — the electrolyte and fluid shifts reverse. Parkland uses lactated Ringer's, not normal saline — the formula is specific to crystalloid choice.

Clinical Pearl

Emergent phase = everything leaves the vessels (hypovolemia, edema, hyperkalemia). Acute phase = everything floods back in (hypervolemia, hemodilution, hypokalemia). The shift flips at 48 hours.

Burn Depth Classification

Burn depth is classified by which skin layer is destroyed, and each depth has a signature appearance, sensation, and healing trajectory. Superficial (first-degree) burns damage only the epidermis — think sunburn: red, dry, painful, blanches with pressure, heals in 3-7 days without scarring. Superficial partial-thickness (second-degree) burns extend into the upper dermis, producing blisters, weeping, intense pain, and a pink moist wound bed that blanches; these heal in 7-21 days with minimal scarring. Deep partial-thickness burns reach the lower dermis — the wound appears mottled red to waxy white, may or may not blister, and sensation is decreased because deeper nerve endings are damaged; healing takes more than 21 days and often requires grafting. Full-thickness (third-degree) burns destroy the entire dermis: the wound is white, brown, or charred, feels leathery and dry, does NOT blanch, and is painless at the center because nerve endings are destroyed. The patient may report pain only at wound edges where partial-thickness injury borders full-thickness. Fourth-degree burns extend into muscle, tendon, or bone and appear charred or blackened. The critical clinical reasoning: pain level inversely correlates with depth once you pass partial-thickness injury. A painless burn is never a good sign.

Key Distinctions

Don't confuse decreased pain with improvement — painless burns indicate full-thickness nerve destruction, not healing. Students mix up superficial partial-thickness (blisters, very painful, moist pink base) with deep partial-thickness (decreased sensation, waxy white, may need grafting). Full-thickness burns do NOT blanch because dermal capillaries are destroyed; blanching indicates viable dermis and a shallower depth.

Clinical Pearl

Pain means nerves are alive. No pain in a burn wound means the nerves are gone — that's full-thickness until proven otherwise.

Burn Extent Calculation

Total body surface area (TBSA) burned drives fluid resuscitation calculations, transfer criteria, and mortality estimates, so accurate estimation is a critical first nursing assessment. The Rule of Nines divides the adult body into regions of 9% or multiples: each arm 9%, each leg 18%, anterior trunk 18%, posterior trunk 18%, head 9%, and perineum 1%. For rapid bedside estimates in adults, this is the standard. However, children have proportionally larger heads and smaller legs. An infant's head is 18% (double the adult value), while each leg is only about 14%. The Lund-Browder chart adjusts percentages by age and is the most accurate method for pediatric burns. For scattered or irregular burns, the patient's own palm (including fingers) represents approximately 1% TBSA — useful for estimating small or patchy areas. Only second-degree (partial-thickness) and third-degree (full-thickness) burns are counted toward TBSA; superficial (first-degree) burns like sunburn are excluded from the calculation. Document the percentage immediately — the Parkland formula and transfer decisions depend on this number.

Key Distinctions

Students often include first-degree burns in TBSA — only partial-thickness and full-thickness burns count. Don't apply the adult Rule of Nines to children; an infant's head is 18%, not 9%, and legs are smaller proportionally. The palm method estimates 1% TBSA using the patient's palm, not the nurse's hand — patient body size matters.

Clinical Pearl

Nine lives for adults, Lund-Browder for little ones. If the patient is under 10 years old, put down the Rule of Nines and pick up the age-adjusted chart.

Burn Wound Care & Infection Prevention

Burn wounds lose the skin's barrier function, creating a protein-rich, warm, moist environment ideal for bacterial and fungal colonization. The priority nursing intervention is strict aseptic wound care using sterile technique during dressing changes. Topical antimicrobials are the first line of defense: silver sulfadiazine (Silvadene) is most commonly used but is contraindicated in sulfa allergy and should not be used on the face; mafenide acetate (Sulfamylon) penetrates eschar and is preferred for deep burns and ears/cartilage but causes significant pain on application and can produce metabolic acidosis through carbonic anhydrase inhibition; silver nitrate (0.5%) stains everything black and can cause electrolyte imbalances (hyponatremia, hypokalemia). Wound infection progresses from colonization to invasive burn wound sepsis — the key warning sign is conversion of a partial-thickness wound to full-thickness (wound deepening), along with dark brown or black discoloration, rapid eschar separation, and hemorrhagic fat necrosis. Systemic signs include temperature instability (hypothermia or fever >39°C), rising WBC or sudden leukopenia, hyperglycemia in a non-diabetic patient, and altered mental status. Wound cultures are obtained via tissue biopsy, not surface swabs — a colony count >10⁵ organisms per gram of tissue confirms invasive infection. Hydrotherapy (wound cleansing) is performed at warm temperatures to prevent hypothermia, and loose necrotic tissue is debrided during sessions.

Key Distinctions

Don't confuse wound colonization (expected bacteria on surface, no systemic signs) with invasive burn wound sepsis (tissue destruction, systemic inflammatory response). Silvadene is broad-spectrum but superficial — Sulfamylon penetrates eschar, so they are not interchangeable. Students often choose surface swab cultures, but tissue biopsy with quantitative culture (>10⁵/g) is the gold standard for diagnosing invasive burn wound infection.

Clinical Pearl

Silvadene for surfaces, Sulfamylon for depth. If the wound gets worse instead of better — deepens, darkens, or separates early — think infection, not poor healing.

Burn Complications

Major burn complications extend well beyond the wound itself and follow a timeline. In the first 24-72 hours, the greatest threats are airway compromise from inhalation injury (singed nasal hairs, hoarse voice, carbonaceous sputum, stridor) and compartment syndrome from circumferential burns causing eschar to act as a tourniquet — the intervention is escharotomy, not fasciotomy. Curling's ulcer (stress ulcer) develops within days due to decreased GI perfusion and requires prophylactic proton pump inhibitors or H2 blockers. Sepsis becomes the leading cause of death after the resuscitation phase; watch for altered mental status, fever or hypothermia, tachycardia, and hyperglycemia before wound cultures confirm it. Acute kidney injury results from myoglobin release in electrical and deep burns — dark tea-colored urine signals rhabdomyolysis, and the nursing priority is aggressive IV fluids to maintain urine output of 75-100 mL/hr for myoglobinuria. Contractures develop during rehabilitation when scar tissue shortens across joints; early splinting and ROM exercises are preventive nursing actions, not afterthoughts.

Key Distinctions

Don't confuse escharotomy (cutting through eschar to release pressure, performed bedside, no anesthesia needed because full-thickness burns lack sensation) with fasciotomy (surgical incision into fascia for true compartment syndrome). Students mix up Curling's ulcer (burn-related stress ulcer) with Cushing's ulcer (brain injury-related). Dark urine in burns signals myoglobinuria requiring increased fluids — not decreased fluids for fluid overload.

Clinical Pearl

Think timeline: airway first, compartment syndrome in hours, Curling's ulcer in days, sepsis in weeks, contractures in months. The burn complication clock never stops ticking.