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Integumentary

Burns

High-yield Verified · Sep 2026

A burn is damage to the body’s tissues caused by heat, chemicals, electricity, sunlight, or radiation — and once it involves more than about 20% of the body surface, the injury triggers a systemic response called burn shock.

The highest-yield integumentary disorder: depth classification, the rule of nines, airway-first priorities, carbon monoxide, the Parkland formula with its injury-time clock, and urine output as the number that actually steers the fluids.

What’s going wrong in the body

The normal physiology, where it fails, and why the body’s compensation backfires.

01 A burn is three zones — one of them salvageable

Most burns are thermal — skin injured by excessive heat from hot surfaces, hot liquids, steam, or flame — but chemicals, electricity, sunlight, and radiation burn tissue by the same end result: cell death. Locally, the wound is not uniform. It forms three concentric zones: an innermost zone of coagulation (necrosis — irreversible cell death), a surrounding zone of stasis (decreased circulation, ischemic but alive), and an outer zone of hyperemia (vasodilation that usually recovers).

The zone of stasis is the reason resuscitation matters at the tissue level: it is at risk of progressing to necrosis if perfusion falters, and it is the zone good fluid management protects. A burn managed badly literally gets deeper.

02 Burn shock — the whole body springs a leak

Burns over roughly 20% TBSA trigger a systemic response. Thermal injury releases inflammatory mediators — histamine, leukotrienes, damage to the vascular glycocalyx — into the circulation, producing vasodilation and increased capillary permeability throughout the body, not just at the wound. Plasma pours out of the intravascular compartment into the interstitium (third-spacing); intravascular proteins leak with it. Once the burn exceeds about 25% BSA, edema is generalized — the whole body swells.

The result is burn shock: marked hypovolemia and hypoperfusion, decreased cardiac output, and increased systemic vascular resistance — a mix of hypovolemic, distributive, and cardiogenic components at once. And the destroyed cells add an electrolyte emergency: massive cellular injury releases intracellular potassium into the extracellular space (the same mechanism as crush injury), so hyperkalemia is an early threat — tall peaked T waves on the monitor are the first rung of a ladder that ends in sine waves and arrest.

Burn shock: systemic capillary leak empties the vessels into the tissues while dying cells release potassium — hypovolemia and early hyperkalemia arrive together.

03 Depth and size — the two numbers that drive everything

Depth decides pain, healing, and surgery. Superficial (first-degree) burns — epidermis only — are pink-to-red, dry, blanching, without blisters, moderately painful, and heal in 5–10 days without scarring. Superficial partial-thickness burns reach the papillary dermis: homogeneously red or pink, moist, blistered, blanching — and very painful — healing in 2–3 weeks with minimal scarring. Deep partial-thickness burns reach the reticular dermis: mottled, blanching only sluggishly, with minimal pain (sensation may exist only to deep pressure), prolonged healing, unavoidable scarring. Full-thickness (third-degree) burns go through the dermis into subcutaneous tissue: white, brown, or charred; leathery, stiff, and dry; no blanching — the blood supply is destroyed — and no pain at the burn itself, because the dermal nerve endings are gone. They take more than 8 weeks and require surgical grafting.

The exam-favorite paradox falls straight out of the anatomy: pain tracks with surviving nerve endings, so the shallow burns hurt the most and the deepest burn is insensate at its center (the shallower zones around it still hurt). A patient who says the worst-looking area "doesn’t hurt" is describing full-thickness injury, not good news.

Size is estimated with the adult rule of nines — and only partial- and full-thickness burns count toward the TBSA; superficial burns are excluded. For scattered burns, the patient’s palm with fingers adducted ≈ 1% TBSA (it can overestimate by 10–20%). Children are proportioned differently — bigger heads, smaller legs — so the adult nines misallocate; use the age-adjusted Lund-Browder chart (the more accurate pediatric method) or, for infants under 10 kg, a "Rule of Eights." Know also that clinicians systematically overestimate burn size, especially extremity burns in obese patients.

The adult rule of nines — head 9, each arm 9, each trunk surface 18, each leg 18, perineum 1. Superficial burns never count toward the total.

04 The course of the injury — from the moment of the burn

Physiologically the injury runs in two phases. The burn-shock ("ebb") phase occupies the first 24–48 hours of a major burn: low cardiac output, high systemic vascular resistance, intravascular volume pouring into the tissues. Then the body flips into the hypermetabolic ("flow") phase beginning 48–72 hours after injury: cardiac output climbs to 2–3× normal, oxygen consumption and CO₂ production soar, catabolic hormones and insulin resistance dominate — and this state can persist for up to 2 years.

Clinical care follows the same clock. First comes ATLS airway-first stabilization — airway before fluids, fluids before wound care. The first 24–48 hours are reserved for resuscitation and physiologic correction. Then, on post-burn days 2–12, comes the pivotal operation: early excision and grafting — removing dead tissue halts the inflammatory cascade, and in one study excising and grafting full-thickness burns within 3 days cut mortality from 45% to 9% versus delayed grafting. Infection surveillance and aggressive nutrition own this window. What remains is the long recovery: physical and occupational therapy, scar and contracture management, for as long as the hypermetabolic state lasts.

The injury course and the resuscitation clock — both start at the moment of the burn, not at hospital arrival.

Causes & risk factors

Modifiable factors are teaching targets — the patient can act on them.

Fire/flame (~43% of burns) and scalds from hot liquids or steam (~34%) Contact with hot objects (~9%) Electrical injury (~4%) — external size does not reflect internal damage Chemical exposure (~3%) — alkalis burn deeper than acids Smoke inhalation — an injury category of its own, affecting about one-third of burn victims Sunlight and radiation Residential fires — the source of 72% of US burn deaths Age 1–4 years — burns are the 2nd leading cause of accidental death in this group

Signs & symptoms

Each finding tied to the mechanism that produces it — and the triage it calls for.

Pink-to-red, dry, blanching burn without blisters, moderately painful Expected
Why: Superficial (first-degree) injury — epidermis only. Heals in 5–10 days without scarring and is excluded from the TBSA count.
Red or pink, moist, blistered burn that blanches and is very painful Expected
Why: Superficial partial-thickness injury into the papillary dermis — exposed dermal nerve endings make this the most painful depth. Heals in 2–3 weeks.
Mottled burn with sluggish blanching and surprisingly little pain
Why: Deep partial-thickness injury into the reticular dermis — sensation may remain only to deep pressure. Prolonged healing; scarring is unavoidable.
White, brown, or charred, leathery, dry burn — no blanching, no pain centrally Hold & notify
Why: Full-thickness injury: the dermal blood supply and nerve endings are destroyed, so the center cannot blanch or hurt. Requires surgical grafting.
Facial burns, singed nasal hair, soot in the mouth, hoarseness, or a fire in an enclosed space early Report immediately
Why: The inhalation-injury cluster. Upper-airway edema is progressive over the first 24–48 h, resuscitation fluids worsen it, and obstruction can be sudden — these cues drive early, preemptive intubation.
Stridor, carbonaceous (sooty) sputum, respiratory distress early Report immediately
Why: The airway is already narrowing — thermal injury above the larynx plus chemical smoke injury below it. Respiratory failure is the leading cause of death from fire injuries.
Headache, nausea, dizziness, or confusion with a normal SpO₂ after smoke exposure Report immediately
Why: Carbon monoxide: carboxyhemoglobin binds hemoglobin 200–250× more avidly than oxygen and shifts the dissociation curve left — tissue hypoxia the pulse oximeter cannot see. Headache is the most common symptom; "cherry-red" skin is typically a postmortem finding, not a bedside sign.
Tall, peaked T waves on the cardiac monitor early Report immediately
Why: Early hyperkalemia — burned and crushed cells dump intracellular potassium. The ECG ladder runs peaked T waves (K⁺ 5.5–6.5) → lost P waves → widened QRS → sine wave/asystole.
Urine output falling below 0.5 mL/kg/h Hold & notify
Why: The resuscitation gauge reading "under-filled" — intravascular volume is still leaking into the tissues faster than the fluids replace it.
Generalized (whole-body) edema early Expected
Why: Once the burn exceeds ~25% BSA the capillary leak is systemic — swelling appears far from the wound. Expected during the leak phase, but it is also the mechanism behind airway swelling and compartment pressure.
Dark, tea-colored urine after an electrical burn Report immediately
Why: Rhabdomyolysis: current destroys muscle along deep bone paths, releasing myoglobin (dipstick positive for "blood" with no RBCs on microscopy) that obstructs renal tubules — pigment-induced acute kidney injury unless flushed with aggressive fluids.
Tense, circumferential burn with pain out of proportion, paresthesia, pallor, or a fading distal pulse Report immediately
Why: Compartment syndrome: inelastic eschar plus tissue edema strangles the limb — the "Ps." A circumferential full-thickness chest burn restricts ventilation the same way. Anticipate escharotomy.
Coffee-ground emesis, hematemesis, or melena days into a major burn Report immediately
Why: Curling ulcer — stress ulceration of gastric/duodenal mucosa from splanchnic hypoperfusion and a failed mucosal barrier; burns > 30% TBSA carry the major risk. These ulcers run deep and can perforate.
A wound that is swollen, red and getting more painful, has pus coming from it — or a patient who feels unwell with a high temperature Hold & notify
Why: The destroyed skin barrier makes the wound infection-prone, and burn-wound organisms seed systemic sepsis — these are the surveillance cues that mean the wound has stopped healing and started infecting.

Diagnostics

Test In this disorder Normal
%TBSA estimate (rule of nines / Lund-Browder) Use the age-adjusted Lund-Browder chart for children — the adult nines misallocate their proportions. Estimates tend to run high. Partial- and full-thickness area only — superficial burns are excluded. Adults with more than 20% TBSA need formula-driven fluid resuscitation (more than 10% in children) StatPearls (Parkland Formula; Burn Fluid Resuscitation) —
Carboxyhemoglobin (CO-oximetry) Standard pulse oximetry cannot see it — SpO₂ reads falsely normal because the device cannot distinguish carboxyhemoglobin from oxyhemoglobin. A blood gas with co-oximetry is required. Significant poisoning at > 20% in adults (> 15% in children); levels correlate poorly with symptoms StatPearls < 3% nonsmokers · up to ~10% smokers
Hourly urine output (indwelling catheter) The formula predicts; the urine decides. Cross-check with SBP > 90 mm Hg, base deficit, and lactate clearance — no single number is worshipped. The resuscitation-adequacy gauge: titrate fluids to 0.5–1.0 mL/kg/h in adults (≈ 30–50 mL/h) · 1.0–1.5 mL/kg/h in children · 1–2 mL/kg/h after electrical injury StatPearls —
Bronchoscopy Direct visualization of airway injury — with carboxyhemoglobin, the key test for inhalation injury —
ECG + cardiac monitoring New abnormalities are unlikely to first appear after 24–48 h of clean monitoring. Peaked T waves of early hyperkalemia; after electrical injury, every adult gets an ECG and monitoring — ventricular fibrillation can occur at currents as low as 50–120 mA —
CK, electrolytes/creatinine, urinalysis (electrical burns) Rhabdomyolysis screen: elevated CK; urine dipstick positive for "blood" with no RBCs on microscopy = myoglobin; add troponin when current crossed the chest —

Complications

Warning: Airway obstruction from progressive edema Report immediately
The upper airway swells over the first 24–48 hours, the resuscitation fluids feed the swelling, and obstruction can be sudden.
This is why intubation is early and preemptive on inhalation-injury cues — facial burns, singed nasal hair, soot, hoarseness, enclosed-space fire — rather than a response to obstruction already underway. Waiting for stridor is waiting too long.
Warning: Early hyperkalemia → lethal dysrhythmia Report immediately
Destroyed cells release intracellular potassium; the most life-threatening consequence is cardiac dysrhythmia and sudden arrest.
Watch the monitor for the ladder: peaked T waves → lost P waves → widened QRS → sine wave. A related trap: from roughly 24–48 h post-burn onward, succinylcholine can trigger exaggerated potassium release from burned muscle and is dangerous in these patients.
Warning: Fluid creep — over-resuscitation kills too Hold & notify
Too much fluid causes pulmonary and cerebral edema, extremity compartment syndrome, abdominal compartment syndrome, ARDS, and multi-organ dysfunction.
The formula is a starting point, not a prescription: titrate to urine output and perfusion endpoints. Monitor circumferential burns for compartment syndrome (pressure > 30 mm Hg) and the abdomen for intra-abdominal pressure > 20 mm Hg with organ dysfunction — and anticipate escharotomy for circumferential eschar, including chest eschar restricting ventilation.
Warning: Burn-wound infection → sepsis Hold & notify
The burn destroyed the skin’s barrier; the wound is the seeding ground for systemic infection, and serious burns can end in shock and death.
Surveillance is the nurse’s job: increasing pain, redness, swelling, pus, fever. Topical antimicrobials and early excision of dead tissue exist precisely to close this door.
Caution: Curling ulcer (burns > 30% TBSA) Hold & notify
Stress ulceration of gastric and duodenal mucosa from splanchnic hypoperfusion — presenting as hematemesis, coffee-ground emesis, melena, or peritonitis if perforated.
These ulcers run deep, and perforation approaches 100% mortality without surgery — so prophylaxis is standard: PPI or H2 blocker, sucralfate, and early enteral feeding (which also prevents bacterial gut translocation).

Medications for this condition

Why each class is prescribed here — every card links to its full pharmacology page.

Opioid Analgesics High-alert
Nervous · morphine

Severe burns require IV pain medication — the contrast is depth-driven: superficial burns need only OTC or topical analgesia, while deeper burns hurt wherever nerve endings survive. Burns are a classic indication for IV opioid PCA (morphine is the gold-standard agent): only the patient presses the button, with sedation and respiratory checks every 1–2 h for the first 24–48 h. Dressing changes and pseudoeschar debridement are painful, so pain must be well controlled around wound care.
Wound & Burn Agents
Integumentary · silver sulfadiazine

The burn destroyed the skin’s barrier, so the wound is where systemic infection starts — topical antimicrobials prevent and treat burn-wound infection. Agent choice trades eschar penetration (silver nitrate → silver sulfadiazine → mafenide acetate, least to most) against toxicity and healing delay: silver sulfadiazine, the most commonly used, slows re-epithelialization and builds a painful-to-debride pseudoeschar with repeated use — stop it once healing is visible.

Beyond medications

  • Parkland formula fluid resuscitation — 4 mL × kg × %TBSA of lactated Ringer’s over 24 h; half in the first 8 h, half over the next 16 h — the clock starts at the time of INJURY, and prehospital fluid is subtracted from the first-8-h volume. Worked example: 70 kg × 40% × 4 mL = 11,200 mL, so 5,600 mL by hour 8 post-injury. LR is the recommended fluid at every age; children get 3 mL/kg/%TBSA plus dextrose-containing maintenance (limited glycogen stores). A 2 mL modified-Brooke variant exists on the same structure — either way, formulas are starting points titrated to urine output.
  • Early excision and grafting (post-burn days 2–12) — removing dead tissue halts the inflammatory cascade; grafting full-thickness burns within 3 days cut mortality from 45% to 9% in one study. Split-thickness autograft is the workhorse; cadaveric allograft buys 1–2 weeks of temporary cover while edema resolves.
  • Escharotomy for circumferential partial-to-full-thickness burns threatening compartment syndrome — including vertical chest incisions to free a chest wall splinted by full-thickness eschar.
  • Aggressive nutrition — the flow phase is fiercely catabolic, so calories are estimated by the Curreri formula (25 kcal/kg + 40 kcal × %TBSA), delivered as early enteral feeding (which also prevents bacterial gut translocation and is part of Curling-ulcer prophylaxis), with a required dietary consult.
  • Contracture and scar management — passive stretching and functional splinting from the start; active range of motion and PT/OT once grafts incorporate (postoperative days 3–5); pressure dressings plus silicone gel sheeting for hypertrophic scars (less pain, pruritus, and scar thickness at 6 months), with corticosteroid injection or laser as escalation.
  • Tetanus booster for any partial- or full-thickness burn.

Nursing considerations

The RN-specific layer — each action paired with the reason it matters.

Assessment & monitoring
Assess the airway before anything else: facial burns, singed nasal hair, soot in the mouth, hoarseness, stridor, sooty sputum — and ask whether the fire was in an enclosed space.
Why: Airway edema is progressive over the first 24–48 h, the resuscitation fluids worsen it, and obstruction can be sudden — the cues drive early, preemptive intubation, not watchful waiting.
Never trust the pulse oximeter after smoke exposure — obtain a carboxyhemoglobin level by co-oximetry.
Why: SpO₂ reads falsely normal because the device cannot tell carboxyhemoglobin from oxyhemoglobin; the patient can be profoundly hypoxic at 99%.
Insert an indwelling catheter and track hourly urine output: 0.5–1 mL/kg/h in adults, 1–1.5 in children, 1–2 mL/kg/h after electrical injury.
Why: Urine output is the real resuscitation gauge — the formula only opens the bidding. The doubled electrical target flushes myoglobin through the kidneys before it plugs the tubules.
Keep the patient on a cardiac monitor; report peaked T waves immediately. Every adult with an electrical injury gets an ECG and monitoring.
Why: Cell destruction causes early hyperkalemia whose deadliest expression is dysrhythmia; ventricular fibrillation after electrical injury can occur at currents as low as 50–120 mA.
Check circumferential burns hourly: distal pulses, pain out of proportion, paresthesia, pallor, poikilothermia — and chest expansion when the eschar circles the torso.
Why: Inelastic eschar plus mounting edema strangles limbs and splints the chest; the findings mean escharotomy, not analgesia.
Trend the perfusion endpoints alongside urine: systolic BP > 90 mm Hg, base deficit, lactate clearance.
Why: Urine output alone can mislead; resuscitation is goal-directed across several markers, watching for under-filling and for fluid creep in both directions.
The resuscitation window (first 24–48 hours)
Start lactated Ringer’s per the Parkland calculation — dating the 8-hour clock from the time of injury and subtracting any prehospital fluid from the first-8-h volume.
Why: A patient who arrives 2 hours after the burn has 6 hours left to receive the first half; starting the clock at the door under-resuscitates the leak phase.
Give 100% oxygen by nonrebreather immediately for suspected CO exposure — before the carboxyhemoglobin result is back.
Why: On room air, carboxyhemoglobin’s half-life is ~320 minutes; 100% oxygen at 1 atm cuts it to less than 90 minutes (hyperbaric oxygen at 3 atm to ~23 minutes). Every minute on room air prolongs tissue hypoxia.
Keep the patient warm: warmed IV fluids, forced-air warming, a raised room temperature — and no extensive cooling of large burns.
Why: Burned skin has lost its heat-retention function; large-burn patients slide into hypothermia while the team works.
Apply silver sulfadiazine with sterile gloves in a 1/16-inch layer, 1–2 times daily, to the cleaned and debrided burn — and make sure pain is well controlled around dressing changes.
Why: The wound is the sepsis portal, and SSD is broad-spectrum bactericidal including Pseudomonas — but dressing changes and pseudoeschar debridement are genuinely painful procedures.
Start Curling-ulcer prophylaxis for major burns: PPI or H2 blocker, sucralfate, and early enteral feeding.
Why: Burns > 30% TBSA are the major risk factor for deep, perforation-prone stress ulcers; early enteral feeding both protects the mucosa and prevents bacterial gut translocation.
Enforce PCA safety: only the patient presses the button; check sedation and respiratory status every 1–2 h for the first 24–48 h.
Why: Burns are a classic indication for IV opioid PCA — and a sleepy patient who cannot press the button is the built-in safety; anyone else pressing it defeats it.
Patient & family teaching
For minor thermal burns: hold the burn under cool running water for 20 minutes, as soon as possible (within 3 hours), then lay cling film over it. No creams, oils or butter, no plasters or sticky dressings, and do not burst blisters.
Why: Early cooling limits the injury; greasy remedies and sticky dressings do nothing the wound needs, and a burst blister is an open door for infection.
For major burns: call 911 for any burn that is very large or deep, on the face or genitals, or caused by chemicals or electricity; remove clothing or jewellery near the burn but do not remove anything stuck to it; and avoid extensive cooling of a large burn.
Why: Extensive cooling of a large burn "could lead to hypothermia" once the skin can no longer hold heat; stuck clothing tears the wound bed away with it.
For chemical exposure: irrigate immediately and copiously with water — eyes included, followed by ophthalmology — and never apply "neutralizing" agents.
Why: Alkalis in particular liquefy tissue and keep penetrating; only dilution helps, and chemical eye injuries can scar and blind. Neutralizers add injury.
Teach the infection signals — a wound that is swollen, red and getting more painful, pus, or feeling unwell with a high temperature — and to get urgent advice for any of them.
Why: The barrier is gone until the wound closes; the patient at home is the infection-surveillance system.
Confirm tetanus status: a tetanus booster is part of treatment for partial- and full-thickness burns "if needed."
Why: A tetanus booster is recommended for partial- and full-thickness burns.
Keep the stretching, splinting, and pressure-garment schedule even when it is uncomfortable.
Why: Contractures form whenever burned skin is allowed to heal shortened; pressure dressings with silicone sheeting measurably reduce scar thickness, pain, and itching by 6 months.

How a real nurse thinks

The clinical-judgment loop, worked for a typical presentation — reasoning, not reference.

  1. 1
    Recognize cues

    The airway cluster leads: hoarseness, facial burns, singed nasal hair, soot in the mouth, an enclosed-space fire — five inhalation-injury cues in one line of the chart. The SpO₂ of 99% is not reassurance: the carboxyhemoglobin is 24%, and a pulse oximeter cannot tell carboxyhemoglobin from oxyhemoglobin. K⁺ 5.9 with peaked T waves is the early-hyperkalemia signature. And the painless charred centers are telling you the depth: full-thickness, nerves destroyed.

  2. 2
    Analyze cues

    Three simultaneous stories. Airway: edema is progressive over the first 24–48 h, the resuscitation fluids he is about to receive will worsen it, and obstruction can be sudden — the hoarseness says it has already started. CO: carboxyhemoglobin binds 200–250× tighter than oxygen and shifts the curve left, so his tissues are hypoxic behind a normal-looking saturation. Burn shock: at 40% TBSA the capillary leak is systemic — hypovolemia is coming, and the destroyed cells are already pushing potassium into his blood.

  3. 3
    Prioritize

    The sourced order of operations is explicit: airway before fluids, fluids before wound care. Oxygen and airway evaluation outrank everything — the CO treatment (100% O₂) and the airway assessment are the same first move. Fluids run second, wound dressings last. The potassium rides on the cardiac monitor while the airway is secured.

  4. 4
    Generate solutions

    100% oxygen by nonrebreather now — it cuts carboxyhemoglobin half-life from ~320 minutes to under 90. Provider evaluation for early, preemptive intubation on the inhalation cues. Then the math: 4 mL × 70 kg × 40% = 11,200 mL LR over 24 h, half (5,600 mL) due by hour 8 after injury. Two hours are already gone and EMS gave 600 mL, so 5,000 mL run over the next 6 hours (≈ 833 mL/h). Indwelling catheter for hourly urine, targeting 0.5–1 mL/kg/h (35–70 mL/h for 70 kg). Warm the room and the fluids.

  5. 5
    Take action

    Apply the nonrebreather while calling the provider to the bedside for airway management — do not wait for stridor. Start the calculated LR rate, insert the catheter, keep him on the monitor with the peaked T waves reported, cover the wounds with dry sterile dressings until formal wound care, and confirm tetanus status. Wound dressing decisions come after airway and fluids — that sequencing is the whole point.

  6. 6
    Evaluate

    Success at the 6-hour mark: urine output steady in the 35–70 mL/h band, systolic BP > 90 mm Hg, base deficit and lactate trending down, T waves flattening as potassium is managed, and a secured airway ahead of the edema peak. Urine below 0.5 mL/kg/h means titrate up; boggy lungs, tense extremities, or a tight abdomen mean fluid creep — over-resuscitation is its own killer. The formula predicted; the urine decides.

Scenario — you’re the nurse

Work each question before revealing the answer. Rationales explain the wrong options too.

Emergency department · burn resuscitation bay · 2100

A 42-year-old (70 kg) pulled from a house fire in an enclosed bedroom about 2 hours ago. Partial- and full-thickness burns charted at 40% TBSA (anterior trunk, both arms, part of one leg). EMS infused 600 mL of lactated Ringer’s en route. He is hoarse and keeps clearing his throat; he says the deepest, charred patches "don’t even hurt."

2100 vitals — HR 118 · BP 102/64 · RR 24 · SpO₂ 99% on room air · T 36.1 °C
Airway — hoarse voice · soot around the nares and in the mouth · singed nasal hair · facial burns
Labs — carboxyhemoglobin 24% (co-oximetry) · K⁺ 5.9 mEq/L · creatinine 1.0 mg/dL
Monitor — sinus tachycardia with tall, peaked T waves
Burn chart — 40% TBSA partial- and full-thickness · charred central areas painless to touch
Fluids — 600 mL LR prehospital · no urinary catheter yet
Q1 Select all that apply
Which assessment findings signal possible inhalation injury requiring immediate airway evaluation? Select all that apply.
  1. A. Hoarse voice with frequent throat clearing
  2. B. Singed nasal hair and soot around the mouth
  3. C. The fire occurred in an enclosed bedroom
  4. D. SpO₂ of 99% on room air
  5. E. Charred areas of the trunk that are painless to touch
Reveal answer & rationale
Answer: A, B, C
Hoarseness (A), singed nasal hair with soot (B), and an enclosed-space fire (C) are the classic inhalation-injury cluster — they predict progressive airway edema over the first 24–48 h and justify early, preemptive intubation. The SpO₂ of 99% (D) is not an airway finding and is falsely reassuring here — with a carboxyhemoglobin of 24%, the pulse oximeter is reading carboxyhemoglobin as if it were oxygen. Painless charred burns (E) matter — they mark full-thickness depth — but they describe the skin, not the airway.
Q2 Multiple choice
The SpO₂ reads 99% on room air and the carboxyhemoglobin is 24%. The best immediate action is to:
  1. A. Document the normal saturation — no oxygen is needed
  2. B. Apply 100% oxygen by nonrebreather mask now
  3. C. Titrate oxygen to keep the SpO₂ at 92–96%
  4. D. Recheck the pulse oximeter on a different finger
Reveal answer & rationale
Answer: B
100% oxygen now (B): a carboxyhemoglobin of 24% exceeds the > 20% significant-poisoning threshold, and high-FiO₂ oxygen drops the carboxyhemoglobin half-life from ~320 minutes on room air to less than 90 minutes. Withholding oxygen because the SpO₂ looks fine (A) misses the entire problem — the oximeter cannot distinguish carboxyhemoglobin from oxyhemoglobin, so titrating to SpO₂ (C) is titrating to a broken gauge. Rechecking another finger (D) rechecks the same falsely normal number.
Q3 Multiple choice
It is 2 hours after the burn. Using the Parkland formula (70 kg, 40% TBSA, 600 mL LR given prehospital), the correct plan for lactated Ringer’s is:
  1. A. 5,600 mL over the next 8 hours
  2. B. 5,000 mL over the next 6 hours
  3. C. 11,200 mL over 24 hours starting from arrival
  4. D. 2,800 mL over the next 8 hours
Reveal answer & rationale
Answer: B
4 mL × 70 kg × 40% = 11,200 mL for the first 24 h; half (5,600 mL) is due within 8 hours of the INJURY. Two of those hours are gone and 600 mL is already in, so 5,000 mL runs over the remaining 6 hours (B, ≈ 833 mL/h). Option A restarts the 8-hour clock at the door and ignores the prehospital fluid; option C restarts the whole 24-hour clock at arrival — both under-resuscitate the leak phase the formula exists to cover. Option D halves the correct volume, as if the modified-Brooke 2-mL variant applied to a plan already built on Parkland.
Q4 Put in order
Put the nurse’s first five actions in priority order:
  1. A. Begin the calculated lactated Ringer’s infusion
  2. B. Apply silver sulfadiazine dressings to the burns
  3. C. Assess the airway and apply 100% oxygen by nonrebreather
  4. D. Insert an indwelling catheter and begin hourly urine measurement
  5. E. Notify the provider to evaluate for early intubation
Reveal answer & rationale
Correct order: C → E → A → D → B
The sourced sequence is airway before fluids, fluids before wound care. Airway assessment with 100% oxygen comes first — it treats the CO and screens the airway in one move (C). The provider evaluates for early, preemptive intubation next, before resuscitation fluids worsen the edema (E). Then the Parkland infusion starts (A), the catheter goes in to gauge that infusion (D), and formal wound care with silver sulfadiazine comes last (B). Starting fluids before securing the airway feeds the very edema that closes it; dressing wounds first treats the most visible problem instead of the most lethal one.
Q5 Multiple choice
Six hours into resuscitation, which finding best indicates the fluid plan is adequate?
  1. A. The infusion pump has delivered exactly the volume the Parkland formula predicted
  2. B. Urine output is holding at 40–50 mL/h with a systolic BP above 90 mm Hg
  3. C. The generalized edema is beginning to resolve
  4. D. The patient reports his pain is better controlled
Reveal answer & rationale
Answer: B
Urine output in the 0.5–1 mL/kg/h band (35–70 mL/h at 70 kg) with SBP > 90 (B) is the sourced adequacy standard — resuscitation is goal-directed, titrated to output and perfusion endpoints. Delivering the formula volume exactly (A) is the formula-worship trap: the calculation is a starting point, and following it blindly risks both under-filling and fluid creep. Generalized edema (C) is an expected feature of the systemic leak in burns over ~25% BSA, not an adequacy meter. Pain control (D) matters, but it tracks analgesia, not intravascular volume.

Common questions

What causes burns?
Common causes and risk factors include fire/flame (~43% of burns) and scalds from hot liquids or steam (~34%), contact with hot objects (~9%), electrical injury (~4%) — external size does not reflect internal damage, chemical exposure (~3%) — alkalis burn deeper than acids, smoke inhalation — an injury category of its own, affecting about one-third of burn victims, and others.
What are the early signs of burns?
Early findings include Facial burns, singed nasal hair, soot in the mouth, hoarseness, or a fire in an enclosed space, Stridor, carbonaceous (sooty) sputum, respiratory distress, Tall, peaked T waves on the cardiac monitor, Generalized (whole-body) edema.
Which findings should a nurse report immediately in burns?
Report immediately: Facial burns, singed nasal hair, soot in the mouth, hoarseness, or a fire in an enclosed space, Stridor, carbonaceous (sooty) sputum, respiratory distress, Headache, nausea, dizziness, or confusion with a normal SpO₂ after smoke exposure, Tall, peaked T waves on the cardiac monitor, Dark, tea-colored urine after an electrical burn, and others. These signal deterioration that needs rapid intervention.
Why doesn’t a full-thickness burn hurt?
Pain requires surviving nerve endings, and a full-thickness burn destroys the dermis — nerves included — so its center is insensate and cannot blanch (the blood supply is gone too). The shallower zones surrounding it still hurt. That is why the most painful burns are the superficial and superficial partial-thickness ones, and why a patient calmly reporting that the worst-looking area "doesn’t hurt" is describing the deepest injury on their body.
The patient arrived 2 hours after the burn — does the Parkland 8-hour clock start now?
No. The first half of the 24-hour volume (4 mL × kg × %TBSA of lactated Ringer’s) is due within 8 hours of the injury itself, not of arrival — so a patient arriving 2 hours post-burn has 6 hours left to receive it, and any fluid EMS gave is subtracted from that first-half volume. Then the formula hands control to the patient: fluids are titrated to a urine output of 0.5–1 mL/kg/h, not run blindly to the calculated number.
How should a burn be cooled — and why not a big burn?
Hold a small burn under cool running water for 20 minutes, as soon as possible and within 3 hours (NHS). A large burn is different: with the skin’s heat-retention function destroyed, "extensive cooling… could lead to hypothermia" (StatPearls).

Sources

Reviewed by Hae Suk Lee, RN

Educational summary for nursing students. Scenarios are fictional teaching cases. Always verify against current guidelines and your institution's protocols before acting in practice. Not medical advice.

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