Massive tissue damage & cellular destruction sets off widespread systemic inflammation that makes blood vessels leaky — the fluid pours out of the vessels and fills the body like a water balloon 🎈. Volume inside the vessels crashes → hypovolemic (burn) shock → organ failure → death. Everything on this page is a downstream consequence of that one sentence.
NG-107 (this page) = the WHY. What is physically happening in the tissue, the vessels, the blood and the airway. Mechanism, phases, lab shifts.
NG-123 = the WHAT-YOU-DO. Airway first, the fluid orders, titrating to urine output, wound care, escharotomy, infection control, pain and nutrition. Same disease, hands on the patient.
Numbers and Rule-of-Nines math live on NG-146; life after wound closure lives on NG-164.
🎈 Leaky = water balloonInflammation opens the capillaries. Fluid leaves the vessels and fills the tissues. The patient gets puffier and drier at the same time.
🚨 Hypovolemic shockLow volume inside the vessels → ↓BP, ↑HR, ↓urine → burn shock. This is the #1 killer in the first 24–48 h.
🧪 K↑ · Na↓ · H&H↑Cells burst → potassium out. Sodium follows water into the tissue → Na low. Plasma leaves, cells stay → H&H falsely HIGH.
⏱️ 18–24 h is the peakInterstitial shifting is greatest 18–24 hours after injury. Diuresis (fluid coming back) starts around 48–72 h.
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THE SKIN & HOW DEEP IT WENT
STEP 0 · LEARN THIS PICTURE
A burn is not a surface event. Depth decides everything — pain, healing, grafting, and how much fluid the patient will leak.
🔬 Skin cross-section — what is actually in there
EXAM TIP Nerve endings sit in the DERMIS. That is why a partial-thickness burn is agonising and a full-thickness burn is numb — the full-thickness burn destroyed the very nerves that would report the pain.
epidermisdermisfatnervevessel
🧠 “Everything that hurts and everything that leaks lives in the DERMIS.” Nerves, capillaries, follicles and glands are all dermal — so dermal damage = pain + fluid loss, and dermal destruction = numbness + no regrowth.
🕳️ Burn depth on the SAME skin — four panels, progressively deeper
Compare the four panels below. It is the identical drawing each time; only the gray/black destroyed zone gets deeper. Depth, not appearance, is what decides healing.
🧠 “Pain rises then vanishes.” 1° hurts, 2° superficial hurts the MOST, deep 2° hurts less, 3° does not hurt at all. A painless burn is the worst burn, not the best one.
⭐ What counts as a MAJOR burn
Criteria vary slightly by center, but the widely taught burn-center referral triggers are:
Partial thickness >10% TBSA
Any full-thickness burn
Burns to face, hands, feet, genitalia/perineum, or over a major joint
Electrical (incl. lightning) or chemical burns
Inhalation injury
Burns in patients with cardiac, renal, respiratory or diabetic comorbidity
Burns with trauma, or in children/older adults
🧠 “Face, Fingers, Feet, Front-bottom, Flexures” = the 5 F's that always get referred — cosmetically and functionally too important to guess on.
⚡ Electrical burns — the iceberg
What you see is the tip. Current travels through muscle, nerve and vessel, so the visible entry and exit wounds massively under-estimate the internal damage.
Muscle breakdown → rhabdomyolysis → myoglobin in the urine (tea/port-wine colored) → acute kidney injury
Expect dysrhythmias — put the patient on a cardiac monitor
Suspect spinal/long-bone fracture from tetanic contraction or a fall
Fluid needs are often higher than the Rule of Nines predicts — the formula is only a starting point
🧠 Electric = “dark urine, dark rhythm, dark inside.” Monitor + urine color + more fluid.
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THE LEAK — WHY A BURN CAUSES SHOCK
STEP 1 · THE CORE MECHANISM
One sentence explains 90% of major-burn nursing: the capillaries open, and the fluid goes to the wrong place.
🎈 Capillary leak & third-spacing — normal vs. burned, side by side
Burned tissue releases histamine, prostaglandins, cytokines and bradykinin. These blow the gaps between endothelial cells wide open. Water, electrolytes and plasma proteins (albumin) pour into the interstitium. Albumin leaving drags even more water out osmotically — so the leak feeds itself.
red cellsalbuminwater & Na⁺vessel wall
🧠 “Wet outside, dry inside.” The burn patient is swollen and soaked in the tissues while the blood vessels are running on empty. Never look at the puffiness and think “fluid overloaded” in the first 24 hours.
🚨 The burn-shock cascade — follow the dominoes
Say this chain out loud once and you can answer almost any major-burn question.
🫘 Hypoperfusion → acute kidney injury · gut ischemia · metabolic acidosis · death
Two extras that make it worse early on: a burn also releases myocardial depressant factors that reduce contractility, and it produces massive evaporative water loss straight off the open wound (skin is the body's cling film — it is gone).
🧠 “90 · 30 · 120” — BP at least 90 systolic, urine at least 30 mL/hr, heart rate under 120. Three numbers, one page. Restlessness is hypoxia until proven otherwise.
🧠 Why the whole body swells — not just the burn
Answer first: because the inflammatory mediators are in the bloodstream, not just the wound. Over roughly 20–25% TBSA, the leak becomes systemic.
That is why a patient burned only on the chest arrives with swollen eyelids, hands and legs. The edema is generalized and it is not a sign of too much IV fluid on day one.
Airway swelling → occlusion risk (see the inhalation section)
Limb swelling under circumferential eschar → compartment syndrome
Chest-wall swelling under eschar → can't ventilate
🧠 Small burn = local puddle. Big burn = whole-body flood. Roughly one-fifth of the body burned is the tipping point.
🔥 Jackson's zones — the burn is three rings, and you can save the middle one
A burn wound is not uniform. The classic model describes three concentric zones, and good resuscitation is aimed squarely at the middle one.
The zone of stasis is why fluid resuscitation matters so much. Under-resuscitate (or let the patient get cold, or squash the limb under tight eschar) and the stasis zone dies — the burn converts to a deeper burn over 24–48 h.
🧠 “The middle ring is on the fence.” Fluid, warmth and pressure relief push it back toward life; shock, cold and pressure push it into the graveyard.
⏱️
THE THREE PHASES
STEP 2 · WHAT MATTERS WHEN
The same patient is a completely different nursing problem on day 1, day 10 and month 6. Know which phase you are in.
📈 Timeline — fluid OUT, then fluid BACK
The single most-tested time fact from this topic: fluid shifting into the interstitium is greatest between 18 and 24 hours after the injury. Then it reverses.
🧠 “Out by 24, back by 72.” Fluid leaks OUT and peaks at 18–24 h; it comes BACK (diuresis) at 48–72 h. Every lab value on this page just follows the water.
🔄 Emergent vs. acute — the flip that trips everyone
Same patient, opposite labs, opposite risks. Learn the flip, not the lists.
EMERGENT (0–48/72 h)
ACUTE (diuresis → closure)
Fluid is…
Leaving the vessels → tissue
Returning tissue → vessels
Potassium
HIGH (cells lyse, K⁺ spills out) >5.0
LOW (K⁺ washed out in urine & wound)
Sodium
LOW (Na⁺ follows water into interstitium) <135
Variable; watch as fluids are titrated
H & H
HIGH — hemoconcentration (plasma left, cells stayed)
LOW — hemodilution + RBC destruction
Urine
Scanty & concentrated; may be dark/red-brown
Copious diuresis
Biggest killer
Hypovolemic shock
Infection / sepsis
Nurse's eyes on…
Airway, BP, HR, hourly urine
Temp, WBC, wound appearance, calories & protein
🧠 “High-K first, low-K later.” Cells burst on day one and dump potassium; by the acute phase the kidneys and the weeping wound have washed it away.
🚨 The gut in the emergent phase
Answer first: blood is shunted away from the gut, so the bowel goes quiet.
Paralytic ileus — absent bowel sounds, distension, vomiting. Expect an NG tube for decompression in large burns.
Curling ulcer — the classic burn-related stress ulcer of the stomach/duodenum from ischemia + acid. Prophylaxis with acid suppression is routine.
Watch for coffee-ground NG output or melena.
Feeding is held until bowel sounds return — then enteral nutrition is started, ideally early.
🧠 “Curling iron → Curling ulcer.” Burns → stomach ulcer. (Don't mix it up with Cushing ulcer, which goes with Cranial/head injury.)
📈 Hypermetabolism — the furnace switches on
After the first day or two the burn patient's metabolic rate can climb dramatically and stay up for months. This drives the whole acute phase.
Massive protein catabolism — muscle is burned for fuel; weight and lean mass fall
Hyperglycemia even in non-diabetics (stress hormones + insulin resistance)
Heat loss through the open wound — patients feel cold and shiver, which costs more calories
Nutrition must be high calorie, high protein, with vitamins C and A and zinc for healing
Keep the room warm — this is a therapeutic intervention, not a comfort measure
🧠 “A burn is a furnace with the door open.” It burns fuel, throws heat away, and eats muscle unless you feed it.
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INHALATION INJURY
STEP 3 · WHAT KILLS FIRST
Fluid loss kills in hours. The airway kills in minutes. That is why airway always outranks the burn.
🔥 Airway cutaway — normal vs. inhalation injury
The danger is not the burn you can see, it is the swelling you cannot. Hot gas and soot injure the upper airway; edema then closes it over the next several hours — often after the patient arrives looking fine.
🧠 “Face, hair, soot, voice.” Facial burns · singed nasal hair/eyebrows · carbonaceous (sooty) sputum · hoarseness or stridor. Any one of those four = tell the provider now, before the airway closes.
🚨 Suspect inhalation injury when…
The fire was in an enclosed space (house, car, basement)
Burns to the face, neck or chest; singed nasal hair, eyebrows or lashes
Treatment: 100% oxygen by non-rebreather; hyperbaric oxygen in severe cases
🧠 “Pink patient, normal sat, dying brain.” If someone came out of a burning building confused, give high-flow O₂ and get a CO level — do not be reassured by SpO₂ 99%.
⭐ Priority order in the first minutes — say it in this order
1
AIRWAY — is it patent, and will it stay patent? Look for the four airway signs. Anticipate intubation.
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2
BREATHING — 100% O₂ by non-rebreather. Check for circumferential chest eschar restricting the chest wall.
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3
CIRCULATION — 2 large-bore IVs (through unburned skin if possible), start Lactated Ringer's, indwelling catheter for hourly urine.
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4
STOP THE BURNING & remove clothing/jewelry — but then keep the patient WARM; large burns lose heat catastrophically.
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5
Assess TBSA, weigh the patient, calculate fluids, give tetanus prophylaxis, then pain control IV.
The full hands-on version of these steps — the fluid orders, titration, wound care and escharotomy — is on NG-123 · Major Burns (treatment).
🧠 “Airway before area.” Nobody ever died in the first five minutes from a mis-calculated TBSA. They die from an airway you did not secure.
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THE LABS — AND WHY EACH ONE MOVES
STEP 4 · NCLEX GOLD
Never memorize burn labs as a list. Each value is just the water and the dead cells telling you where they went.
📊 First-24-hour lab picture on a scale
Typical adult reference ranges are shown as a band — exact values vary by laboratory, by sex and by source. The ▲ marker is where a major-burn patient typically sits in the emergent phase.
🧠 “K up, Na down, blood thick.” Three arrows. Everything else on the emergent panel follows from those.
🚨 Hyperkalemia — Potassium Priority Pumps the heart
K⁺ over 5.0 in a burn patient is a cardiac emergency, not a chemistry curiosity. The rhythm change comes before the arrest.
Put the patient on a continuous cardiac monitor — this is a nursing action you can take yourself
Report a K⁺ over 5.0, and report peaked T waves immediately
Other clues: muscle weakness, paraesthesias, bradycardia, GI cramping/diarrhea
Deep/electrical burns with rhabdomyolysis release even more K⁺ — expect it
🧠 “Potassium Priority Pumps the heart.” Three P's. In burns, potassium is a heart problem before it is a lab problem.
🧪 Hyponatremia — Na under 135
Answer first: sodium goes with the water into the swollen tissue, and pours out of the open wound.
Clues: confusion, lethargy, headache, muscle weakness/cramps, seizures if severe
Hydrotherapy and long soaks can worsen it — sodium leaches out into the water
This is a big reason Lactated Ringer's is chosen: it contains sodium and is close to plasma composition
Never correct sodium quickly on your own initiative — rapid correction is dangerous; follow the prescription
🧠 “Na goes where the water goes.” Water into the tissues drags sodium with it, so the serum number falls.
🧾 Definitions worth 5 marks
Third-spacing — fluid that has left the vessels and sits in a space where it is useless (interstitium, blisters, gut wall)
Hemoconcentration — the plasma left, so the same red cells now make up a bigger fraction → H&H rise
Eschar — the leathery, non-elastic dead tissue over a full-thickness burn. It does not stretch, so swelling underneath strangles the limb or the chest
Escharotomy — an incision through eschar to relieve that pressure (see NG-123)
Burn shock — the hypovolemic + distributive shock of the first 24–48 h
Burn wound conversion — a partial-thickness burn deepening into a full-thickness burn because the zone of stasis died
🧠 Eschar = a cast made of dead skin. Casts have to be split when a limb swells — so does eschar.
🧪 K↑ Na↓ H&H↑First 24 h. Then it flips: K↓ H&H↓ in the acute phase.
⏱️ 18–24 h peakInterstitial shift is greatest 18–24 h; diuresis at 48–72 h.
🎯 Cover & check — 8 rapid-fire questions
Q1: In one sentence, why does a major burn cause shock?
Massive tissue destruction triggers systemic inflammation that increases capillary permeability; plasma and protein leak into the interstitium (third-spacing), so intravascular volume falls and the patient goes into hypovolemic shock.
Q2: When is fluid shifting into the interstitium greatest?
Between 18 and 24 hours after the injury. Diuresis (fluid returning to the vessels) typically begins around 48–72 hours.
Q3: Why is the hematocrit HIGH in the first 24 hours?
Hemoconcentration. Plasma has leaked out of the vessels but red cells stayed behind, so red cells make up a larger percentage of the remaining blood. A Hct around 60% is the classic exam finding — it means dehydration of the vascular space, not polycythemia.
Q4: Why is potassium high early and low later?
Early: burned cells rupture and release intracellular potassium into the blood (plus acidosis shifts K⁺ out of cells). Later, in the acute phase: potassium is lost in the diuresis and through the weeping wound, so it falls.
Q5: What ECG change goes with the early potassium problem?
Tall, narrow, peaked T waves — then a flattened P wave and a widening QRS as it worsens. Put the patient on a cardiac monitor and report it.
Q6: A patient escaped a house fire, is confused, and the pulse oximeter reads 99%. What is going on?
Suspect carbon monoxide poisoning. The pulse oximeter cannot distinguish carboxyhemoglobin from oxyhemoglobin, so it reads falsely normal. Give 100% oxygen by non-rebreather and get a carboxyhemoglobin level.
Q7: Name the four bedside signs that make you suspect inhalation injury.
Facial/neck burns, singed nasal hair or eyebrows, carbonaceous (sooty) sputum or soot around the mouth, and a hoarse voice or stridor. Enclosed-space fire is the key history. Anticipate early intubation.
Q8: The burn patient's whole body is swollen on day one. Should you slow the IV fluids?
No — not on the basis of edema. In the emergent phase the swelling IS the disease: fluid is in the wrong compartment while the vessels are empty. You titrate to intravascular indicators — urine output, blood pressure and heart rate — not to how puffy the patient looks. Report and follow the prescription.
📚 Where to go next
NG-123 — Major Burns: assessment & treatment — the hands-on partner to this page: airway, the fluid orders and titration, wound care, escharotomy, infection prevention, pain, nutrition.