NURS 370 Med Surg: Module 6 Burns: Nursing Care for Patients with Burn Injuries

Burns

Occur when skin or deeper tissues are damaged by thermal, chemical, electrical, or radiation energy. Understanding the different causes is important because each type affects tissue differently and may need unique interventions.

Burns Cause

1. Thermal: Dry/Moist Heat

2. Friction/Contact

3. Chemicals

4. Electricity

5. Ionizing radiation (the eyes too)

Key Teaching Point

Each burn cause leads to different patterns of tissue damage and complications. Always identify the source of the burn during assessment—this guides first aid and medical management.

Friction Burns

Caused by skin rubbing against a rough surface (road rash, treadmill injuries).

Combination of mechanical abrasion + heat.

Radiation Burns

Caused by energy waves or particles:

1. Sunburn (most common).

2. Radiation therapy for cancer.

3. Industrial/occupational exposure (x-rays, nuclear accidents).

Damage mechanism: DNA damage → inflammation, cell death, possible long-term cancer risk.

Electrical Burns

Occur when electric current passes through the body.

Can cause both external and internal damage:

1. Small skin marks at entry/exit sites.

2. Deep damage along the current’s path (muscle, bone, nerves, blood vessels).

Risks: Cardiac arrhythmias (e.g., ventricular fibrillation), fractures from muscle contractions, myoglobinuria → kidney injury.

Chemical Burns

Caused by exposure to strong acids or bases.

1. Examples: bleach, ammonia, drain cleaner, battery acid, cement, lime.

Damage mechanism: Chemicals continue to cause tissue destruction until diluted or neutralized.

1. Acids → coagulation necrosis (forms a barrier, limits spread).

2. Alkalis → liquefaction necrosis (deeper penetration, often more severe).

Thermal Burns

Most common type

Caused by direct contact with heat sources

1. Flames (house fires, explosions, accidents with candles or stoves)

2. Hot liquids (scalds from boiling water, coffee, soup)

3. Hot objects (irons, curling irons, heating pads, cooking surfaces)

4. Steam (industrial or cooking accidents)

Damage mechanism: Heat denatures proteins in skin and tissues → cell death.

Burn Injury Depth and Extent Classification

is determined by both the depth (degree of tissue injury) and extent (how much of the body is involved, measured by TBSA) of tissue injury. Depth Classifications:

1. Superficial (1st Degree)

2. Partial Thickness (2nd Degree)

3. Full Thickness (3rd & 4th Degree) Extent Classification: Extent refers to how much of the body is involved, typically measured using Total Body Surface Area (TBSA). This measurement helps estimate fluid requirements and overall severity.

Superficial (1st degree)

1. Layers Involved: Involves only the epidermis

2. Appearance: Red, Dry, and Painful, like a sunburn that heals quickly. No Blisters.

3. Sensation: Painful, hypersensitive to touch and temperature

4. Course of Healing: Heals in 3–6 days without scarring

5. NCLEX PEARLS: Red, painful, blanches with pressure, intact epidermis; heals within days (3-7 days)

Superficial Partial-thickness (2nd degree) 

1. Layers Involved: Extends into the upper dermis

2. Appearance: Presents with Red, blisters, moist, and more intense pain.

3. Sensation: Very painful (nerve endings exposed), sensitive to air and temperature changes

4. Course of Healing: Heals in ~2–3 weeks, usually no scar but pigment changes possible

5. NCLEX PEARLS: Blistered, wet, very painful, sensitive to air/touch; heals in weeks (<21 days for superficial, >21 days for deep).

Deep Partial-Thickness (2nd degree) 

1. Layers Involved: Epidermis and deeper dermis

2. Appearance: Red/White, less moist, may have diminished sensation.

3. Sensation: Less painful (Nerve endings damaged) but still some pressure sensation.

4. Healing: > 3 weeks, often results in scarring and possible contractures. May require grafting.

Full-thickness (3rd degrees)

1. Layers involved: Entire epidermis + dermis (may extend into subcutaneous tissue)

2. Appearance: Waxy, white, tan, charred, leathery; painless (nerves destroyed), non blanching

3. Sensation: painless but may have painful edges where partial-thickness remains.

4. Healing: Cannot regenerate—requires grafting; high risk for infection and fluid loss.

5. Complications: Fluid loss, infection risk, impaired circulation

Deep Full-Thickness Burns (Fourth-Degree)

1. Layers involved: Extends into muscle, bone, or tendon

2. Appearance: Black, charred, eschar, absent sensation. May have exposed muscle, tendon, bone.

3. Sensation: none at burn site (nerves destroyed)

4. Healing: Requires surgical intervention (debridement, grafting, amputation possible)

Burn Appearance, Sensation, and Healing Pearl

1. Superficial → red, painful, heals quickly

2. Partial-thickness → blistered, very painful, heals with time (weeks)

3. Full-thickness → dry, leathery, painless, needs grafting

Extent of Burn Injury

1. is measured as a percentage of total body surface area (TBSA) involved, using methods like the "Rule of Nines" for quick adult estimates and the Lund-Browder Chart for more precise calculations, especially in children.

2. Severity further considers burn depth and critical locations.

3. Severity: Combines both Depth + Extent + Location

4. Burns are dynamic, and initial depth can worsen over the first 24-48 hours.

Rule of Nines (adults)

1. Head & neck: 9%

2. Each arm: 9% (front 4.5%, back 4.5%)

3. Each leg: 18% (front 9%, back 9%)

4. Front torso: 18%

5. Back torso: 18%

6. Perineum: 1%

Lund-Browder Chart

Allows for age-adjusted TBSA estimates, more accurate for children due to growth differences.

Severity Guidelines (ABA / AHA)

1. Minor Burns: <10% TBSA (partial-thickness); no critical areas involved.

2. Moderate Burns: 10-20% TBSA; may require hospitalization.

3. Major Burns: 20% TBSA, or burns involving the face, hands, feet, perineum, airway, or circumferential burns; refer to a burn center.

Burns Special Considerations

1. Location matters: airway burns risk progressive inflammation and require urgent attention.

2. Functional and cosmetic impacts, including psychosocial concerns, affect burn severity evaluation.

3. Depth describes which tissue layers are destroyed; extent is the amount of body affected; severity is a combination of both with location.

4. Burn wounds may convert and deepen over 24-48 hours after injury.

Systemic Response to Burn Injury

1. Severe burns involving more than 20% of the total body surface area (TBSA) set off a cascade of systemic physiologic changes, mainly triggered by inflammation and altered capillary permeability, resulting in multi-organ involvement.

2. This "triple hit" includes a widespread stress response, end-organ effects, and a massive inflammatory/capillary leak, requiring a holistic management approach.

3. Organ Systems Affected:

A) Cardiovascular

B) Respiratory

C) Gastrointestinal

D) Renal

E) Immune System

F) Metabolic

Physiologic Changes: Massive Fluid Shifts and Electrolyte Imbalances

1. Fluid Shifts: Plasma leaks into interstitial space → edema and hypovolemia.

2. Electrolyte Imbalance: ↑ Potassium (cell lysis) initially, then ↓ K⁺ later with fluid replacement.

3. ↓ Sodium (lost in plasma and diluted with fluids)

Burns and the Cardiovascular

1. Systemic Response: Burn Shock = Fluid loss leads to a mix of hypovolemic and distributive shock, This causes Physiologic Changes

2. Physiologic Changes: Decreased cardiac output and preload. Tachycardia, hypotension, and weak pulses are common, with circumferential burns further impairing circulation.

Burns and the Respiratory

1. Physiological Changes: Inhalation injury from smoke or chemicals can cause airway edema and ARDS. Capillary leak may result in pulmonary edema.

2. Systemic Response: Airway edema, bronchospasm, CO2 poisoning, pulmonary edema.

Burns and the Renal

1. Physiologic Changes: Reduced renal perfusion leads to oliguria or acute kidney injury.

2. Systemic Response: Decreased Urine Output; Muscle breakdown (myoglobinuria) can obstruct tubules and cause failure; strict urine output monitoring is key. 

Burns and the Gastrointestinal

Systemic Response: The stress response reduces GI blood flow, causing ileus and increasing the risk for Curling's ulcers. Nutritional requirements surge in a hypermetabolic state.

Burns and the Immune

Systemic Response: Burned skin compromises the body's first barrier, sharply raising infection risk. Immune suppression from cytokine storms and protein loss make sepsis a leading cause of death in burn patients.

Burns and the Metabolic

1. Physiologic Changes: Burns induce a hypermetabolic state, greatly increasing body temperature, oxygen consumption, and caloric needs. Without nutritional support, muscle wasting is likely.

2. Systemic Response: Increased stress hormones (catecholamines, cortisol) cause insulin resistance, catabolism, and muscle wasting. 

Systemic Inflammatory Response (SIRS)

1. Triggered by severe burns

2. Cytokines (histamine, prostaglandins, interleukins, TNF-α) released from injured tissues cause:

Vasodilation

Increased vascular permeability

White blood cell activation

3. Result: capillary leak and worsening edema, sometimes resembling sepsis even without infection.

Capillary Leak Syndrome

1. Burn injury increases capillary permeability → plasma proteins and fluids leak into interstitial space.

2. Results:

   Massive edema (local and systemic)

   Hypovolemia & hemoconcentration (risk for shock)

3. Direct injury + inflammatory mediators → endothelial gaps in capillaries.

   Leads to:

   Plasma proteins (albumin) leak out → ↓ oncotic pressure → worsens edema.

   Fluid shifts from intravascular → interstitial space (third spacing).

   Maximum effect in first 24–48 hours after major burn.

4. Nursing implication: Massive IV fluid resuscitation (e.g., Parkland formula) required to restore intravascular volume and prevent burn shock.

Severe Burns Teaching Pearl

Think of severe burns as a triple hit:

1. Physiologic stress response (shock, fluid/electrolyte imbalance)

2. Systemic organ involvement (heart, lungs, kidneys, GI, immune)

3. Inflammatory + capillary leak (drives all the fluid shifts)

Core Responses to Burns

1. Physiologic and Inflammatory Response: Systemic inflammation and increased vascular permeability cause fluid shifts, third spacing, and multi-system impairment.

2. Clinical Approach: Early management must focus on airway, breathing, circulation (ABC), and aggressive fluid resuscitation. Ongoing care involves preventing infection, supporting nutrition, providing pain control, and facilitating psychosocial recovery.

3. Burns greater than 20% TBSA are not just skin injuries—they are dynamic, whole-body illnesses requiring coordinated, multi-system care.

Capillary Permeability Change from Burns

1. Normal blood capillary only allows small molecules like water to pass freely.

2. Post-Burn Blood Capillary has its permeability drastically increased. This allows larger molecules, such as proteins, to escape easily.

3. This increased capillary permeability is a hallmark of the systemic inflammatory response, contributing to massive fluid shifts, edema, and subsequent complications in burn patients.

4. The escape of proteins and other large molecules from the vascular space plays a central role in burn shock and hypovolemia.

Severe Burns

1. Creates a whole-body crisis, impacting nearly every major organ system.

2. The skin's loss as a protective barrier, massive capillary fluid leakage leading to burn shock, a powerful stress response driving hypermetabolism and organ strain, and heightened long-term infection risk collectively define the pathophysiology of critical burns.

Severe Burns Impact on: Sympathetic Nervous System

1. Activates stress response, increasing heart rate and mobilizing energy stores.

2. Severe burns trigger a fight-or-flight stress response

3. Catecholamine release (epinephrine, norepinephrine) → tachycardia, vasoconstriction, increased blood pressure initially.

4. Maintains perfusion to heart and brain at the expense of skin, kidneys, and gut.

Severe Burns Impact on: Neuro

1. Burn shock and metabolic changes may alter mental status or cause neuropathies.

2. Major burns can cause altered level of consciousness (LOC) due to:

Hypovolemia and hypoxia

Carbon monoxide or cyanide poisoning (from smoke inhalation)

3. Severe pain → anxiety, agitation; requires pain and sedation management.

Severe Burns Impact on: Cardiovascular System

1. Capillary leak causes hypovolemia, decreased cardiac output, and burn shock; tachycardia and hypotension are common.

2. Burn shock: combination of hypovolemic + distributive shock.

3. Capillary leak → ↓ intravascular volume → hypotension and ↓ cardiac output.

4. Tachycardia is common (compensation).

5. Risk of arrhythmias from hyperkalemia or electrical burns.

Severe Burns Impact on: Pulmonary (Respiratory)

1. Inhalation injury can lead to airway edema, bronchospasm, and ARDS.

2. Inhalation injury: airway edema, risk of obstruction (singed nasal hairs, hoarseness, stridor = red flags).

3. Pulmonary edema and bronchospasm.

4. Carbon monoxide poisoning → headache, confusion, cherry-red skin, hypoxia despite normal SpO₂.

5. Risk of ARDS (acute respiratory distress syndrome).

Severe Burns Impact on: Renal

1. Reduced renal perfusion may cause oliguria or acute kidney injury.

2. ↓ Renal perfusion from hypovolemia → oliguria, acute kidney injury.

3. Myoglobinuria from muscle breakdown (especially electrical burns) → dark urine, tubular obstruction.

4. Requires aggressive IV fluids to maintain urine output ≥ 0.5–1 mL/kg/hr.

Severe Burns Impact on: GI

1. Decreased blood flow to the gut (ileus), increased risk for stress ulcers, and sharply increased nutritional needs.

2. Stress response + ↓ perfusion → ileus (paralyzed gut, absent bowel sounds).

3. Risk of Curling’s ulcer (stress-induced gastric ulcer).

4. Nutritional demands skyrocket → early enteral feeding is essential.

Severe Burns Impact on: Metabolic

1. Marked hypermetabolic state increases caloric and oxygen demand; risk of muscle wasting.

2. Hypermetabolic state develops:

↑ Body temperature (reset hypothalamic thermostat).

↑ Oxygen and calorie needs (can double/triple baseline).

Muscle wasting without nutrition support.

3. Insulin resistance → hyperglycemia common.

Severe Burns Impact on: Integumentary & Immunologic

1. Skin injury removes the first defense against pathogens, while immune suppression and protein loss heighten infection risk—the leading long-term threat.

2. Skin barrier destroyed → high risk of infection and sepsis.

3. Loss of fluids, electrolytes, and heat through open wounds.

4. Immune suppression from cytokine storm + protein loss.

5. Burn wounds can progress in depth (“burn wound conversion”) over 24–48 hours.

Prehospital Burn Care

Focuses on stopping the burning process, prioritizing airway and breathing, and protecting the patient from further harm. Early and appropriate interventions can lower mortality and long-term complications in burn patients. "Stop the burn, secure the airway, cool—but don't overcool—and protect." Early care is vital for reducing mortality and minimizing complications. Key Steps:

1. Stop Burning Process

2. ABCs

3. Don't Remove Stuck Materials (Except Dry Chemicals)

4. Do Not Neutralize Chemicals 5. Cool Water Only/Sterile NS Dressings 6. Psychological Support

Key Step Prehospital Burn Care: Stop burning process

1. Remove the source of heat/chemical.

2. Remove the person from the source of the burn (flames, hot liquid, electrical source, chemicals).

3. Extinguish flames by “stop, drop, and roll” or covering with a blanket.

4. Remove smoldering clothing or jewelry, but do not peel away clothing stuck to the skin.

Key Step Prehospital Burn Care: ABCs

Prioritize airway management, evaluate for carbon monoxide poisoning and thermal injury.

1. Airway: Assess for airway compromise (singed nasal hairs, soot in mouth/nose, hoarseness, stridor).

2. Breathing: Consider risk of inhalation injury (smoke, hot gases). Give 100% oxygen if available.

3. Carbon Monoxide: High suspicion in enclosed-space fires; SpO₂ can be misleading — CO binds hemoglobin.

4. Circulation: Check pulses, especially with circumferential burns (risk of compartment syndrome).

Key Step Prehospital Burn Care: Don't remove stuck materials (except dry chemicals)

Only brush off dry chemicals; materials adhering to the wound should not be forcefully removed.

1. Do not attempt to peel off melted clothing or tar/asphalt — this can worsen tissue injury.

2. If dry chemicals are present (e.g., lime, cement powder) → brush off before irrigating with water.

Key Step Prehospital Burn Care: Do NOT neutralize chemicals

Attempting to neutralize chemicals can cause further injury.

1. Neutralizing chemicals can worsen injury due to heat-producing reactions.

2. Instead: remove contaminated clothing and flush copiously with water (after brushing off dry powders).

Key Step Prehospital Burn Care: Cool water only / sterile NS dressings

Use cool (not cold) water for initial cooling; apply sterile normal saline dressings.

1. Apply cool (not ice-cold) water to stop burning and relieve pain.

Avoid ice → can cause vasoconstriction and worsen tissue damage.

2. Cover burns with clean, dry, sterile dressings or sheets to protect from contamination and heat loss.

3. Avoid ointments, butter, or home remedies.

Key Step Prehospital Burn Care: NPO

Keep patient nil per os (NPO) in anticipation of possible procedures or complications.

1. Burn patients are at high risk for surgery and aspiration.

2. Keep the patient NPO until evaluated in hospital.

Key Step Prehospital Burn Care: Psychological support

Address the emotional distress and anxiety common after burn injuries.

1. Burn injuries are traumatic. Provide emotional reassurance and calm communication.

2. Reduce anxiety by explaining what you are doing.

3. If possible, keep family nearby for support.

Acute Phase (Resuscitation/Shock)

1. Begins at time of injury (ER arrival).

2. Lasts for the first 24-48 hours (48-72 Hours).

3. During this time, massive fluid shifts cause burn shock and require aggressive airway and fluid management.

4. The main priority in this stage is airway, breathing, and circulation (the ABCs) — keeping the patient alive while preventing complications from massive fluid shifts.

Acute Phase: Patient Goals

1. Maintain airway, breathing, and circulation (ABC)

2. Restore and maintain effective tissue perfusion

3. Limit further tissue damage and complications

4. Begin infection prevention

Acute Phase Pathophysiology

1. Capillary leak syndrome: Burn injury causes capillaries to become permeable → plasma and proteins leak into interstitial space → massive edema.

2. Hypovolemia/shock risk: Fluid leaves the intravascular space, leading to decreased circulating volume, reduced cardiac output, and potential burn shock.

3. Electrolyte shifts:

Hyperkalemia (from cell destruction releasing K⁺).

Hyponatremia (sodium lost into interstitial fluid).

4. Metabolic acidosis: From tissue hypoperfusion and anaerobic metabolism.

Acute Phase Clinical Manifestations: Vital Signs

1. Tachycardia (from hypovolemia)

2. Hypotension (fluid loss)

3. Increased respiratory rate (pain, anxiety, possible airway involvement)

4. Initially low temperature (heat loss), may rise with infection later

5. Oxygen saturation may be unreliable if carbon monoxide poisoning is present

Acute Phase Clinical Manifestations: Lab Findings

1. Elevated hematocrit/hemoglobin (hemoconcentration from plasma loss)

2. Elevated potassium (hyperkalemia from cell lysis)

3. Low sodium (loss and dilution)

4. Elevated BUN/creatinine (decreased renal perfusion)

5. Elevated lactate and metabolic acidosis (hypoperfusion, anaerobic metabolism)

6. Early phase: monitor for fluid overload and electrolyte shifts during transition to diuresis

Acute Phase Priority Interventions: Airway and Breathing management

1. Highest urgency, especially with facial or inhalation burns

2. Burns to the face, neck, or chest can cause airway edema → risk of obstruction.

3. Assess for airway compromise: burns to face/neck, singed nasal hairs, hoarseness, stridor, carbonaceous sputum.

4. Early intubation may be required before swelling worsens.

5. High-flow oxygen is given, and ABGs and O2Sat are monitored.

Acute Phase Priority Interventions: Aggressive Circulation and Fluid Resuscitation

1. Goal: restore perfusion and prevent shock.

2. To counteract third spacing and prevent or treat burn shock; monitor urine output closely

3. Parkland formula is commonly used:
   4 mL × body weight (kg) × %TBSA burned = total fluids for first 24 hrs.

   Give ½ in first 8 hours, then the rest over 16 hours.

4. Monitor: Urine output (most reliable indicator of perfusion: 0.5–1 mL/kg/hr in adults).

5. Monitor VS: Heart rate, blood pressure, MAP, CVP if available.

Acute Phase Priority Interventions: Disability/Neurological Status

1. neuro checks (especially in cases of hypoxia, hypoperfusion, or carbon monoxide poisoning).

2. Assess mental status changes → may indicate inadequate perfusion or hypoxemia.

Acute Phase Priority Interventions: Monitor labs, ECG, and hemodynamics

1. Correct electrolyte imbalances as needed

2. Vital signs: tachycardia, hypotension, low urine output signal inadequate resuscitation.

3. Labs: potassium, sodium, hematocrit, BUN/creatinine.

4. Anticipate hyperkalemia (cell destruction) and hyponatremia (fluid shifts).

   Monitor CBC, electrolytes, BUN/creatinine, lactate.

Acute Phase Priority Interventions: Prevent infection

1. Maintain aseptic technique, early wound care

2. Initial cleansing and covering wounds with clean, dry sheets.

3. Tetanus prophylaxis if indicated.

4. Avoid aggressive wound debridement until the patient is stabilized.

Acute Phase Priority Interventions: Pain and anxiety management

1. Address physical and psychological stress

2. Severe pain is expected.

3. Use IV opioids (not IM or subcutaneous, due to impaired absorption).

4. Provide reassurance, explain procedures, and acknowledge pain and fear.

   Family support if possible.

Acute Phase Priority Interventions: Temperature regulation

1. Prevent hypothermia with external warming

2. Burn patients lose skin barrier → risk of hypothermia

3. Maintain warm environment, warm IV fluids, and blankets.

Acute Phase Priority Interventions: Nutritional support

Initiate early enteral feeding as soon as stable

Acute Phase Priority Interventions: Frequent reassessment

Watch for airway compromise, worsening hypoperfusion, and transition to diuretic phase

Possible Test Question: Lab findings and vitals in resuscitation phase: Main Problem

Massive fluid shifts from intravascular → interstitial space (“third spacing”) → burn shock.

Possible Test Question: Lab findings and vitals in resuscitation phase: Vital Signs

1. Heart rate: ↑ Tachycardia (compensating for hypovolemia).

2. Blood pressure: ↓ Hypotension as intravascular volume drops.

3. Respiratory rate: ↑ if pain, anxiety, or inhalation injury; may show stridor/hoarseness with airway compromise.

4. Temperature: Often low initially (heat loss through skin and evaporative cooling); may later rise with infection.

5. Oxygen saturation: May be unreliable if carbon monoxide poisoning present → use carboxyhemoglobin levels instead.

Possible Test Question: Lab findings and vitals in resuscitation phase: Lab Findings Early

1. ↑ Hematocrit / ↑ Hemoglobin → hemoconcentration from plasma loss.

2. ↑ Potassium (hyperkalemia) → cell lysis releases K⁺ into bloodstream.

3. ↓ Sodium (hyponatremia) → lost in plasma and diluted by fluid resuscitation.

4. ↑ BUN/Creatinine → decreased renal perfusion.

5. ↑ Lactate & metabolic acidosis → hypoperfusion and anaerobic metabolism.

Possible Test Question: Lab findings and vitals in resuscitation phase: Lab Findings Ongoing

After diuresis begins (transition toward acute phase):

1. ↓ Potassium (hypokalemia) → K⁺ shifts back into cells and is excreted.

2. Dilutional hyponatremia may persist with fluid therapy.

Acute Phase Clinical Focus

1. Think: tachycardia, hypotension, cool skin, low urine output, high Hct, high K+, low Na = resuscitation phase profile. For this phase, airway first, then fluids, to maintain perfusion and prevent burn shock.

2. Pearl: Acute phase priorities are "fight infection, feed the patient, and focus on function".

Acute Phase Meds

"Pain, Prevent Infection, Protect the Gut, Prevent Clots, Provide Nutrition."

Acute Phase Goals: Limit extent of injury

1. Clinical Manifestations: Sympathetic NS stimulation, catecholamine release, stress response

2. Priority Interventions: Protect from further injury; conserve heat

Acute Phase Goals: Maintain vital organ function

1. Clinical Manifestations: ↓ LOC (neuro), airway edema, pulmonary insufficiency, hypoxemia, ↓ lung compliance, risk aspiration

2. Priority Interventions: Protect airway; intubate, ventilate, O₂, NGT for aspiration risk

Acute Phase Goals: ABCs

1. Clinical Manifestations: ↓ MAP, ↓ CO, ↑ HR, dysrhythmias (CV effects)

2. Priority Interventions: Aggressive IVF (crystalloids) to maintain MAP > 60

Acute Phase Goals: Pain management

1. Clinical Manifestations: Severe pain (esp. partial-thickness), anxiety in pt/family

2. Priority Interventions: Proactive IV analgesia; emotional support, info, environmental control

Acute Phase Goals: FEN (fluid/electrolyte/nutrition)

1. Clinical Manifestations: ↓ ECV, Na⁺, ↑ K⁺, acidosis, ↑ BUN/Hct, hypoproteinemia, hyperglycemia

2. Priority Interventions: Monitor/replace F&E; insulin for hyperglycemia, NPO, ↓ acid with meds

Acute Phase Goals: GI

1. Clinical Manifestations: ↓ bowel sounds, ileus, ↑ gastric retention, hyperacidity

2. Priority Interventions: NPO, meds to ↓ acid, NGT as needed

Acute Phase Goals: Renal

1. Clinical Manifestations: Oliguria/anuria (↓ perfusion), hemoglobinuria/myoglobinuria

2. Priority Interventions: Maintain volume/perfusion, monitor output, labs

Acute Phase Goals: Integumentary/Wound

1. Clinical Manifestations: Edema, hypothermia risk, barrier loss, tissue layer disruption, pain, exudates

2. Priority Interventions: Cover wounds, maintain temp, elevate extremities, asepsis

Acute Phase Goals: Psychosocial

1. Clinical Manifestations: Patient/family distress

2. Priority Interventions: Provide info, support, minimize overload

Intermediate Phase

1. Is a transition from "rescue → restore," where the emphasis moves from basic resuscitation to rehabilitation and complication prevention.

2. Timeline:

Starts after initial resuscitation ~48 hours - 72hours and

Ends when wound closure (through healing or grafting)

3. Key Physiologic Event: Defined by fluid remobilization, diuresis, and a restorative/preventive focus.

4. Restorative/preventive priorities: Early ambulation (as soon as stable), wound care, aggressive nutrition, and complication prevention.

Intermediate Phase: Fluid Remobilization and Diuresis

1. Damaged capillaries begin to heal → fluid starts to move back into the vascular system.

2. Diuresis occurs: urine output increases as kidneys excrete the excess fluid.

3. Electrolyte shifts:

Hyponatremia (from dilution with fluid shifts).

Hypokalemia (as K⁺ moves back into cells or is excreted in urine).

4. Careful monitoring needed for fluid overload as fluid returns to circulation.

Intermediate Phase Priority Interventions

1. Restorative Care

2. Preventive Care

3. Mobility and Function 

Intermediate Phase Priority Interventions: Restorative Care

1. Wound management:

Continue dressing changes, debridement, grafting as needed.

Maintain sterile technique to prevent infection.

2. Nutrition:

High-calorie, high-protein diet or enteral support.

Supplements (Vitamin C, zinc) for wound healing.

3. Pain & anxiety management: Adequate analgesia before procedures.

Intermediate Phase Priority Interventions: Preventive Care (Complications)

1. Infection prevention: vigilant wound and systemic monitoring.

2. Contracture prevention: splinting, positioning, early ROM exercises.

3. Stress ulcer prophylaxis: PPIs or H₂ blockers.

4. Monitor labs & fluids: watch sodium, potassium, and renal function closely.

Intermediate Phase Priority Interventions: Mobility and Function

1. Ambulate ASAP once extracellular volume (ECV) is stable.

2. Early mobilization improves circulation, reduces risk of VTE, prevents pulmonary complications, and promotes psychological recovery.

3. Physical and occupational therapy started early for long-term functional outcomes.

Intermediate Phase Goals: Monitor system function

1. Clinical Manifestations: Fluid remobilization and diuresis, peak inflammatory response, secondary complications

2. Treatment/Interventions: Cardiac/hemodynamic monitoring, adjust IV fluid rates, monitor ABGs, pulmonary toilet

Intermediate Phase Goals

1. Monitor systems function

2. Pain management

3. Adjust Rx for fluid shifts

4. Monitor labs

5. Wound care

6. Aggressive nutritional support

7. Prevent complications

8. Psychosocial support

Intermediate Phase Clinical Manifestations and Treatments: Systemic

1. CM: Compensatory systems, Fluid remobilization and diuretic phase, peak inflammatory response, secondary complications

2. Treatment: Cardiac/hemodynamic monitoring, adjust IV fluid rates, monitor ABGs, pulmonary toilet

Intermediate Phase Clinical Manifestations and Treatments: Neuro

1. CM: Restlessness, confusion, lethargy

2. Treatment: Protect from injury

Intermediate Phase Clinical Manifestations and Treatments: Respiratory

1. CM: Increased RR, dyspnea, adventitious BS, purulent sputum, peak potential for airway edema.

2. Treatment: Monitor airway edema peak, ABGs, RX PRN, Pulmonary Toileting.

Intermediate Phase Clinical Manifestations and Treatments: CVS

1. CM: Dysrhythmias, increased HR, increase/decrease BP (volume and status), ECG changes w/electrical injury, Temp. increase (infection).

2. Treatment: Cardiac and hemodynamic monitoring, RX for source of dysrhythmias, monitor fluid rates.

Intermediate Phase Clinical Manifestations and Treatments: GI

1. CM: Curling's Ulcer, decreased motility, ileus.

2. Treatment: TPN, Feed PO, TF, antacids medications.

Intermediate Phase Clinical Manifestations and Treatments: Renal

1. CM: Large diuresis, glycosuria.

2. Treatment: Monitor renal function

Intermediate Phase Clinical Manifestations and Treatments: FEN

1. CM: Hemodilution (decreased BUN and Hct), decreased sodium, decreased potassium, hypoproteinemia, neg. nitrogen balance, acidosis, increased WBCs, coagulopathies and decreased platelets.

2. Treatment: Monitor FEN, Acid/Base, Coags, manage Blood sugar.

Intermediate Phase Clinical Manifestations and Treatments: Integumentary

1. CM: compartment syndrome, immobility pruritus.

2. Treatment: Raise extremities, raise HOB, ROM, Splints, pressure garments.

Intermediate Phase Clinical Manifestations and Treatments: Wound

1. CM: necrosis, sloughing, secondary infections, debridement, granulation, re-epithelialization

2. Treatment: debridement, escharotomy, topical antimicrobial/ABX, skin grafts.

Intermediate Phase Clinical Manifestations and Treatments: Psychosocial

1. CM: control issues, regression, lack of or exhaustion of coping mechanisms, fears.

2. Treatment: effective pain management, referrals to support consults, listen.

The burn Stress Response = Survival Mode

1. Catecholamines speed up the body.

2. Cortisol breaks down fuel.

3. ADH/Aldosterone try to hold onto fluid.

4. Cytokines make vessels leaky.

5. Together, they create the fluid shifts, hypermetabolism, and infection risks that define severe burn injury.

Sequelae of Major Burn Injury: Physiologic Stress Response

Severe burns trigger a massive stress response that affects nearly every body system. This response is driven by activation of the sympathetic nervous system and the endocrine system, which release stress hormones to help the body survive — but these changes also place patients at high risk for complications.

Causes a physiologic stress response triggered by severe burns that results in widespread and dynamic disruption to body homeostasis. Body Systems Include:

1. Cardiovascular

2. Respiratory

3. Immune

4. Integumentary

5. GI

6. Urinary

7. Metabolic

Sequelae of Major Burn Injury: Physiologic Stress Response: Sympathetic Nervous System (SNS) Activation

Burn injury = trauma → immediate “fight-or-flight” response.

Catecholamines (epinephrine, norepinephrine) released:

1. ↑ Heart rate (tachycardia)

2. ↑ Blood pressure (initially, if circulating volume is adequate)

3. Peripheral vasoconstriction (shunts blood to vital organs)

4. Pupillary dilation, sweating, anxiety

Sequelae of Major Burn Injury: Physiologic Stress Response: Endocrine and Hormonal Response

Cortisol (stress hormone) ↑

1. Promotes breakdown of protein and fat (catabolism)

2. Increases blood glucose → stress-induced hyperglycemia

Aldosterone & ADH (antidiuretic hormone) ↑

1. Retain sodium and water to conserve intravascular volume

2. Contribute to edema formation when capillaries are leaky