Burns Trauma & Acute Deterioration – Comprehensive Study Notes
Anatomy & Functions of the Skin
Skin = largest organ of the human body, serving as a protective barrier; composed of three primary layers:
Epidermis: The outermost avascular layer, primarily composed of keratinocytes, providing protection against water loss, infection, and UV radiation.
Dermis: The middle layer, rich in collagen and elastin fibers, containing blood vessels, nerves, hair follicles, and sweat glands. It provides skin strength, elasticity, and sensation.
Subcutaneous tissue (Hypodermis): The innermost layer, composed mainly of adipose (fat) tissue, providing insulation, energy storage, and shock absorption.
Five key functions critically affected by burns, leading to systemic complications when compromised:
Thermoregulation: The skin plays a vital role in maintaining core body temperature through heat preservation (insulation by fat and vasoconstriction) and heat dissipation (sweating and vasodilatation). Burns disrupt this, leading to hypothermia or hyperthermia.
Fluid-electrolyte balance: The intact epidermis acts as a primary barrier against evaporative fluid losses. Extensive burns destroy this barrier, leading to massive fluid and electrolyte shifts from the intravascular space into the interstitial space, potentially causing hypovolemic shock.
Immune defence: The skin provides a crucial physical and cellular barrier (e.g., Langerhans cells) against pathogens. Burn injury compromises this barrier, significantly increasing the risk of local and systemic infections.
Protection against bacterial invasion: The acidic pH of the skin (acid mantle) and continuous shedding of epidermal cells help inhibit bacterial growth. Disruption makes the burn wound an ideal medium for bacterial proliferation.
Neurosensory interface: The skin contains numerous nerve endings and specialized receptors responsible for sensations of touch, pressure, pain, and temperature. Burns can destroy these nerve endings, leading to altered or absent sensation in the affected areas.
Epidemiology & Aetiology
Burns remain a common and potentially life-threatening injury in both adults and children globally, representing a significant public health burden.
The incidence of burns shows a male : female ratio of approximately 1.6:1, indicating a higher prevalence in males, possibly due to occupational hazards or risk-taking behaviors.
Over the last 20 years, overall burn admissions have shown a decrease in high-income nations, likely due to improved safety measures and public awareness campaigns. However, there has been an increase in some high-risk groups, such as children in South-East Asia and Australasia, highlighting disparities in prevention and safety.
In 1997, the global Disability-Adjusted Life Year (DALY) loss from burns exceeded that from common chronic conditions such as diabetes, HIV, and asthma, underscoring the severe and long-term morbidity and mortality associated with burn injuries.
Knowing the precise injury mechanism is crucial for immediate first responders and receiving medical teams as it dictates initial management strategies and anticipates potential complications:
Thermal burns: Caused by contact with flame, hot liquids (scalds), hot objects, or steam. These are the most common type.
Chemical burns: Result from exposure to strong acids, alkalis, or organic compounds. The duration of contact and type of chemical influence the depth and severity (alkalis tend to cause more liquefaction necrosis, acids cause coagulation necrosis).
Electrical burns: Caused by direct contact with electrical current. These can result in deep tissue damage (often more extensive than surface appearance suggests), cardiac arrhythmias, and neurological injury due to the current path through the body.
Radiation burns: Caused by exposure to radiation, such as excessive sunlight (sunburn), industrial radiation, or radiation therapy. Severity depends on dose and duration of exposure.
Mechanical friction burns: Occur when a body part is rubbed against a surface, causing friction and heat generation, leading to skin abrasion and thermal injury (e.g., road rash).
Pathophysiology – Local Response (Jackson’s Model)
Three concentric zones of tissue injury form immediately after thermal trauma, as described by Jackson's Model, critical for understanding wound progression and guiding treatment:
Zone of coagulation: This central zone is the area of irreversible tissue damage. Cells are immediately necrotic due to protein denaturation and cell membrane disruption. Clinically, it appears white or charred and is completely avascular with no perfusion, indicating permanent tissue loss.
Zone of stasis: Surrounding the zone of coagulation, this area is characterized by injured yet potentially viable tissue. Cells here suffer from microvascular compromise, impaired perfusion, and increased capillary permeability. It appears red, may or may not blanch with pressure, and has altered sensation. This zone is highly susceptible to secondary ischaemia, infection, or inadequate resuscitation, which can lead to its conversion into the zone of coagulation within 24-48 hours.
Zone of hyperaemia: The outermost zone, which typically appears red, blanched upon pressure, and is painful. It is characterized by minimal cellular damage and active vasodilatation due to inflammatory mediators, resulting in increased blood flow. Full recovery of this zone is expected within a few days without specific intervention.
The primary treatment priority in local burn management is to preserve the zone of stasis by optimizing tissue perfusion, preventing infection, and reducing edema, thereby minimizing the extent of irreversible tissue damage.
Pathophysiology – Systemic Response
Major burns (typically >20% TBSA in adults or >10-15% in children) trigger a profound systemic inflammatory response, involving the massive release of various vasoactive and inflammatory mediators into the bloodstream. These include:
Histamine: Released from mast cells, causing vasodilation and increased capillary permeability.
Bradykinin: A potent vasodilator and pain mediator, contributing to increased vascular permeability.
Prostaglandins and Thromboxanes: Lipid mediators that contribute to vasodilation, vasoconstriction, platelet aggregation, and inflammation.
Tumor Necrosis Factor (TNF-\alpha) and Interleukins (IL-1, IL-6, IL-8): Pro-inflammatory cytokines that initiate and propagate the systemic inflammatory response, leading to widespread endothelial dysfunction.
Catecholamines (epinephrine, norepinephrine) and Cortisol: Stress hormones released in response to injury, causing widespread vasoconstriction (initially) and metabolic changes (hypermetabolism, insulin resistance).
Glucagon: Contributes to the hypermetabolic state and hyperglycemia.
These circulating mediators lead to several critical systemic consequences:
Capillary permeability increase: The most significant initial consequence, leading to widespread leakage of plasma proteins (especially albumin) and fluid from the intravascular space into the interstitial space. This results in generalized edema in both burned and unburned tissues.
Hypovolaemia and Burn Shock: The massive fluid shift out of the circulation leads to a profound decrease in circulating blood volume (hypovolaemia). This directly reduces venous return (preload) to the heart, leading to decreased cardiac output and compensatory increase in systemic vascular resistance (SVR). If uncorrected, this progresses to burn (hypovolaemic) shock, characterized by inadequate tissue perfusion and cellular hypoxia.
Immune suppression: Despite the inflammatory surge, burn injury paradoxically causes a generalized state of immune suppression, impairing both innate and adaptive immune responses. This significantly increases the patient's susceptibility to local wound infections, sepsis, and multi-organ dysfunction.
Pulmonary complications: Systemic inflammation can directly affect lung endothelium, leading to increased permeability and fluid accumulation in the alveoli. This, combined with direct inhalation injury, can precipitate Acute Respiratory Distress Syndrome (ARDS), a severe form of lung injury characterized by widespread inflammation and impaired gas exchange.
Classification by Depth
Accurate classification of burn depth is crucial for prognosis, treatment planning, and predicting healing time. Terminology:
Superficial (Epidermal) Burn: Involves only the epidermis. Similar to a mild sunburn. Characterized by erythema (redness), pain, and sensitivity to touch. It does not blister. Heals spontaneously within 3-6 days without scarring as the basal layer of the epidermis remains intact.
Partial Thickness Burn: Involves the epidermis and a portion of the dermis. Subdivided based on the depth of dermal involvement:
Superficial Partial Thickness: Affects the epidermis and the superficial (papillary) dermis. Appears pale-pink, often with intact, painful blisters that are fragile. Capillary refill is brisk (indicating good perfusion), and the burn is very painful due to exposed nerve endings. Heals within 7-14 days with minimal to no scarring, as epidermal appendages (hair follicles, sweat glands) in the deeper dermis are spared.
Mid-dermal Partial Thickness: Extends deeper into the dermis. Appears dark-pink to red, often with larger, ruptured, or unroofed blisters. Capillary refill is sluggish, and sensation may be altered (less painful than superficial partial thickness) due to partial nerve damage. Healing can take 2-3 weeks, usually with minimal to moderate scarring and potential for pigmentary changes. Often requires specialized dressings or antimicrobial creams to promote healing and prevent infection.
Deep Partial Thickness (Deep Dermal): Extends near the base of the dermis, damaging most of the dermal structures. Appearance is mottled (patchy red and white), often waxy or pearly white, and typically does not blanch with pressure. Sensation is significantly diminished or absent due to extensive nerve damage. Healing is prolonged, often taking more than 3 weeks, and typically results in significant scarring, hypertrophic scars, and contractures. These burns frequently require surgical intervention, such as skin grafting, to achieve optimal healing and functional outcomes.
Full Thickness Burn: Destroys the entire epidermis and dermis, and may extend into the subcutaneous tissue below. The burn appears leathery, waxy white, tan, brown, or charred black. It is typically anesthetic (painless) due to complete destruction of nerve endings. Does not blanch with pressure. These burns do not heal by re-epithelialization from wound edges and require surgical excision of the non-viable tissue, followed by skin grafting or reconstructive procedures to close the wound. Healing occurs by scarring and contracture formation.
Extended Full-thickness Burn (Fourth-degree burn): Extends beyond the skin layers into underlying fascia, muscle, bone, or even internal organs. This usually results from prolonged contact with extreme heat or high-energy trauma. Requires extensive surgical debridement and often complex reconstructive procedures, potentially including amputation.
Case Study Snapshot
46 y/o male pilot (80 kg) presents following a plane crash with deep partial burns to the head, neck, and both arms, along with signs of inhalation injury (hoarse voice, scorched nasal hair). Vital signs: Respiratory Rate (RR) = 20 breaths/min, oxygen saturation (SpO₂) = 94% on room air, Blood Pressure (BP) = 114/76 mmHg, Heart Rate (HR) = 102 bpm, Capillary Refill Time (CRT) < 2 seconds, Glasgow Coma Scale (GCS) = 15.
Management priorities (prehospital phase) for this patient include immediate life-saving interventions and stabilization:
Scene safety: Ensure the environment is safe for rescuers and the patient before initiating care; stop the burning process immediately (e.g., extricate from wreckage, extinguish flames).
Primary survey (ABCDE) with C-spine consideration: Assess Airway, Breathing, Circulation, Disability, and Exposure. Given the mechanism of injury (plane crash), cervical spine immobilization is critical until cleared.
High-flow Oxygen (O₂): Administer 100% humidified oxygen via a non-rebreather mask to address potential hypoxemia and carbon monoxide poisoning, common with inhalation injury. Continuously monitor for signs of impending airway oedema (e.g., stridor, progressive hoarseness, increasing respiratory effort) and prepare for early definitive airway management (intubation) if these signs progress.
Cool burns: Apply cool (not cold or ice) running tap water to the burn wounds for at least 20 minutes as soon as possible to limit burn progression and relieve pain. Avoid applying ice or ice water, which can cause hypothermia and vasoconstriction.
Prevent hypothermia: Actively warm the patient with blankets and administer warmed intravenous (IV) fluids to counteract heat loss from cooling and open wounds, especially given large TBSA burns.
Remove clothing/jewellery: Carefully remove all clothing and jewellery that is not adhered to the skin, as these can retain heat or become constrictive as oedema develops.
Estimate TBSA: Use the Rule of Nines for adults to estimate burn size: head/neck 9%, each arm 9% (9\%\times2=18\% for both arms). This totals approximately 27% TBSA. This estimation guides fluid resuscitation.
Fluid Resuscitation (Modified Parkland Formula): Calculate fluid requirements. For this patient (27\% TBSA, 80 kg), the formula is V = 2\,\text{ml}\times\%TBSA\times\text{body weight (kg)}. So, V = 2\,\text{ml}\times27\times80 = 4320\,\text{ml} over the first 24 hours. Administer half of this volume (2160\,\text{ml}) over the first 8 hours post-injury (from the time of the burn, not arrival at hospital) and the remaining half over the next 16 hours. Fluid titration is guided by meticulous urine output monitoring, aiming for 0.5\,\text{ml}\,\text{kg}^{-1}\,\text{h}^{-1} in adults.
Analgesia: Administer intravenous analgesia (e.g., opioids like fentanyl or morphine) early and titrate to effect to manage severe pain, which can exacerbate shock.
Cardiac monitoring: Initiate continuous cardiac monitoring, especially given the history of a crash, to detect arrhythmias or signs of myocardial strain.
NEWS2 scoring: Utilize the National Early Warning Score 2 (NEWS2) to continuously assess clinical deterioration and guide escalation of care.
Rapid transfer/teleconsultation: Expedite transfer to a specialized burns centre, as the patient meets major burn referral criteria (>10% TBSA and presence of airway burn).
First Aid & Prehospital Management Principles
Stop, Drop, Roll: Instruct individuals whose clothing is on fire to stop movement, drop to the ground, and roll to smother the flames. This extinguishes the source of injury quickly.
Cooling the burn: Apply cool running tap water to the burn for at least 20 minutes, ideally initiated as soon as possible (within 3 hours of injury) to reduce pain, inflammation, and depth of injury. This helps prevent conversion of the zone of stasis. Avoid using ice or ice water, as this can cause vasoconstriction, further tissue damage, and increased risk of hypothermia, especially in large burns or young children.
Maintain normothermia: After initial cooling, actively prevent hypothermia, which can complicate burn management and increase mortality. This involves removing wet clothing, covering the patient with warm, dry blankets, and administering warmed intravenous fluids during prolonged management or transport.
Cover the burn: After adequate cooling, cover the burn wound with a clean, dry, non-adherent dressing (e.g., cling film/plastic wrap applied longitudinally, not circumferentially) to protect it from contamination, reduce pain by covering exposed nerve endings, and minimize heat loss.
Analgesia: Administer appropriate analgesia early and sufficiently, preferably intravenous opioids (e.g., fentanyl, morphine) or ketamine, based on pain severity and patient condition. Pain can contribute to the shock state.
C-spine precautions: Implement cervical spine precautions (e.g., manual inline stabilization, cervical collar) whenever the burn mechanism suggests associated trauma (e.g., falls, motor vehicle accidents, explosions).
Identify inhalation injury: Be highly suspicious for inhalation injury in patients with facial burns, singed nasal hairs, hoarse voice, stridor, soot around the nostrils or in sputum, or altered mental status in a confined space fire. Early management includes high-flow humidified O₂, continuous monitoring for progressive airway oedema, and readiness for early elective intubation to secure the airway before irreversible swelling occurs. Carbon monoxide (CO) monitoring is also critical.
Electrical burns: Prioritize scene safety by ensuring the power source is switched off. Perform a thorough assessment for entrance and exit wounds. Treat arrhythmias (e.g., ventricular fibrillation, asystole) according to Advanced Cardiac Life Support (ACLS) protocols. Initiate continuous cardiac monitoring for at least 24 hours, as arrhythmias can be delayed. Consider possibility of compartment syndrome due to deep tissue damage and the need for additional fluids to prevent rhabdomyolysis-induced kidney injury.
Chemical burns: Rescuer Personal Protective Equipment (PPE) is mandatory. For dry chemicals, brush off powders before initiating irrigation. Immediately and copiously irrigate the affected area with water for an extended period (at least 30-60 minutes, or longer for alkalis) to dilute and remove the chemical. Remove all contaminated clothing. Prevent run-off onto healthy skin. For eye involvement, irrigate copiously with saline, ensuring the unaffected eye is positioned uppermost to prevent contamination.
Bitumen/friction burns: Cool the burn for 20 minutes with water. Do NOT attempt to peel off adherent bitumen, as this can cause further skin stripping. Focus on cooling the bitumen layer. Prevent hypothermia, especially during prolonged cooling.
Estimating Burn Size – Rule of Nines
The Rule of Nines is a rapid method used to estimate the Total Body Surface Area (TBSA) affected by partial and full-thickness burns in adults. It divides the body into anatomical regions, each representing a multiple of 9\%
Head & neck – 9\%
Each arm – 9\% (anterior surface 4.5\%, posterior surface 4.5\%, totaling 9\% per arm)
Anterior trunk (chest and abdomen) – 18\%
Posterior trunk (back and buttocks) – 18\%
Each leg – 18\% (anterior 9\%, posterior 9\%, totaling 18\% per leg)
Perineum (genitalia and groin area) – 1\%
Paediatric modifications: The Rule of Nines must be modified for children due to their different body proportions. Infants and young children have relatively larger heads (approximately 13\% at birth, decreasing with age) and proportionally smaller legs (approximately 14\% each leg in an infant compared to 18\% in adults). For greater accuracy in children, the Lund–Browder chart is preferred as it accounts for age-related changes in body proportions and allows more precise estimation of TBSA.
Fluid Resuscitation – Modified Parkland Formula
Fluid resuscitation using the Modified Parkland Formula is a cornerstone of management for patients with significant partial or full-thickness burns who are at risk of burn shock.
Indication: For adults with burns >10% TBSA or children with burns >5% TBSA.
Equation: The total volume of intravenous fluid needed over the first 24 hours post-burn is calculated as:
\displaystyle V_{24h}=2\,\text{ml}\times\%TBSA\times\text{body weight (kg)}Administration schedule: Half of the calculated total volume must be administered over the first 8 hours from the time of the burn injury (not from presentation to hospital). The remaining half is given over the subsequent 16 hours.
Type of fluid: Isotonic crystalloids, such as Hartmann’s Solution (Lactated Ringer’s Solution in the US), are the fluids of choice. Colloids are generally not recommended in the initial 24 hours due to increased capillary permeability.
Titration to endpoints: Fluid administration must be continuously titrated based on clinical response to prevent both hypovolemia (under-resuscitation) and fluid overload (over-resuscitation), which can lead to complications such as acute respiratory distress syndrome (ARDS) or abdominal compartment syndrome. Key endpoints for titration include:
Urine output: Aim for \ge 0.5\,\text{ml}\cdot\text{kg}^{-1}\cdot\text{h}^{-1} in adults and \ge 1\,\text{ml}\cdot\text{kg}^{-1}\cdot\text{h}^{-1} in children.
Other parameters: Heart rate, blood pressure, capillary refill time, and mental status are also monitored.
Example: For an 80 kg adult with 20% TBSA burns, the 24-hour fluid requirement is 2\times20\times80=3200\,\text{ml}. This means 1600\,\text{ml} should be administered in the first 8 hours, and the remaining 1600\,\text{ml} over the next 16 hours.
Burn Shock Pathway
Burn shock is a form of hypovolemic shock unique to severe burn injury, resulting from massive fluid and electrolyte shifts that lead to circulatory collapse if untreated.
Trigger: The initial thermal injury triggers a widespread systemic inflammatory response, leading to the release of a cascade of inflammatory mediators (e.g., histamine, bradykinin, prostaglandins, interleukins, TNF-\alpha).
Microvascular changes: These mediators cause significant increases in microvascular permeability (leakiness) primarily in the post-capillary venules, both in the burned and unburned tissues. Simultaneously, there is an increase in hydrostatic pressure within the capillaries due to vasodilation.
Intravascular fluid loss & oedema: The combined effect of increased microvascular permeability and hydrostatic pressure leads to a massive shift of plasma proteins (especially albumin) and fluid out of the intravascular space into the interstitial space. This results in widespread edema, reducing effective circulating blood volume.
Haemodynamic consequences: The reduction in intravascular volume (hypovolaemia) directly leads to a decreased venous return (preload) to the heart and consequently a significant reduction in cardiac output (CO). The body attempts to compensate by increasing systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR) through vasoconstriction. However, this compensatory mechanism is often insufficient, leading to inadequate tissue perfusion and cellular hypoxia, defining the state of shock.
Goal of management: The primary goal of early and aggressive fluid resuscitation is to quickly restore adequate tissue perfusion and oxygen delivery to vital organs while carefully preventing excessive fluid administration, which can lead to severe edema-related complications (e.g., compartment syndrome, pulmonary edema).
Referral / Trauma Centre Criteria (WA example)
Immediate referral to a specialized burns centre or a major trauma centre with burn capabilities is critical for optimal outcomes in patients meeting specific criteria. (Examples based on Western Australia guidelines):
Adults >10% TBSA partial or full thickness burns.
Children >5% TBSA partial or full thickness burns.
Full thickness burns >5% TBSA in any age group, as these require surgical intervention.
Burns involving special areas which are anatomically or functionally critical: face, hands, feet, perineum, genitalia, major joints, or any circumferential burns of limbs or the chest (due to risk of vascular compromise or restricted ventilation).
Presence of inhalation injury, even without extensive skin burns, due to high risk of airway compromise and pulmonary complications.
Electrical or chemical burns, which often have hidden deeper tissue damage or complex management requirements beyond simple thermal burns.
Concomitant trauma (e.g., fractures, head injury, major blunt trauma) where the burn is one of multiple significant injuries.
Extremes of age: Infants, very young children, and elderly patients (generally >60 years old) have higher morbidity and mortality due to reduced physiological reserves.
Pregnancy as a pre-existing condition.
Patients with pre-existing illness that may complicate management or increase mortality (e.g., cardiac, pulmonary, renal, hepatic insufficiency, diabetes, immunocompromised status).
Suspected non-accidental injury (child abuse or neglect) as the cause of the burn, requiring specialized safeguarding and investigation.
Special Situations
Certain burn characteristics or associated injuries necessitate unique management approaches due to their potential for severe complications:
Circumferential burns: Burns that completely encircle a limb or the torso. As edema develops beneath the constricting eschar (hardened burn tissue), these burns pose a significant risk of vascular compromise to the distal limb (leading to ischemia and necrosis) or restricted ventilation if on the chest. Frequent monitoring of distal pulses (e.g., with Doppler ultrasound) and capillary refill is crucial. Urgent surgical intervention, an escharotomy (a full-thickness incision through the eschar), may be required to release the constricting band and restore circulation or chest wall compliance.
Eyes: Chemical burns to the eyes require immediate and copious irrigation with water or saline for at least 20-30 minutes. Thermal burns to the eyes should also be irrigated gently. Prompt ophthalmology referral is essential for all eye burns to assess corneal damage, vision impairment, and provide specialized care.
Compartment syndrome: A severe complication, particularly common in electrical burns or high-voltage injuries due to extensive deep tissue damage and resultant muscle swelling. It involves increased pressure within a confined fascial compartment, compromising blood flow and leading to nerve and muscle ischemia. Clinical signs include pain disproportionate to the injury, pallor, paraesthesia, pulselessness, and poikilothermia (the 5 Ps). Compartment pressures should be measured, and if elevated, an emergency fasciotomy (surgical incision through the fascia) is required to relieve pressure and prevent irreversible tissue damage.
Burns in Children – Key Differences
Managing burns in children requires specific considerations due to significant physiological and anatomical differences compared to adults:
Thinner skin, larger BSA:mass ratio: Children have thinner skin layers, making their burns proportionally deeper and more severe for a given exposure time. Their larger body surface area (BSA) to body mass ratio leads to significantly increased rates of fluid and heat loss through burn wounds.
Rapid development of hypothermia & hypoglycaemia: Due to thinner skin, less subcutaneous fat, and higher metabolic rates, children lose heat more rapidly and are highly susceptible to hypothermia. They also have smaller glycogen stores and higher glucose utilization, making them prone to faster development of hypoglycaemia. Therefore, maintaining warmth and regular monitoring of blood glucose levels are critical.
Fluid resuscitation threshold lower; maintenance fluids: Children require fluid resuscitation for smaller TBSA burns (>5% TBSA compared to >10% in adults). Importantly, children also require concurrent administration of maintenance IV fluids (e.g., D5W 0.45% normal saline) in addition to their burn resuscitation fluids to meet basal metabolic needs and prevent hypoglycaemia, especially during prolonged fasting or transport.
Consider non-accidental injury (NAI): Burns are a common form of child abuse. Healthcare providers must remain vigilant for signs suggestive of NAI, such as:
Geometric shapes or sharp lines: Indicating forced immersion (e.g.,