Physiology of Burns

Original Editor - Carin Hunter based on the course by [TUTOR LINK/ TUTOR NAME]
Top Contributors - Carin Hunter, Jess Bell and Kim Jackson

Pathophysiology of Burns[edit | edit source]

A burns injury depending on the severity of the injury can result in both local and debilitating systemic effects on all other organs and systems distant to the burn area.

Skin Overview[edit | edit source]

Skin is a cutaneous membrane which covers the surface of the  body. It is the largest organ of the body in  terms of weight and surface area.

Table 1. Illustrating the layers of the skin
Figure 1. Layers of the Skin
For more information on the skin, please see Skin
Epidermis Superficial layer Provides a waterproof barrier and contributes to skin tone Composed of epithelial tissue Avascular
Dermis Deeper, thicker layer Connective tissue Contains blood vessels, nerves, glands and hair follicles Highly vascularised
Hypodermis Deepest layer Storage for fat/ insulation

Attaches to underlying facia

Areolar and adipose tissue Contains large blood vessels

Healing Process[edit | edit source]

When treating a burns patient the knowledge of tissue healing is beneficial to the patient and to the possible outcomes. This will influence the decision of when to rest, exercise, stretch and what level to strengthen. These timescales are variable according to the size of the burn, surgical intervention and any complicating factors.  Clinical reasoning is essential when applying the following in practice.




The process of the wound being closed by clotting

Begins when blood leaks out of the body, then blood vessels constrict to restrict the blood flow The platelets aggregate and adhere to the sub-endothelium surface within seconds of the rupture of a blood vessel's epithelial wall.

After that, the first fibrin strands begin to adhere in about sixty seconds.

As the fibrin mesh begins, the blood is transformed from liquid to gel through pro-coagulants and the release of prothrombin.

The formation of a thrombus or clot keeps the platelets and blood cells trapped in the wound area

Reduce heat and  oedema and pain.

Prevent infection and disruption of  wound.

Useful: Immobilisation,  positioning and splinting.

Inflammation 0-5 days Vasoconstriction  

followed by  

vasodilatation and influx  of inflammatory  

mediators and WBCs.  Increased capillary  

permeability. Exudate  leaks into tissues. Pus  may be produced.

Redness, Heat, Swelling,  Pain Reduce heat and  oedema and pain.

Prevent infection and disruption of  wound.

Useful: Immobilisation,  positioning and

splinting. positioning,  


Proliferation  (fibroplasia) Begins day 3- 5.

Lasts 2-6 weeks.

Fibroblasts synthesize  collagen. Laid down  


Angiogenesis continues.

Moist red raised tissue  over wound Early: Positioning  and  


Later: Gentle  

stress with splinting and exercise.

Reduce oedema and prevent  


Remodelling  (maturation) Begins week  4-6.

Lasts up to 2  years.

Synthesis of collagen  balanced by degradation.  Organisation of collagen  fibres along lines of  


Wound closure

Scar red and raised  

progresses to flat pale and  pliable. Scar tissue  


Optimise function Splinting





Table 2 Tissue healing process following burn injury (Glassey 2004)

Figure 2. The 4 Stages of Wound Healing

For more information on the Healing process please read:

Systemic Response to Burns[edit | edit source]

In severe burn injury, >30% TBSA complex reaction occurs both from the burn area and in the area distant to the burn. Cytokines, chemokines and other inflammatory mediators are released in excess resulting in extensive inflammatory reactions within a few hours of injury. The initial response depending on the size of the burn injury is similar to the inflammation that is triggered after tissue destruction such as trauma or major surgery. Different factors contribute to the magnitude of the host response, they include: burn severity (percentage TBSA and burn depth), burn cause, inhalation injury, exposure to toxins, other traumatic injuries, and patient-related factors such as age, pre-existing chronic medical conditions, drug or alcohol intoxication, and timing of presentation to medical aid. This inflammatory response leads to rapid oedema formation which is caused by increased microvascular permeability, increased hydrostatic microvascular pressure, vasodilation, and increased extravascular osmotic activity. These reactions are due to the direct heat effect on the microvasculature and to the chemical mediators of inflammation. Vasodilation and increased venous permeability at the early stage of the injury are caused by the release of histamine. Also, prostaglandin is released by damage to the cell membranes which causes the release of oxygen-free radicals released from polymorphonuclear leucocytes which activate the enzymes catalyzing the hydrolysis of prostaglandin precursor. These hemodynamic changes lead to continuous loss of fluid from the blood circulation causing increased haematocrit levels and a rapid fall in plasma volume, leading to a decrease in cardiac output and hypoperfusion on the cellular level. Burn shock occurs if fluid loss is not adequately restored. (Evers et al 2010)

In addition to the local effects of a burn, a severe burn injury has an effect on different organs and systems in the body. The effects include:

  1. Cardiovascular
  2. Respiratory
  3. Renal
  4. Endocrine
  5. Metabolic
  6. Immunological Changes
  7. Oedema Formation

Burns are a series of pathophysiological changes that start from heat injury. Accompanied by heat damage to the skin and soft tissues, a large amount of inflammatory mediators is released into circulation. Changes in histamine, bradykinin, and platelet-activating factor (PAF), cytokines such as vascular endothelial growth factor (VEGF), metabolic factors such as ATP and activated neutrophils all affect the body’s vascular permeability (5). The essence of burn shock is the rapid and extensive fluid transfer in burn and non-burn tissues (6). After severe burns, the local and systemic vascular permeability increase, causing intravascular fluid extravasation, leading to a progressive decrease in effective circulation volume, an increase in systemic vascular resistance, a decrease in cardiac output, peripheral tissue edema, multiple organ failure, and even death (7,8). The increase in vascular permeability is characterized as a significant change in the permeability of capillaries and post-capillary venules. In other words, the normal physiological barrier function of endothelial cells (ECs) is destroyed

1. Effect on the Cardiovascular System[edit | edit source]

The initial response to a burn injury of more than 30% is shock which results in a decrease in cardiac output and metabolic rate. This decrease in cardiac output, initially, is caused by hypovolemia and a decrease in the venous return. There is also a decrease in contractibility of the muscles in the heart, thought to be cause by an increase of vasoconstrictors in the body. Compromised cardiac function results in organ hypoperfusion, impaired peripheral microcirculation, burn zone extension, and reduced resistance to bacterial infection at the wound site. The damage to the cardiovascular system can cause effects for up to two years post injury.

Hypervolemia is a decrease in blood volume. Hypovolemic Shock is when there is a loss of approximately 1/5 or more of the normal amount of blood in the body. It is caused by:

  1. Blood loss from bleeding, it can be bleeding from a cut, or internal bleeding.
  2. Loss of blood plasma due to severe burns, this happens due to loss of skin and damage to the blood vessels.
  3. Dehydration ie, diarrhea or vomiting (loss of a lot of body fluids may lead to a drop in the amount of circulatory blood).

Hypovolemic shock is treated by replacing the fluid and/or blood, usually done through an IV line, in addition to treating the cause.

For more information on Hypovolemic Shock, please see Burn Shock.

(Kramer GC, Lund T, Beckum O. Pathophysiology of burn shock and burn edema. In: Herndon DN, editor. Total Burn Care. Philadelphia: Saunders Elsevier; 2007. pp. 93–106. [Google Scholar]

9. Guyton AC. Cardiac output, venous return, and their regulation. In: Guyton AC, editor. Textbook of Medical Physiology. Philadelphia: Saunders; 1981. pp. 281–2.) 9 The initial phase involves both right and left heart failure and depression in contractility, thought to be mediated by circulating vasoconstrictors.

10 (Martyn J, Wilson RS, Burke JF. Right ventricular function and pulmonary hemodynamics during dopamine infusion in burned patients. Chest. 1986;89:357–60. [PubMed] [Google Scholar] 11. Adams HR, Baxter CR, Izenberg SD. Decreased contractility and compliance of the left ventricle as complications of thermal trauma. Am Heart J. 1984;108:1477–87.

, 11 The upregulation of catecholamines and other catabolic agents, such as glucagon, and cortisol, induce a hyperdynamic cardiovascular response, and increased oxygen consumption.

1Asch MJ, Feldman RJ, Walker HL, et al. Systemic and pulmonary hemodynamic changes accompanying thermal injury. Ann Surg. 1973;178:218–212

1Harrison TS, Seaton JF, Feller I. Relationship of increased oxygen consumption to catecholamine excretion in thermal burns. Ann Surg. 1967;165:169–72.3 This response is unparalleled to any other forms of injury. While derangements in pulmonary and systemic physiology are known and well described in the literature12,

14,Linares HA. A report of 115 consecutive autopsies in burned children: 1966-80. Burns Incl Therm Inj. 1982;8:263–70. [PubMed] [Google Scholar]

15. Herndon DN, Barrow RE, Rutan TC, et al. Effect of propranolol administration on hemodynamic and metabolic responses of burned pediatric patients. Ann Surg. 1988;208:484–92. 15;

2. Effect on the Respiratory System[edit | edit source]

The effect of burns on respitation is mainly attributed to the following three complications:

  • Heat Injury to the Upper Airway

The result of the injury to these airway structures include extensive swelling of the the tongue, epiglottis, and aryepiglottic folds and accompanying obstruction.

  • Chemical Injury to the Lower Airway

Following smoke inhalation, inflammatory mediators are released in the lungs leading to bronchoconstriction, pulmonary oedema and adult respiratory distress syndrome (ARDS).

  • Systemic Toxicity

Inhalation of chemicals, cytotoxic liquids, fumes, mist and gases can cause systemic toxic changes. Smoke can combine with these toxins and cause increased mortality by promoting tissue hypoxia, metabolic acidosis, and reducing cerebral oxygen consumption and metabolism.

For more information, please read Inhalation Injury

3. Effect on the Renal System[edit | edit source]

Early kidney injury happens because of low blood volume, inflammatory mediators, the release of protein into the bloodstream, extensive tissue destruction, and giving medications that are toxic to the kidneys.

The renal system is affected following alterations in the cardiovascular system. Due to hypervolemia and decreased cardiac output the kidneys get less and less blood flow to them, starting the process of kidney failure. But proper attention paid to the amount of fluid reaching the heart can make a difference in the outcome.   Adding to the presence of decreased cardiac output, is the presence of high circulating amounts of tumor necrosis factor released by the muscle cells due to the burn. An early sign of renal compromise or failure is decreased urine output. Failure to promptly and adequately manage these cases may lead to acute tubular necrosis, renal failure, and mortality.

4. Effect on the Endocrine System[edit | edit source]

The endocrine system is made-up of glands in the body, which secrete hormones. Following a burns trauma, there are distinct responses in the endocrine system.

Trauma can affect the HPA Axis (Hypothalamic-pituitary-adrenal axis), which controls the interaction between the hypothalamus, pituitary gland, and adrenal glands. The hypothalamus and pituitary gland are located just above the brainstem, while the adrenal glands are found on top of the kidneys. Firstly, due to the burn injury, individuals commonly have an elevated sympathetic drive. This is due to an increase in the release of cortisol and glucagon. These hormones effect the metabolic system, mentioned below. Prolonged excess cortisol can result in hypercortisolemia. Which is associated with infection rates in post burn patients and lengthened durations of severe infection. Secondly, oxytocin production is decreased, which is associated with empathy and love. This can cause long term side effects emotionally for the individual.

5. Effects on Metabolic System[edit | edit source]

The metabolic state is initially suppressed by the effects of acute shock. Initial effects to the body following a burn can cause:

  • Impaired gastrointestinal motility
  • Impaired digestion and absorption
  • Increased intragastric pH
  • Feeding difficulties, which exacerbate effects of hyper metabolism (Evers et al 2010)

Hypermetabolism begins approximately five days post burn. Hypermetabolism is when the basal metabolic rate increases up to three times its original rate. The cause of hypermetabolism is not entirely defined and appears very complex and is most likely activated and sustained by stress induced hormonal releases and inflammation. The decreased perfusion among the organs in the abdominal cavity, necessitates early and aggressive enteral feeding to decrease catabolism and maintain gut integrity. It causes muscle wasting, mucosal atrophy, reduced absorptive capacity, and increased surface permeability. Effects can be seen for up to two years post burn.

Hypermetabolism causes:

  • Increased body temperature
  • Increased oxygen and glucose consumption
  • Increased CO2 and minute ventilation
  • Increased heart rate for up to 2 years post burn  

(Jeschke et al 2007; Grisbrook et al 2012a; Hurt et al 2000)

Catabolism occurs when food is digested and the large, complex molecules in the body are broken down into smaller, simple ones to be used as energy.

6. Immunological Changes: (Hettiaratchy and Dziewulski 2004)[edit | edit source]

As mentioned above, following a burn injury, individuals commonly have an elevated sympathetic drive, causing the release of cortisol. Prolonged excess cortisol can result in hypercortisolemia, which is associated with infection rates in post burn patients and lengthened durations of severe infection.

Patients also suffer from a high risk of  infection while wounds are open.

7. Oedema formation[edit | edit source]

A burn wound causes an increased inflammatory response. Blood tests show an increased level of CRP (C-reactive protein) following a burn injury. This protein is made by the liver and assists the inflammation process. CRP causes increased inflammaorty symptoms of When body tissues are burned, histamine is released from mast cells, act on ECs, fibroblasts, and smooth muscle cell tissues, exert a strong vasodilator effect, and can significantly increase the permeability of microvascular endothelium

Why do burns increased capillary permeability?

The major reasons for this systemic microvascular leakage in burns include an increase in vascular permeability triggered by inflammatory mediators and the increase of vascular hydrostatic pressure caused by vessel dilation.

o Capillary permeability is increased

o leads to loss of intravascular proteins and fluids to the interstitial compartment ∙ Hypovolemia

o Secondary to oedema and rapid fluid loss from surface of wound

∙ Peripheral and splanchnic vasoconstriction occurs

Complications of Healing in Burn Patients[edit | edit source]

  1. Oedema
  2. Skin Complications
    1. Hypertrophic Scarring
    2. Keloid Formation
    3. Contractures
  3. Burn Shock
  4. Burn Associated Pain
  5. Wound Infection
  6. Orthopedic Complications
    1. Soft Tissue Injury
    2. Fracture
    3. Joint Contracture
    4. Heterotophic Ossification
    5. Compartment Syndrome

For more information please see:

1. Oedema[edit | edit source]

Oedema may increase post burn for up to 36 hours  

∙ Increased vascular permeability which occurs during the inflammatory response  ∙ Exacerbated if the burn is severe enough to warrant fluid resuscitation (Weinzweig  and Weinzweig 2004; Kamolz et al 2009).

Post severe burn

∙ The resulting scar (eschar) is inflexible

∙ Does not allow skin expansion  

∙ Tissue beneath continues to expand as  

oedema increases  

∙ Rapid increase in compartment pressure

∙ May result in circulatory compromise/nerve  Damage/ necrosis of distal muscles.  

Figure 5. Hand escharotomy (Weinzweig  and Weinzweig 2004)

∙ Severe cases require a surgical procedure known as an escharotomy o Splits the scar and allows for the expansion of the tissues beneath, relieving  pressure (Kamolz et al 2009,Weinzweig and Weinzweig 2004)..


Recognising Vascular Insufficiency: Where oedema and compartment syndrome is causing  vascular insufficiency, the following symptoms may be present

∙ Pain

∙ Loss of sensation

∙ Pale white skin on the dorsum of the hand/ distal to eschar

∙ Loss of peripheral pulses (may also be caused by hypovolaemia or insufficient fluid  resuscitation) (Kamolz et al, 2009)

As compartment syndrome requires immediate attention, all health care professionals must  remain vigilant.

Oedema and the Hand:  

Oedema in the hand results in the position of intrinsic minus (Kamolz et al 2009) 

∙ Wrist flexion

∙ MCP extension

∙ PIP/DIP flexion

MCP joint extension primary position assumed

∙ Joint contact areas minimised  

∙ Joint capsules and ligaments lax

∙ Therefore, in this position, the joint accommodates the maximum amount of intra articular fluid

Figure 6 Intrinsic Minus hand  position (American Society for  Surgery of the hand 2013)

∙ Increases tension in finger/wrist flexors , relaxes extensors

Therefore, PIP/DIP/ Wrist flexion follow (Weinzweig and Weinzweig 2004) ∙ Joint predisposed to contracture

∙ May have significant functional implications

∙ Even after wound healing appears complete, sub-acute and chronic oedema may be  caused by scar maturation and contraction: therefore, oedema management is a long  term concern.


2. Skin Complications[edit | edit source]

2.1 Hypertrophic Scarring[edit | edit source]

Hypertrophic scars are a common complication of burn injuries. A healing wound requires a  balance of several opposing reactions

∙ Degradation of necrotic tissue/proliferation of new cells

∙ Building up/ breaking down of collagen

∙ Creating/controlling of new blood supplies (Linares et al 1996).  

Disequilibrium of any of these processes may result in abnormal scarring. There is a high risk  of a scar becoming hypertrophic if early wound closure is not achieved. Estimates for optimal  closure time vary from 10 days (ANZBA 2007) to 21 days (Procter 2010). Hypertrophic  scarring is accompanied by:

∙ Exaggerated angiogenesis with high blood flow

∙ Increased deposition of collagen

∙ High rates of contraction

∙ Pruritus (Itch)

∙ Dryness

∙ Lack of pliability. (Procter 2010).  

∙ The orientation of new collagen bundles remain  


∙ haphazard structure persists for several months post  

Figure 7. Hypertrophic scar on  dorsum of hand (Procter 2010)


∙ Some degree of chronic inflammation may also persist.

Identifying Hypertrophic Scarring

(Linares et al 1996).

∙ Shapes and sizes depend on location on the body and nature of injury ∙ Edges are raised and end abruptly

∙ Initially may be red or pink in colour

o Blanch over time, as the scar matures

o Never returns to original colour/texture

∙ May exceed the limits of the original injury (Keloid scars).  (Linares et al 1996; Procter 2010)

2.2 Keloid Formation[edit | edit source]
2.3 Contractures[edit | edit source]

3. Burn Shock[edit | edit source]

For more information, please read Burn Shock

4. Burn Associated Pain[edit | edit source]

“The quality of outcome must be worth the pain of survival”

~Prof FM Wood, James Laing Memorial Essay, 1995

∙ 84% of major burn patients suffer “severe or excruciating pain”

∙ 100% suffer daily pain

∙ 92% are woken at night with pain (ANZBA 2007)

1.71 Types of Pain in Burns: (Summer et al 2007; Richardson and Mustard 2009)

Procedural pain: (Primary mechanical hyperalgesia): intense burning and stinging that  continues to a lesser degree, but may be accompanied by intermittent sharp pain for minutes  or hours following dressing changes or physiotherapy/occupational therapy. Throbbing,  excruciating pain may be associated with positioning of burned extremities (i.e. positioned  below the level of the heart); this is thought to be related to pressure associated with  inflamed, oedematous tissue. Procedural pain is the most intense and most undertreated pain associated with burn injuries.

Procedural pain and associated pain anxiety: research indicates pain-anxiety increases over  time in burn injured patients. Strong correlations have been established between pain,  physiological distress and physical and psychological outcomes in both adults and children.  

Background pain: patients with high anxiety have increased levels of background pain.  There is a wide variability in the pain intensity following injury. Background pain is  characterised by prolonged duration, relatively constant mild-moderate intensity pain. The  pain has been described as continuous burning or throbbing, present even when the patient is  relatively immobile. This pain is best treated with regularly scheduled analgesics.

Breakthrough pain: transient worsening of pain frequently associated with movement.  Patients also report spontaneous pain that may be related to changing mechanisms of pain,  over time or inadequate analgesia. The pain can be described as stinging, shooting, pricking  or pounding. Pain following movement can be associated with primary mechanical  hyperalgesia, but most care providers for those with burns consider pain with movement to be  breakthrough pain. Breakthrough pain can be much worse following periods of immobility,  particularly if skin over joints is affected.


For optimal analgesia, it is recommended that patients are assessed for each type of pain  separately and repeatedly throughout the course of the recovery.  




Substance abuse

Drugs factors: Timing


Side effects

Burn wound: Dressing type Dressing tension Infection


Donor sites

Personality type Context: Expectations


Past experience


Rapport with staff










Figure 8. Factors influencing the patient’s perception of pain from a burn wound. (Richardson and Mustard 2009)


1.72 Pain Mechanisms

(Richardson and Mustard 2009)

The pain mechanisms associated with the inflammation process post burn are:

∙ Primary hyperalgesia

∙ Secondary hyperalgesia

∙ Neuropathic pain

∙ Chronic pain/Central Sensitisation

Other factors to consider in pain are:

1.73 Pain intensity: As the inflammation recedes, the quality of the pain may change. The  reporting of pain intensity varies widely and is reported highest in areas of upper/mid-dermal  skin loss, such as areas of skin donation and decreases with wound closure. Infection may  result in increased pain again following revival of the inflammatory process. Growth of new  tissue is associated with paraesthesia and local discomfort. The healed areas show enhanced  mechanical hyperalgesia following subsequent injury.  

1.74 Anxiety and pain experience: result in increased pain perception. The pain experience  will alter according with the burn treatment. Surgery/debridement/excision of the burn will  alter the depth of the burn injury. Covering the burn with grafts or synthetic dressings  typically reduce pain, with the harvest site often being more painful than the burn injury  itself. Poor pain management during therapeutic procedures is associated with poor  compliance with treatment and post-traumatic stress disorder. It then increases anxiety and  worsens the pain experience in subsequent treatment.

5. Wound Infection[edit | edit source]

6. Orthopedic Complications[edit | edit source]

6.1 Soft Tissue Injury[edit | edit source]
6.2 Fracture[edit | edit source]
6.3 Joint Contracture[edit | edit source]
6.4 Heterotophic Ossification[edit | edit source]
6.5 Compartment Syndrome[edit | edit source]

References[edit | edit source]