The 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.
|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|
For more information, please see Skin Anatomy, Physiology, and Healing Process.
When treating a burns patient, it is crucial to understand tissue healing. Your knowledge of tissue healing, combined with the information gathered from your assessment, will influence clinical decisions, including when to rest, exercise, stretch and what level to strengthen during the recovery period. Please note that these timescales are variable, depending on the size of the burn, surgical intervention and any other complicating factors. Clinical reasoning is essential when applying the following in practice.
|Stage||Timescale||Process||Signs and Symptoms||Treatment|
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 an influx of inflammatory mediators and white blood cells. Increased capillary permeability. Exudate leaks into the tissues. Pus may be produced.||Redness, heat, swelling, pain||Reduce heat and oedema and pain.
Prevent infection and disruption of the wound.
Useful: Immobilisation, positioning and splinting.
|Proliferation (Fibroplasia)||Begins day 3- 5.
Lasts 2-6 weeks.
|Fibroblasts synthesize collagen. Laid down
|Moist red raised tissue over wound||Early: Positioning and
Later: Gentle stress with splinting and exercise.
Reduce oedema and prevent contractures.
|Remodelling (Maturation)||Begins week 4-6.
Lasts up to 2 years.
|Synthesis of collagen balanced by degradation. Organisation of collagen fibres along the lines of stress.||Wound closure. Red and raised scar, progresses to flat pale and pliable scar. Scar tissue tightens.||Optimise function, splinting, positioning, exercise, stretching, strengthening.|
Tissue healing process following burn injury
For more information on the healing process, please see:
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. Excess cytokines, chemokines and other inflammatory mediators are released, which results in extensive inflammatory reactions within a few hours of injury. Depending on the size of the burn injury, the initial response 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
- Patient-related factors
- Pre-existing chronic medical conditions
- Drug or alcohol intoxication
- Timing of presentation to care
This inflammatory response leads to rapid oedema formation This is caused by:
- Increased microvascular permeability
- Increased hydrostatic microvascular pressure
- 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 catalysing 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.
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:
- Immunological Changes
- Oedema Formation
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% TBSA 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, this is thought to be caused by an increase of vasoconstrictors in the body. The damage to the cardiovascular system can cause effects for up to two years post injury.
Compromised cardiac function results in:
- Organ hypoperfusion
- Impaired peripheral microcirculation
- Extension of the burn zone
- Reduced resistance to bacterial infection at the wound site.
- 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,
- Hypovolemic shock is treated by replacing the fluid and/or blood, usually done through an IV line, in addition to treating the cause.
- This is caused by:
- Blood loss from bleeding, it can be bleeding from a cut, or internal bleeding.
- Loss of blood plasma due to severe burns, this happens due to loss of skin and damage to the blood vessels.
- Dehydration ie, diarrhea or vomiting (loss of a lot of body fluids may lead to a drop in the amount of circulatory blood).
For more information on Hypovolemic Shock, please see Burn Shock.
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 a heat injury to airway structures includes extensive swelling of the the tongue, epiglottis, and aryepiglottic folds which causes an accompanying obstruction.
- Chemical Injury to the Lower Airway
- Most commonly, 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 due to tissue hypoxia, metabolic acidosis, decreased oxygen supply to the brain and decreased metabolism.
For more information, please read Inhalation Injury
3. Effect on the Renal System[edit | edit source]
Early kidney injury is due to:
- Low blood volume
- Inflammatory mediators
- Increased release of protein in the bloodstream
- Extensive tissue damage
- Medications that are toxic to the kidneys
The renal system complications are caused by the alterations in the cardiovascular system. Blood flow to the kidneys is decreased due to hypervolemia and decreased cardiac output. This marks the beginning of kidney failure. This can be prevented by conducting an accurate assessment for the correct fluid recusitation to be administered. The rehabilitation team should always keep an eye out for decreased urine output as this is an early sign of renal compromise.
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
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.
- Increased body temperature
- Increased oxygen and glucose consumption
- Increased CO2 and minute ventilation
- Increased heart rate for up to 2 years post burn
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[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.
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
- McCann C, Watson A, Barnes D. Major burns: Part 1. Epidemiology, pathophysiology and initial management. BJA education. 2022 Mar 1;22(3):94-103.
- Glassey N. Physiotherapy for burns and plastic reconstruction of the hand. 2004.
- Jeschke MG. Pathophysiology of burn injury. Springer International Publishing; 2021.
- Kumar R, Keshamma E, Kumari B, Kumar A, Kumar V, Janjua D, Billah AM. Burn Injury Management, Pathophysiology and Its Future Prospectives. Journal for Research in Applied Sciences and Biotechnology. 2022 Oct 31;1(4):78-89.
- Noreen S, Maqbool I, Ijaz S. Skin Burns: Pathophysiology, types and Therapeutic Approaches. Pathophysiology. 2010;1(3).
- Martyn J, Wilson RS, Burke JF. Right ventricular function and pulmonary hemodynamics during dopamine infusion in burned patients. Chest. 1986 Mar 1;89(3):357-60.
- Williams FN, Herndon DN, Suman OE, Lee JO, Norbury WB, Branski LK, Mlcak RP, Jeschke MG. Changes in cardiac physiology after severe burn injury. Journal of burn care & research. 2011 Mar 1;32(2):269-74.
- Galeiras R. Smoke inhalation injury: a narrative review. Mediastinum. 2021;5.
- Masch JL, Bhutiani N, Bozeman MC. Feeding during resuscitation after burn injury. Nutrition in Clinical Practice. 2019 Oct;34(5):666-71.
- Herndon DN, Barrow RE, Rutan TC, Minifee PA, Jahoor FA, Wolfe RR. Effect of propranolol administration on hemodynamic and metabolic responses of burned pediatric patients. Annals of surgery. 1988 Oct;208(4):484.
- Noorbakhsh SI, Bonar EM, Polinski R, Amin MS. Educational Case: Burn Injury—Pathophysiology, Classification, and Treatment. Academic pathology. 2021 Nov 26;8:23742895211057239.
- Grisbrook TL, Elliott CM, Edgar DW, Wallman KE, Wood FM, Reid SL. Burn-injured adults with long term functional impairments demonstrate the same response to resistance training as uninjured controls. Burns. 2013 Jun 1;39(4):680-6.
- Jeschke MG, Mlcak RP, Finnerty CC, Norbury WB, Gauglitz GG, Kulp GA, Herndon DN. Burn size determines the inflammatory and hypermetabolic response. Critical care. 2007 Aug;11(4):1-1.
- Hettiaratchy S, Dziewulski P. ABC of burns: Introduction. BMJ: British Medical Journal. 2004 Jun 6;328(7452):1366.
- Hettiaratchy S, Dziewulski P. Pathophysiology and types of burns. Bmj. 2004 Jun 10;328(7453):1427-9.
- Kramer GC, Lund T, Beckum OK. Pathophysiology of burn shock. Total Burn Care. Philadelphia, Pennsylvania: Saunders Elsevier. 2007:93.