Systemic Resonse to Burns
Top Contributors - Carin Hunter, Jess Bell and Kim Jackson
Pathophysiology of Burns
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.
Cutaneous membrane which
covers the surface of the
body
∙ Largest organ of the body in
terms of weight and surface
area
∙ Epidermis
o Superficial layer
o Composed of epithelial tissue o Avascular
Figure 2. Layers of the skin (MD 2009)
o Deepest layer (Stratum Basale) contains ‘Stem cells’
▪ Capable of regeneration
▪ New skin cannot regenerate if injury destroys a large portion of this layer
∙ Dermis
o Deeper, thicker layer
o Connective tissue
o Contains blood vessels, nerves, glands and hair follicles
∙ Subcutaneous layer
o Areolar and adipose tissue
o Storage for fat/ insulation
o Contains large blood vessels
o Attaches to underlying facia
▪ Connective tissue overlying muscle and bone
An in depth knowledge of pathophysiology of burns, and their effects both locally and systemically is necessary to ensure effective management of a patient with a burn injury.
1.61 Normal Healing[edit | edit source]
∙ Use knowledge of tissue healing to decide when rest is required and when exercise, stretching and strengthening will be beneficial to the patient.
∙ Timescales are variable according to the size of the burn and surgical intervention. Clinical reasoning is essential when applying the following in practice.
STAGE | TIMESCALE | PROCESS | SIGNS AND
SYMPTOMS |
TREATMENT |
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. (immobilisation, positioning, splinting) |
Proliferation (fibroplasia) | Begins day 3- 5. Lasts 2-6
weeks. |
Fibroblasts synthesize collagen. Laid down
haphazardly. Angiogenesis continues. |
Moist red raised tissue over wound | Early: positioning and
immobilisation Later: gentle stress (splinting, exercise) Reduce oedema and prevent contracture |
Remodelling (maturation) | Begins week 4-6.
Lasts up to 2 years. |
Synthesis of collagen balanced by degradation. Organisation of collagen fibres along lines of
stress. |
Wound closure
Scar red and raised progresses to flat pale and pliable. Scar tissue tightens. |
Optimise function Splinting
Positioning Exercise Stretching Strengthening. |
Table 2 Tissue healing process following burn injury (Glassey 2004)
Systemic Response[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.
Besides burn shock, the burn injury can result in other types of injury which include inhalation injury. Inhalation injury is caused by heat or inhalation of smoke or chemical products of combustion leading to various degrees of damage. Usually, it is present in conjunction with the burn and can range from a minor injury to a severe injury. Inhalation injury can be divided into three types: systemic toxicity due to products of combustion (carbon monoxide (CO) and cyanide poisoning); upper airway thermal injury; and lower (bronchi and distal) airway chemical injury. Patients can sustain all of these in a closed-space fire. CO poisoning, more accurately categorised as a systemic intoxication, is easily diagnosed from the serum carboxyhaemoglobin level determined as part of the arterial blood gas measurement at hospital admission.
In addition to the effects above, a severe burn injury has an effect on different organs and systems in the body. The effects include:
Effect on the Cardiovascular System
The initial response to a severe burn injury is characterised by hypovolemia and reduced venous return. This concomitantly leads to a decrease in cardiac output, increased heart rate, and peripheral resistance. In addition to the cardiac dysfunction, pulmonary resistance increases causing an increase in right and left-ventricular work-load.
Effect on the Respiratory System
Following smoke inhalation, inflammatory mediators are released in the lungs leading to bronchoconstriction and adult respiratory distress syndrome.
Effect on the Renal System
The renal system is affected following alterations in the cardiovascular system. Renal blood flow and glomerular filtration rate are reduced secondary to hypovolemia, diminished cardiac output, and the effects of angiotensin, vasopressin and aldosterone. These alterations are usually translated in the form of oliguria as an early sign of renal compromise. Failure to promptly and adequately manage these cases may lead to acute tubular necrosis, renal failure, and mortality.
Effect on the Liver
There is substantial depletion of the hepatic proteins, alterations in serum levels of triglycerides and free fatty acids are highlighted, both of which are significantly increased secondary to a decrease in fat transporter proteins rendering the liver susceptible for fatty infiltration and hepatomegaly with resultant increased risk of sepsis and burn mortality.
Effects on Gastrointestinal System/Metabolism
The basal metabolic rate increases up to three times its original rate. This coupled with splanchnic hypoperfusion, necessitates early and aggressive enteral feeding to decrease catabolism and maintain gut integrity. It causes mucosal atrophy, reduced absorptive capacity, and increased surface permeability.
Effect on the Endocrine System
The stress hormones i.e. catecholamine, glucagon and cortisol among other hormones are actively involved at the onset of burns injuries. These hormones display an exponential increase in their levels; sometimes reaching 10 fold their normal values. The significance of such an upsurge resides in its influence on the cardiovascular system and the resultant fluid shifts that follow these changes. The stress hormones are thereby considered as the initiators of the hypermetabolic-catabolic and proteolytic-response.
1.52 Systemic effects
Once the burn covers more than 30% of TBSA, the injury has a systemic effect due to
∙ Molecular structural alterations
o Release of toxic metabolites
o Release of antigen and immunomodulatory agents
▪ Histamine, Serotonin, Bradykinin, Nitric oxide, etc.
Causes systemic shock, cardiovascular, respiratory and renal failure, immunosuppression and hypermetabolism. (Evers et al 2010)
Cardiovascular Changes
∙ Myocardial depression
o Myocardial contractility decreased
∙ Oedema formation
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
o May cause renal failure
These changes may lead to systemic hypotension and end organ hypoperfusion. (Evers et al, 2010)
Respiratory Changes
Inflammatory mediators cause bronchoconstriction and pulmonary oedema
∙ severely burnt adults acute respiratory distress syndrome (ARDS) can occur ∙ Exacerbated in the case of inhalation injury (Evers et al 2010)
Metabolic Changes
Hypermetabolism begins approximately five days post burn
o Metabolic state is initially suppressed by the effects of acute shock
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o Can persist for up to two years post injury
Inflammatory, hormonal and cytokine milieu cause
∙ 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)
This hyper metabolic state leads to energy substrate release from protein and fat stores Protein catabolism
∙ Loss of lean muscle mass and wasting
∙ Potentially fatal if structure and function of organs are compromised (Jeschke et al 2007; Hurt et al 2000)
In adults with burns of 25% TBSA, metabolic rate ranges from 118-210% that of predicted values. At 40% TBSA, the resting metabolic rate in a thermoneutral environment is
o 180% at acute admission
o 150% at full healing
o 140% post 6 months
o 120% at 9 months
o 110% at 10 months (Jeschke et al 2007; Herndon and Tomkins 2004) Gastrointestinal Changes
∙ Impaired gastrointestinal motility
∙ Impaired digestion and absorption
∙ Increased intragastric pH
∙ Feeding difficulties exacerbate effects of hyper metabolism (Evers et al 2010) Immunological Changes: (Hettiaratchy and Dziewulski 2004)
∙ Immune deficiency occurs despite the activation of the immune system. High risk of infection, particularly while wounds are open.
1.62 Complications of Healing in Burn Patients[edit | edit source]
1.621 Oedema
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)..
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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.
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1.622 Hypertrophic scarring
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
∙ haphazard structure persists for several months post
Figure 7. Hypertrophic scar on dorsum of hand (Procter 2010)
Injury.
∙ 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)
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1.7 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)[edit | edit source]
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.
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For optimal analgesia, it is recommended that patients are assessed for each type of pain separately and repeatedly throughout the course of the recovery.
Pre-disposition:
Genetics
Psychosis
Substance abuse
Drugs factors: Timing
Tailoring
Side effects
Burn wound: Dressing type Dressing tension Infection
Movement
Donor sites
Personality type Context: Expectations
Culture
Past experience
Environment
Rapport with staff
Cognition:
Attention
Distraction
Self-belief
reappraisal
Mood:
Depression
Anxiety
Catastrophising
Figure 8. Factors influencing the patient’s perception of pain from a burn wound. (Richardson and Mustard 2009)
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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.