Systemic Resonse to 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

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

∙ 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

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

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

“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.

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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.