Adult burn management

Introduction

The management of the adult burn is a complex and multifaceted endeavour. The burn injury and wound cause both local and systemic effects mediated by the host responses of inflammation, regeneration, and repair. Initial physiological derangement can give rise to shifts in fluids, electrolytes and proteins within body compartments necessitating formal fluid resuscitation in large burns. Following on from this initial physiological derangement subsequent metabolic, hematological, immunological and endocrine disturbances can occur making the care of these patients a difficult and challenging task. The sequelae and in general the severity of the injury is dependant on the aetiology, the size of the burn and the anatomical depth of tissue destruction. Management of the burn wound is key to attenuation of systemic sequelae and the aim of care is to achieve early durable and sound healing. This must be achieved whilst managing the multi system nature of the illness [1].

Epidemiology and aetiology

Burn injury represents a major cause of morbidity and mortality with large societal and economic implications. There are variation in incidence and aetiology that relate to age and geography. The annual

Marc G. Jeschke et al. (eds.), Handbook of Burns

incidence of patients with severe burn injury in Europe has been reported as being between 0.2 and 2.9/10,000 inhabitants. There are no similar estimates from the developing world however it is widely recognised that the burden of burn injury in this setting is much more common. A higher incidence has been associated with lower socioeconomic status and in ethnic minorities.

The incidence of adult burn injury in Europe and North America has decreased over the past 30 years and has been related to increasing socioeconomic status and reduction of injury at work. Adults account for over half of all injuries admitted to hospital with the growth of the elderly population in the Western world being reflected in the increasing numbers of elderly patients being hospitalised. The majority of adult burn injuries (50–75%) occur in males and are often related to work, this ratio changes in children and the elderly with a more even sex distribution.

The commonest causes of burn injury in adults include flame (~ 45%), scald (~ 40%), contact injury (~ 10%) and chemical and electrical (~ 5%). These ratios change with scalds in children accounting for up to 80% and in the elderly. Flame burns are more common in men, whereas scalds are more frequent in women. Up to one third of adult injuries are work related. Self immolation injury accounts for a small but significant cohort of burn patients as they tend to be large body surface area injuries [2].

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Classification

A burn is defined as coagulative destruction of the surface layers of the body.

The skin is made up of the epidermis and dermis with the adenexal structures such as the hair follicles, sweat and sebaceous glands residing in the deeper parts of the dermis. These adenexal structures are important as they are the source of proliferating epithelial cells (keratinocytes), which resurface wound after the skin has been injured. Loss of the barrier function of the skin allows invasion of microorganisms and systemic sepsis.

Burn injury to the skin can be classified as partial or full thickness. If the epidermis and the superficial part of the dermis have been injured (superficial partial thickness injury), the majority of adenexal structures are preserved, epithelialisation is rapid (10 –14 days) and the risk of hypertrophic scarring is low. If the burn extends down into the deeper parts of the dermis more adenexal structures are destroyed, epithelialisation is slower (3 – 6 weeks) and there is a high incidence of hypertrophic scarring. Full thickness burns involve destruction all constituents of the skin and usually will require surgical intervention to achieve wound healing.

Depth of burn injury classification quantifies the amount of tissue damage in anatomical terms. Depth is divided into partial and full thickness skin loss, with partial thickness burns being sub-divided into superficial and deep types.

Erythema (1st degree burn) involves the epidermis only, usually with no blistering although desquamation can occur later on.

Superficial partial thickness (2nd degree) burns involve the epidermis and part of the dermis sparing a significant proportion of hair follicles, sebaceous and sweat glands.

Deep partial thickness (2nd degree) burns destroy a larger proportion the dermis and associated of hair follicles, sebaceous and sweat glands.

Full thickness (3rd degree) burns destroy all of the epidermis, dermis and all adnexal structures

The depth of anatomical tissue destruction is an important determinant of wound healing.

Erythema (1st degree burns) usually resolves in a few days without any untoward effects. Superficial

partial thickness wounds will heal spontaneously by re-epithelialisation from epidermal remnants within two weeks and leave few or no scars.

Deep partial thickness (2nd degree burns) wounds heal by a mixture of granulation, wound contraction and epithelialization from epidermal remnants and the wound edge. If left to heal spontaneously these wounds take 2–4 weeks or longer to heal and are associated with a high incidence of disfiguring hypertrophic scarring and scar contracture. These wounds often need skin grafting.

Full thickness wounds (3rd degree burns) require surgical intervention and split thickness skin grafting. This invariably leads to hypertrophic scarring particularly at the edges of the grafts (marginal hypertrophy).

If left to heal spontaneously these wounds granulate, contract and epithelialise from the wound margins. This process is prolonged, leaves the wound susceptible to invasive infection, and leads to significant functional and aesthetic deformity.

Burn wounds that require skin grafts have a higher incidence of scar hypertrophy if the grafting is performed after 14 days of injury and the wound has no viable dermal elements. Burn wounds that are not going to heal within two weeks should be debrided and covered with autologous split skin grafts to minimize hypertrophic scarring [3, 4].

Pathophysiology

The necrotic tissue resulting from a burn is known as eschar. It separates slowly from underlying viable tissue and is a good substrate for microorganisms. If left untreated it becomes colonized, contaminated and eventually infected. Infection attracts white blood cells that can digest the interface and cause separation of the eschar from the underlying viable tissue. Topical antimicrobial agents reduce bacterial proliferation in the wound and will increase the time to eschar separation.

The initial local effect of a burn injury can be divided histologically into three differential zones of tissue damage and blood flow [5].

1. The zone of necrosis represents tissue necrosis centrally due to destruction of cells and tissues by the burn injury.