Role Of Periosteum
The periosteum plays a crucial role both in the management of the fracture and in the provision of skin cover. In addition to providing an effective barrier to infection, a significant proportion of the blood supply to the superficial cortex of the bone reaches it through the periosteum.
This explains why avascular necrosis of the superficial cortex and surface sequestration regularly occur where bone is left denuded of periosteum by the injury, and also provides the reason why nothing should be done in manipulating and fixing the fracture which might denude more bone or add to the periosteum already damaged. If plates and screws are being used they should be applied on top of the periosteum even though this may add to the technical problems of fixation.
The surgeon has to accept the therapeutic problems posed by the cortical bone denuded by the injury, but he should not add to them by surgically stripping periosteum.
In relation to the role of the periosteum in the
provision of skin cover, cortical bone which is covered with periosteum will accept a split skin graft; cortical bone denuded of periosteum cannot be expected to accept a split skin graft.
The distinguishing feature of a degloving injury is the flaying of the skin, the result of a severe shearing strain, as for example in the ‘running over’ of the limb by a pneumatic tyre. The plane through which the skin is detached is sometimes superficial, sometimes deep to the investing layer of deep fascia, and the skin may tear, creating a flap.
Alternatively, the skin may remain intact, though detached deeply. The effect of detachment is to disrupt the perfusion pattern of the skin and superficial fascia. The vessels which reach the investing layer of deep fascia and through it perfuse the superficial fascia and skin, described on p. 67, are avulsed.
The sudden extreme tension set up by the shearing strain also disrupts the vascular
9 network in the superficial fascia and skin, the combined effect being to produce ischaemic necrosis of the skin which is detached. Depending on the mechanism of the injury there may also be friction burning of part or all of the degloved skin.
At first sight, the severity and extent of the damage to the skin circulation may not be particularly striking, but there is failure of the skin to blanch when pressure is applied, with return of colour when the pressure is released and, when a skin edge is present, no dermal bleeding, both indicating absence of circulation. The skin area demonstrated to be devoid of circulation, although its epidermis at that point in time may be viable, progresses to ischaemic necrosis.
Accurate assessment of the extent of the area lacking circulation is desirable, and fluorescein, administered intravenously, 15mg/kg in 200ml of saline, over a period of 10 min has been used as a visual aid to estimating this. Viewed under ultraviolet light, normally perfused skin clearly fluoresces while avascular skin does not. Unfortunately, difficulty is liable to arise in the areas where help is most needed, where damage is partial. Such areas show a mottled pattern of fluorescence.
Towards the margin of a degloved flap they are likely to go on at least to superficial necrosis, and are probably better managed as part of the frankly ischaemic skin area.
The principle of management in such an injury is that the non-viable skin area should be excised, and the defect split-skin grafted with the minimum of delay.
The patient’s general condition may overshadow the local and dictate at least temporary delay, but a local assessment should be made as soon as possible, and the excision carried out. It is positive evidence of perfusion which decides viability, and in its absence the skin should be excised.
It is not essential that the graft should be
applied immediately following excision.
There may be advantage in waiting for a few days to allow for further excision if any dubious areas remain, either of the degloved skin or of the sur-face exposed by the degloving. Grafting with a minimum of delay is nonetheless desirable. As much skin as possible should be applied, with priority given to the flexures and areas with underlying tendons.
Damage to muscle may also be present,
recognisable by the darkening of the muscle fibres, and failure of the fibres to contract when pinched. Excision to healthy muscle is then required, since it is only on a healthy base that a graft will take. Residual necrotic muscle will mean local graft failure.
The fact that the skin after the injury, though
without a blood supply, remains viable makes it possible to use it on occasion as a free skin graft to resurface the area at least in part. If it appears largely undamaged, it is worth considering its reapplication to the debrided surface as a full thickness skin graft after its subcutaneous fat has been carefully excised.
Successful use of the skin in this way gives a better ultimate result than a split skin graft cut from elsewhere.
It is important that the nature of the injury and
its vascular significance should be recognised, so that the situation is not allowed to drift until a slough forms and separates slowly and spontan-eously. If the injury has not been recognised primarily, and only becomes obvious when a slough forms, it should be excised as soon as it has demarcated, and the area immediately grafted.
Limb trauma predominantly involves skin, muscle and bone. Infection does not loom large as a hazard if the skin is not involved, but it has to be added to the list of possible complications when there is a break in the skin barrier, and this can be particularly serious when a fracture is part of the injury.
It is for this reason that the effective provision of skin cover becomes a matter of urgency, though its provision has to be coordinated with the management of the other damaged structures, each of which carries its own imperative.
When skin loss is a major element in a limb
injury, whether in isolation or as part of combined skin-bone trauma, it usually takes the form of degloving.