Applying full circumferential casts less than twenty four hours post-operatively became a recent issue for me. Following an open reduction and internal fixation (ORIF) procedure which had taken place the previous day, I was asked to apply a full cast to the involved limb.
When I expressed surprise and a clear reluctance to do so, I was informed that it was a standard procedure in the hospital in which I was working. It felt wrong for me to apply a circumferential cast to an injury which had been managed operatively less than twenty four hours previously.
My thoughts are that any fracture fixed by metalwork is held in the ideal alignment. Initially, the fixation will be strong enough to support and hold the bony fragments in their surgeon determined alignment when the bony fragments are not under load.
The application of a plaster splint should be sufficient to protect the surgical repair. Because load bearing will not be sought immediately after bony fixation, there is no requirement to apply a full cast.
Enclosing a freshly injured limb in a circumferential cast will needlessly increase the risk of circulatory and neurological complications. In the face of the local treatment policy, I decided to evaluate the current evidence for the local practice and to reflect on my own position with respect to applying full casts very early in the treatment cycle.
My starting position is this: Applying a full cast to a limb with a fresh injury (or one which has undergone a surgical procedure within the previous twenty four hours) does not permit adequate time for the soft tissues to recover from the insult to them. This method of treating an injured limb does not consider the probable increase in soft tissue oedema in the immediate future after applying the cast.
The inflammatory response needs more time to reach its natural conclusion. The swelling and pain that attends a fresh injury or a surgically fixed injury is expected because we know that the body accommodates tissue injury by means of the inevitable inflammatory response.
The soft tissues swell as an integral part of the healing process. During this phase of healing the application of a full circumferential cast is an activity which is frequently mistakenly undertaken. A swollen limb will cause the cast to feel tight and may impinge upon neurological and vascular structures.
Compartment syndrome is an orthopaedic and a surgical emergency which requires expert and immediate treatment. Pressure on neurological and vascular structures compromises the functional recovery of the patient's limb.
After a full cast has been applied to a swollen limb the cast will be ill-fitting from the outset. The undercast padding compresses and leaves the cast, which was already too large, too loose.
Undercast padding does not magically create a variable change in the finished size of a cast in order to accommodate increasing swelling. When the injured limb is actively swelling it does not and cannot change the internal dimensions of the cast to accommodate the increasing oedema.
It is mistakenly believed that excessive undercast padding will leave room for additional swelling to take place. It does not because the cast size is fixed and compressed tissues remain compressed.
We cut a cast down to the skin when bivalving it where it appears to be too tight. If the padding was left intact it would possibly become a tourniquet. More padding equals less ability to accommodate increasing swelling.
Try this simple test... take your favourite undercast padding and hold two layers together. Try and stretch or tear them while they are together. Now increase the number of layers to four and try the same test. It is much more difficult to tear or stretch the larger number of layers of padding.
Hiding surgically made wounds under a full cast can prevent early identification of wound dehiscence, bleeding or breakdown and infection. Lightweight casting tapes are impervious to blood and infected wound exudates and with the casting tape colours available, some wound issues are likely remain undetected.
A splint constructed from a slab of plaster of Paris will make visible any wound exudates at the moment when they occur. The need to apply a full cast must derive from a knowledge foundation which guides the clinician in selecting any specific treatment modality with a specific treatment objective in mind.
What could be the imperative driving the clinician to request a full cast immediately after a traumatic injury? The cast is usually applied for the purpose of stabilising a fracture and to ensure that the fragments remain in apposition to each other so that the most appropriate healing pathway is facilitated.
Additional consideration will be given to the final functional outcome and the likely duration of treatment leading to full recovery. Fracture patterns are also treated with thought directed to the mobility of the patient. This attention brings a focus upon their ability to manage their injury; especially where they are living independently but alone.
The application of a circumferential 'well-padded' cast within the first twenty four hours is frequently an error of judgement. It will be ill-fitting from the outset because of excessive padding applied to accommodate an increase in swelling and the fit will deteriorate as the oedema subsides.
A closely fitted and expertly applied posterior slab will not increase the risk of neurovascular damage or compartment syndrome. The slab splint can remain in place for the length of time it takes for tissue oedema to subside. The support for the fracture site is adequate and appropriate and the bony injury healing and limb functional recovery will not be imperilled.
The haste to fully enclose a surgically fixed fracture is difficult to understand. The bony fragments have been aligned and held in an ideal position by the surgeon. A supporting plaster slab should be all the assistance that is required.
Lower limb injuries which have been surgically repaired mandate that the patient is kept non weight-bearing, especially where metalwork such as a diastasis screw is concerned. It may be planned to remove the screw at a later date and early load bearing may bend the screw and make it difficult or impossible to remove.
The modern tightrope technique of resolving diastasis of the fibula and tibia at the syndesmosis would not mandate a circumferential lightweight casting tape. These tapes are impervious to fluids and thereby sub-optimal post surgical fixation.
Adequate surgical fixation does not usually require the support of a full cast. The patient may attend an outpatient clinic at ten to fourteen days post-operatively for suture or clip removal. Where the sutures used are absorbable subcuticular sutures, the patient may attend an outpatient clinic for a wound check and full cast application.
Ten to fourteen days is usually enough time for the swelling resulting from the surgery to have resolved. A definitive, well-fitting cast is normally applied at this point in the healing process. The patient does not have to attend a plaster room on two or three separate occasions before their first formal post operative clinic attendance because a full cast was applied too soon and required frequent cast changing.
The medical science should support the work which cast technicians undertake and to that end, I thought it would be instructive to see what the literature has to offer concerning inflammation where there is a bony injury or surgical fixation of bone. Additionally, I would like to consider the potential for disruption to a planned course of orthopaedic treatment where cast change frequency is higher than expected.
The inflammatory response has been the subject of a large amount of intense study and the complexity of the inflammatory response makes a simplified model of how it works rather difficult to portray.
I will illuminate some of the crucial points that the literature has uncovered. I will then review the local decision making and early full cast application while giving due regard to what is known about the inflammatory response in cases of trauma to bones.
According to Mountziaris & Paschalia et al. (2011) inflammation is a biological response which plays a vital role in facilitating bone regeneration after bony injury. Where the inflammation does not go on to resolve as expected, it leads to a chronic inflammatory condition which exerts destructive effects on bone tissue.
These research workers go on to say that a complex balance exists between bone tissue and the immune system and where the inflammatory response is suppressed, damage to the regenerating injured bone ensues. Anti-inflammatory drugs such as Ibuprofen (NSAIDs) and celecoxib are known to affect bone regeneration negatively.
Aspenberg (2005) identified several groups of drugs which impair fracture repair in long bones. Fluoroquinalone antibiotics have a deleterious effect on growing cartilage. Tetracyclines are thought to have an effect on tissue turnover because of their inhibition of matrix metalloproteinases which affects callus formation.
Their antibiotic properties are likely to be subordinate to the inhibition of new bone formation in the case of fractures. NSAIDs (Cox 1 & Cox 2 inhibition) greatly reduce prostaglandin production. Prostaglandins are required in great amounts for inflammation, repair and cell survival.
It was interesting to note that Mountziaris & Paschalia et al. (2011) identified the acute phase of the inflammatory response to bony injury as being one week in duration. This week is apparently critical in priming the bone regeneration process. Note that bone actually regenerates and does not repair itself by forming scar tissue, which is said to be inferior to actual tissue.
Kolar & Schmidt-Bleek et al. (2010) found the early fracture haematoma to contain immune cells. Where the haematoma was removed from the fracture site at days 1, 2, 3 and 4, they found that the fracture went on to delayed or non-union. They stated that the immune cells are located within the haematoma at the time of the fracture and are activated by coagulation.
These research workers found that only a small remnant of fracture haematoma remained at the fracture site on day 14. Where there was a rotational instability at the fracture site, the haematoma remained for longer than fourteen days. Marsell and Einhorn (2011) describe the acute inflammatory response as peaking within the first twenty four hours and being complete after seven days.
What is clear from the current science is that the acute phase of the inflammatory response lasts for around seven days and is essential for the healing of a fracture. It brings into sharp focus why I was unprepared to apply a full cast to the injured arm. I had wanted the inflammatory response to be unrestricted by a cast with all its attendant dangers. I had wanted to prevent the patient developing neurovascular complications.
Where the inflammatory response is permitted to complete its initiation of the healing process, unhindered, we can expect to see short and efficient healing times. The cardinal signs of inflammation are redness (rubor), heat (calor), swelling (tumor) and pain (dolor). The patient had exhibited all of these signs with excrutiating pain being the most obvious.
Following two decades of intense research into the inflammatory response, the science is clear and unequivocal. Inflammation is a vital component in the healing of a fracture. Any inhibition of the inflammatory response results in delayed or non-union of the fracture.
I have always dissuaded patients from taking over the counter ibuprofen for swelling and pain. It has been known for some time that NSAIDs can inhibit fracture healing and the sources cited at the end of this article provide the rationale for not taking NSAIDs during fracture healing.
In general terms, if the splint for a fresh injury or post surgical fixation is well applied, the patient should not really experience any of the pain which was caused by fracture fragment movement or involved limb movement. The use of simple analgesics will usually serve to ease the pain of a surgically fixed fracture.
The use of a full cast will inhibit the soft tissues from swelling as the component parts required for fracture healing move towards the fracture site. I remain unwilling to put a new injury or surgically fixed fracture into a full cast. The neurovascular consequences may be dire and it just may be an iatrogenic act; which delays healing and the patient's subsequent recovery.
I have not found any useful articles concerning the frequency of cast changes and their possible effect on fracture healing. It is easy to see that with each cast change mandated by decreasing oedema in the first two weeks of fracture treatment, that there is a risk of allowing the fractured fragments of bone to move out of alignment where they were not fixed surgically.
It is estimated that we treat about 80% of all fractures non-operatively in the UK. It is clear that cast changes are a trigger for repeated radiographic examinations to check that movement of the fragments has not taken place. Every X-ray examination adds to the patient's cumulative lifetime dose of radiation. It would be good clinical practice to avoid needlessly adding to the patient's lifetime dose of radiation.
The inflammatory response is inevitable and should not be 'cured' by drugs. It is an integral and essential part of the healing of fractures. Applying a full cast too early in the treatment cycle will increase the risk of serious neurovascular complications. The gold standard was once a plaster slab applied to a surgically fixed fracture or a fresh traumatic injury for fourteen days.
Thereafter, a full circumferential cast could be applied to the involved limb and would very likely remain in situ for the duration of the treatment requirement. It is unlikely that a rational case can be made which demands that a full cast be applied on day one or two post trauma or surgical fixation.
In the cases depicted above, I will continue to refuse to apply full circumferential casts, preferring to splint the limb with a plaster splint which will not impede the circulation nor compress the neurological tissues and pathways.
Drugs and Fracture Repair
Acta Orthopaedica 2005; 76 (6): 741-748
Kolar and Schmidt-Bleek et al.
The Early Fracture Hematoma and Its Potential Role in Fracture Healing
Tissue Engineering Part B: Reviews16.4 (Aug 2010): 427-34.
Marsell and Einhorn
The Biology of Fracture Healing
Injury Volume 42, Issue 6, June 2011, 551-555
Mountziaris & Paschalia et al.
Harnessing and Modulating Inflammation in Strategies for Bone Regeneration
Tissue Engineering Part B: Reviews17.6 (Dec 2011): 393-402.