Sprains, strains and dislocations

When a ligament ruptures, the vessels that run within it tear as well, and blood pours into the joint cavity, producing a haemarthrosis — a joint that is swollen, warm and held in a slightly flexed, comfortable position. That effusion is not only a cosmetic problem. The fluid stretches the capsule, and the swelling sends afferent signals to the spinal cord that reflexively switch off the muscle surrounding the joint, a phenomenon called arthrogenic muscle inhibition. The quadriceps, for example, may be unable to generate full force for weeks after a knee injury even though the muscle itself is untouched, and the patient reads this as instability.

At the same time, the ligament carried mechanoreceptors that reported the joint's position to the brain; when it is torn those proprioceptive signals are lost, so the joint no longer knows where it is in space and the protective reflexes fire too late. Healing itself proceeds in three overlapping phases: an inflammatory phase lasting about 72 hours, a proliferative phase in which fibroblasts lay down a disorganised collagen scar over roughly three days to six weeks, and a remodelling phase in which that scar is reorganised along the lines of stress over six weeks to as long as a year. The scar never regains the strength or the elasticity of the original ligament, and it is least tolerant of load in the first weeks. Two clinical consequences follow directly.

First, complete immobilisation protects the repair in the short term but weakens the surrounding muscle and reduces proprioception, which is why guided early movement and rehabilitation are prescribed rather than a cast for months. Second, a joint that has lost its mechanoreceptors and its ligament support keeps giving way: repeated giving-way is what defines chronic instability, and it is the pathway to further dislocation, cartilage damage and premature osteoarthritis. Nursing practice touches this at three points — controlling swelling with ice, elevation and compression during the inflammatory phase, ensuring the prescribed rehabilitation is actually attended, and warning the patient that a joint which feels normal at rest can still fail under load.

The distinction between what a test detects and what the patient actually has is the heart of safe practice here. A plain radiograph is a picture of bone density: it shows fractures, avulsion fragments where the ligament pulled a piece of bone away, joint alignment, and, after a dislocation, that the surfaces are back in place. It does not show a ligament, so a negative film is entirely compatible with a complete tear. Stress radiographs are sometimes taken with the joint pushed in a controlled direction to reveal abnormal opening, but they need trained hands and are painful. Ultrasound, performed by a clinician, visualises ligaments, tendons and effusions dynamically — the operator can watch the tissue move — and it is quick and repeatable, though it depends heavily on the skill of the person holding the probe.

Magnetic resonance imaging is the reference method for soft tissue: it shows the ligament, the cartilage, the menisci, bone bruising and the presence of an effusion, and it is used when surgery is being considered or when the diagnosis remains unclear. The clinically important tool, however, is not an imaging machine at all. The Ottawa ankle rules are a validated decision aid: an ankle radiograph is required only if there is pain in the malleolar zone together with bone tenderness at the posterior edge or tip of either malleolus, or an inability to bear weight for four steps both immediately and in the emergency department. Applied properly, these rules reduce unnecessary radiographs without missing fractures. The nursing lessons are three.

Never tell a patient that “the X-ray was normal, so there is nothing wrong”, because that sentence contradicts everything above and discourages the rehabilitation that decides the outcome. Always record the mechanism and the examination findings, because they, not the film, establish which tissue failed. And remember that a patient with a suspected tear may be sent for further imaging after discharge, so the instructions given at that moment — who to contact, when to return, what to avoid — carry real clinical weight.

The shoulder pays for its range of movement with a shallow socket, and that anatomy explains why it dislocates more often than any other joint — and why the structures passing close to it are at risk. The axillary nerve runs around the surgical neck of the humerus, only millimetres from the glenoid rim, and it supplies the deltoid muscle and the skin over the outer shoulder. A dislocated humeral head can stretch or compress it, so the classic findings are a patch of numbness over the deltoid and weakness when the patient tries to lift the arm. The axillary artery and the brachial plexus run nearby as well.

These structures are the reason the neurovascular examination is documented before and after reduction: a deficit that was present on arrival was caused by the dislocation, while a new deficit that appears after the manoeuvre was caused by the reduction, and the difference determines what the team does next. Reduction is performed under sedation or a short anaesthetic, both to control pain and to relax the muscles that are otherwise splinting the head in the wrong position; the sooner it is done, the less the pressure on the nerve lasts. After reduction, a radiograph confirms the position, the limb is immobilised in a sling for a period chosen by the surgeon, and the patient begins graded rehabilitation. The complication nurses must anticipate is recurrence.

Young patients, especially those under about twenty, and those whose first dislocation followed only minor trauma, have a high rate of repeat dislocation because the labrum — the fibrous rim that deepens the socket — and the capsule are torn. That combined lesion of the labrum is known as a Bankart lesion, and it may be accompanied by an indentation in the humeral head. Recurrent dislocation erodes the glenoid and damages the cartilage, so prevention is surgical or rehabilitative rather than merely expectant.

In practice, the nurse's contribution is precise and limited: immobilise in the position found, document the neurovascular state, give analgesia and keep the patient nil by mouth for the sedation, never attempt reduction, and teach the patient after discharge which activities to avoid and which warning signs — numbness, increasing pain, loss of movement — must bring them back.