Complications
This is common in patients with lesions involving C4 to C6. Other factors that are predictive of dysphagia include age >60 years, surgical approach to treatment, severity of associated neurological deficit, and the need for a tracheostomy.[141]
A dramatic drop in blood pressure is noted when the patient's position is changed from supine to upright sitting. It is more common in the early stages and in patients with lesions above T5 due to disruption of the autonomic pathways. This condition limits the use of upright apparatus during rehabilitation.[142][143]
A painful condition that is very disabling when fully evolved. It occurs due to the spontaneous formation of abnormal osseous tissue in the periarticular soft tissues. This is seen commonly around the hip, knee, elbow, and shoulders. The incidence is higher in patients with complete lesions (50%). The cause is not clear, although overstretching in the acute stages has been suggested as a contributory factor. The condition presents with pain, localised redness, and joint swelling initially, and, when fully evolved, results in a complete ankylosis of the affected joint. Radiographic findings reflect the stage of the process, ranging from speckled calcification in the soft tissues to a bony bridge across the joint. Surgical excision in the fully evolved stage (1-2 years after onset) may help in the rehabilitation process.[144]
Muscles that have lost the innervations from the spinal cord rapidly waste. If passive mobility is not maintained aggressively, the muscles become fibrous and contract, leading to contractures across a non-functioning joint. Secondary effects on the joint capsule lead to very disabling contractures that are resistant to therapy. Early, aggressive, and regular physiotherapy, and stretching and splinting of all affected joints in a functional position, help to prevent contractures. Tizanidine can be used to manage spasticity in combination with physiotherapy.[137]
Insensate skin is at a high risk of breaking down when subjected to high-point loads.[138][139] This typically occurs under a bony prominence such as the sacrum (lying supine), ischial tuberosities (sitting), or trochanters (lying on one side). The clinical presentation is typically as a red area that does not blanch, in the initial stages. Continued pressure could lead to ischaemic necrosis of the skin and the underlying tissues. The skin breakdown occurs later in the process. Other factors that contribute to the formation of pressure ulcers are spasticity, sphincteric incontinence, age, loss of sympathetic tone, poor circulation, oedema, tight garments, infection, and poor nutrition.[140]
Good nursing care, regular changes in position, and padding over the affected areas could prevent further damage. Surgical treatment may be required if tissue necrosis occurs.[77]
May be triggered due to hypercoagulability, loss of venous muscle pump, smoking, and obesity. A regular and intensive therapy protocol ensures a good circulation. Prophylaxis is recommended to prevent DVT. Pulmonary embolism due to DVT is a leading cause of death in patients with spinal cord injuries.[136]
A bilateral pitting oedema in the gravitationally dependent position is noted that may resolve with a change in position. This occurs due to a combination of poor vasomotor control and a lack of normal muscle function-related venous return.
Use of this content is subject to our disclaimer