The history of spinal cord injury (SCI) dates back as far as the ancient Egyptians, who described it as an ‘ailment not to be treated’ ( Eltorai, 2003 ). For a long time, victims of SCI saw a bleak future confined to a wheelchair and a lifetime of comorbidities and poor survival rates ( McDonald and Sadowsky, 2002 ). It was not until after World War II that the outlook for such patients began to improve ( Eltorai, 2003 ). The development of an infrastructure for the emergency transportation of injured patients and advances in acute care and rehabilitation practices have dramatically reduced mortality and morbidity ( Talu et al. 2005 ). Therapies to enhance neurological function following SCI have been extensively investigated by the clinical and scientific community. Subsequently, significant insight has been generated into the pathology and pathophysiology of acute spinal cord trauma. It has been hypothesised that the primary mechanical injury to the spinal cord initiates a cascade of vascular, cellular and biochemical events that cause extension of the injury site. Current interventions for the acutely cord-injured patient attempt to minimise this secondary injury and protect the tissue that initially survived the mechanical injury ( Dumont et al, 2001 ; Kwon et al. 2004 ; Li and Yang, 2009 ).
Spinal cord injury (SCI) is a serious and debilitating condition that affects both patients and their families. Initial management focuses on the ‘ABCs’ of trauma care—airway, breathing and circulation. Although these are aimed at supporting the life of a patient, with regard to trauma of the spinal cord the ABCs sustain the microcirculation of the cord in an attempt to reduce cell death. In addition to these critical procedures, acute management of traumatic SCI involves the appropriate selection of medical and surgical interventions for the patient, with the aim of enhancing eventual recovery.
Rehabilitation for people with spinal cord injuries (SCI) is a lifelong process that starts in the critical care setting and continues into primary care, with the aim of restoring an individual's functional skills and enabling them to regain self-sufficiency and independence. While the injury in itself is life-changing, the major factors affecting morbidity and mortality in the long term are related to complications of the SCI. Previous articles in this series have discussed the occurrence of acute complications and their immediate management, including haemodynamic and respiratory issues. These may become chronic and patients will often have to be readmitted for care. Early management aims to prevent issues arising further along the rehabilitative process; nevertheless, SCI patients are prone to pressure ulcers and neuromusculoskeletal disorders as ambulatory patients. Prevention should be the mainstay of care, and nurses have a pivotal role in this.
A 22-year-old man presented with a 1-day history of severe abdominal pain. He developed a generalised vesicular rash 12 h prior to admission. On examination, he was maximally tender with peritonism in the lower abdomen. Working diagnosis was perforated appendix and a decision to investigate with CT was made, which showed intra-abdominal haemorrhage likely arising from a ruptured spleen. After a period of observation, he subsequently underwent laparotomy and emergency splenectomy. Viral PCR from vesicular fluid was positive for varicella zoster virus. Viral serology was otherwise negative.
Facial nerve palsies can have a dramatic effect on patients’ quality of life, leaving them permanently disfigured. Bell's palsy is thought to be the most common cause of acute unilateral facial paralysis. Its hallmark is its rapid onset, but the exact aetiology of Bell's palsy remains elusive, with some attributing it to viral, inflammatory or autoimmune causes and others to ischaemia. There is also some controversy as to the appropriate treatment. This article provides an overview of each of these areas, with a view to increasing awareness of this usually temprary but often distressing condition.
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