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Spinal Injuries
Published in Ian Greaves, Keith Porter, Jeff Garner, Trauma Care Manual, 2021
Ian Greaves, Keith Porter, Jeff Garner
In acute spinal cord injury, shock may be neurogenic, haemorrhagic, or both. Following injuries at or above T6, there is significant loss of the sympathetic autonomic (adrenergic) outflow. Consequently, vasomotor tone is reduced and, if the lesion is high enough, sympathetic innervation of the heart is lost. This loss of sympathetic tone results in hypotension and also enhances vagal reflexes, causing profound bradycardia. The triad of hypotension, bradycardia and peripheral vasodilatation resulting from the interruption of sympathetic nervous system control is termed neurogenic shock. It is important to consider this cause of shock in the patient with spinal injuries, although spinal injuries are frequently associated with other major injuries, and hypovolaemia must be excluded before attributing persistent hypotension to neurogenic shock. Hypotension associated with injury below the level of T6, and hypotension in the presence of a spinal fracture alone, with no neurological deficit, are invariably caused by a haemorrhage. To complicate matters, patients with injury above T6 may not show the classical physical findings associated with haemorrhage (tachycardia and peripheral vasoconstriction). Thus, neurogenic shock may mask the normal response to hypovolaemia resulting from other injuries, and the two may coexist.
Neurotrauma in the Field
Published in Mansoor Khan, David Nott, Fundamentals of Frontline Surgery, 2021
Neurogenic shock may play a crucial role in these patients due to higher rates of spinal cord injury. This is an interruption to the sympathetic nervous system with resultant bradycardia and hypotension. Any patient not responding to normal fluid resuscitation should be started on inotropes as early as possible. Studies have shown that maintaining a good perfusion pressure to the spinal cord (current British Association of Spine Surgeons guidelines suggest MAP of more than 90 mmHg) will result in better neurological outcome.
Surgical Emergencies
Published in Anthony FT Brown, Michael D Cadogan, Emergency Medicine, 2020
Anthony FT Brown, Michael D Cadogan
Restore the circulatory volume if the patient is hypotensive. First look for sources of blood loss before diagnosing neurogenic shock.Neurogenic shock causes hypotension in a patient with a cervical cord injury due to loss of sympathetic tone with vasodilation and bradycardia.Place a urinary catheter to monitor urinary output.
Cardiac arrhythmias six months following traumatic spinal cord injury
Published in The Journal of Spinal Cord Medicine, 2022
Shane J.T. Balthazaar, Morten Sengeløv, Kim Bartholdy, Lasse Malmqvist, Martin Ballegaard, Birgitte Hansen, Jesper Hastrup Svendsen, Anders Kruse, Karen-Lise Welling, Andrei V. Krassioukov, Fin Biering-Sørensen, Tor Biering-Sørensen
Our results demonstrated no difference in the mean maximum HR between cervical and thoracic participants at Month 6. Maximum HR significantly increased for the cervical group and shows an increasing trend for the thoracic group between Week 4 and Month 6. Studies have shown HR returning to normal at six weeks post-SCI.18 This finding is perhaps in line with previous conclusions made about autonomic function recovery from HR variability analysis.19 Increases in normal sinus beats likely reflect at least partial recovery of descending fibers providing supraspinal sympathetic control over the heart.20 Furthermore, the small associations between injury severity and mean maximum HR, with a trend as early as Week 1 may suggest the onset of cardiac recovery upon treatment of neurogenic shock.12 Indeed, there were associations with medium effect sizes with increased maximum HR and injury severity in the cervical group beyond the Week 1 assessment.
Columbia Icefield Bus Rollover: A Case Study of Wilderness Mass Casualty Triage, Treatment, and Transport
Published in Prehospital Emergency Care, 2022
Jamin M. Mulvey, Brett H. Shaw, Michael Betzner, Eddie Chang, Mackenzie Wardle, Kevin Lobay, Joshua Bezanson
Secondary triage occurred on patient arrival at the CCP, with ongoing evaluation and treatment occurring as additional medical resources arrived. By 4 hours, 20 minutes post incident, all HEMS providers had arrived on scene. There were multiple patients with blunt traumatic injury patterns, particularly of the head, neck, and thorax. The patients were urgently assessed and received emergent interventions for multiple patterns of shock including hemorrhagic, obstructive, and neurogenic shock. On-site advanced treatments included pre-hospital emergency anesthesia (PHEA) and rapid sequence intubation, finger thoracostomies, aggressive analgesia, intraosseous and vascular access, packed red blood cell transfusions, and initiation of vasopressor agents. These were performed by the combined efforts of ground paramedics, HEMS aeromedical teams, and pre-hospital physicians, as required by patient needs.
Controversies regarding mobilisation and rehabilitation following acute spinal cord injury
Published in British Journal of Neurosurgery, 2020
Fardad T. Afshari, David Choi, Antonino Russo
One of the main reasons for bed rest management following acute spinal cord injury is maintaining cord perfusion. In immediate aftermath following spinal cord injury with neurogenic shock, haemodynamic instability may affect spinal cord perfusion. This has led to common practice of bed rest immediately following spinal cord injury to avoid orthostatic hypotension. There are multiple studies investigating the role of maintaining of blood pressure (BP) and mean arterial pressure (MAP) on neurological recovery after spinal cord injury with most studies being retrospective and lacking control groups. The period of maintaining BP above target in most studies ranges from 24 hours up to 7 days.