There is also not a single consensus in regard to penetrating vs. It is unclear if he was wearing a helmet. He was initially resuscitated by bystanders as he was in cardiac arrest, and then intubated in the field prior to arrival GCS 3-T. He became more bradycardia and did not respond to atropine requiring another brief round of cardiopulmonary resuscitation. Although the initial hemoglobin on his arterial blood gas ABG was Computed Tomography CT of the head and cervical spine showed an occipital condyle fracture as well as a type III low dens fracture with 6 mm distraction and a c2 spinous process fracture Figure 2.
Pressor support with norepinephrine was initiated and preparations were made for trans-venous pacing in the event of refractory bradycardia. Magnetic resonance imaging MRI the following day confirmed a likely distraction injury with cord edema and hemorrhage Figure 3. Interestingly, his hemoglobin by hospital day 1 had increased to He continued to have issues with bradycardia but did not require trans-venous pacing.
Considering his severe high cervical spine injury with resultant tetraparesis and complications he was transitioned to comfort directed care on hospital day 3. Sagittal STIR c-spine MRI left pane with noted intra-axial edema and hemorrhage at the base of the odontoid red triangle and top axial slice , more inferior cord edema yellow triangle and bottom axial slice , and significant posterior compartment paravertebral edema yellow star.
Case Discussion: The case above illustrates the complexities in early identification of neurogenic shock as a distinct entity. Because the signs of neurogenic shock are somewhat variable in terms of timeframe from injury to onset, and in light of differences between individual patients and systems in regard to fluid resuscitation in the field, a high index of suspicion is necessary from the time of initial evaluation through the early hours and days of intensive care.
Any patient presenting with a spinal cord injury should be considered to be at risk with those having higher level injuries at higher risk Figure 1. The authors suggest that the American Spinal Injury Association Autonomic Standards Assessment Form [ 14 ] is a reasonable place to start and takes into account blood pressure, heart rate, sweating, temperature regulation, the bronchopulmonary system, and the lower urinary tract and bowel.
As there is no single accepted treatment cutoff for the bradycardia and hypotension, it may be important for systems to consider their patient population in relation to prior studies and establish parameters for automatic physician notification during hemodynamic monitoring with reasonable case reviews to establish the best local standard.
It is agreed, however, that the profound systemic hypotension that characterizes neurogenic shock may lead to hypoperfusion of the spinal cord with subsequent ischemia and secondary injury [ 15 ].
To improve outcomes, prompt and aggressive treatment of hypotension should be undertaken in a monitored intensive care unit, with adequate cardiopulmonary and ventilatory support [ 8 ]. Medical treatment consists of sufficient fluid administration as well as vasopressor therapy for sustaining blood pressure and maintaining perfusion [ 4 ]. That being said, it should be noted that the data regarding pressor use in SCI may be conflicting in this regard, as a distinction needs to be made between pressor use in an attempt to stabilize or improve the motor and sensory loss related to SCI, and that to preclude hypotension and bradycardia related to neurogenic shock from causing complications such as systemic hypoperfusion and cardiac arrest among others.
Fluid resuscitation is the first line therapy for hypotension in the setting of neurogenic shock [ 17 ]. Maintenance of blood volume influences both blood pressure and blood flow around the site of injury [ 8 ]. What is otherwise considered routine care such as suctioning, as well as abdominal changes such as elevated bladder and bowel pressures, are known to produce wide swings in heart rate and blood pressure that may be refractory to treatment [ 18 ].
These changes should be anticipated and prevented as much as possible. Blood pressure can be further augmented through the administration of intravenous vasopressor agents. These include norepinephrine, epinephrine, dopamine, phenylephrine, as well as concurrent atropine in patients with significant bradycardia [ 15 ].
There are some prior reports of transitioning individuals that need extended treatment with a non-intravenous agent to propantheline, aminophylline, theophylline, and ephedrine although the evidence is extremely limited [ 16 ]. Enteral pseudoephedrine has also been used successfully as an adjunctive therapy [ 16 ].
Current management guidelines dictate that mean arterial pressure MAP should be maintained above 85—90 mmHg for the first 5—7 days of therapy [ 19 ]. This resuscitation target has been questioned due to the lack of quality evidence showing a positive effect on outcomes [ 8 ]. Additionally, maintenance for 5—7 days may be insufficient because certain individuals benefit from longer management [ 4 ].
One study has shown that vasopressor therapy achieving the MAP goal is more likely to cause complications than to improve neurological outcomes, with dopamine leading in complications [ 20 ]. As such, the risk of vasopressors should be balanced against their benefits in each individual patient, and there should be clear goals for use in regard to improvement of the sensory and motor deficits vs.
A recent study suggests that maintenance of a spinal cord perfusion pressure mean arterial pressure — cerebral spinal fluid pressure above 50 mmHg is a stronger predictor of neurologic recovery than systemic MAP and may also be useful in guiding management [ 21 ]. More studies with high quality evidence are needed to establish reasonable treatment goals that are linked to improved patient outcome.
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A year-old male without significant past medical history was admitted to the University of Missouri hospital after falling from a height of 35—40 feet.
There was no history of any prodromal symptoms prior to the fall. The patient subsequently lost consciousness and was brought to the hospital. Magnetic resonance imaging MRI of the cervical spine revealed a C5—6 dislocation. Despite an urgent discectomy and anterior cervical arthrodesis, he developed partial quadriplegia.
He subsequently developed respiratory failure requiring mechanical ventilation. This episode resolved spontaneously after one minute. Telemetry revealed sinus bradycardia, followed by sinus arrest, a ventricular escape rhythm, and, subsequently, restoration to normal sinus rhythm. On hospital day 10, he developed asystole lasting 20 seconds with loss of consciousness.
This episode resolved spontaneously with restoration of sinus bradycardia at 50—55bpm. Due to severe hemodynamic collapse caused by this event, a transvenous pacemaker was placed. The patient required continuous ventricular pacing at a rate of 60bpm for the next four days, after which his intrinsic rate increased to 60—70bpm without further episodes of asystole.
He did not require any more pacing support over the next three days and on hospital day 17 the pacemaker was discontinued. The patient did well from a cardiac standpoint at follow-up four weeks after the injury, with no further documented episodes of bradyarrythmias, syncope, or pre-syncope. There are an estimated 10,—12, spinal cord injuries every year in the US.
Some of the most common vasopressors include:. In addition, if you have a slower heart rhythm, your doctor may prescribe you atropine. This medication will help to keep your heartbeat normal. Neurogenic shock can be fatal. A spinal cord injury is damage to the spinal cord that can have a lasting and significant impact on your daily life.
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Vasovagal syncope is the most common cause of fainting. Health Conditions Discover Plan Connect. Neurogenic Shock. Medically reviewed by Daniel Murrell, M.
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