The role of the sympathetic nervous system in pressor responses induced by spinal injury

Young, Wise; DeCrescito, Vincent; Tomasula, John J.; Ho, Victor

doi:10.3171/jns.1980.52.4.0473

Cited by 29 publications

(3 citation statements)

References 29 publications

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“…3 If the curvature radius is too tight, the sublaminar band is introduced too deeply into the medullary canal and risks in cord injury Eur Spine J (2015) 24:1441-1449 1447 models suggest that spinal cord compression gives an alpha-adrenergic mediated response (vasoconstriction of peripheral arterioles and increased venous return). The bradycardia may be explained by the baroreceptor response, induced by hypertension [12][13][14].…”

Section: Discussionmentioning

confidence: 99%

Sublaminar bands: are they safe?

Polirsztok¹,

Gavaret

Gsell

et al. 2014

Eur Spine J

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Background Sublaminar bands (SB) are frequently used as implants in spine deviation correction. Purpose Our purpose is to demonstrate their safety on a large series of patients. Study design This is a retrospective study. Methods Our department treated 378 spine deviations on children and adolescents via a hybrid posterior technique (lumbar screws, hook and thoracic SB). Each surgery was undertaken using anesthesiologic and a neurophysiologic monitoring using somatosensory evoked potentials (SSEP) and neurogenic mixed evoked potentials (NMEP). An alert was described as an amplitude decrease of 50 % and/or a latency increase of 10 %. Data were analyzed using Student or Wilcoxon tests.Results We used 2,223 SB in 378 operative procedures. We described ten neurophysiologic alerts during the passage of the band under the lamina. There were no significative differences between the two groups concerning the age and the severity of the deformation (p [ 0.05). These neurophysiologic alerts were associated with a dysautonomic trouble (hypertension and bradycardia). The lesional level was determined using a spinal electrode. In six cases, the responsible SB was removed. Three patients had postoperative neurologic deficiency (0.8 %) without complete recovery for one of them (localized incomplete sensitive deficiency). Within the group of 378 patients, 21 alerts were reported due to a screw or a hook, or during the correction manoeuver, without dysautonomic trouble. Conclusion SB neurologic complications rate is as high as other implants' complication rate. Simultaneous hemodynamic and neurophysiologic change is an argument for vegetative response due to SB passage. Their optimal use requires a strict learning of their insertion under the lamina to be as less traumatic as possible. SB are as safe as any other spine implants.

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Section: Discussionmentioning

confidence: 99%

Sublaminar bands: are they safe?

Polirsztok¹,

Gavaret

Gsell

et al. 2014

Eur Spine J

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“…Hypotension can lead to decreased cord perfusion and worsen an existing SCI, because the "cord at risk" cannot self-autoregulate. 26,47,48,70,88 Maintaining hypotensive anesthesia to minimize blood loss is contraindicated in patients with preexisting SCIs or who are at high risk for intraoperative SCI. Vasopressors such as dopamine and levophed should be used at the start of induction to maintain the MABP > 80-85 mm Hg in cases where the cord is already injured or at risk for further cord injury.…”

Section: Presurgical Causes Of Poscimentioning

confidence: 99%

Prevention, identification, and treatment of perioperative spinal cord injury

Ahn¹,

Fehlings

2008

FOC

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Object In this report, the authors suggest evidence-based approaches to minimize the chance of perioperative spinal cord injury (POSCI) and optimize outcome in the event of a POSCI. Methods A systematic review of the basic science and clinical literature is presented. Results Authors of clinical studies have assessed intraoperative monitoring to minimize the chance of POSCI. Furthermore, preoperative factors and intraoperative issues that place patients at increased risk of POSCI have been identified, including developmental stenosis, ankylosing spondylitis, preexisting myelopathy, and severe deformity with spinal cord compromise. However, no studies have assessed methods to optimize outcomes specifically after POSCIs. There are a number of studies focussed on the pathophysiology of SCI and the minimization of secondary damage. These basic science and clinical studies are reviewed, and treatment options outlined in this article. Conclusions There are a number of treatment options, including maintenance of mean arterial blood pressure > 80 mm Hg, starting methylprednisolone treatment preoperatively, and multimodality monitoring to help prevent POSCI occurrence, minimize secondary damage, and potentially improve the clinical outcome of after a POSCI. Further prospective cohort studies are needed to delineate incidence rate, current practice patterns for preventing injury and minimizing the clinical consequences of POSCI, factors that may increase the risk of POSCI, and determinants of clinical outcome in the event of a POSCI.

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“…Haemodynamic modifications after a complete spinal cord section at a high dorsal or at a cervical level have been the subject of several animal experiments in recent years (Rawe et al, 1977;Tibbs et al, 1978;Rawe & Perot, 1979;Alderman et al, 1980;Young et al, 1980). The hypertensive phase is usually of short duration, not more than a few minutes, although the plasma norepinephrine values seem to remain elevated up to two hours after transection when performed at the cervical level (Tibbs et al, 1979).…”

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confidence: 99%

Clinical and anatomical observation of a patient with a complete lesion at C1 with maintenance of a normal blood pressure during 40 minutes after the accident

Gschaedler

Dollfus

et al. 1982

Spinal Cord

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Abstract. An unusual case where there was complete section of the cord at the level of CI-C2 is presented. He was admitted in deep coma, approximately 10 to 15 minutes after the accident. Without the use of drugs, the blood pressure was maintained at 130 Torr for 25 minutes after admission, but progressive hypotension ensued.Key words: Spinal cord injury; Tetraplegia; Pressure response; Brain death.Case Report. Mr R., 18 years old, of Portuguese origin, was crossing the street one evening when he was hit by a car. When the emergency mobile squad arrived, approxi mately 6 minutes later, he was found lying face downwards in a state of complete cardio respiratory arrest. He was immediately intubated, manually ventilated and at the same time external cardiac massage caused the heart to start again. The transfer was rapid, the hospital being less than 2 km distant. He was therefore admitted to the emergency department approximately IS to 20 minutes after the accident. He was in a deep comatose state with bilateral mydriasis unresponsive to light. All other reflexes were absent. No spontaneous respiration could be detected but on the haemodynamic side the blood pressure was constant for another 20 minutes at 130 Torr (the maximum only was recorded) and cardiac frequency was 90 per minute. This was particularly interesting as the patient had not received any intravenous solution or drugs before admission, nor during the period when these blood pressure values were recorded. The X-ray examination showed no cranial fracture, no apparent lesion of the cervical spine and only a transverse fracture at the middle third of the left femur which accounted for a concomitant loss of blood of at least It litres. At the end of the radiological examination (20 minutes after his admission and approximately 35 to 40 minutes after the trauma), the blood pressure fell dramatically to 50-40 Torr accompanied by a sinusal brady cardia at a rate of 40 to 35 per minute. Faced with the association of deep coma, total areflexia, bilateral mydriasis and hypotension with bradycardia, the doctor on duty diagnosed the high probability of an irreversible coma. This diagnosis was 'confirmed' by an I.P.P.V. disconnecting and pure oxygen test.These tests were performed for IS minutes. The diagnosis of brain death seemed most evident and the patient was transferred, orally intubated and artificially ventilated, to the resuscitation department. It was expected that death would follow shortly afterwards.It was only a few hours later, next morning, before an EEG was to be performed to confirm brain death, that reappearance of signs of brain function occurred, i.e. opening of the eyelids, myosis and deglutition reflexes caused by the oral intubation tube. The possibility of a spinal cord injury was evoked evidence of priapism (very unusual in coma). The blood pressure remained at 50 Torr and the cardiac frequency still at 40 per minute. Very little renal secretion was recorded.The intravenous perfusion was then increased under central venous pressure monit...

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The role of the sympathetic nervous system in pressor responses induced by spinal injury

Cited by 29 publications

References 29 publications

Sublaminar bands: are they safe?

Sublaminar bands: are they safe?

Prevention, identification, and treatment of perioperative spinal cord injury

Clinical and anatomical observation of a patient with a complete lesion at C1 with maintenance of a normal blood pressure during 40 minutes after the accident

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