Linked Life Data

15475144

Source:http://linkedlifedata.com/resource/pubmed/id/15475144

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2004-10-11
pubmed:abstractText
Although delayed spinal cord injury following high-voltage electrical burn is not a life-threatening sequelae, complete recovery is not the rule and the morbidity is high. In this study, we conducted a detailed analysis of clinical characteristics, radiographic findings and clinical outcomes in 13 patients with delayed spinal cord injury following electrical burns. The following features were notable. In 11 patients whose entry sites were the head and neck area, paraplegia was detected in cases whose exit sites were lower extremity only, while quadriplegia or cervical injury pattern EMG findings were observed in cases whose exit sites were upper extremity. Quadriplegia was also detected in cases whose exit sites were both upper and lower extremities. Quadriplegia was detected in one case whose entry site was hand and the exit site was the contralateral hand. Paraplegia was detected in one case in whom the entry site was the hand and exit site was the contralateral foot. In our patients, no complete loss of sensation was noted. Most of the patients were initially noted to have hypotonia between days 2 and 10 after electrical burn and were characterized by ascending paralysis, i.e., paraplegia followed by quadriplegia. We can postulate that these unique neurological manifestations after electrical injury may be due to the anatomical characteristics of the arterial blood supply of the spinal cord. The anterior gray matter, especially anterior horn cell is particularly susceptible to ischemic injury, because blood is supplied only by the sulcal branch, the longest branch originating from the anterior spinal artery. So, under the condition that all small sized vessels distributed in the spinal cord undergo degenerative change during a similar period of time, any occlusive event caused by thrombus or vascular wall injury in the sulcal branch will enhance the risk of ischemic injury in its distal area. Furthermore, the spinal cord at T4 to T8 levels is more vulnerable to ischemic injury due to poor collateral circulations. In conclusion, our postulates can explain the diverse patterns of delayed spinal cord injury, and enhance the rationale for early administration of prostaglandin E1 or steroid treatment to reduce ischemic spinal cord injury in cases of electrical burns.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0305-4179
pubmed:author
pubmed:issnType
Print
pubmed:volume
30
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
691-5
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Delayed spinal cord injury following electrical burns: a 7-year experience.
pubmed:affiliation
Department of Surgery, Burn Center, Hangang Sacred Heart Hospital, College of Medicine 94-200, Hallym University, Yongdungpo-Dong 2Ga, Yongdungpo-Gu, Seoul 150-719, South Korea.
pubmed:publicationType
Journal Article