Skull Base 2005; 15(2): 106-107
DOI: 10.1055/s-2005-870594
ORIGINAL ARTICLE

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Commentary

Mark E. Linskey1
  • 1Neurological Surgery, University of California, Irvine, Orange, California
Further Information

Publication History

Publication Date:
24 May 2005 (online)

Dr. Wysocki presents a well-done, careful, and systematic microanatomical study on 100 consecutive temporal bone fractures associated with fatal head injury. Autopsy studies with these kind of numbers are becoming increasingly rare, particularly in the United States, yet a tremendous amount of information can come from them. This study is a good example.

He found that 82% of fractures were longitudinal, 11% transverse, and 7% mixed, which is not unexpected. He found a surprising incidence of facial canal disruption (37%) associated with longitudinal fractures, but nerve disruption occurred in only 7% versus 63% of cases of transverse fracture. He also noted a surprising incidence of ossicular disruption, fracture, or both, as well as jugular bulb injury. Both of these latter findings seem significantly higher than clinical experience would suggest and may reflect the severity of temporal bone fractures associated with fatal head injury, as opposed to basilar skull fractures associated with lesser degrees of survivable closed head injury.

The incidence of carotid canal fracture (52%) is very interesting given Dr. Wysocki's finding of carotid artery injury in only 1 case. Clinical experience suggests that angiographic abnormalities will be present in 42% of cases studied for the presence of a basal skull fracture involving the carotid canal,[1] and as many as 18% of patients with carotid canal fractures may develop clinically symptomatic vascular complications.[2] The likely explanation for this discrepancy is that basal skull fractures through the carotid canal probably lead to intimal dissection as the most common injury, subsequently resulting in thrombosis or embolization rather than transmural disruption. I suspect that Dr. Wysocki's autopsy studies are less sensitive to detecting intimal injury as opposed to transmural disruption through the adventitia. From a clinical standpoint, we need to maintain heightened vigilance for vascular sequelae when carotid canal fractures are identified. Whether or not routine further screening (angiography, computed tomography angiography, magnetic resonance angiography) is a cost-effective approach remains the subject of ongoing debate.[1] [3]

REFERENCES

  • 1 Kerwin A J, Bynoe R P, Murray J et al.. Liberalized screening for blunt carotid and vertebral artery injuries is justified.  J Trauma. 2001;  51 308-314
  • 2 Resnick D K, Subach B R, Marion D W. The significance of carotid canal involvement in basilar cranial fracture.  Neurosurgery. 1997;  40 1177-1181
  • 3 Mayberry J C, Brown C V, Mullins R J, Velmahos G C. Blunt carotid artery injury: the futility of aggressive screening and diagnosis.  Arch Surg. 2004;  139 609-612 , discussion 612-613
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