Publication Type Academic Article
Authors Levack A, Klinger C, Gadinsky N, Dyke J, Fung M, Helfet D, Lorich D
Journal J Orthop Trauma
Volume 34
Issue 12
Pagination 662-668
Date Published 12/01/2020
ISSN 1531-2291
Keywords Diaphyses, Tibial Fractures
Abstract OBJECTIVE: Disrupted blood supply has been proposed as an underlying cause for delayed union in tibial shaft fractures (OTA/AO 42). Although tibial blood supply has been qualitatively evaluated, quantitative studies are lacking. The purpose of this project was to quantify the relative contribution of the endosteal supply to the tibial diaphysis. METHODS: The superficial femoral artery of 8 fresh frozen cadaveric matched pair lower extremities was cannulated. The nutrient artery was ligated at its proximal branch point in experimental limbs. Pregadolinium and postgadolinium enhanced magnetic resonance imaging was performed with high resolution fat-suppressed ultrashort echo time magnetic resonance imaging sequences. Perfusion was assessed in 3 zones (outer, central, and inner cortex) for the proximal, middle, and distal diaphysis, respectively, using custom software to quantify and compare signal intensity between experimental and control limbs. RESULTS: On average, the endosteal system supplied 91.4% (±3.9%) of the cortex and was the predominant blood supply for the inner, central, and outer thirds. The dominance of the endosteal contribution was most pronounced in the inner two-third of the cortex, with more than 97% loss of perfusion. Disruption of the nutrient artery also resulted in 76.3% (±11.2%) loss of perfusion of the outer one-third of the cortex. CONCLUSION: This quantitative study revealed a predominance of endosteal blood supply to all areas (inner, middle, and outer thirds) of the tibial diaphyseal cortex. To prevent delayed bone healing, surgeons should take care to preserve the remaining periosteal vascular network in fracture patterns in which the nutrient artery has likely been disrupted.
DOI 10.1097/BOT.0000000000001853
PubMed ID 33079848
PubMed Central ID PMC7880860
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