Between 1976–1979, 87 Type III open fractures (in 75 patients) were treated at the Hennepin County Medical Center. Factors leading to increased morbidity in Type III fractures were: massive soft-tissue damage; compromised vascularity; severe wound contamination; and marked fracture instability. This study demonstrates, because of varied severity and prognosis, that the current designation of Type III open fracture is too inclusive. We recommend, therefore, that Type III open fractures be divided, in order of worsening prognosis, into three subtypes.
Type IIIA—Adequate soft-tissue coverage of a fractured bone despite extensive soft-tissue laceration or flaps, or high-energy trauma irrespective of the size of the wound.
Type IIIB—Extensive soft-tissue injury loss with periosteal stripping and bone exposure. This is usually associated with massive contamination.
Type IIIC—Open fracture associated with arterial injury requiring repair.
Wound sepsis in the three subtypes were: Type IIIA, 4%, IIIB, 52%; and IIIC, 42%; while amputation rates were, respectively, 0%, 16%, and 42%. Only two patients developed osteomyelitis, and 12 patients had delayed or nonunions. Five patients died, all as a result of multisystem trauma.
The bacterial pathogens in infected open fractures have changed dramatically over the years. In the present series (1976–1979), 77% of infections were due to Gram-negative bacteria, compared with 24% previously (1961–1975). A change of antibiotic therapy from a first-generation cephalosporin alone to a combination of a cephalosporin and an aminoglycoside, or a third-generation cephalosporin, is currently indicated in Type III open fractures.
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