Extensor Tendon Injuries
Extensor mechanism—multiple origins and multiple insertions
Extensor digitorum communis (EDC) and proprius tendons—extrinsic origins
Interossei and lumbricals—intrinsic origins
Insertions—direct at the base of the distal phalanx (P3) and the middle phalanx (P2) via sagittal bands at the base of the proximal phalanx (P1)
Juncturae tendinum transverse connections between EDCs at the metacarpal level.
Mechanism of injury
Closed tensile failure rupture (base of P3, P2, sagittal bands)
Open sharp laceration (anywhere)
Segmental loss as part of industrial trauma involving adjacent structures
Active adults of all ages, both sexes, wide spectrum
Mechanism of injury—tensile overload versus sharp laceration versus complex trauma
Closed versus open
Specific object causing open injury
Degree of contamination
Patient demographics/risk factors (diabetes, vascular disease, smoking)
Demonstration of tendon function/lack of function across injury zone (Figure 31.1)
Appearance of early central slip avulsion is subtle (flexible boutonniere), but key is hyperextension of distal interphalangeal (DIP) with attempted proximal interphalangeal (PIP) extension (Figure 31.2).
Active extension versus resistance from initially flexed PIP joint required to prove insertion at base of P2, simply maintaining extension not sufficient
Check for coronal subluxation at metacarpophalangeal joints—ruptured sagittal band
Proximal EDC laceration can be partially substituted by juncturae tendinum.
Distinguish tendon avulsion at base of P3 from shearing impaction fracture of DIP/PIP joint (Figure 31.3).
Not all fracture fragments at the dorsal base of P2 represent loss of central slip continuity (Figure 31.4)—requires physical examination.
Classification (Table 31.1)
FIGURE 31.1 Terminal tendon avulsion leaves patient unable to actively extend distal interphalangeal joint.