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13.4 rFrral HrrFrecroesg o ronf ctrF rFrral geraroc tesf ontFgres 179
13.3.3 Diagnostics
Suspected carpal fractures are investigated using orthogonal radiographs. Soft tissue swelling over
the carpus may be visible on radiographs. SH Type I fractures may be difficult to identify radio-
graphically if they are minimally displaced (Figure 13.4). Early after injury, SH Type V and VI
fractures are generally not visible radiographically, although soft tissue swelling may be present. If
the history and physical exam suggests that these fractures are present, serial radiographs (e.g.
every two weeks) should be performed since a few weeks later premature closure of the physis will
be visible. Ideally radiographs of both limbs are performed allowing to monitor for a length deficit
compared to the contralateral bone. The goal is to monitor for the development of secondary angu-
lar limb deformities and institute treatment early during the progression of the disease.
If the problem is chronic, focal periosteal reaction over the fracture site may be visible and the
joint may be osteoarthritic. For minimally displaced fractures, if the orientation of the radiographic CARPAL REGION
beam approximates the orientation of the fracture plane, a fracture line may be visible on radio-
graphs. CT greatly enhances the sensitivity and precision of the diagnosis of these fractures.
Incomplete ossification of the radial carpal bone may also not be visible on radiographs, and there-
fore a CT may be needed to diagnose the condition.
13.4 Carpal Hyperextension and Other Carpal
Ligamentous Injuries
Carpal hyperextension is the term used to describe an increase of carpal extension. Excessive car-
pal extension can be developmental or acquired. Acquired carpal hyperextension is a frequent
carpal joint problem that most often results from trauma (Bristow et al. 2015). The antebrachiocar-
pal joint is mainly stabilized by the radiocarpal and ulnarcarpal ligaments, the palmar carpal fibro-
cartilage stabilizes the distal carpal joints (Slocum and Devine 1982; Milgram et al. 2012), and the
accessory metacarpal ligament as well as the accessory carpoulnar ligaments stabilizes the acces-
sory carpal bone (Figure 13.6). With traumatic impact, the main structures supporting the normal
angulation of the carpus become damaged, leading to the typical presentation of a palmigrade
stance. Traumatic carpal hyperextension is generally treated with arthrodesis, since external coap-
tation does not seem to allow for healing of the ligaments. Depending on the level of injury, a
partial carpal (i.e. fusion of the distal carpal joints, leaving the antebrachiocarpal joint intact) or
pancarpal (i.e. fusion of all carpal joints) arthrodesis may be performed (Bristow et al. 2015).
Other, less common causes of carpal hyperextension include immune-mediated joint disease
and hyperadrenocorticism (Cushing’s syndrome; Parker et al. 1981; Lotsikas and Radasch 2006;
Shaughnessy et al. 2016). Immune-mediated mono- or polyarthritis may be associated with carpal
hyperextension and thus should be kept in mind during the diagnostic workup. Increased corticos-
teroid levels negatively impact tenocyte proliferation, inhibit collagen synthesis, decrease tenocyte
migration, and induce tendon cell apoptosis (Galdiero et al. 2014). In affected dogs, joint instability
and tendon rupture may also occur elsewhere.
Immobilization in a splint can also result in ligament laxity of the immobilized limb; in one
report, carpal hyperextension was observed in dogs after only 10 days of immobilization
(Altunatmaz and Guzel 2006).
Developmental carpal hyperextension is unusual but has been reported in growing Doberman
Pinchers and Shar-Peis and various other breeds including German Shepherd Dogs (GSD) (Shires
et al. 1985; Altunatmaz and Guzel 2006; Cetinkaya et al. 2007). The problem is often bilateral, and
in severe cases the tarsi can also be affected.