Clinical Conditions Involving the Cuff.
Last updated Wednesday, January 26, 2005
IntroductionAbout cuff defects The requisites for normal cuff function are stringent, including
healthy, strong cuff muscles, normal capsular laxity, intact cuff
tendons, a smooth contour of the undersurface of the coracoacromial
arch, a thin, lubricating bursa, a smooth upper surface of the cuff and
tuberosities, and concentricity of the glenohumeral and
cuff-coracoacromial spheres of rotation (see figures 1-5). Disorders of
this complex mechanism constitute the most common source of shoulder
problems. (Chakravarty and Webley, 1993, Iannotti, 1994)
Cuff disruption may be partial or full thickness, acute or chronic,
and traumatic or degenerative. (Cofield, 1985, Matsen, Lippitt, 1994)
The magnitude of cuff disruption ranges from the mildest strain to
total absence of the cuff tendons. In younger patients, partial
thickness cuff lesions may include the avulsion of a small chip of bone
from the tuberosity, the radiographic appearance of which should not be
confused with that of calcific tendinitis (see figure 6). Contributing
factors may include trauma (Codman, 1911, Codman, 1937) attrition,
(DePalma, Gallery, 1949, Keyes, 1935, Meyer, 1924, Moseley, 1952)
ischemia, (Lindblom, 1939a, Lindblom and Palmer, 1939, Moseley and
Goldie, 1963, Rathbun and Macnab, 1970, Rothman and Parke, 1965) and
subacromial abrasion. (Craig, 1984, Neer, 1972, Neer, 1983, Neviaser
and Neviaser, 1982, Peterson and Gentz, 1983, Watson, 1978)
Degenerative cuff failure almost always starts with a partial
thickness defect on the deep surface near the attachment of the
supraspinatus to the greater tuberosity. Codman's view of the frequency
of this lesion and the potential range of pathology is indicated by the
following passage (Codman, 1934b)
Figure 7 shows an extensive tear so that the rent has come through
to the most superficial fibers of the tendon. The reader should
visualize this vertical section so as to understand that the rent also
extends along the curve of the edge of the joint cartilage to a
considerable extent, leaving the sulcus bare, perhaps for an inch or
more. This condition I like to call a "rim rent," and I am confident
that these rim rents account for the great majority of sore shoulders.
It is my unproved opinion that many of these lesions never heal,
although the symptoms caused by them usually disappear after a few
months. Otherwise, how could we account for their frequent presence at
autopsy?
The anatomically observed prevalence of partial thickness cuff
lesions leads one to Codman's suggestion that commonly-diagnosed
diagnoses of shoulder pain, referred to as "cuff tendinitis",
"bursitis" or "impingement syndrome" may actually represent failure of
the deep surface fibers of the rotator cuff. (Fukuda, Hamada, 1994) The
degree to which the fibers that remain intact may hypertrophy,
strengthen, or adapt (Burkhart, Fischer, 1996) to stabilize the tear
and take up the function of the damaged fibers are not known. It
appears likely that repeated failure of small groups of fibers leads
not only to self-limited, acute symptoms (perhaps interpreted as
"tendinitis," or "bursitis" [Hawkins, Misamore, 1985]) but also to
progressive weakness of the rotator cuff, making it increasingly
susceptible to damage from lesser loads. This gives rise to the
"creeping tendon ruptures" described by Pettersson. (Pettersson, 1942)
The observation by Pettersson (Pettersson, 1942) and others that major
cuff defects may occur without symptoms or recognized injury suggests
that previous minor, often subclinical, fiber failure leaves shoulder
weaker and the cuff tendons progressively less able to withstand the
loads encountered in daily living.
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