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C OPYRIGHT 2012 BY T HE J OURNAL OF B ONE AND J OINT S URGERY, I NCORPORATED

Current Concepts Review

Posttraumatic Elbow Stiffness
Charalambos P. Charalambous, BSc, MBCHB, MSc, MD, FRCS (Tr&Orth), and Bernard F. Morrey, MD

Investigation performed at the Department of Orthopedic Surgery, Mayo Clinic, Rochester, Minnesota

Early posttraumatic elbow contractures may be treated with a combination of manipulation with the patient under
anesthesia followed by bracing.

Extrinsic contractures of the elbow may be treated with open or arthroscopic release, whereas intrinsic and
combined contractures may require tissue release as well as partial or total arthroplasty.

Elbow stiffness commonly occurs following elbow trauma,
which may involve substantial bone and soft-tissue injury but
may also occur after seemingly trivial trauma. An arc of elbow
motion of 100 (from 30 to 130) is required for most daily
activities, with a loss of 50 in the arc of motion causing up to
an 80% loss of function1. Posttraumatic elbow stiffness is
challenging to treat and often involves young, active patients.
In this article, we review the molecular pathogenesis of elbow
stiffness, its presentation and means of assessment, and
the reported outcomes of open and arthroscopic operative
techniques.
Pathology
Posttraumatic elbow stiffness may be due to soft-tissue con-
tracture (skin, capsule, ligaments, muscles, and tendons) or
osseous congruency disruption. The observation of severe
elbow stiffness, even with well-reduced stabilized fractures,
suggests that soft-tissue contracture is a major contributor.
Contractures in immobilized rat knees were mainly capsular
rather than myogenic2, and this may be the case in the elbow
too. In immobilized fractured rabbit knees, posterior capsular
disruption produced more severe, refractory contractures3.
A contracted capsule consists of cellular and extracellular
matrix components, showing substantial changes compared
with normal controls. Contracted capsules are thicker4 and
have increased collagen (type-I, III, and V)4,5 levels, the fibers of
which are disorganized4. These fibers demonstrate increased
collagen cross-linking, decreased proteoglycan and water
content6, an increase in matrix metalloproteinases (MMP-1, 2,
9, 13, and 15), and a reduction in tissue inhibitors of MMP5.
Contracted capsules have greater absolute and proportional
myofibroblast numbers7.
Pathogenesis
Role of the Myofibroblast
Myofibroblasts are important cells in the development of
posttraumatic elbow stiffness. These cells are tissue fibroblasts
that express the intracellular contractile protein alpha-smooth
muscle actin (a-SMA)8 that may interact with the extracellular
matrix through cell membrane integrins influencing matrix
organization9. Myofibroblasts can cause collagen contraction
more readily than can normal fibroblasts10.
Myofibroblast number is typically elevated in musculo-
skeletal fibrosis, such as adhesive capsulitis11 and Dupuytren
disease12, but also in cirrhosis and in pulmonary, corneal, and
cardiac fibrosis13-15. Hildebrand et al.7 showed that actual and
proportional myofibroblast numbers were elevated in elbow
capsules that required operative release compared with normal
controls. A regional variation was seen with greater increase in
the anterior capsule than in the posterior elbow capsule16. This
is consistent with the clinical observation that loss of extension
is more frequently encountered compared with loss of flexion
in elbow stiffness.
Myofibroblast number is inversely related to motion in
posttraumatic elbow stiffness16. Rabbit models of acute knee
contractures showed that the increase in myofibroblast number

Disclosure: None of the authors received payments or services, either directly or indirectly (i.e., via his or her institution), from a third party in support of
any aspect of this work. One or more of the authors, or his or her institution, has had a financial relationship, in the thirty-six months prior to submission of
this work, with an entity in the biomedical arena that could be perceived to influence or have the potential to influence what is written in this work. No
author has had any other relationships, or has engaged in any other activities, that could be perceived to influence or have the potential to influence what
is written in this work. The complete Disclosures of Potential Conflicts of Interest submitted by authors are always provided with the online version of the
article.

J Bone Joint Surg Am. 2012;94:1428-37 d http://dx.doi.org/10.2106/JBJS.K.00711

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Fig. 1
The myofibroblast is considered central in the pathogenesis of posttraumatic elbow stiffness. Multiple complex interactions may exist in influencing
the differentiation and activity of myofibroblasts. 1ve = stimulates, 2ve = inhibits, MSC = mesenchymal stem cell, and TNF-a = tumor necrosis
factor-a.
occurs early and is similar to that observed in chronic animal
and human contractures17.
Differentiation of mesenchymal stem cells and fibro-
blasts into myofibroblasts and the activity of the myofibroblasts
are influenced by a complex system of chemical and mechan-
ical signals (Fig. 1). Chemical regulators of myofibroblast
function are elevated in posttraumatic capsules of human el-
bows and in animal models18. These include transforming
growth factor beta (TGF-b1), connective tissue growth factor19,
and the domain of fibronectin ED-A (extra domain-A). Myo-
fibroblast contracture can activate latent TGF-b1, providing an
interlink between chemical and mechanical signals20. Autocrine
production of TGF-b1 may promote myofibroblastic differ-
entiation21. Tumor necrosis factor-alpha (TNF-a) has also been
shown to promote myofibroblast proliferation at low doses but
inhibit matrix contraction at higher doses22, via the inhibition
of a-SMA and collagen type-I gene expression. These regula-
tory effects of TNF-a were mediated through prostaglandin E2
and inhibited by diclofenac.
Another mechanism contributing to myofibroblast ac-
tivation is the mast cell-neuropeptide fibrosis axis23, docu-
mented in healing skin24. Mast cells occur in joint capsules and
contain granules of profibrotic mediators (platelet growth
factor A, endothelin 1, basic fibroblast growth factor, and
TGF-b125). These can induce myofibroblast differentiation and
P O S T T R AU M AT I C E L B O W S T I F F N E S S
proliferation. Mast cell degranulation is stimulated by neuro-
peptide substance-P and calcitonin-G-related peptide released
from nerve terminals26 in response to injury and pain27.
In animals and human elbows showing posttraumatic
contracture, the proportional numbers of myofibroblasts, mast
cells, and neuropeptide-containing nerve fibers are greater in
contracted capsules than in normal capsules23.
The mast cell may thus be the link between acute in-
flammation and subsequent contracture, and could be an
intervention target. Red Duroc pigs show greater wound con-
traction than Yorkshire pigs28. Ketotifen, an inhibitor of mast
cell degranulation, reduced wound contraction in red Duroc
pigs to a level seen in Yorkshire pigs. Similarly, ketotifen re-
duced mast cell and myofibroblast numbers and the degree of
flexion contractures by 42% to 52% in rabbit knees immobi-
lized for fractures29.
Role of Female Sex Hormones
Female sex hormones may act on extracellular matrix and
myofibroblasts to influence joint laxity and fibrosis. Joint hy-
permobility is more common in females, and increased laxity
occurs in pregnancy30. Estrogen, progesterone, and relaxin re-
ceptors occur in the anterior cruciate ligament (ACL)31-33. In-
creased ACL laxity correlates with menstrual cycle estrogen
and progesterone peaks34,35. Estrogen reduces collagen synthesis,
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whereas relaxin may decrease collagen formation and increase
the expression of MMP36,37. Knee contractures were created in
rats38. After two weeks of immobilization, there was a trend
toward reduced contractures in pregnant rats. The connective
tissue sensitivity to sex hormones may be modulated by injury.
Pregnancy increased the laxity of the medial collateral ligament
(MCL) in uninjured but not in injured rabbit knees39. Sex
hormone receptors are found in myofibroblasts of normal and
pathological tissues. Estrogen prevented cardiac fibrosis via
activation of the myofibroblast estrogen receptor beta40. Relaxin
decreased myofibroblast proliferation and downregulated
a-SMA expression in cell cultures41. Relaxin therapy in vivo
enhanced muscle regeneration and reduced fibrosis after
skeletal muscle injury42.
Role of Mechanical Factors
Differentiation of fibroblasts into myofibroblasts requires a
mechanically stiff substrate. Progenitor stem cells growing on a
substrate whose stiffness corresponds to bone, muscle, or brain
develop into the corresponding cell lineages43. Even in the
presence of TGF-b1, lack of stress inhibits myofibroblast dif-
ferentiation with TGF-b1 upregulating a-SMA only in fibro-
blasts grown on stiff but not compliant collagen44.
Genetic Predisposition
Individuals with similar elbow injuries show varying degrees of
contractures, raising the possibility of genetic predisposition to
stiffness. Nesterenko et al.45 reviewed the cases of 116 patients
with posttraumatic stiffness and identified a subgroup of four
patients who, following a trivial insult, had developed severe
elbow contractures, refractory to multiple operative and non-
operative interventions. This predisposition is supported by
animal studies. Forty rats from four inbred rat strains had knee
immobilization. The mean contracture observed in two of
these strains was significantly greater than that in the other two
(p < 0.05), supporting intrinsic genetic factors influencing the
severity of joint contractures46.
Understanding the molecular pathogenesis of posttrau-
matic stiffness can allow molecular targeting interventions to
prevent stiffness following elbow injury or its recurrence fol-
lowing operative release of established contractures. Under-
standing the genetic influence may shed light on the molecular
pathogenesis but also offer the exciting opportunity of identi-
fying individuals with an inherent susceptibility to stiffness and
allow early selective targeting.
Classification
Posttraumatic elbow stiffness may be classified as occurring
early or late in relation to the time of the injury. Early pre-
sentation, within six months of injury, may be more amenable
to operative intervention. Classification according to the
structures involved (soft tissue, osseous, or combined) is de-
scribed47. Classification of posttraumatic elbow stiffness into
intrinsic, extrinsic, or combined48 allows better understanding
of the cause of stiffness and provides more logical guidance to
management. Intrinsic contractures are secondary to involve-
P O S T T R AU M AT I C E L B O W S T I F F N E S S
TABLE I Intrinsic and Extrinsic Components of
Elbow Contractures*
Intrinsic Components Extrinsic Components
Intra-articular adhesions Capsular and ligamentous
contracture
Articular malalignment Heterotopic ossification
Loss of articular cartilage Extra-articular malunions
Combination of the above Soft-tissue contractures
following burns
*Most contractures are a combination of both intrinsic and
extrinsic components.
ment of the articular surface, whereas extrinsic are those not
involving the articulation. In reality, most are a combination of
both (Table I).
Presentation
Establishing the exact injury mechanism and subsequent treat-
ment of a patient presenting with elbow stiffness after trauma is
important. It is essential to examine elbow flexion-extension and
pronation-supination actively and passively. The functional
limitations and patients expectations of treatment need to be
established. Typical posttraumatic elbow stiffness is painless.
Pain at mid-motion suggests an intrinsic component to stiffness.
Pain at the extremes of motion is consistent with impingement
between the olecranon or coronoid process and the distal end of
the humerus, usually due to osteophyte formation. With previous
operative treatment and internal fixation, the possibility of in-
fection should be considered. Neurological signs such as ulnar
nerve involvement must also be considered48.
Clinical Evaluation
Radiographs are often sufficient to image the stiff elbow.
Computed tomography with three-dimensional reconstruc-
tion may accurately localize loose bodies and/or impinging
osteophytes, assisting in planning arthroscopic debride-
ment49. Checking inflammatory markers (C-reactive protein
level and erythrocyte sedimentation rate) helps in excluding
infection or inflammatory conditions. Examination with the
patient under anesthesia may differentiate an apparent loss of
elbow motion due to pain and apprehension from true me-
chanical stiffness.
Management
Management options involve nonoperative (serial bracing, ex-
amination under anesthesia, and splinting) or operative treat-
ment in the form of open or arthroscopic release, interposition
arthroplasty, or partial (radial head excision and replacement
and capitellar resurfacing) or total elbow arthroplasty. Treat-
ment is guided by the timing of presentation, the symptoms
and expectation of the patient, functional level, and the un-
derlying cause of contracture.
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TABLE II Reported Outcomes After the Use of Splinting for Elbow Stiffness

Mean Range of Mean Flexion Mean Extension

Motion (deg) (deg) (deg)
Study No. of Cases Preop. Postop. Preop. Postop. Preop. Postop.

Static progressive splinting

51
Bonutti et al. 20 115 129 236 217
52
Doornberg et al. 29 71 110 107 130 235 220
53
Green and McCoy 15 62 107 126 133 260 223
54
Ulrich et al. 37 81 107 110 125 230 219
55
Bhat et al. 28 57 102 118 126 259 227
56
Suksathien and Suksathien 3 27 65 97 103 270 238
57
Gelinas et al. 22 76 100 108 127 232 226
Dynamic splinting
58
Gallucci et al. 17 66 107 108 126 242 219
59
Dickson 1 10 110 100 120 290 210

Intervening for loss of the functional arc of elbow motion
(30 to 130) seems appropriate. However, intervention for the
loss of a lesser amount of motion may be needed in individuals
such as professional athletes or musicians for whom motion
beyond the average functional arc is important.
For patients seen within six months of injury, nonoper-
ative treatment with serial bracing and/or examination under
anesthesia is preferable.
Bracing
Braces for improving elbow motion are either dynamic or static
progressive types50. Dynamic splints have an adjustable spring
exerting a constant stretching load, set to an extent not pro-
ducing pain. In static splinting, the maximum load that can be
tolerated comfortably is applied. As the tissue stretches, the
load required to maintain this stretched state reduces, and the
load becomes better tolerated; the splint is readjusted so that
more load is applied and further stretching achieved. Biological
tissues show viscoelastic properties including creep and stress
relaxation. Dynamic splinting is based on creep (an increase in
length with the application of a constant load for prolonged
time50) and static progressive splinting on stress relaxation
(a decrease in load required to maintain a certain length over
time).
Successful results have been reported with both dy-
namic and static splinting, but a controlled comparison
awaits. Table II summarizes several studies51-59 that have de-
scribed serial elbow splinting. We favor static progressive
splitting because it is better tolerated, and shorter utiliza-
tion periods may increase compliance. The exact protocol
for bracing is based on the degree of contracture, splint tol-
erance, personal circumstances, compliance, and rate of de-
formity correction.
Examination with the Patient Under Anesthesia
Examination under anesthesia may be used for elbow con-
tractures presenting early. It involves assessing the passive range
of motion; evaluating for crepitus, surface irregularity, and
stability; and manipulation to improve motion. The presence
of crepitus and surface irregularity may signify an intrinsic
component to the stiffness. Manipulation is attempted only
when there is radiographic evidence of osseous fracture union
and should be avoided with fractures that have not healed.
Regaining elbow flexion is easier to achieve than is elbow ex-
tension. Examination with the patient under anesthesia is
followed by serial bracing. The value of examination under
anesthesia in treating stiffness comes mainly from reports of its
use following operative treatment60,61 rather than following
trauma.
Operative Treatment
Operative treatment is guided by the type of contracture pres-
ent. Extrinsic contractures are usually managed with open or
arthroscopic release. Those with a large intrinsic component
are managed with arthroplasty. In combined contracture, both
methods of treatment may be used.
Open Release
Open release has been the standard treatment for managing
extrinsic contractures. Several open approaches have been de-
scribed, and they have been guided by the cause, anatomical
location, and goals of the treatment.
Lateral Column Procedure
The lateral column procedure62 consists of an arthrotomy,
capsular release, and osteophyte excision. It allows release of
the anterior and posterior capsule. The incision is centered over
the lateral humeral epicondyle, elevating the brachioradialis
muscle from the humerus, the common extensor origin from
the lateral collateral ligament (LCL), and the brachialis muscle
off the anterior elbow capsule. The capsule is entered at the
level of the radiocapitellar articulation, the lateral capsule
is excised, and the medial capsule is incised. Intra-articular
adhesions and coronoid osteophytes are removed. Elevation of
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the triceps and anconeus muscles from the distal end of the
humerus and proximal part of the olecranon allows posterior
capsular release and olecranon fossa debridement. The LCL
is preserved but, if released, it is reattached via drill-holes or
suture anchors. The lateral approach may not give adequate
exposure to the far medial part of the joint.
Medial Approach
A skin incision is made over the medial humeral epicondyle,
and while the ulnar nerve is protected, the pronator teres
muscle is elevated from the common flexor mass, exposing and
releasing the anterior capsule. The triceps muscle is elevated off
the humerus and olecranon, allowing release of the posterior
band of the MCL and posterior capsule and removal of the
olecranon osteophytes. The anterior band of the MCL is pre-
served for stability. This approach is limited, not giving suffi-
cient exposure to the lateral part of the joint48.
Anterior Approach
This approach accesses the anterior capsule to better manage
flexion contractures63. An anterior bayonet incision is made
across the elbow flexion crease. The medial and lateral ante-
brachial cutaneous nerves; brachial artery; and median, radial,
and musculocutaneous nerves are protected. Medially, the in-
terval between the common flexor origin and biceps tendon
and, laterally, the interval between biceps and brachioradialis
muscle are developed. The brachialis muscle is dissected from
the anterior capsule medially to laterally, exposing the capsule,
which is released and excised.
Posterior Approach
This approach allows extensive medial and lateral releases
and can be used to perform interpositional arthroplasty
when indicated. A midline posterior incision is utilized. The
triceps and anconeus muscles are reflected from the ulna.
The common extensor origin is elevated from the anterior
capsule, which is released. The ulnar nerve is decompressed
and the posterior part of the MCL is released. If greater
exposure is necessary, further release of the triceps and
anconeus muscles from the olecranon is performed laterally
to medially. The triceps is reattached to the olecranon via
drill-holes64.
Other descriptions of open releases include isolated MCL
division65, and the transolecranon osteotomy approach66. We
favor the lateral column procedure for most cases of open re-
lease, reserving the posterior approach when lateral and ex-
tensive medial releases are needed or when the ulnar nerve
must be decompressed. The isolated medial release has limited
indications, whereas an anterior approach is used for isolated
anterior ectopic bone excision.
Arthroscopic Surgical Release
Arthroscopic osteocapsular release involves the removal of
osseous components, such as osteophytes and ectopic bone,
and capsular release. Various arthroscopic portals provide
access to the olecranon fossa and elbow joint. Capsular re-
P O S T T R AU M AT I C E L B O W S T I F F N E S S
tractors facilitate exposure and protect neurovascular struc-
tures. Shavers are used in free-flow mode with suction avoided.
Arthroscopic release is a challenging procedure because of
the close proximity of the neurovascular structures. Although
arthroscopic release has been used for the most difficult and
challenging posttraumatic elbow stiffness by experienced
surgeons, it is a procedure with a steep learning curve, as-
sociated with serious complications67-70. For most surgeons,
particularly those who perform few arthroscopic elbow
procedures, it is a procedure to be undertaken with care and
is reserved for the less severe spectrum of posttraumatic
contractures.
Outcomes
We reviewed the English-language literature to identify clinical
studies examining the outcome of open and arthroscopic re-
lease for posttraumatic elbow stiffness. These are summarized
in Tables III and IV63,71-99. These studies describe primarily
Level-IV evidence involving case series, with no randomized
trials identified. Although there has been a variation in the
approaches utilized and in postoperative rehabilitation proto-
cols, both open and arthroscopic procedures can reliably in-
crease elbow flexion and extension (Tables III and IV). The
results of open arthrolysis are durable over time. Sharma
and Rymaszewski71 reviewed the cases of twenty-five patients
treated by open arthrolysis. The improvement in mean elbow
motion from 55 preoperatively to 105 at one year postop-
eratively was maintained over a mean follow-up interval of
7.8 years.
Management of the Ulnar Nerve
Regardless of the surgical technique used, understanding the
status of the ulnar nerve is critical. With a large flexion loss, or
if ulnar nerve symptoms are present prior to operative release,
nerve decompression is performed at the time of surgery, as
motion gain can initiate or exacerbate ulnar nerve symptoms100.
If there is nerve instability, it is transposed.
Continuous Passive Motion
Continuous passive motion is used to reduce stiffness following
operative treatment or trauma. Joint stiffness occurs in four
stages (bleeding, edema, granulation tissue formation, and fi-
brosis). The first two occur early, whereas granulation tissue
and fibrosis occur over days to months. Continuous passive
motion aims to reduce intra-articular bleeding and periartic-
ular edema through a sinusoidal change in intra-articular and
periarticular pressure. Continuous passive motion is effective if
applied early and has very little role to play once granulation
tissue and fibrosis are established101.
Lindenhovius et al.102 reported a case-control study as-
sessing continuous passive motion following open elbow
release. The case group had continuous passive motion im-
mediately set at the level of flexion-extension achieved intra-
operatively. Continuous passive motion was used at home
for two weeks as tolerated. There was no difference between
the continuous passive motion and control groups with
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TABLE III Reported Outcomes Following Open Release for Posttraumatic Elbow Stiffness

Mean Range of Mean Flexion Mean Extension

Motion (deg) (deg) (deg)
Study No. of Cases Mean Follow-up (mo) Preop. Postop. Preop. Postop. Preop. Postop.
71
Sharma and Rymaszewski 25 7.8 55 110 115 135 260 230
72
Ofiaeli 9 6 4 88 234 212
73
Marti et al. 47 120 45 99 73 114 229 215
74
Heirweg and De Smet 16 47 47 87 104 122 257 236
75
Park et al. 27 22.5 46 102 86 121 240 219
76
Tan et al. 52 18 57 116
77
Cikes et al. 18 16 82 122 117 131 235 28.8
78
Stans et al. 37 15 66 94 118 129 252 232
79
Tosun et al. 30 12 35 86 2 2 2 2
80
Ring et al. 46 48 45 103 93 125 248 221
81
Lindenhovius et al. 23 23 51 106 97 129 246 223
82
Gundlach and Eygendaal 21 24 69 113 2
83
Brinsden et al. 23 43 255 232
84
Weizenbluth et al. 13 57 34 85 107 125 273 240
85
Amillo 34 48 45 92
86
Boerboom et al. 12 62 73 112
87
Park et al. 42 39 89 124 234 29
88
Bae and Waters 11 29 53 107 109 123 257 215
89
Mih and Wolf 9 17 55 108 102 124 247 215
90
Cohen and Hastings 22 26 74 129 113 137 239 28
91
Kulkarni et al. 25 63 16 102 64 119 252 217
63
Aldridge et al. 77 33 59 97 111 117 252 220
92
Kayalar et al. 18 47 26 92 81 124 255 232
93
Nobuta et al. 27 18 53 95 83 121 230 226

regard to motion gain and functional scores. However, this The numbers of patients were small (twelve in the continuous
was a retrospective study with no guidelines for treatment passive motion group and ten in the control group). Gates
allocation, inconsistencies in the protocol for the use of con- et al.103 prospectively studied continuous passive motion fol-
tinuous passive motion, and no formal compliance assessment. lowing anterior capsulotomy for elbow flexion contracture.

TABLE IV Reported Outcomes Following Arthroscopic Surgical Release for Posttraumatic Elbow Stiffness

Mean Range of Mean Flexion Mean Extension

Motion (deg) (deg) (deg)
Study No. of Cases Follow-up* (mo) Preop. Postop. Preop. Preop. Postop. Preop.
94
Phillips and Strasburger 15 80 130 117 135 238 26
95
Lapner et al. 12 54 108 126 130 137 222 210
96
Ball et al. 14 12 117 133 235 29
97
Salini et al. 15 18 100 137 260 213
98
Timmerman and Andrews 19 29 123 134 229 211
99
Kim and Shin 33 24 73 123 106 132 233 29

*The data are given as the mean duration of follow-up, except where indicated as the minimum duration of follow-up.
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There was no difference in extension gain between the con-
tinuous passive motion and control groups; however, contin-
uous passive motion significantly increased flexion gain (p =
0.0036). The mean gain in total arc of motion was greater in the
continuous passive motion group (48 preoperatively to 96
postoperatively) compared with controls (69 preoperatively to
94 postoperatively).
Postoperatively, continuous passive motion may be used
in the hospital, under a nerve block to control pain, and then
continued at home. The continuous passive motion machine is
set to allow maximal motion within pain limits. The use of
continuous passive motion requires careful patient monitoring
to avoid neurological injury or wound breakdown. Tight, cir-
cumferential dressings are avoided. Once the patient is able to
actively maintain most of the motion achieved intraoperatively,
continuous passive motion is changed to a program of splint-
ing, usually for three months. Nighttime splinting is continued
for up to six months.
Postoperative Examination with the Patient
Under Anesthesia
If an external fixator was utilized at the time of operative release
to protect ligamentous repair, it is removed approximately
three weeks postoperatively with the patient under anesthesia.
This allows examination under anesthesia and, if needed, fur-
ther manipulation61.
Physiotherapy
The role of physiotherapy in managing the stiff elbow is
uncertain. To our knowledge, there is no comparative study
evaluating the role of therapy in this context. We believe that
uncontrolled therapy may exacerbate pain and inflammation
and inhibit rather than facilitate mobilization. Therapy, if
given, should be done in a controlled manner in close com-
munication with the surgical team, guiding rather than forcing
motion gains.
Management of Intrinsic Contractures
Managing intrinsic posttraumatic stiffness is challenging, as
patients are often young and functionally demanding. The
options in these patients are release of extrinsic contractures
alongside interposition, total, or partial arthroplasty if there is
substantial articular cartilage damage. Resection arthroplasty
and arthrodesis are poorly tolerated options and should be
avoided.
Total elbow arthroplasty or partial arthroplasty will
likely lead to the need for additional operative treatment in
young patients because of wear or loosening, and interposi-
tion arthroplasty may offer a more durable solution. Several
interposition materials have been described. Larson and
Morrey104 reported interposition arthroplasty with fresh-frozen
Achilles tendon allograft in posttraumatic and inflamma-
tory arthritis in forty-five elbows in patients with a mean age
of thirty-nine years. Operative treatment was for pain,
stiffness, and instability, with >50% involvement of the
articular surface of the trochlea and capitellum. At a mean
P O S T T R AU M AT I C E L B O W S T I F F N E S S
follow-up interval of six years, seven elbows required revision.
In those with surviving allografts, the mean flexion-extension
arc improved from 51 preoperatively to 97 postoperatively.
The mean Mayo elbow performance score (MEPS) increased
from 41 to 65 points. Thirteen patients had a good or excellent
result; fourteen, a fair result; and eleven, a poor result. Al-
though improvement in the pain score was only 4 of 45 points
on the MEPS pain component, patients were subjectively
highly satisfied, with nineteen rating their elbow as much
better and twelve, as somewhat better following interposition
arthroplasty.
Interposition arthroplasty can be converted to total el-
bow arthroplasty with results comparable with those of total
elbow arthroplasty performed for other indications. Blaine
et al.105 reported on twelve total elbow arthroplasties following
interposition arthroplasty (average patient age at the time of
total elbow arthroplasty was fifty years, and the average interval
from interposition to total elbow arthroplasty was 9.9 years).
There were no intraoperative or perioperative complications.
Pain was mild or none, and the result was satisfactory in ten.
The mean MEPS improved from 32.1 preoperatively to 80.4
postoperatively. This study supports the potential benefit of
interposition arthroplasty in buying time until the patient is
older before undergoing total elbow arthroplasty.
Total Elbow Arthroplasty
Peden and Morrey106 reported on thirteen patients who un-
derwent total elbow arthroplasty with use of the Coonrad-
Morrey107 total elbow prosthesis (Zimmer, Warsaw, Indiana)
for spontaneous ankylosis. The position of ankylosis ranged
from 35 to 95 of flexion and was posttraumatic in ten pa-
tients and inflammatory in three. Surgery was challenging,
with a mean operating time of 182 minutes and a high rate
of complications (component malposition, humeral epi-
condylar fracture, wound necrosis, skin breakdown, and ulnar
loosening in one patient each; deep infections in three; and
heterotopic ossification in five). However, the mean arc of
motion achieved was 37 of extension to 118 of flexion. The
mean MEPS for ten patients was 74 points at a mean of ap-
proximately ten years, with good to excellent outcomes in
seven of the thirteen patients. Preoperatively, only three of
thirteen patients were able to complete any of the MEPS ac-
tivities of daily living; however, postoperatively, all were able
to complete some activities and seven, all activities, with
varying degrees of difficulty. Figgie et al.108 reported on
nineteen total elbow arthroplasties performed for complete
ankylosis that had been present for an average of five years. A
26% complication rate occurred. Five patients required fur-
ther manipulation to increase motion. The elbows achieved a
mean arc of motion of 80 (range, 35 to 115) that was
maintained at mean follow-up interval of 5.75 years. The
mean Hospital for Special Surgery Score increased from 23 to
84 points, with four excellent, eleven good, and three fair
results and one failure108. The duration of ankylosis before
total elbow arthroplasty was not related to postoperative
motion.
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Partial Elbow Arthroplasty
In patients with articular cartilage destruction of the radio-
capitellar articulation but preservation of the ulnohumeral
articulation, partial elbow arthroplasty may be utilized109. This
is an attractive option in young patients as it is bone-preserving
and could avoid total elbow arthroplasty complications. Iso-
lated radial head, capitellar, or total radiocapitellar replacement
may be performed along with open capsular release.
Heijink et al.110 reported on three patients who under-
went radiocapitellar hemiarthroplasty for arthritis. At a mean
follow-up of eighty-seven months, the MEPS was 80 points for
one patient and 100 points for two patients, and all patients
were satisfied. Pooley111 described lateral elbow resurfacing and
presented his early results112. Fifty-five elbows had lateral elbow
resurfacing (hemiarthroplasty or total) for osteoarthritis, rheu-
matoid arthritis, or posttraumatic arthritis. The mean MEPS
increased from 46 points preoperatively to 90 points postop-
eratively, and mean flexion-extension increased from 79 to
110 by twenty-four months. Forty-eight patients had satis-
factory results, but five with isolated capitellar resurfacing re-
quired conversion to a total lateral elbow resurfacing. Longer
results are pending.
Distraction Arthroplasty
Distraction arthroplasty is used for instability following con-
tracture release and reattachment of the collateral ligaments
and following interposition arthroplasty to protect the graft113.
Gausepohl et al.114 reported on fourteen children or adolescents
treated with isolated distraction using dynamic external fixa-
tion. Intraoperative distraction was followed by a six-day re-
laxation phase and then by elbow mobilization and distraction
for seven weeks. Impinging ectopic bone was removed in four
patients, but no formal arthrolysis was performed. At a mean
follow-up of thirty-four months, the mean flexion-extension
had increased from 37 preoperatively to 108.
Stiffness in the Presence of Instability
It is difficult to treat elbow stiffness occurring secondary to
immobilization for instability, such as after a missed radial
head dislocation with associated ulnotrochlear subluxation.
One option is to address the instability and stiffness at the same
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(Tr&Orth)
Blackpool Victoria Hospital, Whinney Heys Road, Blackpool,
Lancashire FY3 8NR, United Kingdom.
E-mail address: BCharalambos@hotmail.com
Bernard F. Morrey, MD
Department of Orthopedic Surgery, Mayo Clinic,
200 First Street S.W., Rochester, MN 55905
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