Manual Therapy 18 (2013) 594e597

Contents lists available at SciVerse ScienceDirect

Manual Therapy
journal homepage: www.elsevier.com/math

Case report

Adhesive capsulitis of the hip: A case report: An entity in question

Rebecca Lowe*
Manual Therapy of Nashville, LLC, 74 Brookwood Terrace, Nashville, TN 37205, USA

a r t i c l e i n f o

a b s t r a c t

Article history:
Received 27 January 2012
Received in revised form
8 August 2012
Accepted 31 August 2012

Very little has been discussed in the medical literature concerning adhesive capsulitis of the hip (ACH).
There are no articles to date in the physical therapy literature regarding ACH and only a dozen or so in
medical journals. Evidence suggests ACH may present in a similar progression through four stages as
adhesive capsulitis of the shoulder (ACS) (from synovial inammation to capsular brosis). Consensus
does not exist for management of ACS or ACH. However, most clinicians agree that treatment should be
guided by the stage of the disorder, whether medically, surgically, or through physical therapy. A large
part of the confusion for management of adhesive capsulitis (ACS and ACH) is due to the many studies
that have not reported their ndings by stage. Arthroscopy and synovial/capsular biopsy can conrm the
presence and stage of adhesive capsulitis. Primary (idiopathic) ACH is proposed to be caused by
biomechanical dysfunction in the hip or other joints related to the mechanical function of the hip. The
treatment for stages 1 and 2 consists of using techniques to reduce inammation and correct biomechanical faults that affect the hip. In stages 3 and 4 treatment focuses on the biomechanical dysfunction
of the spine, hip(s), pelvic ring, and lower limb, if needed. In this case, the 55-year-old female patient
presenting with probable stage 3 adhesive capsulitis, responded well to manual therapy and has been
able to return to functional activities and maintain them with a home program.
2012 Elsevier Ltd. All rights reserved.

Keywords:
Adhesive capsulitis of the hip
Synovial inammation
Capsular brosis
Biomechanical dysfunction

1. Introduction
Adhesive capsulitis has been dened as a condition that begins
with synovial inammation and ends in capsular brosis (Rodeo
et al., 1997; Kabbabe et al., 2010; Neviaser and Hannan, 2010;
Neviaser and Neviaser, 2011). It is also described as a continuum of
four stages (Hannan and Chiaia, 2000). Hsu et al. (2011) reports
the association between ACS and other diseases/conditions. This
has not been discussed in the literature for the hip.
Caroit et al. (1963) introduced the concept of ACH. Since then
only a dozen or so articles have been published referring to this
diagnosis (Murphy et al., 1977; Lequesne et al., 1981; Grifths et al.,
1984; Chard and Jenner, 1988; Luukkainen and Asikainen, 1992;
Modesto et al., 1995; Mont et al., 1999; McGrory and Endrizzi, 2000;
Byrd and Jones, 2006; Joassin et al., 2008; Luukkainen et al., 2008).
Adhesive capsulitis of the hip has also been referred to as
frozen hip (Chard and Jenner, 1988) or capsular constriction
(Lequesne et al., 1981). Two cases of adhesive capsulitis of the ankle
have been reported (Goldman et al., 1976; Grifths et al., 1984), as
well as one in the wrist (Hanson et al., 1988). Many articles have

* Tel.: 1 240 751 7578; fax: 1 615 356 1524.

E-mail address: m-t-n@comcast.net.
1356-689X/$ e see front matter 2012 Elsevier Ltd. All rights reserved.
http://dx.doi.org/10.1016/j.math.2012.08.006

addressed this condition in the shoulder with recent reviews by

Neviaser and Hannan (2010), Hsu et al. (2011), and Neviaser and
Neviaser (2011). Hannan and Chiaia (2000) and Kelley et al.
(2009) discuss treatment approaches to ACS that include physical
therapy and medical/surgical interventions based on the stage of
the condition.
Shoulder arthroscopy and biopsies of the synovium and capsule
have given physicians the ability to diagnose ACS and its corresponding stage (1e4) (Rodeo et al., 1997; Sakai et al., 2001; Oehler
et al., 2002; Mullet et al., 2007; Kabbabe et al., 2010; Neviaser and
Hannan, 2010; Hsu et al., 2011; Neviaser and Neviaser, 2011).
Arthroscopic appearance and biopsy have also been used to diagnose ACH (Byrd and Jones, 2006). Similar to ACS, the synovium and
capsule of ACH have either a classically inamed or brosed
appearance depending on the stage of the disorder which can be
observed during hip arthroscopy or open surgery. Biopsy of the
synovium and capsule can show the presence and concentration of
cytokines revealing inammation and brosis on the histological
level. Cytokine levels in synovial uid aspirations have also been
shown to conrm the presence of ACS (Mullet et al., 2007). A
detailed discussion of the arthroscopic appearance and histological
ndings of ACS per stage can be found elsewhere (Hannan and
Chiaia, 2000; Kelley et al., 2009; Neviaser and Hannan, 2010;
Hsu et al., 2011; Neviaser and Neviaser, 2011).

R. Lowe / Manual Therapy 18 (2013) 594e597

In ACH, testing often reveals osteopenia of the hip. Other diagnostic tests are most often negative, unless other pathology is
present such as labral tears, chondral injury, and tears of the ligamentum teres (Byrd and Jones, 2006). Unless ACH is diagnosed
through surgery or biopsy, clinicians must rely on the patients
history and clinical ndings to diagnose ACH and aim treatment at
the underlying pathology or pathologies. The literature for ACH
does not discuss the ndings by stage, nor does it report the natural
progression of the disorder. However, clinical characteristics are
proposed to be similar to those of ACS and are listed by stage (see
Table 1).
The medical literature discusses differentiation between
primary (idiopathic) and secondary ACS (Hannan and Chiaia,
2000; Neviaser and Hannan, 2010; Hsu et al., 2011). Hsu et al.
(2011) denes primary ACS as adhesive capsulitis that is present
without known etiology or concomitant pathology. If adhesive
capsulitis is present and a second pathology is already known, then
the clinician should treat both diagnoses appropriately. The
complex presentations of secondary ACH can be challenging and
may require further diagnostic testing.
The literature of ACS and ACH does not discuss biomechanical
dysfunction as a possible etiology, although one article on ACH
reports the presence of back pain in 3 case studies (Joassin et al.,
2008). Evidence in the research shows interrelationships between
the hip and the lumbar spine (Ellison et al., 1990; Sims, 1999; Lee
and Wong, 2002; Shum et al., 2005; Hwang and Kim, 2009;
McGregor and Hukins, 2009; Carvalhais et al., 2011). Primary ACH
is proposed to be caused by biomechanical dysfunction in the hip
and/or in the joints related to the mechanical function of the hip,
including the spine, sacroiliac joint, and lower limb joints. It
would be interesting and informative to evaluate joint biomechanics, muscle weakness/muscle imbalances, pain or reex
inhibition, and leg length discrepancies when considering the
etiology of any adhesive capsulitis. In addition to these, immobility should also be considered as a factor, as it has been shown to
lead to joint contractures produced by the same cytokines that
lead to capsular brosis in adhesive capsulitis (Hagiwara et al.,
2008).
1.1. Case history
At the initial visit in October 2009 the patient was a 55-yearold female who gave a ve-year history of right hip pain that
progressed to bilateral hip pain (see Fig. 1). The patients right
lateral hip pain began suddenly while the patient was sleeping.
The patient described the initial pain as a constant throbbing pain
that kept her awake. On a pain scale she reports that it was 8 out
of 10 and increased with hip movements. For some time the
patients pain was felt only at night, but it gradually began to

595

include times while driving and sitting. At some point the pain
progressed to include the left hip and to include episodic sharp
pain. The patient described the pain as being worse in sitting and
driving and lessened with standing. The patients pain location
began at her lateral hip region and progressed to anterior hip
region. Several months prior to initial consultation with the
author the patients pain had changed again, but to the groin
region (see Fig. 1). This included episodes of sharp pain with
certain hip movements.
The patients past medical history included an episode of low
back pain 20 years prior to initial consultation. The patient had
been reaching for her young son when she felt immediate low
back pain. She was diagnosed with a pulled muscle and
prescribed valium and bed rest. The patient had only one recurrence of low back pain before she began swimming, bicycling, and
walking for exercise. When she was 26-years-old and working as
a nurse, the patient started wearing orthotics for foot pain. A
podiatrist prescribed a 1/3 inch heel lift for her left lower
extremity shortly after the patient developed the hip pain. Overthe-counter Ibuprofen was ineffective for her hip pain. Diagnostic testing by her physician included X-rays and bone density
testing. The X-rays of her hips showed normal wear-and-tear
and the bone density testing was within normal limits. The
patient had seen a different physical therapist several years after
initial onset. The treatment from the prior physical therapist
consisted of stretching of her hips and knees and performing leg
lifts which had minimal effect.
1.2. Objective examination
The patient was 50 400 and weighed 155 pounds. Observation of
the patient in standing demonstrated moderate spinal scoliosis
with convexity to the right in the thoracic spine and convexity to
the left in the lumbar spine. The patient also had increased lumbar
lordosis and increased right foot pronation. The patients scoliosis
was diminished with a heel lift under her left foot.
Observation of the patients gait revealed increased internal
rotation of both femurs throughout the gait cycle accompanied by
circumduction of the hips. Neurological testing, which included
sensory, motor, reex, and Babinski/Ankle Clonus testing was
negative. The range of motion of the lumbosacral spine demonstrated signicantly impaired exion with an inability to atten the
lumbosacral lordosis.
The range of motion of the patients hips was tested using
combined movement tests. The patients hip range of motion was
signicantly reduced bilaterally in combined extension/external
rotation and exion/abduction/external rotation (see Table 2). The
strength of the right hip abduction/extension was 4/5, compared to
the left which was 4/5.

Table 1
Clinical characteristics of ACH by stage.
Symptoms

Irritability

Range of motion

End feel

High

When range of motion (ROM) is performed when

the patient is under anesthesia there is no, or very little,
range of motion decit.

Empty

Stage 2
Freezing Stage

Gradual onset of pain, achy at rest and often

sharp with movement. Night pain is common.
Often patients unable to sleep on affected side.
Patients describe limitation of motion or
limitation of functional activities.
Pain is constant and can be more severe,
particularly at night.

High

Pain is felt prior to

resistance or end feel.

Stage 3
Frozen Stage

Primary complaint is stiffness. Pain occurs

at end of motion.

Moderate

Stage 4
Thawing Stage

Patients report minimal pain. Patients can

have a gradual return to functional activities.

Low

Moderate range of motion limitation. When ROM is

performed under anesthesia it is the same or almost
the same as when the patient is awake.
Signicant range of motion limitation. When ROM
is performed under anesthesia there is no improvement
with testing.
Can have a gradual improvement in range of motion.

Stage 1
Initial Stage

Abnormally rm capsular
end feel. Resistance met
prior to pain.
Similar to Stage 3.

596

R. Lowe / Manual Therapy 18 (2013) 594e597

Fig. 1. Body chart: progression of symptoms.

Joint mobility testing showed decreased arthrokinematic glides

in multiple joints including the thoraco-lumbar junction and
segments L3-S1. The patients hips had decreased joint glides,
particularly in the posteromedial direction.
Palpation of the lumbar spine and hips was signicant for
tightness and tenderness of the paravertebral muscles, the
adductor muscles, the anterior hip musculature, and the Iliopsoas
muscles bilaterally.
The following tests were negative: provocative sacroiliac joint
stress tests, dural testing e slump and SLR, posterior-to-anterior
pressure on the spinous processes, and axial compression/distraction of the spine.
1.3. Treatment

2.
3.

4.

5.

The patient was seen 9 times per year over a two-year span. The
following is a list of the exercises and techniques used for her
treatment.
1. Joint mobilization of the spine and hips. The mobilization of the
spine using grade 4/4 techniques focused on reducing the
patients scoliosis. The mobilizations of the hips were performed
using a sustained technique for 5e7 min for the posterior and
posteromedial glides, to the patients tolerance. While this

6.

technique was being held the patient was instructed to make

her leg longer and then relax. Combined range of motion
testing was repeated at the end of each treatment to note the
improvement in range of motion and symptom reduction.
Soft tissue mobilization of the paraspinals, the hip musculature, and the Iliopsoas muscles.
Strengthening exercises including core strengthening and
specic hip strengthening exercises. The hip strengthening
exercises consisted of standing hip extension/abduction with
a circle of grey theraband around the ankles. The patient was
instructed to perform these exercises on both sides daily.
Hip stretching exercises were given to the patient to perform at
home. These included stretching into hip abduction/external
rotation, extension/external rotation.
The patient was instructed in self-massage techniques to
perform daily to address muscle tightness.
Posture instruction was given as well, focusing on minimizing
the lumbar hyperlordosis.

By the end of the second course of treatment the patient had

a good understanding of how to self-manage her condition and was
performing her home program consistently. Even so, she continues
to need further manual therapy treatment approximately once
every 3 months when the sharp pain returns. The patient has been

Table 2
Results of combined movement testing of the hip e right side.

Flexion/adduction/internal rotation
Flexion/abduction/external rotation
Extension/external rotation
Extension/internal rotation

Passive range of motion

End feel

Symptoms

Reduced
Signicant reduction 0e40 from vertical
Signicant reduction 0e10
No reduction

Capsular
Abnormally rm capsular
Abnormally rm capsular
Capsular

Pinching in groin
Pain in groin and anterior hip
Pain in groin and anterior hip
No symptoms

R. Lowe / Manual Therapy 18 (2013) 594e597

able to continue with ADLs without problems as long as she

stretches 2/day and performs exercises as given by the therapist.
The patient swims 3/week, uses a stationary bike for 30 min 3/
week, and limits walking to 15e20 min/day. She has pain only after
prolonged sitting that she rates as 5/10 on a pain scale and
describes as being aware of soreness.
2. Discussion
The patient in this case was treated for Stage 3 ACH, as determined by the following clinical signs and symptoms: pain history
indicating low irritability, signicantly reduced range of motion
(particularly into combined exion/abduction/external rotation
and extension/external rotation), and the end feel. The end feel was
abnormally rm and pain was produced after resistance was met.
Since the ACH was in the brosed stage with low irritability and
inammation, the hip was managed biomechanically including
treatment for the hips, the spine, and the pelvic ring. The patient
had already received a heel lift and orthotics to address leg length
discrepancy and right foot over-pronation.
It is theorized that if the patient had received earlier intervention for her leg length discrepancy and scoliosis she may not have
developed hip dysfunction. Or, if she had received biomechanical
treatment earlier, the patient may have had full recovery or at least
not required the same level of maintenance at home to prevent
recurrence.
3. Summary
This case discusses adhesive capsulitis of the hip, an underrecognized entity. There has been enough evidence to support
ACH including the clinical presentation, observation of the capsule
on open reduction or hip arthroscopy, and through synovial/
capsular biopsy. In this case report, the patient had sufcient
clinical ndings to support the diagnosis of stage 3 ACH and was
treated biomechanically, which resulted in successful management
of her symptoms and return to functional activities.
The literature is missing a discussion of the different stages and
a description of the ndings and treatment for each stage.
However, by looking at the research on ACS, therapists can make
comparisons and apply evaluation and treatment principles
accordingly until the research can conrm our suppositions more
denitively.
Current studies of ACS, ACH, osteoarthritis, and immobility
report the presence of the same cytokines that result in brosis of
the joint capsule. It is proposed that there are different levels of the
cytokines found in these different conditions.
If future studies examine the biomechanics of the affected joint,
and those joints related mechanically to the affected joint, the
author believes the research will conrm that biomechanical
dysfunction is the etiology in otherwise unexplained ACH or ACS
(primary or idiopathic adhesive capsulitis).
Acknowledgments
I would like to acknowledge Gail Molloy and Jim Meadows for
being exceptional mentors. I would like to thank Bryant Miller and
David Sheer for their time and assistance on this project.

597

References
Byrd JWT, Jones K. Adhesive capsulitis of the hip. Arthrosc Relat Surg 2006;22(1):
89e94.
Caroit M, Dijan A, Hubault A, Nomandin C, De Seze S. Deux cas de capsuite retractile
de la haunche. Rev du Rhum Mal Oseoartic Soc 1963;12:784e9.
Carvalhais VOC, Arajo VL, Souza TR, Gonalves GGGP, Ocarino JM, Fonseca ST.
Validity and reliability of clinical tests for assessing hip passive stiffness. Man
Ther 2011;16:240e5.
Chard MD, Jenner JR. The frozen hip: an underdiagnosed condition. BMJ 1988;
297(6648):596e7.
Ellison JB, Rose SJ, Sahrmann SA. Patterns of hip rotation range of motion:
a comparison between healthy subjects and patients with low back pain. Phys
Ther Sept 1990;70(9):537e41.
Goldman AB, Katz MC, Freiberger RH. Posttraumatic adhesive capsulitis of the
ankle: arthrographic diagnosis. Am J Roentgenol 1976;127:585e8.
Grifths JH, Utz R, Burke J, Bonglio T. Adhesive capsulitis of the hip and ankle. Am J
Roentgenol 1984;144:101e5.
Hagiwara Y, Chimoto E, Takahashi I, Ando A, Sasano Y, Itoi E. Expression of
transforming growth factor-beta 1 and connective tissue growth factor in
the capsule in a rat immobilized knee model. Ups J Med Sci 2008;113(2):
221e34.
Hannan JA, Chiaia T. Adhesive capsulitis: a treatment approach. Clin Orthop Rel
Res 2000;372:95e109.
Hanson EC, Wood VE, Thiel AE, Maloney MD, Sauser DD. Adhesive capsulitis of the
wrist: diagnosis and treatment. Clin Orthop Rel Res Sept 1988;234:51e5.
Hsu JE, Anakdwenze OA, Warrender WJ, Abboud JA. Current review of adhesive
capsulitis. J Shoulder Elbow Surg 2011;20:502e14.
Hwang S, Kim Y. Lower extremity joint kinetics and lumbar curvature during squat
and stoop lifting. BMC Musculoskelet Disord Feb 2009;10:15.
Joassin R, Vandemeulebroucke M, Nisolle J, Hanson P, Deltombe T. Adhesive capsulitis of the hip: concerning three case reports. Ann Radapt Md Phys 2008;
51:308e14.
Kabbabe B, Ramkumar S, Richardson M. Cytogenetic analysis of the pathology of
frozen shoulder. Int J Shoulder Surg JuleSept 2010;4(3):75e8.
Kelley MJ, McClure PW, Leggin BG. Frozen shoulder: evidence and a proposed
model guiding rehabilitation. J Orthopaedic Sports Phys Ther Feb 2009;39(2):
135e48.
Lee RYW, Wong TKT. Relationship between the movements of the lumbar spine and
hip. Hum Move Sci 2002;21:481e94.
Lequesne M, Becker J, Bard M, Witvoet J, Postel M. Capsular constriction of the hip:
arthrographic and clinical considerations. Skel Radiol 1981;6:1e10.
Luukkainen R, Asikainen E. Frozen hip. Scand J Rheumatol 1992;21(2):97.
Luukkainen R, Sipola E, Varjo P. Successful treatment of frozen hip with manipulation and pressure dilatation. Open Rheumatol J 2008;2:31e2.
McGregor AH, Hukins DW. Lower limb involvement in spinal function and low back
pain. J Back Musculoskelet Rehabil 2009;22(4):219e22.
McGrory BJ, Endrizzi DP. Adhesive capsulitis of the hip after bilateral adhesive
capsulitis of the shoulder. Am J Orthop June 2000;29(6):457e60.
Modesto C, Crespo E, Villas C, Aquerreta D. Adhesive capsulitis. Is it possible in
childhood? Scand J Rheum 1995;24:255e6.
Mont MA, Lindsey JM, Hungerford DM. Adhesive capsulitis of the hip. Orthopedics
1999;22:343e5.
Mullet H, Byrne D, Colville J. Adhesive capsulitis: human broblast response to
shoulder joint aspirate from patients with stage II disease. J Shoulder Elbow
Surg MayeJune 2007;16(3):290e4.
Murphy WA, Siegel MJ, Gilula LA. Arthrography in the diagnosis of unexplained
chronic hip pain with regional osteopenia. Am J Roentgenol August 1977;129:
283e7.
Neviaser AS, Hannan JA. Adhesive capsulitis: a review of current treatment. Am J
Sports Med 2010;38:2346e56.
Neviaser AS, Neviaser RJ. Adhesive capsulitis of the shoulder: review article. J Am
Acad Orthop Surg 2011;19:536e42.
Oehler S, Neureiter D, Meyer-Scholten C, Aigner T. Subtyping of osteoarthritic
synoviopathy. Clin Exp Rheumatol SepteOct 2002;20(5):633e40.
Rodeo SA, Hannan JA, Tom J, Warren RF, Wickiewicz TL. Immunolocalization of
cytokines and their receptors in adhesive capsulitis of the shoulder. J Orthop
Res May 1997;15(3):427e36.
Sakai H, Fujita K, Sakai Y, Mizuno K. Immunolocalization of cytokines and growth
factors in subacromial bursa of rotator cuff tear patients. Kobe J Med Sci Feb
2001;47(1):25e34.
Shum GL, Crosbie J, Lee RYW. Effect of low back pain on the kinematics and joint
coordination of the lumbar spine and hip during sit-to-stand and stand-to-sit.
Spine 2005;30(17):1998e2004.
Sims K. Assessment and treatment of hip osteoarthritis. Man Ther 1999;4(3):
136e44.