Although peripheral arthritis is the most common extra-intestinal
manifestation of inflammatory bowel disease, it is very rarely addressed in
the orthopaedic literature. The overwhelming majority of patients with
inflammatory bowel disease present with gastrointestinal symptoms and do not
have any joint involvement until much later. We present the case of a patient
who had joint pain and swelling but lacked any sign of gastrointestinal
involvement. After five months of work-up, the patient was diagnosed with
Crohn disease and the joint symptoms improved with appropriate medical
treatment. We believe that inflammatory bowel disease should be considered in
the differential diagnosis of joint pain and swelling. Our patient was
informed that data concerning the case would be submitted for publication.
A twenty-two-year-old male active-duty sailor in the United States
Navy presented with a six-week history of right knee pain following a twisting
injury that he had sustained while climbing a ladder on a ship; the knee
twisted as the trunk rotated on the planted ipsilateral foot. At the time of
the initial orthopaedic evaluation, the patient reported that pain and
swelling in the right knee had failed to respond to a course of
anti-inflammatory medication and activity modification. There was no history
of clicking, catching, locking, or snapping. A review of systems was negative
for fevers, chills, nausea, vomiting, recent sexual contact, recent weight
loss, loose stools, abdominal pain, or a history of other joint pain or
swelling.
Physical examination of the knee revealed a moderate effusion, normal
appearance of the skin, mild warmth to touch, and decreased range of motion
from 0° to 100° secondary to pain and swelling. There was diffuse
tenderness of the anterior fat pad but no tenderness at the joint line.
Provocative testing of the knee in varus and valgus, the Lachman test, the
McMurray test, and the drawer tests all revealed negative results. Strength
and sensation in the lower extremity were normal. At this point, the patient
was treated nonoperatively with anti-inflammatory medications, activity
modification, and a directed course of physical therapy.
At the four-week follow-up visit, the patient still had pain, swelling, and
persistent effusion of the right knee. Aspiration of the right knee yielded 10
mL of bloody fluid that revealed an inflammatory effusion with a large amount
of red blood cells (165,000), and some white blood cells (22,000). A gram
stain revealed polymorphonuclear leukocytes without organisms, and an analysis
of the synovial fluid showed no crystals. Because of the persistence of pain,
warmth, and effusion but lack of mechanical symptoms, the differential
diagnosis included pigmented villonodular synovitis, traumatic knee injury
(meniscal tear or ligament injury), and advanced patellofemoral pain
syndrome.
A magnetic resonance imaging scan demonstrated intact cruciate and
collateral ligaments and normal menisci. A moderate joint effusion was evident
along with thickening of the synovium that was consistent with synovial
hyperplasia, but no pigmented villonodular synovitis was seen
(Figs. 1-A and 1-B). The
patient underwent arthroscopy of the knee for the performance of partial
synovectomy. On arthroscopic examination, the synovium was found to be
markedly hypertrophic, especially in the anterior and medial and lateral
gutters of the knee (Figs. 2-A and
2-B). Histologic examination of the synovitic material
demonstrated acute and chronic inflammation, granulation tissue, histiocytes,
subsynovial multinucleated giant cells, fibrin deposition, and microscopic
hemosiderin deposition. However, despite the hemosiderin deposition, there was
no nodular or villonodular proliferation consistent with pigmented
villonodular synovitis (Fig.
3). Laboratory data obtained at this time demonstrated a
microcytic anemia (hemoglobin level of 12.1 g/dL [121 g/L], hematocrit of
36.3% [0.363], mean corpuscular volume of 71 fL, an erythrocyte sedimentation
rate of 51 mm/hr, and a C-reactive protein level of 15.7 mg/dL [0.16 mg/L]).
Due to the inflammatory nature of the findings, additional laboratory data
were obtained, including phenotyping for HLA B-27 (human leukocyte antigen
B-27) and testing for antinuclear antibody (ANA) titers and rheumatoid factor,
all of which revealed negative results. Additional physical therapy was
prescribed, and a rheumatologic consult was obtained.
Approximately six weeks after surgery, the patient presented with similar
symptoms in the contralateral knee. The rheumatologic work-up demonstrated a
similar inflammatory knee effusion and a worsening microcytic anemia (the
results of iron studies were consistent with iron deficiency), and an
anteroposterior radiograph of the pelvis demonstrated sclerosis and early
erosive changes of the sacroiliac joints without ankylosis. An upper
gastrointestinal series with small-bowel follow-through was ordered. (With
this test, the patient drinks barium and then radiographs are made as the
contrast medium empties out of the small intestine and into the large
intestine. Although the test is not specifically used to study the colon,
pathological processes can be visualized as the contrast medium travels
through the colon.) The small-bowel follow-through revealed a cobblestone
mucosal pattern of the entire colon with absence of the haustral pattern and
likely backwash ileitis with narrowing of the ileocecal valve. A colonoscopy
demonstrated focal chronic and active colitis with microabscesses and
granulomatous inflammation with necrosis throughout the colon. The
ulcerations, the focal nature of the changes, the granulomatous inflammation,
and the extension of the inflammation below the mucosa were consistent with a
diagnosis of Crohn disease, a chronic inflammatory gastrointestinal disease of
unknown etiology.
Soon thereafter, the patient began to have multiple loose stools, with
cramping, each day, arthralgia in the left hip and right wrist, episcleritis
in the right eye, and approximately ten deep, pus-filled ulcers on the
anterior aspect of the leg. The ulcers each were approximately 1 cm in
diameter and were confirmed by biopsy to be pyoderma gangrenosum. These new
clinical findings, together with the findings of inflammatory arthritis of the
knee and sacroiliitis, further supported the diagnosis of Crohn disease. The
patient was treated with sulfasalazine, high-dose prednisone, azathioprine,
and iron. The knee pain and swelling, diarrhea, episcleritis, synovitis,
anemia, and pyoderma gangrenosum all resolved, and the patient was able to
taper off the oral corticosteroid medication over a two-month period. He
returned to full military duties, without recurrent effusion or pain in either
knee.
Acute knee injuries are common in young adults. We describe the case
of a young man with no pre-injury joint symptoms who presented with a
low-energy injury to the knee along with diffuse swelling, effusion, and loss
of motion that persisted despite rest, physical therapy, and anti-inflammatory
medications. A magnetic resonance imaging scan was ordered to help narrow the
differential diagnoses to either trauma or synovitis. Although there were no
gastrointestinal symptoms, the patient's rheumatologist suspected that the
diagnosis was inflammatory bowel disease on the basis of the findings of
anemia, oligoarthritis, and asymptomatic sacroiliitis; however, it was not
until the colonoscopy was performed that Crohn disease was confirmed.
Musculoskeletal manifestations of inflammatory bowel disease include
peripheral arthritis, granulomatous monarthritis, sacroiliitis, and ankylosing
spondylitis1, with
peripheral arthritis being the most common
manifestation2. The
knees are the most commonly affected
joints2,3,
followed by the ankles, elbows, wrists, and
shoulders1. The
symptoms include pain, swelling, tenderness, and a decreased range of
motion1,2.
As the inflammation in one joint abates, another joint often becomes affected.
The arthritis usually resolves within one to three months after the onset of
symptoms and is self-limited, with approximately 90% of the episodes lasting
four weeks or less4.
Joint erosion is rare. In one series, 71% of thirty-four cases of peripheral
arthritis that occurred with Crohn disease were
oligoarticular4.
Extra-articular manifestations are rare in patients with Crohn disease. In one
study3 of patients
with Crohn disease, the rate of pyoderma gangrenosum was 1.1% (five of 449)
and the rate of iritis or uveitis was 6.4% (twenty-nine of 449) but there were
no cases of hemolytic anemia. However, when cutaneous or ocular symptoms are
seen in addition to articular manifestations, abdominal disease should be
suspected.
The link between inflammatory bowel disease and peripheral arthritis has
been established. Several studies have described the prevalence of peripheral
arthritis in patients with Crohn disease to be 11% (seventeen of 160) to 16%
(eighty-four of
521)5,6.
Crohn disease does not seem to affect one gender more than the other; one
study4 showed that
13% (eight) of sixty-three men and 14% (fifteen) of 104 women had peripheral
arthritis.
Peripheral arthritis usually is manifested only after the inflammatory
bowel disease has been diagnosed for some
time6. The case of
our patient reflects the rare presentation of peripheral arthritis prior to
the onset of gastrointestinal symptoms. The severity of the arthritis usually
mimics the activity of the bowel disease, and the arthritis usually abates
with medical
treatment3,
underscoring a direct relationship between intestinal exacerbations and joint
symptoms2,3.
Extraintestinal manifestations are most frequently encountered with
ileocolitis (28% to 61% of cases), then colitis (range, 26% to 47% of cases),
and then ileitis (13% to 19% of
cases)2,3,6.
Surgery of the affected joint probably does not influence the natural history
of peripheral arthritis; rather, medical management is the mainstay of therapy
because the disease is due to a systemic process.
Various theories have been proposed with regard to the method in which
inflammatory bowel disease causes peripheral arthritis. One such theory
suggests that the gastrointestinal tract acts as a protective barrier between
the gut and the serum until inflammation in the bowel causes an increase in
gut permeability, which leads to transfer of bacterial antigens from the gut
to the serum. Additionally, there may be cross-reactivity between antigens in
the intestine, synovium, skin, eyes, and biliary
tree7. Furthermore,
the bacterial products lead to activation of immunoregulatory cells,
complement, and proinflammatory
cytokines7,8.
The synovial fluid and tissue show nonspecific inflammatory
changes2; however,
several case reports have demonstrated noncaseating granulomas of the
synovium9-11.
The primary care provider is usually the first to diagnose an inflammatory
bowel condition and is therefore more likely to be alert to the
extra-articular manifestations of these
conditions3.
However, on occasion, the orthopaedic surgeon may be the first physician to
evaluate a patient with persistent joint pain and swelling and thus should be
aware of the extra-articular systemic causes of joint pain and swelling.
?