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Rheumatoid arthritis of the cricoarytenoid jointA clinicopathologic study.

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Rheumatoid Arthritis of the Cricoarytenoid Joint:
A Clinicopathologic Study
AND RICHARD
H. FHEYBERG
By HARRY
BIENENSTOCK,
GEDRGEE. EHRLICH
Arthritis del articulation cricoarytenoide
occurre multo plus frequentemente in patientes con morbo rheumatoide gue lo
que es generalmente suspicite. Decesepte de 64 aleatorimente seligite patientes con arthritis rheumatoide habeva
un o plure symptomas de classe considerate como characteristic de arthritis
cricoarytenoide. In le examine post morte, alterationes histopathologic typic de
arthritis rheumatoide esseva trovate in
le articulationes cricoarytenoide de septe
inter octo patientes con arthritis rheumatoide. Es reportate le anormalitates vidite
in laryngoscopia indirecte in tanto que
illos esseva typic de arthritis rheumatoide del articulationes cricoarytenoide.
Le tractamento es discutite.
Arthritis of the cricoarytenoid joint OCcurs much more frequently in patients
with rheumatoid disease than has generally been suspected. Seventeen of 64
randomly selected patients with rheumatoid arthritis had one or more symptoms
considered to be characteristic of cricoarytenoid arthritis. At postmortem examination, histopathologic changes typical of rheumatoid arthritis were seen in
the cricoarytenoid joints in seven of
eight patients with rheumatoid arthritis.
The abnormal findings on indirect laryngoscopy, typical of rheumatoid arthritis
of the cricoarytenoid joints, are reported
and treatment is discussed.
T
HE CRICOARYTENOID JOINT is more frequently involved in rheumatoid arthritis than is generally suspected. The importance of this joint
in phonation and respiration accounts for reports predominately in the
otolaryngologic literature dealing with various types of cricoarytenoid arthritis.2-'bThe following clinicopathologic study was undertaken to determine
the frequency, severity, and types of changes in this joint found in patients
with rheumatoid arthritis.
The anatomic features of the cricoarytenoid joint help explain the signs
and symptoms encountered. The cricoarytenoid joint is diarthrodia1,l with a
ligamentous capsule lined by synovial membrane. Muscles act on the joint
to adduct and abduct the vocal cords. Two types of movement occur during
normal phonation and respiration: 1 ) rotation of the arytenoid on a vertical
axis, which allows the vocal process to move laterally and medially, thereby
increasing and decreasing the glottic space; and 2 ) a gliding movement by
which the arytenoid cartilages approach and recede from each other. Gliding
and rotation are intimately integrated-medial gliding with medial rotation
and lateral gliding with lateral rotation.
METHODOF STUDY
The clinical features of cricoarytenoid arthritis were studied in two groups
of patients with rheumatoid arthritis attending the rheumatic diseases clinic
From the Department oj Rheumatic Diseases, Hospital for Special Surgery, N e w York
Hospital-Cornell Medical Center, New York, N . Y.
This study w m supported in part by u grant from the Ndicmul lnstibute of Arthritis urn1
Metabolic Diseuses, National Institutes of Health, Bethesda, Md.
48
Al ~TIIHl TISAND
RHEUMATISM, V O L . 6, NO. 1 (FEBRUARY),
1963
49
THE CRICOARYTENOID JOINT
of the Hospital for Special Surgery. The first group consisted of 64 patients
with rheumatoid arthritis selected at random and questioned about the occurrence of symptoms considered to be characteristic of cricoarytenoid arthritis: hoarseness, dyspnea, stridor, dysphagia, and fullness in the throat made
worse by swallowing or speaking. Fifty of these patients were female. The
average age was 52.5 years (range: 16 to 87 years) and the average duration of rheumatoid disease was 9.0 years (range: 9 months to 35 years). Indirect laryngoscopy was performed in all patients willing to undergo the
procedure.* In addition to the random survey, a second group consisting of
six patients with rheumatoid arthritis was studied because they complained
of symptoms suggesting laryngeal dysfunction. The average age was 54.8
years (range: 46 to 62 years) and the average duration of rheumatoid disease
was 22.2 years (range: 7 to 33 years) (table 1 ) .
The pathologic features of cricoarytenoid arthritis were studied in eight
patients with rheumatoid arthritis who had been hospitalized for various
reasons. The average age was 58.8 years (range: 35 to 78 years) and the
average duration of rheumatoid disease was 11.7 years (range: 18 months
to 29 years). Tissue changes in the cricoarytenoid joints of all eight patients
were studied a t postmortem examinations. Fifteen other patients had postmortem studies of the cricoarytenoid joints: I1 of these had never had connective tissue disease, three had systemic lupus erythematosus, and one had
progressive systemic sclerosis. The average age was 54.5 years (range: 25 to
89 years). The pathologic interpretation was made independently of the
clinical evaluation.
RESULTS
Clinical Findings
Seventeen of the 64 randomly selected patients with rheumatoid arthritis
(Group I ) reported one or more symptoms of laryngeal disease. Of these 17,
13 patients gave a history of hoarseness; six, dyspnea on exertion; four, stri-
dor;; three, dysphagia; and two, fullness in the throat when speaking (table
2). Indirect laygoscopy was performed on 35 of these patients, 13 of whom
had laryngeal symptoms. One or more physical signs of disease of the cricoarytenoid articulation were seen in six patients, four of whom had symptoms
characteristic of cricoarytenoid arthritis (table 3 ) . Edema of the tissue about
the cricoarytenoid joint was seen in three patients, redness in two, diminished
motion of the cricoarytenoid joint in one, and diminished movement of the
vocal cords in one patient.
Of the patients who were selected for study because they had specifically
drawn attention to symptoms suggesting laryngeal dysfunction (Group II),
all were hoarse; two patients experienced dyspnea on exertion, one patient
had stridor, and one had fullness in the throat when speaking (table 2 ) . Four
~~~
~
~
*The laryngoscopic examinations were performed by members of the Division of Otolaryngology, Department of Surgery, New York Hnspital-Cnrnell Medical Center, whose
collaboration is gratefully acknowledged.
50
BEENENSTOCK, EHRLICH AND FlWYBERG
Table 1.-Sex,
Age, and Duration of Rheumatoid Arthritis
G ~ U ID
Total number of patients
females
males
Age (average in years)
Duration of rheumatoid arthritis
(average in years)
Table 2.-Laryngeal
Group 11
64
6
50
4
2
14
52.5
54.8
9.0
22.2
Symptoms in Patients with Rheumatoid Arthritis
Number
Group I
Group I1
of Patients
with Laryngeal
Symptoms
Hoarseness
Dyspnea
Stridor
Dysphagia
Fullness in
Throat When
Speaking
17
6
13
6
6
4
1
3
0
2
1
2
Table 3.-Findings on Indirect Lamngoscow
Group I
Group I1
Number of Patients
with
Laryngeal Disease
Edema
6
3
4
2
Diminished
C.A.J. Motion
Diminished
Vocal Cord Motion
2
1
1
4
1
0
_-Redness
of these six patients had one or more abnormalities observed by indirect
laryngoscopy (table 3). Edema of the csicoarytenoid joint area was present in
two patients, redness of the tissues about the joint in one, diminished cricoarytenoid motion in four and diminished vocal cord motion in one patient.
The following case history is presented because it emphasizes the severity
of the laryngeal symptoms resulting from cricoarytenoid arthritis.
M. S., female, age 57 years, who had rheumatoid arthritis for 27 years, experienced in
July 1956 nocturnal dyspnea, wheezing, and a sense of obstruction in the throat that interfered with swallowing and breathing. Simultaneously, she experienced an exacerbation of
rheumatoid arthritis, and several new subcutaneous rheumatoid nodules appeared. Indirect
laryngoscopy performed at that time revealed edema, redness and reduced mobility of the
vocal cords. After treatment with hydrocortisone spray (100 mg. in 250 ml. of water) three
or four times daily for 7 days, prednisone 20 mg. daily for 14 days, and acetyl salicylic acid
0.6 Gm. q.i.d., the sense of obstruction and the wheezing subsided, but some degree of
hoarseness persisted. There was improvement in all manifestations of the rheumatoid arthritis and reduction and disappearance of nodules about the elbows. The dose of prednisone
was reduced gradually over a period of 3 months. At that time the consulting otologist reported improvement in the appearance of the larynx. The generalized rheumatoid process
in the patient continued to be well controlled with low doses of prednisone ( 5 mg. daily),
acetyl salicylic acid 0.6 Gm. q.i.d., and hydroxychloroquine sulfate 200 mg. b i d . Indirect
laryngoscopy performed in August 1961 because of persistent hoarseness revealed anterior
displacement of the left arytenoid cartilage and restricted motion in the left cricoarytenoid
joint. The right arytenoid moved normally. A 3 mm. x 5 mm. polyp was present on each vocal
cord. Laboratory studies at that time revealed a latex fixation test for the rheumatoid factor
positive in dilution 1:5280. The erythrocyte sedimentation rate was 15 mm. per hour
(Westergren).
THE CRICOARITENOID JOINT
51
Comment:This patient had characteristic symptoms of severe cricoarytenoid
arthritis, many of which subsided following treatment with local and systemic corticosteroids. Hoarseness persisted, however, and indirect laryngoscopy
performed 5 years later indicated the presence of chronic disease and dysfunction of the cricoarytenoid joint.
Pathologic Findings
Microscopic changes typical of rheumatoid arthritis were seen in the cricoarytenoid joints of sewn of eight patients with rheumatoid disease in whom
postmortem examination of the larynx was performed. In five instances,
arthritis of the cricoarytenoid articulation was clearly recognizabIe on gross
examination of the larynx. Arthritis was unilateral in only two instances.
Gross pathologic changes ranged from synovial thickening without obvious
joint destruction to infiltration and destruction of cartilagenous joint surfaces by pannus. Microscopic examination of the joints revealed diffuse
synovial inflammation characterized by infiltration of mononuclear-predominantly lymphocytes-and plasma cells; proliferation of synovial villi; and
pannus infiltrating and destroying articular cartilage. In one case ( J . C . ) a
zcne of collagen necrosis surrounded by an area of palisading mononuclear
cells characteristic of a rheumatoid nodule was seen in the muscles adjacent
to the arytenoid cartilage.
The cricoarytenoid joints of all 15 patients without rheumatoid arthritis
were normal histologically.
Case Histories
The following abstracts summarize the clinical and pathologic features of
all the patients with rheumatoid arthritis whose cricoarytenoid joints were
studied at necropsy.
Case # I : J. C., female, age 78 years, had had rheumatoid arthritis for 6 years. The course
of her illness had been complicated by recurrent episodes of osteomyelitis of the left elbow
which followed traumatic fracture of the humerus. During the last 3 months of her illness
she had been treated with prednisone in daily oral doses of 5 to 10 mg. and with gold salts.
One year before death the onset of hoarseness caused her physician to suspect cricoarytenoid
arthritis. Fever, a pleural friction rub, and peripheral neuropathy developed a few months
before her death. The hemoglobin ranged between 9 and 11.0 Gm. per cent; E.S.R.between
60 to 110 mm. per hour (Westergren); and the latex fixation test for the rheumatoid factor
was positive 1:5120. She died of progressive renal failure and chronic nonspecific pneumonitis.
Autopsy findings confirmed the diagnosis of rheumatoid arthritis with generalized necrotizing vasculitis. Rheumatoid nodules were found in the epicardium. The cricoarytenoid joints,
on gross examination, were hypermobile. The joint surfaces were irregular with patchy
areas of destruction of articular cartilage. Microscopic examination revealed synovial villous
proliferation and pannus replacing portions of the articular surfaces and infiltrating deep
into the cricoid cartilage (figs. 3a and 3 b ) . These changes were more pronounced in the
left articulation. A zone of collagen necrosis surrounded by an area of palisading mononuclear cells characteristic of a rheumatoid nodule was present in the muscle adjacent to
the left arytenoid cartilage (fig. 3e).
52
BIENENSTOCK, EHRLICH AND FREYBEFiG
Fig. 1.-Anatomy
of the larynx.
Comment: This patient developed symptoms of cricoarytenoid joint clisease while taking small daily doses of corticosteroids. The dosage was not
raised and symptoms eventually subsided. Besides destructive changes in the
cricoarytenoid joints, a rheumatoid nodule was found in the muscle adjacent to
one arytenoid cartilage. In addition, rheumatoid nodules were found in the
epicardium, and diffuse vasculitis was present.
Case #2: M. M., female, age 50 years, had had rheumatoid arthritis for 29 years. Fifteen
months before death she was hospitalized because of cough, dyspnea and hoarseness. Stridor
was observed at that time and mirror examination of the larynx showed the hypopharynx
and endolarynx to be extremely red and slightly edematous. The glottic space was adequate.
Although intravenous fluids, oxygen and antibiotics effected an improvement in the general
condition, hoarseness persisted for 2 months. Eight months before death 4+ albuminuria
and doubly refractile bodies in the urine were reported. The latex fixation test for rheumatoid factor was repeatedly positive in dilution 1:3000 or 1:SOOO. She was hospitalized 6
weeks before death because of nausea, vomiting, cough and severe ankle edema. Chest x-ray
at that time was compatible with pericardial effusion and yielded 100 ml. of turbid yellow
fluid. The blood urea nitrogen gradually rose from 25 to 104 mg. per cent and she died of
progressive renal failure.
Postmortem tissue studies revealed rheumatoid arthritis, amyloidosis of the kidneys and
adrenal glands, and thrombosis of the renal and iliac arteries. The articular surface of the
left arytenoid cartilage was irregular. The right cricoarytenoid joint was normal in appearance. Microscopic tissue examination of the right cricoarytenoid joint revealed synovial
proliferation, and pannus infiltrated and destroyed the articular surface of the joint.
Comment: Although hoarseness, dyspned and stridor were observed,
rheumatoid arthritis of the cricoarytenoid joint was not recognized in life.
THE CRICOARYTENOID JOINT
53
Fig. 2.-The appearance of the normal cricoarytenoid joint. (2Ox). The articular
surfaces are smooth and no evidence of inflammation is present.
Case #3: S. S., male, age 55 years, had rheumatoid arthritis for 8 years. Ten months before
death he was hospitalized for “encephalitis.”Spinal fluid examination at that time was unrevealing and he recovered spontaneously. Three months before death he was hospitalized
because of sore throat, fever and “snowball lesions” in the lung. Monilia were cultured from
the urine and sputum and treatment with chloramphenicol and mycostatin was instituted
with no noticeable improvement in his condition. Three weeks before death he passed a
number of guaiac positive stools. Six units of whole blood were administered and antibiotic
therapy was changed to penicillin, streptomycin and isoniazid but his condition continued
to deteriorate. He was observed to be hoarse during the last few weeks of his illness. He
was found dead in bed.
Postmortem tissue studies revealed rheumatoid arthritis, adrenal gIand atrophy, pulmonary
granulomas with extensive necrosis, and cryptococcal meningitis and encephalitis. The
articular surfaces of the cricoarytenoid joints were irregular on gross examination (fig. 4a).
The capsule of the left cricoarytenoid joint was thickened. Microscopic tissue examination
of the right cricoarytenoid joint revealed destruction of the articular surfaces of the cricoid
cartilage by pannus (fig. 4b). Findings were not as marked in the left articulation.
C m m m t : Hoarseness was observed but cricoarytenoid arthritis was not
recognized in life.
Case #4: W. W., male, age 70 years, had had rheumatoid arthritis for many years. During
the last 10 years of his illness he had experienced shortness of breath attributed to bronchiectasis and pulmonary fibrosis. A surgical drainage of the maxillary sinus was performed
because of purulent sinusitis 7 years before death, at which time the larynx appeared normal.
He was hospitalized on October 2, 1980 because of chills and cough. Signs of intestinal
obstruction developed and exploratory laparotomy revealed small bowel distention. Because
of the patient’s poor condition, complete exploration of the abdomen could not be performed.
54
BIENENSTOCK, EHRLICH AND FREYBERG
Shortly following surgery he experienced increasing difficulty breathing and tracheostomy
was performed. He died late that evening.
Postmortem tissue studies revealed chronic rheumatoid arthritis, generalized necrotizing
arteritis, infarcts of the colon, and emphysema and fibrosis of the lungs. The left cricoarytenoid joint was immobile. The articular surface of the arytenoid cartilage was eroded by
pannus and heavy bands of connective tissue bridged the joint laterally. The mobility of
the right cricoarytenoid articulation was diminished and a moderate amount of pannus was
seen. Microscopic examination of the left cricoarytenoid joint revealed marked synovial proliferation and synovial villous formation. The right articulation was obliterated by fibrous
tissue.
Comment: Arthritis of the cricoarytenoid joints may have contributed to
the respiratory distress experienced by this patient who had a long history
of pulmonary insufficiency. Trauma to these joints, as in endotracheal antsthesia, has been mentioned as a cause of cricoarytenoid arthritis and may
have aggravated the underlying rheumatoid cricoarytenoid joint disease in
this patient.
The three patients to be described below (Cases 5, 6, 7 ) had no known
history of laryngeal complaints, Postmortem studies revealed rheumatoid
arthritis of the cricoarytenoid joints in all three.
Case #5: J. W., male, age 55 years, had had rheumatoid arthritis for 5 years. He was
treated with moderate amounts of corticotropin, corticosteroids and intramuscular gold salt.
There was no history of laryngeal complaints. Four and one-half months before death the
E.S.R. was 66 mm. per hour (Westergren) and the latex hation test for the rheumatoid
factor was 4 + . He was hospitalized 20 days before death because of fever and increasing
weakness. Chest x-ray revealed streaky vertical densities in both lower lung fields and blood
culture grew out Staphylococ~lsa u r w . He was treated with digitalis, penicillin and streptomycin with no improvement in his condition. He died 10 days following an episode of
right-sided hemiparesis.
Postmortem tissue studies revealed rheumatoid arthritis, generalized necrotizing vasculitis,
multiple cerebral infarcts, necrotizing bronchiolitis, and granulomatous splenitis. Gross examination revealed no abnormalities in the cricoarytenoid joints. Microscopic examinaton of
these joints revealed moderate destruction of the articular surfaces by pannus; synovial villi;
and infiltration of synovium by mononuclear cells, predominantly lymphocytes, and plasma
cells. These findings were more marked in the right articulation.
Case #S: N. M., male, age 73 years, had had rheumatoid arthritis for 25 years during
which time he was treated with intramuscular gold salts, phenylbutazone, hydroxychloroquine sulfate and small doses of corticosteroids. Two years before his death he was hospitalized because of postprandial burning and gastric distress, and upper gastrointestinal
series revealed two ulcers in the gastric antrum. Ulcer symptoms subsided following institution of an ulcer diet and antacid therapy. Ten months before death, following Jewett nailing
for fracture of the left femur, he developed hematemesis and melena which subsided following treatment with probanthine, magnesium aluminum hydroxide and an ulcer diet. Fortyfive days after Jewett nailing he developed serum hepatitis secondary to transfusion therapy
from which he recovered without incident over a &month period. Six days before death he
was hospitalized following two episodes of hematemesis. On the third hospital day a Bilroth
I1 operation was performed because of intractable gastrointestinal bleeding, He did well
following surgery until the third post-operative day when he passed a large, loose tarry
stool, his temperature rose to 40.3 C., and signs of peritonitis developed. His condition
deteriorated rapidly and he died on the fourth post-operative day. He had never complained of symptoms referable to the larynx.
55
THE CRICOARYTENOID JOINT
Postmortem tissue studies revealed rheumatoid arthritis, fibrocalcific rheumatic mitral and
aortic disease, gastric ulcer, granulomatous pulmonary nodules and bronchopneumonia.
Gross examination of the cricoarytenoid joints revealed marked irregularity of the articular
surfaces with pannus formation more marked on the right (fig. 5 a ) . Microscopic tissue study
revealed pannus infiltrating and destroying the articular surfaces of the cricoarytenoid joints
bilaterally (figs. 5b and 5 c ) .
Case #7: C. N., male, age 55 years, had had rheumatoid arthritis for 1% years during
which time he had been treated with intramuscular gold salts and small doses of corticosteroids. There was no history of laryngeal complaints. Six months before death the latex
fixation test for rheumatoid factor was positive 1:1280. He was hospitalized because of
thrombophlebitis of the left leg and died 12 hours later following a hypotensive episode.
Autopsy findings confirmed the diagnosis of rheumatoid arthritis. Other findings were:
Arteriosclerotic cardiovasular disease with recent hemorrhage in an atheromatous plaque
of a coronary artery, ulceration of the colon, hyperplasia of lymph nodes and spleen and
pulmonary emphysema. The right cricoarytenoid joint, on gross examination, was normal in
appearance. Synovial proliferation was seen within the left articulation. Microscopic tissue
studies confirmed these findings.
Case #8: L. F., age 35 years, had psoriasis, rheumatoid spondylitis, and peripheral arthritis for 8 years. Three years before death he developed diarrhea and bloody stools and a
diagnosis of ulcerative colitis was made. During the last four years of his illness he had been
treated with prednisone in doses of 7.5 to 20 mg. daily. The latex fixation titer for rheumatoid factor was negative and the erythrocyte sedimentation rate was 88 mm. per hour 6
months before death. He was hospitalized because of a bleeding duodenal ulcer 18 days
before death. The ulcer was plicated and a pyloroplasty was performed. He required numerous blood transfusions and his course was complicated by a wound dehiscence on the ninth
postoperative day. He died of progressive renal failure 17 days after surgery. He had no
history of laryngeal disease, though specifically questioned about it.
Postmortem studies revealed rheumatoid arthritis, rheumatoid spondylitis; amyloidosis of
the kidneys, liver, and spleen; a duodenal ulcer and an acute ulcer of the colon. The cricoarytenoid joints were normal in appearance on gross and microscopic tissue examination.
Comment: Of the eight patients with rheumatoid arthritis examined postmortem, this patient was the only one in whom the cricoarytenoid joints were
normal in appearance. It is of interest to note that psoriasis and ulcerative
colitis were present in this patient who had rheumatoid spondylitis, and
peripheral arthritis indistinguishable from rheumatoid arthritis. One may
legitimately question whether the combination of diseases present in this
patient might not represent a different disease process from that presented
above (Cases 1-7).
DISCUSSION
Infrequent isolated reports of cricoarytenoid arthritis appeared in the literature of the first two decades of the twentieth century and sporadically thereafter. These articles dealt with various forms of arthritis, e.g., “ i n f e c t i ~ u s , ” ~ ~ ~
“rheumatic,”4-6 “post-traumatic.”*In these reports, laryngeal findings were
not correlated with the different types of rheumatic disease.
In 1955, Montgomery and his associatess renewed interest in the problem
of cricoarytenoid arthritis in relation to rheumatoid arthritis. They discussed
the clinical manifestations of four patients with rheumatoid disease who
had arthritis of the cricoarytenoid joint. Hoarseness, dyspnea, pain radiating
Figs. 3a (above) and 3b (below)-See
legends, facing page.
57
THE CRICOARYTENOID JOINT
Fig. 3c.-J. C. A zone of collagen necrosis surrounded by an area of palisading
mononuclear cells characteristic of a rheumatoid nodule is seen adjacent to the left
arytenoid (65~).
to the ears, and fullness in the throat when swallowing or speaking were considered the predominant acute symptoms. Laryngoscopic examination at times
revealed redness and swelling of the tissue adjacent to the arytenoid cartilage
and edema of the vocal cords. When both cricoarytenoid joints were involved, bowing of the vocal cords was seen during the inspiratory phase of
respiration. When cricoarytenoid arthritis became chronic, laryngeal signs
and symptoms depended upon the position of joint fixation. Unilateral disease resulted in slight hoarseness and/or exertional dyspnea. With bilateral
.___
Fig. Sa.-Case #I, J. C. Left cricoarytenoid joint ( l o x ) showing synovial proliferation, villous formation and pannus replacing portions of the cricoid and arytenoid
cartilages. Ossification of the cricoid cartilage has taken place.
Fig. 3b.--J. C. Higher magnification of fig. 3a (65x) showing infiltration of
synovium by mononuclear cells. The articular surface of the cricoid has been completely destroyed.
BJENENSTOCK, EHRLICH AND FREYBEXG
Fig. 4a.-Case #3, S. S. Posterior view showing the gross appearance of the
cricoarytenoid joints. Note the thickening of the capsule of the right joint and the
irregularity of both joint surfaces.
Fig. 4b.-S. S. Right cricoarytenoid joint (2Ox). Synovial proliferation and infiltration of the cricoid by pannus.
THE CRICOARYTENOID JOINT
59
ankylosis of the cricoarytenoid joints and adduction of the vocal cords, dyspnea was the predominant symptom. When the vocal cords became fixed in
adduction, hoarseness or aphonia resulted. Edema and redness of the larynx,
prominent in acute cricoarytenoid arthritis were not features of the chronic
phase. Mobility of the arytenoid cartilage could be tested by using a laryngeal
spatula.
Copeman,lo and Baker and Bywaters’l reported on rheumatoid arthritis
of the cricoarytenoid joint in 1957. The former presented three cases representing the acute, subacute, and chronic phases of cricoarytenoid arthritis
and concluded that “involvement of the cricoarytenoid joints may sometimes occur as an integral part of the polyarthritic process.”
A detailed study of rheumatoid criccmrytenoid arthritis was reported by
Grossman, Martin and Root in 198O.l2They searched for cricoarytenoid joint
disease in 55 patients with rheumatoid arthritis. Seventeen of these patients
had symptoms of laryngeal dysfunction and 38 presented without laryngeal
complaints. On mirror examination there was some suggestive evidence of
cricoarytenoid arthritis in 18 patients.
In our study 35 of 64 randomly selected patients with rheumatoid arthritis
(Group I ) , including 13 of the 17 who reported symptoms of laryngeal dysfunction, underwent indirect laryngoscopy. Physical signs of abnormality of
the cricoarytenoid joint were detectable in six, only four of whom were symptomatic.
A11 six patients who specifically drew attention to laryngeal symptoms
(Group 11) had mirror examinations of the larynx. In four of these patients,
clinically discernible abnormalities in the area of the cricoarytenoid joint
were seen.
Groups I and I1 were similar with respect to age and sex. The average
duration of rheumatoid disease in Group I1 was significantly longer and may
accounf for the higher incidence of physical signs of laryngeal disease in
this group of patients. Combining our two groups reveals that eight (42 per
cent) of 19 symptomatic patients and only two ( 9 per cent) of 22 asymptomatic patients had physical signs of cricoarytenoid joint disease.
Our studies also revealed that seven (88 per cent} of eight patients with
rheumatoid disease who had postmortem tissue studies of the cricoarytenoid
joints had rheumatoid cricoarytenoid arthritis. This incidence is higher than
that reported by Grossman et. a1.l2 who found necropsy evidence of cricoarytenoid arthritis in five of 11 patients with rheumatoid disease. The one
patient in our series whose cricoarytenoid joints were normal in appearance
also had spondylitis, psoriasis and ulcerative colitis and may represent a
variant of rheumatoid disease. In all 15 control autopsy examinations, the
cricoarytenoid joints were normal. These pathologic findings indicate that
the frequency with which the cricoarytenoid joint is involved in rheumatoid
disease is much greater than is generally appreciated.
In the differential diagnosis of rheumatoid cricoarytenoid arthritis, other
causes of hoarseness, dyspnea and stridor need to be considered. These include upper respiratory infections, vocal cord tumors, postoperative laryngeal
trauma and recurrent laryngeal nerve paralysis.
60
BIENENSTOCK, EHRLICH AND PREYBERG
Fig. 5a.-Case #6, N. M. Lateral view of the right cricoarytenoid joint. The
arytenoid has been retracted medialward revealing destruction of the articular surface by pannus.
Based on the current knowledge of this disease, treatment of rheumatoid
cricoarytenoid arthritis should be directed against the systemic disease.
Upper respiratory infections may precipitate acute laryngeal distress in patients with known cricoarytenoid arthritis or may cause laryngeal symptoms
to develop in rheumatoid patients with previously unsuspected cricoarytenoid
joint disease.13 Prompt treatment of the infection and more active treatment
of the rheumatoid disease is required in these circumstances. Tracheostomy
, ~ ~ only one patient
may be needed to relieve laryngeal o b s t r ~ c t i o n ' ~though
whom we studied required it. Polisarl3J5has reported that unilateral arytenoidectomy performed after the acute process has subsided resulted in relief
of respiratory symptoms. Sedatives should never be used in patients who are
having diEculty breathing as they may further depress re~pirati0n.l~
The value of corticosteroids in patients with acute cricoarytenoid arthritis is
Fig. 5b.-N. M. Right cricoarytenoid joint (20x).Pannus infiltrating and destroying the articular surfaces of the cricoarytenoid joint. The cricoid and arytenoid cartilages have undergone partial ossification.
Fig. 5c.-N. M. Left cricoarytenoid joint ( 3 0 ~ )Marked
.
synovial proliferation
with destruction-of the articular surface of the cricoid cartilage.
61
62
BIENENSTOCK, EHRLICH AND FREYBERC
still open to question. A number of case reportssJ3 as well as our own findings
have indicated that acute respiratory distress may develop even when
patients are receiving corticosteroids. At times, temporary increases in corticosteroids and local hydrocortisone spray may prove helpful. Relief of acute
respiratory symptoms as well as diminution of hoarseness was seen in one of
OW patients (M. S . ) following the increase of the daily dose of prednisone
from 10 to 20 mg. and the use of local hydrocortisone spray.
SUMMARY
Arthritis of the cricoarytenoid joints occurs much more frequently in patients with rheumatoid disease than has been generally suspected. Persistent
hoarseness is the most common symptom and evidence of inflammation
and/or dysfunction of the cricoarytenoid joints can often be seen by indirect
laryngoscopy. The correlated autopsy and clinical findings indicate that
rheumatoid cricoarytenoid arthritis may exist in a clinically undetectable
form.
ACKNOWLEDGMENT
The authors wish to acknowledge with gratitude the technical assistance of Miss Brigitta
Lindegren of the Department of Surgical Pathology of the New York Hospital.
REFERENCES
1. Gray, H.: Anatomy of Human Body.
Goss, C. M., ed. Philadelphia, Lea &
Febiger, 1954, pp. 1204-1209.
2. Mygind, S. H.: Ueber Arthritis Cricoarytenoidea Rheumatica Acuta und
mit derselben Verwandte Larynxleiden. Arch. Laryng. u. Rhin. 28:45,
1913.
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THE CRICOARYTENOID JOINT
Harry Bienenstock, M.D., Clinical Instructor of Medicine,
Cornell University Medicd College; Research Fellow in
Rheumatic Diseases, Hospital for Special Surgey, New YoTk
Hospital-Cornell Medical Center, N e w York, N . Y.
George E. Ehrlich, M.D., Clinical Instructor of Medicine, COTnell University Medical College; Teaching Fellow in Rheumatic Diseases, Hospital fm Special Surgey, New York Hosetal-Cornell Medical Center, N e w York, N . Y .
Richard H . Freyberg, M.D., Clinical Professor of Medicine,
Cornel2 University Medical College; Director, Department of
Rheumatic Diseases, Hospital for Special Surgery, New YoTk
HospitaLCornell Medical Center, N a o Ymk, N . Y.
63
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