Download Sudden Enlargement of a Deep Cervical Lymph Node During

suppression of ovulation with oral contraceptives initially
is recommended; however, recurrence of pneumothorax
has been documented frequently.'6"7 Danazol, a weak
androgen, has been used in the management of recurrent
catamenial pneumothorax;'8 however, recurrence of pneumothorax, as occurred in our patient, has been documented.'9
Pleural abrasion and pleurectomy can prevent recurrent
pneumothorax and hemothorax in these patients but cannot affect catamenial chest pain and hemoptysis. Hormonal suppression has been successful in only 40 percent
of patients. Hysterectomy with bilateral salpingooophorectomy, the definitive treatment for thoracic endometriosis, may not be effective if estrogen replacement
is commenced soon after surgery as occurred in our patient;
delaying hormonal replacement therapy by several months
should provide adequate time for the regression of ectopic
endometrial tissue. Chemical pleurodesis with talc insufflation at thoracoscopy or minocycline, doxycycline, or talc
slurry instillation via a chest tube should be considered as
the initial treatment for catamenial pneumothorax and
hemothorax even with intact ovarian function or hormonal
replacement therapy.
REFERENCES
1 Maurer RR, Schall JA, Mendez FL Jr. Chronic recurring spontaneous pneumothorax due to endometriosis of the diaphragm.
JAMA 1972; 168:2012-14
2 Wilkins SB, Bell-Thompson J, Tyras DH. Hemothorax associated with endometriosis. J Thorac Cardiovasc Surg 1985;
89:636-38
3 Elliot DL, Barker AF, Dixon LM. Catamenial hemoptysis: new
methods of diagnosis and therapy. Chest 1985; 87:687-88
4 Horsfield K. Catamenial pleural pain. Eur Respir J 1989;
2:1013-14
5 Mobbs GA, Sydney MB, Pfanner DW. Endometriosis of the
lung. Lancet 1963; 1:472-74
6 Carter EJ, Ettensohn DB. Catamenial pneumothorax. Chest
1990; 98:713-16
7 Laws HL, Fox LS, Younger B. Bilateral catamenial pneumothorax. Arch Surg 1977; 112:627-28
8 Wilhelm JL, Scommegna A. Catamenial pneumothorax: bilateral occurrence while on suppressive therapy. Obstet Gynecol
1977; 50:227-31
9 Rossi NP, Goplerud CP. Recurrent catamenial pneumothorax.
Arch Surg 1974; 109:173-76
10 Lee CY, DiLoreto PC, Beaudoin J. Catamenial pneumothorax.
Obstet Gynecol 1974; 44:407-11
11 Hobbs JE, Bortnick R. Endometriosis of the lung: an experimental and clinical study. Am J Obstet Gynecol 1940; 40:832-43
12 Park W. The occurrence of decidual tissue within the lung: report of a case. J Pathol Bacteriol 1954; 67:563-70
13 Sahn SA. Catamenial pneumothorax and hemoptysis: current
therapy of respiratory disease-3. Philadelphia: BC Decker,
1989;295-98
14 Zaatri GS, Gupta PK, Bhagavan BS, Jarboe BR. Cytopathology
of pleural endometriosis. Acta Cytol 1982; 26:227-32
15 Grangberg I, Willems JA. Endometriosis of lung and pleura
diagnosed by aspiration biopsy. Acta Cytol 1977; 21:295-97
16 Schoenfeld A, Ziv E, Zeelel Y, ans Ovadia J. Catamenial pneumothorax: a literature review and report of an unusual case.
Obstet Gynecol Surv 1986; 41:20-24
17 Muller NL, Neelms B. Post-coital catamenial pneumothorax:
report of a case not associated with endometriosis and success-
1896
fully treated with tubal ligation. Am Rev Respir Dis
1986;134:803-04
18 Hinson JM, Brigham KL, Daniell J. Catamenial pneumothorax
in sisters. Chest 1981; 80:634-35
19 Furman WR, Wang KP, Summer WR, Terry PB. Catamenial
pneumothorax: evaluation by fiberoptic pleuroscopy. Am Rev
Respir Dis 1980; 121:137-40
Sudden Enlargement of a Deep
Cervical Lymph Node During
and After Treatment for
Pulmonary Tuberculosis*
E. Jane Carter, M.D., F.C.C.P.; and Susan Mates, M.D.
A 25-year-old Filipino woman presented with sudden
massive enlargement of a deep cervical lymph node on
two occasions: during adequate treatment of pulmonary
tuberculosis and again 2 years after completion of therapy. Although this immunologic phenomenon is well
known in childhood tuberculosis, occurrence in adults
should also be recognized. (Chest 1994; 106:1896-98)
AFB=acid-fast bacilli
Pathophysiologically, intrathoracic lymph nodes are
probably infected in every case of pulmonary tuberculosis.' In children2 and HIV-infected patients,3 these
nodes are usually or often clinically apparent. In HIVnegative adults, however, the nodes usually remain clinically silent.
When treating pulmonary tuberculosis, it is important to
be aware of the extensive area of lymphatic drainage from
the affected lung (hilar, subcarinal, paratracheal, deep
cervical, and abdominal nodes) and the potential complications from these nodes.
We present a patient with documented pulmonary tuberculosis, whose nodal involvement became dramatically
apparent when she suffered a sudden enlargement of a left
deep cervical node with symptomatic impingement on her
trachea during therapy and enlargement of a contralateral
deep cervical node after completion of therapy.
CASE REPORT
A 25-year-old woman born in the Philippines presented in
September 1988 with a 6-month history of an 8.1-kg weight loss
and fatigue. She had immigrated to the United States 2 years
previously. There was no relevant medical history. She denied all
*From the Divisions of Pulmonary Medicine (Dr. Carter) and
Infectious Diseases (Dr. Mates), Brown University School of
Medicine and the Rhode Island Tuberculosis Clinic, Providence.
Reprint requests: Dr. Carter, 877 Chalkstone Avenue, Providence, RI 02908
Lymph Node Enlargement Durng and After TB Treatment (Carter, Mates)
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of treatment with medications; complianc&was deemed excellent.
At the end of treatment, she had no palpable adenopathy. Chest
radiograph continued to demonstrate bilateral upper lobe nodules
that had remained stable for greater than 6 months.
Twenty-two months following completion of therapy, she developed a 30X40-mm right deep cervical node. At this time she
had no constitutional symptoms. Weight was stable. Chest radiograph was unchanged. The HIV serologic test was negative.
Excisional biopsy of the lymph node was performed. Pathologic study revealed granulomatous inflammation and areas of
caseous necrosis with acute inflammation. The AFB smear and
subsequent culture were negative.
It was elected not to retreat the patient, but to follow her clinically for any further signs of reactivation. She is now 19 months
since excision without recurrence of nodal disease or constitutional symptoms suggestive of tuberculosis infection.
DISCUSSION
The sudden noninfectious enlargement of tuberculous
lymph nodes during the course of adequate chemotherapy
is well described.4-6 This complication occurs in 12 to 13
percent of patients, usually within the first months of
therapy, and resolves without alteration of chemotherapy.
It is postulated to be due to hypersensitivity to tuberculo-
protein.4
FIGURE 1. Top, Chest radiograph demonstrates bilateral upper
lobe reticulonodular infiltrates. Bottom, Chest CT scan obtained
during therapy reveals an enlarged left deep cervical node with
mild tracheal deviation.
other symptoms, including cough, sputum production, fever, or
chills. A chest radiograph (Fig 1, top) revealed bilateral upper lobe
infiltrates without cavitation or intrathoracic adenopathy. The
trachea was midline. Expectorated sputa for acid-fast bacilli were
negative on two occasions. Fiberoptic bronchoscopy was performed; washings and postbronchoscopy sputum were AFB smear
positive. She was started on a regimen of isoniazid, rifampin, and
ethambutol. At this time she had no visible or palpable lymphadenopathy.
Five weeks into treatment the patient suddenly developed a
20X30-mm left deep cervical node with a new cough described
by the patient as due to tracheal impingement. Otherwise, she felt
well. A computed tomographic scan of the neck (Fig 1, bottom)
confirmed the node and demonstrated minimal tracheal displacement. No change was made in the patient's therapy.
Three and a half months into therapy, the deep cervical node
began to recede. Constitutional symptoms had disappeared; the
patient regained her weight. Cultures of the bronchoscopy specimens eventually grew two organisms: a fully sensitive Mycobacterium tuberculosis and a fully resistant M avium. The second
was believed to be a contaminant.
When sensitivities were received 3 months into treatment,
ethambutol therapy was discontinued. She completed 10½/2 months
When an enlarged mediastinal node occurs during the
course of therapy in a child and causes either respiratory
difficulty or a collapse-consolidation lesion, the use of steroids, under the cover of effective antituberculous drugs,
has been suggested.7 In our case, steroids were deferred as
the patient's tracheal compression was mildly symptomatic, it did not threaten the airway, and sensitivities of the
organism were not yet available.
The probable immune mechanism of this phenomenon
is underscored in that both episodes of enlargement
resolved without specific therapy: the first occurred with
characteristic timing in the treatment of a sensitive
organism with adequate chemotherapy, and the biopsy
specimen of the second was smear- and culture-negative.
Our case is of particular interest because it demonstrates
treatment-related node enlargement occurring not only
during, but also after, effective chemotherapy.
Most physicians caring for children with pulmonary
tuberculosis have experienced the occurrence of sudden
mediastinal node enlargement during treatment, usually
presenting as a new infiltrate with an obstructive cause. It
is important that those caring for adult patients also be
aware of this possibility, the range of nodes that may be
involved, and the potential complications. In most cases, no
change in tuberculosis therapy is necessary. In some cases,
steroids may be considered.
ACKNOWLEDGMENTS: Special thanks to Margaret Smith,
M.D., of Tulane University, New Orleans, and Marian Goble,
M.D., of National Jewish Hospital for Immunologic and Respi-
ratory Disease, Denver, for clinical assistance during care of this
patient.
REFERENCES
1 DesPrez RM, Hein CR. Mycobacterium tuberculosis. In:
Mandell GL, Douglas GR Jr, Bennett JE, eds. Principles and
practice of infectious diseases. 3rd ed. New York: Churchill
Livingstone, 1985
2 Starke JR, Jacobs RF, Jereb J. Resurgence of tuberculosis in
CHEST / 106 / 6 / DECEMBER, 1994
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1897
children. J Pediatr 1992; 120:839-55
3 Hill AR, Premkumar S, Brustein S, Vaidya K, Powell S, Li P-W,
et al. Disseminated tuberculosis in the acquired immunodeficiency syndrome era. Am Rev Respir Dis 1991; 144:1164-70
4 Campbell IA, Dyson AJ. Lymph node tuberculosis: a comparison of various methods of treatment. Tubercle 1977; 58:171-79
5 British Thoracic Society Research Committee. Short course
chemotherapy for tuberculosis of lymph nodes: a controlled
trial. BMJ 1985; 290:1106-08
6 Deitel M, Saldanha CF, Borowy ZJ, Ronald AG, Krajden S.
Treatment of tuberculous masses in the neck. Can J Surg 1984;
27:90-3
7 Smith MHD, Marquis JR. Tuberculosis and other mycobacterial infections. In: Feigin RD, Cherry JD, eds. Textbook of pediatric of infectious diseases. Philadelphia: WB Saunders Co,
1981
Acquired Laryngomalacia
as a
Cause of Obstructive Sleep
Apnea*
Kota G. Chetty, M.B., F.C.C.P.; Fady Kadifa,
Richard B. Berry, M.D., F.C.C.P.; and
C. Kees Mahutte, M.D., Ph.D., F.C.C.P.
M.D.;
We describe a patient who, 4 years after a radical neck
dissection and radiotherapy, presented with obstructive
sleep apnea; upon bronchoscopy, he was found to have
acquired laryngomalacia. Inspiration induced upper
airway obstruction due to a large flaccid epiglottis, large
aryepiglottic folds, and edema of the supraglottic area.
We suggest that acquired laryngomalacia can lead to
obstructive sleep apnea. Patients with obstructive sleep
apnea after radical neck dissection need to be evaluated
for
laryngomalacia
with
fiberoptic laryngobronchos-
copy. Examination of the upper airway is useful to determine the nature and extent of any upper airway col-
lapse.
(Chest
1994; 106:1898-1899)
OSA=obstructive sleep apnea
Key
words:
laryngomalacia; obstructive sleep apnea; up-
per airway
The mechanism of obstructive sleep apnea (OSA) appears
to be multifactorial. Anatomic narrowing, increased
compliance, altered reflexes, and inspiratory pharyngeal
muscle dysfunction may all play a role in the pathophysiology
of OSA.' Thus, structural alterations as well as the balance
*From the Departments of Medicine, Long Beach Veterans Affairs Medical Center, Long Beach, Calif, and the University of
California, Irvine, Calif.
Re print requests: Dr. Chetty, Long Beach VAMC-IIIP, 5901
E. 7th Street, Long Beach, CA 90822
1898
between pharyngeal dilating and collapsing forces are important in maintaining upper airway patency. The collapsing
segment itself may vary in location from the oropharynx to the
hypopharynx.' Although the incidence is low, several upper
airway abnormalities can produce the OSA syndrome. Examination of the nasal passages and oropharynx is performed
routinely to detect nasal obstruction, enlarged tonsils or adenoids, macroglossia, and hypopharyngeal masses.
In infants and children, OSA symptoms have been described with congenital laryngomalacia, an entity characterized by inspiratory stridor due to a flaccid epiglottis, redundant aryepiglottic folds, or hypotonia of the larynx. Belmont
and Grundfast2 evaluated 30 such infants with congenital laryngeal stridor. Endoscopy characteristically showed flaccid
supraglottic structures and medial prolapse of the arytenoid
folds or of the epiglottis on inspiration. Seven of these infants
had OSA.
We describe an adult patient who had had a left radical
neck dissection followed by radiotherapy and who years later
presented with OSA. Endoscopy revealed flaccid supraglottic
tissues. Airflow-induced collapse of the epiglottis into the laryngeal inlet causing intermittent obstruction was also noted.
The term acquired laryngomalacia has been used to describe
the preceding findings.3 Our patient suggests that acquired
laryngomalacia due to neck surgery with radiotherapy may
lead to OSA.
CASE REPORT
A 42-year-old man was admitted to the hospital with complaints of mild swelling of the lips, face, and tongue over 3 days.
He had been diagnosed as having carcinoma of the anterior floor
of the mouth 4 years before hospital admission. At that time, he
underwent a left modified radical neck dissection with removal
of the tumor mass and the inner table of the mandible. During the
neck dissection, the omohyoid, geniohyoid, myelohyoid, and genioglossus muscles were sacrificed. A temporary tracheostomy
was done and this closed with time. The patient also received radiation therapy using a 6-MeV linear accelerator. A total dose of
60 Gy was delivered to the midline of the neck and a dose of 50
Gy was delivered to the lower neck. Several months after radiation therapy, he was started on a regimen of levothyroxine (120
,ug each day). He quit smoking. The patient consumed a moderate amount of alcohol.
Examination at the time of hospital admission showed
an oriented afebrile patient with a weight of 105 kg and height of 185
cm. The left side of the neck was deformed and there was mild
edema of the lower lip and left side of the face. No lymph nodes
were palpable. A mild inspiratory stridor was noted. The chest,
cardiovascular, and results of the rest of the examination were
normal. Results of routine laboratory tests as well as thyroid
function tests were normal. Spirometry showed a FEV, of 3.82 L
(83 percent of predicted) and a FVC of 4.29 L (79 percent of
predicted). The flow volume curve, including the inspiratory
limb, was normal. Chest radiograph was normal. A computed
tomographic scan of the neck and chest showed no masses. Angioedema was suspected clinically and the patient was treated
with antihistamines and steroids without any benefit.
On the ward, the patient was noted to snore and have apneic
events. On further questioning, he admitted to mild daytime
sleepiness. Consequently, a nocturnal polysomnography study
was performed. This study showed a an apnea + hypopnea index
of 67 events per hour of sleep. The apneas were associated with
oxygen desaturations from a baseline of 95 percent to a minimum
level of 60 percent. One hundred fifteen episodes of oxygen de-
Laryngomalacia as a Cause of Obstructive Sleep Apnea (Chetty et al)
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