|If we must die--let it not be like hogs Hunted and penned in an inglorious spot, While round us bark the mad and hungry dogs, Making their mock at our accursed lot. If we must die--oh, let us nobly die, So that our precious blood may not b... Read more of If We Must Die at Martin Luther King.ca|| Informational|
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Acute Stenosis Of The Larynx
Source: A Manual Of Peroral Endoscopy And Laryngeal Surgery
Etiology.--Causes of a relatively sudden narrowing of the lumen of
the larynx and subjacent trachea are included in the following list.
Two or more may be combined.
1. Foreign body.
2. Accumulation of secretions or exudate in the lumen.
3. Distension of the tissues by air, inflammatory products, serum,
4. Displacement of relatively normal tissues, as in abductor
paralysis, congenital laryngeal stridor, etcetera.
Edema of the larynx may be at the glottic level, or in the
supraglottic or subglottic regions. The loose cellular tissue is most
frequently concerned in the process rather than the mucosal layer
alone. In children the subglottic area is very vascular, and swelling
quickly results from trauma or inflammation, so that acute stenosis of
the larynx in children commonly has its point of narrowing below the
cords. Dyspnea, and croupy, barking, cough with no change in the tone
or pitch of the speaking voice are characteristic signs of subglottic
stenosis. Edema may accompany inflammation of either the superficial
or deep structures of the larynx. The laryngeal lesion may be primary,
or may complicate general diseases; among the latter, typhoid fever
deserves especial mention.
Acute laryngeal stenosis complicating typhoid fever is frequently
overlooked and often fatal, for the asthenic patient makes no fight
for air, and hoarseness, if present, is very slight. The laryngeal
lesion may be due to cordal immobility from either paralysis or
inflammatory arytenoid fixation, in the absence of edema.
Perichondritis and chondritis of the laryngeal cartilages often follow
typhoid ulceration of the larynx, chronic stenosis resulting.
Laryngeal stenosis in the newborn may be due to various anomalies of
the larynx or trachea, or to traumatism of these structures during
delivery. The normal glottis in the newborn is relatively narrow, so
that even slight encroachment on its lumen produces a serious degree
of dyspnea. The characteristic signs are inspiratory indrawing of the
supraclavicular fossae, the suprasternal notch, the epigastrium, and
the lower sternum and ribs. Cyanosis is seen at first, later giving
place to pallid asphyxia when cardiac failure occurs. Little air is
heard to enter the lungs, during respiratory efforts and the infant,
becoming exhausted by the great muscular exertion, soon ceases to
breathe. Paralytic stenosis of the larynx sometimes follows difficult
forceps deliveries during which stretching or compression of the
recurrent nerves occur.
Acute laryngeal stenosis in infants, from laryngeal perichondritis,
may be a delayed result of traumatism to the laryngeal cartilages
during delivery. The symptoms usually develop within four weeks after
birth. Lues and tuberculosis are possible factors to be eliminated by
the usual methods.
Surgical Treatment of Acute Laryngeal Stenosis.--Multiple puncture
of acute inflammatory edema, while readily performed with the
laryngeal knife used through the direct laryngoscope, is an uncertain
measure of relief. Tracheotomy, if done low in the neck, will
completely relieve the dyspnea. By its therapeutic effect of rest, it
favors the rapid subsidence of the inflammation in the larynx and is
the treatment to be preferred. Intubation is treacherous and
unreliable except in diphtheritic cases; but in the diphtheritic cases
it is ideal, if constant skilled watching can be had.