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404     PART 4: Pulmonary Disorders



                   CHAPTER   Upper Airway Obstruction
                                                                           • Helium-oxygen mixtures reduce the density-dependent pressure
                    47       Brian K. Gehlbach                            required to drive airflow across obstructing upper airway lesions,
                                                                          and may stabilize patients with UAO pending definitive therapy.
                             John P. Kress
                                                                           • Prompt evaluation and management of suspected UAO may pre-
                                                                          vent subsequent complications including cardiac arrest, anoxic
                                                                          brain injury, and negative pressure pulmonary edema.
                  KEY POINTS
                     • Suspected upper airway obstruction (UAO) constitutes a medical
                    emergency. The immediate bedside consultation of a clinician
                    experienced in the management of this condition is indicated.  There are few medical conditions that are as rapidly and predictably
                     • The initial evaluation of UAO is focused on determining the sever-  lethal as the loss of upper airway patency. Because of the relative infre-
                    ity and suspected site of the obstruction. Arterial desaturation is   quency with which upper airway obstruction (UAO) is encountered by
                    a late  manifestation; better indicators of severity include stridor,   most physicians, opportunities to acquire significant clinical experience
                    poor air  movement, accessory muscle use, abnormal mentation or   are limited. This, combined with the frequently subtle presentation of
                    agitation, tachycardia, hypertension, and pulsus paradoxus.  upper airway obstruction and the clinician’s inability to visualize the
                     • Infections represent important causes of oropharyngeal and hypo-  upper airway in its entire extent through routine physical examina-
                    pharyngeal UAO and include Ludwig angina, peritonsillar abscess,   tion, may hamper diagnosis of this condition until a crisis results.
                    and infections of the retropharyngeal and lateral pharyngeal     This chapter describes an approach to diagnosing and treating UAO
                    spaces. Otolaryngology consultation is indicated. Depending on   as it presents in adults. While certain infections of the head, neck, and
                    the initial site of infection, spread to other critical sites (eg, the   upper respiratory tract are considered here as they relate to UAO, the
                    mediastinum) may occur.                            specific approach to their management is considered in greater detail in
                     • While intubation is not always required in adults with epiglottitis,   Chap. 73. A high index of suspicion for UAO, combined with early
                                                                       consultation of anesthesia and otolaryngology services, is critical to the
                    management in an ICU is mandatory, and intubation equipment   successful management of this condition.
                    and a tracheostomy tray should be at the bedside.
                     • Bacterial infections of the larynx are life-threatening. Causative   ANATOMY OF THE UPPER AIRWAY
                    organisms include  Staphylococcus aureus,  Streptococcus pneu-
                    moniae, Haemophilus influenzae, and Corynebacterium diphtheriae.  The  upper  airway  comprises  air-conducting  passages  that  begin at
                                                                                                               1,2
                     • Laryngospasm and laryngeal edema are important causes of   the mouth or nose and end at the mainstem carina.  The thoracic
                    postextubation stridor.  Prophylactic corticosteroids may  be   inlet divides the upper airway into the intrathoracic and extrathoracic
                                                                       airways. The extrathoracic airways are further divided into the naso-
                    effective at preventing this phenomenon in high-risk patients.
                    A reasonable approach is to administer methylprednisolone   pharynx, oropharynx, hypopharynx, larynx, and extrathoracic trachea.
                                                                       Air inspired through the nose passes through the nasal cavities and
                    20 mg IV q4h beginning 12 to 24 hours prior to planned extu-
                    bation and continued until the tube is removed. Patients with   enters the nasopharynx after exiting the nose by way of the posterior
                                                                       nares. Airflow proceeds inferiorly through the  nasopharynx,  passes
                    postextubation stridor from laryngeal edema may be treated
                    with a short (eg, 24 hours) course of corticosteroids.  posterior to the soft palate, and enters the oropharynx. Closure of the
                                                                       soft palate allows inspiration of air through the mouth. Air passes infe-
                     • Long-term intubation may result in a variety of problems related   riorly through the oropharynx to the hypopharynx, which begins just
                    to the upper airway, including endotracheal tube obstruction from   superior to the hyoid bone, and passes the epiglottis, thereby entering
                    secretions, vocal cord injury, subglottic stenosis, and tracheal stenosis.  the larynx.
                     • Risk factors for foreign body aspiration in adults include dimin-  The larynx is constructed of a cartilaginous skeleton consisting of
                    ished level of consciousness; impaired swallowing mechanism or   the thyroid, cricoid, and arytenoid cartilages (Fig. 47-1). This skele-
                    diminished upper airway sensation as a result of neuromuscular   ton surrounds the vocal cords, the movements of which are controlled
                    disorder, prior cerebrovascular accident, or advanced age; and   by the intrinsic muscles of the larynx, with their innervation arising
                    inability to chew food properly because of poor dentition.  from the left and right branches of the recurrent laryngeal nerve. An
                     • All suspected traumatic laryngeal injuries should be evaluated   exception to this rule is the innervation of the cricothyroid muscle,
                                                                       which arises from the  superior laryngeal  nerve.  This  nerve  also
                    promptly to reduce the immediate risk of UAO, as well as to pre-    supplies sensation to the epiglottis and vestibular folds (false cords),
                    vent long-term sequelae such as subglottic stenosis.
                                                                       which lie superior to the true vocal cords. The larynx is divided into
                     • Early laryngoscopic examination of the upper airway is crucial in   the supraglottic portion, the glottis, and the subglottic portion. The
                    the evaluation of burn patients with suspected inhalation injury.   glottis contains the structures within the plane of the true vocal cords
                    The risk of UAO increases throughout the first 24 hours.  and is located at the midpoint of the thyroid cartilage. The supraglot-
                     • Functional upper airway obstruction may occur in patients who   tic region extends from the epiglottis to just above the true vocal
                    exhibit abnormal glottic closure during inspiration and/or expira-  cords, while the subglottic region lies between the vocal cords and the
                    tion. There is a high risk of coincident asthma, complicating the   lower border of the cricoid cartilage.
                    evaluation of such patients.                         The trachea lies between the inferior border of the cricoid cartilage
                                                                       and the main carina, and is 10 to 13 cm in length in adults. The extra-
                     • Angioedema may result from allergy, hereditary or acquired disor-  thoracic trachea is typically 2 to 4 cm long, and comprises the segment
                    ders of the complement cascade, direct release of histamine from   that lies between the cricoid cartilage and the thoracic inlet. The
                    mast cells from nonallergic mechanisms (eg, opiates), and from   normal trachea has roughly the same coronal as sagittal diameter. Normal
                    angiotensin-converting enzyme inhibitors.          coronal tracheal diameter is 13 to 25 mm in men and 10 to 21 mm
                     • Angioedema from angiotensin-converting enzyme inhibitors may   in women.
                    occur at any time during the course of therapy.      This chapter focuses on disorders of the extrathoracic upper airway
                                                                       because of this region’s greater importance to the topic of UAO.








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