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Advances and controversies in the management of supraglottitis and laryngotracheobronchitis
Clinical Review
Advances and Controversies in the Management of Supraglottitis and Laryn g o trach eobro nc hiti s LEE D. ROWE, M.D.*
Recent advances in pediatric airway intubation and the introduction of pharmacotherapeutic agents, active within the larynx and tracheobronchial tree, have created significant controversies in the treatment of acute obstructive inflammatory laryngeal disease. Although the etiology, pathophysiology, and clinical patterns of supraglottitis and laryngotracheobronchitis are no longer confused, decisions concerning their medical management and method of airway control remain controversial. Both inflammatory disorders are critically examined, with a review of current concepts regarding the choice between endotracheal intubation and tracheotomy. Specific problems of anesthetic technique, criteria for extubation or decannulation, and the rationale for the use of corticosteroids, antibiotics, or racemic epinephrine are evaluated. If mechanical airway control is required, careful attention to initial intubation with a relatively small, cuffless polyvinyl chloride endotracheal tube and precise surgical technique when employing tracheotomy will minimize the overall morbidity. Short term intubation in acute obstructive inflammation of the larynx appears to be well tolerated. Tracheotomy is reserved for the few patients with laryngotracheobronchitis who demonstrate persistent significant subglottic edema.
Prior to World War I! acute obstructive inflammatory disease of the larynx was enmeshed in a tangle of confusion regarding its etiology, pathophysiology, and nomenclature. This disorientation, not surprisingly, created significant controversies over management. Even with recent advances in endotracheal intubation, controversies persist, and the physician faces the dilemma of selecting either tracheotomy or intubation of
the airway. Frequently the decision is based upon the availability of skilled ancillary personnel and the physician's own preference and bias. Tracheotomy or bronchotomy, as it was originally termed, was not accepted initially in American medicine. In 1797 George Washington succumbed from acute supraglottitis, in spite of a consulting physician's recommendation to
Accepted for publication December 12, 1979. *Assistant Professor of Otolaryngalogy, University of California, San Francisco. Assistant Chief of Otolaryngology, San Francisco General Hospital, San Francisco, California. American Journal of Otolaryngology- Volume 1, Number 3, May 1980
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perform a tracheotomy. 1 This proposal was rejected by his two personal physicians and instead, leeches, venesection, and "blisters applied to the throat" probably hastened his demise. 2 Interestingly, Chevalier Jackson over 100 years later alluded to the problem with tracheotomy following the recent introduction of intubation2 Today the increasing use of prolonged mechanical ventilation in premature infants with hyaline membrane disease and a variety of congenital defects has conditioned physicians to the relative safety of endotracheal intubation. 4 The movement away from high pressure, low volume cuffs to expandable high volume, low pressure cuffs and the use of cuffless tubes in infants and children has reduced the risk of laryngeal and tracheal injury. Unfortunately the relative indications for either tracheotomy or endotracheal intubation in infants with acute obstructive inflammatory diseases of the larynx have not been critically evaluated. In this article we examine supraglottitis and laryngotracheobronchitis and review current ideas regarding the choice between endotracheal intubation and tracheotomy. In addition, the specific problems of anesthetic technique, the use of antibiotics, corticosteroids, or racemic epinephrine, and criteria for extubation or decannulation are discussed.
HISTORICAL ASPECTS
A continuing theme throughout the early literature relating to acute laryngeal inflammation is confusion regarding its etiology, pathophysiology, and nomenclature with a concomitant aversion to surgical manipulation of the airway (Table 1). 5 Initially physicians were preoccupied with the morbid action of inflammation, and the science of Physik required a detailed theoretical knowledge of the inflammatory process. Boerhave believed that inflammation was produced by an obstruction to the free circulation of the blood in the capillary vessels. By contrast, the great English anatomist John Hunter considered tissue or organ injury of major importance. 5 The cardinal signs of inflammation (calor, dolor, rubor, and tumor) were related by eighteenth and nineteenth century physicians to increasing blood viscosity with vessel dilatation, allowing the entrance of thicker parts of the blood. Methods of treating laryngeal inflammation included venesection and the local applica-
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TABLE 1. Historical Traces of Acute Laryngeal Inflammation DATE 1765 1797 1819 1826 1844 1895 1900
1914 1940 1941 1948 1974
Holme: First use of the term "croup" George Washington: Died of acute epiglottitis Bayle: First clinical description of acute epiglottiffs (termed acute spasmodic croup} Bretonneau: Treatise on croup secondary to diphtheria Mackintosh: Popular American textbook of medicine: confusion of clinical appearance of croup and epiglottitis Semon: Inflammation of larynx and pharynx considered manifestations of the same disease Theisen: First use of the term "acute epiglottitis" w i t h an accurate anatomical description
Lederman: Described acute phlegmonous epiglattiditis Brown: Separated acute epiglottitis from laryngeal abscess Sinclair: Identified Hemophilus influenzae type B as the etiology of acute epiglottitis Rabe: Positive statement, separating croup and epiglottitis as distinctly different clinical entities Buchan: Identified parainfluenza viruses 1,3 and influenza virus as primary etiologic agents of laryngotracheobronchitis
tion of leeches and counterirritants to drain the inflammatory region2 Indeed the Hippocratic doctrine dictated that "spontaneous determination to the external parts of the neck is vital to recovery. ''6 Constitutional therapy, including brisk purgatives (mercurous chloride and antimony) and emetics (syrup of ipecac), were used in addition to hot pediluvia (foot baths). Occasionally the inhalation of steam from hot water, poured on hops or camomile flowers, was recommended2 Although during the early nineteenth century smallpox, scarlet fever, measles, and diphtheria commonly produced acute laryngeal inflammation, their precise mechanism of action was unknown. More importantly, these disorders overshadowed the contributory effect of Hemophilus influenzae and parainfluenza viruses to the spectrum of acute laryngeal disease. Previously the Scottish physician Francis Holme had described the harsh breathing sound associated with odynophagia as "croup," applying an old Scottish word of the same meaning. "Cynache trachealis" had formerly been used to represent this acute laryngeal disorder3 However, in spite of its original precise meaning, the term croup was subsequently applied to all acute laryngeal disorders. Paul Bretonneau's contribution, in 1826, to the
SUPRAGLOTTITIS AND LARYNGOTRACHEOBRONCHITIS
understanding of diphtheria as an etiology of croup was enormous. He accurately noted that the diphtheritic false membrane may extend from the pharynx to involve the entire larynx and trachea and cause obstruction. 8 The first clinical description of acute supraglottitis is attributed by Mackintosh ~ to Bayle, who seven years previously had called acute spasmodic croup "that peculiar affection of the epiglottis, larynx, and rima glottidis." Although Mackintosh contended that croup was secondary to cerebral irritation, producing convulsions and spasms of the nerves supplying the muscles of the throat, his description of a larynx with acute supraglottitis removed at autopsy is classic: "The epiglottis was much swollen, erect, stiff and of a red color. The mucous membrane was found so much swollen as to leave the smallest possible passage for the transmission of air. ''5 In spite of evidence of mechanical laryngeal obstruction and the knowledge of bronchotomy, tracheotomy was not widely used by physicians. In the midnineteenth century incision and drainage of edematous laryngeal regions were recommended. If this technique failed, laryngeal sounds were inserted. Later, after the introduction of the laryngeal mirror, the epiglottis was multiply punctured with a curved bistoury, producing free hemorrhage. 9 At the same time O'Dwyer's laryngeal intubation for diphtheria undoubtedly saved many lives. Although tracheotomy was practiced for 3500 years by the Egyptians and Hindus, Chevalier Jackson 3 is primarily responsible for its reintroduction, noting: "There is no other justifiable life-saving operation whose reign of usefulness had not been extended by modern methods." Competition from MacEwan's recent introduction of peroral endotracheal intubation was strong, however. ~° Although Theisen 11 anatomically described and introduced the term "supraglottitis" at the turn of the century, Semon, TM a leading otolaryngologist of the period, incorrectly considered all pharyngeal and laryngeal inflammation to be a manifestation of the same disease. This misconception continued for many years until Sinclair 13 identified the etiologic agent of acute supraglottitis as Hemophilus influenzae, type B. Rabe 14in 1948 published three articles concerning croup, separating it from acute epiglottitis as a distinct clinical entity. Finally, in 1974 Buchan et al. ~5 identified in culture parainfluenza viruses 1 and 3 and influenza virus as the primary etiologic agents of laryngotracheobronchitis.
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In the past 30 years, however, authors have recapitulated the mistakes of their predecessors and confused the nomenclature and clinical patterns of croup and epiglottitis. Perhaps the newer terminology, supraglottitis and laryngotracheobronchitis, will resolve this problem.
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SUPRAGLOTTITIS
Supraglottitis is an acute inflammatory disorder of the larynx, secondary to Hemophilus influenzae type B, affecting the epiglottis, aryepiglottic folds, arytenoid cartilages, and ventricular bands. Occasionally pyogenic staphylococcus and group A beta hemolytic streptococcus are implicated. Although there is usually no prodromal phase and the disease progresses rapidly to respiratory collapse, an upper respiratory tract syndrome may precede the onset of recognizable symptoms in 50 per cent of the cases for more than 24 hours. Dysphagia, odynophagia, and shortness of breath rapidly progress to drooling, inspiratory stridor, and a muffled but clear voice. 18 The disease primarily affects children two to six years of age but can occur as early as five months or later in adulthood. A slight male predominance with no seasonal predilection is noted in most series, is, 2o As opposed to the situation in laryngotracheobronchitis, most children are extremely toxic, with an elevated temperature and an increased pulse and respiratory rate. Stridor, which is exacerbated by the supine position, is associated with prolongation of the inspiratory phase of respiration. 21 With increasing upper airway obstruction, hypercapnia, and hypoxia, the respiratory rate and heart rate are accelerated along with the development of marked supraclavicular, intercostal, and substernal retractions. The child sits erect, anxious, increasingly exhausted, drooling, and hungry for air. The chin is thrust outward with the neck hyperextended and the tongue protruding. Sudden laryngospasm may occur with aspiration of secretions into an already compromised airway and produce respiratory arrest. 2°, 22 The diagnosis is confirmed by direct inspection. Mirror examination or direct visualization of the larynx, which is not recommended unless the patient is well oxygenated and equipment is available for immediate intubation, reveals a hyperemic edematous epiglottis with the rima glottidis often obscured by edematous aryepiglottic folds. Mucous membrane changes range
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from edema and hyperemia to occasional desquamation, ulceration, sloughing, or rare abscess formation on the anterior or lingual surface of the epiglottis. 23 Infrequently the larynx is tender to palpation. Roentgenographic studies are used to confirm the diagnosis and to exclude other causes of acute airway obstruction. Among the differential possibilities to be eliminated, foreign bodies of the hypopharynx, upper cervical esophagus, larynx, and trachea are the most important. 24' 25 Anteroposterior and lateral soft tissue films demonstrate swelling and rounding of the epiglottis, with thickening and bulging of the aryepiglottic folds and distention of the hypopharynx (Fig. 1). 26 Also upper airway obstruction may produce alveolar hypoventilation with increasing hypoxia, capillary permeability, and negative intraalveolar pressures, which result in acute cardiac enlargement and pulmonary edema, often visible on chest films. 27 The white blood cell count is frequently higher than 16,000 per cubic milli-
Figure 1. Lateral neck roentgenogram in infant with acute supraglottitis demonstrating massive edema and rounding of the epiglottis (arrows) with thickened aryepiglottic folds and hypopharyngeal distention.
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meter with a relative increase in polymorphonuclear leukocytesY ° Unfortunately arterial blood gas levels cannot be relied upon as criteria for airway intervention. Although selective initial medical management of supraglottitis has been advocated, immediate control of the airway is prudent and life saving. 2s-3° In a retrospective review of 64 patients who were observed but not treated the mortality approached 80 per cent. 29 However, if children without signs of cyanosis, exhaustion, or severe sternal retraction are medically managed with the physician in constant attendance for the first two hours, tracheotomy or intubation may be avoided. 3° Nonetheless, up to 60 per cent of children with acute supraglottitis require airway intervention. 31 Patients are given 100 per cent humidified oxygen and an intravenous line is started. Simultaneously blood cultures are obtained. Because the most frequently isolated organism is Hemophilus influenzae, ampicillin (200 mg. per kg. per day intravenously in four divided doses) is the drug of choice. Recently, however, strains of betalactamase producing Hemophilus influenzae with resistance to ampicillin have appeared throughout the United States at an alarming rate. In 1978 middle ear isolates in children with acute otitis media exhibited an 8 per cent incidence of ampicillin resistant Hemophilus influenzae, a marked increase from the 1 per cent incidence reported during the years 1970 to 1976. 32 Therefore, chloramphenicol (100 mg. per kg. per day intravenously in four divided doses) is frequently added to ampicillin, pending the results of blood cultures and sensitivity studies. A new cephalosporin, cephamandole, capable of inhibiting both ampicillin resistant and ampicillin sensitive Hemophilus influenzae, has recently been introduced for parenteral use. 33 The value of this new drug in the treatment of acute supraglottitis is not yet known, however. The use of corticosteroid therapy, although apparently gaining wider acceptance, is not based upon well designed double blind studies.20, 28, 30, ~4, 35 Presumably the antiinflammatory effect, coupled with stabilization of endothelial permeability, decreases extracellular and intracellular edema. 36 One prospective study, however, revealed no significant difference in the number of tracheotomies required for corticosteroid treated patients and for those receiving none. 29 Therapeutic protocols have ranged from dexamethasone (0.5 mg. per kg.), administered as an initial
SUPRAGLOTTITIS AND LARYNGOTRACHEOBRONCHITIS
intravenous bolus or immediately prior to extubation, to hydrocortisone (1 gm. per day intravenously).2o, 28, 34 Although no method is more advantageous than another, a useful protocol that may be employed includes dexamethasone (1 mg. per kg. for the first 5 kg. of body weight and 1 mg. per kg. for each additional 5 kg. of body weight) administered as an initial intravenous bolus; half of this initial dose is repeated every six hours for 48 hours if needed and one-fourth of the initial dose is given every six hours for 24 hours following extubation. 3° If there is no dramatic improvement in supraglottic obstruction within two hours, control of the airway is imperative. Unfortunately the relative value of tracheotomy versus endotracheal intubation is based upon retrospective case analyses. Pediatric tracheotomy has been associated with significant complications, especially w h e n performed under emergency conditions without concomitant airway control. Most significantly pneumothorax, pneumomediastinum, postoperative hemorrhage, and accidental decannulation are potentially life threatening complications. ~9,37-40 Intermediate problems include atelectasis, mucous plug obstruction, severe tracheitis secondarily to Staphylococcus, Pseudomonas, or Monilia, and tracheoinnominate artery fistula. 41 The delayed complications of pediatric tracheotomy, however, are also devastating: tracheal and subglottic stenosis, tracheoesophageal fistula, tracheomalacia, and delayed decannulation. 41"44Many of these problems can be avoided by proper surgical technique. Initial control of the airway with either a bronchoscope or an endotracheal tube is important. A transverse or vertical neck incision is used and the trachea is incised vertically between the third and fourth tracheal rings, the dissection of the pretracheal fascia being limited to the midline. 44"45 A long nonabsorbable traction suture is placed on either side of the tracheal incision so that the tracheotomy can be opened in the event of an accidental decannulation, A postoperative anteroposterior portable chest film is mandatory to exclude pneumothorax and other complications. Humidification, atraumatic suction, and dry aseptic tracheostomy care minimize the risk of tracheobronchial infection. 46"47 A review of 991 tracheotomies for supraglottitis, reported in 12 series during the past 10 years, indicates a mortality range of 0 to 1 per cent.19, 20, ~9,so, ~4,35, 4s-5~ The incidence of complications, including pneumothorax and pneu-
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momediastinum (20 patients), postoperative hemorrhage (5), tracheal granuloma (4), hypertrophic neck scars (7), and excessive tracheobronchial secretions (6), has ranged from 0 to 39 per cent. By contrast, a similar group of 510 patients treated with endotracheal intubation alone demonstrated a mortality range of 0 to 0.92 per cent with complications in 0 to 24 per cent.Z0. 22, 28.30, 34,49, 53-57Included in the reported complications were accidental extubation (11), subglottic stenosis (7), subglottic granuloma (4), lobar atelectasis (4), mucous plug (1), and vocal cord granuloma (1). However, following the introduction of soft polyvinyl chloride cuffless endotracheal tubes, the incidence of delayed irreversible complications, including subglottic and tracheal stenosis, has remained low (1.6 per cent). 31 Although tracheotomy is no longer the primary modality in the treatment of supraglottitis, several objections to the use of endotracheal tubes may be raised: (1) Endotracheal tubes may increase laryngeal edema. (2) Improperly secured tubes are readily dislodged. (3) The absence of an inner cannula increases the risk of obstruction. (4) Endotracheal tubes require increased nursing skills and intensive care facilities. (5) The tracheobronchial tree is more difficult to suction. (6) Airway resistance and dead space are increased. (7) Peroral feeding is impaired. 58 By contrast, the proponents of endotracheal intubation offer the following distinct advantages over tracheotomy: an overall lower mortality, a greater margin of safety with accidental extubation, fewer laryngotracheal complications following the introduction of soft cuffless polyvinylchloride tubes, and decreased hospitalization. 59 Indeed in several recent series the average duration of intubation ranged from 1.5 to 2.8 days as compared to 2.7 to 5.5 days for tracheotomized infants and children. 19~28, 49, 52, 53, 57 Factors contributing to endotracheal tube complications are related primarily to tube design, size, and duration of intubation. In addition, severe tracheitis and systemic disease, including diabetes mellitus, anemia, malnutrition, and dehydration, increase the risk of laryngotracheal injury. The use of newer, smaller diameter endotracheal tubes with minimal mechanical movement and adequate humidification and hydration will reduce the incidence of these complications.4, 60.61 Most importantly the short duration of intubation in acute supraglottitis significantly decreases the associated risk.
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TABLE 2. Anesthetic Techniques in the Management of Supraglottitis Intravenous
Thiopentane (5 mg./kg.) + succinylcholine (1 mg./kg.) Diazepam (0.4 mg./kg.) + succinylcholine (1 mg./kg.) Diazepam (0.2 mg./kg.) + Ketamine (2 mg./kg.) Ketamine (2 mg./kg.) ÷ Xylocaine (3 mg./kg.) topical spray Inhalational
Halothane (1.5-2.0%) Halothane (1.0-2.0%)
+ oxygen ÷ nitrous oxide ÷ oxygen (50%)
Combined intravenous and inhalational
Diazepam (0.2 mg./kg.) + halothane (1.0-1.5%) + oxygen Ketamine (1-2 mg./kg.) ÷ halothane (1-2%) ÷ oxygen Awake intubation
Topical 4% cocaine Premedication
Within 36 to 48 hours the infant's temperature is frequently normal and he is more alert, occasionally coughing around the tube during suctioning. Although a leak often occurs around the endotracheal tube at 20 to 25 cm. of water pressure, this is not a prerequisite for extubat i o n Y If the massive supraglottic edema has significantly resolved, the patient is extubated in the operating room. Racemic epinephrine delivered by intermittent positive pressure breathing is advocated by some physicians following extubation, but no control studies e x istY "64 If corticosteroid therapy was initiated prior to intubation, it is continued for 24 hours after extubation.63, 65
Atropine (0.005-0.01 mg./kg.)
Proper anesthetic and intubation technique is critical. Several protocols are available, including intravenous, inhalation, intravenousinhalational, and awake intubation. 53' 56 Currently inhalational techniques without the use of muscle relaxants are preferred (Table 2).20, 22, 35, 49, 50, 59 Preoxygenation is followed by rapid halothane and oxygen induction. Although muscle relaxants have been successfully employed, there appears to be no rationale for their use except to facilitate immediate nasotracheal tube placement. ~3 Atraumatic oral intubation secures the airway and allows endoscopic inspection to rule out other potential lesions. Following the placement of a nasotracheal tube (one to two sizes smaller than normal [Table 3]) 2 cm. below the level of the true vocal cords, the child is kept sedated (diazepam, 0.2 mg. per kg. intravenously; chloral hydrate, 50 rag. per kg. intravenously; or pentobarbitol, 2 to 4 rag. per kg. intravenously) and the tube position is confirmed with a chest film. 62 Ultrasonically nebulized oxygen is delivered to maintain a 60 per cent saturation at 37 ° C. 61In addition, the tube is aspirated after irrigation with 0.25 to 0.5 ml. of physiological saline every hour to prevent occlusion and retention of secretions. TABLE 3. Endotracheal Tube Size in Acute Obstructive Laryngeal Inflammation
AGE Newborn-6 months 6 months-2 years 2-5 years Over 5 years
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INTERNALDIAMETER 3.0 ram. 3.5 ram. 4.0 mm. 4.5 ram.
ACUTE LARYNGOTRACHEOBRONCHITIS
Acute laryngotracheobronchitis is a viral illness that is far more c o m m o n than acute supraglottitis. The illness occurs primarily in late autumn and winter, and parainfluenza viruses and influenza viruses A and B account for the majority of cases." 3. ,~, 66 In addition, respiratory syncytial virus, adenoviruses, coxsackievirus A, ECHO viruses, and measles virus contribute to the spectrum of disease. I-3' 5, 7. i0. 14 There is also a variation in predominance of the individual viruses from year to year. The principal lesion is subglottic edema with a variable com ponent of tracheobronchial inflammation, occasionally leading to frank desquamating tracheitis and pneumonitis. Because the infant's subglottic larynx forms an isosceles triangle 7 mm. in length and 5 ram. in width, 1 mm. of edema will effectively reduce the area by 65 per cent. 2"67 Infants three months to three years of age are affected primarily, although occasionally older children contract the disease. 6s A 2:1 female:male ratio is seen. 69 The symptoms of a barking cough, hoarseness, inspiratory and expiratory stridor, and substernal retractions are frequently preceded by an insidious u p p e r respiratory tract prodromal period lasting one to seven days. TM In contrast to patients with supraglottitis, the child appears sick but not toxic. The larynx is not tender, no drooling is observed, and stridor is not exacerbated by a change in position. In addition, hypoxia and cyanosis often develop. Not u n c o m m o n l y the disease recurs. Recently small airway dysfunction and exercise induced bronchospasm have SUPRAGLOTTITIS AND LARYNGOTRACHEOBRONCHITIS
been identified in nonallergic children with a history of laryngotracheobronchitis. TM The degree of hypoxemia is related to ventilation-perfusion abnormalities with right to left shunting and is best correlated with an increasing respiratory rate. 71Also, as the relative component of upper respiratory tract obstruction increases, the arterial carbon dioxide content (PaCO2) rises proportionately. TM Anteroposterior and lateral neck films confirm the clinical impression of marked subglottic narrowing and assist in excluding other causes of infant airway obstruction, including foreign bodies in the aerodigestive tract, laryngeal and tracheal tumors, vascular compression of the trachea, and mediastinal tumors (Fig. 2). The peripheral white blood cell count is elevated, with a relative lymphocytosis. Despite its frequency and life threatening nature, there is no consensus of opinion regarding the treatment of laryngotracheobronchitis. If adequate humidification, oxygenation, and hydration can be maintained and there is no severe
stridor, retractions, cyanosis, or hypoxia, the infant may not require hospitalization. On the other hand, patients with a m i n i m u m of two of the following conditions meet criteria for immediate airway intervention: a heart rate greater than 170 beats per minute, a respiratory rate greater than 55 per minute, a PaCO2 level greater than 37 mm. Hg, a PaO2 level less than 50 mm. Hg, and congestive heart failure, severe tracheitis, or pneumonitis. 73 Humidification in either a high humidity or "croup" tent is extremely important. 66 Electrocardiographic monitoring, intravenous fluids, and maintenance of an inspired oxygen content of 30 to 40 per cent are critical. Antibiotics, although they have no significant influence on the outcome, are frequently used. TM Intravenous therapy with ampicillin may be initiated, pending the results of culture of transtracheal or nasotracheal aspirates. Until recently the role of corticosteroids was controversial and of no proven value. Original experimental work in dogs indicated that dex-
Volume 1 Number 3 May 1980
Figure 2. Anteroposterior chest film in an infant with laryngotracheobronchitis revealing marked subglattic narrowing (arrows).
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amethasone administered immediately following extubation and one hour later prevented the development of laryngeal edema. 65 Unfortunately carefully executed control trials applying these experimental findings were lacking. However, a recent prospective double blind study evaluated the efficacy of corticosteroids in the treatment of laryngotracheobronchitis. Patients receiving dexamethasone intramuscularly (0.3 mg. per kg.) on admission and a similar dose two hours later exhibited a statistically significant improvement in signs and symptoms. 75 Unfortunately the value of racemic epinephrine (2.25 per cent solution of dextro- and levorotatory epinephrine hydrochloride) remains controversial. One-half milliliter of a 2.25 per cent racemic epinephrine solution is diluted with sterile water or physiological saline and delivered through a mainstream nebulizer via a mask with intermittent positive pressure breathing for 12 to 15 minutes (Table 4). 6s High inspiratory flows are initially maintained, with a gradual decrease to slow inflation with peak pressures not exceeding 20 cm. of water. 76 Shortly after the beginning of therapy there is a significant decrease in upper airway obstruction; however, relapses occur within two hours in the majority of patients. Racemic epinephrine is repeated one or more times as necessary, but no significant changes in clinical status have been observed at 24 or 36 h o u r s . 69" 77 Because of the beta-adrenergic side effects of the n-isomer, including tachycardia, hypertension, and ventricular arrhythmias, racemic epinephrine should be avoided if the heart rate exceeds 160 beats per minute. 68' 76It is also contraindicated in children with subvalvular aortic stenosis, pulmonic stenosis, idiopathic hypertrophic subaortic stenosis, and the tetralogy of Fallot. 66 Patients with progressive hypoxia, cyanosis, hypercarbia, and increasing respiratory and cardiac rate who fail to respond to racemic epinephrine and dexamethasone are intubated. An inhalational technique is preferred. Previously tracheotomy was required in 3 to 13 per cent of
TABLE 4. WEIGHT (KG.) 5 10 15 20 25 30
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Dosage
RACEMIC EPINEPHRINE (ML.) 0.25 + 0.5 0.75 1.0 1.25 1.5
the cases. 7s-si Currently the need for tracheotomy has been reduced to nearly zero, and this reduction is attributed to the increasing use of nasotracheal intubation and the widespread application of corticosteroids and racemic epinephrine. 69 This reduction, however, may reflect only a change in the viral virulence or earlier clinical recognition and treatment. A recent survey of 815 hospitalized patients with laryngotracheobronchitis revealed a 6.5 per cent incidence of nasotracheal intubation with a mean duration of intubation of 88 hours. There were no mortalities, and the incidence of delayed complications, as determined by postextubation symptoms, peak expiratory flow rates, and laryngeal polytomography, was less than 2 per cent. 3' The criteria for and technique of extubation are similar to those employed in acute supraglottitis. The development of a leak around the endotracheal tube at 25 to 30 cm. of water positive pressure is an encouraging sign. Children are extubated in the operating room or pediatric intensive care unit, with an anesthesiologist and otolaryngologist in attendance. Tracheotomy is performed only if significant obstruction persists to avoid the high risk of subglottic stenosis associated with reintubation.79, s0 Corticosteroids and racemic epinephrine are frequently continued for 24 hours following extubation. Only three patients of an original 150 children with laryngotracheobronchitis (18 per cent intubated with nasotracheal tube) ultimately required a tracheotomy. 82 Thus, the role of tracheotomy in the management of laryngotracheobronchitis is limited to a select number of patients.
SUMMARY
The etiology, pathophysiology, and clinical patterns of supraglottitis and laryngotracheobronchitis are separately reviewed. In addition, the historical aspects of acute inflammatory
Schedule of Racemic Epinephrine SALINE OR WATER (ML.)
TOTAL (ML.)
O./KG./MIN. X 10-15 MIN.
2.75 2.50 2.25 2.0 1.75 1.5
3.0 3.0 3.0 3.0 3.0 3.0
112.0 112.5 112.4 112.5 112.2 112.5
SUPRAGLOTTITIS AND LARYNGOTRACHEOBRONCHITIS
laryngeal disease and controversies surrounding tracheotomy and intubation of the airway are examined. Acute supraglottitis is appropriately managed by short term intubation of the airway and the parenteral administration of antibiotics capable of inhibiting Hemophilus influenzae. By contrast, laryngotracheobronchitis requires initial aggressive medical management, including humidified oxygen, hydration, and the parenteral administration of corticosteroids. Patients with progressive respiratory insufficiency are intubated, and tracheotomy is reserved for the few children with persistent airway obstruction. By avoiding the high risk of subglottic stenosis associated with prolonged intubation and employing a precise tracheotomy technique, the overall morbidity and mortality of this disorder can be minimized.
References 1. Scheidemandel, H. H. E.: Did George Washington die of quinsy? Arch. Otolaryngol., 102:519-521, 1976. 2. Dick, E. C.: Letter to Thomas Semmes, January 10, 1800. Med. Record 92:1128, 1917. 3. Jackson, C.: Tracheotomy. Laryngoscope, 19:285-290, 1909. 4. Conner, G.: Orotracheal intubation in the newborn. Laryngoscope, 87:87-91, 1977. 5. Mackintosh, J.: Principles of Pathology and Practice of Medicine. Philadelphia, Lindsay and Blakiston, 1844, pp. 1-29, 366-367. 6. Frost, E. A. M.: Tracing the tracheostomy. Ann. Otol. Rhinol. Laryngol., 85:618-624, 1976. 7. Holme, F.: An Enquiry into the Natural Causes and C-~re of Croup. Edinburgh, Kincaid and Bell, 1765. 8. Bretonneau, P.: Des Inflammations sp6ciales du tissu muquex, et an particulier de la Diphth6rie, ou inflammation pelliculaire, connue sous le nom de Croup, d'Angine Maligne, d' Angine Gangreneuse. Paris, 1826. 9. Keen, W. W., and White, J. W.: An American Textbook of Surgery. Philadelphia, W. B. Saunders Company, 1900, pp. 615-637. 10. MacEwan, W.: Clinical observations of introduction of tracheal tubes by mouth instead of a tracheotomy. Br. Meal. J., 2:122-124, 163-165, 1880. 11. Theisen, C. F.: Angina epiglottidea anterior: report of 3 cases. Albany Med. Ann., 21:315, 1900. 12. Semon, F.: Probable pathological identity of the various forms of acute septic inflammations of the throat and neck. Med. Chir. Tr. Lond., 78:181-238, 1895. 13. Sinclair, S. E.: Hemophilus influenzae type B, in acute laryngitis with bacteremia. J. Am. Med. Assoc., 117:170-173, 1941. 14. Rabe, E. F.: Infectious croup. II. "Virus croup." Pediatrics, 2:415-427, 1948. 15. Buchan, R. A., Marten, K. W., and Kennedy, D. H.: Aetiology and epidemiology of viral croup in Glasgow, 1966-1972. J. Hyg., 73:143-150, 1974. 16. Lederman, M. D.: Acute phlegmonous epiglottiditis. Laryngoscope, 29:25, 1914. 17. Brown, J. M.: Acute infections of the epiglottis. Arch. Otolaryngol., 32:631-641, 1940. 18. Gross, C. W.: Medical management, nasotraeheal intuba-
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tion, and tracheotomy in the treatment of upper airway obstruction in children. Otolaryngol. Clin. N. Am., 10:157-166, 1977. 19. Cohen, S. R., and Chai, J.: Epiglottitis: twenty year study with tracheotomy. Ann. Otol. Rhinol. Laryngol., 87:461-467, 1978. 20. Cantrell, R. W., Bell, R. A., and Morioka, W. F.: Acute epiglottitis intubation versus tracheostomy. Laryngoscope, 88:994-1005, 1978. 21. Snow, J. B., Jr.: Clinical evaluation of noisy respiration in infancy. Lancet, 2:504-509, 1965. 22. Hannallah, K., and Rosales, J. K.: Acute epiglottitis: current management and review. Can. Anaesth. Soc. J., 25:84-91, 1978. 23. Miller, A. H.: Acute obstructive supraglottic laryngitis in small children caused by Hemophilus influenzae type B. Trans. Am. Acad. Ophthalmol. Otolaryngol., 53:519-526, 1949. 24. Bogard, A. Q., and Potsic, W. P.: Stridor in the first year of life. Clin. Pediatr., 16:913-919, 1977. 25. Fearon, B. W., and Bell, R. D.: Acute epiglottitis: a potential killer. Can. Med. Assoc. J., 112:760-766, 1975. 26. Gevin, J. L., and Lee, F. A.: Radiological case of the month: acute epiglottitis. Am. J. Dis. Child., 130:195196, 1976. 27. Soloman, M. G., and Ricker, P.: Epiglottitis and pulmonary oedema in children. Can. Anaesth. Sac. J., 25:270-275, 1978. 28. Battaglia, J. D., and Lockhart, C. H.: Management of acute epiglottitis by nasotracheal intubation. Am. J. Dis. Child., 129:334-336, 1975. 29. Johnson, G. K., Sullivan, J. L., and Bishop, L. A.: Acute epiglottitis. Arch. Otolaryngol., 100:333-337, 1974. 30. Strome, M., and Jaffe, B.: E p i g l o t t i t i s - individualized management with steroids. Laryngoscope, 84:921928, 1974. 31. Schuller, D. E., and Birck, H. G.: The safety of intubation in croup and epiglottitis and eight year follow-up. Laryngoscope, 85:33-46, 1975. 32. Schwartz, R., et al.: The increasing incidence of ampicillin resistant Hemophilus influenzae. J. Am. Med. Assoc., 239:320-323, 1978. 33. Cephamandole and cefoxitin. Med. Letter, 21:13-15, 1979. 34. Heldtander, P., and Lee, P.: Treatment of acute epiglottitis in children by long-term intubation. Acta Otolaryngol., 75:379-381, 1973. 35. Cantrell, R. W., Bell, R. A., and Morioka, W. T.: Acute epiglottis: intubation versus tracheotomy. Trans. Pac. Coast Oto-ophthalmol. Soc., 57:75-89, 1976. 36. Goodman, L. S., and Gilman, A.: The Pharmacological Basis of Therapeutics. Ed. 4. New York, Macmillan Publishing, Inc., 1970, pp. 1623-1624. 37. Rabuzzi, D. D., and Reed, G. F.: Intrathoracic complications following tracheotomy in children. Laryngoscope, 81:939-946, 1971. 38. Cohen, S. R., et al.: Endoscopy and tracheotomy in the neonatal period. Ann. Otol. Rhinol. Laryngol., 86:577583, 1977. 39. Heroy, J. H., et al.: Airway management in the premature infant. Ann. Otol. Rhinol. Laryngol., 87:53-59, 1978. 40. Hawkins, D. B., and Williams, E. H.: Tracheostomy in infants and young children. Laryngoscope, 86:331340, 1976. 41. Chew, J. Y., and Cantrell, R. W.: Tracheotomy: complications and their management. Arch. Otolaryngot., 96:538-545, 1972. 42. Tucker, J. A., and Silberman, N. D.: Tracheotomy in pediatrics. Ann. Otol. Rhinol. Laryngol., 81:818-824, 1972. 43. Westgate, H. D., and Roux, K. L., Jr.: Tracheal stenosis following tracheotomy, incidence and predisposing factors. Anesth. Analg., 49:393-401, 1970.
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44. Harde, K. L.: Tracheostomy: indications, technics and tubes. Am. J. Surg., 126:300-310, 1973. 45. Bryant, L. R., et al.: Evaluation of tracheal incisions for tracheostomy. Am. J. Surg., 135:675-679, 1978. 46. Snow, J. B., Jr., and Preston, W. J.: Dry, aseptic method of tracheotomy care. Arch. Otolaryngol., 92:191-194, 1970. 47. Perotta, R. J., and Schley, W. S.: Pediatric tracheotomy: a five year comparison study. Arch. Otolaryngol., 104:316-321, 1978. 48. Margolis, C. M., Ingram, D. L., and Meyer, J. H.: Routine tracheotomy in Hemophilus influenzae type B epiglottitis. J. Pediatr., 81:1150-1153, 1972. 49. Oh, T. H., and Motoyama, E. K.: Comparison of nasotracheal intubation and tracheostomy in the management of acute epiglottitis. Anesthesiology, 46:214216, 1977. 50. Benjamin, B., and O'Reilly, B. O.: Acute epiglottitis in infants and children. Ann. Otol. Rhinol. Laryngol., 85:565-572, 1976. 51. Fearon, B., and Cinnamond, M.: Tracheotomy in acute supraglottitis (epiglottitis): the treatment of choice. Laryngoscope, 87:879-883, 1977. 52. Margolis, C. Z., Ingram, D. L., and Mayer, J. H.: Routine tracheotomy in Hemophilus influenzae type B epiglottitis. J. Pediatr., 81:1150-1153, 1972. 53. Milko, D. A., Marshnk, G., and Striker, T. W.: Nasotracheal intubation in the treatment of acute epiglottitis. Pediatrics, 53:674-677, 1979. 54. Fearon, B., et al.: Airway problems in children following prolonged endotracheal tube intubation. Ann. Otol. Rhinol. Laryngol., 75:975-986, 1966. 55. Johnsen, S.: What is prolonged intubation? Acta Otolaryngol., 75:377-378, 1973. 56. Blanc, V. F., Weber, M. L., and Leduc, C.: Acute epiglottitis in children: management of 27 consecutive cases with nasotracheal intubation with special emphasis on anaesthetic considerations. Can. Anaesth. Soc. J., 24:1-11, 1977. 57. Lewis, J. K., Gartner, J. C., and Galvis, A. G.: A protocol for management of acute epiglottitis. Clin. Pediatr., 17:494-496, 1978. 58. Coker, S. B., and Scherz, R. G.: Safe alternative to tracheostomy in acute epiglottitis. Am. J. Dis. Child., 129:136, 1975. 59. Heldtander, P., and Lee, P.: Treatment of acute epiglottitis in children by long-term intubation. Acta Otolaryngol., 75:379-381, 1973. 60. Lewis, F. R., Schlobohm, R. M., and Thomas, A. N.: Prevention of complications from prolonged tracheal intubation. Am. J. Surg., 135:452-457, 1978. 61. Gregory, G. A.: Respiratory care of newborn infants. Pediatr. Clin. North Am., 19:311-324, 1972. 62. Striker, T. W., Stool, S., and Dowries, J. J.: Prolonged nasotrachea] intubation in infants and children. Arch. Otolaryngo]., 85:210-213, 1967. 63. Koka, B. V., et al.: Postintubation croup in children. Anesth. Analg., 56:501-505, 1977. 64. Khan, F., and Reddy, N. C.: Enlarging intratracheal tube cuff diameter: a quantitative roentgenographic study
65. 66. 67. 68. 69. 70.
71. 72. 73. 74. 75. 76.
77.
78. 79. 80. 81. 82.
of its value in the early prediction of serious tracheal drainage. Ann. Thorac. Surg., 24:49-53, 1977. Biller, H., et al.: Laryngeal edema: an experimental study. Ann. Otol. Rhinol. Laryugol., 79:1084-1087, 1970. Lockhart, C. H., and Battaglia, J. D.: Croup and epiglottitis. Pediatr. Ann., 6:262-269, 1977. Crumley, R. L.: Airway management in croup and epiglottitis. West. J. Med., 126:184-189, 1977. Melnick, A., Berger, R., and Green, G.: Spasmodic croup in children. Clin. Pediatr., 11:615-617, 1972. Singer, O. P., and Wilson, W. J.: Laryngotracheobronchitis: two years' experience with racemic epinephrine. Can. Med. Assoc. J., 115:132-134, 1976. Taussig, L. M.: Clinic and physiologic evidence for the persistence of pulmonary abnormalities after respiratory illnesses in infancy and childhood. Pediatr. Res., 11:216-218, 1977. Newth, C. J. L., Levison, H., and Bryan, A. C.: The respiratory status of children with croup. J. Pediatr., 81:1068-1073, 1972. Wesley, A. G.: Interpretation of arterial carbon dioxide tension on laryngotracheobronchitis. S. Afr. Med. J., 48:1152-1154, 1974. Wesley, A. G.: Indications for intubation in laryngotracheobronchitis in black children. S. Afr. Med. J., 49:1126-1128, 1975. Talavera, F. I., and Rapkin, R. H.: Antibiotic usage in the management of acute laryngotracheobronchitis (croup). Clin. Pediatr., 13:1074-1076, 1974. Lejpzig, B., et al.: A prospective randomized study to determine the efficacy of steroids in the treatment of croup. J. Pediatr., 94:194-196, 1979. Jordan, W. S., Graves, C. L., and Elwyn, R. A.: New therapy for postintnbation laryngeal edema and tracheitis in children. J. Am. Med. Assoc., 212:585-588, 1970. Tanssig, L. M., Castro, O., and Beandry, P. H.: Treatment of laryngotracheobronchitis: use of intermittent positive-pressure breathing and racemic epinephrine. Am. J. Dis. Child., 129:790-793, 1975. VerMnelen, V. R., and Birch, H.: Prolonged intubation versus tracheotomy in children. Arch. Otolaryngol., 87:152-154, 1968. Downes, J. J., Stool, S. E., and Striker, T. W.: Complications of nasotracheal intubation in children with croup. N. Engl. J. Med., 274:226-227, 1966. Abbott, T. R.: Complications of prolonged nasotracheal intubation in children. Br. J. Anaesth., 40:347-352, 1968. Oliver, P., et al.: Tracheotomy in children. N. Engl. J. Med., 267:631-637, 1962. Thomson, P. D., and Olinsky, A.: Nasotracheal intubation in acute laryngotracheobronchitis. S. Aft. Med. J., 49:785-788, 1975. Suite A-717 400 Parnassus Avenue San Francisco, California 94143
SUPRAGLOTTITIS AND LARYNGOTRACHEOBRONCHITIS
Advances and Controversies in the Management of Supraglottitis and Laryn g o trach eobro nc hiti s LEE D. ROWE, M.D.*
Recent advances in pediatric airway intubation and the introduction of pharmacotherapeutic agents, active within the larynx and tracheobronchial tree, have created significant controversies in the treatment of acute obstructive inflammatory laryngeal disease. Although the etiology, pathophysiology, and clinical patterns of supraglottitis and laryngotracheobronchitis are no longer confused, decisions concerning their medical management and method of airway control remain controversial. Both inflammatory disorders are critically examined, with a review of current concepts regarding the choice between endotracheal intubation and tracheotomy. Specific problems of anesthetic technique, criteria for extubation or decannulation, and the rationale for the use of corticosteroids, antibiotics, or racemic epinephrine are evaluated. If mechanical airway control is required, careful attention to initial intubation with a relatively small, cuffless polyvinyl chloride endotracheal tube and precise surgical technique when employing tracheotomy will minimize the overall morbidity. Short term intubation in acute obstructive inflammation of the larynx appears to be well tolerated. Tracheotomy is reserved for the few patients with laryngotracheobronchitis who demonstrate persistent significant subglottic edema.
Prior to World War I! acute obstructive inflammatory disease of the larynx was enmeshed in a tangle of confusion regarding its etiology, pathophysiology, and nomenclature. This disorientation, not surprisingly, created significant controversies over management. Even with recent advances in endotracheal intubation, controversies persist, and the physician faces the dilemma of selecting either tracheotomy or intubation of
the airway. Frequently the decision is based upon the availability of skilled ancillary personnel and the physician's own preference and bias. Tracheotomy or bronchotomy, as it was originally termed, was not accepted initially in American medicine. In 1797 George Washington succumbed from acute supraglottitis, in spite of a consulting physician's recommendation to
Accepted for publication December 12, 1979. *Assistant Professor of Otolaryngalogy, University of California, San Francisco. Assistant Chief of Otolaryngology, San Francisco General Hospital, San Francisco, California. American Journal of Otolaryngology- Volume 1, Number 3, May 1980
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perform a tracheotomy. 1 This proposal was rejected by his two personal physicians and instead, leeches, venesection, and "blisters applied to the throat" probably hastened his demise. 2 Interestingly, Chevalier Jackson over 100 years later alluded to the problem with tracheotomy following the recent introduction of intubation2 Today the increasing use of prolonged mechanical ventilation in premature infants with hyaline membrane disease and a variety of congenital defects has conditioned physicians to the relative safety of endotracheal intubation. 4 The movement away from high pressure, low volume cuffs to expandable high volume, low pressure cuffs and the use of cuffless tubes in infants and children has reduced the risk of laryngeal and tracheal injury. Unfortunately the relative indications for either tracheotomy or endotracheal intubation in infants with acute obstructive inflammatory diseases of the larynx have not been critically evaluated. In this article we examine supraglottitis and laryngotracheobronchitis and review current ideas regarding the choice between endotracheal intubation and tracheotomy. In addition, the specific problems of anesthetic technique, the use of antibiotics, corticosteroids, or racemic epinephrine, and criteria for extubation or decannulation are discussed.
HISTORICAL ASPECTS
A continuing theme throughout the early literature relating to acute laryngeal inflammation is confusion regarding its etiology, pathophysiology, and nomenclature with a concomitant aversion to surgical manipulation of the airway (Table 1). 5 Initially physicians were preoccupied with the morbid action of inflammation, and the science of Physik required a detailed theoretical knowledge of the inflammatory process. Boerhave believed that inflammation was produced by an obstruction to the free circulation of the blood in the capillary vessels. By contrast, the great English anatomist John Hunter considered tissue or organ injury of major importance. 5 The cardinal signs of inflammation (calor, dolor, rubor, and tumor) were related by eighteenth and nineteenth century physicians to increasing blood viscosity with vessel dilatation, allowing the entrance of thicker parts of the blood. Methods of treating laryngeal inflammation included venesection and the local applica-
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TABLE 1. Historical Traces of Acute Laryngeal Inflammation DATE 1765 1797 1819 1826 1844 1895 1900
1914 1940 1941 1948 1974
Holme: First use of the term "croup" George Washington: Died of acute epiglottitis Bayle: First clinical description of acute epiglottiffs (termed acute spasmodic croup} Bretonneau: Treatise on croup secondary to diphtheria Mackintosh: Popular American textbook of medicine: confusion of clinical appearance of croup and epiglottitis Semon: Inflammation of larynx and pharynx considered manifestations of the same disease Theisen: First use of the term "acute epiglottitis" w i t h an accurate anatomical description
Lederman: Described acute phlegmonous epiglattiditis Brown: Separated acute epiglottitis from laryngeal abscess Sinclair: Identified Hemophilus influenzae type B as the etiology of acute epiglottitis Rabe: Positive statement, separating croup and epiglottitis as distinctly different clinical entities Buchan: Identified parainfluenza viruses 1,3 and influenza virus as primary etiologic agents of laryngotracheobronchitis
tion of leeches and counterirritants to drain the inflammatory region2 Indeed the Hippocratic doctrine dictated that "spontaneous determination to the external parts of the neck is vital to recovery. ''6 Constitutional therapy, including brisk purgatives (mercurous chloride and antimony) and emetics (syrup of ipecac), were used in addition to hot pediluvia (foot baths). Occasionally the inhalation of steam from hot water, poured on hops or camomile flowers, was recommended2 Although during the early nineteenth century smallpox, scarlet fever, measles, and diphtheria commonly produced acute laryngeal inflammation, their precise mechanism of action was unknown. More importantly, these disorders overshadowed the contributory effect of Hemophilus influenzae and parainfluenza viruses to the spectrum of acute laryngeal disease. Previously the Scottish physician Francis Holme had described the harsh breathing sound associated with odynophagia as "croup," applying an old Scottish word of the same meaning. "Cynache trachealis" had formerly been used to represent this acute laryngeal disorder3 However, in spite of its original precise meaning, the term croup was subsequently applied to all acute laryngeal disorders. Paul Bretonneau's contribution, in 1826, to the
SUPRAGLOTTITIS AND LARYNGOTRACHEOBRONCHITIS
understanding of diphtheria as an etiology of croup was enormous. He accurately noted that the diphtheritic false membrane may extend from the pharynx to involve the entire larynx and trachea and cause obstruction. 8 The first clinical description of acute supraglottitis is attributed by Mackintosh ~ to Bayle, who seven years previously had called acute spasmodic croup "that peculiar affection of the epiglottis, larynx, and rima glottidis." Although Mackintosh contended that croup was secondary to cerebral irritation, producing convulsions and spasms of the nerves supplying the muscles of the throat, his description of a larynx with acute supraglottitis removed at autopsy is classic: "The epiglottis was much swollen, erect, stiff and of a red color. The mucous membrane was found so much swollen as to leave the smallest possible passage for the transmission of air. ''5 In spite of evidence of mechanical laryngeal obstruction and the knowledge of bronchotomy, tracheotomy was not widely used by physicians. In the midnineteenth century incision and drainage of edematous laryngeal regions were recommended. If this technique failed, laryngeal sounds were inserted. Later, after the introduction of the laryngeal mirror, the epiglottis was multiply punctured with a curved bistoury, producing free hemorrhage. 9 At the same time O'Dwyer's laryngeal intubation for diphtheria undoubtedly saved many lives. Although tracheotomy was practiced for 3500 years by the Egyptians and Hindus, Chevalier Jackson 3 is primarily responsible for its reintroduction, noting: "There is no other justifiable life-saving operation whose reign of usefulness had not been extended by modern methods." Competition from MacEwan's recent introduction of peroral endotracheal intubation was strong, however. ~° Although Theisen 11 anatomically described and introduced the term "supraglottitis" at the turn of the century, Semon, TM a leading otolaryngologist of the period, incorrectly considered all pharyngeal and laryngeal inflammation to be a manifestation of the same disease. This misconception continued for many years until Sinclair 13 identified the etiologic agent of acute supraglottitis as Hemophilus influenzae, type B. Rabe 14in 1948 published three articles concerning croup, separating it from acute epiglottitis as a distinct clinical entity. Finally, in 1974 Buchan et al. ~5 identified in culture parainfluenza viruses 1 and 3 and influenza virus as the primary etiologic agents of laryngotracheobronchitis.
LEE D. ROWE
In the past 30 years, however, authors have recapitulated the mistakes of their predecessors and confused the nomenclature and clinical patterns of croup and epiglottitis. Perhaps the newer terminology, supraglottitis and laryngotracheobronchitis, will resolve this problem.
Volume 1 Number 3 May 1980
SUPRAGLOTTITIS
Supraglottitis is an acute inflammatory disorder of the larynx, secondary to Hemophilus influenzae type B, affecting the epiglottis, aryepiglottic folds, arytenoid cartilages, and ventricular bands. Occasionally pyogenic staphylococcus and group A beta hemolytic streptococcus are implicated. Although there is usually no prodromal phase and the disease progresses rapidly to respiratory collapse, an upper respiratory tract syndrome may precede the onset of recognizable symptoms in 50 per cent of the cases for more than 24 hours. Dysphagia, odynophagia, and shortness of breath rapidly progress to drooling, inspiratory stridor, and a muffled but clear voice. 18 The disease primarily affects children two to six years of age but can occur as early as five months or later in adulthood. A slight male predominance with no seasonal predilection is noted in most series, is, 2o As opposed to the situation in laryngotracheobronchitis, most children are extremely toxic, with an elevated temperature and an increased pulse and respiratory rate. Stridor, which is exacerbated by the supine position, is associated with prolongation of the inspiratory phase of respiration. 21 With increasing upper airway obstruction, hypercapnia, and hypoxia, the respiratory rate and heart rate are accelerated along with the development of marked supraclavicular, intercostal, and substernal retractions. The child sits erect, anxious, increasingly exhausted, drooling, and hungry for air. The chin is thrust outward with the neck hyperextended and the tongue protruding. Sudden laryngospasm may occur with aspiration of secretions into an already compromised airway and produce respiratory arrest. 2°, 22 The diagnosis is confirmed by direct inspection. Mirror examination or direct visualization of the larynx, which is not recommended unless the patient is well oxygenated and equipment is available for immediate intubation, reveals a hyperemic edematous epiglottis with the rima glottidis often obscured by edematous aryepiglottic folds. Mucous membrane changes range
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from edema and hyperemia to occasional desquamation, ulceration, sloughing, or rare abscess formation on the anterior or lingual surface of the epiglottis. 23 Infrequently the larynx is tender to palpation. Roentgenographic studies are used to confirm the diagnosis and to exclude other causes of acute airway obstruction. Among the differential possibilities to be eliminated, foreign bodies of the hypopharynx, upper cervical esophagus, larynx, and trachea are the most important. 24' 25 Anteroposterior and lateral soft tissue films demonstrate swelling and rounding of the epiglottis, with thickening and bulging of the aryepiglottic folds and distention of the hypopharynx (Fig. 1). 26 Also upper airway obstruction may produce alveolar hypoventilation with increasing hypoxia, capillary permeability, and negative intraalveolar pressures, which result in acute cardiac enlargement and pulmonary edema, often visible on chest films. 27 The white blood cell count is frequently higher than 16,000 per cubic milli-
Figure 1. Lateral neck roentgenogram in infant with acute supraglottitis demonstrating massive edema and rounding of the epiglottis (arrows) with thickened aryepiglottic folds and hypopharyngeal distention.
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meter with a relative increase in polymorphonuclear leukocytesY ° Unfortunately arterial blood gas levels cannot be relied upon as criteria for airway intervention. Although selective initial medical management of supraglottitis has been advocated, immediate control of the airway is prudent and life saving. 2s-3° In a retrospective review of 64 patients who were observed but not treated the mortality approached 80 per cent. 29 However, if children without signs of cyanosis, exhaustion, or severe sternal retraction are medically managed with the physician in constant attendance for the first two hours, tracheotomy or intubation may be avoided. 3° Nonetheless, up to 60 per cent of children with acute supraglottitis require airway intervention. 31 Patients are given 100 per cent humidified oxygen and an intravenous line is started. Simultaneously blood cultures are obtained. Because the most frequently isolated organism is Hemophilus influenzae, ampicillin (200 mg. per kg. per day intravenously in four divided doses) is the drug of choice. Recently, however, strains of betalactamase producing Hemophilus influenzae with resistance to ampicillin have appeared throughout the United States at an alarming rate. In 1978 middle ear isolates in children with acute otitis media exhibited an 8 per cent incidence of ampicillin resistant Hemophilus influenzae, a marked increase from the 1 per cent incidence reported during the years 1970 to 1976. 32 Therefore, chloramphenicol (100 mg. per kg. per day intravenously in four divided doses) is frequently added to ampicillin, pending the results of blood cultures and sensitivity studies. A new cephalosporin, cephamandole, capable of inhibiting both ampicillin resistant and ampicillin sensitive Hemophilus influenzae, has recently been introduced for parenteral use. 33 The value of this new drug in the treatment of acute supraglottitis is not yet known, however. The use of corticosteroid therapy, although apparently gaining wider acceptance, is not based upon well designed double blind studies.20, 28, 30, ~4, 35 Presumably the antiinflammatory effect, coupled with stabilization of endothelial permeability, decreases extracellular and intracellular edema. 36 One prospective study, however, revealed no significant difference in the number of tracheotomies required for corticosteroid treated patients and for those receiving none. 29 Therapeutic protocols have ranged from dexamethasone (0.5 mg. per kg.), administered as an initial
SUPRAGLOTTITIS AND LARYNGOTRACHEOBRONCHITIS
intravenous bolus or immediately prior to extubation, to hydrocortisone (1 gm. per day intravenously).2o, 28, 34 Although no method is more advantageous than another, a useful protocol that may be employed includes dexamethasone (1 mg. per kg. for the first 5 kg. of body weight and 1 mg. per kg. for each additional 5 kg. of body weight) administered as an initial intravenous bolus; half of this initial dose is repeated every six hours for 48 hours if needed and one-fourth of the initial dose is given every six hours for 24 hours following extubation. 3° If there is no dramatic improvement in supraglottic obstruction within two hours, control of the airway is imperative. Unfortunately the relative value of tracheotomy versus endotracheal intubation is based upon retrospective case analyses. Pediatric tracheotomy has been associated with significant complications, especially w h e n performed under emergency conditions without concomitant airway control. Most significantly pneumothorax, pneumomediastinum, postoperative hemorrhage, and accidental decannulation are potentially life threatening complications. ~9,37-40 Intermediate problems include atelectasis, mucous plug obstruction, severe tracheitis secondarily to Staphylococcus, Pseudomonas, or Monilia, and tracheoinnominate artery fistula. 41 The delayed complications of pediatric tracheotomy, however, are also devastating: tracheal and subglottic stenosis, tracheoesophageal fistula, tracheomalacia, and delayed decannulation. 41"44Many of these problems can be avoided by proper surgical technique. Initial control of the airway with either a bronchoscope or an endotracheal tube is important. A transverse or vertical neck incision is used and the trachea is incised vertically between the third and fourth tracheal rings, the dissection of the pretracheal fascia being limited to the midline. 44"45 A long nonabsorbable traction suture is placed on either side of the tracheal incision so that the tracheotomy can be opened in the event of an accidental decannulation, A postoperative anteroposterior portable chest film is mandatory to exclude pneumothorax and other complications. Humidification, atraumatic suction, and dry aseptic tracheostomy care minimize the risk of tracheobronchial infection. 46"47 A review of 991 tracheotomies for supraglottitis, reported in 12 series during the past 10 years, indicates a mortality range of 0 to 1 per cent.19, 20, ~9,so, ~4,35, 4s-5~ The incidence of complications, including pneumothorax and pneu-
LEE D. ROWE
momediastinum (20 patients), postoperative hemorrhage (5), tracheal granuloma (4), hypertrophic neck scars (7), and excessive tracheobronchial secretions (6), has ranged from 0 to 39 per cent. By contrast, a similar group of 510 patients treated with endotracheal intubation alone demonstrated a mortality range of 0 to 0.92 per cent with complications in 0 to 24 per cent.Z0. 22, 28.30, 34,49, 53-57Included in the reported complications were accidental extubation (11), subglottic stenosis (7), subglottic granuloma (4), lobar atelectasis (4), mucous plug (1), and vocal cord granuloma (1). However, following the introduction of soft polyvinyl chloride cuffless endotracheal tubes, the incidence of delayed irreversible complications, including subglottic and tracheal stenosis, has remained low (1.6 per cent). 31 Although tracheotomy is no longer the primary modality in the treatment of supraglottitis, several objections to the use of endotracheal tubes may be raised: (1) Endotracheal tubes may increase laryngeal edema. (2) Improperly secured tubes are readily dislodged. (3) The absence of an inner cannula increases the risk of obstruction. (4) Endotracheal tubes require increased nursing skills and intensive care facilities. (5) The tracheobronchial tree is more difficult to suction. (6) Airway resistance and dead space are increased. (7) Peroral feeding is impaired. 58 By contrast, the proponents of endotracheal intubation offer the following distinct advantages over tracheotomy: an overall lower mortality, a greater margin of safety with accidental extubation, fewer laryngotracheal complications following the introduction of soft cuffless polyvinylchloride tubes, and decreased hospitalization. 59 Indeed in several recent series the average duration of intubation ranged from 1.5 to 2.8 days as compared to 2.7 to 5.5 days for tracheotomized infants and children. 19~28, 49, 52, 53, 57 Factors contributing to endotracheal tube complications are related primarily to tube design, size, and duration of intubation. In addition, severe tracheitis and systemic disease, including diabetes mellitus, anemia, malnutrition, and dehydration, increase the risk of laryngotracheal injury. The use of newer, smaller diameter endotracheal tubes with minimal mechanical movement and adequate humidification and hydration will reduce the incidence of these complications.4, 60.61 Most importantly the short duration of intubation in acute supraglottitis significantly decreases the associated risk.
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TABLE 2. Anesthetic Techniques in the Management of Supraglottitis Intravenous
Thiopentane (5 mg./kg.) + succinylcholine (1 mg./kg.) Diazepam (0.4 mg./kg.) + succinylcholine (1 mg./kg.) Diazepam (0.2 mg./kg.) + Ketamine (2 mg./kg.) Ketamine (2 mg./kg.) ÷ Xylocaine (3 mg./kg.) topical spray Inhalational
Halothane (1.5-2.0%) Halothane (1.0-2.0%)
+ oxygen ÷ nitrous oxide ÷ oxygen (50%)
Combined intravenous and inhalational
Diazepam (0.2 mg./kg.) + halothane (1.0-1.5%) + oxygen Ketamine (1-2 mg./kg.) ÷ halothane (1-2%) ÷ oxygen Awake intubation
Topical 4% cocaine Premedication
Within 36 to 48 hours the infant's temperature is frequently normal and he is more alert, occasionally coughing around the tube during suctioning. Although a leak often occurs around the endotracheal tube at 20 to 25 cm. of water pressure, this is not a prerequisite for extubat i o n Y If the massive supraglottic edema has significantly resolved, the patient is extubated in the operating room. Racemic epinephrine delivered by intermittent positive pressure breathing is advocated by some physicians following extubation, but no control studies e x istY "64 If corticosteroid therapy was initiated prior to intubation, it is continued for 24 hours after extubation.63, 65
Atropine (0.005-0.01 mg./kg.)
Proper anesthetic and intubation technique is critical. Several protocols are available, including intravenous, inhalation, intravenousinhalational, and awake intubation. 53' 56 Currently inhalational techniques without the use of muscle relaxants are preferred (Table 2).20, 22, 35, 49, 50, 59 Preoxygenation is followed by rapid halothane and oxygen induction. Although muscle relaxants have been successfully employed, there appears to be no rationale for their use except to facilitate immediate nasotracheal tube placement. ~3 Atraumatic oral intubation secures the airway and allows endoscopic inspection to rule out other potential lesions. Following the placement of a nasotracheal tube (one to two sizes smaller than normal [Table 3]) 2 cm. below the level of the true vocal cords, the child is kept sedated (diazepam, 0.2 mg. per kg. intravenously; chloral hydrate, 50 rag. per kg. intravenously; or pentobarbitol, 2 to 4 rag. per kg. intravenously) and the tube position is confirmed with a chest film. 62 Ultrasonically nebulized oxygen is delivered to maintain a 60 per cent saturation at 37 ° C. 61In addition, the tube is aspirated after irrigation with 0.25 to 0.5 ml. of physiological saline every hour to prevent occlusion and retention of secretions. TABLE 3. Endotracheal Tube Size in Acute Obstructive Laryngeal Inflammation
AGE Newborn-6 months 6 months-2 years 2-5 years Over 5 years
240
INTERNALDIAMETER 3.0 ram. 3.5 ram. 4.0 mm. 4.5 ram.
ACUTE LARYNGOTRACHEOBRONCHITIS
Acute laryngotracheobronchitis is a viral illness that is far more c o m m o n than acute supraglottitis. The illness occurs primarily in late autumn and winter, and parainfluenza viruses and influenza viruses A and B account for the majority of cases." 3. ,~, 66 In addition, respiratory syncytial virus, adenoviruses, coxsackievirus A, ECHO viruses, and measles virus contribute to the spectrum of disease. I-3' 5, 7. i0. 14 There is also a variation in predominance of the individual viruses from year to year. The principal lesion is subglottic edema with a variable com ponent of tracheobronchial inflammation, occasionally leading to frank desquamating tracheitis and pneumonitis. Because the infant's subglottic larynx forms an isosceles triangle 7 mm. in length and 5 ram. in width, 1 mm. of edema will effectively reduce the area by 65 per cent. 2"67 Infants three months to three years of age are affected primarily, although occasionally older children contract the disease. 6s A 2:1 female:male ratio is seen. 69 The symptoms of a barking cough, hoarseness, inspiratory and expiratory stridor, and substernal retractions are frequently preceded by an insidious u p p e r respiratory tract prodromal period lasting one to seven days. TM In contrast to patients with supraglottitis, the child appears sick but not toxic. The larynx is not tender, no drooling is observed, and stridor is not exacerbated by a change in position. In addition, hypoxia and cyanosis often develop. Not u n c o m m o n l y the disease recurs. Recently small airway dysfunction and exercise induced bronchospasm have SUPRAGLOTTITIS AND LARYNGOTRACHEOBRONCHITIS
been identified in nonallergic children with a history of laryngotracheobronchitis. TM The degree of hypoxemia is related to ventilation-perfusion abnormalities with right to left shunting and is best correlated with an increasing respiratory rate. 71Also, as the relative component of upper respiratory tract obstruction increases, the arterial carbon dioxide content (PaCO2) rises proportionately. TM Anteroposterior and lateral neck films confirm the clinical impression of marked subglottic narrowing and assist in excluding other causes of infant airway obstruction, including foreign bodies in the aerodigestive tract, laryngeal and tracheal tumors, vascular compression of the trachea, and mediastinal tumors (Fig. 2). The peripheral white blood cell count is elevated, with a relative lymphocytosis. Despite its frequency and life threatening nature, there is no consensus of opinion regarding the treatment of laryngotracheobronchitis. If adequate humidification, oxygenation, and hydration can be maintained and there is no severe
stridor, retractions, cyanosis, or hypoxia, the infant may not require hospitalization. On the other hand, patients with a m i n i m u m of two of the following conditions meet criteria for immediate airway intervention: a heart rate greater than 170 beats per minute, a respiratory rate greater than 55 per minute, a PaCO2 level greater than 37 mm. Hg, a PaO2 level less than 50 mm. Hg, and congestive heart failure, severe tracheitis, or pneumonitis. 73 Humidification in either a high humidity or "croup" tent is extremely important. 66 Electrocardiographic monitoring, intravenous fluids, and maintenance of an inspired oxygen content of 30 to 40 per cent are critical. Antibiotics, although they have no significant influence on the outcome, are frequently used. TM Intravenous therapy with ampicillin may be initiated, pending the results of culture of transtracheal or nasotracheal aspirates. Until recently the role of corticosteroids was controversial and of no proven value. Original experimental work in dogs indicated that dex-
Volume 1 Number 3 May 1980
Figure 2. Anteroposterior chest film in an infant with laryngotracheobronchitis revealing marked subglattic narrowing (arrows).
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America n Journal of Otolaryngology
amethasone administered immediately following extubation and one hour later prevented the development of laryngeal edema. 65 Unfortunately carefully executed control trials applying these experimental findings were lacking. However, a recent prospective double blind study evaluated the efficacy of corticosteroids in the treatment of laryngotracheobronchitis. Patients receiving dexamethasone intramuscularly (0.3 mg. per kg.) on admission and a similar dose two hours later exhibited a statistically significant improvement in signs and symptoms. 75 Unfortunately the value of racemic epinephrine (2.25 per cent solution of dextro- and levorotatory epinephrine hydrochloride) remains controversial. One-half milliliter of a 2.25 per cent racemic epinephrine solution is diluted with sterile water or physiological saline and delivered through a mainstream nebulizer via a mask with intermittent positive pressure breathing for 12 to 15 minutes (Table 4). 6s High inspiratory flows are initially maintained, with a gradual decrease to slow inflation with peak pressures not exceeding 20 cm. of water. 76 Shortly after the beginning of therapy there is a significant decrease in upper airway obstruction; however, relapses occur within two hours in the majority of patients. Racemic epinephrine is repeated one or more times as necessary, but no significant changes in clinical status have been observed at 24 or 36 h o u r s . 69" 77 Because of the beta-adrenergic side effects of the n-isomer, including tachycardia, hypertension, and ventricular arrhythmias, racemic epinephrine should be avoided if the heart rate exceeds 160 beats per minute. 68' 76It is also contraindicated in children with subvalvular aortic stenosis, pulmonic stenosis, idiopathic hypertrophic subaortic stenosis, and the tetralogy of Fallot. 66 Patients with progressive hypoxia, cyanosis, hypercarbia, and increasing respiratory and cardiac rate who fail to respond to racemic epinephrine and dexamethasone are intubated. An inhalational technique is preferred. Previously tracheotomy was required in 3 to 13 per cent of
TABLE 4. WEIGHT (KG.) 5 10 15 20 25 30
242
Dosage
RACEMIC EPINEPHRINE (ML.) 0.25 + 0.5 0.75 1.0 1.25 1.5
the cases. 7s-si Currently the need for tracheotomy has been reduced to nearly zero, and this reduction is attributed to the increasing use of nasotracheal intubation and the widespread application of corticosteroids and racemic epinephrine. 69 This reduction, however, may reflect only a change in the viral virulence or earlier clinical recognition and treatment. A recent survey of 815 hospitalized patients with laryngotracheobronchitis revealed a 6.5 per cent incidence of nasotracheal intubation with a mean duration of intubation of 88 hours. There were no mortalities, and the incidence of delayed complications, as determined by postextubation symptoms, peak expiratory flow rates, and laryngeal polytomography, was less than 2 per cent. 3' The criteria for and technique of extubation are similar to those employed in acute supraglottitis. The development of a leak around the endotracheal tube at 25 to 30 cm. of water positive pressure is an encouraging sign. Children are extubated in the operating room or pediatric intensive care unit, with an anesthesiologist and otolaryngologist in attendance. Tracheotomy is performed only if significant obstruction persists to avoid the high risk of subglottic stenosis associated with reintubation.79, s0 Corticosteroids and racemic epinephrine are frequently continued for 24 hours following extubation. Only three patients of an original 150 children with laryngotracheobronchitis (18 per cent intubated with nasotracheal tube) ultimately required a tracheotomy. 82 Thus, the role of tracheotomy in the management of laryngotracheobronchitis is limited to a select number of patients.
SUMMARY
The etiology, pathophysiology, and clinical patterns of supraglottitis and laryngotracheobronchitis are separately reviewed. In addition, the historical aspects of acute inflammatory
Schedule of Racemic Epinephrine SALINE OR WATER (ML.)
TOTAL (ML.)
O./KG./MIN. X 10-15 MIN.
2.75 2.50 2.25 2.0 1.75 1.5
3.0 3.0 3.0 3.0 3.0 3.0
112.0 112.5 112.4 112.5 112.2 112.5
SUPRAGLOTTITIS AND LARYNGOTRACHEOBRONCHITIS
laryngeal disease and controversies surrounding tracheotomy and intubation of the airway are examined. Acute supraglottitis is appropriately managed by short term intubation of the airway and the parenteral administration of antibiotics capable of inhibiting Hemophilus influenzae. By contrast, laryngotracheobronchitis requires initial aggressive medical management, including humidified oxygen, hydration, and the parenteral administration of corticosteroids. Patients with progressive respiratory insufficiency are intubated, and tracheotomy is reserved for the few children with persistent airway obstruction. By avoiding the high risk of subglottic stenosis associated with prolonged intubation and employing a precise tracheotomy technique, the overall morbidity and mortality of this disorder can be minimized.
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SUPRAGLOTTITIS AND LARYNGOTRACHEOBRONCHITIS