Disclaimer: The information contained within the Grand Rounds Archive is intended for use by doctors and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No guarantees are made with respect to accuracy or timeliness of this material. This material should not be used as a basis for treatment decisions, and is not a substitute for professional consultation and/or peer-reviewed medical literature. Supraglottitis Supraglottitis is a potentially life-threatening infection of the supraglottic structures in children. Classically the disease is caused by Hemophilus influenzae type b, but may be caused by other bacteria. This disorder was recognized as a primary disease process in the early part of this century, and since that time interest in this disorder has lead to a number of articles in the medical literature. The exact incidence of supraglottitis in the United States in not known. In Sweden, Carenfelt et al found the annual incidence for children under the age of 4 to be 13.8 cases per 100,000. In a similar study in Canada, Wurtle estimated the incidence to be 6 cases per 100,000 for children under the age of 18. The disease typically occurs in children between the ages of 2 and 7. The incidence is higher in the winter, with some studies describing higher numbers in the early winter and spring. Regional differences in incidence occur as well, with the incidence and springtime peak being lower in southern climates. For unexplained reasons there is a higher incidence in Navaho Indians and Eskimos. Hemophilus influenza type b is a gram negative pleomorphic facultative anaerobe that requires enriched media for growth, and it may be divided into six types based on capsular polysaccharides. The capsular antigen in type b is polyribose-ribotol phosphate. Hemophilus influenzae type b is the most common cause of invasive bacterial disease in children in the United States. The most common infection is meningitis, followed by epiglottitis, cellulitis, arthritis, pneumonia, and a variety of abscesses. The signs as symptoms of epiglottitis consist of the four "D's": dysphagia, dysphonia, dyspnea, and drooling. Absence of cough is an important symptom that helps distinguish supraglottitis from croup. Classically, in order to lessen the airway obstruction, the child sits erect, flexed at the waist, with the chin forward, mouth open and the tongue protruding from the mouth. Many children are toxemic with high fever. Symptoms progress rapidly, often in less than 24 hours. In a review of 242 cases of acute supraglottitis, Sendi and Crysdale found dysphagia and stridor in over 90% of cases. Fever was less common, occurring in 60%. Drooling was present in only 2% of patients. Symptoms progressed rapidly, with the average duration being 13.7 hours (ranging from 2 to 72 hours). Because of the severity of this disease, the diagnosis of supraglottitis should be made quickly and as early as possible. Laryngotracheitis (croup), retropharyngeal abscess or obstructive tonsillitis may present similarly to supraglottitis. In a review of 155 children presenting to the emergency room with stridor, Mauro et al found absence of spontaneous cough, and the presence of drooling and agitation to be most commonly associated with supraglottitis. Vigorous examination or stimulation of a child with supraglottitis may lead to laryngospasm and airway obstruction. For this reason, the common teaching has been not to examine or stimulate any child suspected of having supraglottitis. In obvious cases examination should be avoided, but in cases where the diagnosis is unclear, gentle physical examination may be helpful. Lateral neck radiographs may also be used in equivocal cases. Whenever this study is performed the child should be accompanied by a physician with equipment necessary to secure the airway. This study should be performed during inspiration. In supraglottitis the epiglottis, aryepiglottic folds, and arytenoids are swollen and thickened, giving the characteristic thumb print sign. Due to the upper airway obstruction, dilation of the hypopharynx occurs secondary to airtrapping. To prevent obstruction, the management of supraglottitis requires control of the airway. At one time tracheotomy was the usual method of airway control, but now most large centers manage patients with nasotracheal intubation and intensive care unit monitoring. If good intensive care unit observation is not available then tracheotomy is safer. Airway management begins in the emergency room where the child is observed at all times by a physician capable of securing an airway. As soon as the operative team can be assembled, the child should be taken to the operating room to secure the airway. This should not be delayed for laboratory tests or x-rays. The child is anesthetized by inhalation techniques and intubated by the anesthesiologist. The otolaryngologist is present in the operating room and ready to perform a tracheotomy if needed. After the airway is secured, a more thorough laryngoscopy may be performed and the supraglottitis cultured. At the end of the procedure, the oral endotracheal tube may be changed to a nasotracheal tube, which is more secure. After obtaining a secure airway the patient is transferred to the ICU for close observation. The child should be kept sedated and some authors favor complete paralysis and mechanical ventilation to prevent accidental extubation. Criteria for extubation vary, with some otolaryngologists performing a repeat laryngoscopy either directly or using a fiberoptic scope. Some authors extubate without laryngeal examination relying on the presence of air leak and improved clinical picture. A number of reports have shown that the period of intubation needed has been reduced to around 48 hours. In a report by Gonzalez et al from Children's Hospital, Pittsburgh, the period of intubation was reduced to an average of 42.1 hours using daily fiberoptic laryngeal examination in the ICU. Children with supraglottitis must be examined for other sites of infection. Meningitis, pneumonia, cervical adenitis, otitis media, and septic arthritis have been reported. Due to the child being sedated while intubated, meningitis may be particularly difficult to detect, with devastating consequences. Most patients have septicemia, with blood cultures being positive in 60 to 80%. After controlling the airway and obtaining cultures the patient is started on appropriate antibiotics. Because of the high rate of ampicillin resistance in Houston (25 to 30%) all patients should have antibiotics effective against these organisms. In the past patients were treated with ampicillin and chloramphenicol until culture results were obtained. The recent introduction of cephalosporins has allowed most patients to be treated primarily with these. Cefotaxime, Cefamandole, Cefuroxime, and Ceftriaxone have been used. A recent report advocates augmented penicillins such as ampicillin and sulbactam for primary treatment of supraglottitis. Most patients are treated with antibiotics for around 5 to 7 days and than may be converted to oral antibiotics. Close contacts of patients with invasive HIB disease have a 500 to 1000 times increased risk of acquiring HIB disease during the first month after exposure. The AAP recommends Rifampin prophylaxis consisting of 20 mg/kg/day for 4 days. Several changes in supraglottitis have been reported. At the Methodist Hospital in Indianapolis, Emmerson noted an increased number of cases of supraglottitis in younger children, with 36% of their cases being found in children less than 2 years of age, and 51% in those less than 3 years of age. In addition, supraglottitis due to candida and herpes simplex virus have been reported in immunocompromised patients. These patients present with symptoms and airway obstruction similar to the bacterial form of the disease. The introduction of the HIB vaccine in 1985 provides a way to prevent the disease. The initial vaccine PRP contained the capsular polysaccharide polyribose ribitol phosphate as the sole immunogen. Because of its inconsistent immune response in younger children its initial use was limited to children over 24 months of age and several reports have documented cases of invasive HIB disease in immunized patients. Subsequently, two new conjugate vaccines have been released. A conjugate vaccine couples the primary immunogen with another compound to elicit a greater immune response. For the two new vaccines, the capsular polysaccharide is conjugated with either Diphtheria toxoid or the capsular polysaccharide of Neisseria meningitidis. These vaccines are given in three doses, beginning at two months of age, which is similar to the DTP vaccine. Despite the problems with the original vaccine, a reduced rate of invasive HIB disease has been reported. Broadhurst et al reported a decreased incidence based on a large study of US Army health care beneficiaries less than 5 years of age. This is roughly a population of around 200,00 children. The incidence of invasive HIB disease decreased from a high of 188 cases per 100,000 in 1986 to 43 cases per 100,000 in 1991. This decrease was most marked in meningitis and supraglottitis, which showed statistically significant decreases over this period. When analyzed by age, several groups showed decreased rates prior to becoming eligible for the vaccine. The incidence of supraglottitis is decreasing and may be related to the increased use and improved quality of the HIB vaccine. The epidemiology of supraglottitis is changing with more cases occurring in younger patients with more atypical presentations. Using a treatment plan of short term intubation and antibiotic therapy, most patients can be successfully managed. Despite advances in management, failure to diagnose supraglottitis may still result in mortality. Case Presentation A 2½-year-old Latin American boy, presented to the TCH Emergency Room with a 24-hour history of sore throat, fever, decreased oral intake and mild inspiratory stridor. One week prior he had been treated for tonsillitis by his pediatrician. A lateral neck x-ray obtained in the emergency room was suspicious for supraglottitis. He was taken emergently to the operating room where he was intubated and underwent direct laryngoscopy. He was found to have supraglottitis with edema of the epiglottis and aryepiglottic folds along with an exudative tonsillitis. Cultures of the pharynx and supraglottis were obtained. He was transferred to the pediatric intensive care unit where he remained intubated, and was started on intravenous ticarcillin/clavulanic acid. Urine CIE was negative for Hemophilus influenzae type b. Supraglottic and tonsillar cultures grew Staphylococcus aureus resistant to ampicillin. Blood cultures had no growth. Repeat flexible laryngoscopy at 60 hours showed resolution of the supraglottic edema and he was extubated. Following several hours of observation, he was transferred to a regular room. After completing seven days of intravenous antibiotics, he was discharged to home. He made an uneventful recovery and currently is doing well. Bibliography Arndal H, Andreassen UK. Acute epiglottitis in children and adults. Nasotracheal intubation, tracheostomy or careful observation? Current status in Scandinavia. J Laryngol Otol 1988;102:1012-1016. Balck SB, Shinefield HR, Hiatt RA, Fireman BH, Kaiser Permanenete Pediatric Vaccine Study Group. Efficacy of Haemophilus influenzae type b capsular polysaccharide vaccine. Pediatr Infect Dis J 1988;7:149-156. Balsam D, Sorrano D, Barax C. Candida epiglottitis presenting as stridor in a child with HIV infection. Pediatr Radiol 1992;22:235-236. Benjamin B, O'Reilly B. Acute epiglottitis in infants and children. Ann Otol 1976;85:565-572. Blackstock D, Adderley RJ, Steward DJ. Epiglottitis in young infants. Anesthesiology 1987;67:97-100. Bogger-Goren S. Acute epiglottitis caused by herpes simplex virus. Pediatr Infect Dis J 1987;6:1133-1134. Bonadio WA, Losek JD. The characteristics of children with epiglottitis who develop the complication of pulmonary edema. Arch Otolaryngol Head Neck Surg 1991;117:205-207. Brilli RJ, Benzing G III, Cotcamp DH. Epiglottitis in infants less than two years of age. Pediatr Emer Care 1989;5:16-21. Broadhurst LE, Erickson RL, Kelley PW. Decreases in invasive Haemophilus influenzae diseases in US Army children, 1984 through 1991. JAMA 1993;269;227-231. Broome CV. Epidemiology of Haemophilus influenzae type b infections in the United States. Pediatr Infect Dis J 1987;6:779-782. Brown JM. Acute infections of the epiglottis. Arch Otolaryngol 1940;32:631-641. Butt W, Shann F, Walker C, Williams J, Duncan A, Philan P. Acute epiglottitis: a different approach to management. Crit Care Med 1988;16:43-47. Cantrell RW, Bell RA, Morioka WT. Acute epiglottitis: intubation versus tracheostomy. Laryngoscope 1978;88:994-1005. Carenfelt C, Sobin A. Acute infectious epiglottitis in children and adults: annual incidence and mortality. Clin Otolaryngol 1989;14:489-493. Crockett DM, Healy GB, McGill TJ, Friedman EM. Airway management of acute supraglottitis at the Children's Hospital, Boston: 1980-1985. Ann Otol Rhinol Laryngol 1988;97:114-119. Crysdale WS, Sendi K. Evolution in the management of acute epiglottitis: a 10-year experience with 242 children. Intl Anesthiol Clin 1988;26:32-38. Emmerson SGP, Richman B, Spahn T. Changing patterns of epiglottitis in children. Otolaryngol Head Neck Surg 1991;104:287-292. Eskola J, Peltola H, Takala AK, Kayhty H, Hakulinen M, Karanko V, et al. Efficacy of Haemophilus influenzae type b polysaccharide-diphtheria toxoid conjugate vaccine in infancy. N Engl J Med 1987;317:717-722. Gerber AC, Pfenninger J. Acute epiglottitis: management by short duration of intubation and hospitalization. Intensive Care Med 1986;12:407-411. Gervaix A, Suter S. Epidemiology of invasive Haemophilus influenzae type b infections in Geneva, Switzerland, 1976 to 1989. Pediatr Infect Dis 1991;10:370-374. Gilbert GL, Clements DA, Broughton SJ. Haemophilus influenzae type b infections in Victoria, Australia, 1985 to 1987. Pediatr Infect Dis J 1990;9:252-257. Goldhagen JL. Supraglottitis in three young infants. Pediatr Emer Care 1989;5:175-177. Gonzalez C, Reilly JS, Kenna MA, Thompson AE. Duration of intubation in children with acute epiglottitis. Otolaryngol Head Neck Surg 1986;95:477-481. Granoff DM, Shackelford PG, Suarez BK, Nahm MH, Cares KL, Murphy TV, et al. Hemophilus influenzae type b disease in children vaccinated with type b polysacccharide vaccine. N Engl J Med 1986;315:1584-1590. Granoff DM, Sheetz K, Pandey JP, Nahm MH, Rambeck JH, Jacobs JL, et al. Host and bacterial factors associated with Haemophilus infleunzae type b disease in Minnesota children vaccinated with type b polysaccharide vaccine. J Infect Dis 1989;159:908-916. Hodge KM, Ganzel TM. Diagnostic and therapeutic efficiency in croup and epiglottitis. Laryngoscope 1987;97:621-625. Knight GJ, Harris MA, Parbari M, O'Callaghan J, Masters IB. Single daily dose ceftriaxone therapy in epiglottitis. J Paediatr Child Health 1992;28:220-222. Losek JD, Dewitz-Zink BA, Melzer-Lange M, Havens PL. Epiglottitis: comparison of signs and symptoms in children less than 2 years old and older. Ann Emerg Med 1990;19:99-102. Marwick C. Haemophilus influenzae vaccines gain favor. JAMA 1990;264:1375. Mauro RD, Poole SR, Lockhart CH. Differentiation of epiglottitis from laryngotracheitis in the child with stridor. Am J Dis Child 1988;142:679-682. Morus Jones H. Acute epiglottitis: a personal study over twenty years. Proc Roy Soc Med 1970;63:14-20. Moxon ER. Haemophilus influenzae vaccine. Pediatrics 1985;77:258-260. Murrage KJ, Janzen VD, Ruby RR. Epiglottitis: adult and pediatric comparisons. J Otolaryngol 1988;17:194-198. Osterholm MT, Rambeck JH, White KE, Jacobs JL, Pierson LM, Neaton JD, et al. Lack of efficacy of Haemophilus b polysaccharide vaccine in Minnesota. JAMA 1988;260:1423-1428. Potondi A, Ribari O. Clinical and medico-legal aspects of acute epiglottiditis. J Laryngol Otol 1969;83:141-148. Schloss MD, Gold JA, Rosales JK, Baxter JD. Acute epiglottitis: current management. Laryngosocpe 1983;93:489-493. Schuh S, Juang A, Fallis JC. Atypical epiglottitis. Ann Emerg Med 1988;7:168-170. Schuller DE, Birch HG. The safety of intubation in croup and epiglottitis: an eight-year follow-up. Laryngoscope 1975;85:33-46. Sendi K, Crysdale WS. Acute epiglottitis: decade of change - a 10-year experience with 242 children. J Otolaryngol 1987;16:196-202. Shapiro ED, Murphy TV, Wald ER, Bracy CA. The protective efficacy of Haemophilus b polysaccharide vaccine. JAMA;260:1419-1422. Trollfors B. Invasive Haemophilus influenzae infections in household contacts of patients with Haemophilus influenzae meningitis and epiglottitis. Acta Paediatr Scand 1991;80:795-797. Trollfors B, Nylen O, Strangert K. Acute epiglottitis in children and adults in Sweden 1981-3. Arch Dis Child 1990;65:491-494. Wald E, Reilly JS, Bluestone CD, Chiponis D. Sulbactam/Ampicillin in the treatment of acute epiglottitis in children. Rev Infect Dis 1986;8(Suppl 5):S617-S619. Walsh RJ, Gray WC. Candidia epiglottitis in immunocompromised patients. Chest 1987;91:482-483. Wurtele P. Acute epiglottitis in children and adults: a large-scale incidence study. Otolaryngol Head Neck Surg 1990;1-3:902-908. Grand Rounds Archive | Department Home page BCM Public | BCM Intranet | Privacy Notices | Contact BCM | BCM Site Map | ©2001-2006 Baylor College of Medicine
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