Updated: Jan 29, 2009
Epiglottitis, also termed supraglottitis, is an inflammation of the epiglottis and/or the supraglottic tissues surrounding the epiglottis, including the aryepiglottic folds, arytenoid soft tissue, and, occasionally, the uvula.
As with many other aspects of the pediatric airway, the epiglottis is significantly different in the child than in the adult. In the infant, the epiglottis is located more anteriorly and superiorly than in the adult, and it is at a greater angle with the trachea. It is also more omega shaped and floppy than the more rigid, U-shaped epiglottis in the adult. Numerous causes of the inflammation exist, but the common problem is airway occlusion caused by the tissue swelling, and, when untreated, can lead to respiratory failure and death. In the young child, this can take place in hours.
Epiglottitis was historically caused by infection of the supraglottic structures by Haemophilus influenza B (see Haemophilus Influenzae Infection). Since the widespread use of the HiB vaccine, the incidence and causative agents of epiglottitis have changed. Both H influenza type B (HiB) and Streptococcus pneumonia (see Causes) can colonize the pharynges of healthy children through respiratory transmission from intimate contact. These bacteria may penetrate the mucosa invading the bloodstream, causing bacteremia and seeding of the epiglottis and surrounding tissues. Bacteremia can also lead to infection of the meninges, skin, lungs, tears, and joints.
Bacterial infection of the epiglottis leads to acute onset of inflammatory edema, beginning on the lingual surface of the epiglottis where the submucosa is loosely attached. Swelling significantly reduces the airway aperture. Edema rapidly progresses to involve the aryepiglottic folds, the arytenoids, and the entire supraglottic larynx. The tightly bound epithelium on the vocal cords halts edema spread at this level. Aspiration of oropharyngeal secretions or mucus plugging can cause respiratory arrest.
Inflammation of any of the structures around the epiglottis may also become inflamed from trauma, mechanical, thermal, or chemical. Reports have been made of epiglottitis caused by blunt injury to the neck.1
The use of the HiB vaccine has reduced the incidence of epiglottitis. Introduction of the polysaccharide vaccine in 1985, followed by the highly effective conjugate vaccine, has dramatically reduced the incidence of epiglottitis, with consequent decline in hospital admissions. Studies show an annual incidence rate of 0.3 cases per 100,000 persons. Studies in children of all ages with epiglottitis report no seasonal variation in incidence.
International incidence varies widely and is significantly more prevalent in countries without universal immunization. In countries with mandatory immunization, the reported incidences are 0.9 cases per 100,000 persons in Sweden and 0.6 cases per 100,000 in the United Kingdom. Recent discussion exists that epiglottitis is increasing in frequency in the United Kingdom.2 The reason for this is unclear and may be due to giving 3 vaccines rather than 4. Recent studies suggest that bacterial tracheitis is now the most common serious airway infection in children.3,4
Mortality rates as high as 10% can occur in children whose airways are not protected by endotracheal incubation. With endotracheal intubation, mortality is less than 1%.
Most studies showed no racial predominance, although a recent study showed higher incidence among African Americans and Hispanics.
Most studies show a 60% male predominance. This has remained true even with the changing epidemiology of epiglottitis.
Historically, epiglottitis occurred most commonly in children aged 2-7 years. However, it may occur at any age. Once believed to occur exclusively in children, adult cases have been reported for years and some evidence suggests the incidence in adults is increasing.
Epiglottitis usually presents abruptly and rapidly with fever, sore throat, dysphagia, respiratory distress, drooling, and anxiety. The classic presentation is a young child who develops a fever and may complain of a sore throat. The child may refuse to eat. As the disease progresses, the patient may not be able to maintain his or her airway and this may lead to airway obstruction.
No one organism is predominant in causing epiglottitis.
| Bacterial tracheitis | Pediatrics, Pertussis |
| Foreign Bodies, Trachea | Pediatrics, Pharyngitis |
| Mononucleosis | Pediatrics, Pneumonia |
| Pediatrics, Anaphylaxis | Peritonsillar Abscess |
| Pediatrics, Croup or
Laryngotracheobronchitis | Retropharyngeal Abscess |
| Pediatrics, Foreign Body Ingestion | Toxicity, Caustic Ingestions |
Pediatrics, bacterial tracheitis
Tracheitis
The first priority for a patient with epiglottitis is securing and providing respiratory support before a definitive airway is obtained. Initially humidified oxygen can be given by a nasal cannula or a nonrebreather mask as required. The patient should have respiratory and cardiac monitoring placed, and the patient should be kept in plain view of medical staff at all times.
Antibiotic therapy is necessary but should be initiated after securing the airway. Prior to culture results, use antibiotics covering the most likely organisms. Following trauma to the epiglottis, S aureus should be suspected. With the presence of white patches, C albicans should be suspected. Sedation for comfort is also required.
Empiric antimicrobial therapy must cover all likely pathogens in the context of the clinical setting. Treatment should continue for 7-10 d in general.
Third-generation cephalosporin with broad-spectrum gram-negative activity. Lower efficacy against gram-positive organisms and higher efficacy against resistant organisms. Arrests bacterial growth by binding to one or more penicillin-binding proteins.
1-2 g IV q12-24h
75-100 mg/kg/d IV q12-24h
Probenecid may increase levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Ceftriaxone displaces bilirubin from binding sites on albumin; adjust dose in renal impairment; caution in breastfeeding women and in allergy to penicillin
Second-generation cephalosporin maintains gram-positive activity that first-generation cephalosporins have. Adds activity against P mirabilis, H influenzae, E coli, K pneumoniae, and M catarrhalis.
Condition of patient, severity of infection, and susceptibility of microorganism determines proper dose and route of administration.
750 mg to 1.5 g IV q8h
100-150 mg/kg/d IV divided tid
Disulfiramlike reactions may occur when alcohol is consumed within 72 h after taking cefuroxime; may increase hypoprothrombinemic effects of anticoagulants; may increase nephrotoxicity in patient receiving potent diuretics such as loop diuretics; coadministration with aminoglycosides increase nephrotoxic potential
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Administer half dose if CrCl is 10-30 mL/min and one-quarter dose if <10 mL/min; fungal and microorganism overgrowth may occur with prolonged therapy
When combined with chloramphenicol, this is an alternative if unable to use cephalosporins. Beta-lactam antibiotic, which has activity against some gram-positive and gram-negative organisms. Inhibits bacterial cell wall synthesis during active multiplication.
1-2 g IV q6-8h
100-200 mg/kg/d IV divided q6h
Probenecid and disulfiram elevate ampicillin levels; allopurinol decreases ampicillin effects and has additive effects on ampicillin rash; may decrease effects of oral contraceptives
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in renal failure; commonly causes rash (evaluate rash and differentiate from hypersensitivity reaction)
When combined with ampicillin, this is an alternative if unable to use cephalosporins. Elicits activity against some gram-positive, gram-negative, and anaerobic organisms. Inhibits protein synthesis by reversibly binding to the 50S ribosomal subunit.
50 mg/kg/d IV divided q6h
50-100 mg/kg/d IV divided q6h
Coadministration with barbiturate may decrease chloramphenicol serum levels, while barbiturate levels may increase causing toxicity; manifestations of hypoglycemia may occur with sulfonylureas; rifampin may reduce serum chloramphenicol levels, presumably through hepatic enzyme induction; may increase effects of anticoagulants; may increase serum hydantoin levels, possibly resulting in toxicity; hydantoins may either increase or decrease chloramphenicol levels
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Serious and fatal blood dyscrasias (aplastic anemia, hypoplastic anemia, thrombocytopenia, granulocytopenia) can occur; evaluate baseline and perform periodic blood studies approximately every 2 d while in therapy; discontinue upon appearance of reticulocytopenia, leukopenia, thrombocytopenia, anemia, or findings attributable to chloramphenicol; adjust dose in liver or kidney dysfunction; caution in pregnancy at term or during labor because of potential toxic effects on fetus (gray syndrome)
Semisynthetic antibiotic produced by 7(S)-chloro-substitution of 7(R)-hydroxyl group of parent compound lincomycin. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Widely distributes in the body without penetration of CNS. Protein bound and excreted by the liver and kidneys.
600-1200 mg/d IV divided bid/qid
25-40 mg/kg/d IV divided q6-8h
Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects of clindamycin; antidiarrheals may delay absorption of clindamycin
Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment; antibiotic-associated colitis
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis by allowing overgrowth of Clostridium difficile
Drug combination of beta-lactamase inhibitor with ampicillin. Interferes with bacterial cell wall synthesis during active replication, causing bactericidal activity against susceptible organisms. Alternative to amoxicillin when unable to take medication orally.
1.5 (1 g ampicillin + 0.5 g sulbactam) to 3 g (2 g ampicillin + 1 g sulbactam) IV/IM q6-8h; not to exceed 4 g/d sulbactam or 8 g/d ampicillin
<3 months: Not established
3 months to 12 years: 100-200 mg ampicillin/kg/d (150-300 mg Unasyn) IV divided q6h
>12 years: Administer as in adults
Probenecid and disulfiram elevate ampicillin levels; allopurinol decreases ampicillin effects and has additive effects on ampicillin rash; may decrease effects of oral contraceptives
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in renal failure; evaluate rash and differentiate from hypersensitivity reaction
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epiglottitis, epiglottis, Hib, supraglottitis, epiglottitis in children, Haemophilus influenzae type b, Hib vaccine, H influenzae, Streptococcus, Streptococcus pneumoniae, S pneumoniae, Klebsiella pneumoniae, K pneumoniae, Candida albicans, C albicans, Staphylococcus aureus, S aureus, Neisseria meningitidis, N meningitidis, Haemophilus parainfluenzae, H parainfluenzae, varicella zoster, herpes simplex type 1, parainfluenza
Robert Allan Felter, MD, FAAP, CPE, FACPE, Professor of Clinical Pediatrics, Department of Pediatrics, Georgetown University College of Medicine; Medical Director, Pediatric Emergency Medicine and Inpatient Services, Inova Loudoun Hospital, Leesburg, Virginia
Robert Allan Felter, MD, FAAP, CPE, FACPE is a member of the following medical societies: American Academy of Pediatrics and American College of Physician Executives
Disclosure: Nothing to disclose.
Ron D Waldrop, MD, MS, FAAP, FACEP, FACPE, Emergency Physician, Commonwealth Emergency Physicians; Director of Pediatric Quality Care Management, INOVA Loudon Hospital; Adjunct Clinical Professor, Georgetown University School of Medicine
Ron D Waldrop, MD, MS, FAAP, FACEP, FACPE is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.
James Li, MD, Former Assistant Professor, Division of Emergency Medicine, Harvard Medical School; Board of Directors, Remote Medicine
Disclosure: Nothing to disclose.
Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner
Wayne Wolfram, MD, MPH,
Wayne Wolfram, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Pediatrics, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Richard G Bachur, MD, Associate Professor of Pediatrics, Harvard Medical School; Associate Chief and Fellowship Director, Attending Physician, Division of Emergency Medicine, Children's Hospital of Boston
Richard G Bachur, MD is a member of the following medical societies: American Academy of Pediatrics, Society for Academic Emergency Medicine, and Society for Pediatric Research
Disclosure: Nothing to disclose.
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