Severe Upper Airway Infections
Stephen J. Krinzman
Sunil Rajan
Richard S. Irwin
I. NOSOCOMIAL SINUSITIS
A. Incidence: seen radiographically in 95% of nasotracheally intubated patients and 25% if orally intubated, although only 40% of those will have positive cultures. With strict criteria, incidence of 10% in long-term intubated patients.
B. Etiology: often polymicrobial, with gram-negative organisms are causative in two-thirds of cases. Anaerobes isolated in 0% to 15% of cases. Staphylococcus aureus is the most common gram-positive organism, and Pseudomonas species are the most common gram negative. Organism isolated from sinusitis is often identical to lower airway cultures. More unusual pathogens include:
1. Zygomycetes such as Mucor: associated with diabetes mellitus with ketoacidosis, burns, and renal and hepatic failure.
2. Aspergillus species: invasive disease in immunocompromised patients.
3. Cryptococcus neoformans: high mortality in immunocompromised patients.
C. Complications.
1. Orbital: orbital cellulitis and abscess, cavernous sinus thrombosis (20% mortality).
2. Intracranial: osteomyelitis, meningitis, epidural abscess, subdural empyema, and brain abscess.
3. Ventilator-associated pneumonia: causative relationship suggested by studies.
4. Fever of unknown origin (FUO): infectious sinusitis found in 53% of patients with FUO and sole cause in 16%.
D. Diagnosis.
1. Opacification on radiographs does not always indicate bacterial infection. CT scans are the imaging modality of choice. Plain films are helpful if patient unable to travel for CT.
2. Ultrasonography: 67% sensitive and 87% to 100% specific for maxillary sinusitis compared to radiographs. Improved performance when patients in semirecumbent.
3. Rhinoscopy and antral aspiration: Cultures from middle meatus do not correlate with antral lavage aspirates. High correlation between cultures obtained by antral puncture and endotracheal specimens suggests invasive sinus cultures are not usually necessary.
E. Treatment: removal of nasal tubes; decongestants; broad-spectrum antibiotics covering nosocomial gram-negative and gram-positive organisms.
With these measures, 67% of patients become afebrile in 48 hours. Surgical intervention reserved for patients who fail to respond.
With these measures, 67% of patients become afebrile in 48 hours. Surgical intervention reserved for patients who fail to respond.
F. Sphenoid sinusitis: fulminant course and high mortality if untreated. May present with severe headache, fever, and neurologic deficits (trigeminal hyperesthesia or hypoesthesia in 33% of cases). Gram-negatives organisms predominate in acute form, and mixed gram negative and positives are more common in the chronic form. Infection can extend to cavernous sinus, pituitary, and optic chiasm. Surgical drainage if symptoms persist or neurologic signs develop while on antimicrobial therapy.
II. OTOGENIC INFECTIONS
A. Mastoiditis.
1. Pathogenesis: Infection spreads from middle ear to mastoid air cells. Closed space infection may cause bone necrosis. Most common organisms are S. pneumonia, group A streptococci, S. aureus, and Pseudomonas.
2. Presentation: postauricular pain and fever. Half the cases follow diagnosis of otitis media. CT scans are diagnostic.
3. Complications: Up to 25% of patients have complications at presentation —subperiosteal abscess, meningitis, cranial nerve involvement, and sigmoid sinus thrombophlebitis.
B. Malignant otitis externa.
1. Presentation: most commonly in diabetic patients, with otalgia, granulation tissue in external auditory canal, and often purulent or fetid otorrhea. Infection spreads anteriorly toward parotid compartment or temporal bone. Extension leads to pain of tissues around the ear.
2. Etiology: Pseudomonas aeruginosa is the most commonly implicated pathogen.
3. Complications: osteomyelitis, cranial nerve paralysis, meningitis, and thrombophlebitis.
4. Diagnosis: CT and/or magnetic resonance imaging and technetium-99 bone scan.
5. Therapy: prolonged antibiotics against P. aeruginosa (semisynthetic penicillin or ceftazidime with an aminoglycoside). Oral fluoroquinolones have also been used. Optimal duration of treatment is unknown. Decision on surgical intervention based on response to antimicrobial treatment and the presence of complications.
III. SUPRAGLOTTITIS (EPIGLOTTITIS)
A. Presentation: infection of the structures located above the glottis, including the epiglottis, aryepiglottic folds, arytenoids, pharynx, uvula, and tongue base. The true vocal cords rarely involved. May progress to abrupt and fatal airway obstruction.
1. Children: usually present between ages 2 and 5 years. Course is often fulminant.
2. Adults: usually present at ages 40 to 60, with male preponderance. Mortality (<5%) usually due to unexpected airway obstruction.
B. Pathogenesis.
1. Children: inflammation mainly restricted to epiglottis because of loose mucosa on its lingual aspect. Swelling reduces the airway aperture by curling the epiglottis posteriorly and inferiorly. When edema spreads to aryepiglottic folds, inspiration draws these structures downward causing upper airway obstruction and respiratory distress.
2. Adults: Adult airway is relatively protected; larynx is larger and the epiglottis is shaped more like a spatula.
C. Etiology.
1. Infectious: H. influenzae type B is the most common cause in both children and adults. Declining incidence of H. influenzae in children since introduction of vaccine in 1995. Other bacteria, viruses, and Candida are also implicated.
2. Noninfectious: thermal injuries related to inhalation drug use, ingestion of hot food, caustic injury from aspiration, and posttransplant lymphoproliferative disorder.
D. Diagnosis.
1. Characteristic presentation.