The frequency of nosocomial sinusitis varies greatly from less than 5% to 100% [5,6], depending on the patient population studied and the diagnostic criteria used. In one series, 95% of nasotracheally intubated patients developed radiographic evidence of pansinusitis [7], as did 25% of patients who were orotracheally intubated. Only 40% of patients with “radiographic
sinusitis” were found to have positive cultures, although some cultures may have been sterilized by prior use of broad-spectrum antibiotics. Using stringent diagnostic criteria based on antroscopy, histopathology, and microbiology, the rate of infectious sinusitis may be closer to 10% in patients on long-term mechanical ventilation [4,5].

Critically ill patients are predisposed to develop nosocomial sinusitis for several reasons. The diameter of the ostia, normally as small as 1 or 2 mm, has been shown to decrease with recumbency as much as 23% because of venous hydrostatic pressures [8]. In addition, the maxillary sinus ostia are poorly located for gravitational drainage [8]. Nasotracheal and nasogastric tubes strongly predispose patients to develop sinusitis. Patients with orotracheal tubes have a lower incidence of bacterial sinusitis than those with nasotracheal tubes [4,9]. In one series, 73% of mechanically ventilated patients developed culture-proven sinusitis within 7 days of placement of nasogastric or nasotracheal tubes [7]. Larger intranasal tubes (tracheal) will induce radiographic sinus changes more quickly than smaller tubes (gastric) [4]. Using multiple logistic regression analysis, risk factors for nosocomial sinusitis, of strongest association, are sedative use, nasogastric feeding tubes, Glasgow coma scale less than 8, and nasal colonization with enteric Gram-negative bacteria [10].

The microbiology of nosocomial sinusitis is quite distinct from that of community-acquired sinusitis. Haemophilus influenzae and Streptococcus pneumoniae are rarely isolated in the nosocomial setting. Nosocomial sinusitis is polymicrobial in 44% to 58% of cases [11,12], with Gram-negative organisms being the causative agents in two thirds of cases, and Gram-positive organisms being implicated in one third [13]. Anaerobes are isolated in 0% to 15% of cases [11,14]. Staphylococcus aureus is the most common Gram-positive organism identified, and Pseudomonas species are the leading Gram-negative pathogens [4,13,15]. The organisms isolated in nosocomial sinusitis are the ones frequently identical to those cultured from the lower respiratory tract [3,14]. Such findings support the concept of general colonization of the airways in critically ill patients.

Specific situations warrant consideration of infection with more unusual pathogens. Rhinocerebral mucormycosis, an invasive infection usually caused by the branching fungus Rhizopus, a Zygomycetes, is seen most often in association with diabetes mellitus with ketoacidosis, burns, chronic renal disease, cirrhosis, and immunosuppression [16,17]. Other fungal infections, primarily with Aspergillus species, can be seen in normal hosts but are usually invasive diseases of immunocompromised patients [18]. Cryptococcus neoformans can cause sinusitis with a high relapse rate and significant mortality in immunocompetent and immunocompromised patients [19]. Candida species [20], Pseudoallescheria boydii and Cytomegalovirus species, and other unusual organisms have been isolated in patients with acquired immunodeficiency syndrome with sinusitis [21].

Complications of acute sinusitis are rare but can be rapidly fatal and are best managed in an ICU. Orbital complications include edema, predominantly of the eyelids, orbital cellulitis, orbital abscess, subperiosteal abscess, and cavernous sinus thrombosis [22,23]. The last one is the most severe, with a mortality of greater than 20% [24,25,26]. Intracranial complications have an overall mortality of 40% and include osteomyelitis, meningitis, epidural abscess, subdural empyema, and brain abscess [24,25,26]. In these cases, sinus drainage is imperative and antibiotics directed by culture result. Several investigators have examined the relationship between nosocomial sinusitis and ventilator-associated pneumonia. When S. aureus and Pseudomonas aeruginosa are isolated in patients with nosocomial sinusitis, the same organisms are identified in lower respiratory tract cultures in one third of cases [12]. Ventilator-associated pneumonia is more frequent in patients with confirmed nosocomial sinusitis [7]. In a prospective, randomized study of a strategy to systematically detect and treat nosocomial sinusitis, both radiographic evidence and bacteriologic evidence of sinusitis were found in 55% of febrile, mechanically ventilated patients [11]. All patients in the study were nasotracheally intubated. Seventy percent of patients with positive radiographs had positive quantitative cultures. Ventilator-associated pneumonia occurred in significantly fewer patients (34% vs. 47%, p = 0.02) in the group in which there was systematic screening for and treatment of sinusitis. Taken together, these findings suggest a causal relationship between nosocomial sinusitis and ventilator-associated pneumonia.

Nosocomial sinusitis may also cause fever of unknown origin (FUO) in mechanically ventilated patients. van Zanten and colleagues prospectively studied 351 orotracheally intubated patients with fever for more than 48 hours despite treatment with broad-spectrum antibiotics [3]. In 198 patients, the cause of the fever remained unknown despite initial investigations that included chest radiographs. Based on the results of sinus radiographs and subsequent sinus cultures, infectious sinusitis was confirmed in 105 of 198 (53%) patients with FUO and was found to be the sole cause of fever in 16% of cases.

Nosocomial sinusitis is most often related to the presence of nasopharyngeal and oropharyngeal catheters and tubes [4,12,33]. Therefore, in addition to antibiotics and decongestants, treatment includes removal of all nasal tubes to eliminate the source of obstruction and irritation in addition to decongestants and antibiotics. Because the spectrum of bacteria causing nosocomial sinusitis is similar to that causing other nosocomial respiratory infections [4,13,15], broad-spectrum Gram-positive and Gram-negative coverage is indicated. With removal of nasal tubes and antibiotic therapy, 67% of patients become afebrile within 48 hours [34]. Because the majority of patients respond to these conservative measures, consideration of surgical drainage can be reserved for patients who fail to respond to medical therapy and in whom no other source of infection is identified.

Acute mastoiditis is an uncommon complication of otitis media, seen primarily in children and young adults. Inflammation spreads from the middle ear to the modified respiratory mucosa lining of the mastoid air cells. The closed space infection leads to accumulation of purulent exudate, increased pressure, and bony necrosis. Pain, typically postauricular, fever, and abnormal tympanic membranes are the most common findings on presentation [39]. In approximately 50% of patients with mastoiditis, acute otitis media was diagnosed within days to weeks of admission [40]. Radiographic abnormalities of the mastoid are common and demonstrate opacification or cloudiness of the mastoid air cells and, less frequently, evidence of bone destruction [40]. CT scan of the temporal bone can identify and confirm intracranial complications [40]. Up to 25% of patients have complications on presentation, including subperiosteal abscess with or without epidural abscess, meningitis, cranial nerve involvement, and sigmoid sinus thrombophlebitis [41]. Lateral sinus thrombosis secondary to mastoiditis [42] has also been associated with septic pulmonary emboli [43,44]. The most common bacterial organisms isolated include S. pneumoniae, group A streptococci, and S. aureus; Pseudomonas may be commonly isolated as well [39]. Treatment includes broad-spectrum antibiotics that can adequately penetrate cerebrospinal fluid and surgical intervention for those who fail to improve within 24 to 72 hours.

Chronic mastoiditis and chronic otitis media result from a progressive inflammatory process that usually leads to obstruction of the communication between the middle ear and mastoid (aditus) or the middle ear and nasopharynx (eustachian tube) [39]. Often a cholesteatoma or epidermal inclusion cyst within the tympanomastoid compartment may be involved and may become secondarily infected [39]. Presenting symptoms include hearing loss, painless otorrhea, and tympanic membrane perforation [39]. Other symptoms (e.g., facial nerve paresis, headache, ear pain, fever) may be present if complications have occurred. Uncomplicated chronic otitis media and mastoiditis are treated medically with local hygiene, topical antibiotics often including a corticosteroid, and oral, or infrequently parenteral, antibiotics [39]. Broad-spectrum antibiotics are required to cover a wide range of aerobic and anaerobic organisms. Surgery is usually reserved for recurrent disease, often associated with a cholesteatoma, which can be identified by CT scan of the temporal bone [39].

Malignant, or necrotizing, external otitis (MEO) most often affects elderly diabetic patients. Diabetic microangiopathy, an altered immune response, the biochemistry of diabetic cerumen, and characteristics of the usual etiologic organism have been implicated in the pathogenesis of MEO [45]. MEO most commonly presents with otalgia; granulation tissue in the external auditory canal, most prominently at the osteocartilaginous junction; and often purulent and fetid otorrhea [45]. Spread of infection is anteriorly toward the parotid compartment or downward into the temporal bone; spread to the mastoid is less common [37]. Extension leads to pain and tenderness of the tissues around the ear. In MEO, P. aeruginosa is the most commonly implicated pathogen [45]. Patients with acquired immunodeficiency syndrome may develop infection from a wider variety of organisms and may accumulate less granulation tissue in the external auditory canal [46]. Aspergillus species have been identified, primarily in immunocompromised patients [47,48]. Osteomyelitis [49], cranial nerve paralysis [50], and central nervous system (meningitis) and vascular (thrombophlebitis) spread [51] are potential severe and fatal complications of MEO.

CT and magnetic resonance imaging scanning, along with technetium-99 bone scans, are valuable components of the diagnostic evaluation of MEO [51]. The therapy for MEO includes prolonged antibiotics directed against P. aeruginosa unless the culture data suggest otherwise. This may include a semisynthetic penicillin or ceftazidime with an aminoglycoside. Oral fluoroquinolones have also been used successfully [51]. The duration of treatment is not clearly defined. Surgical intervention can be complementary and is based on the response to conservative treatment and the presence of complications.

In the post–H. influenzae type B vaccine era, the annual incidence of acute supraglottitis is estimated between 0.6 and 0.78 cases per 100,000 immunized children [58]. In adults, the incidence of acute supraglottitis has increased from 0.79 cases per 100,000 adults in 1986 to 2.1 cases per 100,000 adults in 2005 [58]. Adults with acute supraglottitis usually present in their 40s and 50s, with a male preponderance, and children usually present between the ages of 2 and 5 years [58].

In children, the inflammation is mainly restricted to the epiglottis because of loose mucosa on its lingual aspect. This provides a readily available space for edema to collect within. Swelling reduces the airway aperture by curling the epiglottis posteriorly and inferiorly, accentuating the juvenile omega shape. When edema spreads to involve the aryepiglottic folds, respiratory distress can occur as inspiration draws these structures downward, further exacerbating the obstruction and resulting in stridor. The adult airway is relatively protected because the larynx is larger and the epiglottis is shaped more like a spatula.

Although various bacteria, viruses, and Candida species have been recognized as causes of acute supraglottitis (Table 67.1) [60,61,62,63,64,65,66,67,68], H. influenzae type B is the most common cause identified in pediatric and adult cases [60,68]. Although vaccine failure has been reported in children who had received an early polysaccharide vaccine [61], significant declines in the incidence of this infection have been noted with the use of conjugated vaccines that can be administered to even younger children [60]. In adults, blood cultures are positive in less than 20% of cases, and H. influenzae is the isolate in one third of these cases [62,68].

Noninfectious causes of acute supraglottitis have been described and include thermal injuries related to inhalation drug use, ingestion of hot food, apparent caustic injury from aspiration, and posttransplant lymphoproliferative disorder [63,64]. McKinney and Grigg [66] described a case of epiglottitis after general anesthesia administered via a laryngeal mask.