akut sinusitis

BackgroundSinusitis is characterized by inflammation of the lining of the paranasal sinuses. Because the nasal mucosa is simultaneously involved and because sinusitis rarely occurs without concurrent rhinitis, rhinosinusitis is now the preferred term for this condition.[1, 2]

Rhinosinusitis may be further classified according to the anatomic site (maxillary, ethmoidal, frontal, sphenoidal), pathogenic organism (viral, bacterial, fungal), presence of complication (orbital, intracranial), and associated factors (nasal polyposis, immunosuppression, anatomic variants). (See Anatomy, Pathophysiology, and Etiology.)

Acute sinusitis is a clinical diagnosis; thus, an understanding of its presentation is of paramount importance in differentiating this entity from allergic or vasomotor rhinitis and common upper respiratory infections. No specific clinical symptom or sign is sensitive or specific for acute sinusitis, so the overall clinical impression should be used to guide management. (See Clinical Presentation.)

The primary goals of management of acute sinusitis are to eradicate the infection, decrease the severity and duration of symptoms, and prevent complications. (See Treatment and Management.) Most patients with acute sinusitis are treated in the primary care setting. Further evaluation by an otolaryngologist is recommended in any of the following cases:

When continued deterioration occurs with appropriate antibiotic therapy When episodes of sinusitis recur When symptoms persist after 2 courses of antibiotic therapy When comorbid immunodeficiency, nosocomial infection, or complications of

sinusitis are present

Definition of acute rhinosinusitis

Many classifications, both clinical and radiological, have been proposed in the literature to define acute sinusitis. Although no consensus on the precise definition currently exists subacute sinusitis represents a temporal progression of symptoms for 4-12 weeks. Recurrent acute sinusitis is diagnosed when 2-4 episodes of infection occur per year with at least 8 weeks between episodes and, as in acute sinusitis, the sinus mucosa completely normalizes between attacks. Chronic sinusitis is the persistence of insidious symptomatology beyond 12 weeks, with or without acute exacerbations.[3]

Anatomy To properly diagnose and treat infectious disorders of the paranasal sinuses, the clinician should have knowledge of the developmental milestones. The development of the paranasal sinuses begins in the third week of gestation and continues until early adulthood.

Development of paranasal sinuses

During the third week of embryonic development, proliferation and medial migration of ectodermal cells form the notochord. After the heart tube and pericardium have rotated from the cranial position to lie anteriorly, the notochord, which is initially in the caudal region of

the embryonic disc, rotates to lie posterior to the primitive foregut. The paraxial layer of mesenchyme, which lies adjacent to the notochord, differentiates into the somite ridges, intermediate cell mass, and lateral plate mesoderm. From these mesodermal structures, the branchial arches develop, the first of which gives rise to internal nasal structures.

The paranasal sinuses develop in conjunction with the palate from changes in the lateral wall of the nasal cavity. At 40 weeks' gestation, 2 horizontal grooves develop in the mesenchyme of the lateral wall of the nasal cavity. Proliferation of maxilloturbinate mesenchyme between these grooves results in an outpouching of tissue medially into the nasal lumen. This outpouching is the precursor of the middle and inferior meatus as well as the inferior turbinate. Ethmoidoturbinate folds develop superiorly to give rise to the middle and superior turbinates. Once the turbinate structures are established, sinus development begins and continues until early adult life.

The sinuses open into the nose via small openings called ostia.[2] The maxillary and ethmoid sinuses form at 3-4 months' gestation. Thus, an infant is born with 3-4 ethmoid cells and tiny teardrop-shaped maxillary sinuses. By the teenage years, each maxillary sinus progressively enlarges to an adult capacity of 15 mL. In healthy individuals, the ethmoid sinuses increase in number to 18-20, and each drains by an individual ostium that is 1-2 mm in diameter.

The frontal sinus develops from an anterior ethmoid cell and moves to its supraorbital position when the individual is aged 6-7 years. Frontal sinuses may begin to develop at this age but usually do not appear radiologically until the individual is aged approximately 12 years. The maxillary, anterior ethmoid, and frontal sinuses drain into the middle meatus; the posterior ethmoid and sphenoid sinuses drain into the superior meatus (see the image below).

Sagittal section of the lateral nasal wall demonstrating openings of paranasal sinuses. Conchae have been cut to depict details of meatal structures.

Structure and function of paranasal sinuses

The paranasal sinuses are air-filled bony cavities that extend from the skull base to the alveolar process and laterally from the nasal cavity to the inferomedial aspect of the orbit and the zygoma. The sinus cavities are lined with pseudostratified, ciliated, columnar epithelium that is contiguous, via ostia, with the lining of the nasal cavity. This epithelium contains a number of mucus-producing goblet cells. These goblet cells in the epithelium and the submucosal seromucous glands contribute to the airway surface liquid,[4] which is 5-100 μm thick and covers the epithelium.

Anterior and posterior ethmoid sinuses are composed of multiple air cells separated by thin bony partitions. Each cell is drained by an independent ostium that measures only 1-2 mm in diameter. These small openings are readily clogged by secretions or are occluded by swelling of the nasal mucosa. The sphenoid sinuses sit immediately anterior to the pituitary fossa and just behind the posterior ethmoid.

The arterial supply of the paranasal sinuses is from branches of the internal and external carotid arteries, while the venous and lymphatic drainage path is through the sinus ostia into the nasal cavity plexus. In addition, venous drainage occurs through valveless vessels corresponding to the arterial supply.

All sinus ostia drain into the nares at locations beneath the middle and superior turbinates. The posterior ethmoid and sphenoid sinuses drain into the superior meatus below the superior turbinate. The ostia of the maxillary, anterior ethmoid, and frontal sinuses share a common site of drainage within the middle meatus. This region is called the ostiomeatal complex and can be visualized by coronal CT scan. The common drainage pathway of the frontal, maxillary, and anterior ethmoid sinuses within the middle meatus allows relatively localized mucosal infection processes to promote infection in all these sinuses.

The successful maintenance of sinus drainage represents a complicated interaction between ciliary action, mucus viscosity, size of sinus ostia, and orientation of body structures. Ciliary beat at the rate of 8-15 Hz is continuously moved by the cilia at a speed of 6 mm/min. The ciliary action can be affected due to local factors, such as infection and local hypoxia that is associated with complete occlusion of sinus ostia. The sinus mucosa has less secretory and vasomotor function than the nasal cavity does. Cilia are concentrated near and beat toward the natural sinus ostia. Blockage of the ostium results in stasis of mucous flow, which can lead to development of disease.

The exact function of the paranasal sinuses is not well understood. The possible roles of the sinuses may include reducing the weight of the skull; dampening pressure; humidifying and warming inspired air; absorbing heat and insulating the brain; aiding in sound resonance; providing mechanical rigidity; and increasing the olfactory surface area.

PathophysiologyThe sinuses are normally sterile under physiologic conditions. Secretions produced in the sinuses flow by ciliary action through the ostia and drain into the nasal cavity. In the healthy individual, flow of sinus secretions is always unidirectional (ie, toward the ostia), which prevents back contamination of the sinuses. In most individuals, the maxillary sinus has a single ostium (2.5 mm in diameter, 5 mm2 in cross-sectional area) serving as the only outflow tract for drainage. This slender conduit sits high on the medial wall of the sinus cavity in a nondependent position. Most likely, the edema of the mucosa at these 1- to 3-mm openings becomes congested by some means (eg, allergy, viruses, chemical irritation) that causes obstruction of the outflow tract stasis of secretions with negative pressure, leading to infection by bacteria.

Retained mucus, when infected, leads to sinusitis. Another mechanism hypothesizes that because the sinuses are continuous with the nasal cavity, colonized bacteria in the nasopharynx may contaminate the otherwise sterile sinuses. These bacteria are usually removed by mucociliary clearance; thus, if mucociliary clearance is altered, bacteria may be inoculated and infection may occur, leading to sinusitis.[5, 2]

Data are available that support the fact that healthy sinuses are colonized. The bacterial flora of noninflamed sinuses were studied for aerobic and anaerobic bacteria in 12 adults who underwent corrective surgery for septal deviation.[6] Organisms were recovered from all

aspirates, with an average of 4 isolates per sinus aspirate. The predominant anaerobic isolates were Prevotella, Porphyromonas, Fusobacterium and Peptostreptococcus species. The most common aerobic bacteria were S pyogenes, S aureus, S pneumonia, and H influenzae. In another study, specimens were processed for aerobic bacteria only, and Staphylococcus species and alpha-hemolytic streptococci were isolated.[7] Organisms were recovered in 20% of maxillary sinuses of patients who underwent surgical repositioning of the maxilla.

In contrast, another report of aspirates of 12 volunteers with no sinus disease showed no bacterial growth.[8] Jiang et al evaluated the bacteriology of maxillary sinuses with normal endoscopic findings.[9] Organisms were recovered from 14 (47%) of 30 swab specimens and 7 (41%) of 17 of mucosal specimens. Gordts et al reported the microbiology of the middle meatus in normal adults and children.[10] This study noted in 52 patients that 75% had bacterial isolates present, most commonly coagulase-negative staphylococci (CNS) (35%), Corynebacterium species (23%), and S aureus (8%) in adults. Low numbers of these species were present. In children, the most common organisms were H influenzae (40%), M catarrhalis (34%), and S pneumoniae (50%), a marked difference from findings in adults. Nonhemolytic streptococci and Moraxella species were absent in adults.

The pathophysiology of rhinosinusitis is related to 3 factors:

Obstruction of sinus drainage pathways (sinus ostia) Ciliary impairment Altered mucus quantity and quality

Obstruction of sinus drainage

Obstruction of the natural sinus ostia prevents normal mucus drainage. The ostia can be blocked by mucosal swelling or local causes (eg, trauma, rhinitis), as well as by certain inflammation-associated systemic disorders and immune disorders. Systemic diseases that result in decreased mucociliary clearance, including cystic fibrosis, respiratory allergies, and primary ciliary dyskinesia (Kartagener syndrome), can be predisposing factors for acute sinusitis in rare cases. Patients with immunodeficiencies (eg, agammaglobulinemia, combined variable immunodeficiency, and immunodeficiency with reduced immunoglobulin G [IgG]– and immunoglobulin A [IgA]–bearing cells) are also at increased risk of developing acute sinusitis.

Mechanical obstruction because of nasal polyps, foreign bodies, deviated septa, or tumors can also lead to ostial blockage. In particular, anatomical variations that narrow the ostiomeatal complex, including septal deviation, paradoxical middle turbinates, and Haller cells, make this area more sensitive to obstruction from mucosal inflammation. Usually, the margins of the edematous mucosa have a scalloped appearance, but in severe cases, mucus may completely fill a sinus, making it difficult to distinguish an allergic process from infectious sinusitis. Characteristically, all of the paranasal sinuses are affected and the adjacent nasal turbinates are swollen. Air-fluid levels and bone erosion are not features of uncomplicated allergic sinusitis; however, swollen mucosa in a poorly draining sinus is more susceptible to secondary bacterial infection.

Hypoxia within the obstructed sinus is thought to cause ciliary dysfunction and alterations in mucus production, further impairing the normal mechanism for mucus clearance.

Impaired ciliary function

Contrary to earlier models of sinus physiology, the drainage patterns of the paranasal sinuses depend not on gravity but on the mucociliary transport mechanism. The metachronous coordination of the ciliated columnar epithelial cells propels the sinus contents toward the natural sinus ostia. Any disruption of the ciliary function results in fluid accumulation within the sinus. Poor ciliary function can result from the loss of ciliated epithelial cells; high airflow; viral, bacterial, or environmental ciliotoxins; inflammatory mediators; contact between 2 mucosal surfaces; scars; and Kartagener syndrome.[11]

Ciliary action can be affected by genetic factors, such as Kartagener syndrome. Kartagener syndrome is associated with immobile cilia and hence the retention of secretions and predisposition to sinus infection. Ciliary function is also reduced in the presence of low pH, anoxia, cigarette smoke, chemical toxins, dehydration, and drugs (eg, anticholinergic medications and antihistamines).

Exposure to bacterial toxins can also reduce ciliary function. Approximately 10% of cases of acute sinusitis result from direct inoculation of the sinus with a large amount of bacteria. Dental abscesses or procedures that result in communication between the oral cavity and sinus can produce sinusitis by this mechanism. Additionally, ciliary action can be affected after certain viral infections.

Several other factors can lead to impaired ciliary function. Cold air is said to stun the ciliary epithelium, leading to impaired ciliary movement and retention of secretions in the sinus cavities. On the contrary, inhaling dry air desiccates the sinus mucous coat, leading to reduced secretions. Any mass lesion with the nasal air passages and sinuses, such as polyps, foreign bodies, tumors, and mucosal swelling from rhinitis, may block the ostia and predispose to retained secretions and subsequent infection. Facial trauma or large inoculations from swimming can produce sinusitis as well. Drinking alcohol can also cause nasal and sinus mucosa to swell and cause impairment of mucous drainage.

Altered quality and quantity of mucus

Sinonasal secretions play an important role in the pathophysiology of rhinosinusitis. The mucous blanket that lines the paranasal sinuses contains mucoglycoproteins, immunoglobulins, and inflammatory cells. It consists of 2 layers: (1) an inner serous layer (ie, sol phase) in which cilia recover from their active beat and (2) an outer, more viscous layer (ie, gel phase), which is transported by the ciliary beat. Proper balance between the inner sol phase and outer gel phase is of critical importance for normal mucociliary clearance.

If the composition of mucus is changed, so that the mucus produced is more viscous (eg, as in cystic fibrosis), transport toward the ostia considerably slows, and the gel layer becomes demonstrably thicker. This results in a collection of thick mucus that is retained in the sinus for varying periods. In the presence of a lack of secretions or a loss of humidity at the surface that cannot be compensated for by mucous glands or goblet cells, the mucus becomes increasingly viscous, and the sol phase may become extremely thin, thus allowing the gel phase to have intense contact with the cilia and impede their action. Overproduction of mucus can overwhelm the mucociliary clearance system, resulting in retained secretions within the sinuses.

Acute sinusitis in the intensive care setting

Acute sinusitis in the intensive care population is a distinct entity, occurring in 18-32% of patients with prolonged periods of intubation, and is usually diagnosed during the evaluation of unexplained fever. Cases in which the cause is obstruction are usually evident and can include the presence of prolonged nasogastric or nasotracheal intubation. Moreover, patients in an intensive care setting are generally debilitated, predisposing them to septic complications, including sinusitis. Finally, sinusitis in intensive care settings is associated with nasal catheter placement.

EtiologyPurulent sinusitis can occur when ciliary clearance of sinus secretions decreases or when the sinus ostium becomes obstructed, which leads to retention of secretions, negative sinus pressure, and reduction of oxygen partial pressure. This environment is then suitable for growth of pathogenic organisms. Factors that predispose the sinuses to obstruction and decreased ciliary function are allergic, nonallergic, or viral insults, which produce inflammation of the nasal and sinus mucosa and result in ciliary dysmotility and sinus obstruction.

In individuals with recurrent or persistent sinusitis, suspect other predisposing conditions such as cystic fibrosis, ciliary dyskinesia, allergic inflammation, immunodeficiency, or an anatomic problem. These predisposing factors are also cited by the 2005 practice parameter for diagnosis and management of sinusitis issued by the American Academy of Allergy, Asthma and Immunology (AAAAI), as are cocaine addiction and nasal polyps and other causes of ostiomeatal obstruction.[12]

Acute viral rhinosinusitis

The vast majority of rhinosinusitis episodes are caused by viral infection. Most viral upper respiratory tract infections are caused by rhinovirus, but coronavirus, influenza A and B, parainfluenza, respiratory syncytial virus, adenovirus, and enterovirus are also causative agents. Rhinovirus, influenza, and parainfluenza viruses are the primary pathogens in 3-15% of patients with acute sinusitis. In about 0.5-2% of cases, viral sinusitis can progress to acute bacterial sinusitis.[13, 14]

Viral upper respiratory tract infections are the most important risk factor for the development of acute bacterial sinusitis.[15] Approximately 90% of patients who have viral upper respiratory tract infections have sinus involvement, but only 5-10% of these patients have bacterial superinfection requiring antimicrobial treatment.[16]

Acute bacterial rhinosinusitis

Acute bacterial rhinosinusitis is very frequently associated with viral upper respiratory tract infection, although allergy, trauma, neoplasms, granulomatous and inflammatory diseases, midline destructive disease, environmental factors, dental infection, and anatomic variation, which may impair normal mucociliary clearance, may also predispose to bacterial infection.

S aureus is a common pathogen in sphenoid sinusitis. The vaccination of children with the 7-valent pneumococcal vaccine introduced in 2000 in the United States brought about the decline in the recovery rate of S pneumoniae and an increase in H influenza.[17, 18] In addition, the rate of recovery of S pneumoniae penicillin-resistant strains was different after vaccination.

P aeruginosa and other gram-negative rods have been recovered in acute sinusitis of nosocomial origin (especially in patients who have nasal tubes or catheters), immunocompromised persons, patients with HIV infection, and those with cystic fibrosis.

Sixty-six percent of patients with acute sinusitis grow at least 1 pathogenic bacterial species on sinus aspirates, while 26-30% percent of patients have multiple predominant bacterial species. The bacteria most commonly involved in acute sinusitis are part of the normal nasal flora. These bacteria can become sinus pathogens when they are deposited into the sinuses by sneezing, coughing, or direct invasion under conditions that optimize their growth.

The most common pathogens isolated from maxillary sinus cultures in patients with acute bacterial rhinosinusitis include Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis.Streptococcus pyogenes, Staphylococcus aureus,and anaerobes are less commonly associated with acute bacterial rhinosinusitis; they have been found in fewer than 10% of patients with acute bacterial sinusitis, despite the ample environment available for their growth. The exceptions are in sinusitis resulting from a dental source and in patients with chronic sinus disease, in whom anaerobic organisms are usually isolated.

S pneumoniae are gram-positive, catalase-negative, facultatively anaerobic cocci that account for 20-43% of acute bacterial rhinosinusitis cases in adults. The rise of antimicrobial resistance in S pneumoniae is a major concern.

A 1998 surveillance study of respiratory tract isolates estimated that 12.3% of S pneumoniae isolates obtained from the paranasal sinuses had intermediate resistance to penicillin; 37.4% were penicillin-resistant. The paranasal sinuses represented the anatomic location with the highest resistance rate.[19] Resistance to macrolide, clindamycin, trimethoprim-sulfamethoxazole, and doxycycline was more common in isolates with intermediate penicillin resistance and those that were penicillin-resistant.

H influenzae are gram-negative, facultatively anaerobic bacilli. H influenza type B was a leading cause of meningitis until the widespread use of the vaccine. Nontypeable strains of H influenzae are responsible for 22-35% of acute bacterial rhinosinusitis cases in adults. Beta-lactamase production is the mechanism of antimicrobial resistance for this organism . Of isolates from the paranasal sinus, 32.7% were found to be beta-lactamase–positive for H influenza; other reports suggest a rate of 44%.

M catarrhalis are gram-negative, oxidase-positive, aerobic diplococci. M catarrhalis is the responsible pathogen in 2-10% of acute bacterial rhinosinusitis cases in adults. Beta-lactamase production is the mechanism of antimicrobial resistance for M catarrhalis as well . Of isolates from the paranasal sinus, 98% were found to be beta-lactamase–positive for M catarrhalis.

S aureus, though accounting for 10% of episodes of acute bacterial rhinosinusitis, is now recognized as an increasingly common pathogen in acute bacterial rhinosinusitis.[20] While

methicillin-resistant S aureus (MRSA) still represents a minority of episodes of S aureus rhinosinusitis, increasing trends of drug-resistant S aureus may alter future treatment recommendations.[21]

Gram-negative organisms, including Pseudomonas aeruginosa (15.9%), Escherichia coli (7.6%), Proteus mirabilis (7.2%), Klebsiella pneumoniae, and Enterobacter species, predominate in nosocomial sinusitis, accounting for 60% of cases. Polymicrobial invasion is seen in 25-100% of cultures. The other pathogenic organisms found in nosocomial patients are gram-positive organisms (31%) and fungi (8.5%).

Acute invasive fungal rhinosinusitis

Rarely, sinusitis is caused by fungi. Fungal sinusitis (eg, allergic fungal sinusitis) may appear similar to lower airway disorder and allergic bronchopulmonary aspergillosis.

Fungal agents associated with this condition include Aspergillus and Alternaria species. Bipolaris and Curvularia species are the most common fungi recovered in allergic fungal sinusitis, accounting for 60% and 20%, respectively, in most studies. Curvularia species is occasionally reported as the most common causative organism in the deep southern United States.

Please go to the main article Fungal Sinusitis for more information.

EpidemiologySinusitis affects 1 out of every 7 adults in the United States, with more than 30 million individuals diagnosed each year. Sinusitis is more common from early fall to early spring. Rhinosinusitis affects an estimated 35 million people per year in the United States and accounts for close to 16 million office visits per year.[22]

According to the National Ambulatory Medical Care Survey (NAMCS), approximately 14% of adults report having an episode of rhinosinusitis each year, and it is the fifth most common diagnosis for which antibiotics are prescribed, accounting for 0.4% of ambulatory diagnoses.[23]

In 1996, Americans spent approximately $3.39 billion treating rhinosinusitis.[24] The economic burden of acute sinusitis in children is $1.77 billion per year.[24]

International prevalence

Acute sinusitis affects 3 in 1000 people in the United Kingdom. Chronic sinusitis affects 1 in 1000 people. Sinusitis is more common in winter than in summer. Rhinoviral infections are prevalent in autumn and spring. Coronaviral infection occurs mostly from December to March.

Acute sinusitis in children

An average child is likely to have 6-8 colds (ie, upper respiratory tract infections) per year, and approximately 0.5-2% of upper respiratory tract infections in adults and 6-13% of viral

upper respiratory tract infections in children are complicated by the development of acute bacterial sinusitis.[25, 26]

Sex distribution for acute sinusitis

Women have more episodes of infective sinusitis than men because they tend to have more close contact with young children. The rate in women is 20.3%, compared with 11.5% in men.

Prognosis Sinusitis does not cause any significant mortality by itself. However, complicated sinusitis may lead to morbidity and, in rare cases, mortality.

Approximately 40% of acute sinusitis cases resolve spontaneously without antibiotics. The spontaneous cure for viral sinusitis is 98%. Patients with acute sinusitis, when treated with appropriate antibiotics, usually show prompt improvement. The relapse rate after successful treatment is less than 5%.

In the absence of response within 48 hours or worsening of symptoms, reevaluate the patient. Untreated or inadequately treated rhinosinusitis may lead to complications such as meningitis, cavernous sinus thrombophlebitis, orbital cellulitis or abscess, and brain abscess.

In patients with allergic rhinitis, aggressive treatment of nasal symptoms and signs of mucosal edema, which can cause obstruction of the sinus outflow tracts, may decrease secondary sinusitis. If the adenoids are chronically infected, removing them eliminates a nidus of infection and can decrease sinus infection.

ComplicationsComplications of sinusitis include acute and chronic sequelae. Acute distant effects include toxic shock syndrome. Acute local effects can also occur. Acute orbital complications include the following: cellulitis, proptosis, chemosis, ophthalmoplegia, orbital cellulitis, subperiosteal abscess, and orbital abscess.

Other acute complications include intracranial sequelae such as meningitis; encephalitis; cavernous or sagittal sinus thrombosis; or extradural, subdural, or intracerebral abscesses.

The incidence of intracranial complications in all patients hospitalized with sinusitis has been reported as 3.7%. Sinusitis is implicated as a source of subdural abscess in 35-65% of cases. Bony complications include dental involvement and osteitis or osteomyelitis. Potts puffy tumor refers to swelling of the scalp, caused by an underlying osteitis of the skull or extradural abscess. A classical cause of such a swelling is complicated frontal sinusitis. Toxic shock syndrome is an unusual complication of acute sinusitis. It occurs after surgery for foreign body removal and is associated with S aureus.

Patient Education

For excellent patient education resources, visit eMedicine’s Headache Center. Also, see eMedicine's patient education article Sinus Infection.

HistoryAcute sinusitis is a clinical diagnosis; thus, an understanding of its presentation is of paramount importance in differentiating this entity from allergic or vasomotor rhinitis and common upper respiratory infections. No specific clinical symptom or sign is sensitive or specific for acute sinusitis, so the overall clinical impression should be used to guide management.

A history of occupational or allergic rhinitis, vasomotor rhinitis, nasal polyps, rhinitis medicamentosa, or immunodeficiency should be sought in an evaluation for rhinosinusitis. Rhinosinusitis is more common in individuals with congenital defects that affect humoral immunity and ciliary motility, in those with cystic fibrosis, and in persons with AIDS.

Obtain a history of diabetes or organ transplant if invasive fungal sinusitis is being considered. Fungal infections are more common in people with diabetes and those who are immunocompromised. Clinicians should maintain a high index of suspicion for acute invasive fungal sinusitis in immunocompromised patients with orbital or CNS complications of rhinosinusitis.

Clinical findings may include the following:

Pain over cheek and radiating to frontal region or teeth, increasing with straining or bending down

Redness of nose, cheeks, or eyelids Tenderness to pressure over the floor of the frontal sinus immediately above the inner

canthus Referred pain to the vertex, temple, or occiput Postnasal discharge A blocked nose Persistent coughing or pharyngeal irritation Facial pain Hyposmia

The duration of the condition should be determined. Suspect acute sinusitis in any patient with an upper respiratory tract infection that persists beyond 7-10 days, particularly if the infection is severe and is accompanied by high fever, purulent nasal discharge, or periorbital edema (ethmoid sinusitis).

The condition may start as an upper respiratory tract infection, and the patient may seem to be recovering; however, the condition becomes acutely worse around the seventh day of illness. This should be considered a red flag because most upper respiratory tract infections last 5-7 days. The natural history of rhinovirus infection, as described by Gwaltney et al, lasts from 1-33 days. One fourth of patients have symptoms that last longer than 14 days.[27]

Bacterial and viral sinusitis

During the course of a viral upper respiratory tract infection, 3 three common clinical presentations should prompt the clinician to consider that the patient is experiencing an episode of acute bacterial sinusitis. These presentations are described as onset with persistent symptoms, onset with severe symptoms, or onset with worsening symptoms. What is meant by persistent symptoms, in the context of acute bacterial sinusitis, is respiratory symptoms that last more than 10 days but less than 30 days and which have not begun to improve. Such symptoms include nasal discharge (of any quality, eg, thick or thin, serous, mucoid or purulent) or daytime cough (which may be worse at night) or both.

A consensus statement published in Otolaryngology-Head and Neck Surgery made strong recommendations that clinicians should distinguish between acute rhinosinusitis caused by bacterial causes and those episodes caused by viral upper respiratory infections and noninfectious conditions.[28]

The panel suggests that the diagnosis of acute bacterial sinusitis be entertained when (1) symptoms or signs of acute rhinosinusitis are present 10 days or more beyond the onset of upper respiratory symptoms, or (2) symptoms or signs of acute rhinosinusitis worsen within 10 days after an initial improvement. A history of purulent secretions and facial or dental pain are specific symptoms that may point to a bacterial etiology. In a patient in intensive care, acute sinusitis should be suspected in the presence of sepsis of unknown origin.

The consensus statement is in accordance with the AAAAI 2005 practice parameter for diagnosis and management of sinusitis, which states that upper respiratory tract infections persisting after 10-14 days are suspicious for acute bacterial sinusitis. The likelihood of bacterial disease increases if the infection history includes persistent purulent rhinorrhea, postnasal drainage, and facial pain.[12]

Acute bacterial rhinosinusitis is commonly overdiagnosed. In fact, acute bacterial rhinosinusitis is the correct diagnosis in only 40-50% of cases in which a primary care physician initially classifies a patient as likely having the condition.[29]

Although diagnostic criteria for acute rhinosinusitis have been proposed,[1] no single sign or symptom has strong diagnostic value for bacterial rhinosinusitis.[30] As noted, however, acute bacterial rhinosinusitis should be suspected in patients who exhibit symptoms of viral upper respiratory tract infection that do not improve after 10 days or that worsen after 5-7 days.

Symptoms of acute bacterial rhinosinusitis include the following:

Facial pain or pressure (especially unilateral) Hyposmia/anosmia Nasal congestion Nasal drainage Postnasal drip Fever Cough Fatigue Maxillary dental pain Ear fullness/pressure

A change in the color or characteristic of the nasal discharge is not a specific sign of bacterial rhinosinusitis. A previous diagnosis of rhinosinusitis is not a predictor of acute bacterial rhinosinusitis.[30]

Physical ExaminationAnterior rhinoscopic examination, with or without a topical decongestant, is important to assess the status of the nasal mucosa and the presence and color of nasal discharge. Predisposing anatomical variations can also be noted during anterior rhinoscopy.

Endoscopic examination may reveal the origin of the purulent discharge from the middle meatus and may provide information about the nature of ostiomeatal obstruction. The use of endoscopy may also aid in the etiologic diagnosis of acute sinusitis by allowing the careful attainment of purulent secretions from the sinus ostia for culture. Purulent secretions in the middle meatus (highly predictive of maxillary sinusitis) may be seen using a nasal speculum and a directed light.

Fever is seen in fewer than 2% of individuals with sinusitis. Sinus transillumination and palpation are of little predictive value. Facial tenderness to palpation is present. Complete opacification of maxillary or frontal sinuses may be seen on transillumination; partial opacification is a nonspecific finding, and it is not as reliable. A basic evaluation of ocular and neurological function is also necessary to rule out potential complications.

The following may be noted:

Purulent nasal secretions Purulent posterior pharyngeal secretions Mucosal erythema Periorbital edema Tenderness overlying sinuses Air-fluid levels on transillumination of the sinuses (60% reproducibility rate for

assessing maxillary sinus disease) Facial erythema

Evaluation of the pediatric patient

Sinusitis and upper respiratory tract infections are common pediatric problems. As many as 10% of upper respiratory tract infections can be complicated by acute sinusitis. Untreated chronic sinusitis can lead to life-threatening complications.

Physical examination findings may not be helpful in making a diagnosis of acute bacterial sinusitis in a child because the findings are almost identical to those of a child with viral rhinosinusitis. The presence of pus in the middle meatus suggests involvement of maxillary, frontal, or ethmoid sinuses; pus in the superior meatus suggests involvement of sphenoid or posterior ethmoid cells.

According to a study by Mcquillan et al in which pediatricians were asked how they diagnose and manage nonsevere acute sinusitis in children, on the basis of age group, pediatricians

reported first considering acute sinusitis at the following rates: ages 0-5 (6%), 6-11 (17%), 12-23 (36%), 24-35 (21%), and 36 months or older (20%).[31]

In the Mcquillan study, symptoms thought to be very important included prolonged symptom duration (93%), purulent rhinorrhea (55%), and nasal congestion (43%); 60% reported that symptom duration is more important than symptom combination. Symptom duration before considering the diagnosis were 1-6 days (3%), 7-9 days (17%), 10-13 days (37%), 14-16 days (38%), and 17 or more days (6%).

Mcquillan et al reported that CT scanning was used by 58% in making the diagnosis of acute sinusitis. Antibiotics were used frequently or always by 96% of the respondents. Adjuvants used frequently or always included saline washes (44%), systemic decongestants (28%), nasal corticosteroids (20%), and systemic antihistamines (13%).

In children younger than 6 years, the nasal examination usually consists of evaluating the anterior nasal cavity and middle meatus with anterior rhinoscopy using an otoscope and ear speculum. The superior meatus can never be observed with this technique and is difficult to observe with nasal endoscopy, rigid rhinoscopy, or both. Purulence running into the posterior nasal cavity and nasopharynx, observed only by rigid rhinoscopy, can indicate probable drainage from the sphenoethmoid recess, which drains the posterior ethmoids and sphenoid sinuses.

In persons with acute ethmoiditis, especially in infants and younger children, periorbital cellulitis with edema of the soft tissues and erythema of the overlying skin is not uncommon.

American Academy of Pediatrics (AAP) recommendations do not require imaging in the diagnosis of children aged 6 years or younger to make the diagnosis of uncomplicated acute bacterial sinusitis if they meet the criteria for the diagnosis.

Complications of DiseaseApproximately 75% of orbital or periorbital infections are the result of extending sinusitis. Untreated, inadequately treated, or partially treated rhinosinusitis may lead to chronic rhinosinusitis, meningitis, brain abscess, or other extra-sinus complications. (See Treatment and Management.)

Local complications

Mucoceles are chronic epithelial cysts that develop in sinuses in the presence of either an obstructed sinus ostium or minor salivary gland duct. They have the potential for progressive concentric expansion that can lead to bony erosion and extension beyond the sinus.

Maxillary sinus mucoceles are usually found incidentally on sinus radiographs and are of little significance in the absence of symptomatology or infection. Frontoethmoidal and sphenoethmoidal mucoceles, on the other hand, tend to be symptomatic and have a high potential for bony erosion.

Osteomyelitis is a potential local complication most commonly occurring with frontal sinusitis. Osteomyelitis of the frontal bone is called a Pott puffy tumor and represents a

subperiosteal abscess with local edema anterior to the frontal sinus. This can advance to form a fistula to the upper lid with sequestration of necrotic bone.

Orbital complications

Orbital complications are the most common complications encountered with acute bacterial sinusitis. Infection can spread directly through the thin bone separating the ethmoid or frontal sinuses from the orbit or by thrombophlebitis of the ethmoid veins.

Diagnosis should be based on an accurate physical examination, including ophthalmological evaluation and appropriate radiological studies. CT scanning is the most sensitive means of diagnosing an orbital abscess, although ultrasound has been found to be 90% effective for diagnosing anterior abscesses.[27] The classification by Chandler, which is based on physical examination findings, provides a reasonable framework to guide management. This classification consists of 5 groups of orbital inflammation[30] :

Group 1 - Inflammatory edema (preseptal cellulitis) with normal visual acuity and extraocular movement

Group 2 - Orbital cellulitis with diffuse orbital edema but no discrete abscess Group 3 - Subperiosteal abscess beneath the periosteum of the lamina papyracea

resulting in downward and lateral globe displacement Group 4 - Orbital abscess with chemosis, ophthalmoplegia, and decreased visual

acuity Group 5 - Cavernous sinus thrombosis with rapidly progressive bilateral chemosis,

ophthalmoplegia, retinal engorgement, and loss of visual acuity; possible meningeal signs and high fever

Intracranial complications

Intracranial complications may occur as a result of direct extension through the posterior frontal sinus wall or through retrograde thrombophlebitis of the ophthalmic veins. Subdural abscess is the most common intracranial complication, although cerebral abscesses and infarction that result in seizures, focal neurological deficits, and coma may occur.

Systemic complications

Sinusitis can result in sepsis and multisystem organ failure caused by seeding of the blood and various organ systems. Reports of bacteremia, thoracic empyema, and nosocomial pneumonia have been documented in the intensive-care population with acute sinusitis, and the mortality rate in this group can be as high as 11%.

Diagnostic ConsiderationsWegener granulomatosis involves angiitis associated with focal necrosis and granulomatous reaction, which initially affects the respiratory tract but which may progress to involve other organs.

Ataxia-telangiectasia is an autosomal recessive disorder associated with recurrent sinusitis, pulmonary infections, bronchiectasis, pulmonary fibrosis, tracheomegaly, diminished lymphoid tissue, and cerebral and cerebellar atrophy.

Cystic fibrosis is an autosomal recessive disorder associated with respiratory, GI, cardiovascular and sinus abnormalities, among others.

Immotile cilia syndrome is an autosomal recessive disorder associated with recurrent chest infections and/or pulmonary consolidation, sinusitis, bronchiectasis, and Kartagener syndrome.

Kartagener syndrome is an autosomal recessive disease associated with sinusitis, situs inversus, recurrent respiratory infections, and bronchiectasis, among other abnormalities.

Hyperallergic patients may have innumerable polyps filling the nasal cavity and obstructing the paranasal sinuses, giving a characteristic imaging appearance. This disease is closely associated with asthma. To see complete information on Asthma and Sinusitis, please go to the main article by clicking here.

Wiskott-Aldrich syndrome is an X-linked, recessive, immune deficiency disease associated with recurrent respiratory tract infections and/or pneumonia, sinusitis, and mastoiditis.

Yellow-nail syndrome is associated with recurrent pleural effusions, pericardial effusions, chylothorax, bronchiectasis, and sinusitis.

Young syndrome is associated with azoospermia secondary to epididymal obstruction and recurrent respiratory infections and sinusitis.

Other problems to consider include the following:

Gastroesophageal reflux Cystic fibrosis Immotile cilia syndrome Dental abscess Periapical abscess Migraine headache Sinonasal polyposis Chemical rhinitis Nasal foreign body Chronic invasive fungal sinusitis Sinonasal neoplasm Upper respiratory tract infection Primary ciliary dyskinesia Unilateral choanal atresia Adenoidal hypertrophy Foreign body Immune deficiency (immunoglobulin [Ig]A, IgG subclass)

Differential Diagnoses

Allergic and Environmental Asthma Asthma Bronchitis Haemophilus Influenzae Infections Headache, Cluster Headache, Tension Influenza Migraine Headache Moraxella Catarrhalis Infections Mucormycosis Otitis Media Parainfluenza Virus Rhinitis, Allergic Rhinocerebral Mucormycosis Rhinoviruses Sinusitis, Chronic Staphylococcal Infections

Approach ConsiderationsSome authors have reported on the use of laboratory tests, including sedimentation rate, white blood cell counts, and C-reactive protein levels, to help diagnose acute sinusitis.[32] These tests appear to add little to the predictive value of clinical findings in the diagnosis.

According to the AAAAI 2005 practice parameter, evaluation of acute, chronic, or recurrent sinusitis might include the following laboratory tests: nasal cytology, nasal-sinus biopsy, or tests for immunodeficiency, cystic fibrosis, or ciliary dysfunction.[12]

Imaging studies are not necessary when the probability of sinusitis is either high or low but may be useful when the diagnosis is in doubt, based upon a thorough history and physical examination. Plain sinus radiographs may demonstrate mucosal thickening, air-fluid levels (see the image below), and sinus opacification.

Air-fluid level (arrow) in the maxillary sinus suggests sinusitis.

Limitations of plain films include interobserver variability, inability to distinguish infection from a polyp or tumor disease, and poor depiction of the ethmoid and sphenoid sinuses.

Blood Studies

The erythrocyte sedimentation rate and C-reactive protein level may be elevated in rhinosinusitis, but these findings are nonspecific.

The findings of complete blood cell (CBC) count with differential may be within reference ranges.

Tests for ImmunodeficiencyTests for immunodeficiency are indicated if history findings indicate recurrent infection, to include the following:

Immunoglobulin studies HIV serology

Nasal CytologyNasal cytology examinations may be useful to elucidate the following entities:

Allergic rhinitis[33]

Eosinophilia Nasal polyposis Aspirin sensitivity

Sweat Chloride TestSweat chloride test screening should be performed if cystic fibrosis is suggested.

Cultures of Nasal SecretionsCultures of nasal secretions are of limited value because they are usually contaminated by normal flora. Consequently, cultures are not routinely obtained in the evaluation of acute sinusitis; however, they should be obtained in a patient in intensive care or with immunocompromise, in children not responding to appropriate medical management, and in patients with complications of sinusitis.

Because the nose is colonized with multiple nonpathogenic species of bacteria, care must be taken when evaluating culture results. A specific organism is considered pathogenic when more than 104 colony-forming units of the species are grown on culture or when polymorph counts are greater than 5000 cells/mL. Important to note is that this sample must be taken from the cavity of a paranasal sinus, not nasal secretions, cultures from which are considered useless. Obtaining cultures endoscopically is useful.

Aspiration of the sinus by direct antral puncture is the only accurate way to obtain a culture; however, this is reserved for those with life-threatening illness or an immunocompromised status or those who have disease that is unresponsive to therapy. However, in adults, if attainable, cultures directed at the middle meatus more accurately reflect the contents of the sinuses themselves, according to most studies. This may not be useful in children because the meatus is usually colonized.[34]

Computed TomographyCT scanning is the preferred imaging method for rhinosinusitis. A screening sinus CT scan is adequate for diagnosis and less expensive than other methods but is necessary only in cases of treatment failure or chronic rhinosinusitis. A complete sinus CT scan with frontal and coronal planes is used if an alternative diagnosis (eg, tumors) must be excluded. CT scanning is characteristic in allergic fungal sinusitis and is one of the major criteria for diagnosis.

The 2005 AAAAI practice parameter states that the optimal technique for evaluating the ethmoid sinuses and for preoperative evaluation of the nose and paranasal sinuses, including assessment of the ostiomeatal complex areas, is CT.[12]

CT scanning has poor specificity for the diagnosis of acute sinusitis, demonstrating sinus air-fluid levels in 87% of individuals with simple upper respiratory tract infections and 40% of asymptomatic individuals. CT scanning is the modality of choice, however, in specific circumstances such as in the evaluation of a patient in intensive care, when complications are suspected, or in the preoperative evaluation of surgical candidates.

According to the 2005 AAAAI practice parameter, CT evidence of sinusitis is associated with viral upper respiratory infections 40%-90% of the time. Symptoms of viral upper respiratory tract infections do not differ between patients with CT abnormalities and patients with no CT evidence of sinusitis, and both groups appear to self-resolve without antibiotics within 21 days. It is inappropriate to prescribe antibiotic treatment for uncomplicated viral upper respiratory tract infection. Doing so is strongly discouraged.[12]

CT scanning can provide valuable information regarding the anatomical and mechanical contributions in the development of acute sinusitis. Coronal views with bone windows are the preferred sinus study for evaluating each of the sinuses as well as the ostiomeatal complex. CT scan findings may be used to differentiate orbital cellulitis from periorbital cellulitis as a complication or to evaluate extension into intracranial space.

Delay CT scanning until antibiotics control acute exacerbation; this practice allows correct diagnosis of chronic inflammation, mucoperiosteal thickening, soft tissue swelling, and ethmoid osteitis.

Because of concerns of radiation exposure, use of limited sinus CT scanning (see the image below) is gaining wide acceptance as an alternative to a single Waters view for evaluation of pediatric chronic sinusitis.

CT cuts for a limited CT study.

See the main article Imaging in Sinusitis for more information.

RadiographyBasic radiographic examination includes 3 projections as follows:

Waters view (occipitofrontal) - Primarily useful for evaluation of maxillary and frontal sinuses

Caldwell view (angled posteroanterior) - Only view that visualizes the ethmoid air cells

Lateral view - Primarily for adenoid and/or nasopharyngeal size and sphenoid disease

Radiographic findings in patients with acute sinusitis include diffuse opacification, mucosal thickening (>4 mm), or an air fluid level. These findings, in conjunction with clinical features of acute sinusitis, are helpful in confirming the diagnosis.

When plain film radiographs are compared with the criterion standard (CT scans), however, a 75-80% disagreement occurs. This means that plain film radiography reveals disease in 40% of cases in which no disease is demonstrated on CT scanning and that plain film radiographs appear normal in 35-40% of cases in which disease is found on CT scanning.


Magnetic Resonance ImagingMRI is useful only if fungal infection or a tumor is suggested. MRI is excellent for evaluating soft tissue disease within the sinuses, but it is of little value in the diagnostic workup for acute sinusitis.

This type of imaging may be too sensitive to define soft tissue structures. MRI is not useful for detecting bone pathology. MRI is mainly used to evaluate intracranial extension and can be used as an adjunct to CT scanning in defining allergic fungal sinusitis.

To see complete information on Imaging in Sinusitis, please go to the main article by clicking here.

UltrasonographyUltrasonography is of limited use. A-mode ultrasonography may be useful in screening for fluid in the maxillary sinus. B-mode (gray scale) ultrasonography may be useful in detecting fluid in the cavity, mucosal thickening, or soft tissue mass in the maxillary sinus.


Paranasal BiopsyParanasal biopsy is used to help exclude neoplasia, fungal disease, and granulomatous disease.

Fiberoptic Sinus EndoscopyFiberoptic sinus endoscopy is used to visualize posterior sinonasal structures. This test is useful to help exclude structural lesions, fungal disease, and granulomatous diseases.

Proceed to Treatment & Management

Approach ConsiderationsThe primary goals of management of acute sinusitis are to eradicate the infection, decrease the severity and duration of symptoms, and prevent complications. These goals are achieved through the provision of adequate drainage and appropriate systemic treatment of the likely bacterial pathogens.

Drainage of the involved sinus can be achieved both medically and surgically. Aggressively treat patients in intensive care who develop acute sinusitis in order to avoid septic complications. Consider removal of nasotracheal and nasogastric tubes and promote drainage either medically or surgically.

Sinus puncture and irrigation techniques allow for a surgical means of removal of thick purulent sinus secretions. The purpose of surgical drainage is to enhance mucociliary flow and provide material for culture and sensitivity. A surgical means of sinus drainage should be used when appropriate medical therapy has failed to control the infection and prolonged or slowly resolving symptoms result or when complications of sinusitis occur.

Another indication for sinus puncture is to obtain culture material to guide antibiotic selection if empiric therapy has failed or antibiotic choice is limited. This is particularly important in patients who are immunocompromised or in intensive care. Sinusitis can be a prominent source of sepsis in these patients. In adults, sinus puncture can usually be achieved using local anesthesia; however, in children, a general anesthetic is usually necessary.

Most patients with acute sinusitis are treated in the primary care setting. Further evaluation by an otolaryngologist is recommended when any of the following exist:

When continued deterioration occurs with appropriate antibiotic therapy When episodes of sinusitis recur When symptoms persist after 2 courses of antibiotic therapy When comorbid immunodeficiency, nosocomial infection, or complications of

sinusitis are present

While in the emergency department and upon discharge, patients may obtain significant immediate relief with the administration of first-generation antihistamines, decongestants, and nonsteroidal anti-inflammatory drugs (NSAIDs).

Recommendations for nonantimicrobial therapy

Intranasal steroids have not been conclusively shown to be of benefit in cases of acute sinusitis. One meta-analysis of 4 double-blind, placebo-controlled trials of intranasal

corticosteroid treatment in acute rhinosinusitis supports its use as monotherapy or as an adjuvant therapy to antibiotics.[35] However, a recent randomized, controlled trial of antibiotics and intranasal steroid showed no treatment benefit of intranasal steroids, either alone or with antibiotics.[36]

No available data suggest that antihistamines are beneficial in acute sinusitis. In fact, antihistamines may cause harm by drying mucous membranes and decreasing clearance of secretions. Antihistamines are beneficial for reducing ostiomeatal obstruction in patients with allergies and acute sinusitis; however, they are not recommended for routine use for patients with acute sinusitis. Antihistamines may complicate drainage by thickening and pooling sinonasal secretions.

Medical drainage is achieved with topical and systemic vasoconstrictors. Oral alpha-adrenergic vasoconstrictors, including pseudoephedrine and phenylephrine, can be used for 10-14 days to allow for restoration of normal mucociliary function and drainage.

Because oral alpha-adrenergic vasoconstrictors may cause hypertension and tachycardia, they may be contraindicated in patients with cardiovascular disease. Oral alpha-adrenergic vasoconstrictors may also be contraindicated in competitive athletes because of rules of competition.

Topical vasoconstrictors (eg, oxymetazoline hydrochloride) provide good drainage, but they should be used only for a maximum of 3-5 days, given the increased risk of rebound congestion, vasodilatation, and rhinitis medicamentosa when used for longer periods.

Mucolytic agents (eg, guaifenesin, saline lavage) have the theoretical benefit of thinning mucous secretions and improving drainage. They are not, however, commonly used in clinical practice in the treatment of acute sinusitis.

Recommendations for antimicrobial therapy

Ahovuo-Saloranta et al, in a 2008 Cochrane Review meta-analysis of 57 studies, concluded that antibiotics yield a small treatment effect in a primary care setting in patients with uncomplicated sinusitis whose symptoms have lasted more than 7 days.[37] However, another meta-analysis found no treatment effect of antibiotics, even in patients whose symptoms had persisted for more than 10 days.[38]

In cases of suspected or documented bacterial sinusitis, the second principle of treatment is to provide adequate systemic treatment of the likely bacterial pathogens (ie, Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis). The physician should be aware of the probability of bacterial resistance within their community. Reports range from approximately 33-44% of H influenzae and almost all of M catarrhalis strains have beta-lactamase–mediated resistance to penicillin-based antimicrobials in children.

A study by Garbutt et al evaluated the effect of amoxicillin treatment over symptomatic treatments for adults with clinically diagnosed acute sinusitis. In a randomized, placebo-controlled trial of 166 adults with uncomplicated, acute sinusitis patients received a 10-day course of either amoxicillin (85 patients) or placebo (81 patients). On day 3 of treatment, there was no difference in improvement between placebo-takers and those prescribed antibiotics. On day 7, the antibiotic group reported a slight improvement, but that edge

disappeared by day 10, when 80% of patients in both groups reported they felt better or cured.[39]

The reduced efficacy of amoxicillin led the Infectious Diseases Society of America to generate new guidelines for the treatment of acute rhinosinusits. These guidelines recommend amoxicillin-clavulanate over amoxicillin as empiric antimicrobial therapy in adults and children with acute bacterial rhinosinusitis.[40]

Several systematic reviews have also been published on antimicrobial therapy versus placebo, with at least 5 since 2005. Pediatric studies have also examined antimicrobial treatment. Evaluating the results of meta-analyses is essential to determine the quality of the studies included in the meta-analyses. A review of many of these studies indicates 2 common methodologic flaws: (1) many patients were declared eligible for study with only 7 days of symptoms (without a qualifier regarding whether these symptoms have begun to improve) and (2) images (plain radiographs, CT scans, ultrasounds, MRIs) were often used as diagnostic entry criteria. Accordingly, good logic exists to believe that many patients enrolled in these studies had uncomplicated viral upper respiratory tract infections rather than acute bacterial rhinosinusitis, thereby diluting the results. Nonetheless, most studies do show a modest benefit with the use of antimicrobials. This benefit may possibly be substantiallymagnifiedifmoreofthestudypatients actually had acute bacterial rhinosinusitis.

As many as 64% of S pneumoniae strains are penicillin resistant because of altered penicillin-binding proteins. Multidrug-resistant S pneumoniae strains are also found in substantial numbers of children in daycare settings.[29]

Initial selection of the appropriate antibiotic therapy (see Table 1, below) should be based on the likely causative organisms given the clinical scenario and the probability of resistant strains within a community. The course of treatment is usually 14 days.

First-line therapy at most centers is usually amoxicillin or a macrolide antibiotic in patients allergic to penicillin because of the low cost, ease of administration, and low toxicity of these agents. Amoxicillin should be given at double the usual dose (80-90 mg/kg/d), especially in areas with known S pneumoniae resistance.

Table 1. Dosage, Route, and Spectrum of Activity of Commonly Used First-Line Antibiotics* (Open Table in a new window)

Antibiotic Dosage Streptococcus pneumoniae Haemophilu

s influenzae

Moraxella catarrhali

s

Anaerobic bacteria Sensitive Intermediat

eResistant

Amoxicillin 500 mg PO tid

+++ ++ + ++ + +++

(except beta-lactamase producers)

Clarithromycin 250-500 mg PO bid

++ ++ + ++ +++ +

Azithromycin 500 mg PO first day, then

250 mg/d PO for 4 days

++ ++ + ++ +++ +

*+, low activity against microorganism; ++, moderate activity against microorganism; +++, good activity against microorganism

Patients who live in communities with a high incidence of resistant organisms, those who fail to respond within 48-72 hours of commencement of therapy, and those with persistence of symptoms beyond 10-14 days should be considered for second-line antibiotic therapy (see Table 2, below).

The most commonly used second-line therapies include amoxicillin-clavulanate, second- or third-generation cephalosporins (eg, cefuroxime, cefpodoxime, cefdinir), macrolides (ie, clarithromycin), fluoroquinolones (eg, ciprofloxacin, levofloxacin, moxifloxacin), and clindamycin.

In patients with dental causes of sinusitis or those with foul-smelling discharge, anaerobic coverage using clindamycin or amoxicillin with metronidazole is necessary.

Table 2. Dosage, Route, and Spectrum of Activity of Commonly Used Second-Line Antibiotics* (Open Table in a new window)

Antibiotic Dosage Streptococcus pneumoniae Haemophilus influenzae

Moraxella catarrhalis

Anaerobic bacteria Sensitive Intermediate Resistant

Amoxicillin/

clavulanate

500 mg PO tid

+++ ++ + +++ +++ +++

Cefuroxime 250-500 mg PO bid

+++ ++ + +++ ++ ++

Cefpodoxime

+

cefixime

200 mg PO bid

400 mg/d PO

-

++

+++

-

++

-

+

+++

+++

+++

++

-

Ciprofloxacin 500-750 mg PO bid

++ + + ++ +++ +

Levofloxacin 500 mg/d PO

+++ +++ +++ +++ +++ ++

Trovafloxacin 200 mg/d PO

+++ +++ +++ +++ +++ +++

Clindamycin 300 mg PO tid

+++ +++ ++ - - +++

Metronidazole 500 mg PO tid

- - - - - +++

*+, low activity against microorganism; ++, moderate activity against microorganism; +++, good activity against microorganism; -, no activity against microorganism

Patients with nosocomial acute sinusitis require adequate intravenous coverage of gram-negative organisms (see Table 3, below). Aminoglycoside antibiotics are usually the drugs of choice for the treatment of such patients because of their excellent gram-negative coverage and sinus penetration. Selection of an antibiotic is usually based on the culture results of attained maxillary secretion.

In addition to surgical management, complications of acute sinusitis should be managed with a course of intravenous antibiotics. Third-generation cephalosporins (eg, cefotaxime, ceftriaxone) in combination with vancomycin provide adequate intracranial penetration, making them a good first-line choice.

Table 3. Dosage, Route, and Spectrum of Activity of Commonly Used Intravenous Antibiotics (Second-Line)* (Open Table in a new window)

Antibiotic Dosage Streptococcus pneumoniae

†

Haemophilus influenzae

Moraxella catarrhalis

Gram-negative

Anaerobic bacteria

Piperacillin 3-4 g IV q4-6h

+++ + - +++ +++

Piperacillin/tazobactam 3.375 g IV q6h

+++ +++ +++ +++ ++

Ticarcillin 3 g IV q4h

+++ - - +++ ++

Ticarcillin/clavulanate 3.1 g IV q4h

+++ +++ - +++ ++

Imipenem 500 mg IV q6h

+++ +++ +++ +++ +++

Meropenem 1 g IV q8h

+++ +++ +++ +++ +++

Cefuroxime 1 g IV q8h

+++ +++ +++ ++ ++

Ceftriaxone 2 g IV bid

+++ +++ +++ +++ ++

Cefotaxime 2 g IV +++ +++ +++ +++ ++

q4-6hCeftazidime 2 g IV

q8h+++ +++ +++ +++ ++

Gentamicin 1.7 mg/kg IV q8h

- +++ +++ ++ -

Tobramycin 1.7 mg/kg IV q8h

- +++ +++ ++ -

Vancomycin 1 g IV q6-12h

+++ - - - ++

*+, low activity against microorganism; ++, moderate activity against microorganism; +++, good activity against microorganism; -, no activity against microorganism †Does not take into account penicillin-resistant types.

Symptomatic TreatmentSymptomatic or adjunctive therapies may include the following:

Humidification/vaporizer Warm compresses Adequate hydration Smoking cessation Balanced nutrition Nonnarcotic analgesia

Antihistamines are not recommended and have not been proven beneficial. Topical decongestants such as oxymetazoline can be used to decrease mucosal edema. To prevent rebound congestion, they should not be used for more than 3 days.

A 15- to 21-day course of intranasal corticosteroids may reduce symptom duration when compared to placebo.[13, 41] Mometasone 200, 400, and 800 μg twice daily for 15 days is the usual regimen given, with minimal adverse effects. Systemic steroids have no proven benefit in sinusitis.

Topical ipratropium bromide 0.06% can be used to decrease rhinorrhea. Antihistamines have not been shown to be of benefit in decreasing nasal congestion; in fact, they may cause overdrying of the nasal mucosa. Mucolytics such as guaifenesin can be used to thin secretions, though they have not been definitively shown to be of benefit.

Antimicrobial TherapyAntimicrobial therapy is the mainstay of medical treatment in sinusitis. Choice of antibiotic depends on whether the sinusitis is acute, chronic, or recurrent. The AAAAI 2005 practice parameter states that choice of antibiotic should be based on predicted effectiveness, cost, and side effects.[12]

In clinically diagnosed acute sinusitis, little evidence from randomized, controlled trials supports the use of antibiotics for the treatment of acute sinusitis.[13] Antibiotics have, however, been shown to have a role in the treatment of acute maxillary sinusitis that is diagnosed radiologically or bacteriologically.

Antibiotics are indicated for sinusitis that is thought to be bacterial, including sinusitis that is severe or involves the frontal, ethmoid, or sphenoid sinuses, since this type of sinusitis is more prone to complications.[42] Penicillins, cephalosporins, and macrolides seem to be equally efficacious.[13] A 10- to 14-day regimen of amoxicillin 500 mg 3 times a day is recommended by many as first-line therapy.[43]

One study suggests that a single dose of 2 g of extended-release azithromycin may be more effective than a 10-day course of amoxicillin/clavulanate.[44] However, azithromycin is not likely a good choice in sinusitis because symptoms may improve only because of the anti-inflammatory efficacy of the agent and because it has poor efficacy against S pneumoniae and H influenzae. The risk of adverse effects should be weighed against the severity of disease and patient comorbidities prior to initiating antibiotic treatment.

Patterns of bacterial resistance should also be taken into account in the choice of antibiotic. (See Etiology.)

Overview of Surgical TherapyRecurrent or persistent sinusitis and presence of complications may require surgical therapy. Failure to respond to appropriate antibiotic therapy, especially in chronic and persistent sinusitis (eg, cystic fibrosis), is an indication for surgical intervention.

Functional endoscopic sinus surgery (FESS) has revolutionized the treatment of sinusitis in recent years. The therapeutic benefits of FESS have helped a large number of patients with chronic sinus disease.[45, 46]

See the article on Functional Endoscopic Sinus Surgery for more information.

Acute Frontal Sinusitis Surgical treatment for acute frontal sinusitis is undertaken when the infection fails to respond to conservative therapy (defined as the use of intravenous antibiotics and mucolytic agents along with topical and systemic decongestants for 3-5 days) or when dangerous complications arise. An additional indication is recurrent acute sinusitis, defined as 3-4 infections per year.

Acute Maxillary Sinusitis Several techniques have been described for drainage of the maxillary sinus. The inferior meatus and canine fossae are optimal drainage sites because of their ease of accessibility and relatively thin well-vascularized bone.

Preoperative imaging is necessary to document the presence of acute sinusitis and to guide surgical planning. Place conscious patients in the sitting position to allow for drainage of the sinus contents into a provided basin. Protect the airway and suction the oropharynx during sinus puncture performed on unconscious patients. In patients in the intensive care unit, catheterization of the sinus may be undertaken with puncture to ensure continued adequate drainage.

See the article on Acute Maxillary Sinusitis for more information.

Acute Sphenoid Sinusitis In general, start medical treatment of acute sphenoid sinusitis once the diagnosis is made. Institute antibiotics and decongestants for 24 hours, and if the patient does not improve over this time course, schedule surgical therapy. If the patient has evidence of complications, undertake urgent surgical decompression.

Some individuals advocate early and aggressive surgical and medical treatment for acute sphenoid sinusitis. Hnatuk comments on the aggressive nature of the disease and concludes that nonoperative medical management is not indicated.[47] These conclusions are based on a small number of patients, all in their teenage years.

See the article on Acute Sphenoid Sinusitis for more information.

Acute Ethmoid Sinusitis The typical case of acute ethmoidal sinusitis is treated with medical therapy. Medical treatment can reduce the inflammation and edema of the mucosa, alleviate the pain, combat the infection, open the ostia of the sinuses, and restore normal mucociliary secretions. However, surgery is indicated in the following instances:

Sinusitis not responsive to medical management Rapidly progressing sinusitis Sinusitis that creates an abscess either in the sinus or adjacent areas such as the orbit

or brain Sinusitis that compromises the survival of the patient

See the article on Acute Ethmoid Sinusitis for more information.

Complications Treatment fails in 10-25% of patients. If this occurs, consider taking a repeat history and perform an additional physical examination; consider an imaging study. Start second-line antibiotics. Approximately 75% of orbital or periorbital infections are the result of extending sinusitis. Untreated, inadequately treated, or partially treated rhinosinusitis may lead to chronic rhinosinusitis, meningitis, brain abscess, or other extra-sinus complications.

Local complications

Mucoceles are chronic epithelial cysts that develop in sinuses in the presence of either an obstructed sinus ostium or minor salivary gland duct. They have the potential for progressive concentric expansion that can lead to bony erosion and extension beyond the sinus.

Maxillary sinus mucoceles are usually found incidentally on sinus radiographs and are of little significance in the absence of symptomatology or infection. Surgical treatment is not usually necessary, and these lesions often regress spontaneously over time.

Frontoethmoidal and sphenoethmoidal mucoceles, on the other hand, tend to be symptomatic and have a high potential for bony erosion. Frontoethmoidal mucoceles should be completely removed and the sinus obliterated. Sphenoethmoid mucoceles should be widely opened into the nasal cavity.

Osteomyelitis is a potential local complication most commonly occurring with frontal sinusitis. Osteomyelitis of the frontal bone is called a Pott puffy tumor and represents a subperiosteal abscess with local edema anterior to the frontal sinus. This can advance to form a fistula to the upper lid with sequestration of necrotic bone. This rare complication should be managed with a combination of systemic antibiotics, surgical drainage of affected sinuses, and debridement of necrotic bone.

Orbital complications

Orbital complications are the most common complications encountered with acute bacterial sinusitis. Infection can spread directly through the thin bone separating the ethmoid or frontal sinuses from the orbit or by thrombophlebitis of the ethmoid veins.

Diagnosis should be based on an accurate physical examination, including ophthalmological evaluation and appropriate radiological studies. CT scanning is the most sensitive means of diagnosing an orbital abscess, although ultrasound has been found to be 90% effective for diagnosing anterior abscesses.[27] The classification by Chandler, which is based on physical examination findings, provides a reasonable framework to guide management. This classification consists of 5 groups of orbital inflammation[30] :

Group 1 - Inflammatory edema (preseptal cellulitis) with normal visual acuity and extraocular movement

Group 2 - Orbital cellulitis with diffuse orbital edema but no discrete abscess Group 3 - Subperiosteal abscess beneath the periosteum of the lamina papyracea

resulting in downward and lateral globe displacement Group 4 - Orbital abscess with chemosis, ophthalmoplegia, and decreased visual

acuity Group 5 - Cavernous sinus thrombosis with rapidly progressive bilateral chemosis,

ophthalmoplegia, retinal engorgement, and loss of visual acuity; possible meningeal signs and high fever

Medical management, including sinus drainage and intravenous antibiotics, is advocated for any degree of orbital complication. Among the classifications by Chandler, surgical drainage of both the infected sinuses and the orbit are advocated for groups 3-5 if inadequate improvement or progression of orbital cellulitis occurs despite medical therapy or if the patient has loss of visual acuity.

Intracranial complications

Intracranial complications may occur as a result of direct extension through the posterior frontal sinus wall or through retrograde thrombophlebitis of the ophthalmic veins. Subdural abscess is the most common intracranial complication, although cerebral abscesses and infarction that result in seizures, focal neurological deficits, and coma may occur. Intracranial complications of sinusitis should be managed surgically with drainage of both the affected sinus and the cranial abscess.

In a retrospective review of 23 cases (8 epidural, 10 subdural, 2 intracerebral abscess, and 3 meningitis) of intracranial complications of sinusitis (ICS) to identify the role and effectiveness of endoscopic sinus surgery (ESS) in the acute setting of ICS, DelGuadio et al concluded that ESS did not alter the need for neurosurgical intervention, which was ultimately necessary in most patients, even those with lesions less than 1 cm.[48]

In the study by DelGuadio et al, of the 23 patients, 22 (96%) had radiologic evidence of frontal sinusitis with prefrontal or frontal lobe ICS at presentation. Medical therapy alone was successful in avoiding craniotomy in only 3 of 8 cases, and treatment with endoscopic sinus surgery and intravenous antibiotics was successful in avoiding craniotomy in only 1 of 6 patients. Of 23 patients, 18 required neurosurgical procedures (9 emergent procedures for abscesses more than 1 cm and 9 delayed procedures for persistent disease despite ICS less than 1 cm).

Systemic complications

Sinusitis can result in sepsis and multisystem organ failure caused by seeding of the blood and various organ systems. Reports of bacteremia, thoracic empyema, and nosocomial pneumonia have been documented in the intensive-care population with acute sinusitis, and the mortality rate in this group can be as high as 11%.[#TreatmentConsultations]

ConsultationsEmergent otolaryngology consultation for admission and definitive care should be obtained in all patients with suspected CNS or orbital invasion or fungal infections. These patients may present with the following symptoms:

Abnormal vision Mental status changes Periorbital edema

Consider outpatient referral to an otolaryngologist for patients with subacute or chronic sinusitis. The following consultations are indicated:

Ear, nose, and throat specialist for complications or when routine management techniques fail

Infectious disease specialist in complicated cases Ophthalmological or neurosurgical consultation when either orbital or intracranial

complications develop

Surgical consultation when chronic sinusitis is refractory to maximal medical therapy or a complication such as formation of mucopyocele with orbital or intracranial extension is suspected

Medication SummaryViral rhinosinusitis does not require antimicrobial treatment. Standard nonantimicrobial treatment options include topical steroids, topical and/or oral decongestants, mucolytics, and intranasal saline spray.

Antimicrobial therapy is the mainstay of medical treatment in sinusitis. The choice of antibiotics depends on whether the sinusitis is acute, chronic, or recurrent.

Antibiotic efficacy rates are as follows[49] :

Levofloxacin, moxifloxacin, and amoxicillin/clavulanate - Greater than 90% High-dose amoxicillin, cefpodoxime proxetil, cefixime, cefuroxime axetil, and

trimethoprim-sulfamethoxazole - 80-90% Clindamycin, doxycycline, cefprozil, azithromycin, clarithromycin, and erythromycin

- 70-80% Cefaclor - 50-60%

On the basis of the 2000 Sinus and Allergy Health Partnership treatment guidelines for acute bacterial rhinosinusitis, patients are divided into 3 groups, as follows:

Adults with mild disease who have not received antibiotics: Amoxicillin/clavulanate, amoxicillin (1.5-3.5 g/d), cefpodoxime proxetil, or cefuroxime is recommended as initial therapy.

Adults with mild disease who have had antibiotics in the previous 4-6 weeks and adults with moderate disease: Amoxicillin/clavulanate, amoxicillin (3-3.5 g), cefpodoxime proxetil, or cefixime is recommended.

Adults with moderate disease who have received antibiotics in the previous 4-6 weeks: Amoxicillin/clavulanate, levofloxacin, moxifloxacin, or doxycycline is recommended.

Patients who remain symptomatic despite appropriate antibiotic therapy may be evaluated with sinus endoscopy, CT scanning, or sinus aspiration/culture.

Penicillins

Class Summary

The penicillins are bactericidal antibiotics that work against sensitive organisms at adequate concentrations and inhibit the biosynthesis of cell wall mucopeptide. The penicillins are also available in combination with agents that inactivate beta-lactamase enzymes, extending their antibiotic spectrum.

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Piperacillin and Tazobactam sodium (Zosyn)

The piperacillin-tazobactam combination includes an antipseudomonal penicillin plus beta-lactamase inhibitor. It inhibits biosynthesis of cell wall mucopeptide and is effective during the stage of active multiplication.


Ticarcillin and clavulanate potassium (Ticar)

The ticarcillin-clavulanate combination inhibits the biosynthesis of cell wall mucopeptide and is effective during the stage of active growth. It has antipseudomonal penicillin plus a beta-lactamase inhibitor that provides coverage against most gram-positive, gram-negative, and anaerobic organisms.


Penicillin VK (Beepen-VK, Pen-Vee K)

Penicillin V is a first-line antibiotic choice. It inhibits biosynthesis of cell wall mucopeptide. It is bactericidal against sensitive organisms when adequate concentrations are reached and most effective during the stage of active multiplication. Inadequate concentrations may produce only bacteriostatic effects.


Amoxicillin and clavulanate (Augmentin)

Amoxicillin-clavulanate is a second-line agent; this drug combination treats bacteria resistant to beta-lactam antibiotics.


Amoxicillin (Amoxil, Trimox)

Amoxicillin is a first-line antibiotic choice. It interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.


Piperacillin

Piperacillin inhibits the biosynthesis of cell wall mucopeptides and the stage of active multiplication; it has antipseudomonal activity.

Cephalosporins

Class Summary

Cephalosporins are structurally and pharmacologically related to penicillins. They inhibit bacterial cell wall synthesis, resulting in bactericidal activity. Cephalosporins are divided into first, second, third and fourth generation. First-generation cephalosporins have greater activity against gram-positive bacteria, and succeeding generations have increased activity against gram-negative bacteria and decreased activity against gram-positive bacteria.


Cefprozil (Cefzil)

Cefprozil is a second-line agent. It binds to one or more of the penicillin-binding proteins, which, in turn, inhibits cell wall synthesis and results in bactericidal activity.


Cefuroxime (Ceftin)

Cefuroxime is a second-line agent. It is a second-generation cephalosporin that maintains the gram-positive activity of first-generation cephalosporins, adding activity against Proteus mirabilis, H influenzae, Escherichia coli, Klebsiella pneumoniae, and M catarrhalis.


Cefpodoxime (Vantin)

Cefpodoxime is a second-line agent. It binds to one or more penicillin-binding proteins, which, in turn, inhibits cell wall synthesis and results in bactericidal activity.


Cefixime (Suprax)

Cefprozil is a second-line agent. By binding to one or more penicillin-binding proteins, it arrests bacterial cell wall synthesis and inhibits bacterial growth.


Ceftriaxone (Rocephin)

Ceftriaxone is a third-generation cephalosporin with broad-spectrum, gram-negative activity; it has lower efficacy against gram-positive organisms and higher efficacy against resistant organisms. It arrests bacterial growth by binding to one or more penicillin binding proteins. It has good penetration.


Cefdinir (Omnicef)

Classified as a third-generation cephalosporin, cefdinir inhibits mucopeptide synthesis in the bacterial cell wall. It is typically bactericidal, depending on organism susceptibility, dose, and serum or tissue concentrations.


Cefaclor (Ceclor, Ceclor CD)

Cefaclor is used for treatment of infections caused by susceptible organisms including H influenzae and for treatment of otitis media, sinusitis, and infections involving the respiratory tract. It may not be appropriate in acute sinusitis, owing to less activity and the potential for severe allergic reactions.


Cefotaxime (Claforan)

Cefotaxime is a third-generation cephalosporin with broad gram-negative spectrum, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms. It arrests bacterial cell wall synthesis by binding to one or more of the penicillin-binding proteins, which, in turn, inhibits bacterial growth.


Ceftazidime (Fortaz, Tazicef)

Ceftazidime is a third-generation cephalosporin with broad-spectrum, gram-negative activity, including pseudomonas; lower efficacy against gram-positive organisms; and higher efficacy against resistant organisms. It arrests bacterial growth by binding to one or more penicillin-binding proteins, which, in turn, inhibits the final transpeptidation step of peptidoglycan synthesis in bacterial cell wall synthesis, thus inhibiting cell wall biosynthesis.

Macrolides

Class Summary

Macrolide antibiotics have bacteriostatic activity and exert their antibacterial action by binding to the 50S ribosomal subunit of susceptible organisms, resulting in inhibition of protein synthesis. Macrolide antibiotics are often used in patients allergic to penicillins.


Erythromycin (E.E.S., E-Mycin, Eryc)

Erythromycin is a first-line treatment in patients allergic to penicillin. It inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.


Clarithromycin (Biaxin)

Clarithromycin is a second-line agent. It inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.


Azithromycin (Zithromax, Zmax)

Azithromycin, an advanced-generation macrolide, works similarly to clarithromycin but with shorter dosage time.


Erythromycin and sulfisoxazole (Eryzole, Pediazole)

This agent is used for treatment of susceptible bacterial infections of upper and lower respiratory tract: in children, it is used for otitis media caused by susceptible strains of H influenzae; it is used for many other infections in patients allergic to penicillin.

Fluoroquinolones

Class Summary

Fluoroquinolones have broad-spectrum activity against gram-positive and gram-negative aerobic organisms. They inhibit DNA synthesis and growth by inhibiting DNA gyrase and topoisomerase, which is required for replication, transcription, and translation of genetic material.


Levofloxacin (Levaquin)

Levofloxacin is used to treat acute maxillary sinusitis caused by S pneumoniae, H influenzae, or M catarrhalis. Fluoroquinolones should be used empirically in patients likely to develop exacerbation due to resistant organisms to other antibiotics. This is the L stereoisomer of the D/L parent compound ofloxacin, the D form being inactive. It provides good monotherapy with extended coverage against Pseudomonas species, as well as excellent activity against pneumococcus. The agent acts by inhibition of DNA gyrase activity. The oral form has bioavailability that is reportedly 99%.


Ciprofloxacin (Cipro)

Ciprofloxacin is a broad spectrum antibiotic with activity against gram-positive and gram-negative aerobic organisms. It inhibits bacterial DNA synthesis and, consequently, growth, by inhibiting DNA gyrase and topoisomerase, which are required for replication, transcription, and translation of genetic material.


Moxifloxacin (Avelox)

Moxifloxacin inhibits the A subunits of DNA gyrase, resulting in inhibition of bacterial DNA replication and transcription.

Anti-Infectives

Class Summary

Anti-infectives such as vancomycin, clindamycin, metronidazole, and sulfamethoxazole-trimethoprim are effective against some types of bacteria that have become resistant to other antibiotics.


Trimethoprim and sulfamethoxazole (Bactrim DS, Septra)

Trimethoprim-sulfamethoxazole is a first-line agent with more convenient dosing. It inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid.


Vancomycin (Vancocin, Lyphocin, Vancoled)

Vancomycin is a potent antibiotic directed against gram-positive organisms and active against Enterococcus species (useful in septicemia and skin structure infections; Enterococcus is very rare in sinusitis). Vancomycin is indicated for patients who cannot receive or have failed to respond to penicillins and cephalosporins or who have infections with resistant staphylococci.


Metronidazole

Metronidazole is an imidazole ring-based antibiotic that is active against various anaerobic bacteria and protozoa. It is used in combination with other antimicrobial agents (except C difficile enterocolitis).


Clindamycin

Clindamycin is a semisynthetic antibiotic produced by 7(S)-chloro-substitution of 7(R)-hydroxyl group of parent compound lincomycin. It inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Clindamycin widely distributes in the body without penetration of the CNS. It is protein bound and is excreted by the liver and kidneys.

Carbapenems

Class Summary

Carbapenems are structurally related to penicillins and have broad-spectrum bactericidal activity. The carbapenems exert their effect by inhibiting cell wall synthesis, which leads to cell death. They are active against gram-negative, gram-positive, and anaerobic organisms.


Imipenem and cilastatin (Primaxin)

The imipenem-cilastin combination is used for the treatment of multiple-organism infections in which other agents do not have wide-spectrum coverage or are contraindicated because of the potential for toxicity.


Meropenem (Merrem IV)

A bactericidal broad-spectrum carbapenem antibiotic that inhibits cell-wall synthesis, meropenem is effective against most gram-positive and gram-negative bacteria. Compared with imipenem, meropenem has slightly increased activity against gram-negative organisms and slightly decreased activity against staphylococci and streptococci.

Aminoglycosides

Class Summary

Aminoglycosides are bactericidal antibiotics used to primarily treat gram-negative infections. They interfere with bacterial protein synthesis by binding to 30S and 50S ribosomal subunits.


Gentamicin (Gentacidin, Garamycin)

Gentamicin is an aminoglycoside antibiotic effective against Pseudomonas aeruginosa; E coli; and Proteus, Klebsiella, and Staphylococcus species. Gentamicin is also variably effective against some strains of certain gram-positive organisms, including S aureus, enterococci, and L monocytogenes. Dosing regimens are numerous; adjust the dose based on creatinine clearance and changes in volume of distribution.


Tobramycin (Nebcin)

Tobramycin is used in skin, bone, and skin structure infections caused by S aureus, P aeruginosa, Proteus species, E coli, Klebsiella species, and Enterobacter species. It is indicated in the treatment of staphylococcal infections when penicillin or potentially less-toxic drugs are contraindicated and when bacterial susceptibility and clinical judgment justify its use. Like other aminoglycosides, tobramycin is associated with nephrotoxicity and ototoxicity.

Tetracyclines

Class Summary

Tetracyclines inhibit protein synthesis and, thus, bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria. They may block dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.


Doxycycline (Periostat, Doryx, Bio-Tab, Vibramycin Vibra-tabs)

Doxycycline is has broad-spectrum activity and is a synthetically derived bacteriostatic antibiotic in the tetracycline class. Doxycycline inhibits protein synthesis, and thus bacterial growth, by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria.

Decongestants

Class Summary

These agents cause vasoconstriction, which reduces nasal congestion. Topical agents are locally active vasoconstrictor agents such as phenylephrine and oxymetazoline, which provide immediate symptomatic relief by shrinking the inflamed and swollen nasal mucosa. Oral decongestants such as pseudoephedrine can be used for 10-14 days to allow for restoration of normal mucociliary function and drainage.


Phenylephrine nasal (Neo-Synephrine)

Phenylephrine produces vasoconstriction. It is possibly helpful and is not harmful.


Oxymetazoline (Afrin)

Oxymetazoline is applied directly to mucous membranes. It stimulates alpha-adrenergic receptors and causes vasoconstriction. Decongestion occurs without drastic changes in blood pressure, vascular redistribution, or cardiac stimulation.


Tetrahydrozoline, ophthalmic (Tyzine, Visine)

The alpha-adrenergic effects of tetrahydrozoline on nasal mucosa produce vasoconstriction.


Pseudoephedrine (Sudafed)

Phenylephrine produces vasoconstriction. It is possibly helpful and is not harmful.

Nasal Sprays

Class Summary

Nasal saline spray and steam inhalation help by moistening dry secretions, reducing mucosal edema, and reducing mucus viscosity. The symptomatic relief gained in some patients can be substantial; moreover, these are benign modalities of therapy.

Saline nasal spray (Ayr, Ocean)

Saline nasal sprays loosen mucus secretions to help remove mucus from the nose and sinuses.

Expectorants

Class Summary

Mucolytic agents such as guaifenesin have the theoretical benefit of thinning mucous secretions and improving drainage.


Guaifenesin (Anti-Tuss, Humibid LA, Robitussin)

Guaifenesin increases respiratory tract fluid secretions and helps to loosen phlegm and bronchial secretions. It is indicated for patients with bronchiectasis complicated by tenacious mucous and/or mucous plugs.

Corticosteroids

Class Summary

Intranasal steroids have not been conclusively shown to be of benefit in cases of acute sinusitis. Study results conflict, with some reporting benefit as monotherapy or in combination with antibiotics and others reporting no benefit (combination or monotherapy).

Beclomethasone (Beconase, Vancenase)

Beclomethasone has potent vasoconstrictive and anti-inflammatory activity. It has a weak hypothalamic-pituitary-adrenocortical (HPA) axis inhibitory potency when applied topically.


Triamcinolone inhaled (Nasacort, Nasacort AQ)

Triamcinolone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.


Flunisolide (AeroBid, Nasalide)

Flunisolide inhibits bronchoconstriction mechanisms, producing direct smooth muscle relaxation. It may decrease the number and activity of inflammatory cells, in turn decreasing airway hyperresponsiveness. Flunisolide decreases inflammation by suppressing migration of

polymorphonuclear leukocytes and reversing capillary permeability. It does not depress the hypothalamus.

Anticholinergics

Class Summary

Anticholinergics block interactions between acetylcholine and muscarinic receptors on the smooth muscle preventing increases in cyclic GMP inhibiting bronchoconstriction and mucus secretion.


Ipratropium (Atrovent, Atrovent HFA)

Topical ipratropium bromide can be used to decrease rhinorrhea. Anticholinergics such as ipratropium have anti-secretory properties, and when applied locally, inhibit secretions from serous, and seromucous glands lining the nasal mucosa.

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