eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > Nasal & Sinus Diseases

Sinusitis, Maxillary, Acute, Surgical Treatment

Author: Steven E Sobol, MD, FRCSC, MSc, FAAP, Assistant Professor, Director of Pediatric Otolaryngology, Department of Otolaryngology Head and Neck Surgery, Emory University School of Medicine; Otolaryngologist-In-Chief, Children's Healthcare of Atlanta at Egleston
Coauthor(s): Melvin D Schloss, MD, FRCSC, Director of Pediatric Otolaryngology, Professor, Department of Otolaryngology, McGill University, Canada; Ted L Tewfik, MD, FRCS(C), Professor, Department of Otolaryngology, Director of Continuing Medical Education of Otolaryngology, McGill University Medical School; Director, Director of Professional Affairs of Otolaryngology, Department of Otolaryngology, Montreal Children's Hospital; Senior Staff, Montreal General Hospital and Royal Victoria Hospital
Contributor Information and Disclosures

Updated: Jul 14, 2009

Introduction

Development of the paranasal sinuses begins in the third week of gestation and continues until early adulthood. Knowledge of developmental milestones is important for the clinician to properly diagnose and treat infectious disorders of the paranasal sinuses.

During the third week of embryonic development, the notochord is formed by the proliferation and medial migration of ectodermal cells. The notochord, which is initially in the caudal region of the embryonic disc, rotates to lie posterior to the primitive foregut after the heart tube and pericardium rotate from the cranial position to lie anteriorly. The paraxial layer of mesenchyme, which lies adjacent to the notochord, differentiates into the somite ridges, intermediate cell mass, and lateral plate mesoderm. The branchial arches develop from these mesodermal structures, the first of which gives rise to the 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 is the precursor of the middle and inferior meatus and the inferior turbinate. Ethmoidoturbinate folds develop superiorly to give rise to the middle and superior turbinates. Once turbinate structures are established, sinus development begins and continues until early adulthood.

The maxillary sinus begins developing in the third month of gestation. It arises as an ectodermal invagination in the middle meatal groove and develops laterally, measuring 7 X 4 X 4 mm at birth. After birth, it continues to grow at a rate of 2 mm vertically and 3 mm anteroposteriorly until early adulthood. The sinus grows rapidly for the first 3 years of life and then grows at a slower rate until age 7 years. A second rapid growth phase takes place from age 7-12 years; growth then slows until early adulthood, when the sinus has reached its final adult proportions. The floor of the sinus is level with the floor of the nose at age 12 years and then descends inferiorly into the alveolus as adult teeth begin to erupt. Articles that detail surgical management of the nose, ethmoid sinuses, frontal sinus, and sphenoid sinuses address development of these structures.

Problem

Many classifications, both clinical and radiologic, have been proposed throughout the literature to define acute sinusitis. Although no consensus on the precise definition exists, acute sinusitis may be defined as a bacterial or viral infection of the sinuses of less than 4 weeks' duration that completely resolves with appropriate treatment. 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. 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, and is discussed in the eMedicine article Sinusitis, Chronic, Medical Treatment.

Frequency

Sinusitis affects 1 out of every 7 adults in the United States, with over 30 million individuals diagnosed each year. Acute bacterial sinusitis is the fifth most common diagnosis prompting antibiotic administration and accounts for 0.4% of ambulatory diagnoses. The economic burden of acute sinusitis in children is 1.77 billion dollars per year.

Etiology

The sinuses are normally sterile under physiologic conditions. Purulent sinusitis can occur when ciliary clearance of sinus secretions decreases or 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, and viral insults, which produce inflammation of the nasal and sinus mucosa and result in ciliary dysmotility and sinus obstruction. Approximately 90% of patients who have viral upper respiratory tract infections (URTIs) have sinus involvement, but only 5-10% of these patients have bacterial superinfection requiring antimicrobial treatment.

Microbiology

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 bacterial pathogens in acute sinusitis are Streptococcus pneumoniae (30-40%), Haemophilus influenzae (20-30 %), and Moraxella catarrhalis (12-20%). Staphylococcus aureus and Streptococcus pyogenes are isolated in rare cases.

Cultures from 66% of patients with acute sinusitis grow at least one pathogenic bacterial species from sinus aspirates while 26-30% of cases have multiple predominant bacterial species. Anaerobic organisms have been found in fewer than 10% of patients with acute bacterial sinusitis despite the ample environment available for their growth. The exception is in sinusitis resulting from a dental source or in patients with chronic sinus disease in which anaerobic organisms are usually isolated.

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 include gram-positive organisms (31%) and fungi (8.5%).

Viruses are the most common triggers of acute sinusitis. Rhinovirus, influenza viruses, and parainfluenza viruses are the primary pathogens in 3-15% of cases of acute sinusitis.

Fungal causes of sinusitis are discussed elsewhere (see Allergic Fungal Sinusitis; Sinusitis, Fungal).

Pathophysiology

Anatomic 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. Mechanical obstruction of the ostiomeatal complex from foreign bodies, polyps, or tumors also can result in acute sinus disease. Systemic diseases that result in decreased mucociliary clearance, including cystic fibrosis and Kartagener syndrome, can be predisposing factors for acute sinusitis in rare cases. Patients with deficiencies in their humoral immune system (eg, agammaglobulinemia, combined variable deficiency, immunoglobulin G [IgG] deficiency, immunoglobulin A [IgA] deficiency) are also at increased risk of developing acute sinusitis.

Nosocomial sinusitis occurs in 18-32% of patients who require prolonged periods of intensive care with nasogastric or nasotracheal intubation. Nasotracheal intubation is the greatest risk factor, although patients with prolonged orotracheal intubation are at greater risk than the general population.

Ciliary function also is reduced in the presence of low pH, anoxia, bacterial toxins, smoking, dehydration, foreign bodies, and drugs such as atropine, antihistamines, and phenylephedrine. 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, as can facial trauma or large inoculations from swimming.

Presentation

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 URTIs. No specific clinical symptom or sign is sensitive or specific for acute sinusitis, and the overall clinical impression should be used to guide management.

A recent 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.¹ The panel suggests that the diagnosis of acute bacterial sinusitis be entertained when (a) symptoms or signs of acute rhinosinusitis are present 10 days or more beyond the onset of upper respiratory symptoms or (b) symptoms or signs of acute rhinosinusitis worsen within 10 days after an initial improvement. In the intensive care setting, acute sinusitis should be suspected in the presence of sepsis of unknown origin.

The diagnosis of acute sinusitis can be difficult to make on clinical grounds because of the similarity of presenting symptoms to those of uncomplicated URTIs. In a primary care setting, diagnosis of acute sinusitis usually is based on the constellation of clinical findings and may be overdiagnosed because of the poor predictive value of history and physical examination findings. A history of purulent secretions, dental pain, poor response to decongestants, or examination findings of colored nasal discharge or abnormal sinus transillumination suggests a diagnosis of acute sinusitis. The presence of 4 or more of these clinical findings greatly increases the probability that the patient has sinusitis.

Anterior 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. Documentation of predisposing anatomic variations also can be performed during anterior rhinoscopy. Sinus transillumination and palpation are of little predictive value.

Endoscopic examination may reveal the origin of the purulent discharge from the middle meatus and may provide information about the nature of ostiomeatal obstruction. Endoscopy also may aid in the etiologic diagnosis of acute sinusitis by allowing careful attainment of purulent secretions from the sinus ostia for culture.

Indications

Use a surgical means of sinus drainage when appropriate medical therapy has failed to control the infection, resulting in prolonged or slowly resolving symptoms, or when the patient has complications of sinusitis. Another indication for sinus puncture is to provide culture material to guide antibiotic selection when empiric therapy has failed or when antibiotic choice is limited. This is particularly important in patients who are immunocompromised or under intensive care, in whom sinusitis can be a prominent source of sepsis.

Relevant Anatomy

The paranasal sinuses are air-filled bony cavities extending from the skull base to the alveolar process and laterally from the nasal cavity to the inferomedial aspect of the orbit and the zygoma. They are lined with a pseudostratified columnar epithelium, which is continuous with the lining of the nasal cavity via the ostia. This epithelium contains a number of mucus-producing goblet cells. Branches of the internal and external carotid arteries provide arterial supply to the sinuses, while the venous and lymphatic drainage is through the sinus ostia into the nasal cavity plexi. Venous drainage occurs through valveless vessels corresponding to the arterial supply.

The focal point of sinus drainage is the ostiomeatal complex, which comprises the maxillary, frontal, and anterior ethmoid ostia and is located in the middle meatus. The posterior ethmoid sinuses empty into the superior meatus, and the sphenoid sinuses empty into the sphenoethmoidal recess.

The exact function of the paranasal sinuses is not well understood. Possible roles of the sinuses may involve reducing the weight of the skull, pressure dampening, humidifying and warming inspired air, absorption and heat insulation of the brain, resonance of sound, mechanical rigidity, or increasing olfactory surface area.

The sinus mucosa has less secretory and vasomotor function than the nasal cavity. Cilia are concentrated near the natural sinus ostia and beat toward them. Ostium blockage results in stasis of mucus flow, which can result in development of disease.

The maxillary sinus is a pyramidal cavity, the base of which lies lateral to the nasal cavity. In adults, the dimensions of the sinus are approximately 33 mm in height, 23-25 mm in width, and 34 mm in the anteroposterior axis; the volume is approximately 15 mL. Maxillary sinus size may be asymmetrical within the same individual.

Medial wall

The medial wall of the sinus is composed of a thin plate of maxilla, the inferior turbinate, the uncinate process, the perpendicular plate of the palatine bone, and the lacrimal bone. The ostium is a large opening in the posteromedial aspect of the sinus that is partially covered by the above-mentioned bony structures and by a reduplication of mucosa inferior to the uncinate process. This leaves an opening into the infundibulum of the middle meatus that measures 3-4 mm. The natural ostium usually is found in the posterior third of the infundibulum; 25-30% of individuals have accessory ostia.

Lateral wall

The lateral apex of the sinus extends into the zygomatic process of the maxillary bone or into the zygoma.

Superior wall

The roof of the sinus slopes inferiorly as it passes from base to apex along the floor of the orbit. This orbital surface of the sinus is approximately twice as wide as the floor. The infraorbital nerve forms a groove in the roof of the sinus as it passes anteriorly.

Inferior wall

The floor of the sinus is formed by the alveolar and palatine processes of the maxilla and lies 1-1.2 cm below the level of the floor of the nose in dentulous adults. The maxillary sinus most often is related to the 3 molar teeth. A layer of compact bone usually separates the tooth cavity from the sinus mucosa. This layer of bone may be thin or absent in some individuals, leaving a direct route for dental infections to spread into the sinus. The premolar and canine teeth are not usually a direct relation of the sinus.

Anterior and posterior walls

The anterior and posterior walls of the maxillary sinus are formed by the corresponding surfaces of the maxilla and are directly related to the cheek skin anteriorly and to the infratemporal fossa posteriorly.

Blood supply

The maxillary sinus derives its arterial blood supply from the infraorbital, greater palatine, sphenopalatine, and posterior and anterior superior alveolar branches of the maxillary artery, which penetrate the bone of the sinus. The facial artery gives a smaller contribution to the maxillary sinus blood supply.

Venous drainage of the sinus is to the internal jugular via the maxillary and anterior facial veins and to the pterygoid plexus through contributions from the maxillary vein. The pterygoid plexus communicates with the dural sinuses, providing a root for the spread of sinus infections intracranially. Lymphatic drainage is to the submandibular lymph nodes.

Nerve supply

Sensory innervation of the maxillary sinus is by the infraorbital nerve, posterolateral nasal nerve, and the anterior, middle, and posterior superior alveolar branches of the second division of the trigeminal nerve. Secretomotor innervation of the sinus mucosa is from the intermediate nucleus of the facial nerve through postsynaptic parasympathetic branches of the pterygopalatine ganglion.

Anatomies of the nose, ethmoid sinuses, sphenoid sinuses, and frontal sinus are discussed in articles detailing their surgical management.

Contraindications

No absolute contraindications to maxillary sinus drainage exist; however, prudent evaluation is necessary in patients at high risk of bleeding (eg, low platelet count) or with anatomical variations that increase the risk of injury to adjacent structures (eg, hypoplastic maxillary sinus).

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