Introduction:
Acute frontal sinusitis is defined as inflammation of mucosal lining of frontal sinus and it’s out flow tract of less than 3 weeks duration. The incidence of acute frontal sinusitis is considerably lower when compared with that of maxillary sinusitis in adults and ethmoidal sinusitis in children. Early diagnosis and management of acute frontal sinusitis will go a long way in preventing development of complications.
Incidence:
Acute sinusitis commonly affects 20% of population. Acute frontal sinusitis affects about 4% of these individuals. Acute frontal sinusitis commonly affects adolescent males and young men. The age predilection is due to the fact that frontal sinuses become vascular and enlarge rapidly during 7 – 15 years of life. Male predilection largely remains unexplained.
Etiopathogenesis:
Acute frontal sinusitis is commonly preceded by viral infections of upper respiratory tract. Rhino virus has been commonly implicated. Other viruses like corona virus, respiratory syncitial virus and Para influenza viruses have been implicated. Viral infections up regulate inflammatory cytokines like IL6, IL8, Tumor necrosis factor ά, histamine and bradykinin. These viruses are also known to suppress neutrophils, macrophages and lymphocytic functions inhibiting immune response. The induction of inflammatory cascade causes mucosal oedema, occlusion of sinus Ostia, impairing mucociliary clearance mechanism. This causes stasis of secretions within the frontal sinus. Mucus stasis forms a nidus within the sinus for super added bacterial infections.
Host risk factors involved in the pathogenesis of acute frontal sinusitis:
These factors which predispose to acute frontal sinusitis include
A series of accessory ethmoidal cells line the frontal sinus outflow tract. These cells receive various names according to their position in relation to the sinus outflow tract. These cells include:
1. The agger nasi cell
2. Frontal intersinus septal cells
3. Suprabullar cells
4. Frontal / infundibular cells
Bent and Khun classified frontal infundibular cells based on their proximity to agger nasi cell.
A – Agger nasi cell
I – Type I frontal cell (a single air cell above agger nasi)
II – Type II frontal cell (a series of air cells above agger nasi but below the orbital roof)
III – Type III frontal cell (this cell extends into the frontal sinus but is contiguous with agger nasi cell)
IV – Type IV frontal cell lies completely within the frontal sinus
Diagnosis:
Acute frontal sinusitis is a clinical diagnosis depending on the duration of symptoms, i.e. lasting for less than 4 weeks. CT scans may show false positive results.
Major diagnostic criteria include:
Unless complications are suspected imaging is not a must in the diagnosis of acute frontal sinusitis.
Microbiology: Organisms causing acute infections of frontal sinus include S. Pneumoniae, H. Influenza, and Moraxella Catarrhalis.
Aims of treatment:
Antibiotics chosen should be able to manage the infecting spectrum of organism.
Complications of acute frontal sinusitis:
Should be suspected in patients with:
Meningitis is one of the important intracranial complications of acute frontal sinusitis. Signs and symptoms of meningitis include:
Osteomyelitis is one of the complications of acute frontal sinusitis. This is caused by direct extension of infection or by thrombophlebitis involving the diploic veins. In patients with osteomyelitis of anterior table of frontal bone may lead to formation of subperiosteal abscess which present as swelling over the forehead. This is also known as the “Pott’s puffy tumor”.
Cavernous sinus thrombosis is a complication of acute frontal sinusitis. Thrombophlebitis involves the diploic veins which are valveless. The infection spreads to cavernous sinus causing thrombophlebitis. Patients with cavernous sinus thrombosis present with ophthalmoplegia, proptosis, visual loss, trigeminal nerve deficits.
Surgery is indicated in recalcitrant cases. It includes frontal sinus trephening and endoscopic decompression.