Spinal Care, Neurology, Spinal Medical Advice and Information.

Intracranial Complications of Acute Sinusitis


RATIONAL: Although the incidence of suppurative intracranial complications in patients with sinusitis is unknown, paranasal sinusitis is the source of 35- 65% of subdural empyemas.

Intracranial extension of infection is the second most common complication of acute sinusitis. Infection may enter the intracranial compartment by two routes. Direct extension may occur through necrotic areas of osteomyelitis in the posterior wall of the frontal sinus or roof of the sphenoid sinus. The underlying dura becomes thickened with inflammatory exudate, and a heavy layer of granulation tissue develops. Bacterial penetration may take place along the course of the small vessels that traverse the dura. This results in a subdural empyema.

This direct route of intracranial extension is more commonly associated with chronic otitis rather than sinusitis. An alternative route of intracranial bacterial entry is provided by the valveless venous network which interconnects the intracranial venous system and the vasculature of the sinus mucosa. Thrombophlebitis originating in the mucosal veins progressively involves the emissary veins of the skull, the dural venous sinuses, the subdural veins, and finally the cerebral veins. By this mode of spread, there may be no involvement of intermediary structures and therefore may be no evidence of extradural pus or osteomyelitis. Further intracranial spread of infection depends on the competence of the arachnoid as a barrier to bacterial invasion.

Although subarachnoid infection secondary to subdural empyema is uncommon in young children, extensive cortical thrombophlebitis is a frequent complication. The involved gyri are edematous and hyperemic, often showing small foci of infarction. Sometimes septic thrombosis of a major dural sinus occurs, resulting in massive bilateral cerebral edema and hemorrhagic infarction. This is often accompanied by the appearance of seizures, focal neurologic deficits, and increased intracranial pressure.

About 50% of patients with subdural empyema secondary to sinusitis present with signs and symptoms of acute frontal sinusitis or an acute exacerbation of a chronic pansinusitis. There is usually low grade fever, malaise, frontal headache, often accompanied by marked forehead tenderness. The initial headache worsens despite prolonged treatment with analgesics and oral antibiotics. Vomiting may become intractable and the level of consciousness deteriorates gradually. There is frequently evidence of meningeal irritation including nuchal rigidity and photophobia. Focal neurologic deficits may develop including isolated weakness, contralateral conjugate gaze palsy, and expressive dysphasia. Focal seizures are not uncommon. In more severe cases signs of increased intracranial pressure may be evident.

CT scanning is the most efficient diagnostic method. Lumbar puncture usually reveals CSF pleocytosis and abnormalities of CSF glucose and protein. Both EEG and radionuclide brain scans are too nonspecific to have any true diagnostic value. The most common organisms isolated from subdural empyemas include staph aureus, strep pneumonia, and anaerobes.

Treatment mandates the surgical drainage of the paranasal sinuses and any intracranial abscesses. Antibiotics should be chosen to cover the most common organisms. Most authors recommend an initial antibiotic regimen including a combination of penicillin G, a penicillinase- resistant penicillin, and chloramphenicol. Despite modern diagnostic and surgical capabilities, the mortality associated with subdural empyema and brain abscesses remains over 25%.

Other complications associated with sinusitis include orbital cellulitis, orbital abscess, subperiosteal abscess, and cavernous sinus thrombosis.