disease | Post-traumatic Intracranial Pneumatosis |
alias | Traumatic Pneumocephalus, Post-traumatic Pneumocephalus |
Post-traumatic intracranial pneumatosis, also known as traumatic pneumocephalus, has an incidence rate of approximately 9.7% in cases of craniocerebral injury.
bubble_chart Etiology
This condition is almost always caused by skull base fractures involving the paranasal sinuses or mastoid air cells, often accompanied by cerebrospinal fluid fistula disease. After air enters the intracranial space through the fracture line, it can accumulate in the epidural space, subdural space, subarachnoid space, within the brain, or inside the ventricles, usually unilaterally, though bilateral pneumocephalus may occur in rare cases. The most common site is the anterior fossa ethmoid fracture, leading to frontal subdural pneumocephalus or localized intracerebral pneumatocele, followed by fractures of the posterior ethmoid or sphenoid sinuses. The mechanism of air entry is related to a sudden increase in gas pressure within the damaged sinus cavity, such as during nose blowing, coughing, or sneezing, which can force air into the intracranial space. However, in some cases, it may also result from excessively low intracranial pressure due to hydrodynamic effects when the patient changes position, drawing air into the skull. Additionally, in open head injuries or penetrating gunshot wounds, air can be directly introduced into the intracranial space, forming subdural, intracerebral, or intraventricular pneumocephalus.
bubble_chart Clinical Manifestations
Usually, a small amount of intracranial air does not present with signs of increased intracranial pressure clinically, and the main symptoms are only irritative manifestations such as nausea, vomiting, headache, and sweating. If accompanied by cerebrospinal fluid fistula disease and intracranial infection, symptoms of meningeal inflammation may occur. Sometimes, the hole causing pneumocephalus has a one-way valve characteristic, leading to continuous accumulation of intracranial air and resulting in tension pneumocephalus. Clinically, this manifests as increased intracranial pressure and brain compression, and in severe cases, it can cause brain herniation.
bubble_chart DiagnosisEarly pneumocephalus is prone to misdiagnosis. Diagnosis mainly relies on X-ray or CT scans, which reveal intracranial air accumulation. Small amounts of gas are often scattered in the subarachnoid space of the frontal and temporal regions, while larger accumulations typically occur in the frontal, temporal, and parietal areas, particularly the frontal region. In severe cases, significant air accumulation in both frontal lobes may appear as a "Mount Fuji sign" on CT cross-sectional images, resembling a mountain ridge.
bubble_chart Treatment Measures
The treatment of pneumocephalus depends on the severity of the injury. For open craniocerebral injuries or penetrating gunshot wounds with intracranial gas accumulation, thorough debridement should be performed once to evacuate the gas and properly repair the dura mater. For small amounts of non-tension scattered gas, no special treatment is required aside from antibacterial therapy to prevent infection, as the gas can often be absorbed on its own. For recurrent pneumocephalus accompanied by cerebrospinal fluid fistula disease, surgery should be performed promptly according to the principles of cerebrospinal fluid fistula repair. For patients with large amounts of tension pneumocephalus, early burr hole evacuation is essential. Any delay or hesitation is dangerous, as the patient may experience a sudden increase in intracranial pressure from something as simple as a sneeze, leading to brain herniation or even death.