Continuing Education Activity

Pneumocephalus, also known as pneumatocele or intracranial aerocele, is the presence of air in the epidural, subdural, or subarachnoid spaces, brain parenchyma, or ventricular cavities. This condition can have a traumatic, infectious, neoplastic, iatrogenic, or spontaneous etiology. The "one-way ball-valve theory of Dandy" and the "inverted-soda-bottle effect of Horowitz and Lunsford" are common theories postulated in the pathogenesis of pneumocephalus.

Symptoms depend on the pneumocephalus volume and intracranial area affected. Most patients are asymptomatic. Rarely, patients may describe a splashing sound during head movement, known as "bruit hydroaerique," which is pathognomonic of pneumocephalus. Tension pneumocephalus is a life-threatening condition that may present with altered sensorium, abnormal breathing patterns (Cushing reflex), or cardiorespiratory arrest.

Noncontrast-enhanced computed tomography of the head is the gold standard imaging modality for diagnosing pneumocephalus. The potential complications of this condition include meningitis, seizures, brain abscesses, and brain herniation secondary to tension pneumocephalus. Determining the intracranial location of air and its entry point helps distinguish benign from complex pneumocephalus, guiding management strategies.

This activity for healthcare professionals is designed to enhance learners' proficiency in evaluating and managing pneumocephalus. Participants gain a broader grasp of the condition's etiology, risk factors, pathogenesis, symptomatology, and evidence-based diagnostic and therapeutic strategies. Greater competence equips clinicians to collaborate seamlessly with an interprofessional team caring for patients with this condition.

Objectives:

• Identify the clinical features indicative of pneumocephalus.

• Determine the diagnostic studies appropriate for evaluating pneumocephalus, describing the salient findings.

• Implement individualized, evidence-based management strategies for pneumocephalus.

• Collaborate effectively within an interprofessional team to manage pneumocephalus, formulating short- and long-term strategies to improve clinical outcomes.

Introduction

Pneumocephalus, also known as pneumatocele or intracranial aerocele, is the presence of air in the epidural, subdural, or subarachnoid spaces, the brain parenchyma, or ventricular cavities.[1] Lecat first described this condition in 1741, but Luckett independently coined the term "pneumocephalus" in 1913. Wolff used the same term to describe the condition in 1914.[2][3][4] The term "tension pneumocephalus" was proposed in 1962 by Ectors, Kessler, and Stern (see Image. Tension Pneumocephalus).[5][6]

Pneumocephalus can occur spontaneously or result from trauma or cranial surgery. This condition is classified as simple or tension pneumocephalus, depending on severity and progression. Pneumocephalus may also be acute or delayed based on disease onset. Acute pneumocephalus develops less than 72 hours before presentation, while the delayed type arises more than 72 hours after presentation.[7]

Etiology

Pneumocephalus may be traumatic, infectious, neoplastic, iatrogenic, or spontaneous.[8] The causes are summarized below (see Table. Possible Causes of Pneumocephalus). The most common etiology of pneumocephalus is head or facial trauma, which accounts for almost 75% of cases. Air can enter the cranial cavity through skull fractures.[9] 

Table. Possible Causes of Pneumocephalus

*Hydrogen peroxide can release oxygen and water upon contact with catalase and egress through the epidural or subdural space, resulting in intracranial pneumatosis.

Epidemiology

The incidence of pneumocephalus varies with the underlying etiology. The condition is seen in almost all postcraniotomy patients. The incidence of pneumocephalus following head injury varies by study but ranges from 1% to as high as 82%. Approximately 74% of documented pneumocephalus cases are due to head trauma.[25][26]

Pathophysiology

Several theories regarding the pathogenic mechanisms of pneumocephalus exist. These theories include:

• Air moves unidirectionally through a dural tear from the outside environment and is trapped inside the cranial cavity. This mechanism is responsible for pneumocephalus following positive pressure ventilation, coughing, and sneezing. This theory is called the "one-way ball-valve theory of Dandy."
• Intracranial pressure (ICP) decreases due to excessive CSF loss, which may occur artificially via lumbar drainage or physiologically during Valsalva maneuvers. This intracranial hypotension creates a vacuum that paradoxically draws in atmospheric air and traps it inside the cranium. This state persists until equilibrium is achieved between intracranial and extracranial pressures. This theory is called the "inverted-soda-bottle effect of Horowitz and Lunsford."
• Blowing the nose, coughing, or sneezing causes a sudden pressure increase in the air sinuses. Air is then drawn into the brain through defects in the skull base.
• The loss-of-resistance technique, used to identify the epidural space, is thought to be responsible for the development of pneumocephalus after epidural injections.
• Air entry through the meninges may be due to accidental injection, inadvertent dural puncture, or pressure gradients between the cranial cavity and atmosphere.
• Nitrous oxide may cause pneumocephalus during anesthetic procedures. The blood–gas partition coefficient of nitrous oxide is 34 times greater than that of nitrogen. Therefore, nitrous oxide can diffuse into the cranial cavity faster than nitrogen or air.
• Boyle's law states that pressure and volume are inversely proportional at constant temperature. Pneumocephalus expands during flights because air volume increases when pressure decreases inside the cranial cavity.[27][28]

Intraoperative pneumocephalus can occur during cranial intervention owing to various risk variables, including:

• Concurrent brain atrophy
• Loss of the CSF negative-pressure gradient due to CSF egress
• Semisitting surgical position [29]

The anatomic location and portal of air entry divide the condition into the following categories:

• Intraarterial: Almost 80% of cases occur after surgical or interventional procedures. The SWIFT trial, which investigated the Solitaire and Merci clot retrieval devices, reported a 1.4% incidence of pneumocephalus. Intraarterial pneumocephalus may also arise from paradoxical air embolism due to right-to-left heart or lung shunting (eg, from a patent foramen ovale, atrial septal defect, or pulmonary arteriovenous fistula) or from barotrauma during deep diving.
• Intravenous: Cases typically arise from vascular access procedures (eg, peripheral intravenous or neck central-line placement), with air traveling primarily to the cavernous sinus via the internal jugular vein. The reported incidence is 0.034%. Air often spreads to multiple intracranial and extracranial sites and is usually benign, though air collection in the dural cavernous and sigmoid venous sinuses may result from septic thrombosis linked to infections such as sinusitis, otitis, mastoiditis, or dental infections, potentially presenting as acute cavernous sinus syndrome or thrombosis.
• Subdural and intraparenchymal: These cases comprise the most common forms of postoperative pneumocephalus. These types are mostly benign and often resolve in 3 weeks.
• Epidural: This type occurs mainly through skull fractures, including breaks involving the mastoid air cells or a paranasal sinus. However, gas and fluid-containing collections adjacent to opacified mastoid air cells or a paranasal sinus may be due to empyema.
• Subarachnoid or ventricular: Air can enter from the spine, most often after spinal epidural anesthesia. Cases resulting from mass lesions or infections carry a risk of meningitis. Subarachnoid gas has been reported in meningitis due to pathogens such as Streptococcus pneumonia and other streptococcal spp., as well as Clostridium perfringens. Air may reach the ventricular system through recirculation from the subarachnoid space after surgery or a penetrating injury. Subarachnoid gas with meningitis should prompt consideration of infectious pathologies.[30]

Skull fractures and dural defects leave the cranial cavity vulnerable to air entry. Large air pockets can compress intracranial structures and increase the ICP, leading to herniation syndrome. Air is also a potential source of intracranial infection. Air entering the meninges can likewise irritate the cerebral cortex and produce seizures.

History and Physical

Pneumocephalus is a medical emergency despite its variable presentation. A quick primary survey—assessing the airway, breathing, circulation, disability, and exposure (ABCDE)—must be performed immediately upon receiving the patient. Unconscious individuals without respirations and pulses must be administered resuscitative measures promptly, regardless of cause. Once the patient's emergent needs are addressed, the secondary survey and diagnostic workup may be initiated.

The patient's history is likely to reveal a recent traumatic incident leading to a skull fracture. Symptoms depend on the pneumocephalus volume and intracranial area affected. Most patients are asymptomatic. However, symptomatic conscious patients may have nausea, vomiting, memory loss, speech and sensory changes, rhinorrhea or otorrhea, seizures, headaches, and motor weakness. Though rare, patients may describe a splashing sound during head movement, known as "bruit hydroaerique," which is pathognomonic of pneumocephalus. Cranial auscultation may confirm this sign. Tympany may be evident during skull percussion.[31]

An enlarging pneumatocele can have a mass effect that may lead to intracranial hypertension and neurological deterioration. Such cases are classified as tension pneumatocele, which is life-threatening. Severe tension pneumatocele may present with altered sensorium, abnormal breathing patterns (Cushing reflex), or cardiorespiratory arrest.[32] Tension pneumocephalus involving the posterior fossa manifests with brainstem signs, respiratory irregularities, and cardiac arrest. In individuals without a history of trauma, a recent neurosurgical or spinal procedure, infection symptoms, signs of intracranial mass effects, or a history of ventilator use or congenital anomalies may be elicited.

The head and neck examination may reveal scalp or skin lacerations, evidence of a skull fracture, blood and fluid in the nose or external auditory meatus, and tympanic membrane perforation. Evidence of multiple traumatic injuries includes respiratory distress signs, hypotension, tachycardia, abdominal rigidity, blood in the genitalia, bloody urine, and axioappendicular fractures. In patients with barotrauma, unilaterally decreased breath sounds (pneumothorax) or a positive Hamman sign (pneumomediastinum) may be noted on auscultation. Neurologic and musculoskeletal findings vary, depending on the site affected.

The following features of the patient's history or examination should make clinicians suspicious that the patient may have pneumocephalus:

• CSF leak from the nose, ear, or surgical site
• Persistent headache after cranial or spinal surgery
• Seizures following surgery
• Postoperative meningitis
• Frontal lobe syndrome
• Flapping scalp sign 
• Oculomotor nerve palsy
• Papilledema
• Tinnitus [33][34]

Septic cavernous sinus thrombosis can present with headache, eye pain, ophthalmoplegia, cranial nerve deficits, and signs of infection (sinusitis, otitis, mastoiditis, or dental). Postoperative abscesses may present with fever, headache, altered sensorium, seizure, and purulent drainage from the surgical site. Epidural or subdural empyema may present with seizure, headache, fever, and lethargy alongside intracranial hypertension symptoms, focal neurological deficits, and papilledema.

Evaluation

Monitoring and Laboratory Testing

Individuals who appear unstable require continuous vital sign and cardiac monitoring. A capillary blood glucose must be performed for all unconscious patients to rule out or address hypoglycemia. Individuals requiring oxygen supplementation must be monitored by pulse oximetry. 

Laboratory testing must be performed immediately for patients with trauma, especially if emergency surgery is considered. The initial tests may include a complete blood count, coagulation profile, blood typing, complete metabolic panel, and urinalysis. Arterial blood gases and electrocardiography may be considered if the patient exhibits cardiorespiratory distress. Imaging studies must be immediately scheduled.

Plain Radiography

Skull x-rays have been used to identify pneumocephalus, but plain films usually miss small quantities of air. Still, x-rays help evaluate multiple injuries or show opacities in the air sinuses, suggesting an infection.

Noncontrast Head Computed Tomography

Head computed tomography (CT) without contrast is the gold standard imaging modality in diagnosing pneumocephalus. This study can detect even 0.55 mL of intracranial air, while a skull radiograph requires at least 2 mL to be appreciable.[35] Air has a Hounsfield coefficient of -1000.

Ishiwata et al identified 2 signs as characteristic of tension pneumocephalus. The first is the "Mount Fuji" sign, named after Mount Fuji, the highest volcano in Japan. This sign is diagnostic of tension pneumocephalus and arises from the accumulation of air in the frontal region, separating the frontal lobes' tips in a patient in the supine position (see Image. Mount Fuji Sign in Tension Pneumocephalus). The second is the "air bubble sign," denoting the presence of multiple air bubbles scattered in several cisterns (see Image. Air Bubble Sign in Tension Pneumocephalus).[36]

On the other hand, the "peaking sign" denotes bilateral compression of the frontal lobes without separation of the tips. This sign indicates a less severe condition than the Mount Fuji sign.

Calculation of the Volume of Postoperative Pneumocephalus

The volume of intracranial air may be determined in 2 ways. The first is by computer-assisted volumetric measurement, which requires special software. The second is by using the ABC/2 formula at the bedside, which requires the following steps when determining the parameters:

1. Select a representative image near the center of the pneumocephalus.
2. Measure "A" or the greatest longitudinal length of the pneumocephalus in millimeters in the axial plane.
3. Measure "B" or the maximum width in millimeters of the pneumocephalus from the skull's inner table perpendicular to "A" on the same slice.
4. Measure "C" or the height of the air in the coronal plane, which is the same as the number of CT axial images showing the pneumocephalus multiplied by the slice thickness.
5. Calculate the estimated volume in milliliters using the formula = (A x B x C)/2.

The ABC/2 formula correlates well with computer-derived values.[37]

Brain Magnetic Resonance Imaging

Brain magnetic resonance imaging (MRI) may also be useful but is less sensitive than CT in diagnosing pneumocephalus. On MRI, air may be mistaken for flow voids or blood products, appearing dark in almost all sequences.

Treatment / Management

The Advanced Trauma Life Support (ATLS) protocol is a widely recognized, systematic approach to trauma patient care that focuses on critical interventions during initial patient assessment and resuscitation. The initial management of any head injury should follow this protocol. Once the patient is stabilized and diagnostics have been obtained, the pneumocephalus must be classified to determine the appropriate treatment plan.

Most patients present with simple pneumocephalus, lacking neurological symptoms and signs of increased ICP. The head CT typically reveals intracranial air without tension pneumocephalus indicators like the Mount Fuji sign. Intracranial air disappears over time through tissue absorption. Management is conservative and involves the following measures:

• Bed rest
• Placing the patient in a 30° Fowler position
• Avoiding Valsalva maneuvers like nose-blowing, coughing, and sneezing
• Analgesics and antipyretics
• Osmotic diuretics, if indicated
• High-flow oxygen therapy is given at 5 L/min for at least 5 days via a face tent or 100% nonrebreather mask with absolute avoidance of positive pressure and
• Hyperbaric oxygen therapy [37]

Atmospheric air is composed of 78% nitrogen and 21% oxygen. The rate of nitrogen absorption from intracranial air depends on nitrogen's partial pressure in the blood, which is inversely proportional to the fraction of inspired oxygen.

Oxygen supplementation reduces blood and brain nitrogen concentration, increasing the nitrogen gradient between the pneumocephalus air collection and surrounding brain tissue. Over time, oxygen replaces intracranial nitrogen—which is well-absorbed in brain tissue and blood—by diffusion, facilitating nitrogen absorption and eventual pneumocephalus resolution.[38] Despite the heterogeneity in delivery modes, which include nonrebreather masks, endotracheal tubes, and hyperbaric chambers, oxygen therapy enhances the reabsorption and resolution of pneumocephalus.[39] Serial CT imaging studies may be obtained to monitor the condition.

Although pneumocephalus poses an increased intracranial infection risk, prophylactic antibiotics do not appear to provide a protective advantage in patients with traumatic pneumocephalus. However, emergent surgical decompression is required when clinical signs manifest. In cases of pneumocephalus complicated with abscess and empyema, surgical drainage, eradication of the infection source, and broad-spectrum antibiotics are recommended.

Surgery is also indicated in the following conditions:

• Symptomatic pneumocephalus
• Tension pneumocephalus
• Recurrent pneumocephalus
• Persistent traumatic pneumocephalus lasting more than 1 week
• Tension pneumoventricle (see Image. Pneumocephalus and Pneumoventriculi)

Strategies for surgical decompression include the following:

• Needle aspiration, either blind or under radiological guidance through an existing burr hole or craniotomy 
• Controlled decompression via a subdural drain connected to an underwater seal followed by dural defect closure 
• Ventriculostomy for tension pneumoventricle 
• Emergency decompression by the creation of fresh cranial burr holes
• Decompressive craniectomy 
• Saline-primed Camino bolt insertion
• Subdural evacuating port system (SEPS) insertion 
• Endoscopic endonasal eustachian tube obliteration during lateral skull base surgery 
• Placing the patient in the Trendelenburg position in the presence of a subarachnoid-pleural fistula facilitates the dissipation of some intracranial air into the spinal canal. This maneuver also helps create an epidural patch at the pleural apex, thereby sealing the dural rent and obliterating the fistula.
• Endovascular suctioning of intraarterial air [40][41][42][43]

Specific preventive strategies for preventing the occurrence of pneumocephalus following cranial surgeries include the following:

• Water-tight sealing of the surgical site during endoscopic transsphenoidal surgery
• Using a prophylactic frontal drainage system
• Placing the patient in the recombinant position before opening the dura
• Initiating liberal irrigation of the surgical site and potentially injured venous sinus, with wax closure of the burr holes to prevent air embolism [44][45]

Differential Diagnosis

Pneumocephalus must be differentiated from the following terms:

• Pneumorrhachis, which denotes intraspinal air
• Pneumocele, which is a focal or diffuse paranasal sinus (usually frontal) enlargement with bone thinning and hyperpneumatization
• Pneumosinus dilatans, which may appear the same on imaging as a pneumocele but have the sinus walls intact and normal

Pneumocephalus may be confused with other structures on imaging studies. For example, intracranial fat may appear hypodense on CT scans and be mistaken for pneumocephalus, though it has a much higher density (-90 HU) than air (-1000 HU). Pneumocephalus may also resemble blood products or flow voids on MRI.

Prognosis

Simple pneumocephalus usually resolves spontaneously with conservative therapy. However, this condition occasionally produces seizures and meningitis. Prognosis is generally good even with tension pneumocephalus, provided timely treatment is given.

The presence of pneumocephalus may suggest chemical meningitis following corpus callosotomy.[46] The postsurgical appearance of pneumocephalus is also a predictor of chronic subdural hematoma recurrence after evacuation. Thus, pneumocephalus is a component of the Puerto Rico Recurrence Scale.[47]

Complications

The potential complications of pneumocephalus include meningitis, seizures, brain abscess, brain herniation secondary to tension pneumocephalus, and death. Early intervention can prevent these complications and improve patient outcomes.

Extensive postoperative convexity pneumocephalus increases the risk of recurrent chronic subdural hematoma.[48] In functional surgeries such as deep brain stimulation, pneumocephalus may indicate targeting inaccuracies, leading to suboptimal clinical outcomes.[49]

Deterrence and Patient Education

The following methods can help prevent the development of pneumocephalus during or after surgical procedures:

• Filling of the surgical site with saline at the time of dural closure
• Administering the Valsalva maneuver during closure, before the last dural suture, to allow air to escape outside
• Using a smaller-gauge spinal needle for lumbar puncture to make a smaller dural perforation and minimize CSF leakage
• Keeping the patient in the supine position with no head-end of bed elevation following chronic subdural hematoma evacuation
• Positioning the head during dural closure so that the last part of the dural defect becomes the highest point. This step facilitates the escape of residual air while filling the subdural space with saline.
• Using saline rather than air to identify the epidural space during epidural injections
• Avoiding high airway pressure and hyperventilation during invasive ventilation

The inhalational anesthetic nitrous oxide was previously thought to cause pneumocephalus if not withdrawn before dural closure. However, a randomized control trial demonstrated that nitrous oxide did not cause a significant ICP increase or produce large pneumocephalus volumes even if administered postoperatively.[50]

Evidence does not support the prophylactic administration of ceftriaxone for preventing meningitis in patients with traumatic pneumocephalus.[51]

Neurosurgical procedures may result in residual intracranial air and also cause continuous air entry into the cranial cavity. Hence, patients must be advised to wait at least 7 days before flying, as cabin pressure changes can introduce air intracranially.[52] Air travel is not advisable for patients with an intracranial air volume of more than 30 mL. An intracranial air volume of 20 mL and an initial ICP of 15 mm Hg are considered conservative thresholds for safe air travel among such patients.[53]

The following measures may be recommended to patients at risk to avoid complications from pneumocephalus during a flight:

• Taking a low-level flight or maintaining ground-level cabin pressure during the flight
• Avoiding frequent cabin pressure changes
• Seeking a position that reduces CSF leaks
• Administering supplementary oxygen
• Taking preflight decongestants
• Avoiding Valsalva maneuvers

Healthcare providers may also help avoid complications in these individuals by performing the following:

• Preventing hypoventilation and carbon dioxide accumulation if the patient is ventilated
• Obtaining imaging studies immediately before the flight to assess the volume of pneumocephalus and rule out an extracranial-intracranial fistulous process
• Educating patients regarding patient activity-related pathophysiology and the time course of pneumocephalus
• Reducing the stresses induced by acceleration (including changing g-forces), noise, or hypoxemia [54]

Avoiding air travel for 2 to 8 weeks after intracranial surgery is recommended.[55]

Pearls and Other Issues

The most important points to remember when evaluating and managing pneumocephalus are the following:

• Pneumocephalus has various causes, but most are trauma-related.
• Determining the intracranial location and point of air entry allows for the classification of pneumocephalus into benign or complex subtypes, facilitating the development of specific management algorithms.
• The condition presents variably. Most patients have the simple type and are asymptomatic, but complications can develop if tension pneumocephalus is not treated immediately.
• The management of all patients with suspected head trauma should follow ATLS protocol.
• Noncontrast CT is the imaging modality of choice for pneumocephalus.
• Simple pneumocephalus may be managed conservatively. Antibiotics have little effect on intracranial infection risk in patients with pneumocephalus.
• Surgery is reserved for patients with symptomatic, recurrent, or persistent traumatic pneumocephalus lasting more than a week and tension pneumocephalus or pneumoventricle.
• The prognosis is generally good for patients with simple pneumocephalus. Prompt intervention significantly improves the prognosis of tension pneumocephalus.

Notably, the definitive treatment depends on the specific etiology of pneumocephalus and the patient's clinical condition. Pneumocephalus typically resolves in 3 weeks. Otherwise, a subtle but persistent defect in the skull base or air sinuses should be considered.

Enhancing Healthcare Team Outcomes

The management of pneumocephalus must involve an interprofessional healthcare team to produce the best outcomes. The team members should include the following care providers:

• Emergency medicine physician: often the first healthcare professional to encounter patients with head trauma or acute neurological symptoms. This provider performs the initial assessment, stabilizes the patient, and coordinates with specialists for further management.
• Radiologist: interprets imaging studies to confirm the diagnosis, assess the extent of pneumocephalus, and identify any associated injuries or conditions. The radiologist's expertise is crucial in guiding the treatment plan.
• Neurosurgeon: assesses the extent of pneumocephalus and may perform necessary surgical procedures.
• Intensivist: may treat patients with pneumocephalus in the intensive care unit.
• Anesthesiologists: may be involved in cases requiring surgical intervention.
• Infectious disease specialist: may be consulted to guide the appropriate antimicrobial therapy and overall management if an intracranial infection develops as a complication of pneumocephalus.
• Respiratory therapist: assists in managing ventilator settings, ensuring adequate oxygenation, and monitoring the patient's respiratory status when mechanical ventilation is required.
• Occupational and physical therapists: providers who may be involved in the later stages of care to assess and facilitate the patient's recovery, primarily if neurological deficits or functional impairments exist.
• Primary care physician: monitors patients and coordinates care in the outpatient setting.

Effective communication and collaboration among these healthcare professionals are essential to ensuring a coordinated and well-rounded approach to pneumocephalus's short and long-term management.