Pneumocephalus is a condition in which air accumulates within the cranial cavity. Simple pneumocephalus is a benign disease that commonly occurs after head trauma or postoperative neurosurgery and is usually asymptomatic (1,6). Tension pneumocephalus is a rare and life-threatening disease similar to tension pneumothorax, which involves increased intracranial pressure and herniation of brain structures in human literature (1). Depending on its location, it may be classified as epidural, subdural, subarachnoid, intracerebral, or intraventricular, with the latter being the most common site in humans (1). This can be seen as a complication of craniotomy (3,4) and trauma (5) in dogs, but other causes have been reported in the veterinary literature (6).

This report presents a case of a 12-year-old Spitz-spayed female dog that developed intraventricular tension pneumocephalus secondary to frontal sinusotomy performed to treat frontal sinus and nasal masses.

A 12-year-old, 6-kg, spayed female Spitz dog presented with a facial mass that had begun to appear 3 weeks prior to presentation. The mass was solid in the left frontal sinus on physical examination, with no apparent pain, fever, or crepitus. Additionally, the results of the general physical and neurological examinations were within normal limits. The complete blood count and serum biochemical analysis results were within the respective reference ranges. Three-view thoracic radiography and abdominal ultrasonography revealed no abnormal findings.

Computed tomography (CT) was performed using a 16-channel multidetector CT scanner (GE Brivo 385; GE Healthcare, Chicago, IL, USA) to evaluate the extent of the lesion and the presence of metastasis to the lymph nodes or lungs. The scanning parameters were as follows: 120 kV, 130 mA, 1.25-mm thickness, and 1-s rotation time. After placing the dog in sternal recumbency, head, thoracic, and abdominal CT images were acquired before and after intravenous iohexol injection (600 mg/kg; Omnipaque 300; GE Healthcare, Oslo, Norway). There was a large, complex, soft-tissue mass with a hypodense lesion in the left frontal sinus and nasal cavity. Post-contrast imaging revealed ring enhancement in the left frontal sinus mass. The frontal bone lining the frontal sinuses was severely lysed (Fig. 1). The conchae and turbinate of the left nasal passages had lost structure, and the left dorsal wall of the cribriform plate was lysed with invasion of the soft tissue mass into the olfactory region of the brain (Figs. 2, 3). It was confirmed that the left submandibular and retropharyngeal lymph nodes were slightly thickened compared to those on the right side. No significant abnormalities were identified in the thoracic or abdominal cavities. Multiple biopsies were obtained and subjected to histopathological, bacterial, and fungal cultures. Histopathological biopsy results revealed mixed rhinitis with edema, fibroplasia, and osseous proliferation. No bacterial or fungal organisms were identified, and there was no evidence of foreign bodies.

Figure 1. Transverse bone-window computed tomography (CT) image (A), post-contrast soft tissue-window CT images (B). A soft tissue mass (asterisk) with ring enhancement after contrast and loss of the frontal sinus septum and frontal sinus bone (arrow) are seen in the left frontal sinus.

Figure 2. Dorsal (A) and transverse (B) bone-window computed tomography images showing the mass (asterisk) filling the choanae and occluding the entire left nasal cavity.

Figure 3. Dorsal (A) and transverse (B) bone-window computed tomography images showing lysis of the dorsolateral cribriform plate on the left side with invasion of the soft tissue mass into the frontal cortex of the brain plate (arrow).

Frontal sinus surgery was performed according to the owner's decision after consulting with the surgeon based on the diagnostic results. The patient was anesthetized, and the mass was surgically debulked using frontal sinusotomy and dorsal rhinotomy. A pneumatic burr was used to create a large bone window that provided access to the dorsal nasal cavity. The relatively soft consistency of the mass indicated that appropriate curettage and removal were possible. The majority of the pathological tissue was removed using the dorsal approach. Complete resection was not possible because of the involvement of the rostral calvarium and cribriform plate. Care was taken to prevent further disruption of the cribriform plates. The dog recovered uneventfully from anesthesia and was discharged 3 days after surgery.

Two weeks after the surgery, the dog underwent a follow-up examination and was doing well. However, a clear mucous discharge was found intermittently in the nose, and sneezing continued frequently. The owner was advised to continue cephalexin (20 mg/kg, PO, q12h) and piroxicam (0.3 mg/kg, PO, q24h) for 3 additional months and to return the dog for blood sample collection every 4-6 weeks so that liver function could be monitored by serum biochemical analysis.

One month after surgery, the dog was readmitted owing to the sudden onset of neurological symptoms over the previous 24 h. The owner reported three generalized tonic-clonic seizures. Clinical findings included left-sided aqueous nasal discharge, depressed mental status with an inconsistent menace response, and minimal response to stimuli. Mild proprioceptive ataxia of the pelvic limbs was observed, and the dog leaned against walls when standing, with no tendency to turn in any particular direction. The dog appeared dull, unaware of its surroundings, and had nonpurposeful, unprovoked aggression. The complete blood count and serum chemistry profile were within the normal limits. Owing to the rapid neurological deterioration, the dog was anesthetized for an emergency CT examination. The CT revealed the absence of the nasal turbinate and portions of the nasal and frontal bones (consistent with a previous frontal sinusotomy and dorsal rhinotomy). A defect with sharp borders was detected in the left dorsal aspect of the cribriform plate. The defect was associated with a 7-mm × 6-mm × 10-mm gas pocket in the left frontal lobe. Further, a large amount of gas was present in the bilateral lateral ventricles, and a smaller amount distended the third ventricle. The lateral ventricles were significantly expanded (Fig. 4).

Figure 4. Sagittal bone-window (A) and dorsal (B) and transverse (C) soft tissue-window computed tomography images of a dog that had undergone frontal sinusotomy and dorsal rhinotomy 4 weeks earlier. Notice a gas pocket in the cribriform plate defect and the intraventricular pneumocephalus with dilation of the bilateral ventricles.

A decision was made to attempt definitive repair of the cribriform plate defect. As a graft was not used over the cribriform plate defect, the brain tissue was left in direct contact with the open frontal sinus. The defect was closed by placing a small piece of hemostatic gelatin sponge (Cutanplast; Mascia Brunelli S.p.A., Milan, Italy) and oxidized regenerated cellulose (Surgicel; Ethicon, Inc., Neuchâtel, Switzerland). Grafts previously placed in the frontal sinus defect were viable but hypermobile. It was then replaced and reinforced using a titanium mesh plate. The mesh was secured to the frontal bone defect using two 1.5-mm titanium screws. One screw was placed in the right lateral portion of the left frontal bone, and a second screw was placed in the caudal aspect of the left nasal bone.

The dog recovered from anesthesia without complications and continued to improve neurologically over the subsequent 7 days. Repeat imaging 7 days later demonstrated resolution of the tension pneumocephalus; in the CT scan after 4 days, pneumocephalus was reduced to 40%. In the image after 7 days, a complete disappearance of pneumocephalus was confirmed (Fig. 5). Postoperatively, no seizures were observed, and the dog was considered normal upon neurological examination 2 weeks later. The patient recovered well and was subsequently discharged on cephalexin (20 mg/kg, PO, q12h), prednisone (0.5 mg/kg, PO, q12h), and tramadol (2 mg/kg, PO, q12h). The prednisone dose was slowly decreased. At 3 and 4 months after the second surgery, neurological examination was normal, and the patient did not have additional seizures.

Figure 5. Transverse soft tissue-window computed tomography images. Before the second surgery (A), the lateral ventricles are significantly dilated with gas, whereas 4 days later (B), the gas in the lateral ventricle has decreased by about 40%, and after 7 days (C), the pneumoventricle has completely resolved.

The collection of air in the cranial cavity is known as pneumocephalus. Air accumulation can occur in the epidural, subdural, and subarachnoid spaces and can be intraventricular or intraparenchymal (6). Pneumocephalus is usually caused by a discontinuity in the skull that allows air to enter the cranial cavity (2). It has been associated with a variety of causes, including craniotomy or craniectomy, trauma, otitis media, evacuation of subdural hematoma, cervical laminectomy, ventriculoperitoneal shunting, and as a complication of radiotherapy (1,9).

In 1962, a case of pneumocephalus, which, unlike simple pneumocephalus, caused brain herniation, leading to rapid deterioration and death, was reported (8). They described the term “tension pneumocephalus” as equivalent to tension pneumothorax, requiring immediate intervention. Three mechanisms suggest the development of tension pneumocephalus. The first is the ball-valve mechanism, in which air is permitted to enter, but not exit, the cranial cavity. The second is the inverted soda-bottle effect, in which air fills the cranial cavity due to the negative pressure from CSF leakage. Finally, infections by gas-forming organisms (7).

The most common symptoms of tension pneumocephalus include nausea, vomiting, headache, altered mental status, and convulsions (10). Neurological findings include nuchal rigidity, photophobia, and focal neurological deficit (10). In cases of tension pneumocephalus, clinical deterioration is caused by increased intracranial pressure and the Cushing reflex (11). Patients may present with bradycardia, hypertension, or cardiac arrest (11).

A simple pneumocephalus, even if massive, can be managed conservatively. Conservative management involves the supine position, 100% supplemental oxygen, and frequent neurological monitoring to detect any signs or symptoms of increased intracranial pressure. However, if the patient demonstrates any features of high intracranial pressure that indicate the development of tension pneumocephalus, an early neurosurgical referral, neurosurgical decompression, and repair of the causative defect are recommended. Without timely intervention, tension pneumocephalus can lead to increased intracranial pressure, brainstem herniation, coma, and death (11).

Simple pneumocephalus, an asymptomatic form of intracranial air after a craniotomy, is common in humans (12). However, the transformation of pneumocephalus into tension pneumocephalus (i.e., symptomatic intracranial air) is a rare phenomenon (8).

In veterinary medicine, sporadic cases have been described, and it is considered a rare disease (3). Pneumocephalus due to complications after transfrontal craniotomy has previously been reported in four cases (3), of which only two showed tension pneumocephalus (3). This is the first case report of tension pneumocephalus that likely developed secondary to a frontal sinusotomy in a dog. In this case, the brain was assumed to be directly exposed to air through the cribriform plate defect because the luminal inflammatory mass was removed via frontal sinusotomy. Alternatively, the fistula may have developed as a result of primary surgery because of necrosis or iatrogenic damage to the brain parenchyma.

After the first surgery, the dog developed a watery nasal discharge before tension pneumocephalus was confirmed. It is possible that the patient’s cerebrospinal fluid entered the nasal cavity through the dural opening, resulting in cerebrospinal fluid rhinorrhea. In other words, in the case of cerebrospinal fluid leakage and parenchymal fistula, the pressure within the ventricular system decreases due to the loss of cerebrospinal fluid, which may lead to air inflow, resulting in tension pneumocephalus. The dog also sneezed frequently after the first surgery. If there is a defect in the dura and a fistula in the brain parenchyma, when the dog coughs or sneezes, the extracranial pressure at the defect increases, and air escapes through the dural defect. When coughing or sneezing stops, the intracranial pressure becomes higher than the pressure on the other side of the dura mater defect, and the brain parenchyma seals the defect, trapping air inside, which can cause tension pneumocephalus. Limitation of this study include the difficulty in characterizing the exact pathogenesis of tension pneumocephalus in this case due to the single case and retrospective nature of the investigation. Nevertheless, these are believed to be the possible reasons for the development of catatonic pneumocephalus in dogs. A causal relationship between clinical deterioration and increased intraventricular pressure due to air accumulation must be established for a definitive diagnosis of tension pneumocephalus. This correlation was not possible in the absence of intracranial pressure monitoring. However, comparing pre- and post-operative lateral ventricle sizes on CT scans showed increased intraventricular pressure.

The surgical treatment of pneumocephalus involves relieving tension within the cavity and preventing dural tears. In our case, the defect was repaired by sealing it with surgical foam. This resulted in the immediate post-operative regression of neurological signs and resolution of rhinorrhea.

This case suggests that if tension pneumocephalus is detected and treated immediately, the patient may have an excellent long-term prognosis. Tension pneumocephalus should be considered as a potential complication in patients with deteriorating neurological signs after skull base surgery. An accurate diagnosis requires an appreciation of imaging features and a high index of suspicion. Immediate intervention is essential, and definitive management involves the repair of the defect to allow intracranial air entry.

The authors received no financial support for the research, authorship, and/or publication of this article.

The authors have no conflicting interests.