Postoperative Tension Pneumocephalus with Mt. Fuji Sign: A Case Report

Abstract

Tension pneumocephalus (TP) is an uncommon but potentially lethal complication of the neurosurgical process. The treatment is usually surgical decompression. We describe here a case of TP following evacuation of subdural hematoma (SDH) and its successful nonoperative management. A 75-year-old elderly male presented to the emergency department with a history of progressive weakness of bilateral upper and lower limbs and altered sensorium for 2 months. His Glasgow Coma Scale was E3V4M6, and pupils were bilaterally equal and reactive to light. A noncontrast computed tomography (NCCT) of the head showed bilateral acute-on-chronic SDH with internal septations and mass effect. The patient was planned and taken for bilateral craniotomy with membranectomy with evacuation of SDH. A repeat NCCT head showed development of bilateral TP with a “Mount Fuji” sign. The patient was placed on high-flow oxygen support and positioned with head-end elevation. Subsequent computed tomography scan showed resolution of intracranial air foci and expansion of the brain. Traumatic pneumocephalus is a dreaded complication of post-neurosurgical procedure. A high index of suspicion based on the clinical and radiological findings helps in identifying TP. Nonoperative management with closed observation is a viable option in clinically silent TP.

 

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Keywords

head injury - Mount Fuji sign - neurosurgical procedure - subdural hematoma - tension pneumocephalus

Introduction

Tension pneumocephalus (TP) is an uncommon but potentially lethal complication of the neurosurgical process.[1] The treatment is usually surgical decompression. We describe here a case of TP following evacuation of subdural hematoma (SDH) and its successful nonoperative management.

 

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Case Report

A 75-year-old elderly male presented to the emergency department with a history of progressive weakness of bilateral upper and lower limbs and altered sensorium for 2 months. The patient's relatives gave a history of similar complaints 4 months back following a fall from bed, for which he had undergone bilateral burr-hole surgery with evacuation of subdural hemorrhage in an outside setup.

On presentation, the patient had a pulse rate of 110 and blood pressure of 130/90 mmHg. His Glasgow Coma Scale (GCS) was E3V4M6, and his pupils were bilaterally equal and reactive to light. He was not on any anticoagulants. There were no significant medical comorbidities. Baseline lab parameters showed Hb: 13.2, platelet count: 3.24 lakhs, Na⁺: 129, K⁺: 4.2, urea: 27, creatinine: 1.23, prothrombin time/international normalized ratio: 13/1.1.

A noncontrast computed tomography (NCCT) of the head showed bilateral acute on chronic SDH with internal septations and mass effect ([Fig. 1]). The patient was planned and taken for bilateral craniotomy with membranectomy with evacuation of SDH. Craniotomy was done, membranes removed, and SDH evacuated bilaterally, followed by gentle saline insufflation in the subdural space via an 8-French tube ([Figs. 2],[3]). Two feeding tubes were placed on each side, and the wound was closed. The patient was extubated postoperatively and kept in the intensive care unit. Postoperative GCS was E4V5M6 with pupils bilaterally equal and reactive to light. A repeat NCCT head showed development of bilateral TP with a “Mount Fuji” sign ([Fig. 4]). However, the patient continued to be fully conscious with no sensory or motor deficit in either of the limbs and GCS of E4V5M6. The patient was placed on high-flow oxygen support and positioned with head-end elevation. Drains were removed on postoperative day 1 and underwent strict GCS monitoring. Antibiotic prophylaxis, proton-pump inhibitor, and antiepileptic prophylaxis were given.

Fig. 1 Figure showing bilateral recurrent SDH with internal septations and pre-existing burr hole defect. SDH, subdural hematoma.

Fig. 2 Figure showing SDH membrane with brain parenchyma underneath. SDH, subdural hematoma.

Fig. 3 Figure showing SDH membrane with brain parenchyma underneath. SDH, subdural hematoma.

Fig. 4 Figure showing NCCT head with “Mount Fuji” sign. NCCT, noncontrast computed tomography.

Fig. 5 Follow-up NCCT head showing brain expansion. NCCT, noncontrast computed tomography.

Fig. 6 Figure showing Mount Fuji (image taken from public access via Wikimedia Commons) with CT image of tension pneumocephalus of the case interposed in the top right corner. CT, computed tomography.

Subsequent computed tomography scan showed resolution of intracranial air foci and expansion of the brain ([Fig. 5]). The patient was weaned off oxygen support and actively mobilized. He was shifted to the ward and remained neurologically stable. He was discharged after 14 days in stable condition. Follow-up visits showed normal neurological function with no recurrence of SDH.

 

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Discussion

TP develops due to escape of air via the dural defect in the subdural, epidural, or intraparenchymal space as a one-way valve.[1] The air is particularly in the frontal lobe and creates a mountain silhouette with a volcano on each side, “Mount Fuji” sign ([Fig. 5]). The “Mount Fuji sign” remains a definitive feature of pneumocephalus with compression due to air in the cranium, causing the brain parenchyma to appear like the famed Japanese mountain on NCCT brain ([Fig. 6]). Ishiwata et al described the Mount Fuji sign in four out of five cases with TP.[2] Harvey et al described TP of the cranium as analogous to tension pneumothorax of the chest and is considered a surgical emergency requiring emergent intervention.[3] Yin and Chen explained two mechanisms leading to TP; one due to one-way passage of air through a dural breach, leading to “ball-valve” effect, and the second, “inverted pop bottle effect” due to drainage of cerebrospinal fluid (CSF) through a dural defect. Singh et al presented the anesthetic use of nitrous oxide as another factor contributing to TP.[4] [5]

This air starts compression on the underlying brain and causes pressure symptoms. The clinical presentation can vary from headache, focal neurological deficit, change in level of consciousness to reopening of previously closed CSF leak due to raised intracranial pressure.[6] [7]

Traditionally, surgical decompression with needle, burr hole, or craniotomy was made to relieve the pressure and mass effect.[1] [8] A review of the literature shows that while duraplasty is the definitive treatment of TP, it still requires urgent temporizing measures to prevent neuronal damage. Surgical decompression provides rapid relief of pneumocephalus and includes procedures such as needle aspiration, burr hole, craniotomy, and ventriculostomy.[4] [9] As per a review by Dabdoub et al, there are only a few cases of TP that resolve with nonoperative management in the absence of surgical intervention, with such cases remaining asymptomatic from detection through the course of treatment.[9] The above case met such criteria, remaining asymptomatic and retaining full neurological function and hemodynamic stability. Cerebral decongestants, consistent high-flow oxygen, and appropriate positioning allowed the washout of nitrous oxide, which contributes to pneumocephalus.[5] [9] While emergent surgical intervention remains gold standard for management of symptomatic TP, rarity of the condition demands further studies to explore more expectant treatment options, especially in asymptomatic patients.

 

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Conclusion

Traumatic pneumocephalus is a dreaded complication of post-neurosurgical procedure. A high index of suspicion based on the clinical and radiological findings helps in identifying TP. Nonoperative management with closed observation is a viable option in clinically silent TP.

 

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Conflict of Interest

None declared.

• References

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• 9 Dabdoub CB, Salas G, Silveira EdoN, Dabdoub CF. Review of the management of pneumocephalus. Surg Neurol Int 2015; 6 (01) 155

Publication History

Article published online:
29 August 2025