Tension pneumocephalus: a rare complication after hyperbaric
Ching-Hsing Lee, MD1; Wei-Chun Chen, MD 2; Chao-I Wu, MD 2; Te-Chun Hsia, MD2
Department of Emergency Medicine, Chang Gung Memorial Hospital, Taipei, Chang Gung
University College of Medicine, Taoyuan, Taiwan, R.O.C.
Hyperbaric Oxygen Therapy Center, China Medical University Hospital, Taichung, Taiwan,
Dr. Te-Chun Hsia
Hyperbaric Oxygen Therapy Center, China Medical University Hospital
2, Yuh-Der Road, Taichung 404, Taiwan, R.O.C.
Tel.: 886-4-22033568; Fax: 886-4-22033568; E-mail: email@example.com
Objective: To describe a patient with multiple skull bone fractures and a cerebrospinal fluid
(CSF) leak who received hyperbaric oxygen therapy (HBOT).
Design: Case report.
Patient: A 40-year-old man presented with subdural hemorrhage, skull bone fractures,
facial bone fractures, sinus fractures, and CSF leakage after a one-story fall. He received HBOT
as an adjunctive treatment to reduce brain edema and increase oxygen availability in brain tissue.
Interventions: Craniotomy, external ventricular drainage, and HBOT (2.3 ATA for 80
min/day for 20 sessions).
Main Results: Tension pneumocephalus developed after HBOT. Bur hole drainage was
performed emergently to relieve the tension pneumocephalus. Cranioplasty and repair of skull
base fracture were subsequently performed. The patient was discharged in a vegetative state. We
proposed a possible mechanism by which tension pneumocephalus developed after HBOT
sessions in this patient.
Conclusions: Pneumocephalus, untreated skull base fracture, and CSF leakage should be
considered contraindications to HBOT.
KEY WORDS: hyperbaric oxygen therapy, tension pneumocephalus
Hyperbaric oxygen therapy (HBOT) is the therapeutic administration of 100% oxygen at
pressures higher than 1 ATA while the patient is in an airtight vessel. The treatment protocol
usually involves pressurization to between 1.5 and 3.0 ATA for periods between 60 and 120
minutes, once daily or more often. This therapeutic method is used as an adjunctive treatment for
patients with traumatic brain injury to reduce brain edema, increase oxygen availability in brain
tissue and reduction intracranial pressure (1). Despite the positive effect of HBOT in traumatic
brain injury, it is associated with some risk of adverse effects, including damage to the ears,
sinuses, and lungs, from the effects of pressure and potential oxygen poisoning. Serious adverse
effects have rarely been reported.
We report here on a patient with traumatic brain injury who suffered from tension
pneumocephalus after HBOT.
This case did not require Institutional Review Board (IRB) review according to the Chang
Gung Memorial Hospital IRB protocol. The IRB was, however, contacted regarding the
inclusion of an author (T. C. Hsia) from another institution and granted permission for him to be
given access to patient medical data, without identifying information.
A 40-year-old man presented to the emergency department after a one-story fall. On
physical examination, bilateral otorrhea, rhinorrhea, and paralysis of the left limbs were noted. A
computed tomography (CT) scan of the head disclosed right frontotemporoparietal subdural
hemorrhage (SDH); left frontotemporoparietal decompressed skull fracture; multiple facial bone
fractures with blood in the frontal, ethmoid, and maxillary sinuses; and pneumocephalus. The
patient underwent a craniectomy to remove the SDH, and an external ventricular drain was
inserted. Ten days after injury, he underwent tracheostomy because of ventilator dependent.
Three weeks after injury, the follow up brain CT disclosed residual brain edema in bilateral
frontal lobe and right occipital lobe. Pneumocephalus was resolved at this time. Twenty-six days
after injury, the patient is in bed ridden status with coma scale E1VtM4. He underwent HBOT in
order to reduce brain edema, intracranial pressure and increase oxygen availability in brain tissue.
The treatment profile was 2.3 atm absolute for 80 min/session without air break, 1 session per
day and 5 days a week for total 20 sessions. Bilateral tympanostomy were done before HBOT.
The oxygen was given by mechanical ventilator. Ventricular drain reservoir engorgement and
right temporal scalp protrusion were noticed after the HBOT sessions were completed. A CT
scan of head revealed a significant amount of air trapped in the cranial vault (Figure 1, white
arrow), air over the frontal lobe and subarachnoid space, and cerebral midline shift (Figure 2).
A diagnosis of tension pneumocephalus was made. Burr hole drainage was performed
emergently to relieve tension pneumocephalus. Cranioplasty and repair of skull base fracture
were performed 1 week later. Operative findings included a 3- x 4-cm defect of the inner table of
the frontal sinus with dural defect; and skull base, zygoma, and orbital roof fracture with dural
adhesion to the fracture line. Postoperative follow-up CT scanning of the head showed that most
of the air had been evacuated. The patient was discharged 1 month after the final surgery in a bed
ridden state with coma scale E4VtM5.
Pneumocephalus refers to the presence of intracranial air and tension pneumocephalus
causes the mass effect of air to lead to midline shift. These are usually sequelae of craniotomy,
transsphenoidal surgery, traumatic skull fracture, thoracotomy, nasopharyngeal tumor invasion,
Valsalva maneuver, or infection by a gas-forming organism (2-4). Rapid pressure change during
airplane flight may also cause pneumocephalus (5). Pneumocephalus progressing to tension
pneumocephalus after repeated pressure change, such as HBOT, has never been reported before.
A possible explanation for the occurrence of tension pneumocephalus after repeated
compression–decompression cycles is that pneumocephalus develops when CSF leakage creates
negative pressure within the intracranial space and air enters the cranial vault (6). In a hyperbaric
environment, intracranial air is compressed and creates negative pressure in the intracranial
space. Due to pressure differences, air enters the intracranial space through the skull base
fracture and dural defect. A one-way-valve effect is formed when intracranial air leaves the dural
defect and accumulates in the upper portion of cranial vault. The intracranial air is trapped in the
cranial vault, with no route out. When returning to the normobaric condition, intracranial air
volume expands (Boyle’s law) and CSF is expelled to release the pressure. The volume of CSF is
replaced by air and pneumocephalus becomes severe. In subsequent sessions of compression, the
more intracranial air is compressed, the greater the pressure difference will be. Greater negative
pressure difference leads to more air entering the cranial vault, and a vicious circle occurs. After
serial compression–decompression cycles, intracranial air accumulates to a critical point at which
pressure balance cannot be maintain by CSF leakage. Finally, the mass effect becomes prominent
and tension pneumocephalus develops.
HBOT plays a positive role in the treatment of patients with traumatic brain injuries.
Indeed, although not accepted as a standard treatment for this indication, there are findings
allowing the assumption of a benefit of HBO in brain injury (1,7). We should, however, be
cautious about treating patients within this group who have skull base fracture, pneumocephalus,
or CSF leakage. These patients are at particular risk of progressing to tension pneumocephalus
after HBOT, although currently these conditions are not a contraindication or a relative
contraindication to HBOT (8). Further study and expert discussion are necessary to determine
whether pneumocephalus, untreated skull base fracture, and CSF leakage are contraindications to
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Figure 1. Scout CT scan showed significant amounts of air (white arrow) trapped in the cranial
Figure 2. CT scan of the head revealed air over the bilateral frontal area (black arrow) and
cerebral midline shift (white arrow).