Traumatic tension pneumocephalus – Two cases and comprehensive review of literature

Abstract

Although traumatic pneumocephalus is not uncommon, it rarely evolves into tension pneumocephalus (TP). Characterized by the presence of increasing amounts of intracranial air and concurrent appearance or worsening neurological symptoms, TP can be devastating if not recognized and treated promptly. We present two cases of traumatic TP and a concise review of literature on this topic. Two cases of traumatic TP are presented. In addition, a literature search revealed 20 additional cases, of which 18 had sufficient information for inclusion. Literature cases were combined with the 2 reported cases and analyzed for demographics, mechanism of injury, symptoms, time to presentation (acute <72 h; delayed >72 h), diagnostic/treatment modalities, and outcomes. Twenty cases were analyzed (17 males, 3 females, median age 26, range 8–92 years). Presentation was acute in 13/20 and delayed in 7/20 patients. Injury mechanisms included motor vehicle collisions (6/20), assault/blunt trauma to the craniofacial area (5), falls (4), and motorcycle/ bicycle crashes (3). Common presentations included depressed mental status (10/20), cerebrospinal fluid rhinorrhea (9), headache (8), and loss of consciousness (6). Computed tomography (CT) was utilized in 19/20 patients. Common underlying injuries were frontal bone/sinus fracture (9/20) and ethmoid fracture (5). Intracranial hemorrhage was seen in 5/20 patients and brain contusions in 4/20 patients. Nonoperative management was utilized in 6/20 patients. Procedural approaches included craniotomy (11/20), emergency burr hole (4), endoscopy (2), and ventriculostomy (2). Most patients responded to initial treatment (19/20). One early and one delayed death were reported. Traumatic TP is rare, tends to be associated with severe craniofacial injuries, and can occur following both blunt and penetrating injury. Early recognition and high index of clinical suspicion are important. Appropriate treatment results in improvement in vast majority of cases. CT scan is the diagnostic modality of choice for TP.

Republished with permission from:

Pillai P, Sharma R, MacKenzie L, Reilly EF, Beery II PR, Papadimos TJ, Stawicki SPA. Traumatic tension pneumocephalus: Two cases and comprehensive review of literature. OPUS 12 Scientist 2010;4(1):6-11.

INTRODUCTION

Traumatic pneumocephalus, or abnormal presence of air in the cranial cavity following traumatic injury, occurs frequently.[1] Its pathophysiology involves air entry into the cranial cavity following injury to the brain meninges.[2] Tension pneumocephalus (TP) is a clinical entity characterized by continued buildup of air within the cranial cavity, leading to abnormal pressure exerted on the brain and subsequent neurologic deterioration.[3,4] The accumulation of intracranial air can be acute or delayed.[3,5,6] Knowledge of risk factors, radiographic findings, and clinical signs/symptoms associated with TP is crucial to its prompt identification and treatment.[4,7,8] Clinical diagnostic and treatment delays may result in poor neurologic outcome and mortality.[9] Treatment may involve a combination of (a) surgical removal of intracranial air; (b) supine or Trendelenburg positioning; (c) administration of 100% oxygen; (d) repair of the bone/dural defects; and (e) drain placement into the air-containing space. In this manuscript, we present two cases of traumatic TP and review additional 18 cases previously reported in literature.

METHODS

Two cases of traumatic TP are presented. In addition, a detailed literature search (PubMed, Google™ Scholar, ScientificCommons) revealed a total of 20 other traumatic pneumocephalus cases, of which 18 [Table 1] contained complete data that were sufficient for subsequent collection/analysis of the following variables: (a) patient age; (b) patient gender; (c) mechanism of injury; (d) primary injury associated with TP; (e) associated injuries; (f) signs and symptoms of TP; (g) therapeutic approach to TP; and (h) timing of clinical onset of TP. Cases reported in literature were then combined with two cases reported by our group and analyzed for demographics, mechanism of injury, symptoms, time to presentation (acute or presenting within 72 h of injury versus delayed or presenting after the initial 72 h postinjury), diagnostic and treatment modalities used, and outcomes.

Table 1.

Comprehensive summary of reported cases of traumatic tension pneumocephalus

Case reports

Case 1

An 8-year-old man was admitted to the hospital after being struck by a motor vehicle. During the initial trauma evaluation, he was found to have slight facial deformities and abdominal tenderness. Computed tomography (CT) demonstrated the presence of multiple skull fractures, including right mastoid fracture as well as pneumocephalus [Figure 1a–d]. His other injuries included a Grade II splenic laceration with no evidence of intravenous contrast extravasation. He was admitted to the Surgical Intensive Care Unit (SICU) for observation. The following morning, the patient was found to have dilated and minimally responsive pupils bilaterally. He also experienced several episodes of bradycardia (lowest recorded heart rate of 28 beats/min). He had no other focal neurologic findings (his Glasgow Coma Score [GCS] remained between 14 and 15), with the only major subjective complaint being significant headache.

Figure 1.

Computed tomographic imaging for Case 1: (a-b) admission computed tomography shows small foci of pneumocephalus; (c-d) admission images showing associated skull fractures, including right mastoid process fracture; (e-f) repeat computed tomographic imaging shows the appearance of the “Mount Fuji” sign

The patient underwent an urgent repeat CT of the brain, which demonstrated a marked increase in the volume of pneumocephalus, no intra- or extra-axial hemorrhage, and stable multiple skull fractures [Figure 1e and f]. The patient, who was initially maintained with 30° head elevation, was now repositioned in flat configuration and high-flow oxygen was administered through face mask. His bradycardic episodes resolved after this positional change and his pupillary dilation resolved over the period of approximately 18 h. Therapy directed at TP was continued for 3 days, after which his activity was liberalized without any recurrent symptom. The patient was doing well on 3-month follow-up (Glasgow Outcome Score [GOS] of 5, GCS of 15, no focal neurological deficits).

Case 2

A 20-year-old man was brought to the trauma evaluation area following a high-speed motor vehicle collision. He sustained massive injuries to his midface after striking the steering wheel. His initial GCS was 14 (motor 6, verbal 5, eyes 3) upon hospital arrival. The initial CT of the head and face demonstrated a small to moderate pneumocephalus, brain contusions as well as multiple facial fractures [Figure 2a]. The patient was initially monitored in the SICU. The patient was placed on 100% oxygen therapy. After approximately 24 h, his GCS suddenly declined to 10 (motor 5, verbal 4, eyes 1). He was intubated, and a repeat CT demonstrated increasing pneumocephalus [Figure 2b], with slight midline shift and the classic appearance of the “Mount Fuji” sign [Figure 2c]. No other obvious causes for such rapid deterioration (i.e., opioid administration, rapidly expanding intracranial hematoma, or other traumatic injuries) were noted. The patient was taken to the operating room for repair of a dural tear as well as fixation of multiple facial fractures. Postoperative CT scan demonstrated resolution of the preoperative pathologic findings [Figure 2d]. The patient gradually recovered over a period of 3 weeks and was discharged to a rehabilitation facility with a GCS of 13 and GOS of 3. On 3-month follow-up, the patient was ambulatory, with GCS of 15, GOS of 4, and continued neurologic improvement.

Figure 2.

Computed tomographic imaging for Case 2: (a) initial computed tomography – note the presence of small amounts of intracranial air; (b and c) repeat computed tomography of the brain demonstrating increasing pneumocephalus, with slight midline shift (c) and “Mount Fuji” sign; and (d) postoperative computed tomography showing the resolution of tension pneumocephalus

REVIEW OF LITERATURE

A total of 20 TP reports were identified. Of those, 18 were suitable for inclusion and further comparisons. Cases outlined by the authors were then added to those identified from the literature search, for a total of 20 patients. There were 17 males and 3 females (median age 26, range 8–92 years). Presentation was acute in 13/20 and delayed in 7/20 patients. Injury mechanisms included motor vehicle collisions (6/20), blunt assault to the craniofacial area (5), falls (4), motorcycle/all-terrain vehicle crashes (3), gunshot wounding (1), and stabbing injury (1). The most common presenting symptoms/signs were depressed mental status (10/20), cerebrospinal fluid (CSF) rhinorrhea (9), headache (8), and loss of consciousness (6). Seizures (3/20), cardiac arrest (2), and blindness (2) were reported less frequently. CT was utilized in 19/20 patients, with magnetic resonance imaging used as the primary neuroimaging modality in one case. The most common injuries thought to be directly associated with traumatic TP included frontal bone/sinus fracture (9/20), ethmoid fracture (5), and other facial/orbital fractures (7). External craniofacial injuries (laceration/contusion) were more common (17/20) than intracranial hemorrhage (5) or cerebral contusions (4). Nonoperative management was utilized in 6/20 patients. Invasive therapeutic options included a combination of craniotomy (11/20), emergency burr hole (4), endoscopy (2), and ventriculostomy (2). Most patients improved with treatment (19/20). Overall, two deaths (2/20 or 10%) were reported. One patient died from multiple organ failure not directly related to TP or associated therapy. Another death was related to intracranial pressure (ICP) monitoring-related complication [Table 1].

DISCUSSION

Pneumocephalus is defined as the presence of air in the cranial vault, usually associated with cranial surgery, craniofacial trauma (especially injuries involving basilar skull or sinus fractures), nasopharyngeal tumor invasion, and meningitis.[6,10] Among these pathophysiologic entities, craniofacial trauma is the most common etiologic factor, with as many as 7%–9% of patients in that group demonstrating the presence of intracranial air on advanced (CT) imaging.[11,12,13] Although the precise incidence of TP among patients with craniofacial trauma is not known, and has not been formally reported to date, the figure is likely <1% (i.e., the authors' medical institutions have seen well in excess of 300 patients with craniofacial trauma during the same year as the two reported cases). Plain imaging can diagnose pneumocephalus, but CT scan is the diagnostic modality of choice, with an ability to detect as little as 0.5 cm ³ of air.[13,14] In fact, the reported incidence of posttraumatic pneumocephalus is approximately 10 times greater (i.e., ~10%) when using CT imaging as compared to plain films (0.5%–0.9%).[4] Observed amounts of intracranial air noted in current case reports (ratios of maximal anterior-posterior extent of the pneumocephalus to the corresponding midline anterior-posterior cranial diameter of ~10%) were consistent with previous reports of posttraumatic TP.[9,15,16]

Pneumocephalus generally develops as a result of a cranial or facial fracture through which air enters the intracranial cavity. Two mechanisms have been proposed to explain pneumocephalus.[17,18,19,20] In the first mechanism, the pathophysiologic process starts with CSF leak in the presence of associated discontinuity of the cranium and leptomeningeal disruption. Subsequent development of relative negative ICP results in a sufficient “vacuum effect” to cause additional accumulation of air within the cranial cavity.[17] This air is generally distributed in the subarachnoid space. The second mechanism is based on the presence of a “one-way valve” at the site of the leptomeningeal tear. Here, the positive endotympanic pressure exceeds the ICP, and air is forced from paranasal sinuses into the cranial cavity.[18] When the ICP exceeds the pressure within the air collection, the “one-way valve” closes, thus preventing the egress of the trapped air.[19,20] In this mechanism, the abnormal air is usually distributed in the extradural space.

TP (i.e., intracranial air causing mass effect on the brain) requires conditions that lead to increased air pressure within the intracranial space, and represents further increases in ICP that are assumed to be due to the mechanisms described above.[19,20] The pressure exerted by the intracranial air upon the brain may lead to extra-axial mass effect with subsequent compression of the frontal lobes [and thus, the “Mount Fuji” appearance on CT, Figures 1e f and 2b, c]. Clinical presentation of TP may include agitation, delirium, otherwise altered level of consciousness, pupillary changes, and frontal lobe syndrome.[9] At times, hemodynamic changes may be present, including episodes of bradycardia with or without hypertension (Case 1).[21]

Trauma is the predominant etiologic factor associated with pneumocephalus, accounting for 67%–74% of all pneumocephalus cases in large series.[12,22] While there are no reports large enough to characterize the incidence of presenting symptoms in patients with TP, certain generalizations may be made based on pneumocephalus literature alone. We have noted that headache was the most common, but not universally present, presenting symptom of TP (44% of cases). This is consistent with previously published data, wherein headache was also found to be the most common, but not predominant, symptom (38% of cases) of pneumocephalus.[12] A comparable degree of similarity can also be seen between the current review and previously reported data in terms of the incidence of CSF rhinorrhea (41% vs. 31%).[12] Of note, the only symptom and physical finding, that is, pathognomonic of pneumocephalus is the bruit hydro-aérique (a.k.a. “succussion splash”), defined as the presence of a splashing sound heard only by the patient upon postural change.[9,16] However, bruit hydro-aérique occurs in only about 7% of pneumocephalus cases.[12] Mental status changes were associated with 44% of TP cases in the current report, with 28% experiencing loss of consciousness at some point during their clinical course.

In terms of clinical management, most cases of pneumocephalus tend to resolve spontaneously with conservative management. Nonoperative management involves oxygen therapy, maintaining the patient supine or in Trendelenburg position, prophylactic antimicrobial therapy (especially in posttraumatic cases), adequate analgesia, frequent neurologic checks, and repeated CT scans. The use of continuous high concentration inspired oxygen as a treatment modality for traumatic pneumocephalus may have certain theoretical benefits (i.e., quicker absorption of the trapped cavitary air through the nitrogen washout effect) although the effectiveness of this approach is yet to be clinically proven in the setting of traumatic pneumocephalus.[23,24,25] Prompt decompression of intracranial air is the initial treatment of symptomatic pneumocephalus.[26] The principles of subsequent treatment parallel those for a CSF leak. It is important to identify the site where the communication between the air cavity and the external environment occurs. If the site can be identified, the passage should be sealed off, thereby decreasing the possibility of worsening or recurrent pneumocephalus. Effective therapy of TP through a controlled decompression using a closed water-seal drainage system has also been described.[27,28]

TP is a neurosurgical emergency, and as such, its early identification is crucial. Diagnostically, Ishiwata et al. described the appearance of the “Mount Fuji” sign in a series of patients with TP.[29] The presence of such “Mount Fuji” sign [Figures 1f and 2b, c] on head CT in trauma patients should be considered a critical finding, and its presence should prompt immediate patient evaluation and appropriate reappraisal of the therapeutic plan.[29] To diagnose TP, the CT findings should correlate with clinical signs of neurologic deterioration. In the early 1980s, an attempt was made to explain the mass effect of pneumocephalus based on the volume of gas. It has been proposed that the volume of air as little 65 mL is sufficient enough to produce TP.[30] Subsequent to this finding, however, other authors demonstrated no substantial difference between the volume of air and the occurrence of TP.[29] After both clinical and imaging findings are appropriately recognized and correlated, definitive treatment is initiated. Reported treatment options for TP include a combination of (a) drilling of burr holes; (b) craniotomy; (c) needle aspiration; (d) ventriculostomy placement; (e) administration of 100% oxygen; and (f) closure of dural defect(s).[29] Careful monitoring for clinical deterioration, as well as serial CT scanning of the brain, is recommended. For additional information and case-specific details, the reader is referred to Table 1. A comprehensive summary of literature sources utilized in this report.[1,2,3,4,5,7,8,9,15,31,32,33,34,35,36,37,38,39]

CONCLUSIONS

Posttraumatic TP is rare, tends to be associated with severe cranial base and facial injuries, and can be present following both blunt and penetrating mechanisms of injury. Early recognition and high index of clinical suspicion are important and prompt treatment results in improvement in vast majority of cases. CT is the gold standard for diagnosis of this condition.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.