INTRODUCCION
Pneumocephalus, also known as intracranial aerocele or intracerebral pneumatocele, is defined as the presence of gas within any of the intracranial compartments of the cranial vault (intraventricular, intraparenchymal, subarachnoid, subdural, and epidural).1 The first description of intracranial pneumocephalus was made by Thomas in 1866.1 Chiari, in 1884, reported on the autopsy results of a patient who had pneumocephalus as a complication of chronic ethmoid sinusitis.2 Luckett used plain radiographs of the skull in 1913 for the diagnosis of pneumocephalus. The term pneumocephalus was first coined and used by Wolff in 1914.3
In 1967 Markam conducted a study to classify the etiological factors involved. It analyzed 284 cases of pneumocephalus of which 73.9% (n: 218) were secondary to trauma, 12.9% (n: 38) neoplastic, 8.8% (n: 26) infectious and only 0.7% (n: 2) of unknown cause.5 Among the causes of unknown etiology for Markam, the otological origin is presented. Andrews analyzed 54 cases of otological pneumocephalus and reported that traumatic origin was the main cause and represented 36%, followed by otitis media in 30%, otological surgery in 30%, and congenital defect in 2% .4,6-7
Cerebrospinal fluid (CSF) fistula is relatively common in patients with a skull base fracture. A fistula, defined as the abnormal outflow of CSF to the outside, is generally produced by a tear of the dura and arachnoid, which allows communication of the subarachnoid space with the outside. Thus, there is a solution of continuity between the bone barrier and the meninges (osteomeningeal gap), generating communication between the endocranium and the exocranium. This communication occurs mainly towards the cavities related to the skull base: frontal and sphenoid sinuses, ethmoid cells, Eustachian tube, and mastoid cells.8,9
Fig 1. (A) Brain tomography in axial view and a bone window showing mastoid cells occupied by a fluid due to skull base fracture. (B) Cerebral tomography in coronal view and a parenchymal window showing pneumocephalus predominantly in the left frontal region, in basal cisterns, subarachnoid space, and lateral ventricle, effacement of sulci and fissures, with a slight deviation from the midline.
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Traumatic CSF ear fistula occurs in 1% to 3% of all hospitalized head trauma patients (TBI); its frequency rises to 6% in skull base fractures. Studies have shown an incidence of CSF fistula secondary to temporal bone fracture that ranges between 15% and 45%.1,2 This would occur more frequently in temporal fractures of a transverse feature. However, Dahiya et al10 suggest that the involvement of the otic capsule in temporal bone fractures is a more relevant parameter than the geometry of its line. In most cases, the diagnosis is obvious, based on a history of severe trauma and the development of otorrhea. However, the diagnosis can be difficult and delayed in some patients if the CSF leak by the ear is inconspicuous, intermittent, or with no way out, or when there is an undamaged tympanic membrane. In these situations, the patient may present with recurrent meningitis or fluctuating conductive hearing loss. In doubtful cases, the measurement of glucose in the CSF leak can serve as a guide. A highly sensitive, specific, and non-invasive method to determine the nature of an otorrhea is the qualitative determination of ß2-transferrin, a protein present exclusively in the CSF.11
The images constitute important support in the diagnosis: the high-resolution rock tomography (CT) would reveal 70% of the bone defects in patients with clinical CSF fistula. In those cases, in which the CT scan is negative, the study should be complemented with radioisotopic cisternography or CT-cisternography (intrathecal metrizamide).12 The management of post-traumatic otorrhea is conservative. 77-90% of CSF fistulas resolve spontaneously within two weeks, taking an average of four days to close.13,14 This is especially true for middle fossa fistulas, due to extensive fibrosis promoted by a rich plot of arachnoids in this area.5 Treatment consists of maintaining strict rest in a semi-Fowler position (head elevated), avoiding coughing and sneezing. CSF drainage can be done through repeated punctures or the placement of a spinal catheter.
CLINICAL CASE
History and examination: 38-year-old male patient, native and from Lima, Villa María del Triunfo district, with no medical history who was admitted to the emergency room of this hospital (“María Auxiliadora”) with a clinical picture of 1 h of evolution characterized by intense pain and slight bleeding in the right ear, feeling light-headed, holocranial headache that increases when standing, associated with nausea and vomiting, caused by the explosion of a pyrotechnic object (“whistle”) near his right ear.
On physical examination: Patient awake, complaining, lucid, and oriented in time, space, and person. There was evidence of non-active bleeding through the right external auditory canal (EAC)
During the 11 hours following the trauma, leakage of high-flow crystalline fluid (CSF) was evidenced from the right EAC, as well as a sensation of thermal rise (38.4 ° C). A cerebral tomography (CT) showed the presence of pneumocephalus predominantly in the left frontal region, in cisterns around the brain stem, and in the lateral ventricle, effacement of sulci and fissures, with a slight deviation from the midline (<5 mm). The bone window showed a fracture line in the right sphenoid wing, as well as liquid collection in mastoid cells on the right side. (Fig 1) He was hospitalized with the following diagnoses: Acoustic trauma, skull base fracture, CSF fistula, and pneumocephalus.
Treatment: He received antibiotic therapy: Ceftriaxone 2 gr IV every 24 hours, clindamycin 600 mg IV every 8 hours, for 21 days, acetazolamide 500 mg every 8 hours for 15 days, mannitol 20% with an initial dose of 1 g / kg/day that then it gradually decreased until his retirement on the 6th day of hospitalization.
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