------------------------------------------------------------------------------- TITLE: DIAGNOSIS AND TREATMENT OF CSF LEAKS SOURCE: Dept. of Otolaryngology, UTMB, Grand Rounds DATE: 19 April 1989 RESIDENT PHYSICIAN: Amy Coffey, M.D. FACULTY: F. B. Quinn, Jr., M.D. DATABASE ADMINISTRATOR: Melinda McCracken, M.S. ------------------------------------------------------------------------------- "This material was prepared by resident physicians in partial fulfillment of educational requirements established for the Postgraduate Training Program of the UTMB Department of Otolaryngology/Head and Neck Surgery and was not intended for clinical use in its present form. It was prepared for the purpose of stimulating group discussion in a conference setting. No warranties, either express or implied, are made with respect to its accuracy, completeness, or timeliness. The material does not necessarily reflect the current or past opinions of members of the UTMB faculty and should not be used for purposes of diagnosis or treatment without consulting appropriate literature sources and informed professional opinion." Causes of CSF fistulas: 80% head injuries with skull base fractures- M>F 16% surgery - nasal and paranasal cavities, skull base 4% spontaneous fistulas- F>M I. RHINORRHEA A. Traumatic 2-3% of all head injuries; >11% with skull base fractures. Occurs in areas of thinness of bone and adherence of the dura to the skull: cribiform plate, posterior wall of frontal sinus, sphenoid, sella floor or the great sphenoidal wing (large lateral development of sinus). Compound fractures more commonly associated with persistent leaks than linear fractures Late appearance of a fistula provoked by an elevation of the intracranial pressure and by an enlargement of the frontal ventricular horn as consequence of a frontal lobe contusion. Appearance occurs by the 1st or 2nd day in 55%, one week in 15%, and up to 20 years later in 10%. The remainder present with meningitis. Treatment- stops spontaneously or under treatment usually in 3-5 days when detected on the day of or after the injury; treated usually by "head-up" position, avoidance of coughing sneezing, nose blowing and straining, laxitives, restricting oral intake, use of steroids, diuretics or osmotically active medications and by repeated lumbar CSF drainage with removal of about 150ml daily (should not be done with marked brain edema, increased ICP). Spontaneous cure not likely if persist longer than one week; all should be treated operatively. If leak stops within one week, no fracture or only a small linear fracture on X-ray, and no anosmia then operative treatment is probably not necessary but patient should be followed closely for at least one year for signs of recurrent or occult rhinorrhea and warned about the increased risk for meningitis. If anosmic, surgery is probably better performed. Some authors feel all cases with compound fractures, a defect within the posterior wall of the frontal sinus, the cribiform plate and ethmoidal region, or fractures of the sphenoid should be operated upon even if rhinorrhea has stopped spontaneously due to high risk of recurrence and meningitis. All bullet wounds of the anterior cranial fossa with rhinorrhea require operative treatment. B. Postoperative Most frequently from transsphenoidal approach to pituitary adenomas due to intraoperative damage of the pituitary tentorium diaphragma sellae. Following removal of tumors of the base of the skull. During ENT operations: endoscopic sinus surgery(bone often dehiscent in long standing or severe polypoid disease), septoplasty (must not crack the cribiform plate- most often occurs using the Jansen-Middleton forceps and a rocking motion) Fistulas produced unintentionally during ENT operations can usually be closed from the same approach. Repair should be undertaken at once; use temporalis fascia tucked in through the bony defect after dural edges carefully detached from the bone-covered with second piece of fascia and possibly a mucoperiosteal flap from the nasal septum rotated and allowed to cover the second piece of fascia then packed with Gelfoam and antibiotic-impregnated gauze left in place 10-14 days. Transseptal sphenoidectomy offers a limited approach for repairs in this area requiring radiologic control for orientation. Treatment of choice for CSF leaks associated with empty sella syndrome. The external ethmoid approach to the sphenoid may give better visualization. Posterior ethmoidal lesions are better closed via a transfrontal intradural approach. If leak diagnosed during the immediate postoperative period, a subarachnoid lumber drain may be used to decompress; kept in place 1 to 2 weeks; may use prophylactic antibiotics. If unrecognized until patient develops meningitis, external ethmoidectomy approach indicated. If this approach fails, may need anterior craniotomy (morbidity much higher with this approach due to invariable damage to the olfactory nerve). May need to identify site of lesion to help with planning using diagnostic study. C. Spontaneous Nasal CSF fistula with no evidence of traumatic origin, are not the result of operation, or for no clear reason escapes through or along the olfactory nerves. Almost always located in the ethmoidal region. Seen with high pressure hydrocephalus of markedly raised intracranial pressure from other reasons, tumours of the base of the skull, ethmoidal encephalomeningocele and sphenoidal defects such as the empty sella syndrome (10% associated with CSF rhinorrhea) II. OTORRHEA A. Most frequently following temporal bone fractures. B. Second most frequently seen after intracranial surgery involving the temporal bone. C. Spontaneous CSF otorrhea - two different subgroups 72% childhood type with congenital defects of the otic capsule. 1. median age 4 years old. 2. meningitis occurs in 92% (usually pheumococcal, recurrent) 3. follows myringotomy for a presumed serous effusion 4. Mondini deformity; uni- or bilateral absence of cochlear and vestibular function usually 5. CSF usually enters inner ear through a dural defect in the lateral aspect of the internal auditory canal and exits through the oval window. Treatment- most effective operation is stapedectomy and packing of the vestibule with a muscle graft. If hearing is present, subtotal petrosectomy including a radical mastoidectomy with exenteration of the hypotympanic and pericarotid air cells, obliteration of the eustachian tube, middle ear and mastoid, and blind sac closure of the external auditory canal. 28% adult type with bony dehiscenses, most commonly of the tegmen tympani or tegmen mastoideum (floor of the middle cranial fossa), less commonly of the posterior fossa plate 1. range from 27 to 72 years old; median age 56. 2. Women > men. 3. present after myringotomy for effusion with conductive hearing loss; CSF rhinorrhea; meningitis. 4. meningeal defects are either meningoencephaloceles (associated with middle cranial fossa floor defects, none found in posterior defects) or holes in the dura. 5. 6% of routine autopsies have small, often multiple, bony defects in the floor of the middle fossa yet incidence of spontaneous CSF otorrhea is low. Other factors are size of the defect, the length of time that it is present, and the presence of increased intracranial pressure. Treatment- combined mastoid and transtemporal supralabyrinthine approach. Tiny defects can then be repaired through this approach. If a meningoencephalocele is protruding through the tegmen, it is safer to perform a middle fossa craniotomy. Also possible to do a combined mastoid and mini-craniotomy approach for repair of tegmen defects. III. ANTIBIOTICS A. Used for prophylaxis - controversial. 1. infection rates do not differ significantly comparing treated to nontreated using penicillin (8 and 5%). 2. few antibiotics penetrate the normal meninges in sufficient concentration to be of value 3. increase the risk of antimicrobial resistance 4. may mask the appearance of an acute infection B. Pneumococcus (Streptococcus pheumoniae) frequent cause of meningitis secondary to temporal bone fractures; may be solated on culture in up to 50% of cases. IV. DIAGNOSIS A. Observation of clear watery fluid look for hidden leak: comatose- place in lateral position and bend the face downward; conscious-pressure test, valsalva, etc. B. Handkerchief test moistened with nasal secretions dries stiff; with CSF dries soft. C. Nasal rhinorrhea usually thin, watery, and opalescent and throws down a stringy precipitate secondary to mucin when tested with alcohol or acetic acid; CSF is clear and watery and does not precipitate when tested with alcohol or acetic acid. D. Halo test great amount of CSF discharge is necessary E. Glucose oxidase test Clinistix or Tes-tape introduced into the nares; positive indicates CSF rhinorrhea, negative indicates rhinal or allergic discharge. many false positives and false negatives documented. F. Chemical analysis of glucose and protein content collect several cubic centimeters in test tube; positive when the glucose content exceeds 0.4 g/l and the protein content is from less than 1 g/l to a maximum of 2 g/l; not reliable when CSF is contaminated with blood or wound secretion or excessive nasal or lacrimal secretions (>20%). G. Dyes- Fluorescein can use intaoperatively with darklight high sensitivity some complications (i.e. status epilepticus, etc.) H. Radioisotope cisternography radioactive tracers injected into the lumbar subarachnoid space followed by scintigraphy compare count of cotton pledgets and blood; normal maximum ratio is 0.3; Indium or TC pertechnetate most frequently used; choice for scanning CSF fistulae when identifying questionable, very small, or intermittent leaks. Very sensitive- false-positives (detected in patients with no CSF leak by circulation to nasal mucosa through blood stream after absorption via the arachnoid villi), large amount of technical equipment I. Radiopaque contrast material metrizamide- water soluble; used in conjunction with computerized axial and sagittal tomography; may be performed in "head up" position relatively free of neurotoxicity sensitive scan of choice in localizing active CSF leaks J. Immunofixation techniques- identify B2-transferrin pathognomonic for CSF fluid; has not been found in any other body fluid collected in test tube, on Merocel sponges, or by aspiration through the TM procedure: measure the protein concentration - if >5g/l, precipitation with ammonium sulfate; precipitate dissolved in distilled water; electrophoresis; immunofixation by soaking sample in monospecific antiserum against human transferrin; rinsed, fixed and stained with silver staining solution(more sensitive than earlier used Coomassie brilliant blue dye). must examine the patient's serum also therefore avoiding false positives (liver cirrhosis, genetic protein variance); if high levels of contamination with blood or wound secretions, Merocel sponge is centrifuged; if blood contamination is above 3g/l hemoglobin, the hemoglobin content is reduced by column chromatography. High sensitivity (4ul sample volume sufficient), high level of accuracy, speed of testing (in biochemical lab), can be repeated and it is not hazardous to the patient. ------------------------------------------------------------------------------ BIBLIOGRAPHY Adkins, WY, et.al. Mini-Craniotomy for Management of CSF Otorrhea from Tegmen Defects, LARYNGOSCOPE August 1983, 93:1038-1040. Bret, P., et.al. Treatment of Cerebrospinal Fluid Rhinorrhea by Percutaneous Lumboperitoneal Shunting: Review of 15 Cases, NEUROSURGERY 1985, 16:44-47. Cannon, C.R., & R.A. Jahrsdoerfer Temporal Bone Fractures: Review of 90 Cases, ARCH OTOLARYNGOL May 1983, 109:285-288. Curnes, J.T. et.al. CSF Rhinorrhea: Detection and Localization Using Overpressure Cisternography with Tc-99m-DTPA. RADIOLOGY 1985, 154:795-799. Hasegawa, M. et.al. Transfer of Radioisotope from CSF to Nasal Secretion. ACTA OTOLARYNGOL 1983, 95:359-364. Hubbard, J.L. et.al. Spontaneous Cerebrospinal Fluid Rhinorrhea: Evolving Concepts in Diagnosis and Surgical Management Based on the Mayo Clinic Experience from 1970 through 1981. NEUROSURGERY 1985, 16:314-320. Katz, R.T. and P.E. Kaplan Glucose Oxidase Sticks and Cerebrospinal Fluid Rhinorrhea. ARCH PHYS MED REHABIL 1985, 66:391-393. Loew, F. et.al. Traumatic, Spontaneous and Postoperative CSF Rhinorrhea. Luotonen, J. et.al. Localisation of a CSF Fistula by Metrizamide CT Cisternography. 1986, 100:955-958. Maniglia, A.J. Fatal and Major Complications Secondary to Nasal and Sinus Surgery. LARYNGOSCOPE 1989, 99:276-283. Nishihira, S. and T.V. McCaffrey The Use of Fibrin Glue for the Repair of Experimental CSF Rhinorrhea. LARYNGOSCOPE 1988, 98:625-627. Oberascher, G. Cerebrospinal Fluid Otorrhea-New Trends in Diagnosis. AM J OTOLOGY 1988, 9:102-108. Oberascher, G. and E. Arrer Efficiency of Various Methods of Identifying Cerebrospinal Fluid in Oto- and Rhinorrhea. ORL 1986, 48:320-325. Park, J. et.al. Current Management of Cerebrospinal Fluid Rhinorrhea. LARYNGOSCOPE 1983, 93:1294-1300. Wetmore, S.J. et.al. Spontaneous Cerebrospinal Fluid Otorrhea. AM J OTOLOGY 1987, 8:96-101. Yokoyama, K. et.al. Diagnosis of CSF Rhinorrhea: Detection of tau-Transferrin in Nasal Discharge. OTOLARYNGOL H & N SURG 1988, 98:328-332. --------------------------------END-------------------------------------