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CSF OTORRHEA
GAJALAKSHMI
• • Cerebrospinal fluid (CSF) otorrhea –Presence
of CSF within the confines of the temporal
bone
• Defect in the dura -abnormal communication
between subarachnoid space and
aircontaining space of temporal bone
The causes of CSF otorrhea
– Trauma (temporal bone fracture)
– Iatrogenic( skull base surgery)
– Neoplastic
– Infectious
– Congenital
• Spontaneous CSF otorrhea – Not related to the
above-mentioned causes
• Two categories of spontaneous cerebral spinal
fluid otorhhea:
(1) pediatric: ages 1–5years,
(2) adult: over 50 years of age
preformed pathways
• Pediatric :
– Enlarged fallopian canal
– Patent tympanomeningeal (Hyrtl’s) fissure
– Mondini dysplasia with communication
to internal auditory canal
• The adult form: enlarging arachnoid
granulations through the middle fossa
or posterior fossa surfaces of the temporal
bone.
• The most common locations for aberrant AGs are
1)lateral to the cribriform plate
2) along the floor of the middle fossa from the tegmen
tympani to the lateral surface of the sella turcica.
3)infrequently located in the posterior fossa plate of the
Temporal bone between the sigmoid sinus and bony
labyrinth and in the region of the jugular foramen.
• There may be an increased incidence of the AG on the
right side of the skull-right side predominance of the
venous system.
Pathophysiology of spontaneous CSF
otorrhea
• Congenital defect theory (Rao A et al ,2005) –
Defects of the middle fossa -tegmen enlarged
( constant CSF pressure) – Dural herniation –
thinning out-csf lea
• Arachnoid granulation theory( Gacek, et al
1999) – Abnormally located arachnoid
granulations –Minor CSF reservoirs. Abnormal
locations - decreased return to the venous
systems – Thinning and erosion of bone k
DEMOGRAPHY
• Mean ages: 60 years
• Mean BMI: 36.3 kg/m2
• Female predominance (F:M=2:1)
• association with
idiopathic intracranial hypertension( Schlosser
et al, 2008)
Empty or partially empty sella turcica
(Friedman et al, 2002 & John et al, 2010)
BMI - CSF otorrhea
Clinical presentation
• Young children:
– h/o recurrent Meningitis
– SNHL( Congenital anomalies )
• Obese middle-aged or elderly women: –
Decreased hearing or aural fullness with
middle ear effusions
– Persistent serous or clear discharge after
myringotomy
investigation
• β-2 transferrin
• MR CT WITH CONTRAST
management
• – Restricted nose blowing
• – Avoidance of straining
• – Bed rest and head elevation of 30 degrees –
• Use of antiemetics, antitussives and stool
softeners
• – Diuretics and fluid restriction
• – Lumbar drain
Surgical intervention
• Various approaches
– Transmastoid & translabyrinthine
– Middle fossa craniotomy
• Materials used to correct bony defect: – Bone,
cartilage, fascia, abdominal fat, silastic and
various combinations of autologous tissues.
• Transmastoid– Preferred approach for most
patients.
–Extracranial visualization of middle and posterior
fossa without damage of intracranial tissues
• Translabyrinthine approach – For patients with no
hearing – Remove all middle ear structure –
Occlude Eustachian tube with bone wax, muscle
and fascia – Obliteration of middle ear with
muscle or fat and close EAC
Mcf approach
• Multilayered Closure:
– highest rate of definitive closure
– lowest rate of recurrence
My references
• Richard R. Gacek-Ear Surgery
• Spontaneous Cerebrospinal Fluid Leaks: A Variant of
Benign Intracranial Hypertension Schlosser, Rodney
J;Woodworth, Bradford A;Eileen Maloney
Wilensky;Grady, M Sean;Bolger, William E The Annals
of Otology, Rhinology & Laryngology; Jul 2006; 115, 7;
• Significance of empty sella in cerebrospinal fluid leaks
RODNEY J. SCHLOSSER, MD, and WILLIAM E. BOLGER,
MD, Charleston, South Carolina, and Bethesda,
Maryland
• Adult onset spontaneous CSF otorrhea with
oval window fistula and recurrent meningitis:
MRI findings V. RUPA, DLO, MS, (ENT), A. JOB,
DLO, MS, (ENT), and V. RAJSHEKHAR, MCh,
(NEURO),* Tamil Nadu, India

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CSF OTORRHEA CAUSES, SYMPTOMS AND TREATMENT

  • 2. • • Cerebrospinal fluid (CSF) otorrhea –Presence of CSF within the confines of the temporal bone • Defect in the dura -abnormal communication between subarachnoid space and aircontaining space of temporal bone
  • 3. The causes of CSF otorrhea – Trauma (temporal bone fracture) – Iatrogenic( skull base surgery) – Neoplastic – Infectious – Congenital • Spontaneous CSF otorrhea – Not related to the above-mentioned causes
  • 4. • Two categories of spontaneous cerebral spinal fluid otorhhea: (1) pediatric: ages 1–5years, (2) adult: over 50 years of age
  • 5. preformed pathways • Pediatric : – Enlarged fallopian canal – Patent tympanomeningeal (Hyrtl’s) fissure – Mondini dysplasia with communication to internal auditory canal • The adult form: enlarging arachnoid granulations through the middle fossa or posterior fossa surfaces of the temporal bone.
  • 6. • The most common locations for aberrant AGs are 1)lateral to the cribriform plate 2) along the floor of the middle fossa from the tegmen tympani to the lateral surface of the sella turcica. 3)infrequently located in the posterior fossa plate of the Temporal bone between the sigmoid sinus and bony labyrinth and in the region of the jugular foramen. • There may be an increased incidence of the AG on the right side of the skull-right side predominance of the venous system.
  • 7.
  • 8. Pathophysiology of spontaneous CSF otorrhea • Congenital defect theory (Rao A et al ,2005) – Defects of the middle fossa -tegmen enlarged ( constant CSF pressure) – Dural herniation – thinning out-csf lea • Arachnoid granulation theory( Gacek, et al 1999) – Abnormally located arachnoid granulations –Minor CSF reservoirs. Abnormal locations - decreased return to the venous systems – Thinning and erosion of bone k
  • 9. DEMOGRAPHY • Mean ages: 60 years • Mean BMI: 36.3 kg/m2 • Female predominance (F:M=2:1) • association with idiopathic intracranial hypertension( Schlosser et al, 2008) Empty or partially empty sella turcica (Friedman et al, 2002 & John et al, 2010)
  • 10. BMI - CSF otorrhea
  • 11. Clinical presentation • Young children: – h/o recurrent Meningitis – SNHL( Congenital anomalies ) • Obese middle-aged or elderly women: – Decreased hearing or aural fullness with middle ear effusions – Persistent serous or clear discharge after myringotomy
  • 13. management • – Restricted nose blowing • – Avoidance of straining • – Bed rest and head elevation of 30 degrees – • Use of antiemetics, antitussives and stool softeners • – Diuretics and fluid restriction • – Lumbar drain
  • 14. Surgical intervention • Various approaches – Transmastoid & translabyrinthine – Middle fossa craniotomy • Materials used to correct bony defect: – Bone, cartilage, fascia, abdominal fat, silastic and various combinations of autologous tissues.
  • 15. • Transmastoid– Preferred approach for most patients. –Extracranial visualization of middle and posterior fossa without damage of intracranial tissues • Translabyrinthine approach – For patients with no hearing – Remove all middle ear structure – Occlude Eustachian tube with bone wax, muscle and fascia – Obliteration of middle ear with muscle or fat and close EAC
  • 16.
  • 18. • Multilayered Closure: – highest rate of definitive closure – lowest rate of recurrence
  • 19.
  • 20. My references • Richard R. Gacek-Ear Surgery • Spontaneous Cerebrospinal Fluid Leaks: A Variant of Benign Intracranial Hypertension Schlosser, Rodney J;Woodworth, Bradford A;Eileen Maloney Wilensky;Grady, M Sean;Bolger, William E The Annals of Otology, Rhinology & Laryngology; Jul 2006; 115, 7; • Significance of empty sella in cerebrospinal fluid leaks RODNEY J. SCHLOSSER, MD, and WILLIAM E. BOLGER, MD, Charleston, South Carolina, and Bethesda, Maryland
  • 21. • Adult onset spontaneous CSF otorrhea with oval window fistula and recurrent meningitis: MRI findings V. RUPA, DLO, MS, (ENT), A. JOB, DLO, MS, (ENT), and V. RAJSHEKHAR, MCh, (NEURO),* Tamil Nadu, India

Editor's Notes

  1. in the anterior cranial fossa,
  2. Autopsy: middle fossa tegmen(21%) Posterior fossa(9%) – (arachnoid villi) carrying CSF enlarge with increased age and physical activity as a result of intermittent subarachnoid pressure [7, 9, 10, 12, 22]. This pulsatile pressure is capable of bone erosion over the course of many years [10, 11]. If the bone erosion occurs over a pneumatized part of the skull such as the TB or paranasal sinuses, then CSF otorrhea or rhinorrhea may develop [9, 10].
  3. ESS occurs when dura herniates through the sellar diaphragm into the sella turcica and fills it with CSF. N In ESS the dural herniation compresses the pituitary gland and gives the radiographic appearance of an empty sella due to the perceived absence of the pituitary gland and the presence of CSF within the sella. ESS may represent a sign of elevated ICPs3,4 Empty sella probably represents a sign of elevated intracranial pressure that leads to idiopathic, spontaneous CSF leaks
  4. Benign icp: etiology is Still unknown and multifactorial in nature( Goddard et al, 2010) – Central obesity – Narrowed cerebral venous sinuses – Hormonal dysfunction: association with polycystic ovarian disease( Connor et al, 2008) Progression of morbid obesity to encephalocele:raised intra abdominal preesure-increased thoracic pressure-decreased venous retyrn-increased ict-bening ict raise-tegmen erosion =-dural herniation-dural thinning out-csf leak
  5. CLEAR FLUID FROM EAR VARIES WITH POSITION Salty sentation in throat Clear watery nasal discharge The more common juvenile variety, reportedly seen in 72% of cases, is represented by an infant or young child with a history of recurrent episodes of meningitis, unilateral, or bilateral severe to profound sensorineural hearing loss and an inner ear anomaly, typically, Mondini’s dysplasia.3 In addition, a history of recurrent middle ear infections or frank CSF otorrhea after myringotomy for suspected middle ear effusion may be present.2 An oval window fistula and/or enlarged cochlear aqueduct are often associated findings.3
  6. has emerged as the preferred biochemical marker of CSF. In 1979, Meurman and colleagues46 performed protein electrophoresis of CSF that low-dose fluorescein (50 mg or less) is unlikely to be associated with adverse events, because most complications seem to be dose related. The recommended dilution of fluorescein is 0.1 mL of 10% fluorescein (the intravenous, not the ophthalmic, preparation) in 10 mL of the patient’s own CSF12; this dilution should be infused slowly over 30 minutes. P
  7. Middle fossa craniotomy with extradural elevation of the temporal lobe avoids the sound transmission system and permits complete exposure and closure of the dural defect. Furthermore, additional asymptomatic AG in Fig. 8.9 Coronal CT demonstrates soft tissue herniation into the mastoid antrum through a bony defect in the tegmen mastoidea (arrow) .