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 spinalfluid 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 arachnoidgranulations through the middle fossaor posterior fossa surfaces of the temporalbone.

• The most common locations for aberrant AGs are 1)lateral to the cribriform plate2) 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