Aeration of Prussak's space is independent of the supradiaphragmatic epitympanic compartments.

HYPOTHESIS: This study's aim was to find out how well various microdissection approaches reveal the basic anatomy of the epitympanum, especially the pathways of aeration to Prussak's space, without the help of serial sections, which many find difficult to interpret. BACKGROUND: The basic studies where made during the latter half of the 19th and the first half of the 20th century. Conflicting concepts have later been published, and doubtful information has been included even in textbooks. METHODS: We have studied 145 temporal bones via microdissection to record the state of the soft tissue structures of the epitympanum, particularly upon Prussak's space with its boundaries. A normal surgical otomicroscope was used in the evaluation, and the findings were recorded via black and white and/or color photography; for recent cases, a digital video camera was used. RESULTS: The epitympanic diaphragm separates the large upper floor compartments from the small, laterally placed lower floor unit. The latter consists of Prussak's space and the posterior pouch, at times also of the lower lateral attic. The tympanic isthmus connects the upper unit to the medial tympanum. Defects in the diaphragm create additional airways to the upper unit, in 29% via the tensor fold and in 19% via the lateral incudomalleal fold. In only 7% was there a small opening in the roof of Prussak's space connecting it to the upper unit. Effective aeration of Prussak's space was independent of the upper floor compartments. CONCLUSION: Microdissection is a reliable and sufficient method for teaching epitympanic anatomy. All important structures can be identified and defects in the epitympanic diaphragm verified. Data obtained via serial sections are invaluable in research but not essential in the training of ear surgeons. The two-floor structure of the epitympanum with an independent aeration of the two units should be the starting point for all anatomy teaching.

Meconium contaminated amniotic fluid and infant otitis media. Is it a risk factor in children surviving aspiration and initial distress of respiration?

OBJECTIVE: Histological studies show that amniotic fluid cellular content (AFCC) causes in the middle ear a foreign body reaction, the extent and severity of which depends upon the massiveness of contamination. We studied how factors related to birth and environment affect proneness to acute otitis media (AOM) in infants born through meconium contaminated amniotic fluid. METHODS: From the birth records of infants born from 1996 to 2000 a list was made of those born through meconium contaminated amniotic fluid with pulmonary aspiration and tracheal suctioning, followed by treatment in a neonatal intensive care unit. Thirty-seven such children formed the study group, 43 children matching the study cases but born through clear fluids formed the control group. Birth and environmental factors together with the frequency and number of episodes of AOM were analyzed in all, based on a verified questionnaire. In addition, 27 children in the study group and 21 in the control group received a specialist ENT examination, hearing tests and tympanometry. RESULTS: The events at delivery were highly significantly different between the two groups, manifested by the lower Apgar points in the study group (p<0.001) while other birth and environmental factors appeared equalized. The first episode of AOM in the study group came earlier than in the control group and their frequency was significantly higher during the 1st and 2nd year of life and during the entire observation period (p<0.001). Tympanostomy was performed more often in the study group. Tympanometry showed more cases of reduced static admittance and negative pressure than in the control group and hearing was poorer. CONCLUSIONS: Cases with compromised delivery through meconium contaminated fluids, resulting in pulmonary aspiration and in need of intensive care treatment, form a risk group, which should be closely followed. Early nasopharyngeal suctioning of AFCC may reduce its entry into the middle ear. A prolonged episode of AOM suggests mucosal involvement of several middle ear compartments, shown by histological studies to occur in all cases of massive contamination. Placement of a ventilation tube after the first prolonged AOM allows regression of the granulation tissue in the air spaces together with the secretory elements in the mucosa.

Fate of the mesenchyme in the process of pneumatization.

HYPOTHESIS: This study's aim was to find histologic data that would indicate the mode of disappearance of the embryonal mesenchyme. BACKGROUND: The basic studies made during the first half of the 20th century concluded that mesenchyme disappears by regression and resorption. Recently, it was suggested that mesenchyme disappears by receding, spreading, and thinning to match the enlarging bony spaces. METHODS: We studied 11 serially sectioned temporal bones from newborns to adults and describe detailed findings in a 9-day-old newborn and in a 1.5-year-old infant. The temporal bones were sectioned to 20 mum and stained by hematoxylin and eosin. RESULTS: Histologic evidence of regression was found in the form of degenerating mesenchymal cells and fibers, in areas free of cells, and with empty spaces of varying size between the fibers. Vacuoles differing much in size appeared, and phagocytic cells were frequent. A rich capillary network allowed resorption of hemopoietic cells dispersed from the marrow spaces into the mesenchyme. From the lower lateral attic, from Prussak's space, and from the mastoid air cells, mesenchyme can disappear only by regression-there is no space where it could recede. CONCLUSION: Pneumatization of the middle ear spaces occurs by regression and resorption with an individual speed under genetic guidance. The osteoclastic activity of the periosteum, intertwined with the nearest mesenchyme, is decisive in the mastoid air cell formation. Dispersion and reabsorption of hemopoietic cells is a normal phenomenon in this process. Underpressure in the middle ear spaces, caused either by a meconium-related foreign body otitis media in infancy or by chronic otitis media in childhood, are factors that may lead to a partial or full arrest of pneumatization.