Middle Ear Ventilation after Acute Otitis media

Abstract

The investigation includes 43 children (82 ears) with acute otitis media who were treated with paracentesis and antibiotics. The middle ear pressure was measured 7 days, 14 days, 1 month, and 2 months after the otitis. A follow-up examination was performed 4–12 months after the otitis. The normalization process was extremely slow: 3 months after the otitis only 37% of the ears had a pressure between 0 and -50 mm H₂O, and 24% had flat curves and chronic secretory otitis. 3–12 months after, 49% of the ears had a normal pressure. A discussion on whether the middle ear ventilation had been reduced before the present otitis, or whether the slow normalization process is due to the changes in the mucous membrane is presented. The first assumption seems to be more probable. The significance of poor ventilation in the occurrence of recurrency is emphasized. Tympanometry is recommended 1–3 months after otitis, especially in recurrent otitis media. The literature on acute suppurative otitis media is very extensive and reveals widely differing opinions on treatment, causes of therapeutic failure, and recurrency. Although commonly agreed that it is a bacterial infection, the distribution of the pathogenic bacteria and the frequency of negative bacterial findings in the secretion vary greatly in the different materials (Lundgren, 1972). Today, the treatment follows several different principles: (1)no primary antibiotic treatment or paracentesis (Meistrup-Larsen et al., 1977); (2) primary antibiotic treatment without paracentesis (Lorentzen and Haugsten, 1977); (3) paracentesis and antibiotic timing treatment on signs of complications (Diamant and Diamant, 1974); (4) primary paracentesis without antibiotics; (5) paracentesis with antibiotics (Lundgren, 1972). The therapeutic effect is considered as being successful when the patient is free of symptoms, the eardrum appears normal and mobile in Siegle’s pneumotic otoscope, and hearing is normal. However, the time of evaluation may vary according to the initial appearance of the disease. The aim of this work has been to investigate prospectively ventilation of the middle ear based on tympanometry performed at various stages after acute otitis. Although it appears valuable when judging the therapeutic effect to include ventilation of the middle ear, apparently only Meistrup-Larsen et al. (1978) have done so when investigating the effect of norephedrine on acute otitis. They found that 14 days after the onset of the disease, 8 out of 100 children did not have normal tympanograms and drums.

Upon the relationship between secretory otitis in childhood and chronic otitis and its sequelae in adults

“…The children were re-examined Vi-A years, on an average 1 Vi years, after treatment (Bonding and . (b) 43 children (82 ears) with acute suppurative otitis were treated with paracentesis and antibiotics and followed with tympanometry for up to 1 year (Leth and Tos, 1977). 4.…”

Penicillin Reduces Eustachian Tube Gland Tissue Changes in Acute Otitis Media

“…Acute otitis media is the most important etiologic factor in the development of secretory otitis media, 14,15 which is well in accordance with a highly increased secretory capacity of the middle ear and Eustachian tube mucosa for a long period after acute otitis media, as determined by an increased goblet cell density and an increased mucous gland volume. 7,11,12 An increased secretory capacity is by several indications correlated to a state of mucosal hypersecretion, [16][17][18] which in conjunction with a deteriorated Eustachian tube function 19 is likely to reflect an intermediate stage of transition towards secretory otitis media. A concurrent or subsequent development of secretory otitis media seems accordingly imminent, as it is frequently seen in the clinical situation following AOM.…”

Eustachian tube gland tissue changes are related to bacterial species in acute otitis media

“…The increased Eustachian tube gland volume and increased thickness of subepithelial connective tissues [14,38] may in addition constitute an extrinsic pressure gradient and subsequently narrow the Eustachian tube lumen, which may contribute to mucus accumulation, compromise patency and hamper the functional opening of the tube, concurrently the drainage of the middle ear. The deteriorated ciliary beating and compromised tubal ventilatory function during and after acute otitis media [39][40][41], possibly as a cause of inflammatory mediators [42], may add further to an accumulation of increased mucous components, which is fascilitated by a slowed mucociliary clearance rate due to higher mucus viscoelasticity during inflammation [43]. Clinically, the Eustachian tube function in children is deteriorated during the recovery phase following acute otitis media [39,40].…”

“…The deteriorated ciliary beating and compromised tubal ventilatory function during and after acute otitis media [39][40][41], possibly as a cause of inflammatory mediators [42], may add further to an accumulation of increased mucous components, which is fascilitated by a slowed mucociliary clearance rate due to higher mucus viscoelasticity during inflammation [43]. Clinically, the Eustachian tube function in children is deteriorated during the recovery phase following acute otitis media [39,40]. Only 25% of ears have a normal middle ear pressure one month after acute otitis media, whereas a normal pressure is found in 39% of ears after three months and in 49% after 4-12 months [40].…”

“…Clinically, the Eustachian tube function in children is deteriorated during the recovery phase following acute otitis media [39,40]. Only 25% of ears have a normal middle ear pressure one month after acute otitis media, whereas a normal pressure is found in 39% of ears after three months and in 49% after 4-12 months [40].…”