**2. Pathogenesis**

Numerous factors have been cited in the development of OME in children suffering from CLP, including (1) immature development of the Eustachian tube, (2) abnormalities in the muscle associated with the Eustachian tube, and (3) craniofacial bone abnormalities [3].

#### **2.1. Immature development of the Eustachian tube**

The Eustachian tube of children is not yet fully developed and therefore shorter than that of adults. It is positioned at a more horizontal angle, and the opening to the nasopharynx is narrower. When upper respiratory tract infection causes swelling and inflammation of the respiratory mucosa, the narrow opening of the Eustachian tube can easily be clogged, leading to negative pressure in the middle ear. In addition, the position and length of the Eustachian tube allow viruses and bacteria from the upper respiratory tract to easily pass into the middle ear cavity, which can cause middle ear infection with effusion. Even after infection has been controlled, it is difficult to discharge fluid from the middle ear through the Eustachian tube to the throat, because the Eustachian tube is shorter and more horizontal with a narrow opening. The remaining fluid can lead to OME [6–9].

#### **2.2. Abnormalities of Eustachian tube‐associated muscle**

Anatomical or structural defects associated with cleft palate can affect velopharyngeal func‐ tion. In children with CLP, the abnormal reflux of food and fluid from the mouth into the nasal cavity due to velopharyngeal insufficiency can result in inflammation and edema of the Eustachian orifices and hypertrophy of adenoid pads, leading to tubal obstruction and sec‐ ondary OME [6]. In addition, abnormal development of the tensor veli palatini (TVP) muscle and levator veli palatini muscle in children with CLP can cause maladjustment in the regu‐ lar opening of the Eustachian tube [10, 11]. When the atmospheric pressure of the environ‐ ment changes (e.g., during descent in an airplane) or the gas in the middle ear is absorbed by mucosa, the Eustachian tube is unable to open and thereby relieve pressure in the middle ear. The resulting negative pressure can cause the eardrum to retract, leading to the collection of fluid in the middle ear, which can again lead to OME [6].

#### **2.3. Craniofacial bone abnormalities**

at least once before the first birthday in as many as 90% of the infants born with CLP [2]. In addition, as many as 97% of the infants born with CLP suffer concurrent OME within the first

The clinical significance of OME is often overlooked, and very few studies have explored this condition in depth, despite it being a complication commonly associated with CLP. This chapter reviews pathogenesis, clinical manifestations, consequences, examination, and diag‐ nosis related to OME in children with CLP. Controversies surrounding the treatment of OME in CLP children are also discussed. We also provide a flowchart for management guidance in OME in children with CLP. It is our hope that the results of this study will provide clinicians

Numerous factors have been cited in the development of OME in children suffering from CLP, including (1) immature development of the Eustachian tube, (2) abnormalities in the muscle associated with the Eustachian tube, and (3) craniofacial bone abnormalities [3].

The Eustachian tube of children is not yet fully developed and therefore shorter than that of adults. It is positioned at a more horizontal angle, and the opening to the nasopharynx is narrower. When upper respiratory tract infection causes swelling and inflammation of the respiratory mucosa, the narrow opening of the Eustachian tube can easily be clogged, leading to negative pressure in the middle ear. In addition, the position and length of the Eustachian tube allow viruses and bacteria from the upper respiratory tract to easily pass into the middle ear cavity, which can cause middle ear infection with effusion. Even after infection has been controlled, it is difficult to discharge fluid from the middle ear through the Eustachian tube to the throat, because the Eustachian tube is shorter and more horizontal with a narrow opening.

Anatomical or structural defects associated with cleft palate can affect velopharyngeal func‐ tion. In children with CLP, the abnormal reflux of food and fluid from the mouth into the nasal cavity due to velopharyngeal insufficiency can result in inflammation and edema of the Eustachian orifices and hypertrophy of adenoid pads, leading to tubal obstruction and sec‐ ondary OME [6]. In addition, abnormal development of the tensor veli palatini (TVP) muscle and levator veli palatini muscle in children with CLP can cause maladjustment in the regu‐ lar opening of the Eustachian tube [10, 11]. When the atmospheric pressure of the environ‐ ment changes (e.g., during descent in an airplane) or the gas in the middle ear is absorbed by mucosa, the Eustachian tube is unable to open and thereby relieve pressure in the middle ear. The resulting negative pressure can cause the eardrum to retract, leading to the collection of

two years of life [5].

98 Designing Strategies for Cleft Lip and Palate Care

**2. Pathogenesis**

and patients/parents with a valuable reference.

**2.1. Immature development of the Eustachian tube**

The remaining fluid can lead to OME [6–9].

**2.2. Abnormalities of Eustachian tube‐associated muscle**

fluid in the middle ear, which can again lead to OME [6].

Other abnormalities in the structure of the Eustachian tube in children with CLP have also been associated with the pathogenesis of OME. These abnormalities include increased naso‐ pharyngeal space, alterations to the medial pterygoid plate and hamulus, a shorter tube, larger angle between the cartilage and TVP, higher cartilage cell density, a smaller ratio of lateral and medial lamina area in the cartilage, less curvature of the lumen, less elastin in the hinge portion of the cartilage, and a lower insertion ratio of TVP to the cartilage [12, 13]. Kemaloglu et al. evaluated clinical and cephalometric data of 37 Japanese children with uni‐ lateral complete CLP or isolated cleft palate and compared them to 40 non‐cleft children. They found that differences in the mastoid‐middle ear‐Eustachian tube system are associated with a tendency toward OME in CLP children. This fact helps to elucidate the pathogenesis of OME in children with CLP [14].
