Oral fistula closure

Introduction

Cleft palate closure has evolved over the past several decades. Successful palatoplasty involves repair of the clefted mucosal layers and re-positioning and approximation of aberrant musculature of the palate. Outside of velopharyngeal insufficiency, repair dehiscence resulting in an oronasal fistula (ONF) remains an undesirable complication following primary cleft palate closure. Although ONF may occur at any location along the palate repair, the most common sites are at the junction of the hard and soft palate or between the premaxilla (primary) and secondary palate. The development of ONF is highly correlated with compromised vascularity, scar tissue formation and restricted mobility of regional tissues, all of which impede a tension-free closure. Irrespective of the etiologic factors that may have contributed to the occurrence of a fistula, closure can be challenging for the cleft surgeon as direct repair with local tissues is associated with high failure rates. Consequently, the risk of fistula recurrence increases with each additional surgical attempt at repair. Therefore, prevention is key and efforts should be focused on achieving a successful primary palate repair, through tension-free closure. Management of an ONF should begin with a thorough evaluation of the patient and their palatal tissue, in order to determine the most appropriate treatment strategy.

Clinical features

While small ONFs may remain asymptomatic, larger communications are more likely to manifest with unfavorable clinical symptoms. In general, symptoms depend on the size and location of the fistula, as well as general competence of the velopharyngeal port. Larger fistulas may be associated with nasal regurgitation of foods and liquids, hypernasal speech and audible nasal air escape, recurrent sinus infections, and food lodging in the defect with resultant malodor. The hypernasality, however, may be secondary to air escape through the fistula itself and/or through impaired function of the palate (velopharyngeal insufficiency); therefore, adequate function of the velopharyngeal port must be assessed. In the presence of a long-standing, symptomatic fistula, the velopharyngeal mechanism may demonstrate decreased functioning as the palatal movement declines. Indeed, studies have shown improved soft palate function following fistula repair. Prolonged velopharyngeal insufficiency can result in the development of misarticulations, which can negatively impact speech comprehension, and in turn communication skills and social interactions. The latter underscores the importance of early detection and treatment of a symptomatic ONF.

Etiology

Although ONF formation is multifactorial in nature, tension at the site of repair resulting from either cleft width or deficiency of local tissues is considered by most to be the main factor contributing to fistula formation. Additional factors that may contribute to the formation of ONF include infection, tissue trauma/ischemia, hematoma, as well as overlapping suture lines. Moreover, external predictors of postoperative fistula formation have been identified, including cleft severity/width (as defined as cleft width of 15 mm or more), presence of a syndrome (e.g., Treacher Collins syndrome), and surgeons’ experience.

A link between Staphylococcus aureus and Streptococcus pyogenes colonization and palatal fistula formation has been cited by some studies in the literature. The utility of routine antibiotic prophylaxis is, however, challenged by Rottgers et al ., who demonstrated less than a 1% decrease in rate of ONF following primary palatoplasty. In light of the significant morbidity associated with ONF, the authors still recommend administering a single prophylactic dose before surgery.

The type or severity of cleft has also been demonstrated to be a principal corollary factor, where fistula formation following bilateral cleft lip and palate repair was significantly more common when compared with other cleft types. Furthermore, as evidenced by a 2014 systematic review which included 9294 patients from 44 studies, the presence of a cleft of both the lip and palate had a statistically significant effect on ONF formation, compared to clefts of the palate alone. Similarly, other reports suggested that patients with a palatal cleft involving both hard and soft palate were more likely to develop a fistula when compared with clefts of the soft palate alone.

Incidence

The incidence of ONF following primary palatoplasty has been reported to range from less than 1% to up to 76%. This large variation is likely a reflection of a lack of standardization of ONF classification schemes, detection or reporting, as well as the fact that small asymptomatic fistulas are presumably excluded from reported rates. Most studies also seldom account for the type of cleft, surgeons’ experience, patients’ age at the time of repair, as well as technique used, all of which are factors that could further compound the disparity in incidences described. Additionally, continuity of care from birth to adulthood may not be the standard worldwide, and long-term follow-up may reveal late presentation of fistulas. Therefore, the true incidence of palatal fistulas is expectedly underreported in the literature.

Prevention

The most important factor in minimizing the incidence of ONF is ensuring a tension-free closure. The latter can be facilitated by the use of lateral relaxing incisions, as well as palatine foramina osteotomies or periosteal dissection of the greater palatine artery, all of which assists in further mobilization of the oral mucosal layers. Extensive dissection of the palatal musculature, with release of the tensor aponeurosis from both its mucosal attachments and from the hamulus (or hamulotomy) may also assist in closure. Alternatively, consideration should be given to the decreased vascularity of the tissues with more radical dissection – potentially mitigating the benefits of radical mobilization should proper tissue-handling and dissection not be maintained. Sommerlad popularized the use of vomerine flaps for hard palate closure at the time of cleft lip repair. While this narrows the cleft and thus facilitates soft palate closure, some studies have shown increased rate of fistula between the hard and soft palate. Sommerlad, however, does not report an increased fistula rate with this technique, highlighting the impact of a surgeon’s experience on the rate of fistula formation.

Bolstering the site of repair with additional peripalatal tissue either to decrease suture-line tension or to provide additional vascularized tissue between repaired tissues, has also been described. To that end, both musculomucosal buccal flaps or buccal fat pad flaps (unilateral or bilateral) employed during the primary repair of cleft palate have been employed to reduce the incidence of postoperative fistula. The use of acellular dermal matrix as an inter-positional scaffold has also been shown to decrease the rate of the formation of postoperative fistulas following primary surgical repair of the cleft palate.

Classification

One proposed ONF classification system is the Pittsburgh Fistula Classification System, which describes seven fistula sub-types based on anatomical location ( Fig. 21.6.1 ). Fistulas are then further categorized into functional or non-functional depending on the associated clinical symptoms such as disturbed speech and the presence of nasal regurgitation. ONFs have also been classified according to their size as small (<2 mm in diameter), medium (2–5 mm), and large (>5 mm). For the purposes of this chapter, fistula sizes are grouped into either small (2–3 mm or less) and large (>3 mm) as there is considerable overlap of techniques employed for various fistula sizes. It is generally agreed that larger fistulas (>3 mm) are more prone to failure following attempted repair, and more significant (or additional) tissue mobilization may be required or warranted.