Airway physiology and development

The upper airway

Formation of the cranial vault and base

The skull is a critical factor in the development of the face and upper airway. The skull develops from a membranous and cartilaginous neurocranium ( Fig. 4.1 ). The membranous neurocranium gives rise to the flat bones of the cranial vault and the cartilaginous neurocranium (chondrocranium) forms the skull base. The flat bones of the neurocranium, which form sutures from edge to edge, also form fontanels where more than two bones meet. The base of the skull is formed from the cartilaginous neurocranium, which then becomes the base of the occipital bone, the sphenoid, the ethmoid and petrous bones, and portions of the temporal bone.

The cranial base provides a floor for the calvarium and a roof for the face. The shaping of the skull base and contiguous structures is a dynamic process involving reciprocal influences between the cranial base, the pharynx, the face, and the primary and secondary palates. During fetal life and early childhood, neural influences predominate because of the rapid growth of the brain. During postnatal development of the airway, nasal influences play a major role, and because of speech and feeding activity, the pharynx also influences the development of the skull base. The anterior portion of the skull base is the roof of the nasomaxillary complex, whereas the posterior portion of the cranial base is the roof of the nasopharynx. During development, the depth of the nasopharynx increases as a result of remodeling of the palate and changes in the angulation of the skull base, providing an enlarged nasal airway for the adult.

Craniovertebral development

The paraxial mesoderm, a column of tissue on either side of the midline of the embryo, divides into blocks (somites) at about the fourth week of development. Whereas most of the muscles of the head are derived from branchial arch mesenchyme, the cervical somites form the vertebrae of the neck that, under normal circumstances, undergo segmentation ( Fig. 4.2 ). Current thinking regarding the mechanism of metameric transformation of the presomitic mesoderm (PSM) follows what is called the “clock and wavefront” model, where PSM cells oscillate between a permissive and a nonpermissive state for somite formation. These oscillations are phase-linked and controlled autonomously by a “segmentation clock.” Somite formation is triggered when cells of the rostral PSM, during the permissive phase of the clock, are hit by a wavefront of maturation that slowly moves caudally along the embryonic axis. This periodicity results in the periodic boundaries of the somites. At the molecular level, the phasic oscillation of the segmentation clock is the result of rhythmic expression of cycling genes. which include the fibroblast growth factor gene FGF8 ( ). Failure of such segmentation can result in fusion and shortening with severely limited neck movement.

The face

Just as the neurocranium forms the cranial vault and base, the viscerocranium forms the face and is derived mainly from cartilage of the first two branchial arches ( Fig. 4.3 ). Ectodermally derived neural crest cells of the developing 3- to 4-week-old embryo migrate to branchial arch mesoderm, and the face develops as a result of these massive cell migrations and their interactions. Those cells forming the frontonasal process are derived from the forebrain fold and migrate a relatively short distance as they pass into the nasal region. Those cells that form the mesenchyme of the maxillary and mandibular processes have a considerably longer distance to migrate because they must move into the branchial arches. At 28 days postconception, the face barely shows its eventual relation to the five primordia from which it is derived: the frontonasal prominence, which is the cranial boundary of the primitive mouth (stomodeum); the paired maxillary prominences (the first branchial arch); and the paired mandibular prominences (also the first branchial arch).

The paranasal sinuses begin developing at approximately 40 weeks of gestational age. The completion of turbinate development signals the beginning of sinus development, which continues until early adult life ( Fig. 4.4 ). Although the exact function of the paranasal sinuses is not well understood, inflammatory, infectious, and neoplastic diseases of the sinuses are of major significance to the anesthesiologist, particularly if there is functional impairment before anesthesia and surgery.

The oral cavity—a structure without structures—where much of the anesthesiologist’s attention and skills are focused, has a complex developmental heritage. The mouth (stomodeum) appears as a slight depression in the surface ectoderm, separated from the oral cavity by the oropharyngeal membrane. This membrane ruptures at about 24 to 26 days’ gestation and the primitive foregut then communicates with the amniotic cavity. The involved germ layers are the endoderm internally and the ectoderm externally.

The tongue surface arises primarily from first arch mesenchyme, with significant contributions from the third and fourth arches; hence its complex innervation by the facial nerve in the anterior two-thirds and the hypoglossal nerve in the posterior one-third ( Fig. 4.5 ). The muscle bulk of the tongue arises primarily from occipital somites, explaining the hypoglossal nerve (XII) innervation and its susceptibility to injury from errant placement of dental rolls and pressure injury from overinflated laryngeal mask airway (LMA) cuffs. The thyroid begins as a thickening of the endoderm of the floor of the pharynx, in the midline between the first and second pouches, at the foramen cecum. A thin connection, the thyroglossal duct, remains attached to the oral cavity, and its point of attachment marks the origin of the thyroid gland. The thyroid descends along the thyroglossal duct and reaches the level of the first tracheal ring at about the seventh week of gestation ( Fig. 4.6 ). The thyroglossal duct is then normally obliterated. Accessory thyroid tissue may be deposited anywhere along this path; on the other hand, failure of the thyroid to descend may result in a lingual thyroid.

The upper lip is formed by the merging of the maxillary prominences with the medial nasal prominences, with the lateral basal prominences forming the alae ( Fig. 4.3 ). The intermaxillary segment in the central portion of the upper lip area consists of a labial component (forming the philtrum), a maxillary component (associated with the four incisor teeth), and a palatal component (which becomes the primary palate).

The palate divides the nasomaxillary complex from the oral cavity ( Figs. 4.7 and 4.8 ). The palatal processes advance in a medial direction from the maxillary processes of the first branchial arch, fusing in the midline in an anterior-to-posterior sequence and uniting with the premaxilla and the developing nasal septum. The soft palate forms from continued growth of the posterior edges of these palatal processes, ending with the formation and fusion of the two halves of the uvula.

The nose originates in the cranial ectoderm, which subsequently develops into the frontonasal prominence. The superior portion of the nose is formed from the lateral nasal processes, whereas the inferior portion of the nasal cavity is incomplete until the paired maxillary processes of the first branchial arch grow anteriorly and medially to fuse with the median nasal processes. The nasal cavities extend posteriorly during development, influenced by the posteriorly directed fusion of the palatal processes, thinning out the membrane that separates them from the oral cavity. By the 38th day of development, the two-layer membrane consisting of nasal and oral epithelia ruptures and forms the choanae (posterior nares). Failure of such rupture results in choanal atresia, although these choanae are not in the same location as the definitive choanae, which will eventually be located more posteriorly. Because the normal nasomaxillary complex grows both downward and forward, however, it does explain the unexpectedly anterior location in choanal atresia given the eventual normal development of the choanae ( Fig. 4.8 ).

This complex choreography is driven by numerous influences: cranial neural crest cells, correctly positioned, spatially related and distinctly differentiated tissues, and underlying structures. Among the rapidly evolving knowledge of genetic influences are fibroblast growth factors (FGF), sonic hedgehog (SHH) proteins, and a variety of geographically linked genes ( Fig. 4.9 ). These genes control signaling for cell migration, growth, adhesion, differentiation, and apoptosis, with disruption of the delicate fusion processes resulting in complete or partial clefts of the face, lip, and/or palate. In addition, the developing fetus may be subject to environmental influences at home, in the workplace, or through lifestyle activities (smoking, alcohol and drug intake, allergens, toxic products, heavy metals, etc.).