Trachea Anatomy
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This discussion of tracheal anatomy covers the following aspects:
Development of the Human Trachea: Highlights of the different periods of embryonic and fetal development
Gross anatomy: The structure, dimensions, and anatomic relationships, as well as the neurovascular and lymphatic supply of the upper airway; differences between the child and adult tracheas
Microscopic anatomy and a few ultrastructural points pertinent to the function of the cartilaginous framework of the trachea
Clinical correlations related to tracheal anomalies, tracheal deviation, or shift as well as artificial trachea
Human development is divided into prenatal and postnatal periods. The prenatal period is further subdivided into 2 periods, the embryonic (see the following image) and fetal periods. The embryonic period (first 8 wk after conception) is divided into 23 stages according to the Carnegie system. Each specific stage is defined by specific morphologic criteria.
The respiratory diverticulum (laryngotracheal diverticulum) appears between the 4th and 6th branchial arches. [1] There is no evidence of identifiable respiratory system development during the first 8 stages of the Carnegie system. During stage 4 (day 20 of embryonic period), the foregut begins its appearance and the respiratory diverticulum, from which the respiratory system develops, is identified in a medial position.
With the continuous growth of the respiratory diverticulum, at about 22 days (stage 10), the primitive pharynx is visible, among the branchial arches and pouches. Around 24 days (stage 11), the respiratory diverticulum divides into 2 lung buds. The respiratory diverticulum then migrates caudally into the mesenchyme ventral to the foregut at 26 days of embryonic life (stage 12) (see the image below). According to O’Rahilly and Tucker, this stage marks the period when the “respiratory tap” is turned on. [2, 3]
According to this theory, the lung buds (tracheal bifurcation) descend, whereas the tracheoesophageal separation remains fixed. During this important stage of human development, the respiratory and digestive tracts develop separately. The mesenchymal tissue separating the 2 systems is known as the tracheoesophageal septum. During stage 13 (embryo is 28 days old), the trachea and lung buds become more evident as the esophagus, respiratory tract, and tracheoesophageal septum elongates.
At the beginning of the fetal period (30 mm crown-rump [C-R] stage), the chondrocytes are well identified within the incomplete rings of the trachea. The cartilage of the rings is hyaline. The paries membranaceus (PM) shows primordium of the circular trachealis muscle. The epiglottis, thyroid cartilage, and the tracheal wall, including the cartilaginous rings, are well defined. The circular shape of the trachealis muscle contains spindle-shaped myoblasts with elongated nuclei. Tracheal glands are not identifiable in the submucosa at this stage yet. During the 42-50 mm C-R stages, the circular trachealis muscle is well defined in the paries membranaceus and between the cartilages, but no glands are visible yet.
The circular muscle fibers of the trachealis muscle are attached to the inner surfaces of the cartilages at the 62 mm C-R stage. Some longitudinal muscle fibers are identified posterior to the circular layer. These fibers attach to the lower part of the posterior aspect of the cricoid, and caudally, they insert into the posterior surface of the carina.
At 100 mm C-R stage, both muscular layers are well indicated. However, elastic fibers, lymphocytes, and tracheal glands are not seen in the submucosa or lamina propria.
The structure, dimensions, and anatomic relations of the trachea as well as the neurovascular and lymphatic supply of the upper airway are described below (see the following images). [4, 5, 6] Some differences between the child and adult tracheas are also mentioned. [7, 8, 9, 10, 11, 12, 13, 14]
The trachea is nearly but not quite cylindrical, flattened posteriorly. In cross-section, it is D-shaped, with incomplete cartilaginous rings anteriorly and laterally, and a straight membranous wall posteriorly. The trachea measures about 11 cm in length and is chondromembranous. This structure starts from the inferior part of the larynx (cricoid cartilage) in the neck, opposite the 6th cervical vertebra, to the intervertebral disc between T4-5 vertebrae in the thorax, where it divides at the carina into the right and left bronchi.
Sex differences
The coronal and sagittal tracheal dimensions vary in males and females. The upper limits of the coronal and sagittal diameters in men are 25 and 27 mm, respectively. In women, they are 21 and 23 mm, respectively. The lower limits for both dimensions are 13 and 10 mm for adult males and females, respectively. The trachea’s diameter, from side-to-side, is from 2 to 2.5 cm, always greater in the male than in the female.
Age differences
In small children, body weight correlates better with tracheal growth than height and age. In the child, the trachea is smaller, more deeply placed, and more movable than in the adult. The bifurcation is also at a higher level until age 10-12 years. The subcarinal angle decreases gradually with age, and the right bronchial angle is reported usually to be smaller than the left. The images below depict the length and anteroposterior (AP) diameter of the trachea from birth to age 20 years.
The video below depicts the trachea of a small child.
Initially, the AP diameter is slightly greater than the transverse. Gradually, as the child grows, the adult configuration emerges. At first, the trachea is funnel-shaped. Later, the discrepancy between the subcricoid area and the carina gradually diminishes, and the tracheal lumen changes from the cylindrical to the more adult-shaped ovoid form. The trachea stops growing in females at around age 14 years, but in males, it continues to enlarge in cross-section but not in length.
The shape of the adult trachea varies even without disease. Some remain circular rather than being ovoid. A triangular configuration is rather rare.
The shape of the trachea varies with change in the intraluminal pressure alterations. This may be due to cough, respiration, or ventilation. The cross-sectional configuration may change markedly with age, especially in the presence of chronic obstructive pulmonary disease (COPD).
Other changes related to disease are softening (malacia) of the tracheal cartilages. The “saber-sheath” trachea is flattened from side-to-side, with a narrow lateral diameter and increased AP diameter. These changes may lead to various degrees of obstruction on coughing and expiration. Other unusual forms occur with tracheal disease such as tracheopathia, osteoplastica, and tracheobronchomegaly (Mounier-Kuhn syndrome). The image below depicts different shapes of the trachea in health and disease.
Cartilaginous rings and bands of fibrous and elastic tissue
The trachea has 15-20 U-shaped rings of hyaline cartilage that are responsible for the lateral rigidity of the organ. Behind, where the “rings” are deficient, the tube is flat and is composed of bands of fibrous and elastic tissue and nonstriated muscle fiber. These tissue bands on the posterior surface of the trachea, which face the esophagus, are capable of yielding to esophageal dilatation resulting from the passage of food or liquid. The cartilaginous rings mechanically hold the airway open but also give it flexibility. By preventing the collapse of the conducting pathway, respiration is not impeded.
The cartilaginous rings may become calcified in advanced life. Each of the cartilages is enclosed in perichondrium; this is continuous within a sheet of dense, irregular connective tissue forming a fibrous membrane between adjacent rings of cartilage and at the posterior aspect of the trachea and extrapulmonary bronchi where the cartilage is incomplete.
The cartilages are placed horizontally above each other, separated by narrow intervals. They measure about 4 mm in depth and 1 mm in thickness. Their outer surfaces are flattened in a vertical direction, but the internal surfaces are convex. The cartilages are thicker in the middle than at the margins. Two or more of the cartilages often unite, partially or completely, and they are sometimes bifurcated at their extremities. They are highly elastic but may become calcified in advanced life.
The first cartilage is broader than the rest and often divided at one end; it is connected by the cricotracheal ligament with the lower border of the cricoid cartilage, with which or with the succeeding cartilage, it is sometimes blended.
The last cartilage is thick and broad in the middle, in consequence of its lower border being prolonged into a triangular hook-shaped process, which curves downward and backward between the 2 bronchi. It ends on each side in an imperfect ring, which encloses the commencement of the bronchus. The cartilage above the last is somewhat broader than the others at its center.
Carina
At the bottom of the trachea, there is a keel-like partition called the carina (frequently membranous) separating the 2 bronchi. It is situated to the left of the median line, and the right bronchus appears to be a more direct continuation of the trachea than the left. During intubation, if the endotracheal tube is pushed beyond the carina, it will enter the right side. This tendency is aided by the larger diameter of the right tube as compared with the left. This fact serves also to explain why a foreign body in the trachea falls more frequently into the right bronchus.
Mucous membrane
The mucous membrane is continuous with, and similar to, the larynx above and intrapulmonary bronchi below. It consists of a layer of pseudostratified ciliated columnar epithelium with numerous goblet cells.
In the neck
The surface of the trachea is covered, from above downward, by the isthmus of the thyroid gland, the inferior thyroid veins, the arteria thyroidea ima (if it exists), the sternothyroid and sternohyoid muscles, the cervical fascia, and, more superficially, by the jugular venous arch between the anterior jugular veins; the thyroid isthmus is in front of the 2nd and 3rd tracheal cartilages.
Laterally, in the neck, it is in relation with the common carotid arteries, the right and left lobes of the thyroid gland, the inferior thyroid arteries, and the recurrent nerves. Posteriorly, it is in contact with the esophagus and behind it, to the vertebral column in the neck and thorax.
Zuckerkandl’s tubercle (ZT) is a pyramidal extension of the thyroid gland, present at the most posterior side of each lobe. Won et al published a study on the comparative anatomy of the thyroid gland and ZTs and their relation to the trachea of the same cadavers before and after fixation. [15] They found that ZT was at the posteromedial border or posterior surface of the thyroid lobe in both the fresh and fixed states, contrary to most previous reports.
In the thorax
The trachea lies in the superior mediastinum.
Anteriorly, it is covered from before backward by the manubrium sterni, the remains of the thymus, the left brachiocephalic (innominate) vein, the aortic arch, the brachiocephalic trunk and left common carotid arteries, and the deep cardiac plexus.
Laterally, on the right side, the trachea is in relation with the pleura and right vagus and near the root of the neck with the brachiocephalic trunk. Laterally, on its left side, the trachea is by the left recurrent nerve, the aortic arch, and the left common carotid and subclavian arteries.
Arterial supply
The lateral parts of the trachea and esophagus are supplied via longitudinal vascular anastomoses of interconnected branches along the lateral surface of the trachea from the following arteries (see the images below) [14] :
Inferior thyroid artery
Subclavian artery
Supreme intercostal artery
Internal thoracic artery
Brachiocephalic trunk
Bronchial arteries at the tracheal bifurcation
The lateral and anterior tracheal walls receive their blood supply through transverse segmental vessels that run in the soft tissues between the cartilages. These transverse vessels interconnect the aforementioned longitudinal anastomoses across the midline and feed the submucosal capillary network. This network is arborized richly beneath the endotracheal mucosa. The tracheal cartilages receive nourishment from the capillary bed located on their internal surface. The esophageal arteries and their subdivisions that supply the posterior membranous tracheal wall contribute almost nothing to the circulation of the cartilaginous walls.
Venous and lymphatic drainage
Small tracheal veins join the laryngeal vein or empty directly into the left inferior thyroid vein. The inferior thyroid veins arise as a venous plexus on the anterior surface of the isthmus of the thyroid gland. Left and right descending veins enter the respective brachiocephalic veins. The 2 veins may form a common trunk entering the superior vena cava or the left brachiocephalic vein.
The tracheal lymphatics drain to the pretracheal, paratracheal, and tracheobronchial groups of lymph nodes. The right lower paratracheal lymph nodes drain into the thoracic duct tributaries that course along the azygos vein. Left superior bronchial lymph nodes below the trachea drain directly into the mediastinal thoracic duct or to the arch of the duct via the left recurrent chain. An alternative pathway is to the aortic arch lymph nodes and up along the arch. Tracheobronchial lymph nodes drain through accessory ducts on both sides of the esophagus to the thoracic duct.
Nerve supply
The muscle fibers of the trachea are innervated by the recurrent laryngeal nerve, which also carry sensory fibers from the mucous membrane. Sympathetic nerve fibers are derived mainly from the middle cervical ganglion and have connections with the recurrent laryngeal nerves.
The tracheal cartilages are enclosed in an elastic fibrous membrane, which consists of 2 layers: (1) the thicker layer, passing over the outer surface of the ring, and (2) the other layer over the inner surface. At the upper and lower margins of the cartilages, the 2 layers blend together and connect the rings. Between the ends of the rings, the membrane forms a single layer. [16, 17, 18]
The muscular tissue consists of 2 layers of nonstriated muscle fibers, longitudinal and transverse. The longitudinal fibers are external and consist of a few scattered bundles. The transverse fibers (trachealis muscle) are internal and form a thin layer, which extends transversely between the ends of the cartilages.
The mucous membrane is continuous with that of the larynx superiorly and the bronchi inferiorly. It consists of areolar and lymphoid tissue and presents a well-marked basement membrane, supporting a stratified epithelium, the surface layer of which is columnar and ciliated, whereas the deeper layers are composed of oval or rounded cells. Beneath the basement membrane, there is a distinct layer of longitudinal elastic fibers with a small amount of intervening areolar tissue. The submucous layer is composed of a loose connective tissue, containing large blood vessels, nerves, and mucous glands; the ducts of the latter pierce the overlying layers and open on the surface.
When Roberts et al used scanning electron microscopy (SEM), histochemistry, and equilibrium tensile testing to investigate the relationship between collagen organization and equilibrium tensile modulus within the structure of airway cartilage, they found that the surfaces of tracheal cartilage matrix are collagen rich and surround a proteoglycan-rich core. [18]
Collagen fibrils in the superficial zones are oriented in the plane of the cartilage surface. In deeper layers of the cartilage, collagen fibrils are oriented less regularly. Equilibrium tensile modulus of 100-micron – thick strips of cartilage was measured and was found to decrease with depth, from 13.6 ± 1.5 MPa (MPa = N/mm2) for the abluminal superficial zone to 4.6 ± 1.7 MPa in the middle zone. [18] Stress-strain curves were linear for strains up to 10% with minimal residual strain. [18] This is consistent with a model in which collagen fibers in the outer layers of the cartilage resist tensile forces, and hydrated proteoglycans in the central zone resist compression forces as the cartilage crescent bends. [19]
Causes of tracheal deviation and shift include the following [7, 8, 9, 17] :
Pleural effusion
Pneumothorax
Pulmonary fibrosis
Lung cancer
Pulmonary collapse
Surgical lobectomy
Pulmonary atelectasis
Mediastinal tumor
Kyphoscoliosis
Hiatal hernia
Thoracic aortic aneurysm
Tension pneumothorax
Pulmonary tuberculosis
Lung collapse
Retrosternal thyroid
Congenital tracheal malformations may be intrinsic to the trachea itself or extrinsic. The primary presenting symptom is most commonly biphasic stridor. Other airway-related symptoms (eg, wheezing, cough, pneumonia, and croup) may be present.
Tracheal agenesis and atresia
Tracheal agenesis and atresia are almost uniformly fatal; fortunately, these conditions are very rare. The trachea may be completely absent (agenesis), or it may be partially in place but considerably deformed (atresia). Communication, in either case, between the larynx and the alveoli of the lungs is lacking. Affected newborns survive only if an alternate pathway for ventilation exists. Surgical attempts yield poor results, making this a noncorrectable malformation.
Tracheal web
Tracheal web consists of a thin layer of tissue draped across the tracheal lumen. Although the thickness of the web may vary, no deformity or abnormality of the underlying cartilage framework exists (in contrast to tracheal stenosis). The web is not complete; the degree of ventilatory symptoms present is directly related to the size of the remaining tracheal lumen. Treatment consists of rupturing the web. This may be accomplished via rigid dilatation, through use of a laser, or with other ablative or cutting instruments. Only the most thickened webs require a more invasive open surgical approach; local resection is the treatment of choice.
Tracheal stenosis
Tracheal stenosis is a rather rare condition. The pathologic process continues to a much greater underlying tissue depth when compared with a tracheal web (see the following images). A single tracheal ring, multiple rings, or even the entire length of the trachea may be involved. Although affected patients may be symptomatic at birth, symptoms may be delayed several months until the airway lumen is compromised further by exacerbation of an upper respiratory tract infection.
Severe tracheal stenosis in children is a rare, life-threatening condition that requires surgery. Yong et al (2013) reported on the use of slide tracheoplasty, with lower mortality and morbidity compared with patch tracheoplasty. [20] The survival 2 years after surgery was associated with an excellent outcome.
Symptoms of tracheal stenosis include dyspnea and biphasic stridor with a prolonged expiratory component. If an affected patient requires intubation, efforts should be made to extubate early to prevent development of further edema and acute additional airway narrowing.
Various other abnormalities are associated with tracheal stenosis, including vascular slings, tracheoesophageal fistulas, pulmonary hypoplasia, and trisomy 21. Short stenoses may be removed directly via a tracheal resection with primary end-to-end anastomosis. More severe lesions require tracheal reconstruction or tracheoplasty.
Vascular anomalies are associated with an essentially normal trachea. However, large vessels are extrinsically impinging upon it; the infant may hyperextend the neck in an effort to straighten the compressed airway, thereby stretching the trachea and pushing away the compressive extraluminal vessels. Fortunately, these episodes spontaneously resolve.
Brachiocephalic trunk compression
The most common vascular anomaly is compression from the brachiocephalic trunk. This is likely to occur especially in cases in which the take-off of the brachiocephalic trunk from the aorta is more distal. Operative intervention is reserved for cases of severe cases. Surgical correction (ie, inominopexy or aortopexy) involves suspending the brachiocephalic or the aorta anteriorly to the sternum.
Complete vascular ring (double aortic arch)
The second most common vascular anomaly is the complete vascular ring, also known as the double aortic arch (see the following image). This condition provides circumferential compression of both the trachea and esophagus. Treatment consists of surgically dividing the ring, generally by ligating the smaller of the 2 arches.
Aberrant left pulmonary artery
Another vascular anomaly affecting the trachea is an aberrant left pulmonary artery. In these cases, the left pulmonary artery passes between the trachea and esophagus, resulting in distal tracheal and right bronchus compression. It is associated with the presence of complete tracheal rings. Treatment involves surgical rerouting of the aberrant vessel. Other vascular anomalies include a right aortic arch with a persistent ligamentum arteriosum as well as an anomalous right subclavian artery compressing the airway if it courses immediately anteriorly or posteriorly to the trachea.
Complete or deformed rings occur when a complete tracheal ring exists, so no posterior membranous portion of the trachea is present, leaving only a rigid ring around the airway. Single rings and short segments may be resected primarily with end-to-end anastomosis, whereas longer segments require tracheoplasty or tracheal reconstruction.
Other tracheal anomalies include tracheoesophageal fistulas, tracheal cysts, trachiectasis (congenital tracheal enlargement), tracheal bronchus (incidence is estimated at 3%, with right side bronchus far outnumbering the left), tracheal clefts and congenitally short tracheas.
To assess the size of the trachea among female patients with idiopathic subglottic stenosis (SGS), Zaghi et al used CT scans of the neck and chest from female patients with idiopathic SGS. [21] The diameter of the trachea was measured at the level of the subglottis, mid-cervical level, and level of the mid-thoracic trachea. Patients with idiopathic SGS were found to have a significantly smaller cross-sectional area throughout the course of the cervical and thoracic trachea. Idiopathic SGS is a rare but distinct subclass of subglottic stenosis characterized by smaller cross-sectional area throughout the course of the trachea.
Mounier-Kuhn syndrome (MKS) is a rare disease of unknown etiology characterized by abnormal dilatation of tracheabronchial tree. The diagnosis of MKS is made using CT scanning of chest, on the basis of enlarged diameters of trachea and main bronchi. Kuwal et al published a histologically confirmed case of MKS in which the diameter of right main bronchus was below minimum diameter (mean + 3 standard deviations) required for the diagnosis. [22] They suggested that the diagnosis of MKS should not be solely based on the diameter of airways but on the basis of the overall clinical, pathologic, and radiologic profile.
Artificial trachea
The main indications for tracheal surgery include congenital or posttraumatic stenoses, inflammatory (generally postintubation) or degenerative lesions, and benign or malignant neoplasms. Although surgical resection has now become part of the surgical practice, other treatment modalities are approaching a new clinical application era, in particular tracheal transplantation and bioengineering.
Since the 1980s, tissue engineering has become one of the major areas of endeavor in medical research. Using this technology, various attempts have been made to create and apply tissue-engineered prosthetic trachea. One type of artificial trachea is a spiral stent composed of Marlex mesh made of polypropylene and covered with collagen sponge made from porcine skin.
Patients undergo a 2-stage operation. In the first operation, after resection of the pathologic regions, the edge of the tracheal cartilage is sutured to the edge of the skin. The tracheal lumen is exposed, and a T-shaped cannula is inserted into the large tracheostoma. After a few weeks, the trachea and skin are separated. The trimmed artificial trachea with venous blood and basic fibroblast growth factor (b-FGF) is then implanted into the cartilage defect. [9]
According to Hovatta (2012), [23] many groups have been active in clinical trials with mesenchymal stem cells in Europe. Successful transplantations of trachea using tissue-engineered stem cells have been made recently. Optimizing the stem cell type for these constructs is ongoing.
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Ted L Tewfik, MD Professor of Otolaryngology-Head and Neck Surgery, Professor of Pediatric Surgery, McGill University Faculty of Medicine; Senior Staff, Montreal Children’s Hospital, Montreal General Hospital, and Royal Victoria Hospital
Ted L Tewfik, MD is a member of the following medical societies: American Society of Pediatric Otolaryngology, Canadian Society of Otolaryngology-Head & Neck Surgery
Disclosure: Nothing to disclose.
Yazeed Alghonaim, MD Resident Physician, Department of Otolaryngology-Head and Neck Surgery, McGill University Faculty of Medicine, Canada
Disclosure: Nothing to disclose.
Thomas R Gest, PhD Professor of Anatomy, Department of Medical Education, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine
Disclosure: Nothing to disclose.
Medscape Reference thanks Ravindhra G Elluru, MD, PhD, Associate Professor, Department of Otolaryngology Head and Neck Surgery, University of Cincinnati College of Medicine; Pediatric Otolaryngologist, Department of Otolaryngology, Cincinnati Children’s Hospital Medical Center, for the video contribution to this article.
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