The most common symptom of laryngotracheal stenosis is gradually-worsening breathlessness (dyspnea) particularly when undertaking physical activities (exertional dyspnea). The patient may also experience added respiratory sounds which in the more severe cases can be identified as stridor but in many cases can be readily mistaken for wheeze. This creates a diagnostic pitfall in which many patients with laryngotracheal stenosis are incorrectly diagnosed as having asthma and are treated for presumed lower airway disease. This increases the likelihood of the patient eventually requiring major open surgery in benign disease and can lead to tracheal cancer presenting too late for curative surgery to be performed.

There are three types of tracheomalacia:

- Type 1—congenital, sometimes associated with tracheoesophageal fistula or esophageal atresia

- Type 2—extrinsic compression sometimes due to vascular rings

- Type 3—acquired due to chronic infection or prolonged intubation or inflammatory conditions like relapsing polychondritis

A Saber-sheath trachea is a trachea that has an abnormal shape caused by chronic obstructive pulmonary disease. The posterior area of the trachea increases in diameter while the lateral measurement decreases.

Woodring et al. (1991) suggested the following diagnostic criteria for tracheomegaly in adults based on chest radiography:

- Adult Males: Tracheal transverse diameter > 25 mm and sagittal diameter > 27 mm.

- Adult Females: Tracheal transverse diameter > 21 mm and sagittal diameter > 23 mm.

Tracheomalacia is a condition where the cartilage that keeps the airway (trachea) open is soft such that the trachea partly collapses especially during increased airflow. The usual symptom is stridor when a person breathes out.

The trachea normally opens slightly during breathing in and narrows slightly during breathing out. These processes are exaggerated in tracheomalacia, leading to airway collapse on breathing out.

If the condition extends further to the large airways (bronchi) (if there is also bronchomalacia), it is termed tracheobronchomalacia. The same condition can also affect the larynx, which is called laryngomalacia. The term is from "trachea" and the Greek μαλακία, "softening"

The differential of TO includes amyloidosis, which is typically circumferential, papillomatosis, though this usually occurs in younger patients and can cause lung cavitation when disseminated, granulomatosis with polyangiitis, though this is circumferential as well and often involves distal lung cavitation as well. Relapsing polychondritis can also spare the posterior wall, though it is not typically nodular in appearance.

Laryngotracheal stenosis is an umbrella term for a wide and heterogeneous group of very rare conditions. The population incidence of adult post-intubation laryngotracheal stenosis which is the commonest benign sub-type of this condition is approximately 1 in 200,000 adults per year. The main causes of adult laryngotracheal stenosis are:

Bronchomalacia is a term for weak cartilage in the walls of the bronchial tubes, often occurring in children under six months. Bronchomalacia means 'floppiness' of some part of the bronchi. Patients present with noisy breathing and/or wheezing. There is collapse of a main stem bronchus on exhalation. If the trachea is also involved the term tracheobronchomalacia (TBM) is used. If only the upper airway the trachea is involved it is called tracheomalacia (TM). There are two types of bronchomalacia. Primary bronchomalacia is due to a deficiency in the cartilaginous rings. Secondary bronchomalacia may occur by extrinsic compression from an enlarged vessel, a vascular ring or a bronchogenic cyst. Though uncommon, idiopathic (of unknown cause) tracheobronchomalacia has been described in older adults.

Initially symptoms asymptomatic or some patients do not experience symptoms at all. In a progressive TBM case symptoms include:

- shortness of breath

- a cough

- mucus build up

- wheezing

- difficulty in breathing

- bluish coloration to skin around the nose and mouth

Symptoms may become worse if the patient is stressed, sick, lying down, or forcing a cough.

- Chronic cough

Tracheobronchopathia osteochondroplastica (TO) is a rare benign disease of unknown cause, in which multiple cartilaginous or bony submucosal nodules project into the trachea and proximal bronchi. The nodules usually spare the posterior wall of the airway because they are of cartilaginous origin, while the posterior wall of the airway is membranous (does not contain cartilage). This is as opposed to tracheobronchial amyloidosis, which does not spare the posterior wall.

It usually occurs in men around their fifth decade of life, as opposed to tracheobronchial papillomatosis due to HPV infection, which usually occurs in younger patients. TO can cause airway obstruction, bleeding and chronic cough. Treatment involves the use of bronchodilators, and physical dilatation by bronchoscopy. The patients are also more prone to post-obstructive pneumonia and chronic lung infection in severe cases.

Tracheobronchomegaly is a very rare congenital disorder of the lung primarily characterized by an abnormal widening of the upper airways. The abnormally widened trachea and mainstem bronchi are associated with recurrent lower respiratory tract infection and copious purulent sputum production, eventually leading to bronchiectasis and other respiratory complications.

Bronchomalacia can best be described as a birth defect of the bronchus in the respiratory tract. Congenital malacia of the large airways is one of the few causes of irreversible airways obstruction in children, with symptoms varying from recurrent wheeze and recurrent lower airways infections to severe dyspnea and respiratory insufficiency. It may also be acquired later in life due to chronic or recurring inflammation resulting from infection or other airway disease.

Symptoms include hemoptysis, and/or massive hemorrhage which result from the formation of a fistula between the trachea and the brachiocephalic artery. The primary threat is respiratory compromise leading to dyspnea and cyanosis. Patients can later present with hypovolemic shock which include symptoms of tachycardia, cyanosis, cold and clammy skin, dizziness, confusion, and fatigue. Patients may also develop septicemia.

Tracheobronchomalacia or TBM is a condition characterized by flaccidity of the tracheal support cartilage which leads to tracheal collapse. This condition can also affect the bronchi. There are two forms of this rare condition: primary TB and secondary TB. Primary TB is congenital and starts as early as two years old. It is mainly linked to genetic causes. Secondary TB is acquired and starts in adulthood. It is mainly developed after an accident or chronic inflammation.

On 28 May 2013, it was reported that a cure had been developed via a 3D printed windpipe. This cure has currently saved the lives of at least 3 infants.

Two-thirds of TIF occurs within three weeks of a tracheotomy. A TIF should be on the top of the differential diagnosis in patients with a tracheostomy followed by bleeding. Most effective diagnostic tool is a rigid bronchoscopy, although this may be unnecessary as a massive arterial hemorrhage from the tracheostomy likely indicates the formation of an TIF. However, a rigid brochoscopy can clear the tracheobronchial tree of aspirated blood and may be used to terminate blood flow.

Only 35% of TIF patients exhibit the pathognomonic warning signs which include sentinel bleeding, a small bleed from the tracheostomy in the preceding the TIF, and pulsations of the tracheostomy tube that coincides with the heartbeat.

Tracheobronchial injury (TBI) is damage to the tracheobronchial tree (the airway structure involving the trachea and bronchi). It can result from blunt or penetrating trauma to the neck or chest, inhalation of harmful fumes or smoke, or aspiration of liquids or objects.

Though rare, TBI is a serious condition; it may cause obstruction of the airway with resulting life-threatening respiratory insufficiency. Other injuries accompany TBI in about half of cases. Of those people with TBI who die, most do so before receiving emergency care, either from airway obstruction, exsanguination, or from injuries to other vital organs. Of those who do reach a hospital, the mortality rate may be as high as 30%.

TBI is frequently difficult to diagnose and treat. Early diagnosis is important to prevent complications, which include stenosis (narrowing) of the airway, respiratory tract infection, and damage to the lung tissue. Diagnosis involves procedures such as bronchoscopy, radiography, and x-ray computed tomography to visualize the tracheobronchial tree. Signs and symptoms vary based on the location and severity of the injury; they commonly include dyspnea (difficulty breathing), dysphonia (a condition where the voice can be hoarse, weak, or excessively breathy), coughing, and abnormal breath sounds. In the emergency setting, tracheal intubation can be used to ensure that the airway remains open. In severe cases, surgery may be necessary to repair a TBI.

Signs and symptoms of spontaneous subcutaneous emphysema vary based on the cause, but it is often associated with swelling of the neck and chest pain, and may also involve sore throat, neck pain, difficulty swallowing, wheezing and difficulty breathing. Chest X-rays may show air in the mediastinum, the middle of the chest cavity. A significant case of subcutaneous emphysema is easy to detect by touching the overlying skin; it feels like tissue paper or Rice Krispies. Touching the bubbles causes them to move and sometimes make a crackling noise. The air bubbles, which are painless and feel like small nodules to the touch, may burst when the skin above them is palpated. The tissues surrounding SCE are usually swollen. When large amounts of air leak into the tissues, the face can swell considerably. In cases of subcutaneous emphysema around the neck, there may be a feeling of fullness in the neck, and the sound of the voice may change. If SCE is particularly extreme around the neck and chest, the swelling can interfere with breathing. The air can travel to many parts of the body, including the abdomen and limbs, because there are no separations in the fatty tissue in the skin to prevent the air from moving.

Signs and symptoms vary depending on what part of the tracheobronchial tree is injured and how severely it is damaged. There are no direct signs of TBI, but certain signs suggest the injury and raise a clinician's suspicion that it has occurred. Many of the signs and symptoms are also present in injuries with similar injury mechanisms such as pneumothorax. Dyspnea and respiratory distress are found in 76–100% of people with TBI, and coughing up blood has been found in up to 25%. However, isolated TBI does not usually cause profuse bleeding; if such bleeding is observed it is likely to be due to another injury such as a ruptured large blood vessel. The patient may exhibit dysphonia or have diminished breath sounds, and rapid breathing is common. Coughing may be present, and stridor, an abnormal, high-pitched breath sound indicating obstruction of the upper airway can also occur.

Damage to the airways can cause subcutaneous emphysema (air trapped in the subcutaneous tissue of the skin) in the abdomen, chest, neck, and head. Subcutaneous emphysema, present in up to 85% of people with TBI, is particularly indicative of the injury when it is only in the neck. Air is trapped in the chest cavity outside the lungs (pneumothorax) in about 70% of TBI. Especially strong evidence that TBI has occurred is failure of a pneumothorax to resolve even when a chest tube is placed to rid the chest cavity of the air; it shows that air is continually leaking into the chest cavity from the site of the tear. Air can also be trapped in the mediastinum, the center of the chest cavity (pneumomediastinum). If air escapes from a penetrating injury to the neck, a definite diagnosis of TBI can be made. Hamman's sign, a sound of crackling that occurs in time with the heartbeat, may also accompany TBI.

Pulmonary artery sling is a rare condition in which the left pulmonary artery anomalously originates from a normally positioned right pulmonary artery. The left pulmonary artery arises anterior to the right main bronchus near its origin from the trachea, courses between the trachea and the esophagus and enters the left hilum. Symptoms include cyanosis, dyspnoea and apnoeic spells. It almost always requires surgical intervention. Rarely it is asymptomatic and is detected incidentally in asymptomatic adults.

A vascular ring is a congenital defect in which there is an abnormal formation of the aorta and/or its surrounding blood vessels. The trachea and esophagus are completely encircled and sometimes compressed by a "ring" formed by these vessels, which can lead to breathing and digestive difficulties.

Most often this is because of persistence of the double aortic arch after the second month of fetal life.

The two arches surround the esophagus and trachea which, if sufficiently constrictive, may cause breathing or swallowing difficulties despite medical therapies.

A less common ring is present with a right aortic arch instead of the usual left-sided aortic arch. This compresses the esophagus and trachea because of the persistence of a ductal ligament (from fetal circulation) that may connect between the aorta on the front and the left subclavian artery posteriorly going to the left arm.

Subcutaneous emphysema is when gas or air is in the layer under the skin. "Subcutaneous" refers to the tissue beneath the skin, and "emphysema" refers to trapped air. It is sometimes abbreviated SCE or SE and also called tissue emphysema, or Sub Q air. Since the air generally comes from the chest cavity, subcutaneous emphysema usually occurs on the chest, neck and face, where it is able to travel from the chest cavity along the fascia. Subcutaneous emphysema has a characteristic crackling feel to the touch, a sensation that has been described as similar to touching Rice Krispies; this sensation of air under the skin is known as "subcutaneous crepitation".

Numerous etiologies of subcutaneous emphysema have been described. Pneumomediastinum was first recognized as a medical entity by Laennec, who reported it as a consequence of trauma in 1819. Later, in 1939, at The Johns Hopkins Hospital, Dr. Louis Hamman described it in postpartum woman; indeed, subcutaneous emphysema is sometimes known as Hamman's syndrome. However, in some medical circles, it can instead be more commonly known as Macklin's Syndrome after L. Macklin, in 1939, and M.T. and C.C. Macklin, in 1944, who cumulatively went on to describe the pathophysiology in more detail.

Subcutaneous emphysema can result from puncture of parts of the respiratory or gastrointestinal systems. Particularly in the chest and neck, air may become trapped as a result of penetrating trauma (e.g., gunshot wounds or stab wounds) or blunt trauma. Infection (e.g., gas gangrene) can cause gas to be trapped in the subcutaneous tissues. Subcutaneous emphysema can be caused by medical procedures and medical conditions that cause the pressure in the alveoli of the lung to be higher than that in the tissues outside of them. Its most common causes are pneumothorax and a chest tube that has become occluded by a blood clot or fibrinous material. It can also occur spontaneously due to rupture of the alveoli with dramatic presentation. When the condition is caused by surgery it is called "surgical emphysema". The term "spontaneous subcutaneous emphysema" is used when the cause is not clear.

Subcutaneous emphysema is not typically dangerous in and of itself, however it can be a symptom of very dangerous underlying conditions, such as pneumothorax. Although the underlying conditions require treatment, subcutaneous emphysema usually does not; small amounts of air are reabsorbed by the body. However, subcutaneous emphysema can be uncomfortable and may interfere with breathing, and is often treated by removing air from the tissues, for example by using large bore needles, skin incisions or subcutaneous catheterization.

Bronchogenic cysts are small, solitary cysts or sinuses, most typically located in the region of the suprasternal notch or over the manubrium.

Symptoms are caused by vascular compression of the airway, esophagus or both. Presentation is often within the first month (neonatal period) and usually within the first 6 months of life. Starting at birth an inspiratory and expiratory stridor (high pitch noise from turbulent airflow in trachea) may be present often in combination with an expiratory wheeze. The severity of the stridor may depend on the patient’s body position. It can be worse when the baby is lying on his back rather than its side. Sometimes the stridor can be relieved by extending the neck (lifting the chin up). Parents may notice that the baby’s cry is hoarse and the breathing noisy. Frequently a persistent cough is present. When the airway obstruction is significant there may be episodes of severe cyanosis (“blue baby”) that can lead to unconsciousness. Recurrent respiratory infections are common and secondary pulmonary secretions can further increase the airway obstruction.

Secondary to compression of the esophagus babies often feed poorly. They may have difficulties in swallowing liquids with choking or regurgitating and increased respiratory obstruction during feeding. Older patients might refuse to take solid food, although most infants with severe symptoms nowadays are operated upon before they are offered solid food.

Occasionally patients with double aortic arches present late (during later childhood or adulthood). Symptoms may mimic asthma.

Laryngeal cleft is usually diagnosed in an infant after they develop problems with feeding, such as coughing, cyanosis (blue lips) and failing to gain weight over time. Pulmonary infections are also common. The longer the cleft, the more severe are the symptoms. Laryngeal cleft is suspected after a video swallow study (VSS) shows material flowing into the airway rather than the esophagus, and diagnosis is confirmed through endoscopic examination, specifically microlaryngoscopy and bronchoscopy. If a laryngeal cleft is not seen on flexible nasopharyngoscopy, that does not mean that there is not one there. Laryngeal clefts are classified into four types according to Benjamin and Inglis. Type I clefts extend down to the vocal cords; Type II clefts extend below the vocal cords and into the cricoid cartilage; Type III clefts extend into the cervical trachea and Type IV clefts extend into the thoracic trachea. Subclassification of type IV clefts into Type IVA (extension to 5 mm below the innomate artery) and Type IV B (extension greater than 5 mm below the innominate artery) may help with preoperative selection of those who can be repaired via transtracheal approach (Type IV A) versus a cricotracheal separation approach (type IV B).