Medical diagnosis of pulmonary hypoplasia in utero may use imaging, usually ultrasound or MRI. The extent of hypoplasia is a very important prognostic factor. One study of 147 fetuses (49 normal, 98 with abnormalities) found that a simple measurement, the ratio of chest length to trunk (torso) length, was a useful predictor of postnatal respiratory distress. In a study of 23 fetuses, subtle differences seen on MRIs of the lungs were informative. In a study of 29 fetuses with suspected pulmonary hypoplasia, the group that responded to maternal oxygenation had a more favorable outcome.

Pulmonary hypoplasia is diagnosed also clinically.

Pneumomediastinum is uncommon and occurs when air leaks into the mediastinum. The diagnosis can be confirmed via chest X-ray showing a radiolucent outline around the heart and mediastinum or via CT scanning of the thorax.

Bronchopulmonary sequestration (BPS) is a rare congenital malformation of the lower respiratory tract.

It consists of a nonfunctioning mass of normal lung tissue that lacks normal communication with the tracheobronchial tree, and that receives its arterial blood supply from the systemic circulation.

BPS is estimated to comprise 0.15 to 6.4 percent of all congenital pulmonary malformations, making it an extremely rare disorder.

Sequestrations are classified anatomically.

Intralobar sequestration (ILS) in which the lesion is located within a normal lobe and lacks its own visceral pleura.

Extralobar sequestration (ELS) in which the mass is located outside the normal lung and has its own visceral pleura

The blood supply of 75% of pulmonary sequestrations is derived from the thoracic or abdominal aorta.

The remaining 25% of sequestrations receive their blood flow from the subclavian, intercostal, pulmonary, pericardiophrenic, innominate, internal mammary, celiac, splenic, or renal arteries.

Usually the sequestration is removed after birth via surgery. In most cases this surgery is safe and effective; the child will grow up to have normal lung function.

In a few instances, fetuses with sequestrations develop problematic fluid collections in the chest cavity. In these situations a Harrison catheter shunt can be used to drain the chest fluid into the amniotic fluid.

In rare instances where the fetus has a very large lesion, resuscitation after delivery can be dangerous. In these situations a specialized delivery for management of the airway compression can be planned called the EXIT procedure, or a fetal laser ablation procedure can be performed. During this minimally invasive fetal intervention, a small needle is inserted into the sequestration, and a laser fiber is targeted at the abnormal blood vessel going to the sequestration. The goal of the operation is to use laser energy to stop the blood flow to the sequestration, causing it to stop growing. Ideally, after the surgery, the sequestration steals less blood flow from the fetus, and the heart and lungs start growing more normally as the sequestration shrinks in size and the pleural effusion goes away.

The treatment for this is a wedge resection, segmentectomy, or lobectomy via a VATS procedure or thoracotomy.

Pulmonary sequestrations usually get their blood supply from the thoracic aorta.

Because it is rare and has a wide spectrum of clinical, histological, and imaging features, diagnosing lymphangiomatosis can be challenging. Plain x-rays reveal the presence of lytic lesions in bones, pathological fractures, interstitial infiltrates in the lungs, and chylous effusions that may be present even when there are no outward symptoms.

The most common locations of lymphangiomatosis are the lungs and bones and one important diagnostic clue is the coexistence of lytic bone lesions and chylous effusion. An isolated presentation usually carries a better prognosis than does multi-organ involvement; the combination of pleural and peritoneal involvement with chylous effusions and lytic bone lesions carries the least favorable prognosis.

When lung involvement is suspected, high resolution computed tomography (HRCT) scans may reveal a diffuse liquid-like infiltration in the mediastinal and hilar soft tissue, resulting from diffuse proliferation of lymphatic channels and accumulation of lymphatic fluid; diffuse peribronchovascular and interlobular septal thickening; ground-glass opacities; and pleural effusion. Pulmonary function testing reveals either restrictive pattern or a mixed obstructive/restrictive pattern. While x-rays, HRCT scan, MRI, ultrasound, lymphangiography, bone scan, and bronchoscopy all can have a role in identifying lymphangiomatosis, biopsy remains the definitive diagnostic tool.

Microscopic examination of biopsy specimens reveals an increase in both the size and number of thin walled lymphatic channels along with lymphatic spaces that are interconnecting and dilated, lined by a single attenuated layer of endothelial cells involving the dermis, subcutis, and possibly underlying fascia and skeletal muscle. Additionally, Tazelaar, et al., described a pattern of histological features of lung specimens from nine patients in whom no extrathoracic lesions were identified, which they termed "diffuse pulmonary lymphangiomatosis" (DPL).

Recognition of the disease requires a high index of suspicion and an extensive workup. Because of its serious morbidity, lymphangiomatosis must always be considered in the differential diagnosis of lytic bone lesions accompanied by chylous effusions, in cases of primary chylopericardium, and as part of the differential diagnosis in pediatric patients presenting with signs of interstitial lung disease.

Respiratory diseases may be investigated by performing one or more of the following tests

- Biopsy of the lung or pleura

- Blood test

- Bronchoscopy

- Chest x-ray

- Computed tomography scan, including high-resolution computed tomography

- Culture of microorganisms from secretions such as sputum

- Ultrasound scanning can be useful to detect fluid such as pleural effusion

- Pulmonary function test

- Ventilation—perfusion scan

Lymphatic malformations may be detected in the human fetus by ultrasound if they are of sufficient size. Detection of a cystic malformation may prompt further investigation, such as amniocentesis, in order to evaluate for genetic abnormalities in the fetus. Lymphatic malformations may be discovered postnatally or in older children/adults, and most commonly present as a mass or as an incidental finding during medical imaging.

Verification of the diagnosis may require more testing, as there are multiple cystic masses that arise in children. Imaging, such as ultrasound or MRI, may provide more information as to the size and extent of the lesion.

Management has three components: interventions before delivery, timing and place of delivery, and therapy after delivery.

In some cases, fetal therapy is available for the underlying condition; this may help to limit the severity of pulmonary hypoplasia. In exceptional cases, fetal therapy may include fetal surgery.

A 1992 case report of a baby with a sacrococcygeal teratoma (SCT) reported that the SCT had obstructed the outlet of the urinary bladder causing the bladder to rupture in utero and fill the baby's abdomen with urine (a form of ascites). The outcome was good. The baby had normal kidneys and lungs, leading the authors to conclude that obstruction occurred late in the pregnancy and to suggest that the rupture may have protected the baby from the usual complications of such an obstruction. Subsequent to this report, use of a vesicoamniotic shunting procedure (VASP) has been attempted, with limited success.

Often, a baby with a high risk of pulmonary hypoplasia will have a planned delivery in a specialty hospital such as (in the United States) a tertiary referral hospital with a level 3 neonatal intensive-care unit. The baby may require immediate advanced resuscitation and therapy.

Early delivery may be required in order to rescue the fetus from an underlying condition that is causing pulmonary hypoplasia. However, pulmonary hypoplasia increases the risks associated with preterm birth, because once delivered the baby requires adequate lung capacity to sustain life. The decision whether to deliver early includes a careful assessment of the extent to which delaying delivery may increase or decrease the pulmonary hypoplasia. It is a choice between expectant management and active management. An example is congenital cystic adenomatoid malformation with hydrops; impending heart failure may require a preterm delivery. Severe oligohydramnios of early onset and long duration, as can occur with early preterm rupture of membranes, can cause increasingly severe PH; if delivery is postponed by many weeks, PH can become so severe that it results in neonatal death.

After delivery, most affected babies will require supplemental oxygen. Some severely affected babies may be saved with extracorporeal membrane oxygenation (ECMO). Not all specialty hospitals have ECMO, and ECMO is considered the therapy of last resort for pulmonary insufficiency. An alternative to ECMO is high-frequency oscillatory ventilation.

Respiratory disease is a common and significant cause of illness and death around the world. In the US, approximately 1 billion "common colds" occur each year. A study found that in 2010, there were approximately 6.8 million emergency department visits for respiratory disorders in the U.S. for patients under the age of 18. In 2012, respiratory conditions were the most frequent reasons for hospital stays among children.

In the UK, approximately 1 in 7 individuals are affected by some form of chronic lung disease, most commonly chronic obstructive pulmonary disease, which includes asthma, chronic bronchitis and emphysema.

Respiratory diseases (including lung cancer) are responsible for over 10% of hospitalizations and over 16% of deaths in Canada.

In 2011, respiratory disease with ventilator support accounted for 93.3% of ICU utilization in the United States.

The tissues in the mediastinum will slowly resorb the air in the cavity so most pneumomediastinums are treated conservatively. Breathing high flow oxygen will increase the absorption of the air.

If the air is under pressure and compressing the heart, a needle may be inserted into the cavity, releasing the air.

Surgery may be needed to repair the hole in the trachea, esophagus or bowel.

If there is lung collapse, it is imperative the affected individual lies on the side of the collapse, although painful, this allows full inflation of the unaffected lung.

In several editions of Physical Diagnosis, concerning mediastinal tumors the author writes:

Many signs and symptoms of a mediastinal tumor do not distinguish between these two principal classes of mediastinal tumor. However, on a radiograph usually the former class will have an irregular shape and the latter class will have a smooth spherical or ovoid shape. A large minority of patients with a mediastinal teratoma (including dermoid cyst) will cough up hair. For a differential diagnosis, the key is to exclude aneurism.

Most common primary anterior mediastinal tumor (20%) in adults but rarely seen in children. It can be classified as lymphocytic, epithelial, or spindle cell histologies, but the clinical significance of these classifications is controversial. Tonofibrils seen under electron microscopy can differentiate thymoma from other tumors such as carcinoid, Hodgkin's, and seminoma. Patients are usually asymptomatic but can present with myasthenia gravis-related symptoms, substernal pain, dyspnea, or cough. Invasive tumors can produce compression effects such as superior vena cava syndrome. (3,4) Thymomas are diagnosed with CT or MRI revealing a mass in anterior mediastinum. Therapy in stage I tumors consists of surgical resection with good prognosis. Stage II-III requires maximal resection possible followed by radiation. Stage IV disease requires addition of cisplatin-based chemotherapy in addition to those in stage II and III. For those with invasive thymoma, treatment is based on induction chemotherapy, surgical resection, and post-surgical radiation. 5-year survival for invasive thymoma is between 12-54% regardless of any myasthenia gravis symptoms (5,6).

Thoracocentesis, pericardiocentesis, pleurodesis, ligation of thoracic duct, pleuroperitoneal shunt, radiation therapy, pleurectomy, pericardial window, pericardiectomy, thalidomide, interferon alpha 2b, Total Parenteral Nutrition (TPN), medium chain triglyceride (MCT) and high protein diet, chemotherapy, sclerotherapy, transplant;

A baby with a prenatally diagnosed cystic hygroma should be delivered in a major medical center equipped to deal with neonatal complications, such as a neonatal intensive care unit. An obstetrician usually decides the method of delivery. If the cystic hygroma is large, a cesarean section may be performed. After birth, infants with a persistent cystic hygroma must be monitored for airway obstruction. A thin needle may be used to reduce the volume of the cystic hygroma to prevent facial deformities and airway obstruction. Close observation of the baby by a neonatologist after birth is recommended. If resolution of the cystic hygroma does not occur before birth, a pediatric surgeon should be consulted.

Cystic hygromas that develop in the third trimester, after thirty weeks gestation, or in the postnatal period are usually not associated with chromosome abnormalities. There is a chance of recurrence after surgical removal of the cystic hygroma. The chance of recurrence depends on the extent of the cystic hygroma and whether its wall was able to be completely removed.

Treatments for removal of cystic hygroma are surgery or sclerosing agents which include:

- Bleomycin

- Doxycycline

- Ethanol (pure)

- Picibanil (OK-432)

- Sodium tetradecyl sulfate

Initially, diagnosis can be difficult, especially when other severe injuries are present; thus the condition is commonly diagnosed late. Chest X-ray is known to be unreliable in diagnosing diaphragmatic rupture; it has low sensitivity and specificity for the injury. Often another injury such as pulmonary contusion masks the injury on the X-ray film. Half the time, initial X-rays are normal; in most of those that are not, hemothorax or pneumothorax is present. However, there are signs detectable on X-ray films that indicate the injury. On an X-ray, the diaphragm may appear higher than normal. Gas bubbles may appear in the chest, and the mediastinum may appear shifted to the side. A nasogastric tube from the stomach may appear on the film in the chest cavity; this sign is pathognomonic for diaphragmatic rupture, but it is rare. A contrast medium that shows up on X-ray can be inserted through the nasogastric tube to make a diagnosis. The X-ray is better able to detect the injury when taken from the back with the patient upright, but this is not usually possible because the patient is usually not stable enough; thus it is usually taken from the front with the patient lying supine. Positive pressure ventilation helps keep the abdominal organs from herniating into the chest cavity, but this also can prevent the injury from being discovered on an X-ray.

Computed tomography has an increased accuracy of diagnosis over X-ray, but no specific findings on a CT scan exist to establish a diagnosis. Although CT scanning increases chances that diaphragmatic rupture will be diagnosed before surgery, the rate of diagnosis before surgery is still only 31–43.5%. Another diagnostic method is laparotomy, but this misses diaphragmatic ruptures up to 15% of the time. Often diaphragmatic injury is discovered during a laparotomy that was undertaken because of another abdominal injury. Because laparotomies are more common in those with penetrating trauma then compared to those who experienced a blunt force injury, diaphragmatic rupture is found more often in these persons. Thoracoscopy is more reliable in detecting diaphragmatic tears than laparotomy and is especially useful when chronic diaphragmatic hernia is suspected.

Between 50 and 80% of diaphragmatic ruptures occur on the left side. It is possible that the liver, which is situated in the right upper quadrant of the abdomen, cushions the diaphragm. However, injuries occurring on the left side are also easier to detect in X-ray films. Half of diaphragmatic ruptures that occur on the right side are associated with liver injury. Injuries occurring on the right are associated with a higher rate of death and more numerous and serious accompanying injuries. Bilateral diaphragmatic rupture, which occurs in 1–2% of ruptures, is associated with a much higher death rate (mortality) than injury that occurs on just one side.

Diagnosis is made through a combination of patient history, neurological examination, and medical imaging. Magnetic resonance imaging (MRI) is considered the best imaging modality for Chiari malformation since it visualizes neural tissue such as the cerebellar tonsils and spinal cord as well as bone and other soft tissues. CT and CT myelography are other options and were used prior to the advent of MRI, but they characterize syringomyelia and other neural abnormalities less well.

By convention the cerebellar tonsil position is measured relative to the basion-opisthion line, using sagittal T1 MRI images or sagittal CT images. The selected cutoff distance for abnormal tonsil position is somewhat arbitrary since not everyone will be symptomatic at a certain amount of tonsil displacement, and the probability of symptoms and syrinx increases with greater displacement, however greater than 5 mm is the most frequently cited cutoff number, though some consider 3–5 mm to be "borderline," and symptoms and syrinx may occur above that. One study showed little difference in cerebellar tonsil position between standard recumbent MRI and upright MRI for patients without a history of whiplash injury. Neuroradiological investigation is used to first rule out any intracranial condition that could be responsible for tonsillar herniation. Neuroradiological diagnostics evaluate the severity of crowding of the neural structures within the posterior cranial fossa and their impact on the foramen magnum. Chiari 1.5 is a term used when both brainstem and tonsillar herniation through the foramen magnum are present.

The diagnosis of a Chiari II malformation can be made prenatally through ultrasound.

In the late 19th century, Austrian pathologist Hans Chiari described seemingly related anomalies of the hindbrain, the so-called Chiari malformations I, II and III. Later, other investigators added a fourth (Chiari IV) malformation. The scale of severity is rated I – IV, with IV being the most severe. Types III and IV are very rare.

Other conditions sometimes associated with Chiari malformation include hydrocephalus, syringomyelia, spinal curvature, tethered spinal cord syndrome, and connective tissue disorders such as Ehlers-Danlos syndrome and Marfan syndrome.

Chiari malformation is the most frequently used term for this set of conditions. The use of the term Arnold–Chiari malformation has fallen somewhat out of favor over time, although it is used to refer to the type II malformation. Current sources use "Chiari malformation" to describe four specific types of the condition, reserving the term "Arnold-Chiari" for type II only. Some sources still use "Arnold-Chiari" for all four types.

Chiari malformation or Arnold–Chiari malformation should not be confused with Budd-Chiari syndrome, a hepatic condition also named for Hans Chiari.

In Pseudo-Chiari Malformation, Leaking of CSF may cause displacement of the cerebellar tonsils and similar symptoms sufficient to be mistaken for a Chiari I malformation.

The diagnosis of Boerhaave's syndrome is suggested on the plain chest radiography and confirmed by chest CT scan. The initial plain chest radiograph is almost always abnormal in patients with Boerhaave's syndrome and usually reveals mediastinal or free peritoneal air as the initial radiologic manifestation. With cervical esophageal perforations, plain films of the neck show air in the soft tissues of the prevertebral space.

Hours to days later, pleural effusion(s) with or without pneumothorax, widened mediastinum, and subcutaneous emphysema are typically seen. CT scan may show esophageal wall edema and thickening, extraesophageal air, periesophageal fluid with or without gas bubbles, mediastinal widening, and air and fluid in the pleural spaces, retroperitoneum or lesser sac.

The diagnosis of esophageal perforation could also be confirmed by water-soluble contrast esophagram (Gastrografin), which reveals the location and extent of extravasation of contrast material. Although barium is superior in demonstrating small perforations, the spillage of barium sulfate into the mediastinal and pleural cavities can cause an inflammatory response and subsequent fibrosis and is therefore not used as the primary diagnostic study. If, however, the water-soluble study is negative, a barium study should be performed for better definition.

Endoscopy has no role in the diagnosis of spontaneous esophageal perforation. Both the endoscope and insufflation of air can extend the perforation and introduce air into the mediastinum.

Patients may also have a pleural effusion high in amylase (from saliva), low pH, and may contain particles of food.

Treatment is difficult to define given the number of different causes and the wealth of anecdotal information collected by and from cat breeders. Treatments have hitherto been based on the assumption that FCKS is caused by a muscular spasm, and their effectiveness is impossible to assess because some kittens will recover spontaneously without intervention.

Diaphragmatic spasm is easily tested for and treated by short term interruption of the Phrenic nerve. The nerve runs down the outside of the neck where the neck joins to the shoulder, within a bundle of muscles and tendons at this junction. The cluster can be pinched gently and held for a few seconds each time. Kittens with spasmodic FCKS will show almost immediate improvement, but the treatment may need to be repeated several times over a few days as the spasm may have a tendency to recur. [Um für diapragmatisch Sparmus zu prüfen, Sie müssen der Phrenikus finden (es heisst auch der Zwerchfellnerv), der lauft am aussen des Hals, wo der Hals trifft die Schulter. Da gibt es mehrere Muskeln und Sehnen–da es unmoeglich ist die Nerv allein zu finden bzw. kneifen, müssen Sie die ganze Menge zusammen ruhig kneifen für ein paar Sekunden. Wenn es doch diapragmatisch Spasmus ist und Sie das Phrenikus gut kneifest (manchmal aber nicht immer werde die Katze mit den hinteren Beinen kicken), sollen Sie sofort eine Verbesserung anschauen. Es kann sein, dass die Spasmus wieder kommt nachher im kommenden Tage—in dem Fall müssen Sie es nochmal machen. Wenn Sie aber keine Verbesserung siehst, ist der Problem dann leider etwas anders.]

Continuous positive air pressure (CPAP) is used in human babies with lung collapse, but this is impossible with kittens. It is possible that the success of some breeders in curing kittens by splinting the body, thus putting pressure on the ribcage, was successful as it has created the effect of positive air pressure, thus gradually re-inflating the lungs by pulling them open rather than pushing them open as is the case with CPAP.

The mediastinum (from Medieval Latin "mediastinus", "midway") is the central compartment of the thoracic cavity surrounded by loose connective tissue, as an undelineated region that contains a group of structures within the thorax. The mediastinum contains the heart and its vessels, the esophagus, trachea, phrenic and cardiac nerves, the thoracic duct, thymus and lymph nodes of the central chest.

Diagnosis is by medical imaging with either plain X ray or CT scan.

It is difficult to determine whether a kitten that goes flat will survive or not. A good indicator is the weight of the kitten: those that continue to gain weight generally have a better chance of survival. Supplement feeding is therefore recommended in all cases, together with vitamin supplements, although many of these kittens will not accept hand feeding. Liquid Paraffin to alleviate colic seems to be significant in assisting normal feeding and weight-gain.

Another indicator to the severity of the case is the use of the stomach when breathing: normal kittens use only the ribcage, a flat-chested kitten may manage to breathe only using the ribcage, or may suck the gut upwards with every breath – if the latter is the case then the likelihood of survival seems to be lower, though still not sufficient to warrant immediate euthanasia. If the condition is stable (i.e. the flatness does not increase over time) or improving, the kitten is more likely to survive. If the condition worsens over several days, survival is less likely.

Kittens with FCKS may die (or have to be euthanased) very soon after onset. There are two points at which breeders report kittens that were otherwise doing well deteriorating and dying: at 10 days of age and at 3 weeks. Generally if the kitten is still flat, but survives the 3-week developmental stage, its prognosis is good. Many will have returned to a normal shape by this time. Those retaining some degree of flatness often grow out of the condition at any point in the ensuing 6 months, and the vast majority of survivors appear to lead normal lives with no side-effects, either physical or immunological.

FCKS kittens that survive but who have not been given any drug treatment or support other than supplementary feeding, generally recover over a period of 4–10 weeks, and are usually normal by 12 weeks of age, though some take as long as 6 months to normalise. In the very small number of kittens reported so far treated with steroids, antibiotics and liquid paraffin (to address colic) recovery is usually seen within a matter of days. Given the number of different types of FCKS these kittens (all with the minor form of the condition) may not be representative of all cases. More data is required for statistical analysis.

A small proportion of severe FCKS kittens are left with long-term respiratory problems, kyphosis, and in some cases cardiac issues caused by the compression of the thorax during the early developmental stages (particularly where the condition has been coupled with Pectus Excavatum). Cardiac issues are generally audible on physical examination; further indications include the kitten becoming breathless after play, less active than siblings, and failure to grow and develop normally.

Professional divers are screened for risk factors during initial and periodical medical examination for fitness to dive. In most cases recreational divers are not medically screened, but are required to provide a medical statement before acceptance for training in which the most common and easy to identify risk factors must be declared. If these factors are declared, the diver may be required to be examined by a medical practitioner, and may be disqualified from diving if the conditions indicate.

Asthma, Marfan syndrome, and COPD pose a very high risk of pneumothorax. In some countries these may be considered absolute contraindications, while in others the severity may be taken into consideration. Asthmatics with a mild and well controlled condition may be permitted to dive under restricted circumstances.

"Prenatal diagnosis (fetal ultrasound):"

Today the diagnosis of double aortic arch can be obtained in-utero in experienced centers. Scheduled repair soon after birth in symptomatic patients can relieve tracheal compression early and therefore potentially prevent the development of severe tracheomalacia.

"Chest X-ray:"

Plain chest x-rays of patients with double aortic arch may appear normal (often) or show a dominant right aortic arch or two aortic arches . There might be evidence of tracheal deviation and/or compression. Sometimes patients present with radiologic findings of pneumonia.

"Barium swallow (esophagraphy):"

Historically the esophagram used to be the gold standard for diagnosis of double aortic arch. In patients with double aortic arch the esophagus shows left- and right-sided indentations from the vascular compression. Due to the blood-pressure related movement of the aorta and the two arches, moving images of the barium-filled esophagus can demonstrate the typical pulsatile nature of the obstruction. The indentation from a dominant right arch is usually deeper and higher compared to the dent from the left arch.

"Bronchoscopy:"

Although bronchoscopy is not routinely done in patients with suspected or confirmed double aortic arch, it can visualize sites and severity of pulsatile tracheal compression.

"Echocardiography:"

In babies under the age of 12 months, echocardiography is considered to be sensitive and specific in making the diagnosis of double aortic arch when both arches are open. Non-perfused elements of other types of vascular rings (e.g. left arch with atretic (closed) end) or the ligamentum arteriosum might be difficult to visualize by echocardiography.

"Computed tomography (CT):"

Computed tomography after application of contrast media is usually diagnostically accurate. It shows the relationship of the arches to the trachea and bronchi.

"Magnetic resonance imaging (MRI):"

Magnetic resonance imaging provides excellent images of the trachea and surrounding vascular structures and has the advantage of not using radiation for imaging compared to Computed tomography.

"Cardiac catherization/aortography:"

Today patients with double aortic arch usually only undergo cardiac catherization to evaluate the hemodynamics and anatomy of associated congenital cardiac defects. Through a catheter in the ascending aorta contrast media is injected and the resulting aortography may be used to delineate the anatomy of the double aortic arch including sites of narrowing in the left aortic arch. Aortography can also be used to visualize the origin of all head and arm vessels originating from the two arches.