Symptoms can vary greatly, but they include a persistent dry cough.

Failure to have a pulmonary sequestration removed can lead to a number of complications. These include:

- Hemorrhage that can be fatal.

- The creation of a left-right shunt, where blood flows in a shortcut through the feed off the aorta.

- Chronic infection. Diseases such as bronchiectasis, tuberculosis, aspergillosis, bronchial carcinoid and bronchogenic squamous cell carcinoma.

Alveolar capillary dysplasia (ACD, sometimes denoted ACDMPV when including misalignment of the pulmonary veins) is a type of diffuse developmental disorder of the lung. The other two diffuse developmental disorders are congenital acinar dysplasia and congenital alveolar dysplasia (CAD).

ACD or ACDMPV is the best studied diffuse developmental disorder. It is a very rare congenital malformation involving abnormal development of the capillary vascular system around the alveoli of the lungs. It is a rare cause of persistent pulmonary hypertension in infants. It also may be a rare cause of pulmonary hypoplasia.

Babies with ACD may appear normal at birth but within minutes or hours they develop respiratory distress with persistent pulmonary hypertension. ACD does not respond to standard therapies that resolve simple pulmonary hypertension. The lack of response is an important diagnostic clue.

The symptoms of pulmonary hypertension include the following:

Less common signs/symptoms include non-productive cough and exercise-induced nausea and vomiting. Coughing up of blood may occur in some patients, particularly those with specific subtypes of pulmonary hypertension such as heritable pulmonary arterial hypertension, Eisenmenger syndrome and chronic thromboembolic pulmonary hypertension. Pulmonary venous hypertension typically presents with shortness of breath while lying flat or sleeping (orthopnea or paroxysmal nocturnal dyspnea), while pulmonary arterial hypertension (PAH) typically does not.

Other typical signs of pulmonary hypertension include an accentuated pulmonary component of the second heart sound, a right ventricular third heart sound, and parasternal heave indicating a hypertrophied right atrium. Signs of systemic congestion resulting from right-sided heart failure include jugular venous distension, ascites, and hepatojugular reflux. Evidence of tricuspid insufficiency and pulmonic regurgitation is also sought and, if present, is consistent with the presence of pulmonary hypertension.

The clinical presentation of plastic bronchitis beyond expectoration of casts includes a productive cough, dyspnea, fever and wheezing. Focal wheezing is a characteristic, if not specific, physical examination finding. If the casts completely obstruct the airway, breath sounds will be decreased and dullness will be present with percussion. With partial obstruction, a “fan sound” or “flag flapping” sound can be heard during auscultation. Bronchial casts can sometimes fill the airways of almost an entire lung, and present as an acute, life-threatening emergency.

Scimitar syndrome, or congenital pulmonary venolobar syndrome, is a rare congenital heart defect characterized by anomalous venous return from the right lung (to the systemic venous drainage, rather than directly to the left atrium). This anomalous pulmonary venous return can be either partial (PAPVR) or total (TAPVR). The syndrome associated with PAPVR is more commonly known as "Scimitar syndrome" after the curvilinear pattern created on a chest radiograph by the pulmonary veins that drain to the inferior vena cava. This radiographic density often has the shape of a scimitar, a type of curved sword. The syndrome was first described by Catherine Neill in 1960.

The anomalous venous return forms a curved shadow on chest x-ray such that it resembles a scimitar. This is called the Scimitar Sign. Associated abnormalities include right lung hypoplasia with associated dextroposition of the heart, pulmonary artery hypoplasia and pulmonary sequestration.Incidence is around 1 per 100,000 births.

Anomalous pulmonary venous connection (or anomalous pulmonary venous drainage or anomalous pulmonary venous return) is a congenital defect of the pulmonary veins.

"Total anomalous pulmonary venous connection", also known as "total anomalous pulmonary venous drainage" and "total anomalous pulmonary venous return", is a rare cyanotic congenital heart defect in which all four pulmonary veins are malpositioned and make anomalous connections to the systemic venous circulation. (Normally, pulmonary veins return oxygenated blood from the lungs to the left atrium where it can then be pumped to the rest of the body). A patent foramen ovale, patent ductui arteriosa or an atrial septal defect "must" be present, or else the condition is fatal due to a lack of systemic blood flow.

In some cases, it can be detected prenatally.

There are four variants: Supracardiac (50%): blood drains to one of the innominate veins (brachiocephalic veins) or the superior vena cava; Cardiac (20%), where blood drains into coronary sinus or directly into right atrium; Infradiaphragmatic (20%), where blood drains into portal or hepatic veins; and a mixed (10%) variant.

TAPVC can occur with "obstruction", which occurs when the anomalous vein enters a vessel at an acute angle and can cause pulmonary venous hypertension and cyanosis because blood cannot enter the new vein as easily.

Interstitial lung disease (ILD), or diffuse parenchymal lung disease (DPLD), is a group of lung diseases affecting the interstitium (the tissue and space around the air sacs of the lungs). It concerns alveolar epithelium, pulmonary capillary endothelium, basement membrane, perivascular and perilymphatic tissues. It may occur when an injury to the lungs triggers an abnormal healing response. Ordinarily, the body generates just the right amount of tissue to repair damage. But in interstitial lung disease, the repair process goes awry and the tissue around the air sacs (alveoli) becomes scarred and thickened. This makes it more difficult for oxygen to pass into the bloodstream. The term ILD is used to distinguish these diseases from obstructive airways diseases.

In children, several unique forms of ILD exist which are specific for the young age groups. The acronym chILD is used for this group of diseases and is derived from the English name, Children’s Interstitial Lung Diseases – chILD.

Prolonged ILD may result in pulmonary fibrosis, but this is not always the case. Idiopathic pulmonary fibrosis is interstitial lung disease for which no obvious cause can be identified (idiopathic), and is associated with typical findings both radiographic (basal and pleural based fibrosis with honeycombing) and pathologic (temporally and spatially heterogeneous fibrosis, histopathologic honeycombing and fibroblastic foci).

In 2013 interstitial lung disease affected 595,000 people globally. This resulted in 471,000 deaths.

Pulmonary hypoplasia is incomplete development of the lungs, resulting in an abnormally low number or size of bronchopulmonary segments or alveoli. A congenital malformation, it most often occurs secondary to other fetal abnormalities that interfere with normal development of the lungs. Primary (idiopathic) pulmonary hypoplasia is rare and usually not associated with other maternal or fetal abnormalities.

Incidence of pulmonary hypoplasia ranges from 9–11 per 10,000 live births and 14 per 10,000 births. Pulmonary hypoplasia is a relatively common cause of neonatal death. It also is a common finding in stillbirths, although not regarded as a cause of these.

Plastic bronchitis (PB) is a disorder in which branching casts of the airways are expectorated. PB has been previously identified by many names including fibrinous bronchitis, bronchitis pseudomembranosa, and Hoffmann bronchitis and is now uniformly termed plastic bronchitis. PB is not a single disease with a defined mechanism that explains the cast formation in all conditions. Examples of diseases associated with expectoration of casts, and which sometimes are labeled PB include tuberculosis, atypical mycobacterial disease, allergic bronchopulmonary aspergillosis and asthma.

When casts are very large with many branches, an abnormal communication or leakage of lymphatic fluid into the airway is often the cause. This entity is termed lymphatic plastic bronchitis (LPB). LPB is a lymphatic flow disorder characterized by the recurrent formation of branching, rubbery bronchial casts composed primarily of proteinaceous and sometimes chylous material and lymphocytes. Lymphatic fluids deposited into the airspaces become gelatinous as they cool, forming large string cheese-like casts of the airways, which can obstruct airflow. Attempts to expectorate casts can be quite frightening, leading to fears of asphyxiation.

According to WHO classification there are 5 groups of PH, where Group I (pulmonary arterial hypertension) is further subdivided into Group I' and Group I" classes. The most recent WHO classification system (with adaptations from the more recent ESC/ERS guidelines shown in italics) can be summarized as follows:

WHO Group I – Pulmonary arterial hypertension (PAH)

- Idiopathic

- Heritable (BMPR2, ALK1, SMAD9, caveolin 1, KCNK3 mutations)

- Drug- and toxin-induced (e.g., methamphetamine use)

- Associated conditions:Connective tissue disease, HIV infection, Portal hypertension, Congenital heart diseases, Schistosomiasis

WHO Group I' – Pulmonary veno-occlusive disease (PVOD), pulmonary capillary hemangiomatosis (PCH)

- Idiopathic

- Heritable (EIF2AK4 mutations)

- Drugs, toxins and radiation-induced

- Associated conditions:connective tissue disease, HIV infection

WHO Group I" – Persistent pulmonary hypertension of the newborn

WHO Group II – Pulmonary hypertension secondary to left heart disease

- Left ventricular Systolic dysfunction

- Left ventricular Diastolic dysfunction

- Valvular heart disease

- Congenital/acquired left heart inflow/outflow tract obstruction and congenital cardiomyopathy

- Congenital/acquired pulmonary venous stenosis

WHO Group III – Pulmonary hypertension due to lung disease, chronic hypoxia

- Chronic obstructive pulmonary disease (COPD)

- Interstitial lung disease

- Mixed restrictive and obstructive pattern pulmonary diseases

- Sleep-disordered breathing

- Alveolar hypoventilation disorders

- Chronic exposure to high altitude

- Developmental abnormalities

WHO Group IV – chronic arterial obstruction

- Chronic thromboembolic pulmonary hypertension (CTEPH)

- Other pulmonary artery obstructions

- Angiosarcoma or other tumor within the blood vessels

- Arteritis

- Congenital pulmonary artery stenosis

- Parasitic infection (hydatidosis)

WHO Group V – Pulmonary hypertension with unclear or multifactorial mechanisms

- Hematologic diseases: chronic hemolytic anemia (including sickle cell disease)

- Systemic diseases: sarcoidosis, pulmonary Langerhans cell histiocytosis: lymphangioleiomyomatosis, neurofibromatosis, vasculitis

- Metabolic disorders: glycogen storage disease, Gaucher disease, thyroid diseases

- Others: pulmonary tumoral thrombotic microangiopathy, fibrosing mediastinitis, chronic kidney failure, segmental pulmonary hypertension (pulmonary hypertension restricted to one or more lobes of the lungs)

Pulmonary edema, connective tissue diseases, asbestosis, lymphangitic carcinomatosis, lymphoma, lymphangioleiomyomatosis, drug-induced lung diseases

- Lymphadenopathy

Sarcoidosis, silicosis, berylliosis, lymphangitic carcinomatosis, lymphoma, lymphocytic interstitial pneumonia

In human anatomy, an azygos lobe is a congenital variation of the upper lobe of the right lung.It is seen in 1% of the population. Embryologically, it arises from an anomalous lateral course of the azygos vein in a pleural septum within the apical segment of the right upper lobe or in other words an azygos lobe is formed when the right posterior cardinal vein, one of the precursors of the azygos vein, fails to migrate over the apex of the lung and penetrates it instead, carrying along two pleural layers that invaginates into the upper portion of the right upper lobe . As it has no bronchi, veins and arteries of its own or corresponding alteration in the segmental architecture of the lung, so it is not a true (misnomer), or even accessory, pulmonary lobe, but rather an anatomically separated part of the upper lobe. It is usually an incidental finding on chest x-ray or computed tomography and is as such not associated with any morbidity but can cause technical problems in thoracoscopic procedures .

Pulmonary vein stenosis is a rare cardiovascular disorder. It is recognized as being the stenosis of one or more of the four pulmonary veins that return blood from the lungs to the left atrium of the heart. In congenital cases, it is associated with poor prognosis and high mortality rate. In some people, pulmonary vein stenosis occurs after pulmonary vein ablation for the treatment of atrial fibrillation. Some recent research has indicated that it may be genetically linked in congenital cases.

The symptomatic patient may present with dyspnea, cyanosis, chest pain, pulsus paradoxus, bradycardia or tachycardia. On physical examination, the patient may have the classic “Beck’s triad” – hypotension, raised JVP and distant heart sounds, when complicated by cardiac tamponade. Extension of the mediastinal air to the subcutaneous tissues via the fascial planes may lead to subcutaneous emphysema. When air and fluid mix together in the pericardial sac, a tinkling sound superimposed over a succussion splash is heard. This is known as a “Bruit de Moulin”, which is French for “Mill–wheel” murmur. Air between the anterior parietal pericardium and the thoracic cage may also give rise to the “Hamman’s Sign” – which is a crunching sound typically heard on auscultation of the chest, but may sometimes be heard even with the unaided ear.

ACD commonly is diagnosed postmortem, by a pathologist.

Sometimes ACD is diagnosed clinically. This is common when there is a family history of ACD, but rare otherwise. A clinical differential diagnosis of ACD excludes fetal atelectasis.

ACD is not detectable by prenatal imaging. However, some babies with ACD have associated congenital malformations that are detectable by imaging. The identification of genes involved in ACD offers the potential for prenatal testing and genetic counseling.

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.

Cyanotic heart defect is a group-type of congenital heart defect (CHD) that occurs due to deoxygenated blood bypassing the lungs and entering the systemic circulation or a mixture of oxygenated and unoxygenated blood entering the systemic circulation. It is caused by structural defects of the heart (i.e.: right-to-left, bidirectional shunting, malposition of the great arteries), or any condition which increases pulmonary vascular resistance. The result being the development of collateral circulation.

According to a study in cyanotic congenital heart disease (CCHD) in Sohag University, Upper Egypt. 50 neonates were diagnosed as suffering from cyanotic congenital heart disease (CCHD), they concluded that cyanotic congenital heart disease (CCHD) frequency was significant (9.5%) with D-TGA being the commonest type. Majority of neonates with Cyanotic congenital heart disease (CCHD) showed survival with suitable management.

Respiratory disease is a medical term that encompasses pathological conditions affecting the organs and tissues that make gas exchange possible in higher organisms, and includes conditions of the upper respiratory tract, trachea, bronchi, bronchioles, alveoli, pleura and pleural cavity, and the nerves and muscles of breathing. Respiratory diseases range from mild and self-limiting, such as the common cold, to life-threatening entities like bacterial pneumonia, pulmonary embolism, acute asthma and lung cancer.

The study of respiratory disease is known as pulmonology. A doctor who specializes in respiratory disease is known as a pulmonologist, a chest medicine specialist, a respiratory medicine specialist, a respirologist or a thoracic medicine specialist.

Respiratory diseases can be classified in many different ways, including by the organ or tissue involved, by the type and pattern of associated signs and symptoms, or by the cause of the disease.

Pneumopericardium is a medical condition where air enters the pericardial cavity. This condition has been recognized in preterm neonates, in which it is associated with severe lung pathology, after vigorous resuscitation, or in the presence of assisted ventilation. This is a serious complication, which if untreated may lead to cardiac tamponade and death. Pneumomediastinum, which is the presence of air in the mediastinum, may mimic and also coexist with pneumopericardium.

It can be congenital, or introduced by a wound.

Chronic respiratory diseases (CRDs) are diseases of the airways and other structures of the lung. This disease could be characterized by a high inflammatory cells recruitment (neutrophil) and/or destructive cycle of infection, (e.g. mediated by "Pseudomonas aeruginosa"). Some of the most common are asthma, chronic obstructive pulmonary disease, or acute respiratory distress syndrome . CRDs are not curable, however, various forms of treatment that help dilate major air passages and improve shortness of breath can help control symptoms and increase the quality of life for people with the disease.

it usually lasts for three months to two years

Eisenmenger's syndrome (or ES, Eisenmenger's reaction, Eisenmenger physiology, or tardive cyanosis) is defined as the process in which a long-standing left-to-right cardiac shunt caused by a congenital heart defect (typically by a ventricular septal defect, atrial septal defect, or less commonly, patent ductus arteriosus) causes pulmonary hypertension and eventual reversal of the shunt into a cyanotic right-to-left shunt. Because of the advent of fetal screening with echocardiography early in life, the incidence of heart defects progressing to Eisenmenger's has decreased.

Eisenmenger's syndrome in a pregnant mother can cause serious complications, though successful delivery has been reported. Maternal mortality ranges from 30% to 60%, and may be attributed to fainting spells, thromboembolism, hypovolemia, hemoptysis or preeclampsia. Most deaths occur either during or within the first weeks after delivery. Pregnant women with Eisenmenger syndrome should be hospitalized after the 20th week of pregnancy - or earlier if clinical deterioration occurs.