VAP occurring early after intubation typically involves fewer resistant organisms and is thus associated with a more favorable outcome. Because respiratory failure requiring mechanical ventilation is itself associated with a high mortality, determination of the exact contribution of VAP to mortality has been difficult. As of 2006, estimates range from 33% to 50% death in patients who develop VAP. Mortality is more likely when VAP is associated with certain microorganisms ("Pseudomonas", "Acinetobacter"), blood stream infections, and ineffective initial antibiotics. VAP is especially common in people who have acute respiratory distress syndrome (ARDS).

Between 8 and 28% of patients receiving mechanical ventilation are affected by VAP. VAP can develop at any time during ventilation, but occurs most often in the first week of mechanical ventilation. There is some evidence for gender differences in the course of VAP: men have been found to get VAP more often, but women are more likely to die after contracting VAP.

Patients, families, and caregivers are encouraged to join the NIH Rare Lung Diseases Consortium Contact Registry. This is a privacy protected site that provides up-to-date information for individuals interested in the latest scientific news, trials, and treatments related to rare lung diseases.

Tuberculosis, pneumonia, inhaled foreign bodies, allergic bronchopulmonary aspergillosis and bronchial tumours are the major acquired causes of bronchiectasis. Infective causes associated with bronchiectasis include infections caused by the Staphylococcus, Klebsiella, or Bordetella pertussis, the causative agent of whooping cough and nontuberculous mycobacteria.

Aspiration of ammonia and other toxic gases, pulmonary aspiration, alcoholism, heroin (drug use), various allergies all appear to be linked to the development of bronchiectasis.

Various immunological and lifestyle factors have also been linked to the development of bronchiectasis:

- Childhood Acquired Immune Deficiency Syndrome (AIDS), which predisposes patients to a variety of pulmonary ailments, such as pneumonia and other opportunistic infections.

- Inflammatory bowel disease, especially ulcerative colitis. It can occur in Crohn's disease as well, but does so less frequently. Bronchiectasis in this situation usually stems from various allergic responses to inhaled fungal spores. A Hiatal hernia can cause Bronchiectasis when the stomach acid that is aspirated into the lungs causes tissue damage.

- People with rheumatoid arthritis who smoke appear to have a tenfold increased rate of the disease. Still, it is unclear as to whether or not cigarette smoke is a specific primary cause of bronchiectasis.

- Case reports of Hashimoto's thyroiditis and bronchiectasis occurring in the same persons have been published.

No cause is identified in up to 50% of non-cystic-fibrosis related bronchiectasis.

Pneumonia is due to infections caused primarily by bacteria or viruses and less commonly by fungi and parasites. Although there are more than 100 strains of infectious agents identified, only a few are responsible for the majority of the cases. Mixed infections with both viruses and bacteria may occur in up to 45% of infections in children and 15% of infections in adults. A causative agent may not be isolated in approximately half of cases despite careful testing.

The term "pneumonia" is sometimes more broadly applied to any condition resulting in inflammation of the lungs (caused for example by autoimmune diseases, chemical burns or drug reactions); however, this inflammation is more accurately referred to as pneumonitis.

Conditions and risk factors that predispose to pneumonia include smoking, immunodeficiency, alcoholism, chronic obstructive pulmonary disease, asthma, chronic kidney disease, and liver disease. The use of acid-suppressing medications—such as proton-pump inhibitors or H2 blockers—is associated with an increased risk of pneumonia. The risk is also increased in old age.

In order to prevent bronchiectasis, children should be immunized against measles, pertussis, pneumonia, and other acute respiratory infections of childhood. While smoking has not been found to be a direct cause of bronchiectasis, it is certainly an irritant that all patients should avoid in order to prevent the development of infections (such as bronchitis) and further complications.

Treatments to slow down the progression of this chronic disease include keeping bronchial airways clear and secretions weakened through various forms of pneumotherapy. Aggressively treating bronchial infections with antibiotics to prevent the destructive cycle of infection, damage to bronchial tubes, and more infection is also standard treatment. Regular vaccination against pneumonia, influenza and pertussis are generally advised. A healthy body mass index and regular doctor visits may have beneficial effects on the prevention of progressing bronchiectasis. The presence of hypoxemia, hypercapnia, dyspnea level and radiographic extent can greatly affect the mortality rate from this disease.

Conditions which commonly involve hemoptysis include bronchitis and pneumonia, lung cancers and tuberculosis. Other possible underlying causes include aspergilloma, bronchiectasis, coccidioidomycosis, pulmonary embolism, pneumonic plague, and cystic fibrosis. Rarer causes include hereditary hemorrhagic telangiectasia (HHT or Rendu-Osler-Weber syndrome), Goodpasture's syndrome, and granulomatosis with polyangiitis. In children, hemoptysis is commonly caused by the presence of a foreign body in the airway. The condition can also result from over-anticoagulation from treatment by drugs such as warfarin.

Blood-laced mucus from the sinus or nose area can sometimes be misidentified as symptomatic of hemoptysis (such secretions can be a sign of nasal or sinus cancer, but also a sinus infection). Extensive non-respiratory injury can also cause one to cough up blood. Cardiac causes like congestive heart failure and mitral stenosis should be ruled out.

The origin of blood can be identified by observing its color. Bright-red, foamy blood comes from the respiratory tract, whereas dark-red, coffee-colored blood comes from the gastrointestinal tract. Sometimes hemoptysis may be rust-colored.

The most common cause of minor hemoptysis is bronchitis.

- Lung cancer, including both non-small cell lung carcinoma and small cell lung carcinoma.

- Sarcoidosis

- Aspergilloma

- Tuberculosis

- Histoplasmosis

- Pneumonia

- Pulmonary edema

- Pulmonary embolism

- Foreign body aspiration and aspiration pneumonia

- Goodpasture's syndrome

- Granulomatosis with polyangiitis

- Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)

- Bronchitis

- Bronchiectasis

- Pulmonary embolism

- Anticoagulant use

- Trauma

- Lung abscess

- Mitral stenosis

- Tropical eosinophilia

- Bleeding disorders

- Hughes-Stovin Syndrome and other variants of Behçet's disease

- Squamous Cell Carcinoma Of Esophagus

Bacteria are the most common cause of community-acquired pneumonia (CAP), with "Streptococcus pneumoniae" isolated in nearly 50% of cases. Other commonly isolated bacteria include "Haemophilus influenzae" in 20%, "Chlamydophila pneumoniae" in 13%, and "Mycoplasma pneumoniae" in 3% of cases; "Staphylococcus aureus"; "Moraxella catarrhalis"; "Legionella pneumophila" and Gram-negative bacilli. A number of drug-resistant versions of the above infections are becoming more common, including drug-resistant "Streptococcus pneumoniae" (DRSP) and methicillin-resistant Staphylococcus aureus (MRSA).

The spreading of organisms is facilitated when risk factors are present. Alcoholism is associated with "Streptococcus pneumoniae", anaerobic organisms, and "Mycobacterium tuberculosis"; smoking facilitates the effects of "Streptococcus pneumoniae", "Haemophilus influenzae", "Moraxella catarrhalis", and "Legionella pneumophila". Exposure to birds is associated with "Chlamydia psittaci"; farm animals with "Coxiella burnetti"; aspiration of stomach contents with anaerobic organisms; and cystic fibrosis with "Pseudomonas aeruginosa" and "Staphylococcus aureus". "Streptococcus pneumoniae" is more common in the winter, and should be suspected in persons aspirating a large amount of anaerobic organisms.

Pulmonary aspiration is often followed by bacterial pneumonia. Community-acquired aspiration pneumonia is usually caused by anaerobic bacteria, whereas hospital-acquired aspiration pneumonia is more often caused by mixed flora, including both aerobic and anaerobic bacteria.

Pulmonary aspiration of acidic material (such as stomach acid) may produce an immediate primary injury caused by the chemical reaction of acid with lung parenchyma, and a later secondary injury as a result of the subsequent inflammatory response.

To date, about 420 cases have been reported in the medical literature. Given its unusual nature, the true prevalence of PB is unknown, and it is likely that many patients are undiagnosed. PB does affect patients of all age groups and both genders.

Sources of such lipids could be either exogenous or endogenous.

Exogenous: from outside the body. For example, inhaled nose drops with an oil base, or accidental inhalation of cosmetic oil. Amiodarone is an anti-arrythmic known to cause this condition. Oil pulling has also been shown to be a cause. At risk populations include the elderly, developmentally delayed or persons with gastroesophageal reflux. Switching to water-soluble alternatives may be helpful in some situations.

Endogenous: from the body itself, for example, when an airway is obstructed, it is often the case that distal to the obstruction, lipid-laden macrophages (foamy macrophages) and giant cells fill the lumen of the disconnected airspace.

Hemoptysis is the coughing up of blood or blood-stained mucus from the bronchi, larynx, trachea, or lungs. This can occur with lung cancer, infections such as tuberculosis, bronchitis, or pneumonia, and certain cardiovascular conditions. Hemoptysis is considered massive at . In such cases, there are always severe injuries. The primary danger comes from choking, rather than blood loss.

ILD may be classified according to the cause. One method of classification is as follows:

1. Inhaled substances

- Inorganic

- Silicosis

- Asbestosis

- Berylliosis

- printing workers (eg. carbon bblack, ink mist)

- Organic

- Hypersensitivity pneumonitis

2. Drug-induced

- Antibiotics

- Chemotherapeutic drugs

- Antiarrhythmic agents

3. Connective tissue and Autoimmune diseases

- Rheumatoid arthritis

- Systemic lupus erythematosus

- Systemic sclerosis

- Polymyositis

- Dermatomyositis

4. Infection

- Atypical pneumonia

- Pneumocystis pneumonia (PCP)

- Tuberculosis

- "Chlamydia" trachomatis

- Respiratory Syncytial Virus

5. Idiopathic

- Sarcoidosis

- Idiopathic pulmonary fibrosis

- Hamman-Rich syndrome

- Antisynthetase syndrome

6. Malignancy

- Lymphangitic carcinomatosis

7. Predominantly in children

- Diffuse developmental disorders

- Growth abnormalities deficient alveolarisation

- Infant conditions of undefined cause

- ILD related to alveolar surfactant region

Endogenous lipoid pneumonia and non-specific interstitial pneumonitis has been seen prior to the development of pulmonary alveolar proteinosis in a child.

The morbidity associated with DIPNECH is due to the associated obstructive lung disease. The lung disease tends to be slowly progressive, but given enough time can lead to significant disability and require supplemental oxygen therapy. There have been reports of lung transplantation in the setting of end-stage DIPNECH.

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.

Air in subcutaneous tissue does not usually pose a lethal threat; small amounts of air are reabsorbed by the body. Once the pneumothorax or pneumomediastinum that causes the subcutaneous emphysema is resolved, with or without medical intervention, the subcutaneous emphysema will usually clear. However, spontaneous subcutaneous emphysema can, in rare cases, progress to a life-threatening condition, and subcutaneous emphysema due to mechanical ventilation may induce ventilatory failure.

A pulmonary consolidation is a region of (normally compressible) lung tissue that has filled with liquid, a condition marked by induration (swelling or hardening of normally soft tissue) of a normally aerated lung. It is considered a radiologic sign. Consolidation occurs through accumulation of inflammatory cellular exudate in the alveoli and adjoining ducts. Simply, it is defined as alveolar space that contains liquid instead of gas. The liquid can be pulmonary edema, inflammatory exudate, pus, inhaled water, or blood (from bronchial tree or hemorrhage from a pulmonary artery). It must be present to diagnose pneumonia: the signs of lobar pneumonia are characteristic and clinically referred to as consolidation.

When a pleural effusion has been determined to be exudative, additional evaluation is needed to determine its cause, and amylase, glucose, pH and cell counts should be measured.

- Red blood cell counts are elevated in cases of bloody effusions (for example after heart surgery or hemothorax from incomplete evacuation of blood).

- Amylase levels are elevated in cases of esophageal rupture, pancreatic pleural effusion, or cancer.

- Glucose is decreased with cancer, bacterial infections, or rheumatoid pleuritis.

- pH is low in empyema (<7.2) and may be low in cancer.

- If cancer is suspected, the pleural fluid is sent for cytology. If cytology is negative, and cancer is still suspected, either a thoracoscopy, or needle biopsy of the pleura may be performed.

- Gram staining and culture should also be done.

- If tuberculosis is possible, examination for "Mycobacterium tuberculosis" (either a Ziehl–Neelsen or Kinyoun stain, and mycobacterial cultures) should be done. A polymerase chain reaction for tuberculous DNA may be done, or adenosine deaminase or interferon gamma levels may also be checked.

The most common causes of exudative pleural effusions are bacterial pneumonia, cancer (with lung cancer, breast cancer, and lymphoma causing approximately 75% of all malignant pleural effusions), viral infection, and pulmonary embolism.

Another common cause is after heart surgery, when incompletely drained blood can lead to an inflammatory response that causes exudative pleural fluid.

Conditions associated with exudative pleural effusions:

- Parapneumonic effusion due to pneumonia

- Malignancy (either lung cancer or metastases to the pleura from elsewhere)

- Infection (empyema due to bacterial pneumonia)

- Trauma

- Pulmonary infarction

- Pulmonary embolism

- Autoimmune disorders

- Pancreatitis

- Ruptured esophagus (Boerhaave's syndrome)

- Rheumatoid pleurisy

- Drug-induced lupus

Subcutaneous emphysema is a common result of certain types of surgery; for example it is not unusual in chest surgery. It may also occur from surgery around the esophagus, and is particularly likely in prolonged surgery. Other potential causes are positive pressure ventilation for any reason and by any technique, in which its occurrence is frequently unexpected. It may also occur as a result of oral surgery, laparoscopy, and cricothyrotomy. In a pneumonectomy, in which an entire lung is removed, the remaining bronchial stump may leak air, a rare but very serious condition that leads to progressive subcutaneous emphysema. Air can leak out of the pleural space through an incision made for a thoracotomy to cause subcutaneous emphysema. On infrequent occasions, the condition can result from dental surgery, usually due to use of high-speed tools that are air driven. These cases result in usually painless swelling of the face and neck, with an immediate onset, the crepitus (crunching sound) typical of subcutaneous emphysema, and often with subcutaneous air visible on X-ray.

One of the main causes of subcutaneous emphysema, along with pneumothorax, is an improperly functioning chest tube. Thus subcutaneous emphysema is often a sign that something is wrong with a chest tube; it may be clogged, clamped, or out of place. The tube may need to be replaced, or, when large amounts of air are leaking, a new tube may be added.

Since mechanical ventilation can worsen a pneumothorax, it can force air into the tissues; when subcutaneous emphysema occurs in a ventilated patient, it is an indication that the ventilation may have caused a pneumothorax. It is not unusual for subcutaneous emphysema to result from positive pressure ventilation. Another possible cause is a ruptured trachea. The trachea may be injured by tracheostomy or tracheal intubation; in cases of tracheal injury, large amounts of air can enter the subcutaneous space. An endotracheal tube can puncture the trachea or bronchi and cause subcutaneous emphysema.

Signs that consolidation may have occurred include:

- Expansion of the thorax on inspiration is reduced on the affected side

- Vocal fremitus is increased on the side with consolidation

- Percussion is dull in affected area

- Breath sounds are bronchial

- Possible medium, late, or pan-inspiratory crackles

- Vocal resonance is increased. Here, the patient's voice (or whisper, as in whispered pectoriloquy) can be heard more clearly when there is consolidation, as opposed to in the healthy lung where speech sounds muffled.

- A pleural rub may be present.

- A lower expected Pa02 than calculated in the alveolar gas equation

There is still much debate to whether pulmonary sequestration is a congenital problem or acquired through reccurent pulmonary infection. It is widely believed that extralobar pulmonary sequestrations are a result of prenatal pulmonary malformation while intralobar pulmonary sequestrations can develop due to reccurent pulmonary infections in adolescents and young adults.

To properly treat a patient with tracheobronchomalacia, the subtype must be determined (primary or secondary). After the type is named, the cause must be identified, whether it is from genetics, a trauma accident, or chronic tracheal illness. If a trauma case or chronic tracheal illnesses were the cause, the first steps of treatment would be to fix or help these underlying issues. If the cause is genetic or the previous underlying issues could not be fixed, other treatments would be assessed. More severe treatments include silicone stenting to prevent tracheal constriction, surgery to strengthen or attempt to rebuild the walls, continuous positive airway pressure that has a machine blow small amounts of air into the trachea to keep it open (mainly at night), or a tracheostomy, which is surgically put into your neck that leads to your trachea to help with breathing. People with tracheobronchomalacia who do not experience symptoms do not need treatment and are often undiagnosed.

To date there have been no clinical trials to determine effective treatment for this disease. Some patients have been treated with somatostatin analogs. Although the cough associated with DIPNECH tends to diminish on this treatment, improvement in pulmonary function has not been clearly demonstrated. There are also reports of symptomatic treatment with long- and short-acting beta agonists. Although steroids, both oral and inhaled, have been used in the setting of DIPNECH, there is no clear improvement with this treatment.

It is not uncommon for typical carcinoids to arise within DIPNECH. Due to presence of these tumors, DIPNECH is classified as a pre-malignant condition. Although there have been reports of atypical carcinoids with local lymph node involvement, there are no reports of more aggressive neuroendocrine tumors, such as large cell neuroendocrine or small cell lung cancer, associated with DIPNECH. When isolated bronchial carcinoids are diagnosed, oncology guidelines recommend surgical resection with lymph node sampling. However, as multiple carcinoids may develop in the setting of DIPNECH, a more conservative approach is often considered to preserve lung function.