Working with asbestos is the most common risk factor for mesothelioma. However, mesothelioma has been reported in some individuals without any known exposure to asbestos.

Asbestos can cause lung cancer that is identical to lung cancer from other causes. Exposure to asbestos is associated with all major histological types of lung carcinoma (adenocarcinoma, squamous cell carcinoma, large-cell carcinoma and small-cell carcinoma). The latency period between exposure and development of lung cancer is 20 to 30 years. It is estimated that 3%-8% of all lung cancers are related to asbestos. The risk of developing lung cancer depends on the level, duration, and frequency of asbestos exposure (cumulative exposure). Smoking and individual susceptibility are other contributing factors towards lung cancer. Smokers who have been exposed to asbestos are at far greater risk of lung cancer. Smoking and asbestos exposure have a multiplicative (synergistic) effect on the risk of lung cancer. Symptoms include chronic cough, chest pain, breathlessness, haemoptysis (coughing up blood), wheezing or hoarseness of the voice, weight loss and fatigue. Treatment involves surgical removal of the cancer, chemotherapy, radiotherapy, or a combination of these (multimodality treatment). Prognosis is generally poor unless the cancer is detected in its early stages. Out of all patients diagnosed with lung cancer, only 15% survive for five years after diagnosis.

Pregnancy has been reported to exacerbate LAM in some cases. However, the risk has not been rigorously studied. In a survey of 318 patients who indicated that they had had at least one pregnancy, 163 responded to a second survey focusing on lung collapse. A total of 38 patients reported a pneumothorax with pregnancy, consistent with an incidence of pneumothorax in pregnancy of at least 10% (38 of 318). In one third of patients, the pneumothorax during pregnancy led to the LAM diagnosis. Pneumothoraces were almost twice as frequent on the right as on the left, and four women presented with bilateral spontaneous pneumothorax. Most pneumothoraces took place during the second and third trimesters. This study and others suggest that pregnancy is associated with pleural complications in LAM patients. Few women with a known LAM diagnosis choose to become pregnant and patients in whom LAM is diagnosed during pregnancy rarely have baseline pulmonary function tests available, complicating resolution of this question.

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

The incidence of mesothelioma has been found to be higher in populations living near naturally occurring asbestos. People can be exposed to naturally occurring asbestos in areas where mining or road construction is occurring, or when the asbestos-containing rock is naturally weathered. Another common route of exposure is through asbestos-containing soil, which is used to whitewash, plaster, and roof houses in Greece. In central Cappadocia, Turkey, mesothelioma was causing 50% of all deaths in three small villages—Tuzköy, Karain, and Sarıhıdır. Initially, this was attributed to erionite. Environmental exposure to asbestos has caused mesothelioma in places other than Turkey, including Corsica, Greece, Cyprus, China, and California. In the northern Greek mountain town of Metsovo, this exposure had resulted in mesothelioma incidence around 300 times more than expected in asbestos-free populations, and was associated with very frequent pleural calcification known as "Metsovo Lung".

The documented presence of asbestos fibers in water supplies and food products has fostered concerns about the possible impact of long-term and, as yet, unknown exposure of the general population to these fibers.

Exposure to talc is also a risk factor for mesothelioma; exposure can affect those who live near talc mines, work in talc mines, or work in talc mills.

In the United States, asbestos is considered the major cause of malignant mesothelioma and has been considered "indisputably" associated with the development of mesothelioma. Indeed, the relationship between asbestos and mesothelioma is so strong that many consider mesothelioma a “signal” or “sentinel” tumor. A history of asbestos exposure exists in most cases.

Pericardial mesothelioma may not be associated with asbestos exposure.

Asbestos was known in antiquity, but it was not mined and widely used commercially until the late 19th century. Its use greatly increased during World War II. Since the early 1940s, millions of American workers have been exposed to asbestos dust. Initially, the risks associated with asbestos exposure were not publicly known. However, an increased risk of developing mesothelioma was later found among naval personnel (e.g., Navy, Marine Corps, and Coast Guard), shipyard workers, people who work in asbestos mines and mills, producers of asbestos products, workers in the heating and construction industries, and other tradespeople. Today, the official position of the U.S. Occupational Safety and Health Administration (OSHA) and the U.S. EPA is that protections and "permissible exposure limits" required by U.S. regulations, while adequate to prevent most asbestos-related non-malignant disease, are "not" adequate to prevent or protect against asbestos-related cancers such as mesothelioma. Likewise, the British Government's Health and Safety Executive (HSE) states formally that any threshold for exposure to asbestos must be at a very low level and it is widely agreed that if any such threshold does exist at all, then it cannot currently be quantified. For practical purposes, therefore, HSE assumes that no such "safe" threshold exists. Others have noted as well that there is no evidence of a threshold level below which there is no risk of mesothelioma. There appears to be a linear, dose-response relationship, with increasing dose producing increasing risk of disease. Nevertheless, mesothelioma may be related to brief, low level or indirect exposures to asbestos. The dose necessary for effect appears to be lower for asbestos-induced mesothelioma than for pulmonary asbestosis or lung cancer. Again, there is no known safe level of exposure to asbestos as it relates to increased risk of mesothelioma.

The time from first exposure to onset of the disease, is between 25 and 70 years. It is virtually never less than fifteen years and peaks at 30–40 years. The duration of exposure to asbestos causing mesothelioma can be short. For example, cases of mesothelioma have been documented with only 1–3 months of exposure.

Malignant pleural effusion is a condition in which cancer causes an abnormal amount of fluid to collect between the thin layers of tissue (pleura) lining the outside of the lung and the wall of the chest cavity. Lung cancer and breast cancer account for about 50-65% of malignant pleural effusions. Other common causes include pleural mesothelioma and lymphoma.

The most common causes of transudative pleural effusions in the United States are heart failure and cirrhosis. Nephrotic syndrome, leading to the loss of large amounts of albumin in urine and resultant low albumin levels in the blood and reduced colloid osmotic pressure, is another less common cause of pleural effusion. Pulmonary emboli were once thought to cause transudative effusions, but have been recently shown to be exudative.

The mechanism for the exudative pleural effusion in pulmonary thromboembolism is probably related to increased permeability of the capillaries in the lung, which results from the release of cytokines or inflammatory mediators (e.g. vascular endothelial growth factor) from the platelet-rich blood clots. The excessive interstitial lung fluid traverses the visceral pleura and accumulates in the pleural space.

Conditions associated with transudative pleural effusions include:

- Congestive heart failure

- Liver cirrhosis

- Severe hypoalbuminemia

- Nephrotic syndrome

- Acute atelectasis

- Myxedema

- Peritoneal dialysis

- Meigs' syndrome

- Obstructive uropathy

- End-stage kidney disease

The goal of treatment of malignant pleural effusions is relief of breathlessness. Occasionally, treatment of the underlying cancer can cause resolution of the effusion. This may be the case with types of cancer that respond well to chemotherapy, such as small cell carcinoma or lymphoma. Simple aspiration of pleural fluid can relieve breathlessness rapidly but fluid and symptoms will usually recur within a couple of weeks. For this reason, more permanent treatments are usually used to prevent fluid recurrence. Standard treatment involves chest tube insertion and pleurodesis. However, this treatment requires an inpatient stay of approximately 2–7 days, can be painful and has a significant failure rate. This has led to the development of tunneled pleural catheters (e.g., Pleurx Catheters), which allow outpatient treatment of effusions.

LAM is almost completely restricted to women. While lung cysts consistent with LAM are reported in some men with tuberous sclerosis, very few of these men develop symptoms. The prevalence of LAM is estimated using data from registries and patient groups and is between 3.4-7.8/million women. The number of new cases each year is between 0.23-0.31/million women/year in the US, UK and Switzerland. The variation between countries and between adjacent states in the US, suggest that a significant number of women with LAM remain either undiagnosed or their symptoms are attributed to other diseases. Adult women with tuberous sclerosis are more likely to develop LAM than women without tuberous sclerosis. Cohorts of patients with tuberous sclerosis have been screened for LAM using CT scanning. In a retrospective study of adults with tuberous sclerosis, CT demonstrated lung cysts in 42% of 95 women and 13% of 91 men. In general, lung cysts were larger and more numerous in women than in men. In a further retrospective study of women with TSC who underwent CT scanning to detect LAM, 25% of those in their 20s had lung cysts whereas 80% of women in their 40s were affected, suggesting that the development of LAM is age dependent at least in tuberous sclerosis-related LAM. Although the prevalence of tuberous sclerosis at 1 in 6000 births is much greater than that of LAM, most pulmonary clinics see more cases of sporadic than tuberous sclerosis-LAM: probably due to a combination of low levels of screening for LAM in tuberous sclerosis and in many, the absence of symptoms.

Female sex and tuberous sclerosis are the only known risk factors. Although use of supplemental estrogen is not associated with development of LAM, one study suggested that use of estrogen-containing contraceptive pills was associated with earlier onset.

It occurs in more than 30% of women with tuberous sclerosis complex (TSC-LAM), a heritable syndrome that is associated with seizures, cognitive impairment and benign tumors in multiple tissues. Most LAM patients who present for medical evaluation have the sporadic form of the disease (S-LAM), however, which is not associated with other manifestations of tuberous sclerosis complex.

Mild cystic changes consistent with LAM have been described in 10–15% of men with TSC, but symptomatic LAM in males is rare. Sporadic LAM occurs exclusively in women, with one published exception to date. Both TSC-LAM and S-LAM are associated with mutations in tuberous sclerosis genes.

According to a recent study, the main risk factors for RA-ILD are advancing age, male sex, greater RA disease activity, rheumatoid factor (RF) positivity, and elevated titers of anticitrullinated protein antibodies such as anticyclic citrullinated peptide. Cigarette smoking also appears to increase risk of RA-ILD, especially in patients with human leukocyte antigen DRB1.

A recently published retrospective study by a team from Beijing Chao-Yang Hospital in Beijing, China, supported three of the risk factors listed for RA-ILD and identified an additional risk factor. In that study of 550 RA patients, logistic regression analysis of data collected on the 237 (43%) with ILD revealed that age, smoking, RF positivity, and elevated lactate dehydrogenase closely correlated with ILD.

Recent studies have identified risk factors for disease progression and mortality. A retrospective study of 167 patients with RA-ILD determined that the usual interstitial pneumonia (UIP) pattern on high-resolution computed tomography (HRCT) was a risk factor for progression, as were severe disease upon diagnosis and rate of change in pulmonary function test results in the first 6 months after diagnosis.

A study of 59 RA-ILD patients found no median survival difference between those with the UIP pattern and those without it. But the UIP group had more deaths, hospital admissions, need for supplemental oxygen, and decline in lung function.

Tumor-like disorders of the lung pleura are a group of conditions that on initial radiological studies might be confused with malignant lesions. Radiologists must be aware of these conditions in order to avoid misdiagnosing patients. Examples of such lesions are: pleural plaques, thoracic splenosis, catamenial pneumothorax, pleural pseudotumor, diffuse pleural thickening, diffuse pulmonary lymphangiomatosis and Erdheim-Chester Disease.

Ectopic endometrial tissue reaches the pleural space of the lung or the right hemi-diaphragmatic region and erodes the visceral pleura, causing the formation of a spontaneous pneumothorax. The condition is often cyclical, due to its associations with the beginning of the menstrual cycle.

Affected persons usually present with recurrent spontaneous pneumothorax associated with the onset of the menstrual cycle. Additionally, chest/scapular pain and/or evidence of endometriosis in the abdominopelvic cavity are other manifestations.

On radiological studies, pneumothorax is visualized using conventional chest x-rays and CT scans. In 90% of the cases, the pneumothorax is located on the right side. In some cases, small nodules can be seen in the pleura using CT scans. Confirmation can be done using video assisted thoracoscopic surgery (VATS).

Treatment for the pneumothorax is with chest tube placement. As for the ectopic endometrial tissue, therapy with gonadotropin-releasing–hormone or resection of the lesions can improve symptoms.

Malignant mesothelioma is an aggressive and incurable tumour caused by asbestos arising from mesothelial cells of the pleura, peritoneum (the lining of the abdominal cavity) and rarely elsewhere. Pleural mesothelioma is the most common type of mesothelioma, representing about 75 percent of cases. Peritoneal mesothelioma is the second most common type, consisting of about 10 to 20 percent of cases. Mesothelioma appears from 20 to 50 years after the initial exposure to asbestos. The symptoms include shortness of breath, chronic chest pain, cough, and weight loss. Diagnosing mesothelioma is often difficult and can include physical examination, chest X-ray and lung function tests, followed by CT scan and MRI. A biopsy is needed to confirm a diagnosis of malignant mesothelioma. Mesothelioma has a poor prognosis, with most patients dying within 1 year of diagnosis. The treatment strategies include surgery, radiotherapy, chemotherapy or multimodality treatment. Several tumour biomarkers (soluble mesothelin-related protein (SMRP), osteopontin and fibulin3) have been evaluated for diagnostic purposes to allow early detection of this disease. Novel biomarkers such as volatile organic compounds measured in exhaled breath are also promising.

The mediastinum is the cavity that separates the lungs from the rest of the chest. It contains the heart, esophagus, trachea, thymus, and aorta. The mediastinum has three main parts: the anterior mediastinum (front), the middle mediastinum, and the posterior mediastinum (back).

The most common mediastinal masses are neurogenic tumors (20% of mediastinal tumors), usually found in the posterior mediastinum, followed by thymoma (15-20%) located in the anterior mediastinum.

Masses in the anterior portion of the mediastinum can include thymoma, lymphoma, pheochromocytoma, germ cell tumors including teratoma, thyroid tissue, and parathyroid lesions. Masses in this area are more likely to be malignant than those in other compartments.

Masses in the posterior portion of the mediastinum tend to be neurogenic in origin, and in adults tend to be of neural sheath origin including neurilemomas and neurofibromas.

Lung cancer typically spreads to the lymph nodes in the mediastinum.

Fibrothorax is diffuse fibrosis of the pleural space surrounding the lungs. It can have several causes including hemothorax, pleural effusion and tuberculosis. It may also be induced by exposure to certain substances, as with asbestos-induced diffuse pleural fibrosis. Idiopathic fibrothorax may also occur.

In fibrothorax, scar tissue is formed around the visceral pleura following inflammation due to pleural effusion or other pathology. The scar tissue lies in a sheet between the pleura, then fuses with the parietal pleura and the chest wall. Over time, generally the course of years, the fibrotic scar tissue slowly tightens, which results in the contraction of the entire hemithorax, and leaves the ribs immobilized. Within the chest, the lung is compressed and unable to expand, making it vulnerable to collapse. At the microscopic level, the scar tissue is composed of collagen fibers deposited in a basket weave pattern. The treatment for fibrothorax is decortication, the surgical removal of the fibrous layer of scar tissue. However, since many of the diseases and conditions resulting in fibrothorax are treatable, prevention remains the preferred method of managing fibrothorax.

Second most common primary anterior mediastinal mass in adults. Most are seen in the anterior compartment and rest are seen in middle compartment. Hodgkin's usually present in 40-50's with nodular sclerosing type (7), and non-Hodgkin's in all age groups. Can also be primary mediastinal B-cell lymphoma with exceptionally good prognosis. Common symptoms include fever, weight loss, night sweats, and compressive symptoms such as pain, dyspnea, wheezing, Superior vena cava syndrome, pleural effusions (10,11). Diagnosis usually by CT showing lobulated mass. Confirmation done by tissue biopsy of accompanying nodes if any, mediastinoscopy, mediastinotomy, or thoracotomy. FNA biopsy is usually not adequate. (12,13,14) Treatment of mediastinal Hodgkin's involves chemotherapy and/or radiation. 5 year survival is now around 75%. (15) Large-cell type may have somewhat better prognosis. Surgery is generally not performed because of invasive nature of tumor.

Of all cancers involving the same class of blood cell, 2% of cases are mediastinal large B cell lymphomas.

The incidence of pleural empyema and the prevalence of specific causative microorganisms varies depending on the source of infection (community acquired vs. hospital acquired pneumonia), the age of the patient and host immune status. Risk factors include alcoholism, drug use, HIV infection, neoplasm and pre-existent pulmonary disease. Pleural empyema was found in 0.7% of 3675 patients needing hospitalization for a community acquired pneumonia in a recent Canadian single-center prospective study. A multi-center study from the UK including 430 adult patients with community acquired pleural empyema found negative pleural-fluid cultures in 54% of patients, Streptococcus milleri group in 16%, Staphylococcus aureus in 12%, Streptococcus pneumoniae in 8%, other Streptococci in 7% and anaerobic bacteria in 8%. Given the difficulties in culturing anaerobic bacteria the frequency of the latter (including mixed infections) might be underestimated.

The risk of empyema in children seems to be comparable to adults. Using the United States Kids’ Inpatient Database the incidence is calculated to be around 1.5% in children hospitalized for community acquired pneumonia, although percentages up to 30% have been reported in individual hospitals, a difference which may be explained by an transient endemic of highly invasive serotype or overdiagnosis of small parapneumonic effusions. The distribution of causative organisms does differ greatly from that in adults: in an analysis of 78 children with community acquired pleural empyema, no micro-organism was found in 27% of patients, Streptococcus pneumoniae in 51%, Streptococcus pyogenes in 9% and Staphylococcus aureus in 8%.

Although pneumococcal vaccination dramatically decreased the incidence of pneumonia in children, it did not have this effect on the incidence of complicated pneumonia. It has been shown that the incidence of empyema in children was already on the rise at the end of the 20th century, and that the widespread use of pneumococcal vaccination did not slow down this trend. This might in part be explained by a change in prevalence of (more invasive) pneumococcal serotypes, some of which are not covered by the vaccine, as well a rise in incidence of pneumonia caused by other streptococci and staphylococci. The incidence of empyema seems to be rising in the adult population as well, albeit at a slower rate.

The condition is rare but serious, and appears in all mammals. It results from leakage of lymph fluid from the thoracic duct (or one of its tributaries). This can result from direct laceration (e.g., from surgery) or from nontraumatic causes. The most common nontraumatic cause is malignancy, especially lymphoma. Less common is left-heart failure, infections, and developmental abnormalities such as Down syndrome and Noonan syndrome.

Treatment of hydrothorax is difficult for several reasons. The underlying condition needs to be corrected; however, often the source of the hydrothorax is end stage liver disease and correctable only by transplant. Chest tube placement should not occur. Other measures such as a TIPS procedure are more effective as they treat the cause of the hydrothorax, but have complications such as worsened hepatic encephalopathy.

A number of PPBs have shown trisomy 8 (17 out of 23 cases studied per the PPB registry). Trisomy 2 and p53 mutations/deletions have also been described.

An association with mutations in the DICER1 gene has been reported. Mutations in this gene are found in 2/3 cases.

The pleural space can be invaded by fluid, air, and particles from different parts of the body which fairly complicates the diagnosis. Viral infection (coxsackie B virus, HRSV, CMV, adenovirus, EBV, parainfluenza, influenza) is the most common cause of pleurisy. However, many other different conditions can cause pleuritic chest pain:

- Aortic dissections

- Autoimmune disorders such as systemic lupus erythematosus (or drug-induced lupus erythematosus), Autoimmune hepatitis (AIH), rheumatoid arthritis and Behçet's disease.

- Bacterial infections associated with pneumonia and tuberculosis

- Chest injuries (blunt or penetrating)

- Familial Mediterranean fever, an inherited condition that often causes fever and swelling in the abdomen or the lungs

- Fungal or parasitic infections

- Heart surgery, especially coronary-artery bypass grafting

- Cardiac problems (ischemia, pericarditis)

- Inflammatory bowel disease

- Lung cancer and lymphoma

- Other lung diseases like cystic fibrosis, sarcoidosis, asbestosis, lymphangioleiomyomatosis, and mesothelioma

- Pneumothorax

- Pulmonary embolisms, which are blood clots that enter the lungs

When the space between the pleurae starts to fill with fluid, as in pleural effusion, the chest pain can be eased but a shortness of breath can result, since the lungs need room to expand during breathing. Some cases of pleuritic chest pain are idiopathic, which means that the exact cause cannot be determined.

If left untreated, the condition can progress to a point where the blood accumulation begins to put pressure on the mediastinum and the trachea, effectively limiting the amount that the heart's ventricles are able to fill. The condition can cause the trachea to deviate, or move, toward the unaffected side.

The annual age-adjusted incidence rate (AAIR) of PSP is thought to be three to six times as high in males as in females. Fishman cites AAIR's of 7.4 and 1.2 cases per 100,000 person-years in males and females, respectively. Significantly above-average height is also associated with increased risk of PSP – in people who are at least 76 inches (1.93 meters) tall, the AAIR is about 200 cases per 100,000 person-years. Slim build also seems to increase the risk of PSP.

The risk of contracting a first spontaneous pneumothorax is elevated among male and female smokers by factors of approximately 22 and 9, respectively, compared to matched non-smokers of the same sex. Individuals who smoke at higher intensity are at higher risk, with a "greater-than-linear" effect; men who smoke 10 cigarettes per day have an approximate 20-fold increased risk over comparable non-smokers, while smokers consuming 20 cigarettes per day show an estimated 100-fold increase in risk.

In secondary spontaneous pneumothorax, the estimated annual AAIR is 6.3 and 2.0 cases per 100,000 person-years for males and females, respectively, with the risk of recurrence depending on the presence and severity of any underlying lung disease. Once a second episode has occurred, there is a high likelihood of subsequent further episodes. The incidence in children has not been well studied, but is estimated to be between 5 and 10 cases per 100,000 person-years.

Death from pneumothorax is very uncommon (except in tension pneumothoraces). British statistics show an annual mortality rate of 1.26 and 0.62 deaths per million person-years in men and women, respectively. A significantly increased risk of death is seen in older victims and in those with secondary pneumothoraces.

Since the mechanism behind chylothorax is not well understood, treatment options are limited. Drainage of the fluid out of the pleural space is essential to obviate damage to organs, especially the inhibition of lung function by the counter pressure of the chyle. Another treatment option is pleuroperitoneal shunting (creating a communication channel between pleural space and peritoneal cavity). By this surgical technique loss of essential triglycerides that escape the thoracic duct can be prevented. Omitting fat (in particular FFA) from the diet is essential. Either surgical or chemical pleurodesis are options: the leaking of lymphatic fluids is stopped by irritating the lungs and chest wall, resulting in a sterile inflammation. This causes the lung and the chest wall to be fused together which prevents the leaking of lymphatic fluids into the pleural space. The medication octreotide has been shown to be beneficial and in some cases will stop the chylothorax after a few weeks.

In animals, the most effective form of treatment until recently has been surgical ligation of the thoracic duct combined with partial pericardectomy. There is at least one case report (in a cat) of clinical response to treatment with rutin.

Its cause is usually traumatic, from a blunt or penetrating injury to the thorax, resulting in a rupture of the serous membrane either lining the thorax or covering the lungs. This rupture allows blood to spill into the pleural space, equalizing the pressures between it and the lungs. Blood loss may be massive in people with these conditions, as each side of the thorax can hold 30 to 40% of a person's blood volume or 1.5 to 2 L per side in the average adult. Even minor injury to the chest wall can lead to significant hemothorax.

Less frequently, hemothorax occurs spontaneously. A major vascular cause of hemothorax is aortic dissection or rupture of thoracic aortic aneurysms. It may also follow surgical intervention in the thoracic area. Infrequently, patients with pneumothorax may develop spontaneous hemothorax. Spontaneous hemothorax or hemopneumothorax may be occur with endometriosis, if endometrial tissue implants on the pleural surface, then bleeds in response to cyclical hormonal changes in menstruating women.