About mesothelioma

INTRODUCTION
Mesotheliomas are neoplasms originating from the layer lining the cavity mesotelial srosa (10.13). Eighty percent occur in the pleura, with 20% in the peritoneum (10.13), most of the primary tumor in the pleura is the most malignant mesotheliomas in the pleura are primary mesotheliomas (9.14) are rarely primary sarcomas derived from the elements-unsurjaringan pengandung on pleura (14)
Two types of mesotheliomas are recognized: a benign localized (localized fibrous tumor of the pleura = benign fibrous tumor of the pleura) and the malignant form difuse (malignant pleural mesotheliomas difuse) (6,8,9,10,13). Mesotheliomas arise in the form of benign (15% of all cases) and malignant (85% of all cases) (10). Localized fibrous tumor of the pleura are not associated with asbestos exposure. Benign fibrous tumor of the pleura from the subpleural fibroblast. Visceral pleural more often involved than the parietal pleura. Histologically, benign fibrous tumor of the pleura may show three patterns (the composition of the picture and name): fibrous, cellular (consisting of cells) and mixed (mix) (9). Since 1960, malignant pleural mesotheliomas difuse has been proven to have a relationship with the use of (exposed) to asbestos (8.9). Predominant in men with perbandinagn 2:1 (10.13). Histologically, malignant pleural mesotheliomas difuse divided into 4 categories:
1. Epithelial or tubulopapilari (35-40%), which is associated with pleural effusion and prognosis is slightly better.
2. Fibrosarcomatous or mesenchymal (20%), which is often "dry" mesotheliomas, the worst prognosis.
3. Mixed (35-45%), intermediate prognosis.
4. Undifferentiated (desmoplastik), the worst prognosis (6,8,9,13,14)
Malignant pleural mesotheliomas difuse almost always unilateral (14). Right Hemithorax 60% more often than the left 35% and 5% bilateral (9).
The majority (<90%) pleural tumors are metastatic, with the most common primary tumor of the breast and lung (10.13).


Embryology and microscopic pleural ANATOMY
Cavity (cavum) pleural formed between the third and seventh week of pregnancy and is derived from splanchnopleura and somatopleura, which then form the visceral pleura (splanchonopleura) and parietal pleura (somatopleura.) Visceral pleura. Differences of origin and plera embryology viscaral parietal pleura is responsible for separation supli vascular, lymphatic and neural structures in both these structures are visible on adult time (12.14). At the end of the seventh week of pregnancy, the diaphragm has been separated from the thorax cavity with the peritoneal cavity and in the third month of pregnancy and two had pleural cavity expands scukupnya (14).
In adults, the second thick pleural surface of approximately 30-40 mm and prepared by the layer of cells mesotelial with underlying tissue is connective tissue (connective tissue). Depending on location, these cells may mesotelial flattened (flat), cubridal or columnar. Other characteristic of the cells is mempunayi many mikrovilli mesotelial that plays a message to phagocytosis, which is as good contribution to the natural lubrication in permukaaaan pleura (14).
Layer of connective tissue (connective tissue) contains neurovaskuler and lymphatics that supply the pleura (10.14). There are some important differences in this layer between the visceral pleura and parietal pleura. In the visceral pleura, connective tissue laposan is continued function of the tissue in the lung fibroelastik jarinagn lining the pleura parietal junction may also be attached to very strong in basic structure as the specific nature of the pleura diafragmatika (3.14). Parietal pleura attached to the surface next to the sternum, costa cartilages, and anterior chest wall, laterally and posteriorly by a thin layer with loose connective jarinagn called fascia endothorasic (3,4,12,14).
Visceral pleural blood supply in humans comes from the lung itself with two double arterial supply in both lungs (pulmonary circulation) and bronchial arteries (systemic circulation) (12.14). Pulmonary capillaries form a web of subpleyral on visceral pleural (12). One venous drainage into pulmonary veins (12, 14). Venous drainage is only because of low pulmonary venous pressure (12). Blood supply to the parietal pleural dar only systemic arteries, including posterior intercostal, internal mammaria, the anterior superior mediastinum and phrenica arteries (12,13). Pleural drainage parietale malewati venules and that berhubunagn with systemic venous mainly into the peribronchial and intercostal veins, but may also drainage directly into the vena azygos and vena cava (12, 14).
Pleural receive nerve supply from nerves that supply the structures in which the pleura is attached (5). Visceral pleura diinnervasi by autonomic nerve fibers are vagal nerve fibers and sympatis of pulmonary plexus (4,5,12,14). But it does not have somatic innervation, and therefore are not sensitive (10,12,14). Visceral pleural sensitive only to strain (4.5)
Parietal pleura is innervated by sympathetic nerves and the sympathetic nervous tetpi pleura also dinnervasi somatic (14). Pleural parietale receive from nerve somatic innervasi intercostalis, except the diaphragm and pleura central parietale mediatinal which innervated by the nerve phrenicus (4,5,12). So pleural parietale able to sense and transmit pain "pleritic" in inflammation and pain in the chest tube during insertion and also after that, which is caused by somatic innervasi the pleura paretal (4,10,14). Parietal pleura is sensitive to temperature, touch and pressure (4).
There are also differences in lymphatic drainage between the two layers of pleura. Drain (pipeline) through the visceral pleural lymphatic nets into the pulmonary lymphatics, eventually flowing towards the pulmonary hilum (12.14). Pipe line (drain) into the pleural mediastinal nodes mediastinal and tracheobronchial nodes. Pipe line (drain) to a series of anterior chest and posterior thorax to the inside of the intercostal nodes near the head of the costa. Pipe line (drain) to the parasternal diaphragmatic pleura, phrenic middle and posterior mediastinal lymph nodes (12.14).
Parietal pleura is also different from the visceral pleura by the nature of those seen in Kampmeier foci and stomata. Kampmeier foci is a collection activities mesotelial cells and limponoretikuler, centered on the lymphatics core, which adds pleura.Limfatik core defense capabilities in the concentrate in the lower mediastinal area on pleuara parietal.Stomata is the pore 2 till 6 mm which relate directly to the lymphatic parietal pleura (14). During the respiration of these pores has the ability to stretch and architecture of such pores form a arah.Jadi vakula pores is a very effective system to drain the fluid and particles, including red blood cells and meterofage . The pores are located on the surface of the parietal pleura which makes it the predominant (in power), responsible for cleaning the cells and particulate substances in the pleural space (10.14).


ANATOMY macroscopic
In each hemitoraks, nisceral pleura that covers the whole surface of the lung with a perfect, including fitura (2,5,14). At the hilum pulimonal, visceral pleural be continued-
right as the parietal pleura that is used to coat the inner chest wall (pleura costalis), mediastimum (pleura mediastinalis), diaphragm (pleura diafrag matika) and cupula (pleural cerricalis) in the chest cavity (1,2,3,4,5, 9,12,14). Fig 1-8 AB p. 12 (4). At the hilum, pleura parietal and visceral pleura in the form of a cuft (cuff) that surrounds the Structure-Structure entering and leaving the lung at the base of the lung (2.4) Figure 1 p. 115 (2).
Pleural cavity in humans is completely separate (15.140. Crosscutting pleural cavity with a short distance in the rear half of the corpus sternum (14). 1.Pada simus pig 50-costo costo prenichus and mediastinal parietal pleura turned on itself, providing a potential space where the lung to inflate the lungs during respiration (14). The lungs adjust to the form of the pleural cavity but not full fill the cavity (5). Superior, pleura extends over the bones of the thorax to the base of the neck (Fig 50-2). Antorior, pleural Casta extends until the 7th, until Casta to-9 on the lateral and until Casta to-12 on the posterior (Fig 50-2), (3.14). Fig 22, Fig 23 (3).
Under the base of the lung pleura to form loose folds in kenall as ligament pulimonal providing venous distension on pulimonal.Ligamentum pulimonal could double in the mediastinal pleura is tapered downward from the base of the lung where bersambungdengan visceral pleura, in candal mediastimum (2.14) .
Pleura is a thin serous membrane active and slippery a porous network of blood vessels, nerves and lifatik (1,2,4,5,9,10,11,12,14,). Consists of the parietal pleura and visceral pleura ( 1,4,6,11,12,14). Between the two layers formed a cavity (gap) tertutupyang carum called the pleura (1,3,4,5). Under normal conditions, in carum pleural serous fluid which there is little make the parietal and visceral pleural surfaces become slippery so as to prevent the occurrence of friction during respiration (1,2,4,9,10,12,14). This fluid is in the form as metralfiltrat from plasma but containing molecules in the secretion by cells mesofel pleural which is a sub factor (12.14). Water is carrying protein that gives tissues mukrid properties in pleural fluid (11). Five to ten liters of fluid into the pleural cavity (pleural carum) for 24 hours (12,13).


Physiology and Pathophysiology of pleural
Pleural mechanics and has the function of negative tekakan fisiolopis.Pleura forward from the thorax to the lung, thereby against resilience (recoil elosis) natural lungs and sustain the development of lung during respiration, this function is performed in an environment with very little friction, thereby providing lung sense to move gracefully with lameor on the inner surface of the chest cavity for the lungs inflate and deflate (11.14). pleura jg of environmental control within the chest cavity to maintain fluid balance, prevent clotting and remove air and maintain space remained sterile (14) .
In normal conditions, carum pleura is a potential space with a thickness of 10 to 20mm (14). Lung is maintained in a state expands with the maintenance of negative pressure in the pleural space (9,11,14). This negative pressure makes the chest cavity to overcome the urging force against of resilience (vekril elastic) natural lungs (9,11,14). The pressure recess in the pleural space, a little - 2 to - 5 cm H2O (14). When the measure with an upright posture, there are more negative pressure on chest apelus than siafragma, the possible influence of gravity (9.14). The negative pressure increases from the surface until the end of respiration with a pressure between -25 to-35cm H2O in the capacity of living (14).
At first look strange pleuraakan space where the gas is not pulled from the stomach into the negative pleura.Tekanan space in the pleural space is the lowest partial pressure of gas in the vein on the circulation of the pleura, while the opponent by oraksi, it prevents pnemotorales normal.Perbedaan spontaneously under conditions of partial pressure This is the circulation between the two most fundamental absorption oksigen.Kalau pressure in the pleural space significantly decreased to less than 50cm H2O, the total force under normal conditions help the absorption of the gas out of the pleural space (14).
Fluid friction (transulasi and absorption) through the membrane, the pleura (parietal and visceral pleura) is complicated and not at all but on life (14). Generally determined by the law storling which depends on hydrostatic, colloid and tissue pressure (9.12). Many styles influence each other in the parietal pleura and visceral pleura, including tekana hydrostatic and colloid in each pleura (14). streaming fluid is controlled by the balance of hydrostatic pressure and colloid in the layer of the pleura and pleural space (9,12,14). Differences pressure is the prime mover of fluid from the parietal pleura into the living style pleura.Keseimbangan help from carum pleural fluid absorption through the visceral pleura (12).
In healthy conditions, formed by the pleural fluid and the absorption by the visceral pleura (Figure 19-4) (9). Systemic capillary hydrostatic pressure is 30 cm H2O and intra-pleural pressure is negative on average -5 cm H2O.Bersama together, these Net hydrostatic pressure 35 cm H2O which causes transudation of pleural parietal.Tekanan osumtik colloid in systemic capillary was 34 cm H2O, is in the opponent by 8 cmH2Odari osumtik pressure pleura.Jadi space, clean osumtik pressure 26 cmH2O draw fluid back into the systemic capillary. systemic hydrostatic pressure (35 cmH2O) exceeds osumtik capillary pressure (26 cmH2O) with 9 cmH2O.Jadi net 9 cmH2Omenggerakkan. fluid into the pleural space by a systemic capillary dada.Perhitungan similar to the wall on the visceral pleura covers the low pressure circulation pulimonal will show
that this move is the result of the net with 10 cmH2O interesting pleural fluid into the capillary liquid pulimonal (9). Nevertheless in physiological conditions, fluid reabsorption pleuar mainly through the lymphatics in the parietal pleura because proteins that enter the pleural space can not enter the pleural capillaries Visceral which are relatively impermeable (12.14).
Under normal conditions the pleural space contains very little liquid, about 0.3 ml / kg (12.14). The liquid is usually hipokotik prokin containing approximately 100 mg / dl (9.14). When the protein is increased in some diseases about 1 g / dl, the net colloid osumtik pressure on the visceral pleura same capillary pressure colloid osumtik pleural fluid and pleural fluid reabsorption becomes dependent on lymphatic drainage (9). parietal pleura with limfatiknya have a great capacity to clean protein and fluid (12 , 14). The excess fluid and protein in the pleural space will be pumped out by the lymphatic vessels (which opens directly) from the pleural cavity into the (1) mediastimum (2) the superior surface of the diaphragm dn (3) the lateral surfaces of the pleura parietal.Gambaran 38 - 9 shows the dynamics of the exchange of fluid in the pleural space (11).
Basic causes of this negative pressure is the pumping of fluid from the pleural space by lymphatic vessels (which is also the basis of negative pressure in the space encountered in most tissues of the body). Because of the tendency of deflation in the normal around -4 (-5-6cmH2O), then pleural liquid pressure at least should always senegatif -4 mm / kguntuk maintain lung development (11).
Pleural homeostasis is influenced by other factors, including gravity, niscositas pleural fluid, pleural thickness mebrane, respiration movement and distribution of the lymphatic drainage of the entire parietal pleura (12.14). A little imbalance of pleural fluid accumulation and absorption will play an important role in the development of pleural effusion (12.14).
The mechanism of this imbalance include (1) increased hydrostatic pressure such as in heart failure (7,9,11,12). (2) decrease the negative pressure intrapleura (12). (3) increased capillary permeability, as inflammatory or neoplastic penykit (7,9,11,12). (4) decreased plasma onkotik pressure (9,11,12) and (5 ) reduction or interruption of lymphatic drainage (11.12).
When disturbed dynamic equilibrium in which the speed exceeds the lymphatic to compensation, can stack little by little overcome the pleura (14). Pleural effusion is an accumulation (accumulation) of fluid in the pleural cavity (10.13). Pleural effusion is not an illness but a sign (gesture) influence (effect) in the pleura or systemic disease (13). Pleural effusion may result in dyspnea (7,10,13) pleural effusions were classified as pleural effusion trasudat or exudate (12). Changes in systemic hydrostatic pressures or colloid osumtik pressure upsets the balance of force through surface normal pleural effusion causing low netralfiltrat consisting of plasma proteins were classified as trasudat.Perusakan effusion capillary permeability caused by inflammation or infiltration in the pleural effusions that cause protein-rich effusions classified as exudates (10,12,13). effusions exudate suggesting disruption or loss of integrity intact pleura (12). The distinction between exudates and pleural effusion transudat related diagnosis (13). The nature of the liquid is in getting the diagnosis toraksintesis can help differentiate between effusions and pleural exudate transudat that summarized in table 16.6 ( 13)


Table 16.6
Some differences in the nature and exudate transudat
Transudat exudate
color clear, serous turbid, brown
The number of leukocytes <1000/mm ³> ³ 10000/mm
Total erythrocyte <10000/mm ³> ³ 10000/mm reddish-
> ³-100000/mm grossly bloody
Low normal glucose under certain conditions
Protein <3.0 g / dl> 3.0 g / dl
Comparative <0.5> 0.5
Protein
The density of <1.016> 1.016
Normal LDH> 67% of the upper limit of normal
Comparative <0.6> 0.6
LDH
same as arterial pH <7.20 suggests empyema
Nungkin negative culture positive (empyema)
Negative cytology may psitif (makignant)


* Pleural fluid protein divided by serum protein
** Pleural fluid LDH divided by serum LDH
Etiology of pleural effusion varies widely (12). Some of the many causes listed in tables 55-2 and 55-3 (12), table 16-4 and table 16-5 (13), table 5-6, table 56.1 (14).


Table 56-1 differensional diagnosis of pleural effusions
Pleural effusion transudat
Congestive heart failure Drug-induced lupus
Cirrhosis Immunoblastic lymphadenopathy
Nephrotic Syndrome Sjögren's syndrome
Superior vena cava obstruction Familial Mediterranean fever
Fontan Procedure Churg-Strauss Syndrome
Wegener's granulomatosis Urinothorax
Peritoneal Dialysis Drug-induced pleural disease
Glomerulonephritis nitrofurantoin
Myxedema Dantrolene
Pulmonary embolism Methylsergide
Sarcoidosis bromocriptine
Pleura effusion exudate Amiodanone
Neoplastic disease Procarbazin
Disease Metastasic Methotrexate
Mesothelioma Miscellaneous Diseases and Conditions
Infection Disease Asbestos Exposure
Tuberculosis Post pericardiectomy or
Post myocardial infraction syndrome
Fungal infections Meig's Syndrome
Parasitic infections Yellow nail syndrome
Viral infections sarcoidosis
Pericardial disease, pulmonary embolization
After gastrointestinal disease, coronary artery bypass surgery
After lung transplant pancreatic disease
Susphrenic abcess Fetal pleural effusion
Intrahepatic abcess Uremia
Intrasplenic trapped lung abcess
Radiation therapy of esophageal perforation
After abdominal surgery Ovarian hyperstimulation syndrome
Diaphragmatic hernia post partum pleural effusion
Endoscopic variceal sclerosis amyloidosis
Electrical burns after liver transplant
Collagen vascular disease, iatrogenic injury
Rheumatoid pleuritis hemothorax
Systemic Lupus Erythematosus Chylothorax
Uses the right of the pleura is still not completely understood. In my experience, it is clear that the pleural fluid and gas to maintain homeostasis (14).


PATHOLOGY
Asbestos fibers are strong fiber winding (chrysotik) usually settle to the proximal airway and with easy to clean and reduce the risk of tumor development, although rarely watery like amphibole fibers (crocidolite, amosite, actinolite, and tremolite anthrophylite) and soil silicate zeolite, was found in Anatolia region of Turkey are usually stuck in the terminal airways and migrate to the pleura, thereby increasing the risk of malignant pleural mesotheliomas difuse more than 300 times that of the general population. The period of latent (hidden) after exposure to 15 years to 50 years. Recent research suggests that gensasi (generation) of free radicals (including nitricolida, suppress immune system (both cellular and hormonal), induction of cytokine (TNF-α, IL-1α, IL-1β and IL-6) and produce genetic damage, such as abnormalities kromosome 1,3,4,6,7,9,11,17 (P53) and 22 (includes C-sis) all may play a role in the mechanism of disease associated with asbestos (9).
Malignant pleural mesotheliomas difuse is locally aggressive neoplasms (10.13). Lining the chest cavity until thick (like mass), the union of two layers of pleura and invaginasi between lung lobes (Figure 56-10). Invasive in the lungs, diaphragm, pericardium, chest wall and mediastinal structures (13.14). Having the ability to be hematogenous metastases and limfogen (10,13,14)


CLINICAL
Most patients with malignant pleural mesotheliomas difuse complain dyspneu on exercise and chest wall discomfort (7,9,13,14). Pleural effusion can cause dyspneu but can also asymptomatic at rest. But other symptoms, such as cough, fever (paraneoplastik), malaise, weight loss and dysphagia also occurs. Complaints severe chest wall pain, abdominal distension, pericardial tamponade, and superior vena cava syndrome disease is advanced member impression. Although in most patients with distant metastases arise at some time during the history of the disease, lesions (lesion) is rarely a problem (9).


DIAGNOSIS
Symptoms of mesotheliomas are often vague and nonspecific, dyspneu and pain (8). Pleural thickening (such as mass) found in classical and pleural restriction is a recently discovered (8.13). Chest radiographs clearly showed thickening of the pleura, effusion (75%) and ICS narrowing (9). The discovery of radiographs that include a broad spectrum including pulmonary nodules, chest wall masses, and masses in the mediastinum (Fig. 16-33) (7.13). Radiographic diagnosis is often difficult at an early stage, by finding a bit of pleural effusion (8). CT (computed tomography) are often members suggested the diagnosis of pleural thickening causes irregular difuse (9). By contrast malignant pleural mesotheliomas usually appear multisentrik difuse, with nodulus multiple-nodulus in the pleura which eventually joins in sheet form with a mass of confluent (13). Ct lung may fail to identify some other abnormalities at an early stage (8). Diagnosis with torakosintesis (pleural puncture), cytologic examination (FNA) and pleural biopsy (7,8,9,13,14). The network can easily be taken with a small incision or biopsy technique VAT (Video Assisted Thoracoscopic Surgery) (9). Accurate diagnosis of pathology Immunohistokimia entrusted with dye staining calretinin-specific stem cells mesotelial the original (9.13). Calretinin dyes has become an important clinical tool and performed in all cases of suspected malignant pleural mesotheliomas difuse (9). When Immunohistokimia not produce definitive diagnosis, is required electron microscopic (13). Electron microscopy may also be useful in distinguishing malignant pleural mesotheliomas difuse with metastatic adenocarcinoma (9)


Staging
Butchort staging system created in 1976 had been abandoned by agreeing a new staging system proposed by the International mesotheliomas Interest Group (IMIG), which provides a more accurate description, to the status of the tumor T and N node status (Table 16-10) (13).


Table 16-10
New International Staging System for Malignant Pleural Mesothelioma Difuse
T1 T1a. Tumor limited to the parietal pleura and mediastinal pleura ± ± ipsilateral pleural diaphragm.
Does not involve the visceral pleura.
T1b. Tumor involving the parietal pleura and mediastinal pleura ± ± ipsilateral pleural diaphragm
Tumor involving the visceral pleura.
T2. Tumor involving each ipsilateral pleural surfaces (parietal pleural, pleural
mediastinal, pleural diaphragm and visceral pleura) with at least one
followers:
• Involvement of diaphragmatic muscle
• Expansion of the tumor on the visceral pleura to the base of the lung parenchyma.
T3. Describing advanced on the ground but most likely resectable tumors
(Resektabel).
Tumor involving the entire ipsilateral pleural surfaces (parietal pleura, mediastinal pleura,
Pleural diaphragm, and visceral pleura) with at least one follower:
• Involvement of fascia endotorasik
• Expansion to mediastinal fat
• solitary tumor is focused (centered) can be resected completely extended until the soft tissue
chest wall
• Not involving the pericardium transverse
T4. Describing advanced elsewhere that it is technically not resectable tumors.
Tumor involving mediastinal, ipsilateral pleura (parietal pleura, mediastinal pleura, diaphragm and pleura visceral pleura) with at least one follower:
• Expansion difuse or multifocal tumor mass in the chest wall, with or without associated
destruction costa (rib)
• Expansion of the tumor directly into the peritoneal transdiafragma
• Direct Expansion of the tumor to the contralateral pleura
• Expansion of the tumor directly into mediastinal organs
• Expansion of the tumor directly to the spine
• Expansion of the tumor through (through) the surface of the pericardium with or without pericardial effusion;
or mediastinal tumor myocardium
N: Lymph nodes
Nx: regional lymph glands can not be assessed
N0: No metastasis to regional lymph limmfe
N1: metastases to bronchopulmonal ipsilateral hilar lymph nodes or
N2: metastases to mediastinal lymph nodes subkarina or ipsilateral including gland
ipsilateral internal mammaria
N3: metastases to contralateral mediastinal, contralateral internal mammaria, lymph nodes
ipsilateral or contralateral supraclavicular


M: metastases
Mx: distant metastases can not be assessed
Mo: No distant metastasis
M1: distant metastases


Stage I:
He T1A No Mo
Ib T1b No Mo
Stage II:
T2 No Mo


Stage III:
All T3 All N1 Mo
All N2
Stage IV:
All T34 All All N3 M1


TREATMENT
Treatment of malignant pleural mesotelium difuse is controversial (debatable) because the factors that affect prognosis are known ugly (9.13). Survival in untreated patients between 6 months to 2 years in stage IV disease. Survival of more than 2 years in a stage I tumor of untreated (13).
Injection intrapleura with various chemotherapeutic agents is an example of a new form of treatment is attempted (6). Patients suffering from early-stage tumors (stage He) reported longer survival in giving intrapleura with gamma interferon (13).
Radiation and chemotherapy alone is not having a strong influence for survival in this disease (9). Surgery also has been used to improve survival with significant results (6.9). Surgical resection in the treatment of malignant pleural mesotelium difuse not completely required (13). Two main approaches have been used: radical or pleurektomi pleuropneumonektomi parietal with decortication (6,9,13). Initial experience with radical pleuropneumonektomi demonstrated, outcome (longer survival) are no better than what can be achieved with radical pleurektomi and decortication, but the morbidity is higher pluropneumonektomi radical (9). When the pleura is free, with no adhesions between the layers of visceral and parietal pleura parietaldan tumors, plurektomi enough. When there are adhesions with loss of pleural space, pleural extra pleurektomi preferred (6).
Several surgical sessions are reported survival reaches 14 to 20 months, but this observed increase in survival may be due to patient selection rather than yanh benefits obtained from surgery (6) another session compared to only surgery with chemotherapy or radiotherapy did not show improvement hdup survival, although improvements Small note when the combination of these modalities are used (6). When surgery combined with post-operative chest wall irradiation, the end of the procedure the average survival to 25 months (9). When combined with adjuvant radiation hemitoraks, pneumonektomi ekstrapleura memebrikan best hope with local control. Patients suffering from stage I or II tumors with epithelial histology is likely to be useful in this approach. Giving chemotherapy is not required. Patients with stage I or II tumors who do not have lung function that are resistant to pneumektomi ekstrapleura to dipalatif with talc pleureksis torakoskopi or with pleurektomi / decortication.
At Memorial Sloan - Kattering Cancer Center, the experience in 150 patients managed with pleurektomi / decortication and adjuvant radiation (radiation hemitoraks wide beam with or without intraoperative brachytherapy) suggest that patients who can be dissected ¼ life expectancy may extend this treatment approach. In most patients the disease occurs locally rekurens not lebi than 2 years and the risk of radiation cause pnumonitis or pericarditis is significant. Patients with locally advanced or metastatic mesotheliomas have few treatment options. Radiation therapy is not sending effective dose in patients who do not cause lung pneumonektomi sensitive to high doses of radiation (13). Until now, the average low response who received chemotherapy makes it attractive for treating patients routinely with standard agents (13).
Intraterapi and post-operative chemotherapy (Lung Cancer Study Group, the Cleveland Clinic), photodynamic therapy (MCI) and immunotherapy with TNF-α and Gamma (MCI, SWOG) without a little real work (9). Using trimodalitas with surgery, chemotherapy and radiation therapy, survival to 39% at 5 years was reported. Surgery is used for this protocol is pneumonektomi ekstrapleura requiring en bloc resection of the parietal pleura, lung, pericardium, and the subsequent reconstruction of the diaphragm with an additional Gore-Tex in the diaphragm and the pericardium (14).
Despite the general impression that the therapy is superior multimodalitas than one therapy alone, the combination of the right to choice of treatment in this disease is still being defined (9). Other treatment modalities, including new chemotherapy, radiation therapy, intra-operative, immunotherapy, photodynamic therapy and gene therapy is experimental and being studied (6,9,13,14). Clearly, new therapies are needed (9).


FOLLOW UP
Mesotheliomas tend to local recurrence (8.9)
CT - scans needed to detect recurrence or residual disease following (8).


Prognosis
Prognosis mainly depends on the histology and stage of tumor (13). Histologically, epithelial tumors without involving the chest wall, pericardium, or diaphragm and lymph nodes had the best prognosis (13.14). Mixed Tumor (mixed epithelial and fibrosarcomatous) had an intermediate prognosis and fibrosarcomatous and undifferentiated tumors had the worst prognosis (