THE KURSK STATE MEDICAL UNIVERSITY
DEPARTMENT OF SURGICAL DISEASES № 1
PLEURITIS
Information for self-training of English-speaking students
The chair of surgical diseases N 1 (Chair-head - prof. S.V.Ivanov)
BY ASS. PROFESSOR I.S. IVANOV
KURSK-2010
Pleuritis
(pleurisy)
1.Pleural Effusion
Excess fluid in the pleural space.
Normally, 10 to 20 mL of fluid is spread thinly over the visceral and parietal
pleurae. The fluid is similar in composition to plasma except that it is lower in
protein (< 1.5 g/dL). Pleural fluid enters from the pleural capillaries and exits via
parietal pleural stomas and the lymphatics.
Pleural effusions are classified as transudates or exudates. Transudates are due to
elevations in microvascular pressure or to decreases in oncotic pressure; exudates
are due to pleural inflammation (pleurisy), with an increased permeability of the
pleural surface to proteinaceous fluid. Lymphatic obstruction may also contribute
to accumulation of pleural fluid. Many conditions can produce either transudates or
exudates.
Hemothorax (blood in the pleural space) occurs most often from trauma and
rarely after rupture of a vessel in a parietopleural adhesion associated with
spontaneous pneumothorax. Spontaneous hemothorax occurs rarely as a
complication of a coagulation defect. Rarely, an aortic aneurysm ruptures into the
pleural space. Pleural blood often does not clot and may be easily withdrawn via a
needle or a water-sealed tube thoracostomy.
Chylothorax (a milky or chylous pleural effusion) is caused by traumatic or
neoplastic (most often lymphomatous) injury to the thoracic duct. The lipid content
(neutral fat and fatty acids) of pleural fluid is high; sudanophilic fat droplets are
often seen microscopically. Cholesterol content is low. The diagnosis is confirmed
by a triglyceride level >= 110 mg/dL (1.24 mmol/L) in the effusion.
Conditions Causing Transudates
Heart failure, which increases systemic venous and pulmonary capillary
pressures, is the most common cause of transudative pleural effusions. Usually
bilateral, such effusions tend to be larger on the right side and, if unilateral, are
generally right-sided.
Hypoalbuminemia may cause pleural effusions, which are usually bilateral and
associated with fluid accumulation elsewhere in the body.
Ascites may be associated with pleural effusion because fluid can move from the
peritoneal space into the pleural space through diaphragmatic defects or lymphatic
channels; 70% of para-ascitic effusions are right-sided, 15% left-sided, and 15%
bilateral. They occur in about 5% of patients with cirrhosis and ascites. Meigs'
syndrome (pleural effusion and ascites associated with ovarian fibromas and other
ovarian tumors) has a similar mechanism, but the pleural fluid associated with
ovarian tumors is generally an exudate. The mechanism is also similar for pleural
effusion associated with peritoneal dialysis or acute pancreatitis.
In myxedema, pleural effusions are usually transudates but may be exudates.
After parturition, small effusions, which clear rapidly, may be seen during the
first 24 h.
Iatrogenic pleural effusions result when fluid infused through a catheter meant
for a subclavian vein enters the pleural space. Misplaced small feeding tubes can
sometimes perforate a main bronchus and enter the pleural space. The resulting
pleural fluid is identical to the infusate.
Conditions Causing Exudates
Mycotic pleurisy produces an exudate, and pleural biopsy may show granulomas.
Organisms can be cultured from pleural fluid and tissue. The geographic history,
skin and serologic tests, microbiologic examination of airway secretions, and
histology of other tissues are useful in establishing a diagnosis. About 10% of
patients with blastomycosis have pleural effusions, usually with extensive
underlying parenchymal disease. Pleural effusion, usually large and unilateral,
occurs in about 7% of patients with primary coccidioidomycosis. About 1/2 of
them have an associated parenchymal lesion; erythema multiforme or erythema
nodosum is common. Pleural effusion also occurs at a later stage of
coccidioidomycosis when a coccidioidal cavity ruptures into the pleural space--a
serious complication. Pleural effusion is rare in primary histoplasmosis and in
cryptococcosis, occurring usually as part of disseminated disease or with massive
parenchymal involvement.
In parapneumonic effusions, the visceral pleura overlying a pneumonia becomes
inflamed; often, an outpouring of serous exudative fluid accompanies acute
pleurisy. The fluid contains many neutrophils and may contain bacteria.
Parapneumonic effusions are usually caused by bacteria, but small effusions may
occur with viral or mycoplasmal pneumonia. Viral pleural effusions may also
occur without evident pneumonia.
Pulmonary embolism produces pleural effusions in 30 to 50% of patients. About
80% of the effusions are exudates, which are often blood-tinged. The main
mechanism of pleural fluid formation is increased permeability of the visceral
pleura over the infarcted lung, although about 1/3 of such effusions occur without
evidence of infarction on x-ray. However, a transudate may occur when heart
failure is present. Atelectasis due to pulmonary embolism can also cause a
transudate.
Metastatic neoplasms are the most common cause of exudates in persons > 60 yr.
The most common primary site is the lung, followed by the breast, but carcinomas
from any site can metastasize to the pleura. Lymphatic obstruction by pleural
implants of tumor is the major mechanism of fluid formation. The effusions are
often large and cause dyspnea on exertion. Blood-tinged or grossly bloody
exudates are the rule. Most carcinomatous pleural effusions can be diagnosed by
cytologic fluid examination, but up to three fluid samples may be needed. Pleural
biopsy is less sensitive than pleural fluid cytology but is sometimes positive when
cytology is negative; in difficult cases, both procedures may be needed.
In Hodgkin's disease and non-Hodgkin's lymphoma, pleural effusion is
common; it may be a presenting sign in non-Hodgkin's lymphoma. The mechanism
is varied, with lymphatic obstruction predominating in Hodgkin's disease and
pleural infiltration predominating in non-Hodgkin's lymphoma. Establishing the
neoplastic nature of the process is rarely necessary in Hodgkin's disease, and
pleural biopsy results are rarely positive. The diagnosis of lymphomatous pleural
effusion can occasionally be made by pleural fluid cytology and needle biopsy of
the pleura.
Malignant mesothelioma (a malignant tumor arising from the pleural
mesothelium) is strongly linked to asbestos exposure. Incidence in the USA is
about 2000 cases/yr. Insidious nonpleuritic chest pain and dyspnea are the most
common presenting symptoms. The tumor, which gradually encases the lungs and
invades the chest wall, produces pleural effusion in about 75% of patients. CT
reveals irregular thickening of the pleura. The pleural fluid is a serous or bloodtinged exudate, with glucose < 50 mg/dL (< 2.78 mmol/L) and pH < 7.2 in about
1/3 of patients. Pleural fluid cytology may reveal malignant cells not easily
differentiated from adenocarcinoma. Because needle pleural biopsies are also
difficult to interpret, open biopsy or biopsy visually directed through a
thoracoscope (video-assisted thoracic surgery [VATS]) is often needed to establish
the diagnosis. Immunohistochemistry and electron microscopy can differentiate
this tumor from adenocarcinoma. The prognosis is dismal, with poor response to
radical surgery, chemotherapy, radiation therapy, or combination therapy.
Benign fibrous mesothelioma is a rare solid tumor of the pleura that produces
chest pain, dyspnea, fever, and hypertrophic osteoarthropathy in 50% of patients.
The fluid is an exudate that may be viscid due to the presence of hyaluronate.
Diagnosis and cure are by thoracotomy and excision of the tumor.
SLE or drug-induced lupuslike syndromes (most often with hydralazine,
procainamide, isoniazid, phenytoin, and chlorpromazine) produce pleural effusions
in up to 40% of patients. The drugs have usually been given for long periods, and
the symptoms usually abate within 10 days of stopping the drug. Fever, pleuritic
pain, and some systemic manifestations of lupus are usual; rarely, isolated pleural
disease occurs. A parenchymal lesion is usually but not always present. The pleural
fluid is exudative, with neutrophils predominating early and monocytes late.
Pleural fluid glucose is usually > 80 mg/dL (> 4.44 mmol/L), pH is > 7.35, and
LDH is < 500 IU/L; pleural fluid complement is low, and pleural fluid antinuclear
antibody (ANA) titers tend to be high. An ANA titer > 1:320 with a homogeneous
pattern or a pleural fluid/serum ANA ratio >= 1 is highly suggestive. In druginduced lupus, unlike in standard SLE, antibodies to histones and single-stranded
DNA often occur in the blood. LE cells may be found and are thought to be
diagnostic, but the test is labor-intensive and should not be ordered because the
diagnosis is usually evident from the clinical features and pleural fluid serology.
Drug-induced pleural effusions are uncommon. Nitrofurantoin is occasionally
associated with an acute febrile illness with pulmonary infiltrates, pleural effusion,
and peripheral blood eosinophilia. Chronic interstitial pneumonia with fibrosis
occurs less often and produces pleural effusions less often. It occurs in persons
who have taken the drug for many years. The muscle relaxant dantrolene
occasionally causes unilateral pleural effusion with blood and pleural fluid
eosinophilia but without parenchymal infiltration. Bromocriptine and other
dopamine agonists, amiodarone, and interleukin-2 infrequently cause pleural
effusions, usually with pulmonary infiltrates.
Rheumatoid disease causes pleural effusion more often in males even though the
disease is more common in females. Pleural effusions are small to moderate and
typically occur in older men who have had rheumatoid disease for several years
and who have subcutaneous rheumatoid nodules. The fluid is an exudate with low
glucose (< 40 mg/dL [< 2.22 mmol/L]), high LDH (> 700 IU/L), low pH (< 7.2),
low complement, and a high rheumatoid factor titer (>= 1:320). Cholesterol
crystals are common.
Subdiaphragmatic abscess most often produces a sympathetic pleural effusion, a
sterile exudate with neutrophils predominating. Rarely does such an effusion
become infected; 3/4 of subdiaphragmatic abscesses occur weeks to months after
abdominal surgery. The diagnosis is established by ultrasonography or abdominal
CT.
Acute pancreatitis is complicated by para-ascitic pleural effusion in about 10% of
cases. The pleural exudate is rich in neutrophils, containing much more amylase
than the serum does. The effusions are usually small; about 60% are left-sided,
30% right-sided, and 10% bilateral.
Pancreatic pseudocysts may burrow into the mediastinum through the aortic or
esophageal hiatus and rupture into one or both pleural spaces. Amylase levels in
the pleural fluid are very high (up to 100,000 IU/L), even though serum amylase
may be normal. Abdominal ultrasound and CT scans help diagnose pancreatic
pseudocyst. Because fluid reaccumulates rapidly after thoracentesis, the
pseudocyst must be drained.
Postcardiac injury syndrome is characterized by fever, pleuropericarditis, and
parenchymal infiltrates beginning weeks after injury to the pericardium or
myocardium. It occurs in about 1% of patients who have had MI, cardiac surgery,
blunt chest trauma, pacemaker implantation, or angioplasty. Pleural effusions are
generally small, are bilateral in about 1/2 the cases, and are often a bloody exudate
with normal glucose and pH. The syndrome responds to NSAIDs and
corticosteroids.
Uremia is often complicated by a generalized serositis, and an exudative pleural
effusion may occur with fibrinous pleurisy. The fluid may be grossly bloody and
usually contains few cells, which are mainly mononuclear. The creatinine level is
elevated but lower than that of the serum, distinguishing it from pleural effusion
due to urinary tract obstruction and retroperitoneal accumulation of urine.
Asbestos exposure produces benign pleural effusion in about 3% of asbestos
workers after a latent period ranging from 5 yr to > 30 yr. Patients may be
asymptomatic or have chest pain. Effusions are usually unilateral and small to
moderate. Pleural plaques, generally without calcification, are common, and about
half the patients have evidence of parenchymal disease. The effusion is an exudate,
which may be blood-tinged. The WBC count may be as high as 25,000/µL, with a
variable differential count and many eosinophils. The diagnosis is one of
exclusion, particularly of mesothelioma and metastatic carcinoma.
AIDS causes pleural effusion (usually an exudate) in < 2% of patients. Effusion
may be due to parapneumonic effusion, empyema, TB, Pneumocystis carinii
pneumonia, or Kaposi's sarcoma. Management principles are similar to those for
persons with normal immune systems.
Symptoms, Signs, and Diagnosis
Pleuritic pain and dyspnea are the most common symptoms, but many pleural
effusions are asymptomatic and are discovered during physical examination or on
chest x-ray. Physical examination may disclose percussion dullness, decreased
motion of the hemithorax, absent tactile fremitus, and decreased or absent breath
sounds. Despite extensive diagnostic evaluation, the etiology of an effusion is not
established in about 20% of cases.
Chest x-rays are the most precise way to confirm physical findings and
demonstrate the presence of pleural fluid. When there are no adhesions between
the visceral and parietal pleurae, fluid collects in the most dependent portion of the
thorax. Because of lung recoil, the upper border of the fluid is meniscus-shaped.
With the patient upright, the minimum amount of detectable fluid ranges from 200
to 500 mL. However, in the lateral decubitus view, < 100 mL of fluid is easily
detectable. Large pleural effusions may result in complete opacification of the
hemithorax and in mediastinal shift to the contralateral side. Adhesions between
visceral and parietal pleurae may result in atypical loculated collections.
Loculations in the horizontal or oblique fissure may be confused with an
intrapulmonary tumor and are called "vanishing tumors." Obliteration of the
costophrenic angle usually denotes a fibrosing and healing reaction and may
remain after healing is complete. Pleural plaques due to asbestos exposure present
as localized areas of pleural thickening, are sometimes calcified, and are usually in
the lower 2/3 of the thorax.
CT scan is valuable in evaluating the underlying lung parenchyma in patients with
extensive pleural disease. A lung abscess, pneumonia, or a shadow due to a
bronchogenic carcinoma may be revealed beneath a loculated pleural effusion. A
lung abscess may be differentiated from an empyema with a bronchopleural fistula
and an air-fluid level. Pleural plaques are easily differentiated from parenchymal
lesions, and the pleural densities of mesothelioma are readily identified. Loculated
pleural effusions are clearly seen with CT. MRI is not indicated.
Ultrasonography can also identify and localize a loculated pleural effusion, which
is echo-free in contrast to the lung and chest wall. In difficult cases, the chest wall
can be marked or thoracentesis performed in the ultrasonography suite.
Thoracentesis should almost always be performed to confirm the presence of
fluid and to determine its characteristics. Fluid may be clear yellow (serous), milky
(chylous), blood-tinged (serosanguineous), grossly bloody (sanguineous), or
translucent or opaque and thick (purulent). Specimens should be taken for
chemical, bacteriologic, and cytologic examination (the last uses tubes with
heparin, 3 U/mL fluid, added). After thoracentesis, a sample of Gram-stained
pleural fluid sediment should be examined microscopically for bacteria and fungi.
Cultures for anaerobes should be sent to the laboratory in special transport media
or in a capped syringe.
Exudates have at least one of the following features: (1) pleural fluid/serum
protein ratio > 0.5, with pleural fluid protein usually > 3.0 g/dL; (2) pleural
fluid/serum LDH ratio > 0.6; and (3) pleural fluid LDH > 2/3 of the upper normal
limit for serum. Transudates meet none of these criteria; they are usually clear
and straw-colored but may be blood-tinged, with an RBC count > 10,000/µL.
WBC count is usually < 1000/µL but is between 1,000 and 10,000/µL in about
20% of transudates. The glucose level is similar to that in serum.
Blood-tinged pleural fluid has little diagnostic significance. More than 15% of
pleural transudates and > 40% of exudates are blood-tinged with RBC counts
between 5,000 and 100,000/µL. Only 5,000 to 10,000 RBCs/µL need be present to
make pleural fluid red, and only 1 mL of blood is needed to make 500 mL of
pleural fluid look blood-tinged. Grossly bloody fluids have > 100,000 RBCs/µL;
bloody pleural fluids suggest trauma, malignancy, or pulmonary infarction. A
hematocrit of > 50% in a bloody pleural fluid indicates hemothorax.
If the body's defenses do not control infection in a patient with pneumonia and
parapneumonic effusion, the number of neutrophils and bacteria increases, and the
fluid takes on the gross appearance of pus. The result is empyema of the thorax
(purulent exudate in the pleural space). Fluids with > 100,000 neutrophils/µL,
bacteria seen on Gram stain, and pH < 7.2 may be presumed to be empyema even
if the fluid is not grossly purulent. Most empyemas are caused by anaerobic
bacteria. Empyema can result from contamination of the pleural space by rupture
of a lung abscess; a bronchopleural fistula complicates the process. A
bronchopleural fistula can result from internal drainage of an empyema. Empyema
may be a sequela of a penetrating wound, a thoracotomy, infection from a hepatic
or subdiaphragmatic abscess, or a ruptured viscus (eg, esophagus).
Total cell counts should be obtained routinely for clear or turbid fluids. A
predominance of polymorphonuclear leukocytes (PMNs) suggests an underlying
pneumonia and a parapneumonic effusion that is usually sterile even in bacterial
pneumonia. In the early stages of bacterial infection, fluid is not visibly purulent,
many PMNs are present, and bacteria may be seen in a Gram stain. The presence
of many small mature lymphocytes, particularly with few mesothelial cells,
strongly suggests TB. In pulmonary infarction, there is usually a mixture of
lymphocytes, PMNs, and mesothelial cells; RBCs may be numerous. Eosinophils
in the pleural fluid have little diagnostic significance but are rarely present in a
tuberculous or malignant effusion.
A glucose concentration of < 60 mg/dL (< 3.33 mmol/L) in an exudative pleural
effusion indicates TB, malignancy, parapneumonic effusion, or rheumatoid
disease. In most rheumatoid pleural effusions, glucose is < 30 mg/dL (< 1.67
mmol/L). Very high amylase levels occur in pleural effusions associated with acute
pancreatitis, chronic pancreaticopleural fistulas, and esophageal rupture. The
amylase in pleural effusions due to esophageal rupture is of salivary origin, is
evident within hours of the rupture, and may be the key to early diagnosis and
lifesaving surgery. In about 10% of malignant pleural effusions, amylase is slightly
to moderately elevated. The pH of loculated pleural effusions that complicate
pneumonia tends to be < 7.2. These laboratory tests are most useful when
integrated with all of the clinical data and other appropriate tests, eg, a tuberculin
skin test when pleural effusion from TB is suspected.
Whenever the diagnosis of an exudative pleural effusion is not clear, a needle
biopsy of the parietal pleura should be performed with a Cope's or Abrams' sidehook needle. Several pieces of tissue can be sent for histologic and bacteriologic
examinations. The combination of microscopic examination and culture of pleural
tissue yields a diagnosis in 90% of patients with pleural effusion from TB.
However, repeat cytologic examination of pleural fluid is preferable to pleural
biopsy for establishing pleural carcinomatosis. In obscure cases, larger amounts of
pleural tissue can be obtained through a small thoracotomy incision (open pleural
biopsy). For example, the diagnosis of pleural mesothelioma often is impossible
from a needle biopsy and requires the larger amount of tissue obtained in an open
pleural biopsy. Replacing fluid with air and performing a VATS biopsy is a
comparable procedure. However, even with these more invasive procedures, the
etiology of the pleural effusion may remain unknown.
Pleural effusion complicates many pulmonary conditions. A clinician must judge
whether to focus diagnostic studies on the lung, the pleural space, or both. If
clinical and x-ray findings suggest the presence of important pulmonary disease,
the initial focus should be on the lungs, and fiberoptic bronchoscopy should be
performed early in the assessment. Unless pulmonary disease is evident,
bronchoscopy is unlikely to reveal the etiology of the pleural process. However,
bronchoscopy should be performed before the etiology is declared unknown.
Treatment
Thoracentesis often dramatically relieves dyspnea due to a large pleural effusion.
Because cardiovascular collapse occurs (rarely) if too much fluid is removed too
quickly, removal should be limited to 1200 to 1500 mL at one time. Pneumothorax
may complicate thoracentesis if the visceral pleura is punctured or if air leaks into
the pleural space (which is at subatmospheric pressure) as a result of a break in the
continuity of the thoracentesis system.
Indolent infection in the pleural space must be treated by a long course of
antibiotic therapy. Pleural fluid is usually reabsorbed spontaneously.
Empyema is treated with high doses of parenteral antibiotics and drainage. One or
two needle aspirations daily may be adequate for small collections of thin pus, but
water-sealed tube thoracostomy is usually preferable. When the empyema cavity is
lined by a thick, organizing, fibrinous exudate or cortex, open drainage over weeks
or months through a rib resection or intercostal tube may be necessary. If the lung
is partially collapsed by a thick cortex or if the empyema is loculated, surgical
decortication by thoracotomy or VATS is the best way to expand the lung and
obliterate the space. Decortication for a loculated empyema is best performed
within the first 3 to 6 wk of the illness. Surgery may also be necessary when a
bronchopleural fistula complicates empyema.
Treatment of pleural effusion due to malignant pleural implants is often difficult.
Pleural fluid often reaccumulates after the thorax has been drained, especially if
systemic antitumor therapy has not yet been adequate. When fluid reaccumulates,
the treatment of choice is pleurodesis: The lung is reexpanded by tube
thoracostomy, followed by instillation of a sclerosing agent, such as asbestos-free
talc, given in a slurry, or doxycycline, a tetracycline derivative. The result is an
intense pleuritis that obliterates the pleural space so that fluid cannot reaccumulate.
For hemothorax, water-sealed tube drainage is generally sufficient, provided the
bleeding has stopped. Fibrinolytic enzymes (streptokinase-streptodornase or
urokinase) may be instilled through an intercostal drainage tube to lyse fibrinous
adhesions if the effusion becomes loculated, but thoracotomy and decortication
may be necessary to expand the lung and obliterate the pleural space.
Pneumothorax
Free air between the visceral and parietal pleurae.
Etiology and Pathophysiology
Traumatic pneumothorax: Normally, pressure in the pleural space is less than
atmospheric pressure because of lung recoil. After trauma, air may enter the
pleural space in several ways. Open pneumothorax occurs when a penetrating chest
wound produces a persistent communication between the outside and the pleural
space that allows outside air to enter the pleural space, causing the lung to collapse.
In closed pneumothorax, the chest wall becomes airtight after penetration (eg, by a
thoracentesis needle, central vein percutaneous catheter via the subclavian veins,
fractured rib, or knife), or air may continue to enter the pleural space (eg, from a
lung punctured by a fractured rib). Air may also leak from a ruptured bronchus or
perforated esophagus into the mediastinum and then into the pleural space. Active
TB or other infectious granulomas may (rarely) cause pneumothorax when a cavity
perforates into the pleural space. Pulmonary barotrauma is an important cause of
pneumomediastinum and pneumothorax in patients on mechanical ventilators. It
occurs most often in the adult respiratory distress syndrome, particularly among
patients requiring high peak inspiratory pressure or positive end-expiratory
pressure.
Spontaneous pneumothorax: Air enters the pleural space without antecedent
trauma. Most spontaneous pneumothoraces occur without exertion. Some occur
during diving or high-altitude flying, apparently related to ambient pressure
changes unequally transmitted to different portions of the lung.
Spontaneous pneumothorax is called simple when it occurs in a previously healthy
person. It is usually caused by rupture of a small, localized, usually apical bulla. It
may occur as a complication of an interstitial pulmonary air leak and
pneumomediastinum, which may be spontaneous. Incidence is greatest in tall men
< 40 yr, and the prognosis is excellent.
Spontaneous pneumothorax is called complicated when it occurs in a person with
extensive underlying pulmonary disease. It most often results from rupture of a
bulla in a person with severe generalized emphysema and is thus predominantly a
disease of middle-aged and older persons. It may also occur in persons with other
chronic pulmonary diseases, such as asthma, eosinophilic granuloma, lung abscess
with bronchopleural fistula and empyema, and cystic fibrosis. Because of the
underlying pulmonary disease, physiologic derangements are much greater and the
prognosis is much worse than those in simple spontaneous pneumothorax.
Tension (positive pressure) pneumothorax: A check-valve mechanism in a
bronchopleural fistula allows air to enter but not leave the pleural space, causing
pressure in the space to rise above atmospheric pressure. The result is lung collapse
and mediastinal shift to the opposite side, which may severely compromise
pulmonary and cardiac function.
Induced pneumothorax: Air may be used to replace fluid as a prelude to
thoracoscopy or, rarely, for better x-ray visualization of masses or of intrathoracic
structures.
Symptoms, Signs, and Diagnosis
Symptoms range from minimal disturbance to severe dyspnea, shock, and lifethreatening respiratory failure and circulatory collapse. Sudden sharp chest pain,
dyspnea, and, occasionally, a dry, hacking cough occur at onset. The pain may be
referred to the corresponding shoulder, across the chest, or over the abdomen; it
may simulate an acute MI or an acute abdomen. Symptoms tend to be less severe
in a slowly developing pneumothorax and usually subside as accommodation to the
altered physiologic state occurs.
A small collection of air may produce no detectable physical signs or only
diminution of voice and breath sounds. A large or tension pneumothorax produces
diminished chest wall motion on the affected side, tympany on percussion, and
diminished or absent tactile fremitus. Mediastinal shift may be detectable as
displacement of cardiac dullness and apex beat away from the affected side. Breath
sounds are markedly depressed or absent. Hypoxemia is minimal or absent in
simple spontaneous pneumothorax but may be severe and associated with
hypercapnia in complicated pneumothorax.
The chest x-ray usually shows air without peripheral lung markings laterally,
limited by a sharp visceral-pleural margin, with lung markings medially, indicating
the position of the collapsed lung. A small pneumothorax may be overlooked on a
routine inspiratory x-ray but is obvious on an expiratory x-ray because the size and
density of the lung (but not of the pleural airspace) change during expiration. The
mediastinum shifts to the contralateral side, especially with a large pneumothorax.
Differential diagnosis includes emphysematous bullae, large lung abscess, and
herniation of the stomach, colon, or, much less commonly, small bowel through
the diaphragm. In patients on mechanical ventilators for the adult respiratory
distress syndrome, pneumothorax may develop subtly in loculated form in a
subpulmonic or paracardiac location. Interstitial air within the lung and
pneumomediastinum may precede the development of pneumothorax.
Prognosis and Treatment
A small spontaneous pneumothorax requires no special treatment; the air is
reabsorbed in a few days. Full absorption of a larger airspace may take 2 to 4 wk,
during which time it is uncertain whether the pleural leak is closed and whether
pleural effusion and epipleural fibrinous exudate will develop. The course can be
shortened by simple aspiration of air through a small-bore catheter. If aspiration is
unsuccessful, a chest tube should be introduced with water-sealed drainage or with
a one-way valve.
In both traumatic and spontaneous pneumothorax, the air leak usually closes and
heals quickly as the lung initially collapses. Reexpansion of the lung can also
promote sealing of the air leak because of symphysis of the visceral and parietal
pleurae. If air continues to leak, chest tube drainage with suction may be used in
the hope of expanding the lung rapidly. Reexpansion pulmonary edema is a risk
after application of suction, particularly if the pneumothorax is large and if long-
standing and high suction pressures are used. If a large, persistent fistula is present
or if the pneumothorax becomes loculated, repair of the fistula or excision of the
affected lung segment may be required. A sclerosing agent, such as intrapleural
doxycycline or talc, may be used for persistent or recurrent pneumothorax in
patients who are poor risks for thoracotomy (eg, those with cystic fibrosis or
emphysema).
In tension pneumothorax, quick removal of air may be lifesaving. Air may be
removed simply by inserting into the chest a 19-gauge or larger needle attached
through a three-way stopcock to a large syringe. The needle may be inserted
anteriorly or laterally over a site with absent breath sounds and enhanced
percussion note. When there is time for a chest x-ray, sites where the lung is held
to the chest wall by adhesions should be avoided. Air is alternately withdrawn
from the pleural space and expelled from the syringe into the room until a tube
thoracostomy has been performed and water-sealed drainage of the hemithorax has
been established. A check valve fitted to a catheter inserted into the pleural space
may also be used to withdraw air.
Recurrent pneumothorax may cause considerable disability. Surgical intervention
is generally indicated after two spontaneous pneumothoraces on the same side. The
preferred procedures are thoracotomy--in which bullae are oversewn or excised
and the pleura roughened by rubbing with gauze--or, when bullous disease is
extensive, parietal pleurectomy. The procedures may be performed using video
assistance via a thoracoscope.
Pleuritis
Inflammation of the pleura, usually producing an exudative pleural effusion and
stabbing chest pain worsened by respiration and cough.
Etiology
Pleurisy may result from an underlying lung process (eg, pneumonia, infarction,
TB); direct entry of an infectious agent or irritating substance into the pleural space
(eg, with a ruptured esophagus, amebic empyema, or pancreatitic pleurisy);
transport of an infectious or noxious agent or neoplastic cells to the pleura via the
bloodstream or lymphatics; parietal pleural injury (eg, trauma, especially rib
fracture, or epidemic pleurodynia [due to coxsackievirus B]); asbestos-related
pleural disease in which asbestos particles reach the pleura by traversing the
conducting airways and respiratory tissues; or, rarely, pleural effusion related to
drug ingestion. If the period of disease more than 8 weeks – chronic empyema of
pleura.
Pathology
The pleura usually first becomes edematous and congested. Cellular infiltration
follows, and fibrinous exudate develops on the pleural surface. The exudate may
be reabsorbed or organized into fibrous tissue resulting in pleural adhesions. In
some diseases (eg, epidemic pleurodynia), the pleurisy remains dry or fibrinous,
with no significant exudation of fluid from the inflamed pleura. More often, pleural
exudate develops from an outpouring of fluid rich in plasma proteins from
damaged capillaries. Occasionally, marked fibrous or even calcific thickening of
pleura (eg, asbestos pleural plaques, idiopathic pleural calcification) develops
without an antecedent acute pleurisy.
Exudate

Purulent

Putrefactive
Microflora

Nonspecific (a staphylococcus, diplococcus)

Specific (tubercular, fungoid)

Mixed
Prevalence of process

Free (total, subtotal, small)

Circumscribed (parietal, intralobal, basal, apical, mediastinal, multichamber)
Symptoms and Signs
Sudden pain is the dominant symptom of pleurisy. Typically, pleuritic pain is a
stabbing sensation aggravated by breathing and coughing, but it can vary. It may
be only a vague discomfort, or it may occur only when the patient breathes deeply
or coughs. The visceral pleura is insensitive; pain results from inflammation of the
parietal pleura, which is mainly innervated by intercostal nerves. Pain is usually
felt over the pleuritic site but may be referred to distant regions. Irritation of
posterior and peripheral portions of the diaphragmatic pleura, which are supplied
by the lower six intercostal nerves, may cause pain referred to the lower chest wall
or abdomen and may simulate intra-abdominal disease. Irritation of the central
portion of the diaphragmatic pleura, innervated by the phrenic nerves, causes pain
referred to the neck and shoulder.
Respiration is usually rapid and shallow. Motion of the affected side may be
limited. Breath sounds may be diminished. A pleural friction rub, although
infrequent, is the characteristic physical sign. It need not be accompanied by
pleuritic pain, but it usually is. The friction rub varies from a few intermittent
sounds that may simulate crackles to a fully developed harsh grating, creaking, or
leathery sound synchronous with respiration, heard on inspiration and expiration.
Friction sounds due to pleuritis adjacent to the heart (pleuropericardial rub) may
vary with the heartbeat as well.
When pleural effusion develops, pleuritic pain usually subsides. Percussion
dullness, absent tactile fremitus, decreased or absent breath sounds, and egophony
at the upper border of the fluid are then noticeable. The larger the effusion, the
more obvious the above signs. A large effusion may produce or contribute to
dyspnea through diminished lung volume, especially if there is underlying
pulmonary disease, mediastinal shift to the contralateral side, and diminished
function and recruitment of inspiratory muscles due to an expanded thoracic cage.
Diagnosis
Pleurisy is readily diagnosed when characteristic pleuritic pain occurs. A pleural
friction rub is pathognomonic. Pleurisy that produces referred abdominal pain is
usually differentiated from acute inflammatory abdominal disease by x-ray and
clinical evidence of a respiratory process; absence of nausea, vomiting, and
disturbed bowel function; marked aggravation of pain by deep breathing or
coughing; shallow rapid breathing; and a tendency toward relief of pain by
pressure on the chest wall or abdomen. Intercostal neuritis may be confused with
pleurisy, but the pain is rarely related to respiration and there is no friction rub.
With herpetic neuritis, development of the characteristic skin eruption is
diagnostic. MI, spontaneous pneumothorax, pericarditis, and chest wall lesions
may simulate pleurisy. A pleural friction rub may be confused with the friction rub
of pericarditis (pericardial rub), which is heard best over the left border of the
sternum in the third and fourth interspaces, is characteristically a to-and-fro sound
synchronous with the heartbeat, and is not influenced significantly by respiration.
Chest x-rays are of limited value in diagnosing fibrinous pleurisy. The pleural
lesion causes no shadow, but an associated pulmonary or chest wall lesion may.
The presence of a pleural effusion, generally small, confirms the presence of acute
pleurisy.
Treatment
Treatment of the underlying disease is essential.
Acetaminophen 0.65 g qid or an NSAID is often effective. Oral narcotics may be
necessary, but cough suppression may not be desired.
Adequate bronchial drainage must be provided to prevent pneumonia. A patient
receiving narcotics should be urged to breathe deeply and cough when pain relief
from the drug is maximal. Antibiotics and bronchodilators should be considered
for treatment of associated bronchitis.
Surgical treatment acute empyema of the pleura.
Thoracoscopy must be distinguished from video-assisted thoracic surgery (VATS).
Thoracoscopy is primarily used for surgical treatment of pleural disease,
pleurodesis and drainage. It is most often performed by surgeons but may be
performed by other trained physicians. In contrast, VATS is used exclusively by
surgeons to perform minimally invasive thoracic surgery.
Thoracoscopy may be performed using a local, regional, or general anesthetic.
A general anesthetic is preferred for patients with complex pleural disease, such as
loculated fluid collection, and for those who might not tolerate unilateral
pneumothorax without mechanical ventilation. After draining (2 drain- first in 7
intercostal space, second in 2 intercostal space) the pleural cavity irrigation
solutions of antiseptics and antibiotics is necessary.
Thoracotomy is most helpful in patients with undiagnosed focal or diffuse
pulmonary problems, in which definitive diagnosis is likely to improve the
management plan. It is used in patients with pulmonary problems of unknown
etiology when less invasive procedures have not yielded a diagnosis or when other
procedures are more dangerous or unlikely to yield a diagnosis.
Main surgical methods of treatment at thoracotomy:

Wide thoracotomy with the resection of lung

Early decortication mild (erasion of pleural solderings and adhesion)
Surgical treatment chronic empyema of the pleura.
During 3-4 months make drainage of pleural cavity (with active aspiration and
respiratory gymnastics).
If the drainage is noneffective - operative treatment is necessary.
Surgical treatment
1.pleuroectomy
2.thoracoplasty (a resection of several ribs, a tamponade of a cavity muscles and
soft tissues)
Sometimes apply scalene thoracoplasties .
In the case of bronchopleural fistula the tamponade of a bronchi or a pleurectomy
is necessary.
Pleural Fibrosis And Calcification
Fibrosis of the pleura can occur when inflammatory reactions heal. Even with
long-standing or severe inflammation, often only a slight amount of scar tissue
remains after complete healing, although the lung occasionally becomes encased in
a thick fibrous layer that limits chest wall motion, retracts the mediastinum toward
the side of disease, and impairs pulmonary function. Differentiating localized
pleural thickening from loculated pleural fluid may be impossible except by
thoracentesis, although characteristic differences may be present on ultrasound and
CT scans. Pleural fibrosis should be minimized by early treatment of underlying
pleural disease.
Calcification of the pleura presents as focal, usually fenestrated, irregular plaques
on the costal surfaces after intrapleural hemorrhage or infection, although there is
often no history of an antecedent acute pleural lesion. Focal plaquelike pleural
fibrosis, at times with calcification, occurs 20 or more years after exposure to
asbestos, most often affecting the diaphragmatic pleura; this finding may be the
only evidence of low-dose, relatively brief exposure to inhaled asbestos fibers.