Peculiarities of the physical examination of the patients with pathology of respiratory organs, laboratory tests and instrumental diagnostics of pulmonary disorders.

The main clinical syndromes in case of respiratoty diseases are:

bronchial obstruction, bronchial spasm, inflammatory syndrom, pulmonary infiltration, diffuse lung injury, pulmonary insufficiency.

Thay will be discussed in certain parts of methodological instructions.

PULMONARY FUNCTION TESTS

Pulmonary function testing has progressed from simple spirometry to sophisticated physiologic testing over the past decade. This chapter will attempt to survey the major clinically applicable tests available and then will attempt to identify their role in clinical management, including recommendations for ordering tests.

In the normal respiratory system, the volume and pattern of ventilation are initiated by neural output from the respiratory center in the medulla of the brain-stem. This output is influenced by afferent information from several sources, including higher centers in the brain, carotid chemoreceptors (PaO₂), central chemoreceptors (Paco2 [H⁺]), and neural impulses from moving tendons and joints. Nerve impulses travel via the spinal cord and peripheral nerves to the intercostal and diaphragmatic muscles where appropriate synchronous contraction generates negative intrapleural pressure. If the resulting inspiration is transmitted through structurally sound, unobstructed airways to patent, adequately perfused alveoli, then O₂ and CO₂ are respectively added to and removed from mixed venous blood. This feedback mechanism of control of breathing is normally very sensitive, so that alveolar ventilation is kept proportional to the metabolic rate and the arterial blood gas tensions are maintained within a very narrow range.

Malfunction of the respiratory system at any point in this pathway can result in deviation from this normal range, and consequent respiratory insufficiency. A disturbance at a given point can often be specifically measured if available tests and known patterns of pathophysiologic disturbances are understood. This chapter discusses tests of pulmonary function.

Static Lung Volumes (see Fig. 1)

The vital capacity (VC or "slow VC") is the maximum volume of air that can be expired slowly and completely after a full inspiratory effort. This simply performed test is still one of the most valuable measurements of pulmonary function. It characteristically decreases progressively as restrictive lung disease increases in severity, and, along with the diffusing capacity, can be used to follow the course of a restrictive lung process and its response to therapy.

The forced vital capacity (FVC) is a similar maneuver utilizing a maximal forceful expiration. This is usually performed in concert with determination of expiratory flow-rates in simple spirometry (see Dynamic Lung Volumes and Flow Rates, below).

The (slow) VC can be considerably greater than the FVC in patients with airways obstruction. During the forceful expiratory maneuver, terminal airways can close prematurely (i.e., before the true residual volume is reached), and the distal gas is "trapped" and not measured by the spirometer.

Functional residual capacity (FRC) is physiologically the most important lung volume because it incorporates the normal tidal breathing range. It is defined as the volume of air in the lungs at the end of a normal expiration when all the respiratory muscles are relaxed. It is determined by the balance between the elastic forces (stiffness) of the chest wall, which tend to increase lung volume, and the elastic forces of the lungs, which tend to reduce it. These forces are normally equal and opposite at about 40% of total lung capacity (TLC). Changes in the elastic properties of the lungs or of the chest wall result in changes in the FRC. The loss of elastic recoil of the lung seen in emphysema results in an increase in the FRC. Conversely, the increased lung stiffness of pulmonary edema, interstitial fibrosis, and other restrictive lung processes results in a decreased FRC. Kyphoscoliosis leads to a decrease in FRC and in the other lung volumes because the stiff, noncompliant chest wall restricts ventilation.

table 1. PULMONARY FUNCTION ABBREVIATIONS

Cdyn

c_stat

Dlco

ERV

FEV₁

FEV₃

FVC

FRC

[H+]

IRV

MEF50%vc

MIF50%vc

Closing capacity

Dynamic lung compliance

Static lung compliance

Closing volume (L)

Diffusing capacity for carbon monoxide (ml/min/mm Hg)

Expiratory reserve volume

Forced expiratory volume in 1 sec (L)

Forced expiratory volume in 3 sec (L)

Forced vital capacity

Functional residual capacity

Concentration of hydrogen ions (nanomoles/L)

Inspiratory reserve volume

Mid-expiratory flow at 50% vital capacity (L/sec)

Mid-inspiratory flow at 50% vital capacity (L/sec)

MMEF Mean maximal expiratory flow (L/sec)

MVV Maximal voluntary ventilation

Paco₂ Arterial partial pressure of COs (mmHg)

Pao₂ Arterial partial pressure of 0; (mmHg)

PEF Peak expiratory flow (L/sec)

p_tp Transpulmonary pressure (mmHg)

Q Perfusion (L/min)

r_aw Airway resistance

RV Residual volume

TLC Total lung capacity

V Lung volume (L)

VC Vital capacity

V Ventilation (L/min)

va Alveolar ventilation (L/min)

Vco2 C02 production (L/min)

Vo₂ O2 consumption (L/min)

The FRC has 2 components, the residual volume (RV), the volume of air remaining in the lungs at the end of a maximal expiration, and the expiratory reserve volume (FRC = RV + ERV).

The RV normally accounts for about 25% of the TLC. It changes with the FRC with 2 exceptions. In restrictive lung diseases, RV tends to remain nearer to normal than other lung volumes (shown in fig. Ib). In small airways diseases, presumably because premature closure of the airways leads to air trapping, the RV may be elevated while the FRC and FEV₁ remain normal.

TLC equals the VC + the RV. In obstructive airways disease, RV increases more than does TLC, resulting in some decrease in VC, particularly in severe disease.

In obesity the ERV is characteristically diminished because of a markedly decreased FRC and a relatively well-preserved RV.

fig la. Normal. RV = 25% of TLC; FRC = 40% of TLC. FEV₁ = > 75% of FVC: FEV3 = > 95% of FVC.

fib. lb. Restrictive disease. Lung volumes are all diminished, the RV less so than the FRC, VC. and TLC. FEV₁ is normal or greater than normal. Tidal breathing is rapid and shallow.

Fig. lc. Obstructive disuse. RV and FRC are increased. TLC is also increased, but to a lesser degree, so that VC is decreased. There is prolongation of expiration. FEV, = < 75% of VC. Note the "emphysematous notch."

Fig. 1. Spirograms and lung volumes.

Dynamic Lung Volumes and Flow Rates

Dynamic lung volumes reflect the nonelastic properties of the lungs, primarily the status of the airways. The spirogram (see Fig. la) records lung volume against time on a water or electronic spirometer during an FVC maneuver. The FEV₁ is the volume of air forcefully expired during the first second after a full breath and normally comprises > 75% of the VC. The mean maximal expiratory flow over the middle half of the FVC (MMEF_25-75%) is the slope of the line that intersects the spirographic tracing at 25% and 75% of the VC. The MMEF is less effort-dependent than is the FEV₁ and is a more sensitive indicator of early airways obstruction.

Airway caliber (and therefore flow) is directly related to lung volume, being greatest at TLC, and decreasing progressively to RV. During a forced expiratory maneuver, the airways become further narrowed because of positive intrathoracic pressure. This "dynamic compression of the airways" limits maximum expiratory flow rates. The opposite effect is seen during an inspiratory maneuver, when negative intrathoracic pressure tends to maintain the caliber of the airways. The differences in airway diameter during inspiration and expiration thus result in greater flow rates during inspiration than expiration during much of the breathing cycle (see Fig. 2a). In chronic obstructive pulmonary disease (COPD) and asthma, prolongation of expiratory flow rates is further exaggerated because of airway narrowing (asthma), loss of structural integrity of the airways (bronchitis), and loss of lung elastic recoil (emphysema). In fixed obstruction of the trachea or larynx, flow is limited by the diameter of the stenotic segment rather than by dynamic compression, resulting in equal reduction of inspiratory and expiratory flows.

In restrictive lung disorders, the increased tissue elasticity tends to maintain airway diameter during expiration so that, at comparable lung volumes, flow rates are often greater than normal. (Tests of small airways function, however, may be abnormal—see below.)

Retesting of pulmonary function after inhalation of a bronchodilator aerosol (e.g., isoproterenol) provides information about the reversibility of an obstructive process (i.e., asthmatic component). Improvement in VC and/or FEV₁(L) of > 10% is usually considered a significant response to a bronchodilator.

The maximal voluntary ventilation (MW) is determined by encouraging the patient to breathe at maximal tidal volume and respiratory rate for 12 seconds; the amount of air expired is expressed in L/min. The MW generally parallels the FEV₁ and can be used as a test of internal consistency and as an estimate of patient cooperation (MW = FEV₁[L] X 40). The MW decreases with respiratory muscle weakness and may be the only demonstrable pulmonary function abnormality in moderately severe neuromuscular disease. The MW is considered an important preoperative test as it reflects the severity of airways obstruction as well as being an index of the patient's respiratory reserves, muscle strength, and motivation.

Flow-Volume Loop (see Fig. 2). The disadvantage of the simple measurements discussed above is that they fragment the complex dynamic interrelationships of flow, volume, and pressure into simple dimensions for arbitrary measurement. The continuous analysis of these parameters during forced respiratory maneuvers is more physiologic and can be more revealing. An analogy in cardiology is the additional information obtained by vectorcardiography above that provided by the conventional ECG. For the flow-volume loop the patient breathes into an electronic spirometer and performs a forced inspiratory and expiratory VC maneuver while flow and volume are displayed continuously on an oscilloscope. The shape of the loop reflects the status of the lung volumes and of the airways throughout the respiratory cycle and can be diagnostic. Characteristic changes are seen in restrictive and in obstructive disorders. The loop is especially helpful in the assessment of laryngeal and tracheal lesions. It can distinguish between fixed (e.g., tracheal stenosis) and variable (e.g., tracheomalada, vocal cord paralysis) obstruction. Fio. 30-2 illustrates some characteristic flow-volume loop abnormalities.

Lung Mechanics

Airway resistance (raw) can, with the help of a body plethysmograph, be directly measured in the laboratory by determining the pressure required to produce a given flow. More commonly, however, it is inferred from dynamic lung volumes and expiratory flow rates more easily obtainable in the clinical laboratory.

Static lung compliance (cstat) is defined as volume-change/unit of pressure-change and reflects lung elasticity or stiffness. This requires the use of an esophageal balloon and is seldom utilized in the clinical laboratory. Lung compliance is inferred by the resultant changes in static lung volumes (see Fig. 3).

Maximal inspiratory and expiratory pressures reflect the strength of the respiratory muscles. These are measured by having the patient forcibly inspire and expire through a closed mouthpiece attached to a pressure gauge. Maximal pressures are reduced in neuromuscular disorders (e.g., myasthenia gravis, muscular dystrophy, Guillain-Barre syndrome).

Diffusing Capacity (DLco) DLco is defined as the number of ml of CO absorbed/min/mm Hg. It is determined by having the patient inspire maximally a gas containing a known small concentration of CO, hold his breath for 10 seconds, then slowly expire to RV. An aliquot of alveolar (i.e., end-expired) gas is analyzed for CO and the amount absorbed during that breath is then calculated. It is generally agreed that an abnormally low DLco is not due to physical thickening of the alveolar-capillary membrane alone, but probably reflects abnormal ventilation/perfusion (V/Q) in diseased lungs. DLco is low in processes that destroy alveolar-capillary membranes; these include emphysema and interstitial inflammatory fibrotic processes. The DLco also tends to be diminished in severe anemia (less Hb available to bind the inhaled CO) and will be artifactually lowered if the patient's Hb already is occupied by CO (e.g., smoking within several hours prior to the test). The DLco increases with increases in pulmonary blood flow as occurs during exercise and also in mild (interstitial) congestive heart failure (increase in blood flow to the usually poorly perfused lung apices).

Distribution of Ventilation

The distribution of ventilation is studied by continuously recording the concentration of expired N2 at the mouth following a single maximal inspiration of 100% 0₂. If the distribution of ventilation is normal (i.e., the majority of alveoli fill and empty synchronously), there should be a < 2% increase in N concentration between 750 and 1250 ml of expired breath (see fig. 4). A > 2% change implies asynchronous emptying of alveoli, which most commonly is due to airways obstruction. A more direct though more complex study involves lung scanning after the inhalation of radioactive xenon gas.

Peripheral "Small" Airways Studies

raw and FEV measurements reflect primarily the condition of the large airways. In the normal lung, bronchi < 2 mm in diameter contribute < 10% of the total airways resistance, yet their aggregate surface area is large. Disease affecting primarily the smaller airways can be very extensive and yet not affect the raw or any tests dependent on this such as the FEV₁. This is true of early obstructive lung disease and probably also of interstitial granulomatous, fibrotic, or inflammatory disorders. The status of the small airways is reflected by the MMEF and by expiratory flows in the last 25 to 50% of the FVC, best determined from the flow-volume loop (see fig. 2a). More complex and sophisticated tests of small airways function have been devised. These include frequency-dependent changes in lung compliance (dynamic compliance), closing volume, and closing capacity. The latter can be determined by a modification of the N washout technic (see Distribution of Ventilation, above, and fig. 3), but in general, measurement of these more complex tests adds little to those more readily available (see above) and has little place in the clinical laboratory.

Control of Breathing

Recent emphasis on the clinical importance of obstructive sleep apnea and central hypoventilation (pickwickian syndrome) has brought the study of the control of breathing to the clinical physiology laboratory.

Hypoxic drive (function of the carotid chemoreceptors) can be studied by plotting the ventilatory response to progressive decrements in inspired O₂.

CO₂ sensitivity (function of the central, medullary chemoreceptors) is reflected by the ventilatory response to progressive increments in inspired CO₂.

Expired Volume (L)

fig. 4. Distribution of ventilation, and closing volume. The numbered phases of expiration refer to deadspace gas (I), mixed deadspace and alveolar gas (II), alveolar gas (III), and "airway closure" (IV). Normally, the CV is less than the FRC in both supine and sitting positions and all airways are open during tidal breathing. As the CV increases with progressive disease of the airways, more and more of the dependent airways become closed during part or all of tidal breathing, contributing to hypoxia. The % rise in nitrogen (W between 750 and 1250 ml of expired gas is a reflection of the distribution of ventilation (see text).

Central and obstructive sleep apnea can be distinguished by monitoring respiration during sleep. An ear oximeter monitors Ch saturation. A CO₂ electrode placed in a nostril monitors Pco₂ and also serves as an indicator of air flow. Chest wall motion is monitored by a strain gauge or by impedance electrodes. In obstructive sleep apnea, air flow at the nose ceases despite continued excursion of the chest wall, 02 saturation drops, and Pco₂ increases. In central apnea, chest wall motion and air flow cease simultaneously.

How to Order and Interpret Pulmonary Function Tests

A "complete" set of pulmonary function tests in a good clinical laboratory includes determination of all lung volumes (VC, FRC, RV, TLC), spirometry (FVC, FEV₁, MMEF), diffusing capacity, flow-volume loop, MW, and of maximum inspiratory and expiratory pressures. This extensive testing is tiring, time-consuming, expensive, and often not necessary for adequate clinical assessment.

Any physician who evaluates patients with pulmonary disorders should have access to simple spirometry in the office. Simple spirometry is the backbone of pulmonary function evaluation and usually provides sufficient information. A number of inexpensive electronic spirometers are now available capable of measuring VC, FEV₁, and PEF. The procedure is readily taught to both patient and operator and yields permanent, reproducible, and accurate data. While spirometry alone may not permit specific diagnosis, it can differentiate between obstructive and restrictive disorders and permits estimation of the severity of the process.

With a few simple guidelines, a great deal of useful information can be gathered from the simple spirogram. A low VC in association with normal flow rates ordinarily suggests restrictive disease (see Fig. Ib). COPD and asthma have the characteristic exponentially decreasing flows seen in fig. 30-Ic. In the patient with predominant emphysema, the airways can be intrinsically normal, and expiratory flow is limited by dynamic compression of the airways because of the loss of elastic supporting tissues. A finite amount of time is necessary for the airways (wide open at TLC) to snap shut after the onset of the FVC maneuver. Thus a transient of rapid flow is often reflected by a notch at the beginning of the tracing. The spirogram in Fig.Ic shows such an "emphysematous notch", and suggests that there has been substantial loss of lung elastic recoil; i.e., there is a significant component of emphysema present. In very severe COPD, expiratory flow can be so prolonged as to appear almost linear on visual analysis of the spirographic tracing. Since lung volume is a major determinant of airway caliber, the slope of the spirogram should continuously decrease from TLC to RV. A truly linear decrease in flow from TLC to RV is pathognomonic of fixed obstruction of the larynx or trachea (e.g., tracheal stenosis or tumor). The limitation to maximal flow here is no longer dynamic compression of airways but a fixed area of narrowing in the large airway.

The spirogram can occasionally be misleading in asthma because it may mimic restrictive disease if there is severe obstruction predominating in the smaller airways. Total occlusion of the airways precludes any air flow and much gas is trapped distally, thus underestimating the VC. The larger airways are patent, so the overall raw is not much increased and the FEV₁ is normal.

table 2. CHARACTERISTIC CHANGES IN PULMONARY FUNCTION IN SEVERAL DISORDERS

Test	Restrictive Lung Diseases	Obstructive Airways Diseases		Neuromuscular Disorders	Obesity
Test	Restrictive Lung Diseases	Conventional#	Central, Fixed$	Neuromuscular Disorders	Obesity
VC/FVC	¯*	N for ¯	N	N or¯	N or ¯
TLC	¯*		N	N	¯
RV/FRC	¯/¯*	/*	N/N	N/N	N/¯*
FEV, (%VC)	N or	¯*	¯	N	N
MMEF	¯	¯	¯	N	N
MW	N	¯*	¯	¯*	N
MEF50%vc	N or ¯	¯	¯*	N	N
MIF50%vc	N	N	¯*	N	N
Inspiratory & expiratory pressures	N	N	N	¯*	N
Distribution of ventilation	N	abnormal*	N*	N	N
Dlco	¯*	¯ emphysema N bronchitis	N	N	N or ¯

* Distinctive features. fN – normal. # –COPD. $– tracheal stenosis.

TABLE 3. CHARACTERISTIC CHANGES IN PULMONARY FUNCTION IN RESTRICTIVE AND OBSTRUCTIVE DISEASE OF VARYING SEVERITY

Impairment	Restrictive Disease
Impairment	None	Mild	Moderate	Severe	Very Severe
VC (% predicted)	>80	60-80	50-60	35-50	<35
FEV, (%VC)	>75	>75	>75	>75	>75
MW (% predicted)	>80	>80	>80	60-80	<60
RV (% predicted)	80-120	80-120	70-80	60-70	<60
Dlco	N	¯E	¯R	¯	¯¯
Arterial blood gases Po₂ (during rest & exercise) Pco₂	N N	N N	¯E ¯	¯ ¯	¯¯ ±
Dyspnea (severity)	0	+	++	+++	++++
Obstructive Disease
VC (% predicted)	>80	>80	>80	¯	¯
FEV₁ (%VC)	>75	60-75	40-60	<40	<40
MW (% predicted)	>80	65-80	45-65	30-45	<30
RV (% predicted)	80-120	120-150	150-175	>200	>200
Dlco	N	N	N	¯	¯¯
Arterial blood gases Po₂ : (during rest & exercise) Pco₂	N N	¯E N	¯E N	¯ E	¯¯ R
Dyspnea (severity)	0	+	++	+++	++++

N — normal; R — rest; E — exercise.

The severity of COPD and the potential for response to bronchodilator can be adequately assessed by simple spirometry (± flow-volume loop) before and after inhalation of bronchodilator. Simple spirometry with determination of the FVC, FEV₁, and MW usually suffices as a general preoperative screen and should be performed in all smokers > 40 and in all patients with respiratory symptoms prior to chest or abdominal surgery. The response to treatment during an exacerbation of asthma can and should be monitored by portable (bedside) spirometry or by serial measurement of peak expiratory flow rates.

Patients with suspected laryngeal or tracheal pathology are adequately and specifically studied by a flow-volume loop (see Fig. 2d).

If weakness of the respiratory muscles is suspected, the MW, maximal inspiratory and expiratory pressures, and VC are the appropriate tests.

Full tests should be requested when the clinical picture (history, physical examination, chest x-ray) does not coincide with the data obtained by simple spirometry, or when more complete characterization of an abnormal pulmonary process is desired. They are indicated prior to thoracotomy or extensive abdominal surgery (particularly in the patient with known or suspected pulmonary impairment) and to document the severity of interstitial pulmonary disorders. Periodic VCs and Dlco₂ usually suffice to follow the course of a restrictive process.

The following tables are intended as general guides to the interpretation of pulmonary function tests. table 2 illustrates several simple patterns of pulmonary function abnormality. These are not necessarily mutually exclusive; a patient may have a combination of disorders (e.g., restrictive and obstructive disease), which complicates the interpretation. table 3 details the expected changes in pulmonary function in restrictive and obstructive disorders of varying severity.

Peakfluorymetry– method of estimation of peak expiratory flow (PEF, L/sec) by portable device usually used by patients to estimate the changes of bronchial obstruction.

CHEST RADIOGRAPHY

Chest radiography is often the initial diagnostic study performed to evaluate patients with respiratory symptoms but it can also provide the initial evidence of disease in patients who are free of symptoms Perhaps the most common example of the latter situation is the finding of one or more nodules or masses when the radiograph is performed for a reason other than evaluation of respiratory symptoms

A number of diagnostic possibilities are often suggested by the radiographic pattern. A localized region of opacification involving the pulmonary parenchyma can be described as a nodule (usually <6 cm in diameter) a mass (usually >= 6 cm in diameter) or an infiltrate Diffuse disease with increased opacihcation is usually characterized as having an alveolar an interstitial or a nodular pattern In contrast increased radiolucency can be localized as seen with a cyst or build or generalized as occurs with emphysema The chest radiograph is also particularly useful for the detection of pleural disease especially if manifested by the presence of air or liquid in the pleural space An abnormal appearance of the hilus and/or the mediastinum can suggest a mass or enlargement of lymph nodes

A summary of representative diagnoses suggested by these common radiographic patterns is presented in Table

Additional Diagnostic Evaluation Further information for clarification of radiographic abnormalities is frequently obtained with computed tomographic scanning of the chest. This technique is more sensitive than plain radiography in detecting subtle abnormalities and can suggest specific diagnoses based on the pattern of abnormality Alteration in the function of the lungs as a result of respiratory system disease is assessed objectively by pulmonary function tests and effects on gas exchange are evaluated by measurement of arterial blood gases or by oximetry. As part of pulmonary function testing quantitation of forced expiratory flow assesses the presence of obstructive physiology which is consistent with diseases affecting the structure or function of the airways such as asthma and chronic obstructive lung disease Measurement of lung volumes assesses the presence of restrictive disorders seen with diseases of the pulmonary parenchyma or respiratory pump and with space occupying processes within the pleura.

Table: Major Respiratory Diagnoses with Common Chist Radiography Patterns

Solitary circumscribed density nodule (<6 cm) or mass (>= 6 cm)

Primary or metastatic neoplasm

Localized infection (bacterial abscess mycobacterial or fungal infection)

Wegener’ s granulomatosis (one or several nodules)

Rheumatoid nodule (one or several nodules)

Vascular malformation

Bronchogenic cyst

Localized opacification (infiltrate)

Pneumonia (bacterial, atypical, mycobacterial or fungal infection)

Neoplasm

Radiation pneumonitis

Bronchiolitis obliterans with organizing pneumonia

Bronchocentric granulomatosis

Pulmonary infarction

Diffuse interstitial disease

Idiopathic pulmonary fibrosis

Pulmonary fibrosis with systemic rheumatic disease

Sarcoidosis

Drug induced lung disease

Pneumoconiosis

Hypersensitivity pneumonitis Infection (Pneumocystis, viral pneumonia)

Eosinophilic granuloma

Diffuse alveolar disease

Cardiogenic pulmonary edema

Acute respiratory distress syndrome

Diffuse alveolar hemorrhage

Infection (Pneumocyitis viral or bacterial pneumonia)

Sarcoidosis

Diffuse nodular disease.

Metastatic neoplasm

Hematogenous spread of infection (bacterial mycobacterial fungal)

Pneumoconiosis

Eosinophilic granuloma

Sputum Examination.

Examination of the sputum remains the mainstay of the evaluation of a patient with lung inflammation. Unfortunately expectorated material is frequently contaminated by potentially pathogenic bacteria that colonize the upper respiratory tract (and sometimes the lower respiratory tract) without actually causing disease This contamination reduces the diagnostic specificity of any lower respiratory tract specimen In addition it has been estimated that the usual laboratory processing methods detect the pulmonary pathogen in fewer than 50% of expectorated sputum samples from patients with bacteremic S pneumomae pneumonia This low sensitivity may be due to misidentification of the a hemolytic colonies of S pneumonie as nonpathogenic a hemolytic streptococci ( normal flora ) overgrowth of the cultures by hardier colonizing organisms or loss of more fastidious organisms due to slow transport or improper process ing In addition certain common pulmonary pathogens such as an aerobes mycoplasmas chlamydiae Pneumocystis mycobacteria fungi and legionellae cannot be cultured by routine methods.

Since expectorated material is routinely contaminated by oral an aerobes the diagnosis of anaerobic pulmonary infection is frequently inferred Confirmation of such a diagnosis requires the culture of an aerobes from pulmonary secretions that are uncontammated by oropharyngeal secretions which in turn requires the collection of pulmonary secretions by special techniques such as transtracheal aspiration (TTA) transthoracic lung puncture and protected brush via bronchoscopy These procedures are invasive and are usually not used unless the patient fails to respond to empirical therapy

Gram s staining of sputum specimens screened initially under low power magnification (10X objective and 10X eyepiece) to deter mine the degree of contamination with squamous epithelial cells is of utmost diagnostic importance In patients with the typical pneumonia syndrome who produce purulent sputum the sensitivity and specificity of Gram s staining of sputum minimally contaminated by upper respiratory tract secretions (>25 polymorphonuclear leukocytes and < 10 epithelial cells per low power field) m identifying the pathogen as S pneumomae are 62 and 85% respectively Gram s staining in this case is more specific and probably more sensitive than the accompanying sputum culture The finding of mixed flora on Gram s staining of an uncontammated sputum specimen suggests an anaerobic infection Acid fast staining of sputum should be undertaken when mycobacterial infection is suspected Examination by an experienced pathologist of Glemsa stained expectorated respiratory secretions from patients with AIDS has given satisfactory results in the diagnosis of PCP The sensitivity of sputum examination is enhanced by the use of monoclonal antibodies to Pneumocystis and is diminished by prior prophylactic use of inhaled pentamidine. Blastomycosis can be diagnosed by the examination of wet preparations of sputum. Sputum stained directly with fluorescent antibody can be examined for Legionella but this test yields false negative results relatively often Thus sputum should also be cultured for Legionella on special media

Expectorated sputum usually is easily collected from patients with a vigorous cough but may be scant in patients with an atypical syndrome in the elderly and in persons with altered mental status If the patient is not producing sputum and can cooperate respiratory secretions should be induced with ultrasonic nebulization of 3% saline. An attempt to obtain lower respiratory secretions by passage of a catheter through the nose or mouth rarely achieves the desired results m an alert patient and is discouraged usually the catheter can be found coiled in the oropharynx.

In some cases that do not require the patient s hospitalization an accurate microbial diagnosis may not be crucial and empirical therapy can be started on the basis of clinical and epidemiologic evidence alone This approach may also be appropriate for hospitalized patients who are not severely ill and who are unable to produce an induced sputum specimen Use of invasive procedures to establish a microbial diagnosis carries risks that must be weighed against potential benefits However the decision to initiate empirical therapy without an evaluation of induced sputum should be undertaken with caution and in the case of hospitalized patients should always be accompanied by the culture of several blood samples The ability to understand the cause of a poor response to empirical antimicrobial therapy may be compromised by the lack of initial sputum and blood cultures Establishing a specific microbial etiology in the individual patient is important for it allows institution of specific pathogen directed antimicrobial therapy and reduces the use of broad spectrum combination regimens to cover multiple possible pathogens Use of a single narrow spectrum antimicrobial agent exposes the patient to fewer potential adverse drug reactions and reduces the pressure for selection of antimicrobial resistance Emergence of antimicrobial resistance is a type of adverse drug re action unlike others because it is contagious. In addition establishing a microbial diagnosis can help define local community outbreaks and antimicrobial resistance patterns.

In case of allergic process many eossinophils are found microscopically, frequently arranged in sheets. Eosinophilic granules from disrupted cells may be seen throughout the sputum smear. Elongated dipyramidal crystals (Charcot-Leyden) originaiting from from eosinophils are commonly found.

In case of lung cancer is possible to evaluate the atypical cells.

PLEURAL EFFUSION

Essentials of Diagnosis

• Dyspnea if effusion is large; may be asymptomatic.

• Pain of pleurisy often precedes the pleural effusion.

• Decreased breath sounds, flatness to percussion, egophony.

• The underlying cardiac or pulmonary disease may be the major source of symptoms and signs.

• X-ray evidence of pleural fluid.

General Considerations

Any fluid collection (transudate or exudate) in the pleural space constitutes a pleural effusion. Numerous disease processes of inflammatory, circulatory, and neoplastic origin can cause pleural effusion. Every effort should be directed toward the diagnosis of the primary disease. "Idiopathic" pleural effusion often proves to be of tuberculous origin.

Clinical Findings

A. Symptoms and Signs: There may be no symptoms. Chest or shoulder pain may be present at onset, especially when fibrinous pleuritis precedes the effusion. Dyspnea may be mild or, with large or rap idly forming effusions, severe. Cardiac failure may be associated with effusion. Fever, sweats, cough, and expectoration may occur, depending upon the underlying cause.

Physical findings include decreased motion of the chest and decreased to absent vocal fremitus on the side of the fluid, flat percussion note and decreased to absent breath sounds over the fluid, and egophony (e-to-a sound) at the upper level of the fluid. With large effusions, the mediastinum shifts away from the fluid (as shown by displacement of the trachea and the cardiac apex), although underlying atelectasis may result in a shift toward the fluid. Signs resembling those of consolidation (dullness, bronchial breath sounds, bronchophony) are occasionally elicited over the fluid, presumably as a result of compression of the underlying lung by large, rapidly forming effusions.

B. X-Ray and Sonographic Findings (picture 1-6, figure 3-5) : Three hundred milliliters or more must be present before fluid can be demonstrated by x-ray. Obliteration of the costophrenic angle is the earliest sign. Later, a homogeneous triangular density with a concave medial border extends upward to the axilla; other borders are formed by the lateral chest wall and the diaphragm. The mediastinum shifts away from the fluid (displaced heart and tracheal air shadow). The mobility of the fluid shadow, which ' 'pours'' into dependent areas of pleural space when the patient is placed on the involved side, may aid in the demonstration of small effusions. An atypical distribution of fluid along the interlobar fissures or in loculated areas may be noted.

Picture 1 In this patient there is an obvious right upper lung field opacification which on later work-up was determined to be a primary cancer. Note that the right lower lung field is clear and that the right diaphragm and lateral costophrenic angle seem sharp though it would seem peculiar that the right diaphragm should seem so high. Although pleural effusions are usually expected to blunt the costophrenic angle, occasionally a "subpulmonic" effusion may mimic the surface of the diaphragm which is the case here. When the decubitus film is obtained note the substantial amount of fluid that layers out.

Picture 2. Sonographic images of normal pleura and chest wall using a 5- to 10-MHz linear scanner

(A) Transverse image through the intercostal space. The chest wall is visualized as multiple layers of echogenicity representing muscles and fascia. The visceral and parietal pleura appear as echogenic bright lines that glide during respiration (gliding sign). Reverberation echo artifacts beneath the pleural lines imply an underlying air-filled lung. (B) Longitudinal image across the ribs. Normal ribs are seen as hyperechoic chambered surfaces (arrowheads) with prominent acoustic shadows beneath the ribs. Pp, parietal pleura; Pv, visceral pleura; L, lung.

Figure 3. Sonographic appearance of pleural effusion

(A) Pleural effusion is presented as an echo-free space between the visceral and parietal pleura. Compressive atelectasis of the lung may be seen in a huge effusion. (B-E) The effusion can be subclassified as anechoic (B), complex nonseptated (C), complex septated (D), and homogenously echogenic (E). Note the movable echogenic spots within the complex nonseptated effusion, and the floating strands and septa within the complex septated effusion (arrowheads). (F) The presence of a consolidation is suggestive of parapneumonic effusion. (G) Pleural effusion associated with pleural nodules or nodular thickenings is characteristic of malignant effusion. PE, pleural effusion; D, diaphragm; RLL, right lower lung; L, lung; T, pleural tumor.

Figure 3. Ultrasound (US) images of pleural thickening and pleural tumors

Figure 4. Extension of inflammatory diseases (A, B) or tumors (C, D) to the pleura

(A) Ultrasound (US) shows a chest wall abscess in a patient with liver cirrhosis as an ill-defined lesion with soft-tissue echogenicity that extends to the pleura. Puslike material was obtained with transthoracic aspiration under US guidance, which yielded Aeromonas hydrophila. (B) US shows an irregular and hypoechoic parenchymal lesion with involvement of the pleural cavity. Nocardiosis was proved microbiologically after transthoracic biopsy of the lesion under US guidance. (C) US shows a parenchymal tumor with posterior echo enhancement (PEE). Note that both of the visceral and parietal pleural lines are intact, fulfilling the criteria of ultrasound pattern 1 of Sugama et al.. The respiratory movement of the tumor should be preserved in real-time US. (D) US shows a peripheral mass that extends beyond the pleura. The visceral pleural line is cut off, and the respiratory movement of the tumor is disturbed in real-time US. Invasion of the pleural cavity by the tumor is evident. A, abscess; P, pleura; L, lung; T, tumor; Pv, visceral pleural; Pp, parietal pleura.

Figure 5A. Ultrasound findings in patients with pleuritic chest pain and partial pneumothorax

(A) Ultrasound (US) findings in a patient with pleuritic chest pain. The grayscale US reveals irregularity and interruption of the pleura. (B, C) Sonographic features in a patient with partial pneumothorax. Real-time US of the healthy side of the chest (B) shows normal gliding of the visceral and parietal pleura with respiration. On the other side with partial pneumothorax (C), the gliding sign of the pleura is absent in real-time US. Markedly enhanced comet-tail reverberation artifacts are seen compared with the US image of the healthy side. P, pleura; L, lung; Pv, visceral pleura; Pp, parietal pleura.

Picture 5B. Lateral X-ray of chest with pleural effusion A-effusion B- pleural cavity

Picture 6 Transudative pleural effusions are formed when normal hydrostatic and oncotic pressures are disrupted. Exudative pleural effusions occur when pleural membranes or vasculature are damaged or disrupted therefore leading to increased capillary permeability or decreased lymphatic drainage.

C. Thoracentesis: This is the definitive diagnostic procedure. It demonstrates conclusively the presence of fluid and provides samples for study of physical characteristics, protein content, cells, and infectious agents. Thoracentesis should be done care fully to avoid introducing infection and puncturing the visceral pleura.

1. Removal of fluid for examination-Remove 50-1000 mL. Use a 3-way stopcock to avoid introduction of air. Care must be exercised to avoid contaminating the pleural space.

2. Pleural fluid examination-(Specimen must be fresh.) A specific gravity of more than 1.015 or protein of more than 3 g/dL usually indicates an exudative fluid. More reliable indicators include a ratio of pleural fluid protein to serum protein greater than 0.5; a fluid LDH to serum LDH ratio of more than 0.6; or a pleural fluid LDH of more than 200IU, especially if all 3 conditions are present.

A stained smear should be examined for the detection of organisms and the nature of the cellular content. Collect a specimen in an anticoagulant tube for cell count. Cultures on appropriate media are indicated for all fluids from unexplained pleural effusions to demonstrate the presence of tubercle bacilli, other bacteria, or fungi. Cy tologic examination of the remaining fluid should be done if a neoplasm is suspected.

Lactic dehydrogenase (LDH) levels are frequently increased in effusions due to cancer. Chylous effusions usually signify interruption of the thoracic duct by cancer.

D. Pleural Biopsy: This procedure has become very simple and valuable as a result of the development of better biopsy needles (eg, Abrams' needle) that permit thoracentesis and removal of one or more tissue specimens with the same needle. Pleural biopsy is indicated whenever the diagnosis is in doubt. If the tissue is not diagnostic, several more specimens should be taken. If pleural fluid examination and needle biopsy do not yield a diagnosis, open pleural biopsy must be considered. A portion of the biopsy material should be cultured.

Treatment

A. Postpneumonic and Other Sterile Effusions: Remove readily obtainable fluid by multiple thoracentesis, at daily intervals if necessary. Removal of more than 1000 mL initially is not advisable. Reexamine subsequent fluid specimens to rule out empyema if the pleuritis does not respond to treatment.

B. Tuberculous Effusion: Uncomplicated pleural effusion due to tuberculosis is treated essen tially as minimal pulmonary tuberculosis. A course of isoniazid plus one of the other major antituberculosis drugs is recommended. Many patients with untreated tuberculous effusions develop pulmonary tuberculosis later, usually within 5 years.

Removal of all readily available fluid by thoracentesis is advisable to minimize later pleural fibrosis. When high fever persists for longer than 2 weeks, hematogenous dissemination should be suspected.

C. Effusions Due to Malignant Tumors: These tend to reaccumulate rapidly and require frequent removal. An attempt should be made to control the re-formation of fluid by irradiation of the hemithorax or by the use of intrapleural tetracycline or cytotoxic agents.

Prognosis

The prognosis is that of the underlying disease.

HYDROTHORAX

The term hydrothorax generally denotes the presence of a collection of serous fluid having a specific gravity of less than 1.015 or a protein content of less than 3 g/dL (transudate). The most common cause is congestive heart failure, but lymphatic obstruction and obstruction of the superior vena cava or vena azygos may also cause hydrothorax. The not unusual finding of hydrothorax in hepatic cirrhosis with ascites (6%) is explained by observations of ready transfer of radioiodine-labeled albumin from the peritoneal to the pleural spaces. The initial examination of the pleural fluid should be as described above.

The fluid should be removed by thoracentesis when it causes dyspnea.

The prognosis is that of the underlying disease.

HEMOTHORAX

Hemothorax (pooling of blood in a pleural space) is most commonly due to trauma but may also follow tumor, tuberculosis, and pulmonary infarction. The physical findings are the same as those of pleural effusion. Military experience has shown that early removal of all blood from the pleural space is desirable. If this cannot be accomplished by thoracentesis, an intercostal tube with water-seal drainage is indicated. If bleeding continues, thoracotomy is indicated. Great care must be taken during aspiration to avoid bacterial contamination of the pleural cavity. Surgical removal of residual blood clots may be necessary.

PLEURAL EMPYEMA (Nontuberculous)

Acute infection of the pleural space may result from (1) direct spread from adjacent bacterial pneumonia, (2) postsurgical infection, (3) post-traumatic (including thoracentesis)infection. Underlying chronic obstructive pulmonary disease or broncho-genie carcinoma is frequently present. The availability of early and specific therapy for these conditions has made empyema an uncommon disease. However, the mortality rate remains high (50% in some series). The incidence of anaerobic infection appears to be increasing. Hospital-acquired infections have a more serious prognosis.

The clinical findings are often obscured by the primary underlying disease. Pleural pain, fever, and ' 'toxicity'' after clinical improvement of the primary disease, in association with physical and x-ray signs of pleural fluid, are characteristic. Thoracentesis reveals a frankly purulent exudate from which the causative organism may be cultured. Empyema, like lung abscess, may become chronic, with a prolonged course and little tendency to spontaneous resorption (especially in bronchiectasis and tuberculosis).

The key to nonsurgical treatment of acute empyema is early diagnosis. Any collection of fluid occurring in the course of pulmonary inflammatory disease should be removed at once. If pus is present, a specimen should be obtained for Gram staining and cultures, including cultures for anaerobic organisms. Specimens for anaerobic culture must be collected without exposure to air and must be placed into suitable transport media immediately. (Coagulase-positive Staphylococcus aureus and gram-negative bacilli are the most common aerobic bacteria causing empyema; Bacteroides and peptostreptococci are the most frequently encountered anaerobic organisms.) The empyema should be aspirated as completely as possible. Some early localized empyemas can be treated by thoracentesis and antibiotic therapy alone. Any large or loculated empyema should be drained immediately via an intercostal tube. Open thoracotomy is sometimes required to ensure adequate drainage.

As soon as specimens have been obtained for culture, parenteral antibiotic treatment should be started with penicillin, 600,000 units intramuscularly every 6 hours, or, alternatively, cephalothin, 8 g intravenously daily. When the pus has a foul odor or the empyema is thought to be secondary to an intra-abdominal infection, chloramphenicol, 50 mg/kg daily orally, should be added to the initial treatment. The object is to obliterate the empyema space as soon as possible. Irrigations with saline through the catheter may be necessary. Chronic empyema usually results from inadequately treated acute empyema or from a bronchopleural fistula. Surgical drainage with or without decortication is usually necessary.

PLEURAL PUNCTION

Pleural punction normally is done under the local anesthesia. For this purposes 0,5 – 1,0 % solution of Novocain infiltration of chest tissues is used. First of all anesthesia of skin is done (so called “lemon cover”). After that, changing the needle on “muscular” one is done the anesthesia of muscles. Pleural punction is performed by third needle connected with syringe by rubber or silicone tube. After the punction of pleural cavity the content of it is aspirated. When the syringe is full for prevention of ear income to pleura the transmitter (rubber or silicone tube) is closed by assistant. The syringe is disconnected. It content transmitted to sterile tube for histological and bacteriological analysis.

After the effusion aspiration from pleural cavity it is necessary to infuse the antimicrobal remedies for prevention of infection complications. After the finish of manipulation the needle is removed and the skin is sterilized by alcohol. After the estimating of effusion amount it transmitted to laboratory study.

CLOSED TUBE THORACOTOMY

(Tube Drainage)

Indications: Pneumothorax, spontaneous and traumatic, is the condition most commonly treated with tube drainage. Massive and recurrent pleural effusions unmanageable by needle aspiration also require this treatment; the etiology may be infection, malignancy, chylothorax, etc. Other indications are empyema, hemothorax, and hemopneumothorax.

Contraindications: Adhesions which may prevent introduction of the tube, clotted hemothorax, and/or empyema with pachypleuritis preclude successful tube drainage and require a thoracotomy.

Procedure: The location is chosen for introduction of the tube. For pneumothorax, the anterior chest wall, 2nd or 3rd intercostal space, midclavicular line is used. For pleural effusion, hemothorax, empyema, etc., the axillary line is preferred in the 5th mid or posterior intercostal space. The skin and the intercostal space are infiltrated with 2% procaine or similar agent, a small incision is made, the intercostal muscles are separated, and the tube is introduced through a trocar or directly with the aid of a clamp. The tube is sutured to the skin and connected to an underwater drainage system. Sometimes drainage is promoted by the use of a pump that can generate up to 20 cm H₂O negative pressure.

Complications: Bleeding from an intercostal vessel injured by the trocar, subcutaneous emphysema if the side holes of the drainage tube are not properly placed inside the pleural space, infection of the local skin site, and pain are common.

THORACOSCOPY

Indication: To obtain a biopsy from a peripheral lesion of the lung or pleura under direct vision through a mediastinoscope or similar instrument.

Contraindications: Adhesions, central location of the lesions to be biopsied, bleeding tendency, or air leak.

Procedure: Under general anesthesia, the location is chosen in the anterior or lateral chest wall according to the location of the lesion. A small incision is made in the skin and the intercostal muscles. A mediastinoscope or a bronchoscope is introduced to explore the pleura and the lung. A biopsy is taken through the instrument with a forceps. The lung is then reinflated. Usually, a tube for drainage is left after the procedure.

Complications: Most are due to bleeding or air leak from the location of the biopsy. Infection of the pleural space in the course of the procedure is uncommon except when infected lesions are biopsied.

FIBERBRONCHOSCOPY

Direct visual examination of the tracheobronchial tree using a flexible tube (flexible bronchoscope; fiberbronchoscope) containing light-transmitting glass fibers that return a magnified image (picture 7-8). Fiberbronchoscopes range in external diameter from 3 to 6 mm; the proper diameter depends on the size of the patient. The small caliber of the instrument makes it possible to enter segmental bronchi and to visualize subsegmental bronchi. The central channel of the scope is 2 to 2.5 mm in diameter and is used to aspirate secretions, to give anesthetic agents, to obtain brush or forceps biopsies, and to introduce bronchographic contrast material. It is also possible to obtain uncontaminated cultures through the channel. Lavage fluid, such as saline, acetylcysteine, and heparin can be introduced through the channel. Cuffing of the scope makes it possible to lavage a lobe via its lobar bronchus.

Diagnostic indications: It is used to explore the cause of an unexplained persistent cough, wheeze, or hemoptysis, or unresolved pneumonia or atelectasis, especially in a male smoker above age 30. The flexible bronchoscope is used for small hemoptysis, i.e., blood-tinged sputum or small quantities of blood; for large hemoptysis, rigid bronchoscopy is used. Fiberoptic bronchoscopy is also used to perform transbronchial lung biopsy and/or bronchial lavage in diffuse lung disease of obscure etiology, to investigate paralysis of the recurrent laryngeal or phrenic nerves, to search for the origin of positive cytology obtained from sputum or endobronchial aspiration or of any other suggestion of lung tumor, to determine the state of the tracheobronchial tree after acute inhalation injury, to determine the anatomy of the endobronchial tree, to visualize a bronchiectatic area, and postoperatively to evaluate the stump of a resected bronchus.

Therapeutic indications: Attempt to open atelectasis; attempt to drain lung abscess; assist a weakened patient to raise secretions; performing extensive suction through an endotracheal or tracheostomy tube; removal of certain foreign bodies;

perform lung lavage after aspiration of add or alkaline material especially; and identification of acute laryngeal obstruction to direct treatment. For removal of large amounts of secretions or foreign bodies, a rigid bronchoscope is generally preferred.

Contraindications depend, in part, on the clinical state. A few, such as an intractable bleeding disorder or severe cardiopulmonary failure, are usually absolute contraindications. But even in bleeding disorders, temporary correction of the defect by transfusion may sometimes allow enough time for visualization of the airways, although biopsy is avoided. An uncooperative patient can be made tractable by preoperative medication or general anesthesia. Cardiac arrhythmias, especially bradyarrhythmias, are contraindications unless they can be brought under control by premedication.

Procedure

The patient to be bronchoscoped fasts for at least 8 h before the procedure is done. P-A and lateral chest x-rays should be done within 24 h of the procedure Clotting function should be known to be normal within 24 h of the procedure. Patients with a history of cardiac disease or arrhythmias or > 50 yr of age should be monitored using the ECG.

Premedication consists of atropine average dose 1 mg s.c. and morphine or valium in appropriate dose. Topical anesthesia is accomplished with 2 or 4% lidocaine by first spraying the mouth, throat, and tongue and then through the nose. The patient inhales with each spray and, after one nostril is well sprayed, the other is anesthetized. A nasal Catheter is then placed through the least open nostril to the level of the uvula and O₂ 4 to 6 L/min is given throughout the procedure.

Before inserting the fiberbronchoscope, lidocaine jelly is used as a lubricant to protect both the patient's mucosa and the fiberbronchoscope from abrasion. The scope may be inserted through the nose providing there is no block, and through the mouth providing a simple curved endotracheal tube is used both as guide and protection for the instrument. The fiberbronchoscope is advanced to the epiglottis and anesthesia of the glottis is completed through the bronchoscope. Additional anesthetic is administered through the fiberbronchoscope as sensitive areas are reached by injecting 1 to 2 ml of the agent through the open channel. It is important to avoid excessive anesthetic agent because of the increasing prospect of untoward reactions as dosage increases.

Insertion of the fiberbronchoscope through endotracheal tubes or tracheostomy tubes that are already in place is quite easy; the main concern is to ensure adequate ventilation of the patient while the procedure is going on. Attachments are available to enable ventilation to proceed during the examination.

The entire procedure can be done under general anesthesia if necessary. Even then topical anesthesia of the glottic structures is advised to minimize the possibility of laryngospasm during or after the procedure is completed.

Complications: The main complications include laryngospasm, cardiac arrhythmias (cardiac arrest is a particular threat in asthmatic patients), hemorrhage due either to biopsy or to injury of the bronchial mucosa by the bronchoscope, pneumothorax secondary to bronchial biopsy, arterial hypoxemia due either to obstruction of a major bronchus by the bronchoscope or to spillover in the course of bronchial lavage, allergic reactions either to premedication or to anesthetic agent, urinary retention or respiratory depression due to premedication, bronchospasm due to irritation of the mucosa by the bronchoscope, and infections of the tra-cheobronchial tree and lung introduced during the procedure.

One complication is potentially useful for cytologic or microbiologic studies— the almost invariable mild bronchitis that follows the procedure increases sputum production for a few days.

Since the patient's swallowing and cough reflexes are depressed for an hour or so, care must be taken to prevent aspiration by abstaining from eating or drinking for a few hours after the procedure.

Picture 7 Bronchoscopy. General view.

Picture 8 Bronchoscopy view.

Some more info about Dronchoscopy you may find here:

http://dpi.radiology.uiow http://dpi.radiology.uiowa.edu/nlm/app/atlas/welcome2.htmla.edu/nlm/app/atlas/welcome2.html

MEDIASTINOSCOPY

Indications: The prime indication is the need to biopsy a tumor of the upper mediastinum or to determine whether lymph node metastases have occurred. In systemic diseases (e.g., Hodgkin's disease or lymphoma) both primary diagnosis and staging of the process may be achieved by mediastinoscopy and biopsy.

Contraindications: Superior vena cava syndrome, aneurysm of the aortic arch, and primary tuberculosis of the lung with lymph node involvement are the major conditions that militate against performing this operation. If the indication is urgent enough for the procedure to be performed, even these conditions are not absolute contraindications.

Procedure

Under general anesthesia in supine position with the neck extended, a transverse incision is made in the suprastemal notch. ^Because of anatomic limitations imposed by the aortic arch and the fascial compartments, the operator has easiest access to structures on the right side, particularly those in the same plane as the trachea and anterior to it. The mediastinoscope is introduced, the dissection is performed in the pretracheal fascia and extended under direct vision to the regional lymph nodes, where biopsy is performed. At the close of the procedure, the fascia and skin are sutured without drainage.

Complications are rare. Pneumothorax may occur if the pleura is opened. Local bleeding may be a problem, especially if superior vena caval obstruction exists. Infection is unusual. Arrhythmias may occur if the pericardium and the heart are touched.

MEDIASTINOTOMY

Indications: The same indications apply as for mediastinoscopy. This procedure is used to biopsy areas that cannot be reached by mediastinoscopy, especially the left side of the mediastinum, the subaortic glands, and structures at or below the level of the hili.

Contraindications are the same as for mediastinoscopy (see above).

Procedure

Under general anesthesia, the patient is placed in the supine position. A para-sternal incision is made above the 3rd rib. The cartilage is excised. The approach is extrapleural. If a deeper approach is needed, a mediastinoscope is used. If the pleura is inadvertently entered during the procedure, drainage is established by leaving a catheter in the pleural space at the end of the procedure.

A lung biopsy may be performed through this approach. If indicated, the incision can be extended into a full thoracotomy for better exploration or excision.

Complications: Pneumothorax, bleeding from vessels such as the internal mammary arteries, intercostal arteries, etc., and infection occur infrequently.

RV Residual volume

Dynamic Lung Volumes and Flow Rates

Obstructive Disease

PLEURAL EFFUSION