Thursday, October 21, 2010

Respiratory system examination- Methods of investigation in pulmonology

PULMONARY FUNCTION TESTS

Pulmonary function testing has progressed from simple spirometry to sophisti cated 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, in cluding 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 contrac tion generates negative intrapleural pressure. If the resulting inspiration is trans mitted 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 nor mally very sensitive, so that alveolar ventilation is kept proportional to the meta bolic 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 chap ter discusses tests of pulmonary function.
Static Lung Volumes
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 per formed 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 air ways 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 volumebecauseit 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 elas tic 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.
PULMONARY FUNCTION ABBREVIATIONS
CC- Closing capacity
Cdyn- Dynamic Lung compliance
CSTART- Static Lung COmpliance
Cv- Closing Volume (L)
DIco- Diffuse capacity for Carbon monoxide (ml/min/mmHg)
ERV- Expiratory reserve volume
FEV1- Forced expiratory volume in 1sec (L)
FEV3- Forced expiratory volume in 3s (L)
FVC- forced vital capacity
FRC- Functional residual capacity
[H+]- Concentration of hydrogen ions (monomoles/L)
IRV- Inspiratory reserve volume
MEF50% vc- Mid-expiratory flow at 50% vital capacity (L/sec)
MEF50% vc- Mid-inspiratory flow at 50% vital capacity (L/sec)
MMEF- Mean maximal expiratory flow (L/sec)
MVV- maximal voluntary ventilation
PaCO2- Arterail partial pressure of CO2 (mmHg)
PaO2- Arterial partial pressure of O2 (mmHg)
PEF- peak expiratory flow (L/sec)
PTP- Transpulmonary pressure (mmHg)
Q- Perfusion (L/min)
RAW- Airway resistance
RV- Residual volume
TLC- Total Lung capacity
V- Lung Volume (L)
VC- Vital capacity
V- Ventilation
VA- ALveolar ventilation (L/min)
Vco2- CO2 production (L/min)
VO2- O2 consumption (L/min)
The FRC has 2 components, the residual volume (RV), the volume of air remain ing 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 nor mal 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 de creased FRC and a relatively well-preserved RV.
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 (MMEF25-75%) 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 FEV1and is a more sensitive indicator of early air ways 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 nega tive intrathoracic pressure tends to maintain the caliber of the airways. The differ ences in airway diameter during inspiration and expiration thus result in greater flow rates during inspiration than expiration during much of the breathing cycle . 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 pa tient 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 respira tory 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. 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 respira tory muscles. These are measured by having the patient forcibly inspire and ex pire through a closed mouthpiece attached to a pressure gauge. Maximal pressures are reduced in neuromuscular disorders (e.g., myasthenia gravis, muscu lar dystrophy, Guillain-Barre syndrome).
Diffusing Capacity (DLco) DLco is defined as the number of ml of CO absorbed/min/mm Hg. It is deter mined 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 abnor mal 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 low ered 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 fail ure (increase in blood flow to the usually poorly perfused lung apices).
Distribution of Ventilation
The distribution of ventilation is studied by continuously recording the concen tration 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 be tween 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 air ways. 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 con trol of breathing to the clinical physiology laboratory.
Hypoxic drive (function of the carotid chemoreceptors) can be studied by plot ting 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.
Central and obstructive sleep apnea can be distinguished by monitoring respi ration during sleep. An ear oximeter monitors Ch saturation. ACO2 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 ob structive 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 maxi mum 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 mea suring VC, FEV1, and PEF. The procedure is readily taught to both patient and operator and yields permanent, reproducible, and accurate data. While spirom etry alone may not permit specific diagnosis, it can differentiate between obstruc tive 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 ordi narily 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 ex piratory 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 sug gests 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 narrow ing 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 air ways. 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.

CHARACTERISTIC CHANGES IN PULMONARY FUNCTION IN RESTRICTIVE AND OBSTRUCTIVE DISEASE OF VARYING SEVERITY
Restrictive diseases
VC (% predicted): None (>80), mild (60-80), moderate (50-60), severe (35-50), very severe (<35)
FEV, (%VC): None (>75), mild (>75), moderate (>75), severe (>75), very severe (>75)
MW (% predicted): None (>80), mild (>80), moderate (>80), severe (60-80), very severe (<60)
RV (% predicted): None (80-120), mild (80-120), moderate (70-80), severe (60-70), very severe (<60)
Dlco: None (Normal), mild (reduced at exercise), moderate (reduced at rest), severe (reduced ¯), very severe (badly reduced ¯¯)
Dyspnea (severity): None (0), mild (+), moderate (++), severe (+++), very severe (++++)
Obstructive Diseases
VC (% predicted): None (>80), Mild (>80), Moderate (>80), severe (Low), very severe (Low)
FEV1 (%VC): None (>75), Mild (60-75), Moderate (40-60), Severe (<40), very severe (<40)
MW (% predicted): None (>80), Mild (65-80), Moderate (45-65), severe (30-45), very severe (<30)
RV (% predicted): None (80-120), Mild (120-150), Moderate (150-175), severe (>200), very severe (>200)
Dlco: None (Normal), Mild (Normal), Moderate (Normal), severe (Low -), very severe (Low --)
Dyspnea (severity): None (0), Mild (+), Moderate (++), severe (+++), very severe (++++)

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
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 ex amination, 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 abdomi nal surgery (particularly in the patient with known or suspected pulmonary im pairment) and to document the severity of interstitial pulmonary disorders. Periodic VCs and Dlco2usually suffice to follow the course of a restrictive pro cess.
The following tables are intended as general guides to the interpretation of pulmonary function tests. TABLE 2 illustrates several simple patterns of pul monary 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 RADIOGRAPH
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.

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 Spneumomae 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 toPneumocystis 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 forLegionella 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 PUNCTURE
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, hemo thorax, and hemopneumothorax.
Contraindications: Adhesions which may prevent introduction of the tube, clot ted 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 pre ferred 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, subcu taneous 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 (flexi ble bronchoscope; fiberbronchoscope) containing light-transmitting glass fibers that return a magnified image (picture). 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 persis tent cough, wheeze, or hemoptysis, or unresolved pneumonia or atelectasis, espe cially 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 he moptysis, rigid bronchoscopy is used. Fiberoptic bronchoscopy is also used to perform transbronchial lung biopsy and/or bronchial lavage in diffuse lung dis ease 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 deter mine the state of the tracheobronchial tree after acute inhalation injury, to deter mine 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 ab scess; 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 intrac table 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 trac table 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.
Bronchoscopy view.
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 impor tant 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 possi bility of laryngospasm during or after the procedure is completed.
Complications: The main complications include laryngospasm, cardiac arrhyth mias (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 ob struction 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.
Bronchoscopy. General view


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
Mediastinoscopy is a procedure in which a lighted instrument (mediastinoscope) is inserted through a neck incision to visually examine the structures in the top of the chest cavity and take tissue samples. This procedure can be used to biopsy lymph n
Under general anesthesia in supine position with the neck extended, a trans verse 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 re gional 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
Anterior mediastinotomy: A surgical procedure to look at the organs and tissues between the lungs and between the breastbone and spine for abnormal areas. An incision (cut) is made next to the breastbone and an endoscope (a thin, lighted tube) is ins
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 inci sion can be extended into a full thoracotomy for better exploration or excision.
Complications: Pneumothorax, bleeding from vessels such as the internal mam mary arteries, intercostal arteries, etc., and infection occur infrequently
SOURCES
Alsaeedi A, Sin DD, McAlister FA. The effects of inhaled corticosteroids in chronic obstructive pulmonary disease: a systematic review of randomized placebo-controlled trials. Am J Med. Jul 2002;113(1):59-65. [Medline].Anthonisen NR. Prognosis in chronic obstructive pulmonary disease: results from multicenter clinical trials. Am Rev Respir Dis. Sep 1989;140(3 Pt 2):S95-9. [Medline].Anthonisen NR, Connett JE, Kiley JP. Effects of smoking intervention and the use of an inhaled anticholinergic bronchodilator on the rate of decline of FEV1. The Lung Health Study. JAMA. Nov 16 1994;272(19):1497-505. [Medline].Belman MJ, Botnick WC, Shin JW. Inhaled bronchodilators reduce dynamic hyperinflation during exercise in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. Mar 1996;153(3):967-75. [Medline].Brenes GA. Anxiety and chronic obstructive pulmonary disease: prevalence, impact, and treatment. Psychosom Med. Nov-Dec 2003;65(6):963-70.Burrows B, Bloom JW, Traver GA. The course and prognosis of different forms of chronic airways obstruction in a sample from the general population. N Engl J Med. Nov 19 1987;317(21):1309-14. [Medline].Casaburi R, Mahler DA, Jones PW. A long-term evaluation of once-daily inhaled tiotropium in chronic obstructive pulmonary disease. Eur Respir J. Feb 2002;19(2):217-24. [Medline].Chapman KR. Therapeutic algorithm for chronic obstructive pulmonary disease. Am J Med. Oct 21 1991;91(4A):17S-23S. [Medline].Davis RM, Novotny TE. The epidemiology of cigarette smoking and its impact on chronic obstructive pulmonary disease. Am Rev Respir Dis. Sep 1989;140(3 Pt 2):S82-4. [Medline].Donohue JF, van Noord JA, Bateman ED. A 6-month, placebo-controlled study comparing lung function and health status changes in COPD patients treated with tiotropium or salmeterol. Chest. Jul 2002;122(1):47-55. [Medline].Dunn WF, Nelson SB, Hubmayr RD. Oxygen-induced hypercarbia in obstructive pulmonary disease. Am Rev Respir Dis. Sep 1991;144(3 Pt 1):526-30. [Medline].Fabbri LM, Luppi F, Beghe B. Update in chronic obstructive pulmonary disease 2005. Am J Respir Crit Care Med. May 15 2006;173(10):1056-65.Ferguson GT, Cherniack RM. Management of chronic obstructive pulmonary disease. N Engl J Med. Apr 8 1993;328(14):1017-22. [Medline].Fletcher C, Peto R. The natural history of chronic airflow obstruction. Br Med J. Jun 25 1977;1(6077):1645-8. [Medline].Halbert RJ, Natoli JL, Gano A. Global burden of COPD: systematic review and meta-analysis. Eur Respir J. Apr 12 2006.Karpel JP, Kotch A, Zinny M. A comparison of inhaled ipratropium, oral theophylline plus inhaled beta-agonist, and the combination of all three in patients with COPD. Chest. Apr 1994;105(4):1089-94. [Medline].Lopez-Majano V, Dutton RE. Regulation of respiration during oxygen breathing in chronic obstructive lung disease. Am Rev Respir Dis. Aug 1973;108(2):232-40. [Medline].Mannino DM, Watt G, Hole D. The natural history of chronic obstructive pulmonary disease. Eur Respir J. Mar 2006;27(3):627-43.McKay SE, Howie CA, Thomson AH. Value of theophylline treatment in patients handicapped by chronic obstructive lung disease. Thorax. Mar 1993;48(3):227-32. [Medline].O''Donnell DE, Sanii R, Anthonisen NR. Effect of dynamic airway compression on breathing pattern and respiratory sensation in severe chronic obstructive pulmonary disease. Am Rev Respir Dis. Apr 1987;135(4):912-8. [Medline].O''Donnell DE, Hernandez P, Aaron S. Canadian Thoracic Society COPD Guidelines: summary of highlights for family doctors. Can Respir J. May-Jun 2003;10(4):183-5. [Medline].O''Donnell DE, Parker CM. COPD exacerbations . 3: Pathophysiology. Thorax. Apr 2006;61(4):354-61.O''Donnell R, Breen D, Wilson S. Inflammatory cells in the airways in COPD. Thorax. May 2006;61(5):448-54.Papi A, Luppi F, Franco F. Pathophysiology of exacerbations of chronic obstructive pulmonary disease. Proc Am Thorac Soc. May 2006;3(3):245-51.Pauwels R. Global initiative for chronic obstructive lung diseases (GOLD): time to act. Eur Respir J. Dec 2001;18(6):901-2. [Medline].Peto R, Speizer FE, Cochrane AL. The relevance in adults of air-flow obstruction, but not of mucus hypersecretion, to mortality from chronic lung disease. Results from 20 years of prospective observation. Am Rev Respir Dis. Sep 1983;128(3):491-500. [Medline].Petty TL, Finigan MM. Clinical evaluation of prolonged ambulatory oxygen therapy in chronic airway obstruction. Am J Med. Aug 1968;45(2):242-52. [Medline].Postma DS, Sluiter HJ. Prognosis of chronic obstructive pulmonary disease: the Dutch experience. Am Rev Respir Dis. Sep 1989;140(3 Pt 2):S100-5. [Medline].Prigmore S. End-of-life decisions and respiratory disease. Nurs Times. Feb 14-20 2006;102(7):56, 59, 61. [Medline].Ram FS, Rodriguez-Roisin R, Granados-Navarrete A. Antibiotics for exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2006;CD004403.Rutten FH, Cramer MJ, Lammers JW. Heart failure and chronic obstructive pulmonary disease: An ignored combination?. Eur J Heart Fail. Mar 10 2006.Sanders C. The radiographic diagnosis of emphysema. Radiol Clin North Am. Sep 1991;29(5):1019-30. [Medline].Schachter EN. Cilomilast. Drugs Today (Barc). Apr 2006;42(4):237-47.Sutherland ER, Martin RJ. Airway inflammation in chronic obstructive pulmonary disease: comparisons with asthma. J Allergy Clin Immunol. Nov 2003;112(5):819-27; quiz 828. [Medline].Thurlbeck WM. Pathophysiology of chronic obstructive pulmonary disease. Clin Chest Med. Sep 1990;11(3):389-403. [Medline].Thurlbeck WM. Overview of the pathology of pulmonary emphysema in the human. Clin Chest Med. Sep 1983;DA - 19840127(3):337-50. [Medline].Tsoumakidou M, Siafakas NM. Novel insights into the aetiology and pathophysiology of increased airway inflammation during COPD exacerbations. Respir Res. May 22 2006;7(1):80.Ulrik CS. Efficacy of inhaled salmeterol in the management of smokers with chronic obstructive pulmonary disease: a single centre randomised, double blind, placebo controlled, crossover study. Thorax. Jul 1995;50(7):750-4. [Medline].Vestbo J. Clinical assessment, staging, and epidemiology of chronic obstructive pulmonary disease exacerbations. Proc Am Thorac Soc. May 2006;3(3):252-6.Vincken W, van Noord JA, Greefhorst AP. Improved health outcomes in patients with COPD during 1 yr''s treatment with tiotropium. Eur Respir J. Feb 2002;19(2):209-16. [Medline].Weitzenblum E, Sautegeau A, Ehrhart M. Long-term oxygen therapy can reverse the progression of pulmonary hypertension in patients with chronic obstructive pulmonary disease. Am Rev Respir Dis. Apr 1985;131(4):493-8. [Medline].

1 comment:

  1. You've written in great detail. Good learning experience to read your articles.

    ReplyDelete