(Saline lavage of lung subsegment via fiberoptic bronchoscope) Use For biopsy of endobronchial tumor in which obstruction may cause secondary pneumonia with effusion but still a resectable tumor To obtain bronchial washings for Diagnosis of nonresectable tumors that may be treated with radiation (e.g., oat cell carcinoma, odg!in"s disease), metastatic tumors, peripheral lesions that cannot be reached by bronchoscope. Diagnosis of pulmonary infection, especially when sputum e#amination is not diagnostic. $uantitative bacterial culture and cytocentrifugation for staining slides provides overall diagnostic accuracy of %&' for pulmonary infection. (egative predictive value ) &*'. +iemsa stain ealthy persons show ,-' neutrophils, ./0.' lymphocytes, .1/.&' alveolar macrophages. 201' neutrophils3 indicates acute inflammation (e.g., bacterial infection, including 4egionella, acute respiratory distress syndrome 567DS8, drug reaction). 20' s9uamous epithelial cells3 indicates that a positive culture may reflect saliva contamination. 2.1' macrophages3 common in pulmonary hemorrhage. 6spergillosis is the only infection associated with significant alveolar hemorrhage, which may also be found in 201' of patients with hematologic malignancies. 2-1' lymphocytes3 may indicate hypersensitivity pneumonitis (often up to :1;<1' with more cytoplasm and large irregular nucleus). 201' neutrophils and 2-' eosinophils3 characteristic of idiopathic pulmonary fibrosis= alveolar macrophages predominate. 4ymphocyte percentage may be increased. 201: colony>forming bacteria?m4 indicates bacterial infection if ,0' s9uamous epithelial cells are present on +iemsa stain. +ram stain @any bacteria suggests bacterial infection if there are ,0' s9uamous epithelial cells, especially if culture shows 201* bacteria?m4. (o bacteria suggests that bacterial infection is unli!ely but 4egionella should be ruled out with direct fluorescent antibody (DF6) test if +iemsa stain shows increased neutrophils. Aombined with methenamine silver or Bap stain, &*' sensitivity for diagnosis of Bneumocystis infection= increased to 011' when C64 is combined with transbronchial biopsy. 6cid>fast stain3 positive result may indicate @ycobacterium tuberculosis or @ycobacterium avium>intracellulare infection. Toluidine blue stain3 may show Bneumocystis carinii cysts in Bneumocystis pneumonia or 6spergillus hyphae in immunocompromised host with invasive aspergillosis. Brussian blue/nuclear red stain3 strongly positive result indicates severe alveolar hemorrhage= moderately positive indicates some hemorrhage= absent indicates no evidence of alveolar hemorrhage. DF6 stain for 4egionella, herpes simple# virus (SD) E and EE (stains bronchial epithelial cells and macrophages), and A@D (stains mononuclear cells) may indicate infection with corresponding organism. Bap stain3 atypical cytology may be due to cytoto#ic drugs, radiation therapy, viral infection (intranuclear inclusions of herpesvirus or A@D), tumor. Fil red F stain3 shows many large intracellular fat droplets in one>third to two>thirds of cells in some patients with fat embolism due to bone fractures but in ,-' of patients without embolism. GASES, BLOOD Decreased pO (A!"#e$%a) ypoventilation (e.g., chronic airflow obstruction)3 due to increased alveolar AFG, which displaces FG 6lveolar hypo#ia (e.g., high altitude, gaseous inhalation) Bulmonary diffusion abnormalities (e.g., interstitial lung disease)3 supplemental FG usually improves pFG 7ight>to>left shunt3 supplemental FG has no effect= re9uires positive end>e#piratory pressure Aongenital anomalies of heart and great vessels 6c9uired (e.g., 67DS) Dentilation>perfusion mismatch3 supplemental FG usually improves pFG 6irflow obstruction (e.g., chronic obstructive pulmonary disease 5AFBD8, asthma) Enterstitial inflammation (e.g., pneumonia, sarcoidosis) Dascular obstruction (e.g., pulmonary embolism) Decreased venous o#ygenation (e.g., anemia) I!creased pCO (H&percap!%a) Decreased ventilation 6irway obstruction Drug overdose @etabolic disorders (e.g., my#edema, hypo!alemia) (eurologic disorders (e.g., +uillain>CarrH syndrome, multiple sclerosis) @uscle disorders (e.g., muscular dystrophy, polymyositis) Ahest wall abnormalities (e.g., scoliosis) Encreased dead space in lungs (perfusion decreased more than ventilation decreased) 4ung diseases (e.g., AFBD, asthma, pulmonary fibrosis, mucoviscidosis) Ahest wall changes affecting lung parenchyma (e.g., scoliosis) Encreased production (e.g., sepsis, fever, seiIures, e#cess carbohydrate loads) SP'T'M Aolor in various conditions J 7usty 4obar pneumonia J 6nchovy paste (dar! brown) 6mebic liver abscess rupture into bronchus J 7ed currant Kelly Llebsiella pneumoniae J 7ed (pigment, not blood) Serratia marcescens= rifampin overdose J Clac! Cacteroides melaninogenicus pneumonia= anthracosilicosis J +reen (with MCAs, sweet odor) Bseudomonas infection J @il!y Cronchioalveolar carcinoma J Nellow (without MCAs) Oaundice Smears and cultures for infections (e.g., pneumonias, TC, fungi) must be ade9uate samples of sputum showing ciliated cells, macrophages= neutrophils (usually 2G:?4BF in good specimen) if acute inflammation is present unless patient is neutropenic= monobacterial population if due to bacterial infection= acute inflammation without a definite bacterial pattern may be due to 4egionella or 7SD or influenIa viruses. @ust be promptly refrigerated Saliva contamination may show s9uamous epithelial cells (20&?4BF ) poor specimen= 00/0&?4BF ) fair specimen= ,01?4BF ) good specimen), e#tracellular strands of streptococci, clumps of anaerobic 6ctinomyces, candidal budding yeasts with pseudohyphae. For possible anaerobic aspiration, fine needle aspiration (F(6) or alveolar lavage is needed. Aytology for carcinoma Bositive in *1' on first sample Bositive in %1' with three samples Bositive in .:' with five samples False>positive in ,0' Aytology in bronchogenic carcinoma Bositive in <%/.:' of s9uamous cell carcinoma Bositive in <*/%1' of small>cell undifferentiated carcinoma Bositive in ::' of adenocarcinoma RESPIRATORY DISEASES 6CSAPSS, 4U(+ Sputum3 mar!ed increase= abundant, foul, purulent= may be bloody= contains elastic fibers. +ram stain is diagnostic;sheets of B@(s with a bewildering variety of organisms. Cacterial cultures (including tubercle bacilli);anaerobic as well as aerobic= rule out amebas, parasites. Aytologic e#amination for malignant cells. Clood culture3 may be positive in acute stage. Encreased MCA in acute stages (0:,111/-1,111?cu mm) Encreased PS7 (ormochromic normocytic anemia in chronic stage 6lbuminuria is fre9uent. Findings of underlying disease;especially bronchogenic carcinoma= also drug addiction, postabortion state, coccidioidomycosis, amebic abscess, TC, alcoholism AD'LT RESPIRATORY DISTRESS SYNDROME (ARDS) Defined 6s- 7atio of pFG (partial pressure arterial FG)?FiFG (fraction inspired FG concentration) Q G11 regardless of positive end>e#piratory pressure. This ratio correlates with patient"s outcome. En acute lung inKury (change in lung function) this ratio is Q -11. Cilateral pulmonary infiltrates on frontal radiography Bulmonary wedge pressure Q 0. mm g or no evidence of increased left atrial pressure Breceding or associated event (e.g., sepsis 5most common8, aspiration, infection, pneumonia, pancreatitis, shoc!, fat emboli, trauma, DEA, etc.= more than one cause is often present). Enfection is more li!ely due to gram>negative than gram>positive organisms. Fccurs in G-' of cases of gram>negative bacteremia. Static pulmonary compliance ,:1 m4?cm GF that mar!edly reduces vital capacity, total lung capacity, functional residual capacity. Enitially there is respiratory al!alosis and varying degrees of hypo#emia resistant to supplementary FG= then profound ano#emia with pFG ,:1 mm g on room air. C64 shows increased B@(s (Q .1'). Posinophilia occurs occasionally. Fpportunistic organisms may be found if presents as 67DS. ASTHMA, BRONCHIAL Parliest change is decreased pAFG with respiratory al!alosis with normal pFG. Then pFG decreases before pAFG increases. Mith severe episode yperventilation causes decreased pAFG in early stages (may be ,-: mm g). 7apid deterioration of patient"s condition may be associated with precipitous fall in pFG and rise in pAFG (2*1 mm g). pFG ,<1 mm g may indicate severe attac! or presence of complication. (ormal pAFG suggests that the patient is tiring. 6cidemia and increased pAFG suggest impending respiratory failure. @i#ed metabolic and respiratory acidosis occurs. Mhen patient re9uires hospitaliIation, arterial blood gases should be measured fre9uently to assess status. Posinophilia may be present. Sputum is white and mucoid without blood or pus (unless infection is present). Posinophils, crystals (Aurschmann"s spirals), and mucus casts of bronchioles may be found. 4aboratory findings due to underlying diseases that may be primary and that should be ruled out, especially polyarteritis nodosa, parasitic infestation, bronchial carcinoid, drug reaction (especially to aspirin), poisoning (especially by cholinergic drugs and pesticides), hypogammaglobulinemia. BRONCHIECTASIS MCA usually normal unless pneumonitis is present. @ild to moderate normocytic normochromic anemia with chronic severe infection Sputum abundant and mucopurulent (often contains blood)= sweetish smell Sputum bacterial smears and cultures 4aboratory findings due to complications (pneumonia, pulmonary hemorrhage, brain abscess, sepsis, cor pulmonale) 7ule out cystic fibrosis of the pancreas and hypogammaglobulinemia or agammaglobulinemia. BRONCHITIS, AC'TE Due To Diruses (e.g., rhinovirus, coronavirus, adenovirus, influenIa) cause most cases. @ycoplasma pneumoniae, Ahlamydia pneumoniae, Cordetella pertussis, 4egionella spp. MCA and PS7 may be increased. BRONCHITIS, CHRONIC MCA and PS7 normal or increased Posinophil count increased if there is allergic basis or component Smears and cultures of sputum and bronchoscopic secretions 4aboratory findings due to associated or coe#isting diseases (e.g., emphysema, bronchiectasis) 6cute e#acerbations are most commonly due to Diruses @. pneumoniae aemophilus influenIae S. pneumoniae @ora#ella (Cranhamella) catarrhalis CARCINOMA, BRONCHOGENIC Aytologic e#amination of sputum for malignant cells;positive in *1' of patients on first sample, in %1' with three samples, in .:' with five samples. False>positive tests are ,0'. Sputum cytology gives highest positive yield with s9uamous cell carcinoma (<%/.:'), intermediate with small cell undifferentiated carcinoma (<*/%1'), lowest with adenocarcinoma (::'). Ciopsy of scalene lymph nodes for metastases to indicate inoperable status;positive in 0:' of patients Ciopsy of bronchus, pleura, lung, metastatic sites in appropriate cases Aytology of pleural effusion (eedle biopsy of pleura is positive in :.' of cases with malignant effusion= indicates inoperable status. Transthoracic needle aspiration provides definitive cytologic diagnosis of cancer in .1;&1' of cases= useful when other methods (e.g., sputum cytology, bronchoscopy) fail to provide a microscopic diagnosis. Aancer cells in bone marrow and rarely in peripheral blood Ciochemical tumor mar!ers Serum AP6 is increased in one>third to two>thirds of patients with all four types of lung cancer. Brincipal uses are to monitor response to therapy and to correlate with staging. Dalues ,: ng?m4 correlate with survival over - yrs compared to values 2: ng?m4. Dalues 201 ng?m4 correlate with higher incidence of e#tensive disease and e#trathoracic metastases. 6 fall to normal suggests complete tumor removal. 6 fall to still elevated values may indicate residual tumor. 6n elevated unchanged value suggests residual progressive disease. 6 value that falls and then rises during chemotherapy suggests that resistance to drugs has occurred. Serum neuron>specific enolase may be increased in %&/.%' of patients with small cell cancer and in 01' of those with non/small cell cancer and nonmalignant lung diseases. Bretreatment level correlates with stage of small cell cancer. @ay be used to monitor disease progression= falls in response to therapy and becomes normal in complete remission but not useful for initial screening or detecting early recurrence. Baraneoplastic syndromes Pndocrine and metabolic (primarily due to small cell cancer) 6AT (Aushing"s syndrome) is most commonly produced ectopic hormone (:1' of patients with small cell cancer) ypercalcemia occurs in 20G' of patients (mostly in epidermoid carcinoma)= correlates with large tumor mass that is often incurable and 9uic!ly fatal. (See umoral ypercalcemia of @alignancy.) Serotonin production by carcinoid of bronchus. SE6D occurs in 00' of patients with small cell cancer. Brolactin usually due to anaplastic tumors. +onadotropin production predominantly with large cell carcinoma 7enal tubular dysfunction with glycosuria and aminoaciduria yponatremia due to massive bronchorrhea in bronchoalveolar cell carcinoma Fthers (e.g., melanocyte>stimulating hormone, vasoactive intestinal peptides) Aoagulopathies, e.g., DEA @igratory thrombophlebitis Ahronic hemorrhagic diathesis (euromuscular syndromes (most commonly with small cell cancer), e.g., @yasthenia Pncephalomyelitis;antineuronal antibodies and small cell cancer associated with limbic encephalitis Autaneous, e.g., Dermatomyositis 6canthosis nigricans Syndromes due to metastases (e.g., liver metastases with functional hepatic changes, 6ddison"s disease, diabetes insipidus) Findings of complicating conditions (e.g., pneumonitis, atelectasis, lung abscess) (ormochromic, normocytic anemia in ,01' of patients CRO'P (EPIGLOTTITIS, LARYNGOTRACHEITIS) +roup C . influenIae causes 2&1' of cases of epiglottitis= other bacteria include beta>hemolytic streptococci and pneumococci. Aultures, smears, and tests for specific causative agents Clood cultures should be ta!en at the same time as throat cultures. (eutrophilic leu!ocytosis is present. Alinical picture in infectious mononucleosis or diphtheria may resemble epiglottitis. 4aryngotracheitis is usually viral (especially parainfluenIa) but rarely bacterial in origin. DYSPLASIA, BRONCHOP'LMONARY Usually seen in infants recovering from respiratory distress syndrome (7DS) in whom endotracheal tube and intermittent positive pressure ventilation have been used for 2G* hrs. Stage E (first days of life);severe 7DS is present. Stage EE (late in first wee!);clinical improvement but not asymptomatic Stage EEE (second wee! of life);clinical deterioration, increasing hypo#emia, hypercapnia, acidosis, diffuse radiographic changes in lungs Stage ED (after 0 mo of age);chronic healing phase with further radiographic changes. G:' die, usually due to pneumonia. Symptoms usually resolve by G yrs but abnormal pulmonary function tests and right ventricular hypertrophy may persist for several years. EMPHYSEMA, OBSTR'CTIVE 4aboratory findings of underlying disease that may be primary (e.g., pneumoconiosis, TC, sarcoidosis, !yphoscoliosis, mar!ed obesity, fibrocystic disease of pancreas, alpha>0>antitrypsin deficiency) 4aboratory findings of associated conditions, especially duodenal ulcer 4aboratory findings due to decreased lung ventilation pFG decreased and pAFG increased Ultimate development of respiratory acidosis Secondary polycythemia Aor pulmonale GOODPAST'RE(S SYNDROME (6lveolar hemorrhage and +( 5usually rapidly progressive8 associated with antibody against pulmonary alveolar and glomerular basement membranes) Broteinuria and 7CAs and 7CA casts in urine 7enal function may deteriorate rapidly or renal manifestations may be mild. 7enal biopsy may show characteristic linear immunofluorescent deposits of Eg+ and often complement and focal or diffuse proliferative +(. Serum may show antiglomerular basement membrane Eg+ antibodies by enIyme immunoassay (PE6). Titer may not correlate with severity of pulmonary or renal disease. Posinophilia absent and iron>deficiency anemia more mar!ed than in idiopathic pulmonary hemosiderosis Sputum or C64 showing hemosiderin>laden macrophages may be a clue to occult pulmonary hemorrhage. Fther causes of combined pulmonary hemorrhage and +( are Megener"s granulomatosis ypersensitivity vasculitis S4P Bolyarteritis nodosa Pndocarditis @i#ed cryoglobulinemia 6llergic angiitis and granulomatosis (Ahurg>Strauss syndrome) CehRet"s syndrome enoch>SchSnlein purpura Bulmonary>renal reactions due to drugs (e.g., penicillamine) HANTAVIR'S P'LMONARY SYNDROME HERNIA, DIAPHRAGMATIC @icrocytic anemia (due to blood loss) may be present. Stool may be positive for blood. HISTIOCYTOSIS ) Diagnosis is established by open lung biopsy. Bulmonary disorder is the maKor manifestation of this disease= bone involvement in minority of cases with lung disease. Bleural effusion is rare. C64 shows increase in total number of cells= G/G1' 4angerhans" cells, small numbers of eosinophils, neutrophils, and lymphocytes, and %1' macrophages. @ost adults do not have positive gallium citrate <% (<%+a) scans. @ild decrease in pFG, which falls with e#ercise INTERSTITIAL PNE'MONITIS, DIFF'SE Serum 4D is increased. LARYN) DISEASES Aulture and smears for specific organisms (e.g., tubercle bacilli, fungi) Ciopsy for diagnosis of visible lesions (e.g., leu!opla!ia, carcinoma) @ay be due to any respiratory viruses. LEGIONNAIRES( DISEASE (Due to 4egionella pneumophila, a gram>negative bacillus that is a facultative aerobic, intracellular, opportunistic pathogen widely disseminated in the environment= at least 0G serogroups are !nown.) Fptimal diagnosis combines culture, detection of antigen and DF6 or BA7 of sputum, C64 fluid, or pleural fluid, and detection of antigen in urine. Frganism may be cultured in -/% days on special media from pleural fluid, lung biopsy specimen, transtracheal or bronchial aspirate, blood= isolate can then be identified only by special tests (e.g., DF6). DF6 may demonstrate the organism in sputum, pleural fluid, or lung, or other tissue within G/- days of onset of clinical disease= is e#tremely useful for rapid specific diagnosis (sensitivity ) T%1'). @ay be negative with few organisms present in early or mild cases or after erythromycin treatment. ence negative test is of little value and does not substitute for culture. Specificity is 2..' compared to culture or serologic tests. Urinary antigen assay is &1' sensitive and 011' specific= antigen can be detected for wee!s after acute illness. Detects only serogroup 0, which accounts for large maKority of cases. BA7 can detect 4egionella in urine, serum, C64 fluid. Used on clinical specimens or culture material= reported sensitivity ) %*' and specificity ) 011'. Detects all species= rapid. (egative result does not e#clude diagnosis. EF6 (allows detection of Eg@ versus Eg+ antibody), P4ES6 Titers of ,03<* are considered negative. Single titers of 03<*/03G:< suggest prior infection at undetermined time. Single EF6 titer of 203G:< is strong presumptive evidence. 6ntibody titers (EF6, P4ES6 or agglutination) show fourfold increase to 030G. in two>thirds of patients in - w!s and in all patients in < w!s and such a finding is evidence of recent infection= most useful for retrospective diagnosis or epidemiologic study but too late for clinical use. +ram stain of sputum shows few to moderate number of B@(s= bacteria are not seen because 4egionella stains poorly in clinical specimens. Bleural effusion may be bilateral in Q:1' of patients= usually small e#udates= culture and test for antigen (as in urine) should be performed. MCA ) 01,111/G1,111?cu mm in %:' of cases= leu!openia is a bad prognostic sign. @ild to moderate increase of serum 6ST, 64B, 4D, or bilirubin is found in T:1' of patients. ypoalbuminemia of ,G.: gm?d4. Decreased serum phosphorus and sodium occurs in T:1' of patients. Diagnosis should be suspected in pneumonia patients with decreased serum phosphorus, abnormal liver function tests, and bradycardia. Broteinuria occurs in T:1' of patients= microscopic hematuria. 7enal failure and DEA are unusual complications. ASF is normal. NASOPHARYNGITIS, AC'TE Due To Cacteria (e.g., +roup 6 beta>hemolytic streptococci 5causes 01/-1' of cases seen by doctors8, . influenIae, @. pneumoniae, etc.). (@ere presence of staphylococci, pneumococci, alpha> and beta>hemolytic streptococci 5other than groups 6, A, and +8 in throat culture does not establish them as cause of pharyngitis and does not warrant antibiotic treatment.) Dirus (e.g., PCD, A@D, adenovirus, 7SD, SD, co#sac!ievirus) @. pneumoniae A. pneumoniae (formerly TM67 agent) Fungus, allergy, foreign body, trauma, neoplasm Ediopathic (no cause is identified in T:1' of cases) M%cr"sc"p%c E#a$%!a*%"! "+ S*a%!ed Nasa, S$ear 4arge numbers of eosinophils suggest allergy. Does not correlate with blood eosinophilia. Posinophils and neutrophils suggest chronic allergy with superimposed infection. 4arge numbers of neutrophils suggest infection. +ram stain and culture of pharyngeal e#udate may show significant pathogen. NEONATAL RESPIRATORY DISTRESS SYNDROME (RDS) ypo#emia ypercapnia and acidosis in severe cases pFG is maintained between :1/%1 mm g to minimiIe retinal damage. 4aboratory findings due to complications (e.g., hypoglycemia, hypocalcemia, acidosis, anemia) PLE'RAL EFF'SION See Fig. <>0, Table <>0, Table <>G and Table <>-. Fig. <>0. 6lgorithm for pleural effusion. Table <>0. Bleural Fluid Findings in Darious Alinical Aonditions Table <>G. Aomparison of UTypicalVa Findings in Transudates and P#udatesb Table <>-. Aomparison of Tumor @ar!ers in Darious Bleural Pffusions N"r$a, Va,-es Specific gravity 0.101/0.1G< Total protein 6lbumin 1.-/*.0 gm?d4 +lobulin :1/%1' Fibrinogen -1/*:' p <../%.< The underlying cause of an effusion is usually determined by first classifying the fluid as an e#udate or a transudate. 6 transudate does not usually re9uire additional testing but e#udates always do. Tra!s-da*e Aongestive heart failure (causes 0:' of cases);acute diuresis can result in pseudoe#udate Airrhosis with ascites (pleural effusion in T:' of these cases);rare without ascites (ephrotic syndrome Parly (acute) atelectasis Bulmonary embolism (some cases) Superior vena cava obstruction ypoalbuminemia Beritoneal dialysis;occurs within *. hrs of initiating dialysis Parly mediastinal malignancy @isplaced subclavian catheter @y#edema (rare cause) Aonstrictive pericarditis;effusion is bilateral Urinothora#;due to ipsilateral +U tract obstruction E#-da*e Bneumonia, malignancy, pulmonary embolism, and +E conditions (especially pancreatitis and abdominal surgery, which cause &1' of all e#udates) Enfection (causes G:' of cases) Cacterial pneumonia Barapneumonic effusion (empyema) TC 6bscess (subphrenic, liver, spleen) Diral, mycoplasmal, ric!ettsial Barasitic (ameba, hydatid cyst, filaria) Fungal effusion (Aoccidioides, Aryptococcus, istoplasma, Clastomyces, 6spergillus= in immunocompromised host, 6spergillus, Aandida, @ucor) Bulmonary embolism?infarction (eoplasms (metastatic carcinoma, especially breast, ovary, lung= lymphoma, leu!emia, mesothelioma, pleural endometriosis) (causes *G' of cases) Trauma (penetrating or blunt) emothora#, chylothora#, empyema, associated with rupture of diaphragm Emmunologic mechanisms 7heumatoid pleurisy (:' of cases) S4P 6fter myocardial infarction or cardiac surgery Fther collagen vascular diseases occasionally cause effusions (e.g., Megener"s granulomatosis, SKSgren"s syndrome, familial @editerranean fever, Ahurg>Strauss syndrome, mi#ed connective tissue disease) Dasculitis epatitis Sarcoidosis (rare cause= may also be transudate) Familial recurrent polyserositis Drug reaction (e.g., nitrofurantoin hypersensitivity, methysergide) Ahemical mechanisms Uremic Bancreatic (pleural effusion occurs in T01' of these cases) Psophageal rupture (high salivary amylase and p ,%.-1 that approaches <.11 in *./ %G hrs) Subphrenic abscess 4ymphatic abnormality Erradiation @ilroy"s disease Nellow nail syndrome (rare condition of generaliIed hypoplasia of lymphatic vessels) EnKury 6sbestosis 6ltered pleural mechanics 4ate (chronic) atelectasis Trapped lung Pndocrine ypothyroidism @ovement of fluid from abdomen to pleural space @eigs" syndrome (protein and specific gravity are often at transudate>e#udate border but usually not transudate) Urinothora# Aancer Bancreatitis, pancreatic pseudocyst Un!nown (T0:' of all e#udates) Airrhosis, pulmonary infarct, trauma, and connective tissue diseases comprise T&' of all cases. E#-da*es T.a* Ca! Prese!* as Tra!s-da*es Bulmonary embolism (2G1' of cases);due to atelectasis ypothyroidism;due to my#edema heart disease @alignancy;due to complications (e.g., atelectasis, lymphatic obstruction) Sarcoidosis;stage EE and EEE Bleural fluid analysis results in definitive diagnosis in TG:' and a probable diagnosis in another :1' of patients= may help to rule out a suspected diagnosis in -1'. L"ca*%"! Typically left>sided;ruptured esophagus, acute pancreatitis, 76. Bericardial disease is left>sided or bilateral= rarely e#clusively right>sided. Typically right>sided or bilateral;congestive heart failure (if only on left, consider that right pleural space may be obliterated or patient has another process, e.g., pulmonary infarction). Typically right>sided;rupture of amebic liver abscess. Gr"ss Appeara!ce Alear, straw>colored fluid is typical of transudate. Aloudy, opa9ue appearance indicates more cell components. Cloody fluid suggests malignancy, pulmonary infarct, trauma, postcardiotomy syndrome= also uremia, asbestosis, pleural endometriosis. Cloody fluid from traumatic thoracentesis should clot within several minutes, but blood present more than several hours has become defibrinated and does not form a good clot. (onuniform color during aspiration and absence of hemosiderin>laden macrophages and some crenated 7CAs also suggest traumatic aspiration. Ahylous (mil!y) fluid is usually due to trauma (e.g., auto accident, postoperative) but may be obstruction of duct (e.g., especially lymphoma= metastatic carcinoma, granulomas). Bleural fluid triglyceride 2001 mg?d4 or triglyceride pleural fluid to serum ratio 2G occurs only in chylous effusion (seen especially within a few hours after eating). 6fter centrifugation, supernatant is white due to chylomicrons, which also stain with Sudan EEE. P9uivocal triglyceride levels (<1/001 mg?d4) may re9uire a lipoprotein electrophoresis of fluid to demonstrate chylomicrons diagnostic of chylothora#. Triglyceride ,:1 mg?d4 e#cludes chylothora#. UBseudochylousV in chronic inflammatory conditions (e.g., rheumatoid pleurisy, TC, chronic pneumothora# therapy for TC) due to either cholesterol crystals (rhomboid shaped) in sediment or lipid>containing inclusions in leu!ocytes. Distinguish from chylous effusions by microscopy. Fluid may have lustrous sheen. Mhite fluid suggests chylothora#, cholesterol effusion, or empyema. Clac! fluid suggests 6spergillus niger infection. +reenish fluid suggests biliopleural fistula. Burulent fluid indicates infection. 6nchovy (dar! red>brown) color is seen in amebiasis, old blood. 6nchovy paste in ruptured amebic liver abscess= amebas found in ,01'. Turbid and greenish yellow fluid is classical for rheumatoid effusion. Turbidity may be due to lipids or increased MCAs= after centrifugation, a clear supernatant indicates MCAs as cause= white supernatant is due to chylomicrons. Dery viscous (clear or bloody) fluid is characteristic of mesothelioma. Debris in fluid suggests rheumatoid pleurisy= food particles indicate esophageal rupture. Aolor of enteral tube food or central venous line infusion due to tube or catheter entering pleural space. Od"r Butrid due to anaerobic empyema 6mmonia due to urinothroa# Pr"*e%!, A,/-$%!, Lac*a*e De.&dr"0e!ase See Table <>G. Mhen e#udate criteria are met by 4D but not by protein, consider malignancy and parapneumonic effusions. Dery high pleural fluid 4D (20111 U?4) occurs in empyema, rheumatoid pleurisy, paragonimiasis= sometimes with malignancy= rarely with TC. G,-c"se Same concentration as serum in transudate Usually normal but -1/:: mg?d4 or pleural fluid to serum ratio ,1.: and p ,%.-1 may be found in TC, malignancy, S4P= also esophageal rupture= lowest levels may occur in empyema and 76. Therefore, only helpful if very low level (e.g., ,-1). 1/01 mg?d4 highly suspicious for 76 (see 7heumatoid Pffusion). pH 4ow p (,%.-1) always means e#udate, especially empyema, malignancy, rheumatoid pleurisy, S4P, TC, esophageal rupture. Psophageal rupture is only cause of p close to <.1= collagen vascular disease is only other cause of p ,%.1. p ,%.01 in parapneumonic effusion indicates need for tube drainage. En malignant effusion, p ,%.-1 is associated with short survival time, poorer prognosis, and increased positive yield with cytology and pleural biopsy= tends to correlate with pleural fluid glucose ,<1 mg?d4. A$&,ase Encreased (pleural fluid to serum ratio 20.1 and may be 2: or pleural fluid greater than upper limit of normal for serum) 6cute pancreatitis;may be normal early with increase over time. Bancreatic pseudocyst;always increased, may be 2011,111 U?4. 6lso perforated peptic ulcer, necrosis of small intestine (e.g., mesenteric vascular occlusion)= 01' of cases of metastatic cancer and esophageal rupture. EsoenIyme studies Bancreatic type amylase is found in acute pancreatitis and pancreatic pseudocyst. Salivary type amylase is found in esophageal rupture and occasionally in carcinoma of ovary or lung or salivary gland tumor. Should be determined in undiagnosed left pleural effusions. O*.er C.e$%ca, De*er$%!a*%"!s Aholesterol ,:: mg?d4 is said to be found in transudates and 2:: mg?d4 in e#udates. AP6 201 ng?m4 has specificity of 2&:' and sensitivity of :*/011' for lung cancer, .-' for breast cancer, 011' for +E tract cancers. @ay also be increased in empyema and parapneumonic effusions. A0G: tumor antigen (A6>0G:=) has sensitivity of %0' and specificity of &&' for non>mucinous epithelial ovarian carcinoma. Aombined AP6 and A6>0G: have sensitivity for detection of malignant effusions due to carcinomas of lung, breast, +E tract, and ovary of %:/011' and specificity of &.'. @ay indicate primary site when the source is un!nown or cytology is negative (Table <>-). Fther tumor mar!ers have been suggested for diagnosis of cancer, but value not established (e.g., acid phosphatase in prostatic cancer, hyaluronic acid in mesothelioma, beta G>microglobulin, etc.) 6cid mucopolysaccharides (especially hyaluronic acid) may be increased (20G1 Wg?m4) in mesotheliomas. Emmune comple#es (measured by 7aKi cell, A09 component of A, 7E6, etc.) are often found in e#udates due to collagen vascular diseases (S4P, 76). 76 late# agglutination tests show fre9uent false>positives and should not be ordered. Fccasionally late# agglutination for bacterial antigens is useful. +as>li9uid chromatography has been reported to show butyric, isobutyric, propionic, and isovaleric acids in anaerobic acute bacterial infection and increased lactic and acetic acid levels in aerobic infections. Ce,, C"-!* Total MCA count is almost never diagnostic. 201,111?cu mm indicates inflammation, most commonly with pneumonia, pulmonary infarct, pancreatitis, postcardiotomy syndrome. 2:1,111?cu mm is typical only in parapneumonic effusions, usually empyema. Ahronic e#udates (e.g., malignancy and TC) are usually ,:111?cu mm. Transudates are usually ,0111?cu mm. :111/<111 7CAs?cu mm needed to give red appearance to pleural fluid Aan be caused by needle trauma producing G m4 of blood in 0111 m4 of pleural fluid. 2011,111 7CAs?cu mm is grossly hemorrhagic and suggests malignancy, pulmonary infarct, or trauma but occasionally seen in congestive heart failure alone. emothora# (pleural fluid to venous ct ratio 2G) suggests trauma, bleeding from a vessel, bleeding disorder, or malignancy but may be seen in same conditions as above. S$ears Mright"s stain differentiates B@(s from mononuclear cells= cannot differentiate lymphocytes from monocytes. @ononuclear cells predominate in transudates and chronic e#udates (lymphoma, carcinoma, TC, rheumatoid conditions, uremia). 2:1' is seen in two>thirds of cases due to cancer. 2.:/&1' suggests TC, lymphoma, sarcoidosis, rheumatoid causes. B@(s predominate in early inflammatory effusions (e.g., pneumonia, pulmonary infarct, pancreatitis, subphrenic abscess). 6fter several days, mesothelial cells, macrophages, lymphocytes may predominate. 4arge mesothelial cells 2:' are said to rule out TC (must differentiate from macrophages). 4ymphocytes 2.:' suggests TC, lymphoma, sarcoidosis, chronic rheumatoid pleurisy, yellow nail syndrome, chylothora#. :1/%:' in 2:1' of cases of carcinoma. Posinophils in pleural fluid (201' of total MCAs) is not diagnostically significant. @ay mean blood or air in pleural space (e.g., pneumothora# 5most common8, repeated thoracenteses, traumatic hemothora#). Et also is said to be associated with asbestosis, pulmonary infarction, polyarteritis nodosa. Barasitic disease (e.g., paragonimiasis, hydatid disease, amebiasis, ascariasis). Fungal disease (e.g., histoplasmosis, coccidioidomycosis). Drug>related (e.g., nitrofurantoin, bromocriptine, dantrolene). Ediopathic effusion (in appro#imately one>third of cases= may be due to occult pulmonary embolism or asbestosis). Uncommon with malignant effusions. 7are with TC. (ot usually accompanied by stri!ing blood eosinophilia. @any diseases associated with blood eosinophilia infre9uently cause pleural effusion eosinophilia. Casophils 201' only in leu!emic involvement of pleura. Fccasionally lupus erythematosus (4P) cells ma!e the diagnosis of S4P. +ram stain for early diagnosis of bacterial infection. 6cid>fast smears are positive in G1' of tuberculous pleurisy. Aulture is often positive in empyema but not in parapneumonic effusions. Cacterial antigens may detect . influenIae type b, Streptococcus pneumoniae, several types of (eisseria meningitidis. Useful when viable organisms cannot be recovered (e.g., due to prior antibiotic therapy). C&*","0& Bositive in <1' of malignancies on first tap, .1' by third tap. Therefore should repeat taps with cytologic e#aminations if cancer is suspected. Es more sensitive than needle biopsy. Aombined with needle biopsy, increases sensitivity by ,01'.* (See Aarcinoma, Cronchogenic.) igh yield with adenocarcinoma, low yield with odg!in"s disease. 7heumatoid effusions3 cytologic triad of slender elongated and round giant multinucleated macrophages and necrotic bac!ground material with characteristically low glucose is said to be pathognomonic. @esothelial cells are nearly always absent. Flow cytometry assay for D(6 aneuploidy and staining with monoclonal antibodies (e.g., AP6, cyto!eratin) to distinguish malignant mesothelioma, metastatic tumor, and reactive mesothelial cells can be performed (note3 some malignant cells may be diploid). P,e-ra, F,-%d F%!d%!0s %! Var%"-s C,%!%ca, C"!d%*%"!s See Fig. <>0. T-/erc-,"s%s igh protein content;almost always 2*.1 gm?d4 Encreased lymphocytes 6cid>fast smears are positive in ,G1', and culture is positive in T<%' of cases= culture combined with histologic e#amination establishes the diagnosis in &:' of cases. (eedle biopsy can be performed without hesitation. 4arge mesothelial cells 2:' are said to rule out TC (must differentiate from macrophages). TC often presents as effusion, especially in youth= pulmonary disease may be absent= ris! of active pulmonary TC within : yrs is <1'. Ma,%0!a!c& Aan cause effusion by metastasis to pleura, causing e#udate>type fluid, or by metastasis to lymph nodes, obstructing lymph drainage and giving transudate>type fluid. 4ow p and glucose indicate a poor prognosis with short survival time. Aharacteristic effusion is moderate to massive, fre9uently hemorrhagic, with moderate MCA count with predominance of mononuclear cells= however, only half of malignant effusions have 7CA 201,111?cu mm. Aytology establishes the diagnosis in T:1' of patients. Aombined cytology and pleural biopsy give positive results in &1'. En some instances of suspected lymphoma with negative conventional test results, flow cytometric analysis of pleural fluid showing a monoclonal lymphocyte population can establish the diagnosis. @ucopolysaccharide level may be increased (normal ,0% mg?d4) in mesothelioma. 4ung and breast cancer and lymphoma cause %:' of malignant effusions= in <', no primary tumor is found. Bleural or ascitic effusion occurs in G1/-1' of patients with malignant lymphoma. AP6, A6>0G:;see Table <>-. P-,$"!ar& I!+arc* Pffusion occurs in :1' of patients with pulmonary infarct= is bloody in one>third to two>thirds of patients= often no characteristic diagnostic findings occur. Small volume, serous or bloody, predominance of B@(s, may show many mesothelial cells= this Utypical patternV is seen in only G:' of cases. C"!0es*%1e Hear* Fa%,-re Es predominantly right>sided or bilateral. Ef unilateral or left>sided in patients with congestive heart failure, rule out pulmonary infarct. P!e-$"!%as Barapneumonic effusions (e#udate type of effusion associated with lung abscess, bronchiectasis= T:' of bacterial pneumonias). 6erobic gram>negative organisms (Llebsiella, Pscherichia coli, Bseudomonas) are associated with a high incidence of e#udates (with :111/*1,111?cu mm, high protein, normal glucose, normal p) and resolve with antibiotic therapy. (onpurulent fluid with positive +ram stain or positive blood culture or low p suggests that effusion will become or behave li!e empyema. S. pneumoniae causes parapneumonic effusions in :1' of cases, especially with positive blood culture. Staphylococcus aureus has effusion in &1' of infants, :1' of adults= usually widespread bronchopneumonia. Streptococcus pyogenes has effusion in &1' of cases= massive effusion, greenish color. aemophilus influenIae has effusion in :1/%:' of cases. Diral or @ycoplasma pneumonia;pleural effusions develop in G1' of cases. 4egionnaires" disease;pleural effusion occurs in up to :1' of patients= may be bilateral. B. carinii pneumonia cases often have pleural effusion to serum 4D ratio 20.1 and pleural effusion to serum protein ratio ,1.:. p ,%.1 and glucose ,*1 mg?d4 indicate need for closed chest tube drainage even without grossly purulent fluid. p of %.1/%.G is 9uestionable indication and should be repeated in G* hrs, but tube drainage is favored if pleural fluid 4D 20111 U?4. Tube drainage is also indicated if fluid is grossly purulent or +ram stain or culture is positive. (ormal p is al!aline and may approach %.<. E$p&e$a Usually MCAs 2:1,111?cu mm, low glucose, and low p. Suspect clinically when effusion develops during ade9uate antibiotic therapy. En Broteus mirabilis empyema, high ammonia level may cause a p T..1. R.e-$a*"%d E++-s%"! See Table <>*. Table <>*. Aomparison of Bleural Fluid in 7heumatoid 6rthritis and Systemic 4upus Prythematosus (S4P) Found in T%1' of 76 patients at autopsy. P#udate is fre9uently turbid and may be mil!y. Alassic picture is cloudy greenish fluid with 1 glucose level. 4evel is ,:1 mg?d4 in .1' and ,G: mg?d4 in <<' of patients= is the most useful finding clinically. Failure of level to increase during ED glucose infusion distinguishes 76 from other causes. (onpurulent, nonmalignant effusions not due to TC or 76 almost always have glucose level 2<1 mg?d4. 7F may be present but may also be found in other effusions (e.g., TC, cancer, bacterial pneumonia). 7F titer X03-G1 or e9ual to or greater than serum level suggests rheumatoid pleurisy. 76 cells may be found (see Aytology). Aytologic e#amination for malignant cells and smears and cultures for bacteria, tubercle bacilli, and fungi are negative. (eedle biopsy usually shows nonspecific chronic inflammation but may show characteristic rheumatoid nodule microscopically. Fne>third of cases have parenchymal lung disease (e.g., interstitial fibrosis). Fther laboratory findings of 76 are found. Brotein level is 2- gm?d4. Encreased 4D (usually higher than in serum) is commonly found in other chronic pleural effusions and is not useful in differential diagnosis. S&s*e$%c L-p-s Er&*.e$a*"s-s J 4P cells are specific for S4P but test has poor sensitivity. J 6(6 titer X0<1 or pleural fluid to serum ratio 20.1 is suggestive but not diagnostic. PNE'MOCONIOSIS Ciopsy of lung, scalene lymph node;histologic, chemical, spectrographic, and radiographic diffraction studies, electron microscopy (e.g., silicosis, berylliosis= also metastatic tumor, sarcoidosis, TC, fungus infection) Cacterial smears and cultures of sputum (especially for tubercle bacilli) should be done. Aytologic e#amination of sputum and bronchoscopic secretions for malignant cells, especially s9uamous cell carcinoma of bronchus and mesothelioma of pleura 6sbestos bodies sometimes occur in sputum after e#posure to asbestos dust even without clinical disease. 6cute beryllium disease may show occasional transient hypergammaglobulinemia. Ahronic beryllium disease Secondary polycythemia Encreased serum gamma globulin Encreased urine calcium Encreased beryllium in urine long after beryllium e#posure has ended Encreased MCA if associated infection Secondary polycythemia or anemia Silicosis 6ssociated conditions QG:' have mycobacterial infections, half of which are nontuberculous. Encreased incidence of nocardiosis, cryptococcosis, sporotrichosis. 01' have connective tissue diseases (e.g., progressive systemic sclerosis, 76, S4P). Encreased incidence of 6(6, 7F, hypergammaglobulinemia. 6AP increased in one> third of patients. PNE'MONIA See Table <>:. Table <>:. Fpportunistic Bulmonary Enfections Due To Bac*er%a S. pneumoniae causes <1/%1' of bacterial pneumonia in patients re9uiring hospitaliIation. @ay cause TG:' of hospital>ac9uired cases of pneumonia. Clood culture positive in G:' of untreated cases during first -/* days. Staphylococcus causes ,0' of all acute bacterial pneumonia with onset outside the hospital but more fre9uent after outbrea!s of influenIa= may be secondary to measles, mucoviscidosis, prolonged antibiotic therapy, debilitating diseases (e.g., leu!emia, collagen diseases). Fre9uent cause of nosocomial pneumonia. Cacteremia in ,G1' of patients. . influenIae is important in <> to G*>mo age group= rare in adults e#cept for middle>aged men with chronic lung disease and?or alcoholism and patients with immunodeficiency (ED, multiple myeloma, chronic lymphocytic leu!emia 5A448). Aan mimic pneumococcal pneumonia= may be isolated with S. pneumoniae. +ram>negative bacilli (e.g., L. pneumoniae, enterobacteria, P. coli, B. mirabilis, Bseudomonas aeruginosa) are common causes of hospital>ac9uired pneumonia but unli!ely outside the hospital. L. pneumoniae causes 0' of primary bacterial pneumonias, especially in alcoholic patients and patients with upper lobe pneumonia= tenacious red>brown sputum is typical. Tubercle bacilli 4egionella pneumophila @. pneumoniae;most common in young adult male population (e.g., armed forces camps) A. pneumoniae, Ahlamydia psittaci Fthers (e.g., streptococcosis, tularemia, plague) See Table <>:. V%r-ses EnfluenIa, parainfluenIa, adenoviruses, 7SD, echovirus, co#sac!ievirus, reovirus, A@D, viruses of e#anthems, herpes simple#, hantavirus R%c2e**s%ae $ fever is most common in endemic areas= typhus. F-!0% B. carinii, istoplasma, and Aoccidioides in particular= Clastomyces, 6spergillus. Pr"*"3"a!s To#oplasma Underlying Aondition Frganism Fbstructive cancer S. pneumoniae, . influenIae, @. catarrhalis, anaerobes 6lcoholism S. pneumoniae, . influenIae, Llebsiella spp., 4egionella spp., anaerobes, @. tuberculosis ED infection S. pneumoniae, . influenIae, S. aureus, gram>negative bacilli, B. carinii, @. tuberculosis and @6E (mycobacterium avium> intracellulare), To#oplasma gondii, Aryptococcus, (ocardia, A@D, histoplasmosis, Aoccidioides immitis, 4egionella, @. catarrhalis, 7hodococcus e9ui 6typical pneumonia @. pneumoniae, A. psittaci, A. pneumoniae, Ao#iella bur>netii, Francisella tularensis, many viruses La/"ra*"r& F%!d%!0s MCA is fre9uently normal or slightly increased in nonbacterial pneumonias= considerable increase in MCA is more common in bacterial pneumonia. En severe bacterial pneumonia, MCA may be very high or low or normal. Cecause individual variation is considerable, it has limited value in distinguishing bacterial and nonbacterial pneumonia. Urine protein, MCAs, hyaline and granular casts in small amounts are common. Letones may occur with severe infection. Ahec! for glucose to rule out underlying diabetes mellitus. Sputum reveals abundant MCAs in bacterial pneumonias. +ram stain shows abundant organisms in bacterial pneumonias (e.g., Bneumococcus, Staphylococcus). Aulture sputum for appropriate bacteria. Sputum that contains many organisms and MCAs on smear but no pathogens on aerobic culture may indicate aspiration pneumonia. Sputum is not appropriate for anaerobic culture. En all cases of pneumonia, blood culture and sputum culture and smear for +ram stain should be performed before antibiotic therapy is started. Fptimum specimen of sputum shows 2G: B@(s and Q: s9uamous epithelial cells?4BF (01Y magnification), but 201 B@(s and ,G: epithelial cells may be considered acceptable sputum specimen. 2G: epithelial cells indicate unsatisfactory specimen from oropharyn# which should not be submitted for culture. Ef good sputum specimen is obtained, further diagnostic microbiological tests are usually not performed. (asopharyngeal aspirate may identify S. pneumoniae with few false positives but S. aureus and gram>negative bacilli often represent false>positive findings. En . influenIae pneumonia, sputum culture is negative in 2:1' of patients with positive cultures from blood, pleural fluid, or lung tissue, and may be present in the sputum in the absence of disease. Transtracheal aspiration (puncture of cricothyroid membrane) generally yields a faster, more accurate diagnosis. Brotected brush bronchoscopy and C64 have high sensitivity. Diagnostic lung puncture to determine specific causative agent as a guide to antibiotic therapy may be indicated in critically ill children. Fpen lung biopsy is gold standard with &%' accuracy but 01' complication rate. For pleural effusions that are aspirated, +ram stain and culture should also be performed. 7espiratory pathogens isolated from blood, pleural fluid, or transtracheal aspirate (e#cept in patients with chronic bronchitis) or identified by bacterial polysaccharide antigen in urine may be considered the definite causal agent. Urine testing for capsular antigen from S. pneumoniae or type C . influenIae by late# agglutination may be helpful. Bositive in T&1' of bacteremic pneumococcal pneumonias and *1' of nonbacteremic pneumonias. @ay be particularly useful when antibiotic therapy has already begun. 6cute phase serum should be stored at onset. Ef causal diagnosis is not established, a convalescent phase serum should be ta!en. 6 *Y increase in antibody titer establishes the causal diagnosis (e.g., 4. pneumophila, Ahlamydia spp., respiratory viruses 5including influenIa and 7SD8), @. pneumoniae. Serologic tests to determine whether pneumonia is due to istoplasma, Aoccidioides, etc. PNE'MONIA, LIPID Sputum shows fat>containing macrophages that stain with Sudan. They may be present only intermittently= therefore, e#amine sputum more than once. P'LMONARY ALVEOLAR PROTEINOSIS (7are disease characteriIed by amorphous, lipid>rich, proteinaceous material in alveoli) B6S/positive material appears in sputum. BSB dye inKected intravenously is e#creted in sputum for long periods of time. C64 fluid contains increased total protein, albumin, phospholipids, and AP6. 7ecently antibodies to surfactant protein 6 (P4ES6 assay) in sputum and C64 have been reported to be highly specific. Serum AP6 is increased and correlates with C64 findings. 7eflects severity of disease and decreases with response to treatment. 7outine laboratory test findings are nonspecific. Serum 4D increases when protein accumulates in lungs and becomes normal when infiltrate resolves= correlates with serum AP6. Decreased arterial FG. Secondary polycythemia may occur. Diagnosis usually re9uires open lung biopsy. Plectron microscopy shows many lamellar bodies. 4aboratory findings due to superinfection. P'LMONARY EMBOLISM AND INFARCTION (o laboratory test is diagnostic. ,01' of emboli lead to infarction @easurement of arterial blood gases (obtained when patient is breathing room air) is the most sensitive and specific laboratory test. pFG ,.1 mm g in ..' of cases but normal pFG does not rule out pulmonary embolus. En appropriate clinical setting, pFG ,.. mm g (even with a normal chest radiograph) is indication for lung scans and search for deep vein thromboses. pFG 2&1 mm g with a normal chest radiograph suggests a different diagnosis. (ormal complete lung scans e#clude the diagnosis. ypocapnia and slightly elevated p. Encreased MCA in :1' of patients but is rarely 20:,111?cu mm (whereas in acute bacterial pneumonia is often 2G1,111?cu mm). Encreased PS7 Triad of increased 4D and bilirubin with normal 6ST is found in only 0:' of cases. Serum enIymes differ from those in acute myocardial infarction. Encreased serum 4D (due to isoenIymes 4D>G and 4D>-) in .1' of patients rises on first day, pea!s on second, normal by tenth day. Serum 6ST is usually normal or only slightly increased. cTn not increased. Serum indirect bilirubin is increased (as early as fourth day) to T: mg?d4 in G1' of cases. Bleural effusion may occur. P,as$a D4d%$er (ELISA "r La*e# A00,-*%!a*%"! 5%*s) Use Detects lysis of fibrin clot only, whereas fibrinogen degradation products test detects lysis of both fibrin clot and fibrinogen (see Ahapter 00). 6t appropriate cutoff level, has 2.1' sensitivity but only T-1' specificity. (egative predictive value 2&1'= normal test useful in e#cluding pulmonary embolism in patients with low pretest probability. Dalue less than cutoff level (which varies with assay !it) obviates need for pulmonary angiography. Encreased En Deep venous thrombosis DEA with fibrinolysis 7enal, liver, or cardiac failure @aKor inKury or surgery Enflammation (e.g., arthritis, cellulitis), infection (e.g., pneumonia) Thrombolytic therapy @easurements of serum AL, 4D, and fibrin products are not indicated routinely as they do not have sufficient sensitivity or specificity to be of diagnostic value. Encreased serum 64B (heat labile derived from vascular endothelium) during reparative phase */ 01 days after onset. Serum ++T may similarly increased. Bleural effusion occurs in one>half of patients= bloody in one>third to two>thirds of cases= typical pattern in only one>fourth of cases. These laboratory findings depend on the siIe and duration of the infarction, and the tests must be performed at the appropriate time to detect abnormalities. 4aboratory findings due to predisposing conditions, e.g., @alignant tumors. Bregnancy. Use of estrogens. ypercoagulable conditions, e.g., Bolycythemia vera Dysfibrinogenemias Brotein A or S deficiency 6ntithrombin EEE deficiency Splenectomy with thrombocytosis See discussion of fat embolism and phlebothrombosis of leg veins. SIN'SITIS, AC'TE Due To Fften precipitated by obstruction due to viral U7E, allergy, foreign body. S. pneumoniae and . influenIae cause 2:1' of cases= also anaerobes, S. aureus, S. pyogenes (group 6). @. catarrhalis causes TG1' of cases in children Diruses cause T01/G1' of cases B. aeruginosa and . influenIae are predominant organisms in cystic fibrosis patients. @ucor spp., 6spergillus spp. should be ruled out in patients with diabetes or acute leu!emia and in renal transplant recipients. 6naerobes (e.g., streptococci, Cacteroides spp.) occur in T:1' of cases of chronic sinusitis. (eedle aspiration of sinus is re9uired for determination of organism. Aulture of nose, throat, and nasopharyn# specimens do not correlate well. @ucosal biopsy may be indicated if aspirate is not diagnostic in unresponsive patient with acute infection. 0 Lahn FM, Oones O@. Cronchoalveolar lavage in the rapid diagnosis of lung disease. 4ab @anage Oune 0&.<3-0. G @enIies 7, Aharbonneau @. Thoracoscopy for the diagnosis of pleural disease. 6nn Entern @ed 0&&0=00*3G%0. - Cernard +7, 6rtigas 6, Crigham L4, et al. The 6merican>Puropean Aonsensus Aonference on 67DS3 definitions, mechanisms, relevant outcomes and clinical trial coordination. 6m O 7espir Arit Aare @ed 0&&*=0*&3.0.. * Bra!esh UCS, 7eiman @. Aomparison of needle biopsy with cytologic analysis for the evaluation of pleural effusion3 6nalysis of *0* cases. @ayo Alin Broc 0&.:=<130:..