Laboratory Tests for Respiratory Modif

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LABORATORY TESTS FOR RESPIRATORY SYSTEM DISEASE

BRONCHOSCOPY AND BRONCHOALVEOLAR LAVAGE (BAL) 1

(Saline lavage of lung subsegment via fiberoptic bronchoscope)

Use

For biopsy of endobronchial tumor in which obstruction may cause secondary pneumonia witheffusion 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.

• 21' 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 or6spergillus 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 (S) E and EE (stains bronchial epithelial cellsand macrophages), and A@ (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@), tumor.

il red 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 AG, which

displaces G

6lveolar hypo#ia (e.g., high altitude, gaseous inhalation)

Bulmonary diffusion abnormalities (e.g., interstitial lung disease)3 supplemental G usually

improves pG

7ight>to>left shunt3 supplemental G has no effect= re9uires positive end>e#piratory pressure

• Aongenital anomalies of heart and great vessels

• 6c9uired (e.g., 67DS)

entilation>perfusion mismatch3 supplemental G usually improves pG

• 6irflow obstruction (e.g., chronic obstructive pulmonary disease 5ABD8, asthma)

• Enterstitial inflammation (e.g., pneumonia, sarcoidosis)

• ascular 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., ABD, 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'MAolor 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 7S 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 (F6) 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 pG (partial pressure arterial G)?FiG (fraction inspired G 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. ccurs in G-' of cases of

gram>negative bacteremia.Static pulmonary compliance :1 m4?cm G 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 G= then profound ano#emia with pG :1 mm g on room air.

C64 shows increased B@s (Q 1'). Posinophilia occurs occasionally. pportunistic organisms

may be found if presents as 67DS.

ASTHMA, BRONCHIAL

Parliest change is decreased pAG with respiratory al!alosis with normal pG. Then pG

decreases before pAG increases.

Mith severe episode

• yperventilation causes decreased pAG in early stages (may be -: mm g).

• 7apid deterioration of patient"s condition may be associated with precipitous fall in

pG and rise in pAG (2*1 mm g).

• pG <1 mm g may indicate severe attac! or presence of complication.

• ormal pAG suggests that the patient is tiring.

6cidemia and increased pAG 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 Toiruses (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

• iruses

• @. 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 oflung cancer. Brincipal uses are to monitor response to therapy and to correlate with



staging. alues : ng?m4 correlate with survival over - yrs compared to values 2:

ng?m4. alues 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

thers (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 agentsClood 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 whomendotracheal 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 E (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

• pG decreased and pAG increased

• Ultimate development of respiratory acidosis

• Secondary polycythemia

• Aor pulmonale

GOODPAST'RES 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.

ther 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>Schnlein 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 pG, 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.)

ptimal diagnosis combines culture, detection of antigen and DF6 or BA7 of sputum, C64 fluid,

or pleural fluid, and detection of antigen in urine.

rganism 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

%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 :1' of patients.

ypoalbuminemia of G.: gm?d4.

Decreased serum phosphorus and sodium occurs in :1' of patients.

Diagnosis should be suspected in pneumonia patients with decreased serum phosphorus, abnormal

liver function tests, and bradycardia.

Broteinuria occurs in :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.)

irus (e.g., PC, A@, adenovirus, 7S, S, co#sac!ievirus)

@. pneumoniaeA. pneumoniae (formerly TM67 agent)

Fungus, allergy, foreign body, trauma, neoplasm

Ediopathic (no cause is identified in :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

pG 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 arious Alinical Aonditions

Table <>G. Aomparison of TypicalVa Findings in Transudates and P#udatesb

Table <>-. Aomparison of Tumor @ar!ers in arious 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#udatesalways 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 :' of these cases);rare without ascites

ephrotic syndrome

Parly (acute) atelectasisBulmonary 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*eBneumonia, 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)

• iral, 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

• ther collagen vascular diseases occasionally cause effusions (e.g., Megener"s

granulomatosis, SKgren"s syndrome, familial @editerranean fever, Ahurg>Strauss

syndrome, mi#ed connective tissue disease)

• asculitis

• 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 01' 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 (0:' of all e#udates)

Airrhosis, pulmonary infarct, trauma, and connective tissue diseases comprise &' of all cases.

E#-da*es T.a* Ca! Prese!* as Tra!s-da*es

Bulmonary embolism (2G1' of cases);due to atelectasisypothyroidism;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 G:' 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.





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= collagenvascular 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 <>-).

ther 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.

ccasionally 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 lymphocytesfrom 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.

ccasionally 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 D6 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).

Pe-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 <%' 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 indicatea 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 :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

typical patternV is seen in only G:' of cases.

C"!0es*%e 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=:' 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.

iral 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 .1.

R.e-$a*"%d E++-s%"!

See Table <>*.

Table <>*. Aomparison of Bleural Fluid in 7heumatoid 6rthritis and Systemic 4upus

Prythematosus (S4P)



Found in %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 E glucose infusion distinguishes 76 from

other causes. onpurulent, nonmalignant effusions not due to TC or 76 almost always haveglucose 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. ne>third of cases have parenchymal lung disease (e.g.,

interstitial fibrosis).

ther 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 66 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 66, 7F, hypergammaglobulinemia. 6AP increased in one>

third of patients.

PNE'MONIA

See Table <>:.

Table <>:. pportunistic Bulmonary Enfections

Due To

Bac*er%a

S. pneumoniae causes <1/%1' of bacterial pneumonia in patients re9uiring hospitaliIation. @ay

cause G:' 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 butmore 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 (E, 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

thers (e.g., streptococcosis, tularemia, plague)

See Table <>:.

V%r-ses

EnfluenIa, parainfluenIa, adenoviruses, 7S, echovirus, co#sac!ievirus, reovirus, A@, 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 rganism

bstructive cancer S. pneumoniae, . influenIae, @. catarrhalis, anaerobes

6lcoholism S. pneumoniae, . influenIae, Llebsiella spp., 4egionella spp.,



anaerobes, @. tuberculosis

E infection S. pneumoniae, . influenIae, S. aureus, gram>negative bacilli, B.

carinii, @. tuberculosis and @6E (mycobacterium avium>

intracellulare), To#oplasma gondii, Aryptococcus, ocardia, A@,

histoplasmosis, Aoccidioides immitis, 4egionella, @. catarrhalis,

7hodococcus e9ui6typical 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. ptimum 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.

pen 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 &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 7S8), @. 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 G.

• 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.• pG 1 mm g in ' of cases but normal pG does not rule out pulmonary

embolus. En appropriate clinical setting, pG mm g (even with a normal chest

radiograph) is indication for lung scans and search for deep vein thromboses. pG

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 : mg?d4 in G1' of cases.

Bleural effusion may occur.

Pas$a D4d%$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 21' sensitivity but

only -1' specificity. egative predictive value 2&1'= normal test useful in e#cluding

pulmonary embolism in patients with low pretest probability. alue less than cutoff level (whichvaries 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 nothave 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'TEDue To



ften 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 G1' of cases in children

iruses cause 01/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 :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*&30.

* 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:.

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Laboratory Tests for Respiratory Modif