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 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:..