Principles of Respiratory Medicine Farokh Erach Udwadia, Zarir F Udwadia, Anirudh F Kohli, Khyati Shah
INDEX
Page numbers followed by f refer to figure, fc refer to flowchart, and t refer to table.
A
Abdomen, computed tomography of 226f, 430f, 620f
Abram's needle 914
Abscess 419, 627, 845
hepatic 430f
intrahepatic 904
multiple 370f
subphrenic 904
Accuhalers 471
Acetazolamide 1010
Acetic acid 984
Acetylator status 231
Acetylcholine 941, 1052
Acetylcysteine 787
Achalasia of Cardia 277, 278
Acid 118
concept of 116
gastric contents, aspiration of 268
maltase deficiency 1054
rain 993
Acid-base
balance 115, 118, 119f
normal 115
disturbances 115, 122, 543
clinical features of 122
management of 122
mixed 121
equilibrium 119
homeostasis 115
measurements 119
Acidemia 118, 120f
Acid-fast bacilli 216, 220f, 273f, 316, 360, 659f, 909
Acidosis 192
chronic metabolic 885
compensated
metabolic 121f
respiratory 120f
Acinetobacter 321, 904
baumannii 337, 383, 385
Acquired immunodeficiency syndrome 216, 248, 391, 392, 396, 831, 918, 924
Acrylate glue 1020
Acrylonitrile 606
Actinomyces 266, 276
israelii 276, 911
Acute abdominal distension 283
Acute asthma 462, 476, 483
attack 483
management of 483t
Acute circulatory failure 283
Acute community-acquired pneumonia, complications of 283t
Acute cough
causes of 174t
diagnostic evaluation of 174
Acute crisis 831
Acute dyspnea 190, 192
causes of 192t
Acute hypoxemic respiratory failure 780, 782, 810
causes of 782t
Acute left ventricular failure 192, 283, 284, 537
Acute mediastinitis 957
etiology of 957t
Acute respiratory crisis, management of 543t
Acute respiratory distress syndrome 37, 198, 273, 283, 299, 313, 314, 335, 423426, 433, 434f, 440, 587, 672, 700f, 773, 782, 803, 837, 838, 838t, 841f, 842f, 847t, 854, 867, 893, 906, 998, 1017, 1039, 1047
etiology of 840t
pathogenesis of 843fc
Acute respiratory failure 283, 536, 760, 761, 777, 792, 1057, 1059
clinical features of 785
complications of 786
management of 787, 787t
treatment of cause of 789
Acute severe asthma 482, 483, 490, 537, 570, 783, 810
clinical features of 462
ventilator support in 804
Acute thromboembolic lung disease, ventilator support in 804
Acyclovir 305
Adenocarcinoma 52f, 57f, 610, 611, 611f, 630f, 931
in situ 610, 611f
Adenoid cystic carcinoma 650
Adenopathy 91f, 163f, 214f, 683f
Adenosine
deaminase 901, 913
triphosphate 1007
stores of 136
Adenovirus 292, 302, 305, 311, 534, 580
Adjunctive therapy 297
Adrenal metastatic lesions 620
Adrenaline 483, 485
Adrenocorticotrophic hormone 621
Adriamycin 403
Adventitious sounds 200
Aedes aegypti mosquito 436
Agammaglobulinemia 355
Age-adjusted deaths 559f
Air bronchogram 54, 63, 63f, 270f, 664f
sign 34
Air conditioner lung 719, 720
Air embolism 773
Air-filled space 920
Air pollution 454, 608, 988
amount of 990
index of 989t
indoor 990
outdoor 506
Air quality
index 989t
standards 995t
Airflow
limitation 527, 704
obstruction 198
degree of 558
severe 487f
patterns of 103f
Air-space opacities, diagnosis of 34
Air-trapping, reducing 547
Airways 1034
adverse effects on 1019
and ventilation, management of difficult 798fc
clearance 362
contrasts 34
difficult 795
disease 67, 392, 447, 863, 871
inflammatory 886
obstructive 133, 593t, 782
small 69, 513
dynamic compression of 517f
dysfunction syndrome 984
reactive 982, 984t
emergency 792
ensuring patency of 565
epithelium 512
hyper-reactive 178
hyperresponsiveness 467, 499, 500, 508
measuring 464
infection 511
treatment of 566
inflammation 465t
noninvasive markers of 465
injury 1016
management 790, 800
obstruction 178, 189, 192, 363, 413, 507, 513, 527
diseases causing 189
element of 1043
management of 974
severe chronic 594
severity of 533
small 190
peripheral 515, 535
pressure 812f, 822f, 832
biphasic positive 289
release ventilation 818, 819
remodelling 458
features of 459f
resistance 102, 102, 145
measurement of 145f
sites of 104
responsiveness, methods of measuring 464
stents, bronchoscopic placement of 642
structural changes in 458
thickening 458
Akinesia 1048
Alae nasi 685f
Albumin 738
Albuterol 456
Alcaligenes xylosoxidans 561
Alcohol abuse 397f
Alcoholism 34, 267, 268, 290
Aldactone 556
Alkalemia 118
Alkalosis 118, 893
compensated metabolic 121f
Allergens 453
Allergic alveolitis, extrinsic 190, 306, 579, 656, 657, 987
Allergic aspergillus sinusitis 577
Allergic bronchopulmonary aspergillosis 306, 420, 568, 569, 571t, 572f, 573t, 574f, 575f, 745
diagnosis of 568
pathogenesis of 571fc
Allergic diseases 453
Allergic rhinitis 140, 374
Allergic status, measuring 464
Alpha-1 antitrypsin
deficiency 509, 511f
molecule 510
Alpha-fetoprotein 941
Alveolar arterial oxygen gradient 109, 827
Alveolar capillary membrane 144
Alveolar cells 106
Alveolar hemorrhage 65f, 192, 392, 845, 847, 867
pulmonary-renal syndrome with 885t
Alveolar hyperplasia, atypical 610
Alveolar hyperventilation 821
Alveolar hypoventilation 109, 518, 824, 889
disorders 749
Alveolar infiltrates 318fc
Alveolar macrophages 678
Alveolar microlithiasis 48f, 49f
Alveolar oxygen 108, 109
partial pressure 1007
Alveolar pressure 130f
Alveolar proteinosis 39f, 66f, 711, 845
diagnosis of 712
Alveolar recoil pressure 516f
Alveolar rupture 817
Alveolar ventilation 18, 107, 108
concept of 107f
Alveolar walls 100
Alveolitis
allergic 657
fibrosing 887
Amantadine 296
Ambrisentan 879
Amebiasis 840
pulmonary complication of 429f
Amebic empyema 430f
Amebic infection 427, 431
American College of Chest Physicians 624, 768
American College of Rheumatology 736
American Heart Association Guidelines for Advanced Cardiac Life Support 588
American Journal of Infection Control 332
American Society of Infectious Diseases 278
American Thoracic Society 140, 186, 200, 250, 278, 284, 286, 349, 461, 524, 655, 665t
Amicrofilaremia 415
Amikacin 234, 242, 245
Amino acid 510
Aminoglycoside 566, 1020
Aminophylline 483, 484
intravenous 484
Amiodarone 915, 1021, 1027
toxicity 1021f, 1023
Ammonia 984, 1002
Amniotic fluid embolism 889, 891, 893
Amodiaquine 427
Amoxicillin 242, 287, 340, 363, 374, 379, 443, 566
Amphoric breath sounds 199
Amphotericin 326, 377, 443
liposomal formulation of 432
lyophilized 327, 377
Amplification test 913
Amplified inflammatory response, nature of 519
Amylase 901
Amyloid 708
Amyloidosis 708, 709f
diffuse parenchymal 709, 710
isolated pulmonary 709
secondary 709
Anaphylactic reactions 15
Anaphylaxis 1019
Anaplastic lymphoma kinase 607
Ancylostoma duodenale 412
Anemia 188, 189, 192, 216, 252, 623, 740f
aplastic 312, 313
chronic 588
severe 587, 588
Anesthesia, general 588
Aneurysm 90
arteriovenous 627
cardiac 952
Aneurysmal dilatation 874
Aneurysmal portion, rupture of 181
Angina, unstable 587, 588
Angiocentric disease 61
Angiofollicular lymphoid hyperplasia 953
Angiograms, coronary 11f
Angiomyolipomas 703, 706, 708
Angiotensin-converting enzyme 132, 175, 178, 457, 677, 1051
inhibitors 178, 1019
Ankylosing spondylitis 191, 411, 412, 420, 859, 873, 874f, 886, 1045
Anorexia 233
Anthrax 444
bacillus 276
mediastinitis 959
spores 959
Antibiotic 538
choice of 286
resistance 381, 383, 386
managing 386
therapy 340, 362, 371
duration of 909
use of 340
use of 584
Antibody
defect 313
testing 296
Anti-centromere antibodies 868
Anticholinergic bronchodilator 550, 551, 552f
long-acting 551
Anticholinergic drug
long-acting 551
side effects of 551
Anticoagulant therapy 769t
Antidiuretic hormone 621
production 217
Antidotes, specific 1004
Antiepileptics 1017
Antigen
processing 720
test, rapid 296
Anti-glomerular basement membrane 739
Anti-inflammatory therapy 364
Anti-Koch's treatment 220f
Antimetabolites 1017
Antimicrobial therapy 288, 288t
Antimitotic cytotoxic drugs 1024
Antimony pentachloride 967
Antimony trichloride 967
Antineutrophilic cytoplasmic antibody 183, 735, 741, 746, 884, 918
Antinuclear antibody 741, 865
Antioxidant 553
Antiphospholipid antibody syndrome 759, 868
Antiretroviral drugs 393
Antiretroviral therapy 250, 251, 398
highly active 252, 252f, 351, 392
use of active 393
Anti-TNF therapy 693
Antitoxin, use of 440
Antitrypsin deficiency 509fc
Anti-tuberculosis drugs 233
first-line 229t
in vitro 349t
resistance surveillance 237
side effects of 233
Antiviral drugs 296
Anxiety 194, 786, 890
Aorta 160
arch of 26
ascending 28
Aortic aneurysm, ascending 874f
Aortic arch 25, 26, 751f
Aortic dissection 194
Aortic transection 1035f
Aortic wall 962
Aplasia 77
Apnea
trial of 486
witnessed 1067
Apneustic breathing 123
Appetite, loss of 552
Arachidonic acid 132
Arcolein 967
Arginine 475
Argon plasma cauterization 158
Aromatic amines 606
Arrhythmias 478, 543
cardiac 485, 543, 587, 1070
treatment of 557
ventricular 440
Arsenic 606, 608
Artemether 427
Arterial blood
decreased oxygen content of 588
gas 155, 270, 528, 535f, 750, 751, 759, 761, 762, 827, 846, 975, 1044
effects on 111
studies 1056
pressure 127
Arterial catheterization 168
Arterial oxygen 804
partial pressure of 806, 811, 815, 817, 818
saturation 282
Arteriogram, bronchial 23f
Arteriographic embolization 184, 185
Arteriography 184
Arteriovenous malformation 72f
Artery 32
centrilobular 32
esophageal 31
ipsilateral pulmonary 78
lower branch pulmonary 22f
Artesunate 426, 427
Arthralgia 688, 736, 1020
Arthritis 554
Arthropods 453
Artificial airways 791
disadvantages of 792
indications for 792t
maintaining 799
removal of 829
Artificial ventilation 788
Asbestos 608, 929, 977, 981
classes of 977t
crumbling 928
exposure 608
absence of 929
fibers 968f, 978
Asbestosis 657, 918, 968f, 977, 981
management of 982
risk of 979
Ascarial infection 411
Ascariasis 411
Ascaris lumbricoides 411, 420
Aseptic meningitis 295
Aspergilloma 54f, 180, 306, 308f, 324f
Aspergillosis 305
chronic necrotizing 974
invasive tracheobronchial 324
Aspergillus 266, 568570, 577
antigen 570
candida 313
clavatus 720
conidia 306
disease 306
flavus 323
fumigatus 305, 306, 323, 377, 569, 570, 572, 573, 577, 584, 911
hyphae 306
infection 306t, 308f, 317, 319, 324f, 327
niger 323
pneumonia, chronic necrotizing 306
sinusitis 577
skin test 577
specific immunoglobulin E 570
terreus 323
tracheobronchitis, diagnosis of 326t
Aspiration 267, 268, 332
bronchiolitis 583
pneumonia 268, 334f, 425, 435, 439, 840, 862, 889, 1049, 1058
complications of 367
recurrent 870
Aspirin 457, 1021
avoidance of 497
bronchospasm, severe 1021
Asthamatic pulmonary eosinophilia 420
Asthma 140, 158, 174, 176, 192, 449, 450, 452, 454, 455, 459f, 467, 467t, 472t, 478, 487, 488, 498, 499, 499f, 499t, 562, 584, 591t, 737, 744
allergic 482
mechanisms 496
aspirin induced 457, 496, 497
attack 487, 494, 495
typical 466
cardiac 468
chronic 491, 499, 508
clinical features 461
complementary medicines in 478
control 465, 478, 495
levels of 479t
death audits 494t
diagnosis of 451, 461, 462, 465, 577
differential diagnosis 466
difficult 490
distinguishing 466
drugs
cost 488t
used in 472
during pregnancy, management of 495
effect of 495
endotype, concept of 482
eosinophilic 558
epidemics 454
epidemiology of 449
etiopathogenesis 449, 453
exercise induced 478
fewer exacerbations of 572
genetic factors 452
global epidemiology 450
global initiative for 449
impact of 452
in pregnancy, treatment of 495
infections 453
insights and realities 488
life-threatening 456
like symptoms 463
management 466, 470, 481
mediators of 457
medical management of 489
medication 470, 471
side effects of 495
mild 569
mimic of 468
mistaken for 469
moderate-to-severe 474
non-allergic 482
nutrients 455
obesity 454
occupational 456, 965, 982, 983
pathogenesis of 457, 496
pathology of severe 490
phenotypes 465
physical examination 461
pollution 454
pre-existing 570
prevalence of 449451, 453, 454, 983
pulmonary eosinophilia in
extrinsic 728
intrinsic 728
related deaths 475
respiratory symptoms, epidemiology of 451
severe 462, 478, 577
attack of 463t
life-threatening 490
special types 490
symptoms 450, 451, 461
syndrome 481
treatment of 452, 474
trigger for 453, 455
types of 452, 490, 491
typical of 463
uncomplicated 573
uncontrolled 482t
variant of 175
ventilation in 486
work-aggravated 982
worsening 457
Asthmatic population 497
Astrup technique 119
Atelectasis 38, 40, 335, 439, 821, 824, 844, 898, 903
lower lobe 41, 45
obstructive 41f
right middle 45
round 55, 979
Atelectatic alveoli 110f
Atelectatic lobe 43
Atomic absorption spectrometry 995
Atopic disease 451
Atopy 499
Atovaquone 400
Atresia, bronchial 76
Atrial fibrillation 534
Atrial pressure, elevated right 694
Atropine sulfate 550
Attack
acute severe 462
apneic 439
dangerous 462
Attenuation 630
Atypical pneumonia 845
syndrome 270
Auscultation 199
Autoimmune
bodies, formation of 859
connective tissue disorders 182
disease 182, 688, 735
disorders 1025
Autonomic disturbances, management of 441
Autophagy, inhibitors of 707
Autopositive end-expiratory pressure 822
effects of 822
measurement of 822
methods of reducing 823
Avian flu 298
Avian influenza 298, 298t
Axial interstitium 57
Azathioprine 313, 688, 862, 866, 872, 1017
Azithromycin 350, 351, 363, 400, 445
Azoospermia 564
presence of obstructive 564
Azygous lobe fissure 24, 25f
B
Babesia babesiosis 431
Babesiosis 431
Bacillary disease, prevalence of 211
Bacillus anthracis 444
Bacillus calmette-guerin 345
vaccination 210
BACTEC system 228
Bacteremic spread 367
Bacteria
anaerobic 266, 276, 277
atypical 278
translocation of 846
typical 278
Bacterial infection 271, 354, 392, 394, 401, 431
Bacterial pleural exudates, management of 908
Bacterial pneumonia, secondary 295, 425
Bacterial sinusitis, complications of 376
Bag mask respiration 1032
Bagassosis 719, 720
Baggage malaria 426
Balloon
atrial septostomy 755
catheter 145
tamponade 184
Baloxavir 297
Bamboo spine 1045
Bangladesh short-course regimen 246
Bariatric surgery 1073
Barometric pressure 1007
Baroreceptors, arterial 125
Barotrauma 487, 518, 816, 823, 846
Basaloid 944
Basophils 570
B-cell lymphoma 392, 873f, 947
Beclomethasone 553
dipropionate 473
Bedaquiline 242, 244246
Behçet's disease 735, 747, 874, 874f, 875
Benzene 606
Benzo[a]pyrene 606
Benzodiazepine 848
Berlin definition 838
Berylliosis 657, 689
Beryllium disease 967, 968f
Beta carotene 608
Beta lactamase, extended spectrum 340, 385
Beta-agonists
long-acting 464, 474
short-acting 538
Bhopal gas tragedy 580, 999
Bicarbonate 120, 121
reabsorption of 117
Bilevel positive airway pressure 819, 927
Bilevel pressure ventilators 831
Biliary atresia, primary 876
Bill and Melinda Gates Foundation 254
Biologic therapy 887
Biological dusts 966
Biopsy 624, 626, 660, 740
multiple 901
procedure 164, 941
proof 745
proven pulmonary sarcoid 686f
results 192
Bioterrorism 959
Biotrauma 823
Birbeck granules 698f
Bird breeding 965
Bird-Fancier's disease 719, 720
Birt-Hogg-Dubé syndrome 705
Black lung disease 974
Bladder neck obstruction 688
Blastomyces dermatitidis 281, 305, 308
Blastomycosis 305, 308, 367
diagnosis of 309
skin lesions of 309
Bleaching agent 984
Bleeding 820
gastrointestinal 543, 824
Bleomycin 403, 1018, 1024, 1027
toxicity 1024f, 1025f
Blind nasal intubation 797
Blinded invasive procedures, role of 338
Blomia tropicalis 453
Blood 465
arterial 486
brain barrier 124
count, complete 176, 279, 360, 535, 741
culture 281, 327
positive 338
examination 716
expectoration of 180
flow very less 111
flow, distribution of 129f
gas 115
analysis 282
machine 901
gene signatures 259
glucose concentrations, low 901
loss 537, 824
monocytes, peripheral 969, 970
plasma of 119
pressure 815, 1069
reaches lungs 117
stream infection, central line-associated 331
tests, basic 192
urea-nitrogen 536
Blowing diastolic murmur 524
Blurred vision 1004
B-lymphocytes 521
Bochdalek hernia 73, 78
Body mass index 244, 558, 1064, 1068
Body plethysmography 142
Bone 696
eosinophilic granuloma of 696
marrow transplant 580
mineral density 473
pain 233f
scan 634
Bony rib cage 3
Bordetella pertussis 379
Bormal flow-volume loop 141f
Botulism 779, 1051, 1055
Brachial vein 166
Brachiocephalic artery 28
Brachiocephalic vein, left 29
Brachytherapy 158, 642
Bradycardia 785, 786
Bradykinin 132, 173
Brain
hemosiderin deposits in 1011
natriuretic peptide 752, 845
Brainstem strokes 1047
Breath
condensate 465
exhaled 465
shortness of 186, 196
sounds 199
abnormal 199
cavernous 199
stacking 1058
Breathing 533, 1034
disorders, sleep-related 1061, 1063, 1070
exercises 479, 555
reserve 147
sleep-disordered 749, 1063
test, rapid 155
work of 104, 827
Breathlessness 186, 196, 197, 269, 449, 522, 709, 868, 876, 887, 973f, 1010, 1016
complaint of 1033
British Medical Research Council 207
British Thoracic Society 284, 286
British Thoracic Society Sarcoidosis Study 692
Brittle asthma 490, 491, 491f, 492
types of 491
Brock syndrome 354
Bromocriptine 915
Bronchi 550
anatomy of 32
central 32
mucus plugging of 574
Bronchial artery 21, 184, 562
angiogram 23f
embolization 21
hypertrophy 181
Bronchial asthma 132, 189, 199, 468, 893
acute
episodes of 192
exacerbations of 570
severe 782
allergic 306
Bronchial breath sounds 199
Bronchial carcinoid 627
tumors 623
Bronchial carcinoma, primary 627
Bronchial fistula, biliary 429
Bronchial hyper-reactivity 464, 683
Bronchial hyper-responsiveness 449, 468
Bronchial mucus-secreting glands 951
Bronchial obstruction 38, 276
Bronchial responsiveness, nonspecific 984
Bronchial washing, positive cultures in 326
Bronchiectasis 68, 70f, 178, 181, 190, 225f, 283, 353, 356358, 359f, 360t, 363365, 375, 464, 501, 563f, 568, 569, 583, 864
antibiotics in 363t
bilateral extensive 358
causes of 357t
central 572
chronic suppurative 361
classic features of 359
congenital 356
cylindrical 353
diagnosis of 360
extensive bilateral 360
fibronodular 347
idiopathic 357
pathophysiology of 375f
prevalence of 353
representing traction 59f
types of 353
Bronchiectatic lobe, surgical resection of 365
Bronchiolar abnormalities 578
Bronchiolar disease 61, 69
Bronchiolar ulceration 181
Bronchiolar wall disorders 579t
Bronchioles 550, 578
Bronchiolitis 189, 192, 302, 305, 329, 392, 578, 582, 584, 886, 921
acute 579
infective 579, 580
cryptogenic constrictive 580
differential diagnosis of 584
exudative 70, 71f
obliterans 392, 501, 578, 579, 581f, 582f, 671, 1019
cryptogenic 580
organizing pneumonia 314, 655, 671, 845
obstructive 579
primary 578, 579, 582
secondary 579
Bronchitis 305, 379, 423, 500, 864
Bronchoalveolar lavage 158, 273f, 274, 279, 318, 319, 329, 349, 371, 393, 417f, 419, 432, 435, 449, 584, 625, 663, 678, 701, 716, 741, 972, 980
fluid 157f, 223
studies 724
Bronchoconstrictor agent, choice of 464
Bronchodilator 547, 580
aerosolized 527
effect 485
inhaled 547
long-acting 364
response 140
therapy, inhaled 538
Bronchograms 88f
Broncholith 214
Bronchopleural fistula 87, 88f, 369, 907, 925, 925f, 927t
peripheral 88f
Bronchopneumonia 439
eosinophilic 414f
Bronchoprovocation test 140
Bronchopulmonary infections 505, 507
Bronchoscopy 157, 158t, 182, 319, 369, 370, 624, 626, 642, 663, 931, 1039
fiberoptic 160, 282, 319, 616, 689
flexible 973
indications for 158t
role of 373
urgent 185
Bronchospasm 440, 483, 1043
acute 1019
severe 760
Bronchovascular structures 56
Bronchus 1038
right main 23
Broth-drug susceptibility assay 228
Brovasio enzyme 384
Brugia malayi 412, 413
Budd-Chiari syndrome 876, 903
Budesonide 473
Bulla 38, 66, 68f, 163, 921
Bullectomy 557
Bullous emphysema 66, 68f
Bullous myringitis 272, 277
Bupropion 547
Burkholderia cepacia 561, 567
complex 561, 566
Burkholderia pseudomallei 277, 371, 441443
Burkitt's lymphoma 403
Burns 839, 840
Burnt-out infective pathologies 501
Busulfan 1018
Butadiene 606
Buteyko breathing technique 479
Byssinosis 969, 985
C
Café-au-lait spots 657
Calcinosis 870
Calcium channel blockers 754, 879
Campylobacter 1050
Cancer 689
esophageal 956
registries, population-based 604f
risk of 605
treatment of underlying 621
Candida
albicans 392
glabrata 314, 326
infection 326
krusei 314, 326
parapsilosis 326
tropicalis 314, 326
Cansoni skin 421
Capillary blood, volume of 144
Capillary endothelial cells, membrane of 106
Capillary leak syndrome 436
Capreomycin 234, 242
Capsaicin 173
Carbamazepine 420, 1017
Carbapenem 321, 341, 385
Carbohydrates 109
Carbon dioxide 106, 117, 146, 147, 189, 989
elimination and regulation 810
end-tidal partial pressure of 806
partial pressure of 591
pressure of 486
production 147, 779
retention 524
tension 77
Carbon monoxide 465, 662, 706, 707, 784, 975, 988, 998, 1002, 1005
diffusion 1043
capacity for 467, 1056
poisoning 587, 588, 1002
transfer of 143
Carbonic acid 122
formation of 117
Carboplatin 642
Carcinoembryonic antigen 941
Carcinogens 606t, 610, 966
Carcinoid tumors 580, 610, 627, 648, 648f
multiple 579
Carcinoma
bronchial 668, 669
bronchoalveolar 611f, 713
bronchogenic 15f, 178, 182, 392, 609, 616, 617, 617f, 622, 940
bronchopulmonary 610
develop bronchogenic 981
embryonal 947
esophagus 16f
invasive 610
lung 617f
lymphoepithelioma-like 944
Cardiac arrest 518, 587, 588, 1003
Cardiac disease 192, 1055
causes of 891
Cardiac failure, congestive 288, 468, 759, 898, 899, 1070
Cardiac massage, external 922
Cardiac tamponade 188, 518, 1032, 1034
Cardiomyopathy 188
ischemic 891
Cardiopulmonary exercise testing 146, 148
Cardiopulmonary stress testing 146
Cardiorespiratory medicine 837
Cardiorespiratory support 768, 769
Cardiotoxicity 475
Cardiovascular disease 188190, 533, 1002
Cardiovascular disorders 181
Cardiovascular system 523
Carina 154
Carmustine 1018
Carotid artery, common 28, 29
Caspofungin 326
Castleman's disease 392, 405, 953
Catamenial pneumothorax 893
Cataract 473, 567
Catheter
over-needle device 166, 168
studies 1011
Cavitary tuberculosis 227f
Cefotaxime 880
Ceftazidime 363, 443
Ceftriaxone 340, 363, 374, 383, 434, 566
Cell 457
carcinoma
non-small 636f
small 612f, 618f, 620
cytoplasm of 698f
injury 969
lung cancer 1055
extrathoracic staging of non-small 633
management of non-small 638, 639t
non-small 159, 601, 610
palliative treatment for non-small 642t
prognosis of non-small 638, 640t
staging of non-small 633t
malignant 901
require oxygen 586
Center for Disease Control and Prevention 249, 268, 296, 331, 396
Central controlling system 123
Central hypoventilation syndromes 1074
Central nervous system 272, 277, 322, 622, 698, 730, 738, 778, 803, 1047
disease 215, 252
disorders 1047, 1048
Central sleep apnea, spells of 597
Central venous catheter 166, 338, 853
insertion 922
Central venous pressure 536, 770
Centriacinar emphysema 513, 515f
Cepacia syndrome 561
Cerebellar
ataxia 277
degeneration 621, 623, 930
Cerebral
abscess 283
edema 1047
edema, high-altitude 1011
malaria 840
oxygen toxicity 595
Cerebrospinal fluid 124, 1050
Cervical
adenopathy 197
cord
injury 1048
lesions 1058
lymphadenopathy 272
mediastinoscopy 941
spine injury 800
spondylitis 194, 195
Chamberlain's procedure 941
Chaotic atrial tachycardia 534
Chemical
asphyxiants 1002
inflammation 1002
irritants 1001
worker's lung 719, 720
Chemokines 458
Chemoreceptors
central 124
peripheral 124
Chemotherapeutic regimes 1024
Chemotherapy 206, 208, 312, 313, 396, 645
adjuvant 639, 641
choice of 641
cisplatin-based 946
lung 1017
Chest
and neck, palpation of 198
axial computed tomography of 214f
bellows 518
computed tomography of 63f, 165f, 166f, 194, 221f, 226f, 335, 335f, 370f, 419, 421f, 562, 616f, 618f, 650f, 1017f, 1020f
discomfort 887
causes of 194t
disease, evaluation of 3
examination of 198
high-resolution computed tomography of 192, 196, 223f225f, 324f, 368, 370f, 397f, 563f, 581, 625, 667, 700, 672f, 710f, 723, 723f, 729f
infection 433
infiltrates 839
lateral X-ray of 6f
magnetic resonance imaging of 194
pain 21, 194, 195, 274f, 309f, 616, 706, 955, 1020
severe unilateral 195
radiography 278, 309, 316, 419, 528, 580, 627t, 657, 698, 706, 1036
limitations of 670
tightness 449
trauma 916, 1031, 1032, 1038f
complications of 1032t
therapeutic measures in 1039
tube
drainage 161, 162
insertion, procedure for 161
removal 162
ultrasonography of 18f
wall 3, 33, 929
abnormalities 1044
anterior 45
compliance 1043
deformity 1042
disease 639
disorders 1029, 1041
inner 88
mechanics 1056
pain 194, 195
retraction 930
stabilization 1038
system 99
X-ray 192, 279, 316, 681, 723
limitations of 9
Chevalier Jackson's sign 200, 616
Cheyne-Stokes respiration 597
Chills 233, 269
Chin thrust 790
Chlamydia 281, 534
pneumoniae 277, 279, 280, 286, 386, 534, 912
psittaci 277
Chlamydial infections 178
Chlorambucil 1018
Chloramphenicol 384, 445
Chloride
ions 117
secretion, reduced 561
Chlorine 967, 984, 1001
Chlorofluorocarbon 471, 988
Chloromethyl 608
Chloropicrin 967
Chloroquine 427
Cholesterol 901
Chondroma 627
Choriocarcinoma 947
Chromium 606, 608
Chromosome 452
arms of 929
Chronic airways
disease 564
obstruction 120, 810, 831
Chronic bronchitis 112f, 117, 333, 500, 512, 974
emphysema 121
Chronic cough 358
causes of 176t
diagnostic evaluation of 174, 176t
specific treatment for 179t
Chronic disorders 449, 1049
Chronic dyspnea 192
causes of 192t
Chronic left ventricular failure 175, 192
Chronic necrotizing pulmonary aspergillosis 325
diagnosis of 326t
Chronic obstructive lung disease, global initiative for 526, 549
Chronic obstructive pulmonary disease 18, 125, 135, 140, 174, 189, 199, 268, 277, 296, 324, 347, 353, 393, 458, 466, 467t, 482, 492, 498, 499f, 499t, 500, 500t, 512t, 515, 520t, 526t, 528f, 529f, 530, 532, 536, 545, 547f, 549, 556t, 557, 558, 559f, 578, 586, 591t, 609, 709, 749, 758, 759, 779, 803, 807, 920, 968
exacerbations of 192, 532, 533f, 534, 535, 537, 553, 782
Chronic thromboembolic disease 748
Chrysotile 977
Churg-Strauss syndrome 64, 275f, 420, 727, 729, 735, 743, 745f, 845, 884, 900, 918
Chylothorax 898900, 904, 917
causes of 917t
Chylous ascites 706
Chylous effusion 706, 708
Cicatrization atelectasis 38
Ciclesonide 473
Cidofovir 329
Cilastatin 242, 245
Cilia, normal 356f
Ciliary dyskinesia, primary 355
Ciprofloxacin 349, 363, 566
intravenous 445
Cirrhosis, biliary 688, 876, 880, 881
Cisplatin 641
Cladribine 701
Clarithromycin 350, 351, 401
Clavulanate 242, 374, 379, 566
Clavulanic acid 340, 363
Clindamycin 372, 398
Clinical compression syndromes 959
Clofazamine 242, 243, 245, 246
Closed tracheal suction systems 344
Clostridium
botulinum 1051
difficile infection 372
tetani 437
Coagulation system 843
Coal workers’
lung disease 974
pneumoconiosis 965, 974, 975, 975f
Co-amoxiclav 287
Coccidioides immitis 266, 271, 277, 281, 305, 309, 314, 392
Coccidioidomycosis 309, 367, 911
disseminated 309
Cockroach allergens, avoidance of 471
Coffee-worker's lung 719
Collagen
disorders 859
vascular disease 396
Collapse 38
Colloids 185
Coma 786
Combination therapy 326, 755
Common cold 305, 374
Community-acquired pneumonia 217, 265, 266t, 279t, 285, 288t, 292, 311, 395, 401, 894
etiology of 386t
pathogenesis of 269f
risk factors for 267t
severe 442
Complement-fixing test 281
Compost lung 719, 720
Comprehensive waste management 993
Computed tomography 10, 22f, 194, 279, 311, 318, 325, 370, 379, 397, 572, 611, 723, 737
angiography 752f
contrast-enhanced 29
guided
biopsy 163f
fine-needle aspiration cytology 163f
intercostal drainage insertion 165f
pigtail drainage 164f
trucut biopsy 163f
high-resolution 17f, 55f, 191, 220, 353, 360, 361f, 369f, 416f, 580, 582f, 612, 624, 656, 659, 660, 673, 700, 703, 706, 710, 751, 999
pulmonary angiogram 30f
scan 275, 328, 353, 628f, 656
Confusion 786
Congestion, hypostatic 200
Conglomerated nodular lesions, multiple small 71f
Conglomerative cystic lesions 361f
Conjunctiva 685
Conjunctival suffusion 445
Conjunctivitis 213
Connective tissue 913, 937
disease 749, 904, 918
mixed 859, 872
disorders 356, 580, 859, 860t, 866
Consciousness, altered level of 277
Consolidation 33, 36f, 316
Constrictive bronchiolitis 69, 71f, 469, 579, 580
causes of 580
etiology of 580t
histopathology of 579
Continuous flush system 168
Continuous oxygen therapy 596
indications for 556t
severe hypoxia warrants 594
Continuous peritoneal dialysis 903
Continuous positive airway pressure 289, 668, 812814, 848, 927, 1072
machine 1072f
therapy 1072
Controlled oxygen therapy 539
Contusion 1034
Cor pulmonale 519, 556, 976
Coronary artery disease 1069, 1070
Coronary bypass graft surgery 898, 915
Coronavirus 292, 303, 305, 534
Cortex 123
Corticosteroid 197, 312, 334, 483, 568, 576, 692, 693, 710, 725, 960
dependent asthma 570
dosage of 692, 693
reversibility to 527
role of 854, 869
therapy 313, 396
high dose of 312
use of 288, 538, 553, 584, 692
Corynebacterium diphtheriae 1050
Costophrenic sulcus 80
Co-trimoxazole 384, 443, 912
prophylaxis 261
therapy, role of 250
Cough 173, 175, 178, 196, 216, 269, 273f, 300f, 324, 398f, 461, 511, 553, 615, 657, 668, 688, 706, 709, 729f, 887, 955, 971, 972, 974, 1019
complications of 174
ineffectual 1058
mechanism of 173
nonproductive 178
promotion of 787
receptors 173
reflex 174
test 1057
unexplained 179
Coxiella burnetii 271, 277, 281, 912
Coxsackie virus 292
Crackles 200, 657
C-reactive protein 342, 360, 745, 1069
Cricothyroid membrane 156f, 794f
Cricothyroidotomy 155, 156f, 793
procedure for 794f
Crippling pulmonary hypertension 872
Critical care
polyneuropathy 1050
principles of 775
Crohn's disease 356, 454, 688, 886, 887f
Croup 305, 379
Cryotherapy 158
Cryptococcal infection 328, 395, 443
Cryptococcosis 309
Cryptococcus neoformans 277, 305, 309, 328, 392, 911
Cryptosporidium 401
Cuff
care of 800
pressure 154
Curb index 285t
Cushing's syndrome 469, 622
Cyanide 1004
Cyanosis 462, 761, 786
central 198
Cyclooxygenase theory 496
Cyclophosphamide 403, 693, 862, 960, 1018, 1025
Cycloserine 242, 243, 245
Cyst 421, 921
bronchogenic 627, 951, 951f
enterogenous 952, 952f
infection of 951
large 421
Cysteinyl leukotrienes 474, 496
Cystic adenomatoid malformation 76
Cystic bronchiectasis 68, 347f, 353, 355f, 361f
Cystic fibrosis 278, 347, 355, 356, 375, 464, 478, 501, 560562, 563f, 563t, 564, 565, 566t, 567, 568
clinical manifestations of 564
diagnosis of 564
end-stage 567
features of 568
forme fruste of 565
lacks oxygen 561
mild 567
nonrespiratory features of 562t
progression of 567
respiratory
features of 562t
manifestations of 562
transmembrane conductance 560
treatment for 567
Cystic lesions, differential diagnosis of 66
Cystic lung disease 66
Cytokines 401, 458, 843
inflammatory 971
role of 843
Cytomegalovirus 266, 277, 292, 305, 311, 314f, 319, 392, 443, 1050
diagnosis of 329t
infection 271, 317f, 328, 393, 396, 400, 1024
pneumonia 313
Cytoplasm, endoplasmic 510
Cytotoxic drugs immunosuppressants 313
Cytotoxic therapy 312
low-dose 312
D
Dantrolene 915
Dapsone 400
D-dimer 761, 762
Dead space
concept of 108
ventilation 780
Deafness 233
Deep vein thrombosis 426
Defective chloride transport 560
Delamanid 242, 245, 246
Deliberate hypoventilation, strategy of 486
Dengue
antibody 436
fulminant 436
hemorrhagic fever 433, 436
shock syndrome 436
Deoxyribonuclease 911
Deoxyribonucleic acid 281, 325, 929, 1054
Depression, circulatory 594
Dermatomyositis 621, 622, 859, 871, 872f
Dermatophagoides pteronyssinus 453
Descending aorta 26, 28, 29, 194
aneurysm of 956
Desmoplastic stroma 611f
Desquamative interstitial pneumonia 65f, 655, 662f, 861
Dexamethasone 1010, 1012
Dextrocardia 38f, 355f, 375
Diabetes 216, 268, 1071
flare-up 670
mellitus 241, 290
risk of 1071
uncontrolled 312
Diaphragm 24, 31, 34, 79f, 929
right dome of 43f
rupture of 1039
Diaphragmatic dysfunction, ventilator-induced 137
Diarrhea 270, 272
Diastolic Graham Steele murmur of pulmonary regurgitation 750
Diazepam 441
doses of 441
Diclofenac 1021
Diethylcarbamazine 413, 415
Diethylene triamine penta-acetic acid 884
Diffuse alveolar damage 65f, 314, 655, 669, 861, 1017
Diffuse bilateral interstitial plus alveolar infiltrates 319fc
Digital chest radiography 4
Digital tomosynthesis 9
Digoxin 556
Diisocyanates 720
Dilated mitral annulus 892
Dipalmitoylphosphatidylcholine 100
Directly observed therapy 243
Directly observed treatment short course 207, 207f, 208f, 225, 229, 250, 259, 260
Disability adjusted life years 503
Disaster strikes 891
Discoid atelectasis 38, 46f
Disease causing restrictive lung
disease 190
lesion 189
Disseminated intravascular coagulation 432
Distant extrathoracic metastatic manifestations 619
Dizziness 233, 1012
Dobutamine 289
Dopamine 289
Doxorubicin 403
Doxycycline 363, 445, 693, 912
D-penicillamine 1023
Dressler's syndrome 918
Drowsiness 233, 786
Drugs
addiction 393
costs 244
induced lung toxicity 1015, 1016t
interactions 232, 251
newer 244
reaction 64, 335
resistant tuberculosis 228, 236, 238
second-line 236
sensitivity testing 255
specific 1020
susceptibility test 228, 242, 246
toxicity 244, 314, 864
Dry bronchiectasis 359
Dry cough 360, 681, 1016
Dry powder inhalers 471
Dry sounds 200
Dual-energy subtraction imaging 8
Duchenne's muscular dystrophy 1045, 1053
Dutch hypothesis 499
Dynamic hyperinflation 486, 516, 517, 517f, 533
Dyskinesia, ciliary 356f
Dysphagia 77, 161, 618, 956
Dyspnea 148, 186, 189191, 217, 247f, 298, 300, 398f, 461, 534, 558, 616, 657, 681, 688, 706, 708, 761, 786, 887, 889, 898, 921, 930, 955, 960, 972, 976
causes of 189, 190
chronic progressive 192
differential diagnosis of 189t
exertional 148fc
pathophysiology of 188
reduction of 554, 555
severe 971
symptoms of 192
syndrome, isolated 760
well-marked 554
E
Ear 737
nose and throat 492
Earthquakes 1031
Echinococcus granulosa 420
Echocardiography 406, 531, 750, 751, 761, 762
Eclampsia 889, 893
Ectopic corticotropin hormone syndrome 622
Ectopic hormone production 620
Ectopic mediastinal parathyroid adenoma 940
Edema
acute pulmonary 782, 804, 841
cardiogenic pulmonary 845, 846
high-altitude pulmonary 1008, 1010
re-expansion 925
Effusion lymphoma, primary 392, 404
Ehlers-Danlos syndome 356, 1042
Eisenmenger's syndrome 50
Elastic tissue, presence of 99
Elastin 99
Electrocardiography 191, 194, 406, 713, 750
Electromyography 135, 624
Electron microscopy 697
Electrophysiological testing 134
Elevated urine sodium concentration 622
Embolectomy
catheter-directed 768
surgical 768, 770
Embolism, forms of 773
Empathize 243
Emphysema 17f, 18f, 77, 64, 112f, 392, 500, 503, 513, 529f, 530f, 724, 962
centrilobular 66f, 67f, 513, 530f
compensatory 48
extensive surgical 86f
focal 974
interstitial 487
major patterns of 515f
obstructive 48, 214
severe 163
subcutaneous 487, 1038
Emphysematous bullae, multiple 529f
Empirical antimicrobial therapy 289t
Empyema 80, 82, 82f, 83f, 283, 431, 433, 845, 900, 901, 905, 906, 907f, 908, 908f, 909, 932, 1046
causes of 905t
chronic 932
different locations of 906f
necessitatis 906
Encephalitis 277, 295
Encephalomyelopathy 621, 623
Encephalopathy 295, 1054
Enchondroma 51f
Endemic fungi 311
Endobronchial lesion 931
Endobronchial ultrasound 159, 635
guided biopsy 624
Endocarditis 283
Endocrine system 621
Endodermal sinus 947
Endoesophageal ultrasound 160
Endoscopic bronchial ultrasound guided transneedle bronchial biopsy 689
Endothelial cells 106
Endothelin receptor antagonists 755
Endothelium antagonist, selective 879
Endotracheal intubation 153, 541, 788, 793, 794, 795f, 848, 1038t, 1039
and ventilator support 541t
dangers of 848
head and neck for 154f
Endotracheal tube 183, 184f, 333, 343, 799, 824
estimation of size of 153t
Entamoeba histolytica 266, 427, 905
Enterobacteriaceae 340, 385
Enterococcus faecium 383
Environmental pollution 988, 989, 997
health impact of 991
Environmental tobacco smoke 604, 606, 608
Enzyme
cyclooxygenase 496
linked immunosorbent assay 281, 416, 762
techniques 296
thiopurine methyltransferase 862
Eosinophil 414, 418, 457, 465, 521, 570, 730
extrathoracic 744
peroxidase 465
role of 730
Eosinophilia 477, 744
asthmatic pulmonary 727, 728
peripheral 727
syndrome, pulmonary infiltration with 727
Eosinophilic pneumonia 569, 727, 730, 1017, 1017f, 1022
classification of 727
histopathological section of 414f
transient pulmonary infiltrates of 574
Epiglottitis 153, 192, 380
Epithelial cells 521, 561
Epithelioid 932
histiocytes 722f
Epoprostenol 879
Epoxy resin lung 719, 720
Epstein-Barr virus 292, 403, 1050
Erythema
multiforme 277
nodosum 213, 277, 680, 685f, 886
Erythrocyte sedimentation rate 176, 221f, 278, 316, 360, 535, 403, 729, 761, 887, 1022
Erythromycin 384
use of 584
Escherichia coli 274, 311, 321, 368, 880
Esophageal perforation 897, 915, 957
Esophageal sphincter, lower 456
Esophageotracheal-bronchial neural reflex 177
Esophagus 31, 173, 937, 1038
adenocarcinoma of 623
perforation of 904
Estimated tuberculosis incidence rates 209f
Etanercept 743, 873, 1024
Ethambutol 229, 231233, 237, 242, 244246, 350, 351
Ethionamide 242, 243, 245, 349
Ethmoidal 378
Ethyl carbamate 606
Etoposide 403, 641
Etoricoxib 496
European Respiratory Society 140, 524, 655, 665t
Euvolemia 622
Everolimus 707
Exacerbations
acute 534, 668
risk factors for acute 533t
severe 538
acute 362
Excessive daytime sleepiness 1064, 1066
causes of 1067t
Exercise 365, 530
capacity 558
test, self-paced 530
training 555
Exhaled nitric oxide 465
apparatus 465f
Exocrine gland sarcoid 688
Expiration 98
Expiratory airflow limitation 515, 516
Expiratory flow-volume curve, normal 139f
Expiratory positive airway pressure 831
Extensively drug-resistant tuberculosis 236, 237, 238, 242, 244, 253, 254
Extracorporeal membrane oxygenation 819, 820
Extubation failure 829
causes of 829t
Eye movement, rapid 1044, 1058, 1070
F
Face mask 590
simple 590f
with reservoir bag 590, 591, 591f
Facial
burns 153
nerve palsy, bilateral 680
Falciparum infections, fulminant 424f
Fallot's tetralogy 49
Famciclovir 305
Farmer's lung 718, 719, 720
Fat embolism 773
Fatal asthma 459, 493
Fatigue 206, 360
central 136
differential diagnosis of 148fc
low-frequency 136
peripheral 136
Femoral vein 166
thrombosis 284
Femoral venepuncture 168
Fenoterol 478
Fever 215, 233, 252, 270, 273f, 274f, 324, 334, 398f, 445, 623, 680, 736, 740f, 887, 971, 1016
familial mediterranean 919
hemorrhagic 433
high-grade 270f, 273f, 300f, 301f, 397f
intermittent 309f
low-grade 225f, 360, 616, 714, 729f
Fibrinolytic agents, use of 910, 911
Fibrinolytic therapy 910
Fibroblast 679
growth factor 667
Fibrocystic disease 1045
Fibroelastosis 874f
Fibroma 627
Fibrosis 63, 225f, 356, 723, 844, 1018, 1026
drug-induced pulmonary 1018
idiopathic pulmonary 655, 656, 658f, 665t, 861, 968
interstitial 60f, 192, 968f
interstitial pulmonary 105, 197, 415f
severe 1018
Fibrothorax 1046
Fibrous tissue tumors 957
Fick's principle 113
Filarial infection 411
Filariasis 917
Fine-needle aspiration cytology 55f, 57f, 628f
Finger clubbing 621, 622, 657
Fishman's pulmonary
diseases 680
disorders 680
Fissure 24, 32, 32f
interlobar 40
minor 25f
rotates, oblique 42
thickened 44
Fistula, hepatobronchial 429
Flail chest 810, 1032, 1035, 1036, 1045
diagnosis of 1036
management of 1037t
Flail segment 1036
large 1038
Fleeting opacities 40f
Fleeting shadows 37
Flow-volume
curves 104f
loop 140, 527, 547f
Flu syndrome 233
Fluconazole 401
Fluid
balance 853
collection 164
electrolyte balance 1035
exchange across alveolar capillary membrane 131
glucose concentrations, lowest 900
management strategies 853
restriction, treatment consists of 891
Flu-like syndrome 232, 444
Flunisolide 483
Fluorine 18-deoxyglucose 20
Fluorodeoxyglucose 940
positron emission tomography 691
Fluoroquinolone 234, 237, 242, 246
resistance 384
use group 242
Fluticasone 473
Follicular bronchiolitis 582, 864
Food allergy and additives 456
Food and Drug Administration 255, 748
Food-borne disease 1052
Forced vital capacity 359, 694
Foreign body 192, 627, 957
aspiration 176, 192
Formaldehyde 606
Formoterol 475, 478, 550
Fosfomycin 385
Foul-smelling sputum 277
Fracture 759
femur 537
hairline 174
ribs 194, 537
sternum 194
Francisella tularensis 271
Friedlander's pneumonia 275
Functional residual capacity 123, 142f, 143f, 495, 809, 815f, 837
Functional walk tests 149
Fungal aspergillosis, allergic 376
Fungal balls 306
Fungal infection 305, 392, 401, 1024
chronic primary pulmonary 367
invasive 313
Fungal pneumonia 305
Fungal sensitivity 577
Fungal sinusitis 376
invasive 377
Fungi 266, 311
Fusobacterium necrophorum 368
G
Gag reflex, absent 277
Galactorrhea 621
Gallium 940
scans 1022
Ganciclovir 305, 329
Ganglion tumors, autonomic 940
Ganglioneuroblastoma 955
Ganglioneuromas 955
Gas chromatography 995
Gas dilution technique 141
Gas exchange 106, 777
abnormalities 759
parameters, value of 148
within tissues 778
Gas transport 777
Gastric acid 579
Gastric colonization 333
Gastric decontamination 344
Gastroesophageal reflux 177, 179, 455
cough 177
disease 492, 668, 870
well-marked 278
Gastrointestinal disease, pleural effusion in 915
Gastrointestinal tract 332, 436, 824
Gastrointestinal viruses 293
Gatifloxacin 242
Gaucher disease 749
Gemcitabine 1018
Gene replacement therapy 567
Genetics 560, 703
Genotypic methods 228
Germ cell tumor 90, 940, 945
malignant 945, 946f
Ghon foci 214
Ghon focus 213, 215
Giant cell 739f
arteritis 735, 747
interstitial pneumonia 655
Gibbus 1042
Giemsa stain 398
Glaucoma 473
Glaxosmithkline 475
Glomerular basement membrane 741
Glomerulonephritis, progressive 735
Glucocorticoid therapy 693
Glucocorticosteroid, primary 491
Glucose 900
6-phosphate dehydrogenase deficient 427
control 854
Glycine 475
Glycogen storage disease 749
Glycopyrrolate 551
Glycosaminoglycan 458
Goiter, intrathoracic 940, 949
Golden C-sign 41
Gomori methenamine 398
Gonadotropin-releasing hormone 496
Goodpasture's syndrome 182, 183, 735, 845, 884
Graft vs host disease 314
Graham Steele murmur 524
Gram's stain 270, 279, 316
Gram-negative bacilli 274
nonfermenters 385
Gram-negative bacteria 266, 274, 333, 439
Gram-negative infections 287, 317
fulminant 840
Gram-negative organisms 318, 392, 904
Gram-negative sepsis 442, 840
Gram-positive organisms 318
Granulation tissue formation 643
Granulocyte 410, 679, 711
monocyte 1017
Granuloma 55, 413, 418
eosinophilic 656, 696
formation 418
old-healed 51
Granulomatosis 371, 684, 687, 689, 735, 736, 739f, 742, 746t, 845, 1026
bronchocentric 584
eosinophilic 420, 689, 727, 735, 743, 845
Granulomatous disease 710, 1042
noninfectious 953
Granulomatous lesions 418
Ground-glass around nodule 55f, 631
Ground-glass densities 47f, 63, 397f, 666f, 861f, 872f, 1020f
differential diagnosis of 63
Ground-glass opacities 62, 723
multiple 59f
Growing nodule 631
Growth 630
factor binding protein, insulin-like 679
hormone excess 621
rate of 54
Guillain-Barré syndrome 188, 295, 779, 1049, 1050, 1054
Gynecomastia 621, 946
H
H1N1
infection 296, 299, 300
strain 299
H5N1
infection 299
strain 298
virus 298, 299
Haemophilus influenzae 266, 277, 313, 321, 340, 356, 358, 367, 374, 384, 386, 392, 534, 561, 583, 905
Haemophilus parainfluenzae 380
Halo sign 324, 324f
Hamartoma 54f, 55, 627, 650, 650f
calcification typical of 52f
Hamman's sign 1039
Hamman-Rich syndrome 655, 845, 861, 862
Hand-Schüller-Christian syndrome 696
Hantavirus 266, 292, 304
infection 304
Head injury 1047
Headache 233, 485, 547, 1004, 1012
Heart
disease 753
congenital 29, 76, 188, 189, 749, 1044
ischemic 188, 554, 668, 669
low-output 188
enlargement, right 1044
failure 189, 192, 668, 669, 861
acute right 760, 761
chronic left 190
congestive 190, 268, 597, 897, 899, 903, 969, 976
cycle of 1070
prevention of right 595
prognosis in 148
right-sided 543
treatment of right 545, 556, 556t
lung transplants 580
rate 1069
sarcoid involvement of 686
sound, second 1010
Heerfordt's syndrome 680
Helminthic disease, pulmonary manifestations of 410
Helminthic therapy 454
Helminths 311
Hemagglutination test 429
Hemangiomas 957
Hematogenous stem cell transplant 313, 314
Hematological disorders 396, 749
Hematological stem cell transplant 312314
Hematopoiesis, extramedullary 957
Hematuria 436
asymptomatic 738
Hemiazygos veins 31, 938
Hemiplegia 759
Hemithorax 48, 72, 270f, 324, 899f
Hemodialysis 216
Hemoglobin 111
concentration 112, 853
Hemolytic anemia
autoimmune 688
chronic 749
immune 272
Hemopneumothorax 161
Hemopoietic stem cell transplant 840
Hemoptysis 180182, 216, 306, 442, 568, 615, 698, 706
causes of 180
cryptogenic 182
diagnostic evaluation 182
episodes of 562
iatrogenic 182
investigations for 183t
management 183
occasional 21
Hemorrhage 130, 335, 956, 962
diffuse alveolar 314, 738, 1018, 1019, 1022, 1027
intra-alveolar 180, 192, 314, 435f, 713, 715, 739f
intrapulmonary 34
Hemorrhagic fluid 436
Hemosiderosis, idiopathic pulmonary 714, 715f
Hemothorax 80, 900, 916, 924, 925, 1032, 1033, 1036
etiology 916
traumatic 161
treatment 916
Henderson-Hasselbalch equation 116, 117, 146
Henoch-Schönlein purpura 735
Hepatic disease 876, 903
Hepatic failure, fulminant 880, 881
Hepatitis 232, 233, 434, 876, 886
autoimmune 880
granulomatous 686
infections 454
Hepatobiliary diseases
pulmonary
complication in 881t
manifestations of 876
Hepatopulmonary syndrome 876, 878f
clinical features 876
diagnosis 877
imaging 877
management 879
pathogenesis 877
pathology 877
pathophysiology 877
Hepatotoxicity 232
Herbal cocktail 489
Hernia
congenital diaphragmatic 73
diaphragmatic 73f, 74f
hiatus 75f, 90, 957
large hiatus 278
Herpes simplex 311, 392
virus 305, 313, 329
Herpes zoster 194, 1050
infection 1051
virus 329
High flow nasal cannula 591, 592f
High inspiratory inflation pressures 851
Hilum 23, 24, 40
anteriorly 43
right 44
Hip
and knee surgery 759
replacement surgery 335f
Histamine 457, 458
Histiocytosis X 501, 656
Histocompatibility complex, major 677, 720
Histoplasma capsulatum 266, 271, 277, 281, 305, 306, 308, 314, 392, 959
Histoplasmosis 306, 367
Histotoxic hypoxia 586
Hodgkin's disease 159, 403, 623, 727, 947, 948, 948t
classification of 947
Hodgkin's lymphoma 948, 1050
Homeopathy 479
Honeycomb cysts 59f
Hormonal therapy 707
Hormone replacement therapy 759
Horner's syndrome 195, 197, 634, 939, 956
Host protein amyloid, role of 678
Hughes-Stovin syndrome 874
Human chorionic gonadotropin 941
Human epidermal growth factor 607
Human herpesvirus 392, 953
Human immunodeficiency virus 216, 244, 248, 249, 277, 357, 391, 392, 397, 400, 404, 405
disease 427
epidemic 241
infected, pulmonary infections in 401t
infection 197, 290, 355, 401, 410, 749
programs 261
pulmonary infections in 392t
treatment 250
Human infection 419, 434, 443
Human leukocyte antigen 452, 570, 581, 677
Human lymphocytic T cell virus 676
Human metapneumovirus 266
Human tetanus immunoglobulin 440
Humidifier lung 719, 720
Hyaluronan 458
Hydatid cyst 420, 421, 421f, 627
Hydatid disease 420
Hydatidiform mole, benign 892
Hydatidosis 420
Hydrazaline 1018
Hydrazide 1027
Hydrocarbons 465
Hydrofluoric acid 1002
Hydrogen
arterial potential of 146
chloride 1002
cyanide 1000, 1003, 1005
peroxide 465, 521
sulfide 967, 1004
Hydropneumothorax 84f
Hydrothorax, hepatic 879
Hydroxocobalamin 1004
Hydroxychloroquine 693
Hyperbaric bags 1010
Hyperbaric oxygen 593, 1003
Hyperbaric therapy 1010
Hypercalcemia 621, 687, 930
clinical features of 621
Hypercapnia 146, 189, 514, 518, 519, 597, 785, 786, 786t, 791, 846, 848, 851, 871, 1074
acute 120f
causes of 535t
chronic 120f
control of 556
danger of progressive 594
progressive 594
symptomatic management of severe 545
Hypercapnic respiratory failure 439, 831, 871, 1043, 1046, 1055
causes of 779, 780t
Hypereosinophilic syndrome 420, 727, 730
Hyperglycemia 567, 621, 637
Hyperinfection syndrome 417
Hyperinflation
excessive dynamic 486
severe dynamic 518
Hyperkalemia 556
Hypermetabolism 1006
Hyperparathyroidism 90
Hyperplasia 459
Hyperpyrexia 440
Hypersecretion, chronic mucus 505
Hypersensitivity pneumonia 967
Hypersensitivity pneumonitis 62f, 64, 64f, 306, 348, 656, 689, 718, 720722, 722f, 724f, 861, 969f, 1016, 1022
causes of 719t
Hypersensitivity reaction 306
Hypersomnolescence, idiopathic 1067
Hypertension 550, 551, 554, 786, 821, 1069, 1071
chronic thromboembolic 749, 751, 753
idiopathic pulmonary 191, 748
portal 749
pulmonary 750
Hyperthyroidism 621
Hypertonic saline 176, 565
Hyperventilation 805, 889
purposeful 803
Hypnosis 479
Hypoalbuminemia 883, 903
Hypocapnia 597
Hypoesthesia 377
Hypogammaglobulinemia 355
Hypoglossal nerve stimulation 1073
Hypoglycemia 621, 930
Hypokalemia 478, 487, 550
Hypokalemic metabolic alkalosis 543
Hyponatremia 622, 633
Hypophosphatemia 487
Hypoplasia 71, 77, 918
Hypoplastic lung syndrome 75
Hypoproteinemia 853, 884
Hypotension 337, 486, 543, 765, 767, 786, 823, 891
Hypothyroidism 903, 1067
Hypotonicity 622
Hypoventilated alveoli 111
Hypoventilation 587, 779, 1037, 1043
central alveolar 1074
treatment for 1058
Hypovolemia 130
Hypovolemic shock, severe 436
Hypoxemia 485, 511, 586588, 708, 881, 882, 971, 1037, 1039, 1074
causes of 534t
chronic 594, 1074
life-threatening 1032
mild 33
refractory 848, 852
relief of 539
resting 683
severe 122, 1003, 1010, 1032
Hypoxia 189, 192, 298, 514, 519, 541, 586, 597, 748, 761, 785, 786, 786t, 791, 846, 871, 877, 1005, 1016
acute 1008
chronic 1008
life-threatening 595
relief of 540, 587
severe 435f, 1011
Hypoxic pulmonary vasoconstriction 131
Hypoxic stimulus 540
Hysteresis 99f
I
Ibuprofen 1021
Iced-saline lavage 184
Idiopathic interstitial pneumonia 655, 657t
classification of 655t
Imipenem 242, 245
Immune reconstitution and inflammation syndrome 252f, 252t, 395
mechanism of 252
types of 252
Immunofluorescent test 296
Immunoglobulin 357, 360, 571, 735
E 500
G 276
M 860
Immunoregulatory cells, role of 678
Immunosuppression 268
Immunosuppressive drugs
side-effects of 862
use of 312
Immunosuppressive therapy 870
In vitro pregnancy 892
Incremental shuttle test 149
India's National Tuberculosis Control Program 207
Indian Council of Medical Research 206
Indoor pollution 506
Industrial toxic gases 998t
Infection 192, 274, 418, 453, 627, 823, 884, 966, 974, 1024
endobronchial spread of 225f
hospital-acquired 331
incidence of 211
multiple 394, 908
prevalence of 210
treatment of 789
Infectious Disease Society of America 386
Infertility 375
Inflammation
intraluminal 513
masking of 476
syndrome 251
treatment of 567
Inflammatory bowel disease 356, 579, 580, 759, 886, 887, 1026
pulmonary
complication in 886t
manifestations of 886
Inflammatory cells 520, 520t
accumulation, mechanism of 520f
proliferation of 844
Inflammatory disorder 449, 1025
Inflammatory edema 842
zone of 842
Inflammatory mediators 457, 458, 520, 521
Infliximab 693, 694, 743, 873, 1024
Influenza 293, 305, 311, 534, 580
A 292, 296
virus 293
antiviral against 296t
B 292, 296
virus 292
complications of 295
global impact of 293
infection 294
seasonal 293
vaccine 297, 544
virus 266, 290, 292
A 292, A 299
B 292
Ingestion 978
Inhalation 978
injuries 190, 580, 1004
pneumonia 333
Inhaled corticosteroid 364, 472, 549, 553, 567
preparations 473t
role of 553
use of 545
Inhaled steroids 553
high-dose 483
types of 473
Injectable agents, second-line 242
Injury
extrathoracic 840
severity scoring 1006
Insomnia 485
Inspiration 97, 105
muscle of 97
Inspiratory breath, maximum 1055
Inspiratory flow rate 807
Inspiratory muscle 123
activity 124
fatigue, role of 829
strength 1056
Inspiratory pressure, maximum 784
Inspiratory reserve volume 97
Inspired gas, humidification of 787
Inspired oxygen 486
fraction of 155, 285, 536, 806, 808, 811, 818, 815
pressure of 1007
Intensity projection, maximum 13, 16f, 752f
Intensive care unit 161, 279, 314, 331, 334, 367, 425, 590, 770, 777, 779, 780t, 792, 802, 811
treatment in 290
Intercostal drainage 39f, 164, 165f
Intercostal tube insertion 922
Interferon-gamma release assays 211, 249, 258
Interleukin 571
Intermittent positive-pressure ventilation 802
types of ventilators for 806
International Classification of Sleep Disorders 1063
International Cooperative Pulmonary Embolism Registry 765
International Nosocomial Infection Control Consortium 332
Interstitial lung disease 64, 176, 178, 188190, 192, 392, 582, 655, 658f, 669t, 721, 750, 845, 859, 872, 924
acute exacerbations of 668
complications of 668, 668t
diagnosis of 656, 667t
distribution of 656
features of 669
late stage 783
respiratory bronchiolitis with 579, 655
Interstitial nodules 684f, 690f
extensive 690f
Interstitial pneumonia 48f, 58f, 64, 192, 432, 433, 660f, 661f, 664t, 859, 861, 866, 868, 869, 869f, 871, 880, 887, 1025, 1026
cellular nonspecific 59f
chronic 655
fibrotic nonspecific 58f
lymphocytic 405, 655, 861
lymphoid 392
nonspecific 57, 392, 655, 663f, 666f, 722, 861, 866, 1016
severe 1026
usual 655, 660, 662f, 666f, 722
Interstitial thickening, smooth 57f
Interstitium 32
centrilobular 33f
intralobular 57, 57f
normal anatomy of 33f
peripheral 56
Intra-alveolar hemorrhage, severe 435
Intra-alveolar pressure 516, 518
Intracellular cyclic adenosine 550
Intracranial tension 800
Intralobular interstitial thickening 57f
Intraocular tension 551
Intrapleural pressure 99
negative 524
positive 524
Intrathoracic pressure 921
Intrathoracic spread 617
Intrathoracic staging 634
steps for 634t
Intubating laryngeal mask airway 793
Invasive aspergillosis 306, 322, 323f
Invasive pulmonary aspergillosis 322, 324, 325t
treatment of 326t
Invasive ventilator support
indicators for 1038t
modes of 811
Ionizing radiation 608
Ipratropium 551, 584
bromide 140, 484
Iron deficiency anemia 715
Ischemic attack, transient 1071
Isocyanates 984
Isoenzymes phosphodiesterase 551
Isoniazid 206, 229, 231, 233, 234, 237, 246, 261, 349, 350, 401, 915
monoresistance 236
Isospora belli 399
Itraconazole 326, 443, 576
Ivacaftor 567
J
Jarisch-Herxheimer reaction 419
Jaundice 233, 434, 619
Joint pains 232, 233, 745
Jugular vein 29, 939
internal 166
left 29
Jugular venepuncture, internal 168
K
Kala azar 431
Kallikrein-Kinin clotting cascade 132
Kanamycin 234, 242
Kaplan's syndrome 863
Kaposi's sarcoma 392, 401, 402f, 403f, 918
Kartagener's syndrome 70f, 198, 355, 355f, 375
Kawasaki disease 735
Kernig's sign 283
Ketoacidosis, diabetic 191
Ketoconazole 622
Kidney 117, 434
biopsies 745
disease, chronic 885, 974
Klebsiella 35, 321, 439, 539, 904, 905
infection 275
pneumoniae 34, 274, 275, 275f, 277, 283, 311, 358, 367, 383, 386, 534, 536, 880
carbapenemase 385
infection 288
Klippel-Feil syndrome 1041, 1042, 1044
Koch's infection 219f
Krait snakebite 1055
Kussmaul's breathing 191
Kyphoscoliosis 188, 714, 1041
Kyphoscoliotic deformity 191, 1043
Kyphoscoliotic spinal deformity 1041
Kyphoscoliotic spine 1044
Kyphosis 1041, 1042
Cobb angle of 1042f
Kyphotic deformity 1042, 1043
Kyphotic spine 1044
L
Lactate dehydrogenase 397, 712, 860, 899, 901
Lactic acid acidosis 122, 1054
Lady Windemere's syndrome 347f, 357
Lambert-Eaton Myasthenic syndrome 621, 623, 624
Langerhan's cell 696, 697, 698f
granulomatosi 656
histiocytosis 66, 190, 501, 578, 704
classification of 696t
monoclonal proliferation of 697
Laplace's law 100
Large airway, tumor obstructing 192
Laryngeal axis 794f
Laryngeal mask airway 792, 792f, 797, 798
Laryngeal nerve 941
Laryngeal sarcoid 687
Laryngeal spasm 439, 486
Laryngitis 192, 379
Laryngopharyngeal reflux 177
Larynx 125
Laser 743
therapy 158, 184, 642
Lead 606
Leflunomide 693, 861, 1021
Left upper lobe atelectasis 45
Left ventricular failure 587, 588, 762, 891
function 845
Legionella 266, 313
antigen 274f
infection 283, 905
pneumonia 274, 274f
pneumophila 277, 280, 281, 321, 386
urinary antigen tests 279
Legionnaire's disease 274, 845
Leiomyoma 627
Leishmania donovani 431
Leishmaniasis 431
Leptospira 434, 435
icterohaemorrhagiae 434
in leptospira agglutination test 435
Leptospiral infection 434
Leptospirosis 433, 434, 435f, 840
Lesion
core biopsy of 163f
malignant 51
reactive non-neoplastic 582
types of 634
Letterer-Siwe disease 696
Leukemia 159, 313, 313, 396
acute 312, 313
lymphoblastic 948
childhood 890
chronic
lymphocytic 313
myeloid 623
Leukocyte count, differential 900
Leukocytosis 270, 270f, 276, 344, 442
mild 217, 273f
well-marked 906
Leukopenia 216, 328, 436
Leukotriene 457, 458, 521
metabolites 465
modifiers 474
pathway 496
Levalbuterol 478
tartrate 550
Levofloxacin 234, 242, 245
Lidocaine solution 168
Light pollution 988
Light's criteria 908
Light-emitting diode microscopes 254
Lignocaine 158
Limb movement 1065
Limiting tidal volume 849
Linear opacities, causes of 46t
Linezolid 242, 245, 566
Lipid peroxidation 969
Lipoma 21f, 957
Lipopolysaccharide 520f
Liposomal doxorubicin 403
Lipotropin 621
Liquid chromatography, high performance 995
Liquid oxygen 597
Listeria 392
monocytogenes 399, 1024
Lithium hydride 967
Liver 434
abscess
amebic 428f, 430f, 431
indications for aspiration of 431t
and spleen involvement 686
cell dysfunction 846
cirrhosis of 290, 312, 881, 899, 903
disease 485, 877, 879
disorders, chronic 876
dysfunction 893
failure, drug-induced acute 233
functions 274
metastases 619
organ screening of 634
transplantation 880
Lobar collapse 27, 40
Lobar pneumonia, severe 284
Loeffler's syndrome 411, 727
Löfgren's syndrome 680, 692
severe form of 692
Lomustine 1018
Low molecular weight heparin 768
Low ventilation-perfusion ratios 780, 110
Löwenstein-Jensen medium 255
Lower limb venous compression ultrasonography 761, 762
Lower respiratory tract infection 354, 383
bacteriological examination of 337
Lumefantrine 427
Lung 33, 391, 434, 688, 696, 929, 1058
abscess 37f, 180, 182, 367, 368, 370, 433, 907f, 908, 908f
chronic 371
management of 371
absence of 74
actinomyces infection of 371
adenocarcinoma of 79f, 607, 611f, 612
adverse drug reaction on 1015
and chest wall 133, 135
apex 44
attenuation 56, 64
assessment of 63
basic function of 106
biopsy 282, 701, 716, 725, 922
cancer 54, 178, 194, 404, 601, 604, 604f, 608t, 607, 609t, 614, 621t, 625, 727, 871, 974
cell type of 615
classification of 610t
clinical course of 646, 646t
diagnostic assessment of 624t
early detection of 630
etiology of 605
incidence of 603f
management of 642
pathogenesis of 605
peripheral 613
primary 627
risk of 605
small cell 601, 610, 612, 613, 619, 620, 643
management of 645t
staging of 631
study group 639
symptom in 175
types of 613
use in early 159
capacity
inflammation, subdivisions of total 968f
total 97, 359, 581, 723, 844
carcinoma 981, 981t
primary 617f
cell damage 969
collapses 42
compliance 145, 1043, 1056
contusion 1032, 1034
severe 1034
cross-section of 514f
destruction 63
determine closing pressure of 818
diffusion capacity of 144f
disease 3, 138, 625, 748, 749
acute thromboembolic 782
asbestos-related 978
cavitatory 347
chronic 61
common occupational 965, 968
developmental 749
diffuse 56, 703
parenchymal 655
drug-related 689, 887
end-stage 58
environmental 963
granulomatous 176, 1024
infiltrative 1018
helminthic 409, 410
in cystic fibrosis, natural history of 565
infiltrative 192
nature of 192
obstructive 143
severe 810
elastic properties of 99
fibrosis 66
severe 969
flukes 419
function 413, 535, 546f, 554, 581, 683, 712, 723, 729, 871, 986, 1044
assessment of 138, 524
normal 480
studies 583
test 500, 670, 701, 706, 716, 966, 1044, 1056
gangrene of 369
gas exchange zone of 107f
health study 546, 609
heart study 547
hyperinflated 518
hyperinflation of 547, 556
injury 335, 845, 997
acute 40f, 283, 773, 782, 815f, 837, 838, 838t, 881f
asymptomatic 887
drug-induced 1013
existing 849
inhalational 997
severe acute 845, 848
transfusion-related acute 314, 316f, 335, 840, 1019
involvement 696
lobes of 74
malignancy, disseminated 847
neoplasm, primary 22f, 617f
neuroendocrine tumor of 649f
parenchyma 3, 4f, 15f, 16f, 22, 67f, 164, 190, 414f, 530f, 861f, 920, 1001, 1005
adverse effects on 1016
peripheral 70
parts of 111
pathology 434
periphery 36, 546, 569
physiology 95
pressure-volume curve of 99f, 101f, 105f, 145f
primary lymphoma of 403
protection strategies 850
receptors 124
recoil pressure, low 844
recruitment measures 1058
regional gas exchange in 111
regions, normal 63
remodeling 458
scarring 969
severe 435
small cell carcinoma of 612f, 613f
squamous cell carcinoma of 610f, 646
studies 1056
syndrome, shrinking 865, 865f
tissue 67
toxicity 594, 861, 1024
absence of 1022
drug-related 1016
transbronchial biopsy of 679f
translucency of both 49
transplantation 365, 557, 558, 567, 580, 668, 670, 694, 708
indications for 558t, 756t
tumors 176, 599, 601, 647
staging for small cell 633
unilateral transradiancy of 47
ventilation 589
differential 819, 820
volume 97, 99, 103, 141, 143, 192, 527, 810, 998, 1056
and capacities 98f
measurement of 527
reduction surgery 557, 557t
unknown 141
white-out 37, 435
Lupoid pneumonia 64, 866, 867f
Lupus anticoagulant 759
Lupus pernio 685f
Lymph glands 686
sarcoid involvement of 686
Lymph nodes 696, 932
regional 959
Lymphadenopathy 354, 706, 939
benign mediastinal 953
granulomatous mediastinal 953
peripheral 688
Lymphangioleiomyomas 706
Lymphangioleiomyomatosis 190, 501, 656, 703, 705f, 749, 904, 917
cells 704
extrapulmonary features of 706t
pulmonary features of 706t
Lymphangioma 90
Lymphangitic carcinomatosis 56f, 57, 60
Lymphatics 33f
Lymphedema, peripheral 918
Lymphocytes 418, 570
Lymphoid cells, small 404f
Lymphoma 312, 313, 582, 627, 697, 873f, 900, 904, 917, 947, 948, 1024
body cavity-associated 392, 404
centroblastic 403
large cell 948
lymphoblastic 947
Lymphoproliferative disorders 582
post-transplantation 314
Lymphoproliferative malignant lesions 582
M
MacLeod's syndrome 49, 580
Macrolides 364, 478, 553
Macrophage 418, 457
colony stimulating factor 410, 679, 711
inflammatory proteins 843
Magnesium 483, 485
trisilicate 971
Magnetic resonance imaging 379
Mainstream smoke 606
Maintenance therapy 743
Malabsorption 564
Malaise 233, 360, 736, 1016
Malaria 423, 433
prophylaxis 426
Malarial infection, pulmonary manifestations of 423
Malarial pneumonia 425
existence of 425
Malignancy, assessment of risk of 629
Mallory-Weiss syndrome 957, 958f
Malnutrition 312, 564
Malt-worker's lung 719, 720
Mandibular osteotomy 1073
Mantoux test 228
positive 914
Manubrium sternum 3
Marfan's syndrome 356, 920, 921, 1042, 1044
Mask with reservoir 591
Mass
abdominal 893
esophageal 16f
homogenous 89
lesions 737
prevascular 90, 91
prevertebral 91
Massive atelectasis 192
Massive diffuse intra-alveolar hemorrhage 716
Massive fibrosis, progressive 49f, 975f, 976
Massive hemoptysis 23f, 184, 736
investigations for 183t
Massive injury 1006
Massive intra-alveolar bleeds 716
Massive life-threatening hemoptysis 361
Massive pulmonary embolism 195
syndromes with 760
Mast cells 457
heparin-containing 132
Mastectomy 50f
unilateral 50f
Maternal smoking 504
Mature teratomas 945
Maxillary osteotomy 1073
Maxillary sinusitis 374
May-Giemsa stain 712
McGill forceps 154
McLeod's syndrome, 354
Measles virus 266, 292, 303, 305
Mechanical bronchial obstruction 354
Mechanical insufflator-exsufflator 1058
Mechanical obstruction 354
Mechanical ventilation 483, 485, 541, 543, 802, 805, 821t, 1038
asthma 485
complications of 821
indications for 803, 803t
management of 807
noninvasive 540, 541
principles of 849
purpose of 802
Mediastinal adenopathy 37, 90f, 91f, 48f, 214f, 226f, 635, 682f
malignant 617
Mediastinal border, right 25
Mediastinal compartments 938t
Mediastinal cysts 951
Mediastinal emphysema 925, 925f, 1038
severe 1038
Mediastinal fibrosis 22f, 959, 961f
diagnosis of 960
Mediastinal germ
cell tumor 945
primary 945
Mediastinal gland enlargement 214
Mediastinal hemorrhage 962
Mediastinal lipoma 951f
Mediastinal lymph nodes 30, 638
Mediastinal lymphoma 947
primary 947
Mediastinal masses 940t
investigation of 939, 940t
lesion 194
anterior 941, 942f
posterior 7f, 956
Mediastinal nonseminomatous germ cell tumor 946
Mediastinal pathology 176, 192
Mediastinal pleura 89
Mediastinal pleural reflections 937
Mediastinal seminoma 946
Mediastinal shift, normal 87
Mediastinal silhouette 45
Mediastinal structures, normal 28
Mediastinal teratoma 945
Mediastinal tumors, posterior 954
Mediastinal vasculature 28
Mediastinitis 959
descending necrotizing 958
fibrosing 959
following sternotomy 959
Mediastinoscopic biopsy 624
mediastinoscopy with 690
Mediastinoscopy, anterior 941
Mediastinum 3, 4, 25, 33, 40, 44, 89, 929, 937, 938
anterior 938
diseases of 935, 937
masses in middle 951
metastasize to 954
middle 938
miscellaneous disorders of 957
posterior 938
superior 959
Medical Research Council 595
Medications, several 694
Medullary respiratory center 123, 126
Mefloquine 427
Meigs’ syndrome 904, 918
Melanocyte-producing hormone 621
Melioidosis 433, 441
diagnosis of 443
Mendelson's syndrome 579
Meningeal tuberculosis 215
Meninges, fungal invasion of 378
Meningism 283
Meningitis, acute 283
Mental changes 786
Mental confusion 785
Mental depression 543
Mepolizumab 477, 558
role of 477
Mercury 967
Meropenem 242, 245, 363, 372
Mesalamine 887
Mesenchymal tumors 957
Mesothelin related protein, soluble 931
Mesothelioma 88, 90f, 929, 930f, 932
diagnosis of 931
malignant 928, 930, 931, 932f
risk of 928, 929, 981
stage III 932
Mesothelium 929
Metabisulfites 456
Metabolic acidosis 119, 122, 191, 536, 786, 846
management of 122
Metabolic alkalosis 119, 121, 122
Metabolic causes 1051
Metabolic changes, primary 121
Metabolic derangements in disease 147
Metabolic disorders 749
Metabolic function of lung 132
Metabolic manifestation 217
Metabolic myopathies 1054
Metabolic syndrome 1071
Metabolism 55
Metal dusts 966
Metalloproteinases 609
Metapneumo virus 305
Metastasis 627, 932
cranial 619
Metastatic calcification 885
Metastatic cancer 627
Metastatic lymphadenopathy 953
Metastatic mediastinal adenopathy 92f
Metered-dose inhaler 471, 471f, 493
Methemoglobinemia 112, 587, 588
Methicillin-resistant Staphylococcus aureus 272, 288, 321, 341, 904
Methotrexate 693, 861, 1016, 1017, 1025
lung 864
toxicity 1026f
Methyl isocyanate
gas 580, 967, 997
inhalation of 999
respiratory effects of 999
Methylchrysene 606
Methylprednisolone 693
Methysergide 915
Meticulous asepsis 344
Meticulous examination 1055
Metronidazole 372, 431
Microbiological techniques, newer 281
Microbiology 337
Microepidermoid carcinoma 650
Microfilaremia 415
Microlithiasis, typical of 48f
Micropolyspora polyspora 718
Microsporidium 401
Midazolam 795
Middle east respiratory syndrome 303
Middle lobe
atelectasis, right 43
pneumonia, right 34f
syndrome 354
Miliary lesions, multiple small 215f
Miliary tuberculosis 48f, 61f, 215, 215f, 218f, 698, 840, 913
Miller's lung 719, 720
Mineral dusts 966
Minimally invasive adenocarcinoma 610, 612
Minimum intensity projection 14, 17f
Ministry of Environment and Forests 994
Minocycline 693, 1017
Minute ventilation 486, 780, 784, 807
Mitochondrial myopathy 1054
Mitomycin 1026, 1027
Mitotic disease
progression of underlying 314
spread of 335
Mitral incompetence, functional 891
Mitral stenosis 181, 189
Modalities, newer 828
Moist sounds 200
Molecular diagnostics from culture growth 255
Molecular tests 255
Mometasone furoate 473
Monge's disease 1012
Mononeuritis multiplex 744
Mononuclear cells 414f, 860, 918
Monophonic wheeze 469
Monoresistant tuberculosis 236
Moraxella catarrhalis 266, 276, 277, 358, 374, 384, 386, 534, 539
Morbidity weekly report 391
Morgagni presents 950
Morgagni's hernia 74, 74f, 75f, 90, 950
Mortality rates 211
Mortality weekly report 391
Mosaic attenuation 67
Mosaic perfusion 67
Motor neuron disease 1054
Motor vehicular accidents 1071
Mountain sickness, acute 1008, 1009
Mouthpiece volume ventilator 1058
Moxifloxacin 234, 242, 245, 350
Mucociliary transport 561
Mucoepidermoid carcinoma 610
Mucoid 553
impaction 47, 562
Mucolytic agents 553
Mucopurulent expectoration 553
Mucopurulent sputum 886
Mucormycosis 327
Mucus gland changes 459
Mucus layer 561
Multicentric Castleman's
disease 405
syndrome 953
Multidetector scanners, single-detector to 10
Multidrug-resistant 244, 248, 253
treating 242
tuberculosis 206, 224, 236238, 239f, 240, 242t, 254, 287
epidemiology of 237
treating 243
types of 236
Multifactorial causes 1041
Multigenic disease 758
Multi-organ failure 337, 442
Multiorgan histiocytic disorder 696
Multiplanar reconstructions 12
Multiple drug-resistance pathogens 340t
Multiple system atrophy 1048
Multisystem disease 696
Muscle
bronchial 103, 533
diaphragmatic 136
disorders of 1053
fatigue 136, 783
central 136
ventilator support with severe 804
groups, small 134
internal intercostal 98
pains 687
paralysis of 1049
relaxants 440, 1020
strength
and function, reduced 1057
expiratory 1056
tests
for expiratory 1057
for inspiratory 1057
tumors, smooth 957
twitching 786
weakness 133, 687, 871, 1050
Muscular dystrophy 1041
Musculoskeletal pain 194
Musculoskeletal system 621, 688
Mushroom-worker's lung 719, 720
Musical industries 10
Myalgia 298, 445, 736
Myasthenia gravis 90, 779, 1052
use of prostigmine in 789
Myasthenic crisis, acute 1053
Mycetomas 182
Mycobacteria 254
atypical 311, 313, 347f
growth index 224
rapidly growing 346
Mycobacterial growth indicator tube 255
Mycobacterial infection 322
Mycobacterial lipoarabinomannan 258
Mycobacterial taxonomy 345
Mycobacterial tuberculous 861
Mycobacterium abscessus-pulmonary disease 350
Mycobacterium africanum 345
Mycobacterium avium 281, 395
complex 401
intracellulare 394, 561
complex 357
Mycobacterium bovis 345
Mycobacterium intracellulare 281
Mycobacterium kansasii 281, 357
Mycobacterium malmoense-pulmonary disease 350
severe 351
Mycobacterium scrofulaceum 281
Mycobacterium tuberculosis 208, 213, 224, 237t, 245, 249, 252, 266, 267, 272, 273, 273f, 277, 281, 286, 311, 313, 342, 345, 360, 392, 395, 401, 507, 676, 689, 913
complex 258, 345
infection 270
testing 225
Mycobacterium Xenopi-pulmonary disease 350
severe 350
Mycophenolate 313, 862, 866, 872
mofetil 693, 862
tacrolimus 313
Mycoplasma 178, 277, 311, 313, 534, 713
infection 281
pneumonia 266, 272, 273f, 277, 279, 280, 281, 283, 379, 386, 534
Mycoplasmal infection 272
Mycoplasmal pneumonia 37, 272
Myeloma 194, 313
multiple 16, 312
Myeloperoxidase 735
Myeloproliferative disorders 749
Myocardial dysfunction 844
Myocardial infarction 587, 588, 759, 891, 1070
Myocardial injury 1034
Myocarditis 272, 295
acute 283
Myocyte
changes 459
hypertrophy 459
Myopathy 1050
chronic inherited 1053
inflammatory 1053
Myotonia dystrophica 1053
N
N-acetylcysteine 667
Nails, clubbing of 198
Naproxen 1021
Narcolepsy 1067
Narcotic poisonings, use of naloxone in 789
Nasal cannula 591
Nasal catheters 589
Nasal endoscopy 374, 377
Nasal expiratory positive airway devices 1073
Nasal intubation 154
Nasal mucosa, invasion of 377
Nasal polyps 177
Nasal prongs 589, 590f, 593
Nasopharynx 125
National Ambient Air Quality Standards 990, 992f, 993f
National Cancer Registry Program 604, 604f
National Emphysema Treatment Trial 557
National Healthcare Safety Network 331
National Institute of Communicable Diseases 294
National Institute of Virology 294
National Institutes of Health 396, 748
National Safety Healthcare 331
National Sample Survey 210
National Tuberculosis Control Program, revised 207
National Tuberculosis Institute 206
National Tuberculosis Program, revised 240
Natriuretic peptide 468
Nausea 233, 270, 272, 485
Near-fatal asthma 493, 494
Nebulization, solution for 550
Nebulized colistin 566
Nebulized tobramycin 566
Nebulized β-agonists 483
Nebulizer 488
solution 488
Necator americanus 412
Neck
and axilla 939
extension 790
for lymph glands, palpation of 198
girth 1068
Necrotizing bronchiolitis 580
Necrotizing granulomas 684f, 739f
Necrotizing pneumonia 276, 369
Necrotizing sarcoid granulomatosis 684
Necrotizing sarcoidosis 684f
Neisseria pharyngitis 332
Nematode infections, pulmonary manifestations of 411
Neodymiumyttrium aluminum garnet laser 642
Neonatal hepatitis syndrome, benign 509
Neonatal tetanus 438f
Neoplastic pathologies 863
Neoplastic tissue 929
Nephropathy, contrast induced 15
Nephrotic syndrome 16, 396, 759, 899, 903
Nephrotoxicity 233
Nerve
intercostal 938
peripheral 1050
roots, disorders of 1050
sheath tumors 954
Neurally adjusted ventilatory assist 819
Neuritic pathologies, rarer 1050
Neuroblastoma 955, 955f, 956
Neuroendocrine
carcinoma, large cell 643, 610, 613
cell hyperplasia 579, 580
marker chromogranin 649f
tumor 648, 648f, 649, 649f
intrabronchial extension of 648f
Neurofibroma 954, 955f
Neurofibromatosis 713
diagnosis of 705f
Neurogenic pulmonary edema 1047
Neurogenic tumor 954, 954f
Neuroleptics 1020
Neurological deficits 956
Neurological involvement 738
Neurological syndromes 623
Neuromuscular adverse effects 1020
Neuromuscular blocking agents 487
Neuromuscular disease 174, 189, 192, 1041, 1043, 1055
management of 1057
Neuromuscular disorder 1016, 1047, 1054
chronic 1055
Neuromuscular junction 134, 1051
Neuromuscular paralysis 541, 803
Neuromuscular respiratory system 1057
Neuromuscular weakness 1074
Neuronal discharge 123
Neuropathy
autonomic 621, 623
peripheral 231, 621, 745, 930
Neuropsychiatric complications 1003
Neurosarcoid 686, 688
Neutropenia 313
severe 312
Neutrophil defect, functional 313
Neutrophilic airway diseases 478
Neutrophilic phenotype 478
Neutrophils 358, 362, 458, 513, 521, 843
predominate 513
New York Heart Association 756
Nickel 608
carbonyl 967
Nicotine
replacement therapy 546, 547
side effects of 547
Nifedipine 1011
Nintedanib 667
Nipple 24
shadow 24f, 25f
bilateral 24f
Nitric oxide 458, 465, 521, 749
synthase 1005
Nitrofurantoin 197, 420, 915, 1016, 1020
toxicity 1020f
Nitrogen
concentration 146
high 146
dioxide 534, 967
higher concentration of 146
meter 146
mustards 967
oxide 580, 988, 989, 1001
washout test 142
Nitropropane 606
Nitrotyrosine 465
Nitrous oxide 854, 877
N-nitrosamines 606
N-nitrosodiethylamine 606
N-nitrosodimethylamine 606
Nocardia 311, 313, 392
asteroides 275, 367, 371, 393, 912, 971
species 266, 275, 277
Nocardial infection 322, 627
Nocardial pleural effusions 912
Nocardiosis 275f, 322, 399
Nocturnal asthma 463
Nocturnal choking 1066, 1067
causes of 1067t
Nocturnal hypoventilation, absence of 1045
Nocturnal hypoxemia 1053
Nocturnal myoclonus 1067
Nocturnal oximetry 1068
Nocturnal oxygen 596
therapy 596, 597
trial 595
trial survival data 596f
use of 596
Nocturnal symptoms 479
Nodular lesions, multiple small 48f
Nodular opacities 58
Nodular parenchymal amyloidosis 710
Nodular pleural lesions, multiple 617f
Nodule
centrilobular 62f, 723
cutaneous 277
enhancement 55
morphology 51
multiple 631
Noise
breathing 616
pollution 988
Non-aspergillus filamentous fungal infections 326
Nonasthmatic eosinophilic bronchitis 176
Noncardiorespiratory causes 189
Noncaseating granulomas 675, 677, 679f, 686f, 689
Noncavitatory disease 244
Noncystic fibrosis 362
Non-Hodgkin's lymphoma 159, 394, 403, 404f, 649, 883, 884, 918, 947, 948, 948f, 1026
Non-Hodgkin's variety 649
Non-human immunodeficiency virus, pneumonia in 311
Non-immunohistochemistry biomarkers 931
Nonindustrial mesothelioma 929
Noninvasive tests 325
Nonmalignant disorders 405
Nonmetastatic paraneoplastic manifestations 620
Non-necrotizing granuloma 722f
Nonrespiratory complications 295
Nonrespiratory conditions 537
Nonsteroidal anti-inflammatory drugs 232, 457, 496, 918, 1017, 1021
use of 567, 584
Nonsteroidal inflammatory drugs 861
Nontuberculous adenopathy 354
Nontuberculous mycobacteria 223, 257, 258, 345, 346, 348, 349, 357, 358, 392, 566, 719, 720
disease 348
infection, treatment of 351
lung disease 348
pulmonary
disease 348
infection, treatment of 351
Nontuberculous mycobacterial infections 345
Nose 125, 737
sarcoid involvement of 685f
Nosocomial bloodstream infection 845
Nosocomial infections 334t
Nosocomial isolates, resistance in 385
Nosocomial pneumonia 321, 331, 333, 334f, 334t, 335f, 336, 337, 340, 342, 426, 845
clinical diagnosis of 334t
diagnosis of 845
management of 845
pathogenesis of 332fc
prevention of 342, 343t
severe 340t
No-touch sterile technique 800
Noxious 840
Nucleic acid
amplification techniques 258
hybridization probes 255
testing 296
Numerous diseases 180
Numerous enzymes 609
Nurses 554
Nutrition 268
poor 267
Nutritional guidance 555
Nutritional support 854
Nystagmus 233
O
Obliterative bronchiolitis 863, 863f, 864, 1023
Obstruction, inflammatory 886
Obstructive pulmonary disease, mild chronic 547f
Occupational asthma
immunological IgE-mediated 983
immunological non-IgE-mediated 983
Occupational diseases, treatment of 965
Occupational exposure 507
Occupational lung
disease 176, 963, 965
classification of 966t
prevalence of 966t
disorder, diagnosis of 966
Occupational triggers 456
Ocular sarcoid 685
Ocular toxicity, monitoring for 232
Oils and coke 608
Omalizumab 476, 477
Ondine's curse 1047
Open lung 851
biopsy 664, 667
concept 817, 819
procedure 818t
ventilation 851
Open pneumothorax 923f, 927
Open-heart surgery 1050
Operative mortality 640
Opisthotonos 438f
Opportunistic infections 668, 669, 861
monitor for 743
Optic nerve toxicity 232
Optimal oxygenation 816
Optimized background therapy 246
Optimized smear microscopy 254
Oral
anaerobes 266
antibiotic therapy, prolonged 363
anticoagulation 768
appliances 1073
contraceptives 759
corticosteroid 456
therapy 671f
endotracheal intubation 153
intubation 154
procedure for 153
salbutamol 488
theophylline 481, 488, 539
β2-agonists 478
Organ dysfunction, multiple 114, 342, 845
Organ failure
assessment, sequential 338
multiple 340, 893
Organ systems 868
Organ transplant 918
recipients 290
single 314
Organic dust toxic syndrome 722
Organising pneumonia 392, 426, 578, 655, 671, 861, 886, 1018, 1022
Organisms, multiple 392
Organophosphorus poisoning 839, 1051
Organs and organ systems 687
Oropharyngeal airway 791
Oropharyngeal secretions 344
Oropharynx 553
colonization of 274
Orthodexia 876
Ortho-toluidine 606
Oscillating ventilation, high frequency 850
Oseltamivir 296, 297, 300, 305
Osler's saying 1015
Osler's time 1015
Osseochondrous tumors 957
Osteoarthropathy, hypertrophic pulmonary 621, 622
Osteopathy, hypertrophic pulmonary 623
Osteopontin 931
Osteoporosis 473
Ototoxicity 233
Outpatient department treatment 287
Ovarian enlargement 893
Ovarian hyperstimulation syndrome 892, 916
Ovarian teratomas 946
Overexpands air 45
Overlap syndrome 530, 872
Overlapping toxicity 251
Owl's eye 328
Oxidative stress, role of 521
Oxygen 141, 482, 556, 588, 594, 770, 1010
administration 589
devices, low-flow 589
methods of 589
alveolar pressure of 188
and exhaled gas 142
arterial pressure of 586
concentration of 108, 806, 807
consumption 113, 889
content 112
delivery system, long-term 597
diffusion of 781
dosage of 596
effect of 593t
exchange 106
extraction ratio 114
partial pressure of 155, 285, 591
release, failure of 784
role of 556
saturation 147, 282, 1069
low 397f
stores 586
supplemental 846, 1012, 1027, 1038
tension in arterial blood 777
therapy 555, 586, 591
complications of 594
indications for 586, 587t
long-term 555, 595, 596
routine 589
toxicity 594, 850
transport 113, 188
failure of 783
maximal 816
supramaximal 853
uptake, maximal 147
use of 787, 789
utilization, failure of 784
withdrawal, danger of 594
Oxygenation 809, 827
impaired 877
proof of impaired 877
Oxyhemoglobin
dissociation curve, normal 113f
level 1065
Oxytocin 894
Ozone 534
depletion 993
P
Pacemaker insertion 922
Pacing catheter 166
Paclitaxel 642
eluting stents 1027
Pain 195
abdominal 233
acute severe 195
complaint of 1033
control of 1037
ischemic cardiac 194
relief of 1039
Palisaded histiocytes 739f
Palliative therapy 933
Palpitation 550
P-aminosalicylic acid 245
Panacinar emphysema 67f
Panbronchiolitis, diffuse 578, 583
Pancoast's tumor 194, 195, 616, 618, 619f, 640, 641
Pancreatic diseases, pulmonary manifestations of 876
Pancreatic insufficiency 560, 563
Pancreatic pseudocyst 904
Pancreatitis 840, 904
acute 283, 839, 881, 881f
recurrent acute 564
Pancuronium 441
Panda sign 691
Panlobular emphysema 65, 513
Panton-valentine leukocidin 266, 385
Papilloedema 686f, 786
Papilloma 627
Para influenza 305
Para-aminosalicylic acid 206, 242
Paracardiac masses 90, 91
Paracoccidioides brasiliensis 305
Paradoxical movement 97
Paradoxical reaction 251, 395
Paragangliomas 956
Paraganglionic neoplasms 956
Paragonimiasis 411, 419, 420
Paragonimus worms 419
Parainfluenza 311, 534
virus 266, 292, 302, 580
Paralysis 440
acute
hyperkalemic 1055
hypokalemic 1055
bilateral diaphragmatic 198
irrecoverable diaphragmatic 1058
Paralytic agents, use of 852
Paranasal sinuses 374, 564, 739f
axial computed tomography scan of 377f
X-ray of 374
Paranasal sinusitis 744
Paraneoplastic manifestations 942
Paraneoplastic pemphigus 579, 580
Paraneoplastic syndrome 581, 620, 623, 871, 930, 939, 940t
rare 623
Paraplegia 759
Parapneumonic effusion 900, 904
uncomplicated 903
Parapneumonic pleural effusions 903
Paraquat 967
Paraseptal emphysema 66, 513, 530f
Parasites 266
helminthic 410
Parasitic disease 420, 900
Parasitic helminths 410
Parasitic infections 392
Parasympathetic fibers 1008
Parathyroid
adenoma 949f
hormone-related protein 621
masses 949
Paravertebral tubercular abscess 956
Parenchyma 920, 1043
Parenchymal asbestosis 978, 979, 979t
Parenchymal disease 18
Parenchymal injury 1016
Parenchymal lung
disease 18, 189, 1055
lesions 26
Parenchymal necrosis, suppurative 367
Parenchymal opacification 59f, 61
ground-glass pattern of 62f
Parenteral nutrition, total 385
Parietal pleura 897
Parkinson's disease 1048
Parotid gland enlargement 680
Peak airway pressure 806, 960
Peak alveolar pressure 806
Peak expiratory flow 463, 491f, 494
limitations of 463
rate 827, 985
utility of 463
Peak inspiratory pressure 812f, 818, 822f
Peak oxygen uptake 147
Pemphigus 581
Penicillamine 420, 580, 861, 1018
Penicillin 420
Penicilliosis marneffei 327, 443
Penicillium 443
marneffei 393
Pentamidine 400, 432
Percutaneous dilatational tracheostomy 156
Percutaneous subclavian venepuncture 169f
Percutaneous techniques 166
Percutaneous tracheostomy 793
Percutaneous transthoracic needle puncture 282
Perfusion 877
abnormality 877
inequalities 111, 1047
lung scintigraphy 761
scan 19f
Peribronchial interstitial thickening 59f, 684f
Peribronchial lymphatics 131
Peribronchovascular ground-glass densities 1017f
Peribronchovascular interstitial thickening 56f
Peribronchovascular interstitium 33f, 57
Pericardial cyst 949, 950f
Pericardial disease 188
Pericardial effusion 189
Pericarditis 194, 295, 887
constrictive 903
Pericardium 57f, 929
Perilymphatic nodules 60f
Periodic acid-Schiff 712
reagent 972
Periodic limb movement disorder 1067
Periodontal disease 277, 367
Peripartum cardiomyopathy 891
diagnosis of 891
Peripheral air-space consolidations 36
Peripheral nerve tumors, malignant 954
Peripheral nodule, small 625
Peritoneal cavities 436, 928
Permissive hypercapnia 814, 851
Persistent alveolar leak 925
Persistent bronchopleural fistula 911
Persistent cough 309f
Persistent hypercalcemia 692
Persistent rhinosinusitis 360
Pet allergen avoidance 471
PET scan 701
pH 901
Pharmacopoeia 1015
Pharyngeal axis 794f
Pharyngitis 305
Phenotypic methods 228
Phenylalanine 560
Phenytoin 915, 1017
Pheochromocytoma 940, 956
Phlyctenular conjunctivitis 213
Phosgene 967
Phosphodiesterase
inhibition of 552
type-5 inhibitors 754
Phosphokinase, creatine 435, 1053
Photodynamic therapy 158, 642
Phrenic nerve 1058
injury 1050
Phthalic anhydride 720
Physiotherapists 554
Pigtail catheters 164
Piperacillin 340, 341, 363, 372, 566
Pirbuterol 478
Pirfenidone 667
Pituitary 696
Plague 443, 444, 444f
Plasma 117, 119
bicarbonate 120
oncotic pressure 897
Plasmodium falciparum
infection 825, 840, 841, 847
malaria 433, 841
Plate atelectasis 38, 42f
Plateau pressure 485
Pleura 3, 33, 173, 929
diseases of 895, 1039
functions of 897
Pleural aspiration 931
Pleural biopsy 165, 860, 901, 914, 915, 922
Pleural calcification 88
Pleural cavities 165, 937
Pleural change, type of 979
Pleural disease 864, 900
Pleural effusion 38, 78, 79f81f, 214, 215, 425, 436, 537, 860, 870, 876, 883, 899f, 901, 902, 902fc, 903, 911, 915, 918, 933, 939, 978
causes of 898t
control of 933
hemorrhagic 81f
small 80
small-to-moderate 898
Pleural exudate 883
causes of 904t
etiology of 900t
positive culture of 338
Pleural fibroma 623
Pleural fibrosis, asbestos-related 978
Pleural fluid 281, 897, 901, 913, 914
amylase concentration 901
aspiration of 922
eosinophilia 900
examination 899, 908
lymphocytosis 900
Pleural infections, uncommon 911
Pleural injury 1016
Pleural lesions 51
Pleural mesothelioma 89f, 904, 914, 928, 929, 931, 981t
malignant 928, 929, 931, 932
risk of 928
treatment of 933
Pleural metastases 617f, 904, 914f
Pleural pathology 176, 189
Pleural plaques 979, 980f
Pleural rub 200
Pleural space 909
Pleural thickening 87, 89f
Pleural transudate 883
causes of 903t
Pleural tumor 928
Pleurectomy, partial 933
Pleurisy, drug-induced 915
Pleuritic chest pain 194, 195, 269, 324, 523, 921
Pleuritic pain 971
Pleuritis 887
Pleurodesis 933
Pleuropericarditis 1027
Pleuropulmonary
disease 1045
lesions 431
manifestations 864
symptoms 1020
Pneumatocele 66
multiple 400f
Pneumococcal pneumonia 270f, 280
Pneumococcus 341
Pneumoconiosis 656, 968971
Pneumocystis
carinii 277, 280, 393, 924
infection 831, 924
extrapulmonary 396
infection 321, 861
jirovecii 311, 313, 396, 400, 400f
infection 325
jirovecii pneumonia 36, 39f, 64f, 314f, 316, 319, 392, 393, 395397, 397f, 398f, 399, 400, 400f, 742
prophylaxis, use of 393
pneumonia 391, 443
Pneumomediastinum 487, 889, 960, 962
causes of 960
Pneumonectomy
contralateral 163
extrapleural 933
Pneumonia 64, 174, 180, 214, 265, 268, 269, 276, 278, 290, 302, 305, 312, 319fc, 328, 331, 360, 394, 433, 439, 485, 528, 537, 616, 627, 810, 845, 897, 1024f, 1043
acute 536
eosinophilic 727, 728, 845, 847
interstitial 64f, 65f, 655, 664f, 713, 845
reversible 1022
tuberculous 273f
anaerobic bacterial 276
bacterial 295, 297, 320, 433, 839
chronic 371
eosinophilic 64, 713
cryptogenic
chronic eosinophilic 727, 729
eosinophilic 420, 727, 729
organizing 37, 578, 579, 627, 655, 656, 671673, 713
diagnosis of 435
drug-induced eosinophilic 1018
estimating severity of 284, 284t
etiology of 277t
exogenous lipid 713
healthcare-associated 331
hematogenous 333
hospital-acquired 331
in immunocompromised patients 311t
increased risk of 553
influenzal 292, 296t
lobar 270f
nonbacterial 292, 394
pathogens causing 313t
prevention of 290
primary 295
serious 553
severity index 285
still persists 906
supportive treatment in 289
suppurative 367
syndrome
idiopathic 314
typical 269
type of 664
ventilator-associated 331, 332, 334, 335f, 338, 385
viral causes of 292t
Pneumonitis 265, 354, 883, 999, 1021
drug induced 713
gold-induced 1023
Pneumoperitoneum 487
Pneumotaxic center 123
Pneumothorax 38, 82, 83f, 84, 84f, 85, 85f, 86f, 88f, 164, 165f, 168, 182, 198, 400, 487, 528, 537, 543, 568, 587, 668, 669, 698, 700f, 702, 706, 824, 893, 900, 925f, 999, 1036
benign spontaneous 920
bilateral 925
causes of 922t
chronic 925
complications of 924, 925t
iatrogenic 927
increases 84
loculated 88f, 925
management of 86, 926, 927t
primary 921
spontaneous 85, 920
secondary 920, 921, 923, 926
signifies 920
traumatic 927
Poisoning 839, 840
Poisonous shell-fish 1055
Poland syndrome 48
Poliomyelitis 1049
acute 779
Pollution
adverse effects of 989
control 993
environmental effects 989
forms of 988
health effects 989
outdoor 454
prevention approach 994
Polyangiitis 371, 420, 687, 689, 727, 735, 736, 739f, 743, 746t, 845, 847, 1026
involving lungs 739f
microscopic 735, 746, 884
Polyarteritis nodosa 735, 746, 746t
Polycyclic aromatic hydrocarbons 606
Polycythemia
reduction of 595
secondary 1012
severe 1012
Polydrug-resistant tuberculosis 236
Polymerase chain reaction 160, 205, 266, 279, 317, 325, 329, 348, 430, 929
Polymorphonuclear leucocytosis 729, 900
Polymyositis 580, 621, 622, 735, 859, 871, 1055
acute infective 779
Polyneuropathy 744
Polypeptides 621
Polysomnography 750, 751
monitoring equipment 1068f
Polytrauma 800, 1035
Pompe's disease 1054
Popcorn calcification 51
Porphyria, acute intermittent 1055
Portopulmonary hypertension 876, 879
Portosystemic anastomosis 879
Positive end-expiratory pressure 424, 435, 485, 533, 594, 773, 802, 808, 815, 815f, 816, 817f, 818, 821, 849
complications of 816
use of 809, 814
Positive pressure ventilation
advantage of noninvasive 831
contraindications of noninvasive 831t
implementation of noninvasive 541
noninvasive 540, 540t, 831, 1058
Positron emission tomography 22f, 637, 645
Post stroke 1071
Postbiopsy pneumothorax 164
Postcoronary bypass graft surgery 915
Postdischarge precautions 926
Postextubation tracheal stenosis 800f
Postpoliomyelitis muscular atrophy 1049
Postprimary pulmonary tuberculosis 215
Postsplenectomy state 290
Post-transplant obliterative, management of 581
Post-tussive syncope 174
Postviral fatigue syndrome 1067
Potassium bisulfite 456
Potential asthma 452
Pott's disease 205
Pott's spine 1042
Poverty 267, 268
Pranayama 478
Praziquantel 419
Prednisolone 403, 688, 862
Preeclampsia 889
pulmonary edema in 890
Preexisting cardiac disease 891
Pregnancy 759, 893
and lactation 234
breathlessness, last trimester of 889
cardiomyopathy of 889
effects of 495
respiratory system in 889
trophoblastic disease in 892
tuberculosis in 894
Pressure
esophageal 145
ventilation, positive 922
Pressure-regulated volume control 819
Primary disease, reactivation of 215
Private public mixes 260
Private sector, unregulated 241
Procainamide 915, 1027
Prone posture, use of 850
Prophylactic drug therapy 399
Propionibacterium acnes 676
Prostacyclin 854
analogs 879
Prostaglandin 457, 458
Prostanoids 754
Prosthetic stents, use of 642
Protease-antiprotease imbalance 521
Protein 900
derivative, purified 252
eosinophilic cationic 465
nitrosation 969
Proteinaceous fluid 972
Proteus mirabilis 385
Prothionamide 242, 245
Protozoal infections
pulmonary manifestations of 423
rare 431
Provocation tests 468
Pruritis 232
Pseudochylothorax 899, 917
Pseudoemphysematous lobe 214
Pseudomembranous tracheobronchitis 324
Pseudomonas 288, 341, 904, 905
aeruginosa 35, 274, 275, 311, 313, 315, 321, 333, 356, 358, 363, 370, 383, 439, 534, 536, 539, 561, 564, 566, 567, 583
infection 566, 567
pseudomallei 275, 277
pyocyaneus 367
strains 823
Psychiatrists 554
Psychogenic cough 178
Psychogenic dyspnea 191193
Psychological counseling 555
Psychological stress 456
Public health problem 971
Public sleep laboratories 1065
Puerperium 759
Pulmonary adverse effects 1025
Pulmonary alveolar
hemorrhage 883
microlithiasis 713, 714
proteinosis 157f, 656, 710, 710f, 711f
Pulmonary amyloidosis 708
Pulmonary angiogram 22f
Pulmonary angiography 20, 191, 750, 751, 761, 764, 878, 1022
normal 30f
Pulmonary arterial
branch 32
hypertension 749
pressure 130, 752
Pulmonary arteriopathy 698
Pulmonary arteriovenous
fistulae 418
malformation 71, 72f, 73f
Pulmonary artery 26, 29, 78, 127, 160, 184, 514, 738, 752, 763f, 960
aneurysms of 952
catheterization 184
curved multiplanar reconstruction of 14f
left 12, 14, 27, 28
main 28
occlusion pressure 837
pressure 130, 130f, 1043
right 12, 14, 23, 27, 28
rupture of 182
unilateral absence of 78
Pulmonary atelectasis 314, 537
major 782
Pulmonary blood 129
flow, measurement of 129
Pulmonary calcification 883
Pulmonary circulation 127, 418, 1008, 1016
adverse effects on 1019
hemodynamics of 127
Pulmonary compliance 846
reduced 837
Pulmonary complication 859, 873, 884, 886, 1021, 1036
noninfectious 295
Pulmonary component 1010
Pulmonary contusion 1036
Pulmonary cysts 705
Pulmonary cytokine production 849
Pulmonary disease 510, 753, 971
chronic 506f
obstructive 533t
progressive 308
pathogenesis of chronic obstructive 520fc
prevalence of chronic obstructive 505
severe chronic obstructive 525f, 548f
Pulmonary drug toxicity, diagnosis of 1027
Pulmonary edema 38f, 39f, 131, 189, 314, 335, 425, 434, 713, 844, 846, 881, 883, 889, 890, 897, 1010, 1011, 1018
drug-induced 892
noncardiogenic 998, 999
Pulmonary emboli 764f
small 20
Pulmonary embolism 48, 144, 192, 194, 400, 426, 668, 669, 757, 758, 760t, 766f, 767t, 898, 900, 904, 915
and infarction 865
complicating 536
diagnosis 760
management of 768, 768t
mortality of 765
severity index 767t
simplified 767
sources of 758
syndromes 760, 760t
Pulmonary endarterectomy 755
surgical 755
Pulmonary eosinophilia 411, 727
causes of 420t
Pulmonary features, management of 565
Pulmonary fibrosis 38, 99, 356, 678, 859, 864, 1018
evidence of 868
Pulmonary filariasis 412
Pulmonary function 456, 515, 546, 877, 973, 982
test 14, 138, 472f, 487, 496, 576, 656, 661, 667, 750, 751, 877, 975, 1043t, 1068, 1074
Pulmonary gas exchange 518
Pulmonary hemorrhage 64, 335
complicating renal disease 884
Pulmonary hemosiderosis 714
Pulmonary histiocytosis 749
Pulmonary hydatid cyst 421f
Pulmonary hyperinflation 516
Pulmonary hypertension 144, 188, 189, 191, 192, 195, 405, 418, 514, 519, 535, 562, 684, 694, 702, 748, 750t, 751f, 753, 759, 864, 867, 868, 870, 872, 879, 885, 892, 976
classification of 749t
estimating severity of 752t
history of 748
investigations of 750t
obstructive 879
passive 879
pathogenesis of 749
prevalence of 749
primary 392
signs of 657
therapy for 753, 754t
Pulmonary hypoplasia 78
Pulmonary immune response 392
Pulmonary infarct 36f, 761f
Pulmonary infarction 174, 194, 314, 335, 759, 900
syndrome 760
Pulmonary infection 310, 345, 394, 511, 543, 698, 864, 868, 884, 905
acute 536, 782, 840
chronic 176
epidemiology of 394
risk of 884
treatment of complicating 557
ventilator-associated 342
Pulmonary infiltrates 316t, 575, 744
Pulmonary intravascular abnormalities 878
Pulmonary involvement 433, 709, 737, 865, 874
Pulmonary Langerhans cell histiocytosis 68f, 696, 700f
Pulmonary lobule, secondary 61
Pulmonary lymphangioleiomyomatosis 703
Pulmonary lymphoma 649
Pulmonary manifestations 420, 423, 436, 442, 443, 511, 860, 860t, 864, 883
noninfectious 392t
Pulmonary metastasis 647
role of surgery in 647
Pulmonary nodule 50, 163f, 863, 1022
secondary 56
Pulmonary opacity 33, 33t, 34, 40
bat wing pattern of 36
Pulmonary paragonimiasis 420f
Pulmonary parenchyma 876, 880, 932
Pulmonary perfusion, peripheral 78
Pulmonary physiology 853
Pulmonary rehabilitation 365, 554, 554t, 555t, 668
Pulmonary renal syndrome 1023
Pulmonary sarcoidosis 681, 685
Pulmonary schistosomiasis 418f
Pulmonary sequestration 76, 77f, 278
Pulmonary stretch receptors 124
Pulmonary thromboembolic disease 181, 870, 890
chronic 191, 192
Pulmonary thromboembolism 537, 543, 557, 889, 891
Pulmonary thromboembolus disease 188
Pulmonary toxicity 426, 1022, 1023
diagnosis of 1027
Pulmonary toxoplasmosis 432
Pulmonary tuberculosis 177, 203, 218f, 219f, 221f223f, 345, 347, 393, 409, 442f, 507, 727, 894, 973
primary 213
reactivation of 226f
Pulmonary vascular
disease 192, 870
disorders 733
involvement 867
resistance 128, 128f
Pulmonary vasculature 78
Pulmonary vasculitides, other 747
Pulmonary vasculitis 420, 735, 840, 845
Pulmonary vasoconstriction 535
Pulmonary veins 76
Pulmonary veno-occlusive disease 748, 753, 1020
Pulmonary venous pressure 130
Pulmonary vessels 20, 32, 735, 879, 1008
Pulmonary-renal syndrome 885
Pulmonary-systemic collaterals 78
Pulse oximetry 878
Purulent fluid, tube drainage of 909
Purulent sputum 334
Pyoderma granulosum 886
Pyogenic bacteria 311, 313
Pyogenic meningitis, acute 283
Pyopneumothorax 368, 925
Pyrazinamide 227, 229, 232, 233, 237, 242, 244246
Pyrexia 326
Pyridoxine 233
supplementation 231, 234
Pyrimethamine 427
Q
Q fever 269
Quality microscopy 229
Quinidine 1027
Quinine 427
Quinolone 363
use of 244
R
Rabies 840, 1048
Radial artery catheterization, technique of 168
Radiation fibrosis 41f
Radiation therapy 396, 639
adjuvant 641
Radiation toxicity 314
Radioactive selenomethionine 940
Radiofrequency ablation 165, 166f
Radiographs, portable 8
Radiological disease, prevalence of 211
Raloxifene 759
Randomized controlled trial 553, 754
Rattus rattus 444
Raynaud's phenomena 198, 868, 870
and sclerodactyly 657
Recombinant human deoxyribonuclease 362
Recombinant tissue plasminogen activator 769
Recurrent pneumonia 276, 278, 562
causes of 278t
Red blood cells 425, 738, 877
Reference standards 141
Refractory asthma, monoclonal antibodies in 476
Refractory hydrothorax 880
management of 880
Regulate gas exchange 809
Rehabilitation 554
features of 554
Relapsing polychondritis 859
Relaxation pressure 102
Reliever medications 478
Renal cell cancer, inherited 705
Renal diseases 903
pulmonary
associations of 883t
manifestations of 883
Renal dysfunction 692
Renal failure 234, 854
chronic 268, 290, 768
Renal involvement 738, 868
Renal transplantation 884
Rendu-Osler-Weber disease 72
Reproterol 478
Reslizumab 477
Respiration 1047
Respiratory acidemia 120
Respiratory acidosis 117, 118, 120f, 122, 543, 846
Respiratory alkalosis 117, 122, 192, 889
acute uncompensated 121f
Respiratory arrest 120, 587, 1049
Respiratory bronchiolitis 62f, 64, 515f, 582, 655, 672f, 721
Respiratory cilia 561
Respiratory community pathogens, specific 383
Respiratory complications 438
treatment of 568
Respiratory conditions 537
Respiratory depressants, use of 537
Respiratory disease 115, 503, 587, 978
chronic 559
risk factors for 393
Respiratory distress 298, 587, 786, 927
episodes of severe 440
severe 444
syndrome 837
Respiratory drive 826
Respiratory exchange ratio 147, 148
Respiratory failure 115, 518, 777, 863, 976, 1053, 1054
acute 803
onset of 664f
chronic 532, 596, 1059
hypercapnic 596
diagnosis of 1054
hypoxemic 439, 694, 716, 779, 783, 817, 1025
pathophysiology of acute 533fc
reversal of 826
severe
acute 536
hypoxemic 1034
Respiratory frequency 155
Respiratory infection, severe 1058
Respiratory insufficiency, severe 1074
Respiratory involvement 1049
Respiratory mechanics, monitoring of 831
Respiratory misregistration 11
Respiratory mucosa, erythema of 1006
Respiratory muscle 97, 102, 136, 137, 518, 1043, 1048, 1050, 1055
action of 97
adaptation of 137
fatigue 136, 425, 551, 783, 784, 1037
features of 784t
function 533
testing 133
inefficiency 1037
paralysis 1055
severe 1059
paresis of 1055
strength 827
weakness 133, 487, 1049
Respiratory paralysis 1049, 1055
Respiratory physicians 115
Respiratory physiology 130
Respiratory rate 486, 807
Respiratory secretions 1043
culture of 295
obtaining 281
Respiratory stimulant properties 1074
Respiratory support 289, 820, 848
Respiratory symptoms 433, 688, 976
development of 506
Respiratory syncytial virus 266, 292, 301, 305, 311, 392, 453, 534, 580
infection 301
Respiratory syndrome, severe acute 303, 303f, 409
coronavirus 266
Respiratory system 133, 440, 1000t, 1001t, 1004, 1047
clinical examination of 196
effects on 1000t
examination of 523
Respiratory therapists 554
Respiratory tract 268, 998f
epithelium 453
infection 178, 329
acute 178
acute lower 265
acute upper 174
lower 471, 999
Respiratory viruses 311, 313, 329
common 292, 305t
Respiratory-related deaths 475
Restlessness 786
Restriction fragment length polymorphism 256
Restrictive flow-volume loop 141f, 143f
Restrictive lung
disease 139, 143, 190, 782, 1000
lesion 189, 190
pathology 189, 190t, 582
Resuscitation, cardiopulmonary 803
Reticular opacities 47, 49f, 56
Reticulonodular opacitie 47, 47t, 658f
Retrolental fibroplasia 595
Retroperitoneal fibrosis 959
Retrosternal goiter 949f
Reye's syndrome 297
Rheumatic diseases 974
Rheumatoid arthritis 356, 580, 657, 735, 859, 861f, 1025
clinical features of 860
Rheumatoid disease 356, 579, 580, 863f, 900, 918
Rheumatoid nodule 627, 861f
Rheumatoid pleural effusions 900, 901
Rheumatological manifestations 745
Rhinitis 177
acute 174
atopic 464, 481
sicca 873
Rhinocerebral mucormycosis 377, 378f
Rhinosinusitis 455
Rhinovirus 292, 305, 534
Rhodococcus equi infections 371
Rhonchi 200
Rhythm disturbances 786
Rib 194
chondrosarcoma of 647f
computed tomography of 619f
lesions 51
tumor deposits in 194
Ribavirin 305
Ribonucleic acid 252, 393
Rifampicin 229, 231234, 237, 350, 351, 912
dosing of 233
Right heart catheterization 750, 751
parameters 752
Right ventricular
gallop 524
heave 1010
Risus sardonicus 438f
Rituximab 743, 861, 1025
Road traffic accidents 1031
Rural counterparts 1065
S
Saccharomonospora viridis 718, 720
Saccharopolyspora rectivirgula 718, 720
Saccular bronchiectasis 353
Sacroiliac arthritis 886
Sahaja yoga 478
Salbutamol 478, 538
Salicylate 1021
levels 1021
Saline, use of normal 787
Salivary gland
tumor 650
type, carcinoma of 610
Salmeterol 475, 550, 551
Multicenter Asthma Research Trial 475
Salmonella
choleraesuis 433
infections 433, 840
typhi 433, 434
typimurium 433
Salmonellosis 433
Salvage therapy 326
Sarcoid 627
cardiac 688
chronic pulmonary 692
cutaneous 685
granulomas, extensive 684f
hematogenous 688
hepatic 688
myopathy 692
nodules 685
Sarcoidosis 48f, 57, 59, 61f, 190, 198, 392, 501, 584, 657, 674, 675, 679f, 680, 682f684f, 687, 688, 690, 723, 749
acute 680
asymptomatic 680
classic feature of 679
diagnosis of 690
etiology of 675
extra pulmonary manifestations of 685
genetics in 676
interstitial lesions of 48f
pathognomonic of 691
treatment of 693t
wheeze in 657
Sarcomatoid, carcinoma of 610
Sarcomatous 932
Satellite nodules 54
Scapula laterally 3
Scar cancer 613
Schilling's classification 986t
Schistosomiasis 417, 420, 749
Scimitar syndrome 78, 79f
Sclerodactyly 870
Scleroderma 688, 735
Sclerosing cholangitis 886
Sclerosis
amyotrophic lateral 1049
multiple 454, 1048
Scoliosis 1041
causes of 1042t
Cobb angle of 1042f
Scoliotic deformity 1041
Scrub typhus 445
Sebaceous
glands 945
secretions 945
Secretory leucoprotease inhibitor 510
Sedation 852
daily interruption of 343
Sedatives, use of 440
Segmental atelectasis 1036
Segmental bronchus 76
Seizures 34, 786
Seldinger technique, modified 166, 167f
Sensitive injectables, use of 244
Sensory system 123
Sepsis 821
bacterial 700f
severe 114, 333, 840
syndrome 283
Septal lines 47f
Septal thickening 56, 660f
background of 66f
irregular 58f
smooth 47f
Septic pulmonary emboli 367
Septic shock 342, 442, 805
presence of 290
Septoplasty 1073
Serial lung function 662
Serological tests 258, 435
Serum
angiotensin converting enzyme 691, 953
electrolytes, estimation of 119
precipitin antibodies 573
Shock 760, 769, 824
from any cause 587, 588
Shunt within lungs, right to left 781
Shuttle walking test 530
Shy-Drager syndrome 1048
Sickle cell disease 290
Sickness, chronic mountain 1008, 1012
Silhouette, loss of 28, 34
Silica 971
toxicity of 971
Silicon dioxide 971
Silicosis 49f, 61f, 216, 347, 965, 968, 968f, 971
accelerated 974
acute 971
chronic 972
treating 974
Simian virus 929
Sinus 737
aspergilloma 376
computed tomography of 374
Sinusitis 374, 375, 375f, 744
acute 174, 374, 375f
chronic 375f, 376f
bacterial 374
frontal 374
fungi causing invasive 378
Sirolimus 1016
Sitophilus granarius 720
Situs ambiguus 31
Situs inversus 31
Six minute walk test 149, 752
Sjögren's syndrome 356, 688, 859, 873, 873f
Skeletal data 205
Skeletal muscle
tumors 957
weakness 871
Skeletal thoracic abnormalities 189
Skin 696
examination of 198
involvement 738
lesions 315, 698, 705
manifestations 744
prick test 573
rash with 233
test 451, 500
Sleep
deprivation 1067
impact of 1074
quality of 595
studies 530
Sleep apnea 668, 1068
central 597, 1047, 1063, 1074
obstructive 668, 831, 1063, 1064, 1067, 1069, 1073t
treatment of obstructive 1072
Sleep disorder
breathing 597
types of 1063
Smoke inhalation 153
from fire 534
injury 1004, 1005
Smoker's cough 178
Smoking 267, 268
and lung cancer 606
cessation program 546
habits in world 607
passive 504
to lung cancer, relation of 605t
Snakebite 1051
Sniff inspiratory nasal pressure 1058
Sniff nasal inspiratory pressure test 1057
Sniff pressure 134
Soap bubble appearance 419
Society of Healthcare Epidemiology of America 386
Sodium 456
chloride, absorption of 561
nitrite 1004
reabsorption of 118
sulfite 456
Soft tissue 790
abnormalities 48
tumors 957
Solid nodule 631
Solid organ transplant 312
Solid tumors 1024
Solitary nodule, causes of 627t
Solitary pulmonary
mass 630f
nodule 50, 50f55f, 626, 626f, 628, 629f, 673
Somatostatin release mimicking pancreatic tumor 621
Sonography 16
Sore throat 1004
Specimen brush, protected 282, 338
Sphenoidal sinuses 376f, 378
Sphenoidal sinusitis 376
Spinal cord
injury 759, 1047, 1048
tumors 194
Spinal muscular atrophy 1049
Spine 194
metastatic lesions in 194
tubercle of 194, 195
tumor deposits in 194
Spirometry 138, 192, 463, 467, 524
Splenectomy 749
Splenic granulomas 226f
Spondylitis, advanced ankylosing 873
Spontaneous bacterial empyema 879
Spontaneous breathing 136, 826t
trial 827
failure criteria 827t
Spontaneous pneumomediastinum, treatment of 962
Spontaneous pneumothorax 192, 705, 870
management of 926fc
risk factors for primary 920
Sputum
culture 223, 564
cytology 616, 625
role of 638
eosinophilia 468, 492
examination of 310
expectoration of 358
immunodetection 280
microscopy 221
production 533
smear-positive 225
Squamous carcinoma 54f
Squamous cell 944
cancer, surge of 614
carcinoma 610, 611, 613, 615, 628f
tumor 621
Squamous metaplasia 609
Stable nodule 631
Staphylococcal infection 271f
Staphylococcal pneumonia 271f, 272f, 316f
Staphylococcal species 271
Staphylococcus 341
aureus 35, 36f, 266, 277, 295, 300, 311, 321, 337, 356, 358, 367, 370, 374, 383, 384, 386, 392, 401, 561, 564, 566
infection 737
Starling's equation 131
Starling's law 131
Static hyperinflation 516
Static inspiratory, maximal 133
Steady state exercise test 530
Steam inhalation 1058
Stenotrophomonas maltophilia 561, 566, 567
Stereotactic body radiation therapy 638, 640
Steroid 666, 746, 888
dependent asthma 573
myopathy, acute 487
resistance 492
resistant asthma 491
reversibility to 467
role of 398
use of 538
Stevens-Johnson syndrome 579
Stiff lungs 837
Stomach 173
acute dilatation of 283
Streptococcus 277, 341
anginosus 370
pneumoniae 34, 217, 266, 271, 277, 295, 300, 311, 313, 321, 358, 367, 369, 374, 383, 386, 392, 401, 534, 539, 583, 904, 905
infection 433
pyogenes 271, 383, 384
species 271, 880
Streptomycin 229, 233, 234, 237, 242, 444
Stress ulcer prophylaxis 344
Stridor 200
Stroke 1047, 1070
affecting 1047
like syndromes 1054
volume 1069
Strongyloides
infection 411
stercoralis 277, 311, 313, 401, 410
infection 416
Strongyloidiasis 417f, 420
Stuffiness 177
Subclavian artery 28, 29f
aberrant right 29f
left 28
Subclavian vein 29, 166, 167f
catheterization 167
puncture 167f
right 29
Subclinical toxicity 1024
Subglottic secretions, aspiration of 343
Subglottic stenosis 192, 193, 739f, 742
Subpleural bleb 921
Subpleural soft tissue density lesions 764f
Subpulmonic effusion 80
Subpulmonic pleural effusion 79f
Subsegmental pulmonary
arteries 765f
embolus 765f
Sudden death 440, 760
risk of 475
Suffer nonfatal injuries 1031
Sulcus tumor, superior 195, 618
Sulfa drugs 1017
Sulfadoxine 427
Sulfamethoxazole 443
Sulfasalazine 887, 1021
Sulfhemoglobinemia 587, 588
Sulfur dioxide 456, 506, 534, 984, 988, 989, 1001
Sulfur granules 371
Sulfur mustards 967
Sulphamethoxazole 420
Sulphonamides 420
Superinfection pneumonia 342
Supernumerary bronchus 30
Supranational reference laboratories 223
Surface tension 100
Surgery 326, 327
role of 351
Surgical biopsy 670
techniques 941
Surgical treatment 365
Surveillance, epidemiology and end results 644
Susceptibility testing 224
Swallowing dysfunction 1058
Swan-Ganz catheter 166
Sweat sodium chloride test 563
Swine flu 299
Swyer-James syndrome 49, 71, 72f
Sympathetic ganglia 955
neoplasms 955
Sympathetic trunk 938
Symptomatic pneumothorax 922
Symptomatic therapy 694
Synaptophysin 649f
Synchronized intermittent mandatory ventilation 812, 813
Syncope, prolonged 760
Syndrome of inappropriate antidiuretic hormone
hypersecretion 274
secretion 217, 621
Systemic corticosteroids 538
indications for 692t
Systemic diseases, pulmonary manifestations of 857, 1053
Systemic disorders 749
Systemic glucocorticosteroids 476
Systemic infections 537
Systemic lupus erythematosus 197, 232, 579, 580, 657, 735, 864, 864f867f, 900, 901
drug-induced 1015, 1016, 1020
Systemic sarcoidosis 680
Systemic sclerosis 580, 657, 859, 868, 869f
pulmonary complication of 870
Systemic sepsis 698
Systemic steroid therapy 483
Systemic therapy 692, 693
Systemic thromboembolism 820
Systemic toxicity 1005
Systolic pressure 441
T
T helper cell 912
Tachycardia 274, 429, 462, 550, 786, 844, 891, 1010, 1039
supraventricular 534, 543
ventricular 534
Tachyphylaxis 550, 551
Tachypnea 298, 315, 425, 761, 784, 844, 927
Tacrolimus 313
Tactile fremitus 198
Takayasu's arteritis 735, 747
Tamoxifen 759
Targeted therapy 372
Taxanes 1026
Taxonomy 395
Tazobactum 340, 341, 363, 372, 566
Tea-grower's lung 719
Tear
esophageal 958f
of diaphragm, rupture or 1032
Telangiectasia 870
hemorrhagic 72
triad of 72
Temporal subtraction 8, 9
Tension hydrothorax 76
Tension pneumothorax 87f, 891, 921, 922f, 925, 1032, 1033
features of 922f
Tension time index 784
Teratoma 945f
benign 945
malignant 945
treatment of 946
Teratosarcomas, malignant 945
Terbutaline 478
Terizidone 242, 245
Tetanus 437, 779
facies 438f
fulminant 847
severe 440
toxoid vaccination 440
Tetracycline 384, 445
Thatched roof lung 719, 720
Theophylline 456, 476, 478, 539, 549, 551
blood levels 551
Therapeutic bronchoscopy 157f
Therapeutic drug monitoring 243
Therapeutic interventions 333
Thermoactinomyces
sacchari 718, 720
thalpophilus 718
vulgaris 718, 720
Thermoplasty, bronchial 158
Thioacetazone 242
Thiosulfate detoxifies 1004
Thoracic
cavity 75f
duct 31, 938
endometriosis 920
gas, volume of 143f
pain 194
scoliosis, severe idiopathic 1043t
wall 48
Thoracocentesis, previous 900
Thoracoplasty 1046
Thoracoscopic biopsy, video-assisted 320, 326, 579, 624, 690, 729
Thoracoscopic surgery, video-assisted 667, 740, 741, 923, 931, 941
Thoracoscopy, video-assisted 159, 670, 860
Thoracotomy 1039
indications for 1039, 1039t
Thorax, middle of 937
Three-bottle pleural drainage system 161f, 923f
Throat 737
Thrombocytopenia 436, 868
heparin-induced 768
Thromboembolic disease 868, 874, 887
Thrombolysis 768, 769
Thrombophilia, acquired 759
Thrombophlebitis 624
migratory 930
Thrombosis, recurrent 768
Thrombotic episodes 868
Thrombotic thrombocytopenic purpura 930
Thymic carcinoid 940, 944, 945f
Thymic carcinoma 944, 623
Thymic cysts 944
Thymic hyperplasia 945
Thymic malignancies, staging of 943t
Thymolipoma 944
Thymoma 940942, 943f
diagnosis of 943
gross section of 944f
invasive 942f
noninvasive 941, 942f
presumed 943
Thymus 29, 30f
Thyroid
carcinoma 623
disorders 749
mass 90
intrathoracic 948
lesions 90
Thyrotoxicosis 189, 192
Tidal volume 807
small 541
Tiotropium 140, 551, 584
binds 551
T-lymphocytes 458, 521
Tobacco specific N-nitrosamines 606
Tobacco-worker's lung 719, 720
Tocolytic pulmonary edema 892
Tomosynthesis 8
Tongue
reduction 1073
repositioning devices 1073
Tonic clonic seizures, generalized 705f
Topical medication 184
Toxemia 495
Toxic
air pollutants 991
causes 1051
fumes 966
gases 580
Toxicity
mechanism of 971, 1002
monitor for 743
Toxocara
canis 416
catis 416
Toxoplasma 311, 313
gondii 392, 399, 401, 432
Trachea 23, 30
bubbles 157
divides 23
enters 23
rupture of 1038
volume rendering technique of 14f
Tracheal bronchus 31f
Tracheal deviation 27f
Tracheal intubation 333
Tracheal sounds 1065
Tracheal stenosis 67, 69f, 192, 193
Tracheal tube cuff, design of 343
Tracheitis 379
Tracheobronchial amyloidosis 709
Tracheobronchial mucosa, biopsy of 326
Tracheobronchial submucosal glands 873
Tracheobronchial tree 14f, 15f, 29, 180, 182, 183, 440, 648f, 1005
maximum intensity projection of 739f
minimum intensity projection of 17f
volume rendered image of 15f
Tracheobronchitis 192, 324, 379
acute 195, 379
viral 379
substernal pain with acute 194, 195
ventilator-associated 342
Tracheoesophageal fistula 75
Tracheostomy 343, 441, 791, 798, 1039, 1073
care 799, 800t
complications of 799f
emergency 793
in flail chest 1038t
obstructed 824
tube 156f, 333, 794f
care of 800
wound, care of 800
Traction bronchiectasis 57f, 59f, 353, 360f
Trained doctors, poorly 489
Tranquilizers 537
Transbronchial biopsy 329, 403f, 684f, 689, 922
Transbronchial lung biopsies 159, 663, 664
Transdiaphragmatic pressure 133
Transjugular hepatic portovenous shunting 903
Transjugular intrahepatic
portocaval shunt 880
portosystemic shunt 876
Translucency, unilateral 50f
Transmission 293
Transmural pressure 130
Transpulmonary pressure 99
Transthoracic contrast echocardiography 878
Transtracheal aspiration 282
Transtracheal jet ventilation 796, 797
Transtracheal oxygen delivery 590
Transverse myelitis 194, 295
Trauma 182, 537, 917, 1029
penetrating 368
to chest 782, 1031
Treatment consists 956
Tree in bud appearance 221, 225f, 582, 583
Trematode infections, pulmonary manifestations of 417
Triamcinolone 553
Trichophytosis 946
Trichosporon cutaneum 720
Triglycerides 901
Trimellitic anhydride 720
Trimethoprim 420, 443
sulfamethoxazole 395, 400
Trophozoites 429
Tropical eosinophilia 190, 412, 414f, 415f, 501
end-stage of 415f
Tuberculin skin test 210, 213, 228, 258, 975
Tuberculosis 38f, 181, 196, 198, 205, 215, 224f, 248, 254, 267, 280, 289, 322, 501, 627, 669, 676, 710, 897, 898, 900, 902, 917, 976
burnt-out 190
cavitating 222f
Chemotherapy Center 206
diagnosis, novel technologies for 254
disseminated hematogenous 840
drugs, management of side effects of 233t
endobronchial 216, 224f, 225f
extrapulmonary 215
fibrocalcareous 41f
infection 226f
latent 215, 258, 259, 670
integrate 261
long-term course of primary 215
natural history of 207
nucleic acid, detection of 913
old healed 227f, 228f
past history of 216
prevalence of 991
primary 213
reactivation of 225f, 226f, 670
symptom in 175
treatment of 229
vaccine, new 260
Tuberculous
adenopathy 917
cavity 367
chronic 181
empyema 905
infection 443
lesion 55
pleural 912
pleural effusion 912, 913
diagnosis of 913
pneumonia 273f
subcarinal lymphadenopathy 953f
Tuberous sclerosis 704
Tumor 929
benign 627
body 957
cells 271f, 613f, 649f
esophageal 90
markers 643
necrosis factor 323, 743, 843, 969
alpha 364, 425, 721, 1020
node metastasis 631
proximal 639
rarer 627
Turbuhalers 471
Typhoid 433, 841f
infections, severe 840
U
Ulcerations 1006
Ulcerative colitis 454, 688
Ulcerative tracheobronchitis 324
Umeclidinium 551
Unclear multifactorial mechanisms 749
Unconscious state 34
Unconventional therapy 485
Uniform calcification 52
Unknown origin
pyrexia of 215, 249
sarcoid is pyrexia of 686
Upper airway 1066
and lung 737
examination 1068
injury 1005
obstruction 67, 192, 790, 1019
slowly progressive 192
receptors 125
Upper lobe
bronchus, right 30
collapse, right 23, 44
division 30
pneumonia, right 34f, 35f
predominant disease 557
right 31
Upper respiratory tract 272
colonization of 845
infection 140, 178, 374, 383, 461
Uremic lung 883, 884
Uremic pleurisy 918
Ureteric rupture 884
Urethane 606
Urinary tract infections, catheter-associated 331
Urine 465
orange 233
red 233
Urinoma 884
Urinothorax 899, 903
Uterine tears, large 891
Uveitis 680, 886
Uvulopalatopharyngoplasty 1073
laser-assisted 1073
V
Vague chest discomfort 195
Valsalva, sinus of 952
Valvular heart disease 188, 891
Van Slyke apparatus 119
Vancomycin 321
Varenicline 547
Varicella-zoster 311, 392
infection 271
virus 266, 292, 304, 305
Varicose bronchiectasis 353
Vascular anomalies 182
Vascular changes 459, 514
Vasculitic lesions 887
Vasculitides 904
primary 735
Vasculitis 887, 918
classification of 735t
secondary 735
Vasopressors 289
Vasovagal syncope 899
Veins
collapse sharply 524
techniques for specific 167
Velcro crackles 657
Vena cava
inferior 26
interruption, indications for 772t
superior 3, 26, 28, 29, 938
obstruction 903
syndrome 617, 618f, 959, 960
Venous admixture 110
Venous blood, mixed 126
Venous oxygen saturation, mixed 785
Venous pressure 130f
Venous stasis, Virchow's triad of 758
Venous thromboembolism 758
Venous thrombosis 624
Ventilated lung volumes 528
Ventilation 111, 147, 777, 877
abnormality 877
control of 115, 123
cyclic process of 97
high-frequency 819
inequalities 111, 1047
lung scintigraphy 761
mechanics of 97
noninvasive 343, 485, 669, 1038, 1074
perfusion
imbalance 1037
ratios, distribution of 112, 112f
pressure support 541, 812, 814, 828
pressure-controlled 811, 812
proportional assist 818, 819
scans 20
volume targeted 812f
volume-controlled 811
Ventilator
associated complication 336
associated pneumonia
causes of nonresolution of 342t
treatment of 338fc
circuits, management of 344
modes 850
requirements 542
settings 542
support 441, 789, 802, 808t
initiation of 808
noninvasive 596, 791, 848
objectives of 809
role of noninvasive 828
weaning from 824
unsuccessful weaning from 828
Ventilatory control 518
Ventilatory demands 1043
Ventilatory failure 777, 778, 1043
management of 1045
pathophysiology of 778
ventilator support in primary 803
Ventilatory muscle dysfunction 1058
Ventilatory parameters 827
assessment of 827
Ventilatory pressure 155
Ventilatory response to exercise 126
Ventilatory strategies 486
Ventilatory support
newer modes of 818, 819t
use of 290
Ventimask 592
Ventricular dysfunction, right 514, 543, 765, 767
Venturi mask 593
Vertebrae 3, 42
Vertebral column 937, 938
Vertigo 233
Vessels, aneurysm of major 952
Vicious cycle terminating 1043
Vigorous percussion 537
Vincristine 403
Vinyl chloride 606
Violent bronchospasm 496
Viral bronchiolitis 579
Viral cultures, positive 329
Viral infection 392
acute 580
other 329
Viral pneumonia 37, 266, 292, 839
influenzal 295
primary 295
specific 292
Viral upper respiratory tract infections 292
Virtual bronchoscopy 15f, 16f, 636
Virus 266, 305, 311
B 293
Visceral compartment 938
Visceral larva migrans 416, 416f
Visceral pleura 929
Visceral pleural line 83
Vision, impaired 621
Visual pollution 988
Vital capacity 155, 784
Vital homeostatic function 115
Vitamin
C 608
K 769
Vivax malaria, pulmonary complication of 426
Vocal cord 469
dysfunction 468
edema 153
Vocal fremitus 200
Voice, hoarseness of 617, 941
Volume rendering technique 14f, 15f, 72f
Volume trauma 823
Volume-rendering techniques 12
Volume-targeted support 812
Voluntary ventilation, maximum 140
Volutrauma 849
Vomiting 270, 272, 485
Voriconazole 326, 377, 379
W
Water
logging, severe 543
pollution 988
retention 824
Water-lily sign 421, 421f
Water-soluble chemicals 997
Weaning 487
methods of 827
process of 826
screen 825
Wegener's granulomatosis 37f, 67, 180, 182, 197, 307f, 372f, 375, 627, 656, 735, 736, 739f741f, 845, 884, 918
Weight loss 225f, 252, 623, 971
systemic features of 740f
Westermark sign 761f
Wheelchair-bound 1049
Wheeze 200, 461, 462t, 468, 657, 709
history of 462
tight 523
White blood cell 283, 743
White mater edema 1009
William-Campbell syndrome 356
Wilson's disease 876
Window settings 15
Wood pulp worker's lung 719, 720
Woolsorter's disease 444
World Health Organization 748, 1031
World influenza pandemic, dangers of 301
Worsen hypercapnia 556
Worsen hypoxemia 483
Worsening dyspnea 533, 974
Wrights stain 398
Wuchereria bancrofti 413, 917
X
Xerostomia 680
Xerotrachea 873
Y
Yellow nail syndrome 357, 904, 917, 918
Yersinia pestis 276, 443
Yoga 478
Yolk sac 947
Young's syndrome 355
Z
Zanamivir 296, 305
Ziehl-Neelsen stain 222, 254, 272, 280, 345, 346
Zileuton 474
Zinc chloride 967
Zoledronate 621
×
Chapter Notes

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1Imaging Techniques and Imaging of the Chest2

Imaging Techniques and Imaging of the ChestCHAPTER 1

 
INTRODUCTION
The chest radiograph remains the primary imaging investigation in the evaluation of diseases of the respiratory system. It is a low-radiation, cheap and easily available imaging technique, providing invaluable information regarding the lung parenchyma, pleura, mediastinum and chest wall. It has its share of limitations being a projectional two-dimensional (2D) imaging modality. Computed tomography (CT), a cross-sectional imaging modality provides excellent detail of the lung, pleura, mediastinum as well as chest wall to compensate for the limitations of chest X-ray. The chest X-ray as well as the CT scan suffice for all imaging needs in the chest. Ultrasonography (USG)/magnetic resonance imaging (MRI)/positron emission tomography (PET) have complementary roles in the evaluation of chest diseases.
 
CHEST RADIOGRAPHS
Even after 100 years of technological developments, the chest X-ray remains the primary imaging modality for diseases of the chest. It is obtained with the patient erect, facing the cassette, with the X-ray beam directed from behind the patient, from a distance of 6 feet to avoid magnification of mediastinal structures (Figs. 1 and 2). The X-ray is obtained at deep inspiration. A film obtained in expiration will result in alteration of the mediastinal contour as well as a misleading appearance of diffuse lung disease (Figs. 3A and B). It is important to position the patient well such that he or she is not rotated. A well-centered X-ray will demonstrate the medial ends of the clavicles to be equidistant from the spinous processes of the vertebrae. Rotation to the left results in the manubrium sternum, superior vena cava (SVC) and great vessels appearing prominent—this may simulate a mediastinal mass (Figs. 4A and B). Rotation may also result in one lung appearing more or less translucent (Figs. 5A to C). To minimize the shadow of the scapula on the lungs, the arms are placed on the sides and shoulders rotated forward so as to rotate the scapula laterally.
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Fig. 1: PA view of the chest: Positioning for a PA view of the chest with patient facing the cassette and arms rotated forward to take the scapulae off the film.
A large part of the lungs on a frontal radiograph are obscured by the bony rib cage. To be able to visualize larger areas of lung parenchyma free from significant obscuration by the ribs, high kVp (peak kilovoltage) techniques are used. As the coefficient of X-ray absorption of soft tissue and bone approach each other at high kVp, 4the bony rib cage no longer obscures the lungs to the same extent as on lower kVp films. The mediastinum is also penetrated better in high-kVp films, thereby allowing more details to be viewed of the mediastinum and large airways (Fig. 6). Scattered radiation is higher at high kVp, causing significant degradation of image quality. To minimize this effect a grid or an air gap of 15 cm between the patient and cassette is used, thereby improving image quality. If an air gap is used, the distance between patient and X-ray beam is increased to 12 feet to avoid magnification of the mediastinum. A drawback of high kVp is a lack of demonstration of calcified lesions and small pulmonary nodules. Low-kVp films have the advantage of providing excellent detail in the unobscured lung, as there is excellent contrast resolution between vessels and aerated lung.
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Fig. 2: PA view of the chest: Normal chest X-ray, note scapulae have been rotated off the chest so as to avoid obscuration of lung parenchyma.
Digital chest radiography has now nearly totally replaced analog radiography modalities. There have been compelling reasons for this shift. The availability of data in an electronic form makes it possible to postprocess the image data so as to present optimal image quality, view the images on large high-resolution workstations, archive as well as distribute images across a hospital network or to any remote location. Computed radiography or CR, the first commercially available digital X-ray imaging technique is still the most popular digital imaging technique available today. In this technique, conventional X-ray film is replaced by a phosphor plate. This phosphor plate when exposed to X-rays, stores the X-ray radiation as energy. This phosphor plate is read by a laser beam which releases the energy stored on the phosphor plate as light, producing an image. Recently, flat panel detectors have been introduced.
These do away with the need to have a cassette containing the phosphor plate. The images are instantly available as soon as the X-ray is exposed. The image quality is superior and as no cassette is involved, the work flow is much faster.
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Figs. 3A and B: Inspiratory and expiratory views: PA view of the chest in inspiration (A) and in expiration (B) of same patient. Note change in mediastinal contour as well as diffuse haziness in both lung bases on expiratory view simulating interstitial lung disease.
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Figs. 4A and B: Rotation: (A) To check for rotation on a PA view, a vertical line is drawn along the spinous processes of the vertebrae (blue). Horizontal line is drawn between the medial ends of the clavicles so as to cut the vertical line. The medial ends of the clavicles should be equidistant when there is no rotation (B) Note rotation to left as medial end of right clavicles rotates further away this results in a right paratracheal opacity representing SVC shadow. This opacity may simulate a mass or adenopathy.
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Figs. 5A to C: (A) Chest X-ray reveals haziness in the left mid and lower zones. (B and C) Axial and coronal CT sections revealed absence of any pathology. Left sided haziness in the X-ray was due to the rotation to the left.
 
ADDITIONAL VIEWS
 
Lateral
The utility of this view is to check whether an equivocal frontal chest X-ray shadow is actually present, to position an abnormality seen on a frontal X-ray, and define as to which lobe it is located in. The patient stands perpendicular to the cassette with arms held high and well away from the thorax. The lateral chest X-ray is not of much use in evaluating the apices, as the shoulders overlap this region (Figs. 7 to 10).
 
Lateral Decubitus
Lateral decubitus is a useful view to demonstrate a small pleural effusion which is not visible on the PA view, or differentiate a free pleural effusion from loculated pleural fluid or pleural thickening (Fig. 11). A frontal radiograph is obtained with the patient lying in a decubitus position with the side suspected to have pleural effusion down. Free fluid gravitates along the dependent chest wall between the lungs and chest wall.6
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Fig. 6: High-kVp X-ray demonstrates the lung fields well, the opacity of overlying ribs is reduced considerably; note the detail of the mediastinum and trachea. A disadvantage of this technique is a lower detection rate of pulmonary nodules and calcified granulomas as compared to low-kVp X-ray.
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Fig. 7: Lateral view of chest and positioning for a lateral view: Left side of chest is in contact with the cassette, this reduces cardiac magnification as compared to right side; arms are held up.
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Fig. 8: Lateral X-ray of chest: A normal lateral X-ray of the chest. Important points to note are: (1) Increasing lucency of the descending dorsal vertebrae. Loss of this progressive lucency is indicative of a pathological process in this location. (2) Homogenous cardiac opacity as well as aerated retrosternal region. Loss of homogeneity in this region would indicate the presence of a pathological process.
 
Lateral Shoot Through
This view is useful to demonstrate a small anterior pneumothorax in a supine patient. The X-ray beam is directed horizontally from one lateral chest wall and the cassette is placed along the other lateral chest wall.
 
Lateral Oblique
This view is used to demonstrate rib fractures and rib lesions. The axillary course of a rib is obscured on a frontal radiograph; on oblique view these are well visualized. The patient is rotated by 45° and a frontal radiograph is obtained.
 
Lordotic View
On a frontal radiograph the apices are often obscured by the clavicle and first rib thereby obscuring a lesion in this location. Subtle tubercular lesions hidden beneath the first rib/clavicle can be well-demonstrated on this view (Figs. 12A and B). Additionally, on a PA view it may be difficult to discern between a fibrotic tubercular lesion and costochondral cartilage; a lordotic view would be able to differentiate the two. The patient is positioned upright and the X-ray beam is angled 15° upward or alternatively the X-ray beam is kept horizontal and the patient arched backward resembling the posture of a “lord” (Figs. 13A and B).7
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Figs. 9A and B: (A) PA view of the chest demonstrates a large mass lesion in the right upper and middle zone, silhouetting the right mediastinal border, with a small right pleural effusion; (B) Lateral X-ray demonstrates the large opacity overlying the upper cardiac silhouette as well as partly obliterating the retrosternal air space. The translucency over the lower dorsal vertebrae is lost due to presence of pleural fluid. Note well-defined lower zone pulmonary nodule overlying anterior end of lower dorsal vertebra. This lesion was not appreciated on the PA view.
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Figs. 10A and B: Posterior mediastinal mass: (A) PA view of the chest reveals a large mass lesion occupying and extending beyond the confines of the mediastinum; (B) Lateral view localizes the mass to the posterior mediastinum. The mass lesion is seen as a homogenous opacity posterior to the trachea as well as displacing the trachea anteriorly.
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PORTABLE RADIOGRAPHS
These are extremely useful as they are performed at the patient's bedside. They do have their share of limitations. Due to the shorter tube focus distance, there is mediastinal magnification. High-kVp techniques are not possible as the output of these machines is limited, the exposure time is longer, so that patients may be unable to hold their breath, resulting in motion artifacts. The positioning of these patients is also a challenge as they are often half upright or rotated. Patients also find it difficult to take a deep breath in a semi-erect position. Digital X-rays have fortunately helped considerably to improve image quality of portable X-rays. Similar to X-rays taken in the imaging department using CR, the same CR cassettes can be used in the intensive care unit (ICU), and processed in the same readers available in the imaging department. DR or digital radiography units which do not require a cassette and which are available for an imaging department are also available for portable radiography (Figs. 14A and B). These have a great advantage; they provide an instant image, thereby saving precious time—time taken to transport a cassette to the imaging department, process it, archive the image and transport it back. These however at present are extremely expensive. As a bridge, portable CR readers are being developed, so that at the bedside itself the CR cassette can be read, producing a quick image.
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Fig. 11: Lateral decubitus: PA view of the chest had demonstrated a right basal opacity, ? collapse consolidation, ? pleural fluid. X-ray taken with patient lying on his right side; there is fluid layering along the chest wall indicating a free pleural effusion.
There are newer novel applications developing in digital radiography—Dual Energy, Tomosynthesis and Temporal Subtraction.
 
Dual-energy Subtraction Imaging
The absorption of X-ray by tissues depends upon the kilovoltage (kV) used, as well as on the consistency of the tissues. When kV is varied the response of tissues changes; as a result tissues can be separated from each other at different kVs. In the chest, bone and soft tissue both appear bright on low kV, so that a pulmonary nodule underlying a rib will be obscured due to their similar densities. At higher kV the attenuation of calcium and soft tissue to X-rays differs. This principle is used to generate images using different kVs. The images are subtracted to provide images with only soft tissue. This helps to improve detection of a solitary pulmonary nodule as only soft tissue is seen and no bone.
zoom view
Figs. 12A and B: Lordotic view: (A) PA view of the chest reveals a questionable opacity underlying the first rib on the right side; (B) Lordotic view uncovers the first rib demonstrating ill-defined soft opacities in the right apex due to active tuberculous infection.
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zoom view
Figs. 13A and B: Lordotic X-rays demonstrate two methods of demonstration of the apices without overlap of first rib, in (A) the X-ray beam is horizontal, the patient is arched back simulating a “lord”. In the other method (B) the X-ray beam is angled upwards by 15° to the apex, the patient stands straight with back to the cassette.
 
Digital Tomosynthesis
Digital tomosynthesis is a technique where images of a certain depth in the chest are obtained. The tissues above and below this level are blurred, only tissue at that depth is visualized. This is similar to tomography of the olden days, now using digital techniques to enhance the evaluation.
 
Temporal Subtraction
This technique utilizes subtraction of a previous image from the present image. If there is any interval change it will be demonstrated. Inaccuracies do occur in terms of positioning as well as differences in breathhold.
 
Computer-aided Diagnosis
This is a technique which relies on a pattern recognition approach using artificial intelligence to help detect lesions which may be missed by radiologists. The main applications being evaluated at present are detection of pulmonary nodules, as well as pulmonary emboli (Fig. 15). These techniques are yet to become popular, as there is a high rate of false-positive detection; also the detection rate is similar to that observed by radiologists.
 
LIMITATIONS OF CHEST X-RAY
The limitations of a chest X-ray relate essentially to the fact that the chest X-ray is a 2D modality, imaging a three-dimensional (3D) structure. Nearly 75% of the lungs are covered by ribs, mediastinum and diaphragm; as a result a number of anatomical structures are superimposed reducing the detectability of lesions. From a technical aspect since the chest is a large region to be imaged, approximately 40 cm, as the whole of this area has to be radiated, there is significant scatter radiation resulting in degradation of image quality.
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Figs. 14A and B: Portable chest radiograph: (A) PA view and (B) portable AP view of the chest. Note the change in cardiac outline between a PA view and an AP view. Commenting on cardiomegaly on an AP view may be hazardous.
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Fig. 15: Computer-aided diagnosis (CAD): CAD demonstrates a pulmonary nodule colored in yellow, separate from adjacent vessels. The volume of this nodule can be easily determined. The nodule can be followed up on subsequent examinations to determine rate of growth. CAD helps in detecting lesions which may have been missed by radiologists; at present CAD has a high false-positive detection rate; however, it is extremely useful for volume measurements.
 
COMPUTED TOMOGRAPHY
CT has been heralded as the greatest discovery in medicine following the discovery of X-rays. The history of the development of the CT scanner is extremely unique. Electrical and musical industries (EMI) became famous in the 1960s as they were the record label for the Beatles. At their Abbey Road studios they recorded enough Vinyl for the Beatles to go around the earth's circumference. They became a cash-rich company. Godfrey Hounsfield, an eminent scientist with EMI who had already developed the first all-transistor computer, was keen to develop a product which would more effectively evaluate the attenuation of X-rays through soft tissues. This research was funded directly by profits from the Beatles. In 1972, Godfrey Hounsfield unveiled the first CT scanner to the world named as EMI. That scanner took 4 minutes to acquire a single slice and a further 7 minutes to reconstruct the image. CT has come a long way since those days with the entire thorax being scanned with a dual-source CT in under a second in 2010. Not only did the Beatles spawn an entire shift in musical tastes, outlook, physical appearance and hairstyles for nearly the entire globe, they contributed to one of the greatest advances in medicine since the discovery of X-rays.
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Figs. 16A and B: Helical CT: (A) Demonstrates a conventional CT which obtained slices one by one; (B) Demonstrates a helical CT, all slices are obtained simultaneously in one breathhold.
CT scanners are based on the same principles as X-ray. Tissues attenuate X-rays differently depending on their composition, i.e. atomic number; thereby a CT scanner is able to detect minute differences in attenuation by tissues, providing extremely high anatomical detail. A CT scanner consists of an X-ray tube which emits X-rays, and a detector opposite to the X-ray tube. This combined assembly rotates 360° around the patient acquiring data. Data from one 360° rotation produces a single image. Present-day scanners are helical scanners; data is acquired simultaneously with the table moving and X-ray tube rotating during a single breathhold. This technique has significant advantages over the previous nonhelical scanners. As scans are acquired in a single breathhold, the possibility of missing a pulmonary nodule due to respiratory misregistration does not arise (Figs. 16 and 17). Data is acquired as a volume and therefore can be reconstructed at any slice thickness as well as in any plane which is desired. Additionally, as the scan time is shorter, less intravenous contrast medium is required. Helical scanners have advanced technologically from being single-detector to multidetector scanners (MDCT) (Figs. 18A and B). These MDCT scanners may have from 2 rows to 64 rows of detectors. Increasing the number of rows of detectors enables faster scans, reducing respiratory and motion artifacts.11
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Figs. 17A and B: Multidetector CT: (A) Demonstrates a single-slice helical CT rotation; (B) Demonstrates a multidetector helical CT rotation.
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Figs. 18A and B: Multidetector CT: Comparison between a single-detector CT and a multidetector CT. (A) Single-detector (B) Multidetector CT. Note the increased coverage in a single rotation with a multidetector CT allowing for large volume coverage in shorter time with thinner slices.
Angiographic images may be obtained as well as larger volumes may be covered, with thinner sections obtained. A CT image is a 2D image, but there is a third dimension, depth or slice thickness. A thick slice contains different tissues within the section, which will be averaged to produce the final image. To obtain a high degree of anatomical detail as with high-resolution CT (HRCT) very thin sections are required, 1 mm or less, so that there is no averaging of tissues. These scanners have further revolutionized the diagnostic potential of CT, especially the 16, 64 slice scanners, as these produce thin slices (0.6–0.75 mm) which are isotropic, i.e. reconstruction of these slices in any plane results in no loss of resolution. These scanners have essentially converted CT from an axial cross-sectional technique to a true 3D technique allowing arbitrary selection of scan planes, and volumetric display of data. Newer scanners with 128 rows, 256 rows, 360 rows and dual-source CT have been introduced essentially to facilitate CT coronary angiography. The dual-source CT houses two CT scanners in one CT gantry. The advantage of this is in the performance of CT coronary angiograms without the need to use beta-blockers. As dual-source CT scanners have two X-ray tubes, they can fire at different energies resulting in dual-energy scans (Figs. 19 and 20). This is useful in obtaining lung perfusion scans. These help in the detection of pulmonary embolism. Segmental and subsegmental emboli may only be detected by demonstrating a perfusion defect on dual-energy scans (Figs. 21A and B).
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Fig. 19: Dual-source CT: New generation of CT scanners with two CT tubes, providing faster scans and higher temporal resolution, of particular value in coronary angiograms as there is no need of beta-blockers, and images are of higher resolution.
 
Respiratory Misregistration
Conventional CT scanned the chest slice by slice. With every slice, the patient was asked to hold his or her breath, the table then moved to the next table position and 12another slice was obtained. The illustration demonstrates respiratory misregistration. In the first section, due to an increased inspiratory effort the nodule goes below the slice; in the next slice where the nodule should be visualized, it is not, as the patient has taken only a moderate inspiratory effort. This resulted in a lower accuracy for CT in detecting pulmonary nodules (Fig. 22).
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Fig. 20: Dual-energy CT: Schematic diagram of a dual-energy CT scan, two tubes firing at different kVs, one at 80 kV and other at 140 kV simultaneously.
Multiplanar reconstructions (MPR) allow reconstruction of images in any plane such as the coronal, sagittal or any oblique plane (Figs. 23A to D). Curved multiplanar reconstructions are also possible where a curved structure such as a vessel or airway may be straightened out; its diameter as well as extent of stenosis may be quantified (Figs. 24 and 25).
Volume-rendering techniques (VRTs) are 3D techniques which provide a rendering of the surface of the organ. These are useful for demonstrating the tracheobronchial tree, as well as vasculature, especially the aorta and coronary arteries. An adaptation of this technique is virtual bronchoscopy. A 3D volume of the tracheobronchial tree is obtained, utilizing a fly-through software. The internal contents of the tracheobronchial tree can be visualized similar to an optical bronchoscopy, the advantages of a virtual bronchoscopy being the ability to demonstrate tracheobronchial stenosis, extrinsic compression, intraluminal masses, foreign bodies or intraluminal extension of extrinsic lesions. Internal measurements of the tracheobronchial tree are also possible (Figs. 26 to 31). This helps to determine the length and size of stents required in planning surgery. The main disadvantage is the inability to obtain biopsies and lavages.
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Figs. 21A and B: Dual-energy CT: CT pulmonary angiogram (A) demonstrates bilateral pulmonary emboli, particularly on the right side. Dual-energy CT (B) demonstrates perfusion defects, particularly wedge-shaped defect in right mid-zone. Dual-energy CT provides a CT angiography with a perfusion scan, thereby increasing accuracy in detection of pulmonary embolism, especially subsegmental emboli. CT data in MDCT scanners is acquired as a data volume; this data can be postprocessed to provide a variety of different images(RTPA: Right pulmonary artery; LTPA: Left pulmonary artery).
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zoom view
Fig. 22: Problems of conventional CT scan.
 
Maximum Intensity Projections
The disadvantage of thin-section CT is the inability to differentiate small nodules from vessels. On thicker sections it is possible to differentiate these as the branching appearance of vessels is easily appreciated. Maximum intensity projections (MIPs) create a thicker slab of tissue and highlight structures with high intensity such as vessels and nodules. As the slab is thicker, the branching nature of the vessels is well-appreciated, the detection of nodules is much easier (Figs. 32A and B). The ideal thickness is 3 mm; an additional benefit beyond precise detection is an accurate characterization of the location of the nodules in relation to the vessels—whether centrilobular or perivascular. For detection of miliary nodules or pulmonary metastatic deposits this technique is ideal.
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Figs. 23A to D: (A and B) Axial CT scans reveal an opacity in the right upper lobe. On the axial scans it is difficult to determine the etiology of the lesion; (C and D) Coronal and sagittal reconstructions demonstrate that the opacity represents fluid in the interlobar fissure. An example of how visualization of an abnormality in multiple planes may help establish the location, extent and etiology of the lesion.
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Fig. 24: Curved multiplanar reconstruction (MPR): Curved MPR of aorta demonstrates displaced intimal flap separating true from false lumen, this is also well depicted on the volume rendering technique (VRT) image. The advantage of curved MPR is that a curvilinear structure can be straightened out.
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Fig. 25: Curved multiplanar reconstruction (MPR) of pulmonary arteries: Curved MPR demonstrates main pulmonary artery and both right and left pulmonary arteries in one image. Note multiple pulmonary emboli in right and left pulmonary arteries. The advantage of a curved MPR is that the main, right and left pulmonary arteries can be demonstrated in a single image.
(RTPA: Right pulmonary artery; LTPA: Left pulmonary artery)
 
Minimum Intensity Projections
In emphysema, bronchiolitis obliterans, the contrast between normal and low-attenuation lung parenchyma may be subtle on inspiratory HRCT. Such subtle regional density differences can be highlighted by minimum intensity projections (MinIPs) (Figs. 33 and 34). MinIPs correlate excellently with pulmonary function tests. Another useful application of MinIP is demonstration of tracheobronchial tree stenosis/occlusions (Fig. 35). A window width of 350–500 HU and a window level of −750 to −900 HU is ideal (Fig. 36).
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Fig. 26: Volume rendering technique (VRT) of trachea: Volume-rendered image of the trachea demonstrates an extrinsic mass lesion indenting the right main bronchus, causing significant narrowing of its lumen.
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Fig. 27: Volume rendering technique (VRT) tracheobronchial tree. Volume-rendered 3D image of the tracheobronchial tree, no abnormality was detected. Note the visualization of not only the tracheobronchial tree, but also segmental and subsegmental bronchi.
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Fig. 28: Volume rendering technique (VRT) tracheobronchial tree: Volume-rendered image of tracheobronchial tree and lung parenchyma. Mass lesion seen in left upper lobe infiltrates the left upper lobe bronchus causing significant narrowing of its lumen.
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Fig. 29: Virtual bronchoscopy. Virtual bronchoscopy at the level of the carina reveals marked irregularity and narrowing of the right main bronchus due to a bronchogenic carcinoma.
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Figs. 30A to C: Virtual bronchoscopy: (A) Chest X-ray reveals an area of collapse consolidation in right lower zone. (B) Virtual bronchoscopy reveals a well-defined foreign body in the right bronchus. (C) Post procedure, chest X-ray reveals clearing of collapse consolidation.
 
Window Settings
To visualize body structures the CT images are “windowed”. Two variables are used to select the densities to be viewed: window width and window level. CT density is measured in HU values. Arbitrarily, water is considered as zero and air as −1,000. Window width determines the number of Hounsfield units to be demonstrated. Any densities greater than the upper limit of the window width are displayed as white and any below are displayed as black. Between these two levels all densities are demonstrated in shades of gray.
 
CONTRAST MEDIA
Intravenous contrast enhancement is required to enhance mediastinal vasculature and separate vessels from mediastinal masses as well as demonstrate enhancement within mass lesions. Ionic contrast mediums which had a significant incidence of mild, moderate as well as severe reactions have now been nearly universally replaced by nonionic contrast media which are far safer. Other than anaphylactic reactions, contrast-induced nephropathy (CIN) is an important adverse event.16
Contrast-induced nephropathy is an exacerbation of previously demonstrated impairment in renal function occurring within 3 days following intravascular administration of contrast medium. This is in the absence of an alternative etiology for the deteriorating renal function. An increase in serum creatinine of more than 0.5 mg/dL or 25% above the baseline serum creatinine is considered the criterion to determine the presence of contrast-induced nephropathy. CIN is by no means uncommon. It is the third most common cause of acute renal failure in patients admitted to hospital. The incidence is estimated to be 1% with intravenous contrast medium, and 2–7% with intra-arterial contrast medium. In diabetics with normal renal function it rises to 16%. In patients with preexisting renal insufficiency prior to receiving contrast media, the incidence of developing CIN is 33%. Diabetics with associated renal insufficiency are at the greatest risk for developing CIN. Other risk factors for developing CIN are dehydration, hypotension, nephrotic syndrome, multiple myeloma, use of higher dose of contrast media, repeated doses of contrast media within 48 hours, use of higher osmolar contrast media and concurrent use of nephrotoxic drugs.
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Fig. 31: Virtual bronchoscopy: Virtual bronchoscopy in an individual with carcinoma esophagus. The esophageal mass indents the posterior surface of the trachea as well as infiltrates into the lower trachea. Seen as nodular lesions projecting into the distal aspect of the trachea. This is an excellent non-invasive technique to determine local extension into the tracheobronchial tree.
To minimize the risk of CIN, universal use of nonionic contrast media, a volume expansion and the use of N-acetyl cystine are recommended. If the serum creatinine is greater than 1.4 mg/dL the possibility of another imaging modality should be considered. If a CT with contrast is considered imperative, the risk-benefit ratio should decide the issue.
 
SUPPORTIVE IMAGING TECHNIQUES
 
Sonography
This is a very useful imaging modality to demonstrate pleural fluid, especially at the bedside. Fluid manifests as an anechoic area separating the echogenic margin of lung and diaphragm. The contents of pleural fluid can also be estimated depending upon its echogenicity. Pleural fluid is usually anechoic; exudates are also anechoic but usually have internal septae (Fig. 37). Empyemas have echoes within and a hemothorax has echogenic fluid. Sonography is very useful to determine whether a basal opacity on an X-ray is due to pleural fluid or collapse consolidation.
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Figs. 32A and B: Maximum intensity projection (MIP): (A) Routine high-resolution computed tomography (HRCT) reveals suspicious small nodules in the lung parenchyma. As the slice thickness is very thin, it is difficult to be certain whether these represent nodules or vessels. (B) MIP demonstrates vessels very well as branching structures. The fine nodules are seen well-separate from the vessels. This technique is very useful in detecting subtle miliary nodules.
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Figs. 33A and B: Minimum intensity projection: (A) coronal and (B) axial minimum intensity projections demonstrate ill-defined areas of decreased attenuation in the lung fields representing areas of emphysema.
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Fig. 34: Minimum intensity projections: High-resolution computed tomography (HRCT) demonstrates extensive emphysema; narrow window settings demonstrate emphysematous changes very well. Minimum intensity projections demonstrate the involvement extremely well, providing a global view.
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Fig. 35: Minimum intensity projection of tracheobronchial tree. The entire tracheobronchial tree is demonstrated from the level of the pharynx. There is a mass lesion at the carina indenting the carina, extending to engulf the right lower lobe bronchus with resultant right lower lobe collapse; there is extension to the left to encase the left main bronchus narrowing and obliterating the left main bronchus. Note right lower lobe collapse with elevation of diaphragm.
Sonography is also an excellent guide for thoracocentesis, reducing the incidence of postaspiration pneumothorax.18
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Fig. 36: Ideal window settings displaying emphysema.
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Fig. 37: Ultrasonography (USG) of the chest demonstrates a hypoechoic area representing a pleural effusion.
 
RADIONUCLIDE IMAGING
The main utility of radionuclide imaging in the respiratory system is in the detection of pulmonary embolism. Ventilation/Perfusion scans also known as V/Q scans simultaneously image the pulmonary blood flow as well as alveolar ventilation.
Perfusion imaging is performed by intravenous injection of microparticles or human protein-labeled technetium (Tc-99). These are trapped in the pulmonary capillaries on their first pass. In patients with a right to left shunt there is a small possibility of the particles occluding systemic vessels with resultant tissue ischemia/necrosis. Similarly, in patients with pulmonary hypertension there is a risk of further occlusion of an already depleted vascular bed. In both these situations the quantum of radiotracer particles injected should be reduced, though there is usually a wide safety margin. The radiotracer has a half-life of 6–8 hours; by 24 hours, most of the activity is only visible in the kidneys and gut. The radiotracer is injected with the patient in the supine position; this limits the effect of gravity on regional blood flow. The particles mix in the heart and consequently are trapped by pulmonary precapillary arterioles. The distribution of the particles is proportional to the regional blood flow. At least six views are obtained—anterior, posterior, right lateral, left lateral, right posterior oblique, left posterior oblique. Additionally, right anterior oblique and left anterior oblique views may be obtained, if required. Even though multiple projections are obtained, perfusion scans underestimate perfusion abnormalities. For example, the medial basal segment of the right lower lobe is completely surrounded by normal lung; consequently, a perfusion defect is not detected on planar perfusion imaging.
All parenchymal diseases cause a reduction in pulmonary blood flow in the affected lung zone. In pulmonary embolism, perfusion is reduced whereas ventilation is preserved. Parenchymal lung diseases cause both a ventilation defect and a perfusion defect. Tc-99m radio-labeled aerosols are used for ventilation scans. Approximately 30 mCi of radiotracer in 3 mL of saline is placed within a nebulizer. Oxygen is forced through the nebulizer at high pressure to form aerosolized droplets which are inhaled by the patient via a mouthpiece. The distribution of the radiotracer is proportional to regional ventilation. Images are obtained in multiple planes similar to perfusion imaging.
In pulmonary embolism there are perfusion defects which may be subsegmental, segmental or even involve an entire lobe or lung (Figs. 38 and 39). The ventilation scan in these patients is normal; thereby there are mismatched defects. In patients who have pulmonary embolism with infarcts there would also be a ventilation defect; however, the ventilation defect is smaller in size than the perfusion defect. Matched defects occur in chronic obstructive pulmonary disease (COPD) as there is a ventilation defect as well as reflex hypoperfusion.19
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Fig. 38: Perfusion scan: Perfusions scans demonstrate multiple perfusion defects bilaterally, ventilation scan revealed no abnormality, indicative of ventilation-perfusion mismatch due to pulmonary embolism.
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Fig. 39: Perfusion scan: Perfusion scan demonstrates no evidence of perfusion defect. A normal perfusion scan virtually rules out the possibility of a pulmonary embolism.
CT angiography has virtually replaced ventilation-perfusion scans as the modality of choice in the detection of pulmonary embolism (Table 1).
CT angiography has additional advantages. It is available at most institutions round the clock; many institutions may not have nuclear medicine facilities. Clinical mimics of pulmonary embolism such as aortic dissection and pneumonia can be detected by CT. Concurrent venous imaging to detect lower limb/pelvic venous thrombosis is possible with CT angiography, increasing the sensitivity of CT angiography, though at the cost of a higher radiation dose. The requirement to use contrast in CT angiography is a potential disadvantage, especially in individuals with renal impairment or in patients with a history of anaphylaxis to nonionic contrast media.20
Table 1   Differences between V/Q scan and CT angiography.
V/Q scan
CT angiography
Nondiagnostic
26.5%
6%
Sensitivity, specificity
77%, 98%
83%, 96%
Definitive diagnosis
74%
94%
Source: Acute pulmonary embolism: sensitivity and specificity of ventilation-perfusion scintigraphy in PIOPED II study; Dirk Sostman: Radiology. 2008;246(3):941-6.
Another debatable issue is the quantum of radiation dose in these two modalities. CT angiography has a higher radiation dose ranging from 2.7 mSev to 10.2 mSev depending on the type of scanner and technique used, as compared to radiation dose in V/Q, ranging from 1.2 mSev to 6.8 mSev. The newer dual-source CT scanners utilize a much lower radiation dose, 1.9–2.7 mSev, similar to the radiation dose of V/Q scan. In pregnancy the radiation dose to the fetus in V/Q scans is 0.1–0.8 mGy as compared to CT angiography, 0.01–0.6 mGy. CT angiography is thus preferred over V/Q scan in pregnancy. The dose to maternal breasts is much higher using CT angiography than V/Q scan; however, this can easily be minimized by using bismuth breast shields. In view of these significant advantages with a positive benefit over risk ratio, CT angiography is the preferred modality.
 
MAGNETIC RESONANCE IMAGING
Magnetic resonance imaging (MRI) is making rapid strides in the evaluation of the abdominal pathologies. Its utility in imaging the brain, spine, musculoskeletal system and pelvis is well established. Evaluation for pulmonary pathologies is limited by a number of factors—the lower proton density of lung, and by cardiac and respiratory motion. These limitations are magnified with increasing field strength; the recent shift to 3T by institutions has not helped. Outside the lung parenchyma, MRI can be a useful alternative to CT, especially when intravenous (IV) contrast is contraindicated such as in patients with renal failure or history of anaphylaxis to contrast media. MRI is useful in the evaluation of the chest wall and mediastinum, to detect mass lesions, as well as demonstrate their local extension (Figs. 40A to D). It is also useful to evaluate the pulmonary arteries, aorta and heart (Fig. 41). IV contrast may be used if serum creatinine is not elevated. Advances are occurring rapidly using newer sequences as well as experimenting with gases for ventilation scans.
 
POSITRON EMISSION TOMOGRAPHY-COMPUTED TOMOGRAPHY
Positron emission tomography-computed tomography (PET-CT) combines a PET scanner and a CT scanner in one gantry. Images acquired from both devices can be obtained sequentially in the same session and images superimposed in a single image.
Positron emission tomography imaging is based on the fact that metabolically active cells take up glucose. PET-CT fuses anatomical and functional data to provide an excellent correlation of anatomic and metabolic information. A radionuclide-labeled glucose analog Fluorine 18-deoxyglucose (FDG) is taken up by malignant tumors, inflammation/infection and active tissue repair. Sixty minutes after IV FDG, a CT is acquired over approximately 30 seconds, followed by a slow transit of the patient through the bore of the PET. This data acquisition takes 30–40 minutes. Standard uptake values can be calculated from the PET data. This is useful as a value above 2.5 SUV is considered significant. The main utilities of PET-CT in respiratory medicine are in the staging of neoplastic processes, including lymphoma and mesothelioma. It is also useful in the detection of inflammatory processes which are not detected by other imaging modalities (Figs. 42 and 43).
 
PULMONARY ANGIOGRAPHY
Pulmonary angiography is considered to be the gold standard in the evaluation of pulmonary thromboembolism. This is an invasive procedure with an incidence of 1.5% serious complications. Acute pulmonary emboli are demonstrated as intraluminal filling defects, peripheral occlusion of pulmonary vessels and/or wedge-shaped perfusion defects (Fig. 44). To improve the detection of small pulmonary emboli, dedicated techniques are now available, such as cine angiography, balloon occlusion angiography and superselective angiography.
Many studies using spiral CT angiography have demonstrated a sensitivity and specificity for spiral CT angiogram to match that of pulmonary angiogram. The limitations of both spiral CT angiography and pulmonary angiography are also comparable. It is reported that 10% of spiral CT examinations will be inconclusive compared to 12% for pulmonary angiograms. Three percent of spiral CT angiograms will be technically inadequate compared to 4% for pulmonary angiograms. In view of the less invasiveness and similar sensitivity and specificity of spiral CT angiogram as compared to pulmonary angiograms, spiral CT angiograms have by and large replaced pulmonary angiograms in the detection of pulmonary emboli (Fig. 44).21
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Figs. 40A to D: Lipoma: (A) Chest X-ray demonstrates a large homogenous mass in the right lower zone with no shift of the mediastinum; (B) Lateral X-ray demonstrates opacity in an anterior location; (C and D) MRI characterizes the lesion as a lipoma, as the mass is of fat intensity.
 
BRONCHIAL ARTERY EMBOLIZATION
Bronchial artery embolization is performed to stop massive hemoptysis. The bronchial arteries arise from the intercostobronchial trunk which arises from the aorta at T5. There is a single bronchial artery on the right side and two on the left side. As with most anatomical structures there are variations in the anatomy of the bronchial arteries. These vessels are selectively cannulated and if on angiography, there is extravasation of the dye from an artery or its branch, that vessel is selectively embolized using polyvinyl alcohol or gel foam (Figs. 45A and B). Serious complications following bronchial artery embolization are rare. Patients mainly complain of occasional hemoptysis, transient fever and chest pain.22
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Fig. 41: Mediastinal fibrosis: Contrast-enhanced MRI reveals bilateral superior pulmonary vein narrowing due to mediastinal fibrosis.
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Fig. 42: Positron emission tomography-computed tomography (PET-CT) examination demonstrates uptake in right upper lobe mass lesion and in right paratracheal lymph node representing primary lung neoplasm with nodal spread.
 
APPEARANCES OF A NORMAL CHEST RADIOGRAPH
 
Lung Parenchyma
The lung markings seen on a chest X-ray represent vascular shadows. Occasionally, an accompanying bronchus may be visualized along with the vessels as an air-filled thin tube. Bronchi are best demonstrated end on with the accompanying vessel. In the erect position, the vascular markings are more prominent in the lower zones as the diameters of vessels are larger in the lower zones. In the supine position there is an equalization of the diameters of the vessels in the apices and bases. The vascular markings are a combination of pulmonary arteries and veins. In the upper zones it is not possible to differentiate these as they course similarly in a curvilinear fashion; in the lower zones they may be separated as veins course horizontally and arteries more vertically.
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Fig. 43: Positron emission tomography-computed tomography (PET-CT) demonstrates a lesion in the left lingula with multiple bony lesions in sternum, ribs, vertebral body and soft tissue lesions in the spleen and left costal pleura representing a primary lung neoplasm with metastatic deposits.
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Fig. 44: Pulmonary angiogram: Selective injection of left pulmonary artery demonstrates multiple filling defects in lower branch pulmonary arteries.
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Figs. 45A and B: Bronchial artery angiogram: A patient with active tuberculosis presented with massive hemoptysis. Bronchial arteriogram (A) demonstrates large feeding vessels with extravasation of contrast, indicative of bleeding vessel; (B) The large feeder vessel was occluded with coils to stop the bleeding.
 
Trachea
The trachea enters the thorax 1–3 cm above the level of the suprasternal notch, the intrathoracic portion is 6–9 cm in length. The trachea contains 16–20 incomplete or horseshoe-shaped cartilage rings giving the trachea a corrugated outline—calcification of the cartilage rings occurs after the age of 40 years. The trachea deviates mildly to the right to accommodate the left-sided aortic arch. With unfolding and ectasia of the aorta the trachea deviates more to the right.
The trachea divides into the two mainstem bronchi at the carina, approximately at the level of the T5. The left main bronchus extends up to twice as far as the right main bronchus before giving off its upper lobe division. The right main bronchus is approximately 25 mm long; the left main bronchus is approximately 50 mm long. In children the angles between the bronchi are symmetric, but in adults the right mainstem bronchus has a steeper angle than the left. The segmental bronchi are not well demonstrated on the X-ray unless seen end on; they are well-demonstrated on CT.
 
Hilum
The hilar opacity is mainly due to pulmonary arteries and to a lesser extent due to the pulmonary veins. There is a small contribution by adenopathy, fat and bronchial walls. The left hilum is higher in position than the right hilum; this is because the left pulmonary artery arches over the left bronchus and descends posterior to the left bronchus while the right pulmonary artery extends directly inferiorly, anterior to the right bronchus. In 5% of individuals they may be at the same level. If the left hilum is found to be lower than the right hilum, it is useful to evaluate for left lower lobe collapse or a right upper lobe collapse. There is usually a wide variation in size of the hilum in normal individuals. If there is prominence of a hilar shadow, the possibility that this is due to a technical factor such as rotation or scoliosis should be first excluded. The margins of the hilum are usually smooth; if there is a lobulated contour a mass should be suspected.
The pulmonary arteries descend vertically downwards; the size of the descending vessels is relatively equal to a little finger. If the descending pulmonary artery is not visualized on the right side, always check for right lower lobe collapse. A mass lesion at the hilum in contact with 24the hilar vessels will result in a loss of the hilar silhouette. If the hilum is well-visualized through a mass lesion then the mass has not silhouetted the hilum, indicating that the mass is anterior or posterior to the hilum.
 
Diaphragm
The right dome is normally at the level of the sixth rib anteriorly. The left dome is usually about 1.5–2.5 cm below the right dome. There may be variations in the position of the diaphragm; they may be one interspace higher or lower, they may be at the same level or occasionally, the left is higher than the right but not more than 1 cm. During a respiratory cycle the diaphragm may move between 2.5 cm and 8.0 cm.
 
Nipples
These may be visualized as bilaterally symmetric dense well-defined spherical shadows with a sharp and a non-sharp margin (Fig. 46). If they are asymmetric they may be mistaken for a pulmonary nodule (Fig. 47). To clarify whether a shadow is a nipple or a pulmonary nodule, a marker may be placed on the nipple (Fig. 48), or in a female the breasts are manually elevated. If a nipple casts a shadow, the marker will be on the opacity; if the breasts have been elevated, the nipple will move up, the pulmonary nodule will remain in the same location.
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Fig. 46: PA view of the chest demonstrates bilaterally symmetric dense well-defined rounded shadows with a sharp and a non sharp margin in the lower zones. These represent bilateral nipple shadows.
 
Fissures
Major fissures are present bilaterally and separate the upper from the lower lobes. The fissures run obliquely forward and downward crossing the hilum. They arise from the fifth thoracic vertebrae and end at the diaphragm approximately 3 cm behind the sternum. On a lateral radiograph, often parts or the whole of a fissure may be visualized. On a frontal radiograph the major fissures are rarely visualized.
A minor fissure is present on the right side dividing the upper and middle lobes (Fig. 49). The fissure extends from the hilum anteriorly and laterally. On a frontal radiograph it is seen in nearly 50% of individuals, contacting the lateral chest wall at or near the axillary portion of the sixth rib. It is also seen on the lateral chest radiograph in approximately 50% of individuals extending anteriorly from the hilum.
 
Azygous Lobe Fissure
This fissure develops due to failure of the azygous vein to migrate from the chest wall through the lung into its location at the tracheobronchial angle. The invaginated visceral and parietal pleura persist to form a fissure, at the bottom of which lies the azygous vein (Fig. 50). This may be occasionally seen on the left side with the left superior intercostal vein occupying the bottom of the fissure.
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Fig. 47: Nipple shadow: PA view of the chest demonstrates a well-defined nodular lesion in the left lower zone, this may represent a nipple shadow or a nodular lesion.
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Fig. 48: Nipple shadow: PA view of the chest shows a nipple marker coinciding with nodular lesion indicating that the shadow was a nipple.
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Fig. 49: Minor fissure: Lateral view of chest reveals minor fissure as a horizontal line extending from the hilum anteriorly.
 
Mediastinum
The left mediastinal border above the level of the aortic arch is constituted by the left subclavian and carotid arteries. The left wall of the trachea is not visualized as it is in contact with the vessels. From the level of the aortic arch inferiorly the border is constituted by the aorta, main pulmonary artery, and heart (Fig. 51A). A small nodular well-defined opacity may be seen just below the aortic knuckle; this represents the left superior intercostal vein as it arches around the aorta before entering the left brachiocephalic vein. This should not be misinterpreted for a lymph node. The left border of the descending aorta is visualized through the main pulmonary artery and heart down to the aortic hiatus in the diaphragm.
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Fig. 50: Azygous lobe: PA view demonstrates an azygous fissure in the right upper zone.
The right mediastinal border is formed by the right brachiocephalic vein, SVC and right atrium. The right paratracheal stripe consisting of the tracheal wall and adjacent fat is seen through the brachiocephalic vein and SVC as the lung is in contact with the posterior wall of the trachea. The presence of this stripe excludes the possibility of a paratracheal mass lesion. This stripe is visible in two-thirds of individuals. At the lower end of this stripe is the azygous vein in the tracheobronchial angle.
 
Lateral View
On the lateral view there are three zones to observe. The vertebrae, each thoracic vertebra appears more translucent than the one above. The cardiac shadow is visualized as a homogenous opacity. The retrosternal space is well-aerated, any alteration in this pattern indicates an abnormality (Fig. 51B).
The two domes of the diaphragm overlap each other. It is fairly easy to separate the two. The right is visualized all the way from front to back. The left is only seen from the costophrenic recess posteriorly to the point where it meets the cardiac silhouette. Anterior to this point, it is not visualized as the lung/diaphragm interface is obliterated by the cardiac silhouette. Occasionally, it may be difficult to separate the two domes as they totally overlap. If the diaphragm silhouette is lost, an abnormality in the lower lobes should be suspected.26
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Figs. 51A and B: (A) PA and (B) lateral views of chest demonstrating anatomy.
(PA: Pulmonary artery; AA: Arch of aorta; DA: Descending aorta; LA: Left atrium; RV: Right ventricle; LV: Left ventricle; SVC: Superior venacava; Desc: Descending; IVC: Inferior venacava; Diaph/DIA: Diaphragm)
It is difficult to differentiate the right from the left hilum as they totally overlap each other. The right pulmonary artery traverses anterior to the right bronchus and the left pulmonary artery hooks over and is posterior to the left bronchus. The bronchi are seen end on, the higher ring is the right and the lower the left bronchus. If the hilum is considerably prominent, large in size and lobulated in contour, a hilar mass should be suspected.
The mediastinal opacity is occupied by the heart. The portion behind the hila is the left atrium; the posterior border below the hilum is constituted by the left ventricle, the anterior surface of the shadow constitutes the right ventricle. If the cardiac silhouette does not appear to be homogenous, the possibility of a superimposed pulmonary pathology may be considered.
The aortic arch is well-visualized with the brachiocephalic artery often being visualized arising and extending anterior to the trachea. The left and right brachiocephalic veins are often visualized as an extrapleural bulge beneath the manubrium sternum and should not be mistaken for a sternal/chest wall mass. Similarly, in the inferior part of the chest, the anterior paracardiac fat may simulate a mass lesion posterior to the chest wall. This is because the two lungs do not meet in the midline, the heart and paracardiac fat being interposed.
The horizontal fissure is seen on most lateral chest X-rays. Oblique fissures appear like the blades of a propeller. The right oblique fissure at its most posterior position lies 4–5 cm behind the sternum, the left oblique is positioned slightly more superior (Figs. 49 and 52).
The IVC may be visible as a well-defined vertical line which meets the posterior and inferior aspect of the heart.
 
Interpreting Chest Radiographs
A systematic approach to the interpretation of a chest radiograph is very important. This is particularly so when an obvious abnormality is present. The PA view of the chest is printed as if the patient is facing the interpreter, with the right side facing the interpreter's left side. It is important first to evaluate the radiograph from a technical quality perspective. Important factors to evaluate are (Fig. 53).
Exposure: In a well-exposed radiograph the dorsal intervertebral disks should just be visible through the cardiac shadow. In an overexposed X-ray the vertebral bodies are well-outlined, the lung fields are darkened. The risk of overexposure is that parenchymal lung lesions may not be visible, though the retrocardiac regions are well-visualized. In an underexposed X-ray the mediastinum appears brighter than usual; also, there is no visualization of the dorsal intervertebral disks.27
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Fig. 52: Lateral view of chest demonstrates the normal oblique fissures extending from the fifth dorsal vertebra posteriorly to the cardiophrenic angle crossing the hilum.
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Fig. 53: Normal chest X-ray: A perfectly exposed X-ray as the dorsal interspaces are just visualized. There is no rotation as the clavicles are equidistant from the cervical spinous processes; the inspiratory effort is adequate, as the anterior ends of the sixth ribs are at the mid-diaphragmatic level.
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Fig. 54: Tracheal deviation: PA view of the chest demonstrates tracheal deviation as a result of mass lesion in the neck arising from the thyroid causing significant displacement and compression to the left.
Inspiratory effort: Chest X-rays are obtained in deep inspiration; the midpoint of the right hemidiaphragm should be at the anterior end of the sixth rib.
Rotation: The medial ends of the clavicle should be equidistant from the spinous processes of the cervical vertebrae.
 
Evaluation of Different Structures on a Chest X-ray
Start with the trachea, note its position, mass effect, deviation and caliber (Fig. 54). Then evaluate the mediastinal silhouette, the right border, then the left border from above downwards. Note any loss of silhouette, cardiomegaly. Next evaluate the hilum, again one at a time, position of hilum, right in relation to left, equality in size and density. If a hilum appears larger or denser, a lateral view is very useful to confirm or exclude a mass lesion. For example, if the right hilum is prominent, presence of a mass will be seen on the lateral view as being posterior to the trachea, since the right pulmonary artery is anterior to the trachea. For the left, it is converse as the left pulmonary artery is posterior to the trachea. The lower lobe pulmonary vessels are well-visualized on a radiograph. Absence of this leash of vessels on a well-centered X-ray is a useful clue to lobar collapse. Evaluate the diaphragms for position, 28contour any loss of silhouette. Now evaluate the lungs. A useful method is to examine them in a zigzag fashion from below upward. Evaluate each zone from a size, transradiancy perspective. The position of the horizontal fissure if visible should be noted, as this may also be a clue toward lobar collapse. Finally, evaluate the ribs and chest wall. Before concluding, pitfall areas where abnormalities may lurk should be evaluated. These include the central mediastinum, lungs behind the diaphragm and heart, lung apices, lung and pleura along the inner surface of the chest wall.
 
CT Anatomy of Normal Mediastinum and the Lung
The normal mediastinal structures, heart, blood vessels, tracheobronchial tree, esophagus are always identified on cross-sectional imaging (Figs. 55A to D).
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Figs. 55A to D: CT anatomy of normal mediastinal structures.
(CCA: Common carotid artery; SCA: Subclavian artery; SVC: Superior venacava; AA: Ascending aorta; DA: Descending aorta; MPA: Main pulmonary artery; RPA: Right pulmonary artery; LPA: Left pulmonary artery; RA: Right atrium; RV: Right ventricle; LV: Left ventricle; LA: Left atrium)
 
MEDIASTINAL VASCULATURE
The vertical portions of the ascending and descending aorta are well-visualized as spherical tubes, the diameter of the ascending aorta is 3.5 cm and of the descending aorta 2.5 cm. The descending aorta descends to the left of the vertebrae and then takes a more midline course to enter the abdomen anterior to the vertebrae. The arch of the aorta is seen in cross-section traversing from the ascending aorta to the descending aorta right to left, anterior to the trachea. Above the level of the aortic arch the great vessels are well-visualized in an arc anterior and to the left of the trachea. The left common carotid artery lies to the left of the trachea, left subclavian artery to the left or posterior to the trachea. The brachiocephalic artery is larger than the left common carotid and left subclavian artery. In 0.5% of the population the right subclavian artery has an anomalous origin arising distal to the left 29subclavian artery. It courses from left to right, posterior to the esophagus at the level of the aortic arch; it then ascends in the right paravertebral space to the root of the neck. The brachiocephalic in this situation becomes the right common carotid artery, with a size similar to that of the left common carotid artery. A barium swallow will demonstrate the posterior indentation of the esophagus caused by the anomalous right subclavian artery (Figs. 56A and B). Pressure on the esophagus by this artery may cause dysphagia.
The right subclavian and jugular vein unite to form the right brachiocephalic vein, which descends vertically in the mediastinum to continue as the superior vena cava (SVC) following its union with the left brachiocephalic vein. The SVC is usually half to two-thirds the diameter of the ascending aorta. The left brachiocephalic vein courses through the mediastinum from the left to the right, anterior to the great vessels. In 0.3–0.5% of the population a left SVC is present. This is more commonly seen in individuals with congenital heart disease. The left SVC is formed by the union of the left jugular and subclavian veins, and descends vertically in the left mediastinum to open into the coronary sinus. Due to the increased blood flow, the coronary sinus is increased in size in this situation.
The azygous vein ascends from the diaphragm in the prevertebral space to the right or posterior to the esophagus; it arches over the right main bronchus to open into the posterior wall of the SVC. In 1% of individuals the azygous penetrates the lung as it arches over the bronchus resulting in an azygous lobe. Occasionally, the IVC does not develop, the azygous becomes the conduit to drain blood back to the heart, and is then termed as the azygous continuation of the IVC. The hepatic veins then open directly into the right atrium and the azygous vein dilates. Variants in vascular anatomy such as left-sided SVC, azygous continuation of IVC, left superior intercostal vein, may be mistaken for a mass lesion or adenopathy on an unenhanced scan or chest X-ray. The hemiazygous and accessory hemiazygous veins ascend posterior to the descending aorta. The accessory hemiazygous may cross to the right to open into the azygous or open into the left superior intercostal vein. The left superior intercostal vein is a small vein, which arches around the aorta at the level of the arch and descending aorta to open into the left brachiocephalic vein. It is only occasionally identified on X-ray/CT.
 
Pulmonary Artery
The main pulmonary artery runs backward and upward obliquely to the left of the ascending aorta (Fig. 57). The right branch travels horizontally to the right between the ascending aorta and tracheobronchial tree; it then descends anterior to the right bronchus. The left branch curves upward and posteriorly over the left main bronchus and descends posterior to the left main bronchus. The main pulmonary artery diameter is approximately 2.8 cm. A main pulmonary artery/aortic ratio greater than 1 indicates pulmonary hypertension. The pulmonary artery branches are two-thirds the diameter of the main pulmonary artery.
 
Thymus
The thymus is best visualized in a section at the level of the aortic arch, anterior to the aorta and pulmonary artery, inferior to the left brachiocephalic vein, and superior to the right pulmonary artery (Fig. 58). Till puberty the thymus occupies most of the anterior mediastinum with a density of soft tissue. After puberty the gland starts to get replaced by fatty tissue; by 40 the gland is not visualized as it is replaced by fatty tissue. In individuals on chemotherapy the thymus may be visualized in adults, termed as thymic rebound.
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Figs. 56A and B: Aberrant right subclavian artery: CECT chest demonstrates right subclavian artery arising distal to the left subclavian and courses from left to right, posterior to the trachea and esophagus.
(CECT: Contrast enhanced computed tomography)
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Fig. 57: Computed tomography (CT) pulmonary angiogram demonstrates a normal pulmonary angiography.
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Fig. 58: Thymus: CT scan chest demonstrates a normal thymus. Seen as a triangular well-defined soft-tissue density with internal fat densities.
 
Mediastinal Lymph Nodes
Ninety-five percent of normal mediastinal lymph nodes measure less than 10 mm in short axis diameter. Mediastinal lymph nodes are chiefly located in the paratracheal, prevascular, pretracheal, subcarinal and aortopulmonary regions.
 
Trachea
In cross-section, the trachea is round or oval with a flattened posterior margin formed by the fibromuscular membrane. On expiration there is a significant change in the diameter of the trachea. This is due to forward motion of the posterior wall of the trachea; there is consequent reduction in the AP diameter of the trachea.
The trachea divides into the two mainstem bronchi at the carina, approximately at the level of T5. The left main bronchus extends up to twice as far as the right main bronchus before giving off its upper lobe division. The right main bronchus is approximately 25 mm long, the left main bronchus is approximately 50 mm long. In children the angles between the bronchi are symmetric, but in adults the right mainstem bronchus has a steeper angle than the left. The segmental bronchi are well-demonstrated on CT.
The right upper lobe bronchus divides into the right apical, posterior and anterior segmental upper lobe bronchi (Fig. 59).
The right lower lobe bronchus divides into right lower lobe superior segment bronchus, (middle lobe medial and lateral) segmental bronchi and anterior, lateral, posterior and medial lower lobe segmental bronchi.
On the left side the upper lobe bronchus divides into apicoposterior and anterior upper lobe segmental bronchi as well as the lingular superior and inferior segmental bronchi. The left lower lobe bronchus divides into superior segmental and anterior medial basal, posterior and lateral basal segmental bronchi.
 
VARIATIONS
  • Common origin of right upper/middle bronchus
  • Tracheal bronchus—either a segmental or the entire right upper lobe bronchus arises from the trachea; there may be a displaced or supernumerary bronchus (Figs. 60A and B)31
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    Fig. 59: Anatomy of tracheobronchial tree: AP view of branches of airways beyond the segmental bronchi.
    (LUL: Left upper lobe; RUL: Right upper lobe; RLL: Right lower lobe; ML: Middle lobe; LLL: Left lower lobe)
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    Figs. 60A and B: Tracheal bronchus: (A) Minimum intensity projection and (B) Volume-rendered images of the tracheobronchial tree demonstrate a tracheal bronchus. The right upper lobe bronchus is seen to arise directly from the trachea.
  • Accessory cardiac bronchus arising from the medial aspect of the right main bronchus, usually blind-ended but may supply a small lobule
  • Lateral inversion of right and left-sided airways in “situs inversus
  • Situs ambiguus—airway has either bilateral right-sided or left-sided configuration
  • Bridging bronchus—right lower lobe bronchus arises from the left main bronchus, crosses the mediastinum to reach the right lung.
The segmental bronchi divide progressively into smaller airways till after 6–20 divisions become bronchioles which further divide till terminal bronchioles. These are the last of the conducting airways. Beyond the terminal bronchioles lie the gas exchange units, the acini. The anatomy of the secondary lobule is discussed under the HRCT section of this chapter.
 
Diaphragm
The diaphragm consists of a large dome-shaped central tendon with radiating striated muscle attached to the xiphisternum and to the 7th to 12th ribs. The two crura arise from the first three lumbar vertebrae forming the lateral walls of the aortic hiatus. The aorta, azygous, hemiazygous veins and thoracic duct pass through this hiatus. There are two more hiatuses anterior to the aortic hiatus in the diaphragm—the esophageal hiatus through which pass the esophagus, esophageal arteries and vagus nerve, and the hiatus for the IVC.32
 
Fissures
The major fissures are well-visualized as thin white lines traversing from posterior to anterior and from cephalad to caudal. The minor fissure lies in the plane of the scanning, therefore, the fissure per se is not visualized. Its position can be inferred as there is an avascular zone in the subpleural regions (Figs. 61A and B).
An avascular zone in the right middle lobe points to the site of the minor fissure.
 
Interstitium: Normal HRCT Anatomy
The lung is supported by a network of connective tissue fibers known as the interstitium of the lung. The interstitium is divided into three components, the axial interstitium, the peripheral interstitium and the intralobular interstitium which communicates between the axial and peripheral interstitium. The peripheral interstitium is located beneath the visceral pleura; it envelops the lung like a fibrous sac from which connective tissue septae penetrate into the lung parenchyma. Between each interlobular septa lies a secondary lobule. The axial interstitium consists of the peribronchovascular interstitium which is strong connective tissue encasing the central bronchi and arteries. This interstitium extends from the level of the pulmonary hila to the periphery of the lung, encasing the centrilobular arteries and bronchioles in the secondary lobules (Fig. 62). The secondary lobule is the smallest unit of lung structure varying in size from 1 cm to 2.5 cm containing 10–12 acini. It is polygonal in shape, with its apex pointing to the hilum and base toward the pleural surface. Each is supplied by a small bronchiole and pulmonary arterial branch—centrilobular artery. This is visualized on HRCT sections as a small dot; however, the bronchus is not visualized as it is below the resolution of present-day HRCT scans (Fig. 63). The interlobular septae which marginate the secondary lobules contain pulmonary veins and lymphatics. At the level of the secondary lobule all three connective tissue systems are present.
 
Anatomy of Bronchi and Pulmonary Vessels
The bronchi and pulmonary arteries run parallel to each other. Their appearances depend upon the scan plane they are sectioned in. If the scan plane is perpendicular to their course they will appear as well-defined round structures adjacent to each other. If sectioned in the same plane, they will appear as tubular structures running parallel to each other. The artery is seen as a well-defined round homogenous white structure. The accompanying bronchus has a thin well-defined wall with a lucent center containing air resembling a pipe with air in its lumen. The outer surface of these structures is smooth. The inner diameter of the bronchus to accompanying arterial diameter is usually 0.65/0.7:1. A bronchoarterial ratio of 1:1 is considered normal; greater than this is considered as bronchiectasis (Fig. 64). An increased bronchoarterial ratio greater than 1 may be seen in patients who reside at a high altitude; the mild hypoxemia induces mild bronchial dilatation as well as vasoconstriction, resulting in an altered bronchoarterial ratio. Bronchi are visualized till the peripheral 2 cm of the lung. It is rare to see normal bronchi in the peripheral 2 cm of the lung. Normal bronchi may extend till 1 cm of the mediastinal surface.
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Figs. 61A and B: Fissures: (A) Axial and (B) sagittal reconstructions demonstrate major interlobar fissures. The minor fissure is not seen on the axial scan as it is in the same plane as the slices. The position of this fissure is inferred on the axial images as a zone of avascularity.
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Fig. 62: Normal anatomy of interstitium: Schematic diagram demonstrates peribronchovascular interstitium in green extending to the secondary lobules. In secondary lobules it forms centrilobular interstitium (blue). The periphery of the secondary lobule is bounded by the interlobular interstitium (yellow). Within the secondary lobule the fine bands in brown represent the intralobular interstitium.
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Fig. 63: Anatomy of secondary lobule—schematic diagram demonstrates polygonal secondary lobules. The secondary lobules share common walls with lymphatics and pulmonary veins in their walls. The center of the secondary lobule contains the centrilobular artery and bronchus.
 
RADIOGRAPHIC PATTERNS OF DISEASE PROCESSES
The most important aspects of imaging are to determine the anatomic location of a lesion, whether in the lungs, mediastinum, pleura or chest wall as well as the nature of the lesion. The most common abnormality visualized on a radiograph is a pulmonary opacity (Table 2). An opacity is often ill-defined and is more opaque than the surrounding lung. It is useful to categorize the patterns of pulmonary opacities as it helps to narrow the differential diagnostic possibilities.
 
Consolidation/Air-space Opacities
Air-space opacities represent one or more ill-defined areas of increased density in the lung parenchyma. When they abut the pleura they have a sharp margin. Vascular shadows are obscured by the air-space opacity, as the air-filled dark lung does not contrast with the soft tissue density of vessels.
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Fig. 64: CT chest showing the normal bronchoarterial ratio.
Table 2   Patterns of pulmonary opacities.
  • Consolidation or air-space opacities
  • Atelectasis
  • Linear/band-like opacities
  • Nodular/reticulonodular opacities
  • Nodules/masses
  • Cavitations
  • Cysts/bullae/honeycombing
  • Calcifications
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Similarly, intrapulmonary airways are rarely visible on chest X-rays. With air-space opacification the air in the airways contrasts with the air-space opacity, so that the airways become visible. This appearance is known as an air bronchogram sign. It also confirms the opacity is intrapulmonary. Another useful sign is the silhouette sign. The borders of the heart and domes of the diaphragm are well-visualized as they are contrasted by the interface with the dark lung. If a pulmonary opacity is in contact with the margins of the heart/diaphragm there is an interruption of the margins resulting in a loss of silhouette. This helps in detecting and localizing the abnormality. Conversely, presence of an opacity with preservations of the silhouette would indicate that the pulmonary abnormality is not in contact with the heart border or diaphragmatic surface. Cavitation may occur within air-space opacities. The cavity results following expulsion or drainage of necrotic contents via the bronchial tree. A gas-filled space with or without an air-fluid level is seen in the air-space opacity. CT is more sensitive in detection of air-space opacities; it may detect opacities even when the chest X-ray is normal. The causes of air-space opacities are numerous; any pathological process which results in filling of alveoli will result in an air-space opacity. The differential diagnosis of air-space opacities includes pneumonia, atelectasis, infarction, hemorrhage, neoplasm, and edema (Figs. 65 to 74).
Important points which may help in the differential diagnosis of air-space opacities:
  • Opacities over half a lobe with no loss of lung volume are virtually diagnostic of pneumonia.
  • Widespread pneumonia is invariably accompanied by cough and fever.
  • Lobar consolidation with lobar expansion causing bulging of the fissure is most often seen in infection due to Klebsiella pneumoniae. It is also occasionally seen following infection with Streptococcus pneumoniae, staphylococcus, and other gram-negative bacteria.
  • Neoplastic obstruction of a lobar bronchus usually causes some degree of atelectasis. However, bronchoalveolar carcinoma and lymphoma may appear as lobar pneumonia with no evidence of atelectasis, as the neoplastic process spreads in the alveolar spaces without involvement of the bronchi.
  • Aspiration should be suspected with a history of alcoholism, seizures, unconscious state. Air-space opacities with evidence of associated loss of volume are seen in patients with aspiration pneumonia. Air-space opacities with well-marked hemoptysis may occur in intrapulmonary hemorrhage.
  • Cavitation within a consolidated lobe could represent tuberculosis or a necrotizing pneumonia (Fig. 72). The latter is commonly caused by Klebsiella (Kl.) pneumoniae, Pseudomonas (Ps.) aeruginosa, Staphylococcus aureus and anaerobic bacteria. Cavitation could also arise in relation to noninfectious etiologies such as Wegener's granulomatosis, other forms of vasculitis and in neoplasms (Figs. 75 to 77).
  • Lucencies seen within an air-space opacity could be due to overlying uninvolved lung, areas of centrilobular emphysema within the abnormal lung, necrosis of tissue with cavitation, pneumatoceles.
  • Rib or vertebral body destruction in the absence of a mass points to a metastatic lesion, though tuberculosis or fungal infections can also present similarly, as destructive bone lesions.
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Fig. 65: Right upper lobe pneumonia: PA view of the chest demonstrates a consolidation in the right upper zone with loss of silhouette of right aortic border. Note there is no loss of volume and silhouette of right cardiac border. There is no shift of mediastinal structures. This is a feature of pneumonia.
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Fig. 66: Right middle lobe pneumonia: PA view of the chest demonstrates ill-defined air space opacities in the right lower zone which has an ill-defined inferior margin and sharp superior margin. Air space opacities are ill-defined, however, when they about the pleura in this case, they have a sharp margin. Note there is loss of silhouette of right cardiac border but silhouette of right aortic border is preserved.
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Fig. 67: Right upper and middle lobe pneumonia: Large area of consolidation is seen in the right lung with loss of silhouettes of both right cardiac and right aortic borders and with subtle bronchograms within; note there is no evidence of loss of volume or mediastinal shift.
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Fig. 68: Right lower lobe pneumonia. PA view of the chest demonstrates an ill-defined consolidation in the right lower zone preserving silhouette with cardiac margin but loss of silhouette with diaphragm.
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Fig. 69: Right lower lobe pneumonia. PA view of the chest demonstrates an ill-defined area of consolidation in the right lower zone; there is no loss of the silhouette of the cardiac as well as diaphragmatic surface indicating this consolidation is not in contact with either the diaphragm or cardiac surface.
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Fig. 70: Right upper lobe pneumonia with collapse consolidation: PA view of the chest reveals a triangular shaped consolidation with air bronchograms in the right upper zone associated with elevation of the minor fissure and mild deviation of trachea to the right representing a right upper lobe consolidation with partial collapse.
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Fig. 71: Consolidation. CT chest demonstrates a large consolidation in the right middle lobe with an air bronchogram pattern. There is an associated pleural effusion.
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Fig. 72: Consolidation with cavitation: PA view of the chest reveals ill-defined area of consolidation with cavitation in the right upper zone. Causative organism—Staphylococcus aureus.
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Fig. 73: Pulmonary infarct. PA view of the chest reveals a wedge-shaped area of consolidation in the right lower zone abutting the pleura. The appearance of a wedge-shaped consolidation should raise the possibility of a pulmonary infarct.
 
BAT WING PATTERN OF PULMONARY OPACITY
This is a term used to describe diffuse parahilar opacities which have ill-defined margins. These may be symmetric or asymmetric, being larger on one side. The most common cause for this opacity is pulmonary edema, especially if associated with cardiomegaly/pleural effusion/Kerly A/B lines. Another feature of pulmonary edema is the rapid appearance and disappearance of opacities (Figs. 78 and 79). Other conditions which may present with this type of opacities are aspiration pneumonias, and inhalation exposure to noxious gases. Immunocompromised patients, especially Pneumocystis jirovecii pneumonia can have a similar appearance (Fig. 80). Bat wing opacities unchanged over a long period of time with nonspecific symptoms, suggest the possibility of alveolar proteinosis (Fig. 81) or a neoplastic process such as lymphangitic carcinomatosis.
Peripheral air-space consolidations are considered as a photographic negative of pulmonary edema as the opacities are in the lung periphery. Especially when present in the upper zones the most common possibility is chronic eosinophilic pneumonia.37
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Figs. 74A and B: (A) X-ray chest in a febrile patient demonstrates no abnormality; (B) CT chest reveals multiple bilateral cavitating and subpleural nodular lesions. CT is more sensitive than chest X-rays in detection of focal lesions, as well as demonstrating internal morphology of focal lesions, such as cavitation, necrosis, calcification, and air bronchograms.
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Fig. 75: Lung abscess: PA view of chest reveals thick-walled cavitatory lesions with air-fluid level in the left upper zone as well as in the right lower zone. These lesions represent lung abscesses.
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Fig. 76: Wegener's granulomatosis: PA view of the chest X-ray reveals multiple well-defined rounded nodular lesions in both the mid and lower zones. Some appear solid, some cavitatory and some with air-fluid levels. c-ANCA was strongly positive in this patient confirming Wegener's granulomatosis.
If the opacities are not predominantly in the upper zones, the possibilities include cryptogenic organizing pneumonia, viral pneumonia or a mycoplasmal pneumonia. Fleeting shadows, shadows which come and go, or appear in different regions of the lungs, raise the possibilities of pulmonary edema, eosinophilic pneumonia, asthma, ABPA and vasculitis (Figs. 82A to D).
White-out lungs are typical for acute respiratory distress syndrome (ARDS), especially with associated air bronchograms (Fig. 83). Sarcoid may present with patchy opacities in the lungs which may be spherical and have associated mediastinal adenopathy.38
 
COLLAPSE/ATELECTASIS
Often the words collapse and consolidation are used interchangeably. Consolidation is essentially due to replacement of alveolar air by an exudate, transudate or cellular debris resulting in a homogenous opacity with no loss of volume. Atelectasis or its synonym “collapse” indicates volume loss. The atelectatic/collapsed segment or lobe of the lung will therefore demonstrate a homogenous opacity with accompanying volume loss. Atelectasis is caused by bronchial obstruction which is either due to an intrabronchial pathology, foreign body or extrinsic compression of the bronchus (Figs. 84A and B). Compression atelectasis can be due to compression of adjacent lung by tumor, bulla, pneumothorax or pleural effusion.
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Fig. 77: Tuberculosis: PA view of the chest reveals ill-defined fibrocavitatory lesion in left upper and mid zones as well as patchy nodular consolidation with cavitation in right mid zone. Incidentally note is dextrocradia. The presence of upper/mid zone cavitation in the Indian subcontinent favors the diagnosis of tuberculosis.
 
Cicatrization Atelectasis
Following resolution of an inflammatory/infective process there may be localized atelectasis. This is due to either direct destruction of lung parenchyma or fibrotic contraction, termed as cicatrization fibrosis. This is commonly seen in tuberculosis, radiation fibrosis, interstitial pulmonary fibrosis, and bronchostenosis (Figs. 85 and 86).
Pulmonary fibrosis can cause significant loss of volume due to fibrotic contraction of lung parenchyma.
 
Plate or Discoid Atelectasis
This is a form of atelectasis, which is due to hypoventilation, leading to alveolar collapse. The alveoli in the lung bases as well as posterior aspects of the lung fields are the most prone to collapse. These appear as linear plate or disk-like opacities in the lower zones, occasionally extending across the whole breadth of the lower lobe (Fig. 87). As these are due to hypoventilation they are seen mainly in hospitalized patients, post general anesthesia and in patients with an acute abdomen where the diaphragm is splinted, resulting in reduced respiratory excursion.
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Figs. 78A and B: Pulmonary edema. AP view portable X-ray. (A) demonstrates ill-defined fluffy opacities in both lung fields; within a few hours, on a follow-up X-ray; (B) the opacities regressed.
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Figs. 79A and B: Pulmonary edema. Portable chest X-rays in a patient with left centralvenous catheter in situ. X-ray (A) reveals an ill-defined opacity in the right lower zone; (B) subsequent X-ray a few hours later reveals increasing opacities in the both lungs. This feature of rapidly appearing and disappearing shadows is highly suggestive of pulmonary edema.
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Fig. 80: Pneumocystis jirovecii pneumonia (PCP): Immunocompromised patient with diffuse ill-defined air-space opacities. In the setting of immunocompromise, the most likely etiology would be Pneumocystis jirovecii pneumonia.
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Fig. 81: Alveolar proteinosis. PA view of the chest demonstrates ill-defined airspace opacities in both lung fields sparing the right upper lobe. Intercostal drainage (ICD) seen in situ following thoracoscopic biopsy which revealed pulmonary alveolar proteinosis. Patient presented with cough, fever and mild dyspnea over 3 months. This is an example of bilateral white-out lungs with subacute to chronic symptoms.
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Figs. 82A to D: Fleeting opacities. Serial high-resolution computed tomography (HRCT) chest performed in 30-year-old patient with blood eosinophilia reveal (A) multiple ill-defined areas of consolidation seen in right upper lobe on 30/8/13. (B) resolution of previously seen consolidation with reappearance of lesions of less severe extent on 25/11/13. (C) ill-defined areas of peribronchovascular and subpleural consolidation with air bronchogram and adjacent areas of ground-glass attenuation involving right upper and middle lobes on 17/09/18. (D) regression in the right lung consolidation on 27/09/18. CT-guided biopsy performed on 30/08/13 revealed Churg-Strauss syndrome with vasculitis.
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Fig. 83: Acute lung injury: Typical white-out lung appearance seen in acute lung injury.
 
Lobar Collapse/Atelectasis
The imaging features of lobar collapse are a pulmonary opacity with evidence of volume loss. The pulmonary opacity is due to loss of air in the alveoli of the collapsed segment/lobe and/or due to retained mucous secretions. The loss of volume is demonstrated by a shift of normal structures such as the hilum, interlobar fissures, mediastinum, with crowding of ribs, and of bronchovascular structures and elevation of the dome of the diaphragm. There is hypertranslucency of the normal ipsilateral lung due to compensatory overexpansion, with pulmonary vessels within it being more widely separated when compared to the opposite lung. It is important to note that when there is severe/total collapse of a lobe it may not always be possible to demonstrate the shadow of the lobar collapse on an X-ray, as the signs are too subtle. A shift of the hilum, fissure or the mediastinum should always suggest an underlying atelectasis.41
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Figs. 84A and B: Obstructive atelectasis. Chest X-ray (A) demonstrates an opaque left hemithorax with a shift of the mediastinum to the left indicative collapse of left lung. The most likely cause would be an obstruction to the left main bronchus. Bronchoscopy revealed a mucus plug obstructing the left main bronchus; (B) after aspirating the mucus plug the lung expanded with few residual opacities.
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Fig. 85: Fibrocalcareous tuberculosis (TB). PA view of the chest reveals bilateral apical fibrotic lesions with calcified nodular lesions in both apices. These features of reticular opacities with calcified nodules and loss of volume are typical of old healed tuberculosis.
 
GOLDEN S-SIGN
When there is obstructive collapse by a central neoplasm with consequent peripheral collapse—the shape of the fissure assumes an “S” shape, as the fissure is concave peripherally and convex centrally.
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Fig. 86: Radiation fibrosis. PA view of the chest reveals an ill-defined opacity in the right apical region with associated loss of volume, shift of trachea to the right, with the right hilum pulled up. Patient had received radiation for cancer of the esophagus with resultant radiation fibrosis.
 
Lower Lobe Atelectasis
The appearances of right and left lower lobe atelectasis are similar. The lobes collapse posteromedially in the lower part of the chest. Left lower lobe atelectasis is often difficult to detect as the collapsed lobe is hidden 42by the cardiac silhouette (Fig. 88). A penetrated X-ray would reveal the opacity of the collapsed lower lobe (Figs. 89A and B). As the lobe collapses posteromedially, the oblique fissure rotates backward and medially, the upper portion of the oblique fissure swinging downward. The collapsed lobe is seen as a triangular opacity lying against the mediastinum. On the right side the medial aspect of the diaphragm is obscured, the lateral margin of the adjacent vertebrae is effaced, the ipsilateral hilum is depressed and the ipsilateral lower lobe pulmonary artery is not visualized (Figs. 90 and 91). Lower lobe atelectasis is better demonstrated on a lateral view (Fig. 92). The lung collapses posteriorly, therefore is seen as an opacity overlying the vertebrae. Normally, the vertebrae on a lateral view demonstrate increasing transradiancy of the lower dorsal vertebrae. On CT the collapsed lobe is seen plastered along the vertebral column in a posteromedial location. The major fissure rotates to lie obliquely.
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Fig. 87: Plate atelectasis. PA view of the chest in a postoperative patient reveals a central line in situ. Plate atelectasis is seen in the left lower zone with evidence of loss of volume as evidenced by elevation of left dome of diaphragm.
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Fig. 88: Lower lobe collapse: Schematic diagram of left lower lobe collapse. The lower lobe collapses behind the cardiac silhouette on the PA view. The diaphragm is mildly elevated and the left lung volume is reduced. The diagram of the lateral view demonstrates the posterior collapse of the lower lobe, and a shift of the oblique fissure posteriorly.
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Figs. 89A and B: Left lower lobe collapse. (A) PA view of the chest demonstrates a homogenous opacity with a smooth margin behind the cardiac silhouette due to the collapse of left lower lobe. Note the evidence of volume loss in the left lung. (B) Lateral view of the chest demonstrates obscuration of the density of lower dorsal vertebral bodies due to the posteriorly collapsed left lower lobe.
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Fig. 90: Right lower lobe collapse: Schematic diagram—PA view demonstrates collapsed segment along the right heart border abutting the diaphragm. There is elevation of the right dome of diaphragm, loss of volume in the right lung and a shift of mediastinum to the right. Lateral view reveals the collapsed lung posteriorly with shift of the oblique fissure posteriorly.
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Fig. 91: Right lower lobe collapse. PA view of the chest demonstrates a homogenous opacity in the right paracardiac region with loss of the cardiac and diaphragmatic silhouette. There is evidence of loss of volume, as the right dome of the diaphragm is elevated and the right lung is smaller in size as compared to the left.
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Fig. 92: Right lower lobe collapse. Lateral view demonstrates an ill-defined haze overlying the lower dorsal vertebrae. There is loss of normal increasing translucency of lower dorsal vertebrae due to the collapsed right lower lobe opacity overlapping the vertebrae. Note the elevated right dome of the diaphragm.
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Fig. 93: Right middle lobe collapse. Schematic diagram demonstrates right lower zone opacity abutting the cardiac silhouette with elevation of the diaphragm, and reduction in right lung volume. Lateral view demonstrates minor and major fissure approximate with each other, with a triangular opacity representing the collapsed middle lobe within.
 
Right Middle Lobe Atelectasis
The atelectatic right middle lobe on a chest X-ray is seen as an opacity along the right heart border resulting in a loss of the silhouette of the right cardiac border (Figs. 93 and 94A). There is no significant change in the vasculature; the right hilum does not change in position. Right middle lobe atelectasis is best demonstrated on a lateral view as the horizontal fissure descends with increasing atelectasis (Fig. 94B). The atelectatic lobe is seen as an opaque wedge extending from the hilum anteriorly. Occasionally, when the atelectasis is very severe the appearances may resemble a thickened fissure. On CT, right middle lobe atelectasis is seen as a triangular wedge atelectatic lung, bound by the major fissure posteriorly and minor fissure anteriorly (Fig. 95).44
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Figs. 94A and B: Right middle lobe collapse. (A) PA view demonstrates an ill-defined opacity in the right lower zone; (B) Lateral view of the chest reveals a homogenous opacity overlying the cardiac silhouette bounded by the interlobar fissures representing right middle lobe collapse. Note the marked downward shift of the lesser fissure.
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Fig. 95: Collapse of the lateral segment of the right middle lobe. CT chest reveals a mass lesion in the right hilum causing collapse of the lateral segment of the right middle lobe, seen as a band-like shadow in the right middle lobe.
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Fig. 96: Right upper lobe collapse: Schematic diagram demonstrates on PA view right upper lobe opacity, elevation of minor fissure, right hilum and right dome of diaphragm. Lateral view demonstrates elevation and backward rotation of minor fissure with collapsed right upper lobe opacity within the two fissures.
 
Right Upper Lobe Collapse
The right upper lobe collapses against the mediastinum and lung apex (Fig. 96). As the lobe collapses the silhouette of the superior vena cava is lost. When there is total collapse a wedge of tissue is seen in the right upper zone along the mediastinum (Fig. 97). The right middle and lower lobes demonstrate compensatory expansion and there is elevation of the right hilum. The major and minor 45fissures move upward and toward each other. This is well seen on the lateral view. The collapsed lobe on the lateral view silhouettes the ascending aorta. On CT, the collapsed right upper lobe appears as a triangular soft tissue density lying against the mediastinum and anterior chest wall.
 
Left Upper Lobe Atelectasis
The pattern of collapse is complex, as there is no horizontal fissure. As the lobe collapses it pulls the major fissure forward and the lower lobe expands posterior to the major fissure (Figs. 98A to C). As the left lower lobe expands posterior to the collapsing left upper lobe, on PA radiographs the atelectatic left upper lobe appears as a diffuse haze overlying the left hilum often extending to the lung apex, but fading inferiorly and laterally (Figs. 99A and B). The left cardiac and mediastinal silhouette is lost. As the lower lobe expands the aortic knuckle may be visible and consequently the left apex and upper mediastinum may be visible as the expanded lung occupies these regions.
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Fig. 97: Right upper lobe collapse: PA view of the chest demonstrates triangular opacity in the right apical region with the deviation of the trachea to the right and loss of volume in right hemithorax. This is due to the right upper lobe collapse.
On the lateral view the collapsed lung is seen anteriorly with the major fissure moving anteriorly to be relatively parallel to the chest wall. As the lower lobe overexpands air may be seen between the sternum and the atelectatic lung. The appearances on CT are very similar to those seen with right upper lobe atelectasis (Fig. 99C).
 
Right Middle and Lower Lobe Atelectasis
This type of atelectasis is rare considering the distance between the two bronchi. It may however occur due to separate occlusions of the right middle and lower lobe bronchi. The appearances resemble a right lower lobe atelectasis; the extent of involvement is more extensive, extending to the lateral costophrenic angle on the PA view and to anterior chest wall on the lateral view.
 
Linear and Band-like Opacities
Linear opacities are linear densities less than 5 mm and bands are considered to be linear densities more than 5 mm in thickness (Fig. 100). The causes are tabled in Table 3.
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Figs. 98A to C: Left upper lobe collapse (A) Schematic diagram (B and C) PA views demonstrate an ill-defined haze overlying the left upper lobe. A homogenous opacity is not seen as in other lobar collapses as the compensatory expansion of the left lower lobe occurs posterior to the collapsed left upper lobe. These opacities are summated on a PA view resulting in only a hazy opacity. On the lateral view the opacity of the collapsed left upper lobe is better visualized, though with marked expansion of the lower lobe, the expanded lower lobe may intersperse between the sternum and collapsed left upper lobe. Note the major fissure has moved anteriorly parallel to the anterior chest wall.
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Figs. 99A to C: Left upper lobe collapse. PA view of the chest (A) demonstrates an ill-defined opacity in the left suprahilar region. Lordotic view (B) demonstrates a well-defined opacity plastered against the mediastinum. CT chest (C) demonstrates collapsed lobe abutting mediastinum.
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Fig. 100: Plate or Discoid atelectasis. PA view of the chest reveals linear bands in the right mid and left lower zone due to plate atelectasis, following general anesthesia.
Mucoid impaction appears as one or more band-like opacities pointing toward the hilum, usually 1.0 cm or more in diameter (Fig. 101). The margins are usually sharply demarcated and smooth with a finger-in-glove appearance. This appearance is mainly seen in ABPA but may also be seen as a result of bronchial obstruction in bronchial carcinoid, lung Ca, bronchostenosis, broncholithiasis, and bronchial atresia. If the lung distal to the obstructed segment is consolidated or collapses, the linear bands of mucoid impaction will not be visualized as they are now silhouetted by the collapse/consolidation.
Table 3   Causes of linear opacities.
  • Clothing, tubes, etc.
  • Wall of a bleb or pneumatocele
  • Bronchocele (mucoid impaction)
  • Parenchymal or pleuroparenchymal scar
  • Discoid atelectasis
  • Organizing pneumonia (presenting with a band-like pattern)
  • Anomalous blood vessels or feeding and draining vessels to arteriovenous malformations
  • Thickening of pleural fissures
  • Pleural tail associated with pulmonary nodule
  • Septal lines (Kerley lines) as in pulmonary edema, neoplastic infiltration, lymphangitis carcinomatosis
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Fig. 101: Mucoid impaction chest X-ray reveals well-defined nodular opacities in left lower zone. CT demonstrated the nodular opacities to be due to mucoid impaction. The nodular opacities seen on X-ray are due to end on dilated bronchi with mucoid impaction.
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Septal Lines
Interlobular septa of normal lungs are not visible on chest radiographs or even HRCT. When septa become thickened they become visible. Kerley first described septal lines especially in pulmonary edema. They were named ABC, “A” referred to septal lines which ranged up to 4.0 cm radiating from the hila into the central portions of the lung, more visible in the upper/mid zones of lung. These are now referred to as deep septa. The “B” lines are short, less than 1.0 cm in length, are parallel to each other and at right angles to the pleura. They are referred to as peripheral interlobular septa, and are seen most frequently in the lung bases. Kerley “C” lines have been dropped, as they actually represent many B lines superimposed on each other. It is important to differentiate septal lines from vascular shadows. Kerley B lines are essentially visualized in the last 1 cm of lung parenchyma; lung vessels are not seen in the last 1 cm of the lung. Kerley A lines are differentiated from lung vessels as they are much thinner and do not branch (Figs. 102A and B).
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Figs. 102A and B: Septal lines: (A) Chest X-ray demonstrates cardiomegaly, right pleural effusion and prominent lung markings; (B) CT chest demonstrates smooth septal thickening with ground-glass densities due to pulmonary edema secondary to congestive cardiac failure.
 
Reticular and Reticulonodular Opacities (Table 4) (Figs. 103 to 110)
Table 4   Reticular and reticulonodular opacities.
  • Interstitial lung disease
  • Pulmonary edema or pneumonia
  • Fever with reticular opacities—mycoplasmic or viral pneumonia
  • Lymphangitis carcinomatosis—unilateral reticular opacities
  • Tuberculosis, rarer causes include fungal disease (histoplasmosis), chronic hypersensitivity pneumonitis, ankylosing spondylitis
  • Sarcoidosis
  • Pneumoconiosis
  • Calcified opacities in both lung fields—miliary metastases due to thyroid carcinoma, osteogenic sarcoma, tuberculosis
  • High-density miliary nodules are observed in silicosis, baritosis, microlithiasis
  • Cloud-like punctate calcification is typically seen in alveolar microlithiasis
  • Conglomerate opacities with fibrosis and miliary nodules—progressive massive fibrosis with pneumoconiosis
 
Unilateral Transradiancy of the Lung
The causes for unilateral transradiancy of the lung are:
  • Radiographic artifact: The radiographic output is usually adjusted to increase the output in the region of the bases as compared to the apices. This is known as a heel-toe effect. If this heel-toe effect is horizontally oriented rather than vertically, it will result in one hemithorax being overpenetrated. A similar effect occurs when the patient is rotated. This can be detected by observing the soft tissue in relation to the shoulders; the penetration will be different.48
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    Fig. 103: Interstitial pneumonia: Chest X-ray reveals extensive reticular opacities and ill-defined areas of consolidation more on right mid zone as result of an interstitial pneumonia.
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    Fig. 104: Sarcoidosis: There is evidence of large bilateral hilar adenopathy as well as multiple small nodular lesions in both the mid and lower zones (left>right). These represent mediastinal adenopathy and interstitial lesions of sarcoidosis (Stage 2).
  • Thoracic wall and soft tissue abnormalities: Unilateral mastectomy or congenital absence of pectoralis muscle (Poland syndrome) (Fig. 111).
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    Fig. 105: Miliary tuberculosis. PA view of the chest reveals multiple small nodules in both lung fields as a result of miliary tuberculosis.
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    Fig. 106: Alveolar microlithiasis. PA view of chest reveals extensive small nodular high densities in both lung fields. The very high density is typical of microlithiasis.
  • Overexpansion or increased translucency of one lung:
    • Obstructive emphysema due to a foreign body, or intrabronchial mass lesion
    • Compensatory emphysema due to severe lobar collapse or lobectomy
    • Pulmonary embolism involving one major pulmonary artery49
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      Fig. 107: Alveolar microlithiasis: CT chest in a relatively asymptomatic patient reveals extensive small nodular high-density calcified lesions in both lung fields as a result of alveolar microlithiasis.
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      Fig. 108: Reticular opacities: PA view of chest reveals reticular opacities in both lung fields particularly lung bases. HRCT revealed interstitial pulmonary fibrosis.
    • Pleural effusion in a supine patient, causing an ipsilateral increase in density of the hemithorax, consequently the opposite hemithorax appears to be hypertranslucent (Fig. 112)
    • Macleod's or Swyer-James syndrome.
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      Fig. 109: Progressive massive fibrosis: PA view of the chest reveals bilateral ill-defined parahilar mass lesions with multiple small ill-defined nodular lesions along the periphery of the lesion.
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      Fig. 110: Progressive massive fibrosis: CT chest reveals ill-defined soft tissue mass lesions with internal calcification and cavitation in a patient with progressive massive fibrosis secondary to silicosis.
  • Increased translucency of both lungs:
    • Widespread transradiancy of both lungs may be seen in airway disease such as constrictive bronchiolitis, asthma and emphysema
    • Obstruction of flow from right side of heart with a right to left cardiac shunt such as Fallot's tetralogy, Eisenmenger's syndrome, severe widespread pulmonary arterial stenosis and massive pulmonary embolism.50
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Fig. 111: Unilateral mastectomy: PA view of the chest, note right lung appears more translucent than left lung. This is due to mastectomy on the right side.
 
Solitary Pulmonary Nodule
A pulmonary nodule is referred to as a spherical opacity with relatively well-defined margins with a diameter of up to 3 cm (Fig. 113). Lesions more than 3 cm in size are considered as mass lesions. A well-defined spherical opacity below 1 cm in diameter is referred to as a small SPN.
With increasing use of MDCT and its high spatial resolution, small nodules are being detected with an increasing frequency. Though most are benign in etiology, it is important to remember that 20–30% of lung cancers present as a solitary pulmonary nodule. One of the primary roles of imaging, beyond detection is to accurately differentiate malignant from benign lesions. It is important to obtain 3/5 mm sections as well as thin 1-mm sections through the lung on CT. The thinner sections help to reduce partial volume averaging so as to provide an accurate assessment of the internal contents and margins of the nodule. The thicker 3/5 mm sections are important as it is difficult to differentiate small SPN from vessels in thin 1 mm sections.
The first step in the radiological evaluation is to determine whether the nodule is pulmonary or extrapulmonary, as the chest X-ray gives a 2D image. Skin, pleural or rib lesions can appear as an intrathoracic lesion. Lateral, oblique X-rays or a CT scan would help to localize the lesion (Figs. 114 to 116). Once the lesion is confirmed to be intrapulmonary, the possibilities would essentially be an infective lesion, benign lesion or a malignant lesion. There is a significant overlap in the imaging appearances. To help differentiate, it is useful to look at the clinical and morphological features.
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Fig. 112: Unilateral translucency: Frontal chest X-ray in supine position reveals uniform haziness of right hemithorax with transradiancy of left hemithorax. This is due to a right pleural effusion layering along the chest wall contributing to the right hemithorax opacity and consequent transradiancy of left hemithorax.
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Fig. 113: Solitary pulmonary nodule: Chest X-ray demonstrates a well-defined nodular lesion with calcification along its medial aspect in the right upper zone. The lateral margins of the lesion appear to have obtuse angles with the chest wall, a sign suggesting that the lesion is extrapulmonary.
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Fig. 114: Solitary pulmonary nodule: CT demonstrates that the nodule demonstrated on the chest X-ray is not intrapulmonary. It arose from the posterior end of the rib with calcification along its anterior aspect. The histopathology revealed an enchondroma.
 
Nodule Morphology
Calcification: Presence of calcification in a pulmonary nodule is a useful sign to differentiate benign from malignant nodules. However, 13% of all lung carcinomas demonstrate calcification; only 2% less than 3 cm in size demonstrate calcification. The different types of calcification which may be visualized in a pulmonary nodule are—concentric, popcorn, punctate/eccentric and uniform.
Concentric: The calcification occupies the entire SPN or the entire periphery of the SPN in a laminated manner. This calcification is mainly seen in tuberculous and fungal infections.
Popcorn calcification: Multiple small rings or nodules of calcification which overlap are seen in hamartomas/cartilage tumors (Fig. 117).
Punctate/Eccentric calcification: Punctate/Eccentric calcification is suspicious as it may be seen in infections and malignancies. A malignancy may engulf a calcified focus representing an old-healed granuloma, with calcification appearing on the periphery of the lesion (Fig. 118).
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Figs. 115A and B: Solitary pulmonary nodule (A) PA view demonstrates a solitary pulmonary nodule in right lower zone; (B) lateral view demonstrates nodule is subcutaneous (arrow). This case demonstrates the paramount importance of a lateral X-ray of the chest in determining the location of a nodular opacity.
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Figs. 116A and B: (A) Chest X-ray reveals solitary pulmonary nodule in right lower zone. (B) Lateral view demonstrates nodule in posterior, pleural base with a wide pleural attachment and with obtuse angles against the chest wall. These features favor pleural/extrapleural mass lesion rather than an intrapulmonary lesion.
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Fig. 117: Solitary pulmonary nodule: CT chest demonstrates a well-defined nodule in the right upper lobe. There is a popcorn type of distribution of calcification typical of a hamartoma.
Uniform calcification: The entire SPN is calcified; this is typical of calcified granulomas (Fig. 119).
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Fig. 118: Solitary pulmonary nodule: CT chest reveals a nodular mass lesion in the left lower lobe with a calcific speck along its periphery, an example of an eccentric type of calcification. CT-guided biopsy revealed an adenocarcinoma. The calcific density represented an old granuloma which healed with calcification and was engulfed by the neoplasm.
 
Size
Most malignant nodules are larger than 2 cm in size, however 40% are less than 2 cm, 15% are less than 1 cm, 1% of malignant lesions are less than 7 mm in size. Most 53lesions above 3 cm are likely to be either bronchogenic carcinoma, lung abscess, Wegener's granulomatosis, lymphoma, round atelectasis, focal pneumonia, or hydatid cysts. It is difficult to detect a lesion less than 5 mm in diameter on a chest X-ray. If a lesion which is 5 mm or less is seen on a chest X-ray, it is invariably calcified.
 
Shape
A spiculated margin is very suggestive of carcinoma; the spicules represent spread into the interstitium of the lung (Figs. 120 and 121). Lobulation and notching which indicate unequal growth are suggestive signs for malignancy but may be seen in inflammatory lesions. There is considerable overlap in the findings between benign and malignant. A spiculated lesion though has a predictive value of 90% to be a malignant lesion. An inflammatory lesion with fibrosis may however have a similar appearance. Benign lesions usually have smooth margins. Conversely 20% of primary lung tumors have smooth margins; most metastatic lesions also have smooth margins.
 
Cavitation
Cavitation occurs in inflammatory as well as primary and metastatic tumors. Benign lesions tend to have thinner and smoother walls as compared to malignant lesions, which have thicker and irregular walls (Figs. 122 and 123).
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Fig. 119: Solitary pulmonary nodule: CT chest demonstrates a well-defined pulmonary nodule in the right upper lobe. The nodule is densely calcified, representing a uniform type of calcification, indicating with certainty that the nodule is benign.
 
Fat
Demonstration of fat within a solitary pulmonary nodule is pathognomonic of a hamartoma, (50% of hamartomas demonstrate fat in the lesion) (Fig. 124). Rarely, lipoid pneumonia/metastatic liposarcoma or renal cell carcinoma metastasis may demonstrate fat densities.
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Fig. 120: Solitary pulmonary nodule: Chest X-ray demonstrates a nodule in the left upper lobe. Note its spiculated margin, a relatively specific sign to indicate malignancy.
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Fig. 121: Solitary pulmonary nodule: CT chest demonstrates a nodular lesion in the left apex. There are multiple radiating bands arising from the surface of the nodule resulting in a spiculated appearance. This is typical of a malignant lesion. Rarely, an inflammatory lesion may demonstrate spiculation.
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Fig. 122: Solitary pulmonary nodule: CT chest reveals a well-defined nodular lesion in the right upper lobe abutting the pleura with internal cavitation, the margins of which are smooth. CT-guided biopsy revealed this lesion to be due to Mycobacterium tuberculosis.
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Fig. 123: Solitary pulmonary nodule: CT chest reveals a large nodular lesion with internal necrosis and cavitation in the right lower lobe. The inner margins of the cavitation are irregular: CT-guided biopsy revealed a squamous carcinoma.
 
Satellite Nodules
Multiple small peripheral nodules around an SPN are very useful signs indicating a benign lesion, especially inflammatory in etiology. It has a positive predictive value of 90%.
 
Air Bronchogram
Presence of an air bronchogram does not exclude a neoplasm as this may be seen in a bronchoalveolar carcinoma or in lymphoma. Presence of an air crescent is useful to diagnose an aspergilloma (Fig. 125).
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Fig. 124: Solitary pulmonary nodule: CT chest reveals a small pulmonary nodule in the right chest anteriorly. There is a fat density within the lesion; this is typical of a hamartoma.
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Fig. 125: Solitary pulmonary nodule: Well-defined solitary pulmonary nodule in right mid-zone with an air crescent along superior surface of nodule. The air crescent indicates that the nodule represents a fungal ball in a cavity—aspergilloma.
 
CT Halo Sign
Lung cancers can have a halo around them, though such halos may also be seen in inflammatory lesions, especially in invasive aspergillosis (Fig. 126).
 
Rate of Growth
Lung cancers take from 1 month to 18 months to double in volume, the average time being 4.2–7.3 months. Volume doubling faster than 1 month suggests an infection/infarction/aggressive lymphoma. Doubling 55after 18 months is seen in granuloma/hamartoma/carcinoid/round atelectasis. A lesion which has not grown or has reduced in size in 2 years is likely to be benign. For a nodule to double in volume, the change in nodule diameter is approximately 26% (Figs. 127A and B). A 4 mm nodule which increases to 5 mm would have doubled in volume. Thus accurate measurements are critical in deciding doubling time. There is significant inter- and intraobserver variation in measurements, especially in spiculated lesions. The ideal method to evaluate growth is to evaluate volume, as an irregular-shaped structure is being measured. Automated volume measuring techniques are very useful in this setting. The problems of inter-/intraobserver variations are minimized, as all spiculated and irregular margins are taken into consideration for measurements. Most modern CT workstations have automated software that enables accurate measurements.
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Fig. 126: Solitary pulmonary nodule: High-resolution computed tomography (HRCT) demonstrates a well-defined nodule in the apical segment of the right lower lobe with an ill-defined halo of ground-glass around the nodule. This appearance is seen in invasive aspergillosis.
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Figs. 127A and B: Solitary pulmonary nodule: CT chest studies done 6 months apart reveal progression in size of nodule. CT-guided fine-needle aspiration cytology (FNAC) of lesion revealed a non-small-cell cancer; this is the most important sign in the evaluation of a pulmonary nodule (its progression in a short-period of time). It indicates the need for further intervention, FNAC, biopsy or surgical excision.
 
Nodule Enhancement and Metabolism
There are numerous reports in Western literature on the utility of contrast enhancement to differentiate between benign and malignant SPN. If the enhancement of a nodule following contrast enhancement exceeds 20 HU then it is most likely malignant, whereas if less than 15 HU it is most likely benign. Enhancement is determined by measuring HU values, postcontrast after 1, 2, 3, 4 minutes. The peak HU value is subtracted from the precontrast HU value. Sensitivities of 98%, specificity of 73%, positive predictive value of 77%, and negative predictive value of 98% have been reported. However, these findings do not apply to patients in the Indian subcontinent as the most likely differential diagnosis of a malignant SPN is an inflammatory lesion (in particular a tuberculous lesion). A tuberculoma will enhance to a similar extent as a malignant 56nodule. For the same reason the FDG PET is insensitive in differentiating a malignant from a tuberculous or other inflammatory pathology. Further, PET can be quite insensitive in detecting pulmonary nodules, especially metastatic nodules, less than 1 cm in diameter.
 
High-resolution Computed Tomography Patterns of Diffuse Lung Disease
The detection and diagnosis of diffuse lung diseases is based on the demonstration and recognition of specific abnormal findings. These findings can be classified into essentially two groups, those with increased lung attenuation and those with decreased lung attenuation. Those with increased lung attenuation can be further subdivided into reticular opacities, nodular opacities and parenchymal opacification. Those with decreased lung attenuation can be subdivided into cystic lesions, emphysema, bronchiectasis, mosaic perfusion/attenuation and air trapping.
 
RETICULAR OPACITIES
Thickening of the interstitial fiber network of the lung by inflammation, fluid, fibrous tissue or neoplastic infiltration results in linear/reticular opacities. Thickening of the axial interstitium results in thickening of the interstitium along the walls of the bronchovascular structures (Fig. 128). Since bronchial walls and vessels have similar densities, it is difficult to differentiate the interstitial thickening from the underlying bronchovascular structures. Consequently, the appearances are of thickening of the bronchial wall and an increase in the vessel diameter.
Thickening of the peripheral interstitium is easy to demonstrate, as septal thickening is seen in the subpleural regions, marginating the secondary pulmonary nodule, and interlobular interstitium. This is manifested as radiating bands extending perpendicular to the pleural surface (Figs. 129 and 130).
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Fig. 128: Peribronchovascular interstitial thickening: The vessels appear to be prominent in size with irregular surfaces. This is due to peribronchovascular interstitial thickening. There is extension of the interstitial thickening peripherally into the subpleural regions.
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Fig. 129: Interlobular interstitial thickening: Schematic diagram of secondary lobules demonstrates thickening of walls of secondary lobule as well as centrilobular interstitium.
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Fig. 130: Interlobular interstitial thickening: HRCT in a patient with lymphangitis carcinomatosis reveals smooth thickening of the interlobar interstitium. The walls of the secondary lobule are thickened, and the internal architecture is preserved, demonstrating the anatomy of the secondary lobule very well.
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Thickening of the intralobular interstitium, which lies within the secondary lobule, is seen as a fine haze of linear opacities or may appear as ground-glass opacities (Fig. 131).
The interstitial thickening may be smooth, nodular or irregular. Smooth thickening is seen in pulmonary edema, lymphangitis carcinomatosis (Figs. 132A and B). Nodular thickening is seen in lymphangitis carcinomatosis, sarcoidosis. Irregular septal thickening is seen mainly in patients with lung fibrosis (Fig. 133). Extensive peribronchovascular fibrosis can result in large conglomerate masses of fibrous tissue as seen in sarcoidosis, silicosis, tuberculosis and talcosis. Subtle peribronchovascular interstitial thickening may be difficult to detect.
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Fig. 131: Intralobular interstitium: HRCT demonstrates ill-defined reticular ground-glass densities in the right middle lobe and left lingula associated with traction bronchiectasis. These features are due to intralobular interstitial thickening.
Involvement of the peribronchovascular interstitium predominantly is seen in nonspecific interstitial pneumonias (NSIPs) (Figs. 134A and B) as compared to predominantly subpleural interstitial thickening seen in usual interstitial pneumonia. Another differentiating feature is the lack of honeycombing, seen typically in UIP. Also in UIP, there are no significant ground-glass densities and parenchymal opacification which are seen in the cellular variety of NSIP (Fig. 135).
 
Axial Interstitium
In patients with irregular interstitial thickening, fibrotic tissue along the bronchial walls causes traction resulting in “traction bronchiectasis” (Figs. 136 and 137). A similar involvement of the peripheral bronchioles is termed traction bronchiolectasis. The dilated bronchi have a varicose or a corkscrew appearance.
When there is involvement of the terminal bronchioles, the bronchioles may dilate to occupy the entire secondary lobule, resulting in honeycomb cysts. On HRCT, honeycomb cysts are usually 1.0 cm or more in diameter with thin walls in the subpleural regions.
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Figs. 132A and B: Smooth interstitial thickening: CT chest (A) demonstrates an ill-defined mass lesion in the lingula flush with the pericardium. CT-guided fine-needle aspiration cytology (FNAC) revealed an adenocarcinoma. HRCT (B) reveals smooth septal thickening from the surface of the mass lesion, this represents lymphatic infiltration by the mass lesion. Smooth septal thickening is also present in the right middle lobe with preservation of the secondary lobule. This is due to lymphangitis carcinomatosis secondary to hematogenous spread.
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These honeycomb cysts share their walls and occur in several contiguous layers (Figs. 138 and 139). Honeycombing indicates end-stage lung disease. The location of honeycombing is important in the differential diagnosis of chronic ILD. If the honeycombing is basal and posterior with associated significant fibrosis and architectural distortion, the diagnosis is UIP. If honeycomb cysts are seen in the upper zones the possibility of sarcoid should be considered; if in the mid-zone with a patchy distribution, the diagnosis of chronic hypersensitivity pneumonitis should be entertained. Anterior honeycomb cysts with fibrosis are seen in ARDS since the posterior portions of the lungs are protected by collapse/consolidation and are therefore not exposed to the deleterious effects of mechanical ventilation.
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Fig. 133: Irregular septal thickening: HRCT demonstrates irregular interstitial thickening in both lung bases posteriorly in a subpleural and peribronchovascular location as seen in usual interstitial pneumonia.
 
Nodular Opacities
A nodule is defined as a rounded opacity which can be well- or ill-defined. A small nodule is one which is less than 1.0 cm; a large nodule varies in size between 1.0 cm and 3.0 cm; nodules above 3.0 cm are termed as masses.
Small nodules are of two types: (1) interstitial and (2) air-space. Interstitial nodules are well-defined and discrete, as seen in sarcoidosis, miliary tuberculosis, silicosis and metastatic lesions. Air-space nodules tend to be ill-defined and conglomerative. Airspace nodules may have a soft tissue density or demonstrate a diffuse ground-glass haze. Examples of air-space nodules are seen in exudative bronchiolitis. Despite these differences in appearance, it is often difficult to differentiate interstitial from air-space nodules on HRCT. The distribution of nodules is extremely useful in establishing the differential diagnosis. Nodules may be perilymphatic, random or centrilobular in distribution. Perilymphatic nodules occur in relation to the lymphatics/interstitium (Figs. 140 and 141), i.e. in relation to the perihilar bronchovascular interstitium, interlobular septae, subpleural interstitium.
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Figs. 134A and B: Fibrotic nonspecific interstitial pneumonia (NSIP): Extensive interstitial thickening in the lungs anteriorly in the upper lobes and posteriorly in the lung bases. The predominant interstitial thickening is in the peribronchovascular interstitium and not in the subpleural regions.
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Fig. 135: Cellular nonspecific interstitial pneumonia (NSIP): HRCT demonstrates ill-defined areas of air-space opacification in the peribronchovascular and subpleural regions of both lung bases. There are no honeycomb changes. In view of the parenchymal opacification, lack of honeycomb changes, and significant fibrotic lesions this would represent the cellular variety of nonspecific interstitial pneumonia.
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Fig. 136: Traction bronchiectasis: HRCT demonstrates peribronchovascular interstitial thickening as evidenced by thickening and irregularity of the vessel and bronchial wall. There is dilatation and irregularity secondary to peribronchial interstitial thickening, representing traction bronchiectasis.
The subpleural distribution of nodules is best demonstrated in relation to fissures. These small nodules in the subpleural regions may coalesce to form pseudoplaques along the pleura. These nodules may also coalesce to form large conglomerative masses. Satellite nodules may be seen in relation to these conglomerative masses giving the appearance of a galaxy (Fig. 142). This pattern is seen in sarcoidosis, silicosis/coal workers pneumoconiosis, lymphangitic carcinomatosis, lymphoproliferative disorders. These diseases demonstrate different patterns of perilymphatic involvement, allowing a distinction.
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Fig. 137: Traction bronchiectasis: HRCT demonstrates peribronchovascular interstitial thickening with consequent traction bronchiectasis and multiple ground-glass opacities.
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Fig. 138: Honeycomb cysts: Extensive honeycomb cysts are seen in both lung fields especially the left.
 
Sarcoidosis
Nodules are seen essentially in relation to the peribronchovascular interstitium and subpleural regions.60
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Figs. 139A and B: Dependent densities: Supine HRCT reveals ill-defined opacities in the lung bases posteriorly. (A) These appear as reticular opacities due to interstitial fibrosis. Prone scans at the same level; (B) demonstrate that the opacities have resolved. These opacities in the lung base on a supine scan represent basal atelectasis. It is important to obtain prone scans in all patients with basal posterior opacities to exclude basal atelectasis.
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Fig. 140: Perilymphatic nodules: HRCT demonstrates extensive nodules in a peribronchovascular location along the vascular surfaces as well as the fissures. As the vessels are white and the nodular areas also white, the appearance is of a nodular surface of the vessels.
The central bronchovascular structures and fissures have a nodular appearance. An upper lobe preponderance is common, with the lung involved in a patchy asymmetric fashion, groups of nodules occurring in one region, normal lung in other regions.
 
Silicosis/CWP
Nodules are distributed in a subpleural and centrilobular location, rarely in a peribronchovascular location as compared to sarcoidosis. Nodules tend to be more evenly distributed as compared to sarcoidosis (Fig. 143).
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Fig. 141: Perilymphatic nodules: HRCT demonstrates multiple small well-defined nodules along the surface of the bronchi and vessels. The vessels have a beaded appearance. These represent interstitial nodules along the peribronchovascular interstitium.
 
Lymphangitic Carcinomatosis
There is smooth thickening of the peribronchovascular and interlobular interstitium. Nodules are seen in relation to these thickened septae. The involvement may be unilateral, patchy or bilateral and symmetric.
 
Patterns of Distribution of Nodules
 
Random
The distribution is uniform with no predilection for any anatomic structures, bilateral and symmetric as seen in miliary tuberculosis (Fig. 144), hematogenous metastasis, and fungal infection.61
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Fig. 142: Sarcoidosis: HRCT demonstrates multiple small nodules in an interstitial location, along the fissures, vessels and bronchi as well as in the subpleural regions. The distribution is asymmetric and essentially perilymphatic. The nodules are seen to conglomerate in the right middle lobe with a number of satellite nodules resulting in an appearance akin to a galaxy. This distribution pattern is typical of sarcoidosis.
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Fig. 143: Silicosis: HRCT demonstrates multiple small well-defined nodules distributed evenly in both lung fields. These nodules are along the vessels, fissures and in the subpleural regions, i.e. perilymphatic in location. As compared to the asymmetric distribution of nodules in sarcoidosis the distribution is uniform in silicosis.
 
Centrilobular
Ill-defined small nodules are centered on the centrilobular structures of the secondary pulmonary lobule.
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Fig. 144: Miliary tuberculosis: HRCT demonstrates multiple small nodules in a random distribution. There is no predilection for any anatomic structure; the distribution is uniform. This is typically seen in the miliary tuberculosis.
Nodules which are predominantly centrilobular in location are most likely secondary to bronchiolar/peribronchiolar inflammation resulting in infiltration or fibrosis of the surrounding interstitium and alveoli (Figs. 145A and B). Angiocentric diseases may also manifest as centrilobular nodules. Bronchiolar diseases manifesting as centrilobular nodules are endobronchial spread of tuberculosis, nontuberculous mycobacterial infections, granulomatous infections, bronchopneumonia, panbronchiolitis, bronchiectasis, ABPA, hypersensitivity pneumonitis (Fig. 146), Langerhans’ cell histiocytosis, respiratory bronchiolitis (Fig. 147), endobronchial spread of neoplasm. Angiocentric nodules are due to pulmonary edema and pulmonary hemorrhage.
Centrilobular nodules due to bronchiolar inflammation may have a tree-in-bud appearance; as the bronchioles dilate and are filled with inspissated mucus, a branching pattern is visualized (Figs. 145A and B).
 
Parenchymal Opacification
Diffuse or multifocal increase in lung attenuation is a common finding on HRCT in patients with chronic lung disease. Increased lung opacity may be ground-glass or consolidation. These represent varying degrees of parenchymal opacification, depending upon whether the vessels are obscured or not by the parenchymal opacification.62
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Figs. 145A and B: Centrilobular nodules: HRCT demonstrates multiple small ill-defined nodular lesions in centrilobular location.
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Fig. 146: Hypersensitivity pneumonitis: HRCT demonstrates multiple small nodules in both lung fields distributed uniformly, evenly spaced, representing centrilobular nodules due to hypersensitivity pneumonitis.
Ground-glass opacity is an area of parenchymal opacification not associated with obscuration of the underlying vessels (Fig. 148). Parenchymal consolidation obscures the vessels (Fig. 149).
Ground-glass opacity results from either fluid, inflammatory material within the alveoli/interstitium or the presence of fine interstitial fibrosis in the intralobular interstitium of the secondary lobule. The distribution is usually geographic with areas of spared lung interspersed with areas of affected lung. Detection of ground-glass opacity is of significance as this indicates an ongoing active as well as potentially treatable process. Since ground-glass opacity may also be a manifestation of intralobular interstitial thickening, presence of significant areas of fibrosis/lung destruction in other regions would indicate that the ground-glass densities are more likely due to intralobular fibrosis.
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Fig. 147: Respiratory bronchiolitis: HRCT demonstrates multiple small pulmonary nodules in both lung fields. These nodules are evenly spaced at the centers of the secondary lobule. These represented nodules due to respiratory bronchiolitis.
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Fig. 148: Ground-glass pattern of parenchymal opacification.
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Pitfalls in Diagnosis of Ground-Glass Opacity
There is a reduction in the amount of air in the alveoli during expiration; consequently there is an increase in lung attenuation, mimicking the appearance of ground-glass densities. It is useful to check the shape of the trachea to determine whether the scan has an adequate inspiratory effort. If the posterior tracheal surface is seen to bulge into the tracheal lumen, it is an expiratory scan rather than inspiratory (Figs. 150A and B). The diagnosis of ground-glass opacity is essentially subjective, based on quantitative assessment of lung attenuation. It is important to maintain consistent window settings. Using too low a window mean with a narrow window width may give an appearance of ground-glass densities. Similar appearances may occur with a wider window width without changing the window mean. A useful tip is to see the air in the trachea or bronchi. If the air appears gray rather than black, the apparent increase in attenuation of lung parenchyma is usually not genuine. In patients with patchy areas of emphysema or air-trapping, normal lung regions may appear as areas of increased attenuation due to the contrast with darker areas. This can be avoided by using consistent window settings. Additionally in regions of normal lung attenuation, air bronchograms are not visualized as seen in areas of ground-glass density. Expiratory images are also useful in confirming lucent areas to represent areas of emphysema or air-trapping (Figs. 151A and B).
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Fig. 149: Computed tomography (CT) chest showing consolidation in the left lower lobe with air bronchogram.
 
Differential Diagnosis of Ground-Glass Densities
A large number of diseases may be associated with ground-glass opacities on HRCT as the pathological processes in the early stages are similar (Fig. 152). These disease processes may be acute, subacute or chronic.
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Figs. 150A and B: Pitfall in diagnosis: HRCT (A) reveals ill-defined ground-glass densities in both lung fields. Note shape of trachea; the posterior wall is bulging inwards showing that this is an expiratory scan; (B) HRCT in deep inspiration in same patient at same level. Note trachea is well-distended and there are no ground-glass densities.
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Fig. 151A and B: Hypersensitivity pneumonitis: HRCT reveals ill-defined areas of ground-glass densities in the inspiratory (A) and expiratory phases (B). Note the accentuation of air trapping in the expiratory phase.
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Fig. 152: Pneumocystis jirovecii pneumonia (PCP): Seropositive patient presented with fever and dyspnea. HRCT revealed diffuse ground-glass densities indicative of PCP. confirmed on bronchoalveolar lavage.
Acute disease processes manifesting as ground-glass densities include acute interstitial pneumonia (Figs. 153 and 154), diffuse alveolar damage (Fig. 155), pulmonary edema, ARDS, pulmonary hemorrhage (Fig. 156), pneumonia and early radiation fibrosis. Subacute/chronic disease processes include interstitial pneumonias, especially NSIP, DIP (Fig. 157), respiratory bronchiolitis, interstitial lung disease, hypersensitivity pneumonitis, drug reactions, chronic eosinophilic pneumonia, Churg Strauss syndrome, lupoid pneumonia, sarcoidosis and alveolar proteinosis (Fig. 158).
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Figs. 153: Acute interstitial pneumonia: HRCT chest demonstrates ill-defined areas of increased lung attenuation in an acutely breathless patient.
 
Decreased Lung Attenuation
Pathological processes with decreased lung attenuation may be due to lung cysts, emphysema, bronchiectasis, mosaic attenuation or air-trapping.
 
Emphysema
This is a result of permanent abnormal enlargement of air-spaces with destruction of their walls distal to terminal bronchioles. On HRCT emphysema appears as focal or diffuse areas of decreased attenuation compared to normal lung parenchyma. By modifying the window settings of HRCT (600–800 window mean) emphysema can be very well-demonstrated (Figs. 156 and 158). Emphysema is essentially of four types:65
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Fig. 154: Acute interstitial pneumonia: HRCT of the chest with coronal reconstruction in an acutely breathless patient demonstrates ill-defined areas of ground-glass opacification and consolidation.
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Fig. 155: Diffuse alveolar damage: Drug-induced diffuse alveolar damage seen on HRCT as diffuse ill-defined areas of increased lung attenuation in both lung fields.
  1. Centrilobular: This occurs predominantly in the upper lobes with lung destruction around the centrilobular arterial branches resulting in lucencies grouped around the centers of the secondary pulmonary lobule. With more severe destruction the appearances resemble panlobular emphysema. Centrilobular emphysema occurs in cigarette smokers due to enzymatic destruction of lung parenchyma as there is an imbalance between lung proteases and antiproteases (Figs. 159 and 160).
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    Fig. 156: Alveolar hemorrhage: HRCT in a patient with hemoptysis demonstrates ill-defined areas of ground-glass density in right middle lobe as well as right lower lobe. The ground-glass densities were due to alveolar hemorrhage.
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    Fig. 157: Desquamative interstitial pneumonia: HRCT in a chronic smoker reveals ill-defined areas of parenchymal opacification in the subpleural and peribronchovascular regions. Thoracoscopic biopsy revealed desquamative interstitial pneumonia.
  2. Panlobular emphysema: This is characterized by uniform destruction of the pulmonary lobule leading to widespread areas of low attenuation. The pulmonary vessels appear fewer and thinner in appearance, termed as a diffuse simplification of lung architecture. Panlobular emphysema occurs in individuals with alpha-protease inhibitor deficiency and as an extension of centrilobular emphysema in cigarette smokers (Figs. 161A and B).66
  3. Paraseptal emphysema: The area of destruction involves the alveolar ducts and alveolar sacs marginated by the interlobular septa. On HRCT there are subpleural cysts which share thin walls. These cysts may become fairly large and reach up to a size of 1.0 cm. Paraseptal emphysema may be confused with honeycomb cysts, as both are in a subpleural location. Honeycomb cysts tend to be in several contiguous layers as compared to paraseptal emphysema which tends to occur in a single layer. Additionally, lung fibrosis usually accompanies honeycomb cysts, whereas other forms of emphysema such as centrilobular and panacinar may be present with paraseptal emphysema. Honeycomb cysts tend to be in the lung bases as compared to paraseptal emphysema which tends to be in the upper lobes.
  4. Bullous emphysema is characterized by large bullae, often associated with centrilobular/paraseptal emphysema (Fig. 162).
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Fig. 158: Alveolar proteinosis: HRCT reveals ill-defined ground-glass densities in both lung fields with a background of septal thickening. This appearance simulates a crazy pavement appearance, most commonly seen in alveolar proteinosis.
Bulla represents a sharply demarcated area of emphysema measuring 1.0 cm or more in diameter with a thin wall not more than 1 mm. They may range up to 20 cm in diameter but generally range between 2 cm and 8 cm in diameter (Fig. 163).
Bleb—Bleb refers to a gas-containing space within the visceral pleura.
Pneumatocele is a thin-walled gas-filled space within the lung, occurring from lung necrosis and bronchiolar obstruction. It usually occurs in an acute setting following an acute pneumonia and is often transient. Pneumatocele has a similar appearance to lung cyst or bulla.
 
Differential Diagnosis of Cystic Lesions
The differential diagnosis of diffuse cystic lung diseases includes pulmonary Langerhans’ cell histiocytosis, usual interstitial pneumonia, and centrilobular emphysema. Langerhans’ cell histiocytosis chiefly involves the upper lobes and also shows the presence of nodules (Fig. 164). UIP chiefly involves the lower lobes with cysts subpleural in location. The cystic spaces in centrilobular emphysema do not have well-defined walls. Lymphangioleiomyomatosis occurs in young females with evenly distributed cysts in both lung fields. Cystic bronchiectasis may also enter into the differential diagnosis and is generally easily identified.
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Figs. 159A and B: Centrilobular emphysema: (A) multiple thin-walled air spaces in both lung fields due to centrilobular emphysema (B) These are well-demonstrated on minimum intensity projection.
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Mosaic Attenuation
The lung may have an inhomogenous attenuation pattern with ill-defined areas of increased and decreased lung attenuation intermixed. This may be due to infiltrative diseases with areas of ground-glass density, increased lung attenuation with areas of normal lung attenuation intermixed (Figs. 165A and B).
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Fig. 160: Centrilobular emphysema: Multiple well-defined air spaces are seen with a central vessel within. These findings are typical for centrilobular emphysema. Lung destruction is seen to be occurring around the centrilobular vessel.
Mosaic perfusion is characterized by areas of decreased lung attenuation with areas of normal lung attenuation. Lung density is partially determined by the amount of blood present in lung tissue. Regional perfusion differences may occur due to airway abnormalities or vascular abnormalities. If there is reduced ventilation of a portion of the lung due to narrowing of the airways, there is reflex vasoconstriction resulting in hypoperfusion of the hypoventilated region. This is seen in bronchiolitis obliterans, bronchiolitis, bronchiectasis, and cystic fibrosis. If there is vascular obstruction there would be areas of hypoperfusion resulting in areas of low attenuation as seen in acute and chronic pulmonary thromboembolism.
 
Airway Diseases
 
Upper Airways Obstruction
Tracheal stenosis: Tracheal stenosis can be related to inflammatory or neoplastic causes and is sometimes due to Wegener's granulomatosis. The lesion may occur anywhere within the trachea and may involve the major bronchi also (Figs. 166A and B).
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Figs. 161A and B: Panacinar emphysema: (A) Axial and (B) coronal HRCT images demonstrate large area of lung destruction seen in right lower zone. The density of the lung parenchyma is reduced and there is considerable thinning and separation of the vessels.
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Fig. 162: Bullous emphysema: HRCT demonstrates extensive bullae in both lung fields, especially right with consequent compression of the lung parenchyma. There is extensive centrilobular emphysema in both lung fields.
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Fig. 163: Bulla: HRCT demonstrates a huge thin-walled air space in the right lung field representing a bulla. Also noted are the bronchiectatic changes in the superior segments of both lower lobes.
Clinical features include breathlessness, sometimes accompanied by a wheeze. A stridor is often observed when the obstruction is subglottic or if it involves the main trachea. This condition is often mistaken for asthma because of the presence of a wheeze. Even if the wheeze is present, as for example in a patient with obstruction to the right or left bronchus, it is monophonic in nature and not polyphonic as seen in patients with asthma. Flow volume loop confirms the diagnosis. Initially there is flattening of the inspiratory loop but later a flattening of both inspiratory and expiratory loops of the flow volume curve is observed.
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Fig. 164: Pulmonary Langerhans’ cell histiocytosis: HRCT reveals a right-sided pneumothorax with multiple bizarre-shaped cysts in both lung fields. The bizarre shape of the cysts as well as history of exposure to cigarette smoke helps to differentiate from the thin-walled smooth cysts seen predominantly in females in lymphangioleiomyomatosis.
Bronchiectasis: Bronchiectasis is defined as localized irreversible dilatation of the bronchial tree. There are a wide variety of causes. It is usually as a result of acute, chronic or recurrent infection. Bronchiectasis is classified on the basis of its severity as cylindrical (the walls of the bronchi are dilated but parallel), varicose (there is dilatation of the bronchi with focal constrictions, thereby giving a varicose appearance), and cystic, where the bronchi are ballooned (Figs. 167 to 170).
On HRCT, the dilated bronchi are visualized depending on the plane they are traversing in. If perpendicular to the plane of CT, i.e. running vertically down, they are visualized in cross-section. This appearance has been likened to a signet ring appearance—the dilated bronchus as the ring and the accompanying pulmonary artery as the jewel on the ring. If the bronchi are running parallel to the scan plane, i.e. horizontal they are visualized as tram tracks or parallel lines. There may be associated atelectasis resulting in the bronchi being bunched up, this gives an appearance of multiple cysts. Bronchial wall thickening may also be seen as well as air-fluid levels, especially in cystic bronchiectasis.69
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Figs. 165A and B: (A) HRCT demonstrates subtle inhomogenous areas of attenuation in both lung fields on inspiratory scan. On expiratory scans (B) there is accentuation of the inhomogenous areas of altered attenuation. Focal areas are seen to be darker and focal areas are brighter. The vessels within the areas which are darker are sparse in distribution and thinner in caliber, representing air-trapping. Mosaic attenuation was due to constrictive bronchiolitis.
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Figs. 166A and B: (A) Coronal CT section shows tracheal stenosis at two sites—an upper and a lower one, just above the carina. This patient was a young 23-year-old lady diagnosed as having asthma because of difficulty in breathing and a wheeze on auscultation. Clinical examination revealed noisy breathing, often amounting to a stridor. Auscultation revealed a monophonic wheeze; (B) The flow volume loop demonstrated a marked flattening of the inspiratory and expiratory curve. Surgical correction of this disorder was successfully done. The etiology of this tracheal stenosis was uncertain. It was probably related to Wegener's granulomatosis.
 
Small Airway Diseases: Bronchiolar Diseases
HRCT has revolutionized our ability to diagnose small airway disease. The HRCT findings can be divided into two groups based on the imaging findings:
  1. Constrictive bronchiolitis
  2. Exudative bronchiolitis.
1. Constrictive bronchiolitis: Constrictive bronchiolitis is concentric fibrosis involving the submucosal and peribronchial tissues of the terminal bronchioles resulting in bronchial narrowing and obliteration (Figs. 171A and B).70
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Fig. 167: Bronchiectasis: HRCT chest demonstrates dilated bronchi representing bronchiectasis.
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Fig. 168: Bronchiectasis: HRCT demonstrates dilated bronchi (blue arrows) in both lung bases. Note marked difference in the diameter of the bronchus and accompanying artery. A few dilated bronchi in the left lower lobe demonstrate soft-tissue within their lumen representing mucoid impaction (red arrows).
The HRCT findings reflect the pathophysiology that causes airflow limitation. There is both hypoventilation of the involved segments of the lung and air-trapping. This is seen as areas of mosaic attenuation. The affected segments are dark and demonstrate air-trapping on expiratory scans. Hypoventilation of the involved areas of the lung results in reflex hypoperfusion so that vessels in the involved segments appear attenuated and sparse. The airways in these segments may also demonstrate abnormalities in the form of focal bronchial dilatation and wall thickening.
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Fig. 169: Bronchiectasis: HRCT demonstrates dilated bronchi in both lung fields, note dextrocardia in a case of Kartagener's syndrome.
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Fig. 170: Bronchiectasis: Coronal HRCT demonstrates dilated bronchi in the right upper lobe. There is a linear well-defined tubular opacity extending to the subpleural region representing mucoid impaction in dilated bronchus.
2. Exudative bronchiolitis: There is mucoid impaction in the terminal bronchioles. On chest X-ray these are seen as numerous small (5 mm) ill-defined nodules (Figs. 172 and 173). On HRCT the areas of mucoid impaction are seen as tubular branching structures in the peripheral lung parenchyma resembling toy jacks also termed as tree-in-bud appearance. When seen in cross-section they appear as centrilobular nodules.71
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Figs. 171A and B: Constrictive bronchiolitis: (A) Inspiratory CT chest: areas of inhomogenous attenuation with areas of increased and decreased attenuation; (B) Expiratory scans reveal air-trapping as the areas of decreased attenuation retain their attenuation whereas the areas of increased attenuation become brighter: the air-trapping indicates small-airway disease.
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Fig. 172: Exudative bronchiolitis: HRCT demonstrates multiple small conglomerated nodular lesions representing mucoid impaction in terminal bronchioles as a result of exudative bronchiolitis.
 
Swyer-James Syndrome (Fig. 174)
This condition is usually caused by a viral infection to the immature lung, before it has completed development (below eight years of age). There is obliterative bronchiolitis involving the distal airways. Usually, an entire lung is involved, occasionally segments are spared. There is hypoplasia of the lung together with hypoplasia of the pulmonary artery to the involved lung.
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Fig. 173: Exudative bronchiolitis: HRCT demonstrates multiple small conglomerated nodular lesions representing mucoid impaction in terminal bronchioles with associated ground-glass densities as a result of exudative bronchiolitis with peribronchiolar inflammation.
On the chest X-ray there is unilateral transradiancy, the opposite lung appears to be plethoric. The ipsilateral hilum may be small chiefly because of a hypoplastic pulmonary artery supplying the involved lung.
 
IMPORTANT CONGENITAL MALFORMATIONS AND ANOMALIES
 
Pulmonary Arteriovenous Malformations
Nearly 70% of cases with pulmonary arteriovenous malformations (PAVM) are associated with hereditary 72hemorrhagic telangiectasia (HHT or Rendu-Osler-Weber disease). This is an autosomal dominant disorder characterized by the triad of telangiectasia, recurrent epistaxis and a family history of the disease. There is a wide spectrum of presentations. Patients may be asymptomatic, lesions being detected incidentally on a chest X-ray. If the AVM is large enough to cause a marked right to left shunt, the patient may present with cyanosis, dyspnea, clubbing, hemoptysis, and cardiac failure. Usually, in these cases a distinct bruit is heard over the hemithorax. Patients may also present with cerebral abscesses and cerebral infarction due to paradoxical embolism. An important clinical finding in PAVMs is orthodeoxia—there is a drop in oxygen saturation from the supine to erect position. This is because PAVMs are mainly in the lower zones; this results in an increased right to left shunting of blood within the lungs in the erect position (Figs. 175 and 176).
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Fig. 174: Swyer-James syndrome: Chest X-ray demonstrates unilateral transradiancy on the left side due to infantile bronchiolitis resulting in a Swyer-James syndrome.
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Figs. 175A and B: Pulmonary arteriovenous malformation: (A) Maximum intensity projection (MIP) and (B) Volume rendering technique (VRT) images of CT angiography demonstrate an arteriovenous malformation in the right upper zone with feeding arteries and draining veins.
On chest radiographs AVMs are seen as well-defined nodules ranging in size from 1 cm to more than 1 cm. Peripheral AVMs usually demonstrate feeding arteries and draining veins as curvilinear structures. The more central AVMs are more difficult to detect as they may be overlapped by the hilum; the feeding draining vessels may not be visualized as they traverse a short distance.
CT is extremely sensitive and specific in demonstrating pulmonary AVMs. It is able to demonstrate feeding as well as draining vessels. There is intense enhancement of these lesions; CT scans are also able to detect the presence of multiple lesions. Remy Jardin and colleagues in fact found CT more sensitive than pulmonary angiograms, which have been considered the gold standard for the diagnosis of AVMs. CT detected AVMs in 98% of cases compared to pulmonary angiograms, which detected AVMs in 60%.73
CT additionally assists in deciding further management of these lesions. Using 2D and 3D reconstructions the feeding arteries can be demonstrated. Feeding arteries greater than 3 mm in diameter are embolized interventionally using coils, detachable balloons, to decrease the right to left shunting. Contrast echocardiography can be used to demonstrate complex angioarchitecture as well as provide a road map of the extent of the right to left shunt. MRI is useful in demonstrating larger PAVMs but smaller PAVMs may not be as well detected as in a CT.
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Fig. 176: Pulmonary arteriovenous malformation: Sagittal multiplanar reconstruction (MPR) demonstrates feeding arteries and draining vein of pulmonary arteriovenous malformation.
 
Congenital Diaphragmatic Hernia
The classical congenital diaphragmatic hernia results from failure of the pleuroperitoneal cavity to close with resultant herniation of abdominal contents into the thorax. The incidence is 1:2,400 births, and is most commonly left-sided (90%). In the neonatal period these present as respiratory distress, as the herniated abdominal contents cause compressive effects on the lung and mediastinum. The diagnosis is fairly easy on the chest X-ray as there is evidence of soft tissue and air-filled bowel loops in the left hemithorax. When the stomach is included in the hernial sac, the nasogastric tube rather than descending in the abdomen is seen to take a turn upwards into the thorax from the gastroesophageal junction (Figs. 177 and 178).
Hernias on the right side may be difficult to detect as there is usually herniation of liver; the chest radiograph demonstrates a soft tissue opacity in the lower right hemithorax.
 
Bochdalek Hernia
These result from herniation through a posterior diaphragmatic defect close to the crura. They tend to manifest later in life and may be bilateral and symmetric. The liver prevents herniation on the right side. Occasionally, kidney and/or stomach may herniate on the left side.
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Figs. 177A to C: Diaphragmatic hernia: (A) AP and (B) oblique views demonstrate soft-tissue opacity and bowel loops in the left hemithorax with shift of the mediastinum to the right; (C) Barium study confirms bowel loops in the hemithorax.
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Morgagni's Hernia
These are due to herniation between sternal and costal attachments usually developing in the right anterior cardiophrenic sulcus. On the left herniation is impeded by the heart. Visual contents of the hernia are liver and omentum, occasionally transverse colon. On chest X-ray herniation of liver and omentum is visualized as a paracardiac mass with a D/D of pericardial cyst, paracardiac fat pad or a pleural/pulmonary mass (Figs. 179A and B). When there is herniation of colon, the presence of a gas-filled viscus makes the diagnosis easy. A lateral view of the chest helps to localize the hernia anteriorly. CT is diagnostic as CT demonstrates the herniation of liver/omentum and bowel (Figs. 180 and 181).
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Fig. 178: Diaphragmatic hernia: Chest X-ray in a neonate reveals ill-defined opacities in the left hemithorax with multiple air-filled loops representing a diaphragmatic hernia. There is consequently a shift of the mediastinum to the right.
 
ABSENCE OF LUNG OR LOBES OF LUNGS
Unilateral agenesis is a rare congenital anomaly presenting with minimal clinical problems. It is frequently associated with other congenital anomalies particularly tracheoesophageal fistula and the VACTERL association (non-random association of birth defects). When the bronchus is absent, it is termed as “agenesis”.
When the bronchus is present but rudimentary, it is termed aplasia. The ipsilateral pulmonary artery develops but is usually hypoplastic.
Agenesis of the right lung is often accompanied by esophageal atresia and is twice as common as left lung agenesis (Figs. 182A and B). Left lung agenesis is often accompanied by tracheoesophageal fistula. On imaging there is loss of aeration and volume on the ipsilateral side as evidenced by elevation of the diaphragm, shift of the mediastinum to the ipsilateral side and increase in extrapleural fat to fill the space due to congenital hypoplasia.
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Figs. 179A and B: Morgagni's hernia: (A) PA view and (B) topogram of the chest reveals a bowel loop with an air-fluid level in the right hemithorax.
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Figs. 180A and B: Morgagni's hernia: CT scans show herniation of colon through an anterior abdominal wall defect into the anterior hemithorax, representing a Morgagni's hernia.
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Fig. 181: Hiatus hernia: CT demonstrates a huge hiatus hernia with the stomach extending into the thoracic cavity.
Absence of individual lobes is a form of hypoplastic lung syndrome. When there is absence of a lobe there is compensatory expansion of the rest of the lung, distorting bronchovascular structures. This overexpansion is never adequate to revert the lung to normal size. The size of the ipsilateral lung is always smaller, similar to what is seen in pulmonary hypoplasia. The difference is easily determined on CT as a bronchus is absent, whereas in hypoplasia all segments are present but the tracheobronchial tree is stunted and underdeveloped.
 
Tracheoesophageal Fistula
Tracheoesophageal fistulas are associated with esophageal atresia and are usually diagnosed in the neonatal period. Rarely, tracheoesophageal fistulas are not diagnosed till later in life as the symptoms may be nonspecific. These fistulas are of the “H” type—a short horizontal communication between the trachea and esophagus—the horizontal communication being represented by the H bar. Symptoms are due to recurrent aspiration, paroxysmal cough, feeding difficulties and recurrent pneumonia. The appearances on chest radiographs are of aspiration, excessive air may also pass from the trachea into the esophagus as well as into the gut. This may be visualized also on an X-ray as air in the esophagus and/or gaseous distension of the bowel. An obvious tracheoesophageal fistula is fairly easy to demonstrate. A small tracheoesophageal fistula, especially the “H” variety is best demonstrated in the prone position using a feeding tube which is slowly withdrawn while a nonionic water soluble contrast is injected to demonstrate the fistulous communication.76
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Figs. 182A and B: Agenesis of right lung: (A) CT chest reveals a marked shift of mediastinum to the right with no lung tissue seen in right hemithorax; (B) there is compensatory expansion of left lung. The right pulmonary artery was absent.
The “H” type of tracheoesophageal fistulas is usually associated with other congenital anomalies—these have been designated by acronyms: VATER—vertebral, anal, tracheoesophageal, renal; VACTEL—vertebral, anal, cardiac, tracheoesophageal and limb. Pulmonary hypoplasia, tracheal stenosis and pulmonary sequestration may also be associated.
 
Bronchial Atresia
There is a short segment of atresia involving a segment or subsegmental bronchus. There is consequently dilatation of the bronchus distal to the atresia, resulting in accumulation of mucus in the dilated bronchus. This mucocele is seen on imaging as a mass-like structure; there may be a branching configuration which helps establish the diagnosis. The surrounding lung in the affected segment is hypertranslucent as the lung beyond the atretic segment is aerated by collateral drift and because there is reflex hypoperfusion of the vessels in the affected segment. The vessels appear thinner and less is number in the affected segment. Most patients are asymptomatic. Bronchial atresia has limited clinical significance; the only issue is that it may be mistaken for a mass. CT very effectively demonstrates the central mucous-filled mass, atresia of the segmental bronchus, and the hypertranslucent lung segment.
 
Pulmonary Sequestration
Pulmonary sequestration is characterized by the presence of pulmonary tissue which does not communicate with the central airways through a normal bronchial connection and receives its blood supply via an anomalous systemic artery. Pulmonary sequestration is divided into intralobar and extralobar varieties, based on venous drainage. If the venous drainage is to the pulmonary veins, it is termed “intralobar sequestration” (Figs. 183A and B). If the drainage is to the systemic veins, it is termed “extralobar sequestration”.
Extralobar sequestrations are congenital abnormalities usually associated with other congenital abnormalities, such as congenital heart disease, diaphragmatic hernia, or cystic adenomatoid malformation. They are asymptomatic and therefore discovered incidentally on antenatal ultrasound, chest X-ray, sonography, CT, angiography or during surgical repair of a congenital diaphragmatic hernia with which they are commonly associated. An extralobar sequestration has a complete serosal covering; it may have a narrow vascular pedicle as it is separate from the normal lung. Extralobar sequestrations in 90% of cases occur on the left side. Torsion is a complication and this may result in a tension hydrothorax.
Extralobar sequestrations are seen on imaging as mass lesions of homogenous density. They have well-defined margins, in particular the lateral margin which is covered by pleura.77
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Figs. 183A and B: Pulmonary sequestration: (A) CT scan demonstrates an ill-defined consolidation; (B) CT angiography demonstrates arterial branch arising from aorta feeding the consolidation representing an intralobar sequestration.
The medial margin may be difficult to discern as it abuts the mediastinum, often giving the appearance of a mediastinal mass. Sequestration may be seen in relation to the pericardium, diaphragm, and the retroperitoneum, occasionally communicating with the esophagus or stomach, which can be demonstrated by barium studies.
As compared to extralobar sequestration which is a congenital abnormality, intralobar sequestration is being considered to be more likely an acquired lesion rather than a congenital abnormality. Chronic bronchial obstruction due to foreign body, carcinoid tumor and postobstructive pneumonia are considered to be causes of intralobar sequestration. The chronic inflammatory process “parasites” its blood supply from the systemic circulation, often a branch from the descending aorta or branches from the inferior pulmonary ligament. Therefore, 98% of all sequestrations occur in the lower lobes. As compared to extralobar sequestrations which are asymptomatic, intralobar sequestrations present as an infective lesion or sequelae of an infective lesion. On imaging they appear as round, oval, lobulated mass lesions simulating an intrapulmonary mass lesion. Air and air-fluid levels may be seen within these masses due to communication with bronchi secondary to episodes of infection. CT appearances are similar to those of a chest X-ray; however, CT more frequently detects air, air-fluid levels, and the presence of emphysema adjacent to the sequestration. The emphysema occurs due to impaired ventilation secondary to chronic obstruction with consequent collateral air drift and air-trapping. Occasionally, a pure cystic form of sequestration is detected with air-trapping, focal emphysema and bulla formation. The key in differentiating from other cystic masses is the demonstration of a systemic arterial supply. CT angiography on MDCT scanner has replaced the need for invasive angiography to demonstrate systemic arterial supply, the key to the diagnosis of sequestration. The differential diagnosis of sequestration encompasses infective lesions, pulmonary masses, mediastinal and pleural masses. The clue to the correct diagnosis is location, arterial supply, venous drainage, and a history of repeated infections.
 
Congenital Lobar Overinflation
Previously known as congenital lobar emphysema, it is now termed as congenital lobar overinflation (CLO). The pathophysiology of this condition is characterized by overinflation of normal alveoli most likely due to central airway obstruction, presumably due to aplasia, hypoplasia or dysplasia of the bronchial support structures. A clinically similar condition is polyalveolar lobe—the lobe contains four to five times the number of alveoli normally present, resulting in a large lobe having all the compressive effects seen in CLO. CLO manifests in the neonatal period with respiratory distress. On chest X-ray there is hyperexpansion of a lobe of the lung, usually upper or middle lobe. Involvement of more than one lobe or the lower lobe is extremely rare. The hyperexpanded 78lobe causes mass effect on the adjacent structures, heart, mediastinum and diaphragm (Fig. 184). The main differential diagnosis is obstruction to the bronchus by a foreign body, mucous plug, endobronchial mass, extrinsic compression of the airway or a localized pneumothorax. CT is useful to confirm the diagnosis of hyperinflation of a lobe. CT angiography differentiates CLO from other forms of pulmonary hypoplasia.
 
Pulmonary Hypoplasia
Primary unilateral pulmonary hypoplasia is usually associated with the scimitar syndrome or with other vascular malformations. Patients present with repeated episodes of wheezing and pneumonia. The affected lung is small in size, the mediastinum is displaced toward the ipsilateral hemithorax and the pulmonary vasculature is reduced in size. On the lateral chest X-ray, a sharply marginated opacity is seen behind and parallel to the sternum. This is due to the displacement of the heart and mediastinum into the ipsilateral thorax. Primary bilateral pulmonary hypoplasia is very rare. Chest X-ray reveals bilateral small lungs with a normal-sized abdominal cavity, presenting a bell-shaped appearance of the chest and abdomen.
 
Unilateral Absence of Pulmonary Artery
This is a rare anomaly characterized by the absence of a short segment or atresia of the proximal left or right pulmonary artery; the more distal segments are usually present. Chest radiographs demonstrate reduction in lung volume, shift of mediastinum, small-sized or absent pulmonary hilum; peripheral pulmonary perfusion is reduced. There may be reticular opacities in the affected lung due to pulmonary-systemic collaterals. The normal lung may be plethoric as the entire cardiac output is shunted through the lung. CT will demonstrate the absence of the pulmonary artery and the presence of systemic pulmonary collaterals.
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Fig. 184: Congenital lobar overinflation (CLO). Chest X-ray demonstrates marked overinflation of the left upper lobe causing a shift of the mediastinum to the right and collapse of the left lower lobe. Collapsed left lower lobe is seen along the left cardiac border.
 
Scimitar Syndrome
This is a condition involving essentially the right lung which is hypoplastic, with underdevelopment of the airways as well as vasculature. The characteristic finding which in turn contributes to its name is anomalous pulmonary drainage. A large anomalous pulmonary vein descends vertically inferiorly to open into the inferior vena cava above or below the diaphragm. The vein broadens as it curves medially to enter into the vena cava, thereby simulating the appearance of a Turkish sword—scimitar. The anomalous vein may also drain into the coronary sinus, right atrium, or rarely into hepatic veins. The scimitar syndrome may be associated with other congenital anomalies such as septal defects, eventration, Bochdalek hernia, bronchiectasis and tracheal diverticuli. On a chest radiograph, the key feature is the presence of the anomalous draining vein. Additional features are a small-sized right lung, shift of the mediastinum to the right and a small ipsilateral pulmonary artery (Fig. 185). CT is useful to confirm the diagnosis, demonstrating the anomalous draining vessel and its termination, tracheobronchial anomalies, small ipsilateral pulmonary artery, as well as associated abnormalities such as tracheal diverticuli and bronchiectasis.
 
Imaging of Pleura
 
Pleural Effusions
Free pleural effusions tend to gravitate to the most dependent portions of the pleural cavity. On erect chest X-rays these are seen as homogenous densities in the lower zone with a typical concave or upward-sloping contour (Figs. 186 and 187), the lateral margin being higher than the medial margin. Fluid collects in the subpulmonic space (Fig. 188) then spills into the posterior and finally lateral costophrenic sulcus. The posterior costophrenic (CP) sulcus is the deepest portion of the pleura. This is the site where the fluid tends to first accumulate. Radiologically, this is seen as blunting of the costophrenic angle on the lateral view.79
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Fig. 185: Scimitar syndrome: AP view demonstrates typical curvilinear vascular opacity in right paracardiac region.
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Fig. 186: Pleural effusion: Chest X-ray reveals a large homogenous opacity in left hemithorax and there is mediastinal shift to the right. This is diagnostic of a pleural effusion.
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Fig. 187: Pleural effusion: PA view of chest reveals a left-sided pleural effusion. There is also an underlying spiculated mass which on biopsy was proven to be an adenocarcinoma of lung.
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Fig. 188: Subpulmonic pleural effusion: PA view of the chest demonstrates a homogenous opacity in the right lower zone, appearing as an elevated flattened dome of the diaphragm. This appearance is suggestive of a subpulmonic pleural effusion. Sonography confirmed the presence of a pleural effusion.
At least 200 mL of fluid is required to cause obliteration of the CP angle on a PA view of the chest, though in some cases there is no blunting of the angle even when 500 mL of fluid is present. The lateral decubitus view is the most sensitive X-ray to demonstrate free fluid. Fluid is seen layering the dependent part of the chest wall as a thin uniform opacity. This view however may be technically difficult to obtain in a patient who is critically ill. In patients who are too critically ill to sit erect, a diagnosis of pleural effusion has to be made on a supine X-ray chest. 80The findings in moderate-sized or large effusions are a homogenous opacity of the affected hemithorax with absence of the vascular markings. This is because the fluid is layering posteriorly along the chest wall. Fluid also tends to accumulate along the apex, like an apical pleural cap, and in the base, as these are the most dependent areas on a supine film. Small pleural effusions can be easily missed on a supine radiograph. In fact only 67% sensitivity and 70% specificity have been reported for the detection of a pleural effusion on supine chest X-ray as opposed to a lateral decubitus view.
In critically ill patients who cannot be positioned for a lateral decubitus view, or if a supine radiograph shows equivocal or negative findings, sonography is an excellent means for demonstrating pleural fluid. This imaging modality is portable and can be easily performed at the bedside. Pleural fluid is seen as an anechoic area separating the echogenic line of the diaphragm and the echogenic inferior margin of the lung (Figs. 189 and 190). Sonography is also useful in differentiating a pleural effusion from atelectasis/consolidation which may simulate an effusion on the chest X-ray. Further, it is an excellent guide for thoracocentesis, markedly reducing the incidence of iatrogenic pneumothorax.
Occasionally, free pleural fluid may accumulate in a subpulmonic location between the lung and diaphragm, with the lung floating on the fluid. The upper margin of the fluid may then take the appearance of the diaphragm. There is however a subtle difference from the normal appearance of the diaphragm in a subpulmonic effusion (see Fig. 188). The peak of the diaphragm is more lateral, the medial aspect has a more gradual slope and the lateral aspect a steeper slope. On a lateral X-ray the posterior costophrenic sulcus is obliterated. Left-sided subpulmonic effusions may be detected by noting the wide distance between the stomach air bubble and diaphragm. On the right side differentiation from an enlarged liver pushing the diaphragm upwards may be difficult. In these cases either a lateral decubitus view or sonography is useful to clinch the diagnosis. A loculated effusion may occur when there are adhesions between the visceral and parietal pleura, as a result of which the fluid does not shift with change of the patient's position (Figs. 191A and B). Empyema and hemothorax may appear as loculated effusions. Sonography will demonstrate the fluid is echogenic rather than anechoic in empyemas/hemothorax.
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Fig. 189: Pleural effusion: Sonography demonstrates a hypoechoic appearance of pleural fluid layering above diaphragm.
CT is extremely sensitive in detecting even small pleural fluid collections (Fig. 192). With the patient supine, free fluid accumulates posteriorly as a hypodense layer conforming to the contour of the chest wall. The presence of septae in the pleural fluid (denoting a likely exudate) is however brought out by a sonographic study rather than by a CT scan. Acute hemorrhage in the pleural space can be well-identified by the hyperdensity of blood (Fig. 193). CT is also useful in the assessment of the site, extent and wall thickening of loculated effusions (Fig. 194), and for loculated interlobar effusions. These may simulate a mass lesion on plain X-ray but can easily be differentiated on CT. CT with intravenous contrast medium is very useful in differentiating parenchymal from pleural lesions, especially when a plain radiograph has not been helpful.
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Fig. 190: Pleural effusion: Sonography demonstrates pleural effusion as an echoic fluid collection. There are multiple linear bands within this fluid collection; these represent septae. Presence of septae is highly suggestive of the effusion being an exudate.
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Figs. 191A and B: Interlobar effusion: (A) PA view demonstrates a well-defined opacity in the right mid-zone (B) Lateral view demonstrates the homogenous opacity seen on the PA view, represents loculated fluid in the major interlobar fissure. The inferior part of the fissure as well as the minor fissure is mildly thickened. The homogenous appearance on the PA view of an opacity in the location of the fissure would suggest the need for a lateral view to localize the lesion.
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Fig. 192: Pleural effusion: CT is extremely sensitive in detecting small pleural and pericardial effusion.
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Fig. 193: Hemorrhagic pleural effusion: CT chest without IV contrast reveals a thin pleural effusion on the right side and a moderate-sized pleural fluid collection on the left. The pleural fluid collection on the left is hyperdense indicating hemorrhage and the right side hypodense indicating fluid. CT is useful in differentiating pleural effusion from a hemothorax.
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Empyema
On a chest radiograph an empyema is usually seen as a loculated fluid collection. It tends to be lenticular in shape as compared to a lung abscess which is rounded (Figs. 195 and 196A). Further, an empyema usually forms an obtuse angle with the chest wall while a lung abscess forms an acute angle. CT is very useful in the diagnosis and management of empyema. On CT an empyema appears as a well-defined fluid collection with enhancing parietal and visceral pleura (Fig. 196B). This sign of separation of the pleura is known as the split pleura sign.
Traditionally, empyemas have been treated with insertion of chest tubes. The success rate with chest tube drainage is 35–71%. However, 35% of all patients treated with conventional chest tubes are found to subsequently require either open chest tube drainage or decortication. Several studies have estimated the success rate of fluoroscopy, sonography and CT in image-guided percutaneous insertion of chest tubes to be between 70% and 90%. Under imaging guidance, the chest tube can be placed accurately in the fluid collection. In fact image-guided percutaneous drainage of empyemas is advocated as the primary method of treating empyemas. Patients who show inadequate drainage or progressive persistent pleural thickening may finally require decortication.
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Fig. 194: Loculated pleural effusion: CT chest demonstrates pleural fluid in the right hemithorax loculated along the right lateral chest wall with multiple loculations.
 
Pneumothorax
Pneumothorax may be spontaneous, either primary or secondary. A rupture of an apical pleural bleb is the most likely cause for a primary spontaneous pneumothorax.
The radiographic appearances depend upon the patient's position (air is seen in the most nondependent portion of the pleural cavity) as well as the presence or absence of loculations. In an erect patient, air rises in the pleural space to the apicolateral regions, separating lung from chest wall, allowing the visceral pleural line to become visible (Figs. 197 to 199). The visceral pleural line separates the vessel-containing lung from the avascular pneumothorax. This line remains parallel with the chest wall; therefore, in a shallow pneumothorax it may be difficult to separate the visceral pleural line from the chest wall, especially if covered by ribs. To demonstrate these questionable or subtle pneumothoraxes an expiratory film is very useful (Figs. 200A and B). This increases the volume of the pneumothorax as well as changes the orientation of the ribs.
There are a number of mimics of a pneumothorax on a chest X-ray. Any curvilinear shadow projected over the lung, especially the apex, may mimic a visceral pleural line. Skin folds, tubes, vascular lines, clothing, scapulae, walls of bulla/cavities all may mimic a visceral pleural line. One of the most helpful differentiators is to follow the so-called visceral pleural line beyond the margins of the chest wall. Other helpful differentiators are when the orientation of the line is not in the orientation of the collapsed lung, or vessels are seen beyond the line. The above circumstances negate the diagnosis of a pneumothorax.
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Fig. 195: Empyema: PA view of the chest demonstrates a homogenous lenticular fluid collection along right lateral chest wall with an air-fluid level. Sonography confirmed the homogenous opacity was fluid with internal echoes. An aspiration revealed an empyema.
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Figs. 196A and B: Empyema: Chest X-ray and CT chest demonstrate a loculated fluid collection in the left hemithorax. There are multiple specks of air in the fluid collection. The presence of air in a pleural collection is highly suggestive of infection in the pleural fluid. Air may also be present in pleural fluid if it has been inadvertently introduced during aspiration of the fluid.
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Fig. 197: Pneumothorax: PA view of chest demonstrates a right sided pneumothorax with underlying partial collapse of right upper lobe.
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Fig. 198: Pneumothorax: AP portable erect X-ray reveals a large pneumothorax on the right side with partial collapse of right lung. A central line is seen in situ on the right side. The pneumothorax occurred following placement of the central line.
Skin folds appear as thick linear bands with a sharp outer margin and a fading medial margin.84
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Figs. 199A and B: Hydropneumothorax: (A) Chest X-ray demonstrates a right upper zone pneumothorax with an air-fluid level representing a hydropneumothorax. Intercostal drainage (ICD) was placed to drain the hydropneumothorax; (B) Chest X-ray demonstrates total evacuation of hydropneumothorax.
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Figs. 200A and B: Pneumothorax: (A) Chest X-ray inspiratory PA view demonstrates a suspicious thin visceral pleural line at the left apex. (B) Expiratory PA view demonstrates a large pneumothorax with a well-defined visceral pleural line. Expiratory chest X-rays are very useful to demonstrate a suspicious pneumothorax as well as the extent of the pneumothorax.
The outer margin is transradiant due to air trapped between skin fold and skin (Fig. 201). The scapula edge is a common mimic and must be looked out for. Extrapleural dissection of air from a pneumomediastinum may also be mistaken for a pneumothorax, the linear abnormality is confined to the lung apex and does not progress in size. The most difficult to differentiate are bullae as they appear translucent/avascular, and have thin well-defined margins. One differentiating feature is that the inner margin of a bulla is concave as compared to a pneumothorax, which would be convex, in line with the chest wall. CT is very helpful in excluding these mimics of a pneumothorax (Figs. 202 and 203).
As the pneumothorax increases in size and the lung collapses, the density of the underlying lung increases, till finally in total collapse it appears like a fist-like opacity overlying the hilum.85
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Fig. 201: PA view of the chest revealed a well-defined line in the left hemithorax simulating a pneumothorax. This, however, is a skin fold resembling a pneumothorax as the line is seen to extend beyond the confines of the thorax into the abdomen.
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Fig. 202: Pneumothorax: CT lung window demonstrates a left pneumothorax with a large thin-walled bulla in the left lingula.
As the density of the collapsing lung increases it becomes easier to detect etiological causes for the pneumothorax. For this reason, apical pleural blebs, the most common cause of a primary spontaneous pneumothorax are visible only on 15% of chest X-rays at the time of the pneumothorax. These blebs are best seen on a CT scan, being detected in 85% of cases. On both X-rays and CT scans other causes such as cysts/bullae/bronchiectasis, etc. should also be looked for. It is also important from a management perspective to estimate the size of a pneumothorax. A simple method is to measure hemithorax distance, interpleural distance.
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For example, if the hemithorax distance is 10 cm and the interpleural distance is 2 cm, the size of the pneumothorax is 50%, an indication that the pneumothorax is much larger than what might be apparent on an X-ray chest.
 
Pneumothorax in a Supine Patient
In a number of patients in a critical care setting X-rays can only be done in a supine position. It is important to recognize the signs of a pneumothorax in a supine patient. Air collects in the highest portion of the pleural cavity which in the supine position is anterior or anteriomedially at the base. The displaced visceral pleural line is difficult to demonstrate on a supine X-ray. In the absence of this specific sign, other signs to demonstrate the collection of air are important. As air collects in the anterior costophrenic sulcus there is transradiancy in the hypochondrial region overlying the diaphragm. There is increased sharpness of the adjacent mediastinal margin and diaphragm. The costophrenic sulcus becomes deep with a well-defined margin. The inferior edge of collapsed lung becomes visible. The ipsilateral hemidiaphragm is depressed. Cardiac margins become sharp and pericardial fat pads become well-outlined.
A pneumothorax suspected on a supine film can be confirmed on a cross-table lateral view or lateral decubitus with suspect side uppermost. If there is any doubt a CT will be very useful, as it would be confirmatory (Figs. 204 and 205).
Tension pneumothorax is an absolute emergency and if untreated results in death. A tension pneumothorax occurs when air enters during inspiration but cannot exit during expiration due to a check valve mechanism (Figs. 206 and 207). On a chest X-ray, the entire hemithorax is hypertranslucent, the mediastinum is shifted to the opposite side and the ipsilateral lung is compressed. In addition the diaphragm on the affected side may be deeply inverted.86
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Figs. 203A and B: Pneumothorax: (A) CT lung window and (B) minimum intensity projection demonstrate a loculated pneumothorax with adhesions along the left anterior lateral parietal pleura.
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Fig. 204: Pneumothorax: Supine AP view in a patient who was hemodynamically unstable; an erect view was not possible. The costophrenic and cardiophrenic recess on the right side are deep and well-outlined. The right dome of the diaphragm is well-outlined as compared to the left. These are all features of a pneumothorax in a supine patient.
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Fig. 205: Pneumothorax: Supine AP view reveals bilateral pneumothorax as evidenced by a sharp diaphragmatic contour and sharp deep bilateral costophrenic sulci. There is extensive surgical emphysema.
 
Management of Pneumothorax
Not every pneumothorax requires drainage. An asymptomatic pneumothorax with interpleural distance less than 2.0 cm may be successfully managed by observation with or without oxygen therapy. Larger symptomatic pneumothoraces may resolve if the air is totally aspirated and the two pleural surfaces appose each other.87
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Figs. 206A and B: Tension pneumothorax: (A) Chest PA view reveals a translucency in left hemithorax due to a large pneumothorax. There is a mediastinal shift to right. These are features of a tension pneumothorax; (B) After intercostal drainage (ICD) tube insertion there is expansion of lung with return of mediastinal structures to their normal position.
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Figs. 207A and B: Tension pneumothorax: (A) Axial and (B) coronal CT demonstrate a large pneumothorax on the right side. The pneumothorax is under tension as evidenced by inversion of the right dome of the diaphragm and displacement of the mediastinum. Extensive centrilobular emphysema is seen in both lung fields.
 
Bronchopleural Fistula
A bronchopleural fistula may be central when the communication is between the bronchus and pleura. A peripheral BPF exists when the communication is between lung parenchyma or a peripheral bronchus and the pleura. The chest radiography signs of a bronchopleural fistula are an increase in air in a pneumonectomy space, with a loss of normal mediastinal shift toward the operated side. Occasionally, the only sign is a persistence of air following pneumonectomy. CT is useful to demonstrate the bronchopleural fistula, but may do so in only 30–50% of cases (Figs. 208 to 210).
 
Pleural Thickening
Pleural thickening is seen as a veil-like opacity along the inner margins of the chest wall, sharply marginated along its inner aspect and fading into the chest wall along its lateral aspect. Pleural thickening involving the costophrenic angle is seen as an angular opacity differentiating it from pleural fluid which is seen as a smooth curvilinear margin (Figs. 211A and B). In cases of difficulty, a lateral decubitus or ultrasound would help in differentiation. CT is very sensitive in the detection of pleural thickening. Extrapleural fat can mimic pleural thickening; this is also well-differentiated on CT.88
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Fig. 208: Bronchopleural fistula: PA view of the chest reveals well-defined walled rounded air-space in the left mid zone with an associated another small more lucent air-space along its lateral aspect.
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Fig. 209: Bronchopleural fistula: CT chest with multiplanar reconstruction demonstrates a dilated bronchus communicating with a loculated pneumothorax. The thin-walled large air-space seen on the X-ray represents the located pneumothorax seen on the CT scan. The well-defined smaller lucent air-space along the lateral aspect represents a dilated bronchus communicating with the loculated pneumothorax. These are seen end on the X-ray.
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Fig. 210: Bronchopleural fistula: In a case of pneumothorax, air bronchograms are seen to communicate with the left pleural cavity indicating a peripheral bronchopleural fistula.
 
Pleural Calcification
Pleural calcification is visualized as a sheet of calcification. When visualized en face, it appears as a veil-like opacity; when visualized in profile it is seen as a linear dense band parallel to the inner chest wall (Fig. 212). Following resolution of an empyema, calcification may be seen as a double layer due to calcification of visceral and parietal pleura. This is well-appreciated on CT.
 
Mesothelioma
On imaging, there are plaques/nodules on visceral/parietal pleura forming a lobular sheet of tumor up to several centimeters thick encasing the lung and growing into the interlobar fissure. Invasion of the mediastinum, diaphragm, lung may occur, though late. An important sign is the loss of lung volume on the ipsilateral side, because the mesothelioma grows as a sheet entrapping the lung (Figs. 213 and 214). These appearances are very well demonstrated on a CT, which is useful for detection, as also for demonstration of chest wall and or mediastinal invasion. Occasionally, the only finding may be pleural thickening with a small-sized ipsilateral hemithorax. The pleural masses are seen to creep along the pleural surfaces. MRI is also useful for demonstrating chest wall and mediastinal involvement.89
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Figs. 211A and B: Pleural thickening: (A) PA and (B) lateral views demonstrate thickening of the minor fissure following resolution of an interlobar effusion.
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Fig. 212: Pleural calcification: AP view of chest reveals veil-like calcification in the left hemithorax.
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Fig. 213: Pleural mesothelioma: CT chest shows presence of multiple lobulated enhancing lesions along the entire right pleural surface.
 
MEDIASTINUM
The chest radiograph is usually the first investigation performed for a suspected mediastinal/hilar mass lesion. Mediastinal masses may also be detected incidentally on X-rays done for other reasons. If a mediastinal pathology is suspected and the chest X-ray reveals no abnormality, a cross-sectional imaging technique, ideally a CT scan is required. Mediastinal pathology may be obscured by mediastinal vasculature on an X-ray. A CT scan is very useful to characterize the mass lesion; it also serves as a guide for biopsy of a mediastinal mass. Mediastinal masses appear on chest X-rays as projections from the mediastinal silhouette. Hilar masses are visualized as prominence and or enlargement of the hilum. The first step in the differential diagnosis is to determine if the lesion arises from the mediastinum or lung. A spiculated mass lesion will nearly always be of pulmonary origin. Homogenous masses which project beyond the confines of the mediastinum, have a broad base and form obtuse angles with the mediastinum, arise from the mediastinum or mediastinal pleura. The differential diagnosis of mediastinal masses is based on their location and internal morphology.90
 
LOCATION
 
Prevascular Masses
Prevascular masses are located anterior to the ascending aorta and its branches. These are most commonly thymic masses, thyroid masses, germ cell tumors or lymphadenopathy. Thyroid masses are easy to diagnose as they are seen in the superior mediastinum contiguous with the thyroid in the neck. On unenhanced scans they are of a higher attenuation than adjacent skeletal muscle in view of their iodine content. Internally, thyroid masses are heterogeneous with calcific densities and cysts. Thyroid masses are the most common lesions to cause deviation of the trachea. Thymic and germ cell tumors appear similar on imaging; their differentiation is based on clinical and laboratory features. Thymomas may be clinically associated with myasthenia gravis, red cell aplasia, and hypogammaglobulinemia. An elevated HCG or alpha fetoprotein levels are indicative of a germ cell tumor. Thymoma, germ cell tumors may demonstrate calcification. Presence of fat, cartilaginous calcification, teeth or a fat-fluid level are indicative of a mature teratoma.
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Fig. 214: Mesothelioma: CT chest reveals plaque-like thickening of pleural surface with nodularity of surface in left apical region. Biopsy revealed a mesothelioma. Note vascular encasement of the great vessels by the mesothelioma.
Unusual causes of prevascular masses are parathyroid adenoma (usually evidence of hyperparathyroidism). Lymphangioma (cystic with multiple internal septations). Cystic hygroma should be considered when a cystic mass is seen extending from the neck into the mediastinum.
 
Paracardiac Masses
Chiefly include pericardial cyst, diaphragmatic hernia and lymphadenopathy.
Pericardial cysts are easily diagnosed as they are homogenous, of water attenuation, with thin walls. Diaphragmatic hernias (Morgagni's hernia) are due to a defect in the diaphragm with herniation of a pad of fat and or bowel loops into the thorax. Occasionally, germ cell tumors and thymomas may be visualized in a paracardiac location.
 
Paratracheal, Subcarinal and Paraesophageal Masses
These are considered together as they are contained in one fascial sheath. The group includes lymphadenopathy (Figs. 215 to 219), foregut malformations, esophageal tumors, thyroid mass lesions, hiatus hernia, aneurysms, vascular anomalies and pancreatic pseudocyst. The most common of these is lymphadenopathy. Esophageal carcinoma presents early as dysphagia and generally results in a small mass lesion. Vascular anomalies and aneurysms are visualized as homogenous enhancing structures. Foregut malformations are fluid-filled well-defined lesions in relation to the vertebrae, esophagus or tracheobronchial tree.
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Figs. 215A to C: Mediastinal adeuopathy: Chest X-ray (A) reveals a large right paratracheal mass lesion. Note it is homogenous with a wide mediastinal base and obtuse angles with the lung indicating a mediastinal mass lesion. Lateral view (B) demonstrates the mass lesion to be anterior mediastinum. CT chest (C) confirms that the mass lesion is a large necrotic adenopathy. CT-guided aspiration confirmed the adenopathy to be of tubercular origin.
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Figs. 216A to C: Mediastinal adenopathy: (A) Chest X-ray reveals right paratracheal and left hilar adenopathy (B and C) CT chest confirms adenopathy as well as demonstrates small left prevascular adenopathy and large subcarinal adenopathy, not detected on the X-ray as these were covered by the mediastinum.
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Figs. 217A to C: Mediastinal adenopathy: (A) Chest X-ray demonstrates large right paratracheal and hilar adenopathy; (B) CT chest; (C) confirms adenopathy, which are necrotic, indicating tuberculosis.
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Fig. 218: Mediastinal adenopathy: Chest X-ray demonstrates large hilar and right paratracheal mass lesions representing adenopathy.
 
Prevertebral Masses
These are most commonly neurogenic tumors, or lymph gland masses. Other pathologies include mesenchymal tumors, lesions arising from the pharynx, or vertebra. A paraspinal abscess and an aneurysm of the descending aorta are also observed in the prevertebral location.
Imaging studies of prevascular masses, of paracardiac masses, of paratracheal, subcarinal, paraesophageal masses and of prevertebral masses have been amply illustrated in the chapter on Diseases of the Mediastinum and therefore do not bear repetition.92
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Figs. 219A to E: Metastatic mediastinal adenopathy: (A) Chest X-ray reveals an opacity in the left para-aortic region, however, not silhouetting the aorta; (B) Coronal CT demonstrates a spiculated mass lesion in the left apex; (C) axial CT demonstrates spiculated apical mass lesion very well. CT-guided fine-needle aspiration cytology (FNAC) revealed mass to be squamous cell carcinoma; (D) axial post-contrast CT reveals large anterior mediastinal mass lesion representing metastatic adenopathy; (E) coronal reconstruction demonstrates large anterior mediastinal adenopathy.
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SUGGESTED READING
  1. David MH, Peter A, David L, et al. Imaging of the Diseases of the Chest, 4th edition. Philadelphia: Elsevier Mosby;  2005.
  1. Grenier PA. Imaging of airway diseases. Radiol Clin North Am. 2009;47.
  1. Sanjiv B. Thoracic MDCT comes of age. Radiol Clin North Am. 2010;48.
  1. Webb R, Muller NL, Naidich DP. High Resolution CT of the Lung, 4th edition. Philadelphia: Lippincott Williams and Wilkins;  2008.94