Oxford Case Histories in Respiratory Medicine
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A note from the series editors
Case histories have always had an important role in medical education, but
most published material has been directed at undergraduates or residents. The
Oxford Case Histories series aims to provide more complex case-based learn-
ing for clinicians in specialist training and consultants, with a view to aiding
preparation for entry and exit-level specialty examinations or revalidation.
Each case book follows the same format with approximately 50 cases, each
comprising a brief clinical history and investigations, followed by questions on
differential diagnosis and management, and detailed answers with discussion.
All cases are peer-reviewed by Oxford consultants in the relevant specialty. At
the end of each book, cases are listed by mode of presentation, aetiology and
diagnosis.
We are grateful to our colleagues in the various medical specialties for their
enthusiasm and hard work in making the series possible.
Sarah Pendlebury and Peter Rothwell
Quotes on the first book in the series – “Neurological Case Histories”
“I recommend this excellent volume highly ....... this book will enlighten and
entertain consultants, and all readers will learn something.”
Lancet Neurology 2007; 6: 951
“This short and well-written text is …. designed to enhance the reader’s diag-
nostic ability and clinical understanding …. A well documented and practical
book”
European Journal of Neurology 2007; 14: e19
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Introduction
Postgraduate medical education has changed considerably over the last
30 years. There is greater emphasis on structured learning, but apprenticeship
time has decreased. Thus specialist registrars may reach the end of their training
without having seen cases of either rare diseases, rare presentations of common
diseases or unusual problems in association with common diseases. Most phy-
sicians learn from cases they have seen. This collection of cases is a second-best
alternative, providing vignettes that hopefully will come to mind when a
similar case is encountered in the future.
The cases are not meant to comprehensively cover the ‘syllabus’ of a specialist
registrar in respiratory medicine, but are selected for their interest, or to eluci-
date points that the authors feel are important but may be under-appreciated.
The style of presentation thus inevitably varies depending on the type of message
and some of the problems discussed have no right answer, ours may well be
disputed!
We hope the question-and-answer format will keep the reader on their toes
and make reading through the cases more fun.
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Acknowledgements
Many people have given their time to read through these cases and correct
errors or improve clarity. We are very grateful for their input; in particular
Rachel Benamore has provided considerable help with the radiology, and Rolf
Smith read through all the cases to provide us with invaluable help. These are
the individuals who reviewed one or more cases for us: Lesley Bennett,
Malcolm Benson, Di Bilton, Steve Chapman, Sonya Craig, Ling-Pei Ho, Rob
Davies, Colin Forfar, Maxine Hardinge, Robin Howard, Gary Lee, Raashid
Luqmani, Lorna McWilliam, Grace Robinson, Rana Sayeed, Claire Shovlin,
Catherine Swales, Catherine Thomas, Chris Winearls, and John Wrightson.
Needless to say any errors remain our responsibility.
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Contents
Abbreviations xiii
Normal ranges xvi
Cases 1–44 1
List of cases by aetiology 387
List of cases by diagnosis 388
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Abbreviations
AAFB Acid- and alcohol-fast bacilli CTEPH Chronic thromboembolic
ABG Arterial blood gases pulmonary hypertension
ABPA Allergic bronchopulmonary CTPA Computerized tomographic
aspergillosis pulmonary angiogram
ACE Angiotensin converting CVID Common variable
enzyme immunodeficiency
ANA Anti-nuclear antibody CXR Chest radiograph
ANCA Anti-nuclear cytoplasmic DBP Diastolic blood pressure
antibody DCT Direct Coombs test
ARDS Adult respiratory distress DNA Deoxyribonucleic acid
syndrome DOT Directly observed therapy
ASD Atrial septal defect DPB Diffuse panbronchiolitis
AVM Arteriovenous malformation DVLA Driver vehicle licensing
BAL Bronchoalveolar lavage authority
BAPE Benign asbestos-related pleural DVT Deep vein thrombosis
effusion EIA Enzyme immunoassay
BE Base excess ELCs Emphysema-like changes
BMI Body mass index (kgs/metre2) ELS extralobar sequestration
BMT Bone marrow transplant EPP extrapleural pneumonectomy
BNP Brain natriuretic peptide ESS Epworth sleepiness score
BO bronchiolitis obliterans FEV1 Forced expiratory volume in
BPM Beats per minute one second
Ca++ Calcium FRC Functional residual volume
CBG Capillary blood gases FVC Forced expiratory volume
CCAM Congenital cystic adenomatoid GVHD Graft-versus-host-disease
malformation H&E Haematoxylin and Eosin
CETTE Contrast-enhanced Hb Haemoglobin
transthoracic echo
[HCO3]¯ Bicarbonate
CF Cystic fibrosis
HES Hypereosinophilic syndrome
CFTR Cystic fibrosis transmembrane
HGV Heavy goods vehicle
conductance regulator
HHT Hereditary haemorrhagic
CLL Chronic lymphatic leukaemia
telangiectasia
COP Cryptogenic organizing
HIV Human immunodeficiency
pneumonia
virus
CPAP Continuous positive airway
HLA Human leukocyte antigen
pressure
HP Hypersensitivity pneumonitis
CRP C-reactive protein
HPS Hepatopulmonary syndrome
CT Computerized tomography
xiv ABBREVIATIONS
HRCT High resolution computerized OSA Obstructive sleep apnoea
tomography OSAS Obstructive sleep apnoea
HR Heart rate syndrome
ICS Inhaled corticosteroid OSLER Oxford sleep resistance test
IL1 Interleukin 1 PA Pulmonary artery
ILS intralobar sequestration PaCO2 Partial pressure of arterial
INR International normalized ratio carbon-dioxide
IPF Interstitial pulmonary fibrosis PaO2 Partial pressure of arterial
oxygen
IVC Inferior vena cava
PAP Pulmonary artery pressure
JVP Jugular venous pressure
PAVM Pulmonary arteriovenous
K+ Potassium
malformations
KCO Carbon-monoxide transfer
PCD Primary ciliary dyskinesia
coefficient
PCR Protein creatinine ratio
LAM Lymphangioleiomyomatosis
PEFR Peak expiratory flow rate
LCH Langerhans cell histiocytosis
PH Pulmonary hypertension
LDH Lactate dehydrogenase
PFO Patent foramen ovale
LFTs Liver function tests
PFTs Pulmonary function tests
LIP Lymphoid interstitial
pneumonia PND Post-nasal drip or paroxysmal
nocturnal dyspnoea
LTOT Long-term oxygen therapy
PSP Primary spontaneous
LV Left ventricle
pneumothorax
LVSF Left ventricular systolic
RA-ILD Rheumatoid associated
function
interstitial lung disease
MAC Mycobacteria avium complex
RAW Airway resistance (from body
MCS Microscopy, culture and box)
sensitivity
RBILD Respiratory bronchiolitis–
MCT Medium-chain triglycerides interstitial lung disease
MCV Mean corpuscular volume RPO Re-expansion pulmonary
MDR-TB Multi-drug resistant TB oedema
MGUS Monoclonal gammopathy of RV Residual volume/Right
unknown significance ventricle
MI Myocardial infarction SaO2 Arterial oxygen saturations
MPO Myeloperoxidase SBP Systolic blood pressure
MSLT Multiple sleep latency test SOB Shortness of breath
MWT Maintenance of wakefulness SVC Superior vena cava
test T4 Thyroxine
Na+ Sodium TB Tuberculosis
NSAID Non-steroidal anti- TBB Transbronchial biopsy
inflammatory agent
TLC Total lung capacity
NICE National Institute for Health
TLCO Carbon-monoxide transfer
and Clinical Excellence
factor
NSIP Non-specific interstitial
TNM Tumour/nodes/metastases
pneumonia
classification
NTM Non-tuberculous mycobacteria
SYMBOLS AND ABBREVIATIONS xv
TPN Total parenteral nutrition USS Ultrasound scan
U&Es Urea and electrolytes VATS Video-assisted thoracoscopy
UACS Upper airway cough VCD Vocal cord dysfunction
syndrome VTE Venous thrombo-embolism
UIP Usual interstitial pneumonia V/Q Ventilation/perfusion
Normal ranges
Lower limit Upper limit units
Hb (men) 13 18 g/dL
Hb (women) 11.5 15 g/dL
MCV 83 105 fL
WCC 4 11 ×109/L
Neutrophils 2 7 ×109/L
Lymphocytes 1 4 ×109/L
Eosinophils 0.02 0.5 ×109/L
Platelets 150 400 ×109/L
PTT 10 14 s
APTT 22 34 s
ESR 0 about half the age mm/hr
Na 135 145 mmol/L
K 3.5 5 mmol/L
Urea 2.5 6.7 mmol/L
Creatinine 70 150 umol/L
Bilirubin 3 17 umol/L
AST 3 35 IU/L
ALT 10 45 IU/L
ALP 75 250 IU/L
Albumin 35 50 g/L
GGT (men) 11 51 IU/L
GGT (women) 7 33 IU/L
Ca (corr) 2.12 2.62 mmol/L
PO4 0.8 1.45 mmol/L
Glucose (fasting) 3.5 5.5 mmol/L
CRP 0 8 mg/L
ACE 18 55 IU/L
α1 anti trypsin 107 209 mg/dL
PSA 0 4 ng/mL
PaO2 12 14 kPa
PaCO2 4.7 5.9 kPa
pH 7.36 7.44
Base excess −2 2 meq/L
Bicarbonate 23 27 meq/L
IgG 6 13 g/L
IgA 0.8 3 g/L
IgM 0.4 2.5 g/L
IgE 5 120 kU/L
Case 1
A 42-year-old lady was referred for respiratory review with a history of asthma,
which had become difficult to control over the last 3 years, with increased
nocturnal cough and peak flow variability. She had received multiple courses
of oral antibiotics and steroids to which she would briefly respond, and was on
a long-term combined inhaled steroid and long-acting beta agonist. She used
a nasal steroid for nasal polyps. She had not moved house or changed jobs, she
worked as a gardener and had no pets.
Questions
1a) What reasons could explain this deterioration after many years of good
control?
2 CASE HISTORIES IN RESPIRATORY MEDICINE
Answers
1a) What reasons could explain this deterioration after many years of good
control?
There are multiple reasons to fail to respond to asthma therapy, including
a poor inhaler technique or adherence to therapy. Reasons for deteriora-
tion in symptoms after good control include:
◆ Development of oesophageal reflux
◆ New exposure to asthma triggers, e.g. house-dust-mite, cat fur, pollen
or occupational exposure
◆ New psychological or social pressure
◆ Alternative diagnoses, such as the development of allergic bronchopul-
monary aspergillosis (ABPA) or Churg–Strauss syndrome
◆ Gain in weight.
Investigations showed
◆ Full blood count: Hb, 13.5g/dL
◆ WCC, 7.29 × 109/L
◆ Eosinophils, 3.21 × 109/L
◆ Platelets, 362 × 109/L
◆ Total IgE, 620 ng/ml (normal range 5–120)
◆ Aspergillus RAST (IgE), strongly positive
◆ Aspergillus precipitins (IgG), 2 lines (where 1 line = weakly positive and
6 = strongly positive)
◆ Sputum culture, mucoid Pseudomonas aeruginosa
◆ CF genetic screening, negative for common CF mutations.
Questions
1b) What do the CXR and CT scan in Fig. 1.1 show?
1c) What diagnosis do investigations support?
1d) What are the typical clinical features of this condition?
1e) Discuss treatments options for this lady.
CASE 1 3
(a)
(b)
Fig. 1.1 (a) CXR and (b) CT chest.
4 CASE HISTORIES IN RESPIRATORY MEDICINE
Answers
1b) What do the CXR and CT scan in Fig. 1.1 show?
The CXR shows hyper-expanded lung fields, with widespread bronchiec-
tatic changes. The CT slice shows dilated airways, much larger than the
adjacent blood vessel, in keeping with bronchiectasis. There is also ‘tree
in bud nodularity’, which may be suggestive of small airway chronic or
atypical infection.
Tree-in-bud nodularity
Dilated airways
Fig. 1.2 Portion of CT-chest illustrating features in keeping with allergic
bronchopulmonary aspergillosis.
1c) What diagnosis do investigations support?
Investigations support a diagnosis of allergic bronchopulmonary aspergil-
losis, ABPA. Atopic patients with asthma and cystic fibrosis with IgE-
mediated allergy to inhaled Aspergillus spores are vulnerable to this
condition. They may develop IgE and IgG reactions to Aspergillus in the
airways, provoking mucous plugging with distal consolidation, and then
ABPA, with inflammatory damage to the airways and resultant bron-
chiectasis. Damp conditions, composting organic material and thunder-
storms are associated with high Aspergillus spore counts, and so may lead
to exacerbations. Since simple atopic asthma is at one end of a continuum,
with ABPA at the other, there is no single diagnostic test that defines the
transition. The presence of the features in Box 1.1 would support the diag-
nosis, with the first four being the most important. Many asthmatics and
patients with cystic fibrosis have one or more findings suggestive of ABPA,
but do not fulfil all criteria listed.
ABPA is a complex hypersensitivity reaction, often in patients with asthma
or cystic fibrosis that occurs when bronchi become colonized by Aspergillus.
