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Basic Sciences: Answers
109
References
Rademacher J, Welte T. Bronchiectasis--diagnosis and treatment. Dtsch Arztebl Int.
2011;108:809-15.
Stenbit AE, Flume PA. Pulmonary exacerbations in cystic fibrosis. Curr Opin Pulm Med.
2011;17:442-7.
1.33 Answer: B
Lobar pneumonia is the result of alveolar wall injury with severe haemorrhagic oedema
induced by inhaled infectious organisms that reach the subpleural zone of the lung. This
injury is followed by a rapid multiplication of organisms and invasion of the infected
oedematous fluid by polynuclear leukocytes. The process spreads rapidly through the pores of
Kohn leading to a consolidation of an entire lobe or segment.
Community-acquired pneumonia develops in people with limited or no contact with
medical institutions or settings. The most commonly identified pathogens are Streptococcus
pneumoniae, Haemophilus influenzae, and atypical organisms (i.e., Chlamydia pneumoniae,
Mycoplasma pneumoniae, Legionella species). Symptoms and signs are fever, cough,
dyspnoea, tachypnoea, and tachycardia. Diagnosis is based on clinical presentation and chest
x-ray.
The typical radiological pattern is air space consolidation involving an entire lobe
containing air bronchograms. Because of the use of antibiotics, the pneumonia is limited to
one or more segments within a lobe. Necrosis and cavitation represent the potential
complication of lobar pneumonia. Pulmonary gangrene may occur rarely.
References
Driver C. Pneumonia part 1: Pathology, presentation and prevention. Br J Nurs. 2012;21:103-
6.
Driver C. Pneumonia part 2: signs, symptoms and vaccinations. Br J Nurs. 2012;21:245-9.
1.34 Answer: C
This is a description of the typical 'Ghon complex' of an initial, or primary, tuberculosis
(TB) infection.
Airborne droplet nuclei lodge in subpleural terminal airspaces, predominantly in the
lower lung, usually in only one site. Tubercle bacilli replicate inside macrophages, ultimately
killing them; inflammatory cells are attracted to the area, causing a tubercle and sometimes
pneumonitis. In the early weeks of infection, some infected macrophages are borne to
regional lymph nodes (e.g., hilar, mediastinal). Haematogenous spread to any part of the
body, particularly the apical-posterior portion of the lungs, epiphyses of the long bones,
kidneys, vertebral bodies, and meninges, may occur. In 95% of cases, after about 3 wk of
uninhibited growth, the immune system suppresses bacillary replication before symptoms or
signs develop. Foci of infection in the lung or other sites resolve into epithelioid cell
granulomas, which may have caseous and necrotic centres; tubercle bacilli can survive in this
material for years, the host's resistance determining whether the infection ultimately resolves
without treatment, remains dormant, or becomes active. Foci may leave nodular scars in the
apices of one or both lungs (Simon foci), calcified scars from the primary infection (Ghon
foci), or calcified hilar lymph nodes. The tuberculin skin test is positive.
Shahzad G. Raja
110
Rarely, the primary focus immediately progresses, causing acute illness with pneumonia
(sometimes cavitary), pleural effusion, and marked mediastinal or hilar lymph node
enlargement (which in children may compress bronchi). Small pleural effusions are
predominantly lymphocytic, typically contain few organisms, and clear within a few weeks.
Primary extrapulmonary TB at any site can sometimes present without evidence of lung
involvement. TB lymphadenopathy is the most common extrapulmonary presentation;
however, meningitis is the most feared because of its high mortality in the very young and
very old.
References
Jeong YJ, Lee KS. Pulmonary tuberculosis: up-to-date imaging and management. AJR Am J
Roentgenol. 2008;191:834-44.
Agrons GA, Markowitz RI, Kramer SS. Pulmonary tuberculosis in children. Semin
Roentgenol. 1993;28:158-72.
1.35 Answer: D
Clinical features of pulmonary embolism (PE) are sudden-onset dyspnoea, tachypnoea,
chest pain of "pleuritic" nature (worsened by breathing), cough, haemoptysis, and in severe
cases, cyanosis, tachycardia, hypotension, shock, loss of consciousness, and death. Although
most cases have no clinical evidence of deep venous thrombosis (DVT) in the legs, findings
that indicate DVT may aid in the diagnosis.
The most common sources of embolism are proximal leg deep venous thrombosis or
pelvic vein thromboses. Any risk factor for DVT also increases the risk that the venous clot
will dislodge and migrate to the lung circulation, which happens in up to 15% of all DVTs.
The conditions are generally regarded as a continuum termed venous thromboembolism.
The development of thrombosis is classically due to a group of causes named Virchow‘s
triad (alterations in blood flow, factors in the vessel wall and factors affecting the properties
of the blood). Often, more than one risk factor is present.
Alterations in blood flow: immobilisation (after surgery, injury or long-distance air
travel), pregnancy (also procoagulant), obesity (also procoagulant)
Factors in the vessel wall: of limited direct relevance in venous thromboembolism
Factors affecting the properties of the blood (procoagulant state):
– Oestrogen-containing hormonal contraception
– Genetic thrombophilia (factor V Leiden, prothrombin mutation G20210A,
protein C deficiency, protein S deficiency, antithrombin deficiency,
hyperhomocysteinemia and plasminogen/fibrinolysis disorders).
– Acquired thrombophilia (antiphospholipid syndrome, nephrotic syndrome,
paroxysmal nocturnal haemoglobinuria)
References
Reitsma PH, Versteeg HH, Middeldorp S. Mechanistic view of risk factors for venous
thromboembolism. Arterioscler Thromb Vasc Biol. 2012;32:563-8.
Wolberg AS, Aleman MM, Leiderman K, Machlus KR. Procoagulant activity in hemostasis
and thrombosis: Virchow's triad revisited. Anesth Analg. 2012;114:275-85.
Basic Sciences: Answers
111
1.36 Answer: B
α1-antitrypsin deficiency is congenital lack of a primary lung antiprotease, α1-antitrypsin,
which leads to increased protease-mediated tissue destruction and emphysema in adults. α1-
antitrypsin deficiency is a genetic disorder that affects about one in 2000-5000 individuals. It
is clinically characterised by liver disease and early-onset emphysema. Although α1-
antitrypsin is mainly produced in the liver, its main function is to protect the lung against
proteolytic damage from neutrophil elastase. The most frequent mutation that causes severe
α1-antitrypsin deficiency arises in the SERPINA 1 gene and gives rise to the Z allele. This
mutation reduces concentrations in serum of alpha1 antitrypsin by retaining polymerised
molecules within hepatocytes. Hepatic accumulation of abnormal α1-antitrypsin can cause
liver disease (cirrhosis) in both children and adults. Serum α1-antitrypsin level < 11 μmol/L
(< 80 mg/dL) confirms the diagnosis. In addition to the usual treatments for emphysema,
infusion of purified α1-antitrypsin from pooled human plasma represents a specific treatment
and raises the concentrations in serum and epithelial-lining fluid above the protective
threshold. Evidence suggests that this approach is safe, slows the decline of lung function,
could reduce infection rates, and might enhance survival. However, uncertainty about the
cost-effectiveness of this expensive treatment remains.
References
Stoller JK, Aboussouan LS. Alpha1-antitrypsin deficiency. Lancet. 2005;365:2225-36.
Modrykamien A, Stoller JK. Alpha-1 antitrypsin (AAT) deficiency - what are the treatment
options? Expert Opin Pharmacother. 2009;10:2653-61.
1.37 Answer: A
Most lung abscesses develop after aspiration of oral secretions by patients with gingivitis
or poor oral hygiene who are unconscious or obtunded from alcohol, illicit drugs, anaesthesia,
sedatives, or opioids. Older patients and those unable to handle their oral secretions, often
because of neurologic disease, are also at risk. Lung abscess less commonly complicates
necrotizing pneumonia that may develop from haematogenous seeding of the lungs due to
septic embolism from intravenous drug use or suppurative thromboembolism. In contrast to
aspiration, these conditions typically cause multiple rather than isolated lung abscesses.
The most common pathogens are anaerobic bacteria, but about
1
⁄
2
of all cases involve
both anaerobic and aerobic organisms. The most common aerobic pathogens are streptococci.
Immunocompromised patients with lung abscess are more likely to have infection with
Nocardia, mycobacteria, or fungi. People from developing countries are at risk of abscess due
to Mycobacterium tuberculosis, amoebic infection (Entamoeba histolytica), paragonimiasis,
or Burkholderia pseudomallei.
Lung abscess is suspected based on history, physical examination, and chest x-ray. In
anaerobic infection due to aspiration, chest x-ray classically shows consolidation, with a
single cavity containing an air-fluid level in portions of the lung that are dependent when the
patient is recumbent (e.g., posterior segment upper lobe or superior segment lower lobe). This
pattern helps distinguish anaerobic abscess from other causes of cavitary pulmonary disease,
such as diffuse or embolic pulmonary disease, which may cause multiple cavitations, or TB,
which involves the apices. CT scan is not routinely needed but may be useful when the x-ray
suggests a cavitating lesion or when an underlying pulmonary mass obstructing the drainage
of a lung segment is suspected.
Shahzad G. Raja
112
References
Puligandla PS, Laberge JM. Respiratory infections: pneumonia, lung abscess, and empyema.
Semin Pediatr Surg. 2008;17:42-52.
Mansharamani NG, Koziel H. Chronic lung sepsis: lung abscess, bronchiectasis, and
empyema. Curr Opin Pulm Med. 2003;9:181-5.
1.38 Answer: A
Asbestosis, a form of interstitial pulmonary fibrosis, is much more common than
malignant disease. Shipbuilders, textile and construction workers, home remodelers, workers
who do asbestos abatement, and miners exposed to asbestos fibers are among the many
categories of workers at risk of the disease. Secondhand exposure may occur among family
members of exposed workers and among those who live close to mines. Pathophysiology is
similar to that of other pneumoconioses—alveolar macrophages attempting to engulf inhaled
fibers release cytokines and growth factors that stimulate inflammation, collagen deposition,
and ultimately fibrosis—except that asbestos fibers themselves may also be directly toxic to
lung tissue. Risk of disease is generally related to duration and intensity of exposure and type,
length, and thickness of inhaled fibers.
Asbestosis is initially asymptomatic but can cause progressive dyspnoea, nonproductive
cough, and fatigue; the disease progresses in > 10% of patients after cessation of exposure.
Advanced asbestosis may cause clubbing, dry bibasilar crackles, and, in severe cases,
symptoms and signs of right ventricular failure (cor pulmonale).
Diagnosis is based on history of exposure and chest x-ray or chest CT. Chest x-ray shows
linear reticular or nodular opacities signifying fibrosis, usually in the peripheral lower lobes,
often accompanied by pleural changes. Honeycombing signifies more advanced disease,
which may involve the mid lung fields. As with silicosis, severity is graded on the
International Labor Organization scale based on size, shape, location, and profusion of
opacities. In contrast to silicosis, asbestosis produces reticular opacities with a lower lobe
predominance. Hilar and mediastinal adenopathy are uncharacteristic and suggest a different
diagnosis. Chest x-ray is insensitive; high-resolution chest CT (HRCT) is useful when
asbestosis is a likely diagnosis. HRCT is also superior to the chest x-ray in identifying the
pleural abnormalities. Pulmonary function tests, which may show reduced lung volumes and
transfer factor for carbon monoxide, are nonspecific but help characterise changes in lung
function over time after the diagnosis is made. Bronchoalveolar lavage or lung biopsy is
indicated only when noninvasive measures fail to provide conclusive diagnosis;
demonstration of asbestos fibers indicates asbestosis in people with pulmonary fibrosis,
although such fibers can occasionally be found in lungs of exposed people without disease.
References
Jamrozik E, de Klerk N, Musk AW. Asbestos-related disease. Intern Med J. 2011;41:372-80.
Lazarus AA, Philip A. Asbestosis. Dis Mon. 2011;57:14-26.
1.39 Answer: E
Squamous cell carcinoma accounts for 25-30% of all lung cancers. The classic
manifestation is a cavitary lesion in a proximal bronchus. Histologically, this tumour is
characterised by the presence of keratinization and/or intercellular bridges. Keratinization
Basic Sciences: Answers
113
may take the form of squamous pearls or individual cells with markedly eosinophilic (pink)
dense cytoplasm. These features are prominent in the well-differentiated tumours.
References
Fan Z, Schraeder R. Fan Z, Schraeder R. The changing pathology of lung cancer. Surg Oncol
Clin N Am. 2011;20:637-53.
Idowu MO, Powers CN. Lung cancer cytology: potential pitfalls and mimics - a review. Int J
Clin Exp Pathol. 2010;3:367-85.
1.40 Answer: A
Acute respiratory distress syndrome (ARDS) is a diffuse pulmonary parenchymal injury
associated with noncardiogenic pulmonary oedema and resulting in severe respiratory distress
and hypoxemic respiratory failure. The pathologic hallmark is diffuse alveolar damage, but
lung tissue rarely is available for a pathologic diagnosis. Therefore, diagnosis is made on
clinical grounds, according to the following criteria set forth by the American-European
Consensus Conference:
Acute onset
Bilateral infiltrates
Pulmonary artery wedge pressure less than 19 mm Hg (or no clinical signs of
congestive heart failure)
PaO2/FIO2 ratio less than 200 (ARDS) or less than 300 (acute lung injury [ALI]):
ALI is a milder clinical expression of the injury of ARDS that may or may not
progress to ARDS.
Many conditions have been found to precipitate ARDS. In some cases a predisposing
condition cannot be identified. The following is a list of the most common predisposing
conditions:
Infection - Pneumonia of any aetiology (especially viral) and systemic sepsis
(especially gram negative)
Shock - Any type, particularly septic and traumatic shock
Aspiration - Gastric contents, near drowning, and toxic inhalation
Trauma - Pulmonary contusion, fat embolization, and multiple trauma
Other - Systemic inflammatory response syndrome, pancreatitis,
postcardiopulmonary bypass, massive blood transfusion, drug ingestion (e.g., heroin,
methadone, barbiturates, salicylates)
ARDS is thought to develop when pulmonary or systemic inflammation leads to systemic
release of cytokines and other proinflammatory molecules. The cytokines activate alveolar
macrophages and recruit neutrophils to the lungs, which in turn release leukotrienes, oxidants,
platelet-activating factor, and proteases. These substances damage capillary endothelium and
alveolar epithelium, disrupting the barriers between capillaries and airspaces. Oedema fluid,
protein, and cellular debris flood the airspaces and interstitium, causing disruption of
surfactant, airspace collapse, ventilation-perfusion mismatch, shunting, stiffening of the lungs
Shahzad G. Raja
114
with decreased compliance, and pulmonary hypertension. The injury is distributed
heterogeneously but mainly affects dependent lung zones. Histopathologically, diffuse
alveolar damage results with intra-alveolar neutrophils, red blood cells, and cellular debris
and denuded epithelial basement membranes with formation of hyaline membranes.
References
Saguil A, Fargo M. Acute respiratory distress syndrome: diagnosis and management. Am Fam
Physician. 2012;85:352-8.
Bellani G, Mauri T, Pesenti A. Imaging in acute lung injury and acute respiratory distress
syndrome. Curr Opin Crit Care. 2012;18:29-34.
1.41 Answer: A
Bronchoalveolar or bronchioloalveolar carcinoma (BAC) is a distinct subtype of
adenocarcinoma with the classic manifestation as an interstitial lung disease on a chest
radiograph. Bronchoalveolar carcinoma arises from type II pneumocytes and grows along
alveolar septa. This subtype may manifest as a solitary peripheral nodule, multifocal disease,
or a rapidly progressing pneumonic form. A characteristic finding in persons with advanced
disease is voluminous watery sputum.
Bronchioloalveolar carcinoma disproportionately affects women, never-smokers, and
Asians and is characterized by growth along alveolar septae without evidence of stromal,
vascular, or pleural invasion. Although pure BAC accounts for approximately 4% of lung
cancers, tumors with histologically mixed BAC and adenocarcinoma account for > 20% of all
non-small-cell lung carcinoma (NSCLC), and the incidence of BAC might be increasing.
Bronchioloalveolar carcinoma histology is most commonly found in small lesions identified
incidentally on chest radiographs or computed tomography scans and might represent a
precursor lesion to invasive adenocarcinoma. As with other subsets of NSCLC, surgical
resection is the only potentially curative treatment. Patients with unresectable BAC are more
likely to respond to the epidermal growth factor receptor tyrosine kinase inhibitors gefitinib
and erlotinib than patients with other subtypes of NSCLC. Stage for stage, patients with BAC
have a higher rate of long-term survival but might have an increased rate of intrathoracic
recurrence than patients with other subtypes of NSCLC.
References
Raz DJ, He B, Rosell R, Jablons DM. Bronchioloalveolar carcinoma: a review. Clin Lung
Cancer. 2006;7:313-22.
Garfield DH, Cadranel JL, Wislez M, Franklin WA, Hirsch FR. The bronchioloalveolar
carcinoma and peripheral adenocarcinoma spectrum of diseases. J Thorac Oncol.
2006;1:344-59.
1.42 Answer: C
Sarcoidosis is a multisystemic disorder of unknown cause characterized by the formation
of immune granulomas in involved organs. It is an ubiquitous disease with incidence (varying
according to age, sex, race and geographic origin) estimated at around 16.5/100,000 in men
and 19/100,000 in women. The lung and the lymphatic system are predominantly affected but
virtually every organ may be involved. Other severe manifestations result from cardiac,
neurological, ocular, kidney or laryngeal localizations. In most cases, sarcoidosis is revealed
Basic Sciences: Answers
115
by persistent dry cough, eye or skin manifestations, peripheral lymph nodes, fatigue, weight
loss, fever or night sweats, and erythema nodosum. Abnormal metabolism of vitamin D3
within granulomatous lesions and hypercalcemia are possible. Chest radiography is abnormal
in about 90% of cases and shows lymphadenopathy and/or pulmonary infiltrates (without or
with fibrosis), defining sarcoidosis stages from I to IV. The etiology remains unknown but the
prevailing hypothesis is that various unidentified, likely poorly degradable antigens of either
infectious or environmental origin could trigger an exaggerated immune reaction in
genetically susceptible hosts. Diagnosis relies on compatible clinical and radiographic
manifestations, evidence of non-caseating granulomas obtained by biopsy through
tracheobronchial endoscopy or at other sites, and exclusion of all other granulomatous
diseases. The evolution and severity of sarcoidosis are highly variable. Mortality is estimated
at between 0.5-5%. In most benign cases (spontaneous resolution within 24-36 months), no
treatment is required but a regular follow-up until recovery is necessary. In more serious
cases, a medical treatment has to be prescribed either initially or at some point during follow-
up according to clinical manifestations and their evolution. Systemic corticosteroids are the
mainstay of treatment of sarcoidosis. The minimal duration of treatment is 12 months. Some
patients experience repeated relapses and may require long-term low-dose corticosteroid
therapy during years. Other treatments (immunosuppressive drugs and aminoquinolins) may
be useful in case of unsatisfactory response to corticosteroids, poor tolerance and as sparing
agents when high doses of corticosteroids are needed for a long time. In some strictly selected
cases refractory to standard therapy, specific antiTNF-alpha agents may offer precious
improvement. Some patients benefit from topical corticosteroids.
References
Mihailovic-Vucinic V, Jovanovic D. Pulmonary sarcoidosis. Clin Chest Med. 2008;29:459-
73, viii-ix.
Nunes H, Bouvry D, Soler P, Valeyre D. Sarcoidosis. Orphanet J Rare Dis. 2007;2:46.
1.43 Answer: D
Small cell lung cancer (SCLC) is considered distinct from the other lung cancers, called
non–small-cell lung cancers (NSCLCs), because of their clinical and biologic characteristics.
SCLC exhibits aggressive behavior, with rapid growth, early spread to distant sites, exquisite
sensitivity to chemotherapy and radiation, and frequent association with distinct
paraneoplastic syndromes (shown below in Table). Surgery usually plays no role in its
management, except in rare situations (<5% of patients) in which it presents at a very early
stage as a solitary pulmonary nodule. Even then, adjuvant chemotherapy after surgical
resection is recommended, since SCLC always should be considered a systemic disease.
In this vignette the patient has features of Cushing syndrome secondary to ectopic ACTH
production.
References
Samson DJ, Seidenfeld J, et al.; American College of Chest Physicians. Evidence for
management of small cell lung cancer: ACCP evidence-based clinical practice guidelines
(2nd edition). Chest. 2007;132(3 Suppl):314S-323S.
Walker S. Updates in small cell lung cancer treatment. Clin J Oncol Nurs. 2003;7:563-8.
Shahzad G. Raja
116
Organ System
Syndrome
Mechanism
Frequency
Endocrine
SIADH
Antidiuretic hormone
5-10%
Ectopic secretion of ACTH
Adrenocorticotropic
hormone
5%
Atrial natriuretic factor
Neurological
Eaton-Lambert reverse
myasthenic syndrome
5-6%
Subacute cerebellar
degeneration
Subacute sensory neuropathy
Limbic encephalopathy
Anti-Hu, Anti-Yo
antibodies
1.44 Answer: B
The lung is the most common site of metastatic neoplasms. Pulmonary metastases most
frequently occur with tumours that have rich systemic venous drainage. Examples of such
metastases include renal cancers, bone sarcomas, choriocarcinomas, melanomas, testicular
teratomas, and thyroid carcinomas. Most pulmonary metastases arise from common tumours,
such as breast, colorectal, prostate, bronchial, head-and-neck, and renal cancers.
Resection of pulmonary metastases is reasonable and is commonly performed for patients
whose primary disease is controlled and for whom the metastatic burden in the chest is such
that all disease can be resected safely. The use of video- assisted thoracic surgery rather than
an open approach in metastasectomy, however, is still being debated. In addition,
nonresectional therapies such as radiofrequency ablation and stereotactic body radiation
therapy are being used in centers for patients with oligometastases to the lungs.
References
Zheng Y, Fernando HC. Surgical and nonresectional therapies for pulmonary metastasis. Surg
Clin North Am. 2010;90:1041-51.
Erhunmwunsee L, D'Amico TA. Surgical management of pulmonary metastases. Ann Thorac
Surg. 2009;88:2052-60.
1.45 Answer: B
Transudates are ultrafiltrates of plasma in the pleura caused by a small, defined group of
aetiologies. The following cause transudates:
Congestive heart failure
Cirrhosis (hepatic hydrothorax)
Atelectasis (which may be due to malignancy or pulmonary embolism)
Hypoalbuminaemia
Nephrotic syndrome
Peritoneal dialysis
Myxoedema
Constrictive pericarditis
Basic Sciences: Answers
117
Laboratory testing helps distinguish pleural fluid transudates from exudates; however,
certain types of exudative pleural effusions might be suspected simply by observing the
quality of the fluid obtained during thoracentesis.
Frankly purulent fluid indicates an empyema.
A putrid odor suggests an anaerobic empyema.
A milky, opalescent fluid suggests a chylothorax, resulting most often from
lymphatic obstruction by malignancy or thoracic duct injury by trauma or surgical
procedures.
Grossly bloody fluid indicates the need for a spun hematocrit test of the sample. A
pleural fluid hematocrit level of more than 50% of the peripheral hematocrit level
defines a hemothorax, which often requires tube thoracostomy.
The initial diagnostic consideration is distinguishing transudates from exudates. The fluid
is considered an exudate if any of the following apply:
Pleural fluid to serum protein ratio more than 0.5
Pleural fluid to serum lactate dehydrogenase (LDH) ratio more than 0.6
Pleural fluid LDH more than two thirds of the upper limits of normal serum value
References
Light RW. Pleural effusions. Med Clin North Am. 2011;95:1055-70.
Porcel JM, Light RW. Diagnostic approach to pleural effusion in adults. Am Fam Physician.
2006;73:1211-20.
1.46 Answer: B
Chylothorax refers to the presence of lymphatic fluid in the pleural space secondary to
leakage from the thoracic duct or one of its main tributaries. The aetiology of chylothorax
includes:
Nontraumatic
Malignant etiologies account for more than 50% of chylothorax diagnoses and are
separated into lymphomatous and nonlymphomatous. Lymphoma is the most
common cause, representing about 60% of all cases, with non-Hodgkin lymphoma
more likely than Hodgkin lymphoma to cause a chylothorax. By comparison,
nonlymphomatous causes are rare.
Nonmalignant aetiologies are separated into idiopathic, congenital, and
miscellaneous. Clinicians must rule out all possible malignant causes before
designating the chylothorax as idiopathic.
Congenital chylothorax is the leading cause of pleural effusion in neonates.
Miscellaneous causes include cirrhosis, tuberculosis, sarcoidosis, amyloidosis, and
filariasis.
Shahzad G. Raja
118
Traumatic
Trauma is the second leading cause of chylothorax (25%). Iatrogenic injury to the
thoracic duct has been reported with most thoracic procedures. In particular,
cardiothoracic surgery has been associated with 69-85% of cases of chylothorax in
children.
Nonsurgical traumatic injury is a rare cause, usually secondary to penetrating trauma.
Pseudochylothorax
Chylothorax must be distinguished from pseudochylothorax, or cholesterol pleurisy,
which results from accumulation of cholesterol crystals in a chronic existing effusion.
The most common cause of pseudochylothorax is chronic rheumatoid pleurisy, followed
by tuberculosis and poorly treated empyema.
References
Huggins JT. Chylothorax and cholesterol pleural effusion. Semin Respir Crit Care Med.
2010;31:743-50.
Skouras V, Kalomenidis I. Chylothorax: diagnostic approach. Curr Opin Pulm Med.
2010;16:387-93.
1.47 Answer: A
Sputum cytology examines a sample of sputum (mucus) under a microscope to determine
whether abnormal cells are present. Sputum has some normal lung cells in it. Sputum
cytology may be done as the first diagnostic test to help detect lung cancer and certain
noncancerous lung conditions. A sputum sample may be collected:
By a person coughing up mucus
By breathing in a saltwater (saline) mist and then coughing
During bronchoscopy
Sputum cytology is the least invasive means of obtaining a diagnosis in a patient who is
suspected of having lung cancer. The diagnostic accuracy of sputum cytology, however, is
dependent on rigorous specimen sampling (at least three specimens) and preservation
techniques, as well as on the location (central vs peripheral) and size of the tumour. Patient
characteristics associated with positive cytologic diagnosis on sputum include the following:
bloody sputum; low FEV
1
values; large lung tumours (> 2.4 cm); centrally located tumours;
and squamous cell cancers.
Sputum cytology is particularly useful in patients who present with centrally located
tumours (i.e., SCLC or squamous call carcinoma) and in those who present with haemoptysis.
The sampling of sputum specimens should certainly be considered in a patient who presents
with a central lesion with or without radiographic evidence of metastatic disease, in whom a
semi-invasive procedure such as bronchoscopy or trans-thoracic needle aspiration might pose
a higher risk. The previously published and the more recently performed systematic literature
reviews found 17 studies providing data on the performance characteristics of sputum
cytology for the diagnosis of suspected lung cancer. Sensitivity ranged from 0.42 to 0.97;
specificity ranged from 0.68 to 1.0. The pooled sensitivity was 0.66, and the pooled