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American Manualof Examination
in Medicine(2CK)
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Pne
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American Manualof Examination
in Medicine(2CK)
AuthorPatricia Clares Montn
Amer ican Manual of Examinat ion in Medicine (2CK)
01. Obstructive Pulmonary Diseases .........................................1
1.1. Asthma ..................................................................................................................................................11.2. Bronchiectasis ............................................................................................................................21.3. COPD ........................................................................................................................................................3
02. Restrictive Lung Diseases ..........................................................5
03. Interstitial Diseases ..............................................................................5
3.1. Sarcoidosis.......................................................................................................................................53.2. Hypersensitivity Pneumonitis ............................................................................73.3. Pulmonary Eosinophilia ..............................................................................................7
04. Acute Respiratory Failure ...........................................................7
4.1. Hypoxemia ......................................................................................................................................74.2. Respiratory Distress Syndrome in Adults ............................ 8
05. Pulmonary Vascular Disease ..................................................8
5.1. Pulmonary Hypertension ..........................................................................................85.2. Venous Thromboembolic Disease ...............................................................95.3. Lung Cancer ..............................................................................................................................10
06. Pleural Pathology ................................................................................10
6.2. Pneumothorax.......................................................................................................................11
Index
Pneumology
1
Chapter 01
Obstructive
Pulmonary Diseases
They are characterized by a di culty emptying the lung, keeping a normal air inlet in most cases. They are therefore characterized by a decrease in expiratory fl ow and increased residual volume (RV) (Figure 1, Table 1).
Initi ally midexpiratory fl ows decrease (FEF 25-75%) and next, the Ti e-neau Index (FEV/TLC) lowers; this parameter defi nes and characterizes these diseases.
Among the diseases associated with this breathing patt ern are: asthma, COPD, bronchiectasis and cysti c fi brosis.
TLC
VC
IC
FRC
Volumen (liters)
IRV
ERV
RV
VC
Figure 1. Static pulmonary volumes
1.1. Asthma
Chronic infl ammatory airway disease with bronchial hyperreacti vity, re-versible and variable in its clinical course.
Symptoms
Typical symptoms are dry cough, shortness of breath, wheezing and chest pain.
Characteristi cally, symptoms usually occur more frequently at night or at dawn.
Other forms of atypical manifestati ons are chronic cough and asthma induced by e ort.
Diagnosis
Based on clinical suspicion along with reversible airway obstructi on demonstrati on, bronchial hyperresponsiveness or variability in lung functi on (Figure 2).
Figure 2. Diagnostic algorithm of asthma
Spirometry: the diagnosis is confi rmed by demonstrati ng an obs-tructi ve breathing patt ern accompanied by reversibility (improved lung functi on by more than one 12%) in response to a bronchodi-lator treatment. A normal spirometry does not discard the disease; in this case presence of bronchial hyperreacti vity or lung functi on variability should be investi gated.
Bronchial hyperresponsiveness: it is diagnosed with a bronchopro-vocati on test using histamine, methacholine or exercise. It is positi -ve if FEV1 decreases more than 20%.
TLC RV VC FEV1 TIFFENEAU MIP MEP
Obstructive: N or N or N or (< 70%) N NRestrictive parenchymal: N or N or
(80%)N N
Restrictive inspiratory extraparenchymal or N N or N or (80%)
N or *
N
Restrictive inspiratory and expiratory extraparenchymal
N or Variable N or *
N or *
* Values are reduced in neuromuscular disease (N: normal)
Table 1. Ventilatory function alterations
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2
Treatment in Exacerbations
See Figure 3.
1.2. Bronchiectasis
Abnormal and irreversible bronchial dilati on medium size (greater than 2 mm) because of the destructi on of the elasti c and muscular compo-nents of the wall.
Etiology
Localized bronchiectasis: Infecti ons: adenovirus, measles, rubella and infl uenza. The bac-
teria include staphylococcus, Klebsiella and anaerobes. Endobronchial obstructi on: pulmonary carcinoma, carcinoids. In
children the most common cause is the aspirati on of foreign bodies.
Di use bronchiectasis: Pulmonary origin: toxic, necroti zing bacterial or viral infecti ons,
BPAA. Extrapulmonary origin: BPAA, congenital or acquired immu-
no-defi ciencies, HIV, cysti c fi brosis, primary ciliary dyskinesia, Youngs syndrome, defi ciency of alpha1 anti trypsin.
Symptoms and Diagnosis
They are characterized by the presence of chronic producti ve cough or purulent bronchorrhoea. Hemoptysis is usually mild and appears in nearly half of pati ents.
Variability: it is esti mated by serial measurements of peak fl ow for about 1-2 weeks.
FeNO: indicates eosinophilic airway infl ammati on, although it sti ll has not been establihed as a diagnosti c test as its fi gures will be normal in not-atopic individuals.
Chest x-ray: in intercriti cal period it is usually normal. Occasionally, radiologic signs of air trapping are present.
Treatment
1. General measures: identi fy and avoid specifi c allergens, nonspecifi c irritants and noxious drugs.
2. Drugs: Inhaled corti costeroids: treatment of choice. They reduce symp-
toms, exacerbati ons and bronchial hyperreacti vity. Inhaled beta-adrenergic: they are never to be used in monothera-
py as they may worsen disease monitoring in the long term. They are very e ecti ve associated with inhaled corti costeroids. These include salmeterol, formoterol and indacaterol.
Theophylline: they are drugs with bronchodilator acti on with moderate anti -infl ammatory acti on.
Cromones: they stabilize the membrane with moderate anti -in-fl ammatory acti on. They are e ecti ve in exercise-induced asth-ma.
Monoclonal anti IgE anti bodies: administered subcutaneously. Used in asthma in advanced stages of extrinsic dominance if no control is achieved with common drugs.
Leukotrine receptors antagonist: they are e ecti ve anti -infl am-matories in stress induced asthma.
3. Immunotherapy.
Treatment in Stable Phase (Table 2)
Decrease Therapeutic Stages Increase
STEP 1 STEP 2 STEP 3 STEP 4 STEP 5 STEP 6
MAINTENANCE TREATMENT
Of choice Inhaled glucocorticoid at low doses
Inhaled glucocorticoid a low dose + long-acting adrenergic 2 agonist
Inhaled glucocorticoid at moderate dose + long-acting adrenergic 2 agonist
Inhaled glucocorticoid at high dose + long-acting adrenergic 2 agonist
Inhaled glucocorticoid at high dose + long-acting adrenergic 2 agonist + oral glucocorticoid
Other options
Antileukotriene Inhaled glucocorticoid at moderate doses
Inhaled glucocorticoid at low doses + antileukotriene
Inhaled glucocorticoid at low doses + antileukotriene
Add
Antileukotriene and/or theophylline and/or omalizumab
Add
Antileukotriene and/or theophylline and/or omalizumab
Upon demand
Short-acting adrenergic 2 agonist
Short-acting adrenergic 2 agonist
Short-acting adrenergic 2 agonist
Short-acting adrenergic 2 agonist
Short-acting adrenergic 2 agonist
Short-acting adrenergic 2 agonist
Education, environmental control, treatment of comorbidities
Consider allergen immunotherapy
Table 2. Treatment of asthma according to the level of control
Pneumology
3
The chest x-ray can be normal or show typical images as swallows nest, rail tram or in signet ring; although unspecifi c, they are best observed with high-resoluti on CT.
Bronchoscopy is indicated if there is hemoptysis and when they are localized.
Once the diagnosis is established, the eti ologic study must be made to treat the primary cause.
Treatment
It is based on: Removing, if present, bronchial obstructi on. Improving the removal of secreti ons with hydrati on, chest physio-
therapy and postural drainage. Controlling infecti ons with anti bioti cs in
exacerbati ons for 10-15 days.
1.3. COPD
Characterized by airfl ow limitati on not fully reversible, reversible and progressive, caused by an abnormal reacti on of the lungs upon exposure to certain harmful substances, espe-cially tobacco smoke.
There are two classic phenotypes of the disease:
Chronic bronchiti s is defi ned by the presence of cough and expec-torati on for at least three months a year for two consecuti ve years.
Emphysema: consists of the dilatati on of acini and alveolar wall des-tructi on.
Symptoms and Diagnosis
Most common symptoms are cough, expectorati on and dyspnea. It is very common to show a history of acti ve or past smoking of at least 20 packs/year.
The main di erences between the two phenotypes are collected in Table 3.
Diagnosis is based on the symptoms and the demonstrati on of airfl ow limitati on in spirometry (post-bronchodilator TI less than 0.7).
Figure 3. Management of acute asthma
TYPE ACIUS LOCATION LUNG LOCATION RELATED CAUSES OR FACTORS
Centroacinar Central (respiratory bronchiole)
Upper areas Smoking, elderly
Panacinar Uniform Lower areas Diff use in AAT defi ciency Occasionaly focal in elderly
and smokers, associated with central-acinar in upper lobes
Distal or paraseptal acinar
Distal (alveolar septa, alveolar ducts and alveoli)
Subpleuralin upper areas
Young Spontaneous pneumothorax
for rupture of apical bullae. The airfl ow is usually preserved
Table 3. Variants of emphysema
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The assessment of the severity should be established by evaluati ng the symp-toms with dyspnea scale COPD Assessment Test, the severity of the obstruc-ti on esti mati ng the FEV1 and the risk of exacerbati ons (Table 4, Figure 4).
The pati ent is considered at high risk of exacerbati on if in their clinical history at least two exacerbati ons have been observed in the last year or if FEV1 is less than 50% (Table 5).
DEGREE ACTIVITY
0 Absence of dyspnea except with strenuous exercise
1 Dyspnea when walking fast in plain, or when walking up a gentle slope
2 Dyspnea produces an inability to keep up with others of the same age walking in plain or having to stop a rest when walking in plain at their own pace
3 Dyspnea makes them stop to rest when walking about 100 meters or after a few minutes of walking in plain
4 Dyspnea impedes the patient from leaving home or appears with activities such as dressing or undressing
Table 4. Modi ed Medical Research Council dyspnea scale (mMRC)
Degree FEV1 (% Of theoretical)
I (mild) 80
II (moderate) 50-80
III (severe) 30-50
IV (very severe) 30
Table 5. Assessment of the severity of obstruction to the ow
Based on these three parameters the severity is established in four cat-egories (Figure 5):
Risk
(s
ever
ity o
f obs
truc
tion)
Risk
(e
xace
rbat
ions
)
Symptoms(mMRC or CAT)
mMRC 0-1CAT < 10
4
3
2
1
2
1
0
mMRC 2CAT 10
(A) (B)
(C) (D)
Figure 5. Combined rating of the severity of the COPD
Treatment
Nonpharmacolgic measures: abandonment of tobacco and chronic in-home oxygen therapy are the most important measures and have been shown to increase survival in the disease. Others are respiratory rehabi-litati on, in-home non-invasive mechanical venti lati on, or surgical measu-res such as bullectomy, lung volume reducti on or lung transplantati on.
Pharmacologic measures: pneumococcal vaccinati on and infl uenza. The main drugs in this disease are bronchodilators such as anti cholinergic or beta2-agonists. Other bronchodilators include, even much less e ec-ti ve, theophylline. Anti -infl ammatory drugs may also be used such as corti costeroids or PDE4 inhibitors. The latt er are recommended conco-mitanly with bronchodilators in the most severe stages and with BHR.
In exacerbati ons, therapeuti c management is based on the use of in-haled bronchodilators and systemic corti costeroids. The main cause of exacerbati ons are infecti ons so that in many cases it is advisable to add anti bioti c treatment that covers the germs most frequently involved. Add oxygen therapy and other measures, if necessary, as invasive and nonin-vasive mechanical venti lati on in additi on.
I never cough I am always coughing0 1 2 3 4 5
I do not have phlegm (mucus)in chest
My chest is completely filled with phlegm (mucus)
0 1 2 3 4 5
I do not feel any oppression in my chest
I feel a lot of oppression in my chest
0 1 2 3 4 5
When I climb a slope or a flight of stairs, I am not short of breath
When I climb a slope or a flight of stairs I am very short of breath
0 1 2 3 4 5
I do not feel limitation to perform household activities
I feel very limited for domestic activities0 1 2 3 4 5
I sleep without problemsI have trouble sleeping because of the lung condition that I suffer
0 1 2 3 4 5
I feel safe leaving the house in spite of the lung condition that I suffer
I do not feel safe leaving home because of the lung condition that I suffer
0 1 2 3 4 5
I have great energy I have no energy0 1 2 3 4 5
Figure 4. Questionnaire COPD Assessment Test
Pneumology
5
Chapter 02
Restrictive Lung
Diseases
They are characterized by the di culty in fi lling pulmonary air which causes a decrease in lung volumes, especially the TLC which is what defi nes the disorder.
Chapter 03
Interstitial Diseases
This term encompasses more than 100 diseases that a ect the intersti -ti al ti ssue (Table 6). Symptoms, pathophysiology, functi onal and radio-logic study are very similar in all of them. Certain characteristi c aspects of every enti ty do not help to make a di erence and, therefore, to guide the diagnosis in these pati ents (Figure 6).
BAL may be diagnosti c in certain enti ti es such as histi ocytosis X or alveo-lar proteinosis. In most cases it only orients diagnosis.
The functi onal fi ndings we fi nd are a decreased di usion capacity (DLCO of less than 80%) and on spirometry a restricti ve breathing al-terati on, although in certain diseases, an obstructi ve patt ern can also be seen.
DISEASES INVOLVING INFLAMMATION AND/OR FIBROSIS
Known cause Unknown cause
Asbestosis Drugs Radiation Related to smoking:
- Desquamative interstitial pneumonia
- DILD associated with respiratory bronchiolitis
- Langerhans cell histiocytosis
Idiopathic pulmonary fi brosis* Lymphangioleiomyomatosis Pulmonary eosinophilia Alveolar proneinosis
GRANULOMATOUS DISEASES
Known cause Unknown cause
Silicosis Hypersensitivity Pneumonitis Berylliosis
Sarcoidosis Vasculitis** Bronchocentric granulomatosis
* Included pulmonary fi brosis associated with conjunctivepathies and other idiopathic interstitial pneumonias (except those related to smoking)
** Wegener granulomatosis, Churg-Strauss granulomatosisDILD: diff use interstitial lung disease
Table 6. Classi cation of interstitial lung disease
The treatment is usually supporti ve. In exacerbati ons corti costeroids can be considered and other immunosuppressants can be adminis-tered. Ocasionally, it is necessary to indicate lung transplantati on.
Few intersti ti al diseases have a specifi c established treatment.
3.1. Sarcoidosis
Systemic granulomatous disease of unknown eti ology. It usually a ects women at young ages and it is more common in black people.
Symptoms
Generally a ects the lung.
In approximately 25% of pati ents it presents in an acute form with consti tuti onal symptoms whether or not associated with respiratory symptoms. There are specifi c acute forms such as Lofgrens syndrome or Heerfordt-Waldenstrom syndrome. In other cases it occurs in the chronic form where any organ may be a ected (Figure 7).
Anterior uveitis
Diabetes insipidus
Upper respiratory tract involvement
Parotid hypertrophy
Adenopathies
Interstitial involvement
Splenomegaly
Mild anemiaNeutropenia
Testicular enlargement
Erythema nodosum
Migratory arthritis migration of great joints
Hypercalciuria
Hepatomegaly Enzymatic alterations
Facial paralysis
Lupus pernio
Figure 7. Clinical manifestations of the sarcoidosis
Amer ican Manual of Examinat ion in Medicine (2CK)
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Figure 6. Radiologic patterns of interstitial diseases
Pneumology
7
Diagnosis
It is based on histology. The lung is the organ most frequently biopsied. The presence of caseati ng granulomas needs to be proven in a compat-ible clinical functi onal and radiologic context.
Treatment
It is based on administrati on of corti costeroid treatment in cases in which advanced radiologic evidence is accompanied by relevant func-ti onal or clinical alterati on as well as in cases where a vital organ is com-promised (heart, CNS, etc).
3.2. Hypersensitivity Pneumonitis
It is bronchi and alveoli infl ammati on because of organic dust exposure.
Most of the responsible agents derive from occupati onal exposures.
Hypersiti vity pneumonia clinical presentati on is categorized into: Acute: fever, dyspnea and signifi cant clinical and radiologic a ec-
tati on because of exposure in a short ti me (days or weeks) to high concentrati ons of anti gen. The a ectati on usually predominates in the lung bases.
Subacute: exposures for weeks or months to lower concentrati ons than the acute form. Symptoms are usually asthenia, low-grade fe-ver, weight loss, night sweats, etc.
Chronic: exposure for years to lower concentrati ons than in the above forms. Typical symptoms are chronic and progressive dysp-nea and dry cough, similar to any lung fi brosis. It usually a ects the lung apices.
Diagnosis
It is based on the presence of compati ble clinical, radiologic and func-ti onal picture.
Treatment
Avoid exposure to the responsible agent.
In subacute and chronic forms, systemic corti costeroid.
3.3. PulmonaryEosinophilia
Processes characterized by pulmonary infi ltrates with eosinophils, almost al-ways accompanied by peripheral eo-sinophilia (Table 7).
Characteristi c symptoms are chronic dyspnea, cough with low-grade fe-ver or fever on some occasions.
KNOWN CAUSE
Parasites Drugs (nitrofurantoin, amiodarone,
sulfasalazine) Aspergillosis/allergic bronchopulmonary
mycosis
UNKNOWN CAUSE
Leffl er Syndrome Acute eosinophilic pneumonia Chronic eosinophilic pneumonia Churg-Strauss syndrome (allergic
granulomatosis and angiitis) Hypereosinophilic syndrome
Table 7. Eosinophilic lung diseases
Treatment consists of treati ng the cause of the acute exacerbati ons and concomitant superinfecti ons. If the cause is not identi fi ed corti coste-roids can be used.
Chapter 04
Acute Respiratory
Failure
4.1. Hypoxemia
It is defi ned by the decrease of pO2 below 80 mmHg. If values are lower than 60 mmHg, it is called parti al respiratory failure, type I or hypoxemic (Figure 9).
Global respiratory failure is defi ned by pCO2 values above 45 mmHg.
Hypoxemia
Hypoventilation D(A-a)O2
D(A-a)O2 PaO2 corrects with O2?
FiO2
Yes
Extrapulmonary (Intox. opioids)
Pulmonary (COPD)
Shunt Alt. V/QAlt. diffusion
No
or N
N
N
PaCO2
Figure 9. Diagnostic algorithm of the hypoxemia
Amer ican Manual of Examinat ion in Medicine (2CK)
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Respiratory failure is defi ned by blood gas levels and not by the clinical situati on of the pati ent, since, based on the triggering cause and ti me of evoluti on, we may fi nd asymptomati c pati ents with litt le clinical impact or pati ents with signifi cant respiratory e ort, dyspnea, cyanosis, etc.
It is interesti ng to consider the algorithm in Figure 9 bearing in mind some of the responsible causes and other parameters to be analy-zed.
Treatment
There are two main treatments: Eti ology. Oxygen therapy to try to keep the pO2 above 60 mmHg and sa-
turati ons esti mated by pulse oximetry above 90%. Note that oxygen therapy in pati ents retaining carbon should be establis-hed at the lowest possible oxygen fl ow. If conventi onal oxygen therapy is not su cient, other opti ons should be considered, for example, mechanical venti lati on in invasive and noninvasive modaliti es.
4.2. Respiratory Distress Syndrome in Adults (Table 8, Figure 10)
Diagnosis
Diagnosti c criteria are as follows: Presence of underlying cause (sepsis of any origin being the most
common). Presence of bilateral radiographic infi ltrates (bilateral white
lung). Rule out cardiogenic origin (PCP or custom interlock). PaO2/FiO2 quoti ent lower or equal to 200.
Figure 10. Respiratory distress syndrome in adults
DIRECT INJURY
Pneumonia Inhalation of toxic substances Aspiration of gastric contents Pulmonary contusion
INDIRECT INJURY
Sepsis Polytrauma Burns Pancreatitis Polytransfusions
Table 8. Causes of acute respiratory distress
Treatment
It is based on identi fying the triggering cause, ensuring adequate nu-triti on, preventi on of thromboembolic disease and pulmonary hemor-rhage and the treatment of respiratory failure.
The use of low ti dal volumes, preventi on of alveolar collapse by apply-ing positi ve pressure at the end of expirati on (PEEP) and venti lati on in a prone positi on, stand out among other venti lati on strategies.
Chapter 05
Pulmonary
Vascular Disease
5.1. Pulmonary Hypertension
This is defi ned as an increase in high blood pressure in the pulmonary artery above 25 mmHg at rest.
The current classifi cati on defi nes fi ve PHT types (Table 9).
GROUP 1
PULMONARY ARTERIAL HYPERTENSION
Idiopathic Familial Associated with:
- Connective tissue diseases - Portal hypertension - HIV infection - Congenital left-right shunt - Drugs and toxins - Other (thyroid disorders,
glycogen storage diseases [Gaucher] hemoglobinopathies, myeloproliferative disorders, splenectomy)
Capillary or venous involvement: - Veno-occlusive disease - Pulmonary capillary
hemangiomatosis
Persistent pulmonary hypertension in newborn
Table 9. Classi cation of pulmonary hypertension (continued)
Pneumology
9
GROUP 2
PULMONARY HYPERTENSION SECONDARY TO LEFT HEART
DISEASES
Cardiomyopathies Mitral or aortic valvulopathy
GROUP 3
PULMONARY HYPERTENSION SECONDARY TO CHRONIC LUNG DISEASES AND/OR HYPOXEMIA
COPD Interstitial diseases Alveolar hypoventilation
syndromes Sleep apnea syndrome
GROUP 4
CHRONIC PULMONARY THROMBOEMBOLIC
HYPERTENSION
Proximal thromboembolism Distal thromboembolism Nonthrombotic embolism
GROUP 5
OTHER
Sarcoidosis Langerhans cells pulmonary
Histiocytosis Lymphangiolemyomatosis Extrinsic vascular compression
(lymphadenopathy, tumors, fi brosing mediastinitis)
Table 9. Classi cation of pulmonary hypertension
In primary pulmonary hypertension, the most common clinical mani-festati on is chronic dyspnea. Other manifestati ons may be hemoptysis, angina or syncope.
Complementary examinati ons reveal few specifi c fi ndings, and trans-thoracic echocardiography is the diagnosti c test screening upon high clinical suspicion. Upon an elevated systolic PAP higher than 35 mmHg the test giving the most accurate diagnosis is the catheterizati on of right caviti es when esti mati ng the mean PAP, ruling out other causes of PHT and allowing vasoreacti vity testi ng which indicates initi al treatment in these pati ents.
The treatment of pulmonary hypertension is based on anti coagulant and vasodilator drugs according to its functi onal status.
5.2. VenousThromboembolicDisease (VTD)
This includes both deep vein thrombosis (DVT) and pulmonary throm-boembolism (PT).
It is considered a disease whose incidence is underdiagnosed and in which mortality rate is around 10%.
Risk Factors
History of VTD. Immobilizati on, surgeries (abdominal, pelvic, trauma). Neoplasti c diseases. Taking oral contracepti ves, pregnancy, hormonal treatment in me-
nopause. Emerging risk factors: COPD, smoking, hypertension, obesity.
Economy Class Syndrome. Geneti c: hyperhomocysteinemia, V Leiden factor.
Symptoms
The most common symptom is the sudden onset of dyspnea. Depend-ing on the locati on of the embolus in the vascular system, it may be associated with symptoms such as pleuriti c chest pain, and hemoptysis and others such as syncope and hemodynamic instability in those cases of masive embolism.
We can fi nd calf pain, positi ve Homans sign, enlarged and temperature in member a ected by PVT.
Diagnosis
Chest x-ray: most frequently it is normal or with nonspecifi c alte-rati ons. Specifi c signs would be the hump of Hampton or sign of Westermarck.
ECG: sinus tachycardia is the most common fi nding. T wave in right precordial or the patt ern S1Q3T3 consti tute other fi ndings.
BAG: it usually shows hypoxemia and hypocapnia by hyperventi la-ti on. Furthermore, pCO2 values may be normal or high.
Transthoracic echocardiography and Doppler ultrasound of lower limbs. D-dimers: high sensiti vity and low specifi city. CT angiography of pulmonary arteries: is the fi rst choice screening
test; it is contraindicated in case of renal failure or allergy to con-trast and may be replaced by venti lati on perfusion scinti graphy or pulmonary resonance.
Pulmonary arteriography: it is the most certain diagnosis test.
Diagnosti c algorithm (Figure 11):
Estimation of clinical probability
Medium and low probability
High probability or patients admitted to hospital
D Dimer
Image techniquesHighNormal
ObservationNo RI
or contrast allergyRI
or contrast allergy
Angio-CT Scintigraphy
No diagnosisUltrasonic
of limbs
Treat DVT
Normal or abnormal
diagnosis
Pulmonary angiography
Figure 11. PT diagnostic algorithm
Treatment
Primary: fi brinolysis or embolectomy. Indicated in massive pulmo-nary thromboembolism.
Amer ican Manual of Examinat ion in Medicine (2CK)
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Secondary: anti coagulati on. Indicated in all pati ents. Heparins or oral anti coagulants can be used. Treatment must always be initi ated with heparin to prevent the initi al prothromboti c e ect of OCP unti l they reach adequate levels in blood.
If anti coagulati on is contraindicated, as in pati ents with acti ve blee-ding at the moment of diagnosis or those with recent surgeries of the CNS, the alternati ve is inserti on of a fi lter in the inferior vena cava.
5.3. Lung Cancer
The main cause of death in USA. The most important risk factor is smok-ing.
Pathologic Anatomy
There are four main histologic types: Epidermoid or squamous cells carcinoma. Small-cells anaplasti c carcinoma, oat cell or small cell. Adenocarcinoma, including broncho-alveolar variety. Nonsmall cells undi erenti ated carcinoma.
Symptoms
The most common symptom is cough. Other symptoms depend on the locati on of the primary tumor: in the peripheral locati on of the tumor, symptoms include chest pain and pleural e usion, whereas in the cen-tral locati on hemoptysis, dyspnea or obstructi ve pneumonia prevail.
Symptoms caused by adjacent structures being a ected by producti on of substances causing paraneoplasti c syndromes or by metastases. The most commonly a ected are the liver, central nervous system, bone and adrenal glands.
Diagnosis
It requires histologic confi rmati on generally obtained by bronchoscopy and transbronchial biopsy (Table 10, Table 11).
OCCULT CARCINOMA Tx N0 M0
STAGE 0 Tis N0 M0
STAGE IA T1a-b N0 M0
STAGE IB T2a N0 M0
STAGE IIAT1a-b, T2a N1 M0
T2b N0 M0
STAGE IIBT2b N1 M0
T3 N0 M0
STAGE IIIA
T1-2 N2 M0
T3 N1-2 M0
T4 N0-1 M0
STAGE IIIBT4 N2 M0
Any T N3 M0
STAGE IV Any T Any N M1a-b
Table 10. Stages of CNCP tumor
Once diagnosed, it is essenti al to determine the locati on and the degree of extension as well as the evaluati on of operability in potenti ally oper-able pati ents.
Treatment
It depends on the histology and the extension of the tumor.
In nonsmall cell tumors, stage I and II are resectable. Treatment with che-motherapy must also be added to stage II. Stage III someti mes is resect-able, requiring chemotherapy and radiotherapy, in other cases. Stage IIIB receives treatment with chemo and radiotherapy, and IV only chemother-apy. In localized small-cell tumors, radio and chemotherapy are given and if there is no lymph node tumoral involvement, surgery may be consid-ered. If the disease is widespread, it is treated only with chemotherapy.
Chapter 06
Pleural Pathology
It is the presence of fl uid in the pleural cavity. Typical symptoms are pro-gressive dyspnea and pleuriti c chest pain. During physical examinati on, hypoventi lati on or aboliti on of breath sounds in areas where e usion is located are found.
The diagnosis is performed with chest radiology in which the most common signs are: costophrenic posterior angle obliterati on in lateral projecti on or costophrenic lateral sinuses in PA chest radiology. As the amount of fl uid increases, the opacifi cati on of some hemithorax with the image of Damoiseau meniscus can be observed.
Upon any case of pleural e usion (Figure 12), an eti ologic study by per-forming a diagnosti c thoracentesis must be considered (Figure 13). In the initi al eti ologic study, Lights criteria will be used to determine whether the fl uid complies with the characteristi cs of exudate transudate (Table 12).
Figure 12. Right pleural e usion
Pneumology
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Figure 13. Thoracentesis technique
LIGHTS CRITERIA Proteins in pleural fl uid/protein in serum > 0.5 LDH in liquid/LDH in serum > 0.6 LDH in liquid greater than two-thirds of the normal serum limit
Table 12. Lights criteria
Treatment
It depends on the underlying cause. In complicated cases of pleural ef-fusion, it is necessary to place a drainage tube.
6.2. Pneumothorax
Presence of air in the pleural cavity.
The usual symptoms are sudden onset dyspnea and chest pain. Breath sounds to be heard in the area of the aerial camera.
T: PRIMARY TUMOR
Tx. Primary tumor that cannot be evaluated, or proven by malignant tumor cells in sputum or bronchial aspirate, without the tumor being visible by imaging or bronchoscopy
T0. Without evidence of primary tumor TIs. Carcinoma in situ T1. Tumor 3 cm in diameter, surrounded by healthy lung or visceral pleura, without bronchoscopic evidence of invasion
more proximal than the lobar bronchus (ie, main bronchus is not aff ected). It is subdivided into: - T1a: tumor 2 cm in diameter[1] - T1b: tumor > 2 cm but 3 cm diameter
T2. Tumor > 3 cm but 7 cm diameter, or tumor with any of the following data: - Main bronchus aff ected at a distance of more than 2 cm from the tracheal carina - Invasion of visceral pleura - Atelectasis or obstructive pneumonia extending to the hilar region, without aff ecting the entire lung. It is subdivided into:
T2a: tumor > 3 cm but 5 cm diameter T2b: tumor > 5 cm but 7 cm diameter
T3. Any of the following characteristics: - Tumor > 7 cm diameter - Direct invasion of any of the following structures: chest wall (including tumor of superior ulcus), diaphragm, phrenic nerve,
mediastinal pleura, parietal pericardium - Tumor in main bronchus at less than 2 cm from the tracheal carina, without aff ecting it - Obstructive pneumonia of the entire lung or atelectasis - Presence of tumor node(s) separated from the primary tumor but in the same lobe
T4. Tumor of any size that complies with any of the following characteristics: - Invasion of any of the following: mediastinum, great vessels, heart, recurrent laryngeal nerve, tracheal carina, esophagus,
vertebral body - Presence of tumor node(s) separated from the primary tumor, located in the same lung but in a diff erent lobe
N: REGIONAL GANGLIA
Nx. The presence of regional ganglia metastases cannot be evaluated N0. Absence of regional ganglia metastases N1. Metastases in peribronchial or ipsilateral hilar ganglia (region aff ected by direct extension) N2. Metastases in ipsilateral mediastinal and/or subcarinal ganglia N3. Metastases in contralateral (hilar or mediastinal) ganglia, or in scalene or supraclavicular ganglia (ipsilateral or contralateral)
M: METASTASES AT DISTANCE
Mx. Presence of metastases cannot be evaluated at a distance M0. Absence of metastases at a distance. M1. Presence of metastases at a distance. It is subdivided into:
- M1a: Any of the following: Presence of tumor nodule(s) in the organ contralateral to the primary tumor Presence of pleural tumor nodules Existence of pleural or malignant pericardial[2] eff usion
- M1b: Metastases at a distance[1] The uncommon superfi cial tumor of any size with invasive component limited to bronchial wall is also classifi ed as T1, although it extends proximally
to the main bronchus[2] Most pleural or pericardial eff usions of a patient with lung cancer are caused by the cancer. However, in some cases, eff usion related to the tumor can be
excluded and, therefore, be considered M0. For this purpose, eff usion must not be hematic or exudate and multiple studies of cytopathologic pleural fl uid (or pericardial) must be negative, as well as clinical judgment
Table 11. Classi cation TNM for CNCP
Amer ican Manual of Examinat ion in Medicine (2CK)
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Classiication
Traumati c. It must include iatrogenic (thoracentesis, central vascu-lar access, etc.).
Spontaneous. It occurs without previous trauma. Primary pneumotho-rax is considered to occur in young pati ents, more oft en in males, by rupture of unknown apical bullae. Secondary pneomothorax occurs in other diseases in which previous lung pathology existed.
Hypertensive. Catamenial.
To diagnose it, x-ray chest in special screenings such as forced inspira-tory or expiratory is required (Table 13).
Treatment
In cases of small pneumothorax if it is small in pati ents with litt le clinical impact, conservati ve management with administrati on of oxygen therapy at a high fl ow for 3-6 hours and discharge may be considered if there is no progression.
In case of large pneumothorax or if the pati ent is hemodynamically un-stable, inserti on of transthoracic tube drainage is required.
SMALL LARGE
< 3 cm >_ 3 cm
< 2 cm >_ 2 cm
Table 13. Calculation of the size of a pneumothorax