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American Manualof Examination

in Medicine(2CK)

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ISBN full edition: 978-84-16276-21-9

DISCLAIMER

Medicine is a science subject to constant change. As research and clinical experience widen our knowledge, treatments and pharmacotherapy changes are necessary. The editors of this work have veri ed their results against reliable sources, in an e ort to provide general and complete information, according to the accepted criteria at the time of publication. Nevertheless, given the fact that human error may occur or that some changes may take place in medical sciences, neither the editor nor any of the contributors involved in the preparation or publication- of this work can guarantee that the content herein is accurate and complete in each and every aspect. The editors and the contributing sources cannot be held responsible for any errors, omissions or the outcome derived from the use of the information provided herein. Therefore, readers are recommended to verify the content of this work against other sources. As an example, it is especially advisable to read the package insert of any drug to be administered to ensure that the information furnished by this publication is accurate and no modi cations were made either to the recommended dose or to the contraindications for administering said drug. This recommendation is particularly signi cant in relation to new or seldom used drugs. Readers should also check with their own laboratory about normal values.

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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


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






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


4

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


6

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


8

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.


10

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


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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

usmle 01 1415 manual nm

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