By
Prof. Mohammad Khairy ElBadrawy Professor of Thoracic Medicine Mansoura University 2009
Cardinal symptoms of chest diseases 1. Cough 2. Hemoptysis 3. Chest wheezes 4. Dyspnea 5. Chest pain •Www.MansFans.Com
1. Cough • Cough reflex is almost essential for life and by which the airways are maintained free of foreign matter. • Cough is the commonest symptom in chest diseases.
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Cough • Cough is considered chronic when lasts > 3 weeks. • It is an explosive expiratory maneuver, which may be a voluntary act, involuntary (reflex) or both to clear the airways. •Www.MansFans.Com
Components reflex arc:
of
the
1. Receptor sites: • Larynx, trachea and bronchi: (stretch or irritant receptors). • Terminal bronchioles and alveoli are: receptors sensitive to chemical stimuli, as inhalation or irritant gases. • Pleura & mediastinum.
larnx
trachea
bronchi
TB
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Components of the reflex arc: 1. Extrathoracic receptor sites: • Vagal branches as: • • • • •
Meningeal. Auricular. Buccal. Cardiac. Gastric.
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2. Stimuli: • Mechanical and chemical: irritation at receptor sites or irritation of the cough center by lesions in its locality. 3. Afferent nerves: a) Vagus nerve. b) Glossopharyngeal nerve. c) Trigeminal.
4. Center: • Cough center is present in the medulla oblongata. 5. Efferent: a) Vagus nerves: larynx. b) Intercostal nerves: intercostal respiratory muscles. c) Phrenic nerve: diaphragm. d) Pelvic nerves: pelvic muscles.
Components of cough maneuver: • Deep inspiration. •
Closure of the glottis tightly to entrap air within the lungs.
•
Forceful contraction of expiratory muscles (including abdominal muscles) consequently the pressure in the lungs rise.
•
Sudden opening of the glottis widely so that air under pressure in the lungs explodes outward with very high velocities carrying with it secretion and foreign matter.
Cough reflex is decreased by: • Laryngeal disorders: vocal cord paralysis, tracheostomy, laryngeal tumors and bulbar palsy. • Receptor site affection: Accommodation of cough receptors to repeated stimuli, as in the smoker who only coughs after his first cigarette of the day. • CNS depression: • General anaesthesia. • Alcohol or addict drug over dose. • Elderly. • Respiratory muscle disorders: • Chest pain. • Muscle weakness: myasthenia gravis. • Muscle paralysis: quadriplegia.
Hazards of cough I. To the patient: a) Thoracic: • Emphysema. • Rupture bullae or blebs leading to spontaneous pneumothorax and pneumomediastinum. • Haemothorax from tearing of adhesions. • Stress fracture of a rib. • Rupture of an aneurysm.
b) Extra thoracic: •
•
• •
Increased intraabdominal pressure: hernias, prolapse and stress incontinence. Increased intraocular pressure: subconjunctival and retinal hemorrhage and retinal detachment. Increased intracranial pressure: rupture of mycotic aneurysm. Post-tussive emesis, syncope and convulsions.
c) General: • •
Insomnia. Exhaustion and possibly neurosis.
II. To the community: transmission of infections.
Cough may be classified into: dry and productive: • Dry cough: it may be initiated by respiratory and non respiratory diseases; it is useless cough and should be suppressed. • Productive: it is initiated only from airway disease.
Causes of dry cough A) Respiratory causes: 1- Acute upper and lower respiratory tract infections: • • • •
Common cold. Acute rhinitis and sinusitis. Acute pharyngitis. Acute bronchitis, tracheitis and tracehobronchitis. • Pneumonias.
1. Allergy: • •
Bronchial asthma. Allergic rhinitis.
2. Pulmonary edema: • •
• •
Cadiogenic. ARDS
Pulmonary embolism. Tumors: – Bronchial adenoma – Bronchial carcinoma.
• • • •
FB inhalation. Pleural diseases. IPF and EAA. Mediastinal masses.
B) Non respiratory causes: • • •
Gastroesophageal reflux disease (GERD). Central causes: irritation of the cough center by lesions in its locality. Reflex: due to irritation of vagus branches: – – – – –
Meningeal branches: meningitis. Auricular branches: otitis media. Buccal branches: pharyngitis. Cardiac branches: cardiac arrhythmias. Gastric branches.
4. Drug induced: Use of ACE inhibitors. 5. Psychogenic cough.
Causes of productive cough (expectoration) Productive chough is initiated only from airway disease. 1. Acute upper respiratory tract infections. 2. Chronic sinusitis and allergic rhinitis: postnasal drip syndrome (PNDS). 3. Cigarette smoking. 4. Chronic bronchitis. 5. Pneumonia. 6. T.B. 7. Bronchial asthma.
1. Gastroesophageal reflux disease (GERD). 2. Suppurative lung disease. 3. Recurrent aspiration of eosophageal or oropharyngeal contents. 4. Congenital tracheoesophageal fistulae. 5. Inhaled foreign bodies. 6. Bronchial carcinoma. 7. Pulmonary edema.
• Special characters of cough: • • • • • •
Painful cough Whooping cough Bovine cough non explosive cough Brassy cough Barking cough Emetic cough
2. Special time of cough ocurrence: • Nocturnal cough – Left- sided heart failure and pulmonary edema. – Bronchial asthma. – Aspiration.
• After exertion (15min from start of exercise) exercise-induced asthma or cardiac aetiology. • Occupational asthma. • Early morning. • Emetic cough. •Www.MansFans.Com
Expectoration (productive cough) •
Expectoration entails the passage of sputum out of the respiratory tract. • Sputum is composed of expectorated or swallowed mucus contaminated by saliva, transudations from serum, exfoliated epithelial cells, glycoproteins and serum proteins (mainly albumin) and bacteriostatic proteins (lysozymes, lactoferrin, interferon, secretory IgA).
Differentiation of Sputum 1. Onset, course, duration. 2. Amount. 3. Color. 4. Consistency. 5. Smell. 6. Relation to day- time. 7. Relation to posture. 8. Associated haemoptysis.
Onset, course, duration
2.Onset: Acute: • Acute bronchitis. • Pneumonia. • Acute abscess. • Empyema with bronchopleural fistula. Gradual: • T.B. • Chronic bronchitis. • Bronchiectasis.
2. Course: • Progressive: – Infection uncontrolled by antibiotics.
• Regressive course: – Spontaneous improvement. – Good response to antibiotics.
• Intermittent course: – Chronic bronchitis. – Bronchiectasis.
3. Duration: • Long duration: – Chronic bronchitis – Chronic lung abscess.
• Short duration: – Acute bronchitis. – Pneumonia. – Acute lung abscess.
Amount A patient may swallow large amounts of sputum unconsciously. Volumes of more than 100ml sputum /day are defined as bronchorrhoea.
Causes: 1. Suppurative lung disease. 2. Chronic bronchitis. 3. Asthma. 4. Alveolar cell carcinoma. 5. Acute organophosphorous poisoning.
Relation to day -time 1. Chronic morning expectoration over years: as in chronic bronchitis. 2. Excessive amounts of sputum production mainly in the morning: suppurative lung diseases. 3. Variable morning or nocturnal expectoration: bronchial asthma. 4. Recent onset of sputum production: bronchopulmonary infections.
Relation to posture Only in suppurative lung diseases.
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Color of the sputum: (it may be diagnostic): 1. Green or thick yellow sputum usually means infection (the color and increased viscosity are due to its content of leucocytes). • Sputum stagnation containing leucocytes will turn green. It is due to liberation of the green enzyme verdoperoxidase or (myeloperoxidase) from the broken-down cells. • The first sputum produced in the morning in many patients with chronic bronchitis will be green, while that produced later in the day reverts to a clear color. • Asthmatic sputum laden with eosinophils: yellow or green color.
1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
Rusty sputum (brownish yellow). Red current jelly sputum. Haemoptysis. Anchovy sauce sputum. Black sputum. Reddish tinge of sputum mistaken as haemoptysis. Blue sputum. Watery sputum. Trichoptysis. Expectoration of chalky materials or small stones is characteristic of broncholithiasis.
Consistency of sputum • Thick sticky sputum difficult to expectorate occur in infections and bronchial asthma • Extremely thick tenacious sputum: occur in asthma. • Expectoration of intrabronchial tumors may occur, this is particularly important in metastatic renal carcinoma.
Smell of sputum • Offensive putrid odour: suppurative lung disease due to anaerobic infections. • G-ve infection: distinctive odour to sputum, similar to E-coli on a culture medium. These odors can be used as an initial guide for initial chemotherapy while a waiting the culture results.
Management of cough 1- Investigations: • Since most coughs are transient and related to U.R.T infection, it is normally appropriate to treat such a suspected infection and/or to wait for 2-3w before investigating further. • History will give clues to diagnosis. • ENT examination. • Chest X-ray. • X-ray sinuses if needed. • Sputum examination
Sputum examination a- Differentiation of sputum from saliva b- Bacteriological examination including gram stain and culture, and ZN stain and culture for TB. c- Examinations for fungi or parasites d- Cytological examination
1- Investigations (Cont): • Pulmonary function tests: spirometry. • Barium esophogography and/or 24-hour esophageal pH to monitor for silent gastroesophageal reflux disease (GERD). • Bronchoscopy (in certain cases). • HRCT chest (in cases with suspected bronchiectasis). • Non invasive cardiac studies as echocardiogram and ECG.
2- Treatment of the primary disease
3- Symptomatic treatment of cough a) Dry cough: cough sedatives b) Productive cough: • Expectorants • Mucolytics
Wheezes • •
• • •
Wheezes are musical adventitious lung sounds. It occurs due to airway narrowing either to spasm or endoluminal or extraluminal obstruction. It is a common complaint in patient with airway obstruction. Wheezes can be heard without stethoscope. Wheezes do not always indicate bronchial asthma.
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Mechanism: Fluttering of the airway wall is the mechanism responsible for production of wheezes and rhonchi. It occurs when air flows rapidly through a narrow airway (bronchospasm, thick secretions, edema), causing fluttering of the airway wall at one or more sites.
Causes of wheezy chest Generalized chest wheeze 1. Bronchial asthma. 2. COPD. 3. Bronchitis, tracheobronchitis. 4. Bronchiolitis. 5. Bronchiectasis. 6. Cystic fibrosis. 7. Allergic bronchopulmonary aspergillsis. 8. Carcinoid tumor. 9. Left sided heart failure (cardiac asthma). 10. Uremia (renal asthma). 11. Anaphylaxis.
Localized chest wheeze Localized bronchial obstruction: a) Intralumenal: • • • • •
FB inhalation. Mucus plugs Bronchial carcinoma. Carcinoid tumor. Endobronchial TB.
b) Lumenal. • Bronchial stenosis, stricture.
c) Extralumenal. • Compression by enlarged lymph node or a mediastinal mass.
Stridor • Stridor is a particularly loud musical sound of constant pitch • Most prominent during inspiration, • Heard at a distance from the patient. • Stridor indicates partial central and upper airway obstruction.
Causes of Stridor 1. In children – – – –
Viral croup Inhaled foreign body Acute epiglottitis Diphtheria
2. In adult – Chronic laryngitis – Vocal cord paralysis – Neoplasm of the larynx or trachea
Hoarseness of voice • Hoarseness is a rough, coarse quality of voice, occurring when a normal, smooth vocal cord is not brought into contact with its fellow. • It indicates: – Irregularities on the surface of one or both cords – Disorder of nerves and muscles responsible for vocal cord movement.
• Any patient with more than three weeks of hoarseness should be examined by indirect laryngoscopy.
2. Dyspnea Dyspnea is subjective complaint by the patient that can be expressed as: • • • • •
Difficulty of breathing. Difficult or laboured breathing. Undue awareness of breathing. Need to breath more. Uncomfortable or unpleasant breathing.
Mechanism of dyspnea: The concept of unbalanced demand for ventilation and ventilatory reserve (supply) demonstrates how dyspnea occurs. (A) Increased demand: Increase drive for respiration through stimulation of peripheral and central chemoreceptors by: fever, acidosis, anemia, hypoxemia, and hypercapnea.
(B) Reduced reserve of: • Airways: increased airway resistance that interfere with ventilation. • Lung parenchyma and pleura: decreased compliance that impair diffusion. • Pulmonary circulation: decreased perfusion. • Chest wall: • Respiratory muscle dysfunction (weakness, fatigue). • Kyphoscoliosis and obesity (extrathoracic restriction).
Demand
Demand
Reserve
•Normal
Reserve •Dyspnea
Mechanism of dyspnea: when there is no balance between demand and respiratory reserve
Causes of dyspnea A) Pulmonary causes: 1- Airway diseases: • • • •
Upper airway obstruction. Bronchial asthma. COPD. Localized bronchial obstruction either due to: • Extraluminal obstruction: as in mediastinal syndrome. • Intraluminal obstruction: as in foreign body or thick viscid secretions. • Lesions in the wall itself: as in tumors or stenosis.
2- Lung parenchyma diseases: • • • • • • • •
Pulmonary edema. Consolidation. Collapse. Interstitial pulmonary fibrosis. Post TB fibrosis. Sarcoidosis. Pneumoconiosis. Resection of a lobe or lung.
3- Pleural diseases: • • • •
Pneumothorax. Pleural effusion. Pleurisy. Pleural tumors.
4- Pulmonary circulation diseases: • Pulmonary hypertension. • Pulmonary embolism. • Intrapulmonary shunt.
5- Chest wall diseases: • Kyphoscoliosis and other chest wall deformities. • Respiratory muscles disorders. • Weakness and fatigue. • Diaphragmatic paralysis and eventration. • Myopathies, myasthenia gravis and myotonia.
• Obesity. • Thoracoplasty.
B) Cardiac causes: Left sided heart failure due to: • Increase preload: • Right to left shunt (Eisenminger's syndrome) • Mitral and aortic regurge.
• Increase afterload: mitral stenosis, aortic stenosis, systemic hypertension. • Muscle disorders: cardiomyopathy myocardial infarction. •Www.MansFans.Com
Chest Pain .3 • One of the commonest and important symptoms in cardiopulmonary practice. • Chest It is pain carries unique property as it may be just trivial due to myositis or catastrophic due to acute MI. • To know the etiology and to reach the anatomical origin of chest pain
Causes of chest pain •
Thoracic causes:
2. Chest wall. 3. Pleura. 4. Mediastinum: • • • • • •
Cardiac causes. Vascular causes. Oesophageal causes. Tracheal causes. Mediastinitus. Mediastinal tumors
Extrathoracic causes: •
•
Abdominal causes. Pancreatitis. Cholycystitis. Peptic ulcer. Functional chest pain.
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Management of chest pain: • •
Treatment of the cause. Pleuritic pain: • •
• • • •
Analgesics. Local anaesthetic nerve block.
Anginal pain: nitroglycerine. Myocardial infarction: morphia and nitroglycerine. Oesophageal pain: antispasmadics and antacids. Mediastinitis: analgesics and antibiotics even exploration thoracotomy may be indicated for aetiological treatment.
4. Haemoptysis • Haemoptysis is expectoration or coughing up of blood, or blood-tinged sputum from the lungs or tracheobroncheal tree below the level of vocal cords. • Spurious haemoptysis (false): it is that bleeding from sites above the level of VC. (nose, mouth, pharynx, larynx and must be examined carefully and investigated for any cause of bleeding).
Haemoptysis may be confused with haematemesis Haemoptysis History Previous chest symptoms as cough and expectoration. Color of blood Blood is red, frothy with alkaline pH and mixed with sputum. Sputum contains haemosiderin-laden macrophages. On examination Crepitation is heard over the affected side. After attack Many days after the attack, sputum will be mixed or stained with blood.
Haematemesis Previous history of heart burn, esophageal varices or peptic ulcer. Coffee-brown color, acidic pH and mixed with food.
Chest examination is free After the attack, melena will follow it.
Classification of hemoptysis 1) Based on anatomical basis: • True-haemoptysis: bleeding from tracheobronchial tree or the pulmonary parenchyma. • Pseudohaemoptysis or false haemoptysis: expectoration of blood aspirated into the respiratory tract from supraglottic region or gastroentistinal tract. • Factitious or simulated haemoptysis (voluntary induced by trauma): it is rare but should not be overlooked as a possible explanation of sudden episode of bleeding. It has been described for neurotic and aggressive young women.
2) According to severity: • Fatal haemoptysis. • Non fatal haemoptysis.
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3) According to amount: • Blood streaked sputum. • Mild haemoptysis < 20ml blood per 24 hours. • Moderate haemoptysis 20 - 200ml blood/24 hours. • Massive haemoptysis or life threatening haemoptysis: – Coughing up ≥ 150ml of blood in a single attack, which may fill the dead space of the bronchial tree (the patient may suffocate). – or 400ml blood within 3 hours. – or 500ml blood within 12 hours. – or 600ml blood within 24 hours.
Tuberculosis Bacterial pneumonia
Neoplasms
Miscellaneous
Bronchiectasis Cryptogenic
Bronchitis
Common causes of hemoptysis.
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Less common causes of hemoptysis • • • •
Mitral valve disease Good-pasture syndrome. Foreign body aspiration Primary hemorrhagic disease. • Systemic hypertension. • Lung abscess.
• • • •
Haemosiderosis. Aspergilloma. A-V malformation. Acute left ventricular failure. • Hematogenous amoebiasis. • False hemoptysis (nose, mouth, pharynx, larynx).
Most common causes of massive haemotpysis • Bronchiectasis. • Cavitating lung diseases 2ry to necrotizing infections as TB or fungus (mycetoma) cavity. • Bronchial carcinoma. • Mitral valve disease.
Fatal or exsanguinating haemoptysis • ≥ 150ml / attack. • ≥ 1000ml total loss. • It is the severe form of hemoptysis that may lead to death if not vigorously treated.
Most common causes of fatal hemoptysis: • • • •
Rupture of a bronchial artery in a TB or aspergilloma cavities. Following iatrogenic trauma to vascular tumors by biopsy forceps. Iatrogenic trauma to fibrotic lung with drill or needle. Rupture of aortic even pulmonary artery aneurysm.
Mechanisms of hemoptysis 1.
Intra-alveolar hemorrhage and diapedesis of the RBCs from pulmonary microvasculature into the alveoli (acute pulmonary edema).
3.
Necrosis of lung tissue with hemorrhage into the alveolar spaces (infarction).
5.
Rupture of distended endobronchial blood vessels (bronchial varices) as in mitral stenosis.
7.
Ulceration or erosion of the bronchial epithelium (bronchitis, brocholithiasis).
9.
Sloughing of a caseous tracheobronchial tree (TB).
lesion
into
the
•
Rupture of intrapulmonary collaterals: – Pulmonary A-V fistula (Osler- Weber- Rendu disease). – Bronchial artery -pulmonary venous collateral channels (bronchiectasis). – Systemic blood vessel -pulmonary venous collateral channels (sequestration).
•
Invasion of blood vessels (bronchial carcinoma or adenoma).
•
Necrosis of lung tissue associated with inflammation and rupture of blood vessels (necrotizing pneumonias and some parasitic infestations).
•
•
•
•
Rupture of an aortic aneurysm into the tracheobronchial tree (weeping aneurysm). Anticoagulants and immunosuppressive drugs causing intrapulmonary bleeding. With menstruation due to presence of endobronchial endometriosis (catamanial hemoptysis). Malingering. •Www.MansFans.Com
Clinical points in patients with hemoptysis • Repeated small hemoptysis: bronchial carcinoma, bronchiectasis or pulmonary emboli. • Repeated large hemoptysis: bronchiectasis, aspergilloma, lung abscess, TB. • Single or frequent hemoptysis with purulent sputum: acute bronchitis or acute exacerbation of chronic bronchitis. • Single or infrequent hemoptysis: bronchial carcinoma.
• Pleuritic pain or chest wall pain: pulmonary emboli, chest trauma or spontaneous pneumothorax. • With dyspnea: pulmonary emboli, central bronchial carcinoma or endobronchial tumor. • With wheezes: chronic bronchitis, bronchial carcinoma or adenoma or foreign body aspiration. • Heart disease: mitral stenosis. • Bleeding from other sites: haemostatic failure.
Examination: • Finger clubbing: bronchiectasis or bronchial carcinoma. • Wheezes: unilateral or bilateral. • Signs of consolidation or collapse. • Heart examination and signs of DVT.
Management of haemotysis Investigations: • ENT examination, bleeding time, clotting time and platelet count. • Chest X- ray. • Bronchoscopy is usually advisable unless a non-malignant cause is obvious. It should be carried out in other individuals in whom the hemoptysis is recurrent after an interval of observation. • Sputum cytology for malignant cells. • ZN for acid- fast bacilli may diagnose endobronchial TB. • Iron-containing macrophages in patients with hemosiderosis and Good-Pasture syndrome.
• Other special investigations: – Bronchiectasis: HRCT. – A- V fistula or pulmonary embolism: • Pulmonary or bronchial arteriogram • Spiral CT.
• If the history and physical examination are characteristic of acute bronchitis, the haemoptysis is mild, no further investigations will be required unless the symptoms of cough persist or the bleeding recurs. • If no cause is evident it is called idiopathic hemoptysis.
• If pulmonary embolism is suspected with normal CXR: – ECG. – Chest X-ray. – Ventilation / perfusion scanning. – Spiral CT of the chest. – Pulmonary angiogram.
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Treatment of hemoptysis It depends on diagnosis and treatment of the 1ry condition after control of hemoptysis. 1) Mild and moderate haemoptysis: • Rest, cough suppressants and haemostatic drugs. • Specific treatment: – TB: anti TB. – Abscess or pneumonia or infective exacerbation of chronic bronchitis: antibiotics. – Bronchial carcinoma: • • • • •
External irradiation. Laser beam through rigid bronchoscope or through FOB. Argon- plasma coagulation. Electrotherapy. If controlled, the patient must be investigated later on by the investigations mentioned above and elective surgery will be done if the patient is fit for surgery.
2) Massive haemoptysis: Emergency treatment is life saving: – – – –
Positioning: the bleeder side of the chest is the lower most to prevent the expected aspiration of blood to the healthy side and hence drowning. Sedation: diamorphine is the drug of choice. Diazepam can be used. Set up IV line and collect blood for grouping and possible cross- matching for tranfusion. Endotracheal tube for aspiration of blood.
5. Emergency rigid bronchoscope on theater while preparing for resection in certain cases. The bleeding will be controlled through the rigid bronchoscope by: – Aspiration of blood and cold saline lavage through concomitant FOB. – Fogartey balloon catheter inserted into and inflated in the affected main bronchus or lobar bronchus to isolate the affected site with lavage of the other bronchi and trachea from blood. – Gauze packing by the forceps through the rigid bronchoscope. – Double lumen-tracheal catheter.
6. FOB: It may be used and is considered the procedure of choice in experienced hands since it can be performed rapidly, requires only light sedation, and allow excellent airway visualization. • All patients should be intubated prior to FOB. This optimize airway control, allows effective suctioning and permits the bronchoscope to be removed easily and reinserted if the suction channel become occluded. • A balloon catheter may be used to occlude a segmental or lobar airway alternatively the FOB can be used to intubate selectively and ventilate the non bleeding lung.
7. Emergency lung resection of the bleeding lobe or lung. 8. Induction of artificial pneumothorax on the affected side to collapse the lung.
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3) Bronchial artery embolism by gel foam embolization in cases of bronchiectasis and cystic fibrosis. 4) If no cause can be detected follow up with chest X- ray of the patient for 3-6 months. If no cause can be detected no follow is recommended after that period.
Causes of haemoptysis with normal CXR • Acute bronchitis. • Chronic bronchitis. • Bronchiectasis. • Endobronchial TB. • Tracheal trauma from endotracheal intubation or suction. • Hemorrhagic disorders. • Anticoagulants over dosage. • Tracheal tumors. • Bronchial tumor. • Pulmonary embolism. • Idiopathic.
Chest Signs
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