cough and hemoptysis tranx
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COUGHCOUGH
An explosive expiration that acts to protect lungs from aspiration to propelsecretions and other materials upward through the airways.
Its is a protective mechanism of our body to expel foreign material or infection orsecretions.
It provides a normal protective mechanism for clearing the tracheobronchial treeof secretions and foreign materials. When excessive, it is also one of the most common
symptoms for which patients seek medical attention. Reasons for this include discomfortfrom the cough itself, interference with normal lifestyle and concern for the cause of thecough, especially fear of cancer.
MECHANISM
Cough may be voluntary or reflexiveDefensive reflex: both afferent pathways are activated
Afferent limb: Receptors within sensory distribution of trigeminal,glossopharyngeal, superior laryngeal, and vagus nerves are triggered.
Efferent limb: Recurrent laryngeal nerve and spinal nerves are
activated to cause muscle contraction.
Subject: MedicineTopic: Cough and HemoptysisLecturer:Date of Lecture: August 31, 2011Transcriptionist: Madame and the Super MinionPages: 11
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COUGH: What? How? Why?
How do we cough?
The glottis covering the trachea closes.The diaphragm pushes up in a relaxed positionIntrathoracic pressure builds up to 300mgHg, causingalveoli to squeeze down, pushing air out with expiratoryvelocities approaching 500mph.The glottis opens allowing forceful expulsion of airand/or secretions.
MECHANISM: Irritant triggers
Exogenous sourcee.g. smoke, dust, fumes, foreign bodies
Endogenous origin such as upper airway
secretions, gastric contents, may gounrecognized
Cough can be persistent or inflammation of airway from prolonged exposure canprecipitate cough and sensitize airway to other irritants.
Gastroesophageal reflux disease (GERD)
Irritant of upper airways receptors or aspiration of gastric contents, vagallymediated reflex mechanism secondary to acid in distal esophagus
SIGNS AND SYMPTOMSHistory
Valuable clues for etiology-acute or chronic?-Symptoms of respiratory infection at onset?-Seasonal?Wheezing?-Symptoms of postnasal drip? (Nasal discharge, Frequent throat clearing, Tick lein the throat)-Symptoms of gastroesophageal reflux?-Heartburn or sensation of regurgitation?-Fever or sputum?If sputum is present , what is its volume, character?-Hemoptysis?-Associated diseases or risk fators?
-Cigarrete smoking?-HIV?-Enviromental exposures (e.g. asbestos)-Angiotensin-converting enzyme (ACE) inhibitor?
PHYSICAL EXAMINATION
Signs of postnasal drip may be present ( Oropharyngeal muscus or erythema,Cobblestone appearance to mucosa
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Auscultation of the chest may demonstrate:-Inspiratory stridor (upper airway disease)-Rhonchi or expiratory wheezing (lower airway disease)-Inspiratory crackles (process involving pulmonary parenchyma e.g., insterstitiallung disease, pneumonia, or pulmonary edema)
Temperature-Fever suggests infection (bronchitis, pneumonia)
Check for systemic or nonpulmonary causes
-Heart failure-Primary nonpulmonary neoplasm-AIDS
DIFFERENTIAL DIAGNOSIS
ACUTE COUGH (3 weeks)
Often due to more than one condition. In a nonsmoker (where normal chestradiograph; no ACE inhibitor) most common causes are:
-Postnasal drip-Asthma
-Gastroesophageal reflux disease While in a smoker, suspect:
-Chronic obstructive lung disease-Bronchogenic carcinoma
Eosinophilic bronchitis in absence of asthma
REMEMBER:
3 most common causes of chronic cough identified were:- upper airway cough syndrome (UACS) or Post-nasal drip syndrome- Asthma- GERD
ACUTE COUGH- lasting < 3 weeks
SUBACUTE COUGH- lasting between 3 and 8 weeks
CHRONIC COUGH- lasting > 8 weeks
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CONDITIONS ASSOCIATED WITH COUGH
Airway infections, including Viral bronchitis (cough may last weeks), Pertussisinfection Brochientasis, Lung abscess
Asthma: cough masy occur in absence of wheezing or dsypnea ( cough variantasthma)
Neoplasm infiltrating the airway wall including Bronchogenic carcinoma andCarcinoid tumor
Airway filtration with granulomas including Endobronchial sarcoidosis andTuberculosis
Compression of airways from extrinsic masses including Lymph nodes,Mediastinal tumors, Aortic aneurysms
Parenchymal lung disease including Interstitial lung disease, Pneumonia, Lungabscess
CHF
ACE inhibitors which occurs in 5-20% of patients receiving these drugs. Onsetusually within 1 week and can be delayed up to 6 months
LABORATORY TESTS
SPUTUM: gross and microscopic examination
PURULENT SPUTUM- suggests Chronic Bronchitis, Pneumonia,Bronchiectasis, Lung abscess
BLOOD IN SPUTUM- also seen in above disorders but also withEndobronchial tumor
>3% EOSINOPHILS ON STAINING OF INDUCED SPUTUM INPATIENTS WITHOUT ASTHMA- suggests Eosinophilic bronchitis
GRAM AND ACID-FAST STAINS AND CULTURES- are used to identifyinfectious pathogen
CYTOLOGY- it can provide diagnosis or high suspicions of pulmonarymalignancy
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DIAGNOSTIC PROCEDURES
PULMONARY FUNCTION TESTING
To assess functionalabnormalities:
-Forced expiratory flow rates- reversible airflow obstruction
characteristic of asthma-Lung volumes and diffusing capacity- Restrictive pattern seen with diffuse
interstitial lung disease
BRONCHOPROVOCATION TESTINGWith methacholine or cold-air inhalation
To diagnose asthma when flow rates are normal Demonstrates hyperreactivity of airways to a bronchoconstrictive stimulus
SPIROMETRY
Measures lung volumes and airflow parameters
Procedure:1. Inhale maximally to TLC2. Exhale forcefully to RV for 6 seconds
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BRONCOSCOPY
Types: 1. Flexible Video Bronchoscope2. Rigid Bronchoscope
TREATMENT APPROACH
Definitive treatment: dependent on determining underlying cause
---Specific considerations:-Elimination of exogenous inciting agent (cigarette smoking, ACE inhibitor),
or endogenous trigger (postnasal drip, gastroesophageal reflux)-Usually effective if precipitant can be identified- Treat specific respiratory tract infections-Bronchodilators for potentially reversible airflow obstruction-Inhaled glucocorticoids for eosinophilic bronchitis-Chest physiotherapy and other methods to clear secretions in
bronchiectasis- Treatment of endobronchial tumors or interstitial lung disease if therapy
available and appropriate
Specific treatments: Symptomatic or nonspecific therapy--- Consider when:
-Cause not known or specific treatment not possible and cough performsno useful function or causes marked discomfort---Treat irritative, nonproductive cough with antitussive agents
-Codeine (15mg QID) or nonnarcotics such as Dextromethorphan (15mgQID), increases latency or threshold of cough center; and provides symptomatic relief;interrupts prolonged self-perpetuating paroxysms
-Ipratropium bromide (2-4 puffs QID)- lacks proof of efficacy; possiblyinhibits efferent limb of cough reflex
--- Cough productive of significant quantities of sputum should usually not besuppressed
-retention of sputum may interfere with distribution of ventilation, alveolaraeration and ability of the lung to resist infection
MONITORING
Referral to a pulmonologist may be warranted after:1. No identifiable cause is found in history, physical exam and chest x-ray2. Patient does not respond to sequential or concurrent treatment for
postnasal drip, asthma, and GERD3. Specialized tests such as high-resolution CT scan, modified barium
esophagography, bronchoscopy, and cardiac studies are negative.
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COMPLICATIONS
Exhaustions
Cough syncope- due to markedly positive intrathoracic and alveolarpressures, diminished venous return, and decreased cardiac output.It is occasionally precipitated by paroxysms of coughing
Chest and abdominal wall soreness
Urinary incontinence
Cough fractures of ribs- may occur in otherwise normal patients.Should raise the possibility of pathologic fractures, seen in Multiplemyeloma, Osteoporosis, Osteolytic metastases
HEMOPTYSIS
It comes from the Greek words:
haima- blood
ptysis- spitting
Hemoptysis- expectoration of blood or bloody sputum from the lungs ortracheobronchial tree
DIFFERENTIATING FEATURES OF HEMOPTYSIS AND HEMATEMESIS
HEMOPTYSIS HEMATEMESIS
HISTORY
-absence of nausea and vomiting
-lung disease
-asphyxia possible
-presence of nausea and vomiting
-gastric or hepatic disease
-asphyxia unusual
SPUTUM EXAMINATION
-frothy
-liquid or clotted appearance
-bright red or pink
-rarely frothy
-coffe ground appearance
-brown to black
LABORATORY
-alkaline pH
-mixed with macrophages andneutrophils
-acidic pH
-mixed with food particles
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CLASSIFICATION
Massive Hemoptysis- 200-600 mL/ 24 hours blood loss
Mild or minimal hemoptysis- usually refers to specks of blood or a fewsmall clots in sputum
Moderate hemoptysis- is everything from specks to 200 mL in 24 hours
PRINCIPAL SOURCES OF BLEEDING INTO THE LUNGS
Brochial arteries
Pulmonary arteries
Pulmonary capillaries and veins
Systemic fistulas ( rare )
ANATOMICAL ORIGINS OF HEMOTYSIS
TRACHEOBROCHIAL SOURCE
Neoplasm (bronchogenic carcinoma, endobronchial metastatictumor, Karposi sarcoma, bronchial carcinoid)
Bronchitis (acute or chronic) Bronchiectasis
Broncholithiasis
Airway trauma
Foreign body
PULMONARY PARENCHYMAL SOURCE
Lung abscess
Pneumonia TB
Mycetoma (fungus ball) Goodpastures syndrome
Idiopathic pulmonary hemosiderosis
Wegeners granulomatosis Lupus pneumonitis
Lung contusion
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DIAGNOSTIC CLUES IN HEMOPTYSIS: PHYSICAL HISTORY
CLINICAL CLUES SUGGESTED DIAGNOSIS
Anticoagulant use Medication effect, coagulation disorder
Association with menses Catamenial hemoptysis
Dyspnea on exertion, fatigue, orthopnea,paroxysmal nocturnal dyspnea, frothypink sputum
CHF, left ventricular dysfunction, mitralvalve stenosis
Fever, productive cough Upper respiratory infection, acutesinusitis, acute bronchitis, pneumonia.Lung abscess
History of breast, colon, or renal cancers Endobronchial metastatic disease oflungs
History of chronic lung disease, recurrentlower respiratory track infection, coughwith copious purulent sputum
Bronchiectasis, lung abscess
HIV, immunocompression Neoplasia, TB, Kaposis sarcoma
Always ask about:Medications takenTravel historyWeight lossTobacco use/ smokingAlcoholism (esophageal varices)
Nausea/ vomiting/ melenaOccupational history/ exposure to chemicals
HISTORY
Important points in the history:-Hx of prior lung, cardiac or renal disease-Hx of smoking-Hx of prior hemoptysis, pulmonary symptoms or infectious symptoms-Family hx of hemoptysis or aneurysms
-Skin rash-Hx of exposure to organic chemicals-Hx of exposure to asbestos-Travel hx-Hx of bleeding disorders, use of aspirin or NSAIDS, or anticoagulants-Upper airways of upper GI symptoms
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PHYSICAL EXAMINATIONS
Physical examination points of interest-many telengectasia-skin rash-splinter hemorrhage and needle cracks
-clubbing-chest bruit or chest murmur-augmented P2, Tricuspid regurge, Pulmonary insufficiency, Parasternal
heave-signs of deep vein thrombosis
DIAGNOSTICS
CBC, Platelet count PT, PTT, International Normalized Ratio
Arterial blood gases D-dimer Sputum Gram stain, culture
Acid-fast bacillus smear and culture
Sputum cytology
HIV test Erythrocyte sedimentation rate Consider chest CT scan and bronchoscopy where:
-hemoptysis last longer than 2 weeks-recurrent episodes of hemoptysis-volume of hemoptysis is >30 mL/ day
-patient is a smoker and >40 y.o-suspected brochiectasis
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ALGORITHM FOR NON-MASSIVE HEMOPTYSIS
*Sorry for the poor quality of this picture but you can refer to the book for clearerdiagram
MASSIVE HEMOPTYSISPatients with massive hemoptysis need rapid establishment of airway
patency, prevention of suffocation and control bleedingThe secondary goal is to determine the site of bleeding and cause.
INITIAL MANAGEMENT:
If the bleeding site is known, the patient should be put in lateral decubitusposition with the bleeding side down to protect the other lung from spillageand drowning.
If oxygenation is compromised or bleeding continues, the patient should beintubated and mechanically ventilated.
OTHER OPTIONS IN MANAGEMENT OF MASSIVE HEMOPTYSIS:
Use of double-lumen endotracheal tube Insert a balloon catheter through bronchoscope
Laser phototherapy
Electrocautery
Embolotherapy Surgical resection
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