Definition | Treatment | Management of Disease | Diagnosis | Symptoms | Etiology | Pathophysiology | Procedure



Bronchopneumonia  is a type of lung infection caused by infectious agents and are in the area around the bronchi and alveoli.

In general, individuals who are stricken with bronchopneumonia caused by a decrease in the body's defense mechanism against the virulence of pathogenic organisms. People who have a normal and healthy body's defense mechanisms against respiratory organs which comprises: glottis and the cough reflex, presence of mucous layer, the movement of cilia that move the bacteria out of the organ, and local humoral secretion.
Incidence of bronchopneumonia caused by viruses, bacteria, fungi, protozoa, mycobacteria, mycoplasma, and rickettsial. , among others:
  1. Bacteria: Streptococcus, Staphylococcus, H. Influenzae, Klebsiella.
  2. Virus: Legionella pneumoniae
  3. Fungi: Aspergillus species, Candida albicans
  4. Aspiration of food, oropharyngeal secretions or gastric contents into the lungs
  5. Pulmonary congestion occurs because the old one.

Another cause of pneumonia is caused by the normal flora that occurs in patients whose durability is compromised, or there is aspiration of normal flora present in the mouth and because of the cranii pneumocystis, mycoplasma.

Bronchopneumonia is a secondary infection that usually causes bronchopneumonia caused by viruses that enter the respiratory tract, causing inflammation and alveolar broncus. Inflammation is characterized by accumulation of bronchial secretions, causing fever, productive cough, positive Ronchi and nausea. When the spread of germs reach the alveoli so the complications that occur are the alveoli collapse, fibrosis, emphysema, and atelectasis.
Collapsed alveoli will result in a narrowing of the airways, shortness of breath, and breath Ronchi. Fibrosis can cause decreased lung function and decreased surfactant production as a lubricant function to moisturize fleura cavity. Emphysema (accumulation of fluid or pus in the lung cavity) is the follow-up from surgery. Atelectasis resulting in an increase in respiratory rate, hypoxemia, respiratory acidosis, the client happened cyanosis, dyspnea and fatigue which will result in respiratory failure. Pathophysiology can be described briefly in the process scheme.

Usually preceded by upper respiratory tract infection. This disease usually begins suddenly, rising temperature 39-40°C with chills, shortness of breath and rapid, coughs that are non productive "breath sounds" when percussion dim lung examination, breath sounds during auscultation Ronchi smooth wet and loud.
Cough that may be severe respiratory insufficiency begins to occur with upper tract infections, dry cough, headache, muscle pain, anorexia and difficulty swallowing.

Examination Support
To be able to establish nursing diagnoses can be used to:
1. Laboratory examination
• Blood tests
• Examination of sputum
• Blood gas analysis
• Blood cultures
• Samples of blood, sputum, and urine
2. Radiological examination
• Rontgenogram Thorax
• Laryngoscopy / bronchoscopy
Management of Bronchopneumonia
Chemotherapy for mycoplasma pneumonia, may be given erythromycin 4 x 500 mg daily or Tetracycline 3-4 mg a day.
These drugs ease and speed healing, especially in severe cases. Drugs inhibiting the synthesis of SNA (Sintosin Antapinosin and Indoksi Urudin) and interferon inducer such as polinosimle, poliudikocid.

Symptomatic treatment such as:
  1. Breaks, generally the patient does not need to be treated, get enough rest at home.
  2. Symptomatic of a cough.
  3. A productive cough should not suppressed with antitussive
  4. If there is airway obstruction, and mucus and there is febrile, given broncodilator.
  5. Oxygen administration generally is not required, except for severe cases. The best antibiotic is an antibiotic corresponding to the causes that have a narrow spectrum.
  1. Atelectasis 
  2. Emphysema 
  3. Lung abscess
  4. Systemic Infection
  5. Endocarditis 
  6. Meningitis.

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Pleural Effusion

Pleural Effusion is a collection of fluid in the pleural cavity or cavity between the parietal pleura and visceral pleura, can be fluid transudates or exudates.

Pathophysiology and Etiology
- Transudates:
An extracellular fluid that collects in the pleural lavum passively. With a specific gravity of the liquid is less than 1.015; protein in the fluid of less than 2-3 g / dl. Can occur as part of a general or edema in left heart failure.
Generally the cause is: an increase in pulmonary venous pressure, hypoalbuminaemia and mediastinitis fibrosis or miksedema.
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- Exudate:
Fluid in the pleural cavity caused by infectious diseases or neoplasms, generally protein levels> 3 g / dl, yellow or orange, with or without cells or bacteria.
Generally it can be caused by inflammation, neoplasm, and abnormal lymph drainage.

Clinical Symptoms

  • Shortness of breath is the main symptom, sometimes accompanied by feelings of discomfort in the chest. When pleural fluid is low, can not be detected by clinical examination, but can be detected by radiography.
  • Sometimes accompanied by pleural pain or non-productive cough. But pleural effusion is more often a complication of bacterial pneumonia.

Physical examination.
  • There is usually a symptom of the disease essentially.
  • If shortness of breath that stand out, most likely because the process of malignancy.
  • Effusions shaped bag (pocketed) the fissure interlobaris not give symptoms. Similarly, if efusinya is above the diaphragm.
  • Unilateral pleural effusion is often due to infection in the lung tissue before.
  • Bilateral pleural effusions, possibly due to heart failure, hipoproteinemia, pulmonary embolism.
  • On percussion, the voice sounded faint revealed in accordance with the extent of effusion.
  • On auscultation breath sounds decreased or disappeared.
  • Diminished vocal resonance.

Chest X-Ray photo.
  • PA chest X-ray photos, to see the surface of the pleural fluid.
  • The amount of pleural fluid> 300 cc visible on chest X picture in the decubitus position.
  • Pleural effusions seen on chest X-shaped photo bag (pocketed), still need to be distinguished with the same picture of other diseases, because it must be careful in making conclusions.
  • At least costofrenicus sinus effusions seem dull.
  • Effusions in large quantities causing mediastinal shift towards the healthy. But if there is no shift of the mediastinum, the possibility of lung collapse with effusion.

  • Fluid aspiration and biopsy can be used to diagnose diseases and as a culture.
  • Sometimes torakoskopi examination to aid diagnosis.
  • Viewed with the naked eye, the normal pleural effusion clear yellow. If the pleural effusion showed a lot of turbid PMN cells, or containing cholesterol or fatty items. When white as milk, indicating the existence of chylous fluid.
  • Pleural fluid can be used for cytology and arithmetic types.
  • Effusions containing large amounts of red blood cells, possibly due to malignancy or pulmonary infarction. When the lot containing PMN cells indicating bacterial infection.
Lymphocytes in the pleural fluid is not typical for tuberculosis fluid. Eosinophils in large amounts, the possibility of disease in connective tissue or "eosinophilic pleural effusion".

  • Protein> 3 g / dl --> exudate. Protein <3 g / dl --> transudates
  • Glucose < normal --> "rheumatoid pleural effusion". Another possibility for malignancy or purulent. 
  • Cholesterol --> indicates the process or perhaps because of chronic rheumatoid. 
  • Amylase -->  pancreatitis or pancreatic carcinoma. 
Serologic Tests
Rheumatoid and systemic lupus erythematosus are often given anti-nuclear factor and rheumatoid factor positive.

Differential Diagnosis

Other Pleural effusion
"Chylothorax" pleural effusion is caused due to leakage from the duct torasicus. These leaks can be caused by trauma or blockage filiariasis in the tropics.

Management Of Pleural effusion


  • Usually cured after being given adequate treatment of basic diseases. 
  • Empyema may arise due to lung infections like pneumonia.

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Management Of Pleural Effusion

Management Of pleural Effution :
  • Pleural fluid aspiration performed, to reduce the unpleasant taste or "discomfort" and shortness of breath.  It is advisable to gradually aspirations.Fluids released between 500 - 1000 cc. When taking too many and can quickly lead to pulmonary edema.
  • Incorporating intrapleura chemotherapy for malignancy (eg radioactive gold or Ytrium).
  • More often performed pleurodesis in the process of malignancy or in the frequent recurrence of effusion.
  • By using 500 mg tetracycline powder is dissolved in 50 cc of physiologic saline. Patients shake it so flat, then the liquid removed after clamped for 24 hours or given jodium powder or talc.
  • Pain that occurs because the administration of drugs above can be overcome with the analgesic. If need be given pethidine 100 mg i.m.
  • Provision of steroids combined with antituberculosis can absorb the pleural effusion caused by pulmonary tuberculosis quickly and reduce fibrosis.

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Bronchial Asthma

Bronchial asthma is a disease of the lung inflammation in the airways resulting in airway hiperrespon to various stimuli that can cause constriction of the airways that can arise thorough so shortness of breath that is reversible either spontaneously or with therapy.

  • Genetic factors
  • Environmental factors
  • Materials allergens
  • Respiratory tract infections (especially viruses)
  • Air pollution
  • Food Factor

Trigger factors
  • Allergens
  • Physical
  • Chemicals
  • Infection
  • Mechanical factors
  • Psychological factors
The entry of allergens into the airway will cause a reaction between the allergen with immunoglobulin E. The release of materials from mastosit mediators, which cause the inflammation in the bronchial mucosa and submucosa causing bronchial smooth muscle contraction.

Infiltration of inflammatory cells such as eosinophils, neutrophils, and other airway epithelial damage, resulting in expenditures as well as mediators and thickening of the mucosal and submucosal edema. There is hyperplasia of the glands Goblet cells. Happen "mucous plug" on-line the airways.

Clinical Symptoms
Complaints and symptoms depend on the severity at the time of the attack. In bronchial asthma attacks are mild and without complications, complaints and no typical symptoms.

  • Breath sounds
  • Crowded
  • Cough

Physical examination
Abnormalities of the upper airway, bronchi, thoracic, and skins, can be rhinitis, sinusitis, bronchitis, asthma and alveoler broncho-lung hyperinflation.
General state:
  • Composmentis
  • Anxiety / anxiety / panic / sweating
  • Blood pressure increases
  • Pulse increased
  • Pulsus paradoxus: decrease in systolic blood pressure over 10 mm Hg at the time of inspiration
  • Respiratory frequency increased
  • Cyanosis
  • Auxiliary respiratory muscles hypertrophy
  • Obtained prolonged expiratory
  • Wheezing
  • Increased blood Eosinophils> 250/mm3
  • Analysis of blood gases in status asthmaticus
Radiology: there are no typical signs.
Pulmonary Physiology: decreased FEV1
Skin test: to indicate the presence of allergic
Bronchial provocation test: with inhaled histamine, acetylcholine, allergens.

  1. Anamnesa: complaints of shortness of breath by breath sounds ngiik frequent recurrence. The existence of hereditary factors and the presence of precipitating factors.
  2. Physical examination: a thorough wheezing or prolonged expiratory phase.
  3. Laboratory:
• Sputum: Charcot-Leyden crystals, Spiral Curschmann
• Blood: increased number of eosinophils.
• Physiology lung: airway obstruction (ratio of FEV1 / FVC <75% or PEF <150 liters / minute)
• bronchial provocation tests, skin sensitivity test.
Differential Diagnosis
  • Respiratory infection
  • Atelectasis
  • Pneumothorax, Pneumomediastinum, Emphysema cutis
  • Respiratory failure
  • Arrhythmias (especially if previously existing cardiac abnormalities).

Management / Procedure of Bronchial asthma

Special Treatment of Bronchial Asthma

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Emphysema Lung Is the permanent widening of the structure of pulmonary gas exchange that is distal to the terminal bronchioles, accompanied by destruction of alveolar walls.

  1. Main factors: smokers either active smoking or passive smoking depending on the length, number, how to smoke.
  2. Air pollution, in the form: Particles, These chemicals, Toxic Gas
  3. Infections: viral and bacterial
  4. Genetics:
a. Talent arise emphysema
b. The balance of destructive enzymes (protease) & protective enzymes (alpha-1-antitrypsin).

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Inhalation of cigarette smoke or pollutants stimulate cells in the lung macrophages and neutrophils produce elastase and collagenase is an enzyme that damages the fibers of elastin and collagen, and which is the framework of the alveoli and acini in order not to collapse. Smoking also inhibit the action of alpha-1-antitrypsin, an enzyme that protects elastin fibers against proteases.
In the lung there is a balance between destroying enzyme (protease) and protective enzymes (alpha-1-antitrypsin). Due to destruction of fibers of the lung elastin & collagen loss of elastic recoil.

Complaints and Clinical Symtomps
Progressive shortness of breath, tired easily when moving.
Pure emphysema without coughing, shortness, of breath sounds, sputum.
Breathing by means of "purse lips" aims to breathe more easily because of the onset of back pressure in the bronchioles so easy expiration and prevent "water trapping".

On physical examination found:
Chest barrel shaped chest, the space between the ribs widen.
Lung hyperinflation, the percussion sounds hipersonor, reduced chest expansion, difficulties inspiration, decreased breath sounds, rhonchi could be heard when there is phlegm.

Based on anamnesa, complaints and symptoms, supplemented by investigation as follows:
  • PA chest X-ray photo:
Lung looks hyperaereted.
Reduced vascular picture and not look at the third peripheral lung field, it appears the bulla, where the diaphragm is low, little heart shape in the form of water droplets.
  • Tests pulmonary physiology:
Showed abnormalities obstruction.
FEV1 <80% pred. and restrictive decreased FVC <70%, RV> pred. in accordance with lung hyperinflasi
  • Examination of enzymatic:
Levels of alpha-1-antitrypsin is low.
  • Analysis of blood gases:

There hipercapnea hypoxemia and the alveoli as a result of capillary damage and interference ratio of ventilation / perfusion.

Differential Diagnosis

Management of Emphysema
  • Prevention: stop smoking, reduce exposure to air pollution.
  • There is no effective treatment and satisfactory.
  • Treatment with a new bronchodilator reversibility is given when there is obstruction.
  • Antibiotics are given if there are signs of respiratory tract infection.
  • Oxygen increases when crowded.
  • Rehabilitation of relaxation with breathing exercises, postural drainage, exercise improves breathing capacity.
  • Treatment of the complications.

  • Pneumothorax: outbreak caused superficial bulla
  • Respiratory failure: due to bad ratio of ventilation / perfusion
  • Cor pulmonale: arise due to pulmonary hypertension due to hypoxemia and pulmonary vasospasm
  • Weight loss until emasiasi.

In emphysema caused by deficiency of alpha-1-antitrypsin bad prognosis.
Prognosis is determined by:
  • The rate of progression of the emphysema
  • The degree of bronchial obstruction and reversibilitasnya
  • The presence of complications
  • The accuracy of the management of emphysema.
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Special examination of Chronic bronchitis

Special examination :
  •  X-ray photo PA and left lateral chest
-  Typically show no abnormalities, except when it occurs cor pulmonale or emphysema.
-  It may also seem an increase in "bronchovascular markings".
  • Sputum: direct smear, Gram staining.

Please note: the existence of cells in sputum, whether the material is indeed contaminated with sputum or saliva from the oropharynx. Sputum can be identified because of alveoler macrophages (histiocytes). Macrophages alveoler this form round cells, large, with eccentric nuclei and oval or kidney-shaped near the edge of the cell.
Tues skuamus flat and very large and has a spherical nucleus in the middle. If there were> 25 epithelial cells in sputum skuamus, means contaminated with saliva or secretions from the oropharynx.
In chronic bronchitis who experience eksaserbrasi yellow sputum, bronchial ciliated epithelium that despite apparent in sputum neutrophil and looks.
At the time of remission decreased number of neutrophils, but macrophages alveoler increased, resulting in mucoid sputum and grayish-white color.
When sputum is contaminated, it should be repeated sputum collection or rinsed with water (washed sputum), a new Gram staining was made. Note the presence of neutrophils and bacteria. If the bacteria seemed gather very much and the same morphology, mean as a result of stasis, so sputum should be discarded. If it seems a variety of bacteria and many in the sputum, saliva possible, should be attempted again looking for new specimens. Look for the etiology of bronchial inflammation.
  • If the Gram-positive cocci in pairs or forming short chains means "Streptococcus pneumoniae" (diplococus).
  • If the Gram-positive cocci and form large clusters, meaning "Staphylococci".
  • Basil Gram-negative, such as haemophilus influenza, Seratia, Pseudomonas, Klebsiella, E. Colli, and others.

Guidelines for assessment of sputum on COPD:
  1. Gram staining of pus cells --> <1-5  inflammation (-) and germs (-); seed germ (+) --> not the cause of the disease.
  2. Gram staining (+) and seed (+) --> possible causes of infection.
  3.  Gram staining (-) and seed a little (+) --> sputum contaminated with saliva.
If the sputum culture results did not confirm the results of gram staining on sputum smears are true, then breeding considered untrustworthy. If the breeding is not the same as the results of gram staining, a new specimen should be made when antibiotics are used not deliver results.

Tests pulmonary physiology:
To determine the presence of airflow obstruction in chronic bronchitis, pulmonary physiology need to check:

  • FVC (Forced Vital Capacity)
  • FEV1 (Forced expiratory volume one second)
  • FEF 25-75% (Forced expiratory flow over the mid - 50% of the vital capacity) to detect obstruction in small airways.
  • PEFR (peak expiratory flow rate), only to find out the existence of a large obstruction in the airway, can be done in the clinic.
  • TLC (Total Lung Capacity), can only be examined at a hospital that has a complete facility in the form of "body plethysmograph or by helium dilution or nitrogen washout method technique".

In chronic bronchitis:
  • VC is normal or decreased (<80%)
  • FEV1 is normal or decreased (<80%)
  • FEV1 / FVC is always decreased (<75%)
  • FEF 25-75% was always decreased (<80%)
  • TLC normal / increased (N = 80-120%)
  • RV / TLC% is always increasing (N = 25-40%)

Pulmonary Physiology showed obstruction
  • ECG is necessary to know the existence of right heart hypertrophy, such as in cronic cor pulmonale.
  • Examination Arterial Blood Gases:
- PaO2 decreased to 70-80%, normal 80-100 mm Hg.
- PaCO2 normal / increased to 25-35%. Normal = PaCO2 = 35-45 mm Hg.
- pH is normal or decreased (when the state information). Normal pH = 7.35 to 7.45.
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Chronic Bronchitis

Chronic bronchitis is a disease, characterized by cough with phlegm every day, at least 3 months per year and lasts for 2 consecutive years, and the absence of other diseases with symptoms.

Etiology and pathogenesis
  • Exposure to cigarette smoke, both at the "smoker" or "passive smoker". For the smoker is usually measured by pack year (pack years).
  • Exposure to contaminated air in workplaces (eg dust or gas from industrial or workplace).
  • Social factors and residential solid and air pollution in the settlement area by the gases SO2 and NO2.
  • Respiratory tract infection by the virus will cause eksaserbrasi chronic bronchitis. For example, by class sinsisial respiratory viruses and influenza virus group.
  • Most bacteria that are found in chronic bronchitis are streptococcus pneumonia and haemophilus influenza.

a. Cigarette smoke is a disincentive to the bronchial mucosa, to changes:
  • Lung Defense:
  1. Purge function mukosilia slow,
  2. Alveoler Macrophage numbers are increasing,
  3. Impaired macrophage function,
  4. The process of antigen and antigen response to change.
  • Small airways:
  1. Inflammation,
  2. The increased muscle,
  3. Fibrosis,
  4. Refinement,
  5. The number of goblet cells increases.
  • Alveoli:
  1. The number of neutrophils, macrophages increased,
  2. Emphysema.

b.  Exposure to air polluted by industrial pollution or the disposal of fuel combustion in motor vehicles:
  1. Sulfur dioxide (SO2) and the complex particles (<10 u), derived from: Fossil fuels, power generation, oil refining, tobacco smoke, kerosene heaters, stoves that use wood or coal fuel. These materials cause bronchoconstriction.
  2. Photochemical oxidants, nitrogen oxides, ozone, produced by burning fuel in motor vehicles, power plants, and solar radiation. These materials cause stimulation of the respiratory tract, impaired pulmonary physiology and impaired pulmonary defense.
  3. Carbon monoxide (CO) generated by the combustion of automotive fuel, cigarette smoke. CO causes tissue hypoxia, especially the cardiovascular and nervous systems.

Clinical Symtoms
  • Chronic cough with phlegm mucus, thick, a lot, especially in the morning. Muko-purulent sputum, or purulent if there is infection. These symptoms for cough are considered regular smokers.
  • Shortness of breath with breath sounds due to progressive inflammation and bronchial obstruction.
  • If the disease has continued to grow, especially shortness of running time.
  • Physical examination performed on the patient sitting position:
  • Chest hyperinflation 
  • Percussion hipersonor
  • wet crackles at the time of inspiration
  • Wheezing on expiration time.

Special examination of Chronic bronchitis

Management Of Chronic bronchitis

Diagnosis of chronic bronchitis is based on:
  1. Anamnesa according to the criteria of chronic bronchitis with symptoms of chronic cough and phlegm, especially in the early morning, thick sputum and numerous. Sometimes purulent, especially in heavy smokers. Shortness of breath during activity and occurs slowly but progressively.
  2. Physical examination is not typical, usually chest hyperinflation, hipersonor, wet crackles and sometimes audible wheezing.
  3. Chest X-ray photo showed lung hyperinflation with increased bronchovascular markings.
  4. Examination of sputum Gram to detect bacterial infection in exacerbation.
  5. Lung physiology tests to detect obstruction or restriction.
  6. ECG to determine heart abnormalities.
  7. Arteriel blood gas analysis to detect hypoxemia and hypercapnea.

Differential Diagnosis

  • Depending on the early treatment before the disorder is advanced lung physiology and the presence or absence of complications of emphysema and cor pulmonale.
  • Stop smoking, avoid air pollution and socio-economic improvement of the patient will improve prognosis.
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Management of Chronic Bronchitis

  • Education to patients and their families
  • Stop smoking and avoid air pollution
  • Prevent infection
  • Clean environment
  • Hydration moderation: drink enough water (8-10 glasses a day)
  • Proper nutrition: protein rich diet and avoid heavy meals before bedtime, milk can cause increased bronchial secretions, should be prevented.

Provision of drugs:
1. Bronchodilators:
  • Aminophylline inj. 5.6 mg / kg i.v. or oral loading dose of 3 x 100-200 mg.
  • Terbutaline 3 x 2.5 mg oral or injection 0.25 mg s.c. every 4-6 hours (1 mg / ml; = 2 ml ampoule).
  • 3 x 2 mg salbutamol orally.

2. Expectorant:

  • Water is a good expectorant
  • Glyceryl guaiacolate 4 x 100-200 mg.

3. Mucolytic :

  • Bromhexine HCL: 3 x 1 tablet by mouth.
  • N-acetyl cysteine: 3 x 200 mg orally.

4. Respiratory therapy:

  • Aerosols: Ipratropium Bromide 3 x 2 puffs
  • Oxygen: 1-2 liters / minute via nasal cannula if PaO2 <55 mm Hg.
5. Rehabilitation:
  • Physiotherapy
  • Relaxation exercises
  • Breathing exercises
  • Chest percussion and postural drainage
  • Exercise physical abilities
  • Psychosocial Rehabilitation
  • Vocational Rehabilitation.

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