Definition of Pulmonary Emphysema
Pulmonary emphysema is the most severe form of PPOM characterized by recurrent inflammation that injured and eventually damage the alveolar walls causing a lot of blab or bullae (air space) bronchial collapse on expiration (air trap).
Pulmonary emphysema can also be defined as an abnormal distention of the air spaces beyond the terminal bronchioles with alveoli wall damage. This condition is the final stage of a process that progresses slowly over several years.
Classification of Pulmonary Emphysema
There are two (2) main types of emphysema, which is classified based on the changes that occur in the lungs.
a. Panlobular (panacinar), that there is damage to the bronchial tract, alveolar ducts and alveoli. All air space in the lobes somewhat enlarged, with little inflammatory diseases. His trademark is having chest characterized by hyperinflation and dyspnea on exertion, and weight loss.
b. Sentrilobular (sentroacinar), the pathological changes mainly occur in secondary lobe center and peripheral of acini remain good. Often there is chaos perfusion-ventilation ratio, leading to hypoxia, hypercapnia (increased CO2 in arterial blood), polycythemia, and right heart failure episodes. The condition leads to cyanosis, peripheral edema, and respiratory failure.
Etiology of Pulmonary Emphysema
1.Merokok is the main cause
2.Faktor predisposition. Genetic susceptibility to emphysema associated with abnormalities in plasma protein, alpha-1 antitrypsin deficiency, which is an enzyme inhibitor. Are genetically sensitive to environmental factors (smoking, air pollution, infectious agents, allergens).
Clinical Manifestations
1.Dispnea
2.When inspection: chest shape 'Burrel chest'
3.Pernapasan chest, abnormal breathing is not effective, and the use of accessory muscles of respiration (sternocleidomastoid)
4.Pada percussion: hiperesonans and decreased fremitus in all lung fields.
5.Pada auscultation: audible breath sounds with krekels, crackles, and expiratory extension
6.Anoreksia, weight loss, and general weakness
7.Distensi neck veins during expiration
Diagnosis
a.Sinar x chest: to declare lung hyperinflation; horizontal diaphragms; increased retrosternal air area; decreased vascularity sign / bullae (emphysema); increasing signs bronkovaskuler (bronchitis), were normal during periods of remission (asthma).
b.Tes lung function: to determine the cause of dyspnea, to determine whether the abnormal function is obstruction or restriction, to estimate the degree of dysfunction and to evaluate the therapeutic effects, eg., bronchodilators.
c.TLC: increasing the breadth and sometimes bronchitis in asthma: a reduction in emphysema
d.Kapasitas inspiration: decreased in emphysema
e.Volume residue: increased in emphysema, chronic bronchitis, and asthma
f.FEV1/FVC: strong expiratory volume ratios with strong vital capacity decreased in bronchitis and asthma
g.GDA: estimating progression of chronic disease processes
h.Bronkogram: cylindrical bronchial dilatation may indicate the inspiration, the expiratory bronchial kollaps strong (emphysema); enlarged duct mucosa seen in bronchitis
i.JDL and differential: increased hemoglobin (extensive emphysema), increased eosinophils (asthma)
Blood j.Kimia: Alpha 1-antitrypsin deficiency and to convince primary diagnosis of emphysema
k.Sputum: culture to determine the presence of infection, identify pathogens; sitolitik examination to determine malignancy or allergic disorders
l.EKG: right axis deviation, P wave elevation (severe asthma), atrial dysrhythmias (bronchitis), P wave elevation in leads II, III, AVF (bronchitis, emphysema), the vertical axis of the QRS (emphysema)
m.EKG exercise stress tests: helpful in assessing the degree of lung dysfunction, evaluate the effectiveness of bronchodilator therapy, planning / evaluation of training programs.
Management
The goal of treatment is to improve quality of life, to slow the progress of the disease, and to overcome, to relieve airway obstruction hypoxia. Therapeutic approaches include:
a.Tindakan treatment intended to improve ventilation and reduce breathing effort
b.Pencegahan and prompt treatment of infection
c.Teknik physical therapy to maintain and improve pulmonary ventilation
d.Pemeliharaan appropriate environmental conditions to facilitate breathing
e.Dukungan psychological
f.Penyuluhan patient and sustainable rehabilitation
g.Bronkodilator
Bronchodilators are prescribed to dilate the airway because these preparations against mucosal edema and muscular spasm and helps reduce airway obstruction and improve the exchange gas.Medikasi include β-adrenergic antagonist (metoproterenol, isoproterenol) and metilxantin (theophylline, aminophylline), which results in dilatation of the bronchial .
Bronchodilators may be prescribed by oral, subcutaneous, intravenous, rectal or inhalation. Inhaled medications can be administered through a pressurized aerosol, nebuliser.Bronkodilator may cause unwanted side effects include tachycardia, cardiac dysrhythmias, and central nervous systems of stimulation. Metilxantin can also cause gastrointestinal disturbances such as nausea and vomiting.
• Aerosol Therapy
Aerosolization (dividing process mrnjadi powder particles are very fine) copy of bronchodilators and mucolytics are often used to assist in bronchodilation. Aerosols are dinebulizer eliminate mucosal edema and thin bronchial secretions. This makes the cleaning process bronkhiolus, help control the inflammatory process and improve the function of ventilation.
• Infection Treatment
Patients with pulmonary emphysema susceptible to infection and should be treated at the initial onset of signs of infection such as purulent sputum, increased cough, and fever. The most frequent organism is S. pneumonia, H. influenzae, and Branhamella catarrhalis. Antimicrobial therapy with tetracycline, ampicillin, amoxicillin or trimethoprim-sulfametoxazol (Bactrim) may be prescribed.
• Oxygenation
Oxygen therapy may improve survival in patients with severe emphysema. Severe hypoxemia treated with a low concentration of oxygen to increase the oxygen pressure up to between 65 and 80 mmHg. In severe emphysema, oxygen is given at least 16 hours per day to 24 hours a day
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