Preliminary Report Of Bronchial Asthma
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Transcript of Preliminary Report Of Bronchial Asthma
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BAB I
THEORETICAL BACKGROUND
A. DEFINITIONAsthma bronchial is a disease with increased response cirri trachea and bronchi to various
stimuli with a manifestation of a widespread narrowing of the airway and rank can change
spontaneously or as a result of treatment (The American Thoracic Society, 1962).
(Muttaqin, Arif: 2008)
Asthma bronchial is an inflammatory disease characterized by periods of obstructive
episodic spasms of smooth muscles in the walls of the bronchial airways (bronchial spasms).
Bronchospasm is to narrow the airway, making breathing difficult and cause a wheezing
sound. (Asih, Niluh Gede Yasmin: 2004)
Asthma bronchial is inflammation in the airway. Patients experience episodes of
coughing, wheezing, chest feels like tied, and / or dyspnea (shortness of breath), which is
often worse at night or early morning. There are variations in severity and frequency of
attacks. Asthma can be defined as "Increased bronchial responsiveness to various stimuli,
manifested as a narrowing of the airway that extends the severity changed spontaneously as
well as a variety of treatment effect". (J.P.T. Ward, Richard M. Leach, Charles M.
Wiener: 2006)
B. ETIOLOGYAsthma can be classified as extrinsic asthma, which has a definite external causes, and
intrinsic asthma, which has no external cause can be identified. Extrinsic asthma frequentlyoccur as a result of allergic response, with the formation of IgE antibodies against specific
antigens (allergic or atopic asthma) and tend to begin in childhood with symptoms becoming
less severe with age, 80% of people with asthma are atopic. Intrinsic asthma usually occurs
in adults and is not improve. (P.T. Ward, Richard M. Leach, Charles M. Wiener: 2006)
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1. Factors extrinsic / allergic / stofikAntigen-antibody reaction: Because intalasi allergen (dust, filings, feathers, animal).
2. Intrinsic Factor / non-allergica. Infection : Influenza virus, pneumonia, mycoplasma.
b. Physical : cold weather, changes in temperature.
c. Irritant : chemistry, air pollution (co, air, cigarette smoke, perfume).
d. Emotional : Fear, anxiety, tension.
Excessive activity can also be a factor associated with bronchial asthma trigger factors:
a. Heredity (50%)
b. Psychiatric / psychological
c. Physical stress.
C. PATHOPHYSIOLOGYInitial attack of asthma can occur in childhood or adulthood, acute asthma episodes, which
is referred to as asthma attacks can be triggered by stress, strenuous exercise, infection, or
exposure to allergens or other irritants such as dust and so on. Many clients have a family
history of asthma in allergy. Dyspnea is the main symptom of asthma, but hyperventilation,
headache, numbness, and nausea may also occur.
Asmatik attacks occur due to several physiological changes including changes in
immunological responses, increased airway resistance, lung compliance is increased, the
function mukosilaris damaged, and the exchange of oxygen-carbon dioxide are changing.
Asthma is the result of an immunological antigen-antibody reactions that release chemical
mediators, the mediator led to three major reactions: (1) constriction of smooth muscle in the
airway either small or large, resulting in bronchial spasms (2) the increased permeability
resulting in mucosal edema, which further narrows the airway, (3) increased mucous
secretion kelenjer and increase mucus formation. As a result, individuals with asthma
struggling to breathe through the airway has been narrowed and in a state of spasm. (Asih,
Niluh Gede Yasmin: 2004)
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D. SIGN AND SYMPTOMUsually in patients who are free to attack found no clinical symptoms, but at the time of
the attack the person appears to breathe fast and deep, restless, sitting with a prop forward,
and without a respirator muscles work hard. Classic symptoms of bronchial asthma are
shortness of breath, cough, and in some patients there who feel chest pain. The symptoms
that arise more and more, among other things: a silent chest, cyanosis, impaired
consciousness, chest hyperinflasi tachicardi and rapid shallow breathing. Bronchial asthma
attacks often occur at night.
1. Dyspnea meaningful.2. Coughing, especially at night.3. Breathing is shallow and rapid.4. Wheezing can be heard on lung auscultation. Wheezing usually heard only during
expiration, unless the patient's condition worse.
5. Increased breathing effort, characterized by chest retraction, accompanied by worseningconditions, the breath of the nostrils.
6. Anxiety, related to the inability to get enough air.7. Air trapped due to obstruction of blood flow, especially seen during expiration in
patients with asthma. This condition is seen with a prolonged expiratory time.
8. Among asmatik attack, individuals are usually asymptomatic. However, in examiningchanges in lung function between attacks may be seen even in patients who have
persistent asthma. (Corwin, Elizabeth j: 2009)
E. TREATMENT
1. Non Pharmacology
a. Extension. This extension is intended to enhance the client's knowledge about asthma sothat the client is consciously avoiding trigger factors, use of medication correctly, and
consult on the health team.
b. Avoiding trigger factors. Clients need to be helped to identify the triggers of asthmaattacks that exist in its environment, taught how to avoid and reduce trigger factors,
including adequate fluid intake for the client.
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c. Physiotherapy can be used to facilitate mucus expenditure. This can be done withpostural drainage, percussion, and fibrasi chest.
2. Pharmacologicaltreatmenta. Beta agonists: metaproterenol (alupent, metrapel). The form of aerosols, works very fast,
given as much as 3-4 x spray, and spray distance between the first and the second is 10
minutes.
b. Metilxantin, given adult doses of 125-200 mg 4 times daily. Group metilxantin isaminophylline and theophylline. The drug is given when a class of beta-agonists did not
give satisfactory results.
c. Corticosteroids. If the beta agonists and metilxantin not respond well, should be givencorticosteroids. Steroids in the form of an aerosol with a dose of 4 x spray every day.
Steroids in the long term side effects, then clients who received long-term steroids should
be closely monitored.
d. Cromolyn and Iprutropioum bromide (atroven). Cromolyn an asthma preventermedication, especially for children. Bromide Iprutropioum dose given 1-2 capsules four
times daily (Kee and Hayes, 1994). (Muttaqin, Arif: 2008)
F. DIAGNOSTIC EXAMINATION1. Measurement ofPulmonary Function(Spirometry)
Measurements were made before and after class adrenergic aerosol
bronchodilators. Increase in FEV or FVC by more than 20% indicates a diagnosis of
asthma.
2. Provocationtests bronchiThis test is performed on the internal spirometry. FEV decline by 20% or more after the
provocation test and heart rate 80-90% of maximum is considered meaningful if cause
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decreased PEFR 10% or more. Skin examination To demonstrate the presence of IgE
antibodies specific hypersensitivity in the body.
3. Laboratory examinationa. Blood Gas Analysis (AGD / Astrup).
Only done in severe asthma attacks because there is hypoxemia, hiperkapnea, and
respiratory acidosis.
b. sputumThe existence of kreola body is characteristic for severe asthma attack, because only a
great reaction that causes transudation of mucosal edema, thereby terlepaslah group of
epithelial cells from will stick. Gram staining is important to see the bacteria, the way the
test was followed culture and resistance to multiple antibiotics.
c. Tues eosinophils.Tues eosinophils in the client with status asthmaticus can be reached 1000-1500/mm3
either intrinsic or extrinsic asthma, whereas eosinophil cell count to normal between 100-
200/mm3. Diseratai improvement in lung function decline in eosinophil cell counts
showed the treatment had been appropriate.
d. Examination and routine blood chemistry.Leukocyte cell count is more than 15.000/mm3 due to infection. SGOT and SGPT
increased due to liver damage from hypoxia or hiperkapnea.
4. Radiological ExaminationThe results of radiological examinations in clients with bronchial asthma is usually
normal, but this procedure must still be done to rule out the possibility of a pathological
process diparu or complications of asthma such as pneumothorax, pneumomediastinum,
atelectasis, and others. (Muttaqin, Arif: 2008)
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G. PROGNOSIS
Factors affecting prognosis:
1. Age when the first attacks occur, the frequency of asthma attack severity of asthmaattacks, especially in the 2 years since getting an asthma attack.
2. The number of factors of atopy was found in children and their families.3. Suffering from or had suffered from an intractable aksema infaintel4. The duration of drinking milk5. treatment and mitigation efforts6. Does the mother / father / roommate / layperson smokers - that air pollution can also
affect other homes.
7. Avoidance of allergen is eaten since the pregnancy and during breastfeeding8. Gender, hormonal disorders and others.
H. COMPLICATIONStatus asthmaticus is a state of prolonged bronchial spasm, life-threatening that can not be
restored with treatment may occur in some individuals. In this case, the work of breathing is
greatly increased. If the work of breathing increases, oxygen demand is also increasing.
Because individuals who experience asthma attacks can not meet the oxygen needs of
normal, individuals are increasingly unable to meet the needs of a very high oxygen
required for the inspirational and berekspirasi against bronchial spasm, bronchial
inflammation, and mucus is thick. This situation can lead to pneumothorax due to the
amount of pressure to perform ventilation. If the individual fatigue, respiratory acidosis may
occur, respiratory failure, and death. (Corwin, Elizabeth J: 2009)
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I. NURSING CARE PLAN1. Assessment2. Diagnosesa) Ineffective airway clearance related to bronchospasm.b) Impaired gas exchange related to the bronchial spasms.c) Imbalance nutrition: less than body requirements related to unable to absorb food due to
biological factors.
d) Anxiety associated with death threats (inability to breathe).e) Lack of knowledge (specific) related to the misinterpretation of information.
(Nanda: 2005-2006)
3. Interventiona. Diagnoses 1:1) Open the airway2) Position the patient to maximize ventilation3) Identify of patients need the installation of an artificial airway device4) Perform chest physiotherapy if necessary5) Remove secretions by coughing or suction6) Auscultation of breath sounds7) Give bronchodilators if necessary8) Monitor respiration and O2 status.b. Diagnoses 2:1) Open the airway2) Give position the patient to maximize ventilation3) Remove secretions by coughing or suction4) Auscultation of breath sounds5)
Give bronchodilators if necessary
6) Monitor respiration and O2 status7) Note chest movement8) Monitor breath sounds: bradipnea, tachypnea, hyperventilation.9) Monitor the diaphragm muscle fatigue (paradoxical movement)10)Auscultation of lung sounds after the action to know the results
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c. Diagnoses 3:1) Assesst the presence of food allergies2) Collaborate with a dietitian to determine the amount of calories and nutrients needed
patient
3) Instruct the patient to increase the protein and vitamin C4) Give foods that are selected (already consulted with a nutritionist)5) Teach the patient to make daily food records6) Monitor the amount of nutrients and calories7) Assesst patient's ability to get the nutrients it needs.d. Diagnoses 4:1) Identify the level of anxiety2) Teach relaxation techniques3) Maintain a bright environment4) Teach for expiratory feelings verbally5) Give information about treatment, care and patient6) Explain the procedure performed.7) Give medications to relieve anxiety.e. Diagnose 5:1) Provide an assessment of the patient's level of knowledge about the specific process2) Describe signs and symptoms that may appear on the disease3) Describe the disease process4) Identify possible causes5) Provide information to patients about the condition6) Discuss lifestyle changes that may be necessary to prevent complications in the future or
the process of controlling the disease.
7) Instruct the patient about the signs and symptoms to report on the health care giver in aproper way. (Nanda(Nic & Noc): 2007-2008)