Assessment and Pathophysiology of Asthma

 

Mr. Ajesh Kumar T.K

Assistant Professor, MM College of Nursing, Mullana, Ambala  Haryana

*Corresponding Author Email: ajesh.ktk@gmail.com

 

ABSTRACT:

Asthma is a chronic inflammatory disease of the airways that causes airway hyper responsiveness, mucosal edema, and mucus production. This inflammation ultimately leads to re­current episodes of asthma symptoms: cough, chest tight­ness, wheezing, and dyspnea Asthma occurs in families, which suggests that it is an inherited disorder. Apparently, environmental factors (e.g., viral infection, allergens, and pollutants) interact with inherited factors to produce disease. Other inciting factors can include excitatory states (stress, laughing, crying), exercise, changes in temperature, and strong odors. The incidence of asthma has been increasing. It occurs across the life span, from the very young to the very old. It is a highly complex con­dition that can be a mild nuisance or a very serious, life-threatening condition. When people with asthma are exposed to extrinsic allergens and irritants, their airways become inflamed, produc­ing shortness of breath, chest tightness, and wheezing. This case study is exploring the case of Mrs. X , a 35-year-old-woman, was referred to the clinic with recurrent episodes of shortness of breath. For assessing her present condition a comprehensive history and physical examination with particular focus on the respiratory system will be established. In addition the underlying pathophysiology of the present respiratory problems will be discussed with the support of current literature.

 

KEY WORDS:  Respiratory System, Athma, allergens, Physical assessment, pathosphysiology Bronchodilators

 

 

 


PATIENT DEMOGRAPHICS AND HISTORY:

Mrs. X, a 35-year-old-woman, who lives in suburbs of Haryana, India. She is living with her husband and their 6 year old daughter. She works (since her marriage) as a cleaning clerk in a textile factory, does not smoke, but is exposed to environmental tobacco smoke because her husband and in-laws, with whom she lives, smoke. There are a cat and two dogs where she lives.  She is having an average body built and leading an active life style which includes morning walks and playing tennis.

 

Her asthma symptoms began during childhood and were controlled with Marex, an over-the-counter combination of a bronchodilator and antihistamine used to treat asthma. She never had to be hospitalized, but required frequent visits to the ER for asthma exacerbations. During adolescence her symptoms became quiescent and she was able to practice sports while in high school. Five years prior to this visit her asthma relapsed, with symptoms including chest pressure, cough, shortness of breath and wheezing. She is unable to identify any triggers for her asthma exacerbations. However, her symptoms are worse at the end of the week. Before the asthma exacerbations she frequently develops itching and increased secretions in her eyes and nose.

 

Her asthma symptoms have become progressively worse. She now has symptoms every day and night, and over the past year she has received several courses of oral prednisone to control asthma exacerbations. She is afraid of cortisone side effects, and would rather not use that medication. She was also prescribed inhaled beclomethasone, albuterol, and theophylline. She has not used Beclovent since March 2012, and prior to that she used it very irregularly. She believes Beclovent is a steroid, does not work, and is too expensive.

 

She, was referred to the clinic by a rural health nurse with recurrent episodes of shortness of breath. She had had a history of 'asthma' from childhood consisting of episodes of variable wheezy breathlessness associated with a nonproductive cough. For the past year these episodes had been more severe and lasted longer and she had been increasingly unable to do her normal activities and had lost several weeks from work. Some episodes had been associated with 'dizziness' and lighthead­edness. She had continued her normal inhaled med­ication which sometimes gave her relief, although not as consistently as before. Some episodes were asso­ciated with pain along the left lower chest anteriorly which was also made worse on deep breathing. Many of the episodes were associated with exertion but some occurred at rest. She was waking up repeat­edly at night with wheeze and shortness of breath.

A complete family, environmental, and occupational his­tory is essential. A positive family history and environmental factors, including seasonal changes, high pollen counts, mold, pet dander, climate changes, and air pollution, are pri­marily associated with asthma. 1

 

PHYSICAL ASSESSMENT:

A thorough physical examina­tion of the chest and lungs is es­sential when performing an assessment of the respiratory system. The physical examina­tion should be conducted in a consistent manner. The general examination steps are as follows: inspection, palpation, percus­sion, and auscultation. 2 I made good light available in her cubicle before the examination and put curtains down for ensuring patient privacy. I explained the ongoing physical examination procedure and made her to lie in the bed. The aseptic hand washing was done before the beginning of the assessment.

 

INSPECTION:

Inspection is the process of ob­taining a large amount of infor­mation about the clinical status of the patient through a visual inspection. An inspection is based on observing the chest shape, the breathing rate and pattern, and the skin and mu­cous membranes. The patient looked well although a little anxious. The observation of the skin and mucous membranes shows the no signs of cyanosis. There was no evidence of clubbing in the fingers and toes. Chest symmetry was normal and the apical pulse present. Mrs. X  skin was dry and no signs of varicose veins. She was having a prolonged exhalation and retractions of the intercostal spaces during inspiration. When the patient took 20 deep breaths, there were no additional symptoms.

 

PALPATION:

The Mrs. X temperature was 37 degrees. Then the various pulses were palpated and all were normal and regular. Her brachial pulse was 84 beats/min. She is having normal capillary refilling in fingers and toes. Thoracic expansion was assessed by placing both of the hands on her posterior chest at the level of T9 or T10 and observing movement of the hands during a deep inspiration. It shows chest wall expands symmetri­cally during deep inhalation. On palpation there was some tenderness along the left costal margin that reproduced the pain. Her abdomen was normal. There was no tenderness or swelling of the legs.

 

PERCUSSION:

Percussion notes are commonly referred to as resonance, dullness, or hyperresonance. Resonance is heard over the lungs when the chest wall is percussed.  The percussion note was normal.

 

AUSCULTATION:

The heart sounds were normal and there were no murmurs. On auscultation, there were a few scattered wheezes. The blood pressure was 110/85 mmHg.

 

DIAGNOSTIC TECHNIQUES:

Establishing a diagnosis of asthma is usually accomplished y a careful evaluation of the patient's history, physical exam­ination, laboratory tests (complete blood count with differen­tial, sputum analysis), and pulmonary function tests (PFTs). 3 A "challenge" test may be conducted to assess airway responsive­ness by exposing the patient to a variety of triggers and assess­ing the response. Serum levels of immunoglobulin E may be elevated if allergy is present. Arterial blood gas analysis and pulse oximetry re­veal hypoxemia during acute attacks. PFTs provide useful information in the non-acute setting and can help determine the level and course of treatment. The main components for a PFT for an asthma patient are the forced expiratory volume (FEV1), which mea­sures the volume of air that is forcibly exhaled in one second, and the peak expiratory flow (PEF), defined as the maximum flow rate at the outset of forced expiration.4 The diagnosis of asthma is established by demonstrating reversible airway obstruction. Positive wheal and flare reactions to skin tests can be demonstrated to various allergens, but such findings do not necessarily correlate with the intrapulmonary events. Mrs. X results on PFT were FEV1 ≥ 60% and PEF variability was 30%. The arterial blood gases (ABG) analysis shows that carbon dioxide level (PC02) level 50mm Hg.

 

PATHOPHYSIOLOGY OF PATIENT’S CONDITION:

Pa­tients with asthma periodically have acute episodes, or attacks, of varying intensity. Asthma is essentially a hypersensitivity response to a va­riety of stimuli. Because of previous exposures and the development of an antigenic response, repeated ex­posure to such stimuli causes inflammation, which in turn leads to both constriction of the bronchial smooth muscle and a hypersensitivity to stimuli.5  Attacks have two distinct phases. The early phase of an acute episode begins when triggers activate the inflamma­tory process. The airways constrict and become edematous. Mucus secre­tion increases, forming plugs in the airways, and tena­cious sputum is produced. Obstruction causes air to be trapped in the alveoli, creating a ventilation-perfusion mismatch.6 The effect is hypoxemia with compensatory hyperventilation. In the acute phase of an asthma attack, when a stimulus is inhaled, mast cells lining the bronchiole create an antigen re­sponse. The antigen response from the mast cells causes a rapid bronchiole constriction, usually within 10 to 20 minutes. In addition, mast cells are stimulated to increase mucus produc­tion, further occluding the already constricted airway. Increased vascular permeability causes more mucosal edema formation, while parasympathetic stimulation increases bronchoconstriction.7

 

The late phase of an asthma attack usually develops from four to eight hours after exposure to a stimulus and may last for hours to weeks after the initial attack when airway inflammation is pro­nounced. Red and white blood cells infiltrate the swol­len tissues of the airways.8 The bronchial muscles and mucous glands enlarge; thick tenacious sputum is produced; and the alveoli hyperinflate. Some patients have airway subbasement membrane fibro­sis. This is called airway "remodeling" and occurs in re­sponse to chronic inflammation. The fibrotic changes in the airway lead to airway narrowing and potentially irre­versible airflow limitation. The pathophysiologic hallmark of asthma is a reduction in airway diameter brought about by contraction of smooth muscle, vascular congestion, edema of the bronchial wall, and thick, tenacious secretions. The net result is an increase in airway resistance, a decrease in forced expiratory volumes and flow rates, hyperinflation of the lungs and thorax, increased work of breathing, alterations in respiratory muscle function, changes in elastic recoil, abnormal distribution of both ventilation and pulmonary blood flow with mismatched ratios, and altered arterial blood gas concentrations. 2

 

Features of the Mrs. X suggest that something new are the change in severity of the disease and the failure to control it as well as previously. In addition, there are two new symptoms, chest pain and light-headedness, neither of which is primary features of asthma. On the other hand, the nocturnal wheeze and breathlessness is a very powerful pointer to asthma. It is common for asthmatics to complain bitterly about their sleep disturbance but appeared normal by the next morning. The asthma out of control because the she was using the inhalers inadequately to provide maximum benefit. Hyperventilation is suggested by the light-head­edness. In addition she is having, palpitations, tingling in the fingers or weakness in the legs. Breathlessness is usually at rest rather than on exer­tion and waking at night is unusual. 6 Chest pain is often associated and is caused by the additional strain on the ribs and musculature. It can sometimes occur in patients with asthma and, when it does, the hyper­ventilation can make the asthma worse and the con­comitant anxiety then makes the hyperventilation worse. 9

 

 

Complications of asthma may include status asthmaticus, respiratory failure, pneumonia, and atelectasis. Airway obstruction, particularly during acute asthmatic episodes, often results in hypoxemia, requiring the administration of oxygen and the monitoring of pulse oximetry and arterial blood gases. Fluids are administered because people with asthma are frequently dehydrated from diaphoresis and insensible fluid loss with hyperventilation.

 

After finalizing the diagnosis that Mrs. X  suffering with asthma, I stated to give client and family education. The main focuses on my education was in identification and avoidance of known triggers of asthma attack. Avoidance of identified or suspected allergens, such as tobacco smoke, per­fumes, and chemicals, may prevent many acute asthma attacks. Exercise-induced asthma is thought to be caused by the loss of heat and water from the bronchial tree and is often exacerbated by cold.  In addition I educated her and family about the need for a use of a written action plan. Such plans have led to reductions in emergency room visits and hospital­izations as well as improvements in lung function. I also educated the warning signs of impending acute attacks. Awareness of the signs and symptoms of an attack are im­portant, because the attack may be dealt with by administer­ing of drugs. I was very cautious about following all the ethical principles while educating Mrs. X and her family.  During these activities I respected Mrs. X autonomy and was highly vigilant on her participation in the treatment programmes. Mrs. X was very relaxed during the consultation with me and she maintained good eye to eye contact.

 

The main problem I identified in case of Mrs. X her inability to do the regular follow up since she is living in a very sub coastal area where health care facilities are very limited. Despite many rural and remote initiatives over recent years, the health needs of many Australian communities are still not adequately met. Many rural and remote communities experience ongoing difficulties in recruiting and retaining an appropriate and adequately trained medical and health workforce, while residents face increasing difficulties in accessing appropriate care in situations where integration and continuity of care are woefully inadequate. Health workforce shortages and maldistribution and higher out-of-pocket expenses are particular barriers, especially in more remote areas. A rural health nurse visiting Mrs. X and family should be skilled as much as necessary to perform his/her duties and responsibilities and the nurses should be equipped with up-to-date knowledge and clinical skills in order to perform the complex services.

 

CONCLUSION:

Asthma is the chronic inflammation of the airway characterized by repeated episodes of the symptoms: cough, chest tight­ness, wheezing, and dyspnea.  This can be associated with familial, environmental and certain other factors. Chronic inflammation of the airway leads to mucosal edema, mucosal secretion, produc­ing shortness of breath, chest tightness, and wheezing. The patient presented in this case study also suffering from asthma since her childhood. The history, physical examination and laboratory studies confirmed the diagnosis. This case study discussed the major pathophysiological concepts related to the clinical manifestations, diagnostic measures and problems identified. The detailed patient assessment also included. The main problems identified were lack of health care facilities since she is living in suburbs. The rural health nurse visiting the nurse should pay special attention in Mrs. X case for making them in adhering with the follow up and preventing the episodes.

 

REFERENCES:

1.       Bostock-Cox, B. (2010). Revisiting diagnosis and assessment of asthma. Practice Nursing21(6), 285.

2.       Lewis LS, Heitkemper M, Driksen SR (2008). Asthma. Medical Surgical Nursing. 7thEdn: Mosby Publication, St. Lousin. 842-88.

3.       Cartier, A., and Sastre, J. (2011). Clinical assessment of occupational asthma and its differential diagnosis. Immunology and Allergy Clinics Of North America31(4), 717-728

4.       McCormack, M., and Enright, P. (2008). Making the diagnosis of asthma. Respiratory Care53(5), 583-592.

5.       Sims, J. (2006). An overview of asthma. Dimensions Of Critical Care Nursing25(6), 264-268.

6.       Murphy, D., and O'Byrne, P. (2010). Recent advances in the pathophysiology of asthma. Chest137(6), 1417-1426. doi:10.1378/chest.09-1895

7.       Hill, V., and Wood, P. (2009). Asthma epidemiology, pathophysiology, and initial evaluation. Pediatrics In Review30(9), 331-336. doi:10.1542/pir.30-9-331

8.       Kaufman, G. (2011). Asthma: pathophysiology, diagnosis and management. Nursing Standard26(5), 48-56.

9.       Papiris, S., Manali, E., Kolilekas, L., Triantafillidou, C., and Tsangaris, I. (2009). Acute severe asthma: new approaches to assessment and treatment. Drugs69(17), 2363-2391. doi:10.2165/11319930-000000000-00000

10.     Barrios, R., Kheradmand, F., Batts, L., and Corry, D. (2006). Asthma: pathology and pathophysiology. Archives Of Pathology and Laboratory Medicine130(4), 447-451.

 

 

 

Received on 22.06.2014           Modified on 25.06.2014

Accepted on 30.06.2014           © A&V Publication all right reserved

Int. J. Nur. Edu. and Research 2(2): April- June 2014; Page 117-120