Introduction
Flexible fiberoptic bronchoscopy (FB) is a valuable tool in the investigation, diagnosis and monitoring of children with inflammatory lung disease [1-2]. Bronchoalveolar lavage (BAL) is a significant component of the procedure [3]. It is useful not only for the microbiological investigation, but also for the analysis of cellular and noncellular inflammatory mediators. Various studies have assessed the cellular profiles and have analyzed the levels of inflammatory mediators of BAL from children with respiratory diseases and normal children [4-5]. Furthermore, there is a solid interest in the investigation of inflammatory mediators in BALF samples in an attempt to clarify the underlying mechanisms of lung disease.
Lung infection attracts neutrophils to the site of inflammation as infected cells and macrophages release a wide range of chemotactic factors. Accumulation of neutrophils at the site of inflammation leads to the release of a wide range of pro-inflammatory cytokines and chemokines, including IL-8, IL-6, TNF-a, and tissue degradation proteases like matrix metalloproteinase-9 (MMP-9). The elevation of such mediators has a positive feedback to the neutrophilic influx on the inflamed site and to the lung injury. Bacterial infection plays a crucial role in neutrophilic inflammation of the lung and moreover the subclinical infection in healthy subjects could explain symptoms like chronic non specific cough. β-Glucuronidase is a lysosomal enzyme that catalyzes the hydrolysis of glycosaminoglycans [6] and thus is responsible for the degradation of extracellular matrix components. It is situated intracellularly [7] and during inflammation, β-glucuronidase is released from the lysosomes in the extracellular fluid [8]...
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Hospital-acquired infections (HAI) are preventable and pose a threat to hospitals and patients; increasing the cost, nominally and physically, for both. Pneumonia makes up approximately 15% of all HAI and is the leading cause of nosocomial deaths. Pneumonia is most frequently caused by bacterial microorganisms reaching the lungs by way of aspiration, inhalation or the hematogenous spread of a primary infection. There are two categories of Hospital-Acquired Pneumonia (HAP); Health-Care Associated Pneumonia (HCAP) and Ventilator-associated pneumonia (VAP).
Cystic Fibrosis (CF) Pathophysiology: Cystic fibrosis is a genetic disease of the secretory glands that affects the respiratory and digestive system. It mainly affects the lungs, pancreas, liver, intestines, sinuses, and reproductive organs. Cystic fibrosis affects the cells that produce sweat, mucus, and digestive fluids. Mucus becomes thick and sticky, causing build-up in the lungs and blocking airways, making it easier for bacteria to develop. This prompts repeated lung infections and can cause severe lung damage after some time.
Sequeiros, IM, Jarad, NA. 2009. Home intravenous antibiotic treatment for acute pulmonary exacerbations in cystic fibrosis-Is it good for the patient?. Annals of Thoracic Medicine 4(3), pp. 111-114.
Ventilator Associated Pneumonia (VAP) is a very common hospital acquired infection, especially in pediatric intensive care units, ranking as the second most common (Foglia, Meier, & Elward, 2007). It is defined as pneumonia that develops 48 hours or more after mechanical ventilation begins. A VAP is diagnosed when new or increase infiltrate shows on chest radiograph and two or more of the following, a fever of >38.3C, leukocytosis of >12x10 9 /mL, and purulent tracheobronchial secretions (Koenig & Truwit, 2006). VAP occurs when the lower respiratory tract that is sterile is introduced microorganisms are introduced to the lower respiratory tract and parenchyma of the lung by aspiration of secretions, migration of aerodigestive tract, or by contaminated equipment or medications (Amanullah & Posner, 2013). VAP occurs in approximately 22.7% of patients who are receiving mechanical ventilation in PICUs (Tablan, Anderson, Besser, Bridges, & Hajjeh, 2004). The outcomes of VAP are not beneficial for the patient or healthcare organization. VAP adds to increase healthcare cost per episode of between $30,000 and $40,000 (Foglia et al., 2007) (Craven & Hjalmarson, 2010). This infection is also associated with increase length of stay, morbidity and high crude mortality rates of 20-50% (Foglia et al., 2007)(Craven & Hjalmarson, 2010). Currently, the PICU has implemented all of the parts of the VARI bundle except the daily discussion of readiness to extubate. The VARI bundle currently includes, head of the bed greater then or equal to 30 degrees, use oral antiseptic (chlorhexidine) each morning, mouth care every 2 hours, etc. In the PICU at children’s, the rates for VAP have decreased since the implementation of safety ro...
Ventilator-associated pneumonia (VAP) remains to be a common and potentially serious complication of ventilator care often confronted within an intensive care unit (ICU). Ventilated and intubated patients present ICU physicians, nurses, and respiratory therapists with the unique challenge to integrate evidence-informed practices surrounding the delivery of high quality care that will decrease its occurrence and frequency. Mechanical intubation negates effective cough reflexes and hampers mucociliary clearance of secretions, which cause leakage and microaspiration of virulent bacteria into the lungs. VAP is the most frequent cause of nosocomial infections and occurs within 48 hours of intubation. VAP is a major health care burden with its increased morbidity, mortality, longer ventilator days and hospital stay, and escalating health care cost.
Croup: Croup is another common airway inflammation caused by virus that can affect the trachea, larynx and possibility the bronchi (Murray, Sidani, & Zoorob, 2011) thus causing infection in the upper respiratory tract. Murray et al. describes it as the most common illness in children under the age of 6 to 36 months and cause for cough mostly when a child cries; acute stridor and hoarseness in febrile children (Murray et al., 2011). It can be a life-threatening situation in the life of the young infant and the family. Croup symptoms exhibit as hoarseness, barking cough, inspiratory stridor, and respiratory distress. I chose this diagnosis as my first preference because when I read the mother’s subjective report it matches that of croup symptoms: a barking cough, no fever, severe at night and when the baby cries, fatigue due to excessiveness of the tears, pain due to inflames and swollen of the airway. Murray et al., led us to understand that the etiologies of this viral causing agent can be traced to the parainfluenza viruses, type 1. (2011). This virus is commonly spread through contact or droplet secretion.
My disease is Streptococcal pneumonia or pneumonia is caused by the pathogen Streptococcus pneumoniae. Streptococcus pneumoniae is present in human’s normal flora, which normally doesn’t cause any problems or diseases. Sometimes though when the numbers get too low it can cause diseases or upper respiratory tract problems or infections (Todar, 2008-2012). Pneumonia caused by this pathogen has four stages. The first one is where the lungs fill with fluid. The second stage causes neutrophils and red blood cells to come to the area which are attracted by the pathogen. The third stage has the neutrophils stuffed into the alveoli in the lungs causing little bacteria to be left over. The fourth stage of this disease the remaining residue in the lungs are take out by the macrophages. Aside from these steps pneumonia follows, if the disease should persist further, it can get into the blood causing a systemic reaction resulting in the whole body being affected (Ballough). Some signs and symptoms of this disease are, “fever, malaise, cough, pleuritic chest pain, purulent or blood-tinged sputum” (Henry, 2013). Streptococcal pneumonia is spread through person-to-person contact through aerosol droplets affecting the respiratory tract causing it to get into the human body (Henry, 2013).
Haas, D. F. (1990). The Chronic Bronchitis And EMPHYSEMA. New York,NY: John Wiley and Sons, Inc.
...pecific leukotriene receptors on bronchial tissues, therefore preventing bronchoconstriction, mucus secretion, and oedema. These treatments also reduce the influx of eosinophils, which results the ability to limit inflammatory damage being caused in the airway. These oral, non-steroidal, anti-inflammatory drugs reduce the incidence of acute asthma attacks when taken on a regularly basis. Although in cases of acute asthmatic attacks medical intervention and treatment is required. The type of intervention depends on the severity of the attack itself.
Imagine a young child competing with his or her fellow classmates during recess and immediately losing the ability to breathe normally. He or she stops in the middle of the competition and falls to the ground while holding his or her chest trying to find air. When you are young, being able to keep up with your peers during recess and sporting events is very important, however, having asthma restricts this. Asthma has a significant impact on childhood development and the diagnosis of asthma for children 18 years and younger has dramatically increased over the years. Asthma is known as a “chronic inflammation of the small and large airways” with “evident bronchial hyper-responsiveness, airflow obstruction, and in some patients, sub-basement fibrosis and over-secretion of mucus” (Toole, 2013). The constant recreation of the lung walls can even occur in young children and “lead to permanent lung damages and reduced lung function” (Toole, 2013). While one of the factors is genetics, many of the following can be prevented or managed. Obesity, exposure to secondhand smoke, and hospitalization with pneumonia in the early years of life have all been suggested to increase children’s risk of developing asthma.
Liam is a previously healthy boy who has experienced rhinorrhoea, intermittent cough, and poor feeding for the past four days. His positive result of nasopharyngeal aspirate for Respiratory Syncytial Virus (RSV) indicates that Liam has acute bronchiolitis which is a viral infection (Glasper & Richardson, 2010). “Bronchiolitis is the commonest reason for admission to hospital in the first 6 months of life. It describes a clinical syndrome of cough tachypnoea, feeding difficulties and inspiratory crackles on chest auscultation” (Fitzgerald, 2011, p.160). Bronchiolitis can cause respiratory distress and desaturation (91% in the room air) to Liam due to airway blockage; therefore the infant appears to have nasal flaring, intercostal and subcostal retractions, and tachypnoea (54 breathes/min) during breathing (Glasper & Richardson, 2010). Tachycardia (152 beats/min) could occur due to hypoxemia and compensatory mechanism for low blood pressure (74/46mmHg) (Fitzgerald, 2011; Glasper & Richardson, 2010). Moreover, Liam has fever and conjunctiva injection which could be a result of infection, as evidenced by high temperature (38.6°C) and bilateral tympanic membra...
In patients infected with K. pneumonia, inflammatory mechanisms can cause tissue damage that is related with a release of “alarm proteins” (Achouiti, 2012). These alarm proteins are known as the Damage Associated Molecular Patters (DAMPs) and are seen in neutrophils where they potentially affect up to 45 percent of the cytoplasmic protein (Achouiti, 2012). This is harmful because it inhibits the body’s ability to fight the infection, as neutrophils are the body’s natural immunity defense.
Chronic obstructive pulmonary disease (COPD) is preventable disease that has a detrimental effects on both the airway and lung parenchyma (Nazir & Erbland, 2009). COPD categorises emphysema and chronic bronchitis, both of which are characterised by a reduced maximum expiratory flow and slow but forced emptying of the lungs (Jeffery 1998). The disease has the one of the highest number of fatalities in the developed world due to the ever increasing amount of tobacco smokers and is associated with significant morbidity and mortality (Marx, Hockberger & Walls, 2014). Signs and symptoms that indicate the presence of the disease include a productive cough, wheezing, dyspnoea and predisposing risk factors (Edelman et al., 1992). The diagnosis of COPD is predominantly based on the results of a lung function assessment (Larsson, 2007). Chronic bronchitis is differentiated from emphysema by it's presentation of a productive cough present for a minimum of three months in two consecutive years that cannot be attributed to other pulmonary or cardiac causes (Marx, Hockberger & Walls, 2014) (Viegi et al., 2007). Whereas emphysema is defined pathologically as as the irreversible destruction without obvious fibrosis of the lung alveoli (Marx, Hockberger & Walls, 2014) (Veigi et al., 2007).It is common for emphysema and chronic bronchitis to be diagnosed concurrently owing to the similarities between the diseases (Marx, Hockberger & Walls, 2014).
Chronic bronchitis is a disorder that causes inflammation to the airway, mainly the bronchial tubules. It produces a chronic cough that lasts three consecutive months for more than two successive years (Vijayan,2013). Chronic Bronchitis is a member of the COPD family and is prominently seen in cigarette smokers. Other factors such as air pollutants, Asbestos, and working in coal mines contributes to inflammation. Once the irritant comes in contact with the mucosa of the bronchi it alters the composition causing hyperplasia of the glands and producing excessive sputum (Viayan,2013). Goblet cells also enlarge to contribute to the excessive secretion of sputum. This effects the cilia that carry out the mechanism of trapping foreign bodies to allow it to be expelled in the sputum, which are now damaged by the irritant making it impossible for the person to clear their airway. Since the mechanism of airway clearance is ineffective, the secretion builds up a thickened wall of the bronchioles causing constriction and increasing the work of breathing. The excessive build up of mucous could set up pneumonia. The alveoli are also damaged enabling the macrophages to eliminate bacteria putting the patient at risk for acquiring an infection.
Nursing Diagnosis I for Patient R.M. is ineffective airway clearance related to retained secretions. This is evidenced by a weak unproductive cough and by both objective and subjective data. Objective data includes diagnosis of pneumonia, functional decline, and dyspnea. Subjective data include the patient’s complaints of feeling short of breath, even with assistance with basic ADLs. This is a crucial nursing diagnosis as pneumonia is a serious condition that is the eighth leading cause of death in the United States and the number one cause of death from infectious diseases (Lemon, & Burke, 2011). It is vital to keep the airway clear of the mucus that may be produced from the inflammatory response of pneumonia. This care plan is increasingly important because of R.M.'s state of functional decline; he is unable to perform ADL and to elicit a strong cough by himself due to his slouched posture. Respiratory infections and in this case, pneumonia, will further impair the airway (Lemon, & Burke, 2011). Because of the combination of pneumonia and R.M's other diagnoses of lifelong asthma, it is imperative that the nursing care plan of ineffective airway clearance be carried out. The first goal of this care plan was to have the patient breathe deeply and cough to remove secretions. It is important that the nurse help the patient deep breathe in an upright position; this is the best position for chest expansion, which promotes expansion and ventilation of all lung fields (Sparks and Taylor, 2011). It is also important the nurse teach the patient an easily performed cough technique and help mobilize the patient with ADL's. This helps the patient learn to cough and clear their airways without fatigue (Sparks a...