2.4.1 Short Answer Exam based on one case study of acute life-threatening and/or traumatic complex health condition
Explain the pathogenesis causing the clinical manifestations with which Poppy presents.
Asthma is a chronic inflammation of lungs. Various allergens result in asthmatic response. Bronchoconstriction is the dominant event in physiology that causes the clinical manifestations (King et al., 2018). This narrows the airways and interferes in airflow process. When acute asthma exacerbations occur as diagnosed in Poppy’s case, bronchial smooth muscles contract quickly and make airways narrowed as a response to have exposure to a broader range of stimuli that includes allergens and irritants (Caperell et al., 2019). Mast cells release the IgE-dependent mediators that results in allergen-induced bronchoconstriction. The mediators or antibody receptors consist of histamine, leukotrienes, prostaglandins, and tryptase contracting the airway smooth muscles directly. In allergic asthma pathogenesis, the mast cells play the important role. Histamine is the central mediator and player in obstructing the airway via smooth muscle contraction, bronchial secretion and airway mucosal edema (Yamauchi & Ogasawara, 2019). At the same time, other cytokines from the mast cells signal other inflammatory cells. The immunoglobin antibodies that have allergens get attached to mast cells. Histamine and other mediator receptors lead to allergic reaction and causes airway inflammation, mucus secretion, wheezing, bronchospasm, and increased vascular permeability (Caperell et al., 2019). Further, inflammation process is continued by multiple inflammatory cells such as activated eosinophils and T-cells. Cytokines maintain the inflammatory process being secreted by the antigen induced T helper cells as suggested by Yamauchi & Ogasawara (2019). Slowly, inflammation results in the development of mucus plugging into airway and this increases mucus in alveoli. The severity of asthma attack makes the patient have difficulty in breathing out and also feels harder in breathing and this progress the airway obstruction. Air also gets trapped behind the obstructed and narrowed airways. This results in lung hyperinflation (Caperell et al., 2019). This led to deteriorated vital signs of Poppy as making her tachycardic at 160 beats per minute, decrease in oxygen saturation SpO2 at 87% on air and raised respiration rate at 42 breaths per minute (King et al., 2018).
Due to respiratory infection, lung sensitivity increases that makes compel to cough and breathe. It occurs also in the form of reduced auscultation AE bibasally and inspiratory and expiratory wheezing as evident in the case. Poppy is also speaking in single words (King et al., 2018). This could be due to airway hyperresponsiveness that means bronchoconstrictor response has exaggerated to the stimuli. The hyperresponsiveness level depends on the contractile responses to the various challenges present with methacholine that correlates with the severity of clinical asthma (Caperell et al., 2019). Inflammation, dysfunctional neuro-regulation and structural changes influence airway hyperresponsiveness, but inflammation to be the major factor (Caperell et al., 2019). This hyperresponsive releases mucus in increased amount that contributes to exacerbation. If this inflammation and exacerbation continues, factors such as oedema also make contribution to complex breathing, specifically with symptoms of expiration and wheezing evident in case. More power is required in the body for relieving this tension (King et al., 2018). This is causing Poppy little distressed using accessory muscle and shoulder shrugging on inspiration and using tracheal tug. This has also contributed to tachycardia. Poppy is a child with lesser alveoli in comparison to adults that increase the body pressure. It increases oxygen demand making decline in patient’s respiratory function as reported (Yamauchi & Ogasawara, 2019). This also makes patient hypoxic as Poppy is due to the mismatch of gases and impairment of gas exchange making her PaCO2 high. This further developed respiratory acidosis as her lungs are not capable to eliminate carbon dioxide due to respiratory failure (Yamauchi & Ogasawara, 2019).
1. Sit Poppy in a High Fowlers position
– How does positioning a patient with acute asthma in a High Fowlers position assist to alleviate respiratory distress?
This position for patient with acute asthma helps in alleviating respiratory distress as it relaxed the tension of abdominal muscles, permitting for enhanced breathing. In the immobile patients and infants, this position also alleviates chest compression that occurs because of gravity that assists in enhancing respiratory status of patient (Caperell et al., 2019).
2. Apply and titrate oxygen
– What oxygen delivery device will you use?
I will use the high-flow nasal cannula (HFNC) device for delivering oxygen as it is a proven device for effectiveness and safety in managing asthma in children (Fergeson, Patel & Lockey, 2017).
– Why did you choose this device?
Poppy’s SpO2 is 87% and HFNC is effective in increasing expiratory flow and raising ventilation and perfusion ratio that will enhance SpO2 of the child in a dramatic way (Durham et al., 2017).
– How does providing supplemental oxygen work and, how will it assist Poppy?
Poppy’s oxygen saturation is 87% and it needs supplemental oxygen in child and HFNC will assist in enhancing saturation value and will decrease the respiratory acidosis of Poppy (Fergeson et al., 2017).
For each medication below explain
– The mechanism of action.
– Why your patient is receiving this medication in relation to her symptoms and diagnosis?
– What are the nursing considerations for this medication?
– What clinical response you expect?
– What continuing clinical observations will you need to undertake?
Salbutamol via nebuliserà
Salbutamol binds with β2 adrenoceptor certainly with relatively low affinity, but moderate efficacy and act as an agonist. This has shorter half-life because of faster re-equilibration of the drug at active site having restricted residency time (Durham et al., 2017). The activation of β2 adrenoceptor results in increase in the intracellular cAMP and also activates protein kinase A causing smooth muscle relaxation. The protein kinase A is also fund to activate Na/K ATPase that facilitates K+ transportation throughout the cell membrane in the cell and stabilizes the potential membrane (Katsunuma et al., 2019).
Poppy has asthma and her respiratory muscles need relaxation through salbutamol and it will also raise her oxygen saturation level (Caperell et al., 2019).
The nursing considerations must focus on assessing lung sounds, blood pressure, pulse rate prior drug administration and during medication peak; observation of paradoxical spasm; administration of PO medications with meals to reduce gastric irritation; and to allow 1 minutes atleast between aerosol drug inhalation (Katsunuma et al., 2019).
The expected clinical response is relief in asthma, and wheezing and improved SpO2 values and no use of accessory muscles for respiration (Katsunuma et al., 2019).
Comprehensive monitoring is required with regular check of side effects like anxiety, fine tremor, muscle cramps, headache, palpitation and dry mouth (Caperell et al., 2019).
Its short term effects are reduced vasodilation and permeability of capillaries and reduced leukocyte migration towards inflammation sites. This drug binds with glucocorticoid receptor and mediates the changes in the gene expression that results in multiple downstream impacts over hours to days (Doymaz et al., 2020). This drug inhibits demargination and neutrophil apoptosis and inhibits phospholipase A2 that reduces the arachidonic acid derivative formation. They further inhibit NF-Kappa B and several other inflammatory transcription factors. They also promote anti-inflammatory genes such as interleukin-10. The lower corticosteroid dose gives anti-inflammatory impact and higher dosage to be immunosuppressive (Fergeson et al., 2017).
Poppy is suffering from hyperinflation of both her lungs and inflammation of bronchus and this drug needs to be administered to reduce inflammation (Fergeson et al., 2017).
The nursing considerations primarily focus on taking Poppy’s history and physical assessment to assure that she is fit to be administered with this drug. It should be given daily prior 9am to mimic normal peak of diurnal corticosteroid levels and reduce HPA suppression (Doymaz et al., 2020). Its side effects must be closely observed like increased appetite, difficulty sleeping, irritability, stomach upset, mood swings and raised BGL. The nurse also has to assess the signs of raised intracranial pressure as mandatyory in children including the alterations in behaviour and mood, reduced consciousness, lethargy, headache, vomiting and seizures. This needs to be notified immediately to physician if occurs (Doymaz et al., 2020).
The expected clinical response is that Poppy will have reduction in inflammatory airway and there will be rise in her SpO2 level and her wheezing will also reduce (Doymaz et al., 2020).
Clinical observations should focus on regular checking of side effects and Poppy’s response to therapy. Moreover, periodic blood work must be monitored through complete blood count (CBC) test and kidney and liver function test (Doymaz et al., 2020). Moreover, side effects of headache, nausea, heartburn, trouble sleeping, dizziness, acne or increased sweating needs to be monitored. This drug weakens the immune system and can reduce the capability to fight infections (Durham et al., 2017).
Ipratropium Bromide via nebuliserà
Ipratropium bromide is the anticholinergic (parasympatholytic) agent that blocks acetylcholine’s muscarinic receptors and inhibits vagally mediated reflexes through the action of antagonizing by acetylcholine that is the transmitter agent being released through the vagus nerve (Suruki et al., 2017).
Poppy is having the diagnosis of asthma and there is higher chance of airway narrowing that means the constriction of airway. Thus, ipratropium bromide assists in brocnhidilation by raising the levels of SpO2 (Fergeson et al., 2017).
The nursing considerations must primarily focus on managing the side effects of this drug as dry mouth, buccal ulceration, urinary retention, headache, nausea, paralytic ileus, nasal dryness, paradoxical bronchospasm, constipation, trachycardia and immediate hypersensitivity reactions (Suruki et al., 2017). The nurse should repeat the dosage every 4-6 hours as per doctor’s prescription. The nurse has to assure that Poppy has adequate hydration with better control over environmental temperature. Poppy should be made void prior taking this drug to prevent urinary retention (Suruki et al., 2017).
The expected response in decrease in bronchodilation and secretion with rise in SpO2 value (Suruki et al., 2017).
The clinical observations for symptoms of bladder pain, breathlessness, lower back or side pain breathing difficulty, cough producing mucus, bloody or cloudy urine, frequent urge for urination, and difficulty in urinating (Durham et al., 2017).
Caperell, K., Pettigrew, J., Gerughty, A., & Stevenson, M. (2019). Provider Prediction of Disposition for Children With an Acute Exacerbation of Asthma Presenting to the Pediatric Emergency Department. Pediatric emergency care, 35(2), 108-111.
Doymaz, S., Ahmed, Y., Gist, R., Pinto, R., Steinberg, M., & Giambruno, C. (2020). 1182: COMPARISON OF DIFFERENT TYPES OF INTRAVENOUS STEROIDS IN PEDIATRIC ACUTE SEVERE ASTHMA TREATMENT. Critical Care Medicine, 48(1), 569.
Durham, C. O., Fowler, T., Smith, W., & Sterrett, J. (2017). Adult asthma: Diagnosis and treatment. The Nurse Practitioner, 42(11), 16-24.
Fergeson, J. E., Patel, S. S., & Lockey, R. F. (2017). Acute asthma, prognosis, and treatment. Journal of Allergy and Clinical Immunology, 139(2), 438-447.
Katsunuma, T., Fujisawa, T., Maekawa, T., Akashi, K., Ohya, Y., Adachi, Y., ... & Sako, M. (2019). Low-dose l-isoproterenol versus salbutamol in hospitalized pediatric patients with severe acute exacerbation of asthma: A double-blind, randomized controlled trial. Allergology International, 68(3), 335-341.
King, G. G., James, A., Harkness, L., & Wark, P. A. (2018). Pathophysiology of severe asthma: We’ve only just started. Respirology, 23(3), 262-271.
Suruki, R. Y., Daugherty, J. B., Boudiaf, N., & Albers, F. C. (2017). The frequency of asthma exacerbations and healthcare utilization in patients with asthma from the UK and USA. BMC pulmonary medicine, 17(1), 74.
Yamauchi, K., & Ogasawara, M. (2019). The Role of Histamine in the Pathophysiology of Asthma and the Clinical Efficacy of Antihistamines in Asthma Therapy. International journal of molecular sciences, 20(7), 1733.