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Group 3 Ala Ards
Group 3 Ala Ards
CASE SCENARIO
Mr. Juan is a 50 year old man who presents to his primary care provider (PCP)
on Monday with complaints of a productive cough for 3 days with fever, chills, fatigue
beginning in the last 24 hours. His PCP hears coarse rhonchi in Mr. Juan’s lungs and decides
to take a chest x-ray. The X-ray shows right lower lobe infiltrates. His rapid flu swab is
negative. Mr. Juan’s vital signs were as follows:
BP 122/73 mmHg
HR 102 bpm
RR 27 bpm
Temp 38.6°C
Mr. Juan s diagnosed with pneumonia and sent home on Azithromycin. Two days later,
on Wednesday, Mr. Juan still has the cough, fever, chills, and fatigue and is now having body
aches on and off and is short of breath intermittently. He calls his PCP concerned that the
antibiotics are not working. His PCP agrees and changes his antibiotic to Amoxicillin.
On Thursday, Mr. Juan’s wife calls his PCP again because he is struggling to even get out of
bed and is very fatigued and feverish. She reports a fever of 102.9°F. The PCP tells him to
come into the clinic. He arrives at the clinic 20 minutes later.
Upon further assessment, Mr. Juan has rhonchi throughout his lung fields, with occasional
expiratory wheezes. He appears pale and is lethargic. His skin is tenting on his sternum and
his nail beds are pale. The following data are gathered:
Subjective:
Complains shortness of breath, inability to lie flat and diffuse abdominal pain.
Objective:
BP 100/60 mmHg HR 116 bpm
RR 30 bpm
Temp 38.8°C
Diagnostic findings:
PaO2 59mmHg
PaCO2 27mmHg
HCO3 16 mEq/L
O2 Sat 89%
In ARDS, fluid builds up inside the tiny air sacs of the lungs, and surfactant breaks
down. Surfactant is a foamy substance that keeps the lungs fully expanded so that a
person can breathe. These changes prevent the lungs from filling properly with air and
moving enough oxygen into the bloodstream and throughout the body. The lung tissue
may scar and become stiff.
ARDS may develop over a few days, or it can get worse very quickly. The first
symptom of ARDS is usually shortness of breath. Other signs and symptoms are low
blood oxygen, rapid breathing, and clicking, bubbling, or rattling sounds in the lungs
when breathing.
ARDS can develop at any age. To diagnose ARDS, the physician will do a physical
exam, review the patient’s medical history, measure blood oxygen levels, and order a
chest X-ray. Supplying oxygen is the main treatment for ARDS. Other treatments
help make the patient more comfortable or aim to eliminate the cause of ARDS.
Treatments for ARDS may help prevent serious or life-threatening complications,
including organ damage or organ failure.
Statistical Data
Related Implications
Nursing Education
This will help to provide students and clinical instructors to expand and improved
essential knowledge about effective ways to deliver health care to patient and aiming
of nursing education for the development of nursing profession.
Nursing Practice
This will help health care providers determine effective best practices, correct old
misunderstanding studies, pave new treatment, procedure protocols, and create new
methodology – all which patient care who received a diagnosis of ARDS.
Nursing Research
This will serve as a guide for future researchers-students, clinical instructors and
health care providers to provide services and treatments for future generation to help
develop new test for diagnosis, treatments and procedure.
IV. DISCHARGE PLANNING
Acute respiratory distress syndrome (ARDS) remains a major cause of morbidity and
mortality in critically ill patients. Over the past several decades, alcohol abuse and cigarette
smoke exposure have been identified as risk factors for the development of ARDS. The most
common cause of ARDS, a serious infection in the lungs (pneumonia) or other organs with
widespread inflammation. Aspiration pneumonia: Aspiration of stomach contents into the
lungs may cause severe lung damage and ARDS. The coronavirus (COVID-19): The
infection COVID-19 may develop into severe ARDS.
The Florence’s theory of environment was used to guide this study. Florence’s theory of
environment which suggests that an individual’s health is the outcome of his environmental
alteration. Hence, health care professionals particularly nurses, need to modify the
environment in favor of individual’s wellbeing to promote faster recovery and health. It
defined Nursing as “the act of utilizing the environment of the patient to assist him in his
recovery.” It involves the nurse’s initiative to configure environmental settings appropriate
for the gradual restoration of the patient’s health and that external factors associated with the
patient’s surroundings affect the life or biologic and physiologic processes and his
development. The Environment Theory of nursing is a patient-care theory. That is, it focuses
on the care of the patient rather than the nursing process, the relationship between patient and
nurse, or the individual nurse.
Nursing in Nightingale's view is an art of how to let nature work on humans to make the
ill healthy and the healthy remain the same. However a nurse is the one who makes such
conditions in which these laws are easily applicable on patients to achieve the desired health
status. As Nightingale (1860) in notes of nurses says, “If a patient is cold, if a patient is
feverish, if a patient is faint, if he is sick after taking food, if he has a bed-sore, it is generally
the fault not of the disease, but of the nursing”. On this Selanders (2010), comments by
saying “The implication is clear, the nurse is responsible for maintaining the environment in
such a manner as to maintain the health of the patient”. So a nurse should identify why
patient is having the suffering and which of the nature's law is the need of the patient and
how this can be achieved by changing the environment. That is why Nightingale proposed the
assumptions that nursing is an art and a science, nursing is achieved through environmental
alteration, and nursing requires a specific educational base.
B. Roy Adaptation Theory
Many patients confront physical, cognitive, and emotional problems after acute
respiratory distress syndrome (ARDS). No proven therapies for these problems exist, and
many patients manage new disability and recovery with little formal support. According to
Roy adaptation model, the aim of nursing is to increase compliance and life expectancy. Roy
Adaptation Model evaluates the patient in physiologic mode, self-concept mode, role
function mode and interdependence mode aiming to provide holistic care.
The goal of nursing is to promote adaptation for individual(s) in four adaptive modes, thus
contributing to health, quality of life, and dying with dignity. This is done by assessing
behaviour and factors that influence adaptive abilities and by intervening to expand those
abilities and to enhance environmental inter-actions (Roy, 2005). As a practice discipline, the
goal of nursing is to promote adaptation by enhancing human system and environment
interaction. Using information from this study to build a predictive model will help nurses in
assessing adaptive behaviors and the stimuli that influence adaptation behaviour. This
information will be useful for nursing interventions, plans to manage stimuli and enhance
coping processes for patients with ARDS. In this study, life stress events and social support
were defined as the residual stimuli. Stress has a strong effect on coping (Lazarus &
Folkman, 2009), and social support are believed to be components of the social network that
can effect the way patients with ARDS deal with their conditions.
VI. REVIEW OF RELATED LITERATURE
Until recently, a mortality rate in excess of 50% had been consistently documented for
ARDS patients (Brandstetter, Sharma, DellaBadia, Cabreros, & Kabinoff, 1997; Sloane et al.,
1992). More recent reports, however, suggest that this may be changing favorably to less than
40% (Abel et al., 1998; Amato et al., 1998; Amato et al., 1995; ARDS Network, 2000;
Callister & Evans, 2002; McIntyre et al., 2000; Milberg, Davis, Steinberg, & Hudson, 1995).
In order to sustain this trend of declining mortality, a better understanding of the relationships
between various structures and processes of care for ARDS to outcomes of this care is
needed. Evaluation of the quality of care for patients with ARDS requires an understanding
of the disease process as well as the associated components and outcomes of care.
Mechanical ventilation and monitoring as processes of care are especially important in the
identification of potential quality indicators. This section will include a review of the
literature related to the use of mechanical ventilation and monitoring as interventions for
ARDS as well as relationships between associated patient characteristics and outcomes
pertinent to the study.
Ashbaugh and colleagues (Ashbaugh, Bigelow, Petty, & Levine, 1967) are generally
credited with introducing ARDS in their report of 12 patients exhibiting a similar clinical
pattern of acute respiratory distress who did not respond to known treatment. Noted that the
clinical and pathologic features of this syndrome were strikingly similar to those seen in
infantile respiratory distress syndrome (RDS), and included acute onset of tachypnea,
hypoxemia, and loss of compliance. Necropsy 18 findings revealed areas of alveolar
atelectasis, interstitial and intraalveolar edema, intraalveolar hemorrhage, hyaline
membranes, and interstitial inflammation with fibrosis. Since that time, ARDS continues to
be the focus of much investigation to identify etiologic factors and pathophysiologic
processes. ARDS is now known to result from a diffuse inflammatory process leading to
pulmonary microvascular permeability accompanied by pulmonary interstitial and
intraalveolar edema and microatelectasis (Aberle & Brown, 1990; Bachofen & Weibel, 1982;
Bone, Gravenstein, & Kirby, 1980; Sugarman, Rogers, & Miller, 1972; Tomashefski, 1990).
Progressive alveolar collapse, decreased functional residual capacity (FRC), and increased
intrapulmonary shunt are the predominant manifestations of this pathogenesis. Clinically,
patients experience profound arterial hypoxemia and noncompliant or “stiff” lungs
(Brandstetter et al., 1997; Ware & Matthay, 2000). The severity of the clinical findings
associated with ARDS is testimony to the diffuse nature of the parenchymal damage. It has
been estimated that 50-70% of the lung units are poorly aerated or non-aerated in the ARDS
lung (Gattinoni, Pesenti, Avalli, Rossi, & Bombino, 1987). This diffuse injury is
heterogeneously distributed with pockets of normally aerated and compliant lung units
interspersed throughout (Gattinoni et al., 1987; Marcy & Marini, 1991). Such heterogeneity
of lung injury has been identified as a primary source of difficulty in providing optimal
mechanical ventilation for this patient population (MacIntyre, 1996a; Shapiro & Peruzzi,
1995). The respiratory mechanics of aerated lung units are more favorable to inflation than
those that are partially or non-aerated. The application of traditional positive 19 pressure
mechanical ventilation techniques thus results in a non-uniform distribution of ventilation
with overdistention of some units and underventilation of others which creates an
environment favoring the development of ventilator-induced lung injury (VILI) (Shapiro &
Peruzzi, 1995). This propensity for hyperinflation of aerated lung units is aggravated by large
tidal volumes and elevated airway pressures (MacIntyre, 1996; Marini, 1996; Sessler, 1998).
Interestingly, many forms of VILI are indistinguishable histologically from those lesions
incurred during the initial ARDS insult (Tsuno, Miura, Takeya, Kolobow, & Morioka, 1991)
(According to Aaron, S., et al., 2012), Acute respiratory distress syndrome manifests as
rapidly progressive dyspnea, tachypnea, and hypoxemia. Diagnostic criteria include acute
onset, profound hypoxemia, bilateral pulmonary infiltrates, and the absence of left atrial
hypertension. Acute respiratory distress syndrome is believed to occur when a pulmonary or
extrapulmonary insult causes the release of inflammatory mediators, promoting neutrophil
accumulation in the microcirculation of the lung. Neutrophils damage the vascular
endothelium and alveolar epithelium, leading to pulmonary edema, hyaline membrane
formation, decreased lung compliance, and difficult air exchange. Most cases of acute
respiratory distress syndrome are associated with pneumonia or sepsis. It is estimated that 7.1
percent of all patients admitted to an intensive care unit and 16.1 percent of all patients on
mechanical ventilation develop acute lung injury or acute respiratory distress syndrome. In-
hospital mortality related to these conditions is between 34 and 55 percent, and most deaths
are due to multiorgan failure. Acute respiratory distress syndrome often has to be
differentiated from congestive heart failure, which usually has signs of fluid overload, and
from pneumonia. Treatment of acute respiratory distress syndrome is supportive and includes
mechanical ventilation, prophylaxis for stress ulcers and venous thromboembolism,
nutritional support, and treatment of the underlying injury. Low tidal volume, high positive
end-expiratory pressure, and conservative fluid therapy may improve outcomes. A
spontaneous breathing trial is indicated as the patient improves and the underlying illness
resolves. Patients who survive acute respiratory distress syndrome are at risk of diminished
functional capacity, mental illness, and decreased quality of life; ongoing care by a primary
care physician is beneficial for these patients.
Acute respiratory distress syndrome (ARDS) is a rapidly progressive disorder that initially
manifests as dyspnea, tachypnea, and hypoxemia, then quickly evolves into respiratory
failure. The American-European Consensus Conference (AECC) has published diagnostic
criteria for ARDS: acute onset; ratio of partial pressure of arterial oxygen to fraction of
inspired oxygen (PaO2/FiO2) of 200 or less, regardless of positive end-expiratory pressure;
bilateral infiltrates seen on frontal chest radiograph; and pulmonary artery wedge pressure of
18 mm Hg or less when measured, or no clinical evidence of left atrial hypertension. Acute
lung injury is a slightly less severe syndrome characterized by less profound hypoxemia but
otherwise similar diagnostic criteria to ARDS. Because more than one-half of intensive care
units (ICUs) in the United States are not staffed with intensivists, many primary care
physicians provide care for patients with ARDS or acute lung injury. Because the presenting
symptoms of ARDS are nonspecific, physicians must consider other respiratory, cardiac,
infectious, and toxic etiologies. Patient history (e.g., comorbidities, exposures, medications)
in conjunction with a physical examination focusing on the respiratory and cardiovascular
systems can help narrow the differential diagnosis and determine the optimal course of
treatment. Often, ARDS must be differentiated from congestive heart failure and pneumonia.
Congestive heart failure is characterized by fluid overload, whereas patients diagnosed with
ARDS, by definition, do not show signs of left atrial hypertension or overt volume overload.
Patients with congestive heart failure may have edema, jugular venous distension, third heart
sound, an elevated brain natriuretic peptide level, and a salutary response to diuretics.
Patients with ARDS would not be expected to have these findings. Because pneumonia is a
leading cause of ARDS, distinguishing patients with uncomplicated pneumonia from those
who have pneumonia complicated by ARDS presents a greater diagnostic challenge. In
general, a patient with uncomplicated pneumonia may have signs of systemic and pulmonary
inflammation (i.e., fever, chills, fatigue, sputum production, pleuritic chest pain, and
localized or multifocal infiltrates); accompanying hypoxia should respond to oxygen
administration. If hypoxia does not correct with oxygen administration, ARDS should be
suspected and confirmed based on AECC diagnostic criteria. In those with combined
pneumonia and ARDS, treatment entails antibiotics and ventilator management.
No drug has proved beneficial in the prevention or management of acute respiratory distress
syndrome (ARDS). Early administration of corticosteroids to septic patients does not prevent
the development of ARDS. A study by Martin-Loeches et al concluded that the early use of
corticosteroids was also ineffective in patients with the pandemic H1N1 influenza A
infection, resulting in an increased risk of superinfections. This finding was also echoed in a
study by Brun-Buisson et al, who found no evidence of benefit associated with
corticosteroids in patients with ARDS secondary to influenza pneumonia but did find that
early corticosteroid therapy may be harmful.Numerous pharmacologic therapies, including
the use of inhaled synthetic surfactant, intravenous (IV) antibody to endotoxin, interferon-
beta-1a, IV prostaglandin E1, neutrophil elastase inhibitors, ketoconazole, simvastatin, and
ibuprofen, have been tried and are not effective. (Eloise, H., et al., 2020)
Other pharmacologic therapies for ARDS have also been trialled, with various degrees of
success. Maintaining a conservative fluid balance in tandem with use of diuretics has been
shown to reduce the duration of mechanical ventilation and improve lung function in patients
with ARDS, and should be considered routinely. Inhaled nitric oxide may theoretically
reduce pulmonary vascular resistance and ventilation–perfusion mismatch, although
randomized data do not support a mortality benefit, and may in fact suggest harm. Finally, the
use of aerosolized prostacyclin for ARDS has been studied, but further study of its effects is
required before it could be recommended for routine use. (Shannon, M., et al., 2021)
VII. REFERENCES
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Berbiglia, V. (2014). Orem’s self-care deficit theory in nursing practice. In M. R.
Alligood. (Ed.), Nursing theory utilization & application (5th ed.) (p. 222-244). St. Louis:
Mosby
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Aberle, D. R., & Brown, K. (1990). Radiologic considerations in the adult respiratory
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