CORONA VIRUS

A Clinical Report Presented to the Nursing Department to San Pedro College

In Partial Fulfillment of the Requirements in

NCM 212- LEC

OXYGENATION CONCEPT

Submitted to:

MONALIZA JOSON LEE, RN, MN

Clinical Instructor

Submitted by:

HAZEL GWEN B. LLAIT,ST.N

BSN-3B

August 5, 2022
 On March 11, 2020, the World Health Organization declared COVID-19 a

global pandemic indicating a large global spread of an infectious disease. Since

the virus was so virulent and spreads quickly, it leads to death in the most

susceptible individuals,especially those older than 60 and those with underlying

problems.

The novel coronavirus from the family Coronaviridae was quickly identified

as the pathogen causing these atypical infections, and because of its high

homology to SARS-CoV, it was given the name severe acute respiratory

syndrome coronavirus-2 (SARS-CoV-2). By the reason that the virus originated

in Wuhan, China, the virus first appeared on a limited scale in November 2019,

followed by the first significant cluster in December 2019. SARS-CoV-2 was

initially believed to have transferred to humans at one of Wuhan, China's outdoor

"wet markets.". According to Peiris et al. SARS is transmitted to and among

humans by direct contact, droplet, and airborne routes. SARS-CoV-2 infected

people who hadn't had any direct contact with animals as it spread both inside

and outside of China. That indicated that a human being can spread the infection

to another. That being so, people are now unintentionally contracting and

spreading the coronavirus around the world. That which is now a pandemic.

Since the pandemic's start, cases have been reported across all

continents. Globally, there have been believed to be over 500 million confirmed

cases and over 6 million deaths. When the outbreak first started, instances of

COVID-19 were primarily found in the elderly. As the outbreak continued, cases

among those 65 and older grew further, but it was also noted that cases among
children under the age of 18 had grown to some extent. Although there were

initially more male patients, there was no discernible gender difference as the

number of cases rose. The prevalence of seropositivity among healthcare

personnel ranged from 1.6% to 31.6 percent, and the incidence of infection

ranged from 0% to 49.6%. However, compared to White people, being of a non-

White race or Hispanic ethnicity was strongly linked to a higher incidence of

infection. Frontline workers, prolonged or direct patient contact, and working in a

hospital unit with COVID-19 patients were also linked to a higher risk of infection.

In most studies, exposure in a household or private context posed a greater risk

than exposure at work.

Clinical Manifestation

SARS has a characteristic clinical course. Flu-like symptoms such as

fever, chills, coughing, and malaise are common in patients. The remaining 30%

of patients experience clinical improvement after the first week, while

approximately 70% experience continued shortness of breath and recurrent or

chronic fever. However, the lower respiratory tract has a severe clinical

manifestation of a severe acute respiratory syndrome (SARS), an emerging

infectious viral illness. The pathogenesis of SARS is extremely complex, with a

number of variables contributing to serious lung damage and the spread of the

virus to several other organs. Diffuse alveolar damage results from the SARS

coronavirus's targeting of the respiratory tract's epithelial cells. In the course of

the illness, numerous organs and cell types, such as the mucosal cells of the
intestines, the tubular epithelial cells of the kidneys, the neurons in the brain, and

various types of immune cells, may get infected.

Pathophysiology
 People can spread the virus to one another by exchanging respiratory

droplets and aerosols. When a virus enters the body, it binds to host receptors

and enters host cells by engaging in endocytosis (cell drinking/eating). The spike

(S), membrane (M), envelop (E), and nucleocapsid (N) proteins are the four

structural proteins that makeup coronaviruses. The S protein, which is the most

crucial for host attachment and penetration, is visible sticking out from the viral

surface. Two functional subunits (S1 and S2) make up this protein; S1 is in

charge of binding to the host cell receptor, and S2 is involved in the fusing of the

viral and host cellular membranes. As a functional SARS-CoV receptor,

angiotensin-converting enzyme 2 (ACE-2) has been found to be significantly

expressed in pulmonary epithelial cells. The S protein first attaches to this host

receptor to initiate the virus's invasion of the host cell. The S protein is activated

by a two-step protease cleavage process after SARS-CoV-2 binds to ACE-2: the

first cleavage is for priming at the S1/S2 cleavage site, and the second is for

activation at a region close to a fusion peptide inside the S2 subunit. The initial

cleavage stabilizes the S2 subunit at the attachment point, while the following

cleavage cleaves the S protein and likely activates it, triggering conformational

changes that fuse the membranes of the host cell and the virus. The viral

contents are released inside the pulmonary alveolar epithelial cells after

membrane fusion by the virus. Now that the virus is inside the host cell, it

replicates and uses the active RNA polymerase to create a negative-strand RNA

from the single-strand positive RNA that already exists (transcription). This

freshly generated negative strand RNA serves to generate new strands of

positive RNA, which in turn cause the cell cytoplasm to synthesize new proteins

(translation). The M protein aids in integration to the cellular endoplasmic

reticulum while the viral N protein binds the new genomic RNA. These freshly

created nucleocapsids are subsequently sealed in the ER membrane and moved

to the lumen, where they are moved to the cell membrane via Golgi vesicles and

ultimately to the extracellular environment by exocytosis. The newly formed virus

particles are now prepared to attack the nearby epithelial cells and produce new

infectious material for respiratory droplet transmission to the population.

Management

Healthcare professionals can use the COVID-19 Treatment Guidelines

from the National Institutes of Health (NIH) to collaborate with their patients and

choose the most appropriate course of action. For management of patients

presenting with respiratory distress due to COVID-19, Oxygen therapy is

administered according to the severity of presentation. For patients presenting

with mild breathlessness and a SpO2 level between 94% and 97%, a simple face

mask or a nasal cannula can be used for oxygen delivery. To stop the spread of

the virus, patients with moderate illness (SpO2 of 90 to 94 percent in room air)

should be isolated. A thorough clinical history should be obtained, including

information on any prior concomitant conditions. Monitoring of vital signs and

oxygen saturation (SpO2 levels), as well as diagnostic tests such as a complete

blood count, ECG, and a chest X-ray, are necessary.

Medical Management

Certain antiviral drugs and monoclonal antibodies have been approved by the

FDA to treat mild to moderate COVID-19 in those who are more likely to get very

ill.

 Antibiotics are an ideal and efficient antibiotic regimen that helps avoid or

control secondary bacterial infections and sepsis, while it isn't usually

advised in viral pneumonia. In addition to having a considerable anti-

inflammatory effect on the airways, macrolides like azithromycin are

extremely successful at preventing pulmonary infections in patients with viral

cases of pneumonia.

 Corticosteroid for 3-5 days, steroids may be administered to individuals who

exhibit rapid worsening of chest imaging characteristics, enhanced pro-

inflammatory response activation, and gradual deterioration of oxygen

saturation. The first and only steroid recommended at first was

methylprednisolone, with doses not to exceed 0.5–1 mg/kg/day for mild

instances and 1-2 mg/kg/day for severe cases. Given the delay in virus

clearance caused by steroid-mediated immunosuppression, higher doses

were not advised.

 Antiviral drugs target particular virus components to stop them from

proliferating in the body, reducing the risk of serious disease and death.
Nursing Interventions

Nursing interventions for COVID-19 should focus on maintaining the respiratory

function, managing hyperthermia, monitoring vital signs, and preventing

transmission.

1. Monitor vital signs

Rationale: Because of the prevalent COVID-19 symptoms of fever and dyspnea,

temperature and respiratory rate should be monitored closely.

2. Monitor O2 saturation

Rationale: Patients with severe COVID-19 symptoms might develop hypoxia,

with levels falling low enough to necessitate supplementary oxygen. Normal O2

saturation as measured with a pulse oximeter should be 94 or greater.

3. Manage fever

Rationale: Use the proper treatment for hyperthermia, which includes regulating

the room's temperature, removing excess clothing and blankets, using cooling

mattresses, placing cold packs over the body's major blood vessels, starting or

increasing intravenous (IV) fluids as permitted, giving antipyretic medications as

directed, and getting oxygen therapy ready in case respiratory issues arise from

the body's need for oxygen during a fever.

4. Maintain respiratory isolation

Rationale: All those entering the restricted-access area should wear personal

protective equipment, such as masks and gowns; isolation rooms should be

clearly designated with limited access.

5. Enforce strict hand hygiene

Rationale: Patients and everyone entering or leaving the room should wash their

hands after coughing in order to lessen or prevent the spread of the coronavirus.

6. Provide information

Rationale: Inform the patient and the patient's family members of the

transmission of COVID-19, the diagnostic procedures, the course of the illness,

any potential side effects, and effective coronavirus prevention measures.