Infectious Diseases I

Risk factors for COVID-19–related hospitalization span several comorbidities, including hypertension,

diabetes, cardiovascular disease, COPD, obesity, and chronic kidney disease. Patients with comorbidities

are at increased risk of hospitalization, ICU admission, and mortality.

The most common complication of COVID-19 in ICU patients is hypoxemic respiratory failure

from viral pneumonia, usually bilateral. Cytokine release syndrome or “cytokine storm” with mul-

tiorgan failure may be the primary presentation in some patients.

Between 25% and 90% of patients admitted to the ICU require MV.

Additional acute complications: Septic shock, liver dysfunction, bleeding and coagulation dysfunc-

tion, cytokine release syndrome, lymphopenia, and acute cerebrovascular disease

In-hospital crude mortality for COVID-19 is generally 15%–60%. Rates have declined in areas with

higher levels of immunity.

Mortality approaches 40% in ICU patients with COVID-19.

Age-related in-hospital mortality ranges from less than 5% for individuals younger than 40 to great-

er than 60% for those older than 80.

SARS-CoV-2 is a coronavirus; coronaviruses are relatively large, enveloped, single-stranded RNA vi-

ruses. Clinically, coronaviruses are usually associated with the common cold and mild to moderate

gastrointestinal illness. Common seasonal strains include coronaviruses 229E, HKU1, NL63, and OC43.

coronaviruses to cause severe respiratory infection.

SARS-CoV-2 predominantly targets nasal and bronchial epithelial cells and lower respiratory tract epi-

thelial pneumocytes.

SARS-CoV-2 pathogenicity is mediated through binding of the viral structural spike protein (S protein)

to membrane angiotensin-converting enzyme 2 (ACE2) receptors, predominant in alveolar type II cells.

Subsequently, serine protease type 2 transmembrane serine protease (TMPRSS2) cleaves the ACE2

receptor–S protein complex, leading to activation of the viral S protein and enhanced cellular uptake.

Once intracellular, SARS-CoV-2 RNA is incorporated into the host nucleus, and viral replication en-

sues. Activation of the ACE2 receptor may also implicate the contact pathway and complement system,

perhaps through an ACE2-mediated increase in bradykinin, in the pathophysiology of COVID-19. This

has been hypothesized to be the primary mechanism of cytokine release syndrome in patients with

COVID-19.

Mutations in SARS-CoV-2 continue to be reported.

One of the first reported variants was D614G, which has a modified S protein that may increase

cellular viral uptake. Many areas worldwide are concurrently experiencing multiple SARS-CoV-2

variants.

To date, the Delta variant (B.1.617.2) has demonstrated increased transmissibility (about 2-fold) and

pathogenicity compared with the wild-type SARS-CoV-2 strain.

SARS-CoV-2 is primarily transmitted from human to human through respiratory secretions, most likely

through droplets. Transmission is also possible through direct surface contact, though this is less likely.

contact precautions in medical environments are recommended to decrease transmission.

Clinicians caring for patients undergoing aerosol-generating procedures (e.g., endotracheal intubation;

bronchoscopy) should don respirator masks together with eye protection and full-body gowning. Nega-

tive-pressure patient rooms are preferred during aerosol-generating procedures.