π¦ Coronavirus SARS-CoV-2 (COVID-19): As of October 2020, there are insufficient data to recommend for or against specific antiviral or immune-based therapies for patients with mild COVID-19. Management is largely supportive except in severe/critical illness.
π About
- COVID-19 is caused by SARS-CoV-2, a novel coronavirus identified in late 2019.
- It spreads via droplets, aerosols, and fomites, with a high potential for human-to-human transmission.
π Origin
- First identified in Wuhan, China, December 2019, linked to wet markets with close contact between humans and live animals.
π¬ Aetiology
- SARS-CoV-2 has four key structural proteins:
- Spike (S) ποΈ β binds ACE2 receptors (lungs, GI, kidneys, brain).
- Envelope (E) π¦ β viral assembly & release.
- Matrix (M) π§± β structural stability.
- Nucleocapsid (N) 𧬠β protects viral RNA.
- Primary pathology = viral pneumonia, mortality β 1% (higher in elderly/comorbid).
π§« Pathology
- Hyaline membranes, pneumocyte desquamation, mononuclear infiltrates, and fibroblastic proliferation.
- ACE2 receptor expression beyond lungs explains multi-organ involvement (kidneys, heart, brain, liver).
β οΈ Groups at Higher Risk
- π΅ Elderly & nursing home residents.
- Comorbidities: diabetes, obesity, hypertension, chronic lung disease, cancer, immunosuppression.
- Higher risk in some ethnic groups (South Asian, Afro-Caribbean).
- Possible role of low vitamin D and immune variation under study.
π©Ί Clinical Features
- Incubation: 2β14 days (avg ~5 days).
- Common: fever π‘οΈ, dry cough, dyspnoea, fatigue, myalgia, headache, confusion.
- Less common: sore throat, rhinorrhoea, chest pain, diarrhoea, nausea/vomiting.
- Complications: viral pneumonia β type 1 RF, myocarditis β€οΈ, AKI π§½.
π Severity Classification
- Asymptomatic: PCR+ but no symptoms.
- Mild: fever/cough, no hypoxia.
- Moderate: lower respiratory disease, SpOβ β₯94% RA.
- Severe: RR >30, SpOβ <94%, PaOβ/FiOβ <300, >50% lung infiltrates.
- Critical: respiratory failure, septic shock, MODS.
π Complications
- Cytokine Storm πͺοΈ β hyperinflammatory response β ARDS, shock.
- Cardiac β€οΈ β myocarditis, arrhythmias, ACS-like syndromes.
- Renal/Liver π§½ β AKI, liver enzyme rise; ~15% critical cases need renal replacement therapy.
π Investigations
- Bloods: lymphopenia, β CRP, β D-dimer, Β± deranged LFTs.
- Imaging: CXR β patchy bilateral opacities. CT β ground-glass opacities π«οΈ. CTPA β rule out PE (common complication).
- Diagnostic: RT-PCR nasal/throat swabs; antibody testing (past exposure).
- Biomarkers: β troponin/BNP if cardiac involvement.
π‘οΈ Prevention
- π· Masks, π€² hand hygiene, βοΈ social distancing.
- π Contact tracing & isolation of exposures.
- Environmental: PPE, aseptic technique, waste & linen safety, regular cleaning/disinfection.
π Management
- Supportive: IV fluids, Oβ therapy π, treat sepsis.
- Respiratory support: β High-flow Oβ / NIV π· if needed. β Intubation/ventilation in critical cases (low tidal volume + prone).
- Drugs: β Dexamethasone 6 mg OD Γ up to 10 days if requiring Oβ e.g. sats < 92-94%. β Remdesivir = limited/experimental.
- Thromboprophylaxis π©Έ: LMWH due to high VTE risk.