COVID-19

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

SARS-CoV-2 infects respiratory epithelium and can cause local viral symptoms, diffuse pneumonitis, endothelial and coagulation activation and systemic inflammation. Current population immunity has changed baseline severity, but age, immune suppression and chronic disease continue to define high-risk groups. Variant, vaccine and treatment policy evolve faster than static prescribing tables.

The management sequence is severity, illness timing, antiviral eligibility and complications. Stable low-risk illness usually needs symptom care and safety-netting. High-risk early disease may benefit from commissioned antivirals. Hospitalised hypoxaemic disease requires oxygen-targeted supportive care, thrombosis assessment and phase-appropriate treatments under current national policy.

Recovery is heterogeneous. Persistent breathlessness, fatigue, cognitive symptoms, palpitations or reduced function require a fresh assessment for organ injury, thromboembolism, anaemia, dysautonomia and deconditioning rather than assuming either ongoing viral replication or a purely psychological cause.

Key points

COVID-19 ranges from asymptomatic infection to viral pneumonitis and multi-organ critical illness; vaccination and previous infection modify but do not remove severe risk.
Confirm current infection with a validated test when the result changes treatment, infection control or diagnosis, recognising that detection can persist after infectious illness.
Assess respiratory rate, oxygen saturation, work of breathing, mental state, hydration and trajectory; older or immunosuppressed adults may deteriorate without high fever.
High-risk non-hospitalised patients may qualify for early antiviral treatment through current NHS pathways; eligibility, ranking and preferred agent change and must be checked live.
Nirmatrelvir with ritonavir has extensive interactions and renal limits. Complete medication reconciliation and use the current product and commissioning guidance before prescribing.
Hospital treatment depends on oxygen requirement and inflammatory phase; do not use corticosteroids routinely in patients who do not require supplemental oxygen for COVID-19.
Evaluate new deterioration for bacterial pneumonia, pulmonary embolism, myocarditis, acute coronary disease and decompensated comorbidity rather than attributing everything to the positive test.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

SARS-CoV-2 exposure

Inhaled respiratory particles transmit virus, with risk shaped by proximity, ventilation, infectious phase and individual immunity.

Host vulnerability

Age, immune suppression, obesity and chronic organ disease increase the probability of lower-respiratory and systemic complications.

Immune escape and waning protection

Viral evolution and time since vaccination or infection alter susceptibility, while retained immune memory still reduces severe disease for many people.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Cell entry and replication
Viral spike binding and host proteases permit entry into susceptible respiratory cells, where replication disrupts epithelial defence.
2
Innate and adaptive inflammation
Interferon, cytokine, antibody and T-cell responses control infection but can also injure alveolar and systemic tissues.
3
Alveolar and endothelial injury
Pneumonitis, capillary leak, microvascular activation and thrombosis impair ventilation-perfusion matching, oxygen transfer and pulmonary vascular function.
4
Repair or persistent dysfunction
Most tissue recovers, but severe injury or dysregulated recovery can leave organising change, autonomic symptoms and reduced exercise tolerance.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Mild acute infection

Cough, fever, sore throat, anosmia, fatigue or myalgia with stable breathing and hydration can be managed outside hospital when host risk and support permit.

Viral pneumonitisRed flag

Increasing breathlessness, hypoxaemia, tachypnoea and bilateral infiltrates indicate lower-respiratory involvement and need hospital severity assessment.

High-risk early diseaseRed flag

Significant immune suppression, older age and specified comorbidities may meet current NHS criteria for prompt community antiviral assessment.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Validated SARS-CoV-2 molecular or antigen testFirst step
Why
Confirm current infection when diagnosis changes treatment, isolation or cohorting.
Interpretation and limitations
Interpret method, timing and previous infection. Prolonged positivity can outlast infectious symptoms, while an early negative result may require repeat testing when probability is high.
02
Pulse oximetry and serial observations
Why
Identify lower-respiratory disease and changing physiological risk.
Interpretation and limitations
Trend resting saturation, oxygen requirement, respiratory rate, work of breathing and mental state; home readings require device-quality and red-flag advice.
03
Renal and hepatic function with medication review
Why
Determine antiviral eligibility, dose and interaction safety and establish organ-injury baseline.
Interpretation and limitations
Nirmatrelvir with ritonavir has important renal restrictions and CYP-mediated interactions; use a current interaction tool and product information.
04
Chest imaging
Why
Assess pneumonitis, focal bacterial pneumonia, oedema or another thoracic cause in moderate or severe illness.
Interpretation and limitations
Imaging patterns overlap and do not prove active viral disease. Use CTPA only through a thromboembolic probability pathway.
05
FBC, inflammatory, coagulation and cardiac tests when indicated
Why
Assess severity and investigate complications rather than ordering a fixed panel for every infection.
Interpretation and limitations
D-dimer may rise in COVID-19 and should not independently diagnose embolism. Troponin elevation requires clinical and electrocardiographic interpretation.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Influenza and other viruses

Clinical symptoms overlap; epidemiology and validated respiratory testing distinguish pathogens when antiviral or isolation decisions differ.

Bacterial pneumonia

Focal consolidation, recurrent fever, purulent sputum and bacterial cultures support superinfection, which may coexist with positive SARS-CoV-2 testing.

Pulmonary embolism

Abrupt pleuritic pain, unexplained hypoxaemia and thrombotic risk require a probability-led vascular pathway rather than D-dimer interpretation alone.

Cardiac or inflammatory disease

Myocarditis, acute coronary syndrome, heart failure and non-infectious pneumonitis can resemble COVID-19 deterioration and need directed testing.

Additional chapter-specific clues

Alternative emergencyRed flag

Pleuritic pain, unilateral swelling, focal consolidation, shock, arrhythmia or disproportionate deterioration suggests thromboembolism, bacterial infection or cardiac disease in addition to COVID-19.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Stable community illnessSupport and safety-netFirst stepCOVID-19 is confirmed or likely, observations are stable and no current high-risk treatment criterion is met.

1Assess duration, breathing, hydration, comorbidity, pregnancy and support; advise symptom care and current infection-control behaviour.
2Explain urgent triggers including worsening breathlessness, hypoxaemia, confusion, persistent chest pain, fainting or inability to drink.
3Review if symptoms fail to improve, and assess persistent functional problems rather than repeatedly testing without a clinical question.

02High-risk early infectionAccess current antiviral treatmentA non-hospitalised patient may meet current NHS high-risk eligibility within the treatment window.

1Confirm symptom onset and infection, exact immune or comorbidity criterion, renal and hepatic function, pregnancy and full medicines list.
2Use the live NHS policy to select nirmatrelvir with ritonavir, remdesivir or another commissioned option and resolve interactions before the first dose.
3Provide adverse-effect, rebound and deterioration advice and ensure the patient knows antiviral treatment does not prevent every complication.

03Hypoxaemic or deteriorating illnessTreat respiratory disease and search for complicationsOxygen need, tachypnoea, shock, confusion or another organ abnormality develops.

1Perform ABCDE, give oxygen to an individual target, obtain imaging and laboratories and use hospital COVID-19 and critical-care pathways.
2Assess bacterial infection, pulmonary embolism, cardiac injury and fluid status; use antimicrobials or anticoagulation only when their own indications are met.
3Apply current national recommendations for corticosteroids, immunomodulation and thromboprophylaxis based on oxygen need, phase and contraindications.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Early antiviral treatment for eligible high-risk non-hospitalised adults under the current NHS commissioning pathway.

Nirmatrelvir with ritonavir

Start within the commissioned early-treatment window; the standard adult course is 300 mg nirmatrelvir with 100 mg ritonavir orally twice daily for 5 days when renal function permits.

Use the current renal regimen and avoid in severe hepatic impairment. Ritonavir strongly inhibits CYP3A: reconcile antiarrhythmics, anticonvulsants, rifamycins, transplant medicines, anticoagulants, statins, sedatives, herbal and recreational drugs with a live interaction resource. Potent inducers and some narrow-therapeutic-index substrates make an alternative antiviral necessary; do not improvise withholding.

Provides a non-ritonavir antiviral option for selected high-risk non-hospitalised adults when oral treatment is unsuitable.

Remdesivir for early high-risk community treatment

When selected by the current commissioned pathway, give 200 mg intravenously on day 1 then 100 mg intravenously daily on days 2 and 3, starting within the eligible symptom window.

Use a monitored infusion pathway; review hepatic and renal function, prothrombin time and hypersensitivity, and stop or withhold for clinically significant liver injury according to current product guidance. Pregnancy and complex organ failure require specialist benefit-risk review.

Reduces mortality in hospitalised hypoxaemic COVID-19 when used in the inflammatory phase.

Dexamethasone

Give 6 mg orally or intravenously once daily for up to ten days in eligible patients requiring supplemental oxygen.

Do not use routinely for non-hypoxaemic COVID-19; monitor glucose, delirium, secondary infection and gastrointestinal risk and stop at discharge when the course indication ends.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Acute respiratory failure

Diffuse pneumonitis and shunt can cause escalating oxygen need, respiratory muscle exhaustion and prolonged critical-care ventilatory support.

Thromboembolism

Inflammation, endothelial activation and immobility increase venous and arterial thrombosis during severe acute illness, sometimes causing sudden circulatory deterioration.

Secondary infection and treatment harm

Immune therapy, devices and prolonged admission increase bacterial or fungal infection, hyperglycaemia, delirium and medicine interactions.

Post-acute functional illness

Fatigue, breathlessness, cognitive symptoms and dysautonomia may persist and require exclusion of remediable organ disease and rehabilitation.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Trend respiratory rate, work of breathing, oxygen requirement, consciousness and haemodynamics; escalate trajectory rather than waiting for one threshold.
During antiviral treatment, review renal change, adherence, vomiting and interaction management, including when temporarily withheld medicines should restart.
In hospital, monitor glucose, secondary infection, thrombosis, renal and hepatic injury and complications of oxygen or immune treatment.
Reassess a second deterioration with cultures, imaging or vascular and cardiac testing selected from the new syndrome.
After acute illness, document functional baseline, exertional symptoms and red flags and arrange rehabilitation or specialty evaluation when recovery is incomplete.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

A positive test is not a full diagnosis

SARS-CoV-2 can coexist with embolism, bacterial sepsis and myocardial infarction, especially when the clinical pattern is disproportionate.

Ritonavir changes other medicines

Its potent enzyme inhibition can rapidly raise concentrations of interacting drugs, so a casual prescription-list glance is unsafe.

Steroids depend on oxygen need

Benefit is linked to inflammatory hypoxaemic disease; routine use in mild non-hypoxaemic infection can cause harm.

Persistent symptoms need phenotype

Post-acute breathlessness may reflect lung injury, clot, cardiac disease, dysautonomia, anaemia or deconditioning and deserves a structured reassessment.

11Common pitfallsFrequent interpretation and management errors.

01
Prescribing nirmatrelvir with ritonavir without a complete interaction and renal review.
02
Giving dexamethasone routinely to a patient who does not require oxygen.
03
Using raised D-dimer alone to diagnose pulmonary embolism.
04
Assuming a positive test explains every new physiological abnormality.
05
Dismissing persistent symptoms without checking organ and functional complications.