Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Recognise viral lower-respiratory disease, separate it from bacterial coinfection and non-infective mimics, deliver organism-specific antiviral or anti-inflammatory treatment when eligible, and apply current UK infection-control and escalation pathways.
Viral pneumonitis ranges from a self-limiting febrile illness to diffuse alveolar injury and multiorgan disease. Presentation alone rarely identifies the virus. The decision model therefore asks four questions: is respiratory support needed, is an organism-specific treatment time-sensitive, is there bacterial or fungal coinfection, and what infection-control or public-health action applies today?
Treatment is unusually volatile. Influenza recommendations respond to circulating susceptibility and COVID-19 eligibility changes with evidence, variants and commissioning. Before each prescription, check same-day NICE, UKHSA, BNF and local policy, including pregnancy, renal function and interactions.
Influenza, SARS-CoV-2, respiratory syncytial virus and other viruses spread through respiratory particles and can infect lower airways directly.
Older age, pregnancy, immune suppression, obesity and chronic cardiac, respiratory or metabolic disease increase the likelihood of severe lower-respiratory involvement.
Close-contact exposure, outbreaks and waning or absent variant-relevant immunity shape infection risk and clinical severity, whose relevance depends on the complete exposure and clinical history.
Viral epithelial damage and altered immune defence permit bacterial superinfection, which may develop during or after initial viral illness.
Virus enters susceptible airway or alveolar cells, replicates and disrupts mucosal and ciliary defence, and the downstream physiological effect determines clinical severity.
Interferon and inflammatory pathways recruit immune cells, causing fever, systemic symptoms and local epithelial injury, which links the underlying lesion to the observed respiratory dysfunction.
Diffuse inflammation, oedema and microatelectasis impair ventilation-perfusion matching and oxygen diffusion, contributing to the resulting loss of respiratory reserve.
Severe viral illness can activate endothelium and coagulation, contributing to microvascular injury and thromboembolism, with effects that increase as the pathological process progresses.
Most inflammation resolves, but severe injury may progress to ARDS, organising pneumonia or persistent physiological impairment.
Abrupt fever, myalgia, headache and cough progressing to dyspnoea or diffuse infiltrates, with particular concern in pregnancy, older age, immunocompromise and chronic cardiac, neurological or respiratory disease.
Fever, cough, breathlessness and hypoxaemia with bilateral peripheral or diffuse opacities; thromboembolism, myocarditis and inflammatory deterioration may complicate the course.
New focal consolidation, purulent sputum, recurrent fever or deterioration after initial viral improvement suggests bacterial superinfection, including pneumococcus or post-influenza Staphylococcus aureus.
Prolonged shedding, muted fever, lower-airway disease despite a negative nasal sample, mixed infection and antiviral resistance are more likely after transplant, chemotherapy or substantial immunosuppression.
Focal consolidation, purulent sputum and microbiological evidence support bacterial infection, but coinfection can accompany confirmed viral disease.
Sudden deterioration, pleuritic pain or disproportionate hypoxaemia with thrombotic risk warrants probability-led imaging despite viral positivity.
Orthopnoea, oedema and cardiac congestion suggest hydrostatic fluid, which infection may precipitate, with targeted examination and testing used to resolve the uncertainty.
Medicine timing, autoimmune features or negative serial virology may support non-infective inflammation with a similar imaging pattern.
Chronic symptoms, epidemiological risk and upper-zone or cavitating disease require mycobacterial assessment and infection-control measures, while chronology and directed testing distinguish the competing explanation.
Pulmonary oedema, embolism, drug pneumonitis, organising pneumonia and diffuse alveolar haemorrhage can resemble viral pneumonitis and may coexist.
Diffuse alveolar and endothelial injury may produce severe non-cardiogenic oedema, shunt and prolonged ventilation, with severity determined by its extent and the patient's underlying reserve.
Damaged epithelium and altered immunity permit secondary pneumonia, sepsis, empyema or necrotising infection, particularly when baseline cardiopulmonary reserve is limited.
Inflammation, endothelial activation and immobility increase venous and arterial thrombotic events in severe illness, particularly when baseline cardiopulmonary reserve is limited.
Systemic stress, myocarditis, ischaemia and arrhythmia can complicate severe viral infection, with severity determined by its extent and the patient's underlying reserve.
Breathlessness, fatigue, cognitive symptoms and reduced exercise capacity may continue after acute infection through multiple biological and functional mechanisms.
Influenza antivirals are most effective early but remain indicated in severe or at-risk illness under UKHSA guidance; COVID therapies each have their own timing and severity window.
Dexamethasone helps hypoxic COVID-19 but is not routine influenza treatment and can harm when given to non-hypoxic COVID without another indication.
Detection may coexist with oedema, embolism or bacterial pneumonia; in prolonged immunocompromised shedding it may not explain every new deterioration.
Sampling timing and compartment matter, especially in severe lower-airway disease after transplant; discuss lower-respiratory testing rather than declaring the virus excluded.
Resistance patterns, circulation thresholds and commissioned drugs change. A regimen copied from last winter is not a safe substitute for the current UKHSA document.
Giving dexamethasone for uncomplicated COVID-19 without an oxygen requirement.
Withholding influenza antivirals from a severely ill patient because symptoms began more than 48 hours ago.
Using a viral diagnosis to dismiss new focal bacterial consolidation or shock.
Starting antibiotics automatically for every viral pneumonitis without evidence of bacterial coinfection.
Failing to recheck current national eligibility and interaction guidance before prescribing COVID therapeutics.
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An adult has confirmed COVID-19, normal oxygen saturation on room air and no other indication for steroids. What is the best dexamethasone plan?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes
Start promptly and do not delay for testing in severe suspected influenza. Adjust for renal function; persistent infection in immunocompromise may need resistance testing and specialist duration.
Do not use solely for COVID-19 without oxygen requirement. Monitor glucose, delirium, secondary infection and gastrointestinal risk; consider pregnancy and existing steroid therapy.
Exclude uncontrolled non-COVID infection and review neutrophils, platelets, liver tests and bowel-perforation risk. National criteria and supply arrangements can change.