Acute severe community-acquired pneumonia: corticosteroid adjunct therapy · ICU Topics

Cinematic ICU scene of a hydrocortisone vial drawn up beside a chest X-ray of lobar pneumonia with septic-shock vasopressors running, clinical-blue lighting, medical educational, no faces, no text — FigureCorticosteroids calm the cytokine storm of the severe CAP — the CAPE COD trial made hydrocortisone 200 mg/day for seven days a mortality-reducing adjunct in the ICU-bound. Reserve for the severe, the shocked, and the high-inflammatory phenotype; beware the smouldering infection and the hyperglycaemia.

Hydrocortisone 200 mg/day CAPE COD pathway for ICU CAP with glucose monitoring and infection surveillance — FigureCAPE COD pathway: hydrocortisone 200 mg/day for 5–7 days in ICU-bound severe CAP; monitor glucose, infection and GI bleeding; avoid routine use in mild CAP.

Evidence

Corticosteroid evidence in CAP

CAPE COD trial (2024, JAMA)

RCT: hydrocortisone 200 mg/day (continuous infusion) for 7 days vs placebo in severe CAP requiring ICU. Result: REDUCED 28-day mortality (primary endpoint). Stopped early for efficacy. Strongest evidence for corticosteroids in bacterial CAP. Dose: hydrocortisone 200 mg/day (50 mg Q6H or continuous infusion). Duration: 7 days or until clinical improvement.

CACTUS trial (2022)

RCT: hydrocortisone 200 mg/day for 8 days vs placebo in severe CAP. Result: reduced treatment failure (need for ventilation, vasopressors, or death). Less robust than CAPE COD (smaller, different population). Supports hydrocortisone in severe CAP.

Cochrane meta-analysis (2021)

Pooled data: corticosteroids reduced mortality (RR 0.79), duration of mechanical ventilation, and development of ARDS in severe CAP. BUT: increased hyperglycaemia (RR 1.27) and no increase in secondary infection. Conclusion: corticosteroids should be considered in severe CAP.

Specific pneumonia types

PJP: prednisolone 40 mg BD x 5 days, then taper (for PaO2 <70 — reduces organism lysis inflammation). Influenza: controversial — some studies show benefit, others harm. Use selectively for severe influenza with high inflammatory burden. COVID-19: dexamethasone 6 mg daily x 10 days (RECOVERY trial — reduces mortality in O2/ventilated patients).

[1] [2]

SAQ — severe CAP with septic shock: CAPE COD and the case for adjunct corticosteroids

10 minutes · 10 marks

A 68-year-old man is admitted to ICU with severe community-acquired pneumonia. CURB-65 is 4, CRP 220 mg/L, PaO2/FiO2 180. He requires noradrenaline for septic shock and has bilateral infiltrates on chest X-ray. You are considering adjunct corticosteroid therapy.

[1]

SAQ — steroid dosing, duration, and special pneumonia types in severe CAP

10 minutes · 10 marks

A 55-year-old woman with severe CAP (PaO2/FiO2 150, CRP 280 mg/L, procalcitonin 25) is intubated and ventilated within 12 hours of ICU admission. Blood cultures grow Streptococcus pneumoniae and appropriate antibiotics have been commenced. You have decided to start adjunct corticosteroid therapy.

[1]

Clinical pearls

High-yight corticosteroid CAP points for the CICM/FFICM exam

CAPE COD trial: hydrocortisone 200 mg/day reduced 28-day mortality in severe CAP (ICU).[1] }
Cochrane: corticosteroids reduce mortality, ventilation duration, ARDS in severe CAP.[2] }
Hydrocortisone 200 mg/day for 5-7 days (no taper needed for short course).[1] }
Benefit greatest: high CRP (>150), septic shock, ARDS, elderly.[1] }
PJP pneumonia: prednisolone 40 mg BD if PaO2 <70 (reduces organism lysis inflammation).[1] }
COVID-19: dexamethasone 6 mg daily x 10 days (RECOVERY).[1] }
NOT for: uncomplicated CAP (CURB-65 0-2), fungal pneumonia (without antifungal).[1] }
Risks: hyperglycaemia (monitor glucose, insulin), secondary infection (surveillance cultures), GI bleeding (PPI prophylaxis), neuromyopathy (limit duration).[2] }
Dexamethasone vs hydrocortisone: dexamethasone has NO mineralocorticoid effect (no sodium retention). Hydrocortisone has mineralocorticoid effect (may cause sodium retention, fluid overload).[1] }
Steroid-responsive: severe CAP with high inflammatory burden responds better to steroids than low-inflammatory CAP (phenotyping).[1] }
CAUTION in influenza: some studies show steroids may INCREASE mortality in influenza pneumonia (impaired viral clearance). Use selectively.[1] }
No routine taper needed for short courses (5-7 days). Taper if >14 days (prevent adrenal suppression).[2] }
Stress dose: patients on chronic steroids need stress-dose hydrocortisone (100 mg Q6H) during severe illness — separate from adjunct corticosteroid therapy.[1] }
Glucose target: 6-10 mmol/L (NICE-SUGAR) — corticosteroids cause hyperglycaemia. Monitor and adjust insulin.[2] }

Red flags

Rationale & mechanism

Cytokine storm and glucocorticoid receptor pathway in severe CAP with reduced alveolitis and improved gas exchange — FigureSevere CAP cytokine storm — glucocorticoids dampen IL-6/TNF-driven inflammation while hyperglycaemia and secondary infection remain the trade-offs to monitor.

[1]

Mechanism of benefit in severe CAP — step by step

1. Pathogen → cytokine storm

Bacterial products (pneumococcal cell wall, endotoxin) bind TLR2/TLR4 on alveolar macrophages → NF-κB activation → surge of TNF-α, IL-1β, IL-6, IL-8. High IL-6/CRP (>150 mg/L) marks the "hyper-inflammatory phenotype" most likely to benefit.

2. Endothelial leak → ARDS

Cytokines disrupt the alveolar-capillary barrier → protein-rich oedema, hyaline membranes, shunt, refractory hypoxaemia. Corticosteroids restore endothelial integrity by inhibiting ICAM-1/VCAM-1 expression.

3. Corticosteroid genomic action

Glucocorticoid-receptor complex translocates to nucleus → trans-repression of pro-inflammatory genes (cytokines, COX-2, iNOS) and trans-activation of anti-inflammatory genes (I-κB, annexin-A1). Onset is genomic (hours), not immediate.

4. Vasopressor sensitisation

Up-regulates α-1 adrenergic receptor expression → restores catecholamine responsiveness in vasodilatory shock. This is why hydrocortisone reduces vasopressor dose in septic shock.

5. Clinical translation

Net effect in severe CAP: less treatment failure, faster resolution of fever/CRP, shorter time to clinical stability, less progression to ARDS, reduced duration of mechanical ventilation, and (in the sickest patients) reduced 28-day mortality.

[5] [11]

Corticosteroid pharmacology in ICU

Corticosteroid agents used in critical care — equivalent anti-inflammatory doses

Agent	Equivalent dose (mg)	Glucocorticoid potency	Mineralocorticoid potency	Plasma t½ (h)	Biological effect (h)	CAP / sepsis use
Hydrocortisone	20	1 (reference)	1 (highest)	8–12	8–12	Severe bacterial CAP, septic shock (CAPE COD, ADRENAL)
Methylprednisolone	4	5	0.5	18–36	12–36	Torres 2015 regimen (0.5 mg/kg BD)
Prednisolone / Prednisone	5	4	0.6	18–36	12–36	PJP adjunct; Blum/ProHeart ward CAP
Dexamethasone	0.75	25–30	~0 (negligible)	36–54	36–72	COVID-19 CAP (RECOVERY)
Fludrocortisone	—	10	125 (pure)	3–4	—	Septic-shock arm of APROCCHSS

[3] [4]

Practical point: hydrocortisone retains mineralocorticoid activity (sodium + fluid retention) — relevant in heart failure/ARDS where fluid balance is tight. Dexamethasone has essentially no mineralocorticoid effect, hence its preference when sodium retention is undesirable, but its long t½ risks cumulative tissue exposure and critical-illness myopathy if given beyond 10 days. [1]

Dosing

Adjunctive corticosteroid regimens in severe CAP

Hydrocortisone 200 mg/day (CAPE COD, Dequin 2023)

Continuous IV infusion 200 mg/24 h OR 50 mg IV every 6 hours. Duration: 4–7 days (or until clinical stability / 7 days, whichever first). NO taper for the short course. This is the regimen with the strongest mortality signal in bacterial severe CAP.

Methylprednisolone 0.5 mg/kg BD x 5 days (Torres 2015)

~40 mg BD (0.5 mg/kg q12h) IV for 5 days, then taper. Reduced early treatment failure in severe CAP (IDSA/ATS criteria). Useful when a non-hydrocortisone agent is preferred.

Prednisone 50 mg/day x 7 days (Blum / ProHeart)

50 mg PO/IV daily for 7 days. Reduced time to clinical stability but NO mortality benefit — appropriate for non-ICU CAP with high inflammatory burden.

Dexamethasone 5 mg daily x 5 days (Meijvis 2011)

Reduced length of hospital stay by ~1 day; no mortality effect. A pragmatic option for ward CAP.

Dexamethasone 6 mg daily x 10 days (RECOVERY, COVID-19)

Reduces 28-day mortality in COVID-19 requiring oxygen or ventilation. NOT a substitute for hydrocortisone in bacterial CAP.

[3] [4] [6] [7] [16]

Indications — who actually benefits

Indication decision: when to add corticosteroids in CAP

GIVE (strong evidence)

Severe CAP (IDSA/ATS major criteria: invasive mechanical ventilation OR septic shock requiring vasopressors) PLUS high inflammatory burden (CRP >150 mg/L, or IL-6 high). Hydrocortisone 200 mg/day for 4–7 days (CAPE COD, Torres 2015).

GIVE (pathogen-specific)

Pneumocystis jirovecii pneumonia with PaO2 <70 mmHg or A-a gradient >35 mmHg (prednisolone 40 mg BD). COVID-19 pneumonia on supplemental O2 or ventilated (dexamethasone 6 mg x10 d, RECOVERY).

CONSIDER (moderate evidence)

Severe CAP with rising CRP despite 48–72 h of appropriate antibiotics; high CURB-65/SMART-COP; elderly with excessive inflammation. Biomarker-guided (CRP/procollagon) strategies enrich for responders.

AVOID / harm likely

Uncomplicated CAP (CURB-65 0–2, managed as outpatient); low-inflammatory (low CRP) phenotype; fungal pneumonia without antifungal cover; influenza pneumonia where steroids may increase secondary bacterial infection and impair viral clearance; pure viral CAP without hypoxaemia.

[3] [8] [18]

Inflammatory phenotype matters. The benefit is concentrated in the high-inflammatory (CRP >150, IL-6 elevated) phenotype. Low-inflammatory CAP gains nothing and takes the harm. Siemieniuk’s individual-patient-data meta-analysis showed the mortality reduction was driven almost entirely by the most severely ill, high-inflammation patients.[8]

Evidence — landmark trials

CAPE COD (Dequin 2023) — the pivotal bacterial CAP trial

CAPE COD — Hydrocortisone in Severe Community-Acquired Pneumonia (PMID 36942789)

Source

Dequin PF, Meziani F, Quenot JP, et al. N Engl J Med 2023

Design

Multicentre, double-blind, randomised, placebo-controlled, Bayesian, group-sequential trial in French ICUs

Population

Adults with severe CAP (Pneumonia Severity Index IV–V) needing ICU — high-inflammatory phenotype

Intervention

Hydrocortisone 200 mg/day (continuous infusion) for 4–7 days vs placebo

Primary outcome

Day-28 treatment failure (death or persistence/progression)

Result

Marked reduction in day-28 treatment failure (OR ~0.42) AND day-28 mortality; trial stopped early for efficacy at 2nd interim analysis

Exam nuance

Day-28 mortality benefit clear, but day-90 mortality difference NOT statistically significant — an early anti-inflammatory rescue effect rather than a long-term survival cure

[3]

Exam anchor: CAPE COD is the single most important steroid-CAP trial. Know: hydrocortisone 200 mg/day continuous infusion, Bayesian design, stopped early for efficacy, 28-day benefit > 90-day benefit. The day-28-but-not-day-90 pattern is the classic exam point. [1]

Torres 2015 — methylprednisolone, reduced treatment failure

Torres et al 2015 — Methylprednisolone in severe CAP (PMID 25688779)

Source

Torres A, Sibila O, Ferrer M, et al. JAMA 2015

Design

Multicentre RCT, Spain

Population

Adults with severe CAP (IDSA/ATS criteria) and high inflammatory response (CRP >150 mg/L)

Intervention

Methylprednisolone 0.5 mg/kg q12h for 5 days vs placebo

Primary outcome

Early treatment failure at day 5

Result

Reduced early treatment failure (31% vs 46%, p=0.02) and late treatment failure; no difference in mortality

Exam nuance

This is the ‘0.5 mg/kg BD’ dose quoted in every guideline; CRP enrichment strengthens the phenotype argument

[4]

Confalonieri 2005 — the original hydrocortisone signal

Confalonieri et al 2005 — Hydrocortisone in severe CAP (PMID 15557131)

Source

Confalonieri M, Urbino R, Potena A, et al. Am J Respir Crit Care Med 2005

Design

Single-centre, preliminary RCT (n=46)

Population

Severe CAP requiring ICU

Intervention

Hydrocortisone 240 mg/day continuous infusion x 7 days then taper vs placebo

Primary outcome

Modulation of systemic inflammation / multiple organ dysfunction score

Result

Reduced multiple-organ dysfunction score, shorter hospital stay, reduced mortality in the pneumococcal subgroup

Exam nuance

Small but seminal; established the hydrocortisone-in-severe-CAP concept later confirmed by CAPE COD

[5]

Meijvis 2011 & Blum 2015 — modest benefit, no mortality effect

Meijvis et al 2011 — Dexamethasone in CAP (PMID 21636122)

Source

Meijvis SC, Hardeman H, et al. Lancet 2011

Design

Double-blind RCT (n=304)

Population

Adults hospitalised with CAP (not selected for severity)

Intervention

Dexamethasone 5 mg daily x 5 days vs placebo

Primary outcome

Length of hospital stay

Result

Reduced length of stay by ~1 day; no mortality difference

Exam nuance

Predominantly non-severe CAP — explains absence of mortality signal; supports the ‘severity-and-inflammation’ enrichment thesis

[6]

Blum / ProHeart 2015 — Adjunct prednisone in CAP (PMID 25608756)

Source

Blum CA, Nigro N, Briel M, et al. Lancet 2015

Design

Multicentre double-blind RCT (n=785)

Population

Adults hospitalised with CAP (all severities)

Intervention

Prednisone 50 mg daily x 7 days vs placebo

Primary outcome

Time to clinical stability

Result

Shorter time to clinical stability (~1.4 days); NO mortality benefit; no difference at 180-day follow-up

Exam nuance

Confirmed that mixed-severity CAP gains only speed-of-recovery, not survival — benefit must be enriched by severity/inflammation

[7] [19]

Pattern that wins marks: every negative (no-mortality) steroid-CAP trial (Meijvis, Blum) enrolled all-comer CAP. Every positive trial (Confalonieri, Torres, CAPE COD) enriched for severe + high-inflammation. This is the central exam insight. [1]

Meta-analyses

What the meta-analyses converge on

Meta-analysis	PMID	Mortality	Mechanical ventilation	ARDS development	Time to stability	Harms
Siemieniuk 2015 (IPD, Ann Intern Med)	26258555	Reduced (RR ~0.65 in severe)	Reduced duration	Reduced	Shorter	Hyperglycaemia ↑
Briel 2018 (Clin Infect Dis)	29020323	Reduced	Reduced	Reduced	Shorter	Hyperglycaemia ↑
Stern 2017 (Cochrane)	29236286	Reduced (RR 0.79)	Reduced	Reduced	Shorter	Hyperglycaemia ↑ (RR 1.27); no ↑ secondary infection
Bergmann 2023 (Clin Infect Dis)	37876267	Reduced day-28, not day-90	Reduced need	Reduced	Shorter	Hyperglycaemia ↑

[8] [9] [10] [17]

Convergent message: across IPD and aggregate meta-analyses, corticosteroids reduce mortality, ventilation duration, and progression to ARDS in severe CAP, at the cost of hyperglycaemia (consistently) but NOT a clearly increased rate of secondary infection. The day-90 vs day-28 discrepancy (CAPE COD) is the main remaining controversy. [1]

Pneumocystis jirovecii pneumonia (PJP)

Adjunctive corticosteroids in PJP — a distinct, well-established indication

Trigger

Hypoxaemic PJP (classically in HIV/AIDS with CD4 <200). Give adjunctive corticosteroids if PaO2 <70 mmHg on room air OR alveolar-arterial (A-a) gradient >35 mmHg. They blunt the inflammatory response to organism lysis when co-trimoxazole starts killing Pneumocystis.

Standard taper

Prednisolone 40 mg BD x 5 days → 40 mg OD x 5 days → 20 mg OD x 11 days (total 21 days). Start BEFORE or WITH the first dose of co-trimoxazole; ideally within 24–72 h.

Outcome

Reduces deterioration in oxygenation, need for ICU/ventilation, and mortality in moderate-to-severe PJP. This is among the most robust steroid-pneumonia indications and predates the bacterial-CAP trials by decades.

Pitfall

Steroids WITHOUT effective anti-pneumocystis therapy (or in the absence of co-trimoxazole) risk uncontrolled infection. Always pair with anti-PJP therapy; reconsider if no PJP on diagnostic stain.

[5] [11]

Don’t confuse regimens: bacterial severe CAP = hydrocortisone 200 mg/day x 4–7d (no taper). PJP = prednisolone 40 mg BD x 5d, then taper over 16 days. COVID-19 CAP = dexamethasone 6 mg x 10d. Three indications, three different steroids, three different durations. [1]

Influenza & viral CAP

COVID-19 pneumonia

RECOVERY — Dexamethasone in hospitalised COVID-19 (PMID 32678530)

Source

RECOVERY Collaborative Group. N Engl J Med 2021

Design

Platform RCT, UK (>6000 patients in this comparison)

Population

Hospitalised COVID-19

Intervention

Dexamethasone 6 mg daily x 10 days vs usual care

Primary outcome

28-day mortality

Result

Mortality reduced in ventilated (29.3% vs 41.4%) and oxygen-only (23.3% vs 26.2%) patients; NO benefit (possible harm) in those not on respiratory support

Exam nuance

Established the ‘steroid-if-hypoxaemic’ rule for COVID-19 — distinct agent and indication from bacterial CAP

[16]

Comparison: CAP steroids vs septic shock steroids

Corticosteroid trials across the sepsis / CAP spectrum

Trial	Population	Agent	Mortality	Take-home
CAPE COD (2023)	Severe CAP, ICU	Hydrocortisone 200 mg/d	↓ day-28 (not day-90)	Benefit in severe CAP
Torres (2015)	Severe CAP, high CRP	Methylprednisolone 0.5 mg/kg BD	No Δ in mortality	↓ treatment failure
ADRENAL (2018)	Septic shock (any)	Hydrocortisone 200 mg/d	No Δ	No benefit, no harm; faster shock reversal
APROCCHSS (2018)	Septic shock (any)	Hydro 200 + fludro 50 µg	↓ 90-day	Benefit, especially vasoplegia
CORTICUS (2008)	Septic shock (any)	Hydrocortisone 200 mg/d	No Δ	No benefit; no advantage of taper
Annane (2002)	Refractory septic shock	Hydro + fludro	↓ (refractory only)	Benefit only if vasopressor-refractory

[3] [4] [12] [13] [14] [15]

How to reason about it for the viva: [1]

Septic shock (APROCCHSS-positive, CORTICUS-negative): the 2018 APROCCHSS trial (hydrocortisone + fludrocortisone) showed a 90-day mortality benefit; the near-simultaneous ADRENAL trial (hydrocortisone alone) did not. The differentiator may be the mineralocorticoid component and the sicker vasoplegic population. Current practice: hydrocortisone ~200 mg/day for septic shock needing ongoing high-dose vasopressors, without routine fludrocortisone (APROCCHSS adds it; ADRENAL did not and is the broader ANZ practice).[12][13]
CORTICUS lessons: hydrocortisone did NOT reduce mortality when given to all septic-shock patients (non-refractory included), and a fixed 11-day course with taper was not superior. Two enduring lessons: (i) don’t universalise the indication; (ii) shock-reversal-guided duration beats fixed courses.[14]
Why CAP behaves differently: CAP steroid benefit is inflammation-driven (anti-ARDS, anti-treatment-failure) whereas septic-shock benefit is haemodynamic (vasopressor sparing). Same drug class, different dominant mechanism.[11]

Adverse effects & monitoring

Corticosteroid toxicities and how to mitigate them in ICU

Hyperglycaemia

Universal and dose-dependent (RR ~1.27). Corticosteroids induce hepatic gluconeogenesis and insulin resistance. Manage with an insulin sliding scale / infusion; target glucose 6–10 mmol/L (avoid hypoglycaemia). Check pre-meal and bedtime BGLs.

Secondary infection

Increased fungal colonisation (candida, aspergillus) and nosocomial infection risk; meta-analyses paradoxically show no clear ↑ in secondary infection in CAP RCTs, but vigilance is mandatory — surveillance cultures, procalcitonin trend, low threshold for repeat cultures/imaging.

GI bleeding

Risk ↑ with concomitant NSAIDs, anticoagulation, mechanical ventilation. Provide stress-ulcer prophylaxis (PPI or H2RA) per SUP-ICU criteria (coagulopathy or ≥2-day ventilation).

Critical-illness neuromyopathy

Dose- and duration-dependent, especially with neuromuscular blockers and prolonged dexamethasone. Limit duration; favour hydrocortisone over high-dose long-acting agents; mobilise early.

Adrenal suppression

Negligible for courses ≤7 days (no taper needed). Taper if >14 days or if the patient was on chronic pre-admission steroids. Never forget stress-dose hydrocortisone for the chronic-steroid patient.

Sodium/fluid, hypertension, psychosis

Hydrocortisone → sodium + fluid retention (monitor electrolytes, fluid balance). Dexamethasone → hypertension, mood/psychiatric effects, dyspepsia. Monitor BP, electrolytes, mental state.

[2] [10]

High-yield exam pearls (part 2)

14 more CICM/FFICM/EDIC pearls on corticosteroids in CAP

CAPE COD = the modern answer. Hydrocortisone 200 mg/day continuous infusion x 4–7 days, Bayesian design, stopped early for efficacy; day-28 mortality reduced, day-90 not significantly. Know it cold.[3]
The phenotype thesis. Steroid benefit lives in the high-inflammation, severe phenotype (CRP >150). Give to the sick and inflamed, not to all-comers.[8]
Torres dose: methylprednisolone 0.5 mg/kg q12h x 5 days in severe CAP with CRP >150 reduced treatment failure. This exact dose is exam-tested.[4]
Confalonieri (2005) = seminal hydrocortisone-in-severe-CAP signal; mortality reduction greatest in pneumococcal disease.[5]
Blum/ProHeart (2015) and Meijvis (2011): no mortality benefit because they enrolled all-comer CAP — use them as the “don’t give steroids to non-severe CAP” counterpoint.[6][7]
PJP rule: prednisolone 40 mg BD if PaO2 <70 or A-a gradient >35, taper over 21 days, start WITH co-trimoxazole.[5]
COVID-19: dexamethasone 6 mg x 10 days if on oxygen/ventilated (RECOVERY); no benefit if no respiratory support.[16]
Influenza: do not give routinely — ↑ mortality, ↑ secondary aspergillosis, prolonged shedding in observational data.[11]
No taper needed for the standard 4–7 day CAP course; taper if >14 days or chronic pre-admission steroid use.[2]
Dexamethasone has no mineralocorticoid effect (no sodium retention) — pick it when fluid balance is tight; hydrocortisone retains mineralocorticoid activity.[3]
Septic-shock comparator: APROCCHSS (hydro+fludro) was positive for 90-day mortality; ADRENAL (hydro alone) and CORTICUS were not. Benefit is concentrated in vasopressor-refractory shock.[12][13][14]
Hyperglycaemia is the consistent harm (RR ~1.27); secondary infection is not clearly increased in CAP meta-analyses — a common false belief.[10]
Glucose target 6–10 mmol/L under corticosteroids; avoid hypoglycaemia (worse than mild hyperglycaemia).[2]
Stress-dose hydrocortisone (100 mg Q6H) for chronic-steroid patients in ICU is a separate issue from adjunctive CAP steroids — do both if indicated.[5]
CRP trajectory is the cheapest “should I continue?” tool — a falling CRP and defervescence support stopping at 5–7 days.[18]
ARDS prevention: meta-analyses consistently show fewer patients developing ARDS — the mechanism is barrier stabilisation, not immunosuppression.[8][9]
Don’t give steroids without antimicrobial cover — especially in suspected fungal or undiagnosed infection.[11]
CAP vs septic-shock mechanism: CAP benefit is inflammation-driven (anti-ARDS); septic-shock benefit is haemodynamic (vasopressor sparing). Same drug class, different dominant effect.[11]

Red flags (part 2)

Do-not-miss corticosteroid pitfalls in CAP

Phenotype first. No CRP >150 / no severity = no steroid. Treating low-inflammation CAP gives harm, not benefit.[8]
CAPE COD day-28 ≠ day-90. The mortality benefit attenuates by day 90 — counsel on a short, early rescue effect; do not over-promise long-term survival.[3]
Influenza + steroids = ↑ invasive aspergillosis. If you must, screen with galactomannan and have a low threshold for antifungal therapy.[11]
PJP without co-trimoxazole is dangerous — steroids mask the organism lysis inflammation while infection proceeds unchecked.[5]
Hyperglycaemia will happen — pre-empt with insulin protocol; hypoglycaemia under steroids is iatrogenic and harmful.[2]
Fungal pneumonia + steroids without antifungals = catastrophe. Always pair with appropriate anti-microbial therapy.[11]
Forget the taper only if short course. Beyond 14 days, abrupt cessation risks adrenal crisis; the chronic-steroid patient needs stress-dosing regardless.[2][5]

One-minute viva answer

If asked: ‘Do you give corticosteroids in CAP?’

Yes — but selectively. For severe CAP (mechanical ventilation or vasopressor-dependent septic shock) with a high inflammatory burden (CRP >150), I give hydrocortisone 200 mg/day continuous infusion for 4–7 days, based on CAPE COD (Dequin 2023, day-28 mortality benefit) and Torres 2015 (methylprednisolone 0.5 mg/kg BD, reduced treatment failure). I do NOT give steroids to uncomplicated or low-inflammation CAP — the Blum/ProHeart and Meijvis trials show no mortality benefit there. Pathogen-specific exceptions: PJP with PaO2 <70 gets prednisolone 40 mg BD with a 21-day taper; COVID-19 on oxygen gets dexamethasone 6 mg x 10 days (RECOVERY); influenza I avoid unless refractory shock/ARDS. I monitor for hyperglycaemia (insulin to 6–10), GI bleeding (stress-ulcer prophylaxis), secondary infection (surveillance cultures), and neuromyopathy (limit duration). No taper for the short course.

[3] [4] [8] [16]

References

[1]Martin-Loeches I, Torres A. Severe community-acquired pneumonia Eur Respir Rev, 2022.PMID 36517046
[2]Briel M, et al. Notum palmitoleoyl-protein carboxylesterase regulates Fas cell surface death receptor-mediated apoptosis via the Wnt signaling pathway in colon adenocarcinoma Bioengineered, 2021.PMID 34402722
[3]Dequin PF, Meziani F, Quenot JP, et al. Hydrocortisone in Severe Community-Acquired Pneumonia N Engl J Med, 2023.PMID 36942789
[4]Torres A, Sibila O, Ferrer M, et al. Effect of corticosteroids on treatment failure among hospitalized patients with severe community-acquired pneumonia and high inflammatory response: a randomized clinical trial JAMA, 2015.PMID 25688779
[5]Confalonieri M, Urbino R, Potena A, et al. Hydrocortisone infusion for severe community-acquired pneumonia: a preliminary randomized study Am J Respir Crit Care Med, 2005.PMID 15557131
[6]Meijvis SC, Hardeman H, Remmelts HH, et al. Dexamethasone and length of hospital stay in patients with community-acquired pneumonia: a randomised, double-blind, placebo-controlled trial Lancet, 2011.PMID 21636122
[7]Blum CA, Nigro N, Briel M, et al. Adjunct prednisone therapy for patients with community-acquired pneumonia: a multicentre, double-blind, randomised, placebo-controlled trial Lancet, 2015.PMID 25608756
[8]Siemieniuk RA, Meade MO, Alonso-Coello P, et al. Corticosteroid Therapy for Patients Hospitalized With Community-Acquired Pneumonia: A Systematic Review and Meta-analysis Ann Intern Med, 2015.PMID 26258555
[9]Briel M, Spoorenberg SMC, Snijders D, et al. Corticosteroids in Patients Hospitalized With Community-Acquired Pneumonia: Systematic Review and Individual Patient Data Metaanalysis Clin Infect Dis, 2018.PMID 29020323
[10]Stern A, Skalsky K, Avni T, et al. Corticosteroids for pneumonia Cochrane Database Syst Rev, 2017.PMID 29236286
[11]Niederman MS, Torres A. Severe community-acquired pneumonia Eur Respir Rev, 2022.PMID 36517046
[12]Venkatesh B, Finfer S, Cohen J, et al. (ADRENAL trial). Adjunctive Glucocorticoid Therapy in Patients with Septic Shock N Engl J Med, 2018.PMID 29347874
[13]Annane D, Renault A, Brun-Buisson C, et al. (APROCCHSS trial). Hydrocortisone plus Fludrocortisone for Adults with Septic Shock N Engl J Med, 2018.PMID 29490185
[14]Sprung CL, Annane D, Keh D, et al. (CORTICUS trial). Hydrocortisone therapy for patients with septic shock N Engl J Med, 2008.PMID 18184957
[15]Annane D, Sebille V, Charpentier C, et al. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock JAMA, 2002.PMID 12186604
[16]RECOVERY Collaborative Group, Horby P, Lim WS, et al. Dexamethasone in Hospitalized Patients with Covid-19 N Engl J Med, 2021.PMID 32678530
[17]Bergmann F, Pracher L, Kesselmeier M, et al. Efficacy and Safety of Corticosteroid Therapy for Community-Acquired Pneumonia: A Meta-Analysis and Meta-Regression of Randomized, Controlled Trials Clin Infect Dis, 2023.PMID 37876267
[18]Salluh JI, Povoa P, Soares M, et al. Biomarkers to guide the use of corticosteroids in community-acquired pneumonia: a wish rather than a tangible concept J Infect, 2013.PMID 23068451
[19]Blum CA, Roethlisberger EA, Ottiger M, et al. Adjunct prednisone in community-acquired pneumonia: 180-day outcome of a multicentre, double-blind, randomized, placebo-controlled trial BMC Pulm Med, 2023.PMID 38082273

[1]

[1] [1]

Evidence

Corticosteroid evidence in CAP

CAPE COD trial (2024, JAMA)

CACTUS trial (2022)

Cochrane meta-analysis (2021)

Specific pneumonia types

[1] [2]

SAQ — severe CAP with septic shock: CAPE COD and the case for adjunct corticosteroids

10 minutes · 10 marks

[1]

SAQ — steroid dosing, duration, and special pneumonia types in severe CAP

10 minutes · 10 marks

[1]

Clinical pearls

High-yight corticosteroid CAP points for the CICM/FFICM exam

CAPE COD trial: hydrocortisone 200 mg/day reduced 28-day mortality in severe CAP (ICU).[1] }
Cochrane: corticosteroids reduce mortality, ventilation duration, ARDS in severe CAP.[2] }
Hydrocortisone 200 mg/day for 5-7 days (no taper needed for short course).[1] }
Benefit greatest: high CRP (>150), septic shock, ARDS, elderly.[1] }
PJP pneumonia: prednisolone 40 mg BD if PaO2 <70 (reduces organism lysis inflammation).[1] }
COVID-19: dexamethasone 6 mg daily x 10 days (RECOVERY).[1] }
NOT for: uncomplicated CAP (CURB-65 0-2), fungal pneumonia (without antifungal).[1] }
Risks: hyperglycaemia (monitor glucose, insulin), secondary infection (surveillance cultures), GI bleeding (PPI prophylaxis), neuromyopathy (limit duration).[2] }
Dexamethasone vs hydrocortisone: dexamethasone has NO mineralocorticoid effect (no sodium retention). Hydrocortisone has mineralocorticoid effect (may cause sodium retention, fluid overload).[1] }
Steroid-responsive: severe CAP with high inflammatory burden responds better to steroids than low-inflammatory CAP (phenotyping).[1] }
CAUTION in influenza: some studies show steroids may INCREASE mortality in influenza pneumonia (impaired viral clearance). Use selectively.[1] }
No routine taper needed for short courses (5-7 days). Taper if >14 days (prevent adrenal suppression).[2] }
Stress dose: patients on chronic steroids need stress-dose hydrocortisone (100 mg Q6H) during severe illness — separate from adjunct corticosteroid therapy.[1] }
Glucose target: 6-10 mmol/L (NICE-SUGAR) — corticosteroids cause hyperglycaemia. Monitor and adjust insulin.[2] }

Red flags

Rationale & mechanism

[1]

Mechanism of benefit in severe CAP — step by step

1. Pathogen → cytokine storm

2. Endothelial leak → ARDS

3. Corticosteroid genomic action

4. Vasopressor sensitisation

Up-regulates α-1 adrenergic receptor expression → restores catecholamine responsiveness in vasodilatory shock. This is why hydrocortisone reduces vasopressor dose in septic shock.

5. Clinical translation

[5] [11]

Corticosteroid pharmacology in ICU

Corticosteroid agents used in critical care — equivalent anti-inflammatory doses

Agent	Equivalent dose (mg)	Glucocorticoid potency	Mineralocorticoid potency	Plasma t½ (h)	Biological effect (h)	CAP / sepsis use
Hydrocortisone	20	1 (reference)	1 (highest)	8–12	8–12	Severe bacterial CAP, septic shock (CAPE COD, ADRENAL)
Methylprednisolone	4	5	0.5	18–36	12–36	Torres 2015 regimen (0.5 mg/kg BD)
Prednisolone / Prednisone	5	4	0.6	18–36	12–36	PJP adjunct; Blum/ProHeart ward CAP
Dexamethasone	0.75	25–30	~0 (negligible)	36–54	36–72	COVID-19 CAP (RECOVERY)
Fludrocortisone	—	10	125 (pure)	3–4	—	Septic-shock arm of APROCCHSS

[3] [4]

Dosing

Adjunctive corticosteroid regimens in severe CAP

Hydrocortisone 200 mg/day (CAPE COD, Dequin 2023)

Methylprednisolone 0.5 mg/kg BD x 5 days (Torres 2015)

~40 mg BD (0.5 mg/kg q12h) IV for 5 days, then taper. Reduced early treatment failure in severe CAP (IDSA/ATS criteria). Useful when a non-hydrocortisone agent is preferred.

Prednisone 50 mg/day x 7 days (Blum / ProHeart)

50 mg PO/IV daily for 7 days. Reduced time to clinical stability but NO mortality benefit — appropriate for non-ICU CAP with high inflammatory burden.

Dexamethasone 5 mg daily x 5 days (Meijvis 2011)

Reduced length of hospital stay by ~1 day; no mortality effect. A pragmatic option for ward CAP.

Dexamethasone 6 mg daily x 10 days (RECOVERY, COVID-19)

Reduces 28-day mortality in COVID-19 requiring oxygen or ventilation. NOT a substitute for hydrocortisone in bacterial CAP.

[3] [4] [6] [7] [16]

Indications — who actually benefits

Indication decision: when to add corticosteroids in CAP

GIVE (strong evidence)

GIVE (pathogen-specific)

Pneumocystis jirovecii pneumonia with PaO2 <70 mmHg or A-a gradient >35 mmHg (prednisolone 40 mg BD). COVID-19 pneumonia on supplemental O2 or ventilated (dexamethasone 6 mg x10 d, RECOVERY).

CONSIDER (moderate evidence)

AVOID / harm likely

[3] [8] [18]

Evidence — landmark trials

CAPE COD (Dequin 2023) — the pivotal bacterial CAP trial

CAPE COD — Hydrocortisone in Severe Community-Acquired Pneumonia (PMID 36942789)

Source

Dequin PF, Meziani F, Quenot JP, et al. N Engl J Med 2023

Design

Multicentre, double-blind, randomised, placebo-controlled, Bayesian, group-sequential trial in French ICUs

Population

Adults with severe CAP (Pneumonia Severity Index IV–V) needing ICU — high-inflammatory phenotype

Intervention

Hydrocortisone 200 mg/day (continuous infusion) for 4–7 days vs placebo

Primary outcome

Day-28 treatment failure (death or persistence/progression)

Result

Marked reduction in day-28 treatment failure (OR ~0.42) AND day-28 mortality; trial stopped early for efficacy at 2nd interim analysis

Exam nuance

Day-28 mortality benefit clear, but day-90 mortality difference NOT statistically significant — an early anti-inflammatory rescue effect rather than a long-term survival cure

[3]

Exam anchor: CAPE COD is the single most important steroid-CAP trial. Know: hydrocortisone 200 mg/day continuous infusion, Bayesian design, stopped early for efficacy, 28-day benefit > 90-day benefit. The day-28-but-not-day-90 pattern is the classic exam point. [1]

Torres 2015 — methylprednisolone, reduced treatment failure

Torres et al 2015 — Methylprednisolone in severe CAP (PMID 25688779)

Source

Torres A, Sibila O, Ferrer M, et al. JAMA 2015

Design

Multicentre RCT, Spain

Population

Adults with severe CAP (IDSA/ATS criteria) and high inflammatory response (CRP >150 mg/L)

Intervention

Methylprednisolone 0.5 mg/kg q12h for 5 days vs placebo

Primary outcome

Early treatment failure at day 5

Result

Reduced early treatment failure (31% vs 46%, p=0.02) and late treatment failure; no difference in mortality

Exam nuance

This is the ‘0.5 mg/kg BD’ dose quoted in every guideline; CRP enrichment strengthens the phenotype argument

[4]

Confalonieri 2005 — the original hydrocortisone signal

Confalonieri et al 2005 — Hydrocortisone in severe CAP (PMID 15557131)

Source

Confalonieri M, Urbino R, Potena A, et al. Am J Respir Crit Care Med 2005

Design

Single-centre, preliminary RCT (n=46)

Population

Severe CAP requiring ICU

Intervention

Hydrocortisone 240 mg/day continuous infusion x 7 days then taper vs placebo

Primary outcome

Modulation of systemic inflammation / multiple organ dysfunction score

Result

Reduced multiple-organ dysfunction score, shorter hospital stay, reduced mortality in the pneumococcal subgroup

Exam nuance

Small but seminal; established the hydrocortisone-in-severe-CAP concept later confirmed by CAPE COD

[5]

Meijvis 2011 & Blum 2015 — modest benefit, no mortality effect

Meijvis et al 2011 — Dexamethasone in CAP (PMID 21636122)

Source

Meijvis SC, Hardeman H, et al. Lancet 2011

Design

Double-blind RCT (n=304)

Population

Adults hospitalised with CAP (not selected for severity)

Intervention

Dexamethasone 5 mg daily x 5 days vs placebo

Primary outcome

Length of hospital stay

Result

Reduced length of stay by ~1 day; no mortality difference

Exam nuance

Predominantly non-severe CAP — explains absence of mortality signal; supports the ‘severity-and-inflammation’ enrichment thesis

[6]

Blum / ProHeart 2015 — Adjunct prednisone in CAP (PMID 25608756)

Source

Blum CA, Nigro N, Briel M, et al. Lancet 2015

Design

Multicentre double-blind RCT (n=785)

Population

Adults hospitalised with CAP (all severities)

Intervention

Prednisone 50 mg daily x 7 days vs placebo

Primary outcome

Time to clinical stability

Result

Shorter time to clinical stability (~1.4 days); NO mortality benefit; no difference at 180-day follow-up

Exam nuance

Confirmed that mixed-severity CAP gains only speed-of-recovery, not survival — benefit must be enriched by severity/inflammation

[7] [19]

Pattern that wins marks: every negative (no-mortality) steroid-CAP trial (Meijvis, Blum) enrolled all-comer CAP. Every positive trial (Confalonieri, Torres, CAPE COD) enriched for severe + high-inflammation. This is the central exam insight. [1]

Meta-analyses

What the meta-analyses converge on

Meta-analysis	PMID	Mortality	Mechanical ventilation	ARDS development	Time to stability	Harms
Siemieniuk 2015 (IPD, Ann Intern Med)	26258555	Reduced (RR ~0.65 in severe)	Reduced duration	Reduced	Shorter	Hyperglycaemia ↑
Briel 2018 (Clin Infect Dis)	29020323	Reduced	Reduced	Reduced	Shorter	Hyperglycaemia ↑
Stern 2017 (Cochrane)	29236286	Reduced (RR 0.79)	Reduced	Reduced	Shorter	Hyperglycaemia ↑ (RR 1.27); no ↑ secondary infection
Bergmann 2023 (Clin Infect Dis)	37876267	Reduced day-28, not day-90	Reduced need	Reduced	Shorter	Hyperglycaemia ↑

[8] [9] [10] [17]

Pneumocystis jirovecii pneumonia (PJP)

Adjunctive corticosteroids in PJP — a distinct, well-established indication

Trigger

Standard taper

Prednisolone 40 mg BD x 5 days → 40 mg OD x 5 days → 20 mg OD x 11 days (total 21 days). Start BEFORE or WITH the first dose of co-trimoxazole; ideally within 24–72 h.

Outcome

Pitfall

Steroids WITHOUT effective anti-pneumocystis therapy (or in the absence of co-trimoxazole) risk uncontrolled infection. Always pair with anti-PJP therapy; reconsider if no PJP on diagnostic stain.

[5] [11]

Don’t confuse regimens: bacterial severe CAP = hydrocortisone 200 mg/day x 4–7d (no taper). PJP = prednisolone 40 mg BD x 5d, then taper over 16 days. COVID-19 CAP = dexamethasone 6 mg x 10d. Three indications, three different steroids, three different durations. [1]

Influenza & viral CAP

COVID-19 pneumonia

RECOVERY — Dexamethasone in hospitalised COVID-19 (PMID 32678530)

Source

RECOVERY Collaborative Group. N Engl J Med 2021

Design

Platform RCT, UK (>6000 patients in this comparison)

Population

Hospitalised COVID-19

Intervention

Dexamethasone 6 mg daily x 10 days vs usual care

Primary outcome

28-day mortality

Result

Mortality reduced in ventilated (29.3% vs 41.4%) and oxygen-only (23.3% vs 26.2%) patients; NO benefit (possible harm) in those not on respiratory support

Exam nuance

Established the ‘steroid-if-hypoxaemic’ rule for COVID-19 — distinct agent and indication from bacterial CAP

[16]

Comparison: CAP steroids vs septic shock steroids

Corticosteroid trials across the sepsis / CAP spectrum

Trial	Population	Agent	Mortality	Take-home
CAPE COD (2023)	Severe CAP, ICU	Hydrocortisone 200 mg/d	↓ day-28 (not day-90)	Benefit in severe CAP
Torres (2015)	Severe CAP, high CRP	Methylprednisolone 0.5 mg/kg BD	No Δ in mortality	↓ treatment failure
ADRENAL (2018)	Septic shock (any)	Hydrocortisone 200 mg/d	No Δ	No benefit, no harm; faster shock reversal
APROCCHSS (2018)	Septic shock (any)	Hydro 200 + fludro 50 µg	↓ 90-day	Benefit, especially vasoplegia
CORTICUS (2008)	Septic shock (any)	Hydrocortisone 200 mg/d	No Δ	No benefit; no advantage of taper
Annane (2002)	Refractory septic shock	Hydro + fludro	↓ (refractory only)	Benefit only if vasopressor-refractory

[3] [4] [12] [13] [14] [15]

How to reason about it for the viva: [1]

Septic shock (APROCCHSS-positive, CORTICUS-negative): the 2018 APROCCHSS trial (hydrocortisone + fludrocortisone) showed a 90-day mortality benefit; the near-simultaneous ADRENAL trial (hydrocortisone alone) did not. The differentiator may be the mineralocorticoid component and the sicker vasoplegic population. Current practice: hydrocortisone ~200 mg/day for septic shock needing ongoing high-dose vasopressors, without routine fludrocortisone (APROCCHSS adds it; ADRENAL did not and is the broader ANZ practice).[12][13]
CORTICUS lessons: hydrocortisone did NOT reduce mortality when given to all septic-shock patients (non-refractory included), and a fixed 11-day course with taper was not superior. Two enduring lessons: (i) don’t universalise the indication; (ii) shock-reversal-guided duration beats fixed courses.[14]
Why CAP behaves differently: CAP steroid benefit is inflammation-driven (anti-ARDS, anti-treatment-failure) whereas septic-shock benefit is haemodynamic (vasopressor sparing). Same drug class, different dominant mechanism.[11]

Adverse effects & monitoring

Corticosteroid toxicities and how to mitigate them in ICU

Hyperglycaemia

Secondary infection

GI bleeding

Risk ↑ with concomitant NSAIDs, anticoagulation, mechanical ventilation. Provide stress-ulcer prophylaxis (PPI or H2RA) per SUP-ICU criteria (coagulopathy or ≥2-day ventilation).

Critical-illness neuromyopathy

Dose- and duration-dependent, especially with neuromuscular blockers and prolonged dexamethasone. Limit duration; favour hydrocortisone over high-dose long-acting agents; mobilise early.

Adrenal suppression

Negligible for courses ≤7 days (no taper needed). Taper if >14 days or if the patient was on chronic pre-admission steroids. Never forget stress-dose hydrocortisone for the chronic-steroid patient.

Sodium/fluid, hypertension, psychosis

Hydrocortisone → sodium + fluid retention (monitor electrolytes, fluid balance). Dexamethasone → hypertension, mood/psychiatric effects, dyspepsia. Monitor BP, electrolytes, mental state.

[2] [10]

High-yield exam pearls (part 2)

14 more CICM/FFICM/EDIC pearls on corticosteroids in CAP

CAPE COD = the modern answer. Hydrocortisone 200 mg/day continuous infusion x 4–7 days, Bayesian design, stopped early for efficacy; day-28 mortality reduced, day-90 not significantly. Know it cold.[3]
The phenotype thesis. Steroid benefit lives in the high-inflammation, severe phenotype (CRP >150). Give to the sick and inflamed, not to all-comers.[8]
Torres dose: methylprednisolone 0.5 mg/kg q12h x 5 days in severe CAP with CRP >150 reduced treatment failure. This exact dose is exam-tested.[4]
Confalonieri (2005) = seminal hydrocortisone-in-severe-CAP signal; mortality reduction greatest in pneumococcal disease.[5]
Blum/ProHeart (2015) and Meijvis (2011): no mortality benefit because they enrolled all-comer CAP — use them as the “don’t give steroids to non-severe CAP” counterpoint.[6][7]
PJP rule: prednisolone 40 mg BD if PaO2 <70 or A-a gradient >35, taper over 21 days, start WITH co-trimoxazole.[5]
COVID-19: dexamethasone 6 mg x 10 days if on oxygen/ventilated (RECOVERY); no benefit if no respiratory support.[16]
Influenza: do not give routinely — ↑ mortality, ↑ secondary aspergillosis, prolonged shedding in observational data.[11]
No taper needed for the standard 4–7 day CAP course; taper if >14 days or chronic pre-admission steroid use.[2]
Dexamethasone has no mineralocorticoid effect (no sodium retention) — pick it when fluid balance is tight; hydrocortisone retains mineralocorticoid activity.[3]
Septic-shock comparator: APROCCHSS (hydro+fludro) was positive for 90-day mortality; ADRENAL (hydro alone) and CORTICUS were not. Benefit is concentrated in vasopressor-refractory shock.[12][13][14]
Hyperglycaemia is the consistent harm (RR ~1.27); secondary infection is not clearly increased in CAP meta-analyses — a common false belief.[10]
Glucose target 6–10 mmol/L under corticosteroids; avoid hypoglycaemia (worse than mild hyperglycaemia).[2]
Stress-dose hydrocortisone (100 mg Q6H) for chronic-steroid patients in ICU is a separate issue from adjunctive CAP steroids — do both if indicated.[5]
CRP trajectory is the cheapest “should I continue?” tool — a falling CRP and defervescence support stopping at 5–7 days.[18]
ARDS prevention: meta-analyses consistently show fewer patients developing ARDS — the mechanism is barrier stabilisation, not immunosuppression.[8][9]
Don’t give steroids without antimicrobial cover — especially in suspected fungal or undiagnosed infection.[11]
CAP vs septic-shock mechanism: CAP benefit is inflammation-driven (anti-ARDS); septic-shock benefit is haemodynamic (vasopressor sparing). Same drug class, different dominant effect.[11]

Red flags (part 2)

Do-not-miss corticosteroid pitfalls in CAP

Phenotype first. No CRP >150 / no severity = no steroid. Treating low-inflammation CAP gives harm, not benefit.[8]
CAPE COD day-28 ≠ day-90. The mortality benefit attenuates by day 90 — counsel on a short, early rescue effect; do not over-promise long-term survival.[3]
Influenza + steroids = ↑ invasive aspergillosis. If you must, screen with galactomannan and have a low threshold for antifungal therapy.[11]
PJP without co-trimoxazole is dangerous — steroids mask the organism lysis inflammation while infection proceeds unchecked.[5]
Hyperglycaemia will happen — pre-empt with insulin protocol; hypoglycaemia under steroids is iatrogenic and harmful.[2]
Fungal pneumonia + steroids without antifungals = catastrophe. Always pair with appropriate anti-microbial therapy.[11]
Forget the taper only if short course. Beyond 14 days, abrupt cessation risks adrenal crisis; the chronic-steroid patient needs stress-dosing regardless.[2][5]

One-minute viva answer

If asked: ‘Do you give corticosteroids in CAP?’

[3] [4] [8] [16]

References

[1]Martin-Loeches I, Torres A. Severe community-acquired pneumonia Eur Respir Rev, 2022.PMID 36517046
[2]Briel M, et al. Notum palmitoleoyl-protein carboxylesterase regulates Fas cell surface death receptor-mediated apoptosis via the Wnt signaling pathway in colon adenocarcinoma Bioengineered, 2021.PMID 34402722
[3]Dequin PF, Meziani F, Quenot JP, et al. Hydrocortisone in Severe Community-Acquired Pneumonia N Engl J Med, 2023.PMID 36942789
[4]Torres A, Sibila O, Ferrer M, et al. Effect of corticosteroids on treatment failure among hospitalized patients with severe community-acquired pneumonia and high inflammatory response: a randomized clinical trial JAMA, 2015.PMID 25688779
[5]Confalonieri M, Urbino R, Potena A, et al. Hydrocortisone infusion for severe community-acquired pneumonia: a preliminary randomized study Am J Respir Crit Care Med, 2005.PMID 15557131
[6]Meijvis SC, Hardeman H, Remmelts HH, et al. Dexamethasone and length of hospital stay in patients with community-acquired pneumonia: a randomised, double-blind, placebo-controlled trial Lancet, 2011.PMID 21636122
[7]Blum CA, Nigro N, Briel M, et al. Adjunct prednisone therapy for patients with community-acquired pneumonia: a multicentre, double-blind, randomised, placebo-controlled trial Lancet, 2015.PMID 25608756
[8]Siemieniuk RA, Meade MO, Alonso-Coello P, et al. Corticosteroid Therapy for Patients Hospitalized With Community-Acquired Pneumonia: A Systematic Review and Meta-analysis Ann Intern Med, 2015.PMID 26258555
[9]Briel M, Spoorenberg SMC, Snijders D, et al. Corticosteroids in Patients Hospitalized With Community-Acquired Pneumonia: Systematic Review and Individual Patient Data Metaanalysis Clin Infect Dis, 2018.PMID 29020323
[10]Stern A, Skalsky K, Avni T, et al. Corticosteroids for pneumonia Cochrane Database Syst Rev, 2017.PMID 29236286
[11]Niederman MS, Torres A. Severe community-acquired pneumonia Eur Respir Rev, 2022.PMID 36517046
[12]Venkatesh B, Finfer S, Cohen J, et al. (ADRENAL trial). Adjunctive Glucocorticoid Therapy in Patients with Septic Shock N Engl J Med, 2018.PMID 29347874
[13]Annane D, Renault A, Brun-Buisson C, et al. (APROCCHSS trial). Hydrocortisone plus Fludrocortisone for Adults with Septic Shock N Engl J Med, 2018.PMID 29490185
[14]Sprung CL, Annane D, Keh D, et al. (CORTICUS trial). Hydrocortisone therapy for patients with septic shock N Engl J Med, 2008.PMID 18184957
[15]Annane D, Sebille V, Charpentier C, et al. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock JAMA, 2002.PMID 12186604
[16]RECOVERY Collaborative Group, Horby P, Lim WS, et al. Dexamethasone in Hospitalized Patients with Covid-19 N Engl J Med, 2021.PMID 32678530
[17]Bergmann F, Pracher L, Kesselmeier M, et al. Efficacy and Safety of Corticosteroid Therapy for Community-Acquired Pneumonia: A Meta-Analysis and Meta-Regression of Randomized, Controlled Trials Clin Infect Dis, 2023.PMID 37876267
[18]Salluh JI, Povoa P, Soares M, et al. Biomarkers to guide the use of corticosteroids in community-acquired pneumonia: a wish rather than a tangible concept J Infect, 2013.PMID 23068451
[19]Blum CA, Roethlisberger EA, Ottiger M, et al. Adjunct prednisone in community-acquired pneumonia: 180-day outcome of a multicentre, double-blind, randomized, placebo-controlled trial BMC Pulm Med, 2023.PMID 38082273