Dynamic prediction of early antibiotic treatment failure in ischemic stroke-associated pneumonia: development and internal validation of a 48-h landmark model

Q: What are the key findings of this study?

A 48-h landmark model combining CRP change, NLR change, and oxygen escalation improved antibiotic failure prediction over baseline.

Q: What is the clinical evidence from this study?

Study design: Cohort. Population: Ischemic stroke-associated pneumonia (n=199). Intervention: 48-hour landmark reassessment model (combining CRP change, NLR change, and oxygen-support escalation) vs. Baseline (T0) prediction model. Primary outcome: Composite of initial antibiotic-treatment failure between 48 and 72 hours after treatment initiation (efficacy-driven escalation, replacement or addition of systemic antibiotics; persistent clinical instability at 72 hours with uncontrolled pneumonia; or pneumonia-related death) (OR 1.89 per 20 mg/L increase in 48-h CRP change, 95% CI 1.52-2.34, p=<0.001).

Q: What does this research mean for the field?

A 48-hour landmark model incorporating changes in CRP, NLR, and oxygen support escalation predicts early antibiotic treatment failure in ischemic stroke-associated pneumonia significantly better than baseline assessment. Novelty: ClaimNovelty.METHODOLOGICAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

Q: What question did this study set out to answer?

To develop and internally validate a baseline model and a 48-h landmark model for predicting early antibiotic treatment failure between 48 and 72 h after starting empirical antibiotics in ischemic stroke-associated pneumonia.

Jufeng Qiu; Mingjiao Tang; 李思思; Quanchan Li; Cuiling Tang; Xuebin Qin; Haili Feng; Jinsong Li; Tengxiang Zhu; Yuqing Li; Hao Li; Chunhua Lai

doi:10.1080/07853890.2026.2753847

November 12, 2026Annals of MedicineOpen Access

Dynamic prediction of early antibiotic treatment failure in ischemic stroke-associated pneumonia: development and internal validation of a 48-h landmark model

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Key result

Dynamic 48-hour landmark model improves antibiotic failure prediction, with rising CRP linked to ~89% higher odds.

OR 1.89 per 20 mg/L increase in 48-h CRP change
95% CI 1.52-2.34
P<0.001
n=199

Why the study?

Existing stroke-associated pneumonia scores estimate pneumonia occurrence rather than early treatment response after antibiotics have been initiated.

Does a structured 48-hour landmark reassessment combining inflammatory biomarker trajectories (CRP and NLR changes) and oxygen-support escalation improve the prediction of early antibiotic treatment failure between 48 and 72 hours compared to baseline assessment alone in patients with ischemic stroke-associated pneumonia?

Key Points

To develop and internally validate a baseline model and a 48-h landmark model for predicting early antibiotic treatment failure between 48 and 72 h after starting empirical antibiotics in ischemic stroke-associated pneumonia.
Retrospective observational cohort study of 199 acute ischemic stroke patients with stroke-associated pneumonia receiving empirical systemic antibiotics at a single center in Guilin, China between 1 December 2021 and 1 December 2025.
Logistic ridge regression with a fixed penalty (C = 1.0) was used to model the composite primary endpoint of treatment failure between 48 ± 8 h and 72 ± 8 h.
Internal validation and optimism-corrected performance evaluations were conducted using 500 bootstrap resamples.
Treatment failure occurred in 102 of 199 patients (51.3%), with failure at baseline associated with mechanical ventilation before antibiotic initiation and a higher platelet-to-lymphocyte ratio.
The optimism-corrected area under the receiver operating characteristic curve increased from 0.697 for the baseline model to 0.889 for the 48-h landmark model.

Study Design

Type

Cohort (n=199)

Multicenter

No

Structured PICO

Does a structured 48-hour landmark reassessment combining inflammatory biomarker trajectories (CRP and NLR changes) and oxygen-support escalation improve the prediction of early antibiotic treatment failure between 48 and 72 hours compared to baseline assessment alone in patients with ischemic stroke-associated pneumonia?

P

Population

199 adults (median age 70 years, 27.6% female) with acute ischemic stroke who developed stroke-associated pneumonia within 7 days of onset and received empirical systemic antibiotics, followed through a 72-hour assessment window.

E

Exposure

48-hour (T48) landmark dynamic prediction model incorporating baseline variables plus 48-h change in C-reactive protein (ΔCRP), 48-h change in neutrophil-to-lymphocyte ratio (ΔNLR), and 48-h oxygen-support escalation, fitted using ridge logistic regression (C=1.0).

C

Comparator

Baseline (T0) prediction model at antibiotic initiation incorporating age, pre-stroke mRS, admission NIHSS, mechanical ventilation before T0, late SAP timing, diagnosis-to-antibiotic delay, broad-spectrum initial therapy, and baseline platelet-to-lymphocyte ratio (PLR).

O

Outcome

Composite of initial antibiotic-treatment failure after completion of the 48-h (T48) landmark assessment and by the nominal 72-h (T72 ± 8 h) assessment, defined as at least one of: (1) efficacy-driven escalation, replacement, or addition of systemic antibiotics; (2) persistent clinical instability at T72 together with documented uncontrolled pneumonia, ongoing infection activity, or poor response; or (3) pneumonia-related death.composite

Main Result

Odds Ratio: 1.89 (95% CI 1.52–2.34)

p-value: p=<0.001

Limitations

Retrospective single-center design with internal bootstrap validation rather than external validation.
T48 and T72 observations were extracted from routine clinical care within ±8-h target windows, and exact measurement timestamps were not systematically recorded.
Potential residual predictor-outcome overlap and shared clinical information because treating clinicians had access to routine biomarkers and oxygen-support status.
Incomplete microbiological data prevented incorporation of microbiological findings into the failure analysis.
Formal inter-reviewer agreement for initial stroke-associated pneumonia diagnosis could not be calculated across the entire screened population.
Single-center retrospective observational design without external multicenter validation
Routine clinical measurements extracted within ±8-h windows around T48 and T72 without exact timestamps retained in the dataset
Potential predictor-outcome overlap and shared clinical information since treating clinicians were aware of routine biomarkers and oxygen requirements
Microbiological data were incompletely available and not incorporated into the multivariable models
Separate reviewer-specific diagnostic classifications for the entire screened population were not retained, precluding calculation of formal inter-reviewer agreement for SAP diagnosis

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Implication

A structured 48-hour landmark reassessment incorporating routine CRP and NLR trajectories alongside oxygen-support escalation markedly improves short-term prediction of initial antibiotic treatment failure in ischemic stroke-associated pneumonia compared with baseline assessment alone.

Abstract

BACKGROUND: Existing stroke-associated pneumonia scores estimate pneumonia occurrence rather than early response after antibiotics have started. We aimed to develop and internally validate a baseline model and a 48-h landmark model for first antibiotic treatment failure between 48 and 72 h after treatment initiation. METHODS: = 1.0) was used, and 500 bootstrap resamples estimated optimism-corrected performance. RESULTS: Among 199 patients, 102 (51.3%) experienced treatment failure. At baseline, mechanical ventilation before antibiotic initiation and a higher platelet-to-lymphocyte ratio were associated with failure. In the 48-h model, each 20 mg/L increase in C-reactive protein change was associated with greater failure odds (adjusted odds ratio 1.89, 95% confidence interval 1.52-2.34), as were each five-unit increase in neutrophil-to-lymphocyte ratio change (1.98, 1.25-3.13) and escalation of oxygen support (4.56, 1.09-19.01). The optimism-corrected area under the receiver operating characteristic curve increased from 0.697 at baseline to 0.889 at 48 h. Treatment failure was associated with longer hospitalization, higher hospital cost, and longer antibiotic exposure. CONCLUSIONS: In this single-center retrospective study, a structured 48-h reassessment combining routinely available inflammatory trajectories and oxygen-support change improved short-horizon prediction of antibiotic treatment failure. The model should prompt clinical review rather than automatic antibiotic escalation; multicenter external validation and prospective impact evaluation are required before clinical implementation.

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Cite This Study

Qiu et al. (2026) conducted a cohort in Ischemic stroke-associated pneumonia (n=199). 48-hour landmark reassessment model (combining CRP change, NLR change, and oxygen-support escalation) vs. Baseline (T0) prediction model was evaluated on Composite of initial antibiotic-treatment failure between 48 and 72 hours after treatment initiation (efficacy-driven escalation, replacement or addition of systemic antibiotics; persistent clinical instability at 72 hours with uncontrolled pneumonia; or pneumonia-related death) (OR 1.89 per 20 mg/L increase in 48-h CRP change, 95% CI 1.52-2.34, p=<0.001). A 48-h landmark model combining CRP change, NLR change, and oxygen escalation improved antibiotic failure prediction over baseline.

synapsesocial.com/papers/6af7fac1a3236dc65aee8230 https://doi.org/10.1080/07853890.2026.2753847

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Dynamic prediction of early antibiotic treatment failure in ischemic stroke-associated pneumonia: development and internal validation of a 48-h landmark model

Key Points

Study Design

Structured PICO

Main Result

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

Dynamic prediction of early antibiotic treatment failure in ischemic stroke-associated pneumonia: development and internal validation of a 48-h landmark model

Key Points

Study Design

Structured PICO

Main Result

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

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