Fever / Suspected Sepsis
From recognizing organ dysfunction to source identification and time-sensitive empiric therapy.
An educational representation of clinical reasoning, not a diagnostic algorithm or personalized medical advice — always apply clinical judgment and institutional protocols.
Caution
Escalate — Red Flags & Critical Warnings
- Hypotension refractory to an initial fluid bolus — start vasopressors promptly rather than continuing large-volume fluid resuscitation alone.
- A source amenable to drainage or debridement (abscess, empyema, necrotizing infection) — antibiotics alone will not control it; escalate for procedural or surgical source control.
Related Bedside Clinical Problems (21)
Bedside PresentationsRapid bedside hemodynamic categorization: confirming MAP < 65 mmHg, assessing peripheral perfusion, POCUS cardiac/IVC profiling, and differentiating hypovolemic, distributive, cardiogenic, and obstructive etiologies.
Advanced multimodal hemodynamic rescue: second-line vasopressors (vasopressin, angiotensin II), inotropic augmentation, stress-dose steroids, metabolic correction, and mechanical circulatory support evaluation.
Algorithmic triage of acute heart rates > 100–150 bpm: stability screen (immediate cardioversion if unstable), narrow vs wide QRS differentiation, Brugada VT rules, and sinus tachycardia etiology search.
Linked Deep-Dive Topics (8)
Reference KnowledgeLife-threatening organ dysfunction caused by a dysregulated host response to infection — recognized by an acute rise in SOFA score, not by infection plus fever alone.
The subset of sepsis with profound circulatory and cellular/metabolic abnormality — clinically identified by a vasopressor requirement to maintain MAP ≥ 65 mmHg plus lactate > 2 mmol/L despite adequate fluid resuscitation.
Molecular resistance mechanisms (ESBL, AmpC, KPC, NDM, OXA-48, DTR-Pseudomonas, CRAB), the MERINO trial, and modern novel beta-lactamase inhibitor therapeutics.
A surgical source-control emergency: recognize rapidly progressive deep infection, involve surgery immediately, start broad antimicrobials, resuscitate shock, and re-explore until source control is complete.
Nosocomial pneumonia developing ≥ 48 hours after admission in non-ventilated patients, host and antibiogram MDR risk tailoring, nasal MRSA PCR screening, and 7-day de-escalation.
Quantitative lower tract sampling (ETA vs BAL), rapid multiplex PCR panels and stewardship interpretation, PK/PD extended beta-lactams, 7-day duration, and the SHEA prevention bundle.
CT-before-LP criteria, CSF interpretation matrix, de Gans Dexamethasone timing, empiric age/host antimicrobial coverage + Ampicillin + Acyclovir, and neurocritical ICP management.
Cellular dysoxia, DO2/VO2 physiology, the 4 shock phenotypes, dynamic fluid responsiveness (PLR/PPV) vs fluid tolerance (VExUS), and vasoactive pharmacology.
Evidence status
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