17:I[462708,["/_next/static/chunks/3yo3kiro3bmlp.js","/_next/static/chunks/3vr2wvd8f2efb.js","/_next/static/chunks/2vtmb68_vu-9t.js","/_next/static/chunks/2s8mt6_8wrpfo.js","/_next/static/chunks/3vkulz2i3l61y.js","/_next/static/chunks/1cqw2i1silz0i.js","/_next/static/chunks/14dbm3lm_t629.js","/_next/static/chunks/335_v2mb569ld.js","/_next/static/chunks/3ykn5ops9bft5.js","/_next/static/chunks/3cmavum774kjt.js","/_next/static/chunks/3th-0-a2xf9qs.js","/_next/static/chunks/0p0xpwde6kzmv.js","/_next/static/chunks/401-sxxnzbtf_.js","/_next/static/chunks/0wywtv698a1v0.js","/_next/static/chunks/2botzqwpnrzyj.js"],"ArticleReader"] 18:T56e7,## Summary The ABCDE approach—**Airway, Breathing, Circulation, Disability, Exposure**—is a rapid, repeatable method for recognizing and treating immediate threats to life in a deteriorating or critically ill patient. Its value is procedural: identify a life-threatening abnormality, intervene immediately, assess the response, then restart from A because treatment and disease progression can change physiology within minutes.[1,2] ABCDE is not a diagnostic endpoint and is not a substitute for a cardiac-arrest pathway. If an adult is unresponsive with absent or abnormal breathing, activate the resuscitation response, start high-quality cardiopulmonary resuscitation, and attach a defibrillator rather than completing a conventional survey first.[2] Run the assessment with **parallel team activity** whenever staff are available. While one clinician leads the sequence, others can attach ECG, blood-pressure and oxygen-saturation monitoring, obtain IV or intraosseous access, draw blood, check glucose, prepare airway equipment and emergency medications, control hemorrhage, obtain a 12-lead ECG, and call senior or critical-care support.[1,2] At each step, distinguish three questions: **Is there an immediate threat? What intervention is needed now? What definitive treatment or escalation must be prepared next?** A temporarily normal finding is not a clearance certificate. Airway edema, respiratory fatigue, occult bleeding, shock, intracranial deterioration, and temperature-related illness can evolve after an initially reassuring assessment. Oxygen should be prescribed to a target rather than given indefinitely at maximal concentration. In most acutely ill adults who need supplemental oxygen, a target saturation of **94–98%** is appropriate; in patients at risk of hypercapnic respiratory failure, **88–92%** is commonly used pending blood-gas assessment and individualized targets.[1,3] Life-threatening hypoxemia takes priority over concerns about hyperoxia. Circulatory treatment should follow the physiologic problem. Give fluid when intravascular volume depletion or fluid responsiveness is plausible, but reassess after each bolus. Do not treat every hypotensive patient with repeated crystalloid: major hemorrhage requires hemorrhage control and blood products; distributive shock may require early vasopressor support; cardiogenic or obstructive shock may worsen with indiscriminate fluid loading.[4] > **Clinical pearl:** The sequence is a loop, not a checklist completed once. After every major intervention—airway manipulation, ventilation, fluid or blood administration, vasopressor initiation, anticonvulsant treatment, or transfer—return to A and reassess. ## When to use ABCDE Use a structured ABCDE assessment when a patient: - appears critically ill or has rapidly changing vital signs; - has new altered consciousness; - develops respiratory distress, hypoxemia, hypotension, or shock; - deteriorates unexpectedly on a ward or procedural area; - presents after major trauma, poisoning, severe infection, anaphylaxis, or another potentially unstable event; - requires post-resuscitation stabilization after return of spontaneous circulation.[1,2] The approach is useful across emergency departments, wards, critical-care areas, procedural units, clinics, and prehospital systems. The exact interventions depend on setting, staff skills, local protocols, and available equipment. ## Before A: immediate global check Before a detailed sequence, establish within seconds: - personal and scene safety; - responsiveness; - whether breathing is normal; - whether there is catastrophic external hemorrhage; - whether signs of life are present; - whether immediate resuscitation-team activation is required. If there is **no sign of life or any doubt about cardiac arrest**, enter the current resuscitation pathway immediately.[2] If signs of life are present, begin ABCDE while help, monitoring, vascular access, and essential equipment are obtained concurrently. ### Parallel tasks during the first minutes When resources permit: - place continuous ECG and pulse-oximetry monitoring; - cycle noninvasive blood pressure frequently or establish invasive monitoring when appropriate; - obtain IV access; use intraosseous access when urgent vascular access cannot be achieved promptly; - obtain bedside glucose early in altered consciousness; - collect blood for targeted investigations; - obtain a 12-lead ECG when cardiovascular or metabolic disease is possible; - prepare airway and ventilation equipment; - document time, interventions, response, and escalation decisions.[1,2] ## A — Airway ### Objective Determine whether the airway is **patent, maintainable, and protected from aspiration**. Airway obstruction is a medical emergency and must be treated before moving on.[1] ### Rapid airway assessment Listen for the patient’s voice and for abnormal airway sounds. Look for chest movement, facial or neck swelling, blood, vomit, secretions, foreign material, burns, trauma, or a rapidly expanding hematoma. Danger signs include: - inability to speak or markedly altered voice; - stridor; - snoring or gurgling in a patient with reduced consciousness; - absent or minimal airflow despite respiratory effort; - inability to handle secretions; - rapidly progressive tongue, oropharyngeal, facial, or neck swelling; - severe maxillofacial injury or active airway bleeding; - reduced consciousness with loss of protective reflexes; - progressive inhalation injury. A patient who speaks clearly has a currently patent airway, but this does not establish that the airway will remain safe. ### Immediate actions Depending on cause and expertise: 1. Position the patient appropriately and open the airway. 2. Suction blood, vomit, or secretions. 3. Remove a visible obstructing foreign body when appropriate. 4. Use an oropharyngeal or nasopharyngeal airway when indicated and not contraindicated. 5. Provide bag-mask ventilation if ventilation is inadequate. 6. Call experienced airway support early when deterioration is likely. 7. Prepare tracheal intubation when the airway cannot be maintained or protected, oxygenation or ventilation is failing, or the clinical course predicts imminent loss of airway. 8. Prepare a rescue supraglottic airway and emergency front-of-neck access strategy according to local airway protocols when conventional oxygenation or ventilation may fail. In trauma with possible cervical-spine injury, minimize unnecessary neck movement while preserving oxygenation and airway patency. Spinal precautions must never prevent effective airway management. ### Reassessment after airway intervention After an advanced airway is placed: - confirm effective ventilation; - use continuous waveform capnography when available and expected by local resuscitation standards; - reassess chest movement and breath sounds; - secure the device; - review oxygenation, ventilation, blood pressure, and sedation because positive-pressure ventilation and induction drugs can worsen hemodynamics.[2] > **Caution:** A threatened airway is often easier to secure before severe edema, bleeding, fatigue, or distorted anatomy progresses. Escalate early rather than waiting for complete obstruction. ## B — Breathing ### Objective Assess whether oxygenation and ventilation are adequate and identify immediately reversible causes of respiratory failure. ### Bedside assessment Assess: - respiratory rate and trend; - work of breathing, accessory-muscle use, paradoxical movement, and fatigue; - ability to speak; - chest expansion and symmetry; - air entry and added sounds; - oxygen saturation with attention to waveform quality; - end-tidal carbon dioxide when appropriate; - arterial or venous blood gas when the result will change management. A normal oxygen saturation does **not** establish adequate ventilation. Supplemental oxygen can preserve SpO₂ while carbon dioxide rises in hypoventilation. ### Immediate respiratory threats Act immediately for suspected: - tension pneumothorax; - severe bronchospasm with exhaustion or a silent chest; - massive hemothorax; - critical upper-airway obstruction; - pulmonary edema with severe hypoxemia; - opioid- or sedative-related ventilatory failure; - neuromuscular respiratory failure; - severe pneumonia or acute respiratory distress with impending exhaustion. Do not delay emergency treatment of a clinically apparent tension pneumothorax for routine imaging in an unstable patient. ### Oxygen For patients who require supplemental oxygen:[1,3] - target **94–98%** for most acutely ill adults; - target **88–92%** initially in patients at risk of hypercapnic respiratory failure while obtaining blood-gas data and establishing an individualized goal; - in severe hypoxemia, provide sufficient oxygen immediately and titrate once reliable measurements are available. Pulse oximetry has limitations in poor peripheral perfusion and can overestimate arterial saturation in some patients with darker skin pigmentation; interpret the number with waveform quality and the clinical picture.[2] ### Ventilatory support Escalate according to physiology and cause: - optimize position and airway patency; - assist ventilation with bag-mask support when spontaneous ventilation is inadequate; - use noninvasive respiratory support for appropriate syndromes when airway protection, cooperation, and hemodynamics permit; - intubate and provide invasive ventilation when oxygenation or ventilation cannot be maintained, consciousness deteriorates, airway protection fails, or work of breathing is unsustainable. ### Reassess B After oxygen, bronchodilator therapy, pleural decompression, ventilatory support, or airway intervention, reassess: - respiratory rate and effort; - SpO₂; - chest movement and air entry; - capnography when used; - blood gas when indicated; - blood pressure and perfusion, because positive-pressure ventilation can reduce venous return. ## C — Circulation ### Objective Determine whether organ perfusion is adequate, identify shock physiology and hemorrhage, and restore circulation while treating the cause. ### Rapid circulatory assessment Assess: - heart rate and rhythm; - blood pressure and trend; - peripheral temperature and capillary refill; - pulse quality; - mental status; - urine output when available; - jugular venous pressure when interpretable; - external or concealed bleeding; - skin mottling or cyanosis; - bedside lactate and acid-base status when useful. Hypotension is a late or absent finding in some shock states. Tachycardia, altered mentation, cool peripheries, oliguria, rising lactate, or a narrowing pulse pressure can signal inadequate perfusion before profound hypotension appears. ### Think in shock mechanisms | Pattern | Typical clues | Immediate direction | |---|---|---| | Hypovolemic | fluid loss, hemorrhage, flat neck veins, small hyperdynamic ventricle | replace appropriate volume and correct source | | Distributive | warm vasodilated skin early, infection or anaphylaxis, low systemic vascular tone | source-specific therapy, judicious fluid, early vasopressor when needed | | Cardiogenic | pulmonary edema, elevated venous pressure, ischemia, severe ventricular dysfunction | avoid blind fluid loading; treat pump/ischemic/arrhythmic cause | | Obstructive | tension pneumothorax, tamponade, massive pulmonary embolism | definitive relief of obstruction is priority | Mixed shock is common. ### Vascular access and investigations Obtain IV access promptly; use intraosseous access if urgent access is otherwise delayed. Depending on the syndrome, collect: - CBC; - electrolytes and renal function; - glucose; - blood gas and lactate; - coagulation studies; - type and screen/crossmatch when bleeding is possible; - cultures when severe infection is suspected and sampling will not materially delay antimicrobial treatment; - cardiac biomarkers when indicated. Obtain a 12-lead ECG early when arrhythmia, ischemia, electrolyte disturbance, poisoning, or unexplained shock is possible. ### Fluids Use fluids as a **therapeutic trial with reassessment**, not an automatic response to every low blood pressure. A practical adult approach when volume depletion or fluid responsiveness is plausible is a small bolus of isotonic crystalloid, commonly **250–500 mL**, followed immediately by reassessment of blood pressure, perfusion, lungs, venous congestion, and the underlying diagnosis.[1,4] Smaller aliquots may be preferable in heart failure, renal failure, pregnancy with pulmonary edema risk, or uncertain volume tolerance. Stop repeated boluses when: - perfusion no longer improves; - pulmonary congestion develops; - venous congestion is substantial; - cardiogenic or obstructive physiology is more likely; - definitive source control, blood products, or vasopressor therapy is required. ### Major hemorrhage For life-threatening bleeding: - control external hemorrhage immediately; - activate the local major-hemorrhage pathway; - provide blood components according to the institutional protocol; - correct hypothermia and clinically important coagulopathy; - obtain urgent surgical, endoscopic, interventional-radiology, obstetric, or trauma source control as appropriate. Repeated crystalloid alone is not adequate resuscitation for ongoing major blood loss. ### Vasopressors In distributive shock that remains hypotensive during appropriate initial fluid resuscitation, do not delay vasopressors solely to complete an arbitrary fluid volume. Contemporary sepsis guidance supports **norepinephrine as the first-line vasopressor** for septic shock, titrated to organ perfusion and an initial mean arterial pressure target commonly around 65 mmHg in adults, then individualized.[4] ## D — Disability ### Objective Rapidly identify neurologic failure and immediately reversible causes of altered consciousness. ### Assessment Record: - level of consciousness using an institutionally familiar scale such as Alert–Voice–Pain–Unresponsive or Glasgow Coma Scale; - pupils: size, symmetry, and reactivity; - limb movement and gross focal deficit; - seizure activity; - bedside glucose; - temperature when not already obtained; - medication, toxin, or sedative exposure when relevant. ### Time-critical reversible causes Immediately consider and treat: - hypoxemia or hypercapnia; - hypoglycemia; - ongoing seizure/status epilepticus; - opioid toxicity with ventilatory failure; - stroke or intracranial hemorrhage; - meningitis/encephalitis; - severe electrolyte or acid-base disturbance; - poisoning; - hyperthermia or hypothermia. A falling level of consciousness can also signal worsening shock and should trigger return to A, B, and C rather than a neurologic-only response. ### Airway implications Neurologic deterioration can remove airway protection and ventilatory drive. When consciousness is worsening, prepare definitive airway management before complete loss of protective reflexes if the trajectory is unsafe. ## E — Exposure and environment ### Objective Identify important findings that require adequate exposure while preventing iatrogenic harm from heat loss, loss of dignity, or delayed definitive treatment. Inspect as clinically indicated for: - rash, urticaria, petechiae, purpura, or cellulitis; - wounds, pressure injury, burns, bruising, or occult trauma; - surgical sites, drains, vascular catheters, and stomas; - external hemorrhage; - limb ischemia, swelling, or compartment tension; - abdominal distension or peritonism; - back or perineal findings when relevant; - medication patches, injection sites, or toxin exposure clues. Measure temperature. Prevent avoidable hypothermia after exposure, especially in trauma, hemorrhage, older adults, infants, and prolonged resuscitation. ## Reassessment loop After completing E, return to A and compare the new state with baseline. ### Reassess sooner when - an intervention was performed; - vital signs change; - consciousness worsens; - transport or transfer occurs; - a new drug, sedative, vasopressor, fluid bolus, or blood product is given; - respiratory support changes. ### Trend variables that matter Track the variables most relevant to the syndrome, commonly: - respiratory rate and work; - SpO₂ and oxygen requirement; - heart rate and rhythm; - blood pressure and perfusion; - mental status; - urine output; - lactate or blood-gas trajectory when indicated; - temperature. Response to treatment is itself diagnostic information. Failure to improve should prompt reconsideration of mechanism, not just repetition of the same intervention. ## Focused diagnostic phase after immediate threats are controlled Once life-threatening physiology is treated, move from syndromic stabilization to cause-specific evaluation. Common next steps include: - structured history from the patient, family, emergency personnel, or records; - medication and allergy review; - focused bedside ultrasound when trained operators and a clinical question are present; - chest imaging, CT, ultrasound, or other targeted imaging; - serial ECG and cardiac biomarkers when indicated; - microbiology and source evaluation in suspected infection; - toxicology testing when results alter management; - specialty consultation and definitive source control. Do not allow diagnostic completeness to delay a treatment that is already indicated by unstable physiology. ## Special clinical contexts ### Trauma Catastrophic external hemorrhage may need control before the conventional airway step. Apply trauma-system priorities while maintaining the logic of immediate threat treatment. Protect the cervical spine when indicated without compromising airway opening, oxygenation, or ventilation. ### Pregnancy Pregnancy alters airway anatomy, oxygen reserve, venous return, and resuscitation priorities. In later pregnancy, significant supine aortocaval compression can worsen hypotension; manual left uterine displacement or lateral positioning can improve venous return while obstetric causes of instability are assessed. Early obstetric, anesthesia, and critical-care involvement is appropriate for major deterioration. ### Sepsis Use ABCDE to stabilize physiology while cultures, antimicrobials, source control, lactate assessment, and shock treatment proceed in parallel. Hypotension after reasonable initial volume resuscitation should trigger vasopressor treatment rather than unlimited crystalloid.[4] Related topic: [Sepsis and Septic Shock](../critical-care/sepsis-and-septic-shock.md). ### Anaphylaxis Airway edema, bronchospasm, and distributive shock can evolve simultaneously. Give intramuscular epinephrine promptly according to the anaphylaxis pathway; airway preparation, oxygen, fluid, and escalation occur in parallel. Related topic: [Anaphylaxis](../allergy-immunology/anaphylaxis.md). ### Suspected poisoning ABCDE stabilization precedes toxidrome identification. Some poisons require antidotes during the primary survey when delay is dangerous. Obtain ECG and glucose early in altered or unstable patients. ## Escalation and disposition Escalate early when any of the following is present: - threatened or unprotected airway; - escalating oxygen or ventilatory requirement; - persistent hypotension or shock; - recurrent arrhythmia or ischemia; - worsening consciousness; - repeated seizure; - suspected major hemorrhage; - severe metabolic derangement; - need for invasive monitoring, vasopressor support, or mechanical ventilation; - deterioration despite initial treatment. The destination should match the anticipated next failure: resuscitation area, operating theatre, interventional suite, coronary care, stroke pathway, critical care, or another specialist environment. A patient should not be considered safe for ward transfer or discharge merely because a single ABCDE cycle normalized. Confirm stability over an appropriate interval, establish the cause and treatment plan, reconcile medications, and define monitoring and escalation criteria. ## Acute ABCDE checklist 1. **Global:** responsiveness, normal breathing, catastrophic bleeding, call for help. 2. **A:** airway patent and protected? Suction, adjuncts, early definitive airway if threatened. 3. **B:** rate, effort, symmetry, air entry, SpO₂, ventilation; treat immediate thoracic and respiratory threats. 4. **C:** pulse, pressure, perfusion, bleeding, ECG, access; choose fluid, blood, vasopressor, or definitive source control according to mechanism. 5. **D:** consciousness, pupils, focal deficit, seizure, glucose; correct immediately reversible causes. 6. **E:** temperature, rash, wounds, lines, abdomen, occult bleeding; prevent heat loss. 7. **Restart at A:** document response, anticipate deterioration, arrange definitive care. ## Related library topics - [Adult Cardiac Arrest](adult-cardiac-arrest.md) - [Sepsis and Septic Shock](../critical-care/sepsis-and-septic-shock.md) - [Anaphylaxis](../allergy-immunology/anaphylaxis.md) - [Acute Respiratory Distress Syndrome](../critical-care/acute-respiratory-distress-syndrome.md) - [Cardiogenic Shock in Adults](../critical-care/cardiogenic-shock-in-adults.md) - [Post–Cardiac Arrest Care in Adults](../critical-care/post-cardiac-arrest-care-in-adults.md) ## References 1. Resuscitation Council UK. **The ABCDE Approach.** Updated July 2024. https://www.resus.org.uk/library/abcde-approach 2. Resuscitation Council UK. **Guidelines 2025: Adult advanced life support and adult in-hospital resuscitation.** Published October 27, 2025. https://www.resus.org.uk/library/2025-resuscitation-guidelines/adult-advanced-life-support-guidelines 3. O'Driscoll BR, Howard LS, Earis J, Mak V; British Thoracic Society Emergency Oxygen Guideline Group. BTS guideline for oxygen use in adults in healthcare and emergency settings. *Thorax.* 2017;72(Suppl 1):ii1-ii90. doi:10.1136/thoraxjnl-2016-209729. PMID:28507176. 4. Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. *Intensive Care Med.* 2021;47:1181-1247. doi:10.1007/s00134-021-06506-y. PMID:34599691.19:T570b,## Summary The ABCDE approach—**Airway, Breathing, Circulation, Disability, Exposure**—is a rapid, repeatable method for recognizing and treating immediate threats to life in a deteriorating or critically ill patient. Its value is procedural: identify a life-threatening abnormality, intervene immediately, assess the response, then restart from A because treatment and disease progression can change physiology within minutes.[1,2] ABCDE is not a diagnostic endpoint and is not a substitute for a cardiac-arrest pathway. If an adult is unresponsive with absent or abnormal breathing, activate the resuscitation response, start high-quality cardiopulmonary resuscitation, and attach a defibrillator rather than completing a conventional survey first.[2] Run the assessment with **parallel team activity** whenever staff are available. While one clinician leads the sequence, others can attach ECG, blood-pressure and oxygen-saturation monitoring, obtain IV or intraosseous access, draw blood, check glucose, prepare airway equipment and emergency medications, control hemorrhage, obtain a 12-lead ECG, and call senior or critical-care support.[1,2] At each step, distinguish three questions: **Is there an immediate threat? What intervention is needed now? What definitive treatment or escalation must be prepared next?** A temporarily normal finding is not a clearance certificate. Airway edema, respiratory fatigue, occult bleeding, shock, intracranial deterioration, and temperature-related illness can evolve after an initially reassuring assessment. Oxygen should be prescribed to a target rather than given indefinitely at maximal concentration. In most acutely ill adults who need supplemental oxygen, a target saturation of **94–98%** is appropriate; in patients at risk of hypercapnic respiratory failure, **88–92%** is commonly used pending blood-gas assessment and individualized targets.[1,3] Life-threatening hypoxemia takes priority over concerns about hyperoxia. Circulatory treatment should follow the physiologic problem. Give fluid when intravascular volume depletion or fluid responsiveness is plausible, but reassess after each bolus. Do not treat every hypotensive patient with repeated crystalloid: major hemorrhage requires hemorrhage control and blood products; distributive shock may require early vasopressor support; cardiogenic or obstructive shock may worsen with indiscriminate fluid loading.[4] > **Clinical pearl:** The sequence is a loop, not a checklist completed once. After every major intervention—airway manipulation, ventilation, fluid or blood administration, vasopressor initiation, anticonvulsant treatment, or transfer—return to A and reassess. ## When to use ABCDE Use a structured ABCDE assessment when a patient: - appears critically ill or has rapidly changing vital signs; - has new altered consciousness; - develops respiratory distress, hypoxemia, hypotension, or shock; - deteriorates unexpectedly on a ward or procedural area; - presents after major trauma, poisoning, severe infection, anaphylaxis, or another potentially unstable event; - requires post-resuscitation stabilization after return of spontaneous circulation.[1,2] The approach is useful across emergency departments, wards, critical-care areas, procedural units, clinics, and prehospital systems. The exact interventions depend on setting, staff skills, local protocols, and available equipment. ## Before A: immediate global check Before a detailed sequence, establish within seconds: - personal and scene safety; - responsiveness; - whether breathing is normal; - whether there is catastrophic external hemorrhage; - whether signs of life are present; - whether immediate resuscitation-team activation is required. If there is **no sign of life or any doubt about cardiac arrest**, enter the current resuscitation pathway immediately.[2] If signs of life are present, begin ABCDE while help, monitoring, vascular access, and essential equipment are obtained concurrently. ### Parallel tasks during the first minutes When resources permit: - place continuous ECG and pulse-oximetry monitoring; - cycle noninvasive blood pressure frequently or establish invasive monitoring when appropriate; - obtain IV access; use intraosseous access when urgent vascular access cannot be achieved promptly; - obtain bedside glucose early in altered consciousness; - collect blood for targeted investigations; - obtain a 12-lead ECG when cardiovascular or metabolic disease is possible; - prepare airway and ventilation equipment; - document time, interventions, response, and escalation decisions.[1,2] ## A — Airway ### Objective Determine whether the airway is **patent, maintainable, and protected from aspiration**. Airway obstruction is a medical emergency and must be treated before moving on.[1] ### Rapid airway assessment Listen for the patient’s voice and for abnormal airway sounds. Look for chest movement, facial or neck swelling, blood, vomit, secretions, foreign material, burns, trauma, or a rapidly expanding hematoma. Danger signs include: - inability to speak or markedly altered voice; - stridor; - snoring or gurgling in a patient with reduced consciousness; - absent or minimal airflow despite respiratory effort; - inability to handle secretions; - rapidly progressive tongue, oropharyngeal, facial, or neck swelling; - severe maxillofacial injury or active airway bleeding; - reduced consciousness with loss of protective reflexes; - progressive inhalation injury. A patient who speaks clearly has a currently patent airway, but this does not establish that the airway will remain safe. ### Immediate actions Depending on cause and expertise: 1. Position the patient appropriately and open the airway. 2. Suction blood, vomit, or secretions. 3. Remove a visible obstructing foreign body when appropriate. 4. Use an oropharyngeal or nasopharyngeal airway when indicated and not contraindicated. 5. Provide bag-mask ventilation if ventilation is inadequate. 6. Call experienced airway support early when deterioration is likely. 7. Prepare tracheal intubation when the airway cannot be maintained or protected, oxygenation or ventilation is failing, or the clinical course predicts imminent loss of airway. 8. Prepare a rescue supraglottic airway and emergency front-of-neck access strategy according to local airway protocols when conventional oxygenation or ventilation may fail. In trauma with possible cervical-spine injury, minimize unnecessary neck movement while preserving oxygenation and airway patency. Spinal precautions must never prevent effective airway management. ### Reassessment after airway intervention After an advanced airway is placed: - confirm effective ventilation; - use continuous waveform capnography when available and expected by local resuscitation standards; - reassess chest movement and breath sounds; - secure the device; - review oxygenation, ventilation, blood pressure, and sedation because positive-pressure ventilation and induction drugs can worsen hemodynamics.[2] > **Caution:** A threatened airway is often easier to secure before severe edema, bleeding, fatigue, or distorted anatomy progresses. Escalate early rather than waiting for complete obstruction. ## B — Breathing ### Objective Assess whether oxygenation and ventilation are adequate and identify immediately reversible causes of respiratory failure. ### Bedside assessment Assess: - respiratory rate and trend; - work of breathing, accessory-muscle use, paradoxical movement, and fatigue; - ability to speak; - chest expansion and symmetry; - air entry and added sounds; - oxygen saturation with attention to waveform quality; - end-tidal carbon dioxide when appropriate; - arterial or venous blood gas when the result will change management. A normal oxygen saturation does **not** establish adequate ventilation. Supplemental oxygen can preserve SpO₂ while carbon dioxide rises in hypoventilation. ### Immediate respiratory threats Act immediately for suspected: - tension pneumothorax; - severe bronchospasm with exhaustion or a silent chest; - massive hemothorax; - critical upper-airway obstruction; - pulmonary edema with severe hypoxemia; - opioid- or sedative-related ventilatory failure; - neuromuscular respiratory failure; - severe pneumonia or acute respiratory distress with impending exhaustion. Do not delay emergency treatment of a clinically apparent tension pneumothorax for routine imaging in an unstable patient. ### Oxygen For patients who require supplemental oxygen:[1,3] - target **94–98%** for most acutely ill adults; - target **88–92%** initially in patients at risk of hypercapnic respiratory failure while obtaining blood-gas data and establishing an individualized goal; - in severe hypoxemia, provide sufficient oxygen immediately and titrate once reliable measurements are available. Pulse oximetry has limitations in poor peripheral perfusion and can overestimate arterial saturation in some patients with darker skin pigmentation; interpret the number with waveform quality and the clinical picture.[2] ### Ventilatory support Escalate according to physiology and cause: - optimize position and airway patency; - assist ventilation with bag-mask support when spontaneous ventilation is inadequate; - use noninvasive respiratory support for appropriate syndromes when airway protection, cooperation, and hemodynamics permit; - intubate and provide invasive ventilation when oxygenation or ventilation cannot be maintained, consciousness deteriorates, airway protection fails, or work of breathing is unsustainable. ### Reassess B After oxygen, bronchodilator therapy, pleural decompression, ventilatory support, or airway intervention, reassess: - respiratory rate and effort; - SpO₂; - chest movement and air entry; - capnography when used; - blood gas when indicated; - blood pressure and perfusion, because positive-pressure ventilation can reduce venous return. ## C — Circulation ### Objective Determine whether organ perfusion is adequate, identify shock physiology and hemorrhage, and restore circulation while treating the cause. ### Rapid circulatory assessment Assess: - heart rate and rhythm; - blood pressure and trend; - peripheral temperature and capillary refill; - pulse quality; - mental status; - urine output when available; - jugular venous pressure when interpretable; - external or concealed bleeding; - skin mottling or cyanosis; - bedside lactate and acid-base status when useful. Hypotension is a late or absent finding in some shock states. Tachycardia, altered mentation, cool peripheries, oliguria, rising lactate, or a narrowing pulse pressure can signal inadequate perfusion before profound hypotension appears. ### Think in shock mechanisms | Pattern | Typical clues | Immediate direction | |---|---|---| | Hypovolemic | fluid loss, hemorrhage, flat neck veins, small hyperdynamic ventricle | replace appropriate volume and correct source | | Distributive | warm vasodilated skin early, infection or anaphylaxis, low systemic vascular tone | source-specific therapy, judicious fluid, early vasopressor when needed | | Cardiogenic | pulmonary edema, elevated venous pressure, ischemia, severe ventricular dysfunction | avoid blind fluid loading; treat pump/ischemic/arrhythmic cause | | Obstructive | tension pneumothorax, tamponade, massive pulmonary embolism | definitive relief of obstruction is priority | Mixed shock is common. ### Vascular access and investigations Obtain IV access promptly; use intraosseous access if urgent access is otherwise delayed. Depending on the syndrome, collect: - CBC; - electrolytes and renal function; - glucose; - blood gas and lactate; - coagulation studies; - type and screen/crossmatch when bleeding is possible; - cultures when severe infection is suspected and sampling will not materially delay antimicrobial treatment; - cardiac biomarkers when indicated. Obtain a 12-lead ECG early when arrhythmia, ischemia, electrolyte disturbance, poisoning, or unexplained shock is possible. ### Fluids Use fluids as a **therapeutic trial with reassessment**, not an automatic response to every low blood pressure. A practical adult approach when volume depletion or fluid responsiveness is plausible is a small bolus of isotonic crystalloid, commonly **250–500 mL**, followed immediately by reassessment of blood pressure, perfusion, lungs, venous congestion, and the underlying diagnosis.[1,4] Smaller aliquots may be preferable in heart failure, renal failure, pregnancy with pulmonary edema risk, or uncertain volume tolerance. Stop repeated boluses when: - perfusion no longer improves; - pulmonary congestion develops; - venous congestion is substantial; - cardiogenic or obstructive physiology is more likely; - definitive source control, blood products, or vasopressor therapy is required. ### Major hemorrhage For life-threatening bleeding: - control external hemorrhage immediately; - activate the local major-hemorrhage pathway; - provide blood components according to the institutional protocol; - correct hypothermia and clinically important coagulopathy; - obtain urgent surgical, endoscopic, interventional-radiology, obstetric, or trauma source control as appropriate. Repeated crystalloid alone is not adequate resuscitation for ongoing major blood loss. ### Vasopressors In distributive shock that remains hypotensive during appropriate initial fluid resuscitation, do not delay vasopressors solely to complete an arbitrary fluid volume. Contemporary sepsis guidance supports **norepinephrine as the first-line vasopressor** for septic shock, titrated to organ perfusion and an initial mean arterial pressure target commonly around 65 mmHg in adults, then individualized.[4] ## D — Disability ### Objective Rapidly identify neurologic failure and immediately reversible causes of altered consciousness. ### Assessment Record: - level of consciousness using an institutionally familiar scale such as Alert–Voice–Pain–Unresponsive or Glasgow Coma Scale; - pupils: size, symmetry, and reactivity; - limb movement and gross focal deficit; - seizure activity; - bedside glucose; - temperature when not already obtained; - medication, toxin, or sedative exposure when relevant. ### Time-critical reversible causes Immediately consider and treat: - hypoxemia or hypercapnia; - hypoglycemia; - ongoing seizure/status epilepticus; - opioid toxicity with ventilatory failure; - stroke or intracranial hemorrhage; - meningitis/encephalitis; - severe electrolyte or acid-base disturbance; - poisoning; - hyperthermia or hypothermia. A falling level of consciousness can also signal worsening shock and should trigger return to A, B, and C rather than a neurologic-only response. ### Airway implications Neurologic deterioration can remove airway protection and ventilatory drive. When consciousness is worsening, prepare definitive airway management before complete loss of protective reflexes if the trajectory is unsafe. ## E — Exposure and environment ### Objective Identify important findings that require adequate exposure while preventing iatrogenic harm from heat loss, loss of dignity, or delayed definitive treatment. Inspect as clinically indicated for: - rash, urticaria, petechiae, purpura, or cellulitis; - wounds, pressure injury, burns, bruising, or occult trauma; - surgical sites, drains, vascular catheters, and stomas; - external hemorrhage; - limb ischemia, swelling, or compartment tension; - abdominal distension or peritonism; - back or perineal findings when relevant; - medication patches, injection sites, or toxin exposure clues. Measure temperature. Prevent avoidable hypothermia after exposure, especially in trauma, hemorrhage, older adults, infants, and prolonged resuscitation. ## Reassessment loop After completing E, return to A and compare the new state with baseline. ### Reassess sooner when - an intervention was performed; - vital signs change; - consciousness worsens; - transport or transfer occurs; - a new drug, sedative, vasopressor, fluid bolus, or blood product is given; - respiratory support changes. ### Trend variables that matter Track the variables most relevant to the syndrome, commonly: - respiratory rate and work; - SpO₂ and oxygen requirement; - heart rate and rhythm; - blood pressure and perfusion; - mental status; - urine output; - lactate or blood-gas trajectory when indicated; - temperature. Response to treatment is itself diagnostic information. Failure to improve should prompt reconsideration of mechanism, not just repetition of the same intervention. ## Focused diagnostic phase after immediate threats are controlled Once life-threatening physiology is treated, move from syndromic stabilization to cause-specific evaluation. Common next steps include: - structured history from the patient, family, emergency personnel, or records; - medication and allergy review; - focused bedside ultrasound when trained operators and a clinical question are present; - chest imaging, CT, ultrasound, or other targeted imaging; - serial ECG and cardiac biomarkers when indicated; - microbiology and source evaluation in suspected infection; - toxicology testing when results alter management; - specialty consultation and definitive source control. Do not allow diagnostic completeness to delay a treatment that is already indicated by unstable physiology. ## Special clinical contexts ### Trauma Catastrophic external hemorrhage may need control before the conventional airway step. Apply trauma-system priorities while maintaining the logic of immediate threat treatment. Protect the cervical spine when indicated without compromising airway opening, oxygenation, or ventilation. ### Pregnancy Pregnancy alters airway anatomy, oxygen reserve, venous return, and resuscitation priorities. In later pregnancy, significant supine aortocaval compression can worsen hypotension; manual left uterine displacement or lateral positioning can improve venous return while obstetric causes of instability are assessed. Early obstetric, anesthesia, and critical-care involvement is appropriate for major deterioration. ### Sepsis Use ABCDE to stabilize physiology while cultures, antimicrobials, source control, lactate assessment, and shock treatment proceed in parallel. Hypotension after reasonable initial volume resuscitation should trigger vasopressor treatment rather than unlimited crystalloid.[4] Related topic: [Sepsis and Septic Shock](../critical-care/sepsis-and-septic-shock.md). ### Anaphylaxis Airway edema, bronchospasm, and distributive shock can evolve simultaneously. Give intramuscular epinephrine promptly according to the anaphylaxis pathway; airway preparation, oxygen, fluid, and escalation occur in parallel. Related topic: [Anaphylaxis](../allergy-immunology/anaphylaxis.md). ### Suspected poisoning ABCDE stabilization precedes toxidrome identification. Some poisons require antidotes during the primary survey when delay is dangerous. Obtain ECG and glucose early in altered or unstable patients. ## Escalation and disposition Escalate early when any of the following is present: - threatened or unprotected airway; - escalating oxygen or ventilatory requirement; - persistent hypotension or shock; - recurrent arrhythmia or ischemia; - worsening consciousness; - repeated seizure; - suspected major hemorrhage; - severe metabolic derangement; - need for invasive monitoring, vasopressor support, or mechanical ventilation; - deterioration despite initial treatment. The destination should match the anticipated next failure: resuscitation area, operating theatre, interventional suite, coronary care, stroke pathway, critical care, or another specialist environment. A patient should not be considered safe for ward transfer or discharge merely because a single ABCDE cycle normalized. Confirm stability over an appropriate interval, establish the cause and treatment plan, reconcile medications, and define monitoring and escalation criteria. ## Acute ABCDE checklist 1. **Global:** responsiveness, normal breathing, catastrophic bleeding, call for help. 2. **A:** airway patent and protected? Suction, adjuncts, early definitive airway if threatened. 3. **B:** rate, effort, symmetry, air entry, SpO₂, ventilation; treat immediate thoracic and respiratory threats. 4. **C:** pulse, pressure, perfusion, bleeding, ECG, access; choose fluid, blood, vasopressor, or definitive source control according to mechanism. 5. **D:** consciousness, pupils, focal deficit, seizure, glucose; correct immediately reversible causes. 6. **E:** temperature, rash, wounds, lines, abdomen, occult bleeding; prevent heat loss. 7. **Restart at A:** document response, anticipate deterioration, arrange definitive care. ## Related library topics - [Adult Cardiac Arrest](adult-cardiac-arrest.md) - [Sepsis and Septic Shock](../critical-care/sepsis-and-septic-shock.md) - [Anaphylaxis](../allergy-immunology/anaphylaxis.md) - [Acute Respiratory Distress Syndrome](../critical-care/acute-respiratory-distress-syndrome.md) - [Cardiogenic Shock in Adults](../critical-care/cardiogenic-shock-in-adults.md) - [Post–Cardiac Arrest Care in Adults](../critical-care/post-cardiac-arrest-care-in-adults.md) ## References 1. Resuscitation Council UK. **The ABCDE Approach.** Updated July 2024. https://www.resus.org.uk/library/abcde-approach 2. Resuscitation Council UK. **Guidelines 2025: Adult advanced life support and adult in-hospital resuscitation.** Published October 27, 2025. https://www.resus.org.uk/library/2025-resuscitation-guidelines/adult-advanced-life-support-guidelines 3. O'Driscoll BR, Howard LS, Earis J, Mak V; British Thoracic Society Emergency Oxygen Guideline Group. BTS guideline for oxygen use in adults in healthcare and emergency settings. *Thorax.* 2017;72(Suppl 1):ii1-ii90. doi:10.1136/thoraxjnl-2016-209729. PMID:28507176. 4. Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of [Sepsis and Septic Shock](/library/sepsis-and-septic-shock) 2021. *Intensive Care Med.* 2021;47:1181-1247. doi:10.1007/s00134-021-06506-y. PMID:34599691.1a:T9ea4,## One-minute summary **Sepsis** is life-threatening organ dysfunction caused by a dysregulated host response to infection. Operationally, Sepsis-3 identifies organ dysfunction as an acute increase in **SOFA score ≥2 points** attributable to infection.[1] **Septic shock** is a high-risk subset in which, despite adequate volume resuscitation, the patient requires vasopressors to maintain **MAP ≥65 mm Hg** and has **lactate >2 mmol/L**; this phenotype carries very high mortality.[1] The bedside priority is not to “prove sepsis” before acting. In a patient with suspected infection and organ dysfunction, **recognize physiologic threat, stabilize ABCs, obtain cultures without materially delaying therapy, give appropriate antimicrobials when infection is sufficiently likely, restore perfusion, identify the source, and obtain source control early**.[2,3] ### Core treatment sequence 1. **Recognize possible infection + organ dysfunction.** 2. **Assess airway, breathing, circulation and perfusion immediately.** 3. **Measure lactate** when sepsis is suspected; interpret in context.[2] 4. **Obtain appropriate cultures** before antibiotics if this does not cause a clinically important delay. 5. **Antimicrobials:** immediately, ideally within 1 hour for septic shock or high-likelihood sepsis; in possible sepsis without shock, perform rapid diagnostic assessment and treat within 3 hours if concern persists.[2] 6. **Fluids:** crystalloids are first line; balanced crystalloids are generally preferred. For sepsis-induced hypoperfusion/septic shock, SSC suggests at least **30 mL/kg IV crystalloid within the first 3 hours**, followed by frequent reassessment rather than automatic repeated boluses.[2] 7. **Vasopressor:** **norepinephrine** is first line; initial MAP target is usually **65 mm Hg**.[2] 8. **Source control:** drain, debride, remove infected hardware/device, or operate as soon as medically and logistically practical when indicated.[2] 9. **Reassess repeatedly** using mentation, capillary refill, urine output, lactate trend, hemodynamics, dynamic fluid-responsiveness measures and organ function.[2] ★ **High yield:** qSOFA is **not recommended as a stand-alone screening test** for sepsis or septic shock.[2] --- ## Definition and classification ### Sepsis Sepsis-3 defines sepsis as **life-threatening organ dysfunction caused by a dysregulated host response to infection**.[1] Operationally: - Suspected or confirmed infection **plus** - Acute increase in **SOFA ≥2 points** attributable to the infection.[1] The old term **“severe sepsis”** is redundant under Sepsis-3; once organ dysfunction is present, the patient has sepsis.[1] ### Septic shock Septic shock is a subset of sepsis with profound circulatory, cellular and metabolic abnormalities. Sepsis-3 clinical criteria are:[1] - Vasopressor requirement to maintain **MAP ≥65 mm Hg**, **and** - Serum lactate **>2 mmol/L (18 mg/dL)**, - Despite adequate volume resuscitation. ### Infection without sepsis A patient can have pneumonia, pyelonephritis, cellulitis or another infection without meeting criteria for sepsis if there is no infection-related life-threatening organ dysfunction. Conversely, organ dysfunction may be the first clue to an occult infection. --- ## Epidemiology and risk factors Sepsis is among the leading causes of critical illness and infection-related death worldwide. Risk rises substantially with age, frailty, chronic disease and impaired host defense.[1,2] Important risk factors include: - Age extremes and advanced age - Immunosuppression: neutropenia, hematologic malignancy, solid-organ or stem-cell transplantation, high-dose corticosteroids, biologic immunomodulators, advanced HIV - Diabetes mellitus - Chronic kidney disease and dialysis - Cirrhosis - Chronic lung disease - Cancer - Recent surgery or invasive procedures - Indwelling vascular, urinary or biliary devices - Recent hospitalization or antimicrobial exposure - Prior colonization/infection with multidrug-resistant organisms - Functional impairment, frailty, nursing-home residence - Pregnancy/postpartum state (with different physiologic thresholds and dedicated pathways) ### Common infection sources | Source | Typical clues | Important source-control question | |---|---|---| | Lung | Cough, hypoxemia, infiltrate, focal crackles | Empyema? Obstructed airway? Abscess? | | Urinary tract | Dysuria, flank pain, pyuria, hydronephrosis | Obstructed infected collecting system? | | Abdomen | Pain, ileus, peritonism, free air/fluid | Perforation, ischemia, abscess, cholangitis? | | Skin/soft tissue | Cellulitis, wound, pain, crepitus | Necrotizing infection or abscess needing surgery? | | Bloodstream/catheter | Rigors, line tenderness, no other focus | Remove infected line/device after alternate access? | | CNS | Meningism, altered consciousness, seizures | Need immediate meningitis/encephalitis pathway? | | Bone/joint | Focal pain, prosthesis, effusion | Drainage, debridement, prosthetic infection? | | Endocardium | Murmur, emboli, prosthetic valve/device | Echo, surgery/device management? | --- ## Pathophysiology Sepsis is not simply “too much inflammation.” It is a dysregulated host-pathogen interaction involving simultaneous inflammatory and immunosuppressive pathways, endothelial injury, microvascular dysfunction, coagulation abnormalities, altered cellular metabolism and organ-specific responses.[1] ### Mechanistic chain ```text Infection / pathogen products ↓ Innate immune recognition + cytokine signaling ↓ Endothelial activation and injury ↓ Vasodilation + capillary leak + altered vascular tone ↓ Relative/absolute intravascular volume deficit ↓ Microcirculatory heterogeneity + coagulation activation ↓ Impaired tissue oxygen delivery/utilization ↓ Cellular/metabolic dysfunction ↓ Organ dysfunction ± shock ``` ### Why lactate rises Elevated lactate can reflect tissue hypoperfusion and adrenergic-driven glycolysis, but it is **not a pure measure of anaerobic metabolism**. Liver dysfunction, seizures, beta-agonists, epinephrine and impaired clearance can elevate lactate. Therefore a falling lactate may support improving physiology, but a single value should never be interpreted in isolation.[2] ### Why hypotension may be late Compensatory vasoconstriction and tachycardia may preserve blood pressure early. A patient can have clinically important hypoperfusion with apparently acceptable BP; examine mentation, skin perfusion, urine output, capillary refill, lactate and trajectory. --- ## Clinical presentation There is no single sepsis phenotype. Presentation depends on source, age, comorbidity, medications and stage of illness. ### Symptoms and signs suggesting infection - Fever or hypothermia - Rigors - Cough, sputum, pleuritic pain - Dysuria, frequency, flank pain - Abdominal pain, vomiting, diarrhea - Skin/wound pain or erythema - Headache, photophobia, neck stiffness - Device-related pain or discharge - New confusion, weakness or functional decline ### Features of organ dysfunction | Organ/system | Concerning findings | |---|---| | Neurologic | Confusion, reduced GCS, delirium | | Respiratory | Tachypnea, hypoxemia, increased work of breathing, ARDS | | Cardiovascular | Hypotension, prolonged capillary refill, mottling, cool or abnormally warm peripheries | | Renal | Oliguria, rising creatinine | | Hematologic | Thrombocytopenia, DIC pattern | | Hepatic | Rising bilirubin, coagulopathy | | Metabolic | Elevated lactate, worsening acidosis | ### Red flags for immediate escalation - Airway compromise or rapidly falling consciousness - Severe hypoxemia or impending ventilatory failure - Persistent hypotension or signs of shock - Marked mottling, prolonged capillary refill, cold peripheries - Lactate significantly elevated or rising despite treatment - New oliguria/anuria - Purpura, rapidly progressive soft-tissue pain, crepitus - Meningism with altered mental state - Suspected neutropenic sepsis - Suspected obstructed infected urinary or biliary system - Severe abdominal pain/peritonism - Rapidly progressive organ dysfunction --- ## Recognition and screening ### SOFA SOFA evaluates six systems: respiratory, coagulation, liver, cardiovascular, CNS and renal function. An acute rise by **≥2 points** in the context of infection operationalizes sepsis in Sepsis-3.[1] ### qSOFA qSOFA assigns one point each for: - Respiratory rate **≥22/min** - Altered mentation - Systolic BP **≤100 mm Hg** It identifies higher-risk patients but has insufficient sensitivity as a sole screening strategy. SSC recommends **against qSOFA as the single screening tool** compared with SIRS, NEWS or MEWS.[2] ### NEWS2 and the UK approach NICE NG253, published **19 November 2025**, uses **NEWS2 plus clinical judgment** for adults aged 16 years and older who are not currently/recently pregnant. In acute hospital settings, suspected/confirmed infection with NEWS2 ≥7 is high risk; a lower total can still be high risk when a single parameter scores 3 or there are other clinical reasons for concern.[3] **Guideline difference:** Sepsis-3/SCCM use SOFA conceptually for organ dysfunction and advise against qSOFA alone; NICE emphasizes NEWS2-based risk stratification in its UK recognition pathway. These approaches are complementary rather than interchangeable. --- ## Initial assessment: a practical first 10 minutes | Component | Assess | Interpret | Immediate action | Anticipate deterioration | |---|---|---|---|---| | Airway | Patency, voice, secretions, consciousness | Loss of airway reflexes, obstruction | Suction, adjunct, airway team, definitive airway when indicated | Fatigue, encephalopathy, aspiration | | Breathing | RR, SpO₂, work, chest exam, blood gas if needed | Pneumonia, ARDS, pulmonary edema, fatigue | Oxygen to appropriate target; ventilatory support if failing | Rapid ARDS progression | | Circulation | HR, BP/MAP, cap refill, skin, urine, lactate | Shock/hypoperfusion | IV/IO access, cultures/labs, crystalloid if indicated, vasopressor if hypotension persists | Fluid overload, refractory vasoplegia | | Disability | GCS/AVPU, glucose, pupils | Sepsis encephalopathy vs mimics | Correct glucose/oxygen/perfusion; consider CNS infection/stroke/toxin | Seizures, coma | | Exposure/source | Full examination, wounds, lines, abdomen, back | Hidden source, necrotizing infection, device infection | Source-specific imaging/consult; remove triggers/devices when indicated | Need for emergency operation/drainage | --- ## Diagnostic work-up ### Core tests The exact panel is source- and severity-dependent. Common initial tests include: - CBC with differential - Electrolytes, urea/BUN, creatinine - Liver panel and bilirubin - Venous or arterial blood gas when clinically indicated - **Lactate** - Glucose - Coagulation studies - Blood cultures - Urinalysis and urine culture where relevant - Source-specific microbiology: sputum, CSF, wound, joint fluid, stool, respiratory viral PCR, etc. ### Blood cultures Obtain blood cultures before antimicrobials **when this can be done promptly and does not materially delay treatment**. Draw adequate volume and appropriate sets according to local laboratory policy. If endocarditis is suspected, follow a dedicated multi-set culture strategy. ### Imaging Use the fastest test that will meaningfully identify source or complication: - Chest radiograph or lung ultrasound - Renal ultrasound/CT for obstruction - CT abdomen/pelvis for intra-abdominal source - RUQ ultrasound or MRCP/CT for biliary source - Echocardiography for suspected endocarditis or shock phenotype - CT brain/LP pathway for CNS infection as appropriate - Soft-tissue imaging only if it will not delay surgery in suspected necrotizing infection ★ **High yield:** In suspected necrotizing fasciitis or another source requiring emergency surgery, **do not delay definitive source control for low-value imaging** when the clinical diagnosis is sufficiently concerning. --- ## Differential diagnosis: sepsis mimics | Mimic | Clues | Discriminator | |---|---|---| | Hemorrhagic shock | Bleeding, trauma, GI loss | Imaging/exam, falling Hb may lag | | Cardiogenic shock | ACS, pulmonary edema, low EF | ECG, troponin, echo | | Pulmonary embolism | Sudden dyspnea, RV strain | CTPA/echo, risk factors | | Adrenal crisis | Steroid dependence, hyponatremia/hyperkalemia | Cortisol if feasible; do not delay steroids in crisis | | Anaphylaxis | Urticaria, bronchospasm, exposure | Rapid response to IM epinephrine | | Thyroid storm | Hyperthermia, tachyarrhythmia, thyrotoxic features | Thyroid testing, clinical score | | DKA/HHS | Hyperglycemia, ketones, osmotic symptoms | Glucose/ketones/acid-base | | Drug toxicity | Exposure, toxidrome | ECG, drug levels selectively | | Malignant hyperthermia/NMS/serotonin syndrome | Drug trigger, rigidity/clonus | Medication history, neuromuscular findings | | Pancreatitis | Epigastric pain | Lipase, imaging | | HLH/cytokine syndromes | Cytopenias, extreme ferritin, organomegaly | Specialist work-up | **STANDARD OF CARE:** Continuously reassess whether infection remains the most likely diagnosis; SSC recommends stopping empiric antimicrobials if a convincing alternative diagnosis is established.[2] --- ## Management ### 1. Immediate resuscitation Sepsis and septic shock are medical emergencies; treatment and resuscitation should begin immediately.[2] #### Oxygen and ventilation Treat hypoxemia and respiratory failure according to usual critical-care principles. Sepsis-induced ARDS should receive lung-protective ventilation; prone positioning is recommended for moderate-to-severe ARDS when appropriate.[2] #### Access and monitoring - Peripheral IV access; IO if IV access is not rapidly obtainable in shock - Continuous ECG and pulse oximetry in unstable patients - Frequent or continuous BP monitoring; arterial catheter when practical in septic shock - Urine output monitoring - Serial perfusion reassessment --- ### 2. Antimicrobial therapy #### Timing SSC 2021 recommends:[2] - **Possible septic shock or high likelihood of sepsis:** give antimicrobials immediately, ideally **within 1 hour** of recognition. - **Possible sepsis without shock:** rapidly assess infectious vs noninfectious causes; if concern for infection persists, give antimicrobials **within 3 hours** of recognition. - **Low likelihood of infection without shock:** it is reasonable to defer antimicrobials while monitoring closely. NICE 2025 similarly prioritizes urgent assessment and antibiotic treatment within 1 hour for adults at high risk of severe illness or death from sepsis.[3] #### Empiric selection Choose empiric therapy according to: - Likely anatomic source - Community vs healthcare exposure - Local antibiogram - Prior microbiology/colonization - Recent antibiotics - Risk of MRSA or resistant gram-negative organisms - Immune status - Organ function and drug allergy history Do **not** use a universal “sepsis antibiotic.” The correct regimen for community-acquired pneumonia differs from obstructive pyelonephritis, cholangitis, meningitis, neutropenic sepsis or necrotizing soft-tissue infection. #### Resistant organisms SSC recommends MRSA coverage when risk is high, against routine MRSA coverage when risk is low, and against routine double gram-negative coverage in low-MDR-risk patients. Two gram-negative agents may be considered empirically when MDR risk is high, but double coverage should generally stop once susceptibilities are known.[2] #### Pharmacokinetics Critical illness changes drug volume of distribution and clearance. Use appropriate loading doses, renal/hepatic adjustment after the initial strategy as appropriate, and therapeutic drug monitoring when available. SSC favors prolonged infusion of beta-lactams for maintenance after an initial bolus.[2] #### De-escalation and duration - Review cultures and diagnosis daily. - Narrow spectrum when possible. - Shorter effective durations are generally preferred after adequate source control. - Procalcitonin may support **discontinuation** decisions when duration is uncertain, but SSC advises against using procalcitonin plus clinical evaluation to decide whether to **start** antibiotics.[2] --- ### 3. Fluid resuscitation #### Initial fluid For sepsis-induced hypoperfusion or septic shock, SSC suggests **at least 30 mL/kg IV crystalloid in the first 3 hours**.[2] This is a weak recommendation based on low-quality evidence and should not be interpreted as permission for repeated blind boluses. #### Fluid type - **Crystalloids:** first line.[2] - **Balanced crystalloids:** suggested over 0.9% saline.[2] - **Albumin:** may be considered when very large crystalloid volumes have already been required.[2] - **Hydroxyethyl starch:** avoid.[2] #### Reassessment after initial fluid Use **dynamic measures** when possible rather than static measures alone:[2] - Passive leg raise with stroke-volume/cardiac-output response - Small fluid challenge with objective response - Pulse-pressure or stroke-volume variation in appropriate ventilated patients - Bedside echocardiography Also reassess: - Capillary refill - MAP and pulse pressure - Mental status - Urine output - Mottling/skin temperature - Lung ultrasound/B-lines and respiratory status - Lactate trend #### What recent trials changed The **CLASSIC** trial in ICU septic shock found no 90-day mortality difference between restrictive and standard IV-fluid strategies after initial resuscitation.[5] The **CLOVERS** trial found no significant 90-day mortality difference between an early restrictive strategy emphasizing vasopressors and a liberal-fluid strategy in sepsis-induced hypotension.[4] **Practical interpretation:** after initial stabilization, there is no evidence that either indiscriminately liberal fluid or rigidly restrictive fluid is superior for all patients. Give fluid when there is evidence of hypoperfusion and likely fluid responsiveness; stop when benefit is unlikely or congestion emerges. --- ### 4. Vasopressors and hemodynamic targets #### First line **Norepinephrine** is first-line vasopressor therapy for septic shock.[2] A common starting infusion range is institution-specific; titrate rapidly to perfusion goals rather than waiting for central access. SSC supports short-term administration through a well-sited proximal peripheral vein when necessary rather than delaying vasopressor initiation.[2] #### MAP target Initial target **MAP 65 mm Hg** for most adults on vasopressors.[2] Individualize upward when clinically justified, for example selected patients with chronic severe hypertension and ongoing renal or neurologic hypoperfusion, while recognizing that higher targets can increase vasopressor exposure and arrhythmias. #### Second-line strategy - If MAP remains inadequate on norepinephrine, SSC suggests **adding vasopressin** rather than simply escalating norepinephrine indefinitely; guideline practice commonly adds vasopressin when norepinephrine is around **0.25–0.5 micrograms/kg/min**.[2] - If MAP is still inadequate despite norepinephrine + vasopressin, consider **epinephrine**.[2] - For cardiac dysfunction with persistent hypoperfusion despite adequate volume and BP, consider **dobutamine added to norepinephrine** or epinephrine alone.[2] #### Peripheral perfusion Capillary refill is a useful adjunct to other resuscitation endpoints. The ANDROMEDA-SHOCK trial did not show a statistically significant reduction in 28-day mortality with a capillary-refill-targeted strategy versus lactate-targeted resuscitation, but its findings supported renewed emphasis on bedside peripheral perfusion assessment.[6] --- ### 5. Source control **Source control is definitive therapy when infection persists because of an anatomic focus.** SSC recommends identifying/excluding sources requiring emergent intervention and performing required source control as soon as medically and logistically practical.[2] Examples: - Drain intra-abdominal abscess - ERCP/biliary drainage for obstructed cholangitis - Urgent decompression for infected obstructed urinary tract - Debridement for necrotizing soft-tissue infection - Remove infected vascular catheter after alternate access - Drain empyema - Operate for perforated viscus or ischemic bowel - Manage infected prosthetic material/device with specialists ★ **Board pearl:** Antibiotics cannot sterilize a closed abscess, obstructed infected system or necrotic tissue reliably without source control. --- ### 6. Corticosteroids For septic shock with an ongoing vasopressor requirement, SSC suggests IV corticosteroids. Typical regimen:[2] - **Hydrocortisone 200 mg/day IV**, either - 50 mg every 6 hours, or - continuous infusion. SSC remarks that treatment is often started when norepinephrine/epinephrine is **≥0.25 micrograms/kg/min for at least 4 hours**.[2] #### Evidence - **ADRENAL:** hydrocortisone 200 mg/day shortened time to shock resolution but did not reduce 90-day mortality compared with placebo.[7] - **APROCCHSS:** hydrocortisone plus fludrocortisone reduced 90-day mortality compared with placebo in a more severely shocked population.[8] **Guideline interpretation:** steroids are standard adjunctive therapy for vasopressor-dependent septic shock, not routine therapy for uncomplicated sepsis without shock. --- ### 7. Other organ support and adjuncts #### Red blood cell transfusion SSC recommends a restrictive strategy; a typical trigger is **hemoglobin 7 g/dL (70 g/L)**, but transfusion should reflect the whole clinical context, including active hemorrhage, severe hypoxemia or myocardial ischemia.[2] #### Glucose Start insulin for glucose **≥180 mg/dL (10 mmol/L)**; typical post-initiation target is approximately **144–180 mg/dL (8–10 mmol/L)**.[2] #### Bicarbonate - Do **not** use sodium bicarbonate simply to improve hemodynamics in hypoperfusion-induced lactic acidosis.[2] - Consider it in septic shock with **pH ≤7.2 plus AKI stage 2–3**, where SSC gives a weak recommendation.[2] #### Renal replacement therapy Use standard indications such as refractory hyperkalemia, severe acidemia, volume overload or uremic complications. Do not start RRT solely because AKI is present without a definitive indication.[2] #### VTE and stress-ulcer prophylaxis Use pharmacologic VTE prophylaxis unless contraindicated; LMWH is generally preferred over UFH. Stress-ulcer prophylaxis is for patients with GI-bleeding risk factors, not automatically for every sepsis admission.[2] #### Vitamin C and extracorporeal “blood purification” SSC suggests **against IV vitamin C** and against polymyxin-B hemoperfusion; evidence for other blood purification techniques remains insufficient.[2] --- ### Reassessment and monitoring #### Perfusion endpoints No single number defines successful resuscitation. Reassess the pattern: - Mental status - Capillary refill and mottling - Peripheral temperature - MAP - Heart rate - Urine output - Lactate trend - Acid-base status - Bedside echo/dynamic fluid responsiveness - Respiratory status and signs of fluid accumulation #### Urine output Oliguria is a marker of possible renal hypoperfusion or AKI, but urine output also changes with CKD, obstruction, medications and hormonal response. Persistent oliguria warrants evaluation rather than automatic fluid boluses. #### Lactate SSC suggests guiding resuscitation toward decreasing lactate when lactate is elevated, while explicitly noting that lactate must be interpreted in context.[2] --- ### Anticipation of deterioration | Pattern | What it may mean | Next actions | |---|---|---| | Rising vasopressor requirement | Ongoing vasoplegia, missed source, cardiogenic/obstructive component, bleeding | Reassess volume, echo, source control, diagnosis, steroids | | Persistent lactate elevation | Ongoing hypoperfusion or non-hypoxic lactate production | Re-examine perfusion; do not chase lactate with fluid blindly | | Worsening oxygenation after fluids | ARDS or hydrostatic pulmonary edema | Stop indiscriminate fluid, lung ultrasound/echo, ventilatory strategy | | New oliguria | AKI, hypoperfusion, obstruction | Hemodynamics, urinalysis, bladder scan/renal imaging as indicated | | New thrombocytopenia/coagulopathy | DIC, marrow suppression, liver dysfunction, drug effect | Coags/fibrinogen, bleeding assessment, source control | | Persistent fever/hypothermia | Uncontrolled source, resistant organism, noninfectious mimic | Repeat source search and microbiology review | --- ### Complications - Septic shock - ARDS - Acute kidney injury - Disseminated intravascular coagulation - Acute liver dysfunction - Myocardial dysfunction and arrhythmia - Delirium/encephalopathy - Critical illness polyneuropathy/myopathy - Pressure injury and deconditioning - Secondary/nosocomial infections - Malnutrition - Thromboembolism #### Post-sepsis syndrome Survivors may experience persistent weakness, exercise limitation, cognitive impairment, anxiety, depression, PTSD, sleep disturbance and recurrent hospitalization. Discharge planning should include medication reconciliation, rehabilitation needs, recovery education and follow-up for physical, cognitive and emotional sequelae.[2] --- ### Special populations #### Neutropenic sepsis Treat fever/instability in neutropenia as an emergency. Antipseudomonal empiric coverage and local neutropenic-sepsis protocols take priority; do not wait for neutrophil recovery or culture confirmation. #### Pregnancy and postpartum Normal pregnancy physiology changes heart rate, respiratory rate, BP and laboratory reference ranges. Use obstetric sepsis pathways and involve obstetrics early; maternal stabilization remains the priority. #### Cirrhosis Patients may have baseline vasodilation, thrombocytopenia, renal vulnerability and unusual infections. Consider spontaneous bacterial peritonitis, bacteremia and hepatorenal physiology; fluid and vasopressor decisions need particular caution. #### Advanced CKD/heart failure Initial shock treatment is still urgent, but repeated fluid boluses should be guided by dynamic responsiveness, congestion and bedside echo rather than fear of all fluid or routine large-volume administration. #### Immunosuppression Broaden the differential for opportunistic and fungal infection and involve infectious-diseases/microbiology expertise early when appropriate. --- ### Acute management checklist #### First hour: suspected septic shock / high-likelihood sepsis - [ ] ABCDE assessment and immediate stabilization - [ ] Call senior/critical-care help early - [ ] Continuous monitoring; IV/IO access - [ ] Lactate - [ ] Blood cultures and source cultures if they will not delay treatment - [ ] Appropriate empiric antimicrobials immediately, ideally within 1 hour - [ ] Crystalloid for hypoperfusion; balanced crystalloid preferred - [ ] Reassess after each bolus using dynamic/perfusion markers - [ ] Norepinephrine promptly if hypotension persists; do not delay for central line - [ ] Initial MAP target about 65 mm Hg - [ ] Identify source and emergency source-control need - [ ] Glucose, CBC, renal/liver profile, coagulation, blood gas as appropriate - [ ] Imaging focused on source without delaying life-saving intervention #### Following hours - [ ] Repeat lactate if elevated and clinically useful - [ ] Trend capillary refill, urine output, mentation and hemodynamics - [ ] Add vasopressin if norepinephrine requirement rises and MAP remains inadequate - [ ] Consider hydrocortisone for ongoing vasopressor-dependent shock - [ ] De-escalate/target antibiotics when microbiology returns - [ ] Reassess for ARDS, AKI, DIC and occult source - [ ] Re-evaluate diagnosis if response is atypical --- ### Diagnostic and management algorithm ```text Suspected infection ↓ Any acute organ dysfunction / concerning physiology? ├─ No → treat infection; monitor for deterioration └─ Yes ↓ Immediate ABCDE + lactate + cultures/labs + source assessment ↓ Shock / high likelihood of sepsis? ├─ Yes → antimicrobials immediately (ideally ≤1 h) │ + crystalloid if hypoperfusion │ + norepinephrine if hypotension persists │ + urgent source control └─ No → rapid infectious vs noninfectious assessment if concern persists → antimicrobials within 3 h ↓ Reassess perfusion dynamically ↓ Fluid responsive? ├─ Yes + hypoperfused → cautious additional fluid └─ No / congested → avoid further routine bolus ↓ MAP still inadequate? → norepinephrine → add vasopressin → consider epinephrine ↓ Persistent vasopressor-dependent shock? → hydrocortisone 200 mg/day ↓ Repeat source search + organ support + de-escalation + recovery planning ``` --- ### Common pitfalls | Pitfall | Why it is dangerous | Better approach | |---|---|---| | Treating qSOFA as a rule-out test | Misses sepsis | Use broad clinical assessment/NEWS or local screening plus organ dysfunction evaluation | | Waiting for hypotension before recognizing shock | BP can be preserved early | Assess perfusion and trajectory | | Delaying antibiotics in septic shock for “perfect cultures” | Time-sensitive mortality risk | Cultures quickly, then treat; do not materially delay | | Giving repeated automatic 30 mL/kg boluses | Fluid accumulation may worsen outcomes | Initial resuscitation + dynamic reassessment | | Chasing lactate with fluid alone | Lactate has non-hypoperfusion causes | Integrate cap refill, echo, urine, MAP and clinical context | | Delaying vasopressors until central line placement | Prolongs hypotension | Use appropriate proximal peripheral access short-term | | Ignoring source control | Antibiotics alone may fail | Drain/debride/decompress/remove source early | | Continuing broad-spectrum antibiotics indefinitely | Resistance/toxicity/C. difficile | Daily de-escalation and shortest effective duration | --- ### Guideline conflicts and practice variation #### Fluid volume SSC retains a suggestion for at least 30 mL/kg within 3 hours for sepsis-induced hypoperfusion/septic shock.[2] However, CLASSIC and CLOVERS show that after initial resuscitation, restrictive and liberal strategies produce similar major outcomes in broad trial populations.[4,5] Contemporary practice is therefore shifting toward **individualized, physiology-guided fluid** after the initial phase. #### Screening - **SSC:** do not use qSOFA alone; institutional screening and performance-improvement programs are recommended.[2] - **NICE 2025:** uses NEWS2 thresholds plus clinical judgment to stratify risk in adults.[3] #### Antibiotic timing Both SSC and NICE prioritize the fastest treatment in shock/high-risk sepsis. SSC is more explicit about allowing a short diagnostic window (up to 3 hours) for possible sepsis **without shock** when the likelihood of infection is uncertain.[2,3] --- ### STANDARD OF CARE vs emerging vs experimental #### STANDARD OF CARE - Early recognition and organ-supportive resuscitation - Appropriate cultures without clinically important antibiotic delay - Timely empiric antimicrobials based on source and resistance risk - Crystalloids for hypoperfusion, with reassessment - Norepinephrine first-line vasopressor - Initial MAP target around 65 mm Hg - Early source control when indicated - Hydrocortisone for persistent vasopressor-dependent septic shock - De-escalation and shorter appropriate antimicrobial courses #### EMERGING / EVOLVING PRACTICE - Earlier vasopressor initiation with less routine fluid after initial resuscitation - Greater use of capillary refill, bedside echo and dynamic fluid-responsiveness testing - Precision resuscitation based on shock phenotype rather than a fixed fluid recipe - Biomarker- and rapid-diagnostic-guided antimicrobial stewardship #### EXPERIMENTAL / INVESTIGATIONAL - Routine extracorporeal cytokine adsorption/blood purification - Immune-phenotype-directed immunomodulation - Broad metabolomic/genomic sepsis endotyping for bedside treatment selection These should not displace proven infection control, antimicrobials, source control and organ support outside trials or specialist protocols. --- ### Exam-focused review #### USMLE Step 1 Understand: - Vasodilation + capillary leak → decreased effective circulating volume - Endothelial and microcirculatory dysfunction - Why lactate can rise - DIC and organ dysfunction mechanisms #### Step 2 CK / Step 3 Prioritize: - Unstable patient → resuscitate before extensive diagnostics - Septic shock → antibiotics + perfusion support immediately - Persistent hypotension after appropriate fluid → norepinephrine - Obstructed infected system → decompression/source control #### MRCP / ABIM / boards Know: - Sepsis-3 definition and septic shock criteria - SOFA vs qSOFA role - 30 mL/kg recommendation is a **weak initial-resuscitation recommendation**, not a maintenance strategy - Norepinephrine first line; vasopressin add-on - Hydrocortisone 200 mg/day for ongoing vasopressor need - Hb 7 g/dL is a typical restrictive transfusion threshold, modified by clinical context --- ### Original MCQs #### Question 1 A 68-year-old man with pyelonephritis has MAP 56 mm Hg, lactate 4.2 mmol/L, mottled extremities and worsening confusion. He has received an appropriate initial crystalloid resuscitation. What is the best next hemodynamic treatment? A. Dopamine as first-line vasopressor B. Norepinephrine infusion C. Additional 2 L saline without reassessment D. Sodium bicarbonate for the lactate E. Wait for central venous access before starting a vasopressor **Answer: B. Norepinephrine infusion.** **Explanation:** Norepinephrine is first-line vasopressor therapy for septic shock. Vasopressor treatment should not be delayed solely to obtain central access; a suitable proximal peripheral IV can be used briefly with monitoring.[2] #### Question 2 A patient with suspected infection has RR 26/min, SBP 98 mm Hg and normal mentation. Which statement about qSOFA is most accurate? A. qSOFA ≥2 confirms sepsis B. qSOFA <2 excludes sepsis C. qSOFA should be the sole screening test D. qSOFA can identify risk but is not recommended as the sole screening test E. qSOFA replaces SOFA for defining organ dysfunction **Answer: D.** **Explanation:** qSOFA is a prognostic bedside signal, not a definitive diagnostic test. SSC advises against qSOFA as the single screening tool.[2] #### Question 3 A patient with septic shock remains hypotensive despite norepinephrine and appropriate reassessment of volume status. What vasopressor strategy is favored next by SSC? A. Add vasopressin B. Switch to phenylephrine routinely C. Stop norepinephrine and use dopamine D. Give repeated fluid regardless of fluid responsiveness E. Start terlipressin **Answer: A. Add vasopressin.** **Explanation:** For inadequate MAP on norepinephrine, SSC suggests adding vasopressin rather than simply escalating norepinephrine indefinitely.[2] #### Question 4 Which patient most clearly requires urgent source control in addition to antimicrobials? A. Uncomplicated cellulitis without abscess B. Viral bronchitis C. Obstructed infected ureter with hydronephrosis and shock D. Asymptomatic bacteriuria E. Mild cystitis **Answer: C.** **Explanation:** An infected obstructed urinary system is a source-control emergency; decompression is essential because antimicrobials alone may not control infection. #### Question 5 A patient with septic shock is receiving norepinephrine 0.35 micrograms/kg/min for several hours with persistent vasopressor requirement. Which adjunct is guideline-supported? A. Routine IV vitamin C B. Hydrocortisone 200 mg/day IV C. Polymyxin-B hemoperfusion D. Hydroxyethyl starch E. Routine bicarbonate regardless of pH **Answer: B.** **Explanation:** SSC suggests IV corticosteroids for septic shock with ongoing vasopressor need; hydrocortisone 200 mg/day is the typical regimen.[2] --- ### Recent guideline and practice updates - **19 November 2025:** NICE published NG253 for suspected sepsis in people aged 16 or over, replacing the prior all-age structure and emphasizing NEWS2 plus clinical judgment and rapid antibiotics for high-risk patients.[3] - Contemporary post-SSC evidence from **CLASSIC (2022)** and **CLOVERS (2023)** supports a move away from automatic repeated fluid boluses after initial resuscitation toward individualized fluid/vasopressor decisions.[4,5] - As of this review date, the **Surviving Sepsis Campaign 2021 adult guideline remains the principal international comprehensive management guideline** listed by SCCM; local institutions may have more recent operational pathways.[2] --- ### Landmark and influential research - **Sepsis-3 (2016):** modern definition centered on infection-related organ dysfunction and defined septic shock phenotype.[1] - **ProCESS, ARISE, ProMISe (2014–2015):** showed no benefit from mandatory early goal-directed therapy protocols compared with contemporary usual care, helping shift practice toward early recognition/resuscitation without fixed invasive targets.[9-11] - **ADRENAL and APROCCHSS (2018):** clarified the role of corticosteroids in vasopressor-dependent septic shock.[7,8] - **ANDROMEDA-SHOCK (2019):** brought peripheral perfusion/capillary refill back into resuscitation discussions.[6] - **CLASSIC (2022) and CLOVERS (2023):** challenged the assumption that more fluid is inherently better after initial resuscitation.[4,5] --- ### References 1. Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). *JAMA*. 2016;315(8):801-810. doi:10.1001/jama.2016.0287. https://jamanetwork.com/journals/jama/fullarticle/2492881 2. Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. *Intensive Care Med*. 2021;47:1181-1247. doi:10.1007/s00134-021-06506-y. SCCM recommendations: https://www.sccm.org/clinical-resources/guidelines/guidelines/surviving-sepsis-guidelines-2021 3. National Institute for Health and Care Excellence. Suspected sepsis in people aged 16 or over: recognition, assessment and early management. NICE guideline NG253. Published 19 November 2025. https://www.nice.org.uk/guidance/NG253 4. National Heart, Lung, and Blood Institute PETAL Clinical Trials Network. Early Restrictive or Liberal Fluid Management for Sepsis-Induced Hypotension (CLOVERS). *N Engl J Med*. 2023;388:499-510. doi:10.1056/NEJMoa2212663. 5. Meyhoff TS, Hjortrup PB, Wetterslev J, et al. Restriction of Intravenous Fluid in ICU Patients with Septic Shock (CLASSIC). *N Engl J Med*. 2022;386:2459-2470. doi:10.1056/NEJMoa2202707. 6. Hernández G, Ospina-Tascón GA, Damiani LP, et al. Effect of a Resuscitation Strategy Targeting Peripheral Perfusion Status vs Serum Lactate Levels on 28-Day Mortality Among Patients With Septic Shock: ANDROMEDA-SHOCK. *JAMA*. 2019;321(7):654-664. doi:10.1001/jama.2019.0071. 7. Venkatesh B, Finfer S, Cohen J, et al. Adjunctive Glucocorticoid Therapy in Patients with Septic Shock (ADRENAL). *N Engl J Med*. 2018;378:797-808. doi:10.1056/NEJMoa1705835. 8. Annane D, Renault A, Brun-Buisson C, et al. Hydrocortisone plus Fludrocortisone for Adults with Septic Shock (APROCCHSS). *N Engl J Med*. 2018;378:809-818. doi:10.1056/NEJMoa1705716. 9. ProCESS Investigators. A Randomized Trial of Protocol-Based Care for Early Septic Shock. *N Engl J Med*. 2014;370:1683-1693. doi:10.1056/NEJMoa1401602. 10. ARISE Investigators; ANZICS Clinical Trials Group. Goal-Directed Resuscitation for Patients with Early Septic Shock. *N Engl J Med*. 2014;371:1496-1506. doi:10.1056/NEJMoa1404380. 11. Mouncey PR, Osborn TM, Power GS, et al. Trial of Early, Goal-Directed Resuscitation for Septic Shock (ProMISe). *N Engl J Med*. 2015;372:1301-1311. doi:10.1056/NEJMoa1500896. --- ### Related topics to build next - Shock: classification and hemodynamic approach - Community-acquired pneumonia - Neutropenic sepsis - Acute respiratory distress syndrome - Disseminated intravascular coagulation - Vasopressors and inotropes - Source control in severe infection1b:T943a,## One-minute summary An **asthma exacerbation** is an acute or subacute worsening of dyspnea, wheeze, cough or chest tightness with a fall in expiratory airflow compared with the patient’s usual state.[1] The attack is caused by variable airflow obstruction from **bronchial smooth-muscle constriction, airway-wall inflammation/edema and mucus**, with dynamic hyperinflation becoming critical in severe disease. The immediate priorities are: 1. **Assess severity while starting treatment.** Do not wait for full history, chest radiography or spirometry. 2. **If anaphylaxis is present, give epinephrine first**, then treat bronchospasm.[1] 3. Give a rapid-acting inhaled bronchodilator. **Salbutamol/albuterol remains the usual acute bronchodilator**; pMDI + spacer is effective for many mild/moderate attacks.[1] 4. In **moderate/severe exacerbations**, give **systemic corticosteroids early**; in adults, GINA 2026 recommends prednisone/prednisolone **40–50 mg/day for 5–7 days**.[1] 5. Add **ipratropium** during the first 1–2 hours for severe acute asthma; this lowers admission risk when combined with SABA.[1] 6. GINA 2026 suggests supplemental oxygen when **SpO₂ <92%**, targeting **92–95%**; avoid unnecessary hyperoxia.[1] 7. Consider **IV magnesium sulfate 2 g over ~20 minutes** in selected severe attacks with poor initial response; it is not routine therapy for every exacerbation.[1] 8. A **normal or rising PaCO₂ in a severely dyspneic patient is ominous**: acute asthma usually causes hypocapnia; normal/high CO₂ suggests fatigue and impending ventilatory failure.[1] 9. Before discharge, ensure **ICS-containing therapy**, inhaler technique, action plan, trigger/risk review and early follow-up. GINA prefers ICS-formoterol-based anti-inflammatory reliever strategies for most adults/adolescents where available.[1,2] ★ **High yield:** A “quiet” or **silent chest** in a distressed patient is not improvement; it can mean critically reduced airflow. --- ## Definition GINA defines an asthma exacerbation as an episode of progressive worsening in shortness of breath, cough, wheeze and/or chest tightness with a progressive decrease in lung function, representing a clinically important departure from the patient’s baseline that requires a change in treatment.[1] Exacerbations may occur: - In a patient with known asthma - As the first presentation of asthma - Despite apparently mild or previously well-controlled symptoms The term **acute severe asthma** describes a high-risk clinical state requiring urgent treatment; **life-threatening/near-fatal asthma** involves features such as altered consciousness, exhaustion, severe hypoxemia, marked airflow limitation or hypercapnia and may require invasive ventilation. --- ## Core pathophysiology ### What narrows the airway? Three mechanisms act together: 1. **Bronchial smooth-muscle contraction** — rapidly reversible with beta₂-agonists. 2. **Airway inflammation and edema** — improved over hours by corticosteroids, not by bronchodilator alone. 3. **Mucus hypersecretion/plugging** — especially important in severe and fatal asthma. ### Dynamic hyperinflation Severe obstruction prolongs expiration. The next inspiration begins before the lungs fully empty, creating **air trapping** and intrinsic PEEP (auto-PEEP). Consequences include: - Increased work of breathing - Respiratory-muscle fatigue - Increased intrathoracic pressure - Reduced venous return and hypotension - Barotrauma/pneumothorax This physiology explains why aggressive mechanical ventilation can be dangerous: the priority is often to permit adequate expiratory time rather than normalize PaCO₂ immediately. ### Gas exchange Early/moderate attacks commonly cause: - V/Q mismatch → hypoxemia - Hyperventilation → **low PaCO₂** As fatigue develops, PaCO₂ normalizes and then rises. In a patient who is still clinically very unwell, that trend should trigger concern for impending respiratory failure.[1] --- ## Triggers and risk factors ### Common exacerbation triggers GINA 2026 lists common triggers including viral respiratory infections, allergen exposure, outdoor air pollution, seasonal changes and poor adherence to inhaled corticosteroid (ICS) treatment.[1] Other triggers include: - Tobacco smoke and vaping exposure - Occupational irritants - Exercise/cold air in susceptible patients - NSAIDs in aspirin/NSAID-exacerbated respiratory disease - Nonselective beta-blockers - Medication nonadherence or incorrect inhaler technique - Thunderstorm asthma in sensitized populations - Pregnancy-related treatment interruption ### Risk factors for severe or fatal exacerbation - Previous intubation/ICU admission for asthma - ED visit or hospitalization in the past year - Recent systemic corticosteroid use - Excess SABA use - Poor/no ICS adherence - Low baseline lung function - Food allergy/anaphylaxis risk - Major psychosocial barriers or poor access to care - Incorrect inhaler technique - Smoking/vaping - Multiple comorbidities GINA emphasizes that dispensing **≥3 SABA canisters/year** is associated with increased exacerbation risk, while very high SABA dispensing is associated with markedly increased mortality risk.[1] --- ## Clinical assessment Treat while assessing. A patient who looks exhausted, confused or cyanotic does not need a prolonged severity checklist before resuscitation. ### Key history - Onset and rate of progression - Trigger: infection, allergen, smoke, medication, exercise - Reliever doses already taken and response - Current controller therapy and adherence - Previous ICU/intubation - Recent steroid courses/admissions - Anaphylaxis symptoms: urticaria, angioedema, hypotension, GI symptoms after exposure - Fever, pleuritic pain or focal infectious symptoms - Pregnancy - Cardiac disease, COPD or other alternative diagnosis ### Examination | Component | Assess | Interpretation | Immediate action | Anticipate deterioration | |---|---|---|---|---| | Appearance | Ability to speak, posture, agitation, drowsiness | Short phrases/words = severe; altered consciousness = life-threatening | Treat immediately; senior/critical care help | Exhaustion, arrest | | Respiratory rate | Trend, not one value | Tachypnea common; slowing with distress can be fatigue | Bronchodilator, O₂ if indicated | Respiratory muscle failure | | Work of breathing | Accessory muscles, retractions, paradoxical movement | Increasing effort = severity; decreasing effort can be fatigue | Repeated bronchodilation | Impending failure | | Air entry | Bilateral intensity, wheeze, silent chest | Quiet chest can mean minimal airflow | Escalate urgently | Need for ventilation | | SpO₂ | Room air if safe; trend | <92% is a GINA 2026 oxygen threshold | Controlled oxygen to 92–95% | Worsening V/Q mismatch | | PEF/FEV₁ | If patient can perform without delaying care | Objective airflow limitation and response | Repeat after treatment | Failure to improve | | HR/BP | Tachycardia, pulsus, hypotension | Severe distress, drug effect, tension PTX, hyperinflation | Monitor; evaluate shock causes | Dynamic hyperinflation | --- ## Severity: practical categories Exact labels vary across guidelines and age groups, but clinical decisions should center on **mild/moderate vs severe vs life-threatening** physiology. ### Mild–moderate pattern - Speaks in phrases/sentences - Alert - Increased work of breathing but not exhausted - SpO₂ often preserved - PEF typically >50% predicted/personal best, often >60% ### Severe pattern - Speaks only words/short phrases - Marked accessory-muscle use - Tachypnea/tachycardia - SpO₂ reduced - PEF ≤50% predicted/personal best is concerning ### Life-threatening pattern Any of the following should prompt immediate escalation: - Drowsiness, confusion, collapse - Exhaustion or poor respiratory effort - Cyanosis - Silent chest/very poor air movement - Severe hypoxemia - Hypotension or arrhythmia - Normal or rising PaCO₂ despite severe distress - Respiratory arrest ★ **Exam pearl:** The loudness of wheeze does **not** reliably correlate with severity. Less wheeze with worsening distress can mean less airflow. --- ## Differential diagnosis | Diagnosis | Clues against uncomplicated asthma | Useful test/action | |---|---|---| | Anaphylaxis | Sudden exposure, urticaria/angioedema, hypotension | **IM epinephrine first** | | COPD exacerbation | Older age, smoking history, chronic fixed obstruction | Prior spirometry, blood gas | | Vocal cord dysfunction / inducible laryngeal obstruction | Inspiratory noise, throat tightness, poor bronchodilator response | Laryngoscopy when stable | | Pneumothorax | Sudden pleuritic pain, unilateral absent breath sounds | POCUS/CXR; emergency decompression if tension physiology | | Pulmonary edema | Crackles, orthopnea, cardiac disease | POCUS, ECG, BNP selectively | | Pulmonary embolism | Sudden dyspnea, risk factors, pleuritic pain | PE pathway | | Pneumonia | Fever, focal crackles, infiltrate | CXR if clinically indicated | | Foreign body | Sudden onset, focal wheeze, choking | Airway evaluation/imaging | | Central airway obstruction | Stridor, fixed monophonic sound | Imaging/bronchoscopy | | Hyperventilation/panic | Paresthesia, normal airflow | Diagnosis of exclusion in acute distress | | Metabolic acidosis | Deep breathing, little wheeze | Blood gas/metabolic work-up | --- ## Investigations ### Peak expiratory flow / spirometry PEF is useful for objective severity and response when the patient can perform it safely. Do **not** delay treatment in severe disease to obtain a number. Repeated values are more informative than one value: - Compare with predicted or personal best - Look for improvement after bronchodilator - Failure to improve should lower the threshold for admission/escalation ### Pulse oximetry Continuous monitoring is appropriate in severe attacks or when oxygen is required. Be aware of potential pulse-oximeter bias and overestimation in some patients with darker skin pigmentation, particularly near clinical thresholds.[1] ### Blood gas GINA 2026 states ABGs are **not routinely required**. Consider them when:[1] - PEF/FEV₁ <50% predicted - Poor response to initial therapy - Clinical deterioration - Suspected ventilatory failure Interpretation: - Low PaCO₂: expected in many acute attacks - Normal PaCO₂ in a very distressed patient: concerning - **PaCO₂ >45 mm Hg (6 kPa)**: respiratory failure signal in this context[1] - PaO₂ <60 mm Hg (8 kPa): significant hypoxemia[1] A VBG may help assess pH/CO₂ trend in selected settings, but arterial sampling is required when exact oxygenation is necessary. ### Chest radiograph Not routine. GINA recommends considering CXR when:[1] - Alternative/complicating cardiopulmonary disease is suspected - The patient is not responding as expected - Pneumothorax may be difficult to diagnose clinically ### Other testing - ECG in older patients, significant tachycardia, chest pain or electrolyte concern - Electrolytes if severe/repeated beta₂-agonist use, diuretics, arrhythmia or critical illness - Viral testing when it changes isolation/antiviral decisions - Pregnancy test when relevant to imaging/medications --- ## Acute management ### First principle: treat concurrently The main acute therapies are administered together rather than sequentially: bronchodilation, oxygen when indicated, systemic anti-inflammatory therapy and escalation planning.[1] --- ### 1. Oxygen #### GINA 2026 update GINA 2026 suggests supplemental oxygen when **SpO₂ <92%** and recommends a target saturation on oxygen of **92–95%** for adults/adolescents/children 6–11 years.[1] In adults with severe exacerbations, controlled low-flow oxygen targeting approximately **93–95%** has better physiologic outcomes than indiscriminate high-concentration oxygen.[1] **Practical point:** If the patient is critically hypoxemic and pulse oximetry is not immediately available, do not withhold oxygen while waiting for a reading.[1] #### Why avoid hyperoxia? Excess oxygen can worsen V/Q relationships and is unnecessary when saturation is already adequate. Titrate rather than automatically using 100% oxygen for every attack. --- ### 2. Rapid bronchodilation #### Salbutamol/albuterol For mild-to-moderate exacerbations, repeated inhaled SABA is highly effective. Common GINA-based adult/adolescent acute dosing is **4–10 puffs (100 micrograms/puff) by pMDI + spacer every 20 minutes for up to 3 doses in the first hour**, adjusted to response.[1] GINA 2026 primary-care flowcharts further stratify dosing, with severe presentations receiving **6–10 puffs by pMDI + spacer or 5 mg by nebulizer**, repeated every 20–30 minutes if needed.[1] #### pMDI + spacer vs nebulizer For many non-life-threatening exacerbations, pMDI + spacer produces similar lung-function improvement to nebulized SABA and is more resource-efficient.[1,8] Nebulization remains appropriate when the patient cannot effectively use a spacer, requires very high/continuous delivery, or is critically ill according to local protocol. #### Adverse effects - Tremor - Tachycardia - Hypokalemia with high cumulative doses - Lactic acidosis with very intensive beta₂-agonist exposure ⚠ **Common trap:** Persistent tachypnea after heavy salbutamol therapy is not always persistent bronchospasm. Consider beta₂-agonist-associated lactate elevation if airflow has improved but tachypnea remains. --- ### 3. Ipratropium bromide Add inhaled **ipratropium** to SABA during the **first 1–2 hours** for severe acute asthma. GINA notes that this combination reduces hospital admission risk compared with SABA alone.[1] Typical adult severe-attack regimens vary by delivery system/local policy, for example: - Ipratropium **0.5 mg nebulized**, often repeated with initial SABA treatments, or - pMDI + spacer dosing according to local protocol. There is generally **no benefit from continuing ipratropium after the initial 1–2 hours** once the acute phase has improved.[1] --- ### 4. Systemic corticosteroids Give systemic corticosteroids early for **moderate or severe exacerbations**, especially when response to initial bronchodilator is incomplete.[1] #### Adults GINA 2026 discharge/acute guidance recommends: - **Prednisone/prednisolone 40–50 mg orally once daily for 5–7 days**.[1] Oral therapy is preferred when the patient can absorb/tolerate medication; IV corticosteroids are not inherently superior if oral delivery is reliable. #### Why early? Corticosteroids reduce airway inflammation, accelerate recovery and reduce relapse risk. Their onset is not immediate, which is why they should be given early rather than “after bronchodilators fail.” #### Taper? A short 5–7-day adult course generally does not require tapering when the patient is not on chronic systemic steroids; chronic steroid exposure requires individualized adrenal-axis planning. --- ### 5. IV magnesium sulfate **Not routine for every attack.** Consider IV magnesium in severe exacerbations with inadequate response to initial intensive treatment, particularly persistent hypoxemia or very low lung function.[1] Typical adult regimen: - **Magnesium sulfate 2 g IV over ~20 minutes once**.[1] Evidence supports reduced hospital admission in selected severe patients; nebulized magnesium has not shown consistent benefit.[1] --- ### 6. Epinephrine when asthma is part of anaphylaxis A major 2026 emphasis is explicit: **if the patient has features of anaphylaxis and asthma, give epinephrine first**.[1] Bronchodilators treat bronchospasm but do not treat the airway edema, vasodilation and cardiovascular collapse of anaphylaxis. Use the standard anaphylaxis pathway; IM epinephrine dosing is weight-based and protocol-specific. --- ### Treatments that are NOT routine #### Antibiotics Do not prescribe antibiotics routinely for an asthma exacerbation. Use them only when there is evidence of a bacterial infection such as pneumonia, bacterial sinus disease requiring treatment, or another defined indication.[1] #### Aminophylline/theophylline Not recommended routinely because it adds toxicity with little additional benefit over modern inhaled bronchodilator therapy.[1] #### Sedatives Avoid sedatives in severe acute asthma unless required for a controlled airway procedure: respiratory depression can precipitate arrest. #### Routine mucolytics Not recommended; airway irritation may worsen cough/bronchospasm. --- ## Reassessment after initial treatment Reassess at approximately **1 hour or earlier** in severe disease.[1] #### Reassess - Symptoms and ability to speak - Mental status - Respiratory rate and work of breathing - SpO₂ and oxygen requirement - Air entry/wheeze - PEF/FEV₁ if feasible - HR/BP - Need for ongoing SABA #### Favorable response - Marked symptom improvement - Normalizing work of breathing - Adequate oxygenation without escalating oxygen - PEF improving toward >60–80% predicted/personal best - Reliever effect persists #### Poor response / deterioration - Persistent inability to speak - Increasing fatigue/drowsiness - Silent chest - Persistent hypoxemia - PEF persistently <50% or falling - Normal/rising PaCO₂ - Hemodynamic instability → Escalate to senior respiratory/critical-care support and prepare for ventilatory support. --- ### Noninvasive ventilation Evidence for NIV in acute asthma is less robust than in COPD exacerbation. A closely monitored trial may be considered in selected cooperative patients in experienced units, but **NIV must not delay intubation** in a deteriorating patient. Avoid NIV in: - Reduced consciousness - Inability to protect airway - Severe agitation/uncooperativeness - Hemodynamic instability - Impending arrest - Copious secretions/vomiting risk --- ### Indications to consider intubation There is no single mandatory numeric threshold. Intubate for clinical failure, including: - Respiratory arrest/peri-arrest - Progressive exhaustion - Declining consciousness - Inability to maintain oxygenation - Progressive hypercapnia/acidosis with clinical deterioration - Severe hemodynamic instability - Failure of maximal medical therapy Call anesthesia/critical care early; severe asthma is a high-risk airway and ventilation problem. --- ### Mechanical ventilation in status asthmaticus #### Key objective Avoid dangerous dynamic hyperinflation. #### Principles - Lower respiratory rate - Modest tidal volume - High inspiratory flow / short inspiratory time - Long expiratory time - Monitor plateau pressure and auto-PEEP - Accept **permissive hypercapnia** when necessary if pH/hemodynamics remain acceptable - Treat bronchospasm aggressively - Deep sedation initially; neuromuscular blockade only when necessary #### Sudden hypotension after intubation Think immediately of: 1. **Dynamic hyperinflation/auto-PEEP** 2. Tension pneumothorax 3. Sedative-induced vasodilation 4. Hypovolemia If severe auto-PEEP is suspected, disconnecting briefly from the ventilator to allow exhalation can be diagnostic/temporizing while definitive ventilator changes are made by experienced clinicians. --- ### Complications #### From the disease - Respiratory failure/arrest - Pneumothorax/pneumomediastinum - Mucus plugging/atelectasis - Hypoxic injury - Cardiac arrest #### From treatment | Therapy | Important adverse effects | |---|---| | High-dose beta₂-agonist | Tremor, tachycardia, hypokalemia, lactate elevation | | Systemic corticosteroid | Hyperglycemia, mood change, infection risk with repeated courses | | Ipratropium | Dry mouth, ocular exposure issues | | Magnesium | Flushing, hypotension; toxicity in major renal impairment with repeated dosing | | Mechanical ventilation | Barotrauma, hypotension, auto-PEEP | --- ## Disposition ### Consider discharge when - Symptoms substantially improved - No life-threatening features - Oxygenation adequate without supplemental oxygen - Lung function has improved substantially (often PEF >60–80% predicted/personal best, integrated with clinical state) - Reliever need is not excessive - Patient can use inhalers correctly - Safe follow-up and medications are available ### Admit when - Severe or incompletely responsive exacerbation - Persistent hypoxemia - PEF remains low or deteriorates - Significant comorbidities or pregnancy with concern - Previous near-fatal asthma plus concerning current course - Social barriers make outpatient treatment unsafe ### ICU / high-dependency care - Life-threatening features - Hypercapnia/acidosis - Need for NIV or invasive ventilation - Hemodynamic instability - Rapid deterioration despite treatment --- ## Discharge management: preventing the next attack An exacerbation is a sentinel event. The goal is not simply to stop wheezing; it is to reduce future severe attacks and preventable death. #### 1. ICS-containing therapy is mandatory GINA 2026 emphasizes ICS-containing treatment for all adults/adolescents with asthma and prefers **ICS-formoterol anti-inflammatory reliever strategies** where available.[1,2] For adults/adolescents after acute care, GINA recommends initiating or optimizing ICS-containing therapy before discharge; **MART (maintenance-and-reliever therapy) with ICS-formoterol** is preferred for many patients because it reduces future exacerbations compared with SABA-reliever regimens.[1] #### 2. Oral steroid course Adults: prednisone/prednisolone **40–50 mg/day for 5–7 days** when indicated.[1] #### 3. Reliever strategy Return the patient to **as-needed**, not scheduled, reliever use. Patients who use ICS-formoterol as reliever should resume it before/on discharge if SABA was temporarily substituted in acute care.[1] #### 4. Action plan Provide/review a written plan explaining: - Daily controller regimen - How to recognize worsening asthma - How to increase reliever/controller according to the plan - When to seek urgent/emergency care #### 5. Technique and adherence Watch the patient use the inhaler. “Do you know how?” is not equivalent to demonstration. #### 6. Follow-up GINA recommends follow-up **within 2–7 days** after discharge for adults/adolescents (earlier for many high-risk patients).[1] Refer for specialist review after: - ICU/intubation - Recurrent exacerbations - ≥1 exacerbation requiring oral corticosteroids/urgent care in the previous 12 months despite treatment - Diagnostic uncertainty - Suspected difficult-to-treat/severe asthma --- ### Why ICS-formoterol changed asthma care Large trials in mild asthma demonstrated that as-needed budesonide-formoterol substantially reduces severe exacerbations compared with SABA-only treatment while using less total ICS than daily maintenance regimens in some populations.[4-7] These data underpin the modern move away from **SABA-only asthma treatment**. The 2024 BTS/NICE/SIGN chronic asthma guideline similarly states that SABA should not be prescribed without concomitant ICS and favors anti-inflammatory reliever approaches in appropriate patients.[3] **Guideline convergence:** GINA and BTS/NICE/SIGN differ in exact algorithms and licensed products, but both reject SABA-only management as an adequate long-term strategy. --- ### Special populations #### Pregnancy Treat exacerbations aggressively: maternal hypoxemia is a greater fetal risk than standard asthma medicines. Continue ICS-containing treatment. Do not undertreat because of pregnancy. #### Children 6–11 years Use age/weight-specific pathways. GINA 2026 uses controlled oxygen targets and age-specific bronchodilator/steroid dosing; avoid simply copying adult doses.[1] #### Children ≤5 years Acute wheeze has a broad differential. GINA 2026 specifies salbutamol dosing by spacer/nebulizer and age-specific corticosteroid doses; pMDI + spacer is preferred when feasible.[1] #### Older adults Consider competing diagnoses: heart failure, ACS, PE, COPD, medication effects. Beta₂-agonist tachycardia and hypokalemia may be more consequential. #### Aspirin/NSAID-exacerbated respiratory disease Avoid culprit COX-1 inhibitors and refer for specialist management; acute bronchospasm is treated conventionally, but prevention requires recognition of the phenotype. --- ### Anticipation of deterioration | Finding | Meaning | Action | |---|---|---| | Increasing SABA need with shorter relief | Uncontrolled obstruction | Reassess severity; systemic steroid/escalation | | Falling wheeze + falling air entry | Less airflow, not necessarily improvement | Urgent senior/critical-care review | | Drowsiness/confusion | Hypoxemia/hypercapnia/exhaustion | Airway/ventilation planning | | Normalizing PaCO₂ while still distressed | Fatigue | Treat as impending respiratory failure | | Hypotension | Auto-PEEP, tension PTX, dehydration, anaphylaxis | Immediate focused evaluation | | Rising lactate after very high SABA dose with improving airflow | Beta₂-agonist effect possible | Reassess bronchospasm before escalating SABA blindly | --- ### Acute management checklist #### Immediate - [ ] Sit patient upright if tolerated - [ ] Rapid ABC assessment - [ ] Identify anaphylaxis → **epinephrine first** - [ ] SpO₂, HR, RR, BP, mental status - [ ] PEF if feasible without delaying treatment - [ ] Inhaled salbutamol/albuterol promptly - [ ] Oxygen if SpO₂ <92%; target 92–95% (GINA 2026) - [ ] Add ipratropium for severe exacerbation - [ ] Systemic corticosteroid early for moderate/severe attack - [ ] Senior/critical-care help for life-threatening features #### At 1 hour or earlier - [ ] Repeat clinical severity assessment - [ ] Repeat PEF/FEV₁ if feasible - [ ] Check oxygen requirement - [ ] Consider blood gas if PEF/FEV₁ <50%, poor response or deterioration - [ ] Consider IV magnesium 2 g for selected severe poor responders - [ ] Consider CXR only if alternative/complication suspected - [ ] Decide discharge vs admission vs ICU #### Before discharge - [ ] ICS-containing controller/reliever plan - [ ] Complete appropriate OCS course - [ ] Demonstrate inhaler technique - [ ] Written asthma action plan - [ ] Trigger/risk review - [ ] Avoid SABA-only long-term management - [ ] Follow-up within 2–7 days --- ### Diagnostic / management algorithm ```text Acute dyspnea/wheeze in patient with possible asthma ↓ ABC + severity + SpO₂ + PEF if feasible ↓ Anaphylaxis features? ├─ Yes → epinephrine FIRST + anaphylaxis pathway + bronchodilator └─ No ↓ Life-threatening features? ├─ Yes → emergency transfer/ICU + intensive bronchodilator │ + ipratropium + systemic steroid + controlled O₂ │ + consider Mg + early airway plan └─ No ↓ SABA by pMDI+spacer (or nebulizer when appropriate) + systemic steroid if moderate/severe + O₂ only if hypoxemic ↓ Reassess ≤1 hour ↓ Good response? ├─ Yes → observe → discharge plan with ICS-containing therapy └─ No → repeat/escalate bronchodilator + ipratropium + blood gas if severe + consider IV Mg + admit / critical-care review ↓ Fatigue, altered consciousness, rising PaCO₂, refractory hypoxemia? → prepare for invasive ventilation with long expiratory time strategy ``` --- ### Common pitfalls | Pitfall | Why dangerous | Better approach | |---|---|---| | Judging severity by wheeze volume | Silent chest may be near-fatal | Assess air entry, effort, mentation, PEF, gas exchange | | Waiting for CXR before bronchodilator/steroid | Delays effective treatment | Treat first; image selectively | | Routine 100% oxygen | Hyperoxia is unnecessary and potentially harmful | Controlled O₂ to 92–95% when SpO₂ <92% | | Repeated SABA without reassessment | Can worsen tachycardia/hypokalemia/lactate and miss fatigue | Reassess airflow and physiology | | Missing anaphylaxis | Bronchodilator does not treat systemic anaphylaxis | Epinephrine first | | Withholding steroids until “very severe” | Steroids take hours to work | Give early in moderate/severe attacks | | Discharging on SABA alone | Does not treat airway inflammation; higher future risk | ICS-containing regimen | | Intubating then ventilating at high rate | Causes dynamic hyperinflation/hypotension | Slow rate, long expiration, permissive hypercapnia | --- ### STANDARD OF CARE vs emerging vs experimental #### STANDARD OF CARE - Rapid severity assessment and repeated reassessment - Inhaled rapid bronchodilator - Controlled oxygen for hypoxemia - Early systemic corticosteroids for moderate/severe exacerbations - Ipratropium in severe acute asthma during first 1–2 hours - Selective IV magnesium in severe poor responders - Early airway/critical-care involvement in life-threatening disease - ICS-containing therapy and action plan at discharge #### EMERGING / RECENTLY EVOLVING PRACTICE - **2026 GINA acute-care oxygen threshold/target revision:** oxygen suggested below 92%, target 92–95%.[1] - Addition of **ICS-formoterol as an alternative reliever treatment for some mild acute presentations** in 2026 GINA flowcharts, while SABA remains the usual bronchodilator in acute care.[1] - Increasing use of anti-inflammatory reliever/MART strategies immediately after an exacerbation to reduce recurrence.[1-7] #### EXPERIMENTAL / SPECIALIST-ONLY - Extracorporeal support for refractory near-fatal asthma - Heliox in selected refractory cases (not routine) - Advanced bronchoscopic mucus-clearance approaches in exceptional cases - Biologic therapy is important for long-term severe asthma prevention but is **not a substitute for standard acute resuscitation** during a life-threatening attack --- ### Guideline differences and jurisdiction notes #### GINA 2026 - International strategy document - Strong emphasis on ICS-containing therapy for all asthma - Prefers Track 1 ICS-formoterol reliever strategy in adults/adolescents where available - 2026 acute oxygen approach: treat when SpO₂ <92%, target 92–95%[1] #### BTS/NICE/SIGN (UK) The 2024 joint chronic-asthma guideline does not itself replace all retained BTS/SIGN acute-attack recommendations, but it explicitly recommends against prescribing SABA without concomitant ICS and supports anti-inflammatory reliever/MART pathways.[3] #### Local formularies Exact inhaler strengths, approved age groups, AIR/MART licensing and nebulized medication doses differ by country. Always reconcile international strategy with local product labeling and emergency protocols. --- ### Exam-focused review #### Step 1 Know: - Reversible bronchoconstriction + inflammation + mucus - V/Q mismatch → hypoxemia - Severe obstruction → air trapping and dynamic hyperinflation - Beta₂ agonism → bronchodilation, tremor, tachycardia, hypokalemia #### Step 2 CK / Step 3 Priorities: - Acute severe asthma → bronchodilator + systemic steroid early - Anaphylaxis with wheeze → **epinephrine**, not “more albuterol only” - Tension pneumothorax → decompress - Drowsy patient with rising CO₂ → impending respiratory failure #### MRCP / ABIM / boards Remember: - Normal PaCO₂ can be abnormal in severe acute asthma - CXR and ABG are selective, not routine - IV magnesium is for selected severe poor responders - Aminophylline is not routine - Discharge without ICS-containing therapy is poor modern asthma care --- ### Original MCQs #### Question 1 A 24-year-old woman with asthma is speaking in single words, using accessory muscles and has SpO₂ 89% on room air. Which initial plan is best? A. Chest radiograph before treatment B. Oral antibiotic + observe C. Inhaled rapid bronchodilator, controlled oxygen, systemic corticosteroid, add ipratropium and reassess urgently D. Sedative to reduce respiratory drive E. SABA only, discharge when wheeze decreases **Answer: C.** **Explanation:** This is severe acute asthma. Treatment should begin immediately and concurrently. Imaging is selective and must not delay bronchodilation/anti-inflammatory therapy.[1] #### Question 2 A severely dyspneic patient initially had PaCO₂ 28 mm Hg. Two hours later she remains exhausted and PaCO₂ is 42 mm Hg. What is the best interpretation? A. Clear improvement because CO₂ normalized B. Impending ventilatory failure C. Metabolic alkalosis D. SABA toxicity only E. Normal finding requiring no escalation **Answer: B.** **Explanation:** Acute asthma usually causes hypocapnia. A normalizing/rising CO₂ in a patient who remains severely distressed indicates loss of ventilatory reserve and fatigue.[1] #### Question 3 A man presents with wheeze, lip swelling, generalized urticaria and hypotension minutes after eating peanuts. What should be given first? A. Inhaled salbutamol B. IV magnesium C. IM epinephrine D. Prednisolone E. Ipratropium **Answer: C.** **Explanation:** This is anaphylaxis with bronchospasm. GINA 2026 explicitly emphasizes epinephrine first; bronchodilators are adjuncts.[1] #### Question 4 Which is the strongest indication for a chest radiograph in an asthma exacerbation? A. Every patient with wheeze B. Mild attack responding to one bronchodilator dose C. Poor response with sudden unilateral chest pain and markedly reduced breath sounds D. Known asthma and normal exam after treatment E. Need to confirm bronchospasm **Answer: C.** **Explanation:** Routine CXR is not recommended, but suspected pneumothorax or another complicating process is a clear indication.[1] #### Question 5 An adult improves after ED treatment for a moderate exacerbation. Which discharge strategy best reduces future severe attacks? A. SABA alone B. Stop all inhalers after steroid course C. Ensure ICS-containing therapy, preferably an ICS-formoterol-based strategy where appropriate, plus action plan and early follow-up D. Daily antibiotics E. Maintenance oral prednisone indefinitely **Answer: C.** **Explanation:** Modern GINA strategy centers on anti-inflammatory reliever/controller treatment rather than SABA-only care; follow-up and self-management are essential.[1-7] --- ### What changed recently? #### GINA 2026 acute asthma GINA’s 2026 report added/revised acute asthma flowcharts and made several clinically important changes:[1] - If asthma occurs with anaphylaxis, **epinephrine is explicitly prioritized first**. - Supplemental oxygen is suggested when **SpO₂ <92%**, with target **92–95%**. - For mild exacerbations, **ICS-formoterol was added as an alternative reliever option** in appropriate adults/adolescents/children 6–11 depending on formulation/setting. - Discharge strategy increasingly emphasizes **MART/anti-inflammatory reliever treatment** rather than returning patients to SABA dependence. These are meaningful changes from older teaching that routinely targeted higher oxygen saturations and reflexively used SABA as the only acute reliever option in all mild presentations. --- ### Landmark and influential research - **SYGMA 1 (2018):** as-needed budesonide-formoterol reduced severe exacerbation risk versus SABA-only therapy in mild asthma, establishing the anti-inflammatory reliever concept.[4] - **SYGMA 2 (2018):** as-needed budesonide-formoterol was noninferior to maintenance budesonide for severe exacerbations with lower corticosteroid exposure, though symptom-control differences remained.[5] - **Novel START (2019):** in a pragmatic population, as-needed budesonide-formoterol reduced exacerbations versus albuterol-only therapy.[6] - **PRACTICAL (2019):** as-needed budesonide-formoterol reduced severe exacerbations compared with maintenance budesonide plus SABA in a pragmatic open-label trial.[7] - Spacer-vs-nebulizer evidence supports pMDI + spacer as an effective route for many non-life-threatening acute attacks.[8] --- ### References 1. Global Initiative for Asthma (GINA). *Global Strategy for Asthma Management and Prevention: 2026 Update*. 2026. https://ginasthma.org/2026-gina-strategy-report/ 2. Global Initiative for Asthma (GINA). *2026 Summary Guide for Asthma Management and Prevention*. 2026. https://ginasthma.org/2026-gina-summary-guide/ 3. British Thoracic Society, National Institute for Health and Care Excellence, Scottish Intercollegiate Guidelines Network. *Asthma: diagnosis, monitoring and chronic asthma management (BTS, NICE, SIGN)*. NICE NG245. Published 27 November 2024; minor update November 2025. https://www.nice.org.uk/guidance/ng245 4. O'Byrne PM, FitzGerald JM, Bateman ED, et al. Inhaled Combined Budesonide-Formoterol as Needed in Mild Asthma (SYGMA 1). *N Engl J Med*. 2018;378:1865-1876. doi:10.1056/NEJMoa1715274. 5. Bateman ED, Reddel HK, O'Byrne PM, et al. As-Needed Budesonide-Formoterol versus Maintenance Budesonide in Mild Asthma (SYGMA 2). *N Engl J Med*. 2018;378:1877-1887. doi:10.1056/NEJMoa1715275. 6. Beasley R, Holliday M, Reddel HK, et al. Controlled Trial of Budesonide-Formoterol as Needed for Mild Asthma (Novel START). *N Engl J Med*. 2019;380:2020-2030. doi:10.1056/NEJMoa1901963. 7. Hardy J, Baggott C, Fingleton J, et al. Budesonide-formoterol reliever therapy versus maintenance budesonide plus terbutaline reliever therapy in adults with mild to moderate asthma (PRACTICAL). *Lancet*. 2019;394:919-928. doi:10.1016/S0140-6736(19)31948-8. 8. Cates CJ, Welsh EJ, Rowe BH. Holding chambers (spacers) versus nebulisers for beta-agonist treatment of acute asthma. *Cochrane Database Syst Rev*. 2013;(9):CD000052. doi:10.1002/14651858.CD000052.pub3. --- ### Related topics to build next - Chronic asthma: diagnosis and long-term management - Difficult-to-treat and severe asthma - Anaphylaxis - COPD exacerbation - Respiratory failure and mechanical ventilation - Pneumothorax - Inhaler pharmacology and device technique1c:T7b05,## One-minute summary **Acute bacterial meningitis** is infection-driven inflammation of the leptomeninges and cerebrospinal fluid (CSF). It can progress over hours to **sepsis, shock, cerebral edema, seizures, raised intracranial pressure, herniation, hearing loss, neurologic disability, and death**. WHO's first global meningitis diagnosis/treatment guideline was released in 2025, followed by a practical implementation manual in May 2026.[1,2] WHO estimates bacterial meningitis causes death in roughly **1 in 6 affected people**, and about **1 in 5 survivors** develops long-term complications.[1] ### The core emergency sequence 1. **Recognize the syndrome**: fever, headache, neck stiffness, altered mental status, photophobia, vomiting, seizure, focal deficit, non-blanching rash, or sepsis; not every patient has the classic triad. 2. **Stabilize ABCs** and treat shock/seizures immediately. 3. Obtain **blood cultures and key blood tests**, but never allow diagnostics to cause a clinically significant antibiotic delay. 4. Perform **lumbar puncture before antibiotics if safe and immediately feasible**. 5. **Do not routinely obtain CT before LP.** Image first only when specific features suggest a space-occupying lesion or dangerous raised intracranial pressure. 6. Start **IV antibiotics as soon as meningitis is suspected**; NICE specifies within **1 hour of hospital arrival**.[3] 7. Give **IV dexamethasone with or before the first antibiotic dose if possible** in strongly suspected bacterial meningitis (age >3 months in NICE guidance); never delay antibiotics for dexamethasone.[3] 8. Narrow therapy once Gram stain, PCR, culture, and susceptibility data return. 9. Assess for **hearing and neurologic sequelae** and involve public health for meningococcal disease. ★ **High-yield principle:** If CT is needed before LP, **take bloods and start antibiotics first**. Imaging must not become a treatment-delay ritual.[3] --- ## Definition Meningitis is inflammation of the meninges and CSF, usually infectious. **Bacterial meningitis** refers to acute meningitis caused by bacteria, most often acquired in the community but sometimes related to neurosurgery, skull defects, penetrating trauma, CSF devices, or bacteremia. This article focuses primarily on **acute community-acquired bacterial meningitis in children beyond the neonatal period and adults**, with emphasis on adult clinical reasoning. Neonatal, post-neurosurgical, TB, cryptococcal, and chronic meningitis require specialized protocols. --- ## Epidemiology and major pathogens The pathogen distribution varies with age, vaccination, immune status, geography, and healthcare exposure. | Population / risk state | Important organisms | Practical implication | |---|---|---| | Adolescents / younger adults | *Neisseria meningitidis*, *Streptococcus pneumoniae* | Consider meningococcal sepsis/rash; droplet precautions and public-health actions | | General adults | *S. pneumoniae*, *N. meningitidis* | Pneumococcus is a major cause of severe adult disease | | Older adults / cell-mediated immune impairment | Above + *Listeria monocytogenes* | Add anti-Listeria therapy | | Asplenia / complement deficiency | Encapsulated organisms, especially meningococcus/pneumococcus | Higher invasive-disease risk | | Cochlear implant / CSF leak | Pneumococcus | Recurrent meningitis risk; vaccination/prevention critical | | Neurosurgery / CSF shunt | Staphylococci, resistant gram-negative bacilli | Not a standard community-acquired regimen; use healthcare-associated CNS infection guidance | #### Risk factors - Extremes of age - Asplenia or hyposplenia - Complement deficiency or complement-inhibitor therapy - HIV or other immunocompromise - Alcohol use disorder - Diabetes and chronic disease - Otitis, mastoiditis, sinusitis, pneumonia - Basilar skull fracture or CSF leak - Cochlear implant - Recent neurosurgery or CSF device - Crowded living environments for meningococcal transmission - Under-immunization --- ## Pathophysiology The disease usually follows: **nasopharyngeal colonization or local infection → mucosal invasion/bacteremia → crossing of the blood–brain/CSF barriers → bacterial replication in CSF → intense host inflammatory response → endothelial injury and blood–brain barrier disruption → vasogenic/cytotoxic/interstitial edema + impaired CSF flow + vasculitis/thrombosis → increased intracranial pressure and reduced cerebral perfusion.** Bacterial cell-wall products trigger cytokines and neutrophilic inflammation. Complications arise not only from bacterial burden but also from the inflammatory response, which is why appropriately timed corticosteroids can reduce selected neurologic sequelae. --- ## Clinical presentation ### Classic adult features - Fever - Severe headache - Neck stiffness - Altered mental status - Photophobia - Nausea/vomiting The “classic triad” of fever, neck stiffness, and altered consciousness is **not sensitive enough to rule out disease when incomplete**. #### Additional features - Seizure - Focal neurologic deficit - Cranial nerve palsy - Reduced GCS - Petechial or purpuric rash - Shock/DIC - Limb pain or rapidly progressive sepsis in meningococcal disease #### Infants and children Presentation may be nonspecific: irritability, poor feeding, lethargy, high-pitched cry, fever or hypothermia, vomiting, seizures, bulging fontanelle, abnormal tone. #### Older or immunocompromised adults Fever and meningeal signs may be muted. New delirium, sepsis, seizure, or unexplained decline may dominate. --- ## Red flags requiring immediate resuscitation / ICU-level concern - GCS ≤9 or rapidly declining consciousness - Recurrent/prolonged seizure - Abnormal pupils or posturing - Focal neurologic deficit - Shock, rising lactate, DIC - Purpura fulminans / rapidly spreading non-blanching rash - Respiratory failure - Signs of impending herniation - Severe hyponatremia or other metabolic complication --- ## Initial assessment and “what to do next” | Component | Assessment | Interpretation | Immediate action | Anticipate deterioration | |---|---|---|---|---| | A — Airway | GCS, protective reflexes, vomiting | Airway loss risk | Airway support/intubation when indicated | Aspiration, herniation physiology | | B — Breathing | RR, SpO₂, work of breathing | Sepsis, aspiration, pulmonary complication | Oxygen/ventilation as needed | Fatigue, ARDS | | C — Circulation | HR, BP, perfusion, rash, lactate | Septic shock/DIC | IV/IO access, sepsis resuscitation | Refractory shock, adrenal hemorrhage | | D — Disability | GCS, pupils, focal deficit, seizure, glucose | Raised ICP, stroke mimic, hypoglycemia | Treat seizure/glucose; decide LP safety | Herniation, status epilepticus | | E — Exposure | Rash, infection source, trauma/CSF leak | Meningococcus, source clue | Droplet precautions if suspected meningococcus; source management | Rapid purpura/DIC | --- ## Diagnostic strategy ### Blood tests before antibiotics when feasible NICE recommends the following in suspected bacterial meningitis:[3] - Blood culture - WBC with neutrophils - CRP, or procalcitonin if CRP unavailable - Blood glucose - Whole-blood diagnostic PCR including meningococcal and pneumococcal targets where available - HIV testing according to local policy Do **not** rule out meningitis because WBC, CRP, or procalcitonin is normal.[3] Additional tests often include electrolytes, renal/liver profile, lactate, coagulation studies, and type/screen if severe DIC or critical illness is present. --- ## Lumbar puncture: do it early, but safely NICE states that LP should be performed before antibiotics **unless it is unsafe or would cause a clinically significant delay**. If antibiotics have already been started, perform LP as soon as safely possible.[3] ### Stabilize before LP Treat/stabilize these first:[3] - Unprotected airway - Respiratory compromise - Shock - Uncontrolled seizures - Bleeding risk ### Do not perform immediate LP when there is - Extensive/rapidly spreading purpura - Infection at the LP site - Risk factors for an evolving intracranial space-occupying lesion - Clinical signs suggesting dangerous raised ICP requiring imaging first --- ## CT before lumbar puncture: NOT routine NICE explicitly advises **against routine neuroimaging before LP**.[3,4] #### Image before LP when there is - Risk of an evolving space-occupying lesion - New focal neurologic features, including seizure or posturing - Abnormal pupillary reactions - **GCS ≤9** - Progressive sustained or rapid fall in consciousness[3] #### Critical sequence when imaging is required **Bloods → antibiotics (and dexamethasone when indicated) → stabilization → neuroimaging → LP when safe.** ⚠ **Common trap:** “Possible meningitis = CT first.” This delays antibiotics and is not recommended for most patients. --- ## CSF investigations NICE recommends:[3] - RBC and WBC count with differential - Total protein - CSF glucose **with paired blood glucose** to calculate CSF:blood glucose ratio - Gram stain - Culture and antimicrobial susceptibility - PCR for relevant pathogens Store remaining CSF for additional testing if needed.[3] ### Typical CSF patterns | Feature | Bacterial | Viral | TB/fungal (typical) | |---|---|---|---| | Opening pressure | Often high | Normal or mildly high | Often high | | WBC | High, usually neutrophilic | Lymphocytic | Lymphocytic/mononuclear | | Protein | High | Mild–moderately high | High | | Glucose | Low | Usually normal | Low | | CSF:blood glucose ratio | Reduced | Usually preserved | Reduced | | Gram stain/culture | May identify organism | Negative for bacteria | Specialized stains/culture/PCR | **Exceptions are common.** Early bacterial disease can be less neutrophilic; partially treated bacterial meningitis can have altered CSF findings; immunocompromised patients can have weak pleocytosis. --- ## Empiric antibiotics ### STANDARD OF CARE: treatment must not wait NICE recommends IV antibiotics as soon as bacterial meningitis is suspected, **within 1 hour of hospital arrival**.[3] #### UK/NICE approach Before the organism is known:[3] - **Ceftriaxone** at the highest meningitis dose recommended by formulary/local guidance - If ceftriaxone is contraindicated, consider **cefotaxime** - Add **IV amoxicillin** when there are risk factors for *Listeria monocytogenes* NICE does **not** recommend routine aciclovir unless herpes simplex encephalitis is strongly suspected.[3] #### Common adult meningitis doses used internationally These are common adult regimens; always verify local guidance, renal function, body size, allergy and resistance patterns: | Drug | Common adult meningitis dosing | Role | |---|---:|---| | Ceftriaxone | **2 g IV every 12 h** (or total 4 g/day in some protocols) | Core empiric agent / pneumococcus, meningococcus, Hib coverage | | Ampicillin / amoxicillin | **2 g IV every 4 h** (local protocols may vary) | *Listeria* coverage | | Vancomycin | Weight- and renal-function based; dose/monitor to local AUC or trough protocol | Added in many North American regimens for resistant pneumococcus | | Dexamethasone | **10 mg IV every 6 h** in adults | Adjunct, ideally before/with first antibiotic | #### U.S./North American vs UK/WHO nuance Many North American empiric adult protocols use **vancomycin + a third-generation cephalosporin**, adding ampicillin when Listeria risk is present because of concern for cephalosporin-resistant pneumococci. NICE uses ceftriaxone (or cefotaxime) as its core empiric regimen and recommends specialist input for resistance risks.[3] **Do not blindly merge regimens.** Use the guideline adopted in your jurisdiction and local pneumococcal susceptibility data. --- ## Dexamethasone NICE recommends IV dexamethasone for people **over 3 months** with strongly suspected or confirmed bacterial meningitis.[3] #### Timing - Give **with or before the first antibiotic dose if possible**. - Do **not** delay antibiotics to administer dexamethasone. - If delayed by <12 hours after antibiotics, NICE advises giving it as soon as possible; if >12 hours late, obtain infection-specialist advice.[3] #### Adult dose A widely used adult regimen, supported by the landmark randomized trial and common clinical guidance, is **dexamethasone 10 mg IV every 6 hours for 4 days**.[5] #### Continue or stop when organism known NICE recommends:[3] - **Continue** if *S. pneumoniae* or *H. influenzae* type b - **Stop** for other identified organisms - If no organism is identified, seek infection-specialist advice #### Why timing matters Antibiotic-induced bacterial lysis can amplify meningeal inflammation. Steroids are most useful when present before or at the onset of this inflammatory burst. --- ## Pathogen-specific treatment and duration Exact definitive therapy depends on susceptibility and jurisdiction. | Organism | Typical targeted approach | NICE duration concept | |---|---|---| | *N. meningitidis* | Ceftriaxone/cefotaxime; penicillin/ampicillin if susceptibility proven in some systems | **5 days** if recovered[3] | | *S. pneumoniae* | Ceftriaxone/cefotaxime ± vancomycin depending susceptibility/local resistance | **10 days** if recovered[3] | | Hib | Ceftriaxone/cefotaxime | **7 days**, extend to 10 if not recovered[3] | | Group B streptococcus | Ceftriaxone/cefotaxime; specialist input | **14 days** if recovered[3] | | *Listeria monocytogenes* | Ampicillin/amoxicillin-based therapy; specialist guidance | Often prolonged, commonly ~21 days depending disease/response | | Gram-negative bacilli | Susceptibility-guided 3rd/4th-gen cephalosporin or other agent | Often ~21 days; specialist management | NICE states that when CSF suggests bacterial meningitis but blood culture/PCR are negative, initial antibiotics can be continued for **10 days**, stopping if recovered or seeking specialist advice if not.[3] --- ## Meningococcal disease Meningococcal infection may present as meningitis, meningococcemia, or both. ### Clues - Rapidly progressive sepsis - Petechiae/purpura - Limb pain - Shock - DIC - Meningism may be absent in bloodstream-predominant disease #### Infection control Use appropriate **droplet precautions** for suspected meningococcal disease according to local infection-prevention policy. #### Treatment CDC guidance updated in 2026 states empiric treatment should include an extended-spectrum cephalosporin such as **ceftriaxone or cefotaxime**. Once susceptibility is known, penicillin or ampicillin may be used when susceptible.[6] #### Public-health actions Urgently notify public health according to jurisdiction. Close contacts may require chemoprophylaxis, and vaccination may be required depending on serogroup/outbreak context. ★ **Important:** Ceftriaxone treatment effectively clears carriage after a dose; if treatment used cefotaxime or penicillin/ampicillin, additional eradication therapy may be required before discharge according to CDC guidance.[6] --- ## Supportive and critical care ### Sepsis / shock Treat according to current sepsis principles: - Rapid IV/IO access - Lactate when indicated - Appropriate fluids with repeated reassessment - Norepinephrine for persistent vasodilatory shock when indicated - Source-directed antimicrobial therapy - Organ support ### Fluids NICE advises **not routinely restricting fluids below maintenance needs** in bacterial meningitis.[3] ⚠ **Common trap:** Historic reflex fluid restriction can worsen perfusion. Correct true SIADH/hyponatremia thoughtfully, but do not impose routine dehydration. ### Intracranial pressure NICE advises against routine glycerol and against routine use of osmotic agents such as mannitol or hypertonic saline for all meningitis patients.[3] Osmotherapy is reserved for selected patients with suspected impending herniation/raised ICP under critical-care/neurospecialist guidance. General neuroprotective principles include: - Avoid hypoxemia - Avoid hypotension - Treat fever and seizures - Elevate head of bed in selected patients - Maintain appropriate ventilation; avoid unnecessary prolonged hyperventilation - Urgent neurocritical care when herniation is suspected ### Seizures Treat status epilepticus promptly with standard protocols. Persistent altered consciousness may require EEG to detect nonconvulsive seizures. --- ## Complications ### Acute neurologic - Raised ICP / cerebral edema - Brain herniation - Seizures/status epilepticus - Ischemic stroke from vasculitis/thrombosis - Cerebral venous thrombosis - Hydrocephalus - Subdural effusion/empyema - Cranial neuropathies ### Systemic - Septic shock - DIC - Purpura fulminans - Acute kidney injury - ARDS - Waterhouse–Friderichsen syndrome in fulminant meningococcemia ### Long-term WHO highlights long-term complications in approximately **20%** of bacterial meningitis survivors.[1] Important sequelae: - Sensorineural hearing loss - Cognitive impairment - Epilepsy - Motor deficits - Visual/cranial nerve deficits - Learning/behavioral problems in children - Psychological sequelae and reduced quality of life --- ## Hearing and follow-up All survivors require structured assessment for neurologic and functional sequelae. Hearing evaluation is especially important after pneumococcal/Hib disease and in children, because hearing loss can be clinically silent initially but profoundly affect development. Follow-up should address: - Audiology - Cognitive and neurologic function - Seizure recurrence - Rehabilitation needs - Vaccination status - Evaluation for predisposing CSF leak, asplenia, complement deficiency, cochlear implant issues, or immune deficiency when clinically indicated --- ## Prevention ### Vaccination Major prevention tools include: - Pneumococcal vaccination - Hib vaccination - Meningococcal ACWY vaccination - Meningococcal B vaccination in indicated populations Schedules vary by age, country, risk group, and evolving public-health recommendations. ### Meningococcal contact prophylaxis Close contacts and people exposed directly to oral/respiratory secretions can require antibiotic prophylaxis. CDC options include rifampin, ciprofloxacin, or ceftriaxone, with selection based on age, pregnancy, resistance, and local public-health advice.[6] --- ## Special populations ### Immunocompromised / older adult Have a lower threshold for *Listeria* coverage and for atypical presentation. Consider broader differential: cryptococcal, TB, fungal, viral, malignant, and drug-related meningitis. ### Pregnancy *Listeria* risk is important. Antibiotic and prophylaxis choices should be coordinated with infectious disease and obstetrics. ### Asplenia / complement inhibitor therapy High risk of invasive encapsulated organisms. Prevention with vaccination and education about urgent fever management is essential. ### Cochlear implants / CSF leak Recurrent pneumococcal meningitis risk may be elevated. Investigate anatomical predisposition and ensure appropriate vaccination. ### Neurosurgical patients Do not use a routine community-acquired pathway. Post-craniotomy, shunts, drains, and penetrating trauma raise concern for staphylococci and resistant gram-negative bacilli; use healthcare-associated ventriculitis/meningitis guidance. --- ## Important mimics and alternative diagnoses | Condition | Clues | Key discriminator | |---|---|---| | Viral meningitis | Often less toxic, normal glucose | PCR; clinical course | | HSV encephalitis | Altered behavior, focal seizures, temporal signs | Brain MRI + CSF HSV PCR; empiric aciclovir when strongly suspected | | TB meningitis | Subacute course, cranial neuropathies, low glucose | TB testing, imaging, epidemiology | | Cryptococcal meningitis | HIV/immunocompromise, high opening pressure | CSF cryptococcal antigen | | Subarachnoid hemorrhage | Thunderclap headache | CT ± LP for blood/xanthochromia | | Brain abscess | Focal deficit, seizures, source infection | MRI/CT; LP may be unsafe/unhelpful | | Autoimmune encephalitis | Psychiatric symptoms, seizures, dyskinesia | CSF/serology/EEG/MRI | | Drug-induced aseptic meningitis | Temporal medication relationship | Exclusion + history | --- ## Diagnostic / management algorithm ```text Fever/headache/neck stiffness/AMS/seizure/rash → suspect meningitis ↓ ABC stabilization ↓ Blood cultures + CBC/CRP(or PCT) + glucose + chemistries ± PCR ↓ Is immediate LP safe, and can it occur without significant antibiotic delay? ├── YES → LP: cells/diff, protein, CSF glucose + paired blood glucose, │ Gram stain, culture/susceptibility, PCR │ ↓ │ IV antibiotics immediately + dexamethasone with/before first dose │ └── NO → IV antibiotics immediately + dexamethasone when indicated ↓ Does patient meet imaging-before-LP criteria? ├── YES → stabilize + CT/MRI → LP when safe └── NO → LP as soon as safely feasible Then: Gram stain/PCR/culture + susceptibility → narrow therapy Assess seizures/ICP/shock continuously Meningococcus? → droplet precautions + public health + contact management Recovery → hearing + neurologic follow-up + prevention evaluation ``` --- ## Acute management checklist - [ ] ABCs; treat hypoxemia, shock, uncontrolled seizures - [ ] Droplet precautions if meningococcal disease suspected - [ ] Blood cultures before antibiotics if this does not delay therapy - [ ] CBC, CRP/PCT, blood glucose, chemistries; lactate/coagulation if ill - [ ] LP immediately if safe and feasible - [ ] **No routine CT before LP** - [ ] If focal signs, abnormal pupils, GCS ≤9, rapid consciousness decline, or mass-lesion risk → image first, but **antibiotics first** - [ ] IV ceftriaxone-based empiric therapy per local guideline - [ ] Add Listeria coverage when risk factors present - [ ] Add vancomycin when required by local pneumococcal-resistance policy (common North American practice) - [ ] Dexamethasone with/before first antibiotic dose if indicated; never delay antibiotics - [ ] CSF cell count/diff, protein, glucose + paired serum glucose, Gram stain, culture, PCR - [ ] Narrow regimen and define duration once organism/susceptibility known - [ ] Monitor sodium, renal function, neurologic status, seizures, perfusion - [ ] Public-health notification/contact prophylaxis if meningococcus - [ ] Arrange hearing and neurologic follow-up --- ## Common pitfalls | Pitfall | Why dangerous | Better approach | |---|---|---| | Waiting for the classic triad | Triad is insensitive | Use overall syndrome and risk state | | CT on every suspected case | Delays LP and antibiotics | CT only for defined risk features | | Delaying antibiotics until after imaging/LP | Mortality/neurologic harm | Treat within 1 hour; diagnostics only if they do not delay | | Normal CRP/WBC “rules out” disease | False reassurance | NICE explicitly warns against this | | No paired serum glucose with CSF | Loses useful CSF:blood ratio | Draw blood glucose with LP | | Forgetting Listeria in older/immunocompromised patient | Cephalosporins do not reliably cover Listeria | Add ampicillin/amoxicillin when risk present | | Routine aciclovir for all meningitis | Unnecessary treatment | Use when HSV encephalitis is strongly suspected | | Giving dexamethasone hours later without thought | Benefit depends on timing/pathogen | Give with/before antibiotics; follow guideline if delayed | | Routine fluid restriction | May worsen perfusion | Maintain appropriate fluids; treat specific sodium disorder | | Missing meningococcal public-health actions | Preventable secondary cases | Isolation + urgent notification + contact prophylaxis | --- ## Current guideline changes ### WHO 2025 guideline + 2026 practical manual WHO issued its **first global guideline on meningitis diagnosis, treatment and care on 10 April 2025**, covering community-acquired acute meningitis across ages >1 month and including diagnostics, antibiotics, adjunctive therapy, supportive care, and long-term effects.[1] On **26 May 2026**, WHO released a practical manual with job aids and decision algorithms to operationalize these recommendations.[2] **STANDARD OF CARE implications:** rapid recognition, prompt effective antibiotics, rational LP/imaging, supportive care, and active management of sequelae. ### NICE NG240 (2024) Important UK practice points include:[3] - Antibiotics within 1 hour of hospital arrival - Ceftriaxone as core empiric therapy; add amoxicillin for Listeria risk - No routine CT before LP - Explicit criteria for imaging-first cases - Dexamethasone for strongly suspected/confirmed bacterial meningitis >3 months, with/before antibiotics if possible - Pathogen-specific durations including 5 days for meningococcus and 10 days for pneumococcus if recovered - No routine fluid restriction - No routine osmotic therapy ### Jurisdiction differences The major difference clinicians encounter is empiric pneumococcal resistance coverage: **many U.S. protocols add vancomycin**, whereas NICE does not use routine vancomycin in its baseline community-acquired regimen. This reflects antimicrobial-resistance assumptions and local epidemiology, not a fundamental disagreement that therapy should be broad enough to cover likely resistant pathogens. --- ## Evidence classification ### STANDARD OF CARE - Immediate IV antibiotics once bacterial meningitis is suspected - LP as early as safely possible - Selective, not routine, neuroimaging before LP - Dexamethasone given before/with first antibiotic dose in appropriate patients - Pathogen-directed narrowing - Public-health intervention for meningococcal disease - Hearing/neurologic follow-up ### EMERGING EVIDENCE - Faster multiplex molecular diagnostics and metagenomic testing - Biomarker-assisted bacterial-vs-viral differentiation - Improved neurocritical-care phenotyping and individualized ICP management - Better long-term neurocognitive rehabilitation strategies ### EXPERIMENTAL / INVESTIGATIONAL Novel host-directed anti-inflammatory strategies, precision diagnostics, and new adjunctive therapies should not replace immediate antibiotics, dexamethasone when indicated, and basic neurocritical/sepsis care outside trials. --- ## Exam-focused review ### Step 1 / Foundations Know: - Bacterial entry into CSF and inflammatory BBB injury - Neutrophilic CSF response - Low CSF glucose from bacterial/leukocyte metabolism and impaired transport - Raised protein from BBB disruption - Encapsulated organisms and splenic/complement defense ### Step 2 CK Classic next-best-step questions: - Suspected meningitis, stable, no focal deficit/ICP sign → **LP promptly**, then immediate antibiotics; do not order routine CT. - Focal deficit or GCS ≤9 → **blood cultures + antibiotics first**, image, then LP when safe. - Older/immunocompromised adult → add **Listeria coverage**. - Meningococcal rash/sepsis → antibiotics immediately + droplet precautions + public health. ### Step 3 / Resident Add: - Empiric regimen selection by age/immunity/resistance - Dexamethasone timing - Interpretation of partially treated CSF - Sepsis/ICP/seizure management - Contact prophylaxis - De-escalation and duration ### MRCP / ABIM / boards Expect nuance on: - CT-before-LP criteria - Pneumococcal vs meningococcal durations - Dexamethasone continuation by organism - Listeria risk - CSF patterns and exceptions - Public-health management --- ## Original MCQs #### 1. A 23-year-old has fever, headache, photophobia and neck stiffness. GCS 15, no focal deficits, normal pupils, stable vital signs. Best next step? A. CT head before any other test B. Lumbar puncture promptly if immediately available and safe, without delaying antibiotics C. MRI brain D. Discharge with oral antibiotics **Answer: B.** Routine neuroimaging before LP is not recommended. LP should precede antibiotics only when safe and when it will not cause clinically significant delay. #### 2. A 67-year-old with suspected meningitis has a new right arm weakness and GCS 8. Best sequence? A. LP first, then antibiotics B. CT first, then blood cultures, then antibiotics C. Blood cultures + immediate antibiotics/dexamethasone as indicated + stabilization, then imaging, then LP when safe D. EEG only **Answer: C.** Focal deficit/GCS ≤9 are imaging-before-LP criteria, but antibiotics must not wait for the scan. #### 3. Which additional empiric coverage is especially important in an older or cell-mediated immunocompromised adult? A. Metronidazole for *C. difficile* B. Ampicillin/amoxicillin for *Listeria monocytogenes* C. Oseltamivir D. Doxycycline for Lyme disease in every case **Answer: B.** Listeria is not reliably covered by third-generation cephalosporins. #### 4. When should dexamethasone ideally be administered? A. Only after culture confirms pneumococcus B. 24 hours after antibiotics C. Before or with the first antibiotic dose D. Only at discharge **Answer: C.** Benefit is linked to blunting the inflammatory response triggered by bacterial lysis. #### 5. CSF shows 2,400 WBC/µL (90% neutrophils), high protein, low glucose, and a low CSF:serum glucose ratio. Most likely diagnosis? A. Typical bacterial meningitis B. Migraine C. Normal CSF D. Isolated peripheral neuropathy **Answer: A.** This is the classic bacterial pattern, although real cases can vary. --- ## References 1. World Health Organization. **WHO guidelines on meningitis diagnosis, treatment and care.** 10 April 2025. ISBN **978-92-4-010804-2**. https://www.who.int/publications/i/item/9789240108042 2. World Health Organization. **WHO practical manual on meningitis diagnosis, treatment and care.** 26 May 2026. ISBN **978-92-4-012102-7**. https://www.who.int/publications/i/item/9789240121027 3. National Institute for Health and Care Excellence (NICE). **Meningitis (bacterial) and meningococcal disease: recognition, diagnosis and management. NG240.** Published March 2024. https://www.nice.org.uk/guidance/ng240 4. NICE. **Rationale and impact: neuroimaging and lumbar puncture, NG240.** 2024. https://www.nice.org.uk/guidance/ng240/chapter/rationale-and-impact 5. de Gans J, van de Beek D; European Dexamethasone in Adulthood Bacterial Meningitis Study Investigators. **Dexamethasone in adults with bacterial meningitis.** *N Engl J Med.* 2002;347:1549–1556. doi: **10.1056/NEJMoa021334**. 6. Centers for Disease Control and Prevention. **Clinical Guidance for Meningococcal Disease.** Updated 2026. https://www.cdc.gov/meningococcal/hcp/clinical-guidance/index.html 7. Médecins Sans Frontières. **Bacterial meningitis — Medical Guidelines.** Current online edition. https://medicalguidelines.msf.org/en/viewport/CG/english/bacterial-meningitis-16689907.html 8. World Health Organization. **Defeating meningitis by 2030: a global road map.** Geneva: WHO; 2021. https://www.who.int/initiatives/defeating-meningitis-by-2030 --- **Review trigger:** Re-review when WHO, NICE, CDC, IDSA/ESCMID, or national antimicrobial guidance changes empiric regimens, dexamethasone recommendations, LP/imaging criteria, meningococcal prophylaxis, or vaccine schedules.1d:T76cc,## One-minute summary **Acute coronary syndrome (ACS)** is the clinical spectrum caused most often by acute coronary atherothrombosis after plaque rupture or erosion and includes **ST-elevation myocardial infarction (STEMI), non-ST-elevation myocardial infarction (NSTEMI), and unstable angina (UA)**. Modern care is built around five simultaneous priorities: **recognize ischemia, obtain/interpret a 12-lead ECG rapidly, use high-sensitivity cardiac troponin serially, start evidence-based antithrombotic/anti-ischemic therapy, and choose the correct revascularization strategy without delay**.[1–4] The 2025 ACC/AHA/ACEP/NAEMSP/SCAI ACS guideline emphasizes DAPT, radial access for PCI, intravascular imaging for PCI guidance, complete revascularization in appropriate multivessel disease, prompt revascularization in cardiogenic shock, intensive lipid lowering, and cardiac rehabilitation.[1,2] The 2023 ESC ACS guideline similarly integrates STEMI and NSTE-ACS in one pathway and stresses high-sensitivity troponin algorithms and time-sensitive invasive care.[3] ### Immediate priorities 1. **ABCs + monitor + IV access**; treat shock, malignant arrhythmia, pulmonary edema, or cardiac arrest first. 2. **12-lead ECG promptly** and repeat if symptoms continue or the first tracing is nondiagnostic. 3. **High-sensitivity troponin** with an assay-specific accelerated serial algorithm; do not use a single universal numeric cutoff across assays. 4. **Aspirin immediately** unless true contraindication. 5. Determine whether this is **STEMI/occlusion requiring immediate reperfusion** versus **NSTE-ACS requiring risk-stratified invasive management**. 6. Add a **P2Y12 inhibitor + parenteral anticoagulation** according to the reperfusion/invasive strategy and bleeding risk. 7. Start **high-intensity statin** and secondary prevention early. ★ **High-yield principle:** In suspected ACS, the ECG determines the urgent reperfusion pathway; troponin helps diagnose myocardial injury/infarction but should **not delay reperfusion** for a clear STEMI pattern with an appropriate clinical presentation. --- ## Definition and classification ACS describes acute myocardial ischemia caused predominantly by an unstable atherosclerotic coronary lesion and thrombosis. The 2025 U.S. guideline focuses mainly on **type 1 ACS**, where plaque disruption and coronary thrombosis are the mechanism.[1] | Syndrome | ECG pattern | Troponin | Core concept | |---|---|---|---| | STEMI | Persistent ST elevation or an accepted STEMI-equivalent/occlusion pattern in the right context | Usually rises, but may initially be normal | Acute coronary occlusion or near-occlusion requiring immediate reperfusion | | NSTEMI | No persistent ST elevation; may show ST depression, T-wave inversion, transient elevation, or a nondiagnostic ECG | Rise/fall with ≥1 value above assay-specific 99th percentile plus evidence of ischemia | Myocardial infarction without classic persistent ST elevation | | Unstable angina | No persistent ST elevation | No biomarker evidence meeting MI criteria | Ischemic symptoms without detectable acute myocardial necrosis; less common in the high-sensitivity troponin era | ### Myocardial injury is not automatically myocardial infarction Troponin elevation means **myocardial injury**, not necessarily ACS. MI requires acute myocardial injury plus evidence of ischemia. Important alternative causes include sepsis, tachyarrhythmia, myocarditis, pulmonary embolism, acute heart failure, severe anemia, renal disease with dynamic injury, and supply-demand mismatch (type 2 MI). --- ## Pathophysiology The usual sequence is: **lipid-rich atherosclerotic plaque → plaque rupture or endothelial erosion → platelet adhesion/activation → thrombin generation → fibrin-rich thrombus → abrupt reduction in coronary blood flow → myocardial ischemia → myocyte necrosis if ischemia persists.** Ischemia begins subendocardially because wall stress and perfusion vulnerability are highest there. With sustained complete occlusion, necrosis can progress toward the epicardium. Infarct size is influenced by occlusion duration, collateral supply, myocardial oxygen demand, ischemic preconditioning, reperfusion timing, and microvascular obstruction. ### STEMI vs NSTEMI is an ECG phenotype, not a complete anatomy report Some acute coronary occlusions do not produce classic ST elevation. Conversely, ST elevation can be caused by pericarditis, early repolarization, left ventricular aneurysm, Takotsubo syndrome, electrolyte disorders, and other mimics. Clinical reasoning and serial ECGs matter. --- ## Risk factors Major atherosclerotic risk factors include: - Age and family history of premature ASCVD - Cigarette smoking - Hypertension - Diabetes mellitus - Dyslipidemia - Chronic kidney disease - Obesity and physical inactivity - Established coronary, cerebrovascular, or peripheral arterial disease - Chronic inflammatory disease Additional precipitants or modifiers include cocaine/amphetamine exposure, severe emotional or physiologic stress, acute infection, anemia, uncontrolled hypertension, and perioperative stress. --- ## Clinical presentation ### Typical ischemic symptoms - Retrosternal pressure, heaviness, squeezing, burning, or tightness - Radiation to arm(s), shoulder, neck, jaw, back, or epigastrium - Dyspnea - Diaphoresis - Nausea/vomiting - Sense of impending doom - Symptoms provoked by exertion and persistent at rest in acute presentations ### Atypical or less obvious presentations Older adults, women, and patients with diabetes or CKD may present with: - Dyspnea without prominent pain - Weakness or fatigue - Syncope/presyncope - Nausea or epigastric discomfort - Acute heart failure - Confusion Do not dismiss ACS because pain is described as “burning,” “indigestion,” or is not left-sided. ### Red flags for immediate instability - Hypotension, cool extremities, altered mentation - Ongoing severe chest pain despite initial therapy - Ventricular tachycardia/fibrillation - High-grade AV block or severe bradycardia - Acute pulmonary edema - Mechanical complication murmur - Recurrent dynamic ST changes - Cardiac arrest --- ## Initial assessment: first 10 minutes ### Core workflow | Component | Assessment | Interpretation | Immediate action | Anticipate deterioration | |---|---|---|---|---| | Airway/Breathing | Work of breathing, SpO₂, lung exam | Pulmonary edema, hypoxemia, alternative diagnosis | Oxygen only when clinically indicated; ventilatory support if needed | Acute LV failure, respiratory fatigue | | Circulation | HR, BP, perfusion, pulses, JVP | Shock, RV infarction, mechanical complication, arrhythmia | Monitor, IV access, cautious fluids if appropriate, shock pathway | Cardiogenic shock, VT/VF, AV block | | ECG | 12-lead ECG; right/posterior leads when indicated | STEMI/occlusion, ischemia, alternate diagnosis | Activate reperfusion pathway when indicated | Dynamic evolution; repeat ECG | | Biomarkers | hs-cTn serially | Acute myocardial injury pattern | Use validated assay-specific algorithm | Early presenters may have initially normal value | | History | Onset, quality, duration, bleeding history, anticoagulants, PDE5 inhibitors, prior stroke/TIA, allergy | Determines differential and treatment safety | Do not delay reperfusion for exhaustive history | Bleeding, medication contraindications | #### ECG Obtain a 12-lead ECG as early as possible in suspected ACS. Repeat ECGs if symptoms persist or recur, and consider: - **Right-sided leads (especially V4R)** for inferior MI with possible RV involvement - **Posterior leads V7–V9** when posterior MI is suspected, e.g., ST depression V1–V3 with a compatible presentation #### High-sensitivity troponin Use the laboratory's validated **high-sensitivity cardiac troponin (hs-cTn)** assay and accelerated serial algorithm. ESC guidance supports 0/1-hour or 0/2-hour pathways with assay-specific thresholds.[3,4] Interpretation requires: - Absolute concentration relative to the assay's 99th percentile - Rise/fall (delta) - Time since symptom onset - Renal function and chronic structural heart disease - Clinical/ECG evidence of ischemia ⚠ **Common trap:** A chronically elevated troponin in CKD does not prove NSTEMI. Look for a dynamic change and ischemic context. --- ### Differential diagnosis of acute chest pain | Diagnosis | Clues favoring diagnosis | Distinguishing test/findings | Immediate hazard | |---|---|---|---| | ACS | Pressure, diaphoresis, dynamic ECG/troponin | Serial ECG + hs-cTn | Arrhythmia, infarction, shock | | Aortic dissection | Abrupt tearing pain, pulse/BP differential, neuro deficit | CT angiography/TEE | Rupture; anticoagulation can be catastrophic | | Pulmonary embolism | Pleuritic pain, dyspnea, tachycardia, VTE risk | CT pulmonary angiography or V/Q | Obstructive shock | | Pericarditis | Pleuritic/positional pain, diffuse ST elevation/PR depression | ECG, echo | Tamponade if effusion | | Myocarditis | Viral prodrome, variable ECG, troponin, noncoronary pattern | CMR, echo, selective biopsy | Ventricular arrhythmia/shock | | Tension pneumothorax | Sudden dyspnea, unilateral absent breath sounds, shock | Clinical diagnosis | Immediate death without decompression | | Esophageal rupture | Severe pain after vomiting, systemic toxicity | CT/esophagram | Mediastinitis/sepsis | | GI/musculoskeletal pain | Reproducible or meal-related features may occur | Diagnosis of exclusion in high-risk cases | Risk is missed ACS | ★ **Exam pearl:** Do not give antithrombotics reflexively to undifferentiated tearing chest pain before considering dissection. --- ## STEMI and acute coronary occlusion ### Primary PCI is preferred when timely Primary PCI is the preferred reperfusion strategy when it can be performed within an appropriate system delay. ESC guidance recommends primary PCI when achievable within **120 minutes from STEMI diagnosis**; if timely PCI cannot be achieved and symptom onset is within 12 hours with no contraindication, fibrinolysis is indicated, followed by immediate transfer to a PCI-capable center.[3,5] #### STEMI network principles - Activate the cath lab early. - EMS should preferentially transport to a PCI-capable center when system targets can be met. - Do not wait for troponin when the clinical/ECG diagnosis is clear. - After fibrinolysis, transfer to PCI capability even if symptoms improve. - Rescue PCI is required for failed fibrinolysis or ongoing instability/ischemia. #### Cardiogenic shock Prompt revascularization remains a **Class 1** principle in ACS-related cardiogenic shock.[1,2] Shock management requires a multidisciplinary approach: airway/ventilation when necessary, invasive hemodynamic assessment in selected cases, vasopressor/inotrope support, and mechanical circulatory support only in carefully selected patients because benefit and complications vary by device and phenotype. --- ## NSTE-ACS: risk-stratified invasive management NSTE-ACS includes NSTEMI and unstable angina. An invasive strategy is recommended for ACS, but timing depends on risk.[3] #### Very high-risk features: immediate invasive evaluation Examples include: - Hemodynamic instability/cardiogenic shock - Recurrent or refractory chest pain despite medical treatment - Life-threatening arrhythmia or cardiac arrest attributed to ischemia - Mechanical complication - Acute heart failure clearly driven by ongoing ischemia - Recurrent dynamic ST-segment changes, particularly intermittent ST elevation #### High-risk features Features supporting early/inpatient invasive care include confirmed NSTEMI, significant dynamic ST/T changes, and high clinical risk (e.g., elevated GRACE risk). ESC guidance states an early invasive strategy (<24 h) should be considered in high-risk NSTE-ACS.[3] #### GRACE risk score The GRACE score estimates mortality using age, heart rate, systolic BP, creatinine, Killip class, cardiac arrest, ST deviation, and biomarkers. It is useful for prognosis and invasive-timing decisions, but it does not replace clinical judgment. --- ## Acute pharmacotherapy ### STANDARD OF CARE #### Aspirin The 2025 ACC/AHA guideline dosing table recommends:[1] - **Loading:** **162–325 mg orally**, non-enteric coated; chew when possible for faster effect. - **Maintenance:** **75–100 mg orally daily**. Aspirin is generally continued long term unless contraindicated or a specific antithrombotic strategy modifies it. #### P2Y12 inhibitors For patients undergoing PCI, **ticagrelor or prasugrel is preferred over clopidogrel** when not contraindicated.[1,2] | Agent | Loading | Maintenance | Key cautions | |---|---:|---:|---| | Ticagrelor | 180 mg PO | 90 mg PO twice daily | Dyspnea, bleeding; keep aspirin maintenance ≤100 mg/day | | Prasugrel | 60 mg PO | 10 mg daily if ≥60 kg and <75 y; 5 mg daily if <60 kg or age ≥75 y with caution | **Contraindicated with prior stroke/TIA**; higher bleeding risk | | Clopidogrel | 300 or 600 mg PO without fibrinolysis | 75 mg daily | Variable response; used when potent agents unsuitable | | Clopidogrel with fibrinolysis | 300 mg if age ≤75 y; 75 mg initial dose if >75 y | 75 mg daily | Standard P2Y12 option with fibrinolysis | #### DAPT duration For ACS patients **without high bleeding risk**, aspirin plus an oral P2Y12 inhibitor for **at least 12 months** is the default.[1,2] Bleeding-reduction strategies include: - PPI in patients at GI bleeding risk - In selected patients tolerating ticagrelor-based DAPT after PCI, transition to ticagrelor monotherapy ≥1 month after PCI - If chronic oral anticoagulation is required, discontinue aspirin 1–4 weeks after PCI and continue a P2Y12 inhibitor (preferably clopidogrel) with anticoagulation, individualized to ischemic and bleeding risk.[2] #### Anticoagulation Parenteral anticoagulation is part of acute ACS management, selected according to strategy and renal function (e.g., UFH, enoxaparin, or bivalirudin in appropriate settings). Dosing should follow the local PCI/fibrinolysis protocol because the required dose depends on whether the patient is proceeding to PCI, has already received anticoagulant, renal function, and activated clotting time targets. #### Nitrates For ischemic discomfort or hypertensive pulmonary congestion, sublingual nitroglycerin is commonly used if hemodynamically appropriate. The 2025 guideline cautions against nitrates when: - SBP <90 mmHg or >30 mmHg below baseline - Suspected RV infarction - Recent PDE5 inhibitor exposure: approximately **12 h after avanafil, 24 h after sildenafil/vardenafil, 48 h after tadalafil**.[1] Nitrates improve symptoms; they are **not a substitute for reperfusion** and have not been shown to reduce mortality in modern ACS care. #### Analgesia Opioids are reserved for persistent severe pain despite other anti-ischemic therapy. The 2025 guideline notes morphine **2–4 mg IV**, repeat every 5–15 minutes if needed, with careful monitoring; opioids can delay absorption/effect of oral P2Y12 inhibitors.[1] #### Oxygen Do **not** use routine oxygen solely because ACS is suspected when oxygenation is adequate. Give supplemental oxygen for hypoxemia or respiratory distress and titrate according to the patient's condition and local protocol. #### Beta-blocker In ACS without contraindications, the 2025 guideline recommends **early oral beta-blocker initiation within 24 hours** to reduce reinfarction and ventricular arrhythmias.[1] Delay/avoid in cardiogenic shock, decompensated acute HF, severe bradycardia, high-grade AV block without pacing, or other contraindications. #### High-intensity statin High-intensity statin therapy is recommended for all ACS patients unless contraindicated.[2] Common high-intensity regimens include: - **Atorvastatin 40–80 mg daily** - **Rosuvastatin 20–40 mg daily** The 2025 guideline recommends adding a nonstatin lipid-lowering agent when LDL-C remains **≥70 mg/dL (≥1.8 mmol/L)** on maximally tolerated statin; adding a nonstatin is also reasonable at **55–69 mg/dL** in selected patients.[2] #### ACE inhibitor / ARB and mineralocorticoid receptor antagonist ACEi/ARB is indicated particularly in higher-risk ACS patients (e.g., LVEF ≤40%, hypertension, diabetes, or anterior STEMI). An MRA is indicated for LVEF ≤40% with HF symptoms and/or diabetes when renal function and potassium permit.[1] --- ## PCI and revascularization ### Access and imaging The 2025 guideline recommends **radial access over femoral access** for PCI in ACS to reduce bleeding, vascular complications, and death.[1,2] **Intravascular imaging-guided PCI** is now a **Class 1, Level A** recommendation in the 2025 U.S. guideline.[2] ### Complete revascularization For appropriate STEMI and NSTE-ACS patients with multivessel disease, a strategy of complete revascularization is recommended/strongly favored, with timing and method determined by anatomy, comorbidities, shock status, renal function, lesion complexity, and surgical candidacy.[1,2] ⚠ **Shock exception:** Immediate multivessel PCI in cardiogenic shock is not automatically beneficial; culprit-vessel revascularization remains the immediate priority in many cases, with staged treatment of nonculprit disease according to anatomy and stability. --- ## Complications ### Electrical - Ventricular tachycardia/fibrillation - Accelerated idioventricular rhythm after reperfusion - Sinus bradycardia - AV block, especially inferior MI - Atrial fibrillation Treat unstable arrhythmias according to ACLS while correcting ischemia, hypoxia, potassium, magnesium, and acid-base abnormalities. ### Mechanical — think days after MI, sudden collapse or new murmur | Complication | Typical clue | Hemodynamics / echo | Action | |---|---|---|---| | Papillary muscle rupture → acute MR | Sudden pulmonary edema, shock, new systolic murmur | Severe eccentric MR | Emergency surgery; stabilize with afterload reduction/mechanical support when appropriate | | Ventricular septal rupture | New harsh holosystolic murmur, shock | Left-to-right shunt | Urgent surgical/interventional consultation | | Free-wall rupture | Sudden PEA, tamponade | Pericardial blood/effusion | Emergency surgical management | | LV aneurysm/pseudoaneurysm | Persistent ST changes, HF/embolism | Structural abnormality on echo/CT/CMR | Specialist management; pseudoaneurysm has rupture risk | ### Pump failure - Acute LV failure/pulmonary edema - RV infarction with preload sensitivity - Cardiogenic shock #### RV infarction pearl Suspect with inferior MI, hypotension, elevated JVP, and clear lungs. Obtain right-sided leads. Avoid aggressive nitrates/diuresis if preload dependent; give cautious fluid only if clinically appropriate and reassess frequently. --- ## Special populations ### Older adults and frailty Do not withhold evidence-based ACS care based solely on age. Balance invasive benefit against frailty, cognition, bleeding risk, kidney disease, goals of care, and functional status. ### Chronic kidney disease - hs-cTn may be chronically elevated; rely on dynamic change and clinical context. - Adjust renally cleared drugs. - Minimize contrast burden while avoiding harmful delays in indicated revascularization. ### Patients requiring oral anticoagulation Triple therapy markedly increases bleeding. The 2025 guideline favors early aspirin discontinuation (1–4 weeks after PCI) with continuation of oral anticoagulation plus a P2Y12 inhibitor, usually clopidogrel, when long-term anticoagulation is required.[2] ### Prior stroke/TIA **Prasugrel is contraindicated.** Choose another P2Y12 inhibitor when indicated. ### Pregnancy ACS in pregnancy is uncommon and more likely to involve mechanisms such as spontaneous coronary artery dissection. Management requires a pregnancy-heart team; maternal stabilization and indicated reperfusion take priority, while medication and radiation choices are individualized. --- ## Secondary prevention after ACS ### Before discharge - Smoking cessation treatment - Blood pressure optimization - Diabetes management - High-intensity statin ± nonstatin therapy - Antiplatelet plan documented with duration and bleeding strategy - Echocardiographic assessment of LVEF when appropriate - Cardiac rehabilitation referral - Exercise, weight, diet, and adherence counseling - Review driving/work restrictions per jurisdiction The 2025 guideline recommends a fasting lipid panel **4–8 weeks** after starting or adjusting lipid-lowering therapy and recommends referral to cardiac rehabilitation before discharge.[2] #### Cardiac rehabilitation Cardiac rehabilitation reduces recurrent events, improves functional status and quality of life, and is a Class 1 component of contemporary ACS secondary prevention.[2] --- ## Current guideline changes and areas of nuance ### 2025 ACC/AHA/ACEP/NAEMSP/SCAI — major practical updates **STANDARD OF CARE** - DAPT remains foundational. - Ticagrelor/prasugrel preferred over clopidogrel for PCI when appropriate. - Default DAPT ~12 months when bleeding risk is not high. - Radial PCI access favored. - Intravascular imaging-guided PCI elevated to Class 1. - Complete revascularization emphasized. - High-intensity statin for all ACS. - More aggressive nonstatin lipid-lowering thresholds. - Cardiac rehab referral before discharge.[1,2] ### 2023 ESC vs 2025 U.S. guideline Both support rapid hs-cTn pathways, invasive management for high-risk ACS, potent antiplatelet therapy, radial access, and complete revascularization in appropriate patients. Important practical differences may arise in preferred P2Y12 timing, exact invasive-timing categories, local fibrinolysis systems, and antithrombotic de-escalation strategies. Follow the locally adopted guideline and cath-lab protocol. ### EMERGING EVIDENCE - Individualized antiplatelet de-escalation and monotherapy strategies continue to evolve. - Mechanical circulatory support for selected AMI cardiogenic shock remains an area of active patient-selection research. - Physiology- and imaging-guided complete revascularization strategies continue to be refined. ### EXPERIMENTAL / INVESTIGATIONAL No investigational therapy should replace timely reperfusion, guideline antithrombotic treatment, and secondary prevention outside a trial or specialist protocol. --- ## Acute management checklist ### Suspected ACS - [ ] ABCs; identify shock, pulmonary edema, arrhythmia, cardiac arrest - [ ] Cardiac monitor + defibrillator availability - [ ] IV access - [ ] 12-lead ECG promptly; repeat if nondiagnostic - [ ] Right/posterior leads if indicated - [ ] hs-cTn serial algorithm - [ ] CBC, electrolytes, creatinine, glucose; coagulation studies when relevant - [ ] Aspirin 162–325 mg chewed unless contraindicated - [ ] Determine STEMI/occlusion vs NSTE-ACS pathway - [ ] P2Y12 inhibitor based on strategy and bleeding risk - [ ] Parenteral anticoagulation based on strategy - [ ] Nitrate only if appropriate; check BP/RV infarct/PDE5 exposure - [ ] Oxygen only if indicated - [ ] High-intensity statin - [ ] Early beta-blocker if stable and no contraindication - [ ] Echocardiography for LV function/complications as indicated - [ ] Document DAPT duration and bleeding mitigation - [ ] Cardiac rehab + secondary prevention plan --- ## Diagnostic / management algorithm ```text Acute chest discomfort / dyspnea / ischemic equivalent ↓ ABCs + monitor + IV + 12-lead ECG + hs-cTn ↓ Persistent ST elevation / occlusion pattern with compatible syndrome? ├── YES → STEMI reperfusion pathway │ ├─ Primary PCI achievable within system target → PCI │ └─ PCI not achievable within ~120 min, onset ≤12 h, │ no contraindication → fibrinolysis + transfer to PCI center │ └── NO → NSTE-ACS pathway ↓ Serial hs-cTn + repeat ECG + risk assessment ↓ Very high risk / instability? → Immediate invasive strategy High risk? → Early/inpatient invasive strategy Low risk / ACS ruled out? → Evaluate alternative diagnosis / safe disposition At all stages: Aspirin + strategy-appropriate P2Y12 + anticoagulation + high-intensity statin Treat shock/arrhythmia/HF immediately; reassess continuously ``` --- ## Common pitfalls | Pitfall | Why it is dangerous | Better approach | |---|---|---| | Waiting for troponin before activating clear STEMI | Delays reperfusion | Treat ECG + clinical syndrome as time-critical | | Treating every troponin elevation as type 1 NSTEMI | Causes diagnostic anchoring/bleeding risk | Distinguish injury, type 1 MI, type 2 MI, myocarditis, PE, etc. | | One normal ECG ends the workup | ACS can be dynamic | Repeat ECG during symptoms and use posterior/right leads when indicated | | Routine oxygen in normoxemia | No benefit; potential harm | Give for hypoxemia/respiratory distress | | Nitrates in RV infarction or after PDE5 inhibitor | Severe hypotension | Check hemodynamics and medication history | | Prasugrel in prior stroke/TIA | Major bleeding risk | Use alternative P2Y12 agent | | Ignoring bleeding risk when planning DAPT | Preventable hemorrhage | Use PPI, shortened/modified strategies when appropriate | | Discharge without rehab/lipid plan | Misses high-value prevention | Document secondary prevention before discharge | --- ## Exam-focused review ### Foundation / Step 1 Know plaque rupture/erosion, platelet activation, thrombin/fibrin, subendocardial vulnerability, transmural progression, and the physiologic consequences of reduced coronary blood flow. ### Step 2 CK Priority questions usually ask: **What must happen next?** - STEMI ECG → reperfusion, not stress testing. - Ongoing ischemia with instability → invasive management. - Troponin rise/fall + ischemic evidence without ST elevation → NSTEMI. - Inferior MI + hypotension + clear lungs → consider RV infarction; obtain right-sided leads and avoid nitrates. - New murmur + shock days after MI → mechanical complication. ### Step 3 / Resident Add strategy details: reperfusion timing, fibrinolysis contraindications, antithrombotic selection, bleeding mitigation, shock phenotype, mechanical complications, secondary prevention. ### MRCP / ABIM / boards Expect nuance around: - Type 1 vs type 2 MI - Dynamic hs-cTn interpretation - GRACE risk - Antiplatelet contraindications - DAPT duration in bleeding risk / anticoagulation - Post-MI LV dysfunction therapy - Mechanical complications --- ## Original MCQs #### 1. A 61-year-old man has 90 minutes of crushing chest pain. ECG shows 3 mm ST elevation in V2–V5. Initial hs-cTn is within the reference range. What is the best next step? A. Repeat troponin in 3 hours before treatment B. Exercise stress testing C. Activate immediate reperfusion/primary PCI pathway D. CT coronary angiography first **Answer: C.** Early troponin can be normal. A diagnostic STEMI pattern with an appropriate syndrome requires immediate reperfusion; biomarkers must not delay treatment. #### 2. A patient with inferior STEMI becomes hypotensive after sublingual nitroglycerin. Lungs are clear and JVP is elevated. Best next diagnostic step? A. V4R right-sided ECG lead B. D-dimer C. CT pulmonary angiography D. Stress echocardiography **Answer: A.** The pattern strongly suggests RV infarction with preload dependence. #### 3. Which P2Y12 inhibitor is contraindicated in a patient with prior ischemic stroke? A. Clopidogrel B. Ticagrelor C. Prasugrel D. Cangrelor **Answer: C.** Prasugrel is contraindicated after prior stroke/TIA because of bleeding risk. #### 4. A stable ACS patient undergoes PCI and has no high bleeding risk. What is the contemporary default DAPT duration? A. 48 hours B. 1 month C. 6 weeks D. At least 12 months **Answer: D.** The 2025 ACC/AHA guideline uses at least 12 months as the default in patients without high bleeding risk. #### 5. A patient with NSTEMI has shock, ongoing ischemic pain, and recurrent VT despite initial therapy. What invasive strategy is appropriate? A. Outpatient angiography B. Immediate invasive evaluation C. Stress testing before angiography D. Coronary calcium score **Answer: B.** Very high-risk NSTE-ACS features require immediate invasive care. --- ## References 1. Rao SV, O'Donoghue ML, Ruel M, et al. **2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes.** *J Am Coll Cardiol.* 2025;85(22):2135–2237. doi: **10.1016/j.jacc.2024.11.009**. https://www.jacc.org/doi/10.1016/j.jacc.2024.11.009 2. American College of Cardiology / American Heart Association. **Top Things to Know: 2025 Guideline for Acute Coronary Syndromes.** Updated February 27, 2025. https://professional.heart.org/en/science-news/2025-guideline-for-the-management-of-patients-with-acute-coronary-syndromes/top-things-to-know 3. Byrne RA, Rossello X, Coughlan JJ, et al. **2023 ESC Guidelines for the management of acute coronary syndromes.** *Eur Heart J.* 2023;44(38):3720–3826. doi: **10.1093/eurheartj/ehad191**. PMID: **37622654**. https://www.escardio.org/guidelines/clinical-practice-guidelines/all-esc-practice-guidelines/acute-coronary-syndromes/ 4. Thygesen K, Alpert JS, Jaffe AS, et al. **Fourth Universal Definition of Myocardial Infarction (2018).** *Circulation.* 2018;138:e618–e651. doi: 10.1161/CIR.0000000000000617. 5. European Society of Cardiology. **Essential Messages from the 2023 ESC Guidelines for the Management of Acute Coronary Syndromes.** 2023. https://www.escardio.org/ 6. Kumbhani DJ, Cibotti-Sun M, Moore MM. **2025 Acute Coronary Syndromes Guideline-at-a-Glance.** *J Am Coll Cardiol.* 2025;85(22):2128–2134. doi: **10.1016/j.jacc.2025.01.018**. 7. Bikdeli B, Ujueta F, Rashedi S, et al. **Antiplatelet and Anticoagulant Therapy in the 2025 ACC/AHA Guideline for Acute Coronary Syndromes: Key Recommendations.** *J Am Coll Cardiol.* 2025. doi: **10.1016/j.jacc.2025.04.002**. --- **Review trigger:** Re-review whenever ACC/AHA or ESC ACS guidance changes, or when major trials alter PCI strategy, cardiogenic-shock support, antiplatelet duration/de-escalation, or lipid-lowering recommendations.7:["$","$L17",null,{"article":{"id":"medical-abcde-approach","title":"ABCDE Approach","slug":"abcde-approach","description":"The ABCDE approach—Airway, Breathing, Circulation, Disability, Exposure—is a rapid, repeatable method for recognizing and treating immediate threats to life in a deteriorating or critically ill patient. 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