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The most important new clinical guidelines — distilled and expanded with the reasoning behind each recommendation, for practice and for exams.

37 guidelines9 specialties200+ recommendationsUpdated 2026
142clinical guidelines & scientific statements across 15 specialties — every recommendation explained, with the reasoning and exam pearls.

Cardiology & Vascular24 guidelines

▸Fifth Universal Definition of Myocardial Infarction (2026)CardiologyESC/ACC/AHA/WHF · 2026
Clinical takeaway

The first update in eight years retires the Type 1–5 numbering in favour of three clinical categories — primary, secondary and procedure-related MI — and formally endorses sex-specific troponin thresholds.

Background — why it changed

The Fourth Universal Definition (2018) split myocardial infarction into Types 1–5. In practice the numbering caused confusion — especially Type 2 MI versus plain myocardial injury — and didn't map onto how clinicians actually reason at the bedside. Unveiled at the ESC Congress 2026 and published simultaneously in the European Heart Journal and Circulation, the Fifth Universal Definition (a joint ESC/ACC/AHA/WHF task force) reframes the diagnosis around mechanism and clinical context rather than a number.

What's new

  • Three clinical types replace Types 1–5: Primary MI (an atherothrombotic plaque event), Secondary MI (ischaemia from a supply–demand mismatch — tachyarrhythmia, anaemia, hypotension, hypoxaemia, sepsis), and Procedure-related MI (PCI or cardiac surgery). The label now aligns with the evaluation and the management pathway.
  • Sex-specific cardiac troponin thresholds are formally recommended, improving diagnostic accuracy — particularly in women, who are under-diagnosed when a single male-derived cut-off is used.
  • Clearer acute vs chronic myocardial injury: refined criteria emphasise the underlying mechanism — a rising/falling troponin pattern for acute injury versus a stable elevation for chronic injury.
  • Procedure-related MI no longer hinges on arbitrary biomarker multiples; the definition is now comparable for percutaneous and surgical procedures, integrating biomarkers with ischaemic symptoms/signs, ECG, angiographic and imaging evidence.

What still defines an MI

Troponin above the 99th-percentile upper reference limit with a rise and/or fall, plus at least one marker of ischaemia: ischaemic symptoms, new ischaemic ECG changes, pathological Q waves, imaging evidence of new loss of viable myocardium or a regional wall-motion abnormality, or intracoronary thrombus.

At the bedside

  • Don't call every troponin rise an "MI": separate myocardial injury (troponin up, no ischaemia) from infarction (troponin up + ischaemia).
  • Then separate primary (plaque → antiplatelets, anticoagulation, angiography) from secondary (supply–demand → treat the trigger first).
  • Use the sex-specific threshold your laboratory reports, and act on the rise/fall, not a single value.
Bottom line / exam pearl

Think in three buckets — primary (plaque), secondary (supply–demand), procedure-related — layered on the injury-vs-infarction distinction, with sex-specific troponin cut-offs. The Type 1–5 numbers are out; the mechanism is in.

References

  • Fifth Universal Definition of Myocardial Infarction (2026). Circulation. ahajournals.org
  • European Heart Journal advance article (ESC 2026). academic.oup.com
  • ACC Journal Scan — Global CV Societies Release Updated Universal Definition of MI (Aug 2026). acc.org
▸AHA/ACC Guideline on Pulmonary EmbolismCardiologyJACC · 2026
Clinical takeaway

The first-ever AHA/ACC PE guideline replaces "submassive/massive" with a graded A–E classification (plus a respiratory modifier) that maps directly onto how aggressively to treat.

Background — why it changed

Until now, US practice used low / submassive / massive (AHA) while Europe used low / intermediate / high risk (ESC). Both lump very different patients together — a young person with a tiny subsegmental clot and a normotensive patient with a strained, failing right ventricle could both be "submassive." In Feb 2026 the AHA and ACC (with a dozen societies) issued a single evidence-based framework built around one insight: a patient can be in serious trouble even with a normal blood pressure, because the right ventricle can be failing before systemic hypotension appears.

The A–E clinical categories

  • A — Subclinical: incidental / asymptomatic PE.
  • B — Symptomatic, low severity (low clinical severity score); B1 subsegmental, B2 non-subsegmental.
  • C — Symptomatic, elevated severity — graded C1 (normal RV + normal biomarkers), C2 (abnormal RV or ≥1 abnormal biomarker), C3 (abnormal RV and ≥1 abnormal biomarker).
  • D — Incipient cardiopulmonary failure — D1 transient hypotension, D2 normotensive shock (raised lactate, low urine output, altered mentation, low cardiac index, MAP <60, rising shock score).
  • E — Cardiopulmonary failure — E1 cardiogenic shock, E2 refractory shock / cardiac arrest.
  • "R" respiratory modifier — appended (e.g. C3R, D2R) when there is hypoxaemic respiratory failure or a high supplemental-oxygen need. This is the guideline's flagship innovation.

Key recommendations

  • Rule out PE with an age-adjusted D-dimer or YEARS when clinical pretest probability is <50%; CTPA is the first-line test, V/Q SPECT if CT is contraindicated.
  • To place a patient in a category, weigh symptoms, a severity score (e.g. simplified PESI), clot location, troponin, RV strain on echo/CT, transient/normotensive shock and respiratory status.
  • A–B: home treatment or early discharge on a DOAC is reasonable (use a tool such as HESTIA to confirm suitability).
  • C1–E1 (hospitalised): LMWH is preferred over unfractionated heparin (more predictable, no infusion).
  • Reperfusion (catheter-directed fibrinolysis, mechanical thrombectomy) is reasonable for haemodynamic instability (E1); its value in less-sick C2–D2 patients is still uncertain.
  • E2 (refractory shock/arrest): consider ECMO as a bridge. IVC filter only when anticoagulation is absolutely contraindicated.
  • Duration: continuing anticoagulation beyond 3–6 months is decided by cancer, whether the provoking factor was transient or persistent, and bleeding risk.
Bottom line / exam pearl

Map the letter to the plan: A–B → DOAC, often at home; C–D → admit & anticoagulate (LMWH); E → reperfusion/ECMO. The "R" is the reminder that a normotensive, hypoxic patient is sicker than their blood pressure suggests.

▸2025 Hypertension Guideline (AHA/ACC + 11 societies)CardiologyHypertension · 2025
Clinical takeaway

Confirm hypertension out of the office, risk-stratify with the new PREVENT calculator, and treat most adults to <130/80 — earlier and more assertively.

Background

This reaffirms the 2017 redefinition of hypertension as ≥130/80 (down from ≥140/90). That lower bar was controversial, but subsequent trials (SPRINT and others) have repeatedly shown fewer cardiovascular events with tighter control, so the guideline doubles down while adding better tools for deciding who to treat and how hard.

Definitions & diagnosis

  • Normal <120/80 · Elevated 120–129/<80 · Stage 1 130–139 or 80–89 · Stage 2 ≥140 or ≥90.
  • Confirm out of office — home or ambulatory BP with a validated oscillometric monitor; proper technique (seated, back supported, feet flat, correct cuff, no talking, averaged readings).
  • Cuffless devices (smartwatches, rings) are NOT recommended for diagnosis or titration — they are not validated.

Work-up & risk

  • New diagnosis: check urine albumin-to-creatinine ratio and HbA1c in addition to FBC, electrolytes, renal function, lipids, TSH, urinalysis and ECG.
  • Screen for primary aldosteronism (aldosterone-to-renin ratio) — strongly in resistant hypertension, hypokalaemia, OSA, adrenal nodule or early stroke; and consider it in all stage 2.
  • Use the PREVENT calculator (replaces the pooled cohort equations) to inform treatment in stage 1.

Treatment

  • Lifestyle for everyone: weight loss, low sodium, DASH-style diet, exercise, alcohol moderation, tobacco cessation, stress reduction.
  • Stage 1, low-risk (no diabetes/CKD, 10-yr risk <7.5%): 3–6 months of lifestyle first; otherwise start a drug.
  • Target <130/80 for most (strong when 10-yr risk ≥7.5%).
  • Stage 2: begin with two first-line agents in a single-pill combination — first-line classes are thiazide-type diuretics, ACE inhibitors/ARBs and dihydropyridine calcium-channel blockers.
  • Dedicated recommendations for pregnancy, severe hypertension and comorbidities (diabetes, CKD, recent stroke).
Bottom line / exam pearl

Diagnose on home BP, risk-stratify with PREVENT, and get most patients to <130/80 — starting stage 2 on a single-pill dual combination. Don't forget to screen stage 2 for primary aldosteronism.

▸ACC/AHA Lipid Management & ASCVD PreventionCardiologyJACC · 2026
Clinical takeaway

Cholesterol is reframed as a lifelong, cumulative exposure — treat earlier, to target, guided by the PREVENT calculator.

Background

The first ACC/AHA lipid guideline since 2018 moves away from betting everything on a 10-year risk number. Because LDL exposure is cumulative — every year of high LDL adds atherosclerotic burden — the new emphasis is lifetime risk, cumulative LDL and subclinical atherosclerosis. It adopts PREVENT (usable from age 30; gives 10- and 30-year risk) and supports coronary artery calcium (CAC), lipoprotein(a) and apoB for individualising decisions.

Primary prevention

  • 10-year ASCVD risk bands via PREVENT: Low <3% · Borderline 3–<5% · Intermediate 5–<10% · High ≥10%.
  • Statins remain first-line — strong for high risk; generally recommended at intermediate risk after a clinician–patient discussion; at borderline risk, consider if there are risk enhancers or a positive CAC.
  • Under 60 with a reassuring 10-year number but 30-year risk ≥10%: earlier treatment is reasonable (don't be lulled by a low short-term score in a young patient).
  • Measure lipoprotein(a) at least once in a lifetime to catch inherited risk.

LDL targets & intensification

  • <100 mg/dL — borderline/intermediate primary prevention.
  • <70 mg/dL — high-risk primary prevention.
  • <55 (or <70) mg/dL — secondary prevention, depending on cardiovascular risk.
  • Goals not met on a maximally-tolerated statin → add stepwise: ezetimibe → PCSK9 inhibitor / inclisiran → bempedoic acid.
Bottom line / exam pearl

Think lifetime, not just 10 years: treat earlier, drive LDL to target for the risk band, and escalate beyond statins when needed. CAC and Lp(a) help decide the grey-zone (borderline/intermediate) patient.

▸Peripheral Artery Disease in Adults with DiabetesVascularACC statement · 2025
Clinical takeaway

Screen these high-risk patients actively for PAD — it stays silent until a foot ulcer or critical ischaemia forces the issue.

Background

Diabetic neuropathy blunts the claudication that would otherwise warn of PAD, so disease is often first noticed as a non-healing ulcer or gangrene. The USPSTF found insufficient evidence to screen asymptomatic adults generally, but the 2024 ACC/AHA PAD guideline endorsed screening selected high-risk groups. This statement extends that to the diabetic population and pairs detection with modern medical therapy.

Screening & diagnosis

  • Comprehensive foot exam (inspection + pulse palpation) at least annually.
  • Screen asymptomatic diabetics with risk enhancers* using the ankle–brachial index (ABI): ≤0.9 = PAD; >1.4 = non-compressible, calcified vessels → do a toe–brachial index.
  • Exertional leg symptoms but borderline/normal resting ABI → exercise treadmill ABI (unmasks flow-limiting disease).

*Age ≥65, smoking, diabetes ≥10 years, microvascular disease, foot complications or other end-organ damage.

Management

  • Aggressive risk-factor control: SBP <120 (if safely achievable), LDL <55 mg/dL, and above all tobacco cessation.
  • Refer symptomatic patients to supervised exercise therapy — it improves walking distance and quality of life as much as some procedures.
  • Prioritise SGLT2 inhibitors and GLP-1 agonists for cardiovascular/renal benefit; semaglutide reduces some adverse limb events and improves function.
  • Consider rivaroxaban 2.5 mg twice daily + low-dose aspirin in symptomatic PAD (dual-pathway inhibition; particularly beneficial in diabetes) — use antiplatelet monotherapy instead if bleeding risk is high.
Bottom line / exam pearl

Feet + ABI at least yearly in diabetes. ABI ≤0.9 = PAD; >1.4 = calcified → check toe pressures. Then: stop smoking, LDL <55, SBP <120, supervised exercise, SGLT2/GLP-1, and consider low-dose rivaroxaban + aspirin.

▸Acute Coronary Syndromes in Premenopausal WomenCardiologyCirculation · 2026
Clinical takeaway

ACS in young women is a distinct entity — frequently non-atherosclerotic — needing mechanism-specific treatment, not a reflex stent-and-DAPT.

Background

Premenopausal women with ACS are understudied and often mislabelled as "non-cardiac chest pain." The AHA statement reframes them as a distinct group in whom non-obstructive and non-atherosclerotic causes predominate and female-specific factors (pregnancy-related conditions, hormonal influences) play a major role — driving diagnostic difficulty, treatment uncertainty and trial under-representation.

Aetiology & diagnosis

  • Higher prevalence of SCAD (spontaneous coronary artery dissection), MINOCA (MI with non-obstructive coronary arteries) and coronary vasospasm; classic atherosclerosis still occurs but is proportionally less common than in older patients.
  • A standard angiogram can miss SCAD and plaque erosion — intracoronary imaging (OCT/IVUS) and multimodality imaging are often needed to find the mechanism.

Cause-specific treatment

  • Atherosclerotic ACS: standard guideline-directed medical therapy.
  • SCAD: conservative management is preferred — most heal spontaneously; avoid routine PCI (the dissected vessel is fragile) and avoid prolonged DAPT unless a stent was placed or plaque disruption is present. β-blockers may reduce SCAD recurrence.
  • MINOCA / vasospasm: treat the identified mechanism (e.g. calcium-channel blockers for vasospasm); DAPT is not indicated for vasospastic mechanisms.
  • Prevention: aggressive lifetime risk reduction (LDL <55–70, SBP <120 if tolerated); address preeclampsia, early menopause and pregnancy-related risks.
Bottom line / exam pearl

In a young woman with ACS, think SCAD, MINOCA, vasospasm — image beyond the angiogram and tailor therapy to the mechanism. SCAD is usually managed conservatively, not stented.

▸NICE Hypertension in Adults (NG136)CardiologyNICE · UK
Clinical takeaway

The UK approach — confirm with ABPM/HBPM, treat by age and ethnicity with the A/C/D ladder, and keep the <140/90 threshold (NICE has not adopted the US 130/80 cut-off).

Background

NICE keeps a higher diagnostic threshold than the US ACC/AHA guideline and leans heavily on out-of-office measurement to avoid over-diagnosis from white-coat hypertension. Knowing both frameworks matters for MRCEM/UK practice, where NG136 is the standard.

Key recommendations

  • Diagnose: clinic BP ≥140/90 → confirm with ambulatory (ABPM) or home (HBPM) monitoring. Stage 1 = clinic ≥140/90 and ABPM/HBPM ≥135/85; Stage 2 = clinic ≥160/100 and ABPM/HBPM ≥150/95; severe = clinic ≥180/120.
  • Who to treat: all Stage 2; Stage 1 in under-80s with target-organ damage, established CVD, renal disease, diabetes, or a 10-year QRISK ≥10%.
  • Targets: <80 yrs → clinic <140/90 (ABPM/HBPM <135/85); ≥80 yrs → clinic <150/90; type 2 diabetes → <140/90.
  • Drug steps: Step 1 — ACEi/ARB if <55 or type 2 diabetes, CCB if ≥55 or of Black African/Caribbean family origin (without diabetes). Step 2 — A + C. Step 3 — A + C + thiazide-like diuretic. Step 4 (resistant, confirm adherence) — add spironolactone if K⁺ ≤4.5, otherwise an alpha- or beta-blocker.
  • Offer lifestyle advice and check for secondary causes / end-organ damage.
Bottom line / exam pearl

NICE = confirm with ABPM/HBPM, threshold stays 140/90, and treat with A (ACEi/ARB) if young or diabetic, C (CCB) if older or Black African/Caribbean, then A+C, then add a thiazide-like diuretic, then spironolactone.

▸Acute Coronary Syndromes (ESC/ACC)CardiologyESC 2023 · unified ACS
Clinical takeaway

One ACS spectrum — the ECG and high-sensitivity troponin split STEMI (immediate reperfusion) from NSTE-ACS (risk-stratified early invasive), and everyone gets dual antiplatelet + anticoagulation.

Background

The 2023 ESC guideline unified STEMI and NSTE-ACS into a single continuum, driven by how quickly you can open the artery and how high the risk is.

Key recommendations

  • ECG within 10 minutes. STEMI → primary PCI within 120 min of diagnosis; if unavailable, fibrinolysis then transfer.
  • Use high-sensitivity troponin 0/1 h (or 0/2 h) algorithms to rule NSTE-ACS in or out.
  • NSTE-ACS: very-high-risk (instability, ongoing ischaemia) → immediate invasive; high-risk (raised troponin, GRACE >140) → invasive within 24 h.
  • Antithrombotics: aspirin + a P2Y12 inhibitor (ticagrelor or prasugrel preferred over clopidogrel) + parenteral anticoagulation.
  • Give oxygen only if SpO₂ < 90% (routine oxygen is out); nitrates/morphine for symptoms.
  • Secondary prevention: high-intensity statin, ACEi/ARB, beta-blocker, and 12 months of DAPT.
Bottom line / exam pearl

STEMI = clock starts, reperfuse fast (PCI <120 min). NSTE-ACS = hs-troponin + GRACE decide how urgently to catheterise. Ticagrelor/prasugrel > clopidogrel; oxygen only if hypoxic.

▸Atrial Fibrillation (ESC / AHA)CardiologyESC 2024 · AF-CARE
Clinical takeaway

Follow AF-CARE: manage Comorbidities, Avoid stroke (anticoagulate by CHA₂DS₂-VASc), Reduce symptoms (rate/rhythm), and Evaluate/reassess.

Background

The 2024 ESC guideline reorganised AF care around the AF-CARE pathway, stressing that risk-factor control and stroke prevention matter as much as rate/rhythm decisions.

Key recommendations

  • Stroke prevention: anticoagulate if CHA₂DS₂-VASc ≥2 (men) / ≥3 (women) — a DOAC is preferred over warfarin. Use HAS-BLED to flag modifiable bleeding risk, not to withhold anticoagulation.
  • Rate control: beta-blocker or diltiazem/verapamil; a lenient target of < 110 bpm is acceptable initially.
  • Rhythm control: cardioversion or ablation for symptoms; early rhythm control benefits recently-diagnosed AF (EAST-AFNET 4).
  • Acute / unstable (shock, ischaemia, pulmonary oedema) → synchronised DC cardioversion.
  • Anticoagulate for ≥3 weeks before elective cardioversion, or exclude thrombus on TOE, if AF > 48 h.
Bottom line / exam pearl

Anticoagulate by CHA₂DS₂-VASc with a DOAC, control rate to <110, consider early rhythm control, and DC cardiovert the unstable patient. Treat the comorbidities that drive AF.

▸Acute Heart Failure (ESC)CardiologyESC · Heart Failure
Clinical takeaway

Classify by congestion and perfusion (wet/dry, warm/cold): most are 'wet & warm' — treat with IV diuretics and vasodilators; 'cold' needs inotropes.

Background

Acute heart failure is a haemodynamic emergency; rapid classification directs whether the problem is congestion, low output, or both.

Key recommendations

  • Wet & warm (congested, perfusing) — IV loop diuretic (furosemide) ± vasodilator (GTN) if SBP adequate.
  • Wet & cold (congested, hypoperfused) — cautious diuresis + inotrope/vasopressor; consider mechanical support.
  • Oxygen if SpO₂ < 90%; NIV (CPAP) for acute cardiogenic pulmonary oedema and respiratory distress.
  • Find the precipitant — CHAMPIT (ACS, Hypertension emergency, Arrhythmia, Mechanical, PE, Infection, Tamponade).
  • Start/continue the four pillars of chronic therapy once stable: ARNI/ACEi, beta-blocker, MRA, SGLT2 inhibitor.
Bottom line / exam pearl

Sort by wet/dry & warm/cold: diuretics + vasodilators for wet-and-warm, inotropes for cold, CPAP for pulmonary oedema — and always hunt the CHAMPIT precipitant.

▸Mechanical Complications of Acute Myocardial InfarctionCardiologyAHA Scientific Statement (Circulation) & 2025 AATS Expert Consensus · 2026
Clinical takeaway

Post-MI mechanical complications (ventricular septal rupture, papillary muscle rupture, free-wall rupture/pseudoaneurysm) are rare in the primary-PCI era but remain among the most lethal cardiac emergencies. Survival depends on rapid echocardiographic diagnosis, early mechanical circulatory support in shock, and urgent multidisciplinary (heart-team) intervention.

Background — why it changed

With timely primary PCI these complications now occur in well under 1% of STEMI, but mortality remains extremely high, especially with cardiogenic shock. Most events cluster in the first days after infarction, and risk is higher with late-presenting, non-reperfused, first anterior infarcts. Recent AHA and AATS consensus documents standardise recognition and management; transatlantic debate persists over the optimal timing of ventricular septal rupture repair.

Key recommendations

  • Suspect a mechanical complication with new murmur, abrupt haemodynamic deterioration or recurrent shock after MI; obtain urgent transthoracic +/- transoesophageal echocardiography as the first-line diagnostic test.
  • Ventricular septal rupture: confirm with echo (left-to-right shunt); surgical or transcatheter closure is definitive. Timing is contested - early repair carries high mortality through friable tissue, so stabilise with mechanical circulatory support where feasible, individualising timing via the heart team.
  • Acute mitral regurgitation from papillary muscle rupture: typically the posteromedial muscle (single blood supply); usually needs emergency surgical mitral repair/replacement - medical therapy alone has very poor survival.
  • Free-wall rupture: often catastrophic with tamponade/PEA arrest; contained rupture (pseudoaneurysm) needs urgent surgery. Pericardiocentesis may temporise tamponade.
  • Mechanical circulatory support (IABP, and increasingly micro-axial pumps or VA-ECMO) is used to bridge shocked patients to definitive repair rather than as destination therapy.
  • Manage in centres with cardiac surgery and structural/interventional expertise; early transfer of the deteriorating post-MI patient is advised.

At the bedside

  • A new harsh systolic murmur plus shock days after MI is a mechanical complication until proven otherwise - get bedside echo immediately.
  • Do not delay for a coronary lab work-up: haemodynamic stabilisation and surgical/structural consultation run in parallel.
  • Vasodilators/afterload reduction (if BP permits) and MCS can buy time in acute MR or VSR while arranging repair.
  • PEA arrest in a recent-MI patient should prompt thought of free-wall rupture with tamponade.
Bottom line / exam pearl

Think mechanical complication for any post-MI patient with a new murmur or sudden collapse; echo first, heart team fast, and support the circulation as a bridge to urgent repair.

References

▸Inflammation in Coronary SyndromesCardiologyESC / Association for Acute CardioVascular Care (ACVC) Clinical Consensus Statement · 2026
Clinical takeaway

Residual inflammatory risk is a modifiable driver of recurrent events in coronary disease. The statement supports hsCRP as a practical marker of residual inflammation and low-dose colchicine as an adjunct in selected secondary-prevention patients, while acknowledging genuine uncertainty about timing and patient selection.

Background — why it changed

A decade of translational and clinical work (CANTOS, LoDoCo2, COLCOT) established inflammation as a treatable component of atherosclerosis, acting largely through the NLRP3 inflammasome and the IL-1beta/IL-6 axis. This ESC/ACVC clinical consensus statement translates that evidence for everyday practice across acute and chronic coronary syndromes. It follows the 2024 ESC chronic coronary syndrome guidance that gave low-dose colchicine a (weak/IIb) recommendation.

Key recommendations

  • Recognise residual inflammatory risk (persistently elevated hsCRP despite guideline lipid-lowering) as distinct from residual cholesterol risk and a target in its own right.
  • hsCRP is the most accessible biomarker for identifying low-grade inflammation; measure when the patient is clinically stable and away from acute infection.
  • Low-dose colchicine 0.5 mg once daily may be considered as an adjunct for secondary prevention in patients with residual inflammatory risk after optimised standard therapy.
  • Colchicine evidence is not uniform: benefit in COLCOT/LoDoCo2 contrasts with the neutral CLEAR-SYNERGY (OASIS-9) post-PCI trial, so timing, dose and patient selection remain unsettled.
  • Screen for and counsel on gastrointestinal intolerance, avoid colchicine in significant renal or hepatic impairment, and check for interacting drugs (strong CYP3A4/P-gp inhibitors).
  • Optimise conventional anti-inflammatory levers first - high-intensity statins, smoking cessation, weight and glycaemic control - as foundational to lowering inflammatory burden.

At the bedside

  • In recurrent ACS despite good LDL control, an elevated hsCRP flags residual inflammatory risk worth addressing at follow-up.
  • Colchicine is an outpatient secondary-prevention adjunct, not an acute intervention; do not start it reflexively in the acute admission.
  • Ask about diarrhoea and renal function before recommending colchicine, and review the medication list for interactions.
Bottom line / exam pearl

Inflammation is a real, measurable (hsCRP) and modifiable residual risk in coronary disease; low-dose colchicine is a reasonable adjunct in selected patients, but the evidence is mixed - individualise.

References

  • ESC/ACVC Clinical Consensus Statement, EHJ Acute Cardiovasc Care (zuag086). doi.org
  • Colchicine in cardiovascular disease, Eur Heart J 2026;47(4):526. academic.oup.com
  • EHJ Acute Cardiovascular Care (journal home). academic.oup.com
▸Coronary Microvascular Obstruction: Prevention and ManagementCardiologyESC Working Groups on Coronary Pathophysiology & Microcirculation and Thrombosis, with EAPCI - Clinical Consensus Statement · 2026
Clinical takeaway

Microvascular obstruction (MVO / 'no-reflow') persists in a large share of reperfused STEMI despite a patent epicardial artery and is a strong, independent predictor of adverse LV remodelling and heart failure. Prevention and early recognition matter more than any single rescue therapy.

Background — why it changed

Even with timely primary PCI, suboptimal myocardial reperfusion is common, driven by distal embolisation, ischaemia-reperfusion injury, microvascular spasm and intramyocardial haemorrhage. The result - the no-reflow phenomenon - impairs infarct healing and worsens prognosis. This ESC consensus statement synthesises pathophysiology, diagnosis and management to standardise an area with limited high-quality trial evidence.

Key recommendations

  • Diagnose MVO by angiographic no-reflow (reduced TIMI flow/myocardial blush despite a patent vessel), invasive microvascular indices (e.g. index of microcirculatory resistance), and, as reference standard, late-gadolinium and T2* cardiac MRI.
  • Prevention is the priority: prompt reperfusion, effective platelet inhibition, and avoidance of manoeuvres that worsen distal embolisation.
  • Routine manual thrombus aspiration is not recommended for unselected STEMI (no mortality benefit and a signal of stroke harm in trials).
  • For established no-reflow, intracoronary vasodilators (such as adenosine, nitroprusside, verapamil or nicardipine) may improve flow, though evidence on hard outcomes is limited.
  • Avoid microvascular injury from over-aggressive or oversized ballooning/stenting; deferred stenting is not supported as a routine strategy for outcomes.
  • Identify high-risk patients early and reserve intensive strategies for them; no single agent reliably reverses no-reflow, so expectations should be tempered.

At the bedside

  • Persisting ST-elevation or ongoing chest pain after a technically successful PCI should raise suspicion of MVO.
  • MVO on post-PCI imaging predicts worse LV function - flag these patients for closer heart-failure surveillance and guideline-directed medical therapy.
  • Intracoronary vasodilators are the practical bedside lever in the cath lab; systemic support addresses haemodynamics.
  • Do not reach for routine thrombus aspiration to prevent no-reflow - it is not evidence-supported.
Bottom line / exam pearl

No-reflow means the artery is open but the myocardium is not perfused; prevent it, recognise it (angiography, IMR, CMR), and accept that reversal options are limited and their outcome benefit unproven.

References

  • ESC Clinical Consensus Statement, Eur Heart J (ehag334). doi.org
  • ESC Clinical Practice Guidelines (all). www.escardio.org
▸Management of Blunt Thoracic Aortic Injury (Focused Update)VascularSociety for Vascular Surgery (SVS), Journal of Vascular Surgery · 2026
Clinical takeaway

This SVS focused update refines a grade-based strategy for blunt thoracic aortic injury (BTAI): non-operative management for minimal (grade 1-2) injuries, TEVAR as the mainstay for higher grades, and repair timing driven by haemodynamic stability and competing traumatic injuries.

Background — why it changed

BTAI is a leading cause of death after blunt trauma, usually at the aortic isthmus. TEVAR has replaced open repair as first-line for most anatomically suitable injuries. This focused update revises the 2011 SVS guideline with 13 updated recommendations reflecting evidence accrued over the intervening years, published in the Journal of Vascular Surgery (March 2026).

Key recommendations

  • Grade 1 (intimal tear): definitive non-operative management, with no routine follow-up imaging required.
  • Grade 2 (intramural haematoma): non-operative management with one follow-up CT angiogram to confirm stability/resolution.
  • Grade 3 (pseudoaneurysm), haemodynamically stable: delayed TEVAR (>24 h) is suggested, allowing management of concomitant injuries first.
  • Grade 3 with instability attributable to the aorta, or grade 4 (rupture): urgent/emergent repair (TEVAR preferred where anatomy allows).
  • Prefer TEVAR over open repair for anatomically suitable injuries requiring intervention.
  • In patients with concomitant TBI or solid-organ injury, take a collaborative, individualised approach to intraprocedural anticoagulation during TEVAR.
  • Employ impulse (anti-impulse) control - blood-pressure and heart-rate reduction - as a temporising measure while awaiting definitive repair.

At the bedside

  • On the trauma CT, grade the injury (1-4): minimal injuries are managed medically, not with a stent.
  • Start beta-blockade / strict BP and HR control early in stable BTAI to reduce aortic wall stress while other injuries are addressed.
  • A stable grade 3 can usually wait >24 h - treat the immediately life-threatening injuries (brain, abdomen) first.
  • Escalate for emergent repair if the aorta is the source of instability or if there is frank rupture (grade 4).
Bottom line / exam pearl

Grade the BTAI: 1-2 medical, stable 3 delayed TEVAR, unstable/grade 4 emergent - and control blood pressure and heart rate while you decide.

References

▸Diuretic Therapy in Acute Heart Failure with Worsening Renal FunctionCardiologyAHA/ACC/HFSA HF guideline plus recent cardiorenal reviews (Circulation; Nephrol Dial Transplant; Am J Kidney Dis) · 2025
Clinical takeaway

In a congested AHF patient, a modest creatinine rise during effective decongestion is usually pseudo-worsening renal function and should not trigger premature diuretic withdrawal -- keep decongesting while congestion persists and natriuretic peptides fall.

Background — why it changed

Worsening renal function (a creatinine rise of about >=0.3 mg/dL) during diuresis is common, but its meaning depends on context. Venous congestion, not low cardiac output, drives most cardiorenal syndrome, so under-decongestion is the greater danger. Recent evidence (natriuresis-guided decongestion, ADVOR, PUSH-AHF) has refined how diuretics are titrated and escalated.

Key recommendations

  • Start IV loop diuretics promptly and dose to achieve effective decongestion; do not withhold for mild or asymptomatic changes in renal function.
  • Interpret rising creatinine in context: WRF with resolving congestion and a falling NT-proBNP (pseudo-WRF) carries a benign-to-good prognosis, whereas WRF with persistent congestion is concerning.
  • Assess diuretic response early with a spot urine sodium (~1-2 h) and urine output (~6 h); a poor natriuretic response prompts escalation.
  • For inadequate response or diuretic resistance, escalate the loop dose then add sequential nephron blockade (thiazide, acetazolamide, or an SGLT2 inhibitor) rather than stopping diuretics.
  • A large, sustained rise (roughly a doubling of creatinine or an increase of >1 mg/dL, oliguria, or hyperkalemia) suggests true injury and warrants workup and reassessment.
  • Do not routinely discontinue RAAS inhibitors or other GDMT for small, asymptomatic creatinine rises.
  • Reserve ultrafiltration / renal replacement for genuinely refractory congestion or diuretic-resistant AKI with metabolic or volume indications.

At the bedside

  • Congestion, not creatinine, drives outcomes -- treat the volume and watch the trend.
  • Falling NT-proBNP + improving congestion + a small creatinine bump = keep going.
  • Check a spot urine sodium after the first IV loop dose to see if the diuretic is working before blindly doubling it.
  • Red flags for true injury: oliguria despite adequate dosing, a big creatinine jump with ongoing congestion, or hyperkalemia.
Bottom line / exam pearl

Don't stop diuretics for a small creatinine rise in a still-congested patient -- pseudo-WRF during decongestion is expected and prognostically benign.

References

  • AKI in acute heart failure -- when to worry (Nephrol Dial Transplant, 2025). academic.oup.com
  • Kidney Dysfunction in Heart Failure: Core Curriculum 2025 (Am J Kidney Dis). www.ajkd.org
  • 2022 AHA/ACC/HFSA Heart Failure Guideline (Circulation). www.ahajournals.org
▸Prevention and Treatment of New-Onset Postoperative Atrial Fibrillation After Cardiac SurgeryCardiologySociety of Thoracic Surgeons (STS), The Annals of Thoracic Surgery · 2026
Clinical takeaway

Postoperative AF is the most common complication after cardiac surgery and drives longer stays, cost, and morbidity; the STS now endorses a proactive, phase-based approach favoring perioperative amiodarone and posterior pericardiotomy for prevention.

Background — why it changed

Postoperative atrial fibrillation (POAF) affects a large share of cardiac-surgery patients yet practice has varied widely. Using a PICO/GRADE framework across preoperative, intraoperative, and postoperative domains, the STS synthesized RCT and observational evidence into a single comprehensive document. The result is 15 graded recommendations meant to standardize prevention and treatment and to flag remaining evidence gaps.

Key recommendations

  • Perioperative oral amiodarone is recommended for prophylaxis (a Class I recommendation); reported preventive benefit is seen with a cumulative dose in the range of roughly 3-6 g.
  • Cardioversion is recommended for hemodynamically unstable POAF (Class I).
  • Perioperative beta-blockers are reasonable for prevention (Class IIa).
  • Posterior pericardiotomy is a reasonable intraoperative adjunct to reduce POAF (Class IIa).
  • The document totals 15 recommendations - 8 on prevention, 3 on intraoperative adjuncts, and 4 on postoperative management.
  • Eight Class IIb recommendations mark areas of uncertainty and three Class III recommendations identify therapies without demonstrated benefit.
  • Postoperative care centers on rhythm monitoring, early rate or rhythm control, and individualized anticoagulation, with optimal anticoagulation timing/duration acknowledged as unresolved.

At the bedside

  • Start prophylaxis planning preoperatively: consider an amiodarone loading strategy and continue/optimize beta-blockade unless contraindicated.
  • For a patient who becomes hemodynamically unstable in new POAF, move to cardioversion rather than temporizing with rate control.
  • Weigh anticoagulation individually against post-surgical bleeding risk - the guideline stresses shared, case-by-case decisions given uncertain optimal timing.
  • Discuss posterior pericardiotomy with the surgical team as a low-cost intraoperative option in appropriate cases.
Bottom line / exam pearl

Be more aggressive about POAF prevention - perioperative amiodarone (Class I) plus beta-blockers and posterior pericardiotomy (Class IIa) - and cardiovert unstable POAF.

References

▸Ethical Considerations for Heart Organ Allocation: Current Landscape and Future Policy GuidanceCardiologyAmerican Heart Association (AHA) Scientific Statement, Circulation · 2026
Clinical takeaway

Donor hearts are a scarce public resource, and the statement argues that the traditional sickest-first priority must be balanced against post-transplant utility, equity, and responsible stewardship.

Background — why it changed

The heart transplant allocation system is under pressure from rising demand, new technologies (durable and temporary mechanical support), and broader geographic sharing. This AHA statement, chaired by Prateeti Khazanie, reviews the ethics of past and current allocation systems and reframes allocation as an ongoing ethical - not purely medical - question. Its goal is to inform future, more transparent and equitable policy.

Key recommendations

  • Treat donor hearts as a scarce shared resource requiring responsible stewardship and fair distribution, not just clinical urgency.
  • Periodically reassess the historical 'sickest patients first' principle, weighing it against post-transplant outcomes and utility.
  • Explicitly address socioeconomic and geographic disparities in access to listing and transplantation.
  • Recognize that expanded donor pools and wider geographic sharing bring new costs and access barriers that need ongoing evaluation.
  • Embed ethical principles through multidisciplinary collaboration, bioethics education, and data-driven allocation modeling.
  • Align allocation with UNOS mandates for equitable distribution in order of decreasing medical urgency while safeguarding public trust.

At the bedside

  • When counseling candidates, be transparent that listing status and allocation reflect ethical trade-offs between urgency, utility, and equity - not urgency alone.
  • Watch for how socioeconomic and geographic factors may disadvantage your patient's access, and advocate accordingly.
  • Frame mechanical support and status decisions knowing they interact with allocation priority and fairness.
  • Engage bioethics and multidisciplinary teams for contested or borderline candidacy decisions.
Bottom line / exam pearl

Modern heart allocation is shifting from pure 'sickest first' toward a balance of urgency, utility, and equity - stewardship of a scarce resource is now an explicit ethical mandate.

References

▸Evaluation and Management of Acute Pulmonary Embolism in AdultsCardiologyAHA/ACC with ACCP, ACEP, CHEST, SCAI, SHM, SIR, SVM and SVN; published in Circulation and JACC · 2026
Clinical takeaway

The first joint US PE guideline retires 'massive/submassive' and introduces a five-category (A-E) physiology-based classification to match therapy intensity to risk, while formalising PE response teams.

Background — why it changed

This is a de novo, multi-society guideline covering evaluation, treatment and follow-up of adults with acute PE. It replaces anatomy/clot-burden thinking with a scheme built on clinical severity, biomarkers, RV imaging, haemodynamics and respiratory compromise, so that decisions turn on physiological impact rather than clot size.

Key recommendations

  • Use the new Clinical Categories A-E: A = asymptomatic, B = symptomatic low-severity, C = elevated severity with raised biomarkers and/or RV dysfunction, D = incipient cardiopulmonary failure, E = overt failure with persistent hypotension.
  • Category A can typically be discharged from the ED and B is generally suitable for early discharge, while C-E warrant admission.
  • For oral anticoagulation, DOACs are recommended over vitamin K antagonists unless contraindicated, to cut recurrent VTE and major bleeding.
  • When parenteral anticoagulation is needed, LMWH is recommended over unfractionated heparin in most patients.
  • Advanced therapies (systemic thrombolysis, catheter-directed thrombolysis, mechanical thrombectomy, surgical embolectomy) are reasonable for high-risk Category E and may be considered in Category D.
  • PE response teams (PERTs) are recommended to improve timeliness and coordination of care for higher-risk PE.

At the bedside

  • Stop saying 'submassive' - assign an A-E category using severity score, biomarkers, RV assessment and haemodynamics.
  • Start a DOAC rather than warfarin for most patients moving to oral therapy.
  • For the crashing hypotensive patient (Category E), activate the PERT and consider thrombolysis or thrombectomy urgently.
  • Screen low-risk Category A/B patients for safe early or outpatient discharge instead of routine admission.
Bottom line / exam pearl

Category drives disposition and reperfusion: E gets advanced therapy, D may, and A/B often go home - all coordinated through a PERT.

References

▸Intra-operative Haemodynamic Monitoring and Management for Noncardiac SurgeryCardiologyEuropean Society of Anaesthesiology and Intensive Care (ESAIC), published in European Journal of Anaesthesiology · 2025
Clinical takeaway

Manage intra-operative haemodynamics around mean arterial pressure, keeping MAP above roughly 60 mmHg, and individualise fluids and cardiac-output targets to signs of perfusion rather than to fixed numbers.

Background — why it changed

Developed by 25 international experts across seven domains (arterial pressure, heart rate, stroke volume/cardiac output and more), the guideline responds to strong evidence linking intra-operative hypotension to organ injury. It reframes management toward personalised, perfusion-oriented goals instead of one-size-fits-all thresholds or maximised cardiac output.

Key recommendations

  • Base arterial-pressure management on MAP and keep intra-operative MAP above ~60 mmHg, individualising higher targets for at-risk patients.
  • Identify and treat the underlying cause of hypotension (hypovolaemia, vasodilation, low cardiac output) rather than reflexively giving fluid or pressor.
  • Use continuous invasive arterial monitoring in high-risk patients; otherwise use properly performed oscillometric measurement.
  • Judge heart rate by its haemodynamic impact, not a fixed cutoff.
  • Guide fluid challenges by stroke-volume or cardiac-output response, and do not give fluid on fluid-responsiveness alone - confirm signs of hypovolaemia.
  • Link stroke-volume/cardiac-output monitoring to a meaningful therapeutic decision, and do not universally maximise cardiac output.

At the bedside

  • Watch the MAP trend and intervene to keep it above ~60 mmHg, aiming higher in chronically hypertensive or high-risk patients.
  • When the pressure drops, diagnose why (preload, afterload, contractility) before choosing fluid versus vasopressor.
  • Place an arterial line for continuous pressure in high-risk or major cases rather than relying on intermittent cuff readings.
  • Give a fluid bolus only as a challenge tied to a stroke-volume response - stop if there is no meaningful rise.
Bottom line / exam pearl

Keep MAP above ~60 mmHg, treat the cause of hypotension, and tailor fluids/cardiac output to perfusion instead of maximising a number.

References

  • ESAIC intra-operative haemodynamic monitoring and management guideline (European Journal of Anaesthesiology, Ovid). www.ovid.com
  • Overview of the 2025 ESAIC haemodynamic guidelines. campusvygon.com
▸Infective Endocarditis: Diagnosis, Antibiotic Therapy, and ManagementCardiologyAmerican Heart Association (AHA) Scientific Statement, published in Circulation · 2026
Clinical takeaway

This statement, the first comprehensive AHA update since 2015, endorses the 2023 Duke-ISCVID criteria for greater diagnostic sensitivity and reinforces a multimodality imaging and multidisciplinary team approach to endocarditis.

Background — why it changed

Infective endocarditis remains highly lethal, and both microbiology and imaging have changed substantially since the 2000 modified Duke criteria and the 2015 AHA statement. The writing group incorporated the 2023 Duke-ISCVID diagnostic framework, newer molecular diagnostics, and advanced imaging, and updated antimicrobial guidance to reflect current evidence.

Key recommendations

  • Apply the 2023 Duke-ISCVID criteria, which add molecular/microbiologic and imaging elements and are more sensitive than the 2000 modified Duke criteria (with comparable or modestly reduced specificity).
  • Echocardiography remains first-line; transesophageal echo is preferred when transthoracic imaging is non-diagnostic, for prosthetic valves, or when intracardiac complications are suspected.
  • Use multimodality imaging (cardiac CT, and PET/CT or leukocyte-labeled imaging in prosthetic-valve/device cases) for added diagnostic yield when echo is inconclusive.
  • Tailor antimicrobial therapy to organism and valve type; a consensus judged that the risks of gentamicin outweigh benefit in staphylococcal prosthetic-valve IE.
  • Long-acting lipoglycopeptides (e.g., dalbavancin, oritavancin) are alternative options but may carry higher relapse rates, especially in non-operated prosthetic-valve enterococcal disease.
  • Manage patients through a multidisciplinary Endocarditis Team to guide diagnosis, antibiotic selection, and timing/indication for surgery.
  • Early surgical evaluation is advised for heart failure, uncontrolled infection, or high embolic risk (e.g., large mobile vegetations).

At the bedside

  • Draw at least 3 sets of blood cultures from separate sites before antibiotics whenever IE is suspected in a febrile patient with a new murmur or risk factors.
  • If transthoracic echo is negative but suspicion stays high, do not stop -- pursue TEE and involve the endocarditis team early.
  • Reassess for embolic and heart-failure complications daily; new neurologic deficits or worsening regurgitation change management and surgical urgency.
  • Confirm valve type (native vs prosthetic) up front, because it changes both antibiotic choice and the imaging pathway.
Bottom line / exam pearl

Suspected endocarditis = cultures before antibiotics, echo first (TEE if needed), 2023 Duke-ISCVID criteria, and an early multidisciplinary team decision on surgery.

References

▸Criteria for the Diagnosis of Cardiogenic Shock -- European PerspectiveCardiologyESC Clinical Consensus Statement (ACVC, HFA, EAPCI of the ESC), published in European Heart Journal: Acute Cardiovascular Care · 2026
Clinical takeaway

This consensus offers a pathophysiology-based, standardized definition of cardiogenic shock built on three diagnostic pillars, aiming to speed recognition and treatment of a syndrome whose heterogeneous presentation delays diagnosis.

Background — why it changed

Cardiogenic shock carries very high mortality, yet its presentation is heterogeneous and its diagnosis has not been standardized, so treatment is often started late. The statement proposes explicit criteria to define the syndrome and situates them alongside the SCAI SHOCK severity stages.

Key recommendations

  • Diagnose cardiogenic shock using three essential pillars: (1) evidence of end-organ hypoperfusion at rest, (2) primarily caused by a haemodynamic abnormality, that is (3) a direct consequence of underlying cardiac dysfunction commensurate with the shock state.
  • End-organ hypoperfusion is central -- look for clinical and biochemical markers (e.g., altered mentation, cold/mottled skin, oliguria, rising lactate) rather than blood pressure alone.
  • The haemodynamic abnormality is typically low cardiac output, which may occur with or without frank hypotension (hypotension is not required for the diagnosis).
  • Confirm a cardiac cause of adequate severity and exclude non-cardiac shock states that can mimic the picture.
  • Layer the SCAI SHOCK stages on top for severity/prognosis: Stage C = hypoperfusion requiring vasoactive drugs or MCS; Stage D = deteriorating, needing escalation; Stage E = refractory despite multiple vasoactives/MCS.
  • Standardized criteria are intended to enable earlier diagnosis and consistent enrollment/comparison across shock cohorts and trials.

At the bedside

  • Check a lactate and assess perfusion (mentation, skin, urine output) early -- hypoperfusion, not just a low BP number, defines shock.
  • Remember a patient can be in cardiogenic shock with a 'normal' blood pressure if they are hypoperfused on vasoactive support.
  • Use the SCAI letter (C/D/E) to communicate trajectory to the team and trigger timely escalation or MCS/transfer decisions.
  • Actively rule out distributive, hypovolemic, or obstructive shock before anchoring on a cardiac cause.
Bottom line / exam pearl

Cardiogenic shock = end-organ hypoperfusion from a haemodynamic abnormality due to cardiac dysfunction -- hypotension is not mandatory, and SCAI C-E tracks severity.

References

▸ESC Guidelines for the Management of Heart FailureCardiologyEuropean Society of Cardiology (ESC) with the Heart Failure Association (HFA), published in European Heart Journal · 2026
Clinical takeaway

The 2026 ESC guideline simplifies HF classification and reframes treatment into foundational medical therapy, additional medical therapy, and guideline-directed interventional therapy -- with the HFrEF 'four pillars' as the foundational base to start and up-titrate early.

Background — why it changed

Building on the flood of trial evidence since 2021, the guideline replaces the older GDMT language with a therapy taxonomy designed to stay durable as new drugs and devices arrive. It streamlines phenotype/staging and, notably, defines foundational therapy for HFpEF as well as HFrEF.

Key recommendations

  • Diagnose HF from symptoms/signs plus objective evidence of cardiac dysfunction; use natriuretic peptides and echocardiography, and classify by ejection fraction phenotype within a staged framework.
  • For HFrEF, start all four foundational (pillar) therapies early: a beta-blocker, a RAAS inhibitor (ACE-I / ARNI / ARB), a mineralocorticoid receptor antagonist, and an SGLT2 inhibitor.
  • For HFpEF, foundational therapy now includes an MRA and an SGLT2 inhibitor.
  • Additional medical therapy (AMT) covers agents with narrower or mainly symptom/quality-of-life indications, layered on top of foundational therapy.
  • Guideline-directed interventional therapy (GDIT) consolidates device and procedural care -- including ICD/CRT and mitral transcatheter edge-to-edge repair (TEER).
  • In decompensated/acute HF, treat congestion with diuretics, support perfusion, and identify and correct precipitants.
  • Systematically screen and treat comorbidities (iron deficiency, atrial fibrillation, diabetes, CKD) and refer advanced HF patients early for transplant/MCS evaluation.

At the bedside

  • Aim to get an HFrEF patient on all four pillars quickly rather than one drug at a time over many months -- early combination is the goal.
  • Do not forget the SGLT2 inhibitor and MRA in HFpEF -- foundational therapy now extends beyond HFrEF.
  • Check iron studies and rhythm in every HF patient; correcting iron deficiency and managing AF changes symptoms and outcomes.
  • Flag the advanced-HF patient (recurrent admissions, escalating diuretics, low output) for early referral before they become too sick for options.
Bottom line / exam pearl

Start the four HFrEF pillars (beta-blocker, ACE-I/ARNI/ARB, MRA, SGLT2i) early -- and remember HFpEF now has foundational MRA + SGLT2i.

References

  • European Heart Journal: 2026 ESC Guidelines for Heart Failure (Oxford Academic). academic.oup.com
  • TCTMD: Updated ESC Heart Failure Guideline Brings Big Changes. www.tctmd.com
  • touchCARDIO: New ESC HF Guidelines Introduce Foundational Therapy. touchcardio.com
▸ESC Guidelines for the Management of Cardiovascular Disease and Chronic Kidney DiseaseCardiologyEuropean Society of Cardiology (ESC), in collaboration with the European Renal Association (ERA); published in the European Heart Journal · 2026
Clinical takeaway

This first dedicated ESC/ERA cardiorenal guideline urges that every patient with cardiovascular disease be screened for CKD (eGFR + urine albumin-to-creatinine ratio), and that a foundational combination of a RAAS inhibitor, an SGLT2 inhibitor, and statin therapy be used to slow renal decline and cut cardiovascular risk.

Background — why it changed

CKD affects an estimated 100 million people in Europe and independently raises the risk of coronary syndromes, heart failure, arrhythmias, stroke, peripheral arterial disease, and sudden cardiac death, yet cardiac and renal care have historically been siloed. This is the first ESC guideline devoted to CVD in CKD, built around the 'STAMP on CKD' framework: Screen for disease, Triage/assess risk, Address CKD progression, Modify CVD interventions, and Plan multidisciplinary care. It was presented at ESC Congress 2026 and published online in the European Heart Journal in August 2026.

Key recommendations

  • Screen every CVD patient for CKD using a creatinine-based eGFR plus a spot (morning) urine albumin-to-creatinine ratio, classify by GFR and albuminuria category, and confirm persistence over ~3 months.
  • Base kidney-protective care on a foundational triad: a RAAS inhibitor (ACE inhibitor or ARB), an SGLT2 inhibitor, and statin-based lipid-lowering therapy.
  • SGLT2 inhibitors can be initiated at an eGFR of 20 mL/min/1.73 m2 or higher and continued below that threshold until kidney replacement therapy begins.
  • Offer intensive statin-based therapy, with or without ezetimibe, routinely to non-dialysis CKD patients irrespective of baseline lipid levels to reduce atherosclerotic risk.
  • In patients with type 2 diabetes or heart failure, add a nonsteroidal MRA (finerenone) and/or a GLP-1 receptor agonist to further reduce cardiorenal risk.
  • Target a systolic blood pressure of 120-129 mmHg when tolerated (e.g., in a patient with eGFR around 30 mL/min/1.73 m2), individualized to tolerability.
  • Use an SGLT2 inhibitor in heart failure regardless of ejection fraction, and coordinate care across cardiology and nephrology.

At the bedside

  • Order an eGFR and a spot urine ACR on your cardiac patients; a normal creatinine alone does not exclude significant albuminuric CKD.
  • When starting or up-titrating a RAAS inhibitor, SGLT2 inhibitor, or nonsteroidal MRA, recheck eGFR and serum potassium within a few weeks, and expect a small initial eGFR dip with SGLT2 inhibitors that does not warrant stopping the drug.
  • Do not withhold statins or SGLT2 inhibitors purely because of a reduced eGFR; use the eGFR 20 threshold for SGLT2 initiation and continue therapy down to dialysis.
  • Reserve added MRA (finerenone) and GLP-1 RA specifically for the diabetes/heart-failure cardiorenal population, and monitor potassium when combining RAAS blockade with an MRA.
Bottom line / exam pearl

Screen every cardiac patient for CKD and build therapy on RAAS inhibition + an SGLT2 inhibitor (start at eGFR >=20) + a statin, adding finerenone or a GLP-1 RA in diabetes or heart failure.

References

  • 2026 ESC Guidelines for the management of cardiovascular disease and chronic kidney disease (ESC guideline page). www.escardio.org
  • Full text, European Heart Journal (advance article, DOI 10.1093/eurheartj/ehag098). academic.oup.com
  • ESC press release: new guidelines recommend all heart-disease patients be tested for kidney disease. www.escardio.org
▸HRS/PACES Scientific Statement on the Use of Antiarrhythmic Drugs in Understudied Clinical ScenariosCardiologyHeart Rhythm Society (HRS) with the Pediatric and Congenital Electrophysiology Society (PACES); published in Heart Rhythm · 2026
Clinical takeaway

This statement offers practical, consensus-based guidance for prescribing antiarrhythmic drugs in patients and situations poorly represented in clinical trials, making explicit that most of the advice rests on expert experience and mechanistic reasoning rather than high-quality randomized evidence.

Background — why it changed

Landmark antiarrhythmic-drug trials enrolled narrow populations, leaving clinicians without evidence for many everyday scenarios and special populations. Recognizing these gaps, HRS and PACES convened a diverse expert panel to identify common but understudied situations and to give the best available practical advice, pairing whatever evidence exists with pooled clinical proficiency and a stated rationale for each recommendation. It was published in Heart Rhythm in 2026.

Key recommendations

  • Treat the low evidence base explicitly: recommendations here are consensus-driven guidance for gaps in the trial evidence, not equivalent to guideline Class I directives.
  • Individualize antiarrhythmic selection and dosing to the specific scenario and patient, since trial-derived dosing may not transfer to underrepresented populations.
  • Reflecting PACES collaboration, the statement extends guidance to pediatric and congenital heart disease patients, who are especially poorly served by adult drug trials.
  • Give particular attention to patients with structural heart disease and other special populations, where proarrhythmia and negative inotropy risks shape drug choice.
  • Screen for and manage drug-drug interactions, QT prolongation, and organ-based dose adjustment (renal and hepatic) as core safety steps when trial data are absent.
  • Decide the setting of initiation (inpatient telemetry vs outpatient) based on proarrhythmic risk and the individual clinical scenario rather than assuming trial protocols apply.
  • Document the rationale for each off-trial prescribing decision and reassess as new evidence emerges.

At the bedside

  • Before starting an antiarrhythmic in an off-trial patient, obtain a baseline ECG (QTc, QRS), assess renal and hepatic function, and review the full medication list for interactions.
  • Match the monitoring intensity to proarrhythmic risk: consider inpatient rhythm monitoring during initiation of higher-risk agents or in patients with structural heart disease.
  • For pediatric, congenital, pregnant, or organ-impaired patients, seek electrophysiology (and, where relevant, PACES-aligned pediatric EP) input rather than extrapolating adult doses blindly.
  • Tell patients and colleagues when a choice is expert-consensus based rather than trial-proven, and re-evaluate the plan as the clinical picture or evidence changes.
Bottom line / exam pearl

When the trials do not cover your patient, this HRS/PACES statement gives structured expert consensus, not proof, so individualize the drug, dose, and monitoring setting and document your reasoning.

References

  • 2026 HRS/PACES scientific statement on the use of antiarrhythmic drugs in understudied clinical scenarios (Heart Rhythm). www.heartrhythmjournal.com
  • Heart Rhythm journal (HRS publications portal). www.hrsonline.org
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Resuscitation & Critical Care36 guidelines

▸2025 AHA Advanced Cardiac Life Support (ACLS)ResusCirculation · 2025
Clinical takeaway

No new drugs or algorithm overhaul — but several practical refinements that change what you do at the bedside.

Key changes & the reasoning

  • Opioid overdose — don't delay CPR. In cardiac arrest, high-quality chest compressions come first; naloxone is an adjunct, not a substitute, and fetching it must not interrupt compressions.
  • Mechanical CPR not routine for out-of-hospital arrest — trials show no benefit over good manual CPR, which stays the default; reserve devices for special situations (moving/transport, cath lab, prolonged ECPR).
  • IV preferred over IO for ACLS drugs — recent trials suggest better drug delivery and outcomes with a peripheral IV first; use IO only if IV access fails or is inaccessible.
  • Defibrillation / cardioversion:
    • Start synchronised cardioversion for AF/flutter at 200 J biphasic.
    • Do not use vector change or double sequential defibrillation for refractory VF (insufficient evidence to recommend routinely).
    • Polymorphic VT is unstable — defibrillate immediately (don't attempt synchronised cardioversion on a chaotic rhythm the machine can't sync to).
  • POCUS — an experienced operator may use it to identify reversible causes (pneumothorax, tamponade, PE), only if it does not interrupt compressions; misuse to inappropriately stop CPR is explicitly discouraged.
  • Post-ROSC: targeted temperature management at 36 °C for at least 36 hours (avoid fever, which worsens brain injury).
  • Education: children as young as 12 can learn effective CPR/AED use; cognitive aids (checklists, algorithm apps) are recommended for professionals during codes — but lay rescuers should focus on compressions.
Bottom line / exam pearl

Remember the shifts: CPR before naloxone · manual over mechanical CPR · IV before IO · 200 J for AF cardioversion · shock polymorphic VT immediately · POCUS only if it doesn't stop CPR · TTM 36 °C ≥36 h.

▸Surviving Sepsis Campaign — Sepsis & Septic ShockCritical careSSC · Crit Care Med
Clinical takeaway

Screen early, deliver the sepsis bundle fast, resuscitate to MAP ≥65 with balanced fluids and noradrenaline — then de-escalate.

Background

Sepsis is life-threatening organ dysfunction from a dysregulated response to infection; septic shock adds a vasopressor requirement plus lactate >2 despite fluids. The Campaign frames care around rapid recognition and a time-critical bundle, with the latest emphasis on avoiding over-resuscitation.

Key recommendations

  • Screen with a validated tool; act on suspicion, don't wait for confirmation.
  • Bundle (within the first hour): measure lactate (repeat if >2); take blood cultures before antibiotics; give broad-spectrum antibiotics; start 30 mL/kg balanced crystalloid for hypotension or lactate ≥4; start vasopressors if hypotensive during/after fluids to keep MAP ≥65 (a range of 60–70 is practical).
  • Vasopressors: noradrenaline first-line; add vasopressin, then adrenaline; add hydrocortisone for ongoing pressor need.
  • Fluids: balanced crystalloids preferred over saline; use dynamic measures to guide further fluid and avoid over-resuscitation.
  • Then de-escalate: narrow antibiotics on cultures, source control, and active fluid removal in the later phase.
Bottom line / exam pearl

Recognise fast → lactate, cultures, antibiotics, balanced fluids, noradrenaline to MAP ≥65 → then de-escalate antibiotics and remove excess fluid. Steroids for refractory shock.

▸Anaphylaxis (Resuscitation Council UK / WAO)ResusResus Council UK
Clinical takeaway

IM adrenaline into the anterolateral thigh is the immediate, life-saving treatment — give it early and repeat after 5 minutes if needed.

Background

Anaphylaxis is a severe, life-threatening systemic hypersensitivity reaction with rapid Airway/Breathing/Circulation compromise, usually with skin changes.

Key recommendations

  • IM adrenaline 1:1000 into the anterolateral thigh, repeat after 5 minutes if no improvement. Adult/>12 y: 500 mcg (0.5 mL); 6–12 y: 300 mcg; 6 mo–6 y: 150 mcg.
  • Remove the trigger, give high-flow oxygen, lie flat with legs raised (sit up if breathing difficulty), and a rapid IV crystalloid bolus (500–1000 mL adult).
  • Refractory (no response to 2 IM doses) → adrenaline infusion + expert/critical-care help.
  • Antihistamines and steroids are NOT first-line — steroids are no longer routinely recommended for the acute reaction.
  • Observe for a biphasic reaction (2–12 h), measure mast cell tryptase, prescribe two adrenaline auto-injectors and refer to allergy.
Bottom line / exam pearl

Adrenaline IM early and repeated is everything; fluids and oxygen support it. Antihistamines/steroids are adjuncts, not treatment. Two auto-injectors + allergy referral on discharge.

▸Major Haemorrhage & Massive TransfusionCritical careMajor haemorrhage protocol
Clinical takeaway

Activate the protocol early, give balanced blood products (roughly 1:1:1) and tranexamic acid, control the source, and keep the patient warm.

Background

Uncontrolled haemorrhage kills through the 'lethal triad' of hypothermia, acidosis and coagulopathy — modern damage-control resuscitation targets all three while stopping the bleeding.

Key recommendations

  • Recognise early (mechanism, shock index, ongoing loss) and activate the major haemorrhage protocol.
  • Tranexamic acid within 3 hours of injury (1 g over 10 min, then 1 g over 8 h).
  • Transfuse RBC : FFP : platelets ≈ 1 : 1 : 1; minimise crystalloid.
  • Permissive hypotension (SBP ~80–90) until surgical control — except in traumatic brain injury, where perfusion must be maintained.
  • Prevent/treat the lethal triad: keep warm, correct acidosis, give calcium, and monitor coagulation.
  • Reverse anticoagulants — PCC for warfarin (and DOAC factor-Xa where indicated), idarucizumab for dabigatran.
  • Definitive control: damage-control surgery or interventional radiology.
Bottom line / exam pearl

TXA early, blood in balanced ratios (1:1:1), permissive hypotension (not in TBI), stop the bleeding, and fight the lethal triad — warmth, calcium, correct coagulopathy.

▸Adult Sepsis and Septic Shock (Surviving Sepsis Campaign 2026)Critical careSCCM/ESICM (Critical Care Medicine / Intensive Care Medicine) · 2026
Clinical takeaway

Norepinephrine remains first-line and can be started peripherally to avoid delaying MAP restoration; balanced crystalloids are preferred over saline, and after an initial ~30 mL/kg either a restrictive or liberal fluid strategy is now acceptable, individualised to the patient.

Background — why it changed

This is a major refresh of the 2021 guidance, developed by a large international panel spanning many countries with substantial low- and middle-income representation. It contains around 129 statements, of which roughly 46 are new, and adds bedside quick-reference graphics and clearer strong-versus-conditional labelling. New trial evidence on fluid strategy, peripheral vasopressors and antimicrobial timing drove several changes.

Key recommendations

  • Initial fluids: suggest at least 30 mL/kg IV crystalloid within the first 3 hours for sepsis-induced hypoperfusion or septic shock (low certainty), individualised and with frequent reassessment.
  • Fluid strategy after initial resuscitation: for persistent hypoperfusion after ~30 mL/kg, suggest either a restrictive or a liberal approach guided by patient and health-system factors.
  • Crystalloid choice: suggest balanced crystalloids over 0.9% saline (moderate certainty).
  • First-line vasopressor: recommend norepinephrine over dopamine/others; suggest starting vasopressors peripherally rather than waiting for central access.
  • Add-on vasopressors: suggest adding vasopressin on escalating norepinephrine, then adrenaline if MAP remains inadequate.
  • Corticosteroids: suggest IV corticosteroids in septic shock (low certainty).
  • Antimicrobials: for probable/definite sepsis, give immediately, ideally within 1 hour; for possible sepsis without shock, a time-limited rapid work-up with antimicrobials within 3 hours if concern persists.

At the bedside

  • You no longer have to wait for a central line: start norepinephrine peripherally through a good large-bore cannula while resuscitating.
  • Reassess dynamically after the first bolus rather than reflexively chasing a fixed total volume - both over- and under-resuscitation cause harm.
  • Reach for balanced fluids (e.g. Hartmann's/Plasma-Lyte) in preference to normal saline.
  • Distinguish 'possible' from 'probable' sepsis: the 1-hour antibiotic clock is for shock or probable sepsis, with a permissible short diagnostic window (up to 3 h) for equivocal cases without shock.
Bottom line / exam pearl

Norepinephrine first (peripherally if needed), balanced crystalloids, individualised fluid volume, and antibiotics within 1 hour for probable sepsis or shock.

References

▸Paediatric Sepsis and Septic Shock (Surviving Sepsis Campaign 2026)Critical careSCCM/ESICM (Pediatric Critical Care Medicine / Intensive Care Medicine) · 2026
Clinical takeaway

The paediatric update introduces graded definitions - probable sepsis, suspected septic shock, and septic shock with persistent hypoperfusion - and emphasises early lactate, prompt antimicrobials, point-of-care ultrasound and structured follow-up for the many survivors left with lasting morbidity.

Background — why it changed

This revises the first dedicated paediatric SSC guidelines (2020). A panel of around 68 international experts produced roughly 61 statements, applying to children from term birth (>=37 weeks) to 18 years with acute infection and organ dysfunction. New evidence and a push for practical, resource-aware bedside criteria drove the update.

Key recommendations

  • New tiered definitions: probable sepsis, suspected septic shock, and septic shock with persistent hypoperfusion, intended to capture essentially all children with acute infection plus organ dysfunction.
  • Measure blood lactate at initial assessment as part of recognition and risk stratification.
  • Early antimicrobial therapy once sepsis is recognised.
  • Point-of-care ultrasound (cardiac and lung POCUS) to guide haemodynamic and respiratory management.
  • Conservative oxygenation: an SpO2 target of around 88-92% is suggested.
  • Early rehabilitation and attention to post-sepsis morbidity, with long-term follow-up.
  • Emphasis on hospital performance-improvement programmes to embed timely recognition and treatment.

At the bedside

  • Check a lactate early in the unwell febrile child - it now sits within the recognition pathway.
  • Use POCUS to decide whether ongoing shock is fluid-responsive versus needing early vasoactive support, rather than repeated blind boluses.
  • Avoid hyperoxia: titrate oxygen to roughly 88-92% SpO2 once stabilised.
  • Flag survivors for follow-up - counsel families that recovery can involve physical, cognitive and emotional sequelae.
Bottom line / exam pearl

Recognise early with lactate and the new tiered definitions, treat promptly with antibiotics and POCUS-guided support, avoid hyperoxia, and plan for post-sepsis follow-up.

References

▸Definition of Refractory Septic Shock (Delphi Consensus)Critical careSCCM/ESICM Delphi Consensus (Critical Care Medicine / Intensive Care Medicine) · 2026
Clinical takeaway

Refractory septic shock is defined by persistent tissue hypoperfusion (raised lactate and/or prolonged capillary refill) in a fluid-unresponsive patient requiring a noradrenaline-equivalent dose > 0.5 mcg/kg/min, with critical-care ultrasound to confirm when mixed shock is suspected.

Background — why it changed

Until now there has been no agreed definition of when septic shock becomes 'refractory', hampering trials of rescue therapies and consistent bedside recognition. A multinational, multiprofessional panel (around 56 experts from 22 countries) used a structured five-round Delphi process during 2025, reaching consensus on 13 criteria across perfusion, organ dysfunction, adequate volume/fluid responsiveness and vasoactive drug use.

Key recommendations

  • Vasopressor threshold: a noradrenaline-equivalent dose greater than 0.5 mcg/kg/min is central to the definition.
  • Persistent hypoperfusion: persistently elevated lactate and/or prolonged capillary refill time despite treatment.
  • Optimised volume state: the patient must be fluid unresponsive with adequate intravascular volume before the label applies.
  • Confirm the shock type: use critical-care ultrasound (CCUS) when mixed (e.g. cardiogenic) shock is suspected, to avoid mislabelling.
  • The 13 consensus criteria span four domains: markers of tissue perfusion, markers of organ dysfunction, adequate fluid resuscitation/intravascular volume, and vasoactive drug use.
  • Intended to standardise identification for enrolment into trials of rescue/adjunctive therapies, not to prescribe a specific treatment.

At the bedside

  • Before calling shock 'refractory', confirm the patient is genuinely fluid-optimised and not simply under-resuscitated.
  • Track a noradrenaline-equivalent dose - crossing >0.5 mcg/kg/min with ongoing hypoperfusion should trigger escalation and senior review.
  • Use bedside echo/CCUS to exclude an unrecognised cardiogenic or obstructive component.
  • Persisting lactate and prolonged capillary refill are the perfusion red flags to watch, not blood pressure alone.
Bottom line / exam pearl

Refractory = fluid-unresponsive septic shock needing noradrenaline-equivalent > 0.5 mcg/kg/min with persistent lactate/capillary-refill abnormality; confirm it is not missed mixed shock.

References

▸Allocation of Critical Care Resources During Crisis-Level ShortagesCritical careSCCM (American College of Critical Care Medicine) - Critical Care Medicine · 2026
Clinical takeaway

These guidelines offer an evidence-based framework for triaging ICU admission when products, staff or beds are critically scarce, aiming to maximise survival while preserving ethical, equitable care - though the panel stresses the underlying evidence is largely low or very low certainty.

Background — why it changed

Pandemic experience exposed the lack of rigorous, evidence-based triage guidance for genuine crisis conditions. A 21-member multidisciplinary panel (physicians, nursing, advanced practice providers, respiratory therapists, ethicists, a lawyer and patient/family representatives) reviewed the evidence for triaging critically ill adults during crisis-level shortages of essential resources.

Key recommendations

  • Defines crisis-level shortage as severe deficits of products (e.g. blood, ventilators), personnel (e.g. nurses, respiratory therapists) and facilities (e.g. ICU beds) that materially degrade care.
  • Triage should prioritise strategies that maximise survival while remaining ethical and equitable.
  • Recommends a structured, transparent triage process rather than ad hoc bedside rationing by individual clinicians.
  • Explicitly notes that certainty of evidence was low or very low across all questions, so recommendations are cautious and context-dependent.
  • Frames triage as a system/institutional responsibility with attention to fairness and avoidance of discriminatory criteria.
  • Intended to be activated only under declared crisis conditions, distinct from conventional or contingency care.

At the bedside

  • Crisis triage is an institutional, pre-declared protocol - individual clinicians should not improvise rationing at the bedside.
  • Know your hospital's surge/crisis-standards trigger and who authorises activation before you need it.
  • Decisions should rest on survival benefit and objective clinical factors, applied consistently and transparently to all patients.
  • Document the crisis context and criteria used; separate the treating role from the triage-decision role where possible.
Bottom line / exam pearl

A framework for fair, survival-oriented ICU triage in true resource crises - but built on weak evidence, so it emphasises transparent process over rigid scoring.

References

▸Transfer of the Critically Ill Adult, 5th Edition (ICS)Critical careIntensive Care Society (ICS), endorsed by FICM and HSSIB · 2026
Clinical takeaway

A major expansion of UK transfer guidance with new chapters defining minimum equipment, medications, documentation and pre-transfer checklists, reinforcing that every acute hospital must be able to resuscitate, stabilise and transfer critically ill patients 24/7.

Background — why it changed

This is a substantial revision of the previous (4th) edition, reflecting changes in critical care transfer since the COVID-19 pandemic, including the growth of dedicated transfer services. It is endorsed by the Faculty of Intensive Care Medicine and the Health Services Safety Investigations Body, and is accompanied by new companion pathways such as maternal transfers.

Key recommendations

  • System readiness: all acute hospitals must have systems and resources to resuscitate, stabilise and transfer critically ill patients 24 hours a day, 7 days a week.
  • New dedicated chapters setting minimum standards for equipment, medications, and paperwork/documentation.
  • Stabilise before you go: emphasis on resuscitation, stabilisation and structured patient preparation prior to any transfer.
  • Checklists: formal pre-transfer checklists to standardise safety and reduce omissions.
  • Monitoring in transit should match the standard of care the patient was receiving, with attention to continuity of monitoring and drug delivery.
  • Safety, documentation and handover chapters strengthen structured clinical handover at the receiving unit.
  • New companion guidance (e.g. maternal transfers) to be used alongside the core 5th edition.

At the bedside

  • Treat the transfer as a period of ongoing intensive care - stabilise (airway, access, haemodynamics) before moving, not en route.
  • Run the pre-transfer checklist every time: equipment, oxygen/battery reserve, drugs, notes/imaging, and an appropriately trained escort.
  • Maintain the same monitoring standard in the ambulance/corridor as on the unit; anticipate deterioration and pack for it.
  • Give a structured handover to the receiving team and ensure documentation travels with the patient.
Bottom line / exam pearl

Stabilise first, use the checklist, take the right kit, drugs and trained escort, and maintain ICU-standard monitoring throughout - transfer is intensive care on the move.

References

  • ICS - 5th edition announcement. ics.ac.uk
  • ICS - Transfer of the Critically Ill Adult, 5th edition (PDF). ics.ac.uk
▸Major Bleeding on Direct Oral Anticoagulants in the ED (ACEP Clinical Policy)ResusAmerican College of Emergency Physicians (ACEP) - Annals of Emergency Medicine · 2026
Clinical takeaway

For life-threatening DOAC-associated bleeding, use agent-specific reversal where available - idarucizumab for dabigatran, and a factor Xa reversal strategy for apixaban/rivaroxaban (specific antidote or, where that is unavailable, prothrombin complex concentrate) - alongside standard haemorrhage control and resuscitation.

Background — why it changed

DOAC use is now widespread, so emergency physicians frequently face major or intracranial haemorrhage in anticoagulated patients, and the reversal-agent landscape has shifted (including changes in availability of specific factor Xa antidotes). This ACEP clinical policy addresses the critical questions around reversal and assessment in adult ED patients on DOACs.

Key recommendations

  • Dabigatran: reverse life-threatening/uncontrolled bleeding with idarucizumab (a fixed 5 g IV dose), the specific antidote.
  • Factor Xa inhibitors (apixaban, rivaroxaban, edoxaban): use a specific factor Xa reversal agent where available; 4-factor prothrombin complex concentrate is the practical alternative where a specific antidote is not available or not stocked.
  • Availability caveat: access to specific factor Xa antidotes varies by region and over time, so know your own institution's stocked agent and protocol in advance.
  • Coagulation testing is limited: routine PT/aPTT do not reliably quantify DOAC effect, so do not use a normal standard coagulation screen to exclude clinically significant drug levels.
  • Reserve reversal for major/life-threatening bleeding (including intracranial haemorrhage) or genuinely urgent procedures - not for minor or stable bleeding.
  • Combine any reversal with standard measures: source control, transfusion/haemostatic support, and correction of contributing factors.

At the bedside

  • Establish the specific DOAC, last dose timing and renal function early - these drive both risk and reversal decisions.
  • Do not be reassured by a normal PT/aPTT; it does not rule out a significant DOAC effect.
  • Know today, before the resus, which reversal agent your ED actually stocks for factor Xa inhibitors and how to access it fast.
  • In DOAC-associated intracranial haemorrhage, move immediately on reversal plus neurosurgical/critical-care involvement rather than waiting on assays.
Bottom line / exam pearl

Idarucizumab reverses dabigatran; for factor Xa inhibitor bleeding give the available specific antidote or PCC - and never rely on a normal PT/aPTT to exclude a DOAC effect.

References

▸Unscheduled Procedural Sedation: Clinical Practice (Part 2)ResusACEP / multidisciplinary Delphi consensus, Ann Emerg Med · 2026
Clinical takeaway

This multidisciplinary consensus reaffirms that ED procedural sedation is safe when done systematically: do not delay sedation based on fasting time, monitor oxygenation and ventilation, and ketamine and propofol are both endorsed as safe in adults and children.

Background — why it changed

Part 2 of ACEP's Unscheduled Procedural Sedation Multidisciplinary Delphi Consensus Guidelines (approved by the ACEP Board of Directors 29 April 2026, published Ann Emerg Med Sept 2026) was developed with a 20-member panel across 14 organisations. It addresses clinical practice - assessment, monitoring, drug selection and recovery - across all settings and all ages.

Key recommendations

  • Do not delay procedural sedation based on preprocedural fasting time in adults or children; aspiration risk in sedation is low relative to operative anaesthesia.
  • Verify ventilatory adequacy by continual observation of the airway and chest-wall motion, plus pulse oximetry and capnography.
  • Ketamine, propofol, and the propofol-ketamine combination can each be safely used for adults and children.
  • In patients at higher-than-usual risk, ketamine alone is a logical choice as it uniquely tends to preserve protective airway reflexes.
  • Perform a focused pre-sedation assessment and match agent, depth and personnel to procedure and patient risk.
  • Recovery and discharge should be criteria-based, with monitoring continued until the patient returns to a safe baseline.

At the bedside

  • Stop delaying fracture reductions and cardioversions for NPO status - the evidence does not support fasting-based cancellation.
  • Set up capnography routinely; it detects hypoventilation before desaturation.
  • For the crashing or high-risk airway patient needing sedation, reach for ketamine.
  • Have reversal agents, suction, airway kit and a dedicated monitoring provider ready before the first drug.
Bottom line / exam pearl

Fasting time should not delay ED sedation; capnography plus pulse oximetry and clinical observation are core monitoring, and ketamine/propofol are the workhorse agents.

References

▸Unscheduled Procedural Sedation: Principles, Oversight & Quality Monitoring (Part 1)ResusACEP / multidisciplinary Delphi consensus, Ann Emerg Med · 2026
Clinical takeaway

Part 1 sets the governance framework for unscheduled sedation: competency-based privileging, multidisciplinary institutional oversight, and continuous quality monitoring, applicable across specialties, settings and all ages.

Background — why it changed

Companion to Part 2, Part 1 (approved by the ACEP Board of Directors 29 April 2026, published Ann Emerg Med Sept 2026) addresses the underlying principles and oversight of procedural sedation - competencies, privileging and quality monitoring - as a scientific, evidence-based framework to inform hospital and ED sedation policies.

Key recommendations

  • Institutional oversight of sedation should be collaborative and multidisciplinary, typically via a local procedural sedation committee.
  • Privileging should be competency-based rather than specialty-based, focused on demonstrated skills (assessment, monitoring, rescue).
  • Practitioners must be able to rescue a patient from a level of sedation deeper than intended, including airway management.
  • A structured quality-monitoring programme should track adverse events, interventions and outcomes to drive improvement.
  • Policies should apply uniformly across clinical settings and patient age groups, rather than differing by department.
  • Sedation systems should ensure appropriate personnel, monitoring equipment and recovery processes are consistently available.

At the bedside

  • Know your institution's sedation privileging and rescue-competency requirements before sedating.
  • Report and log sedation adverse events - the quality programme depends on complete capture.
  • Advocate for consistent monitoring and staffing standards regardless of which department performs the sedation.
  • Skills to rescue from over-sedation (bag-mask, airway adjuncts, reversal) are the safety net the framework assumes you have.
Bottom line / exam pearl

Safe sedation is a system: competency-based privileging, multidisciplinary oversight and quality monitoring, not just drug choice.

References

▸Quantitative Lung Ultrasound in the ICUCritical careESICM-ESPNIC international expert consensus; Intensive Care Medicine (2025;51(6):1022-1049) · 2025
Clinical takeaway

This consensus formalises quantitative lung ultrasound (LUS) scoring as a reproducible bedside tool to grade lung aeration and track change over time across adult, paediatric and neonatal ICUs.

Background — why it changed

LUS has been used qualitatively for years, but scoring methods and technique varied widely, limiting comparability and research use. ESICM (European Society of Intensive Care Medicine) and ESPNIC (paediatric/neonatal society) convened ~20 experts plus methodologists to address 14 prioritised clinical questions on technique and clinical application. The result standardises how the aeration score is generated and where it is clinically useful.

Key recommendations

  • Score aeration in each region on a 0-3 scale: 0 = A-lines/normal (up to 2 B-lines), 1 = >2 discrete B-lines (mild loss), 2 = coalescent B-lines over >half the pleural line (moderate loss), 3 = consolidation (severe loss).
  • In adults the standard survey uses 12 thoracic regions (6 per lung); both simplified and extended regional protocols are endorsed.
  • Use quantitative LUS to monitor lung aeration over time and response to interventions (e.g. recruitment, diuresis, PEEP changes), not for one-off labelling alone.
  • Standardise probe choice, depth and reference lines to maximise reproducibility and inter-operator agreement.
  • Apply LUS scoring within a defined clinical question (e.g. ARDS severity, weaning/extubation readiness, congestion) rather than as an isolated number.
  • Adapt region counts and interpretation for paediatric and neonatal patients, for whom aeration scores also carry prognostic value.
  • Interpret scores alongside clinical context and other imaging; a score is a semiquantitative aeration estimate, not a diagnosis.

At the bedside

  • Learn the 0-3 aeration score and sweep a consistent 12-zone map so serial exams are truly comparable.
  • Track the trend: a rising total LUS score signals worsening aeration/de-recruitment before oxygenation may fall.
  • Use a low LUS score at the lung bases as supportive evidence of readiness when assessing extubation.
  • Keep probe settings and patient position fixed between studies to avoid artefactual score change.
Bottom line / exam pearl

Quantitative LUS grades aeration region-by-region from 0 (normal) to 3 (consolidation) and is best used to follow trends, not as a stand-alone diagnosis.

References

▸Non-Invasive Intracranial Pressure Monitoring in Traumatic Brain Injury (B-ICONIC)Critical careB-ICONIC (Brussels) consensus of international TBI experts; Intensive Care Medicine · 2025
Clinical takeaway

When invasive ICP monitoring is unavailable, the B-ICONIC consensus recommends a multimodal non-invasive strategy: use at least two concordant nICP modalities plus clinical exam and imaging to guide ICP-directed therapy.

Background — why it changed

Invasive ICP monitoring is the reference standard but is unavailable in many centres, especially in low- and middle-income settings. A panel of 41 experts who routinely use non-invasive ICP (nICP) tools built practical guidance and management algorithms for TBI care without an intraparenchymal or ventricular device. It defines which modalities to combine and how to escalate or de-escalate therapy.

Key recommendations

  • No single non-invasive method is sufficient; require at least two concordant nICP modalities, giving priority to the most concerning value.
  • Core modalities are optic nerve sheath diameter (ONSD), transcranial Doppler (TCD/TCCD) pulsatility index, and automated pupillometry (Neurological Pupil index, NPi).
  • An ONSD >= 6 mm is suggestive of ICP >= 20 mmHg.
  • A TCD pulsatility index >= ~1.4 correlates with predicted ICP >= 20 mmHg.
  • A low/abnormal NPi (approximately <= 3) supports poor intracranial compliance/raised ICP.
  • Integrate nICP findings with clinical examination and neuroimaging (CT); do not act on a single isolated measurement.
  • Use the concordant multimodal signal to drive escalation or de-escalation of ICP-directed therapy via the consensus algorithm.

At the bedside

  • Pair modalities: e.g. confirm a widened ONSD with an elevated TCD pulsatility index or a dropping NPi before escalating osmotherapy.
  • Trend serial NPi with automated pupillometry to catch deterioration earlier than manual pupil checks.
  • Anchor thresholds to clinical picture and CT; treat the patient and concordant signals, not one borderline number.
  • Reserve non-invasive assessment for when an invasive device is unavailable or being arranged, and hand off findings clearly.
Bottom line / exam pearl

Without an invasive monitor, suspect raised ICP when at least two of ONSD >=6 mm, TCD PI >=~1.4, and a low NPi agree with the clinical and CT picture.

References

▸Gastric Point-of-Care Ultrasound for Aspiration RiskCritical careASRA Pain Medicine narrative review and expert practice recommendations; Regional Anesthesia & Pain Medicine · 2025
Clinical takeaway

Gastric POCUS lets clinicians individualise aspiration risk in medically complex patients by imaging the antrum, grading it, and estimating gastric volume when fasting status is uncertain.

Background — why it changed

Fasting guidelines poorly predict actual gastric contents in many at-risk groups, and the surge in GLP-1 receptor agonist use has heightened concern about delayed emptying. ASRA Pain Medicine reviewed the evidence and issued expert practice recommendations for using gastric POCUS to guide decisions in medically complex patients undergoing regional anaesthesia and pain procedures. It targets seven populations: pregnant, obese, diabetic, GERD, emergency, enterally fed, and GLP-1RA patients.

Key recommendations

  • Scan the gastric antrum in supine and right lateral decubitus (RLD) positions to classify contents.
  • Use the Perlas 3-point grade: grade 0 = empty in both positions, grade 1 = clear fluid seen only in RLD (small volume), grade 2 = clear fluid in both positions (larger volume).
  • Estimate antral cross-sectional area (CSA) from anteroposterior x craniocaudal diameters (CSA = pi x AP x CC / 4); an antral CSA cutoff ~340 mm2 flags a higher-risk (full) stomach.
  • Interpret volume thresholds: < 1.5 mL/kg is typical of a fasted, low-risk stomach, while > 1.5 mL/kg or any solid content indicates increased aspiration risk.
  • Solid or thick ('frosted-glass') content, or grade 2 fluid, indicates a full stomach regardless of stated fasting time.
  • Prioritise gastric POCUS in GLP-1RA users, active labour/urgent caesarean, and diabetics, where residual content is more likely.
  • Let findings guide management (proceed, delay, or treat as full stomach with rapid-sequence precautions) rather than replacing clinical judgement.

At the bedside

  • Use a curvilinear probe with the patient in RLD to maximise sensitivity for antral fluid; identify aorta and rectus abdominis as landmarks.
  • Empty antrum (grade 0) in both positions supports a low-risk stomach; grade 2 or solids means treat as full stomach.
  • Reach for gastric POCUS specifically when a GLP-1 agonist patient presents with uncertain hold or GI symptoms.
  • Document the grade, CSA and estimated volume to justify proceeding, delaying, or applying aspiration precautions.
Bottom line / exam pearl

In uncertain or high-risk patients, an empty antrum (Perlas 0) reassures, while grade 2 fluid, CSA >~340 mm2, >1.5 mL/kg, or any solid means treat as a full stomach.

References

▸Adult Critical Care UltrasonographyCritical careSociety of Critical Care Medicine (SCCM) Guidelines - Focused Update; Critical Care Medicine (2025;53(2)) · 2025
Clinical takeaway

SCCM suggests using critical care ultrasonography (CCUS) to guide management in shock and respiratory failure, and specifically favours ultrasound-guided volume management over usual care, citing a signal toward improved mortality.

Background — why it changed

CCUS has become central to ICU practice, and this focused update refreshes the prior SCCM recommendations with current evidence. An interprofessional panel of 36 (including two patient/family representatives) addressed five high-yield scenarios: cardiac arrest, sepsis/septic shock, acute dyspnoea/respiratory failure, volume management, and cardiogenic shock. The guideline assumes operators already have appropriate equipment, training and competency.

Key recommendations

  • In septic shock, suggest using CCUS to guide management.
  • In acute dyspnoea / respiratory failure, suggest using CCUS to guide management.
  • In cardiogenic shock, suggest using CCUS to guide management.
  • For volume management, suggest CCUS-guided assessment over usual care, given evidence suggesting a mortality benefit.
  • Recommendations presuppose operator competency - appropriate training and equipment are assumed prerequisites.
  • CCUS is positioned as a management-guiding adjunct integrated with the full clinical assessment, across the five defined scenarios.
  • Recommendations are largely conditional/suggested, reflecting moderate-to-low certainty evidence.

At the bedside

  • Fold focused cardiac, lung and IVC/venous ultrasound into the bedside assessment of undifferentiated shock and dyspnoea.
  • Use dynamic ultrasound measures rather than static numbers to steer fluids, and reassess after each intervention.
  • Do not exceed your trained scope - the guideline assumes competency, so obtain credentialed help for advanced views.
  • Treat CCUS findings as one input alongside exam, labs and haemodynamics, not as a stand-alone verdict.
Bottom line / exam pearl

SCCM 2024 focused update: use CCUS to guide management in sepsis, respiratory failure and cardiogenic shock, and prefer ultrasound-guided over usual-care volume management.

References

▸Emergency Department Observation ServicesResusAmerican College of Emergency Physicians (ACEP) policy statement; State-of-the-Art interim practice update (JACEP Open) · 2026
Clinical takeaway

A dedicated, protocol-driven ED observation unit is a best practice that shortens length of stay and reduces avoidable admissions while keeping short-stay patients under emergency-physician oversight.

Background — why it changed

ACEP policy supports observing appropriate ED patients in a dedicated observation area rather than in inpatient or acute ED beds. A 2026 interim practice update to ACEP's earlier resource paper reviews structure, staffing, billing, and expanding applications across chest pain, toxicology, geriatrics, psychiatry, and oncology. The model is a time-limited diagnostic and therapeutic trial, not a holding area.

Key recommendations

  • Observe appropriate ED patients in a dedicated ED observation unit rather than general inpatient or acute ED beds.
  • Governance in writing: medical and nursing leadership, admission and discharge criteria, the responsible physician and nurse, and handoff/documentation rules.
  • Use condition-specific observation protocols (e.g., chest pain, asthma, dehydration, TIA, cellulitis) to standardize care.
  • Set a maximum allowable length of stay with clear criteria to admit or discharge.
  • APPs (PA/NP) staffing the unit should be directly supervised by an emergency physician, in person or via telehealth.
  • Define which clinical changes trigger physician notification.
  • Continuously monitor utilization and quality metrics.

At the bedside

  • Observation is for a defined question with an expected short answer -- if the patient clearly needs admission, admit; if clearly dischargeable, discharge.
  • Set the disposition clock and re-evaluate against protocol endpoints rather than leaving it open-ended.
  • Know the unit's inclusion and exclusion criteria before placing a patient in observation.
Bottom line / exam pearl

Observation is a time-limited, protocol-driven trial under EM oversight -- not a parking spot for undecided admissions.

References

▸Transfer of Critically Ill Adults to Their Preferred Place of DeathCritical careIntensive Care Society (ICS) - supplementary guidance to the Transfer of the Critically Ill Adult · 2025
Clinical takeaway

A minority of dying ICU patients wish to die at home or another meaningful place, and with careful multidisciplinary decision-making a planned, compassionate critical care transfer can honour that wish. Feasibility, safety and family support must be balanced against the patient's expressed preference.

Background — why it changed

Published July 2025 by a joint intensive care and palliative medicine group, this supplementary guidance fills a long-standing gap. Teams increasingly face requests to facilitate death outside the ICU but previously had little structured guidance on how to decide on and safely execute such transfers under time pressure and clinical uncertainty.

Key recommendations

  • Use a structured five-stage approach: multidisciplinary review, communication, planning and preparation, the transfer itself, and anticipation of potential complications.
  • Confirm the decision through multidisciplinary review and repeated dialogue with the patient (where able) and family about end-of-life preferences.
  • The escorting team must meet the standards of the ICS Transfer of the Critically Ill Adult guideline and be appropriately senior, experienced and capable of working in a non-clinical environment.
  • Escort staff must be experienced in the end-of-life care of critically ill adults, including managing the possibility of death during transit.
  • Plan explicitly for foreseeable complications (deterioration or death en route) and agree a management plan in advance.
  • Prepare the receiving location, ambulance service and family, ensuring symptom-control medications and documentation travel with the patient.

At the bedside

  • Ask early and revisit: does this patient have a preferred place of death, and is transfer realistically achievable in the time available?
  • Hold an MDT and palliative discussion and document the plan, including what happens if the patient dies before or during transfer.
  • Send a senior, end-of-life-experienced escort with symptom-control drugs, and brief the family that death may occur en route.
Bottom line / exam pearl

A planned transfer to a preferred place of death is a legitimate critical care intervention when an experienced MDT judges it safe, feasible and aligned with the patient's wishes.

References

  • ICS - The decision making and transfer of critically ill adults to their preferred place of death. ics.ac.uk
  • ICS guidance PDF. ics.ac.uk
▸Repatriation of International Critical Care Patients to UK HospitalsCritical careIntensive Care Society (ICS) · 2025
Clinical takeaway

UK residents who become critically ill abroad have a right to timely NHS care, and repatriation to the hospital serving their home should be treated with the same urgency as an internal network transfer. Where overseas care may be substandard, expedite repatriation.

Background — why it changed

Updated May 2025, this guidance sets out principles for coordinating the return of UK residents from overseas critical care units, where resources and standards of care vary widely and may fall below what is acceptable in UK units.

Key recommendations

  • All UK residents, including those taken ill abroad, have a right to timely access to NHS facilities.
  • Aim to repatriate to the hospital serving the patient's home residence within the timeframe used for internal transfers in that ODN - normally around 48 hours.
  • Every repatriation request must involve direct discussion with the receiving critical care consultant, in line with local ODN guidelines.
  • Where overseas care is, or is likely to be, below acceptable UK standards, make all efforts to repatriate immediately.
  • Coordinate through the operational delivery network (ODN) and critical care transfer service rather than through ad hoc arrangements.

At the bedside

  • Establish the patient's home hospital and ODN early, and route the request through it.
  • Speak consultant-to-consultant with the receiving unit before accepting or arranging transfer.
  • Assess whether current overseas care is adequate; if not, escalate the urgency of return.
Bottom line / exam pearl

Treat international repatriation like an internal network transfer - consultant-led, ODN-coordinated, and generally within about 48 hours.

References

  • ICS - Repatriation of International Critical Care Patients to UK Hospitals (May 2025). ics.ac.uk
  • ICS repatriation guidance asset (PDF). ics.ac.uk
▸A Code of Practice for the Diagnosis and Confirmation of DeathCritical careAcademy of Medical Royal Colleges (AoMRC), with the Faculty of Intensive Care Medicine · 2025
Clinical takeaway

The first full rewrite since 2008 confirms death as the permanent loss of the capacity for consciousness combined with the permanent loss of the capacity to breathe, diagnosable by somatic, circulatory or neurological criteria, and tightens apnoea-test parameters and the recording of time of death.

Background — why it changed

Published January 2025, this Code updates the 2008 version for the first time. It harmonises the three criteria sets across all ages and clinical settings and clarifies the timing of observation, apnoea-testing thresholds and how the time of death is recorded.

Key recommendations

  • Death may be confirmed using one of three criteria sets: somatic, circulatory, or neurological.
  • Circulatory death: after cardiorespiratory arrest, observe for a minimum of 5 minutes of continuous mechanical asystole (mechanical, not electrical) before confirmation, with absent pulse, heart sounds and pupillary responses.
  • Neurological (brainstem) death requires two full sets of clinical tests, including two apnoea tests, performed by two suitably qualified doctors.
  • Apnoea-test targets: starting PaCO2 at least 5.3 kPa, a rise of at least 2.7 kPa from baseline, an end PaCO2 of at least 8.0 kPa, with arterial pH below 7.3.
  • Preconditions must exclude reversible causes (drugs, hypothermia, endocrine or metabolic derangement) before neurological testing.
  • Time of death is recorded as the completion of the second set of neurological tests (or the point of confirmation for circulatory death).

At the bedside

  • For circulatory or DCD death, time the 5-minute observation from mechanical asystole and do not intervene during it.
  • Correct temperature, drug effects and metabolic derangements before starting brainstem testing.
  • Use the standard ABG apnoea targets (end PaCO2 >= 8.0 kPa, rise >= 2.7 kPa, pH < 7.3) and repeat the full test set.
Bottom line / exam pearl

Death is permanent loss of consciousness plus permanent loss of the capacity to breathe - confirm circulatory death after 5 minutes of asystole, and neurological death with two test sets meeting strict apnoea targets.

References

▸Fluid Therapy in Adult Critically Ill Patients, Part 2: The Volume of Resuscitation FluidsCritical careEuropean Society of Intensive Care Medicine (ESICM); Intensive Care Medicine · 2025
Clinical takeaway

In sepsis or septic shock, give up to 30 mL/kg of IV crystalloid in the initial phase with frequent reassessment, then individualise - the evidence does not favour a blanket restrictive or liberal strategy in the optimisation phase. Most recommendations rest on very-low-certainty evidence.

Background — why it changed

Published in Intensive Care Medicine (March 2025), this is Part 2 of a three-part ESICM series (Part 1 covers fluid type, Part 3 covers fluid removal and de-escalation). An international panel used PICO questions and the GRADE approach across the phases of resuscitation.

Key recommendations

  • Conceptualise fluid therapy in four phases: initial resuscitation, optimisation, stabilisation, and recovery.
  • In sepsis or septic shock, suggest up to 30 mL/kg IV crystalloid in the initial phase, adjusted to clinical context with frequent reassessment (very low certainty).
  • In the optimisation phase, no recommendation for or against a restrictive versus liberal strategy (moderate certainty of no meaningful difference between the tested approaches).
  • Use an individualised approach to fluid volume in the optimisation phase (very low certainty).
  • Favour frequent reassessment over fixed large-volume boluses, reflecting the very-low-certainty evidence base.

At the bedside

  • Start with about 30 mL/kg crystalloid in septic shock, but reassess after each bolus rather than front-loading blindly.
  • Beyond the initial phase, tailor further fluid to dynamic response and organ perfusion, not a fixed liberal or restrictive protocol.
  • Treat fluid as a drug with a harm ceiling - consider early vasopressors rather than over-resuscitating.
Bottom line / exam pearl

About 30 mL/kg crystalloid up front in septic shock, then individualise - neither routine liberal nor routine restrictive fluids proved superior.

References

▸Referring Patients with Severe Eating Disorders to Critical Care for Assisted NutritionCritical careIntensive Care Society & College of Intensive Care Medicine (CoICM, formerly Faculty of Intensive Care Medicine) · 2026
Clinical takeaway

A framework for the ethically and medico-legally complex situation of patients with severe eating disorders referred to critical care for assisted feeding, sometimes under restraint and mental health legislation. Engaging the eating-disorder behaviours is as important as the physiological refeeding.

Background — why it changed

Issued August 2026 in response to repeated enquiries about managing severe eating-disorder patients who need assisted nutrition with restraint under mental health law. It addresses the complex ethical, medico-legal, clinical and logistical challenges and the sparse evidence base in this area.

Key recommendations

  • Manage refeeding to avoid refeeding syndrome: MEED-based safe refeeding suggests increasing intake by about 5 kcal/kg/day every ~2 days toward roughly 60 kcal/kg/day, aiming for weight gain greater than 0.5 kg/week, with close biochemical monitoring.
  • Monitor and replace electrolytes closely (phosphate, potassium, magnesium) and give thiamine; note that underfeeding also causes harm.
  • Any use of restraint or forced/covert feeding must sit within the appropriate legal framework (e.g. Mental Health Act or Mental Capacity Act) with psychiatric involvement.
  • Actively address the eating-disorder behaviours - failure to do so can paradoxically escalate the intensity, invasiveness and restrictiveness of care required.
  • Decisions should be multidisciplinary, involving intensive care, eating-disorder and psychiatry specialists, with clear documentation of capacity and legal basis.
  • Treat critical care referral as being for specific interventions (safe assisted nutrition, monitoring, restraint) rather than a default pathway, weighing benefits against risks and least-restrictive options.

At the bedside

  • Before feeding, confirm the legal framework and capacity assessment and involve the eating-disorder or psychiatry team.
  • Start cautiously and monitor phosphate, potassium and magnesium with thiamine cover, escalating calories gradually per MEED.
  • Plan restraint and sedation with the MDT, document the least-restrictive rationale, and treat behaviours, not just biochemistry.
Bottom line / exam pearl

Assisted nutrition under restraint in severe eating disorders is a joint critical care-psychiatry, law-bound intervention where gradual MEED-guided refeeding and behavioural engagement matter as much as electrolyte control.

References

  • ICS/CoICM - Framework for referring patients with eating disorders to critical care for assisted nutrition (Aug 2026). ics.ac.uk
  • Journal of Eating Disorders - NG tube feeding under restraint: systematic scoping review. link.springer.com
▸Collaborative Sustainability and Resource Stewardship in the ICUCritical careANZICS in collaboration with the Intensive Care Society (UK); ANZICS/ICS toolkit · 2026
Clinical takeaway

Critical care is resource- and carbon-intensive, and this ANZICS/ICS toolkit gives multidisciplinary teams practical, evidence-informed strategies to cut environmental impact while maintaining high-quality patient care.

Background — why it changed

Endorsed by the ANZICS Board and the Intensive Care Society (UK) in March 2026, this guide builds on earlier 'Green Teams in the ICU' work. It shifts emphasis to the domains with the greatest impact potential - energy, travel, medical supplies, pharmaceuticals, diagnostics, and waste - and pairs case studies with actionable steps. It is aimed at clinicians, managers, educators, and sustainability leads to move units from intention to implementation.

Key recommendations

  • Energy: measure ICU power use, partner with engineers to cut HVAC demand, install efficient lighting, power down idle equipment, and design/refurbish units for efficiency.
  • Anaesthetic gases: move away from high-global-warming-potential agents such as desflurane and nitrous oxide toward lower-impact alternatives.
  • Pharmaceuticals: reduce medication waste, favor lower-carbon options, and educate staff on correct disposal (e.g., metered-dose inhaler propellants are potent greenhouse gases; consider dry-powder inhalers where appropriate).
  • Waste: make correct segregation as easy as possible at the bedside and recycle where feasible (e.g., pharmaceutical glass).
  • Reduce low-value diagnostics and supplies through value-based care and de-implementation of unnecessary tests.
  • Address travel/logistics (staff and sample transport, telehealth) as a contributor to the unit's footprint.
  • Embed a sustainability mindset and multidisciplinary Green Team collaboration into everyday ICU practice.

At the bedside

  • Right-size daily investigations - cut reflexive daily bloods, films, and repeat tests that will not change management.
  • Avoid desflurane/nitrous oxide when a lower-impact agent is clinically equivalent.
  • Sort waste correctly at the bedside and turn off monitors, pumps, and lights not in use.
  • Join or start a unit Green Team and champion value-based, lower-waste choices as routine practice.
Bottom line / exam pearl

Sustainable intensive care means less waste, less energy, greener anaesthetic and inhaler choices, and fewer low-value tests - delivered without compromising patient care.

References

  • ANZICS/ICS - Collaborative Sustainability and Resource Stewardship in the ICU (PDF). www.anzics.org
  • Intensive Care Society - collaborative sustainability work. ics.ac.uk
▸Caring for Older Adults in the ICUCritical careSociety of Critical Care Medicine (SCCM), Critical Care Medicine · 2026
Clinical takeaway

For critically ill adults aged 65 and older, embed a geriatric model of care built on the 4Ms and do not use antipsychotics to prevent delirium; chronological age alone should not drive decisions.

Background — why it changed

Older adults make up a large and growing share of ICU patients but have historically been under-served by generic critical-care protocols. A 22-member interprofessional SCCM/ACCM panel used the GRADE framework across five PICO questions to align ICU practice with Age-Friendly Health Systems principles. The evidence base is sparse, so most guidance is conditional or consensus-based.

Key recommendations

  • Apply a geriatric model of care built on the 4Ms - What Matters Most, Medications, Mentation, Mobility - for all older adults in the ICU (conditional).
  • Do not use antipsychotics to prevent delirium in critically ill older adults (conditional).
  • No recommendation for or against antipsychotics to treat established delirium.
  • No recommendation for a MAP target of 60-65 mm Hg vs usual care in older adults with vasodilatory shock.
  • No recommendation for or against specialised post-ICU follow-up for older survivors.
  • Guidance was built by an interprofessional panel (including a geriatrician, pharmacist, PT/OT and patient representative) using GRADE for adults aged >=65.

At the bedside

  • Ask 'what matters most' early and align goals of care with it; review medications and deprescribe high-risk or anticholinergic drugs.
  • Screen for and manage delirium with non-pharmacologic measures first - do not start antipsychotics as prophylaxis.
  • Prioritise early mobility and daily cognitive engagement to preserve function.
  • Let baseline frailty and function, not age alone, inform goals-of-care conversations.
Bottom line / exam pearl

In older ICU patients, operationalise the 4Ms and avoid antipsychotics for delirium prevention - age by itself should not dictate care.

References

▸Post-Resuscitation Care After Cardiac ArrestResusEuropean Resuscitation Council & European Society of Intensive Care Medicine (ERC-ESICM), published in Resuscitation / Intensive Care Medicine · 2025
Clinical takeaway

After ROSC, care is a bundle: find and treat the cause, avoid hypoxia and hyperoxia, maintain perfusion, and actively prevent fever rather than deep hypothermia, while delaying neuroprognostication.

Background — why it changed

The 2021 ERC-ESICM guidelines (updated 2025) consolidated post-arrest management into a structured pathway. The biggest shift followed the TTM2 trial: routine targeted hypothermia to 33 C was abandoned in favour of controlled normothermia with fever prevention, since 33 C showed no mortality or functional-outcome benefit over treating fever alone.

Key recommendations

  • Titrate oxygen to an SpO2 of 94-98% once it can be measured reliably; avoid both hypoxaemia and hyperoxaemia.
  • Ventilate to normocapnia (PaCO2 35-45 mmHg / 4.5-6.0 kPa).
  • Support haemodynamics to maintain adequate perfusion (urine output, normalising lactate), generally targeting MAP above ~65 mmHg; avoid hypotension.
  • Perform emergency coronary angiography in patients with suspected cardiac cause and ST-elevation on ECG.
  • Use continuous core-temperature monitoring and actively prevent fever (>37.7 C) for at least 72 h; routine hypothermia at 33 C is not recommended, and do not actively rewarm mild spontaneous hypothermia to normothermia.
  • Treat seizures (EEG-guided) and manage glucose, avoiding hypoglycaemia.
  • Delay neuroprognostication and use a multimodal approach no earlier than 72 h after ROSC in a patient off sedation.

At the bedside

  • Don't chase 100% SpO2 - dial FiO2 back to keep 94-98% once the saturation reading is trustworthy.
  • Set the ventilator for normocapnia and recheck an ABG rather than trusting end-tidal CO2 alone.
  • Put an antipyretic/cooling plan in place early to keep temperature at/below ~37.5 C and block fever - not to force 33 C.
  • Warn the family and team that meaningful neurological prognosis cannot be called in the first 72 hours.
Bottom line / exam pearl

Prevent fever, not induce deep hypothermia - and never prognosticate too early.

References

▸Management of Unanticipated Difficult Tracheal Intubation in AdultsResusDifficult Airway Society (DAS), published in British Journal of Anaesthesia · 2025
Clinical takeaway

The updated DAS algorithm shifts the emphasis from rescuing a failed airway to preventing failure and maximising first-attempt success, keeping the familiar linear Plan A-B-C-D pathway.

Background — why it changed

This is the first major revision of the 2015 DAS guideline, built from a 3-year systematic review of ~1,240 papers and a Delphi consensus, yielding roughly 65 recommendations. It reflects the routine availability of videolaryngoscopy and a stronger focus on human factors, preoxygenation and declaring failure early.

Key recommendations

  • Videolaryngoscopy is the recommended first choice for asleep tracheal intubation.
  • Limit intubation attempts to a maximum of three, plus one further attempt by a more experienced operator (3+1), to avoid airway trauma and the can't-intubate-can't-oxygenate (CICO) spiral.
  • Optimise the first attempt (Plan A): positioning, preoxygenation, neuromuscular block, and an adjunct such as a bougie, stylet or flexible scope with a hyperangulated blade.
  • Plan B: oxygenate and rescue with a second-generation supraglottic airway device.
  • Plan C: revert to facemask ventilation and, if the situation allows, wake the patient.
  • Plan D (CICO): declare emergency front-of-neck access and perform a scalpel-bougie-tube cricothyroidotomy without delay.
  • Use a 'stop and think' pause and clear communication between plans, treating declaring failure early as good practice rather than defeat.

At the bedside

  • Reach for the videolaryngoscope from the outset for the anticipated tricky asleep airway, not only after a failed direct look.
  • Count your attempts out loud - at three, call for a more experienced colleague and prepare the neck.
  • Have a second-generation SGA and a scalpel-bougie-tube FONA kit physically ready before induction.
  • Verbally declare 'CICO' to mobilise the whole team and commit to the front-of-neck airway.
Bottom line / exam pearl

Optimise attempt one, cap attempts at 3+1, and cut the neck with a scalpel-bougie-tube the moment CICO is declared.

References

▸Administration of Neuromuscular Blockade in Adults With ARDSCritical careSociety of Critical Care Medicine (SCCM), published in Critical Care Medicine · 2026
Clinical takeaway

Neuromuscular blockade is a targeted, short-term rescue for patients with moderate-to-severe ARDS who stay hypoxaemic or dyssynchronous despite optimised ventilation and sedation - not a routine early continuous infusion for everyone.

Background — why it changed

After conflicting trials (ACURASYS suggested benefit, ROSE showed none versus light sedation), SCCM re-appraised the evidence. A meta-analysis of seven RCTs supported a reduction in 28-day mortality, and the panel framed NMBAs as a conditional, low-certainty option reserved for persistent hypoxaemia rather than blanket use.

Key recommendations

  • Suggest using NMBAs over not using them in adults with ARDS and PaO2/FiO2 < 150 who remain persistently hypoxaemic and/or cannot meet ventilation targets on sedation alone (conditional recommendation, low certainty).
  • First optimise the ventilator and sedation (lung-protective settings, dyssynchrony control) before starting a paralytic.
  • If used, limit duration and do not routinely exceed 48 hours.
  • Either a fixed-dose strategy without depth-of-block monitoring or a titration strategy with train-of-four monitoring is acceptable.
  • Ensure deep analgesia and sedation before and during paralysis; either scale-based or non-scale evaluation of sedation depth may be used.
  • There is insufficient evidence to mandate one specific agent, though cisatracurium is the most-studied choice.

At the bedside

  • Before paralysing, confirm the ventilator and sedation are truly optimised - many patients settle without an NMBA.
  • Guarantee adequate sedation is running first; never paralyse an under-sedated patient.
  • Plan a stop date - aim to discontinue by ~48 hours and reassess daily.
  • Whether you monitor train-of-four or dose fixed, watch for prolonged weakness and minimise concurrent steroids where possible.
Bottom line / exam pearl

Reserve paralysis for P/F < 150 with refractory hypoxaemia or dyssynchrony, keep it deeply sedated, and stop by ~48 hours.

References

▸Fluid Therapy in Critically Ill Adults, Part 3: Fluid Removal at De-escalationCritical careEuropean Society of Intensive Care Medicine (ESICM); Intensive Care Medicine · 2025
Clinical takeaway

After the acute resuscitation phase, actively de-escalate fluids and favor protocolized diuretic-driven fluid removal over usual care, rather than defaulting to a positive or neutral balance.

Background — why it changed

This is the third and final part of the ESICM fluid-therapy guideline series, addressing what to do once shock has stabilized. It was built from 13 RCTs with a literature search through February 2025 using GRADE methodology. The impetus is growing evidence that cumulative positive fluid balance and tissue edema worsen outcomes, so de-resuscitation is now treated as an active, deliberate phase of care.

Key recommendations

  • Suggest de-escalation of fluid therapy over no de-escalation in critically ill adults after the acute phase of resuscitation (conditional, low certainty).
  • Suggest protocolized fluid removal using diuretics over usual care once patients are past the acute resuscitation phase (conditional, moderate certainty).
  • Suggest against routine ultrafiltration or extracorporeal fluid removal for the sole purpose of de-resuscitation when there is no other indication for renal replacement therapy (conditional, low certainty).
  • All recommendations are conditional; none reached strong-recommendation status given the limited certainty of evidence.
  • Evidence was insufficient to make specific recommendations for particular subgroups (e.g., ARDS, sepsis, AKI), so decisions there remain individualized.
  • De-resuscitation is framed as a distinct, active phase of fluid management rather than passive fluid restriction.

At the bedside

  • Once shock has resolved and the patient is hemodynamically stable, stop maintenance/creep fluids and shift the goal to a negative or even balance.
  • Use a diuretic protocol (rather than ad hoc dosing) to drive fluid removal, monitoring for hypovolemia, electrolyte shifts, and hemodynamic tolerance.
  • Do not start ultrafiltration/RRT purely to remove fluid unless a standard RRT indication (e.g., refractory hyperkalemia, acidosis, uremia, true diuretic-resistant overload) is present.
  • Track cumulative fluid balance daily and reassess de-escalation targets against perfusion and organ function.
Bottom line / exam pearl

In the recovery phase, de-resuscitate with a diuretic protocol and reserve ultrafiltration for genuine RRT indications, not fluid removal alone.

References

  • ESICM CPG on fluid therapy Part 3 (Intensive Care Medicine, Springer). link.springer.com
  • ESICM announcement of fluid therapy Part 3 guideline. www.esicm.org
▸Circulatory Shock and Haemodynamic MonitoringCritical careEuropean Society of Intensive Care Medicine (ESICM); Intensive Care Medicine · 2025
Clinical takeaway

Shock is a clinical diagnosis of tissue hypoperfusion; assess it with capillary refill time and skin signs, and escalate to cardiac-output and venous-oxygenation monitoring in patients who do not respond to initial therapy.

Background — why it changed

These 2025 ESICM guidelines update guidance on diagnosing shock and monitoring hemodynamics in adult critically ill patients. An international panel used PICO questions with GRADE, issuing ungraded good practice statements (UGPS) where strong evidence was lacking. In total the panel issued 50 statements spanning clinical assessment, perfusion markers, cardiac-output monitoring, and fluid responsiveness.

Key recommendations

  • Monitor skin perfusion using capillary refill time, which may be complemented by assessment of skin temperature and mottling.
  • In patients with a central venous catheter, perform serial measurements of (central) venous oxygen saturation and of the veno-arterial CO2 partial pressure difference (PvaCO2 gap).
  • Cardiac output and/or stroke volume should be monitored in patients who do not respond to initial therapy, to determine shock type and assess response to treatment.
  • Perform serial echocardiographic evaluations to add information on cardiac function, even when cardiac output is already monitored.
  • Blood lactate is a central marker of acute circulatory failure and should be used to gauge severity and track response.
  • Many statements are ungraded good practice statements (UGPS) reflecting the limited high-certainty evidence in hemodynamic monitoring.

At the bedside

  • At the bedside, act on a prolonged capillary refill time plus mottling as early markers of hypoperfusion, not just blood pressure.
  • In a non-responder, get an echo early to sort cardiogenic from hypovolemic/distributive shock and to trend cardiac function.
  • Use ScvO2 and the PvaCO2 gap together to judge adequacy of flow relative to metabolic demand in patients with a central line.
  • Reserve advanced/invasive cardiac-output monitoring for patients failing initial resuscitation rather than applying it routinely.
Bottom line / exam pearl

Diagnose shock clinically (CRT, mottling, lactate) and reserve cardiac-output and venous-oxygenation monitoring for patients not responding to initial therapy.

References

  • ESICM guidelines on circulatory shock and hemodynamic monitoring 2025 (Intensive Care Medicine, Springer). link.springer.com
  • ESICM guideline announcement page. www.esicm.org
▸PADIS Focused Update: Pain, Anxiety, Agitation/Sedation, Delirium, Immobility, SleepCritical careSociety of Critical Care Medicine (SCCM); Critical Care Medicine · 2025
Clinical takeaway

This focused update to the 2018 PADIS guideline reinforces light sedation with dexmedetomidine over propofol when reducing delirium is a priority, adds anxiety as a new domain, and favors opioid-sparing analgesia, enhanced mobilization, and melatonin for sleep.

Background — why it changed

The SCCM task force updated the 2018 PADIS guidelines to incorporate newer evidence, reviewing pain, anxiety (a newly added topic), agitation/sedation, delirium, immobility, and sleep disruption in adult ICU patients. It uses GRADE and issues mostly conditional recommendations, reflecting evolving evidence in sedation and delirium since 2018.

Key recommendations

  • Suggest dexmedetomidine over propofol for sedation in mechanically ventilated adults when light sedation and/or reduction in delirium are the highest priorities (weigh against bradycardia risk).
  • Suggest nefopam (where available) as an adjunct or replacement for opioids to reduce opioid use and opioid-related harms.
  • Suggest low-dose ketamine as an adjunct to opioids in postsurgical ICU adults to reduce opioid consumption (cited regimen: 0.5 mg/kg IV push once, then 1-2 mcg/kg/min infusion).
  • Recommend a neuropathic pain agent (e.g., gabapentin, pregabalin, carbamazepine) with opioids for neuropathic pain.
  • Unable to recommend for or against antipsychotics for treating delirium, as evidence shows minimal or no effect on patient-important outcomes.
  • Suggest enhanced mobilization/rehabilitation over usual care; vasoactive infusions or mechanical ventilation are not automatic barriers to mobilizing an otherwise stable patient.
  • Suggest melatonin over no melatonin and a multicomponent sleep-promoting protocol; suggest not using propofol to improve sleep.

At the bedside

  • For the agitated ventilated patient where you want light sedation and less delirium, prefer a dexmedetomidine-based strategy and monitor for bradycardia.
  • Build an opioid-sparing analgesia plan: add nefopam or low-dose ketamine, and use gabapentinoids for neuropathic pain.
  • Do not treat pressors or the ventilator as reasons to keep a stable patient in bed; escalate mobilization/rehab.
  • For sleep, use a bundled non-pharmacologic protocol plus melatonin rather than propofol; there is insufficient evidence to routinely give benzodiazepines for anxiety.
Bottom line / exam pearl

Light, dexmedetomidine-favored sedation, opioid-sparing analgesia, early mobilization, and melatonin-based sleep care define the 2025 PADIS update.

References

  • A Focused Update to the PADIS Guidelines (Critical Care Medicine, LWW, 2025). journals.lww.com
  • SCCM: A Focused Update to the PADIS Guideline. sccm.org
▸Management of Very Old Patients in Intensive Care (VIP)Critical careEuropean Society of Intensive Care Medicine (ESICM); Intensive Care Medicine · 2025
Clinical takeaway

For patients aged 80 and older, chronological age alone should never decide ICU admission; base decisions on frailty, comorbidity, functional status, and the patient's own preferences, and use time-limited trials when prognosis is uncertain.

Background — why it changed

Very old patients (age >= 80) are the fastest-growing ICU cohort, yet high-quality trial evidence is scarce because of their heterogeneity and complex geriatric syndromes. Because classical evidence-based methods fall short here, ESICM used a two-round Delphi consensus (28-member steering group, 110 experts) to produce consensus-based recommendations. Strong consensus required >= 90% agreement and moderate consensus >= 80%.

Key recommendations

  • Chronological age alone should not determine ICU admission; decisions should weigh acute and chronic conditions together.
  • Assess frailty, chronic multimorbidity, and pre-existing functional impairment as critical factors shaping management (endorsed by ~97% of experts).
  • Prioritize patient preferences regarding functionality, quality of life, and life-sustaining treatment when planning care.
  • Use time-limited trials of intensive care for patients with uncertain prognosis, with predefined goals and reassessment.
  • Clarify treatment-escalation plans at (or soon after) ICU admission rather than deferring these conversations.
  • Deliver patient-centered care that accounts for biological and functional heterogeneity among older adults, avoiding one-size-fits-all protocols.
  • The recommendations are consensus-based (Delphi), reflecting expert agreement in the absence of robust trial evidence.

At the bedside

  • When triaging an 80+ patient, document frailty (e.g., a frailty score), baseline function, and comorbidity rather than deciding on age.
  • Have an early goals-of-care conversation and record patient/surrogate preferences and an escalation plan on admission.
  • Offer a time-limited trial with explicit endpoints when the trajectory is unclear, and reassess at the agreed checkpoint.
  • Individualize intensity of care to the specific older patient, integrating geriatric syndromes into the plan.
Bottom line / exam pearl

Judge the very old ICU patient by frailty, function, and preferences with time-limited trials, not by age alone.

References

  • ESICM consensus-based recommendations for management of very old patients in intensive care (Intensive Care Medicine, Springer, 2025). link.springer.com
  • ABCDE-Frailty: summary of the 2025 ESICM expert consensus recommendations (PubMed). pubmed.ncbi.nlm.nih.gov
▸Guidelines for the Provision of Intensive Care Services (GPICS), Third EditionCritical careUK Intensive Care Society (ICS) & Faculty of Intensive Care Medicine (FICM) - standards document (not a journal) · 2026
Clinical takeaway

GPICS V3 is the UK reference standard for planning and delivering adult intensive care, now framed around auditable minimum standards ('must-do' statements) covering infrastructure, workforce and processes. It reaffirms core safety staffing: 1:1 nursing for Level 3 patients and 1:2 for Level 2.

Background — why it changed

GPICS V3 (published January 2026) builds on the 2015, 2019 and 2022 (v2.1) editions, incorporating lessons from COVID-19, emerging evidence and changing practice. It is the first edition co-produced with patients and families, whose lived experience is embedded in the editorial board, and it adds material on sustainability and on equality, diversity and inclusion. The document was restructured so each chapter presents a minimum standard, recommendations for a quality service, and a background/explanation section to improve auditability and consistency.

Key recommendations

  • Standards are recast as minimum standards that every UK ICU is expected to meet, each expressed as a single 'must-do' statement supported by background and explanation.
  • Content is organised into five sections: intensive care structure, workforce, clinical care, service development, and preparedness.
  • Registered nurse-to-patient ratio of 1:1 for Level 3 (including all ventilated) patients and 1:2 for Level 2 patients for direct care.
  • A consultant in Intensive Care Medicine must be available 24/7, with consultant-delivered care and dedicated ICU sessions.
  • Care must be delivered by a multiprofessional team (medical, nursing, pharmacy, physiotherapy, dietetics, microbiology and others) with defined access standards.
  • New emphasis on sustainability and on equality, diversity and inclusion as service considerations.
  • Patient and family lived experience is embedded into service design, follow-up and rehabilitation standards.

At the bedside

  • Use the minimum-standard 'must-do' statements as a self-audit checklist for your unit's staffing and infrastructure.
  • Confirm ventilated and Level 3 patients have 1:1 registered-nurse cover on every shift, escalating when acuity outstrips staffing.
  • Know your 24/7 route to a consultant intensivist and to the wider MDT (pharmacy, physio, microbiology).
  • Reference GPICS V3 when commissioning, business-planning, or challenging unsafe staffing/capacity locally.
Bottom line / exam pearl

GPICS V3 is the UK benchmark for what 'safe' intensive care looks like - if a unit cannot meet a minimum standard, that is an auditable safety gap, not a local preference.

References

▸Management of Emergencies in Patients on ECMOCritical careBritish societies (Intensive Care Society and partner organisations); published in Intensive Care Medicine · 2025
Clinical takeaway

This UK multi-society guideline gives the first national framework for emergencies in ECMO patients, stressing that standard advanced life support algorithms may not apply and that rapid recognition of arrest, team prioritisation and early circuit troubleshooting are the life-saving priorities.

Background — why it changed

Emergencies in patients on extracorporeal membrane oxygenation (ECMO) are complex because the altered circulation means conventional ALS may not be appropriate. Through collaboration between all UK ECMO centres and eight national societies, the current evidence was assessed and, using a modified Delphi consensus process, national guidance was produced. It was published in Intensive Care Medicine (2025) and is intended for all staff and all ECMO types in the UK, used alongside appropriate training.

Key recommendations

  • Recognise that usual ALS algorithms may not be applicable on ECMO; management must be adapted to the circuit and cannulation type.
  • Prioritise early recognition of cardiac arrest and clear team role allocation during the emergency.
  • Perform early ECMO circuit troubleshooting (pump, oxygenator, cannulae, flows and pressures) as part of the initial response.
  • Assess whether the circuit is still providing adequate systemic perfusion before defaulting to conventional chest compressions.
  • Be alert to ECMO-specific complications such as differential hypoxia (Harlequin/north-south syndrome) in VA-ECMO, circuit air, and cannula displacement or bleeding.
  • Deliver the guidance in conjunction with structured training and local emergency protocols across the ECMO service.

At the bedside

  • Keep an ECMO emergency algorithm and hand-crank at every bedside, and rehearse roles as a team.
  • In a deteriorating VA-ECMO patient, check circuit flow and pressures early and sample right-hand/upper-body oxygenation to detect differential hypoxia.
  • Do not reflexively disconnect or clamp the circuit - troubleshoot systematically and call the ECMO/perfusion team.
  • Confirm cannula position and look for bleeding, air, or access insufficiency ('chatter') as reversible causes.
Bottom line / exam pearl

On ECMO, the circuit is part of the patient - recognise arrest fast, troubleshoot the circuit early, and remember that standard ALS may not apply.

References

▸Family-Centered Care for Adult ICUsCritical careSociety of Critical Care Medicine (SCCM); Critical Care Medicine · 2024
Clinical takeaway

The panel makes one strong recommendation - liberalized family presence as the default in adult ICUs (upgraded from conditional in 2017) - plus 14 conditional recommendations and 2 best-practice statements to engage, support and communicate with families.

Background — why it changed

These 2024 SCCM guidelines (published in Critical Care Medicine, February 2025) update the 2017 family-centered care guidelines and are organised into four domains: engagement of families, support of family needs, communication support, and support of the ICU clinicians who provide family-centered care. Meta-analysis found liberalized presence increased family (and possibly patient) satisfaction and reduced anxiety and depression symptoms, with no signal of harm to mortality or length of stay - justifying the upgrade to a strong recommendation.

Key recommendations

  • Strong recommendation: adopt liberalized (open) family presence policies as the default in adult ICUs (low certainty evidence).
  • Offer families the option to be present on ICU rounds and to participate in bedside care.
  • Offer family presence during resuscitation, with a dedicated staff member assigned to support the family.
  • Provide ICU diaries and family educational programs to support understanding and recovery.
  • Provide mental health, bereavement and spiritual support for families.
  • Use structured, regularly scheduled family meetings/conferences and standardized communication approaches, including specialized ICU communication staff.
  • Provide communication skills training for ICU clinicians and support their wellbeing in delivering family-centered care.

At the bedside

  • Default to open/flexible visiting; document any restriction as a specific clinical exception rather than the norm.
  • Invite family to rounds and offer a defined role in simple bedside care (mouth care, range-of-motion, orientation).
  • Start an ICU diary early and signpost bereavement, spiritual and mental-health support proactively.
  • Schedule structured family meetings rather than waiting for a crisis, and assign a support person if family witness resuscitation.
Bottom line / exam pearl

Open family presence is now the strong-recommendation default in the adult ICU - families are partners in care, not visitors.

References

  • SCCM - Guidelines on Family-Centered Care for Adult ICUs: 2024. sccm.org
  • SCCM Guidelines on Family-Centered Care for Adult ICUs: 2024 - Critical Care Medicine. journals.lww.com
▸Adult End-of-Life Care in the ICUCritical careSociety of Critical Care Medicine (SCCM); Critical Care Medicine · 2025
Clinical takeaway

The first major SCCM update since the 2008 consensus statement recommends proactive palliative care and/or ethics involvement, protocolized withdrawal of life-sustaining treatment with structured symptom management, and structured shared decision-making for adult ICU end-of-life care.

Background — why it changed

Published in Critical Care Medicine (December 2025; 53(12):e2734-e2746), these clinical practice guidelines update the 2008 American College of Critical Care Medicine consensus statement on end-of-life (EOL) care. They are motivated in part by evidence that at least ~20% of ICU patients have goals that are not medically attainable or a treatment plan misaligned with achievable goals. An accompanying editorial notes the recommendations rest largely on low-certainty evidence, so most are conditional.

Key recommendations

  • Proactively consult Palliative Care/Palliative Medicine and/or an Ethics service (where available) to help define goals of care for patients who may no longer benefit from critical care.
  • Implement institutional policies to address conflicts over futile or potentially inappropriate treatments.
  • Use protocolized approaches to withdrawal of life-sustaining treatment and symptom management.
  • Assess and manage symptoms across the whole withdrawal pathway - pre-extubation, during weaning, and after extubation.
  • Use structured tools to facilitate shared decision-making for EOL treatment decisions.
  • Explore and support patients' and families' cultural, spiritual and family traditions at the end of life.

At the bedside

  • When goals may no longer be achievable, trigger an early palliative care / ethics conversation rather than waiting for crisis.
  • Follow a written withdrawal-of-treatment protocol so analgesia and sedation for symptoms are titrated proactively, not reactively.
  • Anticipate and pre-emptively treat dyspnea and distress before and after extubation with a symptom-management plan.
  • Use a structured shared-decision framework and ask about cultural, spiritual and family rituals early.
Bottom line / exam pearl

Good ICU dying is planned, protocolized and multidisciplinary - proactive palliative/ethics input plus structured symptom control at withdrawal is the standard.

References

  • SCCM - Clinical Practice Guidelines on Adult End-of-Life Care in the ICU. sccm.org
  • SCCM Clinical Practice Guidelines on Adult End-of-Life Care in the ICU - Critical Care Medicine. journals.lww.com
  • Editorial: End-of-Life Care in the ICU - Getting Good Recommendations From Bad Evidence (PubMed). pubmed.ncbi.nlm.nih.gov
▸Delirium in the Critically Ill PatientCritical careUK Intensive Care Society (ICS) - guidance document · 2025
Clinical takeaway

ICS delirium guidance prioritises routine screening with validated tools (CAM-ICU or ICDSC) and non-pharmacological, bundle-based prevention as first-line, reserving drug therapy for when patient or staff safety is at risk or a withdrawal state is contributing.

Background — why it changed

Released by the Intensive Care Society on 24 February 2025, this multiprofessional guidance updates earlier UK delirium recommendations and incorporates current evidence. Delirium affects a large proportion of critically ill patients (cited as up to ~74% of ventilated patients), is frequently underdiagnosed, and is associated with long-term cognitive impairment, increased mortality and significant burden on patients, families and staff.

Key recommendations

  • Screen routinely for delirium using validated tools - CAM-ICU or the ICDSC - as part of daily assessment.
  • Make non-pharmacological, multicomponent strategies first-line (orientation, early mobilisation, sleep promotion, sensory aids, family involvement), aligned with the ABCDEF bundle.
  • Minimise modifiable and environmental triggers (over-sedation, immobility, noise, disrupted sleep, restraints).
  • Reserve pharmacological therapy for when patient or staff safety is at risk, or when a withdrawal state is thought to be contributory.
  • Do not use antipsychotics routinely to prevent delirium in all critically ill adults.
  • Deliver care via a coordinated multidisciplinary team with personalised, structured assessment and management.

At the bedside

  • Screen every patient every shift with CAM-ICU (or ICDSC) and act on a positive result.
  • Bundle non-drug measures first: lighten sedation, mobilise, restore day/night cues, give back glasses/hearing aids, involve family.
  • Hunt for reversible causes (pain, hypoxia, sepsis, drugs, retention, alcohol/benzodiazepine withdrawal) before reaching for medication.
  • If a drug is truly needed for dangerous agitation, use it short-term and targeted - not as routine prevention.
Bottom line / exam pearl

Screen, prevent and de-trigger first - drugs are a last resort for safety, and antipsychotics do not prevent ICU delirium.

References

  • Intensive Care Society - Guidance for Delirium in the Critically Ill Patient. ics.ac.uk
  • ICS - Guidance for Delirium in the Critically Ill Patient (Feb 2025 PDF). ics.ac.uk

Neurology15 guidelines

▸AHA/ASA Early Management of Acute Ischaemic StrokeNeurologyAHA/ASA · Stroke
Clinical takeaway

Time is brain — rapid CT, thrombolysis within 4.5 h (tenecteplase increasingly preferred), and thrombectomy for large-vessel occlusion out to 24 h in selected patients.

Background

The guideline covers the first hours of ischaemic stroke, where reperfusion saves neurons. Speed and systems (prehospital routing, prenotification, door-to-needle targets) drive outcomes.

Key recommendations

  • Assess: NIHSS, non-contrast CT to exclude haemorrhage, capillary glucose (hypoglycaemia is a classic mimic).
  • IV thrombolysis: alteplase within 4.5 hours of onset — tenecteplase 0.25 mg/kg is a reasonable, increasingly preferred alternative. BP must be <185/110 before lysis and kept <180/105 for 24 h after.
  • Mechanical thrombectomy for anterior large-vessel occlusion within 6 hours, and up to 24 hours in selected patients using perfusion imaging (DAWN/DEFUSE-3 criteria).
  • BP if not for reperfusion: permissive hypertension — treat only if >220/120 or end-organ compromise.
  • Antiplatelets: aspirin within 24–48 h (after 24 h if thrombolysed); dual antiplatelet (aspirin + clopidogrel) for 21 days after minor stroke / high-risk TIA.
  • Maintain glucose 140–180, treat fever, screen swallowing before oral intake, and give VTE prophylaxis.
Bottom line / exam pearl

CT first to exclude bleed → thrombolyse (tenecteplase/alteplase) within 4.5 h with tight BP control → thrombectomy for LVO up to 24 h in selected patients. Always exclude hypoglycaemia.

▸Status Epilepticus (NCS / ILAE)NeurologyNeurocritical Care Soc.
Clinical takeaway

Time-critical staged treatment — a benzodiazepine at 5 minutes, a second-line antiepileptic at 20 minutes, and anaesthesia by 40 minutes.

Background

Convulsive status epilepticus (a seizure > 5 min or repeated seizures without recovery) becomes harder to stop and more damaging the longer it runs, so treatment is time-boxed.

Key recommendations

  • Stage 1 (5 min): IV lorazepam 4 mg (repeat once); if no IV — IM midazolam 10 mg, buccal midazolam, or rectal diazepam.
  • Stage 2 (20 min): IV levetiracetam, valproate, or (fos)phenytoin.
  • Stage 3 — refractory (40 min): RSI and an anaesthetic infusion (midazolam / propofol / thiopental) with continuous EEG.
  • Check glucose and correct it; give thiamine before glucose if alcohol/malnutrition; pyridoxine in young children.
  • Look for and treat the cause (hyponatraemia, eclampsia, toxins, CNS infection, structural).
Bottom line / exam pearl

Benzo → second-line AED → anaesthesia, on a 5/20/40-minute clock. Don't under-dose the benzodiazepine, and always check the glucose.

▸Subarachnoid Haemorrhage & Spontaneous ICH (AHA/ASA)NeurologyAHA/ASA · Stroke
Clinical takeaway

Thunderclap headache → urgent non-contrast CT (near 100% sensitive within 6 h); if negative but still suspicious, LP for xanthochromia or CT angiography.

Background

Aneurysmal SAH and spontaneous intracerebral haemorrhage are time-critical haemorrhagic strokes where early diagnosis and BP/complication control change outcome.

Key recommendations

  • SAH: non-contrast CT first (highest sensitivity < 6 h); if negative, LP at ≥12 h for xanthochromia (or CTA). Confirm the aneurysm (CTA/DSA) and secure it early (coil/clip) within 24–72 h.
  • SAH supportive care: oral nimodipine (reduces delayed cerebral ischaemia), BP control before securing, and treat hydrocephalus (EVD).
  • Spontaneous ICH: rapid, careful BP lowering (target ~140 systolic, avoid dropping < 130), reverse anticoagulation immediately, and urgent neurosurgical review.
  • Avoid hyperglycaemia and fever; give VTE prophylaxis once bleeding is stable.
Bottom line / exam pearl

Thunderclap headache = CT then LP. Secure the aneurysm early and give nimodipine for SAH; for ICH, lower BP to ~140 and reverse any anticoagulant fast.

▸Bacterial MeningitisNeurologyEmpirical management
Clinical takeaway

Do not delay antibiotics — give ceftriaxone (plus amoxicillin for Listeria in the vulnerable) and dexamethasone as soon as meningitis is suspected.

Background

Bacterial meningitis is rapidly fatal; time-to-antibiotics drives survival, so treatment must not wait for imaging or LP when those will be delayed.

Key recommendations

  • Recognise fever, headache, neck stiffness, photophobia, altered consciousness ± a non-blanching rash.
  • Take blood cultures, then LP — unless contraindicated (focal signs, GCS < 9, immunocompromise, seizures, signs of raised ICP) → CT first / treat empirically without delay.
  • Empirical IV ceftriaxone 2 g; add amoxicillin/ampicillin for Listeria cover if > 50 y, pregnant or immunosuppressed.
  • Dexamethasone with or just before the first antibiotic dose (reduces complications, esp. pneumococcal).
  • Add IV aciclovir if encephalitis is possible. Notify public health and arrange prophylaxis for close contacts (meningococcal).
Bottom line / exam pearl

Antibiotics first, imaging second — ceftriaxone (+ amoxicillin if vulnerable) and dexamethasone immediately; never let a CT or LP delay the first dose.

▸Aneurysmal Subarachnoid HaemorrhageNeurologyESO/EANS/ESMINT joint guideline, European Stroke Journal 2026;11(5) · 2026
Clinical takeaway

Treat the ruptured aneurysm early (ideally within 24 h) by a dedicated team, give oral nimodipine to all, and favour endovascular coiling over clipping when both are equally suitable. aSAH still carries a case-fatality of roughly 40%.

Background — why it changed

This 2026 joint guideline of the European Stroke Organisation, European Association of Neurosurgical Societies and European Society for Minimally Invasive Neurological Therapy updates management of aneurysmal subarachnoid haemorrhage using GRADE methodology. It covers aneurysm securing, prevention of rebleeding and delayed cerebral ischaemia, and systems of care. Survivors frequently have lasting functional, cognitive and emotional sequelae.

Key recommendations

  • Secure the ruptured aneurysm as early as feasible, suggested within 24 h of ictus, provided the most experienced team is available.
  • In good-grade patients (awake/mildly drowsy, at most mild deficit) where both modalities are suitable, coiling without adjunctive devices is preferred over microsurgical clipping.
  • For selected ruptured wide-neck aneurysms unsuitable for simple coiling, balloon-assisted coiling and intrasaccular flow-disruption devices are reasonable options.
  • Give all patients oral nimodipine to reduce delayed cerebral ischaemia and improve outcome.
  • Do not use antifibrinolytics (e.g. tranexamic acid) routinely to prevent rebleeding - they reduce rebleeding rates without improving outcome (ULTRA trial).
  • Avoid statins, magnesium sulphate, tirilazad and endothelin-receptor antagonists for DCI prevention (no outcome benefit).
  • Manage patients in a dedicated neuro-ICU/high-care unit in a centre with adequate case volume (suggested >=70 aSAH/year, or >=35/year in geographically remote areas).

At the bedside

  • Suspect aSAH with sudden 'thunderclap' headache; non-contrast CT is highly sensitive early, LP for xanthochromia if CT is negative and suspicion remains.
  • Start oral nimodipine promptly and arrange urgent transfer to a high-volume neurovascular centre for definitive aneurysm treatment.
  • Do not delay aneurysm securing - rebleeding risk is highest in the first hours; antifibrinolytics are not a substitute for early definitive treatment.
  • Watch for and treat acute hydrocephalus (external ventricular drain) and monitor for delayed cerebral ischaemia.
Bottom line / exam pearl

Early aneurysm securing (favouring coiling), universal oral nimodipine, and care in a high-volume neuro-ICU are the pillars; antifibrinolytics, statins and magnesium are not recommended.

References

▸Blood Pressure Management in Acute Stroke (2025 Update)NeurologyEuropean Stroke Organisation (ESO) guideline update, European Stroke Journal 2026;11(5) · 2026
Clinical takeaway

Do not lower BP pre-hospital in suspected stroke. For thrombolysis keep BP <185/110 mmHg before and <180/105 mmHg during/24 h after; in ICH, early systolic reduction to <140 mmHg is suggested for small-to-moderate haematomas.

Background — why it changed

This 2025 update to the ESO blood-pressure guideline addresses eight clinical questions across acute ischaemic stroke and intracerebral haemorrhage, developed with GRADE methodology and systematic review. It reflects evidence from major BP-lowering trials (including INTERACT and ATACH-era data) and recent reperfusion-therapy studies.

Key recommendations

  • Advise against routine pre-hospital BP lowering in suspected acute stroke (moderate-certainty evidence).
  • Before intravenous thrombolysis, keep BP <185/110 mmHg.
  • During and for 24 h after intravenous thrombolysis and/or mechanical thrombectomy, keep BP <180/105 mmHg (low-certainty evidence).
  • In acute ICH with small-to-moderate haematomas, early systolic BP reduction to <140 mmHg is supported (largely expert consensus) to limit haematoma expansion.
  • Avoid abrupt or excessively intensive BP drops, and avoid large BP variability, particularly around reperfusion therapy.
  • Recommendations are calibrated to certainty of evidence - many are conditional/low-certainty, so individualise to clinical context.

At the bedside

  • In the field, treat the stroke, not the number - do not give antihypertensives simply for a high reading in suspected stroke.
  • Before giving alteplase/tenecteplase, confirm BP <185/110; use titratable IV agents (e.g. labetalol) to reach target, then maintain <180/105 for 24 h.
  • For a hyperacute ICH with a modest haematoma, aim for smooth systolic control around <140 mmHg; avoid overshoot and hypotension.
  • Treat pain, agitation and full bladder - common reversible drivers of acute hypertension.
Bottom line / exam pearl

No pre-hospital lowering; <185/110 pre-lysis and <180/105 peri-reperfusion for ischaemic stroke; early smooth systolic control toward <140 mmHg for small-to-moderate ICH.

References

▸Minimally Invasive Evacuation of Spontaneous ICHNeurologyAmerican Heart Association Science Advisory, 2026 · 2026
Clinical takeaway

Minimally invasive surgery appears to confer a mortality benefit, with functional benefit best supported for lobar haemorrhages. The clearest indication is early (<24 h) evacuation in ENRICH-type patients: lobar supratentorial ICH, ~30-80 mL, by a trained team.

Background — why it changed

This 2026 AHA science advisory updates the evidence on minimally invasive surgical (MIS) evacuation of supratentorial spontaneous ICH following the contemporary randomised trials ENRICH and MIND. ENRICH used a trans-sulcal parafascicular approach with a tubular retractor and neuronavigation; MIND used endoscopic aspiration. It refines patient selection, timing and platform choice relative to the 2022 AHA/ASA ICH guideline.

Key recommendations

  • The best-supported indication is early (<24 h) MIS evacuation of lobar supratentorial ICH, ~30-80 mL, in patients resembling the ENRICH cohort.
  • Functional-outcome benefit is supported chiefly for lobar haemorrhages; evidence for deep (e.g. basal ganglia) ICH is weaker/inconsistent.
  • Across current data, MIS evacuation appears to reduce mortality compared with medical management.
  • ENRICH showed a 6-month functional benefit (utility-weighted mRS) driven by the lobar subgroup, plus improved 30-day mortality.
  • In MIND, MIS improved 30-day function but the effect was not sustained at 90 and 180 days; technical efficacy was high (~80% volume reduction) with fewer serious adverse events.
  • Success depends on a trained team using a standardised workflow (parafascicular/endoscopic) with good haematoma clearance and haemostasis.

At the bedside

  • For a patient with a moderate-to-large lobar ICH (~30-80 mL) presenting within hours, urgently involve neurosurgery to consider early MIS evacuation.
  • Continue guideline-based medical care in parallel - aggressive BP control, reversal of anticoagulation, and airway/ICP management.
  • Set realistic expectations: mortality benefit is more consistent than functional benefit, and deep ICH evidence remains uncertain.
  • Refer to centres with a trained MIS team and appropriate imaging/navigation rather than attempting evacuation without the platform.
Bottom line / exam pearl

Early minimally invasive evacuation of a ~30-80 mL lobar supratentorial ICH by an experienced team is the clearest evidence-based indication; mortality benefit is supported, functional benefit mainly in lobar bleeds.

References

▸Neuroprognostication After Acute Ischaemic StrokeNeurologyNeurocritical Care Society (NCS) & DGNI joint guideline, Neurocritical Care 2026 · 2026
Clinical takeaway

No single predictor reliably forecasts outcome after critical AIS - avoid premature prognostication and use multimodal assessment. Early neurological improvement within 24 h of revascularisation is a moderately reliable marker of good functional outcome.

Background — why it changed

This NCS/DGNI guideline (GRADE-based narrative systematic review) addresses neuroprognostication in critically ill adults with acute ischaemic stroke, focusing on the reliability of individual predictors and multivariate models used when counselling patients and surrogates. It emphasises timing, confounders, language during counselling and disclosure of uncertainty, given wide practice variation and the risk of self-fulfilling prophecy.

Key recommendations

  • Avoid premature neuroprognostication and minimise confounders (sedation, metabolic derangement) before formulating a prognosis.
  • Use multimodal assessment rather than any single clinical variable, score or model.
  • Early neurological improvement within 24 h of revascularisation was identified as a moderately reliable predictor of good functional outcome.
  • No other individual predictor was judged reliable for predicting mortality or functional outcome in isolation.
  • Good-practice statements address predicting recovery of swallowing and tracheostomy decannulation, and counselling patients with large hemispheric (malignant) infarction and their surrogates before neurological decline.
  • Communicate uncertainty explicitly and be alert to the self-fulfilling prophecy created by early withdrawal-of-care decisions based on weak predictors.

At the bedside

  • Do not offer a firm prognosis in the first hours/days of a large infarct while sedation and other confounders are present.
  • In malignant MCA territory infarction, counsel early about the trajectory and decompressive hemicraniectomy before deterioration.
  • Track early neurological improvement after thrombolysis/thrombectomy - it is one of the more reliable favourable signs.
  • Frame prognosis probabilistically to families and avoid a single number driving early care-limitation decisions.
Bottom line / exam pearl

Prognosticate late and multimodally: only early post-revascularisation improvement is a moderately reliable good-outcome sign, and no single predictor should drive care-limiting decisions.

References

▸Neuroprognostication in Status EpilepticusNeurologyNeurocritical Care Society (NCS) & DGNI joint guideline, Neurocritical Care 2026 · 2026
Clinical takeaway

No individual clinical variable or prediction model reliably predicts in-hospital mortality in status epilepticus. STESS and EMSE should not drive prognosis for individual patients, and prognostic pessimism must not justify under-treatment.

Background — why it changed

This NCS/DGNI guideline (GRADE-based narrative systematic review) outlines principles of neuroprognostication in critically ill adults with status epilepticus and reviews the reliability of clinical predictors and scores for counselling surrogate decision-makers. It examines the Status Epilepticus Severity Score (STESS) and the Epidemiology-based Mortality score in SE (EMSE), among other predictors.

Key recommendations

  • No single clinical variable or prediction model reliably predicts in-hospital mortality in status epilepticus.
  • STESS discrimination is modest and inconsistent across validation cohorts, with high false-positive rates for predicting death - do not use it to prognosticate for individuals.
  • Insufficient evidence to use EMSE for counselling individual surrogates on in-hospital mortality, though it may outperform STESS in some cohorts.
  • Aetiology of status epilepticus is a major determinant of outcome and should be central to any prognostic discussion.
  • Avoid prognostic self-fulfilling prophecy: a predicted poor outcome should not, by itself, trigger less aggressive seizure treatment, as under-treatment worsens outcome.
  • Counsel surrogates with explicit acknowledgement of prognostic uncertainty and reassessment over time.

At the bedside

  • Treat status epilepticus aggressively regardless of an unfavourable score - controlling seizures takes priority over early prognostication.
  • Identify and treat the underlying cause; aetiology matters more for outcome than any severity score.
  • Do not quote STESS or EMSE as a mortality prediction to families for the individual in front of you.
  • Give prognosis time - reassess after seizures are controlled and confounders (sedation, metabolic factors) resolve.
Bottom line / exam pearl

In status epilepticus, no score or single variable reliably predicts death - prognosticate cautiously, prioritise treating the cause and the seizures, and never let a poor predicted outcome justify under-treatment.

References

  • NCS/DGNI Neuroprognostication in Status Epilepticus (Springer, Neurocrit Care 2026). link.springer.com
  • NCS/DGNI Neuroprognostication series (Springer collection). link.springer.com
▸Intravenous Management of Headache Disorders in Hospitalised PatientsNeurologyASRA Pain Medicine (American Society of Regional Anesthesia and Pain Medicine) practice advisory; Regional Anesthesia & Pain Medicine · 2026
Clinical takeaway

For hospitalised patients with intractable primary headache, ASRA advises structured IV multimodal therapy led by dopamine-receptor antagonists and magnesium rather than reflexive opioids, which are not recommended as routine abortive agents.

Background — why it changed

Inpatient IV headache care has long been highly variable and opioid-heavy despite weak supporting evidence. This ASRA Pain Medicine consensus (proposal approved 2023, published for 2026) is the first multidisciplinary practice advisory dedicated to IV abortive strategies in admitted patients, assembling neurologists, pain physicians, anaesthesiologists and a patient representative. It synthesises the evidence for antiemetic/neuroleptic infusions, magnesium, valproate and dihydroergotamine and standardises dosing and monitoring.

Key recommendations

  • Use IV prochlorperazine or metoclopramide 10 mg as a core abortive agent; doses may be repeated approximately every 6 hours.
  • Co-administer diphenhydramine or benztropine before dopamine-receptor antagonists to reduce akathisia and dystonic reactions.
  • Give IV magnesium sulfate 1-2 g over 15 minutes for migraine (with or without aura); check pre-infusion magnesium level and blood pressure first.
  • Consider IV sodium valproate 500-1000 mg over 20 minutes, repeatable after about 8 hours, in appropriate patients.
  • Dihydroergotamine (DHE) is an option for refractory primary headache and may be combined with antiemetic pretreatment; observe ergot contraindications (vascular disease, pregnancy, recent triptan use).
  • Avoid routine opioids and barbiturates as first-line inpatient abortive therapy.
  • Individualise adjuvant combinations, as data on combining magnesium with metoclopramide are conflicting.

At the bedside

  • Screen for QT prolongation before repeated dopamine-antagonist dosing and give an antihistamine/anticholinergic pre-med to prevent akathisia.
  • Draw a magnesium level and check BP before magnesium infusion; run it slowly (over ~15 min) to limit flushing and hypotension.
  • Exclude secondary/red-flag headache (thunderclap, focal deficit, fever, papilloedema) before committing to an infusion pathway.
  • Set a clear response endpoint and taper plan rather than escalating to opioids when infusions partially work.
Bottom line / exam pearl

Inpatient intractable headache is treated with scheduled IV neuroleptic/antiemetic infusions plus magnesium and pre-medication for akathisia, not with opioids.

References

  • Practice advisory for intravenous management of headache disorders in hospitalized patients (PMC). pmc.ncbi.nlm.nih.gov
  • ASRA Pain Medicine - Guidelines landing. asra.com
▸Acute Management of Status Epilepticus in AdultsNeurologyIntensive Care Society (ICS, UK) guidance; Journal of the Intensive Care Society · 2025
Clinical takeaway

Status epilepticus is a time-critical emergency: give a full-dose benzodiazepine immediately, then load a full-dose second-line antiseizure medication early, because timing and adequate dosing matter more than which agent is chosen.

Background — why it changed

UK practice in status epilepticus (SE) had been inconsistent, with frequent benzodiazepine under-dosing and delayed second-line therapy. The Intensive Care Society convened acute medicine, neurology, intensive care and emergency medicine specialists to produce cross-specialty guidance for patients over 16, using ILAE definitions and covering stabilisation, investigation, drug therapy, sedation and critical-care transfer. Diagnosis of the underlying cause is emphasised, especially in refractory SE.

Key recommendations

  • Treat as SE using ILAE timing: a convulsive seizure lasting >= 5 minutes (or recurrent seizures without recovery) mandates immediate treatment.
  • First line: IV lorazepam ~0.1 mg/kg (up to ~4 mg), or IV diazepam 0.15 mg/kg (up to 10 mg); if no IV access, IM midazolam ~0.2 mg/kg (up to 10 mg) or buccal midazolam.
  • Give a full weight-based benzodiazepine dose and one repeat if needed; under-dosing is a common, avoidable failure.
  • If seizures persist, load a full-dose second-line ASM early (levetiracetam, sodium valproate, or (fos)phenytoin), which are broadly equivalent in efficacy (per ESETT-type evidence).
  • Avoid under-dosing levetiracetam in particular; use adequate weight-based loading.
  • For refractory SE, proceed to anaesthetic infusions (e.g. midazolam, propofol) with intubation and continuous EEG, and transfer to critical care.
  • Actively investigate and treat the underlying cause (imaging, metabolic, infective, autoimmune) in parallel, especially in refractory/super-refractory SE.

At the bedside

  • Start the clock at 5 minutes and give the benzodiazepine at full weight-based dose - do not split or delay for IV access (use IM/buccal midazolam).
  • Have the second-line ASM drawn up and ready to load before the benzodiazepine has even declared failure.
  • Send glucose, electrolytes, calcium/magnesium, drug levels and consider pregnancy, toxidromes and CNS infection early.
  • Escalate to anaesthesia/intubation and continuous EEG promptly once SE is refractory; arrange critical care transfer.
Bottom line / exam pearl

SE = seizure >=5 min: full-dose benzodiazepine now, full-dose second-line ASM (levetiracetam/valproate/(fos)phenytoin) early - speed and dose beat drug choice.

References

  • ICS guidance: acute management of status epilepticus in adults (SAGE / J Intensive Care Soc). journals.sagepub.com
  • Intensive Care Society - status epilepticus guidance. ics.ac.uk
▸Seizure Prophylaxis in Patients Undergoing Supratentorial NeurosurgeryNeurologyNeurocritical Care Society (NCS) Guideline, Neurocritical Care · 2026
Clinical takeaway

In seizure-naive adults having supratentorial neurosurgery, the NCS makes only a conditional recommendation: either prophylactic antiseizure medication or no prophylaxis is acceptable, reflecting low-quality evidence.

Background — why it changed

Antiseizure medication (ASM) prophylaxis after supratentorial surgery has long been practiced inconsistently. The NCS performed a systematic review and meta-analysis in adults with no prior seizures, structured around three PICO questions: ASM versus no ASM, agent choice (levetiracetam vs phenytoin/fosphenytoin), and duration (7 days or less vs more than 7 days). The overall evidence base was weak, so recommendations are conditional.

Key recommendations

  • For ASM versus no ASM, the guideline suggests either primary prophylaxis or no prophylaxis is reasonable - a conditional recommendation with low quality of evidence.
  • The choice should be individualized to patient- and procedure-specific seizure risk rather than applied reflexively to all cases.
  • If an ASM is used, the guideline addressed levetiracetam versus phenytoin/fosphenytoin; levetiracetam is commonly favored in practice for its more favorable tolerability and drug-interaction profile.
  • The guideline evaluated duration of prophylaxis (7 days or less versus more than 7 days), reflecting a general trend toward short-course rather than prolonged prophylaxis when ASM is used.
  • There is no high-quality evidence that routine prophylaxis reduces late/remote seizures, so benefit is uncertain.
  • Decisions should weigh ASM adverse effects and cost against uncertain seizure-prevention benefit.

At the bedside

  • Do not treat post-craniotomy ASM prophylaxis as mandatory - decide case by case with the neurosurgical team based on seizure risk.
  • When prophylaxis is chosen, levetiracetam is the practical default over phenytoin for tolerability and fewer interactions.
  • Favor a short course rather than open-ended prophylaxis, and have an explicit stop plan.
  • Counsel that evidence is low-quality and monitor for ASM side effects that may outweigh benefit.
Bottom line / exam pearl

For seizure-naive supratentorial surgery, prophylaxis is optional (conditional, low-quality evidence) - individualize, prefer levetiracetam if used, and keep it short.

References

▸Stroke-Associated Pneumonia: Diagnosis and ManagementNeurologyEuropean Stroke Organisation (ESO), European Stroke Journal · 2026
Clinical takeaway

Treat diagnosed stroke-associated pneumonia (SAP) with prompt empirical antibiotics guided by local protocols, but do not use prophylactic antibiotics - prevention relies on positioning, mobilisation, nutrition and dysphagia management.

Background — why it changed

SAP is a common, outcome-worsening complication of acute stroke, yet practice has varied widely and the evidence base is thin. This ESO guideline standardises the approach to diagnosis and treatment and formally rejects routine preventive antibiotics after trials showed no benefit on SAP incidence or clinical outcomes. Because robust data are limited, many recommendations rest on expert consensus.

Key recommendations

  • Use standardised diagnostic criteria for SAP rather than a purely subjective bedside call.
  • Chest CT and plasma C-reactive protein (CRP) may add diagnostic value but are supportive, not standalone tests.
  • Do not give prophylactic/preventive antibiotics - no benefit on SAP incidence or outcomes.
  • Start empirical antibiotics promptly once SAP is diagnosed or strongly suspected, guided by local protocols targeting aspiration-associated pathogens.
  • Prevention centres on positioning, early mobilisation and individualised nutrition.
  • Dysphagia screening and swallowing management remain core preventive measures (detailed in the separate ESO/ESSD post-stroke dysphagia guideline).
  • Adjunctive therapies are not standard care but may be considered in selected patients.

At the bedside

  • Do not reach for antibiotics in every dysphagic or ventilated stroke patient - reserve them for diagnosed or suspected SAP.
  • Screen swallowing before any oral intake, keep the patient upright, and mobilise early as tolerated.
  • When SAP is suspected, begin empirical therapy per your local antibiogram without waiting for confirmatory imaging.
  • Anchor the diagnosis to a standardised definition; use CRP and chest CT to support, not replace, clinical judgement.
Bottom line / exam pearl

Prompt empirical antibiotics for diagnosed SAP - but no prophylaxis; prevention is positioning, mobilisation, nutrition and dysphagia management.

References

▸Pharmacologic Treatment for Migraine Prevention in AdultsNeurologyAmerican Academy of Neurology (AAN) and American Headache Society (AHS), published in Neurology and Headache · 2026
Clinical takeaway

This guideline replaces the 2012 recommendations and, for the first time in AAN/AHS guidance, places CGRP-targeted therapies alongside traditional oral preventives, with selection driven by whether the patient prioritizes efficacy or tolerability.

Background — why it changed

Since 2012, gepants (oral CGRP antagonists) and anti-CGRP monoclonal antibodies have transformed migraine prevention. The updated guideline grades these newer agents against established options and emphasizes individualized, shared decision-making rather than a rigid step-therapy order.

Key recommendations

  • Offer preventive therapy to adults with at least 4 migraine days/month, at least 4 moderate-to-severe headache days/month, or substantial migraine-related disability (Level B).
  • When efficacy is the priority in episodic migraine (Level B): atogepant, the CGRP mAbs (eptinezumab, erenumab, fremanezumab, galcanezumab), propranolol, topiramate, or valproate.
  • When tolerability is the priority in episodic migraine (Level B): atogepant, eptinezumab, erenumab, fremanezumab, or galcanezumab.
  • For chronic migraine: atogepant, the four CGRP mAbs, onabotulinumtoxinA, topiramate, or valproate.
  • Evidence-supported options may be offered without first requiring failure of older/less expensive drugs.
  • There is insufficient head-to-head evidence to name any single preventive as clearly superior; choose based on efficacy, tolerability, safety, cost, comorbidities, contraindications, route, and patient preference.
  • Address special populations (e.g., pregnancy/lactation, older adults, comorbidities such as fibromyalgia) individually, with attention to safety (avoid valproate/topiramate in pregnancy).

At the bedside

  • Ask about monthly migraine days and disability at the visit -- crossing ~4 days/month or significant disability is the trigger to start prevention.
  • Frame the choice around the patient's own priority: 'best chance of fewer attacks' vs 'fewest side effects,' since the Level B lists differ.
  • Do not gatekeep CGRP therapies behind failed older drugs if the evidence and patient priorities support them first-line.
  • Set expectations: give a preventive an adequate trial and reassess response with a headache diary before switching.
Bottom line / exam pearl

Prevention is indicated at roughly 4+ migraine days/month; pick the agent by the patient's priority (efficacy vs tolerability), and CGRP therapies no longer require failing older drugs first.

References

▸Guideline for Adult Stroke Rehabilitation and RecoveryNeurologyAmerican Heart Association / American Stroke Association (AHA/ASA), published in Stroke · 2026
Clinical takeaway

Replacing the 2016 guideline, this 248-recommendation update frames recovery as a continuum and stresses early, intensive, organized interprofessional rehabilitation, prevention of secondary complications, and mental-health screening.

Background — why it changed

Rehabilitation evidence has grown considerably since 2016, spanning technology-enabled therapy, comorbidity management, and long-term participation. The guideline reorganizes care across five recovery phases and broadens scope to caregiver support, return to work/driving, fall/fracture risk, and telerehabilitation access.

Key recommendations

  • Deliver organized, coordinated interprofessional rehabilitation for eligible patients to maximize functional independence.
  • Structure care across five phases: hyperacute (0-24 h), acute (1-7 days), early subacute (7 days-3 months), late subacute (3-6 months), and chronic (>6 months).
  • Emphasize early and appropriately intensive rehabilitation, with task-specific and dose-adequate training.
  • Screen for and treat post-stroke depression and anxiety, integrating mental-health care into recovery.
  • Prevent secondary complications -- venous thromboembolism, skin breakdown, falls, and fracture risk -- as part of routine rehab care.
  • Use telerehabilitation and technology-enabled therapies (including functional electrical stimulation) to extend access and support recovery.
  • Support caregivers and address participation goals, including safe return to work and driving.

At the bedside

  • Start planning rehabilitation early in the admission rather than treating it as a discharge afterthought.
  • Screen every stroke survivor for depression and anxiety, and re-screen over time -- mood disorders are common and treatable.
  • Build the VTE, skin, and fall-prevention bundle into daily rehab orders from the start.
  • Use validated tools to counsel on return to driving and work, and offer telerehab when in-person access is limited.
Bottom line / exam pearl

Stroke recovery is a five-phase continuum: organized interprofessional rehab started early, complications prevented, and mood disorders screened and treated throughout.

References

Endocrine, Metabolic & Renal7 guidelines

▸ADA Standards of Care in Diabetes — 2026EndocrineDiabetes Care · 2026
Clinical takeaway

Diabetes technology moves earlier and wider — CGM at diagnosis for insulin users, and automated insulin delivery reaches type 2.

Technology — the headline change

  • Offer a continuous glucose monitor (CGM) at diagnosis for most patients using insulin, and for any patient in whom "CGM helps management."
  • Consider automated insulin delivery (AID) systems — historically a type 1 tool — for type 2 patients not meeting goals on basal insulin.

Glycaemic targets — beyond HbA1c

  • Targets now incorporate CGM metrics: most adults aim HbA1c <7% and time-in-range (70–180 mg/dL) >70%, with time-below-range <4%; looser goals for older adults with complex health status.
  • Specific time-in-range / below-range / above-range targets are given for different clinical scenarios (e.g. pregnancy, frailty).

Drug selection & BP

  • Choose agents by comorbidity, not by HbA1c — with more emphasis on GLP-1 receptor agonists for HFpEF and metabolic dysfunction–associated steatohepatitis (MASH).
  • Blood-pressure goal <120 for those at high cardiovascular/renal risk; <130/80 for most others when safely achievable.
Bottom line / exam pearl

Start CGM early, target time-in-range >70% (not just HbA1c), and pick drugs by the patient's comorbidities (GLP-1 for heart failure/MASH, SGLT2 for CKD/HF) rather than the sugar number.

▸KDIGO 2026 — Anaemia in Chronic Kidney DiseaseNephrologyKidney Int · 2026
Clinical takeaway

A welcome update after >10 years — but most recommendations rest on low-certainty evidence, so let symptoms guide you, not cut-offs alone.

Background

Anaemia in CKD is common (reduced erythropoietin, functional iron deficiency, inflammation, shortened red-cell survival). The previous KDIGO guidance was over a decade old; this update blends graded recommendations with "practice points" (expert opinion), with certainty ratings shown — and they are mostly "very low."

Diagnosis & monitoring

  • Screen with FBC, reticulocytes, ferritin and transferrin saturation (TSAT) — at least annually (stage 3), twice yearly (stage 4), 3-monthly (stage 5).
  • Anaemia = Hb <12 g/dL (women) / <13 g/dL (men). Ferritin <45 ng/mL or microcytosis → hunt for a blood-loss source.

Iron

  • On haemodialysis: start iron if ferritin ≤500 and TSAT ≤30% (IV iron preferred).
  • Not on HD: start iron if ferritin <100 and TSAT <40%, or ferritin 100–300 and TSAT <25%.
  • Monitor iron indices 1–3 monthly (HD) / 3-monthly (non-HD); hold iron during systemic infection (iron feeds pathogens).

Erythropoiesis-stimulating agents (ESAs)

  • Consider ESAs in dialysis patients when Hb ≤9–10 g/dL.
  • ESAs are favoured over HIF-PH inhibitors. If medications are used, keep Hb <11.5 g/dL — a firm ceiling, because higher targets raise stroke risk.
  • Consider pausing ESAs when thromboembolic risk is high (e.g. acute stroke).
Bottom line / exam pearl

Screen with ferritin/TSAT, replace iron by the stage-specific thresholds (IV in dialysis), reach for ESAs at Hb ≤9–10, and never chase Hb above 11.5 — overshooting causes strokes, not benefit.

▸ADA Standards of Care in Overweight & Obesity — 2026EndocrineADA · Diabetes Care
Clinical takeaway

A dedicated ADA standard treating obesity as a chronic disease — structured assessment, effective GLP-1/GIP pharmacotherapy, and surgery, with weight-loss targets tied to organ benefit.

Background

The ADA has split obesity care into its own standards, reflecting the arrival of highly effective incretin therapies. The emphasis is on obesity as a chronic, relapsing disease managed long-term — and on reducing weight stigma.

Key recommendations

  • Diagnose & assess: BMI plus waist circumference and complications; take a respectful, stigma-free history and screen for weight-related comorbidity.
  • Foundational care: individualised nutrition, physical activity and behavioural support for all.
  • Pharmacotherapy when BMI ≥30, or ≥27 with a weight-related comorbidity: prefer highly effective agents — GLP-1 receptor agonists (semaglutide) and the dual GIP/GLP-1 agonist (tirzepatide) — which also benefit diabetes, cardiovascular and renal outcomes.
  • Metabolic/bariatric surgery for BMI ≥35 (or ≥30 with poorly-controlled comorbidity such as type 2 diabetes).
  • Targets: aim for ≥5% loss for metabolic benefit; ≥10–15% can drive remission of comorbidities and organ-level benefit.
Bottom line / exam pearl

Treat obesity as a chronic disease: lifestyle for all, and offer GLP-1 / GIP-GLP-1 agents (BMI ≥27 with comorbidity or ≥30) or surgery (BMI ≥35), targeting ≥10–15% weight loss.

▸KDIGO 2026 — Acute Kidney Injury & Acute Kidney DiseaseNephrologyKDIGO · draft 2026
Clinical takeaway

Refined AKI/AKD definitions, cause-directed work-up, supportive management (optimise haemodynamics, stop nephrotoxins), and no routine early dialysis — plus follow-up to catch progression to CKD.

Background

KDIGO updates the AKI framework and formalises acute kidney disease (AKD) — the <3-month window that bridges AKI and CKD. Recent trials settled the long-running question of when to start dialysis.

Key recommendations

  • Define AKI: creatinine rise ≥26.5 µmol/L (0.3 mg/dL) in 48 h, OR ≥1.5× baseline within 7 days, OR urine output <0.5 mL/kg/h for ≥6 h. Stage 1–3 by the worst of creatinine/urine output.
  • AKD: acute kidney abnormalities lasting <3 months that don't meet AKI criteria — a prompt to follow up rather than discharge and forget.
  • Work-up: classify pre-renal / intrinsic / post-renal; assess volume, review and stop nephrotoxins, urinalysis, and renal ultrasound to exclude obstruction.
  • Manage: optimise haemodynamics and volume with balanced crystalloids, treat the cause, dose-adjust drugs, and correct hyperkalaemia, acidosis and fluid overload.
  • Dialysis (KRT): do not start early routinely (STARRT-AKI/AKIKI) — start for refractory hyperkalaemia, acidosis, fluid overload or uraemic complications.
  • Contrast: don't withhold clinically indicated contrast for fear of contrast-associated AKI (risk is lower than once believed). Emerging cell-cycle-arrest biomarkers (TIMP-2·IGFBP7) aid early detection.
  • Follow-up: AKI survivors need monitoring — they are at high risk of progressing to CKD.
Bottom line / exam pearl

Define AKI by creatinine/urine output, find and treat the cause, optimise volume and stop nephrotoxins, and don't rush to dialyse — start KRT for the classic emergencies. Follow survivors up for CKD.

▸DKA & HHS (JBDS / ADA)EndocrineJBDS · 2026
Clinical takeaway

Fix fluid and potassium first, clear ketones with fixed-rate insulin, and watch potassium and glucose closely; HHS is fluid-led with cautious insulin.

Background

Diabetic ketoacidosis and the hyperosmolar hyperglycaemic state are the two hyperglycaemic emergencies — different tempos, overlapping principles.

Key recommendations

  • DKA diagnosis: glucose > 11 (or known diabetes), ketones ≥ 3 (or significant ketonuria), and pH < 7.3 or bicarbonate < 15.
  • Fluids first: IV 0.9% saline (cautious rate in the young, elderly or cardiac). Fixed-rate insulin 0.1 unit/kg/h; add 10% glucose when BG < 14.
  • Potassium: replace in the fluids; do not run insulin if K⁺ < 3.5 until replaced (insulin drives K⁺ into cells).
  • Find the precipitant (infection, missed insulin, MI), give VTE prophylaxis, and avoid bicarbonate. Resolution: ketones < 0.6, pH > 7.3.
  • HHS: older, insidious, glucose often > 30 with osmolality > 320 and little ketosis/acidosis — fluids are the mainstay, insulin lower-dose/later, and VTE risk is high.
Bottom line / exam pearl

DKA = fluids + fixed-rate insulin + potassium, glucose added at BG <14, no bicarbonate. HHS = fluid-led, gentle insulin, high clot risk.

▸Hyperkalaemia — Emergency ManagementNephrologyUK Renal / ACC
Clinical takeaway

ECG changes or K⁺ ≥ 6.5 mmol/L is an emergency — protect the heart with calcium first, then shift potassium into cells and remove it from the body.

Background

Severe hyperkalaemia can cause fatal arrhythmia with little warning; management follows a fixed three-step logic.

Key recommendations

  • Recognise ECG evolution: peaked T waves → PR prolongation → wide QRS → sine wave → arrest.
  • 1 — Stabilise the myocardium: IV calcium gluconate (or chloride) if ECG changes or K⁺ ≥ 6.5 (repeat as needed).
  • 2 — Shift K⁺ into cells: insulin 10 units + 25 g glucose IV, and nebulised salbutamol.
  • 3 — Remove K⁺: potassium binders (patiromer / sodium zirconium cyclosilicate); haemodialysis if refractory or in renal failure.
  • Stop the culprits (ACEi/ARB, K⁺-sparing diuretics, NSAIDs, trimethoprim) and treat the cause; recheck K⁺ and glucose.
Bottom line / exam pearl

Calcium to protect the heart → insulin-glucose + salbutamol to shift → binders/dialysis to remove. Always recheck glucose after insulin.

▸Adrenal Crisis & Thyroid EmergenciesEndocrineEndocrine emergencies
Clinical takeaway

In suspected adrenal crisis, give hydrocortisone immediately — never wait for a cortisol result. Thyroid storm and myxoedema coma are clinical diagnoses needing prompt treatment.

Background

These endocrine emergencies are easy to miss and rapidly fatal, but respond dramatically to early empirical treatment.

Key recommendations

  • Adrenal crisis: hypotension with hyponatraemia, hyperkalaemia and hypoglycaemia → IV hydrocortisone 100 mg stat then 200 mg/24 h, IV fluids, and treat the precipitant. Teach sick-day rules (double oral steroids when unwell).
  • Thyroid storm: fever, tachyarrhythmia and agitation → beta-blocker (propranolol), an antithyroid drug (propylthiouracil/carbimazole), iodine given AFTER the antithyroid drug, hydrocortisone, and active cooling.
  • Myxoedema coma: hypothermia, bradycardia and reduced consciousness → IV levothyroxine ± liothyronine, IV hydrocortisone (until adrenal insufficiency excluded), and supportive care.
  • Always give steroids with or before thyroid hormone in myxoedema coma to avoid precipitating adrenal crisis.
Bottom line / exam pearl

Adrenal crisis → hydrocortisone now, ask questions later. Thyroid storm → block (beta-blocker + antithyroid), then iodine + steroid. Myxoedema coma → thyroid hormone + steroid + warmth.

Hepatology & GI11 guidelines

▸Acute-on-Chronic Liver Failure — Global Multisociety ConsensusHepatologyEASL/AASLD/APASL/ALEH/SOLDA · Hepatology International · 2026
Clinical takeaway

The five major liver societies (EASL, AASLD, APASL, ALEH, SOLDA) agree a single global definition of ACLF: liver failure (bilirubin ≥5 mg/dl and INR ≥1.5) developing on advanced chronic liver disease (≥F3 fibrosis / cirrhosis) together with one or more extrahepatic organ dysfunctions/failures, usually after a precipitant — graded 1–3 by the number of failing organs, with higher grades carrying higher short-term mortality.

What it is

ACLF is a life-threatening syndrome of acute deterioration, organ failure, systemic inflammation and high short-term mortality in a patient with chronic liver disease. This harmonisation initiative replaces competing regional definitions (CLIF-C, APASL/AARC, NACSELD) with one evidence-based framework for clinical practice, research and clinical-trial endpoints — developed by Delphi consensus (≥70% agreement) and aligned with the FDA/EMA.

Harmonised definition & grading

  • Core syndrome = liver failure — bilirubin ≥5 mg/dl and INR ≥1.5 — on advanced chronic liver disease (ACLD, ≥F3 fibrosis or cirrhosis), plus ≥1 extrahepatic organ dysfunction or failure.
  • Type A: ACLF arising in compensated ACLD / cirrhosis with no prior decompensation (acute insult precedes overt decompensation, typically within ~4 weeks). Type B: ACLF on previously decompensated cirrhosis.
  • Grade 1: liver failure + one extrahepatic organ dysfunction (circulatory/respiratory count only if monitored in a high-dependency/ICU setting).
  • Grade 2: liver failure + one extrahepatic organ failure.
  • Grade 3: liver failure + two or more extrahepatic organ failures.

Extrahepatic organ failure thresholds (at the bedside)

  • Kidney: AKI stage 2–3 (KDIGO) or new renal replacement therapy.
  • Brain: hepatic encephalopathy West Haven grade 3–4, or mechanical ventilation for HE.
  • Circulatory: vasopressor requirement (not for hepatorenal syndrome–AKI treatment alone).
  • Respiratory: PaO₂/FiO₂ ≤225 (or SpO₂/FiO₂ ≤244 if PaO₂ unavailable), or need for mechanical ventilation.
  • Immune dysregulation and gut failure are recognised but not yet formally defined.

Precipitants & diagnosing the underlying liver disease

  • Bacterial infection is the commonest trigger; others include ongoing alcohol use, hepatitis B reactivation/superinfection, drug-induced liver injury, GI bleeding and major surgery/invasive procedures. No identifiable trigger is found in a substantial proportion.
  • Diagnose ACLD by histology (≥F3/F4), known cirrhosis, or non-invasive tests (VCTE/MRE/SWE) — but interpret non-invasive stiffness with caution in the acute setting, as acute liver injury can falsely raise it; integrate all clinical, laboratory and imaging data.
Bottom line / exam pearl

Suspect ACLF when a patient with cirrhosis or advanced chronic liver disease develops jaundice + coagulopathy (bilirubin ≥5 mg/dl, INR ≥1.5) after a precipitant (most often infection). Grade by extrahepatic organ failures — 1 = one dysfunction, 2 = one failure, 3 = ≥2 failures — treat the trigger, support failing organs early, and assess transplant candidacy, because mortality rises steeply with grade.

References

  • Acute-on-chronic liver failure: a global multisociety consensus on definitions (EASL · AASLD · APASL · ALEH · SOLDA). Hepatology International, published 30 Oct 2026. doi.org/10.1007/s12072-026-11169-2
▸ACG Clinical Guideline — Hepatic EncephalopathyHepatologyACG · Am J Gastro 2026
Clinical takeaway

Diagnose clinically, hunt and treat the precipitant, use lactulose first-line and add rifaximin to prevent recurrence — and do not protein-restrict.

Background

Hepatic encephalopathy (HE) is reversible neuropsychiatric dysfunction in liver failure / portosystemic shunting, driven largely by ammonia. Most episodes are triggered by a precipitant, so finding it is central to management.

Key recommendations

  • Diagnose clinically (West Haven grades; covert/minimal HE needs specific testing) and exclude other causes of altered mental status. A normal ammonia argues against HE, but a level isn't required to diagnose and shouldn't guide titration.
  • Find & treat the precipitant: infection (incl. SBP), GI bleeding, constipation, dehydration/electrolyte disturbance (esp. hypokalaemia), diuretic excess, sedatives, renal failure, TIPS, and non-adherence.
  • First-line treatment: lactulose, titrated to 2–3 soft stools/day (oral or enema).
  • Prevent recurrence (secondary prophylaxis): add rifaximin to lactulose after a second episode.
  • Nutrition: do not restrict protein — aim for adequate protein (≈1.2–1.5 g/kg/day); consider branched-chain amino acids in selected patients.
  • Refractory HE: consider LOLA, embolisation of large portosystemic shunts, and referral for liver transplant assessment. Routine primary prophylaxis is generally not recommended (except selected situations, e.g. during a GI bleed).
Bottom line / exam pearl

Treat the trigger, give lactulose to 2–3 soft stools/day, add rifaximin to prevent recurrence, and feed protein — don't restrict it.

▸Acute Upper GI Bleeding (NICE / ACG)GastroenterologyNICE · ACG
Clinical takeaway

Resuscitate, risk-score with Glasgow-Blatchford, endoscopy within 24 h, and transfuse restrictively (Hb 70) — variceal bleeds also need terlipressin and antibiotics.

Background

Upper GI bleeding is common and the approach differs sharply between variceal and non-variceal causes.

Key recommendations

  • Glasgow-Blatchford Score 0–1 → consider outpatient management; otherwise admit and resuscitate.
  • Restrictive transfusion — threshold Hb 70 g/L (80 if cardiovascular disease); over-transfusion worsens variceal bleeding.
  • Endoscopy within 24 h (immediately after resuscitation if unstable).
  • Variceal: terlipressin + prophylactic antibiotics before endoscopy, then band ligation (or sclerotherapy).
  • Non-variceal: endoscopic haemostasis; PPI after endoscopy (not routinely before). Use the Rockall score for rebleeding/mortality risk.
  • Correct coagulopathy, but avoid reflexive platelet/FFP over-transfusion.
Bottom line / exam pearl

Blatchford to triage, Hb 70 transfusion trigger, scope within 24 h. Variceal = terlipressin + antibiotics + banding; non-variceal = endoscopic haemostasis + PPI after scope.

▸Acute Pancreatitis (ACG / IAP)GastroenterologyACG · IAP-APA
Clinical takeaway

Diagnose on any 2 of 3 (typical pain, lipase ≥ 3× ULN, imaging); give goal-directed fluids and analgesia, treat the cause, and avoid prophylactic antibiotics.

Background

Most pancreatitis is mild and self-limiting, but early fluid strategy and cause-directed care shape outcomes in severe disease.

Key recommendations

  • Diagnosis = 2 of 3: characteristic pain, lipase/amylase ≥ 3× upper limit, or characteristic imaging.
  • Assess severity (persistent SIRS, CRP, Glasgow/APACHE II) and monitor for organ failure.
  • Goal-directed (moderate) IV fluid resuscitation — avoid over-aggressive fluids; give early enteral nutrition once tolerated.
  • No prophylactic antibiotics — reserve antibiotics for infected necrosis or cholangitis.
  • Gallstone cause: urgent ERCP if cholangitis/obstruction; same-admission cholecystectomy for mild gallstone pancreatitis.
  • Manage local complications (necrosis, pseudocyst) with a step-up (drainage before surgery) approach.
Bottom line / exam pearl

2-of-3 to diagnose, fluids that are goal-directed not torrential, feed early, no prophylactic antibiotics, and fix the gallstones (ERCP for cholangitis, same-admission cholecystectomy).

▸Endoscopic Management of Oesophageal and Gastric VaricesHepatology & GIASGE (American Society for Gastrointestinal Endoscopy), Standards of Practice / Gastrointestinal Endoscopy; aligned with AASLD 2023 and Baveno VII · 2014
Clinical takeaway

In acute variceal bleeding, combine a vasoactive drug, prophylactic antibiotics, and endoscopic band ligation within 12 hours; gastric fundal varices are best treated with cyanoacrylate injection rather than banding.

Background — why it changed

Variceal haemorrhage remains a leading cause of death in portal hypertension. ASGE guidance defines the role of endoscopy in screening, primary prophylaxis, and acute haemostasis, and has been reinforced by more recent AASLD and Baveno VII consensus that emphasise earlier risk stratification and pre-emptive TIPS. The approach differs for oesophageal versus gastric varices because of vessel calibre and shunt anatomy.

Key recommendations

  • For acute oesophageal variceal bleeding, perform endoscopic band ligation (EBL) as the endoscopic therapy of choice, ideally within 12 hours of presentation after resuscitation.
  • Give a vasoactive drug (octreotide, terlipressin, or somatostatin) started at presentation and continued for up to 3-5 days, plus antibiotic prophylaxis with ceftriaxone 1 g daily for up to 7 days.
  • For bleeding gastric fundal varices, use endoscopic variceal obturation with tissue adhesive (cyanoacrylate) where available; EBL is an alternative but generally less effective for fundal varices.
  • For primary prophylaxis of high-risk oesophageal varices when non-selective beta-blockers are not tolerated, use EBL, repeated every 2-4 weeks until variceal eradication.
  • After eradication, perform surveillance endoscopy at 3-6 months in the first year, then periodically thereafter.
  • Consider TIPS (or balloon-occluded retrograde transvenous obliteration for some gastric varices) when bleeding cannot be controlled endoscopically or recurs despite combined pharmacological and endoscopic therapy.
  • Use a restrictive transfusion strategy targeting haemoglobin around 7 g/dL in haemodynamically stable patients.

At the bedside

  • Start the vasoactive drug and IV ceftriaxone before endoscopy - do not wait for the scope.
  • Protect the airway in the actively vomiting or encephalopathic patient before endoscopy.
  • If endoscopic control fails, a balloon tamponade tube or oesophageal stent is a bridge to definitive TIPS, not a treatment.
  • Ask specifically whether the varix is oesophageal or gastric fundal - it changes the endoscopic technique (band vs glue).
Bottom line / exam pearl

Drug + antibiotic + band within 12 hours for oesophageal varices; glue (cyanoacrylate) for gastric fundal varices; TIPS for failure.

References

  • ASGE Guideline: The role of endoscopy in the management of variceal hemorrhage (Gastrointestinal Endoscopy). www.giejournal.org
  • ASGE - Top Recommendations for the Diagnosis and Management of Esophagogastric Variceal Bleeding. www.asge.org
  • ACG & AASLD Joint Clinical Guideline: Varices and Variceal Hemorrhage in Cirrhosis (summary). acgcdn.gi.org
▸Management of Oesophageal PerforationHepatology & GIWSES (World Society of Emergency Surgery), World Journal of Emergency Surgery · 2019
Clinical takeaway

Oesophageal perforation is a surgical emergency where early diagnosis (within 24 hours) and timely intervention drive survival; management is individualised across non-operative, endoscopic (stent/vacuum) and surgical routes based on stability, contamination and delay.

Background — why it changed

There is no widely adopted recent society guideline dedicated solely to oesophageal perforation from the STS; the most cited multidisciplinary emergency guidance is the WSES 'Esophageal emergencies' guideline, supported by recent systematic reviews. Perforation carries high mortality (historically up to 30%, now nearer 15%) because mediastinal and pleural contamination progresses rapidly to sepsis. Improved stents, minimally invasive surgery and endoscopic vacuum therapy have broadened options.

Key recommendations

  • Obtain CT of the chest/abdomen with oral contrast and/or a water-soluble contrast oesophagogram to confirm the diagnosis, site and extent, and any leak of contrast.
  • Start immediate supportive care: NPO, IV broad-spectrum antibiotics and antifungal cover, fluid resuscitation, and nutritional support (parenteral or distal enteral).
  • Consider non-operative management only for a contained perforation with free drainage back into the lumen, a stable non-septic patient, and no untreated distal obstruction or malignancy.
  • Offer surgery as soon as possible for patients not meeting non-operative criteria; primary repair (with buttressing) is preferred when tissue is viable, ideally early.
  • Use endoscopic therapy - covered self-expanding stents, clips, or endoscopic vacuum therapy - for selected contained leaks or as an adjunct/alternative in poor surgical candidates.
  • Reserve oesophagectomy or diversion for extensive necrosis, malignancy, or unreconstructable injury; ensure adequate mediastinal/pleural drainage in all approaches.
  • Treatment choice depends on location, size, degree of contamination, time from injury to diagnosis, and physiological status.

At the bedside

  • Suspect Boerhaave in a patient with chest/epigastric pain after vomiting plus subcutaneous emphysema or a left pleural effusion.
  • Time is prognosis - flag the interval from perforation to diagnosis, and escalate to surgery/thoracics urgently.
  • Do not give barium if perforation is suspected; use a water-soluble agent first (CT is more sensitive).
  • Ensure chest drainage and sepsis-6 measures run in parallel with definitive planning.
Bottom line / exam pearl

Early CT/contrast study, aggressive resuscitation and antibiotics, and prompt surgical or endoscopic control - delay beyond 24 hours sharply worsens outcome.

References

▸Management of Portal HypertensionHepatology & GIBSG (British Society of Gastroenterology), with BSIR & BASL; Frontline Gastroenterology / Gut · 2026
Clinical takeaway

Risk-stratify with non-invasive tests, use carvedilol as the preferred non-selective beta-blocker to prevent decompensation and variceal bleeding, and refer early for TIPSS in refractory ascites or uncontrolled/high-risk variceal bleeding.

Background — why it changed

The BSG has updated UK guidance on portal hypertension and on TIPSS (with BSIR and BASL), building on the Baveno VII consensus which shifted management toward earlier detection of clinically significant portal hypertension (CSPH) and treating portal pressure rather than just varices. Non-invasive markers (liver stiffness, platelet count) now identify who can avoid endoscopy. Carvedilol has emerged as first-line because it lowers portal pressure more effectively than traditional beta-blockers.

Key recommendations

  • Define clinically significant portal hypertension by HVPG >= 10 mmHg (varices and variceal bleeding risk rise sharply at >= 12 mmHg); use non-invasive surrogates where HVPG is unavailable.
  • In compensated advanced chronic liver disease, the Baveno VII 'rule': liver stiffness < 15-20 kPa with platelets > 150 makes high-risk varices unlikely and can defer screening endoscopy.
  • Use carvedilol as the preferred NSBB to prevent first decompensation/variceal bleeding in patients with CSPH; the CALIBRE trial showed no significant difference between carvedilol and band ligation for primary prophylaxis of medium/large varices.
  • For acute variceal bleeding, combine vasoactive drugs, prophylactic antibiotics, and endoscopic band ligation, with a restrictive transfusion threshold of ~7 g/dL.
  • Consider pre-emptive (early) TIPSS within 72 hours in high-risk bleeders (e.g. Child-Pugh C < 14, or Child-Pugh B with active bleeding at endoscopy).
  • Refer for TIPSS for refractory/recurrent variceal bleeding despite combined therapy, and for refractory or recurrent ascites, after multidisciplinary patient selection.
  • Screen for and manage precipitants and complications (infection, hepatic encephalopathy, renal dysfunction) as part of portal hypertension care.

At the bedside

  • Check the platelet count and liver stiffness together - they can spare a patient an unnecessary screening endoscopy.
  • Carvedilol titrated to tolerated blood pressure/heart rate is doing more than 'rate control' - it is lowering portal pressure.
  • In an acute bleed, remember the whole bundle: terlipressin/octreotide + ceftriaxone + band ligation + restrictive transfusion.
  • Flag Child-Pugh C or actively bleeding Child-Pugh B patients early for an interventional radiology (TIPSS) discussion.
Bottom line / exam pearl

Detect CSPH early, use carvedilol to prevent decompensation, and escalate to pre-emptive TIPSS in high-risk variceal bleeding.

References

  • BSG guideline on portal hypertension (Frontline Gastroenterology, 2026). www.bsg.org.uk
  • BSG/BSIR/BASL Guidelines: TIPSS in the management of portal hypertension (Gut, 2020). www.bsg.org.uk
  • Guideline review: TIPSS in portal hypertension - a BSG guideline (PubMed). pubmed.ncbi.nlm.nih.gov
▸Colonic DiverticulitisHepatology & GIACG (American College of Gastroenterology), American Journal of Gastroenterology · 2026
Clinical takeaway

Confirm the diagnosis with CT, and withhold routine antibiotics in low-risk, uncomplicated diverticulitis, reserving them for high-risk, immunocompromised, or systemically unwell patients.

Background — why it changed

The 2026 ACG guideline provides evidence-based recommendations for managing colonic diverticulitis largely in the outpatient/gastroenterology setting. It reflects a major shift away from reflexive antibiotics for uncomplicated disease, supported by randomised trials showing no benefit in selected low-risk patients. It also refines who needs interval colonoscopy and elective surgery.

Key recommendations

  • Use CT imaging to confirm the diagnosis of acute diverticulitis, particularly at first presentation and when severe or complicated disease is suspected.
  • Do not routinely give antibiotics for low-risk, acute uncomplicated diverticulitis managed as an outpatient.
  • Do give antibiotics for complicated disease and for patients with high-risk features - immunocompromise, frailty, significant comorbidity, or inability to manage safely as an outpatient.
  • Perform interval colonoscopy after recovery from complicated diverticulitis to exclude missed colorectal cancer or a premalignant lesion.
  • After uncomplicated diverticulitis, offer colonoscopy if there are alarm features or the patient is not up to date with colorectal cancer screening.
  • Refer patients with recurrent uncomplicated diverticulitis significantly affecting quality of life for surgical consultation to discuss elective resection (individualised, not based on episode count alone).
  • Advise lifestyle measures to reduce recurrence: a fibre-rich diet (fruit, vegetables, whole grains, legumes; limited red/processed meat), physical activity, healthy weight, smoking cessation, and minimising NSAIDs where clinically appropriate.

At the bedside

  • For a well, low-risk patient with CT-confirmed uncomplicated diverticulitis, supportive care without antibiotics is now standard.
  • Escalate to antibiotics (and imaging for abscess/perforation) if the patient is septic, immunosuppressed, frail, or failing outpatient care.
  • Book interval colonoscopy after complicated disease - do not assume it was 'just diverticulitis'.
  • Elective surgery is a quality-of-life decision made with the patient, not an automatic rule after two episodes.
Bottom line / exam pearl

CT to confirm, skip antibiotics in low-risk uncomplicated disease, and scope after complicated diverticulitis to rule out cancer.

References

▸Hepatic EncephalopathyHepatology & GIACG (American College of Gastroenterology), American Journal of Gastroenterology; complements AASLD guidance · 2026
Clinical takeaway

Lactulose is first-line for overt hepatic encephalopathy (titrated to 2-3 soft stools/day), with rifaximin added for treatment of acute episodes and for prevention of recurrence; always hunt for and treat the precipitant.

Background — why it changed

The 2026 ACG guideline updates the diagnosis and management of hepatic encephalopathy (HE) in chronic liver disease, complementing AASLD guidance. HE is usually precipitated (infection, GI bleeding, constipation, electrolyte disturbance, dehydration, sedatives). Rifaximin's role has expanded from secondary prophylaxis to an early adjunct in acute overt HE based on trial data showing faster reversal, shorter admissions and lower mortality when combined with lactulose.

Key recommendations

  • Treat hospitalised acute overt HE with lactulose, titrated to 2-4 soft bowel movements per day, as first-line therapy.
  • Add rifaximin (550 mg twice daily) to lactulose for acute overt HE - combination therapy improves complete reversal, shortens hospital stay and reduces mortality versus lactulose alone.
  • Identify and treat precipitating factors (infection/SBP, GI bleeding, constipation, hypokalaemia/hyponatraemia, dehydration, renal dysfunction, sedatives) in every episode.
  • For secondary prophylaxis after an episode of overt HE, use lactulose (titrated to 2-3 soft stools/day) as first-line maintenance therapy.
  • Add rifaximin to lactulose for patients with recurrent overt HE despite lactulose - strongly recommended to reduce recurrence.
  • Avoid prophylactic protein restriction; maintain adequate protein/calorie intake, as malnutrition and sarcopenia worsen HE.
  • Titrate lactulose carefully - overuse can cause dehydration, hypernatraemia and hypokalaemia, which can themselves precipitate or worsen HE.

At the bedside

  • Every episode of HE means 'find the trigger' - culture, look for a bleed, check electrolytes, review sedatives, treat constipation.
  • Titrate lactulose to stool output (2-3 soft stools/day), not to a fixed dose - and watch for over-purging.
  • Add rifaximin for recurrent HE or as an early adjunct in the acute overt episode, not as monotherapy.
  • Do not starve the cirrhotic patient of protein - feed them; malnutrition worsens encephalopathy.
Bottom line / exam pearl

Lactulose titrated to 2-3 soft stools/day plus rifaximin for acute and recurrent overt HE - and always treat the precipitant.

References

  • ACG Clinical Guideline: Hepatic Encephalopathy (American Journal of Gastroenterology). journals.lww.com
  • ACG Clinical Guideline on Hepatic Encephalopathy (PMC). pmc.ncbi.nlm.nih.gov
  • AASLD Practice Guideline: Hepatic Encephalopathy in Chronic Liver Disease. www.aasld.org
▸Tranexamic Acid in Gastrointestinal BleedingHepatology & GIHALT-IT trial (The Lancet); reflected in NICE and UK guideline positions · 2020
Clinical takeaway

Do not use tranexamic acid to treat acute GI bleeding - the HALT-IT trial found no reduction in death due to bleeding and a significant increase in venous thromboembolism (and seizures).

Background — why it changed

Earlier small trials and a Cochrane meta-analysis had suggested a mortality benefit from tranexamic acid (TXA) in GI bleeding, but the evidence was low quality. HALT-IT was a large international RCT (about 12,000 adults with significant upper or lower GI bleeding) designed to settle the question. It used a high-dose 24-hour regimen and overturned the earlier optimism, so current UK/NICE and international positions do not recommend TXA for GI bleeding.

Key recommendations

  • Do not routinely give tranexamic acid to treat acute gastrointestinal bleeding outside a clinical trial.
  • HALT-IT showed no significant reduction in death due to bleeding (about 4% in both TXA and placebo groups).
  • TXA was associated with a significant increase in venous thromboembolic events (DVT and pulmonary embolism).
  • TXA was also associated with an increased risk of seizures.
  • The trial studied a high-dose regimen (a loading dose followed by a 24-hour infusion), so lack of benefit is not explained by underdosing.
  • NICE does not recommend TXA as part of standard management of acute upper GI bleeding, consistent with these findings.
  • Standard care - resuscitation, PPI where indicated, urgent endoscopy, and variceal-specific measures - remains the priority rather than antifibrinolytics.

At the bedside

  • Reach for endoscopy, PPI and resuscitation in a GI bleed - not tranexamic acid.
  • If TXA is being considered for another reason, weigh the increased clot (DVT/PE) and seizure risk in this population.
  • Do not extrapolate the trauma (CRASH-2) TXA benefit to gastrointestinal bleeding.
  • Focus resources on early risk stratification and definitive haemostasis.
Bottom line / exam pearl

HALT-IT put a stop to TXA for GI bleeding: no mortality benefit, more clots and seizures - so don't use it.

References

  • HALT-IT: high-dose 24-h tranexamic acid infusion in acute GI bleeding (The Lancet, 2020). www.ncbi.nlm.nih.gov
  • HALT-IT trial - ClinicalTrials.gov (NCT01658124). clinicaltrials.gov
  • NICE CG141: Acute upper gastrointestinal bleeding in over 16s - Recommendations. www.nice.org.uk
▸Management of Symptomatic Walled-Off Pancreatic NecrosisHepatology & GISAGES with AHPBA (Society of American Gastrointestinal and Endoscopic Surgeons / Americas Hepato-Pancreato-Biliary Association); Surgical Endoscopy · 2026
Clinical takeaway

For symptomatic walled-off pancreatic necrosis, the panel makes conditional recommendations favouring endoscopic (transmural) intervention over image-guided drainage, and image-guided or minimally invasive approaches over open surgery - though all recommendations rest on very low certainty evidence.

Background — why it changed

Walled-off pancreatic necrosis (WON) is a late (typically >4 weeks) complication of necrotising pancreatitis; symptomatic or infected collections require intervention. This 2026 SAGES/AHPBA guideline, with an accompanying systematic review and meta-analysis, addressed four comparisons: image-guided vs endoscopic, image-guided vs surgical, endoscopic vs surgical, and pure endoscopic vs step-up approaches. The shift reflects the move away from early open necrosectomy toward minimally invasive, step-up strategies.

Key recommendations

  • Conditional recommendation for endoscopic management over image-guided (percutaneous) intervention for suitable collections.
  • Conditional recommendation for image-guided intervention over open surgery.
  • Conditional recommendation for either minimally invasive surgery or image-guided intervention (rather than open surgery) when surgery is chosen.
  • The review also compared pure endoscopic versus step-up approaches, informing modality sequencing.
  • Endoscopic drainage is typically achieved with EUS-guided lumen-apposing metal stents (LAMS), enabling direct endoscopic necrosectomy when solid debris or infection is present.
  • All recommendations are based on very low certainty of evidence, so individualised, multidisciplinary decision-making is emphasised.
  • Intervention generally follows maturation of the collection wall in the appropriate clinical context rather than immediate debridement.

At the bedside

  • Manage WON through a multidisciplinary team (interventional endoscopy, HPB surgery, interventional radiology) - modality choice is individualised.
  • Favour a minimally invasive/step-up path over upfront open necrosectomy whenever anatomy and local expertise allow.
  • For endoscopically accessible collections adjacent to the stomach/duodenum, EUS-guided LAMS drainage (with necrosectomy if needed) is the typical first step.
  • Reserve percutaneous drainage for collections not amenable to endoscopy or as part of a combined/step-up strategy, and open surgery as a last resort.
Bottom line / exam pearl

Step up, do not cut first: endoscopic transmural drainage is favoured over percutaneous, and both are favoured over open surgery - all on very low certainty evidence.

References

Respiratory & Allergy9 guidelines

▸VA/DoD Primary-Care Asthma Guideline (2025)RespiratoryAnn Intern Med · 2026
Clinical takeaway

Falls in line with GINA — ICS/formoterol as reliever and maintenance; it is time to retire albuterol-only rescue.

Background

SABA-only rescue treats the bronchospasm but ignores the underlying inflammation, and heavy SABA use is linked to worse outcomes and death. GINA has for years recommended anti-inflammatory reliever therapy (an ICS given with every reliever dose). This VA/DoD guideline brings US primary care into step (it does not cover severe/biologic asthma, which stays with specialists).

Key recommendations

  • Prefer ICS + a rapid-onset LABA (e.g. formoterol) over albuterol monotherapy for rescue.
  • Mild asthma: ICS/formoterol as a reliever alone (anti-inflammatory reliever).
  • Moderate–severe: ICS/formoterol as both maintenance and reliever — MART — with a variable ICS dose that rises when symptoms do.
  • Not controlled on medium–high-dose MART → add a LAMA (long-acting antimuscarinic; "triple therapy").
  • Well controlled for 3 months → consider step-down.
  • Treat the modifiers: obesity and symptomatic GORD.
  • Exercise-induced bronchoconstriction: a pre-exertional short-acting beta-agonist is suggested; patients already on ICS/formoterol can use that pre-exercise.
Bottom line / exam pearl

ICS/formoterol is now the backbone — reliever alone in mild asthma, MART in moderate–severe, add LAMA if still uncontrolled. If you're still handing out a SABA-only inhaler, update the plan.

▸Acute Allergic Reactions — Epinephrine & When to Call EMSAllergyJACI · Intl consensus
Clinical takeaway

Scenario-based rules for community settings: when to use adrenaline, and when adrenaline alone is enough vs when to call an ambulance.

Background

There are no randomised trials of adrenaline in anaphylaxis (it would be unethical to withhold it), so this is expert consensus aimed at patients and carers at home. Adrenaline is the first-line, life-saving treatment; antihistamines and steroids are adjuncts that do not treat airway or circulatory compromise.

Give adrenaline (epinephrine) if the patient has

  • Any cardiovascular or neurological feature — altered responsiveness, dizziness, collapse.
  • Moderate/severe GI symptoms — repeated vomiting or abdominal pain.
  • Any respiratory feature — cyanosis, cough, dyspnoea, hoarseness/stridor.

Activate EMS (when adrenaline is needed) if the patient is

  • Alone, or more than 30 minutes from a hospital.
  • Needing multiple doses or lacking backup doses.
  • Having severe or residual cardiorespiratory symptoms after adrenaline.

Adrenaline NOT required for

  • Isolated mild skin symptoms (a few hives / mild swelling).
  • Mild mucosal symptoms (rhinorrhoea, mild mouth/throat itch).
  • Mild GI upset (vomiting once, mild abdominal pain, nausea).
Bottom line / exam pearl

Any respiratory, cardiovascular/neuro, or moderate–severe GI feature = give adrenaline. Isolated mild skin/mucosal/GI symptoms can be observed. Call EMS if the patient is alone, far from help, needs repeat doses, or isn't settling.

▸GOLD 2026 — COPD Diagnosis & ManagementRespiratoryGOLD · 2026 report
Clinical takeaway

Confirm with post-bronchodilator spirometry, group patients A/B/E, start most on LABA+LAMA, and let blood eosinophils decide on inhaled steroids.

Background

GOLD grades airflow limitation but drives treatment by symptoms and exacerbation risk. The ABE assessment (which replaced ABCD) and eosinophil-guided ICS are the framework's core, with biologics now entering for the eosinophilic phenotype.

Key recommendations

  • Diagnose: post-bronchodilator FEV₁/FVC < 0.70 plus symptoms/risk factors; grade severity by FEV₁ (GOLD 1–4).
  • Assess with ABE: symptoms (mMRC / CAT) + exacerbation history → Group A (low symptoms/risk), B (high symptoms, low risk), E (high exacerbation risk: ≥2 moderate or ≥1 hospitalisation).
  • Initial therapy: A → a bronchodilator; B → LABA+LAMA; E → LABA+LAMA, adding ICS if blood eosinophils ≥300.
  • Follow-up by trait: persistent dyspnoea → LABA+LAMA; persistent exacerbations → add ICS if eosinophils ≥100 (triple therapy); consider roflumilast or azithromycin in selected patients; dupilumab for the eosinophilic, exacerbating phenotype.
  • Exacerbations: SABA, prednisolone 40 mg for 5 days, antibiotics if increased sputum purulence/volume or ventilated; controlled O₂ to SpO₂ 88–92%; NIV for hypercapnic respiratory failure.
  • Foundational: smoking cessation (the single most effective intervention), vaccinations (influenza, pneumococcal, COVID-19, RSV, pertussis), pulmonary rehabilitation and physical activity.
Bottom line / exam pearl

Spirometry to confirm (FEV₁/FVC <0.70) → group A/B/E → LABA+LAMA for most, add ICS if eosinophils high. Exacerbation = steroids ± antibiotics + O₂ 88–92% ± NIV. Stop smoking, vaccinate, rehab.

▸Community-Acquired Pneumonia (BTS / IDSA-ATS)RespiratoryBTS · IDSA/ATS
Clinical takeaway

Score severity with CURB-65, match antibiotics and setting to severity, and don't reach for broad-spectrum cover unnecessarily.

Background

CAP severity scoring guides where the patient is treated and how broadly they are covered, avoiding both under- and over-treatment.

Key recommendations

  • CURB-65 — Confusion, Urea > 7, RR ≥ 30, BP < 90/60, age ≥ 65: 0–1 usually home, 2 consider admission, ≥ 3 severe / consider critical care (CRB-65 in the community).
  • Low severity: amoxicillin. Moderate/high: add a macrolide or use co-amoxiclav; cover atypicals when suspected.
  • Give oxygen to target saturations; look for complications (parapneumonic effusion / empyema).
  • De-escalate on cultures; 5 days is often sufficient if improving and afebrile.
  • Consider corticosteroids in severe CAP (recent evidence of mortality benefit) in selected patients.
Bottom line / exam pearl

CURB-65 sorts site and severity; amoxicillin for mild, broaden for moderate/severe, cover atypicals when suspected, and stop at ~5 days if improving.

▸Noninvasive Respiratory Support in Acute Respiratory FailureRespiratoryAmerican Thoracic Society (ATS) Clinical Practice Guideline, Am J Respir Crit Care Med · 2026
Clinical takeaway

Using GRADE, the ATS gives a strong recommendation for HFNC over standard oxygen in de novo acute hypoxaemic respiratory failure and a strong recommendation for NIV in acute hypercapnic failure, with structured advice on preoxygenation and post-extubation support.

Background — why it changed

Noninvasive respiratory support - high-flow nasal cannula (HFNC), non-invasive ventilation (NIV) and CPAP - can avert intubation but risks delaying it if misapplied. This multidisciplinary ATS guideline (approved May 2026; AJRCCM 212(9):2135) addresses hypoxaemic and hypercapnic failure, preoxygenation before intubation, and post-extubation support.

Key recommendations

  • De novo acute hypoxaemic respiratory failure: HFNC recommended over standard oxygen (strong recommendation, moderate certainty).
  • In the same population, NIV (facemask or helmet) and CPAP (facemask or helmet) are each suggested over standard oxygen (conditional, low certainty).
  • Acute hypercapnic respiratory failure: NIV strongly recommended to reduce mortality and the need for intubation.
  • HFNC in hypercapnic failure only for less severe hypercapnia with mild acidaemia (pH >7.25), and only where close monitoring and prompt NIV escalation are available (conditional).
  • Preoxygenation before intubation: HFNC or NIV strongly recommended over standard oxygen to prevent peri-intubation hypoxaemia.
  • Post-extubation: HFNC suggested for low-risk patients and NIV for high-risk patients to reduce reintubation after critical illness.

At the bedside

  • Reach for HFNC first in de novo hypoxaemic failure - but set a clear time-limited trial and watch for failure (rising ROX-type concern) so intubation is not delayed.
  • In a COPD exacerbation with respiratory acidosis, NIV is the strong, first-line intervention.
  • Preoxygenate the difficult/critically ill patient with HFNC or NIV rather than plain facemask oxygen.
  • Match post-extubation support to risk: high-risk (e.g. hypercapnia, comorbidity) to NIV; low-risk to HFNC.
Bottom line / exam pearl

HFNC first for hypoxaemic failure, NIV first for hypercapnic failure - and use HFNC/NIV to preoxygenate and to prevent reintubation, always with a low threshold to escalate.

References

▸BTS Guideline for Pleural Disease in AdultsRespiratoryBritish Thoracic Society (BTS), published in Thorax (with an accompanying BTS Quality Standard for Pleural Disease) · 2023
Clinical takeaway

The 2023 BTS guideline shifts spontaneous pneumothorax care toward a symptom-based, often conservative/ambulatory approach and standardises management of pleural infection and malignant effusion.

Background — why it changed

This guideline replaced the 2010 BTS pleural disease guidance after more than a decade of new evidence, and was published alongside a BTS Clinical Statement on pleural procedures in 2023. A dedicated BTS Quality Standard for Pleural Disease was subsequently developed (working group convened March 2024) to support implementation. Major drivers of change included trials supporting conservative management of pneumothorax and intrapleural enzyme therapy for pleural infection.

Key recommendations

  • Manage spontaneous pneumothorax by a symptom-based approach: conservative management is appropriate for patients who are asymptomatic or only mildly symptomatic, rather than defaulting to intervention based on size alone.
  • Ambulatory management and needle aspiration are options that can reduce the need for chest drain insertion and hospital admission in selected patients.
  • Investigate an undiagnosed unilateral pleural effusion systematically, using pleural fluid analysis and image-guided sampling, with thoracic ultrasound to guide procedures.
  • For pleural infection, use a small-bore chest tube for initial drainage; intrapleural tPA plus DNase should be considered for residual/loculated collections.
  • The RAPID score (Renal, Age, Purulence, Infection source, Dietary/albumin) may be used to risk-stratify pleural infection.
  • In malignant pleural effusion, offer definitive management (indwelling pleural catheter and/or talc pleurodesis) guided by patient preference; where IPC pleurodesis and removal is the goal, daily drainage improves pleurodesis rates.
  • Use thoracic ultrasound for all pleural interventions to improve safety and success.

At the bedside

  • A small, minimally symptomatic pneumothorax in a stable patient often does not need a drain - reassess symptoms rather than reflexively intervening.
  • Always use ultrasound guidance for pleural aspiration/drain insertion; never mark a "blind" site from an old film.
  • Send pleural fluid for pH, protein/LDH (Light's criteria), glucose, cytology and microbiology; a low pH or frank pus signals the need for drainage.
  • For empyema not clearing on antibiotics plus a small-bore drain, escalate to intrapleural tPA/DNase or surgical referral rather than waiting.
Bottom line / exam pearl

Treat spontaneous pneumothorax by symptoms (conservative when mild), drain pleural infection with a small-bore tube plus tPA/DNase for loculated collections, and always image with ultrasound before any pleural procedure.

References

▸WAO Guidelines for the Classification, Diagnosis, and Treatment of Hereditary AngioedemaAllergyWorld Allergy Organization (WAO); published in the World Allergy Organization Journal (building on the WAO/EAACI guideline lineage) · 2025
Clinical takeaway

Every patient with confirmed HAE should have on-demand therapy available at all times, treating attacks early, while long-term prophylaxis follows a treat-to-target approach aimed at complete disease control.

Background — why it changed

The 2025 WAO guideline updates the prior international WAO/EAACI guideline (2021 revision) and was developed by an international panel of experts from many countries, with explicit attention to worldwide disparities in access to therapy. It reframes management around a treat-to-target philosophy - aiming for no attacks, normal quality of life, and normalised disease burden - with shared decision-making and regular reassessment. Newer targeted therapies have expanded the prophylaxis options since earlier guidelines.

Key recommendations

  • All confirmed HAE patients should have access to on-demand treatment for acute attacks, including asymptomatic patients, and any attack affecting or potentially affecting the airway should be treated.
  • Treat attacks as early as possible after onset with an effective on-demand agent.
  • Recommended on-demand options include C1-inhibitor concentrate, icatibant (bradykinin B2-receptor antagonist), and ecallantide where available.
  • Consider individualised long-term prophylaxis (LTP) for patients with ongoing disease burden, using a treat-to-target framework with regular reassessment.
  • First-line LTP options include plasma-derived C1-inhibitor, lanadelumab, or berotralstat.
  • Confirm the diagnosis biochemically (C4 and C1-inhibitor level/function; C1-INH-HAE type 1 vs type 2), and evaluate for HAE with normal C1-INH where suspected.
  • Patient self-administration and a written individualised action plan should be supported to enable early home treatment.

At the bedside

  • HAE angioedema does not respond to antihistamines, corticosteroids, or adrenaline - do not rely on the usual anaphylaxis kit; give a targeted HAE agent (C1-INH or icatibant).
  • Any laryngeal or tongue swelling is a potential airway emergency - treat immediately and prepare for airway management.
  • Ask about family history and prior attacks (recurrent abdominal pain, non-urticarial swelling without itch) to distinguish HAE from histaminergic angioedema.
  • Ensure the patient always carries on-demand medication and knows how to self-administer it early.
Bottom line / exam pearl

HAE swelling is bradykinin-mediated and unresponsive to antihistamines/steroids/epinephrine - every patient needs early on-demand C1-INH or icatibant, with treat-to-target long-term prophylaxis for those with significant burden.

References

▸Managing Acute Asthma: A Practical Guide to GINA RecommendationsRespiratoryGlobal Initiative for Asthma (GINA), GINA Global Strategy for Asthma Management and Prevention · 2025
Clinical takeaway

Assess exacerbation severity while starting treatment immediately - repeated inhaled SABA, controlled oxygen, and early systemic corticosteroids - and before discharge always step up ICS-containing controller therapy because an attack is a red flag for the next one.

Background — why it changed

GINA is an annually updated global strategy report rather than a fixed guideline. It frames acute asthma management around rapid severity triage and prompt reliever therapy, and it has shifted maintenance care toward ICS-containing (anti-inflammatory) reliever strategies to reduce exacerbation risk. Discharge planning and early follow-up are treated as core parts of exacerbation care.

Key recommendations

  • Assess severity while treating - speech, work of breathing, mental status, oxygen saturation, and peak flow where feasible - and identify high-risk patients (prior near-fatal asthma, recent OCS, over-use of SABA).
  • Inhaled SABA is first-line: repeated/frequent salbutamol (e.g. via pMDI-spacer or nebulizer), given every 20 minutes in the first hour for moderate-severe attacks.
  • Add ipratropium bromide for moderate-severe exacerbations (e.g. 4 puffs with each of up to 3 salbutamol doses / nebulized) for greater bronchodilation.
  • Give systemic corticosteroids early to all but the mildest exacerbations (oral is as effective as IV); a short course is continued after discharge.
  • Titrate controlled oxygen to a target saturation of 93-95% in adults/adolescents (at least 94% in young children) rather than high-flow to 100%.
  • Consider IV magnesium sulfate for severe exacerbations not responding to initial treatment (including children 2 years and older).
  • Before discharge, start or step up ICS-containing therapy; in patients 12 years and older, ICS-formoterol maintenance-and-reliever therapy is preferred, and arrange follow-up within about 2-7 days.

At the bedside

  • Reassess response at or before 1 hour; improving patients can be considered for discharge, deteriorating ones escalated.
  • Do not send a patient home on SABA alone after an attack - ensure an ICS-containing controller is prescribed to cut re-exacerbation risk.
  • Treat any exacerbation needing urgent care or OCS as a prompt to review and step up maintenance therapy and inhaler technique.
  • Watch for silent chest, exhaustion, drowsiness, or falling saturation - signs of life-threatening asthma needing critical-care input.
Bottom line / exam pearl

Repeated SABA plus ipratropium, early systemic steroids, and controlled oxygen to 93-95% get the patient through the attack - but the exam pearl is that no one leaves without an ICS-containing controller and early follow-up.

References

▸Global Strategy for Prevention, Diagnosis and Management of COPD (GOLD Report)RespiratoryGlobal Initiative for Chronic Obstructive Lung Disease (GOLD) · 2026
Clinical takeaway

GOLD 2026 moves beyond a spirometry-centric model toward early diagnosis and multi-dimensional assessment, formally treating disease activity as a therapeutic target and using blood eosinophils to guide inhaled corticosteroid use.

Background — why it changed

GOLD continues to refine COPD care around personalized, exacerbation-focused management. The 2026 report keeps the ABE assessment scheme but sharpens it, integrates eosinophil-guided ICS decisions, and broadens assessment to include multimorbidity and disease activity.

Key recommendations

  • Confirm diagnosis with post-bronchodilator spirometry (FEV1/FVC < 0.70) in a patient with compatible symptoms and risk exposure; emphasize earlier case-finding.
  • Assess across five domains: airflow-obstruction severity, current symptoms, exacerbation history, blood eosinophil count, and multimorbidity.
  • Use the ABE groups: Group A and B require no exacerbations in the past year and differ by symptom burden (A = CAT <10 and mMRC <2; B = CAT >=10 or mMRC >=2); Group E = a significant exacerbation history regardless of symptoms.
  • Initial therapy: Group A -- a bronchodilator; Group B -- LABA + LAMA; Group E -- LABA + LAMA.
  • Consider adding an inhaled corticosteroid when the blood eosinophil count is elevated (about >= 300 cells/uL), and avoid ICS with very low eosinophils/recurrent pneumonia.
  • For acute exacerbations, treat with short-acting bronchodilators, systemic corticosteroids, and antibiotics when indicated, plus oxygen/ventilatory support as needed, and address the trigger.
  • Prevent future exacerbations with inhaler optimization, smoking cessation, vaccination, pulmonary rehabilitation, and physical activity.

At the bedside

  • Do not classify a COPD patient without the exacerbation history and a blood eosinophil count -- both steer the inhaler choice.
  • Most symptomatic and exacerbating patients start on dual bronchodilation (LABA+LAMA); reserve ICS for those with higher eosinophils or an asthma-COPD overlap picture.
  • At every exacerbation, ask why now -- infection, non-adherence, or a comorbidity -- and reassess inhaler technique.
  • Layer in the non-drug essentials each visit: quit smoking, vaccinate, refer to pulmonary rehab, and confirm the patient can actually use their device.
Bottom line / exam pearl

GOLD 2026 ABE with eosinophil-guided ICS: A gets a bronchodilator, B and E get LABA+LAMA, and add ICS mainly when eosinophils are ~>=300 cells/uL.

References

Trauma & Injury2 guidelines

▸Major Trauma (ATLS / NICE)TraumaATLS · NICE NG39
Clinical takeaway

Work <C>ABCDE — catastrophic haemorrhage first — with damage-control resuscitation and rapid transfer to definitive care.

Background

Trauma deaths cluster early from airway loss and haemorrhage; a structured primary survey with simultaneous resuscitation prevents avoidable deaths.

Key recommendations

  • <C> Catastrophic haemorrhage — direct pressure, tourniquet, haemostatic dressing.
  • A Airway with C-spine control; B Breathing — decompress tension pneumothorax, seal open chest wounds; C Circulation — control bleeding, pelvic binder, blood products, TXA, permissive hypotension.
  • D Disability — GCS, pupils, glucose; E Exposure/Environment — full exposure while preventing hypothermia.
  • Activate the major haemorrhage protocol and use eFAST; whole-body CT for the significantly injured.
  • Team-based care: primary survey and resuscitation together, then a thorough secondary survey; early transfer to a major trauma centre.
Bottom line / exam pearl

Catastrophic bleeding before airway; decompress the chest, bind the pelvis, give blood + TXA, keep them warm, and get the significantly injured to CT and a trauma centre fast.

▸Head Injury (NICE NG232)TraumaNICE NG232
Clinical takeaway

Use the NICE criteria to select a CT head within 1 hour or within 8 hours — and remember anticoagulation lowers the threshold to scan.

Background

Most head injuries are minor, but a small number harbour a surgical bleed; NICE criteria identify who needs imaging and when.

Key recommendations

  • CT head within 1 hour if: GCS < 13 on arrival, GCS < 15 at 2 h, suspected open/depressed or basal skull fracture, post-traumatic seizure, focal neurological deficit, or > 1 episode of vomiting.
  • CT head within 8 hours (if any LOC or amnesia) for: age ≥ 65, a dangerous mechanism, or > 30 min of retrograde amnesia.
  • On anticoagulants/antiplatelets with any LOC or amnesia → CT within 8 hours even without other features.
  • Consider CT cervical spine alongside per the criteria; admit/observe those with abnormal imaging, persistent symptoms or ongoing concern.
  • Give clear written head-injury discharge advice and safety-netting to those sent home.
Bottom line / exam pearl

Know the 1-hour vs 8-hour NICE CT triggers; being on an anticoagulant with any LOC/amnesia buys a scan on its own. Always give written safety-netting.

Toxicology & Environmental4 guidelines

▸Paracetamol OverdoseToxicologyTOXBASE / RCEM
Clinical takeaway

Treat single acute ingestions by the nomogram at 4 hours; give N-acetylcysteine empirically for staggered, late or unknown-time overdoses.

Background

Paracetamol is a leading cause of acute liver failure yet is highly treatable if NAC is given in time.

Key recommendations

  • Single acute ingestion: take a paracetamol level at 4 hours post-ingestion and plot on the 100 mg/L treatment line; treat if above it.
  • Staggered (> 1 h) or unknown-time overdose: start NAC immediately — the nomogram does not apply.
  • Give N-acetylcysteine IV (watch for anaphylactoid reactions — slow/pause the infusion, give an antihistamine).
  • Monitor INR, LFTs, creatinine, venous pH and lactate; consider activated charcoal if presenting within 1 h of a large ingestion.
  • Use the King's College Criteria to flag transplant referral (pH < 7.3, or INR > 6.5 + creatinine > 300 + grade III–IV encephalopathy).
Bottom line / exam pearl

Nomogram for a clean single ingestion; NAC empirically for staggered/late/unknown. Track INR/pH/creatinine and refer to a liver unit using the King's College Criteria.

▸Alcohol Withdrawal & Delirium TremensToxicologyWithdrawal management
Clinical takeaway

Benzodiazepines are the mainstay — ideally symptom-triggered (CIWA-Ar) — and parenteral thiamine prevents Wernicke's encephalopathy.

Background

Alcohol withdrawal ranges from tremor and anxiety to seizures and life-threatening delirium tremens; early, adequate treatment prevents escalation.

Key recommendations

  • Assess severity with CIWA-Ar; give benzodiazepines — chlordiazepoxide or diazepam (use lorazepam in significant liver disease) by symptom-triggered or fixed-dose regimen.
  • Give parenteral thiamine (Pabrinex) BEFORE any glucose to prevent Wernicke's encephalopathy (confusion, ataxia, ophthalmoplegia).
  • Correct magnesium, potassium and phosphate; treat dehydration.
  • Withdrawal seizures → benzodiazepines (not long-term anticonvulsants).
  • Delirium tremens (severe agitation, autonomic instability, hallucinations) → high-dose benzodiazepines, consider phenobarbital or dexmedetomidine, and manage in a high-care/ICU setting.
Bottom line / exam pearl

Benzodiazepines (symptom-triggered) control withdrawal; thiamine before glucose prevents Wernicke's; replace Mg/K/PO₄; DT needs high-dose benzos and close monitoring.

▸Treatment of Heat StrokeEnvironmentalSociety of Critical Care Medicine (SCCM); Critical Care Medicine · 2025
Clinical takeaway

Rapid active cooling is the priority - cold or ice-water immersion cools fastest and should be used where available, aiming for a cooling rate of at least 0.155 deg C/min and core temperature below about 39 deg C within roughly 30 minutes. Antipyretics and dantrolene are ineffective and should be avoided.

Background — why it changed

Published in Critical Care Medicine (February 2025), this is the first SCCM guideline dedicated to heat stroke. The panel issued two strong recommendations, five good practice statements and one research-only statement covering both classic and exertional heat stroke.

Key recommendations

  • Use active cooling over passive cooling, prioritising cold- or ice-water immersion as the fastest method where feasible.
  • Similar cooling strategies apply to both classic and exertional heat stroke.
  • Target a cooling rate of at least 0.155 deg C/min and reach target temperature within about 30 minutes of recognition (observational data link reaching <= 38.9 deg C within 1 hour to lower mortality).
  • Avoid antipyretics (acetaminophen, NSAIDs, salicylates) - hyperthermia here is failed thermoregulation, not cytokine-mediated fever.
  • Recommend against dantrolene; there is no evidence supporting pharmacologic temperature control in heat stroke.
  • Control shivering or seizure activity with benzodiazepines as needed during cooling.

At the bedside

  • Cool first and cool fast: get the patient into cold or ice-water immersion immediately and monitor core temperature continuously.
  • Do not waste time on paracetamol, NSAIDs or dantrolene - they do not help.
  • Give benzodiazepines for shivering to keep cooling effective, while supporting airway, circulation and organ function concurrently.
Bottom line / exam pearl

In heat stroke, immediate cold-water immersion to a cooling rate of at least 0.155 deg C/min beats drugs - antipyretics and dantrolene have no role.

References

▸Laboratory Testing for Drugs of Misuse to Support the Emergency DepartmentToxicologyAssociation for Diagnostics & Laboratory Medicine (ADLM, formerly AACC/NACB) - Guidance Document, Journal of Applied Laboratory Medicine · 2026
Clinical takeaway

Emergency-department urine drug screens are presumptive immunoassays that rarely change acute management of the undifferentiated patient: a positive can reflect exposure hours to days earlier and results carry meaningful false-positive and false-negative rates, so treat the patient, not the screen.

Background — why it changed

This ADLM guidance replaces the 2003 NACB document (23 years out of date) and modernises ED drug-of-misuse testing for the fentanyl era. It updates recommended test menus, turnaround times, cutoffs, and reporting language, and stresses that immunoassay screens have inherent limitations that must be communicated to ED clinicians for correct interpretation.

Key recommendations

  • Include a modern menu covering amphetamines/amphetamine-type stimulants, benzodiazepines, cocaine, opiates, oxycodone, and fentanyl (fentanyl and oxycodone were missing from the 2003 guidance).
  • Provide results within a mutually agreed window, generally <60 minutes, so testing is clinically actionable; a single urine specimen on arrival is generally sufficient.
  • Report immunoassay results qualitatively as 'presumptive positive' (or 'unconfirmed positive') with the assay cutoff and interpretive comments, never as a definitive diagnosis.
  • Recognise the detection window far exceeds the duration of clinical/physiological effects - a positive screen may reflect exposure hours to days earlier and does not prove current intoxication.
  • Account for false positives (cross-reacting compounds) and false negatives (poorly detected drugs); laboratories should give the ED assay-specific lists of common interferents and gaps.
  • Use definitive/confirmatory testing (e.g. LC-MS/MS) to resolve discrepant or clinically important results, understanding it is usually not available in the acute timeframe.
  • Educate ED staff on what each assay can and cannot detect so screens are ordered and interpreted appropriately rather than driving reflexive management changes.

At the bedside

  • Manage acute poisoning clinically (toxidrome, vitals, glucose, ECG) - do not wait on or over-rely on the urine screen, which seldom alters immediate resuscitation.
  • Before acting on a surprising result, ask the lab about cross-reactants (e.g. common causes of a false-positive amphetamine screen) and whether the drug of concern is even reliably detected.
  • Remember a negative screen does not exclude a dangerous ingestion - many agents (e.g. synthetic opioids/novel drugs beyond the assay, some benzodiazepines) are poorly detected.
  • Interpret a positive as 'exposure at some point,' not 'currently intoxicated by this drug', and confirm important findings before they drive disposition or legal decisions.
Bottom line / exam pearl

The ED urine drug screen is a presumptive, delayed marker of exposure - treat the patient clinically and confirm before letting a screen change management.

References

Exam prep · MD · DNB · JIPMERPG Theory CourseTheory MCQs with detailed, why-the-others-are-wrong explanations. Open ›

Screening & Musculoskeletal3 guidelines

▸ACP Breast Cancer Screening RecommendationsScreeningAnn Intern Med · 2026
Clinical takeaway

Biennial mammography for average-risk women 50–74, with shared decision-making for younger and older women — deliberately more conservative than some other bodies.

Background

Guidelines genuinely disagree here, and patients notice. The USPSTF (2024) lowered the start age to 40 (biennial); the American College of Radiology favours annual screening from 40. The ACP, synthesising the same systematic reviews, holds to starting at 50 and screening every 2 years, weighing the modest mortality benefit against false positives and overdiagnosis. All recommendations are low-to-moderate certainty and apply to average-risk people assigned female at birth.

Key recommendations

  • 50–74 years: biennial screening mammography (moderate certainty of net benefit in reducing breast-cancer mortality).
  • 40–49 years: shared decision-making — those who remain uncertain after counselling should defer; those who choose to screen do so biennially.
  • ≥75 years: discuss stopping — uncertain mortality benefit and real overdiagnosis risk.
  • Dense breasts (an independent risk factor present in 40–50%): consider supplemental digital breast tomosynthesis (DBT); supplemental MRI or ultrasound is not recommended.
Bottom line / exam pearl

ACP = biennial 50–74, individualised at 40–49 and ≥75. Know that this differs from USPSTF/ACR (earlier / annual) — the exam (and your patients) will ask why the advice varies.

▸Subacromial Pain Syndrome (Dutch Orthopaedic Assoc.)MSKActa Orthop · 2026
Clinical takeaway

Manage most patients non-operatively — a few exam tests, ultrasound if needed, then a stepped programme; surgery is a last resort.

Background

Subacromial pain syndrome (SAPS, formerly "shoulder impingement") is non-traumatic, non-rheumatological shoulder pain that is worst when the arm is raised above the shoulder — it spans supraspinatus tendinosis, calcific tendinitis and degenerative cuff tears. Crucially, high-quality trials have shown subacromial decompression surgery adds little over placebo/exercise, so this multidisciplinary guideline (which included primary care) is firmly conservative.

Diagnosis

  • A combination of physical tests is slightly more accurate than any single one; the empty-can test and resisted external rotation have the highest positive predictive value.
  • Ultrasound is the preferred imaging for suspected rotator-cuff tears; MRI only if ultrasound is unavailable.

Treatment (stepped)

  • Exercise is the mainstay for long-term resolution; educate about limiting aggravating movements (forward flexion, abduction above the shoulder, rotation) and the effect of smoking, obesity and deconditioning on healing.
  • NSAIDs and subacromial corticosteroid injections short-term only — to enable pain-free exercise, not as long-term therapy.
  • Calcific tendinitis: corticosteroid injection first; if unsuccessful, ultrasound-guided barbotage (needle, break up and aspirate the calcium).
  • Suprascapular nerve block when other non-operative measures fail.
  • Surgery for an isolated non-traumatic supraspinatus tear only after 3–6 months of failed conservative care.
Bottom line / exam pearl

Diagnose with a couple of exam manoeuvres ± ultrasound, then education + exercise, short-term NSAIDs/injections, barbotage for calcific disease. Decompression surgery adds little — reserve surgery for refractory cases.

▸Identification and Management of Sarcopenia in Patients With MultimorbidityScreeningEuropean Federation of Internal Medicine (EFIM) critically appraised and adapted guideline, European Journal of Internal Medicine · 2026
Clinical takeaway

In multimorbid patients, proactively case-find for sarcopenia and use muscle strength (handgrip or chair-stand) as the entry point to assessment, then treat with individualized exercise and nutrition rather than waiting for overt frailty.

Background — why it changed

Sarcopenia - loss of muscle mass and strength - is common and under-recognized in patients with multiple chronic conditions and drives disability and poor outcomes. EFIM's Multimorbidity Working Group critically appraised and adapted four high-quality clinical practice guidelines to produce recommendations tailored to internal-medicine practice. Eight PICO questions covered case-finding, screening, diagnosis, prevention, iatrogenic complications, and nutritional, exercise, and pharmacologic interventions.

Key recommendations

  • Undertake proactive case-finding in adults 65 years and older, and in multimorbid adults under 65 with specific risk factors.
  • Use muscle strength - handgrip dynamometry or the chair-stand (sit-to-stand) test - as the entry point to assessment.
  • Apply flexible, individualized diagnostic pathways rather than a single rigid algorithm, confirming with muscle mass/quality measures where available.
  • Prescribe individualized multimodal physical activity, with resistance/progressive exercise as a cornerstone of management.
  • Provide nutritional intervention, including attention to adequate protein and energy intake, alongside exercise.
  • Attend to iatrogenic contributors (e.g. immobilization, polypharmacy, undernutrition) that worsen sarcopenia in multimorbid patients.
  • Recognize that most recommendations rest on limited evidence: of 37 adapted recommendations (30 strong, 7 weak), only 8 were based on high-quality evidence, so individualize and reassess.

At the bedside

  • Screen older or multimorbid inpatients with a quick chair-stand test or handgrip rather than relying on appearance alone.
  • Pair any diagnosis of sarcopenia with a concrete resistance-exercise and protein/nutrition plan, not just observation.
  • Review the medication list and mobilization plan for iatrogenic drivers of muscle loss during admission.
  • Reassess strength and function over time to gauge response, since evidence for specific thresholds is weak.
Bottom line / exam pearl

Think of sarcopenia early in multimorbidity - screen with muscle strength (grip or chair-stand) and treat with individualized exercise plus nutrition.

References

Obstetrics3 guidelines

▸Initial Management of Amniotic Fluid EmbolismObstetricsSociety for Maternal-Fetal Medicine (SMFM) Special Statement · 2026
Clinical takeaway

The updated SMFM checklist frames AFE as a sudden cardiorespiratory collapse with consumptive coagulopathy near delivery, prioritising immediate high-quality resuscitation aligned with ACLS, prompt delivery, and aggressive DIC/haemorrhage management.

Background — why it changed

AFE is a rare, catastrophic syndrome of abrupt cardiorespiratory collapse during labour or soon after delivery, often followed by disseminated intravascular coagulation. This 2026 Special Statement updates the 2021 checklist with revised terminology and intervention criteria, closer alignment with current ACLS guidance, and integration of newer epidemiology and pathophysiology. It is intentionally focused on the first minutes of management on the labour-and-delivery unit.

Key recommendations

  • Recognise AFE clinically as sudden hypoxia/hypotension/cardiovascular collapse plus coagulopathy around labour/delivery; it remains a diagnosis of exclusion.
  • Deliver high-quality resuscitation aligned with ACLS, including manual left uterine displacement and preparation for perimortem/expedited caesarean if there is no rapid response to arrest.
  • Anticipate and treat severe DIC / obstetric haemorrhage early with a massive transfusion approach (balanced products, fibrinogen replacement).
  • Assign clear team roles and call for help early (obstetrics, anaesthesia, critical care, neonatology, blood bank).
  • The 'A-OK' regimen (atropine, ondansetron, ketorolac) is of unproven benefit; SMFM notes cautions - atropine is relatively contraindicated with tachycardia, and ketorolac may impair platelet function in DIC/thrombocytopenia.
  • Consider advanced support (e.g. echocardiography-guided management, ECMO/mechanical circulatory support) for refractory cardiogenic shock.

At the bedside

  • Call the arrest/massive-transfusion team the moment AFE is suspected - minutes determine survival.
  • Maintain left uterine displacement and prepare for perimortem caesarean within minutes of maternal cardiac arrest that does not respond immediately.
  • Expect profound coagulopathy: activate MTP and give fibrinogen (concentrate or cryoprecipitate) early.
  • Treat A-OK as adjunctive and unproven - do not let it delay ACLS, delivery or haemorrhage control.
Bottom line / exam pearl

AFE = abrupt collapse plus DIC around delivery; the wins are immediate ACLS, left uterine displacement, rapid delivery and aggressive coagulopathy management, not any single 'magic' drug.

References

▸Maternal Stroke in Pregnancy and PostpartumObstetricsAmerican Heart Association Scientific Statement (ACOG-endorsed), Stroke · 2026
Clinical takeaway

This AHA statement stresses that pregnancy should not delay evidence-based stroke care: treat severe hypertension promptly, and offer IV thrombolysis and thrombectomy to eligible pregnant/postpartum patients when benefit outweighs risk.

Background — why it changed

Published 28 January 2026 in Stroke (2026;57:e127-e145) and endorsed by ACOG, the statement addresses prevention, rapid diagnosis, acute treatment and recovery of maternal stroke. Stroke complicates roughly 20-40 per 100,000 pregnancies and accounts for an estimated 4-6% of pregnancy-related deaths in the US, with hypertensive disorders implicated in nearly half of pregnancy-associated stroke hospitalisations.

Key recommendations

  • Treat severe hypertension (>=160/110 mmHg) promptly in pregnancy and postpartum; aggressive BP control is central to prevention.
  • For acute ischaemic stroke within 4.5 hours, IV thrombolysis is recommended when benefit outweighs risk; tenecteplase is now an option, with single-bolus dosing advantages.
  • Do not withhold indicated acute stroke interventions (thrombolysis, mechanical thrombectomy, safe neuroimaging) solely because of pregnancy.
  • Manage recovery/delivery with a multidisciplinary team (maternal-fetal medicine, neurology/neurocritical care, anaesthesiology, neonatology, nursing).
  • Promote pre-pregnancy and antenatal primary prevention per Life's Essential 8 (BP, smoking cessation, activity, healthy weight/diet).
  • Maintain a high index of suspicion for stroke with new severe headache, focal deficits or seizures peripartum, given overlap with preeclampsia/eclampsia.

At the bedside

  • A pregnant or postpartum patient with focal neurological signs gets the same rapid stroke pathway - imaging and thrombolysis eligibility - as anyone else.
  • Severe-range BP (>=160/110) is an emergency: treat within minutes to reduce haemorrhagic stroke risk.
  • Do not let pregnancy talk you out of CT/CTA or thrombectomy referral when indicated.
  • New worst-ever headache or seizure peripartum: think stroke and cerebral venous thrombosis, not just eclampsia.
Bottom line / exam pearl

Pregnancy is not a contraindication to standard stroke care - control severe hypertension fast and offer thrombolysis/thrombectomy to eligible patients.

References

▸Heart Failure Occurring in the Perinatal PeriodObstetricsAmerican Heart Association (AHA) Scientific Statement, Circulation · 2026
Clinical takeaway

Perinatal heart failure - including peripartum cardiomyopathy - is frequently missed because its symptoms mimic normal pregnancy, and delayed recognition drives preventable maternal death, arrhythmia, and stroke.

Background — why it changed

This AHA scientific statement addresses heart failure with reduced and mildly reduced ejection fraction arising from pregnancy through about one year postpartum, spanning both pre-existing disease and de novo cardiomyopathy such as PPCM. It was written because dyspnea, fatigue, and edema of normal pregnancy overlap with true heart failure, so diagnosis is delayed. The statement pushes for standardized definitions, better screening tools, and attention to maternal health equity.

Key recommendations

  • Maintain a low threshold to investigate dyspnea, orthopnea, exercise intolerance, or edema that seem out of proportion to normal pregnancy.
  • Use ECG, cardiac biomarkers, and echocardiography to distinguish physiologic pregnancy changes from genuine heart failure.
  • Medications generally considered acceptable in pregnancy include beta-blockers, diuretics, vasodilators (e.g., hydralazine/nitrates), and anticoagulation when indicated.
  • ACE inhibitors, ARBs, ARNI, and SGLT2 inhibitors are contraindicated in pregnancy because of fetal toxicity; guideline-directed agents are (re)introduced postpartum, with lactation-compatibility considered.
  • Anticoagulation should be considered given the elevated thromboembolic risk of pregnancy plus low ejection fraction.
  • Care should be delivered by a multidisciplinary pregnancy heart team (cardiology, maternal-fetal medicine, obstetrics, anesthesia) with a plan spanning delivery and the postpartum year.
  • The statement emphasizes standardized disease definitions, screening tools, and maternal health equity to close diagnostic and outcome gaps.

At the bedside

  • Do not attribute new or worsening dyspnea/edema in a peripartum patient to 'normal pregnancy' by default - obtain an ECG, natriuretic peptide, and echo.
  • Before prescribing, check pregnancy/lactation status: avoid ACE inhibitors/ARBs/ARNI/SGLT2 antenatally and pivot to pregnancy-compatible agents.
  • Activate a pregnancy heart team early and plan the mode/timing of delivery collaboratively rather than reactively.
  • Counsel on postpartum follow-up and future-pregnancy risk, since dysfunction and recurrence can persist beyond delivery.
Bottom line / exam pearl

In a pregnant or recently postpartum patient, treat unexplained dyspnea or edema as possible heart failure until echo and biomarkers say otherwise - early recognition saves lives.

References

Infectious Diseases6 guidelines

▸COVID-19 Treatment and ManagementInfectious diseasesInfectious Diseases Society of America (IDSA), Clinical Infectious Diseases · 2026
Clinical takeaway

The IDSA living guideline continues to prioritise early antiviral therapy for outpatients at high risk of progression - nirmatrelvir/ritonavir preferred - and immunomodulation for hospitalised patients needing oxygen, with attention to drug-drug interactions and renal dosing.

Background — why it changed

IDSA maintains a continuously updated ('living') COVID-19 treatment guideline using GRADE. Recent updates address antiviral treatment of mild-to-moderate disease in adults and focused comparisons of immunomodulators (e.g. baricitinib vs tocilizumab), reflecting an evolving virus, population immunity and shifting evidence.

Key recommendations

  • Mild-to-moderate COVID-19 at high risk of progression: nirmatrelvir/ritonavir recommended over no antiviral (strong recommendation, moderate certainty), started as early as possible within the labelled window.
  • Screen rigorously for drug-drug interactions with ritonavir; many are manageable by dose adjustment or temporary interruption, but some preclude use.
  • Adjust nirmatrelvir/ritonavir dose for renal function per eGFR; it is not recommended in severe renal impairment.
  • Remdesivir is an alternative outpatient antiviral for high-risk patients when nirmatrelvir/ritonavir is unsuitable; molnupiravir is reserved for when preferred agents cannot be used.
  • Hospitalised patients requiring supplemental oxygen: corticosteroids (e.g. dexamethasone) plus an immunomodulator such as baricitinib or tocilizumab in appropriate severity strata.
  • Antiviral benefit is greatest in those genuinely at high risk of severe disease; routine antivirals are not recommended for low-risk patients.

At the bedside

  • In the ED/urgent care, identify high-risk outpatients early and start nirmatrelvir/ritonavir promptly - time from symptom onset matters.
  • Before prescribing, run a formal interaction check (statins, anticoagulants, antiarrhythmics, immunosuppressants) and confirm eGFR.
  • For the patient on new oxygen, think dexamethasone plus an immunomodulator per severity, not antivirals alone.
  • Molnupiravir is a last-line antiviral option; avoid in pregnancy.
Bottom line / exam pearl

High-risk outpatient with COVID to early nirmatrelvir/ritonavir (check interactions and renal function); hospitalised on oxygen to steroids plus an immunomodulator.

References

▸WHO Guidelines for MalariaInfectious diseasesWorld Health Organization (WHO), consolidated living guidelines · 2025
Clinical takeaway

Confirm every suspected case with a parasitological test (RDT or microscopy) before treating, and treat severe malaria with IV artesunate for at least 24 hours, then complete a full 3-day ACT course.

Background — why it changed

WHO maintains malaria guidance as a continuously updated "living guideline," with the consolidated version most recently reissued on 13 August 2025 (superseding the 30 November 2024 version). The recommendations consolidate diagnosis, uncomplicated and severe treatment, chemoprevention and elimination guidance into one document. Parenteral artesunate replaced quinine as the standard of care for severe malaria on the basis of large trials (SEAQUAMAT, AQUAMAT) showing a mortality benefit.

Key recommendations

  • All suspected malaria should be confirmed by a parasitological test (RDT or microscopy) before treatment wherever feasible; both should be supported by quality assurance.
  • Uncomplicated P. falciparum malaria: treat with an artemisinin-based combination therapy (ACT) for 3 days (options include artemether-lumefantrine, artesunate-amodiaquine, artesunate-mefloquine, dihydroartemisinin-piperaquine, artesunate-SP, artesunate-pyronaridine).
  • Severe malaria (adults and children, including infants, pregnant and lactating women): give IV or IM artesunate for at least 24 hours and until oral therapy is tolerated, then complete a full 3-day ACT.
  • Artesunate dosing: children <20 kg should receive a higher dose of 3 mg/kg per dose, versus 2.4 mg/kg per dose for larger children and adults, to achieve equivalent drug exposure.
  • If artesunate is unavailable, use artemether in preference to quinine for severe malaria.
  • Pre-referral treatment: where a full course cannot be given and oral therapy is not tolerated, give a single dose of rectal artesunate to children under 6 years with suspected severe malaria and refer urgently.
  • Pregnant women with uncomplicated P. falciparum malaria should be treated with artemether-lumefantrine.

At the bedside

  • Do not treat on clinical suspicion alone if a test is available - a negative RDT/smear should prompt a search for another cause.
  • In severe malaria, start parenteral artesunate immediately and do not wait to switch to oral until the patient can reliably tolerate it (minimum 24 hours parenteral).
  • Weigh the child: the <20 kg threshold changes the mg/kg artesunate dose.
  • For a sick child who cannot be treated on site and cannot swallow, a rectal artesunate dose buys time - but it is a bridge to referral, not definitive therapy.
Bottom line / exam pearl

Confirm parasitologically, treat uncomplicated disease with a 3-day ACT, and treat severe malaria with at least 24 hours of IV/IM artesunate (higher weight-based dose if <20 kg) followed by a full ACT course.

References

  • WHO Guidelines for malaria (living guideline landing page). www.who.int
  • WHO guidelines for malaria, 13 August 2025 (IRIS full PDF). iris.who.int
  • WHO guidelines for malaria, 13 August 2025 (NCBI Bookshelf). www.ncbi.nlm.nih.gov
▸Initial Antifungal Treatment of Severe HistoplasmosisInfectious diseasesIDSA (Infectious Diseases Society of America); Clinical Infectious Diseases · 2007
Clinical takeaway

For severe acute pulmonary or disseminated histoplasmosis, start liposomal amphotericin B 3 mg/kg IV daily for induction, then step down to oral itraconazole for a total of at least 12 months. (The 2025 IDSA update covers only mild/moderate pulmonary disease and pulmonary nodules, so severe disease is still governed by the 2007 guideline.)

Background — why it changed

Histoplasma capsulatum is endemic to river valleys (classically the Ohio and Mississippi in the US) and can cause severe pneumonia or disseminated disease, especially in immunocompromised hosts. The IDSA 2007 guideline remains the authoritative source for severe/disseminated disease; a 2025 IDSA update deliberately addressed only asymptomatic nodules and mild-to-moderate acute pulmonary disease, leaving the severe-disease algorithm unchanged.

Key recommendations

  • For severe/moderately severe disease, use liposomal amphotericin B 3.0 mg/kg IV daily as preferred induction therapy.
  • Give amphotericin induction for roughly 1 to 2 weeks (until clinical improvement), then transition to oral azole.
  • Step-down: itraconazole 200 mg three times daily for 3 days, then 200 mg twice daily.
  • Continue itraconazole for a total of at least 12 months in disseminated disease.
  • Consider methylprednisolone (about 0.5-1 mg/kg/day IV) during the first 1-2 weeks for severe respiratory complications/hypoxaemia.
  • An alternative lipid amphotericin formulation at ~5.0 mg/kg/day may be substituted for cost or tolerability.
  • Monitor itraconazole serum levels to confirm adequate absorption during maintenance.

At the bedside

  • In a febrile patient from an endemic area with severe pneumonia or multi-organ disease, send urine/serum Histoplasma antigen and consider empiric liposomal amphotericin.
  • Do not use itraconazole as sole initial therapy for severe disease - it is a step-down agent.
  • Watch amphotericin toxicities: renal function, potassium, and magnesium; liposomal formulation is preferred for CNS and severe disease.
  • Reserve adjunctive corticosteroids for severe respiratory compromise, not routine cases.
Bottom line / exam pearl

Severe histoplasmosis: liposomal amphotericin B 3 mg/kg induction, then itraconazole for at least a year.

References

▸Staphylococcus aureus Bacteraemia - Risk Stratification and ManagementInfectious diseasesIDSA & ESCMID joint consensus (Infectious Diseases Society of America / European Society of Clinical Microbiology and Infectious Diseases) · 2026
Clinical takeaway

This guidance replaces the old 'complicated vs uncomplicated' dichotomy with a risk-stratification framework, and supports a 14-day course for low-risk SAB with no deep-seated or metastatic focus after adequate work-up.

Background — why it changed

Released in September 2026, this is the first in a planned IDSA/ESCMID series on S. aureus bacteraemia and focuses on risk stratification, diagnostic evaluation (follow-up cultures, echocardiography, whole-body imaging) and duration of therapy. The panel judged the traditional complicated/uncomplicated split inadequate to guide work-up and treatment, favouring an individualised assessment of risk for deep-seated or metastatic infection and relapse. Future manuscripts will address specific MRSA and MSSA antibiotic management.

Key recommendations

  • Stratify adults into low risk vs increased risk for deep-seated/metastatic foci rather than labelling SAB complicated/uncomplicated.
  • Obtain at least 2 sets of follow-up blood cultures at 48 hours after the first positive set, then repeat 1-2 sets every 24-48 hours until clearance is documented.
  • Perform TTE routinely in all adults with SAB, since no subgroup could be defined as being at very low risk of endocarditis.
  • TEE may be unnecessary when a good-quality TTE is negative and there are no increased-risk features for endocarditis.
  • Consider whole-body imaging such as [18F]FDG-PET/CT in increased-risk patients with an unidentified focus after initial evaluation.
  • For low-risk SAB without deep-seated or metastatic foci after evaluation, treat for 14 days rather than a longer or shorter course.
  • Diagnostic evaluation, not a single label, should drive both the extent of work-up and the treatment duration.

At the bedside

  • Every SAB patient needs source control thinking plus a TTE and documented blood-culture clearance - not just antibiotics.
  • Draw the 48-hour follow-up cultures reliably; persistent positivity flags a deep-seated focus and reclassifies the patient as increased-risk.
  • In increased-risk patients with fever/positive cultures but no obvious source, escalate imaging (TEE and/or FDG-PET/CT) to find metastatic foci.
  • Involve infectious diseases early - risk stratification changes duration from 14 days to substantially longer.
Bottom line / exam pearl

Risk-stratify rather than label: low-risk SAB with a clean work-up gets 14 days, but everyone gets follow-up cultures and a TTE.

References

▸Treatment of Antimicrobial-Resistant Gram-Negative InfectionsInfectious diseasesInfectious Diseases Society of America (IDSA) guidance, Clinical Infectious Diseases · 2024
Clinical takeaway

Match the drug to the specific resistance mechanism: reserve newer beta-lactam/beta-lactamase-inhibitor agents and cefiderocol for true carbapenem-resistant organisms, and do not use them empirically for ESBL infections where carbapenems still work.

Background — why it changed

This living IDSA guidance document (updated in 2024, with a further 2026 refresh) replaces a formal guideline and is revised as new agents and data emerge. It covers ESBL-producing Enterobacterales, AmpC producers, carbapenem-resistant Enterobacterales (CRE), difficult-to-treat Pseudomonas aeruginosa (DTR-P. aeruginosa), carbapenem-resistant Acinetobacter baumannii (CRAB), and Stenotrophomonas maltophilia. It gives preferred and alternative regimens by organism, site, and susceptibility, and applies to adults and children (doses listed for adults).

Key recommendations

  • ESBL-E: uncomplicated cystitis - nitrofurantoin or trimethoprim-sulfamethoxazole preferred; pyelonephritis/complicated UTI - ertapenem, meropenem, imipenem-cilastatin, ciprofloxacin, levofloxacin, or TMP-SMX; infections outside the urinary tract - a carbapenem is preferred.
  • CRE (KPC or carbapenemase status unknown): ceftazidime-avibactam or meropenem-vaborbactam are preferred; imipenem-cilastatin-relebactam is an alternative.
  • CRE producing metallo-beta-lactamases (e.g. NDM): aztreonam-avibactam, or ceftazidime-avibactam plus aztreonam, with a slight preference for aztreonam-avibactam.
  • DTR-P. aeruginosa: ceftolozane-tazobactam, ceftazidime-avibactam, imipenem-relebactam, or cefiderocol, guided by susceptibility.
  • CRAB: sulbactam-durlobactam is preferred, generally combined with a carbapenem (meropenem or imipenem-cilastatin); high-dose ampicillin-sulbactam-based combination therapy is an alternative.
  • Stenotrophomonas maltophilia: options in order include TMP-SMX, minocycline, cefiderocol, and levofloxacin, often using combination therapy for severe disease.
  • Reserve newer agents (aztreonam-avibactam, ceftazidime-avibactam, meropenem-vaborbactam, imipenem-relebactam, ceftolozane-tazobactam, cefiderocol) for carbapenem-resistant infections to preserve activity.

At the bedside

  • Ask the micro lab which resistance mechanism is present - KPC vs metallo-beta-lactamase changes the whole regimen (avibactam-based agents fail against MBLs unless aztreonam is added).
  • For an ESBL isolate causing a bloodstream or serious non-urinary infection, step up to a carbapenem rather than piperacillin-tazobactam.
  • Involve infectious diseases and antimicrobial stewardship early for any CRE, DTR-Pseudomonas, or CRAB isolate.
  • Confirm source control and de-escalate to the narrowest effective, ideally oral, agent once susceptibilities return.
Bottom line / exam pearl

Resistance mechanism plus infection site drives the choice - carbapenems for ESBL, avibactam/vaborbactam agents for KPC-CRE, add aztreonam for metallo-beta-lactamases, and sulbactam-durlobactam for CRAB.

References

  • IDSA 2024 Guidance on Treatment of Antimicrobial-Resistant Gram-Negative Infections (Clin Infect Dis). academic.oup.com
  • IDSA Antimicrobial-Resistant Gram-Negative Guidance (living document). www.idsociety.org
▸Infection Prevention and Control of Candida auris in Pediatric SettingsInfectious diseasesSociety for Healthcare Epidemiology of America (SHEA) consensus statement, Antimicrobial Stewardship & Healthcare Epidemiology · 2026
Clinical takeaway

Candida auris is a multidrug-resistant, environmentally persistent fungus, and this SHEA consensus fills a gap by giving pediatric-specific infection-prevention guidance across acute-care, non-acute, and congregate settings.

Background — why it changed

C. auris causes high morbidity and mortality and spreads readily in healthcare environments, yet prior guidance was largely adult-focused. A multidisciplinary SHEA expert panel used a structured Delphi consensus process, informed by literature and practical considerations, to produce pediatric recommendations. The statement was endorsed by APIC, ASM, IDSA, PIDS, PCCA, and Ronald McDonald House Global.

Key recommendations

  • Use targeted screening to identify at-risk pediatric patients (e.g. transfers from facilities or regions with known C. auris, or those epidemiologically linked to a case).
  • Place colonized or infected patients in a single room with contact precautions where feasible, with appropriate room placement and cohorting.
  • Emphasize meticulous hand hygiene and reinforce it given the caregiver-child contact typical of pediatric care.
  • Perform effective environmental cleaning and disinfection with an agent active against C. auris (EPA List P-type sporicidal/fungal products), including high-touch surfaces.
  • Carefully manage shared medical equipment, toys, and common spaces, which are important reservoirs in pediatric units.
  • Address child-specific issues - visitors, breastfeeding, skin-to-skin contact, and caregiver-child interactions - while maintaining precautions.
  • Coordinate promptly with infection prevention and public health partners whenever C. auris is suspected or confirmed.

At the bedside

  • Flag high-risk transfers on admission and screen before cohorting with other children.
  • Confirm your unit's disinfectant is specifically labeled as effective against C. auris - many routine agents are not.
  • Dedicate or rigorously disinfect shared toys and equipment, and limit shared play spaces for affected patients.
  • Notify infection prevention immediately on a positive result so isolation and public-health reporting start without delay.
Bottom line / exam pearl

For pediatric C. auris, combine targeted screening, contact isolation, obsessive hand hygiene, and C. auris-active environmental cleaning - and loop in infection prevention and public health early.

References

Haematology & Coagulation8 guidelines

▸Reversal of Direct Oral Anticoagulants in Life-Threatening BleedingHaematologyESAIC (European Society of Anaesthesiology and Intensive Care); European Journal of Anaesthesiology (EJA) · 2024
Clinical takeaway

In DOAC-associated life-threatening bleeding, give specific reversal first when available - idarucizumab for dabigatran, andexanet alfa for factor Xa inhibitors - and do not wait for DOAC level results before starting haemostatic treatment.

Background — why it changed

DOACs (dabigatran, rivaroxaban, apixaban, edoxaban) are now first-line for many indications, so emergency clinicians increasingly face DOAC-related major bleeding and urgent surgery. This 2024 ESAIC guideline synthesises evidence across the four agents to standardise when and how to reverse them, moving away from reliance on non-specific global coagulation tests.

Key recommendations

  • In life-threatening/urgent settings, start haemostatic or reversal treatment without waiting for DOAC-level monitoring.
  • For dabigatran, idarucizumab is recommended to normalise coagulation; if unavailable, PCC or activated PCC (aPCC) may be used.
  • For factor Xa inhibitors (apixaban, rivaroxaban, edoxaban), andexanet alfa, PCC or aPCC is suggested when relevant residual drug is suspected.
  • Use DOAC-specific assays (e.g. dilute thrombin time, anti-Xa) to estimate drug level; global coagulation tests should not be used to exclude clinically relevant DOAC levels.
  • A plasma concentration above 50 ng/mL may be considered a threshold to justify haemostatic or antidote intervention.
  • Tranexamic acid and fresh frozen plasma may assist in massive bleeding but are not substitutes for routine specific reversal.
  • Time since last dose and renal function help estimate residual anticoagulant effect when levels are unavailable.

At the bedside

  • Establish the agent, last dose time, and renal function immediately - this drives both drug level and reversal choice.
  • Do not delay reversal or definitive haemostasis (surgery/endoscopy) waiting for coagulation assays in a crashing patient.
  • Know your hospital's stock: idarucizumab and andexanet alfa are agent-specific, and PCC/aPCC is the fallback when antidotes are unavailable.
  • Add adjuncts (mechanical/surgical control, tranexamic acid, transfusion) rather than relying on reversal agents alone in massive haemorrhage.
Bottom line / exam pearl

Match the antidote to the drug (idarucizumab for dabigatran, andexanet alfa for factor Xa inhibitors), fall back to PCC/aPCC, and treat before the level comes back.

References

▸Therapeutic Apheresis and Plasma Exchange - IndicationsHaematologyASFA (American Society for Apheresis), Writing Committee; Journal of Clinical Apheresis (Ninth Special Issue) · 2023
Clinical takeaway

ASFA grades each condition by category (I-IV) and evidence grade to say whether therapeutic apheresis is first-line, adjunctive, of unestablished benefit, or ineffective/harmful - so the category label, not the diagnosis alone, drives whether to call the apheresis service.

Background — why it changed

The Ninth Edition is the reference framework for indications for therapeutic plasma exchange (TPE) and other apheresis modalities. It comprises 91 fact sheets and 166 graded, categorised indications, adding seven new fact sheets and updating several categories using systematic-review methodology. It exists to bring consistency and evidence grading to a field where many recommendations still rest on low-quality evidence.

Key recommendations

  • Category I = apheresis is accepted first-line therapy (alone or with other treatment); Category II = accepted as second-line.
  • Category III = optimal role not established, decision individualised; Category IV = published evidence suggests apheresis is ineffective or harmful.
  • An accompanying evidence grade (1A to 2C) conveys strength of recommendation and quality of evidence separately from category.
  • Thrombotic thrombocytopenic purpura (TTP) remains the archetypal Category I, Grade 1A indication for urgent TPE and is treated as a medical emergency.
  • Neurologic emergencies such as Guillain-Barre syndrome and myasthenic crisis are recognised TPE indications alongside IVIG.
  • Most of the 166 indications (about 55%) fall into Category III, underscoring that many uses are individualised rather than proven.
  • Category assignment guides both whether to perform apheresis and its priority/urgency.

At the bedside

  • For suspected TTP, treat as a Category I emergency: activate TPE urgently rather than delaying for confirmatory ADAMTS13 results.
  • When consulting the apheresis service, state the working diagnosis so they can apply the ASFA category and prioritise.
  • Recognise that a Category III label means benefit is uncertain - weigh line placement, citrate/anticoagulation, and volume risks against expected gain.
  • Confirm modality (plasma exchange vs cytapheresis vs other) matches the indication, since the category is modality-specific.
Bottom line / exam pearl

Ask 'what ASFA category is this?' - Category I means start apheresis now, Category IV means do not.

References

▸Andexanet Alfa for Factor Xa Inhibitor ReversalHaematologyBritish Society for Haematology (BSH) position statement, Br J Haematol · 2026
Clinical takeaway

The BSH concludes that for most patients with a factor Xa inhibitor-associated bleed, the risks of andexanet alfa appear to outweigh its benefits, driven by a significant excess of thromboembolic events, particularly ischaemic stroke.

Background — why it changed

Andexanet alfa is the only licensed specific reversal agent for apixaban- and rivaroxaban-associated life-threatening or uncontrolled bleeding, but it is not licensed for edoxaban, heparins, or reversal before urgent surgery. UK reimbursement is inconsistent: NICE (2021) supports use only in gastrointestinal bleeding in England, whereas NHS Scotland reimburses bleeding at any site. This statement responds to accumulating safety-signal and rebound-anticoagulation concerns.

Key recommendations

  • For most oral factor Xa inhibitor-associated major bleeds, the BSH judges that the benefit-risk balance does not favour andexanet alfa over prothrombin complex concentrate (PCC).
  • Andexanet is associated with a significantly increased risk of thromboembolic events, especially ischaemic stroke, and with rebound anti-Xa activity as levels fall.
  • Licensing is limited to apixaban and rivaroxaban; it is not licensed for edoxaban, heparin-based anticoagulants, or pre-surgical reversal.
  • Where a reversal/haemostatic agent is used, PCC remains a reasonable and widely available alternative alongside standard bleeding management.
  • Restarting anticoagulation should be considered as soon as safe after haemostasis, given the thrombotic hazard in this population.
  • Local protocols should reflect the restricted evidence base and inconsistent UK reimbursement, and use should be individualised.

At the bedside

  • Prioritise the fundamentals: stop the anticoagulant, direct haemostasis/source control, transfusion support, and reversal of any contributing factors.
  • For life-threatening bleeding, PCC is an immediately available option; do not assume andexanet is superior.
  • Counsel and monitor for arterial and venous thrombosis (stroke, MI, VTE) after any reversal, and plan early anticoagulation restart.
  • Check your local/NICE/SMC funding status before assuming andexanet is available for a non-GI bleed.
Bottom line / exam pearl

For factor Xa inhibitor bleeding, the BSH considers andexanet's thromboembolic risk to outweigh benefit for most patients, positioning PCC plus standard care as the pragmatic default.

References

▸Factor Concentrates for Perioperative BleedingHaematologyISTH SSC Subcommittee on Perioperative and Critical Care Thrombosis and Haemostasis · 2026
Clinical takeaway

This ISTH guidance gives pragmatic advice on using coagulation factor concentrates (fibrinogen concentrate, PCC, rFVIIa, factor XIII) for surgically acquired coagulopathy, favouring targeted, viscoelastic-guided replacement over empirical plasma.

Background — why it changed

Factor concentrates have been increasingly incorporated into perioperative bleeding algorithms because of rapid availability, standardised dosing, low infusion volumes and pathogen inactivation, reducing reliance on plasma. This document updates ISTH's 2018 guidance to reflect newer trials and systematic reviews, focusing on major surgery including cardiac surgery.

Key recommendations

  • Correct fibrinogen deficiency first: low fibrinogen prolongs clot formation and can render PCC less effective; fibrinogen concentrate is a rapid, standardised option.
  • Use viscoelastic testing (ROTEM/TEG) and targeted algorithms to guide which concentrate to give and when, rather than fixed empirical dosing.
  • 4-factor PCC is the predominant concentrate for perioperative major bleeding and has theoretical advantages over rFVIIa (broader mechanism, lower adverse-event rates).
  • Recombinant activated factor VII (rFVIIa) is reserved for refractory bleeding after conventional measures, given its thrombotic risk.
  • Consider factor XIII replacement in the setting of ongoing bleeding with documented or likely deficiency.
  • Important evidence gaps remain for optimal dose, timing, viscoelastic targets, sequencing with fibrinogen concentrate, and cost-effectiveness.

At the bedside

  • In massive perioperative bleeding, treat hypofibrinogenaemia early - it is often the first factor to become critically low.
  • Point-of-care viscoelastic testing lets you target the right product instead of blanket plasma transfusion.
  • Weigh thrombotic risk whenever escalating to PCC or rFVIIa, especially in cardiac surgery.
  • These are concentrate-selection principles; they do not replace surgical haemostasis and the wider massive-transfusion protocol.
Bottom line / exam pearl

Think fibrinogen first, then goal-directed PCC, with rFVIIa as rescue only - guided by viscoelastic testing rather than empirical plasma.

References

▸Laboratory Diagnosis and Monitoring of Thrombotic Thrombocytopenic Purpura (TTP)HaematologyBritish Society for Haematology (BSH), British Journal of Haematology · 2026
Clinical takeaway

When TTP is suspected, send an urgent ADAMTS13 activity before starting plasma exchange; a severely low result (activity <10 IU/dL) confirms the diagnosis and should trigger reflex anti-ADAMTS13 antibody testing to separate immune (acquired) from congenital TTP.

Background — why it changed

This BSH guidance is a laboratory-focused companion to the 2023 BSH management guideline for TTP and thrombotic microangiopathies. It standardises how ADAMTS13 activity and anti-ADAMTS13 antibody assays are performed, reported and used for monitoring, because timely and correctly interpreted ADAMTS13 results drive urgent treatment decisions in a condition that is rapidly fatal if untreated.

Key recommendations

  • Perform urgent ADAMTS13 activity testing whenever there is clinical suspicion of TTP, ideally on a sample taken before plasma exchange, so treatment is not delayed.
  • An ADAMTS13 activity <10 IU/dL indicates severe deficiency consistent with TTP; higher levels make TTP unlikely and should prompt consideration of other thrombotic microangiopathies.
  • When activity is <10 IU/dL, perform an anti-ADAMTS13 antibody (IgG) assay within 72 hours of presentation to distinguish immune-mediated TTP from congenital (hereditary) TTP.
  • Use validated, quality-assured ADAMTS13 assays with defined reference ranges and participate in external quality assurance; report results in a way clinicians can act on urgently.
  • Repeat anti-ADAMTS13 antibody testing when activity remains low despite treatment for acute immune TTP, to help guide escalation of immunosuppression.
  • Monitor ADAMTS13 activity (and antibody where relevant) during follow-up to detect subclinical relapse, and test in any patient with suspected clinical relapse.

At the bedside

  • Draw the ADAMTS13 sample before the first plasma exchange or plasma infusion, then start treatment on clinical suspicion without waiting for the result.
  • Do not let a normal platelet count or absent classic pentad reassure you: microangiopathic haemolytic anaemia plus thrombocytopenia with no other cause should prompt ADAMTS13 testing.
  • Flag the request as urgent and tell the lab it is for suspected TTP so the assay is prioritised and turnaround is minimised.
  • In a confirmed immune TTP patient who is not recovering, ask the lab to re-check ADAMTS13 activity and antibody to inform whether to intensify immunosuppression.
Bottom line / exam pearl

Activity <10 IU/dL confirms TTP; a positive anti-ADAMTS13 antibody means immune (acquired) TTP, and a negative antibody with severe deficiency points to congenital TTP.

References

  • BSH guideline page: Diagnosis and monitoring of TTP - guidance for laboratories. b-s-h.org.uk
  • British Journal of Haematology (Wiley), doi:10.1111/bjh.70727. onlinelibrary.wiley.com
  • BSH 2023 companion guideline: Diagnosis and management of TTP and TMAs (bjh.19026). onlinelibrary.wiley.com
▸Anticoagulation for Cardiac Surgery in Patients with Heparin-Induced Thrombocytopenia (HIT)HaematologyISTH SSC on Perioperative and Critical Care Haemostasis and Thrombosis, Journal of Thrombosis and Haemostasis · 2026
Clinical takeaway

The safest approach depends on HIT phase: for elective cardiopulmonary bypass in a patient with a positive HIT functional assay, postpone surgery until the functional assay is negative; when surgery cannot wait, use a parenteral nonheparin anticoagulant (bivalirudin has the strongest supporting evidence).

Background — why it changed

Patients with HIT who need cardiac surgery are a high-risk group because unfractionated heparin is normally the anticoagulant of choice for cardiopulmonary bypass. This ISTH SSC guidance is based on a systematic review (about 30 included studies) of intraoperative strategies, and it frames choices around whether HIT is acute, subacute or remote and whether functional (platelet-activation) assays are still positive.

Key recommendations

  • For elective CPB in a patient with a positive HIT functional assay, delay surgery until the functional assay becomes negative so that heparin can potentially be used safely.
  • For urgent or emergent surgery in acute or subacute HIT, prefer perioperative anticoagulation with a parenteral nonheparin agent rather than heparin.
  • Of the nonheparin options, bivalirudin (a direct thrombin inhibitor) has the strongest data and appears effective for CPB.
  • Weigh bivalirudin's drawbacks: increased bleeding risk and no reversal agent, plus practical monitoring and circuit-stasis considerations on bypass.
  • In subacute HIT B or remote HIT, a strategy of brief intraoperative heparin re-exposure (for the bypass run only) followed by an alternative anticoagulant postoperatively is reasonable.
  • Alternative reviewed strategies include heparin after therapeutic plasma exchange to lower antibody levels, and heparin combined with a potent antiplatelet agent; these have weaker or more limited evidence.
  • Base the choice on the phase of HIT and current functional-assay status, coordinating haematology, cardiac surgery, anaesthesia and perfusion.

At the bedside

  • Confirm the HIT phase and re-test the functional assay before scheduling: a patient who has seroconverted to a negative functional assay may tolerate a single intraoperative heparin exposure.
  • If bivalirudin is used on bypass, plan for higher bleeding risk, careful anticoagulation monitoring, and awareness that there is no antidote if bleeding occurs.
  • Restrict any heparin re-exposure strategy to the bypass run only, and avoid heparin before and after surgery, using a nonheparin agent for peri-operative anticoagulation.
  • Escalate early to a multidisciplinary team (haematology, surgery, perfusion) because the optimal plan is patient- and timing-specific.
Bottom line / exam pearl

Delay elective bypass until the HIT functional assay is negative; when you cannot wait, bivalirudin is the best-supported nonheparin option despite its bleeding risk and lack of a reversal agent.

References

  • Journal of Thrombosis and Haemostasis (ScienceDirect), ISTH SSC guidance on HIT and cardiac surgery with CPB. www.sciencedirect.com
  • PubMed record: ISTH SSC guidance on anticoagulation for HIT requiring cardiac surgery with CPB. pubmed.ncbi.nlm.nih.gov
  • ASH Education Program 2024: Approaches to management of HIT in complex scenarios, including cardiac surgery. ashpublications.org
▸Perioperative Anaemia and Blood Management in Cardiac SurgeryHaematologyAmerican Heart Association (AHA) Scientific Statement, Circulation · 2026
Clinical takeaway

Treat preoperative anaemia and iron deficiency as modifiable risk factors: screen and correct them before elective cardiac surgery, and combine restrictive transfusion thresholds with a structured intraoperative blood-conservation bundle to reduce transfusion and its complications.

Background — why it changed

Preoperative anaemia affects up to about 50% of adults presenting for cardiac surgery and, along with red-cell transfusion, is linked to worse outcomes including acute kidney injury, stroke and death. This AHA scientific statement summarises current evidence on preoperative anaemia assessment, intraoperative blood conservation and special populations, positioning patient blood management as a multidisciplinary, patient-centred part of Enhanced Recovery After Cardiac Surgery (ERAS).

Key recommendations

  • Screen for anaemia and iron deficiency preoperatively: anaemia is present in up to ~50% and iron deficiency in ~20-50% of cardiac surgery patients, with or without anaemia.
  • Treat preoperative anaemia (including iron therapy for iron deficiency) to reduce the likelihood of red-cell transfusion and transfusion-related complications such as alloimmunisation.
  • Apply restrictive red-cell transfusion thresholds, consistent with surgical-society guidelines, because liberal transfusion is associated with acute kidney injury, stroke and increased mortality.
  • Use a structured intraoperative bundle to minimise haemodilution, including CPB-circuit refinements and autologous techniques.
  • Give antifibrinolytic therapy (e.g. tranexamic acid) to reduce perioperative blood loss.
  • Use goal-directed transfusion algorithms guided by point-of-care viscoelastic testing to reduce bleeding and transfusion.
  • Consider acute normovolaemic haemodilution and intraoperative cell salvage / autologous donation as part of blood conservation.

At the bedside

  • Order iron studies plus a full blood count in the anaemia clinic weeks ahead of elective surgery so there is time to give iron and re-check the haemoglobin.
  • Do not transfuse on a fixed number alone: apply a restrictive threshold and assess the whole clinical picture before giving red cells.
  • Have viscoelastic (ROTEM/TEG) testing available in theatre to target the specific bleeding defect rather than giving empirical blood products.
  • Treat blood conservation as a team sport within ERAS: surgeon, anaesthetist, perfusionist and haematology all contribute to minimising loss and transfusion.
Bottom line / exam pearl

Correct anaemia and iron deficiency before surgery and pair a restrictive transfusion threshold with antifibrinolytics, viscoelastic-guided transfusion and autologous techniques to cut red-cell use.

References

  • AHA Professional Heart Daily hub: Perioperative Anemia and Patient Blood Management in Cardiac Surgery. professional.heart.org
  • AHA 'Top Things to Know': Perioperative Anemia and Patient Blood Management in Cardiac Surgery. professional.heart.org
  • PubMed record: AHA Scientific Statement, Perioperative Anemia and Patient Blood Management in Cardiac Surgery. pubmed.ncbi.nlm.nih.gov
▸Peri-Operative Venous Thromboembolism (VTE) ProphylaxisHaematologyEuropean Society of Anaesthesiology and Intensive Care (ESAIC), with ESRA input and ISTH endorsement; European Journal of Anaesthesiology · 2024
Clinical takeaway

Base peri-operative VTE prophylaxis on individualised risk assessment (procedure risk plus patient risk factors, e.g. a Caprini-type model) rather than a blanket approach, and use mechanical prophylaxis (especially IPC) whenever pharmacological prophylaxis is limited or contraindicated by bleeding risk.

Background — why it changed

This is the first major update (2024) of the 2018 European guidelines, rebuilt with a more rigorous methodology and expanded to new areas including plastic surgery, urology, non-ambulatory orthopaedic surgery and trauma. It reflects newer evidence on DOACs, aspirin and fast-track surgery, and harmonises prophylaxis timing with neuraxial anaesthesia safety. The recommendations are graded (GRADE-style, e.g. Grade 1B, 2C).

Key recommendations

  • Stratify every surgical patient using both procedure-related and patient-related VTE risk; validated clinical prediction tools such as the Caprini model are recommended to guide the intensity of prophylaxis.
  • Mechanical prophylaxis, particularly intermittent pneumatic compression (IPC), is emphasised when pharmacological prophylaxis is contraindicated or the bleeding risk is high, and as an adjunct in higher-risk patients.
  • LMWH is preferred as first-line pharmacological prophylaxis over unfractionated heparin, partly because of the lower risk of heparin-induced thrombocytopenia, notably in cardiac and vascular surgery (Grade 2B).
  • After fast-track total hip or knee arthroplasty, pharmacological prophylaxis with LMWH (Grade 1B), a DOAC (Grade 1B) or aspirin (Grade 1C) is recommended over no prophylaxis.
  • In cardiac surgery, early initiation of pharmacological prophylaxis between 6 and 24 h postoperatively is recommended if there is no significant bleeding risk (Grade 1C); in vascular surgery, consider early initiation within 24 h in higher procedural or patient VTE risk (Grade 2C).
  • When neuraxial anaesthesia or a deep peripheral nerve block is planned, prefer starting pharmacological prophylaxis postoperatively rather than preoperatively to reduce spinal/epidural haematoma risk (Grade 2C).
  • For higher-risk procedures, a minimum 7-day duration of prophylaxis is recommended over 3-day or single-dose protocols (Grade 1B).

At the bedside

  • Do a documented VTE risk assessment (patient + procedure) on every surgical admission and reassess if bleeding or mobility status changes.
  • If bleeding risk is high or pharmacological agents are contraindicated, start IPC and switch to or add LMWH once haemostasis is secure.
  • Coordinate LMWH/DOAC timing with the anaesthetist around neuraxial blocks: favour post-operative dosing and respect the drug-specific needle-to-dose intervals.
  • Do not stop prophylaxis prematurely for higher-risk cases; plan for extended (at least 7-day, and longer after major orthopaedic/cancer surgery) duration and arrange it at discharge.
Bottom line / exam pearl

Peri-operative VTE prevention is individualised: risk-stratify every patient, lean on IPC when you cannot anticoagulate, prefer LMWH, and time pharmacological prophylaxis post-operatively around neuraxial blocks to protect the spinal cord.

References

  • ESAIC guideline hub - Peri-operative VTE prophylaxis (first update, 2024). esaic.org
  • European guidelines on peri-operative VTE prophylaxis: first update - Introductory chapter (Eur J Anaesthesiol 2024; PubMed). pubmed.ncbi.nlm.nih.gov
  • Executive summary - Eur J Anaesthesiol 2024;41(8):561-569, DOI 10.1097/EJA.0000000000002025. doi.org

Paediatrics12 guidelines

▸Community-Acquired Pneumonia in Infants and ChildrenPaediatricsIDSA/PIDS (Infectious Diseases Society of America / Pediatric Infectious Diseases Society), published in Clinical Infectious Diseases · 2026
Clinical takeaway

The 2026 IDSA/PIDS update revises the landmark 2011 guideline and centers on parapneumonic effusion/empyema: small uncomplicated effusions in stable children can be observed rather than drained, and when drainage is needed, chest tube plus fibrinolytics is favored over surgery. Amoxicillin (ampicillin/penicillin inpatient) remains the core empiric therapy for the fully immunized child with uncomplicated CAP.

Background — why it changed

The original 2011 IDSA/PIDS pediatric CAP guideline was the field standard for over a decade. The 2026 revision is the first installment of a broader update, focusing on the diagnosis and management of pneumonia with parapneumonic effusion using newer evidence. Five of six effusion-related recommendations changed from 2011.

Key recommendations

  • For moderate-to-large parapneumonic effusion on chest radiograph, use chest ultrasonography to characterize complexity rather than CT or MRI.
  • For small, uncomplicated effusions in a clinically stable child, observation is suggested over invasive pleural drainage.
  • When drainage is indicated for empyema, use chest tube plus intrapleural fibrinolytics as first-line rather than upfront surgical (VATS) debridement in most cases.
  • When a chest tube is placed, favor small-bore (<=12 Fr) tubes over large-bore (>=14 Fr) tubes.
  • For pneumonia-associated empyema requiring fibrinolysis, the panel suggests tPA alone over tPA plus DNase.
  • Empiric therapy for the fully immunized child with uncomplicated CAP remains amoxicillin (outpatient) or ampicillin/penicillin G (inpatient), reflecting continued S. pneumoniae predominance.
  • Reserve broader-spectrum agents and macrolide add-on (atypical coverage) for specific clinical or epidemiologic indications.

At the bedside

  • Get a bedside chest ultrasound before reaching for CT when you see a moderate/large effusion; it spares radiation and characterizes loculation.
  • A small effusion in a well-appearing, stable child does not automatically need a drain; treat the pneumonia and reassess.
  • If drainage is needed, ask for a small-bore pigtail catheter with fibrinolytics rather than defaulting to surgery.
  • Do not narrow to azithromycin monotherapy; amoxicillin/ampicillin still covers the most likely pathogen in immunized kids.
Bottom line / exam pearl

Small, stable effusion = observe; when you must drain, small-bore chest tube + fibrinolytics beats going straight to surgery.

References

▸Preseptal and Orbital Cellulitis in Otherwise Healthy Children and YouthPaediatricsCanadian Paediatric Society (CPS), published in Paediatrics & Child Health · 2026
Clinical takeaway

Distinguish preseptal (eyelid erythema/edema, tenderness, normal eye movements) from orbital cellulitis (painful/limited extraocular movements, proptosis, chemosis, reduced acuity, or an afferent pupillary defect) - orbital signs mandate admission, IV antibiotics, imaging, and specialist involvement.

Background — why it changed

Left untreated, orbital cellulitis can cause vision loss, cavernous sinus thrombosis, and intracranial spread. This CPS statement gives practical, Canadian-context guidance for the healthy child, tailoring antibiotic choice to immunization status (Hib), local resistance, and clinical severity, and clarifying when imaging is truly needed.

Key recommendations

  • Clinically differentiate preseptal from orbital disease at the bedside: orbital red flags are painful/restricted EOM, proptosis, chemosis, diminished visual acuity, or a relative afferent pupillary defect.
  • Mild atraumatic preseptal cellulitis can be treated with narrow-spectrum oral antibiotics; escalate to a beta-lactam/beta-lactamase inhibitor (e.g., amoxicillin-clavulanate) if no improvement or the child is underimmunized against Hib or in a high H. influenzae type a area.
  • Children with severe infection or orbital involvement should be admitted for IV antimicrobials, diagnostic work-up, and specialty (ophthalmology/ENT) consultation.
  • Reserve contrast CT of the orbits/sinuses for young/toxic children, suspected optic nerve or intracranial involvement, prominent forehead swelling, high WBC/CRP, or diagnostic uncertainty; otherwise consider delaying imaging pending response to antibiotics.
  • Suggested treatment durations: 5-7 days for preseptal and 10-14 days for uncomplicated orbital cellulitis.
  • Tailor antimicrobial selection to the child's antibiotic exposure, immunization status, and the local antibiogram.
  • Consider early surgical drainage of an involved sinus or orbital abscess if orbital signs progress despite IV antibiotics.

At the bedside

  • Test extraocular movements, visual acuity, and pupils on every periorbital swelling - these findings separate a discharge from an admission.
  • Do not reflexively CT every swollen eyelid; a well child with pure preseptal signs can often be imaged only if they fail to respond.
  • Ask about immunization status (Hib) - it changes empiric antibiotic choice toward amoxicillin-clavulanate.
  • Any proptosis, pain on eye movement, or vision change = admit, IV antibiotics, image, and call ophthalmology/ENT.
Bottom line / exam pearl

Painful or restricted eye movements, proptosis, or vision change turn 'red swollen eyelid' into an emergency needing IV antibiotics, imaging, and a specialist.

References

  • CPS Position Statement: Preseptal and Orbital Cellulitis. cps.ca
  • Paediatrics & Child Health 31(6):670. academic.oup.com
▸Brief Resolved Unexplained Events (BRUE) and Evaluation of Lower-Risk InfantsPaediatricsAmerican Academy of Pediatrics (AAP), published in Pediatrics · 2016
Clinical takeaway

The AAP replaced the vague term ALTE with BRUE and defined a lower-risk group who can be safely managed with minimal testing, brief observation, and shared decision-making rather than admission and an extensive work-up.

Background — why it changed

The old label 'apparent life-threatening event' (ALTE) implied severity that most events did not warrant and drove unnecessary testing and hospitalization. BRUE is a diagnosis of exclusion used only when a full history and exam find no explanation, letting clinicians risk-stratify instead of over-investigating.

Key recommendations

  • A BRUE is an event in an infant <1 year that is sudden, brief, and fully resolved, with >=1 of: cyanosis/pallor; absent/decreased/irregular breathing; marked change in tone; or altered responsiveness - and no explanation after history and exam.
  • Classify as lower-risk only if: age >60 days; gestational age >=32 weeks and postconceptional age >=45 weeks; a first, single event lasting <1 minute; no CPR by a trained provider; and a reassuring history and physical exam.
  • In lower-risk infants, do not obtain WBC, blood culture, CSF, chest radiograph, echocardiography, EEG, or admit solely for cardiorespiratory monitoring.
  • For lower-risk infants, clinicians may briefly monitor with continuous pulse oximetry and serial observation, and may obtain a 12-lead ECG and pertussis testing.
  • Educate caregivers and offer CPR training resources; engage in shared decision-making about observation and follow-up.
  • Home cardiorespiratory monitors should not be prescribed for lower-risk infants after a BRUE.
  • Higher-risk infants (younger, prematurity, recurrent events, CPR needed, or abnormal findings) fall outside the lower-risk pathway and warrant tailored evaluation.

At the bedside

  • Confirm the event is truly resolved and unexplained before calling it a BRUE - a feeding cough, reflux, or infection makes it something else.
  • Run the lower-risk checklist (>60 days, term-equivalent, first event, <1 min, no CPR, normal exam) to decide against a big work-up.
  • For a lower-risk infant, a brief oximetry observation, an ECG, and shared decision-making usually replace admission.
  • Do not send home apnea monitors or start empiric anti-reflux therapy for a lower-risk BRUE.
Bottom line / exam pearl

If it fits the lower-risk BRUE criteria, resist labs and admission - observe briefly, consider an ECG, teach CPR, and arrange follow-up.

References

▸Nonemergency Acute Care Delivered Outside of the Medical HomePaediatricsAmerican Academy of Pediatrics (AAP), published in Pediatrics · 2026
Clinical takeaway

The AAP reaffirms the medical home as the preferred setting for nonemergency acute care, and sets standards so that when children are seen in urgent care, retail clinics, or direct-to-consumer telemedicine, the care is safe, pediatric-appropriate, and communicated back to the medical home.

Background — why it changed

Families increasingly use acute care outside their pediatrician's office for convenience, access, or cost, creating risks of fragmented, duplicated, or lower-quality care. This revised policy updates the 2017 statement, catalogs the modern 'medical neighborhood' (urgent care, retail clinics, DTC telemedicine, school-based health, EMS), and defines expectations to preserve continuity.

Key recommendations

  • The medical home remains the preferred setting for most nonemergency acute pediatric care because it offers comprehensive, continuous, coordinated care.
  • Pediatric medical homes should expand access (online self-scheduling, extended/weekend hours, telemedicine, home visits) to reduce reliance on outside acute care.
  • Acute care entities serving children - including telemedicine platforms - should have pediatric-appropriate equipment, staff training, and protocols that ensure timely, competent care.
  • There should be robust communication and record-sharing back to the medical home after any acute care encounter to maintain continuity.
  • Pediatricians should understand the local 'medical neighborhood' - the services, benefits, and limitations of each acute care option - to counsel families.
  • Direct-to-consumer telemedicine outside an existing relationship or coordination with the medical home is discouraged as a substitute for the medical home.
  • Acute care settings should have clear referral and escalation pathways for children needing emergency care or specialty follow-up.

At the bedside

  • When you see a child in urgent care or via telehealth, send a note back to their pediatrician to close the loop.
  • Confirm the acute care site has pediatric-sized equipment and pediatric-trained staff before it is relied on for children.
  • Counsel families that DTC telemedicine is not a replacement for their medical home, especially for young infants or complex problems.
  • Have a clear escalation plan to the ED for red-flag presentations rather than managing beyond the site's capability.
Bottom line / exam pearl

Care outside the medical home is fine when it is pediatric-ready and looped back to the child's own pediatrician - continuity is the safety net.

References

▸Children and Youth Injury Prevention in CanadaPaediatricsCanadian Paediatric Society (CPS), published in Paediatrics & Child Health · 2026
Clinical takeaway

Injury is a leading cause of death and disability in Canadian children aged 1-19, and the CPS frames childhood injuries as predictable and preventable, urging clinicians to embed injury prevention into everyday care with a focus on equity, data, policy, and education.

Background — why it changed

Building on the CPS's 2012 statement, this 2026 framework updates mortality and hospitalization data across injury mechanisms and age groups. It positions injury prevention as a core child-health competency rather than an add-on, and highlights inequities (including for Indigenous children and youth) in injury burden.

Key recommendations

  • Treat childhood injuries as predictable and preventable, and make anticipatory injury-prevention counselling a routine part of paediatric care.
  • Prioritize equity, recognizing that injury burden falls disproportionately on some populations, including Indigenous children and youth.
  • Strengthen injury surveillance and data infrastructure to guide and evaluate prevention efforts.
  • Advocate for policy and legislation (e.g., helmet laws, playground safety standards, restrictions on ATV/off-road vehicle and snowmobile operation by children, graduated driver licensing).
  • Reinforce established measures: correct car seat/booster use and rear-facing seating for young children, back seat until at least age 13, and safe-sleep practices for infants.
  • Promote drowning prevention - isolation (4-sided) pool fencing and swim skills - and safe-storage measures against poisoning and firearm injury.
  • Integrate injury prevention into medical education and training so clinicians are equipped to counsel and advocate.

At the bedside

  • Add a quick age-appropriate safety check to well-child visits: car seat stage, helmets, pool/water access, safe sleep, and safe storage of meds and firearms.
  • Tailor counselling to the child's developmental stage - the leading injury mechanisms shift from falls/suffocation in infants to transport and sport in older youth.
  • Advise against ATV/off-road vehicle operation by children and youth under 16.
  • Frame injuries with families as preventable, not accidental - and connect higher-risk families to community resources.
Bottom line / exam pearl

Injuries are predictable and preventable - build brief, developmentally targeted safety counselling into every visit and advocate for protective policy.

References

  • CPS Position Statement: Children and Youth Injury Prevention in Canada. cps.ca
  • CPS Injury Prevention document collection. cps.ca
▸Prevention of DrowningPaediatricsAmerican Academy of Pediatrics (AAP), published in Pediatrics · 2026
Clinical takeaway

Drowning is a leading cause of injury death in young children, and prevention requires layered protection - because no single measure is fully protective, the AAP stresses barriers, supervision, swim skills, life jackets, and CPR together.

Background — why it changed

This 2026 policy statement updates the AAP's 2019 guidance with new epidemiology and a stronger focus on inequities in drowning risk and swim access. Fatal drowning rates are higher among Native Hawaiian/Pacific Islander and Black children, and children with autism spectrum disorder or epilepsy carry elevated risk.

Key recommendations

  • Use multiple layers of protection - no single intervention prevents all drowning.
  • Install a 4-foot, 4-sided isolation fence that separates the pool from the house and yard, with a self-closing, self-latching gate.
  • Provide close, constant 'touch supervision' of young children in and around water, with an undistracted designated adult.
  • Support swim lessons starting after the first birthday; formal lessons are associated with roughly an 88% lower drowning risk in children aged 1-4.
  • Require US Coast Guard-approved life jackets for boating and open water; inflatable toys and air-filled devices are not safety devices.
  • Encourage CPR training for parents, caregivers, and pool owners, since bystander CPR improves outcomes.
  • Address equity in swim access and target higher-risk groups, including children with autism spectrum disorder and seizure disorders.

At the bedside

  • Counsel families that fences, supervision, swim lessons, life jackets, and CPR are layers - all are needed, none alone is enough.
  • For toddlers, emphasize touch supervision and a 4-sided isolated pool fence at home.
  • Recommend Coast Guard-approved life jackets, not water wings or pool toys, for any open-water or boating activity.
  • Flag children with epilepsy or autism as higher risk and reinforce extra water precautions and CPR training for caregivers.
Bottom line / exam pearl

Layered prevention wins - a 4-sided isolation fence, touch supervision, swim lessons, life jackets, and caregiver CPR, because no single measure is foolproof.

References

▸Preparation for Pediatric Emergencies in the OfficePaediatricsAmerican Academy of Pediatrics (Pediatrics) · 2026
Clinical takeaway

Every office that cares for children should be ready for the common in-office emergencies -- respiratory distress, seizures, and anaphylaxis -- with a written plan, stocked equipment and medications, trained staff, and regular drills.

Background — why it changed

This statement updates the 2007 AAP guidance and is paired with a companion technical report. Office emergencies are uncommon but predictable, and preparedness (self-assessment, protocols, stocked kit, and mock codes) shortens response time and bridges care to EMS. It applies to both primary care and subspecialty pediatric offices.

Key recommendations

  • Perform an annual office-based readiness self-assessment and keep written emergency protocols current.
  • Stock essential equipment: an oxygen source with delivery devices, bag-valve-mask (infant and child sizes), oral airways, suction, and a pulse oximeter.
  • Stock core medications, including epinephrine for anaphylaxis, albuterol for bronchospasm, and oxygen; dose using a length-based / weight-in-kg tool.
  • Train all staff (clinical and non-clinical) to recognize and begin care of a deteriorating child; maintain BLS, and PALS/APLS competency for clinicians per role.
  • Run regular mock codes / drills to build team response and expose system gaps.
  • Establish protocols in advance for rapid response, early EMS activation, family communication, and structured handoff to EMS.
  • Hold a structured debrief after every real event or drill.

At the bedside

  • Keep the emergency cart or kit checked and restocked on a fixed schedule -- know where epinephrine and the BVM are without searching.
  • Anaphylaxis = IM epinephrine to the anterolateral thigh first, then activate EMS; do not delay for antihistamines.
  • Use a length-based tape for weight and drug doses to avoid math errors under stress.
  • Assign roles before an emergency: who runs the code, who calls 911, who documents, who meets EMS.
Bottom line / exam pearl

An office emergency plan is only as good as your last drill -- practice, stock, and reassess annually.

References

▸Pediatric Readiness in the Emergency DepartmentPaediatricsAAP / ACEP / ENA / ACS joint policy statement (Pediatrics; Ann Emerg Med; J Emerg Nurs) · 2026
Clinical takeaway

Every ED, regardless of size, should meet defined pediatric readiness standards; higher ED readiness is associated with substantially lower mortality in critically ill and injured children.

Background — why it changed

This revision of the prior joint statement responds to the fact that most children are seen in general rather than children's EDs, where readiness is uneven. Meeting readiness standards could save an estimated more than 2,100 children's lives per year in the US. It adds emphasis on care coordinators, weight-in-kilograms, dosing tools, and mental health.

Key recommendations

  • Appoint pediatric emergency care coordinators -- both a physician and a nurse PECC -- to drive pediatric QI, policies, education, and equipment familiarity.
  • Weigh and record all children in kilograms only (never pounds); use a length-based method when a child cannot be weighed.
  • Maintain pediatric-specific equipment, supplies, and weight-based dosing tools to cut medication errors.
  • Run a continuous pediatric quality-improvement and patient-safety process.
  • Screen for mental and behavioral health needs and have pathways for pediatric psychiatric emergencies.
  • Keep written interfacility transfer agreements and disaster plans that specifically address children.
  • Ensure staff competencies across the pediatric age range and use the national Pediatric Readiness assessment to measure and improve.

At the bedside

  • Confirm the weight is in kg before ordering any weight-based drug or fluid.
  • Know who your department's PECC is and where the pediatric resuscitation cart and dosing reference live.
  • Use a length-based tape or app for doses and equipment sizes in an unweighable child.
  • Screen at-risk pediatric patients for suicide / behavioral health and know your transfer pathway.
Bottom line / exam pearl

A high pediatric readiness score is one of the few ED-level factors independently linked to lower child mortality -- kilograms, coordinators, and QI are the backbone.

References

▸Premedication for Laryngoscopy in the Newborn InfantPaediatricsCanadian Paediatric Society (CPS) position statement, Paediatrics & Child Health · 2026
Clinical takeaway

For all non-emergent neonatal intubations, give premedication with a vagolytic, a fast-acting opioid, and a short-acting muscle relaxant - it reduces adverse physiologic effects and improves intubation success.

Background — why it changed

Laryngoscopy and intubation are common in the NICU and are associated with bradycardia, hypoxemia, raised intracranial pressure, and pain. Evidence shows premedication blunts these effects and increases first-attempt success, so the CPS recommends it as standard for non-emergent intubations. The statement also addresses less invasive surfactant administration (LISA/MIST), where non-pharmacological measures are prioritized.

Key recommendations

  • In all non-emergent intubations, provide premedication combining a vagolytic, a fast-acting opioid, and a short-acting muscle relaxant.
  • Suggested vagolytic: atropine 0.01-0.02 mg/kg, given before the muscle relaxant to prevent bradycardia.
  • Suggested opioid: fentanyl 2 mcg/kg, given slowly over 2-5 minutes to avoid chest-wall rigidity.
  • Suggested muscle relaxant: succinylcholine 2 mg/kg (rapid onset ~1 min, short duration); avoid in hyperkalemia or family history of malignant hyperthermia.
  • Rocuronium (about 0.5-1 mg/kg) is an alternative relaxant but has a longer, more variable duration, making it less ideal than succinylcholine.
  • For less invasive surfactant administration, prioritize non-pharmacological measures rather than routine deep sedation/paralysis.
  • Laryngoscopy should always be performed or supervised by a skilled provider with continuous cardiorespiratory monitoring.

At the bedside

  • Reserve unpremedicated intubation for true emergencies (e.g. delivery-room resuscitation) where there is no time.
  • Draw up and give atropine first, then the opioid, then the relaxant; push fentanyl slowly to prevent chest-wall rigidity.
  • Screen for hyperkalemia and malignant-hyperthermia history before choosing succinylcholine; use rocuronium if contraindicated.
  • Keep continuous SpO2 and heart-rate monitoring, and ensure a skilled operator or supervisor is present for every attempt.
Bottom line / exam pearl

Non-emergent neonatal intubation should be premedicated with a vagolytic (atropine), a fast opioid (fentanyl, pushed slowly), and a short-acting relaxant (succinylcholine) under continuous monitoring.

References

  • CPS position statement: Premedication for laryngoscopy in the newborn infant. cps.ca
  • Paediatrics & Child Health article (doi:10.1093/pch/pxag041). doi.org
▸Care of Pediatric and Neonatal ICU Patients at the End of LifePaediatricsSociety of Critical Care Medicine (SCCM), Pediatric Critical Care Medicine · 2026
Clinical takeaway

End-of-life care across PICU, cardiac ICU and NICU rests on proactive advance care planning, early palliative care involvement, systematic symptom management, structured bereavement support and explicit attention to health equity.

Background — why it changed

End-of-life care for critically ill children and neonates has been highly variable and under-guided. This SCCM guideline used a GRADE evidence-to-decision framework and a systematic review of literature from 2000-2025 to define principles of practice for most children and families navigating end of life in an ICU. It yielded five conditional recommendations and one good practice statement spanning PICU, CICU and NICU settings.

Key recommendations

  • Support advance care planning with children (as appropriate) and families facing end of life in the ICU.
  • Involve pediatric palliative care through consultation, and invest in palliative care education for ICU teams.
  • Use systematic, protocolised symptom assessment and management rather than ad hoc treatment.
  • Provide structured bereavement support for families.
  • Explicitly address health equity in access to and delivery of end-of-life care.
  • Recommendations apply across PICU, cardiac ICU and neonatal ICU settings.
  • The panel issued five conditional recommendations plus one good practice statement, reflecting generally low-certainty evidence.

At the bedside

  • Bring palliative care in early and proactively, not only in the final hours.
  • Use a systematic symptom-assessment approach so pain and distress are not managed reactively.
  • Build bereavement follow-up for families into the care plan from the outset.
  • Actively watch for and address equity gaps in communication and access.
Bottom line / exam pearl

Proactive advance care planning, early palliative care, systematic symptom control, bereavement support and equity are the pillars of pediatric and neonatal ICU end-of-life care.

References

▸Therapeutic Hypothermia for Neonatal Hypoxic-Ischemic EncephalopathyPaediatricsAmerican Academy of Pediatrics (Committee on Fetus and Newborn; Section on Neurology) - Clinical Report, Pediatrics · 2026
Clinical takeaway

In infants >=36 0/7 weeks with moderate-to-severe HIE, cooling to 33.5-34.5 C started within 6 hours of birth and continued for 72 hours reduces death or moderate-to-severe neurodevelopmental impairment. It is not recommended for mild HIE or preterm infants outside research.

Background — why it changed

This 2026 clinical report updates prior AAP guidance (2014) on therapeutic hypothermia for neonatal HIE. It reaffirms cooling as standard care for moderate-to-severe HIE at term while clarifying persistent uncertainties: whether to treat mild HIE, near-term infants (35 weeks), and infants presenting after the 6-hour window. It also reviews adjunctive therapies and concludes high-dose erythropoietin is not an effective add-on.

Key recommendations

  • Offer therapeutic hypothermia to infants born at >=36 0/7 weeks with moderate-to-severe HIE; target core temperature 33.5-34.5 C.
  • Initiate within 6 hours of birth and continue for 72 hours, then rewarm slowly; earlier initiation maximises benefit.
  • When cooling cannot begin within 6 hours, there is a small benefit to starting later, up to about 24 hours, though evidence is weaker.
  • Therapeutic hypothermia for mild HIE is not recommended outside a research study.
  • Cooling is not recommended for preterm infants <36 weeks; at 35 weeks it may be considered case-by-case with shared decision-making given uncertain benefit/harm.
  • High-dose erythropoietin should not be used as an adjunct to cooling in moderate/severe HIE (no reduction in death or disability).
  • Cooling requires a program with neuromonitoring, neuroimaging, and structured neurodevelopmental follow-up; delivering centres need protocols for prompt recognition and initiation or transfer.

At the bedside

  • Screen every depressed term newborn early: identify moderate-to-severe HIE and start passive cooling and transfer immediately so active cooling begins within the 6-hour window.
  • Do not overshoot - avoid dropping below 33.5 C; monitor for cooling-associated effects (bradycardia, thrombocytopenia, coagulopathy, subcutaneous fat necrosis).
  • Any delivery setting should have a written action plan to recognise possible HIE and either initiate cooling or arrange rapid transfer to a cooling centre.
  • Counsel families that cooling reduces but does not eliminate risk of death or impairment, and that follow-up neurodevelopmental assessment is part of care.
Bottom line / exam pearl

Cool term/near-term babies (>=36 weeks) with moderate-to-severe HIE to 33.5-34.5 C within 6 hours for 72 hours - not for mild HIE, preterm infants, or as a reason to add erythropoietin.

References

▸ESAIC and ESPA Guidelines on Neuromuscular Block in Anaesthetised ChildrenPaediatricsEuropean Society of Anaesthesiology and Intensive Care (ESAIC) and European Society for Paediatric Anaesthesiology (ESPA) - joint guideline, European Journal of Anaesthesiology · 2025
Clinical takeaway

The first paediatric-specific NMB guideline calls for quantitative neuromuscular monitoring whenever any NMBA is given, confirming a train-of-four (TOF) ratio >=0.9 before extubation, and favours rocuronium/vecuronium reversed with sugammadex over neostigmine.

Background — why it changed

Until 2025-2026 no dedicated guideline addressed neuromuscular blockade in anaesthetised children, so practice was extrapolated from adults. This ESAIC/ESPA joint task force (approved 2024, published in the EJA) provides the first structured, child-specific recommendations on indications, monitoring, and reversal, emphasising objective monitoring and safe reversal to reduce residual paralysis.

Key recommendations

  • Use quantitative neuromuscular monitoring (objective, e.g. EMG-based TOF) whenever an NMBA is administered to titrate dosing and exclude residual block.
  • Confirm a TOF ratio >=0.9 plus return of upper-airway reflexes before extubation.
  • When an NMBA is needed, prefer an aminosteroid agent (rocuronium or vecuronium) so it can be antagonised with sugammadex.
  • Give a strong recommendation for sugammadex over neostigmine for reversal of aminosteroid block (faster, more reliable recovery at moderate and deep block).
  • Dose sugammadex using the same weight-based dosing as adults (e.g. ~2 mg/kg at reappearance of the second twitch, ~4 mg/kg for deep block); note it remains off-label in children <2 years.
  • Sugammadex does not remove the need for monitoring - it requires it; monitoring guides both dosing and confirmation of full reversal.
  • Avoid succinylcholine in known or suspected neuromuscular disease (rhabdomyolysis/malignant hyperthermia risk); a non-depolarising agent is preferred, including for rapid-sequence induction.

At the bedside

  • Set up objective TOF monitoring before the first NMBA dose - not just a peripheral nerve stimulator - and document a TOF ratio >=0.9 before you pull the tube.
  • Default to rocuronium plus sugammadex; keep sugammadex readily available for both routine and emergency (deep-block) reversal.
  • Weight-based sugammadex dosing mirrors adults, but flag that use under 2 years is off-label - confirm local policy.
  • In a child with (or suspected of) neuromuscular disease, plan a non-depolarising RSI rather than succinylcholine.
Bottom line / exam pearl

Monitor objectively for every paralysed child, confirm TOF >=0.9 before extubation, and reverse rocuronium/vecuronium with sugammadex rather than neostigmine.

References

Ophthalmology2 guidelines

▸Role of Corticosteroids in the Management of Orbital CellulitisOphthalmologyAmerican Academy of Ophthalmology (AAO) Ophthalmic Technology Assessment; published in Ophthalmology · 2026
Clinical takeaway

Adjunctive systemic corticosteroids appear safe in orbital cellulitis when given with appropriate antibiotics and may speed symptom resolution, but their effect on length of hospital stay remains unclear.

Background — why it changed

This Ophthalmic Technology Assessment was prepared by the AAO Oculofacial and Orbital Surgery Panel and approved by the AAO Board of Trustees on 21 February 2026, based on a PubMed literature search (August 2025). Nine studies met inclusion criteria (one level I, four level II, four level III), reflecting limited and heterogeneous evidence. It was published amid ongoing debate, including a 2026 pediatric meta-analysis that raised concerns about corticosteroid-associated adverse outcomes.

Key recommendations

  • Corticosteroids may be safe in the setting of orbital cellulitis when used alongside appropriate systemic antibiotics.
  • Adjunctive systemic corticosteroids may improve the rate of symptom/inflammation resolution.
  • The impact on duration of hospitalization remains unclear from available evidence.
  • The evidence base is limited and heterogeneous (nine studies, low-to-moderate certainty), precluding a strong, uniform recommendation.
  • Where used, corticosteroids are an adjunct to - not a replacement for - antibiotics, and are generally started after antibiotic therapy has been initiated.
  • A separate 2026 pediatric meta-analysis found corticosteroid use was not associated with reduced length of stay and was associated with higher risks of surgery, PICU admission, and 30-day readmission, underscoring caution in children.

At the bedside

  • Orbital cellulitis is first and foremost a surgical/infectious emergency: start IV antibiotics promptly and obtain imaging (CT with contrast) to assess for subperiosteal or orbital abscess.
  • Do not start steroids before adequate antibiotic cover is on board; treat the infection first.
  • Watch for red flags of orbital (vs preseptal) involvement - proptosis, painful/restricted eye movements, diplopia, and reduced vision or an RAPD - which mandate urgent ophthalmology and possibly surgical drainage.
  • The decision to add steroids should be individualised and made with ophthalmology/ENT input, weighing possible faster inflammation control against uncertain and possibly worse outcomes, especially in children.
Bottom line / exam pearl

In orbital cellulitis, antibiotics (and drainage when indicated) come first; adjunctive systemic steroids appear safe and may hasten inflammation resolution, but the benefit is uncertain and pediatric data urge caution.

References

▸Primary Angle-Closure Disease Preferred Practice PatternOphthalmologyAmerican Academy of Ophthalmology (AAO) Preferred Practice Pattern, Glaucoma Panel; published in Ophthalmology · 2025
Clinical takeaway

In acute angle-closure crisis, lower the IOP promptly with medical therapy, then perform laser peripheral iridotomy (LPI); treat the fellow phakic eye prophylactically, and consider lens extraction for angle-closure with markedly elevated IOP or glaucoma.

Background — why it changed

The Primary Angle-Closure Disease PPP defines the spectrum from primary angle-closure suspect (PACS) through primary angle closure (PAC) to primary angle-closure glaucoma (PACG), and covers acute angle-closure crisis (AACC). This most recent 2025 update in Ophthalmology follows the January 2021 edition and incorporates evidence such as the EAGLE trial (favoring clear lens extraction in some PACG/PAC eyes) and trials refining who benefits from prophylactic LPI. Dark-room dynamic gonioscopy remains the reference standard for diagnosis, supported by anterior-segment imaging.

Key recommendations

  • Diagnose angle-closure with dark-room dynamic gonioscopy; anterior-segment OCT and ultrasound biomicroscopy can complement gonioscopy and help confirm improvement after treatment.
  • For acute angle-closure crisis, first lower IOP promptly with medical therapy (and interventions such as anterior chamber paracentesis or laser iridoplasty as needed), then proceed to LPI once the cornea clears.
  • After an acute attack, the fellow phakic eye should generally undergo prompt prophylactic LPI because of its high risk of a subsequent attack.
  • Lens extraction is an effective treatment for PACG and for PAC with markedly elevated IOP (consistent with the EAGLE trial), and may be offered as a primary intervention in appropriate patients.
  • LPI is the standard initial treatment to relieve pupillary block across the angle-closure spectrum; the benefit of prophylactic LPI in PACS is more modest, so treatment should be individualised.
  • Long-term follow-up is required to monitor for progressive peripheral anterior synechiae, rising IOP, and glaucomatous optic neuropathy.
  • Distinguish PACS/PAC/PACG by the presence of PAS/elevated IOP and glaucomatous optic neuropathy, and manage IOP and neuropathy as in other glaucomas when present.

At the bedside

  • Acute angle closure = red painful eye with a fixed mid-dilated pupil, hazy cornea, high IOP, headache/nausea/vomiting, and halos - treat as an emergency.
  • Start IOP-lowering immediately (topical agents plus systemic acetazolamide, and consider a hyperosmotic such as IV/oral glycerol or mannitol), then add topical pilocarpine once IOP begins to fall and the iris sphincter can respond.
  • Do not forget the other eye: it is at high risk and usually needs prophylactic LPI.
  • Definitive relief of pupillary block requires LPI (or lens extraction) - medication alone is temporising until the laser/surgery can be done.
Bottom line / exam pearl

Acute angle-closure is an ophthalmic emergency: break the attack medically, then secure the angle with laser peripheral iridotomy (or lens extraction), and don't forget prophylactic LPI in the fellow eye.

References

  • Primary Angle-Closure Disease Preferred Practice Pattern (Ophthalmology, full text). www.aaojournal.org
  • Primary Angle-Closure Disease PPP (AAO education page). www.aao.org

Psychiatry & Behavioural1 guideline

▸Suicide and Suicide Risk in AdolescentsPsychiatryAmerican Academy of Pediatrics (Pediatrics), clinical report · 2024
Clinical takeaway

Universally screen youth 12 and older for suicide risk with a validated tool; those who screen positive get a structured brief suicide safety assessment, a safety plan, and lethal-means counseling.

Background — why it changed

Suicide is a leading cause of adolescent death, and this 2024 AAP clinical report reframes screening as universal rather than symptom-triggered. It integrates lethal-means restriction (especially firearms), collaborative safety planning, and linkage to evidence-based treatment. Screening in preteens 8-11 is advised when clinically indicated.

Key recommendations

  • Universally screen adolescents 12+ at health encounters with a validated tool (e.g., ASQ or PHQ-9A); screen preteens 8-11 when clinically indicated.
  • Conduct the screen confidentially, without caregivers present.
  • A positive screen triggers a structured Brief Suicide Safety Assessment (e.g., ASQ-BSSA) or C-SSRS to stratify acuity -- this is not a full psychiatric evaluation.
  • Provide lethal-means counseling: assess access to firearms, medications, and other means and advise safe storage (firearms unloaded and locked, ammunition stored separately) or removal.
  • Collaboratively develop a safety plan with the youth and family.
  • Link to evidence-based treatment (CBT, DBT, family-based interventions) and ensure follow-up and care coordination.
  • No single screening tool is recommended over another -- use any validated instrument that fits the workflow.

At the bedside

  • Ask directly about suicide -- asking does not increase risk.
  • On any positive screen, screen for firearm access and counsel on safe storage or removal.
  • Step the caregiver out of the room so the confidential screen is honest.
  • Have a disposition and safety plan with follow-up in place before the patient leaves.
Bottom line / exam pearl

Screen everyone 12+, assess positives with a structured tool, and never skip lethal-means (firearm) counseling.

References

About this summary. These are independent educational summaries of major recent clinical guidelines and scientific statements, re-written and expanded in our own words for teaching and revision. They are a study aid, not a substitute for the full guideline documents or your local protocols. Guidelines from different bodies sometimes disagree (e.g. breast-screening age, BP targets) — always confirm thresholds, doses and indications against the primary source and your institution's policy before applying them to a patient.

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